Browse result page of ThPDB2
This is the result page of the browse module of ThPDB2. This page gives the information about the query submitted by the user as per the browse category. Further details of the entries can be seen by clicking on the ID or THPP_ID. Further the user can sort the entries on the basis of various fields by clicking on the respective headers. The user can also download the results in various formats.
Tabular representation:
| ID | THPP_ID | Therapeutic Name | Sequence | Molecular Weight | Chemical Formula | Isoelectric Point | Hydrophobicity | Melting Point | Half Life | Description | Disease/Indication | Pharmacodynamics | Mechanism of Action | Toxicity | Metabolism | Absorption | Volume of Distribution | Clearance | Categories | Patent Number | Date of Issue | Date of Expiry | Drug Interaction | Target | Brand Name | Company | Brand Description | Prescribed for | Chemical Name | Formulation | Physical Appearance | Route of Administation | Recommended Dosage | Contraindication | Side Effects | Useful Links 1 | Useful Links 2 | Remarks |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 10005 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | CA1340417 | 2-Mar-1999 | 2-Mar-2016 | Thalomid (thalidomide) | Epidermal growth factor receptor,Low affinity immunoglobulin gamma Fc region receptor III-B,Complement C1r subcomponent,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immunoglobulin gamma Fc region receptor III-A,Complement C1s subcomponent,High affinity immunoglobulin gamma Fc receptor I,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c | Erbitux | ImClone Systems Inc | ImClone Systems Inc | Used for treatment of metastatic colorectal cancer (cancer spread beyond the colon or rectum) that over-expresses the epidermal growth factor receptor (EGFR). Aapproved for the treatment of squamous cell carcinoma of the head and neck. | NA | Formulated in a solution with no preservatives, which contains 8.48 mg/mL sodium chloride, 1.88 mg/mL sodium phosphate dibasic heptahydrate, 0.41 mg/mL sodium phosphate monobasic monohydrate, and Water for Injection, USP. | Sterile, clear, colorless liquid of pH 7.0-7.4, which may contain a small amount of easily visible, white, amorphous cetuximab particulates | Intravenous infusion | Generally given once every week for 6 to 7 weeks. And supplied at a concentration of 2 mg/mL in either 100 mg (50 mL) or 200 mg (100 mL), single-use vials. | allergic | Rash (Acne like), Generalized weakness, malaise, Fever, Low magnesium level are commom (occurring in greater than 30%) for patients taking Erbitux. And less coomon side effects (occurring in about 10-29%) of patients receiving Erbitux are; Nausea and vomitting. | Link | NA | NA |
| 10006 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Aciphex (rabeprazole) | NA | NA | Cardinal Health | Cardinal Health | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10007 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Aciphex Sprinkle (rabeprazole) | NA | NA | Catalent Pharma Solutions | Catalent Pharma Solutions | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10008 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Adrucil (fluorouracil) | NA | NA | Oso Biopharmaceuticals Manufacturing LLC | Oso Biopharmaceuticals Manufacturing LLC | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10009 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | amoxicillin | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10010 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | clarithromycin | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10011 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | lansoprazole | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10012 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Omeprazole | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10013 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Capecitabine | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10014 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Carboplatin | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10015 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Carboplatin Novaplus (carboplatin) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10016 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | cisplatin Dexilant (dexlansoprazole) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10017 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Dexlansoprazole | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10018 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Eloxatin (oxaliplatin) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10019 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Esomeprazole | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10020 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Naproxen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10021 | Th1002 | Cetuximab | >Th1002_Cetuximab QVQLKQSGPGLVQPSQSLSITCTVSGFSLTNYGVHWVRQSPGKGLEWLGVIWSGGNTDYNTPFTSRLSINKDNSKSQVFFKMNSLQSNDTAIYYCARALTYYDYEFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145781.6 | C6484H10042N1732O2023S36 | 8.48 | -0.413 | 71 | 112 hours | It is an epidermal growth factor receptor which binds to FAB region. Cetuximab consists of the variable antigen-binding regions of the 225 murine EGFr monoclonal antibody that is specific for N-terminal part of human EGFr with human IgG1 heavy chain and kappa light chain constant regions. | Used to treat EGFR-expressing metastatic colorectal cancer in patients resistant to irinotecan based chemotherapy regimens. Also used to treat squamous cell carcinoma of the head and neck in combination with radiation therapy. | Cetuximab specifically binds to the epidermal growth factor receptors (EGFr, HER1, c-ErbB-1) on both normal and tumor cells(EGFr is over-expressed in many colorectal cancers). Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. | Cetuximab binds to EGFr (over-expressed in many colorectal cancers) on both normal and tumor cells. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread. | Single doses of cetuximab more than 500 mg/m2 have'nt been tested. There is no report of overdosage in human clinical trials. | Like other monoclonal antibodies, cetuximab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target‐mediated disposition pathway. | After administration of a 400 mg/m2 initial dose followed by a 250 mg/m2 weekly dose, the steady-state levels of cetuximab was reached by the third weekly infusion with mean peak and trough concentrations across studies ranging from 168 µg/mL to 235 µg/mL and 41 µg/mL to 85 µg/mL, respectively.11 Tmax is about 3 hours. | 2-3 L/m2(Independent of dose) | 0.103 L/h( In patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck) | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Epidermal Growth Factor Receptor Antagonist, Globulins, HER1 Antagonists, Immunoglobulins, Immunoproteins, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Fluorouracil | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10038 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty. | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | Gonadotropin-releasing hormone receptor | Eligard | Atrix Labs/QLT In | Atrix Labs/QLT In | Eligard is used to treat the symptoms of prostate cancer in men. | 5-oxo-L-prolyl-L-histidyl-L-tryptophyl-L-seryl-L-tyrosyl-D-leucyl-L-arginyl-N-ethyl-L-prolinamide acetate | ELIGARD is prefilled and supplied in two separate, sterile syringes whose contents are mixed immediately prior to administration. The two syringes are joined and the single dose product is mixed until it is homogenous. One syringe contains the ATRIGEL De | Suspension | Subcutaneous Injection | 7.5mg-1 injection/month, 22.5mg-1 injection per 3 month, 30mg-1 injection per 4 month, 45 mg- 1 injection every 6 month. | Hypersensitivity and pregnancy | Rare pain or unusual sensations in your back; numbness, weakness, or tingly feeling in your legs or feet; muscle weakness or loss of use; loss of bowel or bladder control; or liver problems - nausea, upper stomach pain, itching, tired feeling, loss of apetite. | Link | NA | NA |
| 10039 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Enantone | Takeda | Takeda | NA | NA | NA | Solution | Injection | One3.75 mg DPS mnthly or one 11.25 mg DPS every 3 month as a single SC/IM injection. | Hypersensitivity, undiagnosed abnormal vag bleeding, pregnancy, lactation | Weightloss, Parosmia (distortion of the sense of smell, as in smelling odours that are not present), Nausea (feeling of having an urge to vomit), Musculoskeletal Stiffness (stiffness of the body's muscles, joints, tendons, ligaments and nerves), Mood Swinng. | Link | NA | NA |
| 10040 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Leuplin | Cardinal Health | Cardinal Health | NA | NA | NA | NA | Injection | NA | NA | NA | Link | NA | NA |
| 10041 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | LeuProMaxx | Baxter/Teva | Baxter/Teva | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10042 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Leupromer | Oso Biopharmaceuticals Manufacturing LLC | Oso Biopharmaceuticals Manufacturing LLC | NA | NA | NA | NA | Injection | NA | NA | NA | Link | NA | NA |
| 10043 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Lupron | Abbott/TAP Pharmaceuticals | Abbott/TAP Pharmaceuticals | NA | NA | NA | NA | Injection | 7.5 mg for 1-month, 22.5 mg for 3-month, 30 mg for 4-month, and 45 mg for 6-month administration are prescribed for the palliative treatment of advanced prostate cancer, 3.75 mg for 1-month and 11.25 mg for 3-month administration are used for the manageme. | Allergic, pregnancy, lactation | NA | Link | NA | NA |
| 10044 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Lutrate | Hospira Inc. | Hospira Inc. | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10045 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Memryte | Curaxis | Curaxis | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10046 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Prostap 3 | Sanofi-Aventis Inc. , Sun Pharmaceutical Industries Ltd. , Takeda Pharmaceutical Co. Ltd. , Teva Pharmaceutical Industries Ltd. , Tolmar Inc. | Sanofi-Aventis Inc. , Sun Pharmaceutical Industries Ltd. , Takeda Pharmaceutical Co. Ltd. , Teva Pharmaceutical Industries Ltd. , Tolmar Inc. | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10047 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Prostap SR, Camcevi, Fensolvi, Lupaneta Pack 1-month, Lupron, Lupron Depot-ped, Zeulide Depot | Takeda UK Limited, Eon Labs, Physicians Total Care Inc. | Takeda UK Limited, Eon Labs, Physicians Total Care Inc. | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10048 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Viadur | Bayer AG | Bayer AG | NA | 5-Oxo-L-prolyl-L-histidyl-L-tryptophyl-L-seryl-L-tyrosyl-D-leucyl-Lleucyl-L-arginyl-N-ethyl-L-prolinamide acetate | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10117 | Th1016 | Pegfilgrastim | >Th1016_Pegfilgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 39000 | C845H1343N223O243S9 | 5.65 | 0.209 | 60 | 15-80 hours | PEGylated(at N terminus) form of human G-CSF (Granulocyte colony stimulating factor), 175 residues, produced from E. coli via bacterial fermentation. | Increases leukocyte production, for treatment in non-myeloid cancer, neutropenia and bone marrow transplant | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Pegfilgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment and end cell functional activation. Pegfilgrastim has reduced renal clearance and prolonged persistence in vivo as compared to Filgrastim. | Pegfilgrastim binds to the G-CSF receptor. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Pegfilgrastim also stimulates the release of neutrophils from bone marrowstorage pools and reduces their maturation time. Pegfilgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, pegfilgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | Overdosage of pegfilgrastim may result in leukocytosis and bone pain. Events of edema, dyspnea, and pleural effusion have been reported in a single patient who self-administered pegfilgrastim on 8 consecutive days in error. | It is not know whether pegfilgrastim is metabolized into major metabolites.13 Once it binds to the therapeutic target, pegfilgrastim is internalized by the neutrophil and undergoes nonspecific degradation | lower absolute bioavailability | approximately 170L | 14 mL/h/kg | Adjuvants, Immunologic, Alcohols, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Carbohydrates, Colony-Stimulating Factors, Compounds used in a research, industrial, or household setting, Cytokines, Ethylene Glycols, Glycoconjugates, Glycols, Glycoproteins, Granulocyte Colony-Stimulating Factors, Hematinics, Hematopoietic Cell Growth Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Macromolecular Substances, Pegylated agents, Peptides, Polymers, Proteins | CA1341537 | 31-Jul-2007 | 31-Jul-2024 | NA | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Neulasta | Amgen Inc. | Amgen Inc. | Neulasta is used to prevent neutropenia(lack of certain white blood cells caused by receiving chemotherapy). | NA | Supplied in 0.6 mL prefilled syringes. Each syringe contains 6 mg pegfilgrastim (based on protein weight) in a sterile, clear, colorless, preservative-free solution (pH 4.0) containing acetate (0.35 mg), polysorbate 20 (0.02 mg), sodium (0.02 mg), and sor | Solution | Subcutaneous Injection | Single subcutaneous injection of 6 mg administered once per chemotherapy cycle in adults. Do not administer Neulasta between 14 days before and 24 hours after administration of cytotoxic chemotherapy. | Allergy, or having sickle cell disorder; chronic myeloid leukemia; myelodysplasia (also called preleukemia); or if you are allergic to latex. | Bone pain; pain in your arms or legs; or bruising, swelling, pain, redness, or a hard lump where the injection was given. | Link | NA | NA |
| 10118 | Th1016 | Pegfilgrastim | >Th1016_Pegfilgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 39000 | C845H1343N223O243S9 | 5.65 | 0.209 | 60 | 15-80 hours | PEGylated(at N terminus) form of human G-CSF (Granulocyte colony stimulating factor), 175 residues, produced from E. coli via bacterial fermentation. | Increases leukocyte production, for treatment in non-myeloid cancer, neutropenia and bone marrow transplant | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Pegfilgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment and end cell functional activation. Pegfilgrastim has reduced renal clearance and prolonged persistence in vivo as compared to Filgrastim. | Pegfilgrastim binds to the G-CSF receptor. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Pegfilgrastim also stimulates the release of neutrophils from bone marrowstorage pools and reduces their maturation time. Pegfilgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, pegfilgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | Overdosage of pegfilgrastim may result in leukocytosis and bone pain. Events of edema, dyspnea, and pleural effusion have been reported in a single patient who self-administered pegfilgrastim on 8 consecutive days in error. | It is not know whether pegfilgrastim is metabolized into major metabolites.13 Once it binds to the therapeutic target, pegfilgrastim is internalized by the neutrophil and undergoes nonspecific degradation | lower absolute bioavailability | approximately 170L | 14 mL/h/kg | Adjuvants, Immunologic, Alcohols, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Carbohydrates, Colony-Stimulating Factors, Compounds used in a research, industrial, or household setting, Cytokines, Ethylene Glycols, Glycoconjugates, Glycols, Glycoproteins, Granulocyte Colony-Stimulating Factors, Hematinics, Hematopoietic Cell Growth Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Macromolecular Substances, Pegylated agents, Peptides, Polymers, Proteins | CA1339071 | 29-Jul-1997 | 29-Jul-2014 | NA | NA | Cegfila | Mundipharma Corporation (Ireland) Limited | Mundipharma Corporation (Ireland) Limited | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10119 | Th1016 | Pegfilgrastim | >Th1016_Pegfilgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 39000 | C845H1343N223O243S9 | 5.65 | 0.209 | 60 | 15-80 hours | PEGylated(at N terminus) form of human G-CSF (Granulocyte colony stimulating factor), 175 residues, produced from E. coli via bacterial fermentation. | Increases leukocyte production, for treatment in non-myeloid cancer, neutropenia and bone marrow transplant | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Pegfilgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment and end cell functional activation. Pegfilgrastim has reduced renal clearance and prolonged persistence in vivo as compared to Filgrastim. | Pegfilgrastim binds to the G-CSF receptor. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Pegfilgrastim also stimulates the release of neutrophils from bone marrowstorage pools and reduces their maturation time. Pegfilgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, pegfilgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | Overdosage of pegfilgrastim may result in leukocytosis and bone pain. Events of edema, dyspnea, and pleural effusion have been reported in a single patient who self-administered pegfilgrastim on 8 consecutive days in error. | It is not know whether pegfilgrastim is metabolized into major metabolites.13 Once it binds to the therapeutic target, pegfilgrastim is internalized by the neutrophil and undergoes nonspecific degradation | lower absolute bioavailability | approximately 170L | 14 mL/h/kg | Adjuvants, Immunologic, Alcohols, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Carbohydrates, Colony-Stimulating Factors, Compounds used in a research, industrial, or household setting, Cytokines, Ethylene Glycols, Glycoconjugates, Glycols, Glycoproteins, Granulocyte Colony-Stimulating Factors, Hematinics, Hematopoietic Cell Growth Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Macromolecular Substances, Pegylated agents, Peptides, Polymers, Proteins | NA | NA | NA | NA | NA | Fulphila | Mylan S.A.S, Viatris Limited | Mylan S.A.S, Viatris Limited | decrease the incidence of infection, as manifested by febrile neutropenia, in patients with non-myeloid malignancies receiving myelosuppressive anti-cancer drugs associated with a clinically significant incidence of febrile neutropenia | NA | Fulphila (pegfilgrastim-jmdb) injection is intended for subcutaneous use only and is supplied in a single-dose prefilled syringe with a 29 gauge needle, with UltraSafe Passive Plus ™ Needle Guard. The prefilled syringe does not bear graduation marks and is designed to deliver the entire contents of the syringe (6 mg/0.6 mL). | clear, colorless solution | Fulphila is administered subcutaneously via a single-dose prefilled syringe for manual use. | The recommended dosage of Fulphila is a single subcutaneous injection of 6 mg administered once per chemotherapy cycle. For dosing in pediatric patients weighing less than 45 kg, refer to Table 1. Do not administer Fulphila between 14 days before and 24 hours after administration of cytotoxic chemotherapy. | Fulphila is contraindicated in patients with a history of serious allergic reactions to pegfilgrastim products or filgrastim products. Reactions have included anaphylaxis | Splenic Rupture Acute Respiratory Distress Syndrome Serious Allergic Reactions Use in Patients with Sickle Cell Disorders Glomerulonephritis Leukocytosis Thrombocytopenia Capillary Leak Syndrome Potential for Tumor Growth Stimulatory Effects on Malignant Cells Myelodysplastic syndrome Acute myeloid leukemia Aortitis | Link | NA | NA |
| 10120 | Th1017 | Sargramostim | >Th1017_Sargramostim APARSPSPSTQPWEHVNAIQEALRLLNLSRDTAAEMNETVEVISEMFDLQEPTCLQTRLELYKQGLRGSLTKLKGPLTMMASHYKQHCPPTPETSCATQIITFESFKENLKDFLLVIPFDCWEPVQE | 14434.5 | C639H1006N168O196S8 | 5.05 | NA | NA | NA | Sargramostim (127 residue glycoprotein) is a human recombinant granulocyte macrophage colony-stimulating factor expressed in yeast system. Substitution of Leu23 leads to a difference from native protein. | Used to treat cancer and in bone marrow transplant | Sargramostim is used in the treatment of bone marrow transplant recipients or those exposed to chemotherapy and recovering from acute myelogenous leukemia, Leukine or GM-CSF is a hematopoietic growth factor which stimulates the survival, clonal expansion (proliferation) and differentiation of hematopoietic progenitor cells. GM-CSF is also capable of activating mature granulocytes and macrophages. After a bone marrow transplant or chemotherapy, patients have a reduced capacity to produce red and white blood cells. Supplementing them with external sources of GM-CSF helps bring the level of neutrophils back to normal so that they can better fight infections. | Sargramostim binds to the Granulocyte-macrophage colony stimulating factor receptor which stimulates a JAK2 STAT1/STAT3 signal transduction pathway which leads to the production of hemopoietic cells and neutrophils | NA | NA | NA | NA | 420 mL/min/m2 [Normal people with liquid LEUKINE (IV)] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Colony-Stimulating Factors, Cytokines, Glycoproteins, Granulocyte-Macrophage Colony-Stimulating Factor, Hematopoietic Cell Growth Factors, Immunologic Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Peptides, Proteins | CA1341150 | 5-Dec-2000 | 5-Dec-2017 | NA | Granulocyte-macrophage colony-stimulating factor receptor subunit alpha,Interleukin-3 receptor subunit alpha,Cytokine receptor common subunit beta,Syndecan-2,Bone marrow proteoglycan | Leucomax | Novartis | Novartis | Used for reducing severe, life-threatening, or fatal infections after chemotherapy for acute myelogenous leukemia. It is also used to help increase the success of autologous bone marrow transplant and to help increase survival in patients who have bone ma | NA | NA | Solution | Subcutaneous and Intravenous infusion | In case of Intravenous Chemotherapy-induced neutropenia in adultS, 250 mcg/m2 daily for up to 42 days as required, to be given as IV infusion over 4 hr and in case of Intravenous Treatment and prevention of neutropenia in patients receiving myelosuppressivec chemotherapy. | NA | It is common to have aching bones and joints for 2-3 days starting 1-2 days after the start of the injections. This is usually mild and is caused by the bone marrow working harder to make white cells. Occasionally it is more troublesome and pain killers are required. | Link | NA | NA |
| 10121 | Th1017 | Sargramostim | >Th1017_Sargramostim APARSPSPSTQPWEHVNAIQEALRLLNLSRDTAAEMNETVEVISEMFDLQEPTCLQTRLELYKQGLRGSLTKLKGPLTMMASHYKQHCPPTPETSCATQIITFESFKENLKDFLLVIPFDCWEPVQE | 14434.5 | C639H1006N168O196S8 | 5.05 | NA | NA | NA | Sargramostim (127 residue glycoprotein) is a human recombinant granulocyte macrophage colony-stimulating factor expressed in yeast system. Substitution of Leu23 leads to a difference from native protein. | Used to treat cancer and in bone marrow transplant | Sargramostim is used in the treatment of bone marrow transplant recipients or those exposed to chemotherapy and recovering from acute myelogenous leukemia, Leukine or GM-CSF is a hematopoietic growth factor which stimulates the survival, clonal expansion (proliferation) and differentiation of hematopoietic progenitor cells. GM-CSF is also capable of activating mature granulocytes and macrophages. After a bone marrow transplant or chemotherapy, patients have a reduced capacity to produce red and white blood cells. Supplementing them with external sources of GM-CSF helps bring the level of neutrophils back to normal so that they can better fight infections. | Sargramostim binds to the Granulocyte-macrophage colony stimulating factor receptor which stimulates a JAK2 STAT1/STAT3 signal transduction pathway which leads to the production of hemopoietic cells and neutrophils | NA | NA | NA | NA | 431 mL/min/m2 [Normal people with lyophilized LEUKINE (IV)] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Colony-Stimulating Factors, Cytokines, Glycoproteins, Granulocyte-Macrophage Colony-Stimulating Factor, Hematopoietic Cell Growth Factors, Immunologic Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Peptides, Proteins | NA | NA | NA | NA | NA | Leukine | Berlex , Bayer , Genzyme Corporation , Partner Therapeutics, Inc , Sanofi Aventis , Bayer , Genzyme Corporation , Partner Therapeutics, Inc , Sanofi Aventis | Berlex , Bayer , Genzyme Corporation , Partner Therapeutics, Inc , Sanofi Aventis , Bayer , Genzyme Corporation , Partner Therapeutics, Inc , Sanofi Aventis | NA | NA | NA | NA | NA | NA | NA | Occasionally irritation at the injection site. | Link | NA | NA |
| 10122 | Th1017 | Sargramostim | >Th1017_Sargramostim APARSPSPSTQPWEHVNAIQEALRLLNLSRDTAAEMNETVEVISEMFDLQEPTCLQTRLELYKQGLRGSLTKLKGPLTMMASHYKQHCPPTPETSCATQIITFESFKENLKDFLLVIPFDCWEPVQE | 14434.5 | C639H1006N168O196S8 | 5.05 | NA | NA | NA | Sargramostim (127 residue glycoprotein) is a human recombinant granulocyte macrophage colony-stimulating factor expressed in yeast system. Substitution of Leu23 leads to a difference from native protein. | Used to treat cancer and in bone marrow transplant | Sargramostim is used in the treatment of bone marrow transplant recipients or those exposed to chemotherapy and recovering from acute myelogenous leukemia, Leukine or GM-CSF is a hematopoietic growth factor which stimulates the survival, clonal expansion (proliferation) and differentiation of hematopoietic progenitor cells. GM-CSF is also capable of activating mature granulocytes and macrophages. After a bone marrow transplant or chemotherapy, patients have a reduced capacity to produce red and white blood cells. Supplementing them with external sources of GM-CSF helps bring the level of neutrophils back to normal so that they can better fight infections. | Sargramostim binds to the Granulocyte-macrophage colony stimulating factor receptor which stimulates a JAK2 STAT1/STAT3 signal transduction pathway which leads to the production of hemopoietic cells and neutrophils | NA | NA | NA | NA | 549 mL/min/m2 [Normal people with liquid LEUKINE (SC)] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Colony-Stimulating Factors, Cytokines, Glycoproteins, Granulocyte-Macrophage Colony-Stimulating Factor, Hematopoietic Cell Growth Factors, Immunologic Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Peptides, Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Very rarely a disturbance in the liver function blood tests. | NA | NA | NA |
| 10123 | Th1017 | Sargramostim | >Th1017_Sargramostim APARSPSPSTQPWEHVNAIQEALRLLNLSRDTAAEMNETVEVISEMFDLQEPTCLQTRLELYKQGLRGSLTKLKGPLTMMASHYKQHCPPTPETSCATQIITFESFKENLKDFLLVIPFDCWEPVQE | 14434.5 | C639H1006N168O196S8 | 5.05 | NA | NA | NA | Sargramostim (127 residue glycoprotein) is a human recombinant granulocyte macrophage colony-stimulating factor expressed in yeast system. Substitution of Leu23 leads to a difference from native protein. | Used to treat cancer and in bone marrow transplant | Sargramostim is used in the treatment of bone marrow transplant recipients or those exposed to chemotherapy and recovering from acute myelogenous leukemia, Leukine or GM-CSF is a hematopoietic growth factor which stimulates the survival, clonal expansion (proliferation) and differentiation of hematopoietic progenitor cells. GM-CSF is also capable of activating mature granulocytes and macrophages. After a bone marrow transplant or chemotherapy, patients have a reduced capacity to produce red and white blood cells. Supplementing them with external sources of GM-CSF helps bring the level of neutrophils back to normal so that they can better fight infections. | Sargramostim binds to the Granulocyte-macrophage colony stimulating factor receptor which stimulates a JAK2 STAT1/STAT3 signal transduction pathway which leads to the production of hemopoietic cells and neutrophils | NA | NA | NA | NA | 529 mL/min/m2 [Normal people with lyophilized LEUKINE (SC)] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Colony-Stimulating Factors, Cytokines, Glycoproteins, Granulocyte-Macrophage Colony-Stimulating Factor, Hematopoietic Cell Growth Factors, Immunologic Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Peptides, Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Rare mild flu like symptom, headache, malaise, rigors & nausea. | NA | NA | NA |
| 10124 | Th1017 | Sargramostim | >Th1017_Sargramostim APARSPSPSTQPWEHVNAIQEALRLLNLSRDTAAEMNETVEVISEMFDLQEPTCLQTRLELYKQGLRGSLTKLKGPLTMMASHYKQHCPPTPETSCATQIITFESFKENLKDFLLVIPFDCWEPVQE | 14434.5 | C639H1006N168O196S8 | 5.05 | NA | NA | NA | Sargramostim (127 residue glycoprotein) is a human recombinant granulocyte macrophage colony-stimulating factor expressed in yeast system. Substitution of Leu23 leads to a difference from native protein. | Used to treat cancer and in bone marrow transplant | Sargramostim is used in the treatment of bone marrow transplant recipients or those exposed to chemotherapy and recovering from acute myelogenous leukemia, Leukine or GM-CSF is a hematopoietic growth factor which stimulates the survival, clonal expansion (proliferation) and differentiation of hematopoietic progenitor cells. GM-CSF is also capable of activating mature granulocytes and macrophages. After a bone marrow transplant or chemotherapy, patients have a reduced capacity to produce red and white blood cells. Supplementing them with external sources of GM-CSF helps bring the level of neutrophils back to normal so that they can better fight infections. | Sargramostim binds to the Granulocyte-macrophage colony stimulating factor receptor which stimulates a JAK2 STAT1/STAT3 signal transduction pathway which leads to the production of hemopoietic cells and neutrophils | NA | NA | NA | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Colony-Stimulating Factors, Cytokines, Glycoproteins, Granulocyte-Macrophage Colony-Stimulating Factor, Hematopoietic Cell Growth Factors, Immunologic Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Peptides, Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Rare mild itching and occasional skin rash. | NA | NA | NA |
| 10125 | Th1017 | Sargramostim | >Th1017_Sargramostim APARSPSPSTQPWEHVNAIQEALRLLNLSRDTAAEMNETVEVISEMFDLQEPTCLQTRLELYKQGLRGSLTKLKGPLTMMASHYKQHCPPTPETSCATQIITFESFKENLKDFLLVIPFDCWEPVQE | 14434.5 | C639H1006N168O196S8 | 5.05 | NA | NA | NA | Sargramostim (127 residue glycoprotein) is a human recombinant granulocyte macrophage colony-stimulating factor expressed in yeast system. Substitution of Leu23 leads to a difference from native protein. | Used to treat cancer and in bone marrow transplant | Sargramostim is used in the treatment of bone marrow transplant recipients or those exposed to chemotherapy and recovering from acute myelogenous leukemia, Leukine or GM-CSF is a hematopoietic growth factor which stimulates the survival, clonal expansion (proliferation) and differentiation of hematopoietic progenitor cells. GM-CSF is also capable of activating mature granulocytes and macrophages. After a bone marrow transplant or chemotherapy, patients have a reduced capacity to produce red and white blood cells. Supplementing them with external sources of GM-CSF helps bring the level of neutrophils back to normal so that they can better fight infections. | Sargramostim binds to the Granulocyte-macrophage colony stimulating factor receptor which stimulates a JAK2 STAT1/STAT3 signal transduction pathway which leads to the production of hemopoietic cells and neutrophils | NA | NA | NA | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Colony-Stimulating Factors, Cytokines, Glycoproteins, Granulocyte-Macrophage Colony-Stimulating Factor, Hematopoietic Cell Growth Factors, Immunologic Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Peptides, Proteins | NA | NA | NA | NA | NA | Leukine | Berlex Laboratories Inc | Berlex Laboratories Inc | Leukine is used to increase white blood cells and help prevent serious infection in conditions such as leukemia, bone marrow transplant, and pre-chemotherapy blood cell collection. Leukine is used for adults who are at least 55 years old. | NA | The liquid vial and reconstituted lyophilized vial both contain 40 mg/mL mannitol, USP; 10 mg/mL sucrose, NF; and 1.2 mg/mL tromethamine, USP, as excipients | Sterile, preserved (1.1% benzyl alcohol), injectable solution (500 mcg/mL) and also as sterile, white, preservative free lyophilized powder (250 mcg) that requires reconstitution with 1 mL Sterile water for Injection | Subcutaneous Injection (Subcutaneous) or Intraveno | In Neutrophil Recovery, Chemotherapy in Acute Myelogenous Leukemia, the recommended dose is 250 mcg/m2/day, administered intravenously over a 4 hour period starting approximately on day 11 or four days following the completion of induction chemotherapy, if the day 10 bone marrow is hypoplastic with <5% blasts. | Allergy | High fever, chills, sore throat, stuffy nose, flu symptoms; white patches or sores inside your mouth or on your lips; easy bruising, unusual bleeding (nose, mouth, vagina, or rectum), purple or red pinpoint spots under your skin; swelling, rapid weight gain, chest pain, fast or uneven heart rate, weakness or fainting, black-bloody or tarry stools, coughing up blood, painful urination, clay-colored stools, jaundice, breathing problems and problems with vision, speech, balance or memory. | Link | NA | NA |
| 10126 | Th1017 | Sargramostim | >Th1017_Sargramostim APARSPSPSTQPWEHVNAIQEALRLLNLSRDTAAEMNETVEVISEMFDLQEPTCLQTRLELYKQGLRGSLTKLKGPLTMMASHYKQHCPPTPETSCATQIITFESFKENLKDFLLVIPFDCWEPVQE | 14434.5 | C639H1006N168O196S8 | 5.05 | NA | NA | NA | Sargramostim (127 residue glycoprotein) is a human recombinant granulocyte macrophage colony-stimulating factor expressed in yeast system. Substitution of Leu23 leads to a difference from native protein. | Used to treat cancer and in bone marrow transplant | Sargramostim is used in the treatment of bone marrow transplant recipients or those exposed to chemotherapy and recovering from acute myelogenous leukemia, Leukine or GM-CSF is a hematopoietic growth factor which stimulates the survival, clonal expansion (proliferation) and differentiation of hematopoietic progenitor cells. GM-CSF is also capable of activating mature granulocytes and macrophages. After a bone marrow transplant or chemotherapy, patients have a reduced capacity to produce red and white blood cells. Supplementing them with external sources of GM-CSF helps bring the level of neutrophils back to normal so that they can better fight infections. | Sargramostim binds to the Granulocyte-macrophage colony stimulating factor receptor which stimulates a JAK2 STAT1/STAT3 signal transduction pathway which leads to the production of hemopoietic cells and neutrophils | NA | NA | NA | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Colony-Stimulating Factors, Cytokines, Glycoproteins, Granulocyte-Macrophage Colony-Stimulating Factor, Hematopoietic Cell Growth Factors, Immunologic Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Peptides, Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Mobilization of Peripheral Blood Progenitor Cells, the recommended dose is 250 mcg/m2/day administered IV over 24 hours or SC once daily. | NA | Black, bloody, or tarry stools; coughing up blood or vomit that looks like coffee grounds; painful or difficult urination; dark urine, clay-colored stools, jaundice (yellowing of the skin or eyes); breathing problems; or problems with vision, speech, balance or memory. | Link | NA | NA |
| 10127 | Th1017 | Sargramostim | >Th1017_Sargramostim APARSPSPSTQPWEHVNAIQEALRLLNLSRDTAAEMNETVEVISEMFDLQEPTCLQTRLELYKQGLRGSLTKLKGPLTMMASHYKQHCPPTPETSCATQIITFESFKENLKDFLLVIPFDCWEPVQE | 14434.5 | C639H1006N168O196S8 | 5.05 | NA | NA | NA | Sargramostim (127 residue glycoprotein) is a human recombinant granulocyte macrophage colony-stimulating factor expressed in yeast system. Substitution of Leu23 leads to a difference from native protein. | Used to treat cancer and in bone marrow transplant | Sargramostim is used in the treatment of bone marrow transplant recipients or those exposed to chemotherapy and recovering from acute myelogenous leukemia, Leukine or GM-CSF is a hematopoietic growth factor which stimulates the survival, clonal expansion (proliferation) and differentiation of hematopoietic progenitor cells. GM-CSF is also capable of activating mature granulocytes and macrophages. After a bone marrow transplant or chemotherapy, patients have a reduced capacity to produce red and white blood cells. Supplementing them with external sources of GM-CSF helps bring the level of neutrophils back to normal so that they can better fight infections. | Sargramostim binds to the Granulocyte-macrophage colony stimulating factor receptor which stimulates a JAK2 STAT1/STAT3 signal transduction pathway which leads to the production of hemopoietic cells and neutrophils | NA | NA | NA | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Colony-Stimulating Factors, Cytokines, Glycoproteins, Granulocyte-Macrophage Colony-Stimulating Factor, Hematopoietic Cell Growth Factors, Immunologic Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Peptides, Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Post Peripheral Blood Progenitor Cell Transplantation, the recommended dose is 250 mcg/m2/day administered IV over 24 hours or SC once daily beginning immediately following infusion of progenitor cells and continuing until an ANC>1500 cells/mm3 for three consecutive days is attained. | NA | Nausea, stomach pain, vomiting, diarrhea, loss of appetite; tired feeling; hair loss; weight loss; headache. | Link | NA | NA |
| 10128 | Th1017 | Sargramostim | >Th1017_Sargramostim APARSPSPSTQPWEHVNAIQEALRLLNLSRDTAAEMNETVEVISEMFDLQEPTCLQTRLELYKQGLRGSLTKLKGPLTMMASHYKQHCPPTPETSCATQIITFESFKENLKDFLLVIPFDCWEPVQE | 14434.5 | C639H1006N168O196S8 | 5.05 | NA | NA | NA | Sargramostim (127 residue glycoprotein) is a human recombinant granulocyte macrophage colony-stimulating factor expressed in yeast system. Substitution of Leu23 leads to a difference from native protein. | Used to treat cancer and in bone marrow transplant | Sargramostim is used in the treatment of bone marrow transplant recipients or those exposed to chemotherapy and recovering from acute myelogenous leukemia, Leukine or GM-CSF is a hematopoietic growth factor which stimulates the survival, clonal expansion (proliferation) and differentiation of hematopoietic progenitor cells. GM-CSF is also capable of activating mature granulocytes and macrophages. After a bone marrow transplant or chemotherapy, patients have a reduced capacity to produce red and white blood cells. Supplementing them with external sources of GM-CSF helps bring the level of neutrophils back to normal so that they can better fight infections. | Sargramostim binds to the Granulocyte-macrophage colony stimulating factor receptor which stimulates a JAK2 STAT1/STAT3 signal transduction pathway which leads to the production of hemopoietic cells and neutrophils | NA | NA | NA | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Colony-Stimulating Factors, Cytokines, Glycoproteins, Granulocyte-Macrophage Colony-Stimulating Factor, Hematopoietic Cell Growth Factors, Immunologic Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Peptides, Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Myeloid Reconstitution After Autologous or Allogeneic Bone Marrow Transplantation, the recommended dose is 250 mcg/m2/day administered IV over a 2-hour period beginning two to four hours after bone marrow infusion, and not less than 24 hours after the last dose of chemotherapy or radiotherapy. | NA | Mild skin rash or itching; bone pain; joint or muscle pain; or redness, swelling, or irritation where the injection was given. | Link | NA | NA |
| 10145 | Th1021 | Thyrotropin Alfa | >Th1021_Thyrotropin_Alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 | 25 ± 10 hours | Thyrotropin alfa is a recombinant form of thyroid stimulating hormone used in performing certain tests in patients who have or have had thyroid cancer. It is also used along with a radioactive agent to destroy remaining thyroid tissue in certain patients. | For detection of residueal or recurrent thyroid cancer | Binding of thyrotropin alfa to TSH receptors on normal thyroid epithelial cells or on well-differentiated thyroid cancer tissue stimulates iodine uptake and organification. Thyrogen is an exogenous source of human TSH that offers an additional diagnostic tool in the follow-up of patients with a history of well-differentiated thyroid cancer. | Binding of thyrotropin Alfa to the thyrotropin receptors found on any residual thyroid cells or tissues stimulates radioactive iodine uptake for better radiodiagnostic imaging. | NA | NA | Time to peak: Median: 10 hours (range: 3-24 hours) After a single intramuscular injection of 0.9 mg of thyrotropin alfa: Cmax= 116+38mU/L, Tmax=22+8.5 hours. AUC=5088+1728 mU·hr/L. | NA | Through kidney and liver | Agents used to treat hypothyroidism, Anterior Pituitary Lobe Hormones and Analogues, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Pituitary and Hypothalamic Hormones and Analogues, Pituitary Hormones, Pituitary Hormones, Anterior, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | US5840566 | 24-Nov-1998 | 24-Nov-2015 | NA | Thyrotropin receptor | Thyrogen | Genzyme Corporation , Genzyme Europe Bv | Genzyme Corporation , Genzyme Europe Bv | It is used in performing certain tests in patients who have or have had thyroid cancer. It is also used along with a radioactive agent to destroy remaining thyroid tissue in certain patients who have had their thyroid gland removed because of thyroid canc | NA | Each vial of THYROGEN contains 1.1 mg thyrotropin alfa, 36 mg Mannitol, 5.1 mg Sodium Phosphate, and 2.4 mg Sodium Chloride. | Lyophilized powder | IntramuSubcutaneousular preferably the buttocks | A 0.9 mg intramuscular injection to the buttock followed by a second 0.9 mg intramuscular injection to the buttock 24 hours later. | Allergic | Rash; hives; itching; difficulty breathing; tightness in the chest | Link | NA | NA |
| 10146 | Th1021 | Thyrotropin Alfa | >Th1021_Thyrotropin_Alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 | 25 ± 10 hours | Thyrotropin alfa is a recombinant form of thyroid stimulating hormone used in performing certain tests in patients who have or have had thyroid cancer. It is also used along with a radioactive agent to destroy remaining thyroid tissue in certain patients. | For detection of residueal or recurrent thyroid cancer | Binding of thyrotropin alfa to TSH receptors on normal thyroid epithelial cells or on well-differentiated thyroid cancer tissue stimulates iodine uptake and organification. Thyrogen is an exogenous source of human TSH that offers an additional diagnostic tool in the follow-up of patients with a history of well-differentiated thyroid cancer. | Binding of thyrotropin Alfa to the thyrotropin receptors found on any residual thyroid cells or tissues stimulates radioactive iodine uptake for better radiodiagnostic imaging. | NA | NA | Time to peak: Median: 10 hours (range: 3-24 hours) After a single intramuscular injection of 0.9 mg of thyrotropin alfa: Cmax= 116+38mU/L, Tmax=22+8.5 hours. AUC=5088+1728 mU·hr/L. | NA | Through kidney and liver | Agents used to treat hypothyroidism, Anterior Pituitary Lobe Hormones and Analogues, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Pituitary and Hypothalamic Hormones and Analogues, Pituitary Hormones, Pituitary Hormones, Anterior, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Swelling of the mouth, face, lips, or tongue; confusion; one-sided weakness | Link | NA | NA |
| 10147 | Th1021 | Thyrotropin Alfa | >Th1021_Thyrotropin_Alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 | 25 ± 10 hours | Thyrotropin alfa is a recombinant form of thyroid stimulating hormone used in performing certain tests in patients who have or have had thyroid cancer. It is also used along with a radioactive agent to destroy remaining thyroid tissue in certain patients. | For detection of residueal or recurrent thyroid cancer | Binding of thyrotropin alfa to TSH receptors on normal thyroid epithelial cells or on well-differentiated thyroid cancer tissue stimulates iodine uptake and organification. Thyrogen is an exogenous source of human TSH that offers an additional diagnostic tool in the follow-up of patients with a history of well-differentiated thyroid cancer. | Binding of thyrotropin Alfa to the thyrotropin receptors found on any residual thyroid cells or tissues stimulates radioactive iodine uptake for better radiodiagnostic imaging. | NA | NA | Time to peak: Median: 10 hours (range: 3-24 hours) After a single intramuscular injection of 0.9 mg of thyrotropin alfa: Cmax= 116+38mU/L, Tmax=22+8.5 hours. AUC=5088+1728 mU·hr/L. | NA | Through kidney and liver | Agents used to treat hypothyroidism, Anterior Pituitary Lobe Hormones and Analogues, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Pituitary and Hypothalamic Hormones and Analogues, Pituitary Hormones, Pituitary Hormones, Anterior, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Severe or persistent dizziness or headache; shortness of breath or other breathing problems; slurred speech; vision problems. | Link | NA | NA |
| 10385 | Th1061 | Trastuzumab | >Th1061_Trastuzumab DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPSRFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 145531.5 | C6470H10012N1726O2013S42 | 8.45 | -0.415 | 71 | average 28.5 days | A recombinant IgG1 kappa, humanized monoclonal antibody that selectively binds with high affinity in a cell-based assay (Kd = 5 nM) to the extracellular domain of the human epidermal growth factor receptor protein. Produced in CHO cell culture. | For treatment of early stage HER2-positive breast cancer, or metastatic breast cancer that substantially overexpress HER2. | Used in the treatment of HER2-positive breast cancer. HER2 protein overexpression is observed in 25%-30% of primary breast cancers.Trastuzumab has been shown, in both in vitro assays and in animals, to inhibit the proliferation of human tumorcells that overexpress HER2. It is a mediator of antibody dependent cellular cytotoxicity, in that the binding of the antibody to HER2 overexpressing cells leads to preferential cell death. | Trastuzumab binds to the HER2 (or c-erbB2) proto-oncogene, an EGF receptor-like protein found on 20-30% of breast cancer cells. The binding leads to antibody mediated (complement mediated) killing of the HER2 positive cells. | Administration of trastuzumab can result in ventricular dysfunction and congestive heart failure. Risk of cardiotocity is especially elevated in patients recieving concurrent anthracycline or cyclophosphamide therapy. | Most likely removed by opsonization via the reticuloendothelial system. | Peak and trough plasma concentrations at steady state (between weeks 16 and 32) were approximately 123 and 79 mcg/mL, respectively. At the highest weekly dose studied (500 mg), mean peak serum concentration was 377 mcg/mL | 44 mL/kg | The predicted steady-state clearance of trastuzumab is 0.173 - 0.337 L/day, dependent primarily on the dosing regimen. The clearance rate for subcutaneously administered trastuzumab, formulated with hyaluronidase for improved subcutaneous absorption, is 0.11 L/day. | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Cardiotoxic antineoplastic agents, Globulins, HER2 Receptor Antagonist, HER2/Neu/cerbB2 Antagonists, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | CA2103059 | 22-Mar-2005 | 15-Jun-2012 | Abciximab may increase the risk of a hypersensitivy reaction to Trastuzumab | Receptor tyrosine-protein kinase erbB-2 | Truxima | Celltrion, Cephalon, Inc. | Celltrion, Cephalon, Inc. | Adjuvant Breast Cancer, Metastatic Breast Cancer, Metastatic Gastric Cancer | NA | Each multi-use vial of Herceptin contains 440 mg trastuzumab, 400 mg a,a-trehalose dihydrate, 9.9 mg L-histidine HCl, 6.4 mg L-histidine, and 1.8 mg polysorbate 20, USP. Reconstitution with 20 mL of the appropriate diluent (BWFI or SWFI) yields a solution containing 21 mg/mL trastuzumab, at a pH of approximately 6 | Herceptin is a sterile, white to pale yellow, preservative-free lyophilized powder |  Intravenous administration | Initial dose of 4mg/kg for 90 minutes and after that 2mg/kg weekly for 30 minutes during chemotherapy for the first 12 weeks incase of breast cancer. Last Dose 6mg/kg for 3 weeks. | None | Cardiomyopathy, Infusion reactions, Embryo-fetal Toxicity, Pulmonary toxicity,Exacerbation of chemotherapy-induced neutropenia, ever, nausea, vomiting, infusion reactions, diarrhea, infections, increased cough, headache, fatigue, dyspnea, rash, neutropenia, anemia, and myalgia. | Link | NA | NA |
| 10386 | Th1061 | Trastuzumab | >Th1061_Trastuzumab DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPSRFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 145531.5 | C6470H10012N1726O2013S42 | 8.45 | -0.415 | 71 | average 28.5 days | A recombinant IgG1 kappa, humanized monoclonal antibody that selectively binds with high affinity in a cell-based assay (Kd = 5 nM) to the extracellular domain of the human epidermal growth factor receptor protein. Produced in CHO cell culture. | For treatment of early stage HER2-positive breast cancer, or metastatic breast cancer that substantially overexpress HER2. | Used in the treatment of HER2-positive breast cancer. HER2 protein overexpression is observed in 25%-30% of primary breast cancers.Trastuzumab has been shown, in both in vitro assays and in animals, to inhibit the proliferation of human tumorcells that overexpress HER2. It is a mediator of antibody dependent cellular cytotoxicity, in that the binding of the antibody to HER2 overexpressing cells leads to preferential cell death. | Trastuzumab binds to the HER2 (or c-erbB2) proto-oncogene, an EGF receptor-like protein found on 20-30% of breast cancer cells. The binding leads to antibody mediated (complement mediated) killing of the HER2 positive cells. | Administration of trastuzumab can result in ventricular dysfunction and congestive heart failure. Risk of cardiotocity is especially elevated in patients recieving concurrent anthracycline or cyclophosphamide therapy. | Most likely removed by opsonization via the reticuloendothelial system. | Peak and trough plasma concentrations at steady state (between weeks 16 and 32) were approximately 123 and 79 mcg/mL, respectively. At the highest weekly dose studied (500 mg), mean peak serum concentration was 377 mcg/mL | 45 mL/kg | The predicted steady-state clearance of trastuzumab is 0.173 - 0.337 L/day, dependent primarily on the dosing regimen. The clearance rate for subcutaneously administered trastuzumab, formulated with hyaluronidase for improved subcutaneous absorption, is 0.11 L/day. | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Cardiotoxic antineoplastic agents, Globulins, HER2 Receptor Antagonist, HER2/Neu/cerbB2 Antagonists, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Daunorubicin, Doxorubicin, Epirubicin), Idarubicin, Valrubicin. may increase the cardiotoxicity of drugs with trastuzumab. Signs and symptoms of cardiac dysfunction should be monitored for frequently. Increased risk of heart failure. Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events | NA | Herzuma | Cephalon, Inc., Celltrion Healthcare | Cephalon, Inc., Celltrion Healthcare | to treat the symptoms of Breast Cancer and Gastric Cancer. | NA | HERZUMA (trastuzumab-pkrb) is a humanized IgG1 kappa monoclonal antibody that selectively binds with high affinity to the extracellular domain of the human epidermal growth factor receptor 2 protein, HER2. Trastuzumab-pkrb is produced by recombinant DNA technology in a mammalian cell (Chinese Hamster Ovary) culture. | sterile, white to pale yellow, preservative-free lyophilized powder | intravenous infusion | Initial dose at 8 mg/kg as an intravenous infusion over 90 minutes Subsequent doses at 6 mg/kg as an intravenous infusion over 30–90 minutes every three weeks. Extending adjuvant treatment beyond one year is not recommended | NA | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, dizziness, fatigue, shortness of breath, swelling, chest pain or pressure, fever, sore throat, chills, and fatigue | Link | NA | NA |
| 10387 | Th1061 | Trastuzumab | >Th1061_Trastuzumab DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPSRFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 145531.5 | C6470H10012N1726O2013S42 | 8.45 | -0.415 | 71 | average 28.5 days | A recombinant IgG1 kappa, humanized monoclonal antibody that selectively binds with high affinity in a cell-based assay (Kd = 5 nM) to the extracellular domain of the human epidermal growth factor receptor protein. Produced in CHO cell culture. | For treatment of early stage HER2-positive breast cancer, or metastatic breast cancer that substantially overexpress HER2. | Used in the treatment of HER2-positive breast cancer. HER2 protein overexpression is observed in 25%-30% of primary breast cancers.Trastuzumab has been shown, in both in vitro assays and in animals, to inhibit the proliferation of human tumorcells that overexpress HER2. It is a mediator of antibody dependent cellular cytotoxicity, in that the binding of the antibody to HER2 overexpressing cells leads to preferential cell death. | Trastuzumab binds to the HER2 (or c-erbB2) proto-oncogene, an EGF receptor-like protein found on 20-30% of breast cancer cells. The binding leads to antibody mediated (complement mediated) killing of the HER2 positive cells. | Administration of trastuzumab can result in ventricular dysfunction and congestive heart failure. Risk of cardiotocity is especially elevated in patients recieving concurrent anthracycline or cyclophosphamide therapy. | Most likely removed by opsonization via the reticuloendothelial system. | Peak and trough plasma concentrations at steady state (between weeks 16 and 32) were approximately 123 and 79 mcg/mL, respectively. At the highest weekly dose studied (500 mg), mean peak serum concentration was 377 mcg/mL | 46 mL/kg | The predicted steady-state clearance of trastuzumab is 0.173 - 0.337 L/day, dependent primarily on the dosing regimen. The clearance rate for subcutaneously administered trastuzumab, formulated with hyaluronidase for improved subcutaneous absorption, is 0.11 L/day. | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Cardiotoxic antineoplastic agents, Globulins, HER2 Receptor Antagonist, HER2/Neu/cerbB2 Antagonists, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Paclitaxel may increase the risk of neutropenia and anemia with trastuzumab. Concomitant therapy may also increase Trastuzumab serum concentration and decrease Paclitaxel serum concentrations. Monitor closely for adverse events and therapeutic response | Insulin receptor,Insulin-like growth factor 1 receptor,Insulin-degrading enzyme,HLA class II histocompatibility antigen, DQ alpha 2 chain,HLA class II histocompatibility antigen, DQ beta 1 chain,Retinoblastoma-associated protein,Cathepsin D,Carboxypeptidase E,Neuroendocrine convertase 2,Neuroendocrine convertase 1,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7,Synaptotagmin-like protein 4 | Kanjinti | AMGEN INC | AMGEN INC | to treat the symptoms of Breast Cancer and Gastric Cancer. | NA | Trastuzumab-anns is a humanized IgG1 kappa monoclonal antibody that selectively binds with high affinity to the extracellular domain of the human epidermal growth factor receptor 2 protein, HER2. Trastuzumab-anns is produced by recombinant DNA technology in a mammalian cell (Chinese Hamster Ovary) culture containing the antibiotic geneticin. Geneticin is not detectable in the final product. | sterile, white to pale yellow, preservative-free lyophilized powder with a cake-like appearance | intravenous administration. | Initial dose of 4 mg/kg as an intravenous infusion over 90 minutes then at 2 mg/kg as an intravenous infusion over 30 minutes weekly during chemotherapy for the first 12 weeks (paclitaxel or docetaxel) or 18 weeks (docetaxel and carboplatin). One week following the last weekly dose of KANJINTI, administer KANJINTI at 6 mg/kg as an intravenous infusion over 30–90 minutes every three weeks. | NA | heart problems, nausea, diarrhea, weight loss, headache, trouble sleeping, tiredness, low blood cell counts, rash, fever, chills, cough, blisters or ulcers in your mouth, red or swollen gums, trouble swallowing, altered sense of taste, stuffy nose, sinus pain, and sore throat | Link | NA | NA |
| 10388 | Th1061 | Trastuzumab | >Th1061_Trastuzumab DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPSRFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 145531.5 | C6470H10012N1726O2013S42 | 8.45 | -0.415 | 71 | average 28.5 days | A recombinant IgG1 kappa, humanized monoclonal antibody that selectively binds with high affinity in a cell-based assay (Kd = 5 nM) to the extracellular domain of the human epidermal growth factor receptor protein. Produced in CHO cell culture. | For treatment of early stage HER2-positive breast cancer, or metastatic breast cancer that substantially overexpress HER2. | Used in the treatment of HER2-positive breast cancer. HER2 protein overexpression is observed in 25%-30% of primary breast cancers.Trastuzumab has been shown, in both in vitro assays and in animals, to inhibit the proliferation of human tumorcells that overexpress HER2. It is a mediator of antibody dependent cellular cytotoxicity, in that the binding of the antibody to HER2 overexpressing cells leads to preferential cell death. | Trastuzumab binds to the HER2 (or c-erbB2) proto-oncogene, an EGF receptor-like protein found on 20-30% of breast cancer cells. The binding leads to antibody mediated (complement mediated) killing of the HER2 positive cells. | Administration of trastuzumab can result in ventricular dysfunction and congestive heart failure. Risk of cardiotocity is especially elevated in patients recieving concurrent anthracycline or cyclophosphamide therapy. | Most likely removed by opsonization via the reticuloendothelial system. | Peak and trough plasma concentrations at steady state (between weeks 16 and 32) were approximately 123 and 79 mcg/mL, respectively. At the highest weekly dose studied (500 mg), mean peak serum concentration was 377 mcg/mL | 47 mL/kg | The predicted steady-state clearance of trastuzumab is 0.173 - 0.337 L/day, dependent primarily on the dosing regimen. The clearance rate for subcutaneously administered trastuzumab, formulated with hyaluronidase for improved subcutaneous absorption, is 0.11 L/day. | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Cardiotoxic antineoplastic agents, Globulins, HER2 Receptor Antagonist, HER2/Neu/cerbB2 Antagonists, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Abatacept, Adalimumab, Alemtuzumab, Altretamine, Amsacrine, Anakinra, Asparaginase, Azacitidine, Azathioprine, Basiliximab, Betamethasone, Bleomycin, Busulfan, Capecitabine, Carboplatin, Carmustine, Chlorambucil, Cisplatin, Cladribine, Clofarabine, Corticotropin, Cortisone acetate, Cyclophosphamide, Cyclosporine, Cytarabine, Dacarbazine, Daclizumab, Dactinomycin, Denileukin diftitox, Dexamethasone, Docetaxel, Efalizumab, Erlotinib, Estramustine, Etanercept, Etoposide, Floxuridine, Fludarabine, Fludrocortisone, Fluorouracil, Gefitinib, Gemcitabine, Hydrocortisone, Hydroxyurea, Ibritumomab, Ifosfamide, Imatinib, Infliximab, Irinotecan, Lenalidomide, Lomustine, Mechlorethamine, Melphalan, Mercaptopurine, Methotrexate, Methylprednisolone, Mitomycin, Mitoxantrone, Muromonab, Mycophenolate mofetil, Mycophenolic acid, Natalizumab, Nelarabine, Nilotinib, Oxaliplatin, Pegaspargase, Pentostatin, Prednisolone, Prednisone, Procarbazine, Rilonacept, Rituximab, Sirolimus, Sorafenib, Streptozocin, Sunitinib, Tacrolimus, Temozolomide, Temsirolimus, Teniposide, Thalidomide, Thiotepa, Tioguanine, Tofacitinib, Topotecan, Tositumomab, Tretinoin, Triamcinolone, Vinblastine, Vincristine, Vinorelbine may increase the risk of neutropenia and anemia with trastuzumab. Monitor closely for signs and symptoms of adverse events. | NA | Ogivri | Mylan Institutional LLC, Viatris Limited, Bgp Pharma Ulc | Mylan Institutional LLC, Viatris Limited, Bgp Pharma Ulc | treatment of HER2-overexpressing breast cancer, and the treatment of HER2-overexpressing metastatic gastric or gastroesophageal junction adenocarcinoma. | NA | Ogivri (trastuzumab-dkst) is a humanized IgG1 kappa monoclonal antibody that selectively binds with high affinity to the extracellular domain of the human epidermal growth factor receptor 2 protein, HER2. Trastuzumab-dkst is produced by recombinant DNA technology in a mammalian cell (Chinese Hamster Ovary) culture. | sterile, off-white to pale yellow, preservative-free lyophilized powder | intravenous administration. | Initial dose of 4 mg/kg as an intravenous infusion over 90 minutes then at 2 mg/kg as an intravenous infusion over 30 minutes weekly during chemotherapy for the first 12 weeks (paclitaxel or docetaxel) or 18 weeks (docetaxel/carboplatin). One week following the last weekly dose of Ogivri, administer Ogivri at 6 mg/kg as an intravenous infusion over 30 to 90 minutes every three weeks. | NA | headache, diarrhea, nausea, chills, fever, infection, congestive heart failure, insomnia, cough, rash, low white blood cell count (neutropenia), fatigue, anemia, swelling and sores inside the mouth, weight loss, upper respiratory tract infections, low platelet count (thrombocytopenia), mucosal inflammation, runny or stuffy nose, and changes in taste. | Link | NA | NA |
| 10436 | Th1075 | Capromab | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal antibody that recognizes prostate specific membrane antigen from prostate cancer cells and normal prostate tissue. It is linked to pendetide, a derivative of DTPA. Pendetide acts as a chelating agent for the radionuclide indium-111. Capromab is used to image the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | 4 ± 2.1 L | 42 +/- 22 mL/hr | Indicators, Reagents and Diagnostic Agents | NA | NA | NA | NA | NA | ProstaScint | Jazz Pharmaceuticals, Inc. | Jazz Pharmaceuticals, Inc. | Indium In 111 ProstaScint (capromab pendetide) is indicated as a diagnostic imaging agent in newly-diagnosed patients with biopsy-proven prostate cancer, thought to be clinically-localized after standard diagnostic evaluation (e.g. chest x-ray, bone scan, CT scan, or MRI), who are at high-risk for pelvic lymph node metastases. ProstaScint is not indicated as a screening tool for carcinoma of the prostate nor for readministration for the purpose of assessment of response to treatment. | NA | Each ProstaScint kit consists of two vials which contain all of the non-radioactive ingredients necessary to produce a single unit dose of Indium In 111 ProstaScint, an immunoscintigraphic agent for administration by Intravenous infusion only. The ProstaScint vial contains 0.5 mg of capromab pendetide in 1 mL of sodium phosphate buffered saline solution adjusted to pH 6; a sterile, pyrogen-free, clear, colorless solution that may contain some translucent particles. The vial of sodium acetate buffer contains 82 mg of sodium acetate in 2 mL of Water for Injection adjusted to pH 5-7 with glacial acetic acid; it is a sterile, pyrogen-free, clear, and colorless solution. Neither solution contains a preservative. Each kit also includes one sterile 0.22 μm Millex GV filter, prescribing information, and two identification labels. | Indium In 111 ProstaScint is a sterile, pyrogen-free, clear, colorless solution that may contain some translucent particles. | Intravenous infusion | he recommended dose of ProstaScint (capromab pendetide) is 0.5 mg radiolabeled with 5 mCi of Indium In 111 chloride. Each dose is administered intravenously over 5 minutes and should not be mixed with any other medication during its administration. Indium In 111 ProstaScint may be readministered following infiltration or a technically inadequate scan; however, it is not indicated for readministration for the purpose of assessment of response to treatment . | Indium In 111 ProstaScint (capromab pendetide) should not be used in patients who are hypersensitive to this or any other product of murine origin or to Indium In 111 chloride. | ProstaScint (capromab pendetide) was generally well tolerated in the clinical trials. After administration of 529 single doses of Indium In 111 ProstaScint, adverse reactions were observed in 4% of patients. The most commonly reported adverse reactions were increases in bilirubin, hypotension, and hypertension, which occurred in 1% of patients. Elevated liver enzymes and injection site reactions occurred in slightly less than 1% of patients. Other adverse reactions, listed in order of decreasing frequency, were: pruritus, fever, rash, headache, myalgia, asthenia, burning sensation in thigh, shortness of breath, and alteration of taste. Most adverse reactions were mild and readily reversible. Data from repeat administration in 61 patients revealed a similar incidence of adverse reactions (5%). No deaths were attributable to Indium In 111 ProstaScint administration. | Link | NA | NA |
| 10437 | Th1075 | Capromab | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal antibody that recognizes prostate specific membrane antigen from prostate cancer cells and normal prostate tissue. It is linked to pendetide, a derivative of DTPA. Pendetide acts as a chelating agent for the radionuclide indium-111. Capromab is used to image the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | 4 ± 2.1 L | 42 +/- 22 mL/hr | Indicators, Reagents and Diagnostic Agents | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10455 | Th1082 | Filgrastim | >Th1082_Filgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S9 | 5.65 | 0.209 | 60 | Elimination half-life, healthy subjects and cancer patients, Neopogen = 3.5 hours | 175 amino acid long, recombinant human granulocyte colony stimulating factor (G-CSF) analogue expressed and purified from a strain of E. coli. Neupogen by Amgen. Amino acid sequence is identical to the natural sequence predicted in human genome, with the exception of an N-terminal methionine to aid expression in E coli. Tbo-filgrastim, which is marketed by Sicor Biotech and FDA approved on August 29, 2012, contains the same active ingredient as Neupogen and is biologically similar, but it is formulated to be short-acting. | Filgrastim is used in patients with acute myeloid leukemia receiving induction or consolidation chemotherapy. It is also used in cancer patients receiving bone marrow transplant. In general, filgrastim increases neutrophil counts in order to decrease the risk of infection or duration of neutropenia in the aforementioned patient populations. Infection and neutropenia are adverse events associated with chemotherapy. Furthermore, filgrastim is also indicated for patients with severe chronic neutropenia. It mobilizes hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis to allow for a more rapid engraftment. Tbo-filgrastim has a narrower indication profile than Neupogen - it is a leukocyte growth factor indicated for the reduction in the duration of severe neutropenia in patients with non-myeloid malignancies. | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Filgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment, and end cell functional activation. When tbo-filgrastim is administered to cancer patients, it took 3-5 days to reach maximum absolute neutrophil count (ANC). Levels of neutrophils returned to baseline by 21 days following completion of chemotherapy. In the healthy volunteer trials, doubling the tbo-filgrastim subcutaneous dose from 5 to 10 mcg/kg resulted in a 16-19% increase in the ANCmax and a 33-36% increase in the area under the effect curve for ANC. | Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and reduces their maturation time. Filgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, Filgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | The oral LD50 in mouse and rat was >3 mg/kg. The intravenous LD50 in rat was also >3 mg/kg.11 There is limited information regarding filgrastim overdose. The maximum tolerated dose of filgrastim has not been determined. In clinical trials of patients with cancer receiving myelosuppressive chemotherapy‚ white blood cell counts greater than 100,000/mm3 have been reported in less than 5% of patients‚ but were not associated with any reported adverse clinical effects. Patients in the bone marrow transplantation studies received up to 138 mcg/kg/day without toxic effects‚ although there was a flattening of the dose response curve above daily doses of greater than 10 mcg/kg/day | Like other G-CSF compounds, filgrastim is cleared from plasma via neutrophil-mediated clearance involving internalization via G-CSF receptors and degradation within the neutrophil. Filgrastim is also subject to extracellular proteolytic degradation by neutrophil elastase: this enzyme rapidly cleaves filgrastim and renders it inactive | Filgrastim exhibits nonlinear pharmacokinetics. Subcutaneous administration of 3.45 mcg/kg and 11.5 mcg/kg of filgrastim resulted in maximum serum concentrations of 4 and 49 ng/mL‚ respectively‚ within 2 to 8 hours. Continuous 24-hour intravenous infusions of 20 mcg/kg over an 11 to 20-day period produced steady-state serum concentrations of filgrastim with no evidence of drug accumulation. The absolute bioavailability of filgrastim after subcutaneous administration is 60% to 70% | Vd, healthy subjects and cancer patients = 150 mL/kg | Clearance rates of filgrastim were approximately 0.5 to 0.7 mL/minute/kg after intravenous administration. | Amino Acids, Peptides, and Proteins,Antineoplastic and Immunomodulating Agents,Biological Factors,Colony-Stimulating Factors,Glycoconjugates,Glycoproteins,Granulocyte Colony-Stimulating Factors,Hematologic Agents,Hematopoietic Cell Growth Factors,Increased Myeloid Cell Production,Leukocyte Growth Factor,Peptides,Proteins | CA1341537 | 31-Jul-2007 | 31-Jul-2024 | Topotecan with Filgrastim may increase the adverse effects. Increased risk of prolonged neutropenia. Filgrastim should be administered at least 24 hours following Topotecan therapy. Monitor for signs and symptoms of neutropenia | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Accofil | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10456 | Th1082 | Filgrastim | >Th1082_Filgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S10 | 5.65 | 0.209 | 60 | Elimination half-life, healthy subjects and cancer patients, Neopogen = 3.5 hours | 175 amino acid long, recombinant human granulocyte colony stimulating factor (G-CSF) analogue expressed and purified from a strain of E. coli. Neupogen by Amgen. Amino acid sequence is identical to the natural sequence predicted in human genome, with the exception of an N-terminal methionine to aid expression in E coli. Tbo-filgrastim, which is marketed by Sicor Biotech and FDA approved on August 29, 2012, contains the same active ingredient as Neupogen and is biologically similar, but it is formulated to be short-acting. | Filgrastim is used in patients with acute myeloid leukemia receiving induction or consolidation chemotherapy. It is also used in cancer patients receiving bone marrow transplant. In general, filgrastim increases neutrophil counts in order to decrease the risk of infection or duration of neutropenia in the aforementioned patient populations. Infection and neutropenia are adverse events associated with chemotherapy. Furthermore, filgrastim is also indicated for patients with severe chronic neutropenia. It mobilizes hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis to allow for a more rapid engraftment. Tbo-filgrastim has a narrower indication profile than Neupogen - it is a leukocyte growth factor indicated for the reduction in the duration of severe neutropenia in patients with non-myeloid malignancies. | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Filgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment, and end cell functional activation. When tbo-filgrastim is administered to cancer patients, it took 3-5 days to reach maximum absolute neutrophil count (ANC). Levels of neutrophils returned to baseline by 21 days following completion of chemotherapy. In the healthy volunteer trials, doubling the tbo-filgrastim subcutaneous dose from 5 to 10 mcg/kg resulted in a 16-19% increase in the ANCmax and a 33-36% increase in the area under the effect curve for ANC. | Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and reduces their maturation time. Filgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, Filgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | The oral LD50 in mouse and rat was >3 mg/kg. The intravenous LD50 in rat was also >3 mg/kg.11 There is limited information regarding filgrastim overdose. The maximum tolerated dose of filgrastim has not been determined. In clinical trials of patients with cancer receiving myelosuppressive chemotherapy‚ white blood cell counts greater than 100,000/mm3 have been reported in less than 5% of patients‚ but were not associated with any reported adverse clinical effects. Patients in the bone marrow transplantation studies received up to 138 mcg/kg/day without toxic effects‚ although there was a flattening of the dose response curve above daily doses of greater than 10 mcg/kg/day | Like other G-CSF compounds, filgrastim is cleared from plasma via neutrophil-mediated clearance involving internalization via G-CSF receptors and degradation within the neutrophil. Filgrastim is also subject to extracellular proteolytic degradation by neutrophil elastase: this enzyme rapidly cleaves filgrastim and renders it inactive | Filgrastim exhibits nonlinear pharmacokinetics. Subcutaneous administration of 3.45 mcg/kg and 11.5 mcg/kg of filgrastim resulted in maximum serum concentrations of 4 and 49 ng/mL‚ respectively‚ within 2 to 8 hours. Continuous 24-hour intravenous infusions of 20 mcg/kg over an 11 to 20-day period produced steady-state serum concentrations of filgrastim with no evidence of drug accumulation. The absolute bioavailability of filgrastim after subcutaneous administration is 60% to 70% | Vd, healthy subjects and cancer patients = 150 mL/kg | Clearance rates of filgrastim were approximately 0.5 to 0.7 mL/minute/kg after intravenous administration. | Amino Acids, Peptides, and Proteins,Antineoplastic and Immunomodulating Agents,Biological Factors,Colony-Stimulating Factors,Glycoconjugates,Glycoproteins,Granulocyte Colony-Stimulating Factors,Hematologic Agents,Hematopoietic Cell Growth Factors,Increased Myeloid Cell Production,Leukocyte Growth Factor,Peptides,Proteins | CA1339071 | 29-Jul-1997 | 29-Jul-2014 | NA | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Biograstim | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10457 | Th1082 | Filgrastim | >Th1082_Filgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S10 | 5.65 | 0.209 | 60 | Elimination half-life, healthy subjects and cancer patients, Neopogen = 3.5 hours | 175 amino acid long, recombinant human granulocyte colony stimulating factor (G-CSF) analogue expressed and purified from a strain of E. coli. Neupogen by Amgen. Amino acid sequence is identical to the natural sequence predicted in human genome, with the exception of an N-terminal methionine to aid expression in E coli. Tbo-filgrastim, which is marketed by Sicor Biotech and FDA approved on August 29, 2012, contains the same active ingredient as Neupogen and is biologically similar, but it is formulated to be short-acting. | Filgrastim is used in patients with acute myeloid leukemia receiving induction or consolidation chemotherapy. It is also used in cancer patients receiving bone marrow transplant. In general, filgrastim increases neutrophil counts in order to decrease the risk of infection or duration of neutropenia in the aforementioned patient populations. Infection and neutropenia are adverse events associated with chemotherapy. Furthermore, filgrastim is also indicated for patients with severe chronic neutropenia. It mobilizes hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis to allow for a more rapid engraftment. Tbo-filgrastim has a narrower indication profile than Neupogen - it is a leukocyte growth factor indicated for the reduction in the duration of severe neutropenia in patients with non-myeloid malignancies. | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Filgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment, and end cell functional activation. When tbo-filgrastim is administered to cancer patients, it took 3-5 days to reach maximum absolute neutrophil count (ANC). Levels of neutrophils returned to baseline by 21 days following completion of chemotherapy. In the healthy volunteer trials, doubling the tbo-filgrastim subcutaneous dose from 5 to 10 mcg/kg resulted in a 16-19% increase in the ANCmax and a 33-36% increase in the area under the effect curve for ANC. | Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and reduces their maturation time. Filgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, Filgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | The oral LD50 in mouse and rat was >3 mg/kg. The intravenous LD50 in rat was also >3 mg/kg.11 There is limited information regarding filgrastim overdose. The maximum tolerated dose of filgrastim has not been determined. In clinical trials of patients with cancer receiving myelosuppressive chemotherapy‚ white blood cell counts greater than 100,000/mm3 have been reported in less than 5% of patients‚ but were not associated with any reported adverse clinical effects. Patients in the bone marrow transplantation studies received up to 138 mcg/kg/day without toxic effects‚ although there was a flattening of the dose response curve above daily doses of greater than 10 mcg/kg/day | Like other G-CSF compounds, filgrastim is cleared from plasma via neutrophil-mediated clearance involving internalization via G-CSF receptors and degradation within the neutrophil. Filgrastim is also subject to extracellular proteolytic degradation by neutrophil elastase: this enzyme rapidly cleaves filgrastim and renders it inactive | Filgrastim exhibits nonlinear pharmacokinetics. Subcutaneous administration of 3.45 mcg/kg and 11.5 mcg/kg of filgrastim resulted in maximum serum concentrations of 4 and 49 ng/mL‚ respectively‚ within 2 to 8 hours. Continuous 24-hour intravenous infusions of 20 mcg/kg over an 11 to 20-day period produced steady-state serum concentrations of filgrastim with no evidence of drug accumulation. The absolute bioavailability of filgrastim after subcutaneous administration is 60% to 70% | Vd, healthy subjects and cancer patients = 150 mL/kg | Clearance rates of filgrastim were approximately 0.5 to 0.7 mL/minute/kg after intravenous administration. | Amino Acids, Peptides, and Proteins,Antineoplastic and Immunomodulating Agents,Biological Factors,Colony-Stimulating Factors,Glycoconjugates,Glycoproteins,Granulocyte Colony-Stimulating Factors,Hematologic Agents,Hematopoietic Cell Growth Factors,Increased Myeloid Cell Production,Leukocyte Growth Factor,Peptides,Proteins | CA1339071 | 29-Jul-1997 | 29-Jul-2014 | NA | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Filgrastim Hexal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10458 | Th1082 | Filgrastim | >Th1082_Filgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S10 | 5.65 | 0.209 | 60 | Elimination half-life, healthy subjects and cancer patients, Neopogen = 3.5 hours | 175 amino acid long, recombinant human granulocyte colony stimulating factor (G-CSF) analogue expressed and purified from a strain of E. coli. Neupogen by Amgen. Amino acid sequence is identical to the natural sequence predicted in human genome, with the exception of an N-terminal methionine to aid expression in E coli. Tbo-filgrastim, which is marketed by Sicor Biotech and FDA approved on August 29, 2012, contains the same active ingredient as Neupogen and is biologically similar, but it is formulated to be short-acting. | Filgrastim is used in patients with acute myeloid leukemia receiving induction or consolidation chemotherapy. It is also used in cancer patients receiving bone marrow transplant. In general, filgrastim increases neutrophil counts in order to decrease the risk of infection or duration of neutropenia in the aforementioned patient populations. Infection and neutropenia are adverse events associated with chemotherapy. Furthermore, filgrastim is also indicated for patients with severe chronic neutropenia. It mobilizes hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis to allow for a more rapid engraftment. Tbo-filgrastim has a narrower indication profile than Neupogen - it is a leukocyte growth factor indicated for the reduction in the duration of severe neutropenia in patients with non-myeloid malignancies. | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Filgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment, and end cell functional activation. When tbo-filgrastim is administered to cancer patients, it took 3-5 days to reach maximum absolute neutrophil count (ANC). Levels of neutrophils returned to baseline by 21 days following completion of chemotherapy. In the healthy volunteer trials, doubling the tbo-filgrastim subcutaneous dose from 5 to 10 mcg/kg resulted in a 16-19% increase in the ANCmax and a 33-36% increase in the area under the effect curve for ANC. | Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and reduces their maturation time. Filgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, Filgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | The oral LD50 in mouse and rat was >3 mg/kg. The intravenous LD50 in rat was also >3 mg/kg.11 There is limited information regarding filgrastim overdose. The maximum tolerated dose of filgrastim has not been determined. In clinical trials of patients with cancer receiving myelosuppressive chemotherapy‚ white blood cell counts greater than 100,000/mm3 have been reported in less than 5% of patients‚ but were not associated with any reported adverse clinical effects. Patients in the bone marrow transplantation studies received up to 138 mcg/kg/day without toxic effects‚ although there was a flattening of the dose response curve above daily doses of greater than 10 mcg/kg/day | Like other G-CSF compounds, filgrastim is cleared from plasma via neutrophil-mediated clearance involving internalization via G-CSF receptors and degradation within the neutrophil. Filgrastim is also subject to extracellular proteolytic degradation by neutrophil elastase: this enzyme rapidly cleaves filgrastim and renders it inactive | Filgrastim exhibits nonlinear pharmacokinetics. Subcutaneous administration of 3.45 mcg/kg and 11.5 mcg/kg of filgrastim resulted in maximum serum concentrations of 4 and 49 ng/mL‚ respectively‚ within 2 to 8 hours. Continuous 24-hour intravenous infusions of 20 mcg/kg over an 11 to 20-day period produced steady-state serum concentrations of filgrastim with no evidence of drug accumulation. The absolute bioavailability of filgrastim after subcutaneous administration is 60% to 70% | Vd, healthy subjects and cancer patients = 150 mL/kg | Clearance rates of filgrastim were approximately 0.5 to 0.7 mL/minute/kg after intravenous administration. | Amino Acids, Peptides, and Proteins,Antineoplastic and Immunomodulating Agents,Biological Factors,Colony-Stimulating Factors,Glycoconjugates,Glycoproteins,Granulocyte Colony-Stimulating Factors,Hematologic Agents,Hematopoietic Cell Growth Factors,Increased Myeloid Cell Production,Leukocyte Growth Factor,Peptides,Proteins | CA1339071 | 29-Jul-1997 | 29-Jul-2014 | NA | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Filgrastim Ratiopharm | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10459 | Th1082 | Filgrastim | >Th1082_Filgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S10 | 5.65 | 0.209 | 60 | Elimination half-life, healthy subjects and cancer patients, Neopogen = 3.5 hours | 175 amino acid long, recombinant human granulocyte colony stimulating factor (G-CSF) analogue expressed and purified from a strain of E. coli. Neupogen by Amgen. Amino acid sequence is identical to the natural sequence predicted in human genome, with the exception of an N-terminal methionine to aid expression in E coli. Tbo-filgrastim, which is marketed by Sicor Biotech and FDA approved on August 29, 2012, contains the same active ingredient as Neupogen and is biologically similar, but it is formulated to be short-acting. | Filgrastim is used in patients with acute myeloid leukemia receiving induction or consolidation chemotherapy. It is also used in cancer patients receiving bone marrow transplant. In general, filgrastim increases neutrophil counts in order to decrease the risk of infection or duration of neutropenia in the aforementioned patient populations. Infection and neutropenia are adverse events associated with chemotherapy. Furthermore, filgrastim is also indicated for patients with severe chronic neutropenia. It mobilizes hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis to allow for a more rapid engraftment. Tbo-filgrastim has a narrower indication profile than Neupogen - it is a leukocyte growth factor indicated for the reduction in the duration of severe neutropenia in patients with non-myeloid malignancies. | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Filgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment, and end cell functional activation. When tbo-filgrastim is administered to cancer patients, it took 3-5 days to reach maximum absolute neutrophil count (ANC). Levels of neutrophils returned to baseline by 21 days following completion of chemotherapy. In the healthy volunteer trials, doubling the tbo-filgrastim subcutaneous dose from 5 to 10 mcg/kg resulted in a 16-19% increase in the ANCmax and a 33-36% increase in the area under the effect curve for ANC. | Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and reduces their maturation time. Filgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, Filgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | The oral LD50 in mouse and rat was >3 mg/kg. The intravenous LD50 in rat was also >3 mg/kg.11 There is limited information regarding filgrastim overdose. The maximum tolerated dose of filgrastim has not been determined. In clinical trials of patients with cancer receiving myelosuppressive chemotherapy‚ white blood cell counts greater than 100,000/mm3 have been reported in less than 5% of patients‚ but were not associated with any reported adverse clinical effects. Patients in the bone marrow transplantation studies received up to 138 mcg/kg/day without toxic effects‚ although there was a flattening of the dose response curve above daily doses of greater than 10 mcg/kg/day | Like other G-CSF compounds, filgrastim is cleared from plasma via neutrophil-mediated clearance involving internalization via G-CSF receptors and degradation within the neutrophil. Filgrastim is also subject to extracellular proteolytic degradation by neutrophil elastase: this enzyme rapidly cleaves filgrastim and renders it inactive | Filgrastim exhibits nonlinear pharmacokinetics. Subcutaneous administration of 3.45 mcg/kg and 11.5 mcg/kg of filgrastim resulted in maximum serum concentrations of 4 and 49 ng/mL‚ respectively‚ within 2 to 8 hours. Continuous 24-hour intravenous infusions of 20 mcg/kg over an 11 to 20-day period produced steady-state serum concentrations of filgrastim with no evidence of drug accumulation. The absolute bioavailability of filgrastim after subcutaneous administration is 60% to 70% | Vd, healthy subjects and cancer patients = 150 mL/kg | Clearance rates of filgrastim were approximately 0.5 to 0.7 mL/minute/kg after intravenous administration. | Amino Acids, Peptides, and Proteins,Antineoplastic and Immunomodulating Agents,Biological Factors,Colony-Stimulating Factors,Glycoconjugates,Glycoproteins,Granulocyte Colony-Stimulating Factors,Hematologic Agents,Hematopoietic Cell Growth Factors,Increased Myeloid Cell Production,Leukocyte Growth Factor,Peptides,Proteins | CA1339071 | 29-Jul-1997 | 29-Jul-2014 | NA | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Granix | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10460 | Th1082 | Filgrastim | >Th1082_Filgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S10 | 5.65 | 0.209 | 60 | Elimination half-life, healthy subjects and cancer patients, Neopogen = 3.5 hours | 175 amino acid long, recombinant human granulocyte colony stimulating factor (G-CSF) analogue expressed and purified from a strain of E. coli. Neupogen by Amgen. Amino acid sequence is identical to the natural sequence predicted in human genome, with the exception of an N-terminal methionine to aid expression in E coli. Tbo-filgrastim, which is marketed by Sicor Biotech and FDA approved on August 29, 2012, contains the same active ingredient as Neupogen and is biologically similar, but it is formulated to be short-acting. | Filgrastim is used in patients with acute myeloid leukemia receiving induction or consolidation chemotherapy. It is also used in cancer patients receiving bone marrow transplant. In general, filgrastim increases neutrophil counts in order to decrease the risk of infection or duration of neutropenia in the aforementioned patient populations. Infection and neutropenia are adverse events associated with chemotherapy. Furthermore, filgrastim is also indicated for patients with severe chronic neutropenia. It mobilizes hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis to allow for a more rapid engraftment. Tbo-filgrastim has a narrower indication profile than Neupogen - it is a leukocyte growth factor indicated for the reduction in the duration of severe neutropenia in patients with non-myeloid malignancies. | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Filgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment, and end cell functional activation. When tbo-filgrastim is administered to cancer patients, it took 3-5 days to reach maximum absolute neutrophil count (ANC). Levels of neutrophils returned to baseline by 21 days following completion of chemotherapy. In the healthy volunteer trials, doubling the tbo-filgrastim subcutaneous dose from 5 to 10 mcg/kg resulted in a 16-19% increase in the ANCmax and a 33-36% increase in the area under the effect curve for ANC. | Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and reduces their maturation time. Filgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, Filgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | The oral LD50 in mouse and rat was >3 mg/kg. The intravenous LD50 in rat was also >3 mg/kg.11 There is limited information regarding filgrastim overdose. The maximum tolerated dose of filgrastim has not been determined. In clinical trials of patients with cancer receiving myelosuppressive chemotherapy‚ white blood cell counts greater than 100,000/mm3 have been reported in less than 5% of patients‚ but were not associated with any reported adverse clinical effects. Patients in the bone marrow transplantation studies received up to 138 mcg/kg/day without toxic effects‚ although there was a flattening of the dose response curve above daily doses of greater than 10 mcg/kg/day | Like other G-CSF compounds, filgrastim is cleared from plasma via neutrophil-mediated clearance involving internalization via G-CSF receptors and degradation within the neutrophil. Filgrastim is also subject to extracellular proteolytic degradation by neutrophil elastase: this enzyme rapidly cleaves filgrastim and renders it inactive | Filgrastim exhibits nonlinear pharmacokinetics. Subcutaneous administration of 3.45 mcg/kg and 11.5 mcg/kg of filgrastim resulted in maximum serum concentrations of 4 and 49 ng/mL‚ respectively‚ within 2 to 8 hours. Continuous 24-hour intravenous infusions of 20 mcg/kg over an 11 to 20-day period produced steady-state serum concentrations of filgrastim with no evidence of drug accumulation. The absolute bioavailability of filgrastim after subcutaneous administration is 60% to 70% | Vd, healthy subjects and cancer patients = 150 mL/kg | Clearance rates of filgrastim were approximately 0.5 to 0.7 mL/minute/kg after intravenous administration. | Amino Acids, Peptides, and Proteins,Antineoplastic and Immunomodulating Agents,Biological Factors,Colony-Stimulating Factors,Glycoconjugates,Glycoproteins,Granulocyte Colony-Stimulating Factors,Hematologic Agents,Hematopoietic Cell Growth Factors,Increased Myeloid Cell Production,Leukocyte Growth Factor,Peptides,Proteins | CA1339071 | 29-Jul-1997 | 29-Jul-2014 | NA | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Grastofil | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10461 | Th1082 | Filgrastim | >Th1082_Filgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S10 | 5.65 | 0.209 | 60 | Elimination half-life, healthy subjects and cancer patients, Neopogen = 3.5 hours | 175 amino acid long, recombinant human granulocyte colony stimulating factor (G-CSF) analogue expressed and purified from a strain of E. coli. Neupogen by Amgen. Amino acid sequence is identical to the natural sequence predicted in human genome, with the exception of an N-terminal methionine to aid expression in E coli. Tbo-filgrastim, which is marketed by Sicor Biotech and FDA approved on August 29, 2012, contains the same active ingredient as Neupogen and is biologically similar, but it is formulated to be short-acting. | Filgrastim is used in patients with acute myeloid leukemia receiving induction or consolidation chemotherapy. It is also used in cancer patients receiving bone marrow transplant. In general, filgrastim increases neutrophil counts in order to decrease the risk of infection or duration of neutropenia in the aforementioned patient populations. Infection and neutropenia are adverse events associated with chemotherapy. Furthermore, filgrastim is also indicated for patients with severe chronic neutropenia. It mobilizes hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis to allow for a more rapid engraftment. Tbo-filgrastim has a narrower indication profile than Neupogen - it is a leukocyte growth factor indicated for the reduction in the duration of severe neutropenia in patients with non-myeloid malignancies. | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Filgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment, and end cell functional activation. When tbo-filgrastim is administered to cancer patients, it took 3-5 days to reach maximum absolute neutrophil count (ANC). Levels of neutrophils returned to baseline by 21 days following completion of chemotherapy. In the healthy volunteer trials, doubling the tbo-filgrastim subcutaneous dose from 5 to 10 mcg/kg resulted in a 16-19% increase in the ANCmax and a 33-36% increase in the area under the effect curve for ANC. | Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and reduces their maturation time. Filgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, Filgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | The oral LD50 in mouse and rat was >3 mg/kg. The intravenous LD50 in rat was also >3 mg/kg.11 There is limited information regarding filgrastim overdose. The maximum tolerated dose of filgrastim has not been determined. In clinical trials of patients with cancer receiving myelosuppressive chemotherapy‚ white blood cell counts greater than 100,000/mm3 have been reported in less than 5% of patients‚ but were not associated with any reported adverse clinical effects. Patients in the bone marrow transplantation studies received up to 138 mcg/kg/day without toxic effects‚ although there was a flattening of the dose response curve above daily doses of greater than 10 mcg/kg/day | Like other G-CSF compounds, filgrastim is cleared from plasma via neutrophil-mediated clearance involving internalization via G-CSF receptors and degradation within the neutrophil. Filgrastim is also subject to extracellular proteolytic degradation by neutrophil elastase: this enzyme rapidly cleaves filgrastim and renders it inactive | Filgrastim exhibits nonlinear pharmacokinetics. Subcutaneous administration of 3.45 mcg/kg and 11.5 mcg/kg of filgrastim resulted in maximum serum concentrations of 4 and 49 ng/mL‚ respectively‚ within 2 to 8 hours. Continuous 24-hour intravenous infusions of 20 mcg/kg over an 11 to 20-day period produced steady-state serum concentrations of filgrastim with no evidence of drug accumulation. The absolute bioavailability of filgrastim after subcutaneous administration is 60% to 70% | Vd, healthy subjects and cancer patients = 150 mL/kg | Clearance rates of filgrastim were approximately 0.5 to 0.7 mL/minute/kg after intravenous administration. | Amino Acids, Peptides, and Proteins,Antineoplastic and Immunomodulating Agents,Biological Factors,Colony-Stimulating Factors,Glycoconjugates,Glycoproteins,Granulocyte Colony-Stimulating Factors,Hematologic Agents,Hematopoietic Cell Growth Factors,Increased Myeloid Cell Production,Leukocyte Growth Factor,Peptides,Proteins | CA1339071 | 29-Jul-1997 | 29-Jul-2014 | NA | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Neupogen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10462 | Th1082 | Filgrastim | >Th1082_Filgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S10 | 5.65 | 0.209 | 60 | Elimination half-life, healthy subjects and cancer patients, Neopogen = 3.5 hours | 175 amino acid long, recombinant human granulocyte colony stimulating factor (G-CSF) analogue expressed and purified from a strain of E. coli. Neupogen by Amgen. Amino acid sequence is identical to the natural sequence predicted in human genome, with the exception of an N-terminal methionine to aid expression in E coli. Tbo-filgrastim, which is marketed by Sicor Biotech and FDA approved on August 29, 2012, contains the same active ingredient as Neupogen and is biologically similar, but it is formulated to be short-acting. | Filgrastim is used in patients with acute myeloid leukemia receiving induction or consolidation chemotherapy. It is also used in cancer patients receiving bone marrow transplant. In general, filgrastim increases neutrophil counts in order to decrease the risk of infection or duration of neutropenia in the aforementioned patient populations. Infection and neutropenia are adverse events associated with chemotherapy. Furthermore, filgrastim is also indicated for patients with severe chronic neutropenia. It mobilizes hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis to allow for a more rapid engraftment. Tbo-filgrastim has a narrower indication profile than Neupogen - it is a leukocyte growth factor indicated for the reduction in the duration of severe neutropenia in patients with non-myeloid malignancies. | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Filgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment, and end cell functional activation. When tbo-filgrastim is administered to cancer patients, it took 3-5 days to reach maximum absolute neutrophil count (ANC). Levels of neutrophils returned to baseline by 21 days following completion of chemotherapy. In the healthy volunteer trials, doubling the tbo-filgrastim subcutaneous dose from 5 to 10 mcg/kg resulted in a 16-19% increase in the ANCmax and a 33-36% increase in the area under the effect curve for ANC. | Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and reduces their maturation time. Filgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, Filgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | The oral LD50 in mouse and rat was >3 mg/kg. The intravenous LD50 in rat was also >3 mg/kg.11 There is limited information regarding filgrastim overdose. The maximum tolerated dose of filgrastim has not been determined. In clinical trials of patients with cancer receiving myelosuppressive chemotherapy‚ white blood cell counts greater than 100,000/mm3 have been reported in less than 5% of patients‚ but were not associated with any reported adverse clinical effects. Patients in the bone marrow transplantation studies received up to 138 mcg/kg/day without toxic effects‚ although there was a flattening of the dose response curve above daily doses of greater than 10 mcg/kg/day | Like other G-CSF compounds, filgrastim is cleared from plasma via neutrophil-mediated clearance involving internalization via G-CSF receptors and degradation within the neutrophil. Filgrastim is also subject to extracellular proteolytic degradation by neutrophil elastase: this enzyme rapidly cleaves filgrastim and renders it inactive | Filgrastim exhibits nonlinear pharmacokinetics. Subcutaneous administration of 3.45 mcg/kg and 11.5 mcg/kg of filgrastim resulted in maximum serum concentrations of 4 and 49 ng/mL‚ respectively‚ within 2 to 8 hours. Continuous 24-hour intravenous infusions of 20 mcg/kg over an 11 to 20-day period produced steady-state serum concentrations of filgrastim with no evidence of drug accumulation. The absolute bioavailability of filgrastim after subcutaneous administration is 60% to 70% | Vd, healthy subjects and cancer patients = 150 mL/kg | Clearance rates of filgrastim were approximately 0.5 to 0.7 mL/minute/kg after intravenous administration. | Amino Acids, Peptides, and Proteins,Antineoplastic and Immunomodulating Agents,Biological Factors,Colony-Stimulating Factors,Glycoconjugates,Glycoproteins,Granulocyte Colony-Stimulating Factors,Hematologic Agents,Hematopoietic Cell Growth Factors,Increased Myeloid Cell Production,Leukocyte Growth Factor,Peptides,Proteins | CA1339071 | 29-Jul-1997 | 29-Jul-2014 | NA | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Nivestim | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10463 | Th1082 | Filgrastim | >Th1082_Filgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S10 | 5.65 | 0.209 | 60 | Elimination half-life, healthy subjects and cancer patients, Neopogen = 3.5 hours | 175 amino acid long, recombinant human granulocyte colony stimulating factor (G-CSF) analogue expressed and purified from a strain of E. coli. Neupogen by Amgen. Amino acid sequence is identical to the natural sequence predicted in human genome, with the exception of an N-terminal methionine to aid expression in E coli. Tbo-filgrastim, which is marketed by Sicor Biotech and FDA approved on August 29, 2012, contains the same active ingredient as Neupogen and is biologically similar, but it is formulated to be short-acting. | Filgrastim is used in patients with acute myeloid leukemia receiving induction or consolidation chemotherapy. It is also used in cancer patients receiving bone marrow transplant. In general, filgrastim increases neutrophil counts in order to decrease the risk of infection or duration of neutropenia in the aforementioned patient populations. Infection and neutropenia are adverse events associated with chemotherapy. Furthermore, filgrastim is also indicated for patients with severe chronic neutropenia. It mobilizes hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis to allow for a more rapid engraftment. Tbo-filgrastim has a narrower indication profile than Neupogen - it is a leukocyte growth factor indicated for the reduction in the duration of severe neutropenia in patients with non-myeloid malignancies. | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Filgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment, and end cell functional activation. When tbo-filgrastim is administered to cancer patients, it took 3-5 days to reach maximum absolute neutrophil count (ANC). Levels of neutrophils returned to baseline by 21 days following completion of chemotherapy. In the healthy volunteer trials, doubling the tbo-filgrastim subcutaneous dose from 5 to 10 mcg/kg resulted in a 16-19% increase in the ANCmax and a 33-36% increase in the area under the effect curve for ANC. | Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and reduces their maturation time. Filgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, Filgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | The oral LD50 in mouse and rat was >3 mg/kg. The intravenous LD50 in rat was also >3 mg/kg.11 There is limited information regarding filgrastim overdose. The maximum tolerated dose of filgrastim has not been determined. In clinical trials of patients with cancer receiving myelosuppressive chemotherapy‚ white blood cell counts greater than 100,000/mm3 have been reported in less than 5% of patients‚ but were not associated with any reported adverse clinical effects. Patients in the bone marrow transplantation studies received up to 138 mcg/kg/day without toxic effects‚ although there was a flattening of the dose response curve above daily doses of greater than 10 mcg/kg/day | Like other G-CSF compounds, filgrastim is cleared from plasma via neutrophil-mediated clearance involving internalization via G-CSF receptors and degradation within the neutrophil. Filgrastim is also subject to extracellular proteolytic degradation by neutrophil elastase: this enzyme rapidly cleaves filgrastim and renders it inactive | Filgrastim exhibits nonlinear pharmacokinetics. Subcutaneous administration of 3.45 mcg/kg and 11.5 mcg/kg of filgrastim resulted in maximum serum concentrations of 4 and 49 ng/mL‚ respectively‚ within 2 to 8 hours. Continuous 24-hour intravenous infusions of 20 mcg/kg over an 11 to 20-day period produced steady-state serum concentrations of filgrastim with no evidence of drug accumulation. The absolute bioavailability of filgrastim after subcutaneous administration is 60% to 70% | Vd, healthy subjects and cancer patients = 150 mL/kg | Clearance rates of filgrastim were approximately 0.5 to 0.7 mL/minute/kg after intravenous administration. | Amino Acids, Peptides, and Proteins,Antineoplastic and Immunomodulating Agents,Biological Factors,Colony-Stimulating Factors,Glycoconjugates,Glycoproteins,Granulocyte Colony-Stimulating Factors,Hematologic Agents,Hematopoietic Cell Growth Factors,Increased Myeloid Cell Production,Leukocyte Growth Factor,Peptides,Proteins | CA1339071 | 29-Jul-1997 | 29-Jul-2014 | NA | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Nivestym | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10464 | Th1082 | Filgrastim | >Th1082_Filgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S10 | 5.65 | 0.209 | 60 | Elimination half-life, healthy subjects and cancer patients, Neopogen = 3.5 hours | 175 amino acid long, recombinant human granulocyte colony stimulating factor (G-CSF) analogue expressed and purified from a strain of E. coli. Neupogen by Amgen. Amino acid sequence is identical to the natural sequence predicted in human genome, with the exception of an N-terminal methionine to aid expression in E coli. Tbo-filgrastim, which is marketed by Sicor Biotech and FDA approved on August 29, 2012, contains the same active ingredient as Neupogen and is biologically similar, but it is formulated to be short-acting. | Filgrastim is used in patients with acute myeloid leukemia receiving induction or consolidation chemotherapy. It is also used in cancer patients receiving bone marrow transplant. In general, filgrastim increases neutrophil counts in order to decrease the risk of infection or duration of neutropenia in the aforementioned patient populations. Infection and neutropenia are adverse events associated with chemotherapy. Furthermore, filgrastim is also indicated for patients with severe chronic neutropenia. It mobilizes hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis to allow for a more rapid engraftment. Tbo-filgrastim has a narrower indication profile than Neupogen - it is a leukocyte growth factor indicated for the reduction in the duration of severe neutropenia in patients with non-myeloid malignancies. | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Filgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment, and end cell functional activation. When tbo-filgrastim is administered to cancer patients, it took 3-5 days to reach maximum absolute neutrophil count (ANC). Levels of neutrophils returned to baseline by 21 days following completion of chemotherapy. In the healthy volunteer trials, doubling the tbo-filgrastim subcutaneous dose from 5 to 10 mcg/kg resulted in a 16-19% increase in the ANCmax and a 33-36% increase in the area under the effect curve for ANC. | Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and reduces their maturation time. Filgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, Filgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | The oral LD50 in mouse and rat was >3 mg/kg. The intravenous LD50 in rat was also >3 mg/kg.11 There is limited information regarding filgrastim overdose. The maximum tolerated dose of filgrastim has not been determined. In clinical trials of patients with cancer receiving myelosuppressive chemotherapy‚ white blood cell counts greater than 100,000/mm3 have been reported in less than 5% of patients‚ but were not associated with any reported adverse clinical effects. Patients in the bone marrow transplantation studies received up to 138 mcg/kg/day without toxic effects‚ although there was a flattening of the dose response curve above daily doses of greater than 10 mcg/kg/day | Like other G-CSF compounds, filgrastim is cleared from plasma via neutrophil-mediated clearance involving internalization via G-CSF receptors and degradation within the neutrophil. Filgrastim is also subject to extracellular proteolytic degradation by neutrophil elastase: this enzyme rapidly cleaves filgrastim and renders it inactive | Filgrastim exhibits nonlinear pharmacokinetics. Subcutaneous administration of 3.45 mcg/kg and 11.5 mcg/kg of filgrastim resulted in maximum serum concentrations of 4 and 49 ng/mL‚ respectively‚ within 2 to 8 hours. Continuous 24-hour intravenous infusions of 20 mcg/kg over an 11 to 20-day period produced steady-state serum concentrations of filgrastim with no evidence of drug accumulation. The absolute bioavailability of filgrastim after subcutaneous administration is 60% to 70% | Vd, healthy subjects and cancer patients = 150 mL/kg | Clearance rates of filgrastim were approximately 0.5 to 0.7 mL/minute/kg after intravenous administration. | Amino Acids, Peptides, and Proteins,Antineoplastic and Immunomodulating Agents,Biological Factors,Colony-Stimulating Factors,Glycoconjugates,Glycoproteins,Granulocyte Colony-Stimulating Factors,Hematologic Agents,Hematopoietic Cell Growth Factors,Increased Myeloid Cell Production,Leukocyte Growth Factor,Peptides,Proteins | CA1339071 | 29-Jul-1997 | 29-Jul-2014 | NA | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Nypozi | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10465 | Th1082 | Filgrastim | >Th1082_Filgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S10 | 5.65 | 0.209 | 60 | Elimination half-life, healthy subjects and cancer patients, Neopogen = 3.5 hours | 175 amino acid long, recombinant human granulocyte colony stimulating factor (G-CSF) analogue expressed and purified from a strain of E. coli. Neupogen by Amgen. Amino acid sequence is identical to the natural sequence predicted in human genome, with the exception of an N-terminal methionine to aid expression in E coli. Tbo-filgrastim, which is marketed by Sicor Biotech and FDA approved on August 29, 2012, contains the same active ingredient as Neupogen and is biologically similar, but it is formulated to be short-acting. | Filgrastim is used in patients with acute myeloid leukemia receiving induction or consolidation chemotherapy. It is also used in cancer patients receiving bone marrow transplant. In general, filgrastim increases neutrophil counts in order to decrease the risk of infection or duration of neutropenia in the aforementioned patient populations. Infection and neutropenia are adverse events associated with chemotherapy. Furthermore, filgrastim is also indicated for patients with severe chronic neutropenia. It mobilizes hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis to allow for a more rapid engraftment. Tbo-filgrastim has a narrower indication profile than Neupogen - it is a leukocyte growth factor indicated for the reduction in the duration of severe neutropenia in patients with non-myeloid malignancies. | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Filgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment, and end cell functional activation. When tbo-filgrastim is administered to cancer patients, it took 3-5 days to reach maximum absolute neutrophil count (ANC). Levels of neutrophils returned to baseline by 21 days following completion of chemotherapy. In the healthy volunteer trials, doubling the tbo-filgrastim subcutaneous dose from 5 to 10 mcg/kg resulted in a 16-19% increase in the ANCmax and a 33-36% increase in the area under the effect curve for ANC. | Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and reduces their maturation time. Filgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, Filgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | The oral LD50 in mouse and rat was >3 mg/kg. The intravenous LD50 in rat was also >3 mg/kg.11 There is limited information regarding filgrastim overdose. The maximum tolerated dose of filgrastim has not been determined. In clinical trials of patients with cancer receiving myelosuppressive chemotherapy‚ white blood cell counts greater than 100,000/mm3 have been reported in less than 5% of patients‚ but were not associated with any reported adverse clinical effects. Patients in the bone marrow transplantation studies received up to 138 mcg/kg/day without toxic effects‚ although there was a flattening of the dose response curve above daily doses of greater than 10 mcg/kg/day | Like other G-CSF compounds, filgrastim is cleared from plasma via neutrophil-mediated clearance involving internalization via G-CSF receptors and degradation within the neutrophil. Filgrastim is also subject to extracellular proteolytic degradation by neutrophil elastase: this enzyme rapidly cleaves filgrastim and renders it inactive | Filgrastim exhibits nonlinear pharmacokinetics. Subcutaneous administration of 3.45 mcg/kg and 11.5 mcg/kg of filgrastim resulted in maximum serum concentrations of 4 and 49 ng/mL‚ respectively‚ within 2 to 8 hours. Continuous 24-hour intravenous infusions of 20 mcg/kg over an 11 to 20-day period produced steady-state serum concentrations of filgrastim with no evidence of drug accumulation. The absolute bioavailability of filgrastim after subcutaneous administration is 60% to 70% | Vd, healthy subjects and cancer patients = 150 mL/kg | Clearance rates of filgrastim were approximately 0.5 to 0.7 mL/minute/kg after intravenous administration. | Amino Acids, Peptides, and Proteins,Antineoplastic and Immunomodulating Agents,Biological Factors,Colony-Stimulating Factors,Glycoconjugates,Glycoproteins,Granulocyte Colony-Stimulating Factors,Hematologic Agents,Hematopoietic Cell Growth Factors,Increased Myeloid Cell Production,Leukocyte Growth Factor,Peptides,Proteins | CA1339071 | 29-Jul-1997 | 29-Jul-2014 | NA | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Ratiograstim | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10466 | Th1082 | Filgrastim | >Th1082_Filgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S10 | 5.65 | 0.209 | 60 | Elimination half-life, healthy subjects and cancer patients, Neopogen = 3.5 hours | 175 amino acid long, recombinant human granulocyte colony stimulating factor (G-CSF) analogue expressed and purified from a strain of E. coli. Neupogen by Amgen. Amino acid sequence is identical to the natural sequence predicted in human genome, with the exception of an N-terminal methionine to aid expression in E coli. Tbo-filgrastim, which is marketed by Sicor Biotech and FDA approved on August 29, 2012, contains the same active ingredient as Neupogen and is biologically similar, but it is formulated to be short-acting. | Filgrastim is used in patients with acute myeloid leukemia receiving induction or consolidation chemotherapy. It is also used in cancer patients receiving bone marrow transplant. In general, filgrastim increases neutrophil counts in order to decrease the risk of infection or duration of neutropenia in the aforementioned patient populations. Infection and neutropenia are adverse events associated with chemotherapy. Furthermore, filgrastim is also indicated for patients with severe chronic neutropenia. It mobilizes hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis to allow for a more rapid engraftment. Tbo-filgrastim has a narrower indication profile than Neupogen - it is a leukocyte growth factor indicated for the reduction in the duration of severe neutropenia in patients with non-myeloid malignancies. | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Filgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment, and end cell functional activation. When tbo-filgrastim is administered to cancer patients, it took 3-5 days to reach maximum absolute neutrophil count (ANC). Levels of neutrophils returned to baseline by 21 days following completion of chemotherapy. In the healthy volunteer trials, doubling the tbo-filgrastim subcutaneous dose from 5 to 10 mcg/kg resulted in a 16-19% increase in the ANCmax and a 33-36% increase in the area under the effect curve for ANC. | Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and reduces their maturation time. Filgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, Filgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | The oral LD50 in mouse and rat was >3 mg/kg. The intravenous LD50 in rat was also >3 mg/kg.11 There is limited information regarding filgrastim overdose. The maximum tolerated dose of filgrastim has not been determined. In clinical trials of patients with cancer receiving myelosuppressive chemotherapy‚ white blood cell counts greater than 100,000/mm3 have been reported in less than 5% of patients‚ but were not associated with any reported adverse clinical effects. Patients in the bone marrow transplantation studies received up to 138 mcg/kg/day without toxic effects‚ although there was a flattening of the dose response curve above daily doses of greater than 10 mcg/kg/day | Like other G-CSF compounds, filgrastim is cleared from plasma via neutrophil-mediated clearance involving internalization via G-CSF receptors and degradation within the neutrophil. Filgrastim is also subject to extracellular proteolytic degradation by neutrophil elastase: this enzyme rapidly cleaves filgrastim and renders it inactive | Filgrastim exhibits nonlinear pharmacokinetics. Subcutaneous administration of 3.45 mcg/kg and 11.5 mcg/kg of filgrastim resulted in maximum serum concentrations of 4 and 49 ng/mL‚ respectively‚ within 2 to 8 hours. Continuous 24-hour intravenous infusions of 20 mcg/kg over an 11 to 20-day period produced steady-state serum concentrations of filgrastim with no evidence of drug accumulation. The absolute bioavailability of filgrastim after subcutaneous administration is 60% to 70% | Vd, healthy subjects and cancer patients = 150 mL/kg | Clearance rates of filgrastim were approximately 0.5 to 0.7 mL/minute/kg after intravenous administration. | Amino Acids, Peptides, and Proteins,Antineoplastic and Immunomodulating Agents,Biological Factors,Colony-Stimulating Factors,Glycoconjugates,Glycoproteins,Granulocyte Colony-Stimulating Factors,Hematologic Agents,Hematopoietic Cell Growth Factors,Increased Myeloid Cell Production,Leukocyte Growth Factor,Peptides,Proteins | CA1339071 | 29-Jul-1997 | 29-Jul-2014 | NA | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Tevagrastim | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10467 | Th1082 | Filgrastim | >Th1082_Filgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S10 | 5.65 | 0.209 | 60 | Elimination half-life, healthy subjects and cancer patients, Neopogen = 3.5 hours | 175 amino acid long, recombinant human granulocyte colony stimulating factor (G-CSF) analogue expressed and purified from a strain of E. coli. Neupogen by Amgen. Amino acid sequence is identical to the natural sequence predicted in human genome, with the exception of an N-terminal methionine to aid expression in E coli. Tbo-filgrastim, which is marketed by Sicor Biotech and FDA approved on August 29, 2012, contains the same active ingredient as Neupogen and is biologically similar, but it is formulated to be short-acting. | Filgrastim is used in patients with acute myeloid leukemia receiving induction or consolidation chemotherapy. It is also used in cancer patients receiving bone marrow transplant. In general, filgrastim increases neutrophil counts in order to decrease the risk of infection or duration of neutropenia in the aforementioned patient populations. Infection and neutropenia are adverse events associated with chemotherapy. Furthermore, filgrastim is also indicated for patients with severe chronic neutropenia. It mobilizes hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis to allow for a more rapid engraftment. Tbo-filgrastim has a narrower indication profile than Neupogen - it is a leukocyte growth factor indicated for the reduction in the duration of severe neutropenia in patients with non-myeloid malignancies. | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Filgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment, and end cell functional activation. When tbo-filgrastim is administered to cancer patients, it took 3-5 days to reach maximum absolute neutrophil count (ANC). Levels of neutrophils returned to baseline by 21 days following completion of chemotherapy. In the healthy volunteer trials, doubling the tbo-filgrastim subcutaneous dose from 5 to 10 mcg/kg resulted in a 16-19% increase in the ANCmax and a 33-36% increase in the area under the effect curve for ANC. | Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and reduces their maturation time. Filgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, Filgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | The oral LD50 in mouse and rat was >3 mg/kg. The intravenous LD50 in rat was also >3 mg/kg.11 There is limited information regarding filgrastim overdose. The maximum tolerated dose of filgrastim has not been determined. In clinical trials of patients with cancer receiving myelosuppressive chemotherapy‚ white blood cell counts greater than 100,000/mm3 have been reported in less than 5% of patients‚ but were not associated with any reported adverse clinical effects. Patients in the bone marrow transplantation studies received up to 138 mcg/kg/day without toxic effects‚ although there was a flattening of the dose response curve above daily doses of greater than 10 mcg/kg/day | Like other G-CSF compounds, filgrastim is cleared from plasma via neutrophil-mediated clearance involving internalization via G-CSF receptors and degradation within the neutrophil. Filgrastim is also subject to extracellular proteolytic degradation by neutrophil elastase: this enzyme rapidly cleaves filgrastim and renders it inactive | Filgrastim exhibits nonlinear pharmacokinetics. Subcutaneous administration of 3.45 mcg/kg and 11.5 mcg/kg of filgrastim resulted in maximum serum concentrations of 4 and 49 ng/mL‚ respectively‚ within 2 to 8 hours. Continuous 24-hour intravenous infusions of 20 mcg/kg over an 11 to 20-day period produced steady-state serum concentrations of filgrastim with no evidence of drug accumulation. The absolute bioavailability of filgrastim after subcutaneous administration is 60% to 70% | Vd, healthy subjects and cancer patients = 150 mL/kg | Clearance rates of filgrastim were approximately 0.5 to 0.7 mL/minute/kg after intravenous administration. | Amino Acids, Peptides, and Proteins,Antineoplastic and Immunomodulating Agents,Biological Factors,Colony-Stimulating Factors,Glycoconjugates,Glycoproteins,Granulocyte Colony-Stimulating Factors,Hematologic Agents,Hematopoietic Cell Growth Factors,Increased Myeloid Cell Production,Leukocyte Growth Factor,Peptides,Proteins | CA1339071 | 29-Jul-1997 | 29-Jul-2014 | NA | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Zarxio | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10468 | Th1082 | Filgrastim | >Th1082_Filgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S10 | 5.65 | 0.209 | 60 | Elimination half-life, healthy subjects and cancer patients, Neopogen = 3.5 hours | 175 amino acid long, recombinant human granulocyte colony stimulating factor (G-CSF) analogue expressed and purified from a strain of E. coli. Neupogen by Amgen. Amino acid sequence is identical to the natural sequence predicted in human genome, with the exception of an N-terminal methionine to aid expression in E coli. Tbo-filgrastim, which is marketed by Sicor Biotech and FDA approved on August 29, 2012, contains the same active ingredient as Neupogen and is biologically similar, but it is formulated to be short-acting. | Filgrastim is used in patients with acute myeloid leukemia receiving induction or consolidation chemotherapy. It is also used in cancer patients receiving bone marrow transplant. In general, filgrastim increases neutrophil counts in order to decrease the risk of infection or duration of neutropenia in the aforementioned patient populations. Infection and neutropenia are adverse events associated with chemotherapy. Furthermore, filgrastim is also indicated for patients with severe chronic neutropenia. It mobilizes hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis to allow for a more rapid engraftment. Tbo-filgrastim has a narrower indication profile than Neupogen - it is a leukocyte growth factor indicated for the reduction in the duration of severe neutropenia in patients with non-myeloid malignancies. | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Filgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment, and end cell functional activation. When tbo-filgrastim is administered to cancer patients, it took 3-5 days to reach maximum absolute neutrophil count (ANC). Levels of neutrophils returned to baseline by 21 days following completion of chemotherapy. In the healthy volunteer trials, doubling the tbo-filgrastim subcutaneous dose from 5 to 10 mcg/kg resulted in a 16-19% increase in the ANCmax and a 33-36% increase in the area under the effect curve for ANC. | Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and reduces their maturation time. Filgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, Filgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | The oral LD50 in mouse and rat was >3 mg/kg. The intravenous LD50 in rat was also >3 mg/kg.11 There is limited information regarding filgrastim overdose. The maximum tolerated dose of filgrastim has not been determined. In clinical trials of patients with cancer receiving myelosuppressive chemotherapy‚ white blood cell counts greater than 100,000/mm3 have been reported in less than 5% of patients‚ but were not associated with any reported adverse clinical effects. Patients in the bone marrow transplantation studies received up to 138 mcg/kg/day without toxic effects‚ although there was a flattening of the dose response curve above daily doses of greater than 10 mcg/kg/day | Like other G-CSF compounds, filgrastim is cleared from plasma via neutrophil-mediated clearance involving internalization via G-CSF receptors and degradation within the neutrophil. Filgrastim is also subject to extracellular proteolytic degradation by neutrophil elastase: this enzyme rapidly cleaves filgrastim and renders it inactive | Filgrastim exhibits nonlinear pharmacokinetics. Subcutaneous administration of 3.45 mcg/kg and 11.5 mcg/kg of filgrastim resulted in maximum serum concentrations of 4 and 49 ng/mL‚ respectively‚ within 2 to 8 hours. Continuous 24-hour intravenous infusions of 20 mcg/kg over an 11 to 20-day period produced steady-state serum concentrations of filgrastim with no evidence of drug accumulation. The absolute bioavailability of filgrastim after subcutaneous administration is 60% to 70% | Vd, healthy subjects and cancer patients = 150 mL/kg | Clearance rates of filgrastim were approximately 0.5 to 0.7 mL/minute/kg after intravenous administration. | Amino Acids, Peptides, and Proteins,Antineoplastic and Immunomodulating Agents,Biological Factors,Colony-Stimulating Factors,Glycoconjugates,Glycoproteins,Granulocyte Colony-Stimulating Factors,Hematologic Agents,Hematopoietic Cell Growth Factors,Increased Myeloid Cell Production,Leukocyte Growth Factor,Peptides,Proteins | CA1339071 | 29-Jul-1997 | 29-Jul-2014 | NA | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Zarzio | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10484 | Th1091 | Bevacizumab | >Th1091_Bevacizumab EVQLVESGGGLVQPGGSLRLSCAASGYTFTNYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPHYYGSSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6538H10034N1716O2033S44 | NA | NA | 61 (FAB fr | 20 days (range of 11-50 days) | Recombinant (derived from CHO-gentamycin), humanized, monoclonal IgG1 antibody. It Inhibits the biologic activity of human vascular endothelial growth factor (VEGF) by binding to it. Comprises human framework regions and murine complementarity-determining regions. | As part of combination therapy for metastatic colorectal cancer and HER2-negative metastatic breast cancer. | Bevacizumab prevents or reduces the formation of blood vessels (angiogenesis) thereby preventing or reducing metatstatic disease progressing. Bevacizumab binds VEGF and prevents vascular endothelial growth and endothelial cell proliferation. | Bevacizumab binds VEGF and prevents the interaction of VEGF to its receptors (Flt-1 and KDR) on the surface of endothelial cells. This prevents blood vessel proliferation and tumour metastasis. | Bevacizumab toxicities are distinct from the effects of cytotoxic agents used in chemotherapy, and are normally linked to impaired VEGF function.18,19 Common toxicities associated with bevacizumab include hypertension, gastrointestinal perforation, arterial thromboembolism, reversible posterior leukoencephalopathy syndrome (RPLS), venous thromboembolism, proteinuria, bleeding/hemorrhage, and wound-healing complications | There are several pathways through which monoclonal antibodies (mAbs) may be cleared. Non-specific clearance of mAbs refers to target independent pinocytosis, and proteolysis of the protein into small amino acids and peptides in the reticuloendothelial system (RES) and the liver. Target-mediated clearance is a result of specific interactions between the mAb and its target antigen. Once bound, the antibody-antigen complex may be cleared via lysosomal degradation. Additionally, the production of anti-drug antibodies (ADA), which are a result of an immunogenic response to mAb-based treatment, can form complexes with mAb’s and may impact the rate of mAb clearance | Monoclonal antibodies (mAbs) are large in size, do not readily cross cell membranes, and are unable to withstand proteolysis in the gastrointestinal tract.Given these characteristics, mAbs are poorly absorbed via the oral route and are instead administered intravenously, intramuscularly or subcutaneously.In a single dose (1mg/kg) pharmacokinetic study assessing the bioequivalence of bevacizumab and TAB008 (a biosimilar product), the pharmacokinetic parameters of Avastin (bevacizumab) were as follows: Geometric mean Cmax = 17.38 ug/mL Geometric mean AUCinf = 5,358 ugxh/mL Geometric mean Tmax = 2.50 hrs | The volume of distribution of bevacizumab is approximately 3.29 L and 2.39 L for the average male and female, respectively. | The clearance (CL) of bevacizumab is approximately 0.207 L/day. The CL of bevacizumab can increase or decrease by 30% in patients who weigh >114 kg or <49 kg respectively. Males tend to clear bevacizumab at a faster rate than females (26% faster on average). Other factors including alkaline phosphatase (ALP), serum aspartate aminotransferase (AST), serum albumin, and tumor burden may cause the CL to fluctuate | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Cardiotoxic antineoplastic agents,Experimental Unapproved Treatments for COVID-19,Globulins,Growth Inhibitors,Immunoglobulins,Immunoproteins,Immunotherapy,Narrow Therapeutic Index Drugs,Proteins,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors,Vascular Endothelial Growth Factor-directed Antibody Interactions | CA2286330 | 10-Jun-2008 | 3-Apr-2018 | NA | Vascular endothelial growth factor A,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c | Avastin | Genentech | Genentech | Metastatic Colorectal Cancer (mCRC): Avastin is indicated for the first- or second-line treatment of patients with metastatic carcinoma of the colon or rectum. Non-Squamous Non-Small Cell Lung Cancer (NSCLC), glioblastoma with progressive disease in adult patients. Metastatic Renal Cell Carcinoma (mRCC): Avastin is indicated for the treatment of metastatic renal cell carcinoma in combination with interferon alfa. Persistent, Recurrent, Or Metastatic Carcinoma Of The Cervix: Avastin in combination with paclitaxel and cisplatin or paclitaxel and topotecan is indicated for the treatment of persistent, recurrent, or metastatic carcinoma of the cervix. | NA | 100 mg product is formulated in 240 mg a,a-trehalose dihydrate, 23.2 mg sodium phosphate (monobasic, monohydrate), 4.8 mg sodium phosphate (dibasic, anhydrous), 1.6 mg polysorbate 20, and Water for Injection, USP. The 400 mg product is formulated in 960 mg a,a-trehalose dihydrate, 92.8 mg sodium phosphate (monobasic, monohydrate), 19.2 mg sodium phosphate (dibasic, anhydrous), 6.4 mg polysorbate 20, and Water for Injection, USP. | Slightly opalescent, colorless to pale brown, sterile, pH 6.2 solution | Intravenous infusion | First infusion: Administer infusion over 90 minutes. Subsequent infusions: Administer second infusion over 60 minutes if first infusion is tolerated; Recommended Doses And Schedules: Metastatic Colorectal Cancer (mCRC).The recommended doses are 5 mg/kg or 10 mg/kg every 2 weeks when used in combination with intravenous 5-FU-based chemotherapy. Administer 5 mg/kg when used in combination with bolus-IFL. Administer 10 mg/kg when used in combination with FOLFOX4. Administer 5 mg/kg every 2 weeks or 7.5 mg/kg every 3 weeks when used in combination with a fluoropyrimidine-irinotecan or fluoropyrimidine-oxaliplatin based chemotherapy regimen in patients who have progressed on a first-line Avastin-containing regimen. Non-Squamous Non-Small Cell Lung Cancer (NSCLC): The recommended dose is 15 mg/kg every 3 weeks in combination with carboplatin and paclitaxel. Glioblastoma: The recommended dose is 10 mg/kg every 2 weeks. Metastatic Renal Cell Carcinoma (mRCC): The recommended dose is 10 mg/kg every 2 weeks in combination with interferon alfa. Cervical Cancer: The recommended dose of Avastin is 15 mg/kg every 3 weeks as an Intravenous infusion administered in combination with one of the following chemotherapy regimens: paclitaxel and cisplatin, or paclitaxel and topotecan. | Do not administer as an intravenous push or bolus. Administer only as an intravenous (IV) infusion.. Do not initiate Avastin until at least 28 days following major surgery. Administer Avastin after the surgical incision has fully healed. | headache, confusion, vision problems, feeling very weak or tired, fainting, and seizure (blackout or convulsions) | Link | NA | NA |
| 10485 | Th1091 | Bevacizumab | >Th1091_Bevacizumab EVQLVESGGGLVQPGGSLRLSCAASGYTFTNYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPHYYGSSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6538H10034N1716O2033S45 | NA | NA | 62 (FAB fr | 20 days (range of 11-50 days) | Recombinant (derived from CHO-gentamycin), humanized, monoclonal IgG1 antibody. It Inhibits the biologic activity of human vascular endothelial growth factor (VEGF) by binding to it. Comprises human framework regions and murine complementarity-determining regions. | As part of combination therapy for metastatic colorectal cancer and HER2-negative metastatic breast cancer. | Bevacizumab prevents or reduces the formation of blood vessels (angiogenesis) thereby preventing or reducing metatstatic disease progressing. Bevacizumab binds VEGF and prevents vascular endothelial growth and endothelial cell proliferation. | Bevacizumab binds VEGF and prevents the interaction of VEGF to its receptors (Flt-1 and KDR) on the surface of endothelial cells. This prevents blood vessel proliferation and tumour metastasis. | Bevacizumab toxicities are distinct from the effects of cytotoxic agents used in chemotherapy, and are normally linked to impaired VEGF function.18,19 Common toxicities associated with bevacizumab include hypertension, gastrointestinal perforation, arterial thromboembolism, reversible posterior leukoencephalopathy syndrome (RPLS), venous thromboembolism, proteinuria, bleeding/hemorrhage, and wound-healing complications | There are several pathways through which monoclonal antibodies (mAbs) may be cleared. Non-specific clearance of mAbs refers to target independent pinocytosis, and proteolysis of the protein into small amino acids and peptides in the reticuloendothelial system (RES) and the liver. Target-mediated clearance is a result of specific interactions between the mAb and its target antigen. Once bound, the antibody-antigen complex may be cleared via lysosomal degradation. Additionally, the production of anti-drug antibodies (ADA), which are a result of an immunogenic response to mAb-based treatment, can form complexes with mAb’s and may impact the rate of mAb clearance | Monoclonal antibodies (mAbs) are large in size, do not readily cross cell membranes, and are unable to withstand proteolysis in the gastrointestinal tract. Given these characteristics, mAbs are poorly absorbed via the oral route and are instead administered intravenously, intramuscularly or subcutaneously. In a single dose (1mg/kg) pharmacokinetic study assessing the bioequivalence of bevacizumab and TAB008 (a biosimilar product), the pharmacokinetic parameters of Avastin (bevacizumab) were as follows20: Geometric mean Cmax = 17.38 ug/mL Geometric mean AUCinf = 5,358 ugxh/mL Geometric mean Tmax = 2.50 hrs | The volume of distribution of bevacizumab is approximately 3.29 L and 2.39 L for the average male and female, respectively. | The clearance (CL) of bevacizumab is approximately 0.207 L/day. The CL of bevacizumab can increase or decrease by 30% in patients who weigh >114 kg or <49 kg respectively. Males tend to clear bevacizumab at a faster rate than females (26% faster on average). Other factors including alkaline phosphatase (ALP), serum aspartate aminotransferase (AST), serum albumin, and tumor burden may cause the CL to fluctuate | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Cardiotoxic antineoplastic agents,Experimental Unapproved Treatments for COVID-19,Globulins,Growth Inhibitors,Immunoglobulins,Immunoproteins,Immunotherapy,Narrow Therapeutic Index Drugs,Proteins,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors,Vascular Endothelial Growth Factor-directed Antibody Interactions | CA2145985 | 16-Sep-2003 | 28-Oct-2012 | NA | Vascular endothelial growth factor A,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c | Abevmy | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10486 | Th1091 | Bevacizumab | >Th1091_Bevacizumab EVQLVESGGGLVQPGGSLRLSCAASGYTFTNYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPHYYGSSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6538H10034N1716O2033S45 | NA | NA | 62 (FAB fr | 20 days (range of 11-50 days) | Recombinant (derived from CHO-gentamycin), humanized, monoclonal IgG1 antibody. It Inhibits the biologic activity of human vascular endothelial growth factor (VEGF) by binding to it. Comprises human framework regions and murine complementarity-determining regions. | As part of combination therapy for metastatic colorectal cancer and HER2-negative metastatic breast cancer. | Bevacizumab prevents or reduces the formation of blood vessels (angiogenesis) thereby preventing or reducing metatstatic disease progressing. Bevacizumab binds VEGF and prevents vascular endothelial growth and endothelial cell proliferation. | Bevacizumab binds VEGF and prevents the interaction of VEGF to its receptors (Flt-1 and KDR) on the surface of endothelial cells. This prevents blood vessel proliferation and tumour metastasis. | Bevacizumab toxicities are distinct from the effects of cytotoxic agents used in chemotherapy, and are normally linked to impaired VEGF function.18,19 Common toxicities associated with bevacizumab include hypertension, gastrointestinal perforation, arterial thromboembolism, reversible posterior leukoencephalopathy syndrome (RPLS), venous thromboembolism, proteinuria, bleeding/hemorrhage, and wound-healing complications | There are several pathways through which monoclonal antibodies (mAbs) may be cleared. Non-specific clearance of mAbs refers to target independent pinocytosis, and proteolysis of the protein into small amino acids and peptides in the reticuloendothelial system (RES) and the liver. Target-mediated clearance is a result of specific interactions between the mAb and its target antigen. Once bound, the antibody-antigen complex may be cleared via lysosomal degradation. Additionally, the production of anti-drug antibodies (ADA), which are a result of an immunogenic response to mAb-based treatment, can form complexes with mAb’s and may impact the rate of mAb clearance | Monoclonal antibodies (mAbs) are large in size, do not readily cross cell membranes, and are unable to withstand proteolysis in the gastrointestinal tract. Given these characteristics, mAbs are poorly absorbed via the oral route and are instead administered intravenously, intramuscularly or subcutaneously. In a single dose (1mg/kg) pharmacokinetic study assessing the bioequivalence of bevacizumab and TAB008 (a biosimilar product), the pharmacokinetic parameters of Avastin (bevacizumab) were as follows20: Geometric mean Cmax = 17.38 ug/mL Geometric mean AUCinf = 5,358 ugxh/mL Geometric mean Tmax = 2.50 hrs | The volume of distribution of bevacizumab is approximately 3.29 L and 2.39 L for the average male and female, respectively. | The clearance (CL) of bevacizumab is approximately 0.207 L/day. The CL of bevacizumab can increase or decrease by 30% in patients who weigh >114 kg or <49 kg respectively. Males tend to clear bevacizumab at a faster rate than females (26% faster on average). Other factors including alkaline phosphatase (ALP), serum aspartate aminotransferase (AST), serum albumin, and tumor burden may cause the CL to fluctuate | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Cardiotoxic antineoplastic agents,Experimental Unapproved Treatments for COVID-19,Globulins,Growth Inhibitors,Immunoglobulins,Immunoproteins,Immunotherapy,Narrow Therapeutic Index Drugs,Proteins,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors,Vascular Endothelial Growth Factor-directed Antibody Interactions | CA2145985 | 16-Sep-2003 | 28-Oct-2012 | NA | Vascular endothelial growth factor A,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c | Alymsys | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10487 | Th1091 | Bevacizumab | >Th1091_Bevacizumab EVQLVESGGGLVQPGGSLRLSCAASGYTFTNYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPHYYGSSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6538H10034N1716O2033S45 | NA | NA | 62 (FAB fr | 20 days (range of 11-50 days) | Recombinant (derived from CHO-gentamycin), humanized, monoclonal IgG1 antibody. It Inhibits the biologic activity of human vascular endothelial growth factor (VEGF) by binding to it. Comprises human framework regions and murine complementarity-determining regions. | As part of combination therapy for metastatic colorectal cancer and HER2-negative metastatic breast cancer. | Bevacizumab prevents or reduces the formation of blood vessels (angiogenesis) thereby preventing or reducing metatstatic disease progressing. Bevacizumab binds VEGF and prevents vascular endothelial growth and endothelial cell proliferation. | Bevacizumab binds VEGF and prevents the interaction of VEGF to its receptors (Flt-1 and KDR) on the surface of endothelial cells. This prevents blood vessel proliferation and tumour metastasis. | Bevacizumab toxicities are distinct from the effects of cytotoxic agents used in chemotherapy, and are normally linked to impaired VEGF function.18,19 Common toxicities associated with bevacizumab include hypertension, gastrointestinal perforation, arterial thromboembolism, reversible posterior leukoencephalopathy syndrome (RPLS), venous thromboembolism, proteinuria, bleeding/hemorrhage, and wound-healing complications | There are several pathways through which monoclonal antibodies (mAbs) may be cleared. Non-specific clearance of mAbs refers to target independent pinocytosis, and proteolysis of the protein into small amino acids and peptides in the reticuloendothelial system (RES) and the liver. Target-mediated clearance is a result of specific interactions between the mAb and its target antigen. Once bound, the antibody-antigen complex may be cleared via lysosomal degradation. Additionally, the production of anti-drug antibodies (ADA), which are a result of an immunogenic response to mAb-based treatment, can form complexes with mAb’s and may impact the rate of mAb clearance | Monoclonal antibodies (mAbs) are large in size, do not readily cross cell membranes, and are unable to withstand proteolysis in the gastrointestinal tract. Given these characteristics, mAbs are poorly absorbed via the oral route and are instead administered intravenously, intramuscularly or subcutaneously. In a single dose (1mg/kg) pharmacokinetic study assessing the bioequivalence of bevacizumab and TAB008 (a biosimilar product), the pharmacokinetic parameters of Avastin (bevacizumab) were as follows20: Geometric mean Cmax = 17.38 ug/mL Geometric mean AUCinf = 5,358 ugxh/mL Geometric mean Tmax = 2.50 hrs | The volume of distribution of bevacizumab is approximately 3.29 L and 2.39 L for the average male and female, respectively. | The clearance (CL) of bevacizumab is approximately 0.207 L/day. The CL of bevacizumab can increase or decrease by 30% in patients who weigh >114 kg or <49 kg respectively. Males tend to clear bevacizumab at a faster rate than females (26% faster on average). Other factors including alkaline phosphatase (ALP), serum aspartate aminotransferase (AST), serum albumin, and tumor burden may cause the CL to fluctuate | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Cardiotoxic antineoplastic agents,Experimental Unapproved Treatments for COVID-19,Globulins,Growth Inhibitors,Immunoglobulins,Immunoproteins,Immunotherapy,Narrow Therapeutic Index Drugs,Proteins,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors,Vascular Endothelial Growth Factor-directed Antibody Interactions | CA2145985 | 16-Sep-2003 | 28-Oct-2012 | NA | Vascular endothelial growth factor A,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c | Aybintio | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10488 | Th1091 | Bevacizumab | >Th1091_Bevacizumab EVQLVESGGGLVQPGGSLRLSCAASGYTFTNYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPHYYGSSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6538H10034N1716O2033S45 | NA | NA | 62 (FAB fr | 20 days (range of 11-50 days) | Recombinant (derived from CHO-gentamycin), humanized, monoclonal IgG1 antibody. It Inhibits the biologic activity of human vascular endothelial growth factor (VEGF) by binding to it. Comprises human framework regions and murine complementarity-determining regions. | As part of combination therapy for metastatic colorectal cancer and HER2-negative metastatic breast cancer. | Bevacizumab prevents or reduces the formation of blood vessels (angiogenesis) thereby preventing or reducing metatstatic disease progressing. Bevacizumab binds VEGF and prevents vascular endothelial growth and endothelial cell proliferation. | Bevacizumab binds VEGF and prevents the interaction of VEGF to its receptors (Flt-1 and KDR) on the surface of endothelial cells. This prevents blood vessel proliferation and tumour metastasis. | Bevacizumab toxicities are distinct from the effects of cytotoxic agents used in chemotherapy, and are normally linked to impaired VEGF function.18,19 Common toxicities associated with bevacizumab include hypertension, gastrointestinal perforation, arterial thromboembolism, reversible posterior leukoencephalopathy syndrome (RPLS), venous thromboembolism, proteinuria, bleeding/hemorrhage, and wound-healing complications | There are several pathways through which monoclonal antibodies (mAbs) may be cleared. Non-specific clearance of mAbs refers to target independent pinocytosis, and proteolysis of the protein into small amino acids and peptides in the reticuloendothelial system (RES) and the liver. Target-mediated clearance is a result of specific interactions between the mAb and its target antigen. Once bound, the antibody-antigen complex may be cleared via lysosomal degradation. Additionally, the production of anti-drug antibodies (ADA), which are a result of an immunogenic response to mAb-based treatment, can form complexes with mAb’s and may impact the rate of mAb clearance | Monoclonal antibodies (mAbs) are large in size, do not readily cross cell membranes, and are unable to withstand proteolysis in the gastrointestinal tract. Given these characteristics, mAbs are poorly absorbed via the oral route and are instead administered intravenously, intramuscularly or subcutaneously. In a single dose (1mg/kg) pharmacokinetic study assessing the bioequivalence of bevacizumab and TAB008 (a biosimilar product), the pharmacokinetic parameters of Avastin (bevacizumab) were as follows20: Geometric mean Cmax = 17.38 ug/mL Geometric mean AUCinf = 5,358 ugxh/mL Geometric mean Tmax = 2.50 hrs | The volume of distribution of bevacizumab is approximately 3.29 L and 2.39 L for the average male and female, respectively. | The clearance (CL) of bevacizumab is approximately 0.207 L/day. The CL of bevacizumab can increase or decrease by 30% in patients who weigh >114 kg or <49 kg respectively. Males tend to clear bevacizumab at a faster rate than females (26% faster on average). Other factors including alkaline phosphatase (ALP), serum aspartate aminotransferase (AST), serum albumin, and tumor burden may cause the CL to fluctuate | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Cardiotoxic antineoplastic agents,Experimental Unapproved Treatments for COVID-19,Globulins,Growth Inhibitors,Immunoglobulins,Immunoproteins,Immunotherapy,Narrow Therapeutic Index Drugs,Proteins,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors,Vascular Endothelial Growth Factor-directed Antibody Interactions | CA2145985 | 16-Sep-2003 | 28-Oct-2012 | NA | Vascular endothelial growth factor A,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c | Bambevi | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10489 | Th1091 | Bevacizumab | >Th1091_Bevacizumab EVQLVESGGGLVQPGGSLRLSCAASGYTFTNYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPHYYGSSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6538H10034N1716O2033S45 | NA | NA | 62 (FAB fr | 20 days (range of 11-50 days) | Recombinant (derived from CHO-gentamycin), humanized, monoclonal IgG1 antibody. It Inhibits the biologic activity of human vascular endothelial growth factor (VEGF) by binding to it. Comprises human framework regions and murine complementarity-determining regions. | As part of combination therapy for metastatic colorectal cancer and HER2-negative metastatic breast cancer. | Bevacizumab prevents or reduces the formation of blood vessels (angiogenesis) thereby preventing or reducing metatstatic disease progressing. Bevacizumab binds VEGF and prevents vascular endothelial growth and endothelial cell proliferation. | Bevacizumab binds VEGF and prevents the interaction of VEGF to its receptors (Flt-1 and KDR) on the surface of endothelial cells. This prevents blood vessel proliferation and tumour metastasis. | Bevacizumab toxicities are distinct from the effects of cytotoxic agents used in chemotherapy, and are normally linked to impaired VEGF function.18,19 Common toxicities associated with bevacizumab include hypertension, gastrointestinal perforation, arterial thromboembolism, reversible posterior leukoencephalopathy syndrome (RPLS), venous thromboembolism, proteinuria, bleeding/hemorrhage, and wound-healing complications | There are several pathways through which monoclonal antibodies (mAbs) may be cleared. Non-specific clearance of mAbs refers to target independent pinocytosis, and proteolysis of the protein into small amino acids and peptides in the reticuloendothelial system (RES) and the liver. Target-mediated clearance is a result of specific interactions between the mAb and its target antigen. Once bound, the antibody-antigen complex may be cleared via lysosomal degradation. Additionally, the production of anti-drug antibodies (ADA), which are a result of an immunogenic response to mAb-based treatment, can form complexes with mAb’s and may impact the rate of mAb clearance | Monoclonal antibodies (mAbs) are large in size, do not readily cross cell membranes, and are unable to withstand proteolysis in the gastrointestinal tract. Given these characteristics, mAbs are poorly absorbed via the oral route and are instead administered intravenously, intramuscularly or subcutaneously. In a single dose (1mg/kg) pharmacokinetic study assessing the bioequivalence of bevacizumab and TAB008 (a biosimilar product), the pharmacokinetic parameters of Avastin (bevacizumab) were as follows20: Geometric mean Cmax = 17.38 ug/mL Geometric mean AUCinf = 5,358 ugxh/mL Geometric mean Tmax = 2.50 hrs | The volume of distribution of bevacizumab is approximately 3.29 L and 2.39 L for the average male and female, respectively. | The clearance (CL) of bevacizumab is approximately 0.207 L/day. The CL of bevacizumab can increase or decrease by 30% in patients who weigh >114 kg or <49 kg respectively. Males tend to clear bevacizumab at a faster rate than females (26% faster on average). Other factors including alkaline phosphatase (ALP), serum aspartate aminotransferase (AST), serum albumin, and tumor burden may cause the CL to fluctuate | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Cardiotoxic antineoplastic agents,Experimental Unapproved Treatments for COVID-19,Globulins,Growth Inhibitors,Immunoglobulins,Immunoproteins,Immunotherapy,Narrow Therapeutic Index Drugs,Proteins,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors,Vascular Endothelial Growth Factor-directed Antibody Interactions | CA2145985 | 16-Sep-2003 | 28-Oct-2012 | NA | Vascular endothelial growth factor A,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c | Equidacent | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10490 | Th1091 | Bevacizumab | >Th1091_Bevacizumab EVQLVESGGGLVQPGGSLRLSCAASGYTFTNYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPHYYGSSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6538H10034N1716O2033S45 | NA | NA | 62 (FAB fr | 20 days (range of 11-50 days) | Recombinant (derived from CHO-gentamycin), humanized, monoclonal IgG1 antibody. It Inhibits the biologic activity of human vascular endothelial growth factor (VEGF) by binding to it. Comprises human framework regions and murine complementarity-determining regions. | As part of combination therapy for metastatic colorectal cancer and HER2-negative metastatic breast cancer. | Bevacizumab prevents or reduces the formation of blood vessels (angiogenesis) thereby preventing or reducing metatstatic disease progressing. Bevacizumab binds VEGF and prevents vascular endothelial growth and endothelial cell proliferation. | Bevacizumab binds VEGF and prevents the interaction of VEGF to its receptors (Flt-1 and KDR) on the surface of endothelial cells. This prevents blood vessel proliferation and tumour metastasis. | Bevacizumab toxicities are distinct from the effects of cytotoxic agents used in chemotherapy, and are normally linked to impaired VEGF function.18,19 Common toxicities associated with bevacizumab include hypertension, gastrointestinal perforation, arterial thromboembolism, reversible posterior leukoencephalopathy syndrome (RPLS), venous thromboembolism, proteinuria, bleeding/hemorrhage, and wound-healing complications | There are several pathways through which monoclonal antibodies (mAbs) may be cleared. Non-specific clearance of mAbs refers to target independent pinocytosis, and proteolysis of the protein into small amino acids and peptides in the reticuloendothelial system (RES) and the liver. Target-mediated clearance is a result of specific interactions between the mAb and its target antigen. Once bound, the antibody-antigen complex may be cleared via lysosomal degradation. Additionally, the production of anti-drug antibodies (ADA), which are a result of an immunogenic response to mAb-based treatment, can form complexes with mAb’s and may impact the rate of mAb clearance | Monoclonal antibodies (mAbs) are large in size, do not readily cross cell membranes, and are unable to withstand proteolysis in the gastrointestinal tract. Given these characteristics, mAbs are poorly absorbed via the oral route and are instead administered intravenously, intramuscularly or subcutaneously. In a single dose (1mg/kg) pharmacokinetic study assessing the bioequivalence of bevacizumab and TAB008 (a biosimilar product), the pharmacokinetic parameters of Avastin (bevacizumab) were as follows20: Geometric mean Cmax = 17.38 ug/mL Geometric mean AUCinf = 5,358 ugxh/mL Geometric mean Tmax = 2.50 hrs | The volume of distribution of bevacizumab is approximately 3.29 L and 2.39 L for the average male and female, respectively. | The clearance (CL) of bevacizumab is approximately 0.207 L/day. The CL of bevacizumab can increase or decrease by 30% in patients who weigh >114 kg or <49 kg respectively. Males tend to clear bevacizumab at a faster rate than females (26% faster on average). Other factors including alkaline phosphatase (ALP), serum aspartate aminotransferase (AST), serum albumin, and tumor burden may cause the CL to fluctuate | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Cardiotoxic antineoplastic agents,Experimental Unapproved Treatments for COVID-19,Globulins,Growth Inhibitors,Immunoglobulins,Immunoproteins,Immunotherapy,Narrow Therapeutic Index Drugs,Proteins,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors,Vascular Endothelial Growth Factor-directed Antibody Interactions | CA2145985 | 16-Sep-2003 | 28-Oct-2012 | NA | Vascular endothelial growth factor A,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c | Mvasi | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10491 | Th1091 | Bevacizumab | >Th1091_Bevacizumab EVQLVESGGGLVQPGGSLRLSCAASGYTFTNYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPHYYGSSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6538H10034N1716O2033S45 | NA | NA | 62 (FAB fr | 20 days (range of 11-50 days) | Recombinant (derived from CHO-gentamycin), humanized, monoclonal IgG1 antibody. It Inhibits the biologic activity of human vascular endothelial growth factor (VEGF) by binding to it. Comprises human framework regions and murine complementarity-determining regions. | As part of combination therapy for metastatic colorectal cancer and HER2-negative metastatic breast cancer. | Bevacizumab prevents or reduces the formation of blood vessels (angiogenesis) thereby preventing or reducing metatstatic disease progressing. Bevacizumab binds VEGF and prevents vascular endothelial growth and endothelial cell proliferation. | Bevacizumab binds VEGF and prevents the interaction of VEGF to its receptors (Flt-1 and KDR) on the surface of endothelial cells. This prevents blood vessel proliferation and tumour metastasis. | Bevacizumab toxicities are distinct from the effects of cytotoxic agents used in chemotherapy, and are normally linked to impaired VEGF function.18,19 Common toxicities associated with bevacizumab include hypertension, gastrointestinal perforation, arterial thromboembolism, reversible posterior leukoencephalopathy syndrome (RPLS), venous thromboembolism, proteinuria, bleeding/hemorrhage, and wound-healing complications | There are several pathways through which monoclonal antibodies (mAbs) may be cleared. Non-specific clearance of mAbs refers to target independent pinocytosis, and proteolysis of the protein into small amino acids and peptides in the reticuloendothelial system (RES) and the liver. Target-mediated clearance is a result of specific interactions between the mAb and its target antigen. Once bound, the antibody-antigen complex may be cleared via lysosomal degradation. Additionally, the production of anti-drug antibodies (ADA), which are a result of an immunogenic response to mAb-based treatment, can form complexes with mAb’s and may impact the rate of mAb clearance | Monoclonal antibodies (mAbs) are large in size, do not readily cross cell membranes, and are unable to withstand proteolysis in the gastrointestinal tract. Given these characteristics, mAbs are poorly absorbed via the oral route and are instead administered intravenously, intramuscularly or subcutaneously. In a single dose (1mg/kg) pharmacokinetic study assessing the bioequivalence of bevacizumab and TAB008 (a biosimilar product), the pharmacokinetic parameters of Avastin (bevacizumab) were as follows20: Geometric mean Cmax = 17.38 ug/mL Geometric mean AUCinf = 5,358 ugxh/mL Geometric mean Tmax = 2.50 hrs | The volume of distribution of bevacizumab is approximately 3.29 L and 2.39 L for the average male and female, respectively. | The clearance (CL) of bevacizumab is approximately 0.207 L/day. The CL of bevacizumab can increase or decrease by 30% in patients who weigh >114 kg or <49 kg respectively. Males tend to clear bevacizumab at a faster rate than females (26% faster on average). Other factors including alkaline phosphatase (ALP), serum aspartate aminotransferase (AST), serum albumin, and tumor burden may cause the CL to fluctuate | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Cardiotoxic antineoplastic agents,Experimental Unapproved Treatments for COVID-19,Globulins,Growth Inhibitors,Immunoglobulins,Immunoproteins,Immunotherapy,Narrow Therapeutic Index Drugs,Proteins,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors,Vascular Endothelial Growth Factor-directed Antibody Interactions | CA2145985 | 16-Sep-2003 | 28-Oct-2012 | NA | Vascular endothelial growth factor A,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c | Onbevzi | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10492 | Th1091 | Bevacizumab | >Th1091_Bevacizumab EVQLVESGGGLVQPGGSLRLSCAASGYTFTNYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPHYYGSSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6538H10034N1716O2033S45 | NA | NA | 62 (FAB fr | 20 days (range of 11-50 days) | Recombinant (derived from CHO-gentamycin), humanized, monoclonal IgG1 antibody. It Inhibits the biologic activity of human vascular endothelial growth factor (VEGF) by binding to it. Comprises human framework regions and murine complementarity-determining regions. | As part of combination therapy for metastatic colorectal cancer and HER2-negative metastatic breast cancer. | Bevacizumab prevents or reduces the formation of blood vessels (angiogenesis) thereby preventing or reducing metatstatic disease progressing. Bevacizumab binds VEGF and prevents vascular endothelial growth and endothelial cell proliferation. | Bevacizumab binds VEGF and prevents the interaction of VEGF to its receptors (Flt-1 and KDR) on the surface of endothelial cells. This prevents blood vessel proliferation and tumour metastasis. | Bevacizumab toxicities are distinct from the effects of cytotoxic agents used in chemotherapy, and are normally linked to impaired VEGF function.18,19 Common toxicities associated with bevacizumab include hypertension, gastrointestinal perforation, arterial thromboembolism, reversible posterior leukoencephalopathy syndrome (RPLS), venous thromboembolism, proteinuria, bleeding/hemorrhage, and wound-healing complications | There are several pathways through which monoclonal antibodies (mAbs) may be cleared. Non-specific clearance of mAbs refers to target independent pinocytosis, and proteolysis of the protein into small amino acids and peptides in the reticuloendothelial system (RES) and the liver. Target-mediated clearance is a result of specific interactions between the mAb and its target antigen. Once bound, the antibody-antigen complex may be cleared via lysosomal degradation. Additionally, the production of anti-drug antibodies (ADA), which are a result of an immunogenic response to mAb-based treatment, can form complexes with mAb’s and may impact the rate of mAb clearance | Monoclonal antibodies (mAbs) are large in size, do not readily cross cell membranes, and are unable to withstand proteolysis in the gastrointestinal tract. Given these characteristics, mAbs are poorly absorbed via the oral route and are instead administered intravenously, intramuscularly or subcutaneously. In a single dose (1mg/kg) pharmacokinetic study assessing the bioequivalence of bevacizumab and TAB008 (a biosimilar product), the pharmacokinetic parameters of Avastin (bevacizumab) were as follows20: Geometric mean Cmax = 17.38 ug/mL Geometric mean AUCinf = 5,358 ugxh/mL Geometric mean Tmax = 2.50 hrs | The volume of distribution of bevacizumab is approximately 3.29 L and 2.39 L for the average male and female, respectively. | The clearance (CL) of bevacizumab is approximately 0.207 L/day. The CL of bevacizumab can increase or decrease by 30% in patients who weigh >114 kg or <49 kg respectively. Males tend to clear bevacizumab at a faster rate than females (26% faster on average). Other factors including alkaline phosphatase (ALP), serum aspartate aminotransferase (AST), serum albumin, and tumor burden may cause the CL to fluctuate | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Cardiotoxic antineoplastic agents,Experimental Unapproved Treatments for COVID-19,Globulins,Growth Inhibitors,Immunoglobulins,Immunoproteins,Immunotherapy,Narrow Therapeutic Index Drugs,Proteins,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors,Vascular Endothelial Growth Factor-directed Antibody Interactions | CA2145985 | 16-Sep-2003 | 28-Oct-2012 | NA | Vascular endothelial growth factor A,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c | Oyavas | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10493 | Th1091 | Bevacizumab | >Th1091_Bevacizumab EVQLVESGGGLVQPGGSLRLSCAASGYTFTNYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPHYYGSSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6538H10034N1716O2033S45 | NA | NA | 62 (FAB fr | 20 days (range of 11-50 days) | Recombinant (derived from CHO-gentamycin), humanized, monoclonal IgG1 antibody. It Inhibits the biologic activity of human vascular endothelial growth factor (VEGF) by binding to it. Comprises human framework regions and murine complementarity-determining regions. | As part of combination therapy for metastatic colorectal cancer and HER2-negative metastatic breast cancer. | Bevacizumab prevents or reduces the formation of blood vessels (angiogenesis) thereby preventing or reducing metatstatic disease progressing. Bevacizumab binds VEGF and prevents vascular endothelial growth and endothelial cell proliferation. | Bevacizumab binds VEGF and prevents the interaction of VEGF to its receptors (Flt-1 and KDR) on the surface of endothelial cells. This prevents blood vessel proliferation and tumour metastasis. | Bevacizumab toxicities are distinct from the effects of cytotoxic agents used in chemotherapy, and are normally linked to impaired VEGF function.18,19 Common toxicities associated with bevacizumab include hypertension, gastrointestinal perforation, arterial thromboembolism, reversible posterior leukoencephalopathy syndrome (RPLS), venous thromboembolism, proteinuria, bleeding/hemorrhage, and wound-healing complications | There are several pathways through which monoclonal antibodies (mAbs) may be cleared. Non-specific clearance of mAbs refers to target independent pinocytosis, and proteolysis of the protein into small amino acids and peptides in the reticuloendothelial system (RES) and the liver. Target-mediated clearance is a result of specific interactions between the mAb and its target antigen. Once bound, the antibody-antigen complex may be cleared via lysosomal degradation. Additionally, the production of anti-drug antibodies (ADA), which are a result of an immunogenic response to mAb-based treatment, can form complexes with mAb’s and may impact the rate of mAb clearance | Monoclonal antibodies (mAbs) are large in size, do not readily cross cell membranes, and are unable to withstand proteolysis in the gastrointestinal tract. Given these characteristics, mAbs are poorly absorbed via the oral route and are instead administered intravenously, intramuscularly or subcutaneously. In a single dose (1mg/kg) pharmacokinetic study assessing the bioequivalence of bevacizumab and TAB008 (a biosimilar product), the pharmacokinetic parameters of Avastin (bevacizumab) were as follows20: Geometric mean Cmax = 17.38 ug/mL Geometric mean AUCinf = 5,358 ugxh/mL Geometric mean Tmax = 2.50 hrs | The volume of distribution of bevacizumab is approximately 3.29 L and 2.39 L for the average male and female, respectively. | The clearance (CL) of bevacizumab is approximately 0.207 L/day. The CL of bevacizumab can increase or decrease by 30% in patients who weigh >114 kg or <49 kg respectively. Males tend to clear bevacizumab at a faster rate than females (26% faster on average). Other factors including alkaline phosphatase (ALP), serum aspartate aminotransferase (AST), serum albumin, and tumor burden may cause the CL to fluctuate | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Cardiotoxic antineoplastic agents,Experimental Unapproved Treatments for COVID-19,Globulins,Growth Inhibitors,Immunoglobulins,Immunoproteins,Immunotherapy,Narrow Therapeutic Index Drugs,Proteins,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors,Vascular Endothelial Growth Factor-directed Antibody Interactions | CA2145985 | 16-Sep-2003 | 28-Oct-2012 | NA | Vascular endothelial growth factor A,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c | Zirabev | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10588 | Th1121 | Pertuzumab | >Th1121_Pertuzumab EVQLVESGGGLVQPGGSLRLSCAASGFTFTDYTMDWVRQAPGKGLEWVADVNPNSGGSIYNQRFKGRFTLSVDRSKNTLYLQMNSLRAEDTAVYYCARNLGPSFYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 148000 | NA | NA | NA | NA | 18 days | Recombinant, humanized monoclonal antibody that targets the extracellular dimerization domain (Subdomain II) of the human epidermal growth factor receptor 2 protein (HER2). Two heavy chains and two lights chains are composed of 448 and 214 residues respectively. FDA approved June 8, 2012. | Pertuzumab is indicated for use in combination with trastuzumab and docetaxel for the treatment of patients with HER2-positive metastatic breast cancer who have not received prior anti-HER2 therapy or chemotherapy for metastatic disease. | NA | Pertuzumab is a humanized monoclonal antibody designed to bind to the HER2 receptor and inhibit the ability of HER2 to interact with other HER family members (HER1, HER2, HER3, and HER4) on the surface of cancer cells. The HER signaling pathway plays a role in the formation and growth of numerous cancers, and previous clinical trials of pertuzumab in a single agent setting had suggested clinical activity - including stable disease - in heavily pretreated patients with advanced ovarian and breast cancers. | There are no data regarding overdose of pertuzumab. Single doses higher than 25 mg/kg have not been tested.[L14747] Symptoms of overdose are likely to be consistent with pertuzumab's adverse effect profile, and may therefore involve significant diarrhea, alopecia, neutropenia, nausea, fatigue, rash, and/or peripheral neuropathy.[L14642] Pertuzumab has been associated with the development of left ventricular dysfunction (i.e. cardiotoxicity) that may be exacerbated in instances of overdose.[L14642] | The metabolism of pertuzumab has not been studied directly. Monoclonal antibodies are typically subject to catabolism to smaller peptides and proteins prior to elimination.[L14747] | Intravenously administered pertuzumab, given as a loading dose of 840mg followed by a maintenance dose of 420mg every 3 weeks, reaches steady-state concentration following the first maintenance dose.[L14747] In its subcutaneous formulation, in combination with [hylauronidase], the absolute bioavailability of pertuzumab is approximately 0.7 and the median Tmax is 4 days.[L14531] This subcutaneous formulation leverages the benefits of co-administration with hyaluronidase - this enzyme breaks down hylauronic acid, thereby decreasing the viscosity of the extracellular matrix (ECM) and allowing for greater bioavailability with subcutaneous administration.[L14531] | The average steady-state volume of distribution following intravenous administration is 3.53 - 7.5 L.[L14747] | The median clearance of pertuzumab was determined to be 0.24 L/day based on a population pharmacokinetic analysis.[L14642] | Monoclonal antibodies | CA2376596 | 10-Jun-2009 | 23-06-2020 | NA | Receptor tyrosine-protein kinase erbB-2 | Perjeta | Genentech | Genentech | Neoadjuvant Treatment of Breast Cancer, Metastatic Breast Cancer (MBC), | NA | Each single use vial contains 420 mg of pertuzumab at a concentration of 30 mg/mL in 20 mM L-histidine acetate (pH 6.0), 120 mM sucrose and 0.02% polysorbate 20 | Sterile, clear to slightly opalescent, colorless to pale brown liquid | Intravenous infusion | The initial dose of PERJETA is 840 mg administered as a 60-minute Intravenous infusion, followed every 3 weeks by a dose of 420 mg administered as an Intravenous infusion over 30 to 60 minutes. When administered with PERJETA, the recommended initial dose of trastuzumab is 8 mg/kg administered as a 90-minute Intravenous infusion, followed every 3 weeks by a dose of 6 mg/kg administered as an Intravenous infusion over 30 to 90 minutes.PERJETA, trastuzumab, and docetaxel should be administered sequentially. PERJETA and trastuzumab can be given in any order. Docetaxel should be administered after PERJETA and trastuzumab. An observation period of 30 to 60 minutes is recommended after each PERJETA infusion and before commencement of any subsequent infusion of trastuzumab. | NA | Embryo-Fetal Toxicity , Left Ventricular Dysfunction , Infusion-Related Reactions, Hypersensitivity Reactions. | Link | NA | NA |
| 10589 | Th1121 | Pertuzumab | >Th1121_Pertuzumab EVQLVESGGGLVQPGGSLRLSCAASGFTFTDYTMDWVRQAPGKGLEWVADVNPNSGGSIYNQRFKGRFTLSVDRSKNTLYLQMNSLRAEDTAVYYCARNLGPSFYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | NA | NA | NA | NA | NA | 18 days | Recombinant, humanized monoclonal antibody that targets the extracellular dimerization domain (Subdomain II) of the human epidermal growth factor receptor 2 protein (HER2). Two heavy chains and two lights chains are composed of 448 and 214 residues respectively. FDA approved June 8, 2012. | Pertuzumab is indicated for use in combination with trastuzumab and docetaxel for the treatment of patients with HER2-positive metastatic breast cancer who have not received prior anti-HER2 therapy or chemotherapy for metastatic disease. | NA | Pertuzumab is a humanized monoclonal antibody designed to bind to the HER2 receptor and inhibit the ability of HER2 to interact with other HER family members (HER1, HER2, HER3, and HER4) on the surface of cancer cells. The HER signaling pathway plays a role in the formation and growth of numerous cancers, and previous clinical trials of pertuzumab in a single agent setting had suggested clinical activity - including stable disease - in heavily pretreated patients with advanced ovarian and breast cancers. | There are no data regarding overdose of pertuzumab. Single doses higher than 25 mg/kg have not been tested.[L14747] Symptoms of overdose are likely to be consistent with pertuzumab's adverse effect profile, and may therefore involve significant diarrhea, alopecia, neutropenia, nausea, fatigue, rash, and/or peripheral neuropathy.[L14642] Pertuzumab has been associated with the development of left ventricular dysfunction (i.e. cardiotoxicity) that may be exacerbated in instances of overdose.[L14642] | The metabolism of pertuzumab has not been studied directly. Monoclonal antibodies are typically subject to catabolism to smaller peptides and proteins prior to elimination.[L14747] | Intravenously administered pertuzumab, given as a loading dose of 840mg followed by a maintenance dose of 420mg every 3 weeks, reaches steady-state concentration following the first maintenance dose.[L14747] In its subcutaneous formulation, in combination with [hylauronidase], the absolute bioavailability of pertuzumab is approximately 0.7 and the median Tmax is 4 days.[L14531] This subcutaneous formulation leverages the benefits of co-administration with hyaluronidase - this enzyme breaks down hylauronic acid, thereby decreasing the viscosity of the extracellular matrix (ECM) and allowing for greater bioavailability with subcutaneous administration.[L14531] | The average steady-state volume of distribution following intravenous administration is 3.53 - 7.5 L.[L14747] | The median clearance of pertuzumab was determined to be 0.24 L/day based on a population pharmacokinetic analysis.[L14642] | Monoclonal antibodies | CA2579861 | 18-12-2012 | 19-10-2025 | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10598 | Th1123 | Denosumab | >Th1123_Denosumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYAMSWVRQAPGKGLEWVSGITGSGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDPGTTVIMSWFDPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144700 | C6404H9912N1724O2004S50 | NA | NA | NA | 25.4 days | Novel, fully human IgG2 monoclonal antibody, specific to receptor activator of nuclear factor kappa-B ligand (RANKL). It suppresses bone resorption markers in patients suffering from metastatic tumors and is being investigated in multiple clinical trials for the prevention and treatment of bone metastases. Each light chain consists of 215 amino acids and the heavy chain consists of 448 amino acids. FDA approved on June 1, 2010. | Prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It reduces the incidence of vertebral, nonvertebral, and hip fractures. Prolia is also indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. It can also be used in men with osteoporosis at high risk for fracture or in men receiving androgen deprivation therapy for nonmetastatic prostate cancer to increase bone mass. Xgeva is indicated for the prevention of skeletal-related events in patients with bone metastases from solid tumors. | In clinical studies, treatment with 60 mg of Prolia resulted in reduction in the bone resorption marker serum type 1 C-telopeptide (CTX) by approximately 85% by 3 days. Consistent with the physiological coupling of bone formation and resorption in skeletal remodeling, subsequent reductions in bone formation markers (i.e. osteocalcin and procollagen type 1 N-terminal peptide [PlNP]) were observed starting 1 month after the first dose of Prolia. | Denosumab is designed to target RANKL (RANK ligand), a protein that acts as the primary signal to promote bone removal/resorption. In many bone loss conditions, RANKL overwhelms the body's natural defense against bone destruction. Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone. | In patients with postmenopausal osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, pain in extremity, hypercholesterolemia, musculoskeletal pain, and cystitis. Pancreatitis has been reported in clinical trials. In male patients with osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, arthralgia, and nasopharyngitis. In patients experiencing bone loss due to hormone ablation for cancer, the most common adverse reactions (= 10% and more common than placebo) were: arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials | NA | When 60 mg of denosumab was subcutaneously administered to healthy subjects after fasting for 12 hours, the pharmacokinetic parameters are as follows: Cmax = 6.75 mcg/mL; Tmax= 10 days (range of 3 to 21 days); AUC (0-16 weeks) = 316 mcg•day/mL. Denosumab does not accumulate following multiple doses once every 6 months. The pharmacokinetics of denosumab were not affected by the formation of antibodies. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Bone Density Conservation Agents,Cancer immunotherapy,Drugs Affecting Bone Structure and Mineralization,Drugs for Treatment of Bone Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Musculo-Skeletal System,Proteins,RANK Ligand Blocking Activity,RANK Ligand Inhibitor,Serum Globulins | CA2257247 | 9-Nov-2012 | 15-04-2018 | NA | Tumor necrosis factor ligand superfamily member 11 | Xgeva | Amgen. | Amgen. | Bone Metastasis From Solid Tumors, Giant Cell Tumor Of Bone, Hypercalcemia Of Malignancy | NA | Each single-use vial of Xgeva contains 120 mg denosumab, acetate (18 mM), sorbitol (4.6%), Water for Injection (USP), and sodium hydroxide to a pH of 5.2 | Sterile, preservative-free, clear, colorless to pale yellow solution | NA | Bone Metastasis From Solid Tumors: The recommended dose of Xgeva is 120 mg administered as a subcutaneous injection every 4 weeks. Administer calcium and vitamin D as necessary to treat or prevent hypocalcemia.; Giant Cell Tumor Of Bone: The recommended dose of Xgeva is 120 mg administered every 4 weeks with additional 120 mg doses on Days 8 and 15 of the first month of therapy. Administer calcium and vitamin D as necessary to treat or prevent hypocalcemia.; Hypercalcemia Of Malignancy: The recommended dose of Xgeva is 120 mg administered every 4 weeks with additional 120 mg doses on Days 8 and 15 of the first month of therapy. | Xgeva is not indicated for the prevention of skeletal-related events in patients with multiple myeloma. | Hypocalcemia, Osteonecrosis of the Jaw. | Link | NA | NA |
| 10599 | Th1123 | Denosumab | >Th1123_Denosumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYAMSWVRQAPGKGLEWVSGITGSGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDPGTTVIMSWFDPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144700 | C6404H9912N1724O2004S50 | NA | NA | NA | 25.4 days | Novel, fully human IgG2 monoclonal antibody, specific to receptor activator of nuclear factor kappa-B ligand (RANKL). It suppresses bone resorption markers in patients suffering from metastatic tumors and is being investigated in multiple clinical trials for the prevention and treatment of bone metastases. Each light chain consists of 215 amino acids and the heavy chain consists of 448 amino acids. FDA approved on June 1, 2010. | Prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It reduces the incidence of vertebral, nonvertebral, and hip fractures. Prolia is also indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. It can also be used in men with osteoporosis at high risk for fracture or in men receiving androgen deprivation therapy for nonmetastatic prostate cancer to increase bone mass. Xgeva is indicated for the prevention of skeletal-related events in patients with bone metastases from solid tumors. | In clinical studies, treatment with 60 mg of Prolia resulted in reduction in the bone resorption marker serum type 1 C-telopeptide (CTX) by approximately 85% by 3 days. Consistent with the physiological coupling of bone formation and resorption in skeletal remodeling, subsequent reductions in bone formation markers (i.e. osteocalcin and procollagen type 1 N-terminal peptide [PlNP]) were observed starting 1 month after the first dose of Prolia. | Denosumab is designed to target RANKL (RANK ligand), a protein that acts as the primary signal to promote bone removal/resorption. In many bone loss conditions, RANKL overwhelms the body's natural defense against bone destruction. Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone. | In patients with postmenopausal osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, pain in extremity, hypercholesterolemia, musculoskeletal pain, and cystitis. Pancreatitis has been reported in clinical trials. In male patients with osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, arthralgia, and nasopharyngitis. In patients experiencing bone loss due to hormone ablation for cancer, the most common adverse reactions (= 10% and more common than placebo) were: arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials | NA | When 60 mg of denosumab was subcutaneously administered to healthy subjects after fasting for 12 hours, the pharmacokinetic parameters are as follows: Cmax = 6.75 mcg/mL; Tmax= 10 days (range of 3 to 21 days); AUC (0-16 weeks) = 316 mcg•day/mL. Denosumab does not accumulate following multiple doses once every 6 months. The pharmacokinetics of denosumab were not affected by the formation of antibodies. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Bone Density Conservation Agents,Cancer immunotherapy,Drugs Affecting Bone Structure and Mineralization,Drugs for Treatment of Bone Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Musculo-Skeletal System,Proteins,RANK Ligand Blocking Activity,RANK Ligand Inhibitor,Serum Globulins | CA2274987 | 24-01-2012 | 22-12-2017 | NA | Tumor necrosis factor ligand superfamily member 11 | Prolia | Amgen. | Amgen. | Treatment Of Postmenopausal Women With Osteoporosis At High Risk For Fracture,Treatment To Increase Bone Mass In Men With Osteoporosis, Treatment Of Bone Loss In Men Receiving Androgen Deprivation Therapy For Prostate Cancer, Treatment Of Bone Loss In Women Receiving Adjuvant Aromatase Inhibitor Therapy For Breast Cancer | NA | Each 1 mL single-use prefilled syringe of Prolia contains 60 mg denosumab (60 mg/mL solution), 4.7% sorbitol, 17 mM acetate, 0.01% polysorbate 20, Water for Injection (USP), and sodium hydroxide to a pH of 5.2. Each 1 mL single-use vial of Prolia contains 60 mg denosumab (60 mg/mL solution), 4.7% sorbitol, 17 mM acetate, Water for Injection (USP), and sodium hydroxide to a pH of 5.2 | Sterile, preservative-free, clear, colorless to pale yellow solution | NA | NA | Hypocalcemia. Pregnancy. Hypersensitivity | Hypocalcemia, Serious Infections, Dermatologic Adverse Reactions, Osteonecrosis of the Jaw, Atypical Subtrochanteric and Diaphyseal Femoral Fractures | Link | NA | NA |
| 10600 | Th1123 | Denosumab | >Th1123_Denosumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYAMSWVRQAPGKGLEWVSGITGSGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDPGTTVIMSWFDPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144700 | C6404H9912N1724O2004S50 | NA | NA | NA | 25.4 days | Novel, fully human IgG2 monoclonal antibody, specific to receptor activator of nuclear factor kappa-B ligand (RANKL). It suppresses bone resorption markers in patients suffering from metastatic tumors and is being investigated in multiple clinical trials for the prevention and treatment of bone metastases. Each light chain consists of 215 amino acids and the heavy chain consists of 448 amino acids. FDA approved on June 1, 2010. | Prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It reduces the incidence of vertebral, nonvertebral, and hip fractures. Prolia is also indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. It can also be used in men with osteoporosis at high risk for fracture or in men receiving androgen deprivation therapy for nonmetastatic prostate cancer to increase bone mass. Xgeva is indicated for the prevention of skeletal-related events in patients with bone metastases from solid tumors. | In clinical studies, treatment with 60 mg of Prolia resulted in reduction in the bone resorption marker serum type 1 C-telopeptide (CTX) by approximately 85% by 3 days. Consistent with the physiological coupling of bone formation and resorption in skeletal remodeling, subsequent reductions in bone formation markers (i.e. osteocalcin and procollagen type 1 N-terminal peptide [PlNP]) were observed starting 1 month after the first dose of Prolia. | Denosumab is designed to target RANKL (RANK ligand), a protein that acts as the primary signal to promote bone removal/resorption. In many bone loss conditions, RANKL overwhelms the body's natural defense against bone destruction. Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone. | In patients with postmenopausal osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, pain in extremity, hypercholesterolemia, musculoskeletal pain, and cystitis. Pancreatitis has been reported in clinical trials. In male patients with osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, arthralgia, and nasopharyngitis. In patients experiencing bone loss due to hormone ablation for cancer, the most common adverse reactions (= 10% and more common than placebo) were: arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials | NA | When 60 mg of denosumab was subcutaneously administered to healthy subjects after fasting for 12 hours, the pharmacokinetic parameters are as follows: Cmax = 6.75 mcg/mL; Tmax= 10 days (range of 3 to 21 days); AUC (0-16 weeks) = 316 mcg•day/mL. Denosumab does not accumulate following multiple doses once every 6 months. The pharmacokinetics of denosumab were not affected by the formation of antibodies. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Bone Density Conservation Agents,Cancer immunotherapy,Drugs Affecting Bone Structure and Mineralization,Drugs for Treatment of Bone Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Musculo-Skeletal System,Proteins,RANK Ligand Blocking Activity,RANK Ligand Inhibitor,Serum Globulins | CA2285746 | 28-09-2010 | 15-04-2018 | NA | Tumor necrosis factor ligand superfamily member 11 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10601 | Th1123 | Denosumab | >Th1123_Denosumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYAMSWVRQAPGKGLEWVSGITGSGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDPGTTVIMSWFDPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144700 | C6404H9912N1724O2004S50 | NA | NA | NA | 25.4 days | Novel, fully human IgG2 monoclonal antibody, specific to receptor activator of nuclear factor kappa-B ligand (RANKL). It suppresses bone resorption markers in patients suffering from metastatic tumors and is being investigated in multiple clinical trials for the prevention and treatment of bone metastases. Each light chain consists of 215 amino acids and the heavy chain consists of 448 amino acids. FDA approved on June 1, 2010. | Prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It reduces the incidence of vertebral, nonvertebral, and hip fractures. Prolia is also indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. It can also be used in men with osteoporosis at high risk for fracture or in men receiving androgen deprivation therapy for nonmetastatic prostate cancer to increase bone mass. Xgeva is indicated for the prevention of skeletal-related events in patients with bone metastases from solid tumors. | In clinical studies, treatment with 60 mg of Prolia resulted in reduction in the bone resorption marker serum type 1 C-telopeptide (CTX) by approximately 85% by 3 days. Consistent with the physiological coupling of bone formation and resorption in skeletal remodeling, subsequent reductions in bone formation markers (i.e. osteocalcin and procollagen type 1 N-terminal peptide [PlNP]) were observed starting 1 month after the first dose of Prolia. | Denosumab is designed to target RANKL (RANK ligand), a protein that acts as the primary signal to promote bone removal/resorption. In many bone loss conditions, RANKL overwhelms the body's natural defense against bone destruction. Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone. | In patients with postmenopausal osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, pain in extremity, hypercholesterolemia, musculoskeletal pain, and cystitis. Pancreatitis has been reported in clinical trials. In male patients with osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, arthralgia, and nasopharyngitis. In patients experiencing bone loss due to hormone ablation for cancer, the most common adverse reactions (= 10% and more common than placebo) were: arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials | NA | When 60 mg of denosumab was subcutaneously administered to healthy subjects after fasting for 12 hours, the pharmacokinetic parameters are as follows: Cmax = 6.75 mcg/mL; Tmax= 10 days (range of 3 to 21 days); AUC (0-16 weeks) = 316 mcg•day/mL. Denosumab does not accumulate following multiple doses once every 6 months. The pharmacokinetics of denosumab were not affected by the formation of antibodies. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Bone Density Conservation Agents,Cancer immunotherapy,Drugs Affecting Bone Structure and Mineralization,Drugs for Treatment of Bone Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Musculo-Skeletal System,Proteins,RANK Ligand Blocking Activity,RANK Ligand Inhibitor,Serum Globulins | CA2400929 | 31-05-2011 | 23-02-2021 | NA | Tumor necrosis factor ligand superfamily member 11 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10602 | Th1123 | Denosumab | >Th1123_Denosumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYAMSWVRQAPGKGLEWVSGITGSGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDPGTTVIMSWFDPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144700 | C6404H9912N1724O2004S50 | NA | NA | NA | 25.4 days | Novel, fully human IgG2 monoclonal antibody, specific to receptor activator of nuclear factor kappa-B ligand (RANKL). It suppresses bone resorption markers in patients suffering from metastatic tumors and is being investigated in multiple clinical trials for the prevention and treatment of bone metastases. Each light chain consists of 215 amino acids and the heavy chain consists of 448 amino acids. FDA approved on June 1, 2010. | Prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It reduces the incidence of vertebral, nonvertebral, and hip fractures. Prolia is also indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. It can also be used in men with osteoporosis at high risk for fracture or in men receiving androgen deprivation therapy for nonmetastatic prostate cancer to increase bone mass. Xgeva is indicated for the prevention of skeletal-related events in patients with bone metastases from solid tumors. | In clinical studies, treatment with 60 mg of Prolia resulted in reduction in the bone resorption marker serum type 1 C-telopeptide (CTX) by approximately 85% by 3 days. Consistent with the physiological coupling of bone formation and resorption in skeletal remodeling, subsequent reductions in bone formation markers (i.e. osteocalcin and procollagen type 1 N-terminal peptide [PlNP]) were observed starting 1 month after the first dose of Prolia. | Denosumab is designed to target RANKL (RANK ligand), a protein that acts as the primary signal to promote bone removal/resorption. In many bone loss conditions, RANKL overwhelms the body's natural defense against bone destruction. Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone. | In patients with postmenopausal osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, pain in extremity, hypercholesterolemia, musculoskeletal pain, and cystitis. Pancreatitis has been reported in clinical trials. In male patients with osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, arthralgia, and nasopharyngitis. In patients experiencing bone loss due to hormone ablation for cancer, the most common adverse reactions (= 10% and more common than placebo) were: arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials | NA | When 60 mg of denosumab was subcutaneously administered to healthy subjects after fasting for 12 hours, the pharmacokinetic parameters are as follows: Cmax = 6.75 mcg/mL; Tmax= 10 days (range of 3 to 21 days); AUC (0-16 weeks) = 316 mcg•day/mL. Denosumab does not accumulate following multiple doses once every 6 months. The pharmacokinetics of denosumab were not affected by the formation of antibodies. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Bone Density Conservation Agents,Cancer immunotherapy,Drugs Affecting Bone Structure and Mineralization,Drugs for Treatment of Bone Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Musculo-Skeletal System,Proteins,RANK Ligand Blocking Activity,RANK Ligand Inhibitor,Serum Globulins | CA2328140 | 13-03-2012 | 13-05-2019 | NA | Tumor necrosis factor ligand superfamily member 11 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10603 | Th1123 | Denosumab | >Th1123_Denosumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYAMSWVRQAPGKGLEWVSGITGSGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDPGTTVIMSWFDPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144700 | C6404H9912N1724O2004S50 | NA | NA | NA | 25.4 days | Novel, fully human IgG2 monoclonal antibody, specific to receptor activator of nuclear factor kappa-B ligand (RANKL). It suppresses bone resorption markers in patients suffering from metastatic tumors and is being investigated in multiple clinical trials for the prevention and treatment of bone metastases. Each light chain consists of 215 amino acids and the heavy chain consists of 448 amino acids. FDA approved on June 1, 2010. | Prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It reduces the incidence of vertebral, nonvertebral, and hip fractures. Prolia is also indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. It can also be used in men with osteoporosis at high risk for fracture or in men receiving androgen deprivation therapy for nonmetastatic prostate cancer to increase bone mass. Xgeva is indicated for the prevention of skeletal-related events in patients with bone metastases from solid tumors. | In clinical studies, treatment with 60 mg of Prolia resulted in reduction in the bone resorption marker serum type 1 C-telopeptide (CTX) by approximately 85% by 3 days. Consistent with the physiological coupling of bone formation and resorption in skeletal remodeling, subsequent reductions in bone formation markers (i.e. osteocalcin and procollagen type 1 N-terminal peptide [PlNP]) were observed starting 1 month after the first dose of Prolia. | Denosumab is designed to target RANKL (RANK ligand), a protein that acts as the primary signal to promote bone removal/resorption. In many bone loss conditions, RANKL overwhelms the body's natural defense against bone destruction. Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone. | In patients with postmenopausal osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, pain in extremity, hypercholesterolemia, musculoskeletal pain, and cystitis. Pancreatitis has been reported in clinical trials. In male patients with osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, arthralgia, and nasopharyngitis. In patients experiencing bone loss due to hormone ablation for cancer, the most common adverse reactions (= 10% and more common than placebo) were: arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials | NA | When 60 mg of denosumab was subcutaneously administered to healthy subjects after fasting for 12 hours, the pharmacokinetic parameters are as follows: Cmax = 6.75 mcg/mL; Tmax= 10 days (range of 3 to 21 days); AUC (0-16 weeks) = 316 mcg•day/mL. Denosumab does not accumulate following multiple doses once every 6 months. The pharmacokinetics of denosumab were not affected by the formation of antibodies. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Bone Density Conservation Agents,Cancer immunotherapy,Drugs Affecting Bone Structure and Mineralization,Drugs for Treatment of Bone Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Musculo-Skeletal System,Proteins,RANK Ligand Blocking Activity,RANK Ligand Inhibitor,Serum Globulins | NA | NA | NA | NA | Tumor necrosis factor ligand superfamily member 11 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10628 | Th1127 | Buserelin | >Th1127_Buserelin XHWSYXLRP | 1239.447 | C60H86N16O13 | NA | NA | NA | 50-80 minutes by IV dose, 80 mins. By SC dose, 1-2 hrs by Intranasal dose | Buserelin is a luteinizing hormone-releasing hormone (LHRH) agonist. It is a synthetic hormone which stimulates the pituitary gland's gonadotrophin-releasing hormone receptor (GnRHR) and is used in prostate cancer treatment. | Buserelin may be used in the treatment of hormone-responsive cancers such as prostate cancer or breast cancer, estrogen-dependent conditions (such as endometriosis or uterine fibroids), and in assisted reproduction. | NA | Buserelin stimulates the pituitary gland's gonadotrophin-releasing hormone receptor (GnRHR). Buserelin desensitizes the GnRH receptor, reducing the amount of LH and testosterone. However, there is a concomitant surge in LH and testosterone levels with the decrease in androgens, so antiandrogens must administered. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Lutropin-choriogonadotropic hormone receptor,Gonadotropin-releasing hormone receptor | Suprecur (Nasal Spray Solution) | Sanofi-Aventis | Sanofi-Aventis | Treatment of endometriosis – an illness where some of the tissues that line the womb are found elsewhere in the body. As part of a treatment for infertility – it works by stopping the natural production of hormones that control ovulation. Synthetic hormones are then used to artificially stimulate ovulation. Your doctor should give you more information about how your treatment works | NA | Each spray dose contains 150 micrograms of the active substance, buserelin as buserelin acetate. The other ingredients are citric acid, sodium citrate, sodium chloride and benzalkonium chloride in aqueous solution | 150 micrograms Nasal Spray Solution | Nasal spray | Treatment of endometriosis: The usual dose is one spray in each nostril three times each day. This is to make a total daily dose of 900 micrograms; Use the spray in the morning, at mid-day and in the evening; Treatment will be for a maximum of 6 months;Treatment should be started on the first or second day of your menstrual period.This is to lower the chances you may be pregnant. Your doctor may perform a pregnancy test if there is any doubt; You may get a menstrual period after the first few weeks of using this medicine. You may also carry on getting breakthrough bleeding or spotting As part of treatment for infertility. | Do not use this medicine and tell your doctor if: You are allergic (hypersensitive) to buserelin or goserelin, benzalkonium chloride or other ingredients of Suprecur Nasal Spray. Signs of an allergic reaction include: a rash, swallowing or breathing problems, swelling of your lips, face, throat or tongue; You have abnormal menstrual bleeding where the cause is not endometriosis; You have a tumour that is not affected by hormones; You are pregnant or breast-feeding.This medicine is for use in women only. If you are not sure, talk to your doctor or pharmacist before using Suprecur Nasal Spray. | Allergic reaction, diarrhoea, pain, swelling or a feeling of tension in stomach, weight gain, difficulty in breathing, decreased urination. These could be signs of a serious side effect called ’Ovarian Hyperstimulation Syndrome’. This is more likely if you are taking other hormones as well as Suprecur Nasal Spray (buserelin) as part of a treatment for infertility. | Link | NA | NA |
| 10629 | Th1127 | Buserelin | >Th1127_Buserelin XHWSYXLRP | 1239.447 | C60H86N16O13 | NA | NA | NA | 50-80 minutes by IV dose, 80 mins. By SC dose, 1-2 hrs by Intranasal dose | Buserelin is a luteinizing hormone-releasing hormone (LHRH) agonist. It is a synthetic hormone which stimulates the pituitary gland's gonadotrophin-releasing hormone receptor (GnRHR) and is used in prostate cancer treatment. | Buserelin may be used in the treatment of hormone-responsive cancers such as prostate cancer or breast cancer, estrogen-dependent conditions (such as endometriosis or uterine fibroids), and in assisted reproduction. | NA | Buserelin stimulates the pituitary gland's gonadotrophin-releasing hormone receptor (GnRHR). Buserelin desensitizes the GnRH receptor, reducing the amount of LH and testosterone. However, there is a concomitant surge in LH and testosterone levels with the decrease in androgens, so antiandrogens must administered. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Lutropin-choriogonadotropic hormone receptor,Gonadotropin-releasing hormone receptor | Suprecur (injection) | Sanofi-Aventis | Sanofi-Aventis | infertility | NA | Each 1ml of solution contains 1 milligram of the active substance, buserelin as buserelin acetate. The other ingredients are, sodium chloride, sodium dihydrogen phosphate, sodium hydroxide, benzyl alcohol and water for injections | 1mg/ml Injection | Subcutaneous | Treatment starts on day 1 or day 21 of menstrual cycle. Daily dose is: 200 to 500 micrograms given as a single daily injection or 500 micrograms twice a day; Daily injections until blood tests show that levels of sex hormones are lowered. This usually takes one to three weeks; After this other hormones along with Suprecur Injection;Doctor determines the treatment time | Do not have this medicine and tell your doctor if: Allergy (hypersensitive) to buserelin or other similar medicines such as goserelin, or any of the other ingredients of Suprecur Injection. Abnormal menstrual bleeding Pregnancy or breast-feeding A tumour that is not affected by changes in hormone levels. This medicine is for use in women only. However there is another form of this medicine that can be used in men. Men should not use either form of this medicine if they have had their testicles removed. | NA | Link | NA | NA |
| 10643 | Th1133 | Aflibercept | >Th1133_Aflibercept SDTGRPFVEMYSEIPEIIHMTEGRELVIPCRVTSPNITVTLKKFPLDTLIPDGKRIIWDSRKGFIISNATYKEIGLLTCEATVNGHLYKTNYLTHRQTNTIIDVVLSPSHGIELSVGEKLVLNCTARTELNVGIDFNWEYPSSKHQHKKLVNRDLKTQSGSEMKKFLSTLTIDGVTRSDQGLYTCAASSGLMTKKNSTFVRVHEKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 115000 | C4318H6788N1164O1304S32 | NA | NA | NA | Intravitreal half life - 7.13 days | Aflibercept is a vascular endothelial growth factor (VEGF) inhibitor. It is a recombinant dimeric fusion glycoprotein that comprises (VEGF) binding portions from the extracellular domains of human VEGF receptors 1 and 2, this is fused to the Fc portion of human IgG1. It contains approximately 15% glycosylation to give a total molecular weight of 115 kDa (protein part = 96.9 kDa). It has 5 putative N-glycosylation sites on each polypeptide chain and the attached carbohydrates exhibit some degree of chain heterogeneity, including heterogeneity in terminal sialic acid residues, except at the site associated with the Fc domain, which is unsialylated. | The opthalmic agent is used for the treatment of neovascular (wet) age-related mascular degeneration (AMD) and macular edema following central retinal vein occulsion (CRVO). The systemic injection, known as ziv-aflibercept, in combination with 5-fluorouracil, leucovorin, irinotecan-(FOLFIRI), is for the treatment of metastatic colorectal cancer that is resistant to or progressed following treatment with oxaliplatin. | Compared to other anti-VEGF drugs like bevacizumab and ranibizumab, aflibercept has a higher binding affinity to VEGF-A (Kd = 0.5 pM). | Ablibercept is a recombinant fusion protein that acts as a decoy receptor for the ligands, vascular endothelial growth factor-A (VEGF-A) and placental growth factor (PIGF). It prevents these ligands to binding to endothelial receptors, VEGFR-1 and VEGFR-2, to suppress neovascularization and decrease vascular permeability. This ultimately will slow vision loss or the progression of metastatic colorectal cancer. | For all intravitreal VEGF inhibitors, there is increased risk of stroke and myocardial infarction. An increase in intraocular pressure may also occur. When used intravenously, most common adverse reactions were leukopenia, diarrhea, neutropenia, proteinuria, AST increased, stomatitis, fatigue, thrombocytopenia, ALT increased, hypertension, weight decreased, decreased appetite, epistaxis, abdominal pain, dysphonia, serum creatinine increased, and headache. | Because aflibercept is a protein, it is expected to be broken down via proteolysis into smaller peptides and amino acids. The cytochrome P450 enzyme system is not involved in the metabolism of aflibercept. | In patients with wet AMD and CRVO, the mean peak plasma concentration (Cmax) was 0.02 mcg/mL and 0.05 mcg/mL respectively. These concentrations were reached in 1 to 3 days. Aflibercept did not accumulate when administered as repeated doses intravitreally every 4 weeks. | After intravenous injection of aflibercept, the volume of distribution is 6 L. | When cancer patients were given 2-9 mg/kg every 2 or 3 week; 1 hour IV infusion of aflibercept the typical estimated clearances were as follows: CL of free aflibercept (CLf) = 0.88 L/day; CL of bound aflibercept (CLf) = 0.19 L/day; Patients clear free aflibercept faster if they had low albumin or high alkaline phosphatase levels. | Antineoplastic Agents and Ophthalmics | US7306799 | 12-Nov-2007 | 23-05-2020 | NA | Vascular endothelial growth factor A,Placenta growth factor,Vascular endothelial growth factor B | Eylea | Regeneron Pharmaceuticals | Regeneron Pharmaceuticals | Neovascular (Wet) Age-Related Macular Degeneration (AMD), Macular Edema Following Central Retinal Vein Occlusion (CRVO) | NA | EYLEA is supplied as a preservative-free, sterile, aqueous solution in a single-use, glass vial designed to deliver 0.05 mL (50 microliters) of EYLEA (40 mg/mL in 10 mM sodium phosphate, 40 mM sodium chloride, 0.03% polysorbate 20, and 5% sucrose, pH 6.2). | EYLEA is a sterile, clear, and colorless to pale yellow solution. | Intravitreal Injection | The recommended dose for EYLEA is 2 mg (0.05 mL or 50 microliters) administered by intravitreal injection every 4 weeks (monthly) for the first 12 weeks (3 months), followed by 2 mg (0.05 mL) via intravitreal injection once every 8 weeks (2 months). | ocular or periocular infections, active intraocular inflammation, Hypersensitivity | Endophthalmitis and retinal detachments, Increased intraocular pressure, Thromboembolic events | Link | NA | NA |
| 10644 | Th1133 | Aflibercept | >Th1133_Aflibercept SDTGRPFVEMYSEIPEIIHMTEGRELVIPCRVTSPNITVTLKKFPLDTLIPDGKRIIWDSRKGFIISNATYKEIGLLTCEATVNGHLYKTNYLTHRQTNTIIDVVLSPSHGIELSVGEKLVLNCTARTELNVGIDFNWEYPSSKHQHKKLVNRDLKTQSGSEMKKFLSTLTIDGVTRSDQGLYTCAASSGLMTKKNSTFVRVHEKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 115000 | C4318H6788N1164O1304S32 | NA | NA | NA | Intravitreal half life - 7.13 days | Aflibercept is a vascular endothelial growth factor (VEGF) inhibitor. It is a recombinant dimeric fusion glycoprotein that comprises (VEGF) binding portions from the extracellular domains of human VEGF receptors 1 and 2, this is fused to the Fc portion of human IgG1. It contains approximately 15% glycosylation to give a total molecular weight of 115 kDa (protein part = 96.9 kDa). It has 5 putative N-glycosylation sites on each polypeptide chain and the attached carbohydrates exhibit some degree of chain heterogeneity, including heterogeneity in terminal sialic acid residues, except at the site associated with the Fc domain, which is unsialylated | The opthalmic agent is used for the treatment of neovascular (wet) age-related mascular degeneration (AMD) and macular edema following central retinal vein occulsion (CRVO). The systemic injection, known as ziv-aflibercept, in combination with 5-fluorouracil, leucovorin, irinotecan-(FOLFIRI), is for the treatment of metastatic colorectal cancer that is resistant to or progressed following treatment with oxaliplatin. | Compared to other anti-VEGF drugs like bevacizumab and ranibizumab, aflibercept has a higher binding affinity to VEGF-A (Kd = 0.5 pM). | Ablibercept is a recombinant fusion protein that acts as a decoy receptor for the ligands, vascular endothelial growth factor-A (VEGF-A) and placental growth factor (PIGF). It prevents these ligands to binding to endothelial receptors, VEGFR-1 and VEGFR-2, to suppress neovascularization and decrease vascular permeability. This ultimately will slow vision loss or the progression of metastatic colorectal cancer. | For all intravitreal VEGF inhibitors, there is increased risk of stroke and myocardial infarction. An increase in intraocular pressure may also occur. When used intravenously, most common adverse reactions were leukopenia, diarrhea, neutropenia, proteinuria, AST increased, stomatitis, fatigue, thrombocytopenia, ALT increased, hypertension, weight decreased, decreased appetite, epistaxis, abdominal pain, dysphonia, serum creatinine increased, and headache. | Because aflibercept is a protein, it is expected to be broken down via proteolysis into smaller peptides and amino acids. The cytochrome P450 enzyme system is not involved in the metabolism of aflibercept. | In patients with wet AMD and CRVO, the mean peak plasma concentration (Cmax) was 0.02 mcg/mL and 0.05 mcg/mL respectively. These concentrations were reached in 1 to 3 days. Aflibercept did not accumulate when administered as repeated doses intravitreally every 4 weeks. | After intravenous injection of aflibercept, the volume of distribution is 6 L. | When cancer patients were given 2-9 mg/kg every 2 or 3 week; 1 hour IV infusion of aflibercept the typical estimated clearances were as follows: CL of free aflibercept (CLf) = 0.88 L/day; CL of bound aflibercept (CLf) = 0.19 L/day; Patients clear free aflibercept faster if they had low albumin or high alkaline phosphatase levels. | Antineoplastic Agents and Ophthalmics | US7531173 | 5-Dec-2009 | 2-Feb-2026 | NA | Vascular endothelial growth factor A,Placenta growth factor,Vascular endothelial growth factor B | Zaltrap | Sanofi and Regeneron Pharmaceuticals, Inc. | Sanofi and Regeneron Pharmaceuticals, Inc. | metastatic colorectal cancer (mCRC) that is resistant to or has progressed following an oxaliplatin-containing regimen | NA | ZALTRAP is supplied in single-use vials of 100 mg per 4 ml and 200 mg per 8 ml formulated as 25 mg/mL ziv-aflibercept in polysorbate 20 (0.1%), sodium chloride (100 mM), sodium citrate (5 mM), sodium phosphate (5 mM), and sucrose (20%), in Water for Injection USP, at a pH of 6.2. | ZALTRAP is a sterile, clear, colorless to pale yellow, non-pyrogenic, preservative-free, solution for administration by Intravenous infusion. | Intravenous infusion | 4 mg per kg as an intravenous (IV) infusion over 1 hour every two weeks. | NA | Hemorrhage, Gastrointestinal, Compromised Wound Healing, Fistula Formation, Hypertension, Arterial Thromboembolic Events, Proteinuria, Neutropenia and Neutropenic Complications, Diarrhea and Dehydration, Reversible Posterior Leukoencephalopathy Syndrome | Link | NA | NA |
| 10645 | Th1133 | Aflibercept | >Th1133_Aflibercept SDTGRPFVEMYSEIPEIIHMTEGRELVIPCRVTSPNITVTLKKFPLDTLIPDGKRIIWDSRKGFIISNATYKEIGLLTCEATVNGHLYKTNYLTHRQTNTIIDVVLSPSHGIELSVGEKLVLNCTARTELNVGIDFNWEYPSSKHQHKKLVNRDLKTQSGSEMKKFLSTLTIDGVTRSDQGLYTCAASSGLMTKKNSTFVRVHEKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 115000 | C4318H6788N1164O1304S32 | NA | NA | NA | Intravitreal half life - 7.13 days | Aflibercept is a vascular endothelial growth factor (VEGF) inhibitor. It is a recombinant dimeric fusion glycoprotein that comprises (VEGF) binding portions from the extracellular domains of human VEGF receptors 1 and 2, this is fused to the Fc portion of human IgG1. It contains approximately 15% glycosylation to give a total molecular weight of 115 kDa (protein part = 96.9 kDa). It has 5 putative N-glycosylation sites on each polypeptide chain and the attached carbohydrates exhibit some degree of chain heterogeneity, including heterogeneity in terminal sialic acid residues, except at the site associated with the Fc domain, which is unsialylated | The opthalmic agent is used for the treatment of neovascular (wet) age-related mascular degeneration (AMD) and macular edema following central retinal vein occulsion (CRVO). The systemic injection, known as ziv-aflibercept, in combination with 5-fluorouracil, leucovorin, irinotecan-(FOLFIRI), is for the treatment of metastatic colorectal cancer that is resistant to or progressed following treatment with oxaliplatin. | Compared to other anti-VEGF drugs like bevacizumab and ranibizumab, aflibercept has a higher binding affinity to VEGF-A (Kd = 0.5 pM). | Ablibercept is a recombinant fusion protein that acts as a decoy receptor for the ligands, vascular endothelial growth factor-A (VEGF-A) and placental growth factor (PIGF). It prevents these ligands to binding to endothelial receptors, VEGFR-1 and VEGFR-2, to suppress neovascularization and decrease vascular permeability. This ultimately will slow vision loss or the progression of metastatic colorectal cancer. | For all intravitreal VEGF inhibitors, there is increased risk of stroke and myocardial infarction. An increase in intraocular pressure may also occur. When used intravenously, most common adverse reactions were leukopenia, diarrhea, neutropenia, proteinuria, AST increased, stomatitis, fatigue, thrombocytopenia, ALT increased, hypertension, weight decreased, decreased appetite, epistaxis, abdominal pain, dysphonia, serum creatinine increased, and headache. | Because aflibercept is a protein, it is expected to be broken down via proteolysis into smaller peptides and amino acids. The cytochrome P450 enzyme system is not involved in the metabolism of aflibercept. | In patients with wet AMD and CRVO, the mean peak plasma concentration (Cmax) was 0.02 mcg/mL and 0.05 mcg/mL respectively. These concentrations were reached in 1 to 3 days. Aflibercept did not accumulate when administered as repeated doses intravitreally every 4 weeks. | After intravenous injection of aflibercept, the volume of distribution is 6 L. | When cancer patients were given 2-9 mg/kg every 2 or 3 week; 1 hour IV infusion of aflibercept the typical estimated clearances were as follows: CL of free aflibercept (CLf) = 0.88 L/day; CL of bound aflibercept (CLf) = 0.19 L/day; Patients clear free aflibercept faster if they had low albumin or high alkaline phosphatase levels. | Antineoplastic Agents and Ophthalmics | US7374758 | 20-05-2008 | 23-05-2020 | NA | Vascular endothelial growth factor A,Placenta growth factor,Vascular endothelial growth factor B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10646 | Th1133 | Aflibercept | >Th1133_Aflibercept SDTGRPFVEMYSEIPEIIHMTEGRELVIPCRVTSPNITVTLKKFPLDTLIPDGKRIIWDSRKGFIISNATYKEIGLLTCEATVNGHLYKTNYLTHRQTNTIIDVVLSPSHGIELSVGEKLVLNCTARTELNVGIDFNWEYPSSKHQHKKLVNRDLKTQSGSEMKKFLSTLTIDGVTRSDQGLYTCAASSGLMTKKNSTFVRVHEKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 115000 | C4318H6788N1164O1304S32 | NA | NA | NA | Intravitreal half life - 7.13 days | Aflibercept is a vascular endothelial growth factor (VEGF) inhibitor. It is a recombinant dimeric fusion glycoprotein that comprises (VEGF) binding portions from the extracellular domains of human VEGF receptors 1 and 2, this is fused to the Fc portion of human IgG1. It contains approximately 15% glycosylation to give a total molecular weight of 115 kDa (protein part = 96.9 kDa). It has 5 putative N-glycosylation sites on each polypeptide chain and the attached carbohydrates exhibit some degree of chain heterogeneity, including heterogeneity in terminal sialic acid residues, except at the site associated with the Fc domain, which is unsialylated | The opthalmic agent is used for the treatment of neovascular (wet) age-related mascular degeneration (AMD) and macular edema following central retinal vein occulsion (CRVO). The systemic injection, known as ziv-aflibercept, in combination with 5-fluorouracil, leucovorin, irinotecan-(FOLFIRI), is for the treatment of metastatic colorectal cancer that is resistant to or progressed following treatment with oxaliplatin. | Compared to other anti-VEGF drugs like bevacizumab and ranibizumab, aflibercept has a higher binding affinity to VEGF-A (Kd = 0.5 pM). | Ablibercept is a recombinant fusion protein that acts as a decoy receptor for the ligands, vascular endothelial growth factor-A (VEGF-A) and placental growth factor (PIGF). It prevents these ligands to binding to endothelial receptors, VEGFR-1 and VEGFR-2, to suppress neovascularization and decrease vascular permeability. This ultimately will slow vision loss or the progression of metastatic colorectal cancer. | For all intravitreal VEGF inhibitors, there is increased risk of stroke and myocardial infarction. An increase in intraocular pressure may also occur. When used intravenously, most common adverse reactions were leukopenia, diarrhea, neutropenia, proteinuria, AST increased, stomatitis, fatigue, thrombocytopenia, ALT increased, hypertension, weight decreased, decreased appetite, epistaxis, abdominal pain, dysphonia, serum creatinine increased, and headache. | Because aflibercept is a protein, it is expected to be broken down via proteolysis into smaller peptides and amino acids. The cytochrome P450 enzyme system is not involved in the metabolism of aflibercept. | In patients with wet AMD and CRVO, the mean peak plasma concentration (Cmax) was 0.02 mcg/mL and 0.05 mcg/mL respectively. These concentrations were reached in 1 to 3 days. Aflibercept did not accumulate when administered as repeated doses intravitreally every 4 weeks. | After intravenous injection of aflibercept, the volume of distribution is 6 L. | When cancer patients were given 2-9 mg/kg every 2 or 3 week; 1 hour IV infusion of aflibercept the typical estimated clearances were as follows: CL of free aflibercept (CLf) = 0.88 L/day; CL of bound aflibercept (CLf) = 0.19 L/day; Patients clear free aflibercept faster if they had low albumin or high alkaline phosphatase levels. | Antineoplastic Agents and Ophthalmics | US7608261 | 27-10-2009 | 14-06-2027 | NA | Vascular endothelial growth factor A,Placenta growth factor,Vascular endothelial growth factor B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10647 | Th1133 | Aflibercept | >Th1133_Aflibercept SDTGRPFVEMYSEIPEIIHMTEGRELVIPCRVTSPNITVTLKKFPLDTLIPDGKRIIWDSRKGFIISNATYKEIGLLTCEATVNGHLYKTNYLTHRQTNTIIDVVLSPSHGIELSVGEKLVLNCTARTELNVGIDFNWEYPSSKHQHKKLVNRDLKTQSGSEMKKFLSTLTIDGVTRSDQGLYTCAASSGLMTKKNSTFVRVHEKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 115000 | C4318H6788N1164O1304S32 | NA | NA | NA | Intravitreal half life - 7.13 days | Aflibercept is a vascular endothelial growth factor (VEGF) inhibitor. It is a recombinant dimeric fusion glycoprotein that comprises (VEGF) binding portions from the extracellular domains of human VEGF receptors 1 and 2, this is fused to the Fc portion of human IgG1. It contains approximately 15% glycosylation to give a total molecular weight of 115 kDa (protein part = 96.9 kDa). It has 5 putative N-glycosylation sites on each polypeptide chain and the attached carbohydrates exhibit some degree of chain heterogeneity, including heterogeneity in terminal sialic acid residues, except at the site associated with the Fc domain, which is unsialylated | The opthalmic agent is used for the treatment of neovascular (wet) age-related mascular degeneration (AMD) and macular edema following central retinal vein occulsion (CRVO). The systemic injection, known as ziv-aflibercept, in combination with 5-fluorouracil, leucovorin, irinotecan-(FOLFIRI), is for the treatment of metastatic colorectal cancer that is resistant to or progressed following treatment with oxaliplatin. | Compared to other anti-VEGF drugs like bevacizumab and ranibizumab, aflibercept has a higher binding affinity to VEGF-A (Kd = 0.5 pM). | Ablibercept is a recombinant fusion protein that acts as a decoy receptor for the ligands, vascular endothelial growth factor-A (VEGF-A) and placental growth factor (PIGF). It prevents these ligands to binding to endothelial receptors, VEGFR-1 and VEGFR-2, to suppress neovascularization and decrease vascular permeability. This ultimately will slow vision loss or the progression of metastatic colorectal cancer. | For all intravitreal VEGF inhibitors, there is increased risk of stroke and myocardial infarction. An increase in intraocular pressure may also occur. When used intravenously, most common adverse reactions were leukopenia, diarrhea, neutropenia, proteinuria, AST increased, stomatitis, fatigue, thrombocytopenia, ALT increased, hypertension, weight decreased, decreased appetite, epistaxis, abdominal pain, dysphonia, serum creatinine increased, and headache. | Because aflibercept is a protein, it is expected to be broken down via proteolysis into smaller peptides and amino acids. The cytochrome P450 enzyme system is not involved in the metabolism of aflibercept. | In patients with wet AMD and CRVO, the mean peak plasma concentration (Cmax) was 0.02 mcg/mL and 0.05 mcg/mL respectively. These concentrations were reached in 1 to 3 days. Aflibercept did not accumulate when administered as repeated doses intravitreally every 4 weeks. | After intravenous injection of aflibercept, the volume of distribution is 6 L. | When cancer patients were given 2-9 mg/kg every 2 or 3 week; 1 hour IV infusion of aflibercept the typical estimated clearances were as follows: CL of free aflibercept (CLf) = 0.88 L/day; CL of bound aflibercept (CLf) = 0.19 L/day; Patients clear free aflibercept faster if they had low albumin or high alkaline phosphatase levels. | Antineoplastic Agents and Ophthalmics | US7070959 | 7-Apr-2006 | 23-05-2020 | NA | Vascular endothelial growth factor A,Placenta growth factor,Vascular endothelial growth factor B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10648 | Th1133 | Aflibercept | >Th1133_Aflibercept SDTGRPFVEMYSEIPEIIHMTEGRELVIPCRVTSPNITVTLKKFPLDTLIPDGKRIIWDSRKGFIISNATYKEIGLLTCEATVNGHLYKTNYLTHRQTNTIIDVVLSPSHGIELSVGEKLVLNCTARTELNVGIDFNWEYPSSKHQHKKLVNRDLKTQSGSEMKKFLSTLTIDGVTRSDQGLYTCAASSGLMTKKNSTFVRVHEKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 115000 | C4318H6788N1164O1304S32 | NA | NA | NA | Intravitreal half life - 7.13 days | Aflibercept is a vascular endothelial growth factor (VEGF) inhibitor. It is a recombinant dimeric fusion glycoprotein that comprises (VEGF) binding portions from the extracellular domains of human VEGF receptors 1 and 2, this is fused to the Fc portion of human IgG1. It contains approximately 15% glycosylation to give a total molecular weight of 115 kDa (protein part = 96.9 kDa). It has 5 putative N-glycosylation sites on each polypeptide chain and the attached carbohydrates exhibit some degree of chain heterogeneity, including heterogeneity in terminal sialic acid residues, except at the site associated with the Fc domain, which is unsialylated | The opthalmic agent is used for the treatment of neovascular (wet) age-related mascular degeneration (AMD) and macular edema following central retinal vein occulsion (CRVO). The systemic injection, known as ziv-aflibercept, in combination with 5-fluorouracil, leucovorin, irinotecan-(FOLFIRI), is for the treatment of metastatic colorectal cancer that is resistant to or progressed following treatment with oxaliplatin. | Compared to other anti-VEGF drugs like bevacizumab and ranibizumab, aflibercept has a higher binding affinity to VEGF-A (Kd = 0.5 pM). | Ablibercept is a recombinant fusion protein that acts as a decoy receptor for the ligands, vascular endothelial growth factor-A (VEGF-A) and placental growth factor (PIGF). It prevents these ligands to binding to endothelial receptors, VEGFR-1 and VEGFR-2, to suppress neovascularization and decrease vascular permeability. This ultimately will slow vision loss or the progression of metastatic colorectal cancer. | For all intravitreal VEGF inhibitors, there is increased risk of stroke and myocardial infarction. An increase in intraocular pressure may also occur. When used intravenously, most common adverse reactions were leukopenia, diarrhea, neutropenia, proteinuria, AST increased, stomatitis, fatigue, thrombocytopenia, ALT increased, hypertension, weight decreased, decreased appetite, epistaxis, abdominal pain, dysphonia, serum creatinine increased, and headache. | Because aflibercept is a protein, it is expected to be broken down via proteolysis into smaller peptides and amino acids. The cytochrome P450 enzyme system is not involved in the metabolism of aflibercept. | In patients with wet AMD and CRVO, the mean peak plasma concentration (Cmax) was 0.02 mcg/mL and 0.05 mcg/mL respectively. These concentrations were reached in 1 to 3 days. Aflibercept did not accumulate when administered as repeated doses intravitreally every 4 weeks. | After intravenous injection of aflibercept, the volume of distribution is 6 L. | When cancer patients were given 2-9 mg/kg every 2 or 3 week; 1 hour IV infusion of aflibercept the typical estimated clearances were as follows: CL of free aflibercept (CLf) = 0.88 L/day; CL of bound aflibercept (CLf) = 0.19 L/day; Patients clear free aflibercept faster if they had low albumin or high alkaline phosphatase levels. | Antineoplastic Agents and Ophthalmics | US7374757 | 20-05-2008 | 23-05-2020 | NA | Vascular endothelial growth factor A,Placenta growth factor,Vascular endothelial growth factor B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10692 | Th1156 | Abarelix | >Th1156_Abarelix XXXSYNLXPA | 1416.063 | C72H95ClN14O14 | NA | NA | NA | 13.2 ± 3.2 days | Synthetic decapeptide antagonist to gonadotropin releasing hormone (GnRH). It is marketed by Praecis Pharmaceuticals as Plenaxis. Praecis announced in June 2006 that it was voluntarily withdrawing the drug from the market. | For palliative treatment of advanced prostate cancer. | Used in the palliative treatment of advanced prostate cancer. Abarelix is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis | Abarelix binds to the gonadotropin releasing hormone receptor and acts as a potent inhibitor of gonadotropin secretion | NA | NA | NA | NA | NA | Anti-Testosterone Agents | US5968895 | 19-10-1999 | 12-Nov-2016 | Tacrolimus, Thiothixene, Toremifene, Trimipramine, Voriconazole, Vorinostat, Ziprasidone, Zuclopenthixol- All above drugs cause Additive QTc Prolongation and increases the risk of severe ventricular arrythmias | Gonadotropin-releasing hormone receptor | Plenaxis | Speciality european pharma | Speciality european pharma | Plenaxis is indicated for the palliative treatment of men with advanced symptomatic prostate cancer, in whom LHRH agonist therapy is not appropriate and who refuse surgical castration, and have one or more of the following: (1) risk of neurological compromise due to metastases, (2) ureteral or bladder outlet obstruction due to local encroachment or metastatic disease, or (3) severe bone pain from skeletal metastases persisting on narcotic analgesia. | Abarelix is chemically described as acetyl-D-β-naphthylalanyl-D-4-chlorophenylalanyl- D-3-pyridylalanyl-L-seryl-L-N-methyl-tyrosyl-D-asparagyl-L-leucyl-L-N(ε)-isopropyllysyl- L-prolyl-D-alanyl-amide. | The single-dose vial contains 113 mg of anhydrous free base abarelix peptide (net) supplied in an abarelix CMC complex. This complex also contains 19.1 to 31 mg of CMC. After the vial is reconstituted with 2.2 mL of 0.9% sodium chloride injection | Abarelix for injectable suspension is supplied as a white to off-white sterile dry powder | Intramuscular Injection | The recommended dose of Plenaxis is 100 mg administered intramuscularly to the buttock on Day 1, 15, 29 (week 4) and every 4 weeks thereafter. | Plenaxis is not indicated in women or pediatric patients. In addition, Plenaxis may cause fetal harm if administered to a pregnant woman. | Diarrhea, Dizziness, Flushing of Skin, Headache, Constipation, Sleep Disturbance | Link | NA | NA |
| 10701 | Th1160 | Satumomab Pendetide | >Th1160_Satumomab_Pendetide QVQLQQSDAELVKPGASVKISCKASGYTFTDHAIHWAKQKPEQGLEWIGYISPGNDDIKYNEKFKGKATLTADKSSSTAYMQLNSLTSEDSAVYFCKRSYYGHWGQGTTLTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVCPPCKCPAPNLLGGPSVFIFPPKIKDVLMISLSPIVTCVVVDVSEDDPDVQISWFVNNVEVHTAQTQTHREDYNSTLRVVSALPIQHQDWMSGKEFKCKVNNKDLPAPIERTISKPKGSVRAPQVYVLPPPEEEMTKKQVTLTCMVTDFMPEDIYVEWTNNGKTELNYKNTEPVLDSDGSYFMYSKLRVEKKNWVERNSYSCSVVHEGLHNHHTTKSFSR | 141478.9 | C6268H9708N1666O1971S48 | 7.02 | -0.427 | 61 (FAB fr | 0.80 hours(Mammalian reticulocytes) | Tumor associated glycoprotein (TAG) 72 (B72.3) monoclonal antibody conjugated with Indium 111 for radioimaging colon tumors. Satumomab Pendetide (trade name: OncoScint) is no longer commercially available. | For diagnosis of extrahepatic malignant cancers | Binds to the tumor associated glycoprotein 72 antigen, which is a cell surface protein generally over-expressed in colorectal cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of TAG-72 expressing cells and tumors | Satumomab Pendetide is a monoclonal antibody which is attached to the chelator pentetic acid (DTPA) linked to the tripeptide glycine (G) – L-tyrosine (Y) – L-lysine (K), which chelates Indium 111. Satumomab pendetide binds selectively to cell-surface TAG-72 expressed on colorectal tumors. | NA | NA | NA | NA | NA | Diagnostic Agents | NA | NA | NA | NA | Tumor-associated glycoprotein 72 (TAG-72) | OncoScint | Cytogen Corp, Lonza Biologics | Cytogen Corp, Lonza Biologics | Extrahepatic malignant disease (diagnosis)â€â€Indium In 111 satumomab pendetide is indicated for use in immunoscintigraphy in patients with known colorectal or ovarian cancer. | NA | NA | NA | Intravenous Injection | Estimated dose- 0.32 mSv/MBq | NA | Chillls, Diarrhea, Dizziness, Flushing of Skin, Allergic reactions, confusion, hypertension, Skin rashes, hypothermia, nausea, headache. | Link | NA | NA |
| 10710 | Th1163 | Ancestim | >Th1163_Ancestim MEGICRNRVTNNVKDVTKLVANLPKDYMITLKYVPGMDVLPSHCWISEMVVQLSDSLTDLLDKFSNISEGLSNYSIIDKLVNIVDDLVECVKENSSKDLKKSFKSPEPRLFTPEEFFRIFNRSIDAFKDFVVASETSDCVVSSTLSPEKDSRVSVTKPFMLPPVA | 18540 | C1662H2650N422O512S18 | 5.86 | NA | 230ºC | 2-5 hours | Ancestim is a recombinant methionyl human stem cell factor, branded by Amgen as StemGen. It was developed by Amgen and sold to Biovitrium, now Swedish Orphan Biovitrum, in December, 2008. It is a 166 amino acid protein produced by E. coli bacteria into which a gene has been inserted for soluble human stem cell factor. It has a monomeric molecular weight of approximately 18,500 daltons and normally exists as a noncovalently associated dimer. The protein has an amino acid sequence that is identical to the natural sequence predicted from human DNA sequence analysis, except for the addition of an N-terminal methionine retained after expression in E. coli. Because Ancestim is produced in E. coli, it is nonglycosylated. Ancestim is supplied as a sterile, white, preservative-free, lyophilised powder for reconstitution and administration as a subcutaneous (SC) injection and is indicated for use in combination with filgrastim for mobilizing peripheral hematopoietic stem cells for later transplanation in certain cancer patients | Indicated for use in combination with filgrastim for mobilizing peripheral hematopoietic stem cells for later transplanation in certain cancer patients | NA | Recombinant human stem cell factor | Ancestim was not genotoxic for gene mutation or chromosomal damage and it did not have any effect in fertility.[L1089] | Administration of ancestim in preclinical trials have proven that from the excreted dose all of it is formed by degraded ancestim into lower molecular weigth products.[L1089] | The pharmacokinetics of ancestim has a dose-linear profile. After subcutaneous administration, ancestim has an absorption half-life of 35-41 hours following a mean lag of 2 hours. When a dose of 5-25 mcg/kg is administered, the peak concentration of 3.6-13.7 ng/ml is reached after 15-24 hours. In preclinical studies, the bioavailability of ancestim was reported to be greater than 60%. After multiple dosing, the steady state was reached after 4-5 days from the beginning of the treatment.[L1089] | Preclinical reports demonstrate that after intravenous administration of ancestim, the distribution profile is primarily in plasma and kidneys with a subsequent and rapid loss from all tissues.[L1089] | The apparent clearance reported for ancestim is approximately 35-40 ml/h/kg.[L1089] | NA | NA | NA | NA | NA | Mast/stem cell growth factor receptor Kit | Stemgen | Biovitrum Ab (publ) | Biovitrum Ab (publ) | indicated for use in combination with NEUPOGEN® (filgrastim) in the setting of autologous peripheral blood progenitor cell (PBPC) transplantation for patients at risk of poor PBPC mobilisation to increase the number of PBPC collected in the apheresis harvest, thereby increasing the proportion of patients reaching a PBPC target for transplantation. | NA | Reconstitute with 1.2 mL sterlie water for injection to yield a concentration of 1.5 mg/mL with a withdrawable volume of 1 mL. Compatibility with saline or other diluents is unknown. During reconstitution, the vial contents may be gently swirled to avoid foaming during dissolution. Avoid excess or vigorous agitation | NA | Subcutaneous | 20 mcg/kg/day SC | It is contraindicated in patients with known hypersensitivity to E coli-derived proteins, ancestim or any component of the product; increased risk of systemic allergic reactions (greater incidence and severity) when STEMGEN® was administered by the IV route | Injection site reactions (92%); Paresthesia (29%); Respiratory symptoms (28%); Distant skin reactions (21%);Nausea (16%); Headache (13%); Dizziness (12%); Tachycardia (8%) | Link | NA | NA |
| 10780 | Th1181 | Filgrastim-sndz | >Th1181_Filgrastim-sndz MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S9 | 5.65 | NA | NA | Approximately 3.5 hours | NA | Patients with Cancer Receiving Myelosuppressive Chemotherapy: to decrease the incidence of infection, as manifested by febrile neutropenia, in patients with nonmyeloid malignancies receiving myelosuppressive anti-cancer drugs associated with a significant incidence of severe neutropenia with fever. Patients with Acute Myeloid Leukemia Receiving Induction or Consolidation Chemotherapy: to reduce the time to neutrophil recovery and the duration of fever, following induction or consolidation chemotherapy treatment of patients with acute myeloid leukemia (AML). Patients with Cancer Undergoing Bone Marrow Transplantation: to reduce the duration of neutropenia and neutropenia-related clinical sequelae, e.g., febrile neutropenia, in patients with nonmyeloid malignancies undergoing myeloablative chemotherapy followed by bone marrow transplantation. Patients Undergoing Autologous Peripheral Blood Progenitor Cell Collection and Therapy: for the mobilization of autologous hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis. Patients with Severe Chronic Neutropenia: for chronic administration to reduce the incidence and duration of sequelae of neutropenia (e.g, fever, infections, oropharyngeal ulcers) in symptomatic patients with congenital neutropenia, cyclic neutropenia, or idiopathic neutropenia. | In patients with patients with various nonmyeloid malignancies‚ administration of filgrastim resulted in a dose-dependent increase in circulating neutrophil counts over the dose range of 1 to 70 mcg/kg/day. This increase in neutrophil counts was observed whether filgrastim was administered intravenous (1 to70 mcg/kg twice daily)‚ subcutaneous (1 to 3 mcg/kg once daily)‚ or by continuous subcutaneous infusion (3 to 11 mcg/kg/day). With discontinuation of filgrastim therapy‚ neutrophil counts returned to baseline in most cases within 4 days. Isolated neutrophils displayed normal phagocytic (measured by zymosan-stimulated chemoluminescence) and chemotactic (measured by migration under agarose using N-formyl-methionyl-leucyl- phenylalanine [fMLP] as the chemotaxin) activity in vitro. | Colony-stimulating factors are glycoproteins which act on hematopoietic cells by binding to specific cell surface receptors and stimulating proliferation‚ differentiation commitment‚ and some end-cell functional activation. Endogenous G-CSF is a lineage-specific colony-stimulating factor that is produced by monocytes‚ fibroblasts, and endothelial cells. G-CSF regulates the production of neutrophils within the bone marrow and affects neutrophil progenitor proliferation‚ differentiation, and selected end-cell functions (including enhanced phagocytic ability‚ priming of the cellular metabolism associated with respiratory burst‚ antibody-dependent killing, and the increased expression of some cell surface antigens). G-CSF is not species-specific and has been shown to have minimal direct in vivo or in vitro effects on the production or activity of hematopoietic cell types other than the neutrophil lineage. | NA | NA | NA | NA | NA | NA | NA | NA | NA | The risk or severity of adverse effects can be increased when Filgrastim-sndz is combined with Bleomycin; The risk or severity of adverse effects can be increased when Filgrastim-sndz is combined with Cyclophosphamide; The risk or severity of adverse effects can be increased when Filgrastim-sndz is combined with Topotecan. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10781 | Th1181 | Filgrastim-sndz | >Th1181_Filgrastim-sndz MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S9 | 5.65 | NA | NA | Approximately 3.5 hours | NA | Patients with Cancer Receiving Myelosuppressive Chemotherapy: to decrease the incidence of infection, as manifested by febrile neutropenia, in patients with nonmyeloid malignancies receiving myelosuppressive anti-cancer drugs associated with a significant incidence of severe neutropenia with fever. Patients with Acute Myeloid Leukemia Receiving Induction or Consolidation Chemotherapy: to reduce the time to neutrophil recovery and the duration of fever, following induction or consolidation chemotherapy treatment of patients with acute myeloid leukemia (AML). Patients with Cancer Undergoing Bone Marrow Transplantation: to reduce the duration of neutropenia and neutropenia-related clinical sequelae, e.g., febrile neutropenia, in patients with nonmyeloid malignancies undergoing myeloablative chemotherapy followed by bone marrow transplantation. Patients Undergoing Autologous Peripheral Blood Progenitor Cell Collection and Therapy: for the mobilization of autologous hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis. Patients with Severe Chronic Neutropenia: for chronic administration to reduce the incidence and duration of sequelae of neutropenia (e.g, fever, infections, oropharyngeal ulcers) in symptomatic patients with congenital neutropenia, cyclic neutropenia, or idiopathic neutropenia. | In patients with patients with various nonmyeloid malignancies‚ administration of filgrastim resulted in a dose-dependent increase in circulating neutrophil counts over the dose range of 1 to 70 mcg/kg/day. This increase in neutrophil counts was observed whether filgrastim was administered intravenous (1 to70 mcg/kg twice daily)‚ subcutaneous (1 to 3 mcg/kg once daily)‚ or by continuous subcutaneous infusion (3 to 11 mcg/kg/day). With discontinuation of filgrastim therapy‚ neutrophil counts returned to baseline in most cases within 4 days. Isolated neutrophils displayed normal phagocytic (measured by zymosan-stimulated chemoluminescence) and chemotactic (measured by migration under agarose using N-formyl-methionyl-leucyl- phenylalanine [fMLP] as the chemotaxin) activity in vitro. | Colony-stimulating factors are glycoproteins which act on hematopoietic cells by binding to specific cell surface receptors and stimulating proliferation‚ differentiation commitment‚ and some end-cell functional activation. Endogenous G-CSF is a lineage-specific colony-stimulating factor that is produced by monocytes‚ fibroblasts, and endothelial cells. G-CSF regulates the production of neutrophils within the bone marrow and affects neutrophil progenitor proliferation‚ differentiation, and selected end-cell functions (including enhanced phagocytic ability‚ priming of the cellular metabolism associated with respiratory burst‚ antibody-dependent killing, and the increased expression of some cell surface antigens). G-CSF is not species-specific and has been shown to have minimal direct in vivo or in vitro effects on the production or activity of hematopoietic cell types other than the neutrophil lineage. | NA | NA | NA | NA | NA | NA | NA | NA | NA | The risk or severity of adverse effects can be increased when Filgrastim-sndz is combined with Bleomycin; The risk or severity of adverse effects can be increased when Filgrastim-sndz is combined with Cyclophosphamide; The risk or severity of adverse effects can be increased when Filgrastim-sndz is combined with Topotecan. | NA | Zarxio | Sandoz Inc | Sandoz Inc | NA | NA | 300 ug/.5mL Injection | solution | intravenous; subcutaneous | The recommended starting dosage of ZARXIO is 5 mcg/kg/day‚ administered as a single daily injection by subcutaneous injection‚ by short intravenous infusion (15 to 30 minutes)‚ or by continuous intravenous infusion. Obtain a complete blood count (CBC) and platelet count before instituting ZARXIO therapy and monitor twice weekly during therapy. Consider dose escalation in increments of 5 mcg/kg for each chemotherapy cycle‚ according to the duration and severity of the absolute neutrophil count (ANC) nadir. Recommend stopping ZARXIO if the ANC increases beyond 10‚000/mm³ | ZARXIO is contraindicated in patients with a history of serious allergic reactions to human granulocyte colony-stimulating factors such as filgrastim or pegfilgrastim products | Splenic Rupture; Acute Respiratory Distress Syndrome; Serious Allergic Reactions ; Sickle Cell Disorders; Glomerulonephritis; Alveolar Hemorrhage and Hemoptysis; Capillary Leak Syndrome; Thrombocytopenia; Leukocytosis; Cutaneous Vasculitis. | Link | NA | NA |
| 10782 | Th1181 | Filgrastim-sndz | >Th1181_Filgrastim-sndz MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S9 | 5.65 | NA | NA | Approximately 3.5 hours | NA | Patients with Cancer Receiving Myelosuppressive Chemotherapy: to decrease the incidence of infection, as manifested by febrile neutropenia, in patients with nonmyeloid malignancies receiving myelosuppressive anti-cancer drugs associated with a significant incidence of severe neutropenia with fever. Patients with Acute Myeloid Leukemia Receiving Induction or Consolidation Chemotherapy: to reduce the time to neutrophil recovery and the duration of fever, following induction or consolidation chemotherapy treatment of patients with acute myeloid leukemia (AML). Patients with Cancer Undergoing Bone Marrow Transplantation: to reduce the duration of neutropenia and neutropenia-related clinical sequelae, e.g., febrile neutropenia, in patients with nonmyeloid malignancies undergoing myeloablative chemotherapy followed by bone marrow transplantation. Patients Undergoing Autologous Peripheral Blood Progenitor Cell Collection and Therapy: for the mobilization of autologous hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis. Patients with Severe Chronic Neutropenia: for chronic administration to reduce the incidence and duration of sequelae of neutropenia (e.g, fever, infections, oropharyngeal ulcers) in symptomatic patients with congenital neutropenia, cyclic neutropenia, or idiopathic neutropenia. | In patients with patients with various nonmyeloid malignancies‚ administration of filgrastim resulted in a dose-dependent increase in circulating neutrophil counts over the dose range of 1 to 70 mcg/kg/day. This increase in neutrophil counts was observed whether filgrastim was administered intravenous (1 to70 mcg/kg twice daily)‚ subcutaneous (1 to 3 mcg/kg once daily)‚ or by continuous subcutaneous infusion (3 to 11 mcg/kg/day). With discontinuation of filgrastim therapy‚ neutrophil counts returned to baseline in most cases within 4 days. Isolated neutrophils displayed normal phagocytic (measured by zymosan-stimulated chemoluminescence) and chemotactic (measured by migration under agarose using N-formyl-methionyl-leucyl- phenylalanine [fMLP] as the chemotaxin) activity in vitro. | Colony-stimulating factors are glycoproteins which act on hematopoietic cells by binding to specific cell surface receptors and stimulating proliferation‚ differentiation commitment‚ and some end-cell functional activation. Endogenous G-CSF is a lineage-specific colony-stimulating factor that is produced by monocytes‚ fibroblasts, and endothelial cells. G-CSF regulates the production of neutrophils within the bone marrow and affects neutrophil progenitor proliferation‚ differentiation, and selected end-cell functions (including enhanced phagocytic ability‚ priming of the cellular metabolism associated with respiratory burst‚ antibody-dependent killing, and the increased expression of some cell surface antigens). G-CSF is not species-specific and has been shown to have minimal direct in vivo or in vitro effects on the production or activity of hematopoietic cell types other than the neutrophil lineage. | NA | NA | NA | NA | NA | NA | NA | NA | NA | The risk or severity of adverse effects can be increased when Filgrastim-sndz is combined with Bleomycin; The risk or severity of adverse effects can be increased when Filgrastim-sndz is combined with Cyclophosphamide; The risk or severity of adverse effects can be increased when Filgrastim-sndz is combined with Topotecan. | NA | Zarxio | Sandoz Inc | Sandoz Inc | NA | NA | 480 ug/.8mL Injection | solution | intravenous; subcutaneous | The recommended starting dosage of ZARXIO is 5 mcg/kg/day‚ administered as a single daily injection by subcutaneous injection‚ by short intravenous infusion (15 to 30 minutes)‚ or by continuous intravenous infusion. Obtain a complete blood count (CBC) and platelet count before instituting ZARXIO therapy and monitor twice weekly during therapy. Consider dose escalation in increments of 5 mcg/kg for each chemotherapy cycle‚ according to the duration and severity of the absolute neutrophil count (ANC) nadir. Recommend stopping ZARXIO if the ANC increases beyond 10‚000/mm³ | ZARXIO is contraindicated in patients with a history of serious allergic reactions to human granulocyte colony-stimulating factors such as filgrastim or pegfilgrastim products | Splenic Rupture; Acute Respiratory Distress Syndrome; Serious Allergic Reactions ; Sickle Cell Disorders; Glomerulonephritis; Alveolar Hemorrhage and Hemoptysis; Capillary Leak Syndrome; Thrombocytopenia; Leukocytosis; Cutaneous Vasculitis. | Link | NA | NA |
| 10839 | Th1202 | Pembrolizumab | >Th1202_Pembrolizumab QVQLVQSGVEVKKPGASVKVSCKASGYTFTNYYMYWVRQAPGQGLEWMGGINPSNGGTNFNEKFKNRVTLTTDSSTTTAYMELKSLQFDDTAVYYCARRDYRFDMGFDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 149000 | C6504H10004N1716O2036S46 | 6.8-6.9 | NA | NA | 22 days. | Pembrolizumab is an antibody drug that targets the cell surface receptor programmed cell death protein 1 (PD-1) found on T cells. By preventing the binding of its ligands (PD-L1 and PD-L2), pembrolizumab induces an antitumor immune response. Upregulation of PD-1 ligands occurs in some tumors and signaling through this pathway can contribute to inhibition of active T-cell immune surveillance of tumors. Its use is indicated for the treatment of patients with unresectable or metastatic melanoma and disease progression following therapy with ipilimumab and, if BRAF V600 mutation positive, a BRAF inhibitor. Due to its success in clinical trials, pembrolizumab was approved early to allow quick patient access and was given breakthrough therapy and orphan drug designation. Pembrolizumab (as Keytruda) was approved by the U.S. Food and Drug Administration to treat advanced cases of the most common type of lung malignancy, non-small cell lung cancer (NSCLC) on Oct. 2, 2015. | For the treatment of patients with unresectable or metastatic melanoma and disease progression following therapy with ipilimumab and, if BRAF V600 mutation positive, a BRAF inhibitor. It is also for the treatment of patients with metastatic NSCLC (non-small cell lung cancer) whose tumors express PD-L1 (as determined by an approved test) and who have disease progression on or after platinum-containing chemotherapy. | In syngeneic mouse tumor models, blocking PD-1 activity resulted in decreased tumor growth. | Pembrolizumab is an antibody drug that targets the cell surface receptor programmed cell death protein 1 (PD-1) found on T cells. By preventing the binding of its ligands (PD-L1 and PD-L2), pembrolizumab induces an antitumor immune response. Upregulation of PD-1 ligands is a mechanism for tumours to evade antitumor immune response; when PD-1 binds its ligand, the T cell receives an inhibitory signal leading to T cell anergy and blockade of anti tumour immune response. Instead of directly targeting tumor tissue to induce tumor cell death, pembrolizumab acts as a checkpoint inhibitor to stimulate immune responses to eliminate cancer cells. | There are no data regarding overdosage with pembrolizumab. | Pembrolizumab is catalyzed into smaller peptides and amino acids via general protein degradation.[A18829] | When administered intravenously, pembrolizumab is completely bioavailable. When administered in repeated doses every 3 weeks, the systemic accumulation accounts for a 2.2 fold increase.[A18829] Steady-state is reached after approximately 16 weeks.[L38934] The absorption of pembrolizumab increases proportionally with increased dosage.[L38934] | The steady-state volume of distribution of pembrolizumab is approximately 6 liters.[L38934] | Clearance is moderately lower at steady-state (195 mL/day) than after the first dose (252 mL/day), although this decrease is not clinically significant.[L38934] | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Globulins,Immune Checkpoint Inhibitors,Immunoglobulins,Immunoproteins,Immunotherapy,Programmed Death Receptor-1 Blocking Antibody,Programmed Death Receptor-1-directed Antibody Interactions,Proteins,Serum Globulins | US2012135408 | 29-03-2012 | 29-03-2032 | NA | Programmed cell death protein 1 | Keytruda | Merck Sharp & Dohme Corp. | Merck Sharp & Dohme Corp. | KEYTRUDA® (pembrolizumab) is indicated for the treatment of patients with unresectable or metastatic melanoma. | NA | 100 mg of pembrolizumab in 4 mL of solution. | lyophilized powder | Intravenous infusion | The recommended dose of KEYTRUDA is 2 mg/kg administered as an intravenous infusion over 30 minutes every 3 weeks until disease progression or unacceptable toxicity. | NA | Immune-mediated pneumonitis; Immune-mediated colitis; Immune-mediated hepatitis; Immune-mediated endocrinopathies; Immune-mediated nephritis and renal dysfunction; Other immune-mediated adverse reactions; Infusion-related reactions. | Link | NA | NA |
| 10844 | Th1207 | Necitumumab | >Th1207_Necitumumab QVQLQESGPGLVKPSQTLSLTCTVSGGSISSGDYYWSWIRQPPGKGLEWIGYIYYSGSTDYNPSLKSRVTMSVDTSKNQFSLKVNSVTAADTAVYYCARVSIFGVGTFDYWGQGTLVTVSSASTKGPSVLPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144844.9 | C6436H9958N1702O2020S42 | NA | NA | NA | Approx 14 days | Necitumumab is an intravenously administered recombinant monoclonal IgG1 antibody used in the treatment of non-small cell lung cancer (NSCLC) as an EGFR antagonist. It functions by binding to epidermal growth factor receptor (EGFR) and prevents binding of its ligands, a process that is involved in cell proliferation, metastasis, angiogenesis, and malignant progression. Binding of necitumumab to EGFR induces receptor internalization and degradation, thereby preventing further activation of EGFR which is beneficial in NSCLC as many patients have increased protein expression of EGFR. Necitumumab is approved for use in combination with cisplatin and gemcitabine as a first-line treatment for metastatic squamous non-small cell lung cancer (NSCLC). | Necitumumab is approved for use in combination with cisplatin and gemcitabine as a first-line treatment for metastatic squamous non-small cell lung cancer (NSCLC). It is not indicated for treatment of non-squamous NSCLC. | In animal models administration of necitumumab to implanted mice resulted in increased antitumor activity in combination with gemcitabine and cisplatin as compared to mice receiving gemcitabine and cisplatin alone. | Necitumumab is a recombinant human lgG1 monoclonal antibody that binds to the human epidermal growth factor receptor (EGFR) and blocks the binding of EGFR to its ligands. Expression and activation of EGFR has been correlated with malignant progression, induction of angiogenesis, and inhibition of apoptosis. Binding of necitumumab induces EGFR internalization and degradation in vitro. In vitro, binding of necitumumab also led to antibody-dependent cellular cytotoxicity (ADCC) in EGFR-expressing cells. | The poor safety profile of necitumumab has been one of the major limitations of its use. Rigorous monitoring of the following adverse events is recommended for the use of this drug: cardiopulmonary arrest, hypomagnesia, venous and arterial thromboembolic events, dermatologic toxicities, and infusion-related reactions. Due to observations of increased toxicity and mortality in treatment of non-squamous NSCLC, necitumumab is only recommended for the treatment of squamous NSCLC in combination with cisplatin and gemcitabine. Animal studies suggest potential embryo-fetal toxicity. | NA | NA | Steady state volume of distribution is 7.0 L. | 14.1 mL/h | NA | NA | NA | NA | NA | Epidermal growth factor receptor | Portrazza | Eli Lilly and Company | Eli Lilly and Company | PORTRAZZAâ„¢ is indicated, in combination with gemcitabine and cisplatin, for first-line treatment of patients with metastatic squamous non-small cell lung cancer. | NA | Each vial contains 800 mg PORTRAZZA in 50 mL (16 mg/mL) | Sterile, preservative free, clear to slightly opalescent and colorless to slightly yellow solution | intravenous | The recommended dose of PORTRAZZA is 800 mg administered as an intravenous infusion over 60 minutes on Days 1 and 8 of each 3-week cycle prior to gemcitabine and cisplatin infusion. Continue PORTRAZZA until disease progression or unacceptable toxicity. | NA | Cardiopulmonary Arrest; Hypomagnesemia; Venous and Arterial Thromboembolic Events; Dermatologic Toxicities; nfusion-Related Reactions; Non-Squamous NSCLC - Increased Toxicity and Increased Mortality . | Link | NA | NA |
| 10876 | Th1236 | Sipuleucel-T | NA | NA | NA | NA | NA | NA | NA | Sipuleucel-T is a personalized, autologous, cellular immunotherapy. Sipuleucel-T is a therapeutic cancer vaccine for prostate cancer. Sipuleucel-T selectively targets the prostate-specific antigen (PSA) known as prostatic acid phosphatase (PAP) that is expressed in around 95% of prostate cancers. It must be prepared specifically for each patient. In metastatic prostate cancer, it has extended survival by median 4.1 months (IMPACT Phase III trial data). Sipuleucel-T is marketed under the brand name Provenge by Dendreon Corporation. Sipuleucel-T was approved by the U.S. Food and Drug Administration (FDA) on April 29, 2010, to treat asymptomatic or minimally symptomatic metastatic Hormone-Refractory Prostate Cancer (HRPC). The treatment initially cost $93,000 at the time of FDA approval, but rose to over $100,000 in 2014. | Sipuleucel-T is an autologous cellular immunotherapy indicated for the treatment of asymptomatic or minimally symptomatic metastatic castrate resistant (hormone refractory) prostate cancer. | NA | Sipuleucel-T is designed to induce an immune response targeted against PAP, an antigen expressed in most prostate cancers. During ex vivo culture with PAP-GM-CSF, APCs take up and process the recombinant target antigen into small peptides that are then displayed on the APC surface. The precise mechanism remains unknown, however. | NA | NA | NA | NA | NA | Antineoplastic and Immunomodulating Agents | US8153120 | 4-Oct-2012 | 22-03-2027 | The therapeutic efficacy of Sipuleucel-T can be decreased when used in combination with 2-Methoxyethanol, 9-(2-phosphonylmethoxyethyl)-2,6-diaminopurine, Abatacept, abetimus, ABR-215757, Acteoside, Adalimumab, Adefovir Dipivoxil, Afelimomab, Alefacept. | Prostatic acid phosphatase | Provenge | NA | NA | Provenge® (sipuleucel-T) is an autologous cellular immunotherapy indicated for the treatment of asymptomatic or minimally symptomatic metastatic castrate resistant (hormone refractory) prostate cancer | NA | NA | Solution | Intravenous | The recommended course of therapy for PROVENGE is 3 complete doses, given at approximately 2-week intervals. In controlled clinical trials, the median dosing interval between infusions was 2 weeks (range 1 to 15 weeks); the maximum dosing interval has not been established | Hypersensitivity to the active substance | fever;gredness, swelling, oozing, or other signs of infection where the IV needle was placed; orgsigns of infection around the veins your cells were collected from. | Link | NA | NA |
| 11718 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Amino Acids, Peptides, and Proteins | NA | NA | NA | Chlorotrianisene,Conjugated estrogens,Estrone,Dienestrol,Estriol,Quinestrol,Hexestrol,Tibolone,Synthetic Conjugated Estrogens, A,Synthetic Conjugated Estrogens, B,Polyestradiol phosphate,Esterified estrogens,Zeranol,Equol,Promestriene,Methallenestril,Epimestrol,Moxestrol,Estradiol acetate,Biochanin A,Formononetin,Diethylstilbestrol,Estradiol,Ethinylestradiol,Mestranol,Estrone sulfate,Estradiol benzoate,Estradiol cypionate,Estradiol valerate,Estetrol,Leuprolide,Goserelin,Gonadorelin,Nafarelin,Buserelin,Histrelin,Triptorelin,Deslorelin,Danazol,Elagolix,Gestrinone,Flutamide,Nilutamide,Bicalutamide,Enzalutamide,Apalutamide,Darolutamide,Cyproterone acetate,Chlormadinone,Relugolix,Chlormadinone acetate,Cetuximab,Human immunoglobulin G,Omalizumab,Adalimumab,Abciximab,Gemtuzumab ozogamicin,Indium In-111 satumomab pendetide,Infliximab,Trastuzumab,Rituximab,Basiliximab,Muromonab,Digoxin Immune Fab (Ovine),Ibritumomab tiuxetan,Tositumomab,Alemtuzumab,Efalizumab,Antithymocyte immunoglobulin (rabbit),Natalizumab,Palivizumab,Daclizumab,Bevacizumab,Technetium Tc-99m arcitumomab,Eculizumab,Panitumumab,Ranibizumab,Galiximab,Pexelizumab,Afelimomab,Epratuzumab,Bectumomab,Oregovomab,IGN311,Adecatumumab,Labetuzumab,Matuzumab,Fontolizumab,Bavituximab,CR002,Rozrolimupab,Girentuximab,Obiltoxaximab,XTL-001,NAV 1800,Briakinumab,Otelixizumab,AMG 108,Iratumumab,Enokizumab,Ramucirumab,Farletuzumab,Veltuzumab,Ustekinumab,Trastuzumab emtansine,PRO-542,TNX-901,Inotuzumab ozogamicin,RI 624,MYO-029,CT-011,Leronlimab,Glembatumumab vedotin,Olaratumab,IPH 2101,TB-402,Caplacizumab,IMC-1C11,Eldelumab,Lumiliximab,Canakinumab,Ipilimumab,Nimotuzumab,Clenoliximab,Tocilizumab,BIIB015,Sonepcizumab,Motavizumab,Elotuzumab,AVE9633,Carotuximab,XmAb 2513,Coltuximab ravtansine,Lucatumumab,Pertuzumab,Siplizumab,Apolizumab,Sibrotuzumab,Bivatuzumab,Lerdelimumab,Lexatumumab,Reslizumab,Teplizumab,Catumaxomab,Mepolizumab,Denosumab,Volociximab,Ofatumumab,Golimumab,Brentuximab vedotin,Belimumab,Raxibacumab,Obinutuzumab,Secukinumab,Vedolizumab,Nivolumab,Siltuximab,Pembrolizumab,Dulaglutide,Blinatumomab,Anthrax immune globulin human,Dinutuximab,Asfotase alfa,Idarucizumab,Alirocumab,Evolocumab,Antilymphocyte immunoglobulin (horse),Daratumumab,Necitumumab,Ixekizumab,Ravulizumab,Atezolizumab,Tetanus immune globulin, human,Eftrenonacog alfa,Human varicella-zoster immune globulin,Conatumumab,Tabalumab,Ficlatuzumab,Figitumumab,Durvalumab,Bapineuzumab,Depatuxizumab mafodotin,Onartuzumab,Solanezumab,Sarilumab,Tremelimumab,Brodalumab,Sirukumab,Lampalizumab,Guselkumab,Dalotuzumab,Emibetuzumab,Ublituximab,Ligelizumab,Seribantumab,Landogrozumab,Romosozumab,Vadastuximab talirine,Lebrikizumab,Varlilumab,Avelumab,Crenezumab,Rilotumumab,Anifrolumab,Ocrelizumab,Benralizumab,Gantenerumab,Visilizumab,Urelumab,Lorvotuzumab mertansine,Patritumab,Fulranumab,Tarextumab,Sotatercept,Gevokizumab,Duligotuzumab,Simtuzumab,Fasinumab,Dupilumab,Tralokinumab,Etrolizumab,Zalutumumab,Ganitumab,Etaracizumab,Polatuzumab vedotin,Inclacumab,Cixutumumab,Ascrinvacumab,Aducanumab,GS-5745,Vanucizumab,Labetuzumab govitecan,Tanezumab,Ensituximab,Fezakinumab,Dusigitumab,Fresolimumab,Indusatumab vedotin,Bococizumab,Mirvetuximab Soravtansine,Mogamulizumab,Plozalizumab,Inebilizumab,Mavrilimumab,Blosozumab,Bimagrumab,Dacetuzumab,Tovetumab,Lumretuzumab,Ibalizumab,Intetumumab,Carlumab,Demcizumab,Sifalimumab,Abituzumab,Ecromeximab,Naptumomab estafenatox,Crotedumab,Concizumab,Depatuxizumab,Rontalizumab,Amatuximab,Clazakizumab,Ozanezumab,Sacituzumab govitecan,Bimekizumab,Milatuzumab,Robatumumab,Rovalpituzumab tesirine,Namilumab,Racotumomab,Tregalizumab,Olokizumab,Bezlotoxumab,Edrecolomab,Nebacumab,Human cytomegalovirus immune globulin,Emicizumab,Sulesomab,Besilesomab,Tildrakizumab,Burosumab,Erenumab,Eptinezumab,Fremanezumab,Galcanezumab,Fanolesomab,Lecanemab,Lanadelumab,Cemiplimab,Emapalumab,Risankizumab,Camrelizumab,Setrusumab,Gancotamab,Anetumab ravtansine,Isatuximab,Icrucumab,Codrituzumab,Brolucizumab,Xentuzumab,Lintuzumab,Vobarilizumab,Parsatuzumab,Emactuzumab,Bevacizumab zirconium Zr-89,Refanezumab,Rozanolixizumab,Bermekimab,Pamrevlumab,Opicinumab,Trastuzumab deruxtecan,Margetuximab,Dalantercept,Pateclizumab,Gremubamab,Apomab,Tafasitamab,Ipafricept,Abrilumab,Frovocimab,Tezepelumab,Tigatuzumab,Telisotuzumab vedotin,Utomilumab,Zolbetuximab,Ponezumab,Asunercept,Suvratoxumab,Mitazalimab,Nemolizumab,Bleselumab,Gedivumab,Valanafusp alfa,Sofituzumab vedotin,Istiratumab,Pidilizumab,GMA-161,Ladiratuzumab vedotin,Tomaralimab,Vesencumab,Pinatuzumab vedotin,Lulizumab pegol,Lorukafusp alfa,Naratuximab emtansine,Zenocutuzumab,Atoltivimab,Maftivimab,Odesivimab,Belantamab mafodotin,Ansuvimab,Bamlanivimab,Hepatitis B immune globulin,Human Rho(D) immune globulin,Dostarlimab,Certolizumab pegol,Inolimomab,Pentaglobin,Abagovomab,Efungumab,Foralumab,Indatuximab ravtansine,Magrolimab,Olinvacimab,Actoxumab,Volagidemab,Bentracimab,Amivantamab,Ebola Zaire vaccine (live, attenuated),Imdevimab,Casirivimab,Cilgavimab,Tixagevimab | Glutamate carboxypeptidase 2 | ProstaScint Kit for the Preparation of Indium In 111 Capromab Pendetide | Jazz Pharmaceuticals, Inc. | Jazz Pharmaceuticals, Inc. | Intravenous | 0.5 mg/1mL | Indium In 111 ProstaScint® (capromab pendetide) should not be used in patients who are hypersensitive to this or any other product of murine origin or to Indium In 111 chloride. | ProstaScint® (capromab pendetide) was generally well tolerated in the clinical trials. After administration of 529 single doses of Indium In 111 ProstaScint®, adverse reactions were observed in 4% of patients. The most commonly reported adverse reactions were increases in bilirubin, hypotension, and hypertension, which occurred in 1% of patients. Elevated liver enzymes and injection site reactions occurred in slightly less than 1% of patients. Other adverse reactions, listed in order of decreasing frequency, were: pruritus, fever, rash, headache, myalgia, asthenia, burning sensation in thigh, shortness of breath, and alteration of taste. | ProstaScint® (capromab pendetide) is the murine monoclonal antibody, 7E11-C5.3, conjugated to the linker-chelator, glycyl-tyrosyl-(N, ε-diethylenetriaminepentaacetic acid)-lysine hydrochloride (GYK-DTPA-HCl). The 7E11-C5.3 antibody is of the IgG1, kappa subclass (IgG1κ). This antibody is directed against a glycoprotein expressed by prostate epithelium known as Prostate Specific Membrane Antigen (PSMA). | ProstaScint® (capromab pendetide) is indicated as a diagnostic imaging agent in newly-diagnosed patients with biopsy-proven prostate cancer, thought to be clinically-localized after standard diagnostic evaluation (e.g. chest x-ray, bone scan, CT scan, or MRI), who are at high-risk for pelvic lymph node metastases | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | Link | NA |
| 11719 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Antibodies | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11720 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Blood Proteins | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11721 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Compounds used in a research, industrial, or household setting | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11722 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Diagnostic Radiopharmaceuticals | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11723 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Globulins | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11724 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Immunoglobulins | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11725 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Immunoproteins | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11726 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Indicators and Reagents | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11727 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Indium (111In) Compounds | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11728 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Indium Radioisotopes | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11729 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Laboratory Chemicals | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11730 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Prostatic Neoplasms | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11731 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Proteins | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11732 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Serum Globulins | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11733 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Tumour Detection | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11823 | Th1258 | Galiximab | NA | NA | NA | NA | NA | NA | 13 to 24 days | Galiximab is a chimeric monoclonal antibody which is used as an immunosuppressive drug. | Investigated for use/treatment in lymphoma (non-hodgkin's), psoriasis and psoriatic disorders, bone metastases, multiple myeloma, prostate cancer, and rheumatoid arthritis. | Galiximab is a monoclonal antibody that is being studied in the treatment of follicular non-Hodgkin lymphoma. Monoclonal antibodies are made in the laboratory and can locate and bind to cancer cells. Galiximab binds to the protein CD80, which is found on certain normal and cancerous white blood cells. | Galiximab, an IgG(1) anti-CD80 antibody, binds to CD80, a costimulatory molecule involved in T-cell activation. Reduction in lesional, activated T cells induces improvement in psoriatic plaques. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | T-lymphocyte activation antigen CD80 | GVAX | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11824 | Th1258 | Galiximab | NA | NA | NA | NA | NA | NA | 13 to 24 days | Galiximab is a chimeric monoclonal antibody which is used as an immunosuppressive drug. | Investigated for use/treatment in lymphoma (non-hodgkin's), psoriasis and psoriatic disorders, bone metastases, multiple myeloma, prostate cancer, and rheumatoid arthritis. | Galiximab is a monoclonal antibody that is being studied in the treatment of follicular non-Hodgkin lymphoma. Monoclonal antibodies are made in the laboratory and can locate and bind to cancer cells. Galiximab binds to the protein CD80, which is found on certain normal and cancerous white blood cells. | Galiximab, an IgG(1) anti-CD80 antibody, binds to CD80, a costimulatory molecule involved in T-cell activation. Reduction in lesional, activated T cells induces improvement in psoriatic plaques. | NA | NA | NA | NA | NA | Anti-Inflammatory Agents | NA | NA | NA | NA | T-lymphocyte activation antigen CD80 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11825 | Th1258 | Galiximab | NA | NA | NA | NA | NA | NA | 13 to 24 days | Galiximab is a chimeric monoclonal antibody which is used as an immunosuppressive drug. | Investigated for use/treatment in lymphoma (non-hodgkin's), psoriasis and psoriatic disorders, bone metastases, multiple myeloma, prostate cancer, and rheumatoid arthritis. | Galiximab is a monoclonal antibody that is being studied in the treatment of follicular non-Hodgkin lymphoma. Monoclonal antibodies are made in the laboratory and can locate and bind to cancer cells. Galiximab binds to the protein CD80, which is found on certain normal and cancerous white blood cells. | Galiximab, an IgG(1) anti-CD80 antibody, binds to CD80, a costimulatory molecule involved in T-cell activation. Reduction in lesional, activated T cells induces improvement in psoriatic plaques. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | T-lymphocyte activation antigen CD80 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11826 | Th1258 | Galiximab | NA | NA | NA | NA | NA | NA | 13 to 24 days | Galiximab is a chimeric monoclonal antibody which is used as an immunosuppressive drug. | Investigated for use/treatment in lymphoma (non-hodgkin's), psoriasis and psoriatic disorders, bone metastases, multiple myeloma, prostate cancer, and rheumatoid arthritis. | Galiximab is a monoclonal antibody that is being studied in the treatment of follicular non-Hodgkin lymphoma. Monoclonal antibodies are made in the laboratory and can locate and bind to cancer cells. Galiximab binds to the protein CD80, which is found on certain normal and cancerous white blood cells. | Galiximab, an IgG(1) anti-CD80 antibody, binds to CD80, a costimulatory molecule involved in T-cell activation. Reduction in lesional, activated T cells induces improvement in psoriatic plaques. | NA | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | T-lymphocyte activation antigen CD80 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11827 | Th1258 | Galiximab | NA | NA | NA | NA | NA | NA | 13 to 24 days | Galiximab is a chimeric monoclonal antibody which is used as an immunosuppressive drug. | Investigated for use/treatment in lymphoma (non-hodgkin's), psoriasis and psoriatic disorders, bone metastases, multiple myeloma, prostate cancer, and rheumatoid arthritis. | Galiximab is a monoclonal antibody that is being studied in the treatment of follicular non-Hodgkin lymphoma. Monoclonal antibodies are made in the laboratory and can locate and bind to cancer cells. Galiximab binds to the protein CD80, which is found on certain normal and cancerous white blood cells. | Galiximab, an IgG(1) anti-CD80 antibody, binds to CD80, a costimulatory molecule involved in T-cell activation. Reduction in lesional, activated T cells induces improvement in psoriatic plaques. | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | T-lymphocyte activation antigen CD80 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11828 | Th1258 | Galiximab | NA | NA | NA | NA | NA | NA | 13 to 24 days | Galiximab is a chimeric monoclonal antibody which is used as an immunosuppressive drug. | Investigated for use/treatment in lymphoma (non-hodgkin's), psoriasis and psoriatic disorders, bone metastases, multiple myeloma, prostate cancer, and rheumatoid arthritis. | Galiximab is a monoclonal antibody that is being studied in the treatment of follicular non-Hodgkin lymphoma. Monoclonal antibodies are made in the laboratory and can locate and bind to cancer cells. Galiximab binds to the protein CD80, which is found on certain normal and cancerous white blood cells. | Galiximab, an IgG(1) anti-CD80 antibody, binds to CD80, a costimulatory molecule involved in T-cell activation. Reduction in lesional, activated T cells induces improvement in psoriatic plaques. | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | T-lymphocyte activation antigen CD80 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11829 | Th1258 | Galiximab | NA | NA | NA | NA | NA | NA | 13 to 24 days | Galiximab is a chimeric monoclonal antibody which is used as an immunosuppressive drug. | Investigated for use/treatment in lymphoma (non-hodgkin's), psoriasis and psoriatic disorders, bone metastases, multiple myeloma, prostate cancer, and rheumatoid arthritis. | Galiximab is a monoclonal antibody that is being studied in the treatment of follicular non-Hodgkin lymphoma. Monoclonal antibodies are made in the laboratory and can locate and bind to cancer cells. Galiximab binds to the protein CD80, which is found on certain normal and cancerous white blood cells. | Galiximab, an IgG(1) anti-CD80 antibody, binds to CD80, a costimulatory molecule involved in T-cell activation. Reduction in lesional, activated T cells induces improvement in psoriatic plaques. | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | T-lymphocyte activation antigen CD80 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11830 | Th1258 | Galiximab | NA | NA | NA | NA | NA | NA | 13 to 24 days | Galiximab is a chimeric monoclonal antibody which is used as an immunosuppressive drug. | Investigated for use/treatment in lymphoma (non-hodgkin's), psoriasis and psoriatic disorders, bone metastases, multiple myeloma, prostate cancer, and rheumatoid arthritis. | Galiximab is a monoclonal antibody that is being studied in the treatment of follicular non-Hodgkin lymphoma. Monoclonal antibodies are made in the laboratory and can locate and bind to cancer cells. Galiximab binds to the protein CD80, which is found on certain normal and cancerous white blood cells. | Galiximab, an IgG(1) anti-CD80 antibody, binds to CD80, a costimulatory molecule involved in T-cell activation. Reduction in lesional, activated T cells induces improvement in psoriatic plaques. | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | T-lymphocyte activation antigen CD80 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11831 | Th1258 | Galiximab | NA | NA | NA | NA | NA | NA | 13 to 24 days | Galiximab is a chimeric monoclonal antibody which is used as an immunosuppressive drug. | Investigated for use/treatment in lymphoma (non-hodgkin's), psoriasis and psoriatic disorders, bone metastases, multiple myeloma, prostate cancer, and rheumatoid arthritis. | Galiximab is a monoclonal antibody that is being studied in the treatment of follicular non-Hodgkin lymphoma. Monoclonal antibodies are made in the laboratory and can locate and bind to cancer cells. Galiximab binds to the protein CD80, which is found on certain normal and cancerous white blood cells. | Galiximab, an IgG(1) anti-CD80 antibody, binds to CD80, a costimulatory molecule involved in T-cell activation. Reduction in lesional, activated T cells induces improvement in psoriatic plaques. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | T-lymphocyte activation antigen CD80 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11832 | Th1258 | Galiximab | NA | NA | NA | NA | NA | NA | 13 to 24 days | Galiximab is a chimeric monoclonal antibody which is used as an immunosuppressive drug. | Investigated for use/treatment in lymphoma (non-hodgkin's), psoriasis and psoriatic disorders, bone metastases, multiple myeloma, prostate cancer, and rheumatoid arthritis. | Galiximab is a monoclonal antibody that is being studied in the treatment of follicular non-Hodgkin lymphoma. Monoclonal antibodies are made in the laboratory and can locate and bind to cancer cells. Galiximab binds to the protein CD80, which is found on certain normal and cancerous white blood cells. | Galiximab, an IgG(1) anti-CD80 antibody, binds to CD80, a costimulatory molecule involved in T-cell activation. Reduction in lesional, activated T cells induces improvement in psoriatic plaques. | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | T-lymphocyte activation antigen CD80 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11890 | Th1265 | Ranpirnase | NA | NA | NA | NA | NA | NA | NA | Ranpirnase is a ribonuclease enzyme found in Rana pipiens oocytes. It is being studied in the treatment of cancer. It is manufactured by Alfacell Corporation. It is the first ribonuclease to enter cancer clinical trials. | For the treatment of various forms of cancer. | NA | Ranpirnase controls tumour growth by degrading RNA within cancer cells, resulting in inhibition of protein synthesis and arresting mitosis in G(1)phase. | NA | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | DNA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11891 | Th1265 | Ranpirnase | NA | NA | NA | NA | NA | NA | NA | Ranpirnase is a ribonuclease enzyme found in Rana pipiens oocytes. It is being studied in the treatment of cancer. It is manufactured by Alfacell Corporation. It is the first ribonuclease to enter cancer clinical trials. | For the treatment of various forms of cancer. | NA | Ranpirnase controls tumour growth by degrading RNA within cancer cells, resulting in inhibition of protein synthesis and arresting mitosis in G(1)phase. | NA | NA | NA | NA | NA | Egg Proteins | NA | NA | NA | NA | DNA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11892 | Th1265 | Ranpirnase | NA | NA | NA | NA | NA | NA | NA | Ranpirnase is a ribonuclease enzyme found in Rana pipiens oocytes. It is being studied in the treatment of cancer. It is manufactured by Alfacell Corporation. It is the first ribonuclease to enter cancer clinical trials. | For the treatment of various forms of cancer. | NA | Ranpirnase controls tumour growth by degrading RNA within cancer cells, resulting in inhibition of protein synthesis and arresting mitosis in G(1)phase. | NA | NA | NA | NA | NA | Enzyme Inhibitors | NA | NA | NA | NA | DNA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11893 | Th1265 | Ranpirnase | NA | NA | NA | NA | NA | NA | NA | Ranpirnase is a ribonuclease enzyme found in Rana pipiens oocytes. It is being studied in the treatment of cancer. It is manufactured by Alfacell Corporation. It is the first ribonuclease to enter cancer clinical trials. | For the treatment of various forms of cancer. | NA | Ranpirnase controls tumour growth by degrading RNA within cancer cells, resulting in inhibition of protein synthesis and arresting mitosis in G(1)phase. | NA | NA | NA | NA | NA | Enzymes | NA | NA | NA | NA | DNA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11894 | Th1265 | Ranpirnase | NA | NA | NA | NA | NA | NA | NA | Ranpirnase is a ribonuclease enzyme found in Rana pipiens oocytes. It is being studied in the treatment of cancer. It is manufactured by Alfacell Corporation. It is the first ribonuclease to enter cancer clinical trials. | For the treatment of various forms of cancer. | NA | Ranpirnase controls tumour growth by degrading RNA within cancer cells, resulting in inhibition of protein synthesis and arresting mitosis in G(1)phase. | NA | NA | NA | NA | NA | Enzymes and Coenzymes | NA | NA | NA | NA | DNA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11895 | Th1265 | Ranpirnase | NA | NA | NA | NA | NA | NA | NA | Ranpirnase is a ribonuclease enzyme found in Rana pipiens oocytes. It is being studied in the treatment of cancer. It is manufactured by Alfacell Corporation. It is the first ribonuclease to enter cancer clinical trials. | For the treatment of various forms of cancer. | NA | Ranpirnase controls tumour growth by degrading RNA within cancer cells, resulting in inhibition of protein synthesis and arresting mitosis in G(1)phase. | NA | NA | NA | NA | NA | Esterases | NA | NA | NA | NA | DNA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11896 | Th1265 | Ranpirnase | NA | NA | NA | NA | NA | NA | NA | Ranpirnase is a ribonuclease enzyme found in Rana pipiens oocytes. It is being studied in the treatment of cancer. It is manufactured by Alfacell Corporation. It is the first ribonuclease to enter cancer clinical trials. | For the treatment of various forms of cancer. | NA | Ranpirnase controls tumour growth by degrading RNA within cancer cells, resulting in inhibition of protein synthesis and arresting mitosis in G(1)phase. | NA | NA | NA | NA | NA | Hydrolases | NA | NA | NA | NA | DNA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11897 | Th1265 | Ranpirnase | NA | NA | NA | NA | NA | NA | NA | Ranpirnase is a ribonuclease enzyme found in Rana pipiens oocytes. It is being studied in the treatment of cancer. It is manufactured by Alfacell Corporation. It is the first ribonuclease to enter cancer clinical trials. | For the treatment of various forms of cancer. | NA | Ranpirnase controls tumour growth by degrading RNA within cancer cells, resulting in inhibition of protein synthesis and arresting mitosis in G(1)phase. | NA | NA | NA | NA | NA | Protein Synthesis Inhibitors | NA | NA | NA | NA | DNA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11898 | Th1265 | Ranpirnase | NA | NA | NA | NA | NA | NA | NA | Ranpirnase is a ribonuclease enzyme found in Rana pipiens oocytes. It is being studied in the treatment of cancer. It is manufactured by Alfacell Corporation. It is the first ribonuclease to enter cancer clinical trials. | For the treatment of various forms of cancer. | NA | Ranpirnase controls tumour growth by degrading RNA within cancer cells, resulting in inhibition of protein synthesis and arresting mitosis in G(1)phase. | NA | NA | NA | NA | NA | Rana pipiens | NA | NA | NA | NA | DNA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11932 | Th1269 | Oregovomab | NA | NA | NA | NA | NA | NA | NA | Oregovomab is a murine monoclonal antibody that attaches to the tumor-associated antigen CA125. | Investigated for use/treatment in ovarian cancer. | Oregovomab is well tolerated and induces multiple antigen-specific immune responses, maintained during concomitant chemotherapy. A significant survival benefit has been observed in patients mounting a T-cell response to CA125 and/or autologous tumor. Vaccination with oregovomab may stimulate a host cytotoxic immune response against tumor cells that express CA125. | Oregovomab targets the circulating tumour-associated antigen CA 125, which is shed from the surface of human ovarian cancer cells; the antibodies induce broad cellular and humoral immune responses against CA 125 via complex formation. Unlike free CA 125, CA 125-oregovomab complexes can prime dendritic cells, leading to downstream activation of T cells. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Mucin-16 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11933 | Th1269 | Oregovomab | NA | NA | NA | NA | NA | NA | NA | Oregovomab is a murine monoclonal antibody that attaches to the tumor-associated antigen CA125. | Investigated for use/treatment in ovarian cancer. | Oregovomab is well tolerated and induces multiple antigen-specific immune responses, maintained during concomitant chemotherapy. A significant survival benefit has been observed in patients mounting a T-cell response to CA125 and/or autologous tumor. Vaccination with oregovomab may stimulate a host cytotoxic immune response against tumor cells that express CA125. | Oregovomab targets the circulating tumour-associated antigen CA 125, which is shed from the surface of human ovarian cancer cells; the antibodies induce broad cellular and humoral immune responses against CA 125 via complex formation. Unlike free CA 125, CA 125-oregovomab complexes can prime dendritic cells, leading to downstream activation of T cells. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Mucin-16 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11934 | Th1269 | Oregovomab | NA | NA | NA | NA | NA | NA | NA | Oregovomab is a murine monoclonal antibody that attaches to the tumor-associated antigen CA125. | Investigated for use/treatment in ovarian cancer. | Oregovomab is well tolerated and induces multiple antigen-specific immune responses, maintained during concomitant chemotherapy. A significant survival benefit has been observed in patients mounting a T-cell response to CA125 and/or autologous tumor. Vaccination with oregovomab may stimulate a host cytotoxic immune response against tumor cells that express CA125. | Oregovomab targets the circulating tumour-associated antigen CA 125, which is shed from the surface of human ovarian cancer cells; the antibodies induce broad cellular and humoral immune responses against CA 125 via complex formation. Unlike free CA 125, CA 125-oregovomab complexes can prime dendritic cells, leading to downstream activation of T cells. | NA | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | Mucin-16 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11935 | Th1269 | Oregovomab | NA | NA | NA | NA | NA | NA | NA | Oregovomab is a murine monoclonal antibody that attaches to the tumor-associated antigen CA125. | Investigated for use/treatment in ovarian cancer. | Oregovomab is well tolerated and induces multiple antigen-specific immune responses, maintained during concomitant chemotherapy. A significant survival benefit has been observed in patients mounting a T-cell response to CA125 and/or autologous tumor. Vaccination with oregovomab may stimulate a host cytotoxic immune response against tumor cells that express CA125. | Oregovomab targets the circulating tumour-associated antigen CA 125, which is shed from the surface of human ovarian cancer cells; the antibodies induce broad cellular and humoral immune responses against CA 125 via complex formation. Unlike free CA 125, CA 125-oregovomab complexes can prime dendritic cells, leading to downstream activation of T cells. | NA | NA | NA | NA | NA | Antineoplastic Agents, Immunological | NA | NA | NA | NA | Mucin-16 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11936 | Th1269 | Oregovomab | NA | NA | NA | NA | NA | NA | NA | Oregovomab is a murine monoclonal antibody that attaches to the tumor-associated antigen CA125. | Investigated for use/treatment in ovarian cancer. | Oregovomab is well tolerated and induces multiple antigen-specific immune responses, maintained during concomitant chemotherapy. A significant survival benefit has been observed in patients mounting a T-cell response to CA125 and/or autologous tumor. Vaccination with oregovomab may stimulate a host cytotoxic immune response against tumor cells that express CA125. | Oregovomab targets the circulating tumour-associated antigen CA 125, which is shed from the surface of human ovarian cancer cells; the antibodies induce broad cellular and humoral immune responses against CA 125 via complex formation. Unlike free CA 125, CA 125-oregovomab complexes can prime dendritic cells, leading to downstream activation of T cells. | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | Mucin-16 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11937 | Th1269 | Oregovomab | NA | NA | NA | NA | NA | NA | NA | Oregovomab is a murine monoclonal antibody that attaches to the tumor-associated antigen CA125. | Investigated for use/treatment in ovarian cancer. | Oregovomab is well tolerated and induces multiple antigen-specific immune responses, maintained during concomitant chemotherapy. A significant survival benefit has been observed in patients mounting a T-cell response to CA125 and/or autologous tumor. Vaccination with oregovomab may stimulate a host cytotoxic immune response against tumor cells that express CA125. | Oregovomab targets the circulating tumour-associated antigen CA 125, which is shed from the surface of human ovarian cancer cells; the antibodies induce broad cellular and humoral immune responses against CA 125 via complex formation. Unlike free CA 125, CA 125-oregovomab complexes can prime dendritic cells, leading to downstream activation of T cells. | NA | NA | NA | NA | NA | CA-125 Antigen | NA | NA | NA | NA | Mucin-16 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11938 | Th1269 | Oregovomab | NA | NA | NA | NA | NA | NA | NA | Oregovomab is a murine monoclonal antibody that attaches to the tumor-associated antigen CA125. | Investigated for use/treatment in ovarian cancer. | Oregovomab is well tolerated and induces multiple antigen-specific immune responses, maintained during concomitant chemotherapy. A significant survival benefit has been observed in patients mounting a T-cell response to CA125 and/or autologous tumor. Vaccination with oregovomab may stimulate a host cytotoxic immune response against tumor cells that express CA125. | Oregovomab targets the circulating tumour-associated antigen CA 125, which is shed from the surface of human ovarian cancer cells; the antibodies induce broad cellular and humoral immune responses against CA 125 via complex formation. Unlike free CA 125, CA 125-oregovomab complexes can prime dendritic cells, leading to downstream activation of T cells. | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | Mucin-16 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11939 | Th1269 | Oregovomab | NA | NA | NA | NA | NA | NA | NA | Oregovomab is a murine monoclonal antibody that attaches to the tumor-associated antigen CA125. | Investigated for use/treatment in ovarian cancer. | Oregovomab is well tolerated and induces multiple antigen-specific immune responses, maintained during concomitant chemotherapy. A significant survival benefit has been observed in patients mounting a T-cell response to CA125 and/or autologous tumor. Vaccination with oregovomab may stimulate a host cytotoxic immune response against tumor cells that express CA125. | Oregovomab targets the circulating tumour-associated antigen CA 125, which is shed from the surface of human ovarian cancer cells; the antibodies induce broad cellular and humoral immune responses against CA 125 via complex formation. Unlike free CA 125, CA 125-oregovomab complexes can prime dendritic cells, leading to downstream activation of T cells. | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | Mucin-16 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11940 | Th1269 | Oregovomab | NA | NA | NA | NA | NA | NA | NA | Oregovomab is a murine monoclonal antibody that attaches to the tumor-associated antigen CA125. | Investigated for use/treatment in ovarian cancer. | Oregovomab is well tolerated and induces multiple antigen-specific immune responses, maintained during concomitant chemotherapy. A significant survival benefit has been observed in patients mounting a T-cell response to CA125 and/or autologous tumor. Vaccination with oregovomab may stimulate a host cytotoxic immune response against tumor cells that express CA125. | Oregovomab targets the circulating tumour-associated antigen CA 125, which is shed from the surface of human ovarian cancer cells; the antibodies induce broad cellular and humoral immune responses against CA 125 via complex formation. Unlike free CA 125, CA 125-oregovomab complexes can prime dendritic cells, leading to downstream activation of T cells. | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | Mucin-16 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11941 | Th1269 | Oregovomab | NA | NA | NA | NA | NA | NA | NA | Oregovomab is a murine monoclonal antibody that attaches to the tumor-associated antigen CA125. | Investigated for use/treatment in ovarian cancer. | Oregovomab is well tolerated and induces multiple antigen-specific immune responses, maintained during concomitant chemotherapy. A significant survival benefit has been observed in patients mounting a T-cell response to CA125 and/or autologous tumor. Vaccination with oregovomab may stimulate a host cytotoxic immune response against tumor cells that express CA125. | Oregovomab targets the circulating tumour-associated antigen CA 125, which is shed from the surface of human ovarian cancer cells; the antibodies induce broad cellular and humoral immune responses against CA 125 via complex formation. Unlike free CA 125, CA 125-oregovomab complexes can prime dendritic cells, leading to downstream activation of T cells. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | Mucin-16 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11942 | Th1269 | Oregovomab | NA | NA | NA | NA | NA | NA | NA | Oregovomab is a murine monoclonal antibody that attaches to the tumor-associated antigen CA125. | Investigated for use/treatment in ovarian cancer. | Oregovomab is well tolerated and induces multiple antigen-specific immune responses, maintained during concomitant chemotherapy. A significant survival benefit has been observed in patients mounting a T-cell response to CA125 and/or autologous tumor. Vaccination with oregovomab may stimulate a host cytotoxic immune response against tumor cells that express CA125. | Oregovomab targets the circulating tumour-associated antigen CA 125, which is shed from the surface of human ovarian cancer cells; the antibodies induce broad cellular and humoral immune responses against CA 125 via complex formation. Unlike free CA 125, CA 125-oregovomab complexes can prime dendritic cells, leading to downstream activation of T cells. | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | Mucin-16 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11943 | Th1270 | LErafAON | NA | NA | NA | NA | NA | NA | In monkeys, the terminal plasma half-life of 30.36 +/- 23.87 hours was observed at an i.v. dose of 6.25 mg/kg. | NeoPharm is developing liposome-encapsulated, c-Raf antisense oligodeoxynucleotides (LErafAON) for the potential treatment of various solid tumors, including those that have become resistant to radiation or chemotherapy. Phase I/II trials commenced in March 2001 and were ongoing as of June 2003. | Intended for the treatment of various forms of cancer. | NA | Raf-1 protein serine threonine kinase plays an important role in cell survival and proliferation. Antisense inhibition of Raf-1 expression by drugs such as LErafAON has been shown to enhance the cytotoxic effects of radiation and anticancer drugs. | NA | NA | NA | NA | NA | Carbohydrates | NA | NA | NA | NA | RAF proto-oncogene serine/threonine-protein kinase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11944 | Th1270 | LErafAON | NA | NA | NA | NA | NA | NA | In monkeys, the terminal plasma half-life of 30.36 +/- 23.87 hours was observed at an i.v. dose of 6.25 mg/kg. | NeoPharm is developing liposome-encapsulated, c-Raf antisense oligodeoxynucleotides (LErafAON) for the potential treatment of various solid tumors, including those that have become resistant to radiation or chemotherapy. Phase I/II trials commenced in March 2001 and were ongoing as of June 2003. | Intended for the treatment of various forms of cancer. | NA | Raf-1 protein serine threonine kinase plays an important role in cell survival and proliferation. Antisense inhibition of Raf-1 expression by drugs such as LErafAON has been shown to enhance the cytotoxic effects of radiation and anticancer drugs. | NA | NA | NA | NA | NA | Glycosides | NA | NA | NA | NA | RAF proto-oncogene serine/threonine-protein kinase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11945 | Th1270 | LErafAON | NA | NA | NA | NA | NA | NA | In monkeys, the terminal plasma half-life of 30.36 +/- 23.87 hours was observed at an i.v. dose of 6.25 mg/kg. | NeoPharm is developing liposome-encapsulated, c-Raf antisense oligodeoxynucleotides (LErafAON) for the potential treatment of various solid tumors, including those that have become resistant to radiation or chemotherapy. Phase I/II trials commenced in March 2001 and were ongoing as of June 2003. | Intended for the treatment of various forms of cancer. | NA | Raf-1 protein serine threonine kinase plays an important role in cell survival and proliferation. Antisense inhibition of Raf-1 expression by drugs such as LErafAON has been shown to enhance the cytotoxic effects of radiation and anticancer drugs. | NA | NA | NA | NA | NA | Nucleic Acids, Nucleotides, and Nucleosides | NA | NA | NA | NA | RAF proto-oncogene serine/threonine-protein kinase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11946 | Th1270 | LErafAON | NA | NA | NA | NA | NA | NA | In monkeys, the terminal plasma half-life of 30.36 +/- 23.87 hours was observed at an i.v. dose of 6.25 mg/kg. | NeoPharm is developing liposome-encapsulated, c-Raf antisense oligodeoxynucleotides (LErafAON) for the potential treatment of various solid tumors, including those that have become resistant to radiation or chemotherapy. Phase I/II trials commenced in March 2001 and were ongoing as of June 2003. | Intended for the treatment of various forms of cancer. | NA | Raf-1 protein serine threonine kinase plays an important role in cell survival and proliferation. Antisense inhibition of Raf-1 expression by drugs such as LErafAON has been shown to enhance the cytotoxic effects of radiation and anticancer drugs. | NA | NA | NA | NA | NA | Nucleotides | NA | NA | NA | NA | RAF proto-oncogene serine/threonine-protein kinase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11947 | Th1270 | LErafAON | NA | NA | NA | NA | NA | NA | In monkeys, the terminal plasma half-life of 30.36 +/- 23.87 hours was observed at an i.v. dose of 6.25 mg/kg. | NeoPharm is developing liposome-encapsulated, c-Raf antisense oligodeoxynucleotides (LErafAON) for the potential treatment of various solid tumors, including those that have become resistant to radiation or chemotherapy. Phase I/II trials commenced in March 2001 and were ongoing as of June 2003. | Intended for the treatment of various forms of cancer. | NA | Raf-1 protein serine threonine kinase plays an important role in cell survival and proliferation. Antisense inhibition of Raf-1 expression by drugs such as LErafAON has been shown to enhance the cytotoxic effects of radiation and anticancer drugs. | NA | NA | NA | NA | NA | Oligonucleotides | NA | NA | NA | NA | RAF proto-oncogene serine/threonine-protein kinase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11948 | Th1270 | LErafAON | NA | NA | NA | NA | NA | NA | In monkeys, the terminal plasma half-life of 30.36 +/- 23.87 hours was observed at an i.v. dose of 6.25 mg/kg. | NeoPharm is developing liposome-encapsulated, c-Raf antisense oligodeoxynucleotides (LErafAON) for the potential treatment of various solid tumors, including those that have become resistant to radiation or chemotherapy. Phase I/II trials commenced in March 2001 and were ongoing as of June 2003. | Intended for the treatment of various forms of cancer. | NA | Raf-1 protein serine threonine kinase plays an important role in cell survival and proliferation. Antisense inhibition of Raf-1 expression by drugs such as LErafAON has been shown to enhance the cytotoxic effects of radiation and anticancer drugs. | NA | NA | NA | NA | NA | Polynucleotides | NA | NA | NA | NA | RAF proto-oncogene serine/threonine-protein kinase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11949 | Th1271 | M40403 | >Th1271_M40403 MLSRAVCGTSRQLAPALGYLGSRQKHSLPDLPYDYGALEPHINAQIMQLHHSKHHAAYVNNLNVTEEKYQEALAKGDVTAQIALQPALKFNGGGHINHSIFWTNLSPNGGGEPKGELLEAIKRDFGSFDKFKEKLTAASVGVQGSGWGWLGFNKERGHLQIAACPNQDPLQGTTGLIPLLGIDVWEHAYYLQYKNVRPDYLKAIWNVINWENVTERYMACKK | NA | NA | NA | NA | NA | NA | M40403 is a low molecular weight, synthetic manganese containing superoxide dismutase mimetic (SODm) that selectively removes superoxide anion. | Intended for the treatment of pain and possibly various forms of cancer. | M40403 treatment exerts a protective effect against ischaemia-reperfusion-induced myocardial injury, supporting a key role for superoxide anion in reperfusion injuries. | M40403 is the lead candidate in a unique class of compounds known as superoxide dismutase (SOD) mimetics. These stable, low molecular weight compounds mimic the effect of superoxide dismutase, a naturally occurring enzyme designed to destroy superoxide free radicals present in various diseases associated with pain and inflammation. | NA | NA | NA | NA | NA | Elements | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | manganese(2+);(4R,9R,14R,19R)-3,10,13,20,26-pentazatetracyclo[20.3.1.04,9.014,19]hexacosa-1(26),22,24-triene;dichloride | NA | Link | NA | NA |
| 11950 | Th1271 | M40403 | >Th1271_M40403 MLSRAVCGTSRQLAPALGYLGSRQKHSLPDLPYDYGALEPHINAQIMQLHHSKHHAAYVNNLNVTEEKYQEALAKGDVTAQIALQPALKFNGGGHINHSIFWTNLSPNGGGEPKGELLEAIKRDFGSFDKFKEKLTAASVGVQGSGWGWLGFNKERGHLQIAACPNQDPLQGTTGLIPLLGIDVWEHAYYLQYKNVRPDYLKAIWNVINWENVTERYMACKK | NA | NA | NA | NA | NA | NA | M40403 is a low molecular weight, synthetic manganese containing superoxide dismutase mimetic (SODm) that selectively removes superoxide anion. | Intended for the treatment of pain and possibly various forms of cancer. | M40403 treatment exerts a protective effect against ischaemia-reperfusion-induced myocardial injury, supporting a key role for superoxide anion in reperfusion injuries. | M40403 is the lead candidate in a unique class of compounds known as superoxide dismutase (SOD) mimetics. These stable, low molecular weight compounds mimic the effect of superoxide dismutase, a naturally occurring enzyme designed to destroy superoxide free radicals present in various diseases associated with pain and inflammation. | NA | NA | NA | NA | NA | Metals | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | manganese(2+);(4R,9R,14R,19R)-3,10,13,20,26-pentazatetracyclo[20.3.1.04,9.014,19]hexacosa-1(26),22,24-triene;dichloride | NA | Link | NA | NA |
| 11951 | Th1271 | M40403 | >Th1271_M40403 MLSRAVCGTSRQLAPALGYLGSRQKHSLPDLPYDYGALEPHINAQIMQLHHSKHHAAYVNNLNVTEEKYQEALAKGDVTAQIALQPALKFNGGGHINHSIFWTNLSPNGGGEPKGELLEAIKRDFGSFDKFKEKLTAASVGVQGSGWGWLGFNKERGHLQIAACPNQDPLQGTTGLIPLLGIDVWEHAYYLQYKNVRPDYLKAIWNVINWENVTERYMACKK | NA | NA | NA | NA | NA | NA | M40403 is a low molecular weight, synthetic manganese containing superoxide dismutase mimetic (SODm) that selectively removes superoxide anion. | Intended for the treatment of pain and possibly various forms of cancer. | M40403 treatment exerts a protective effect against ischaemia-reperfusion-induced myocardial injury, supporting a key role for superoxide anion in reperfusion injuries. | M40403 is the lead candidate in a unique class of compounds known as superoxide dismutase (SOD) mimetics. These stable, low molecular weight compounds mimic the effect of superoxide dismutase, a naturally occurring enzyme designed to destroy superoxide free radicals present in various diseases associated with pain and inflammation. | NA | NA | NA | NA | NA | Metals, Heavy | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | manganese(2+);(4R,9R,14R,19R)-3,10,13,20,26-pentazatetracyclo[20.3.1.04,9.014,19]hexacosa-1(26),22,24-triene;dichloride | NA | Link | NA | NA |
| 11952 | Th1271 | M40403 | >Th1271_M40403 MLSRAVCGTSRQLAPALGYLGSRQKHSLPDLPYDYGALEPHINAQIMQLHHSKHHAAYVNNLNVTEEKYQEALAKGDVTAQIALQPALKFNGGGHINHSIFWTNLSPNGGGEPKGELLEAIKRDFGSFDKFKEKLTAASVGVQGSGWGWLGFNKERGHLQIAACPNQDPLQGTTGLIPLLGIDVWEHAYYLQYKNVRPDYLKAIWNVINWENVTERYMACKK | NA | NA | NA | NA | NA | NA | M40403 is a low molecular weight, synthetic manganese containing superoxide dismutase mimetic (SODm) that selectively removes superoxide anion. | Intended for the treatment of pain and possibly various forms of cancer. | M40403 treatment exerts a protective effect against ischaemia-reperfusion-induced myocardial injury, supporting a key role for superoxide anion in reperfusion injuries. | M40403 is the lead candidate in a unique class of compounds known as superoxide dismutase (SOD) mimetics. These stable, low molecular weight compounds mimic the effect of superoxide dismutase, a naturally occurring enzyme designed to destroy superoxide free radicals present in various diseases associated with pain and inflammation. | NA | NA | NA | NA | NA | Transition Elements | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | manganese(2+);(4R,9R,14R,19R)-3,10,13,20,26-pentazatetracyclo[20.3.1.04,9.014,19]hexacosa-1(26),22,24-triene;dichloride | NA | Link | NA | NA |
| 11953 | Th1272 | Tigapotide | >Th1272_Tigapotide PGDSTRKCMDLKGNK | NA | NA | NA | NA | NA | 0.35 hours to 1.45 hours | Tigapotide is a synthetic 15-mer peptide that is derived from the natural sequence of amino acids of the prostate secretory protein (PSP94), one of three predominant proteins found in human seminal fluid. | For the treatment of late stage Hormone Refractory Prostate Cancer (HRPC) for which no effective therapy currently exists. | PCK3145 is a synthetic 15-mer peptide that is derived from the natural sequence of amino acids of the prostate secretory protein (PSP94), one of three predominant proteins found in human seminal fluid. PSP94 expression in the prostate is down regulated in patients with advanced prostate cancer, and believed to be a survival mechanism for the cancer cells. Results from an earlier trial conducted in the U.K. showed PCK3145 to be safe and well tolerated at all doses tested and further suggest that it also plays a role in preventing the metastatic process as measured by its effect on MMP-9 levels, a Gelatinase B enzyme involved in angiogenesis, tumor invasion and metastasis. | The mechanism of action and receptor for PCK3145 suggests PCK3145 to be a signal transduction inhibitor with multiple ways (apoptosis, anti-angiogenesis and anti-metastasis) to restrict disease development. | Non-clinical toxicology studies in mice and primates indicated that a treatment for 28 consecutive days by intravenous administration of PCK3145 up to 450 mg/kg/day in mice and 25 mg/kg/day in primates resulted in no clear evidence of toxicity. | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | 40S ribosomal protein SA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11954 | Th1272 | Tigapotide | >Th1272_Tigapotide PGDSTRKCMDLKGNK | NA | NA | NA | NA | NA | 0.35 hours to 1.45 hours | Tigapotide is a synthetic 15-mer peptide that is derived from the natural sequence of amino acids of the prostate secretory protein (PSP94), one of three predominant proteins found in human seminal fluid. | For the treatment of late stage Hormone Refractory Prostate Cancer (HRPC) for which no effective therapy currently exists. | PCK3145 is a synthetic 15-mer peptide that is derived from the natural sequence of amino acids of the prostate secretory protein (PSP94), one of three predominant proteins found in human seminal fluid. PSP94 expression in the prostate is down regulated in patients with advanced prostate cancer, and believed to be a survival mechanism for the cancer cells. Results from an earlier trial conducted in the U.K. showed PCK3145 to be safe and well tolerated at all doses tested and further suggest that it also plays a role in preventing the metastatic process as measured by its effect on MMP-9 levels, a Gelatinase B enzyme involved in angiogenesis, tumor invasion and metastasis. | The mechanism of action and receptor for PCK3145 suggests PCK3145 to be a signal transduction inhibitor with multiple ways (apoptosis, anti-angiogenesis and anti-metastasis) to restrict disease development. | Non-clinical toxicology studies in mice and primates indicated that a treatment for 28 consecutive days by intravenous administration of PCK3145 up to 450 mg/kg/day in mice and 25 mg/kg/day in primates resulted in no clear evidence of toxicity. | NA | NA | NA | NA | Peptides | NA | NA | NA | NA | 40S ribosomal protein SA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11955 | Th1272 | Tigapotide | >Th1272_Tigapotide PGDSTRKCMDLKGNK | NA | NA | NA | NA | NA | 0.35 hours to 1.45 hours | Tigapotide is a synthetic 15-mer peptide that is derived from the natural sequence of amino acids of the prostate secretory protein (PSP94), one of three predominant proteins found in human seminal fluid. | For the treatment of late stage Hormone Refractory Prostate Cancer (HRPC) for which no effective therapy currently exists. | PCK3145 is a synthetic 15-mer peptide that is derived from the natural sequence of amino acids of the prostate secretory protein (PSP94), one of three predominant proteins found in human seminal fluid. PSP94 expression in the prostate is down regulated in patients with advanced prostate cancer, and believed to be a survival mechanism for the cancer cells. Results from an earlier trial conducted in the U.K. showed PCK3145 to be safe and well tolerated at all doses tested and further suggest that it also plays a role in preventing the metastatic process as measured by its effect on MMP-9 levels, a Gelatinase B enzyme involved in angiogenesis, tumor invasion and metastasis. | The mechanism of action and receptor for PCK3145 suggests PCK3145 to be a signal transduction inhibitor with multiple ways (apoptosis, anti-angiogenesis and anti-metastasis) to restrict disease development. | Non-clinical toxicology studies in mice and primates indicated that a treatment for 28 consecutive days by intravenous administration of PCK3145 up to 450 mg/kg/day in mice and 25 mg/kg/day in primates resulted in no clear evidence of toxicity. | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | 40S ribosomal protein SA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11956 | Th1272 | Tigapotide | >Th1272_Tigapotide PGDSTRKCMDLKGNK | NA | NA | NA | NA | NA | 0.35 hours to 1.45 hours | Tigapotide is a synthetic 15-mer peptide that is derived from the natural sequence of amino acids of the prostate secretory protein (PSP94), one of three predominant proteins found in human seminal fluid. | For the treatment of late stage Hormone Refractory Prostate Cancer (HRPC) for which no effective therapy currently exists. | PCK3145 is a synthetic 15-mer peptide that is derived from the natural sequence of amino acids of the prostate secretory protein (PSP94), one of three predominant proteins found in human seminal fluid. PSP94 expression in the prostate is down regulated in patients with advanced prostate cancer, and believed to be a survival mechanism for the cancer cells. Results from an earlier trial conducted in the U.K. showed PCK3145 to be safe and well tolerated at all doses tested and further suggest that it also plays a role in preventing the metastatic process as measured by its effect on MMP-9 levels, a Gelatinase B enzyme involved in angiogenesis, tumor invasion and metastasis. | The mechanism of action and receptor for PCK3145 suggests PCK3145 to be a signal transduction inhibitor with multiple ways (apoptosis, anti-angiogenesis and anti-metastasis) to restrict disease development. | Non-clinical toxicology studies in mice and primates indicated that a treatment for 28 consecutive days by intravenous administration of PCK3145 up to 450 mg/kg/day in mice and 25 mg/kg/day in primates resulted in no clear evidence of toxicity. | NA | NA | NA | NA | Seminal Plasma Proteins | NA | NA | NA | NA | 40S ribosomal protein SA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11957 | Th1273 | IGN311 | NA | NA | NA | NA | NA | NA | NA | IGN311 is a humanized monoclonal antibody (mab) against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. | Intended for the treatment of various forms of cancer. | IGN311 is a fully humanized IgG1 variant 1 of the parent murine IgG3 mab ABL 364. It is an antibody against the Lewis-Y carbohydrate antigen and Igeneon's next-generation antibody, IGN312. | IGN311 is a humanized monoclonal antibody against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. Lewis Y is over-expressed in up to 90% of all epithelial cancers and its expression on adult normal tissues is very restricted; hence IGN311 has the potential to target a broad range of carcinomas. IGN311 is designed to exert clinical effects by destruction of tumor cells by activation of effector functions and by selective growth inhibition via functional receptors. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Epidermal growth factor receptor,Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11958 | Th1273 | IGN311 | NA | NA | NA | NA | NA | NA | NA | IGN311 is a humanized monoclonal antibody (mab) against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. | Intended for the treatment of various forms of cancer. | IGN311 is a fully humanized IgG1 variant 1 of the parent murine IgG3 mab ABL 364. It is an antibody against the Lewis-Y carbohydrate antigen and Igeneon's next-generation antibody, IGN312. | IGN311 is a humanized monoclonal antibody against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. Lewis Y is over-expressed in up to 90% of all epithelial cancers and its expression on adult normal tissues is very restricted; hence IGN311 has the potential to target a broad range of carcinomas. IGN311 is designed to exert clinical effects by destruction of tumor cells by activation of effector functions and by selective growth inhibition via functional receptors. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Epidermal growth factor receptor,Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11959 | Th1273 | IGN311 | NA | NA | NA | NA | NA | NA | NA | IGN311 is a humanized monoclonal antibody (mab) against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. | Intended for the treatment of various forms of cancer. | IGN311 is a fully humanized IgG1 variant 1 of the parent murine IgG3 mab ABL 364. It is an antibody against the Lewis-Y carbohydrate antigen and Igeneon's next-generation antibody, IGN312. | IGN311 is a humanized monoclonal antibody against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. Lewis Y is over-expressed in up to 90% of all epithelial cancers and its expression on adult normal tissues is very restricted; hence IGN311 has the potential to target a broad range of carcinomas. IGN311 is designed to exert clinical effects by destruction of tumor cells by activation of effector functions and by selective growth inhibition via functional receptors. | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | Epidermal growth factor receptor,Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11960 | Th1273 | IGN311 | NA | NA | NA | NA | NA | NA | NA | IGN311 is a humanized monoclonal antibody (mab) against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. | Intended for the treatment of various forms of cancer. | IGN311 is a fully humanized IgG1 variant 1 of the parent murine IgG3 mab ABL 364. It is an antibody against the Lewis-Y carbohydrate antigen and Igeneon's next-generation antibody, IGN312. | IGN311 is a humanized monoclonal antibody against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. Lewis Y is over-expressed in up to 90% of all epithelial cancers and its expression on adult normal tissues is very restricted; hence IGN311 has the potential to target a broad range of carcinomas. IGN311 is designed to exert clinical effects by destruction of tumor cells by activation of effector functions and by selective growth inhibition via functional receptors. | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | Epidermal growth factor receptor,Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11961 | Th1273 | IGN311 | NA | NA | NA | NA | NA | NA | NA | IGN311 is a humanized monoclonal antibody (mab) against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. | Intended for the treatment of various forms of cancer. | IGN311 is a fully humanized IgG1 variant 1 of the parent murine IgG3 mab ABL 364. It is an antibody against the Lewis-Y carbohydrate antigen and Igeneon's next-generation antibody, IGN312. | IGN311 is a humanized monoclonal antibody against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. Lewis Y is over-expressed in up to 90% of all epithelial cancers and its expression on adult normal tissues is very restricted; hence IGN311 has the potential to target a broad range of carcinomas. IGN311 is designed to exert clinical effects by destruction of tumor cells by activation of effector functions and by selective growth inhibition via functional receptors. | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | Epidermal growth factor receptor,Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11962 | Th1273 | IGN311 | NA | NA | NA | NA | NA | NA | NA | IGN311 is a humanized monoclonal antibody (mab) against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. | Intended for the treatment of various forms of cancer. | IGN311 is a fully humanized IgG1 variant 1 of the parent murine IgG3 mab ABL 364. It is an antibody against the Lewis-Y carbohydrate antigen and Igeneon's next-generation antibody, IGN312. | IGN311 is a humanized monoclonal antibody against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. Lewis Y is over-expressed in up to 90% of all epithelial cancers and its expression on adult normal tissues is very restricted; hence IGN311 has the potential to target a broad range of carcinomas. IGN311 is designed to exert clinical effects by destruction of tumor cells by activation of effector functions and by selective growth inhibition via functional receptors. | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | Epidermal growth factor receptor,Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11963 | Th1273 | IGN311 | NA | NA | NA | NA | NA | NA | NA | IGN311 is a humanized monoclonal antibody (mab) against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. | Intended for the treatment of various forms of cancer. | IGN311 is a fully humanized IgG1 variant 1 of the parent murine IgG3 mab ABL 364. It is an antibody against the Lewis-Y carbohydrate antigen and Igeneon's next-generation antibody, IGN312. | IGN311 is a humanized monoclonal antibody against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. Lewis Y is over-expressed in up to 90% of all epithelial cancers and its expression on adult normal tissues is very restricted; hence IGN311 has the potential to target a broad range of carcinomas. IGN311 is designed to exert clinical effects by destruction of tumor cells by activation of effector functions and by selective growth inhibition via functional receptors. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | Epidermal growth factor receptor,Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11964 | Th1273 | IGN311 | NA | NA | NA | NA | NA | NA | NA | IGN311 is a humanized monoclonal antibody (mab) against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. | Intended for the treatment of various forms of cancer. | IGN311 is a fully humanized IgG1 variant 1 of the parent murine IgG3 mab ABL 364. It is an antibody against the Lewis-Y carbohydrate antigen and Igeneon's next-generation antibody, IGN312. | IGN311 is a humanized monoclonal antibody against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. Lewis Y is over-expressed in up to 90% of all epithelial cancers and its expression on adult normal tissues is very restricted; hence IGN311 has the potential to target a broad range of carcinomas. IGN311 is designed to exert clinical effects by destruction of tumor cells by activation of effector functions and by selective growth inhibition via functional receptors. | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | Epidermal growth factor receptor,Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11965 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11966 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11967 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Antigens | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11968 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Antigens, Surface | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11969 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Biological Factors | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11970 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11971 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Carbohydrates | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11972 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11973 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Glycoconjugates | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11974 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Glycoproteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11975 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11976 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11977 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Membrane Glycoproteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11978 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Membrane Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11979 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11980 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11994 | Th1276 | Labetuzumab | NA | NA | NA | NA | NA | NA | NA | Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. | Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from "http://en.wikipedia.org/wiki/Labetuzumab" | NA | labetuzumab could significantly increase the chemosensitivity of human colon and breast cancer cells in vitro to several anticancer drugs. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Carcinoembryonic antigen-related cell adhesion molecule 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11995 | Th1276 | Labetuzumab | NA | NA | NA | NA | NA | NA | NA | Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. | Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from "http://en.wikipedia.org/wiki/Labetuzumab" | NA | labetuzumab could significantly increase the chemosensitivity of human colon and breast cancer cells in vitro to several anticancer drugs. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Carcinoembryonic antigen-related cell adhesion molecule 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11996 | Th1276 | Labetuzumab | NA | NA | NA | NA | NA | NA | NA | Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. | Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from "http://en.wikipedia.org/wiki/Labetuzumab" | NA | labetuzumab could significantly increase the chemosensitivity of human colon and breast cancer cells in vitro to several anticancer drugs. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Carcinoembryonic antigen-related cell adhesion molecule 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11997 | Th1276 | Labetuzumab | NA | NA | NA | NA | NA | NA | NA | Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. | Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from "http://en.wikipedia.org/wiki/Labetuzumab" | NA | labetuzumab could significantly increase the chemosensitivity of human colon and breast cancer cells in vitro to several anticancer drugs. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Carcinoembryonic antigen-related cell adhesion molecule 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11998 | Th1276 | Labetuzumab | NA | NA | NA | NA | NA | NA | NA | Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. | Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from "http://en.wikipedia.org/wiki/Labetuzumab" | NA | labetuzumab could significantly increase the chemosensitivity of human colon and breast cancer cells in vitro to several anticancer drugs. | NA | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | Carcinoembryonic antigen-related cell adhesion molecule 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11999 | Th1276 | Labetuzumab | NA | NA | NA | NA | NA | NA | NA | Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. | Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from "http://en.wikipedia.org/wiki/Labetuzumab" | NA | labetuzumab could significantly increase the chemosensitivity of human colon and breast cancer cells in vitro to several anticancer drugs. | NA | NA | NA | NA | NA | Antineoplastic Agents, Immunological | NA | NA | NA | NA | Carcinoembryonic antigen-related cell adhesion molecule 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12000 | Th1276 | Labetuzumab | NA | NA | NA | NA | NA | NA | NA | Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. | Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from "http://en.wikipedia.org/wiki/Labetuzumab" | NA | labetuzumab could significantly increase the chemosensitivity of human colon and breast cancer cells in vitro to several anticancer drugs. | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | Carcinoembryonic antigen-related cell adhesion molecule 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12001 | Th1276 | Labetuzumab | NA | NA | NA | NA | NA | NA | NA | Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. | Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from "http://en.wikipedia.org/wiki/Labetuzumab" | NA | labetuzumab could significantly increase the chemosensitivity of human colon and breast cancer cells in vitro to several anticancer drugs. | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | Carcinoembryonic antigen-related cell adhesion molecule 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12002 | Th1276 | Labetuzumab | NA | NA | NA | NA | NA | NA | NA | Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. | Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from "http://en.wikipedia.org/wiki/Labetuzumab" | NA | labetuzumab could significantly increase the chemosensitivity of human colon and breast cancer cells in vitro to several anticancer drugs. | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | Carcinoembryonic antigen-related cell adhesion molecule 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12003 | Th1276 | Labetuzumab | NA | NA | NA | NA | NA | NA | NA | Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. | Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from "http://en.wikipedia.org/wiki/Labetuzumab" | NA | labetuzumab could significantly increase the chemosensitivity of human colon and breast cancer cells in vitro to several anticancer drugs. | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | Carcinoembryonic antigen-related cell adhesion molecule 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12004 | Th1276 | Labetuzumab | NA | NA | NA | NA | NA | NA | NA | Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. | Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from "http://en.wikipedia.org/wiki/Labetuzumab" | NA | labetuzumab could significantly increase the chemosensitivity of human colon and breast cancer cells in vitro to several anticancer drugs. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | Carcinoembryonic antigen-related cell adhesion molecule 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12005 | Th1276 | Labetuzumab | NA | NA | NA | NA | NA | NA | NA | Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. | Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from "http://en.wikipedia.org/wiki/Labetuzumab" | NA | labetuzumab could significantly increase the chemosensitivity of human colon and breast cancer cells in vitro to several anticancer drugs. | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | Carcinoembryonic antigen-related cell adhesion molecule 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12006 | Th1277 | Matuzumab | >Th1277_Matuzumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTSHWMHWVRQAPGQGLEWIGEFNPSNGRTNYNEKFKSKATMTVDTSTNTAYMELSSLRSEDTAVYYCASRDYDYDGRYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKS | NA | NA | NA | NA | NA | 196 hours | Matuzumab (formerly known as the experimental drug, EMD 72000) is a humanized monoclonal antibody used in cancer treatment. It has a high affinity for EGFR (epithelial growth factor receptor), frequently associated with the growth of blood vessels in malignancy, facilitating tumor growth and survival. | Investigated for use/treatment in cervical dysplasia/cancer, colorectal cancer, gastric cancer, and lung cancer. | NA | Matuzumab binds the epidermal growth factor receptor (EGFR) with high affinity, competitively blocking natural ligand binding and blocking receptor-mediated downstream signalling, resulting in impaired tumor cell proliferation. Matuzumab (EMD-72000) is a humanized IgG1 MAb that not only binds with high specificity and affinity to EGFR, but also modulates antibody-dependent cellular cytotoxicity (ADCC). | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12007 | Th1277 | Matuzumab | >Th1277_Matuzumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTSHWMHWVRQAPGQGLEWIGEFNPSNGRTNYNEKFKSKATMTVDTSTNTAYMELSSLRSEDTAVYYCASRDYDYDGRYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKS | NA | NA | NA | NA | NA | 196 hours | Matuzumab (formerly known as the experimental drug, EMD 72000) is a humanized monoclonal antibody used in cancer treatment. It has a high affinity for EGFR (epithelial growth factor receptor), frequently associated with the growth of blood vessels in malignancy, facilitating tumor growth and survival. | Investigated for use/treatment in cervical dysplasia/cancer, colorectal cancer, gastric cancer, and lung cancer. | NA | Matuzumab binds the epidermal growth factor receptor (EGFR) with high affinity, competitively blocking natural ligand binding and blocking receptor-mediated downstream signalling, resulting in impaired tumor cell proliferation. Matuzumab (EMD-72000) is a humanized IgG1 MAb that not only binds with high specificity and affinity to EGFR, but also modulates antibody-dependent cellular cytotoxicity (ADCC). | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12008 | Th1277 | Matuzumab | >Th1277_Matuzumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTSHWMHWVRQAPGQGLEWIGEFNPSNGRTNYNEKFKSKATMTVDTSTNTAYMELSSLRSEDTAVYYCASRDYDYDGRYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKS | NA | NA | NA | NA | NA | 196 hours | Matuzumab (formerly known as the experimental drug, EMD 72000) is a humanized monoclonal antibody used in cancer treatment. It has a high affinity for EGFR (epithelial growth factor receptor), frequently associated with the growth of blood vessels in malignancy, facilitating tumor growth and survival. | Investigated for use/treatment in cervical dysplasia/cancer, colorectal cancer, gastric cancer, and lung cancer. | NA | Matuzumab binds the epidermal growth factor receptor (EGFR) with high affinity, competitively blocking natural ligand binding and blocking receptor-mediated downstream signalling, resulting in impaired tumor cell proliferation. Matuzumab (EMD-72000) is a humanized IgG1 MAb that not only binds with high specificity and affinity to EGFR, but also modulates antibody-dependent cellular cytotoxicity (ADCC). | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12009 | Th1277 | Matuzumab | >Th1277_Matuzumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTSHWMHWVRQAPGQGLEWIGEFNPSNGRTNYNEKFKSKATMTVDTSTNTAYMELSSLRSEDTAVYYCASRDYDYDGRYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKS | NA | NA | NA | NA | NA | 196 hours | Matuzumab (formerly known as the experimental drug, EMD 72000) is a humanized monoclonal antibody used in cancer treatment. It has a high affinity for EGFR (epithelial growth factor receptor), frequently associated with the growth of blood vessels in malignancy, facilitating tumor growth and survival. | Investigated for use/treatment in cervical dysplasia/cancer, colorectal cancer, gastric cancer, and lung cancer. | NA | Matuzumab binds the epidermal growth factor receptor (EGFR) with high affinity, competitively blocking natural ligand binding and blocking receptor-mediated downstream signalling, resulting in impaired tumor cell proliferation. Matuzumab (EMD-72000) is a humanized IgG1 MAb that not only binds with high specificity and affinity to EGFR, but also modulates antibody-dependent cellular cytotoxicity (ADCC). | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12010 | Th1277 | Matuzumab | >Th1277_Matuzumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTSHWMHWVRQAPGQGLEWIGEFNPSNGRTNYNEKFKSKATMTVDTSTNTAYMELSSLRSEDTAVYYCASRDYDYDGRYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKS | NA | NA | NA | NA | NA | 196 hours | Matuzumab (formerly known as the experimental drug, EMD 72000) is a humanized monoclonal antibody used in cancer treatment. It has a high affinity for EGFR (epithelial growth factor receptor), frequently associated with the growth of blood vessels in malignancy, facilitating tumor growth and survival. | Investigated for use/treatment in cervical dysplasia/cancer, colorectal cancer, gastric cancer, and lung cancer. | NA | Matuzumab binds the epidermal growth factor receptor (EGFR) with high affinity, competitively blocking natural ligand binding and blocking receptor-mediated downstream signalling, resulting in impaired tumor cell proliferation. Matuzumab (EMD-72000) is a humanized IgG1 MAb that not only binds with high specificity and affinity to EGFR, but also modulates antibody-dependent cellular cytotoxicity (ADCC). | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12011 | Th1277 | Matuzumab | >Th1277_Matuzumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTSHWMHWVRQAPGQGLEWIGEFNPSNGRTNYNEKFKSKATMTVDTSTNTAYMELSSLRSEDTAVYYCASRDYDYDGRYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKS | NA | NA | NA | NA | NA | 196 hours | Matuzumab (formerly known as the experimental drug, EMD 72000) is a humanized monoclonal antibody used in cancer treatment. It has a high affinity for EGFR (epithelial growth factor receptor), frequently associated with the growth of blood vessels in malignancy, facilitating tumor growth and survival. | Investigated for use/treatment in cervical dysplasia/cancer, colorectal cancer, gastric cancer, and lung cancer. | NA | Matuzumab binds the epidermal growth factor receptor (EGFR) with high affinity, competitively blocking natural ligand binding and blocking receptor-mediated downstream signalling, resulting in impaired tumor cell proliferation. Matuzumab (EMD-72000) is a humanized IgG1 MAb that not only binds with high specificity and affinity to EGFR, but also modulates antibody-dependent cellular cytotoxicity (ADCC). | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12012 | Th1277 | Matuzumab | >Th1277_Matuzumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTSHWMHWVRQAPGQGLEWIGEFNPSNGRTNYNEKFKSKATMTVDTSTNTAYMELSSLRSEDTAVYYCASRDYDYDGRYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKS | NA | NA | NA | NA | NA | 196 hours | Matuzumab (formerly known as the experimental drug, EMD 72000) is a humanized monoclonal antibody used in cancer treatment. It has a high affinity for EGFR (epithelial growth factor receptor), frequently associated with the growth of blood vessels in malignancy, facilitating tumor growth and survival. | Investigated for use/treatment in cervical dysplasia/cancer, colorectal cancer, gastric cancer, and lung cancer. | NA | Matuzumab binds the epidermal growth factor receptor (EGFR) with high affinity, competitively blocking natural ligand binding and blocking receptor-mediated downstream signalling, resulting in impaired tumor cell proliferation. Matuzumab (EMD-72000) is a humanized IgG1 MAb that not only binds with high specificity and affinity to EGFR, but also modulates antibody-dependent cellular cytotoxicity (ADCC). | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12013 | Th1277 | Matuzumab | >Th1277_Matuzumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTSHWMHWVRQAPGQGLEWIGEFNPSNGRTNYNEKFKSKATMTVDTSTNTAYMELSSLRSEDTAVYYCASRDYDYDGRYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKS | NA | NA | NA | NA | NA | 196 hours | Matuzumab (formerly known as the experimental drug, EMD 72000) is a humanized monoclonal antibody used in cancer treatment. It has a high affinity for EGFR (epithelial growth factor receptor), frequently associated with the growth of blood vessels in malignancy, facilitating tumor growth and survival. | Investigated for use/treatment in cervical dysplasia/cancer, colorectal cancer, gastric cancer, and lung cancer. | NA | Matuzumab binds the epidermal growth factor receptor (EGFR) with high affinity, competitively blocking natural ligand binding and blocking receptor-mediated downstream signalling, resulting in impaired tumor cell proliferation. Matuzumab (EMD-72000) is a humanized IgG1 MAb that not only binds with high specificity and affinity to EGFR, but also modulates antibody-dependent cellular cytotoxicity (ADCC). | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12014 | Th1277 | Matuzumab | >Th1277_Matuzumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTSHWMHWVRQAPGQGLEWIGEFNPSNGRTNYNEKFKSKATMTVDTSTNTAYMELSSLRSEDTAVYYCASRDYDYDGRYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKS | NA | NA | NA | NA | NA | 196 hours | Matuzumab (formerly known as the experimental drug, EMD 72000) is a humanized monoclonal antibody used in cancer treatment. It has a high affinity for EGFR (epithelial growth factor receptor), frequently associated with the growth of blood vessels in malignancy, facilitating tumor growth and survival. | Investigated for use/treatment in cervical dysplasia/cancer, colorectal cancer, gastric cancer, and lung cancer. | NA | Matuzumab binds the epidermal growth factor receptor (EGFR) with high affinity, competitively blocking natural ligand binding and blocking receptor-mediated downstream signalling, resulting in impaired tumor cell proliferation. Matuzumab (EMD-72000) is a humanized IgG1 MAb that not only binds with high specificity and affinity to EGFR, but also modulates antibody-dependent cellular cytotoxicity (ADCC). | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12015 | Th1277 | Matuzumab | >Th1277_Matuzumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTSHWMHWVRQAPGQGLEWIGEFNPSNGRTNYNEKFKSKATMTVDTSTNTAYMELSSLRSEDTAVYYCASRDYDYDGRYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKS | NA | NA | NA | NA | NA | 196 hours | Matuzumab (formerly known as the experimental drug, EMD 72000) is a humanized monoclonal antibody used in cancer treatment. It has a high affinity for EGFR (epithelial growth factor receptor), frequently associated with the growth of blood vessels in malignancy, facilitating tumor growth and survival. | Investigated for use/treatment in cervical dysplasia/cancer, colorectal cancer, gastric cancer, and lung cancer. | NA | Matuzumab binds the epidermal growth factor receptor (EGFR) with high affinity, competitively blocking natural ligand binding and blocking receptor-mediated downstream signalling, resulting in impaired tumor cell proliferation. Matuzumab (EMD-72000) is a humanized IgG1 MAb that not only binds with high specificity and affinity to EGFR, but also modulates antibody-dependent cellular cytotoxicity (ADCC). | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12026 | Th1279 | Bavituximab | >Th1279_Bavituximab EVQLQQSGPELEKPGASVKLSCKASGYSFTGYNMNWVKQSHGKSLEWIGHIDPYYGDTSYNQKFRGKATLTVDKSSSTAYMQLKSLTSEDSAVYYCVKGGYYGHWYFDVWGAGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | 30 Hrs | Bavituximab is a chimeric Anti-PS monoclonal antibody analog which is used to potentially treat cancers and viral infections. It binds to phosphatidylserine and other exposed host cell lipids when induced by cellular stress. Additional analogs in the class include 3G4, 2aG4, 9d2 and Hu3g4. | Investigated for use/treatment in breast cancer, cancer/tumors (unspecified), HIV infection, hepatitis (viral, C), and solid tumors. | NA | Bavituximab Anti-Cancer is a monoclonal antibody that binds to a basic component of the cell structure called a phospholipid that is exposed only on the surface of tumor blood vessel cells or on cells infected with certain viruses. Bavituximab binding to the tumor blood vessel cells alerts the body’s immune system to attack the tumor and its blood supply. This has been shown to inhibit tumor growth and development. Because in healthy cells the phospholipids are concealed inside the cell, the bavituximab does not bind to them. This targets the bavituximab to the malignant cells and potentially minimizes unwanted side effects. Bavituximab Anti-Viral represents a unique approach to treating viral diseases by recognizing features found only on infected cells and enveloped viruses. Bavituximab is a monoclonal antibody that binds to a basic component of the cell structure called an aminophospholipid that is exposed on the surface of cells only when they are infected with certain viruses or when they are malignant. After binding to these infected cells, the drug alerts the body’s immune system to attack the infected cells. This makes infected cells particularly susceptible to bavituximab treatment, while potentially sparing healthy cells. Also, bavituximab binds to phospholipids which are derived from the host (human) cell and not the virus, which indicates it may not be susceptible to viral drug resistance. In addition to treating an active illness, bavituximab may also confer long-term immunity. Bavituximab induces a pro-inflammatory cytokine profile, defined as an increase in the ratio of TNF alpha and TGF beta. Stimulating an immune response is a key proposed anti-viral mechanism of action of bavituximab. | Direct clearance of free virus and antibody-dependent cellular cytotoxicity of virus-infected cells appear to be the major mechanisms that contribute to the anti-viral effect of bavituximab | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12027 | Th1279 | Bavituximab | >Th1279_Bavituximab EVQLQQSGPELEKPGASVKLSCKASGYSFTGYNMNWVKQSHGKSLEWIGHIDPYYGDTSYNQKFRGKATLTVDKSSSTAYMQLKSLTSEDSAVYYCVKGGYYGHWYFDVWGAGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | 30 Hrs | Bavituximab is a chimeric Anti-PS monoclonal antibody analog which is used to potentially treat cancers and viral infections. It binds to phosphatidylserine and other exposed host cell lipids when induced by cellular stress. Additional analogs in the class include 3G4, 2aG4, 9d2 and Hu3g4. | Investigated for use/treatment in breast cancer, cancer/tumors (unspecified), HIV infection, hepatitis (viral, C), and solid tumors. | NA | Bavituximab Anti-Cancer is a monoclonal antibody that binds to a basic component of the cell structure called a phospholipid that is exposed only on the surface of tumor blood vessel cells or on cells infected with certain viruses. Bavituximab binding to the tumor blood vessel cells alerts the body’s immune system to attack the tumor and its blood supply. This has been shown to inhibit tumor growth and development. Because in healthy cells the phospholipids are concealed inside the cell, the bavituximab does not bind to them. This targets the bavituximab to the malignant cells and potentially minimizes unwanted side effects. Bavituximab Anti-Viral represents a unique approach to treating viral diseases by recognizing features found only on infected cells and enveloped viruses. Bavituximab is a monoclonal antibody that binds to a basic component of the cell structure called an aminophospholipid that is exposed on the surface of cells only when they are infected with certain viruses or when they are malignant. After binding to these infected cells, the drug alerts the body’s immune system to attack the infected cells. This makes infected cells particularly susceptible to bavituximab treatment, while potentially sparing healthy cells. Also, bavituximab binds to phospholipids which are derived from the host (human) cell and not the virus, which indicates it may not be susceptible to viral drug resistance. In addition to treating an active illness, bavituximab may also confer long-term immunity. Bavituximab induces a pro-inflammatory cytokine profile, defined as an increase in the ratio of TNF alpha and TGF beta. Stimulating an immune response is a key proposed anti-viral mechanism of action of bavituximab. | Direct clearance of free virus and antibody-dependent cellular cytotoxicity of virus-infected cells appear to be the major mechanisms that contribute to the anti-viral effect of bavituximab | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12028 | Th1279 | Bavituximab | >Th1279_Bavituximab EVQLQQSGPELEKPGASVKLSCKASGYSFTGYNMNWVKQSHGKSLEWIGHIDPYYGDTSYNQKFRGKATLTVDKSSSTAYMQLKSLTSEDSAVYYCVKGGYYGHWYFDVWGAGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | 30 Hrs | Bavituximab is a chimeric Anti-PS monoclonal antibody analog which is used to potentially treat cancers and viral infections. It binds to phosphatidylserine and other exposed host cell lipids when induced by cellular stress. Additional analogs in the class include 3G4, 2aG4, 9d2 and Hu3g4. | Investigated for use/treatment in breast cancer, cancer/tumors (unspecified), HIV infection, hepatitis (viral, C), and solid tumors. | NA | Bavituximab Anti-Cancer is a monoclonal antibody that binds to a basic component of the cell structure called a phospholipid that is exposed only on the surface of tumor blood vessel cells or on cells infected with certain viruses. Bavituximab binding to the tumor blood vessel cells alerts the body’s immune system to attack the tumor and its blood supply. This has been shown to inhibit tumor growth and development. Because in healthy cells the phospholipids are concealed inside the cell, the bavituximab does not bind to them. This targets the bavituximab to the malignant cells and potentially minimizes unwanted side effects. Bavituximab Anti-Viral represents a unique approach to treating viral diseases by recognizing features found only on infected cells and enveloped viruses. Bavituximab is a monoclonal antibody that binds to a basic component of the cell structure called an aminophospholipid that is exposed on the surface of cells only when they are infected with certain viruses or when they are malignant. After binding to these infected cells, the drug alerts the body’s immune system to attack the infected cells. This makes infected cells particularly susceptible to bavituximab treatment, while potentially sparing healthy cells. Also, bavituximab binds to phospholipids which are derived from the host (human) cell and not the virus, which indicates it may not be susceptible to viral drug resistance. In addition to treating an active illness, bavituximab may also confer long-term immunity. Bavituximab induces a pro-inflammatory cytokine profile, defined as an increase in the ratio of TNF alpha and TGF beta. Stimulating an immune response is a key proposed anti-viral mechanism of action of bavituximab. | Direct clearance of free virus and antibody-dependent cellular cytotoxicity of virus-infected cells appear to be the major mechanisms that contribute to the anti-viral effect of bavituximab | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12029 | Th1279 | Bavituximab | >Th1279_Bavituximab EVQLQQSGPELEKPGASVKLSCKASGYSFTGYNMNWVKQSHGKSLEWIGHIDPYYGDTSYNQKFRGKATLTVDKSSSTAYMQLKSLTSEDSAVYYCVKGGYYGHWYFDVWGAGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | 30 Hrs | Bavituximab is a chimeric Anti-PS monoclonal antibody analog which is used to potentially treat cancers and viral infections. It binds to phosphatidylserine and other exposed host cell lipids when induced by cellular stress. Additional analogs in the class include 3G4, 2aG4, 9d2 and Hu3g4. | Investigated for use/treatment in breast cancer, cancer/tumors (unspecified), HIV infection, hepatitis (viral, C), and solid tumors. | NA | Bavituximab Anti-Cancer is a monoclonal antibody that binds to a basic component of the cell structure called a phospholipid that is exposed only on the surface of tumor blood vessel cells or on cells infected with certain viruses. Bavituximab binding to the tumor blood vessel cells alerts the body’s immune system to attack the tumor and its blood supply. This has been shown to inhibit tumor growth and development. Because in healthy cells the phospholipids are concealed inside the cell, the bavituximab does not bind to them. This targets the bavituximab to the malignant cells and potentially minimizes unwanted side effects. Bavituximab Anti-Viral represents a unique approach to treating viral diseases by recognizing features found only on infected cells and enveloped viruses. Bavituximab is a monoclonal antibody that binds to a basic component of the cell structure called an aminophospholipid that is exposed on the surface of cells only when they are infected with certain viruses or when they are malignant. After binding to these infected cells, the drug alerts the body’s immune system to attack the infected cells. This makes infected cells particularly susceptible to bavituximab treatment, while potentially sparing healthy cells. Also, bavituximab binds to phospholipids which are derived from the host (human) cell and not the virus, which indicates it may not be susceptible to viral drug resistance. In addition to treating an active illness, bavituximab may also confer long-term immunity. Bavituximab induces a pro-inflammatory cytokine profile, defined as an increase in the ratio of TNF alpha and TGF beta. Stimulating an immune response is a key proposed anti-viral mechanism of action of bavituximab. | Direct clearance of free virus and antibody-dependent cellular cytotoxicity of virus-infected cells appear to be the major mechanisms that contribute to the anti-viral effect of bavituximab | NA | NA | NA | NA | Antineoplastic Agents, Immunological | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12030 | Th1279 | Bavituximab | >Th1279_Bavituximab EVQLQQSGPELEKPGASVKLSCKASGYSFTGYNMNWVKQSHGKSLEWIGHIDPYYGDTSYNQKFRGKATLTVDKSSSTAYMQLKSLTSEDSAVYYCVKGGYYGHWYFDVWGAGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | 30 Hrs | Bavituximab is a chimeric Anti-PS monoclonal antibody analog which is used to potentially treat cancers and viral infections. It binds to phosphatidylserine and other exposed host cell lipids when induced by cellular stress. Additional analogs in the class include 3G4, 2aG4, 9d2 and Hu3g4. | Investigated for use/treatment in breast cancer, cancer/tumors (unspecified), HIV infection, hepatitis (viral, C), and solid tumors. | NA | Bavituximab Anti-Cancer is a monoclonal antibody that binds to a basic component of the cell structure called a phospholipid that is exposed only on the surface of tumor blood vessel cells or on cells infected with certain viruses. Bavituximab binding to the tumor blood vessel cells alerts the body’s immune system to attack the tumor and its blood supply. This has been shown to inhibit tumor growth and development. Because in healthy cells the phospholipids are concealed inside the cell, the bavituximab does not bind to them. This targets the bavituximab to the malignant cells and potentially minimizes unwanted side effects. Bavituximab Anti-Viral represents a unique approach to treating viral diseases by recognizing features found only on infected cells and enveloped viruses. Bavituximab is a monoclonal antibody that binds to a basic component of the cell structure called an aminophospholipid that is exposed on the surface of cells only when they are infected with certain viruses or when they are malignant. After binding to these infected cells, the drug alerts the body’s immune system to attack the infected cells. This makes infected cells particularly susceptible to bavituximab treatment, while potentially sparing healthy cells. Also, bavituximab binds to phospholipids which are derived from the host (human) cell and not the virus, which indicates it may not be susceptible to viral drug resistance. In addition to treating an active illness, bavituximab may also confer long-term immunity. Bavituximab induces a pro-inflammatory cytokine profile, defined as an increase in the ratio of TNF alpha and TGF beta. Stimulating an immune response is a key proposed anti-viral mechanism of action of bavituximab. | Direct clearance of free virus and antibody-dependent cellular cytotoxicity of virus-infected cells appear to be the major mechanisms that contribute to the anti-viral effect of bavituximab | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12031 | Th1279 | Bavituximab | >Th1279_Bavituximab EVQLQQSGPELEKPGASVKLSCKASGYSFTGYNMNWVKQSHGKSLEWIGHIDPYYGDTSYNQKFRGKATLTVDKSSSTAYMQLKSLTSEDSAVYYCVKGGYYGHWYFDVWGAGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | 30 Hrs | Bavituximab is a chimeric Anti-PS monoclonal antibody analog which is used to potentially treat cancers and viral infections. It binds to phosphatidylserine and other exposed host cell lipids when induced by cellular stress. Additional analogs in the class include 3G4, 2aG4, 9d2 and Hu3g4. | Investigated for use/treatment in breast cancer, cancer/tumors (unspecified), HIV infection, hepatitis (viral, C), and solid tumors. | NA | Bavituximab Anti-Cancer is a monoclonal antibody that binds to a basic component of the cell structure called a phospholipid that is exposed only on the surface of tumor blood vessel cells or on cells infected with certain viruses. Bavituximab binding to the tumor blood vessel cells alerts the body’s immune system to attack the tumor and its blood supply. This has been shown to inhibit tumor growth and development. Because in healthy cells the phospholipids are concealed inside the cell, the bavituximab does not bind to them. This targets the bavituximab to the malignant cells and potentially minimizes unwanted side effects. Bavituximab Anti-Viral represents a unique approach to treating viral diseases by recognizing features found only on infected cells and enveloped viruses. Bavituximab is a monoclonal antibody that binds to a basic component of the cell structure called an aminophospholipid that is exposed on the surface of cells only when they are infected with certain viruses or when they are malignant. After binding to these infected cells, the drug alerts the body’s immune system to attack the infected cells. This makes infected cells particularly susceptible to bavituximab treatment, while potentially sparing healthy cells. Also, bavituximab binds to phospholipids which are derived from the host (human) cell and not the virus, which indicates it may not be susceptible to viral drug resistance. In addition to treating an active illness, bavituximab may also confer long-term immunity. Bavituximab induces a pro-inflammatory cytokine profile, defined as an increase in the ratio of TNF alpha and TGF beta. Stimulating an immune response is a key proposed anti-viral mechanism of action of bavituximab. | Direct clearance of free virus and antibody-dependent cellular cytotoxicity of virus-infected cells appear to be the major mechanisms that contribute to the anti-viral effect of bavituximab | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12032 | Th1279 | Bavituximab | >Th1279_Bavituximab EVQLQQSGPELEKPGASVKLSCKASGYSFTGYNMNWVKQSHGKSLEWIGHIDPYYGDTSYNQKFRGKATLTVDKSSSTAYMQLKSLTSEDSAVYYCVKGGYYGHWYFDVWGAGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | 30 Hrs | Bavituximab is a chimeric Anti-PS monoclonal antibody analog which is used to potentially treat cancers and viral infections. It binds to phosphatidylserine and other exposed host cell lipids when induced by cellular stress. Additional analogs in the class include 3G4, 2aG4, 9d2 and Hu3g4. | Investigated for use/treatment in breast cancer, cancer/tumors (unspecified), HIV infection, hepatitis (viral, C), and solid tumors. | NA | Bavituximab Anti-Cancer is a monoclonal antibody that binds to a basic component of the cell structure called a phospholipid that is exposed only on the surface of tumor blood vessel cells or on cells infected with certain viruses. Bavituximab binding to the tumor blood vessel cells alerts the body’s immune system to attack the tumor and its blood supply. This has been shown to inhibit tumor growth and development. Because in healthy cells the phospholipids are concealed inside the cell, the bavituximab does not bind to them. This targets the bavituximab to the malignant cells and potentially minimizes unwanted side effects. Bavituximab Anti-Viral represents a unique approach to treating viral diseases by recognizing features found only on infected cells and enveloped viruses. Bavituximab is a monoclonal antibody that binds to a basic component of the cell structure called an aminophospholipid that is exposed on the surface of cells only when they are infected with certain viruses or when they are malignant. After binding to these infected cells, the drug alerts the body’s immune system to attack the infected cells. This makes infected cells particularly susceptible to bavituximab treatment, while potentially sparing healthy cells. Also, bavituximab binds to phospholipids which are derived from the host (human) cell and not the virus, which indicates it may not be susceptible to viral drug resistance. In addition to treating an active illness, bavituximab may also confer long-term immunity. Bavituximab induces a pro-inflammatory cytokine profile, defined as an increase in the ratio of TNF alpha and TGF beta. Stimulating an immune response is a key proposed anti-viral mechanism of action of bavituximab. | Direct clearance of free virus and antibody-dependent cellular cytotoxicity of virus-infected cells appear to be the major mechanisms that contribute to the anti-viral effect of bavituximab | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12033 | Th1279 | Bavituximab | >Th1279_Bavituximab EVQLQQSGPELEKPGASVKLSCKASGYSFTGYNMNWVKQSHGKSLEWIGHIDPYYGDTSYNQKFRGKATLTVDKSSSTAYMQLKSLTSEDSAVYYCVKGGYYGHWYFDVWGAGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | 30 Hrs | Bavituximab is a chimeric Anti-PS monoclonal antibody analog which is used to potentially treat cancers and viral infections. It binds to phosphatidylserine and other exposed host cell lipids when induced by cellular stress. Additional analogs in the class include 3G4, 2aG4, 9d2 and Hu3g4. | Investigated for use/treatment in breast cancer, cancer/tumors (unspecified), HIV infection, hepatitis (viral, C), and solid tumors. | NA | Bavituximab Anti-Cancer is a monoclonal antibody that binds to a basic component of the cell structure called a phospholipid that is exposed only on the surface of tumor blood vessel cells or on cells infected with certain viruses. Bavituximab binding to the tumor blood vessel cells alerts the body’s immune system to attack the tumor and its blood supply. This has been shown to inhibit tumor growth and development. Because in healthy cells the phospholipids are concealed inside the cell, the bavituximab does not bind to them. This targets the bavituximab to the malignant cells and potentially minimizes unwanted side effects. Bavituximab Anti-Viral represents a unique approach to treating viral diseases by recognizing features found only on infected cells and enveloped viruses. Bavituximab is a monoclonal antibody that binds to a basic component of the cell structure called an aminophospholipid that is exposed on the surface of cells only when they are infected with certain viruses or when they are malignant. After binding to these infected cells, the drug alerts the body’s immune system to attack the infected cells. This makes infected cells particularly susceptible to bavituximab treatment, while potentially sparing healthy cells. Also, bavituximab binds to phospholipids which are derived from the host (human) cell and not the virus, which indicates it may not be susceptible to viral drug resistance. In addition to treating an active illness, bavituximab may also confer long-term immunity. Bavituximab induces a pro-inflammatory cytokine profile, defined as an increase in the ratio of TNF alpha and TGF beta. Stimulating an immune response is a key proposed anti-viral mechanism of action of bavituximab. | Direct clearance of free virus and antibody-dependent cellular cytotoxicity of virus-infected cells appear to be the major mechanisms that contribute to the anti-viral effect of bavituximab | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12034 | Th1279 | Bavituximab | >Th1279_Bavituximab EVQLQQSGPELEKPGASVKLSCKASGYSFTGYNMNWVKQSHGKSLEWIGHIDPYYGDTSYNQKFRGKATLTVDKSSSTAYMQLKSLTSEDSAVYYCVKGGYYGHWYFDVWGAGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | 30 Hrs | Bavituximab is a chimeric Anti-PS monoclonal antibody analog which is used to potentially treat cancers and viral infections. It binds to phosphatidylserine and other exposed host cell lipids when induced by cellular stress. Additional analogs in the class include 3G4, 2aG4, 9d2 and Hu3g4. | Investigated for use/treatment in breast cancer, cancer/tumors (unspecified), HIV infection, hepatitis (viral, C), and solid tumors. | NA | Bavituximab Anti-Cancer is a monoclonal antibody that binds to a basic component of the cell structure called a phospholipid that is exposed only on the surface of tumor blood vessel cells or on cells infected with certain viruses. Bavituximab binding to the tumor blood vessel cells alerts the body’s immune system to attack the tumor and its blood supply. This has been shown to inhibit tumor growth and development. Because in healthy cells the phospholipids are concealed inside the cell, the bavituximab does not bind to them. This targets the bavituximab to the malignant cells and potentially minimizes unwanted side effects. Bavituximab Anti-Viral represents a unique approach to treating viral diseases by recognizing features found only on infected cells and enveloped viruses. Bavituximab is a monoclonal antibody that binds to a basic component of the cell structure called an aminophospholipid that is exposed on the surface of cells only when they are infected with certain viruses or when they are malignant. After binding to these infected cells, the drug alerts the body’s immune system to attack the infected cells. This makes infected cells particularly susceptible to bavituximab treatment, while potentially sparing healthy cells. Also, bavituximab binds to phospholipids which are derived from the host (human) cell and not the virus, which indicates it may not be susceptible to viral drug resistance. In addition to treating an active illness, bavituximab may also confer long-term immunity. Bavituximab induces a pro-inflammatory cytokine profile, defined as an increase in the ratio of TNF alpha and TGF beta. Stimulating an immune response is a key proposed anti-viral mechanism of action of bavituximab. | Direct clearance of free virus and antibody-dependent cellular cytotoxicity of virus-infected cells appear to be the major mechanisms that contribute to the anti-viral effect of bavituximab | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12035 | Th1279 | Bavituximab | >Th1279_Bavituximab EVQLQQSGPELEKPGASVKLSCKASGYSFTGYNMNWVKQSHGKSLEWIGHIDPYYGDTSYNQKFRGKATLTVDKSSSTAYMQLKSLTSEDSAVYYCVKGGYYGHWYFDVWGAGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | 30 Hrs | Bavituximab is a chimeric Anti-PS monoclonal antibody analog which is used to potentially treat cancers and viral infections. It binds to phosphatidylserine and other exposed host cell lipids when induced by cellular stress. Additional analogs in the class include 3G4, 2aG4, 9d2 and Hu3g4. | Investigated for use/treatment in breast cancer, cancer/tumors (unspecified), HIV infection, hepatitis (viral, C), and solid tumors. | NA | Bavituximab Anti-Cancer is a monoclonal antibody that binds to a basic component of the cell structure called a phospholipid that is exposed only on the surface of tumor blood vessel cells or on cells infected with certain viruses. Bavituximab binding to the tumor blood vessel cells alerts the body’s immune system to attack the tumor and its blood supply. This has been shown to inhibit tumor growth and development. Because in healthy cells the phospholipids are concealed inside the cell, the bavituximab does not bind to them. This targets the bavituximab to the malignant cells and potentially minimizes unwanted side effects. Bavituximab Anti-Viral represents a unique approach to treating viral diseases by recognizing features found only on infected cells and enveloped viruses. Bavituximab is a monoclonal antibody that binds to a basic component of the cell structure called an aminophospholipid that is exposed on the surface of cells only when they are infected with certain viruses or when they are malignant. After binding to these infected cells, the drug alerts the body’s immune system to attack the infected cells. This makes infected cells particularly susceptible to bavituximab treatment, while potentially sparing healthy cells. Also, bavituximab binds to phospholipids which are derived from the host (human) cell and not the virus, which indicates it may not be susceptible to viral drug resistance. In addition to treating an active illness, bavituximab may also confer long-term immunity. Bavituximab induces a pro-inflammatory cytokine profile, defined as an increase in the ratio of TNF alpha and TGF beta. Stimulating an immune response is a key proposed anti-viral mechanism of action of bavituximab. | Direct clearance of free virus and antibody-dependent cellular cytotoxicity of virus-infected cells appear to be the major mechanisms that contribute to the anti-viral effect of bavituximab | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12106 | Th1286 | Keyhole limpet hemocyanin | >Th1286_Keyhole_limpet_hemocyanin MWTILALLTATLLFEGAFSVDTVVRKNVDSLSSDEVLALEKALDDLQQDDSNQGYQAIAGYHGVPTMCVDKHEKNVACCLHGMPSFPLWHRLYVVQLERALIRKKATISIPYWDWTSELTHLPELVSHPLFVGTEGGKAHDNSWYRADITFLNKKTSRAVDDRLFEKVQPGHHTRLMEGILDALEQDEFCKFEIQFELAHNAIHYLVGGRHTYSMSHLEYTSYDPLFFLHHSNTDRIFAIWQRLQQLRGKDPNSADCAHNLIHTPMEPFDRDTNPLDLTREHAKPADSFDYGRLGYQYDDLSLNGMSPEELNVYLGERAAKERTFASFILSGFGGSANVVVYVCRPAHDEISDDQCIKAGDFFLLGGPTEMKWGFYRAYHFDVTDSVASIDDDGHGHYYVKSELFSVNGSALSNDILRQPTLVHRPAKGHFDKPPVPVAQANLAVRKNINDLTAEETYSLRKAMERFQNDKSVDGYQATVEFHALPARCPRPDAKDRFACCVHGMATFPHWHRLFVTQVEDALLRRGSTIGLPNWDWTMPMDHLPELATSETYLDPVTGETKNNPFHHAQVAFENGVTSRNPDAKLFMKPTYGDHTYLFDSMIYAFEQEDFCDFEVQYELTHNAIHAWVGGSEKYSMSSLHYTAFDPIFYLHHSNVDRLWAIWQALQIRRGKSYKAHCASSQEREPLKPFAFSSPLNNNEKTYHNSVPTNVYDYVGVLHYRYDDLQFGGMTMSELEEYIHKQTQHDRTFAGFFLSYIGTSASVDIFINREGHDKYKVGSFVVLGGSKEMKWGFDRMYKYEITEALKTLNVAVDDGFSITVEITDVDGSPPSADLIPPPAIIFERADAKDFGHSRKIRKAVDSLTVEEQTSLRRAMADLQDDKTSGGFQQIAAFHGEPKWCPSPEAEKKFACCVHGMAVFPHWHRLLTVQGENALRKHGFTGGLPYWDWTRSMSALPHFVADPTYNDAISSQEEDNPWHHGHIDSVGHDTTRDVRDDLYQSPGFGHYTDIAKQVLLAFEQDDFCDFEVQFEIAHNFIHALVGGNEPYSMSSLRYTTYDPIFFLHRSNTDRLWAIWQALQKYRGKPYNTANCAIASMRKPLQPFGLDSVINPDDETREHSVPFRVFDYKNNFDYEYESLAFNGLSIAQLDRELQRRKSHDRVFAGFLLHEIGQSALVKFYVCKHNVSDCDHYAGEFYILGDEAEMPWRYDRVYKYEITQQLHDLDLHVGDNFFLKYEAFDLNGGSLGGSIFSQPSVIFEPAAGSHQADEYREAVTSASHIRKNIRDLSEGEIESIRSAFLQIQKEGIYENIAKFHGKPGLCEHDGHPVACCVHGMPTFPHWHRLYVLQVENALLERGSAVAVPYWDWTEKADSLPSLINDATYFNSRSQTFDPNPFFRGHIAFENAVTSRDPQPELWDNKDFYENVMLALEQDNFCDFEIQLELIHNALHSRLGGRAKYSLSSLDYTAFDPVFFLHHANVDRIWAIWQDLQRYRKKPYNEADCAVNEMRKPLQPFNNPELNSDSMTLKHNLPQDSFDYQNRFRYQYDNLQFNHFSIQKLDQTIQARKQHDRVFAGFILHNIGTSAVVDIYICVEQGGEQNCKTKAGSFTILGGETEMPFHFDRLYKFDITSALHKLGVPLDGHGFDIKVDVRAVNGSHLDQHILNEPSLLFVPGERKNIYYDGLSQHNLVRKEVSSLTTLEKHFLRKALKNMQADDSPDGYQAIASFHALPPLCPSPSAAHRHACCLHGMATFPQWHRLYTVQFEDSLKRHGSIVGLPYWDWLKPQSALPDLVTQETYEHLFSHKTFPNPFLKANIEFEGEGVTTERDVDAEHLFAKGNLVYNNWFCNQALYALEQENYCDFEIQFEILHNGIHSWVGGSKTHSIGHLHYASYDPLFYIHHSQTDRIWAIWQALQEHRGLSGKEAHCALEQMKDPLKPFSFGSPYNLNKRTQEFSKPEDTFDYHRFGYEYDSLEFVGMSVSSLHNYIKQQQEADRVFAGFLLKGFGQSASVSFDICRPDQSCQEAGYFSVLGGSSEMPWQFDRLYKYDITKTLKDMKLRYDDTFTIKVHIKDIAGAELDSDLIPTPSVLLEEGKHGINVRHVGRNRIRMELSELTERDLASLKSAMRSLQADDGVNGYQAIASFHGLPASCHDDEGHEIACCIHGMPVFPHWHRLYTLQMDMALLSHGSAVAIPYWDWTKPISKLPDLFTSPEYYDPWRDAVVNNPFAKGYIKSEDAYTVRDPQDILYHLQDETGTSVLLDQTLLALEQTDFCDFEVQFEVVHNAIHYLVGGRQVYALSSQHYASYDPAFFIHHSFVDKIWAVWQALQKKRKRPYHKADCALNMMTKPMRPFAHDFNHNGFTKMHAVPNTLFDFQDLFYTYDNLEIAGMNVNQLEAEINRRKSQTRVFAGFLLHGIGRSADVRFWICKTADDCHASGMIFILGGSKEMHWAYDRNFKYDITQALKAQSIHPEDVFDTDAPFFIKVEVHGVNKTALPSSAIPAPTIIYSAGEGHTDDHGSDHIAGSGVRKDVTSLTASEIENLRHALQSVMDDDGPNGFQAIAAYHGSPPMCHMXDGRDVACCTHGMASFPHWHRLFVKQMEDALAAHGAHIGIPYWDWTSAFSHLPALVTDHEHNPFHHGHIAHRNVDTSRSPRDMLFNDPEHGSESFFYRQVLLALEQTDFCQFEVQFEITHNAIHSWTGGHTPYGMSSLEYTAYDPLFYLHHSNTDRIWAIWQALQKYRGFQYNAAHCDIQVLKQPLKPFSESRNPNPVTRANSRAVDSFDYERLNYQYDTLTFHGHSISELDAMLQERKKEERTFAAFLLHGFGASADVSFDVCTPDGHCAFAGTFAVLGGELEMPWSFERLFRYDITKVLKQMNLHYDSEFHFELKIVGTDGTELPSDRIKSPTIEHHGGDHHGGDTSGHDHSERHDGFFRKEVGSLSLDEANDLKNALYKLQNDQGPNGYESIAGYHGYPFLCPEHGEDQYACCVHGMPVFPHWHRLHTIQFERALKEHGSHLGIPYWDWTKSMIALPAFFADSSNSNPFYKYHIMKAGHDTARSPSDLLFNQPQLHGYDYLYYLALSTLEEDNYCDFEVHYEILHNAVHLWLGGTETYSMSSLAFSAYDPVFMILHSGLDRLWIIWQELQKLRKKPYNAAKCAGHMMDEPLHPFNYESANHDSFTRANAKPSTVFDSHKFNYHYDNPDVRGNSIQEISAIIHDLRNQPRVFAGFVLSGIYTSANVKIYLVREGHDDENVGSFVVLGGPKEMPWAYERIFKYDITEVANRLNMHHDDTFNFRLEVQSYTGEMVTHHLPEPLIIYRPAKQEYDVLVIPLGSGHKLPPKVIVKRGTRIMFHPVDDTVNRPVVDLGSHTALYNCVVPPFTYNGYELDHAYSLRDGHYYIAGPTKDLCTSGNVRIHIHIEDE | NA | NA | NA | NA | NA | NA | Keyhole limpet hemocyanin is an immune modulator, given as a vaccine to help the body respond to cancer. A natural protein isolated from the marine mollusc keyhole limpet. Keyhole limpet hemocyanin is an immunogenic carrier protein that, in vivo, increases antigenic immune responses to haptens and other weak antigens such as idiotype proteins. | Investigated for use/treatment in bladder cancer and solid tumors. | NA | Keyhole Limpet Hemocyanin (KLH) is generally a very efficient coupling agent. It is the most common carrier protein used in the preparation of hapten conjugates. KLH is composed of five subunits. It is lysine rich with a large number of available primary amines to facilitate conjugation, antibody production and promote peptide attachment after dissociation. | NA | NA | NA | NA | NA | Adjuvants, Immunologic | NA | NA | NA | NA | Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12107 | Th1286 | Keyhole limpet hemocyanin | >Th1286_Keyhole_limpet_hemocyanin MWTILALLTATLLFEGAFSVDTVVRKNVDSLSSDEVLALEKALDDLQQDDSNQGYQAIAGYHGVPTMCVDKHEKNVACCLHGMPSFPLWHRLYVVQLERALIRKKATISIPYWDWTSELTHLPELVSHPLFVGTEGGKAHDNSWYRADITFLNKKTSRAVDDRLFEKVQPGHHTRLMEGILDALEQDEFCKFEIQFELAHNAIHYLVGGRHTYSMSHLEYTSYDPLFFLHHSNTDRIFAIWQRLQQLRGKDPNSADCAHNLIHTPMEPFDRDTNPLDLTREHAKPADSFDYGRLGYQYDDLSLNGMSPEELNVYLGERAAKERTFASFILSGFGGSANVVVYVCRPAHDEISDDQCIKAGDFFLLGGPTEMKWGFYRAYHFDVTDSVASIDDDGHGHYYVKSELFSVNGSALSNDILRQPTLVHRPAKGHFDKPPVPVAQANLAVRKNINDLTAEETYSLRKAMERFQNDKSVDGYQATVEFHALPARCPRPDAKDRFACCVHGMATFPHWHRLFVTQVEDALLRRGSTIGLPNWDWTMPMDHLPELATSETYLDPVTGETKNNPFHHAQVAFENGVTSRNPDAKLFMKPTYGDHTYLFDSMIYAFEQEDFCDFEVQYELTHNAIHAWVGGSEKYSMSSLHYTAFDPIFYLHHSNVDRLWAIWQALQIRRGKSYKAHCASSQEREPLKPFAFSSPLNNNEKTYHNSVPTNVYDYVGVLHYRYDDLQFGGMTMSELEEYIHKQTQHDRTFAGFFLSYIGTSASVDIFINREGHDKYKVGSFVVLGGSKEMKWGFDRMYKYEITEALKTLNVAVDDGFSITVEITDVDGSPPSADLIPPPAIIFERADAKDFGHSRKIRKAVDSLTVEEQTSLRRAMADLQDDKTSGGFQQIAAFHGEPKWCPSPEAEKKFACCVHGMAVFPHWHRLLTVQGENALRKHGFTGGLPYWDWTRSMSALPHFVADPTYNDAISSQEEDNPWHHGHIDSVGHDTTRDVRDDLYQSPGFGHYTDIAKQVLLAFEQDDFCDFEVQFEIAHNFIHALVGGNEPYSMSSLRYTTYDPIFFLHRSNTDRLWAIWQALQKYRGKPYNTANCAIASMRKPLQPFGLDSVINPDDETREHSVPFRVFDYKNNFDYEYESLAFNGLSIAQLDRELQRRKSHDRVFAGFLLHEIGQSALVKFYVCKHNVSDCDHYAGEFYILGDEAEMPWRYDRVYKYEITQQLHDLDLHVGDNFFLKYEAFDLNGGSLGGSIFSQPSVIFEPAAGSHQADEYREAVTSASHIRKNIRDLSEGEIESIRSAFLQIQKEGIYENIAKFHGKPGLCEHDGHPVACCVHGMPTFPHWHRLYVLQVENALLERGSAVAVPYWDWTEKADSLPSLINDATYFNSRSQTFDPNPFFRGHIAFENAVTSRDPQPELWDNKDFYENVMLALEQDNFCDFEIQLELIHNALHSRLGGRAKYSLSSLDYTAFDPVFFLHHANVDRIWAIWQDLQRYRKKPYNEADCAVNEMRKPLQPFNNPELNSDSMTLKHNLPQDSFDYQNRFRYQYDNLQFNHFSIQKLDQTIQARKQHDRVFAGFILHNIGTSAVVDIYICVEQGGEQNCKTKAGSFTILGGETEMPFHFDRLYKFDITSALHKLGVPLDGHGFDIKVDVRAVNGSHLDQHILNEPSLLFVPGERKNIYYDGLSQHNLVRKEVSSLTTLEKHFLRKALKNMQADDSPDGYQAIASFHALPPLCPSPSAAHRHACCLHGMATFPQWHRLYTVQFEDSLKRHGSIVGLPYWDWLKPQSALPDLVTQETYEHLFSHKTFPNPFLKANIEFEGEGVTTERDVDAEHLFAKGNLVYNNWFCNQALYALEQENYCDFEIQFEILHNGIHSWVGGSKTHSIGHLHYASYDPLFYIHHSQTDRIWAIWQALQEHRGLSGKEAHCALEQMKDPLKPFSFGSPYNLNKRTQEFSKPEDTFDYHRFGYEYDSLEFVGMSVSSLHNYIKQQQEADRVFAGFLLKGFGQSASVSFDICRPDQSCQEAGYFSVLGGSSEMPWQFDRLYKYDITKTLKDMKLRYDDTFTIKVHIKDIAGAELDSDLIPTPSVLLEEGKHGINVRHVGRNRIRMELSELTERDLASLKSAMRSLQADDGVNGYQAIASFHGLPASCHDDEGHEIACCIHGMPVFPHWHRLYTLQMDMALLSHGSAVAIPYWDWTKPISKLPDLFTSPEYYDPWRDAVVNNPFAKGYIKSEDAYTVRDPQDILYHLQDETGTSVLLDQTLLALEQTDFCDFEVQFEVVHNAIHYLVGGRQVYALSSQHYASYDPAFFIHHSFVDKIWAVWQALQKKRKRPYHKADCALNMMTKPMRPFAHDFNHNGFTKMHAVPNTLFDFQDLFYTYDNLEIAGMNVNQLEAEINRRKSQTRVFAGFLLHGIGRSADVRFWICKTADDCHASGMIFILGGSKEMHWAYDRNFKYDITQALKAQSIHPEDVFDTDAPFFIKVEVHGVNKTALPSSAIPAPTIIYSAGEGHTDDHGSDHIAGSGVRKDVTSLTASEIENLRHALQSVMDDDGPNGFQAIAAYHGSPPMCHMXDGRDVACCTHGMASFPHWHRLFVKQMEDALAAHGAHIGIPYWDWTSAFSHLPALVTDHEHNPFHHGHIAHRNVDTSRSPRDMLFNDPEHGSESFFYRQVLLALEQTDFCQFEVQFEITHNAIHSWTGGHTPYGMSSLEYTAYDPLFYLHHSNTDRIWAIWQALQKYRGFQYNAAHCDIQVLKQPLKPFSESRNPNPVTRANSRAVDSFDYERLNYQYDTLTFHGHSISELDAMLQERKKEERTFAAFLLHGFGASADVSFDVCTPDGHCAFAGTFAVLGGELEMPWSFERLFRYDITKVLKQMNLHYDSEFHFELKIVGTDGTELPSDRIKSPTIEHHGGDHHGGDTSGHDHSERHDGFFRKEVGSLSLDEANDLKNALYKLQNDQGPNGYESIAGYHGYPFLCPEHGEDQYACCVHGMPVFPHWHRLHTIQFERALKEHGSHLGIPYWDWTKSMIALPAFFADSSNSNPFYKYHIMKAGHDTARSPSDLLFNQPQLHGYDYLYYLALSTLEEDNYCDFEVHYEILHNAVHLWLGGTETYSMSSLAFSAYDPVFMILHSGLDRLWIIWQELQKLRKKPYNAAKCAGHMMDEPLHPFNYESANHDSFTRANAKPSTVFDSHKFNYHYDNPDVRGNSIQEISAIIHDLRNQPRVFAGFVLSGIYTSANVKIYLVREGHDDENVGSFVVLGGPKEMPWAYERIFKYDITEVANRLNMHHDDTFNFRLEVQSYTGEMVTHHLPEPLIIYRPAKQEYDVLVIPLGSGHKLPPKVIVKRGTRIMFHPVDDTVNRPVVDLGSHTALYNCVVPPFTYNGYELDHAYSLRDGHYYIAGPTKDLCTSGNVRIHIHIEDE | NA | NA | NA | NA | NA | NA | Keyhole limpet hemocyanin is an immune modulator, given as a vaccine to help the body respond to cancer. A natural protein isolated from the marine mollusc keyhole limpet. Keyhole limpet hemocyanin is an immunogenic carrier protein that, in vivo, increases antigenic immune responses to haptens and other weak antigens such as idiotype proteins. | Investigated for use/treatment in bladder cancer and solid tumors. | NA | Keyhole Limpet Hemocyanin (KLH) is generally a very efficient coupling agent. It is the most common carrier protein used in the preparation of hapten conjugates. KLH is composed of five subunits. It is lysine rich with a large number of available primary amines to facilitate conjugation, antibody production and promote peptide attachment after dissociation. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12108 | Th1286 | Keyhole limpet hemocyanin | >Th1286_Keyhole_limpet_hemocyanin MWTILALLTATLLFEGAFSVDTVVRKNVDSLSSDEVLALEKALDDLQQDDSNQGYQAIAGYHGVPTMCVDKHEKNVACCLHGMPSFPLWHRLYVVQLERALIRKKATISIPYWDWTSELTHLPELVSHPLFVGTEGGKAHDNSWYRADITFLNKKTSRAVDDRLFEKVQPGHHTRLMEGILDALEQDEFCKFEIQFELAHNAIHYLVGGRHTYSMSHLEYTSYDPLFFLHHSNTDRIFAIWQRLQQLRGKDPNSADCAHNLIHTPMEPFDRDTNPLDLTREHAKPADSFDYGRLGYQYDDLSLNGMSPEELNVYLGERAAKERTFASFILSGFGGSANVVVYVCRPAHDEISDDQCIKAGDFFLLGGPTEMKWGFYRAYHFDVTDSVASIDDDGHGHYYVKSELFSVNGSALSNDILRQPTLVHRPAKGHFDKPPVPVAQANLAVRKNINDLTAEETYSLRKAMERFQNDKSVDGYQATVEFHALPARCPRPDAKDRFACCVHGMATFPHWHRLFVTQVEDALLRRGSTIGLPNWDWTMPMDHLPELATSETYLDPVTGETKNNPFHHAQVAFENGVTSRNPDAKLFMKPTYGDHTYLFDSMIYAFEQEDFCDFEVQYELTHNAIHAWVGGSEKYSMSSLHYTAFDPIFYLHHSNVDRLWAIWQALQIRRGKSYKAHCASSQEREPLKPFAFSSPLNNNEKTYHNSVPTNVYDYVGVLHYRYDDLQFGGMTMSELEEYIHKQTQHDRTFAGFFLSYIGTSASVDIFINREGHDKYKVGSFVVLGGSKEMKWGFDRMYKYEITEALKTLNVAVDDGFSITVEITDVDGSPPSADLIPPPAIIFERADAKDFGHSRKIRKAVDSLTVEEQTSLRRAMADLQDDKTSGGFQQIAAFHGEPKWCPSPEAEKKFACCVHGMAVFPHWHRLLTVQGENALRKHGFTGGLPYWDWTRSMSALPHFVADPTYNDAISSQEEDNPWHHGHIDSVGHDTTRDVRDDLYQSPGFGHYTDIAKQVLLAFEQDDFCDFEVQFEIAHNFIHALVGGNEPYSMSSLRYTTYDPIFFLHRSNTDRLWAIWQALQKYRGKPYNTANCAIASMRKPLQPFGLDSVINPDDETREHSVPFRVFDYKNNFDYEYESLAFNGLSIAQLDRELQRRKSHDRVFAGFLLHEIGQSALVKFYVCKHNVSDCDHYAGEFYILGDEAEMPWRYDRVYKYEITQQLHDLDLHVGDNFFLKYEAFDLNGGSLGGSIFSQPSVIFEPAAGSHQADEYREAVTSASHIRKNIRDLSEGEIESIRSAFLQIQKEGIYENIAKFHGKPGLCEHDGHPVACCVHGMPTFPHWHRLYVLQVENALLERGSAVAVPYWDWTEKADSLPSLINDATYFNSRSQTFDPNPFFRGHIAFENAVTSRDPQPELWDNKDFYENVMLALEQDNFCDFEIQLELIHNALHSRLGGRAKYSLSSLDYTAFDPVFFLHHANVDRIWAIWQDLQRYRKKPYNEADCAVNEMRKPLQPFNNPELNSDSMTLKHNLPQDSFDYQNRFRYQYDNLQFNHFSIQKLDQTIQARKQHDRVFAGFILHNIGTSAVVDIYICVEQGGEQNCKTKAGSFTILGGETEMPFHFDRLYKFDITSALHKLGVPLDGHGFDIKVDVRAVNGSHLDQHILNEPSLLFVPGERKNIYYDGLSQHNLVRKEVSSLTTLEKHFLRKALKNMQADDSPDGYQAIASFHALPPLCPSPSAAHRHACCLHGMATFPQWHRLYTVQFEDSLKRHGSIVGLPYWDWLKPQSALPDLVTQETYEHLFSHKTFPNPFLKANIEFEGEGVTTERDVDAEHLFAKGNLVYNNWFCNQALYALEQENYCDFEIQFEILHNGIHSWVGGSKTHSIGHLHYASYDPLFYIHHSQTDRIWAIWQALQEHRGLSGKEAHCALEQMKDPLKPFSFGSPYNLNKRTQEFSKPEDTFDYHRFGYEYDSLEFVGMSVSSLHNYIKQQQEADRVFAGFLLKGFGQSASVSFDICRPDQSCQEAGYFSVLGGSSEMPWQFDRLYKYDITKTLKDMKLRYDDTFTIKVHIKDIAGAELDSDLIPTPSVLLEEGKHGINVRHVGRNRIRMELSELTERDLASLKSAMRSLQADDGVNGYQAIASFHGLPASCHDDEGHEIACCIHGMPVFPHWHRLYTLQMDMALLSHGSAVAIPYWDWTKPISKLPDLFTSPEYYDPWRDAVVNNPFAKGYIKSEDAYTVRDPQDILYHLQDETGTSVLLDQTLLALEQTDFCDFEVQFEVVHNAIHYLVGGRQVYALSSQHYASYDPAFFIHHSFVDKIWAVWQALQKKRKRPYHKADCALNMMTKPMRPFAHDFNHNGFTKMHAVPNTLFDFQDLFYTYDNLEIAGMNVNQLEAEINRRKSQTRVFAGFLLHGIGRSADVRFWICKTADDCHASGMIFILGGSKEMHWAYDRNFKYDITQALKAQSIHPEDVFDTDAPFFIKVEVHGVNKTALPSSAIPAPTIIYSAGEGHTDDHGSDHIAGSGVRKDVTSLTASEIENLRHALQSVMDDDGPNGFQAIAAYHGSPPMCHMXDGRDVACCTHGMASFPHWHRLFVKQMEDALAAHGAHIGIPYWDWTSAFSHLPALVTDHEHNPFHHGHIAHRNVDTSRSPRDMLFNDPEHGSESFFYRQVLLALEQTDFCQFEVQFEITHNAIHSWTGGHTPYGMSSLEYTAYDPLFYLHHSNTDRIWAIWQALQKYRGFQYNAAHCDIQVLKQPLKPFSESRNPNPVTRANSRAVDSFDYERLNYQYDTLTFHGHSISELDAMLQERKKEERTFAAFLLHGFGASADVSFDVCTPDGHCAFAGTFAVLGGELEMPWSFERLFRYDITKVLKQMNLHYDSEFHFELKIVGTDGTELPSDRIKSPTIEHHGGDHHGGDTSGHDHSERHDGFFRKEVGSLSLDEANDLKNALYKLQNDQGPNGYESIAGYHGYPFLCPEHGEDQYACCVHGMPVFPHWHRLHTIQFERALKEHGSHLGIPYWDWTKSMIALPAFFADSSNSNPFYKYHIMKAGHDTARSPSDLLFNQPQLHGYDYLYYLALSTLEEDNYCDFEVHYEILHNAVHLWLGGTETYSMSSLAFSAYDPVFMILHSGLDRLWIIWQELQKLRKKPYNAAKCAGHMMDEPLHPFNYESANHDSFTRANAKPSTVFDSHKFNYHYDNPDVRGNSIQEISAIIHDLRNQPRVFAGFVLSGIYTSANVKIYLVREGHDDENVGSFVVLGGPKEMPWAYERIFKYDITEVANRLNMHHDDTFNFRLEVQSYTGEMVTHHLPEPLIIYRPAKQEYDVLVIPLGSGHKLPPKVIVKRGTRIMFHPVDDTVNRPVVDLGSHTALYNCVVPPFTYNGYELDHAYSLRDGHYYIAGPTKDLCTSGNVRIHIHIEDE | NA | NA | NA | NA | NA | NA | Keyhole limpet hemocyanin is an immune modulator, given as a vaccine to help the body respond to cancer. A natural protein isolated from the marine mollusc keyhole limpet. Keyhole limpet hemocyanin is an immunogenic carrier protein that, in vivo, increases antigenic immune responses to haptens and other weak antigens such as idiotype proteins. | Investigated for use/treatment in bladder cancer and solid tumors. | NA | Keyhole Limpet Hemocyanin (KLH) is generally a very efficient coupling agent. It is the most common carrier protein used in the preparation of hapten conjugates. KLH is composed of five subunits. It is lysine rich with a large number of available primary amines to facilitate conjugation, antibody production and promote peptide attachment after dissociation. | NA | NA | NA | NA | NA | Antigens | NA | NA | NA | NA | Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12109 | Th1286 | Keyhole limpet hemocyanin | >Th1286_Keyhole_limpet_hemocyanin MWTILALLTATLLFEGAFSVDTVVRKNVDSLSSDEVLALEKALDDLQQDDSNQGYQAIAGYHGVPTMCVDKHEKNVACCLHGMPSFPLWHRLYVVQLERALIRKKATISIPYWDWTSELTHLPELVSHPLFVGTEGGKAHDNSWYRADITFLNKKTSRAVDDRLFEKVQPGHHTRLMEGILDALEQDEFCKFEIQFELAHNAIHYLVGGRHTYSMSHLEYTSYDPLFFLHHSNTDRIFAIWQRLQQLRGKDPNSADCAHNLIHTPMEPFDRDTNPLDLTREHAKPADSFDYGRLGYQYDDLSLNGMSPEELNVYLGERAAKERTFASFILSGFGGSANVVVYVCRPAHDEISDDQCIKAGDFFLLGGPTEMKWGFYRAYHFDVTDSVASIDDDGHGHYYVKSELFSVNGSALSNDILRQPTLVHRPAKGHFDKPPVPVAQANLAVRKNINDLTAEETYSLRKAMERFQNDKSVDGYQATVEFHALPARCPRPDAKDRFACCVHGMATFPHWHRLFVTQVEDALLRRGSTIGLPNWDWTMPMDHLPELATSETYLDPVTGETKNNPFHHAQVAFENGVTSRNPDAKLFMKPTYGDHTYLFDSMIYAFEQEDFCDFEVQYELTHNAIHAWVGGSEKYSMSSLHYTAFDPIFYLHHSNVDRLWAIWQALQIRRGKSYKAHCASSQEREPLKPFAFSSPLNNNEKTYHNSVPTNVYDYVGVLHYRYDDLQFGGMTMSELEEYIHKQTQHDRTFAGFFLSYIGTSASVDIFINREGHDKYKVGSFVVLGGSKEMKWGFDRMYKYEITEALKTLNVAVDDGFSITVEITDVDGSPPSADLIPPPAIIFERADAKDFGHSRKIRKAVDSLTVEEQTSLRRAMADLQDDKTSGGFQQIAAFHGEPKWCPSPEAEKKFACCVHGMAVFPHWHRLLTVQGENALRKHGFTGGLPYWDWTRSMSALPHFVADPTYNDAISSQEEDNPWHHGHIDSVGHDTTRDVRDDLYQSPGFGHYTDIAKQVLLAFEQDDFCDFEVQFEIAHNFIHALVGGNEPYSMSSLRYTTYDPIFFLHRSNTDRLWAIWQALQKYRGKPYNTANCAIASMRKPLQPFGLDSVINPDDETREHSVPFRVFDYKNNFDYEYESLAFNGLSIAQLDRELQRRKSHDRVFAGFLLHEIGQSALVKFYVCKHNVSDCDHYAGEFYILGDEAEMPWRYDRVYKYEITQQLHDLDLHVGDNFFLKYEAFDLNGGSLGGSIFSQPSVIFEPAAGSHQADEYREAVTSASHIRKNIRDLSEGEIESIRSAFLQIQKEGIYENIAKFHGKPGLCEHDGHPVACCVHGMPTFPHWHRLYVLQVENALLERGSAVAVPYWDWTEKADSLPSLINDATYFNSRSQTFDPNPFFRGHIAFENAVTSRDPQPELWDNKDFYENVMLALEQDNFCDFEIQLELIHNALHSRLGGRAKYSLSSLDYTAFDPVFFLHHANVDRIWAIWQDLQRYRKKPYNEADCAVNEMRKPLQPFNNPELNSDSMTLKHNLPQDSFDYQNRFRYQYDNLQFNHFSIQKLDQTIQARKQHDRVFAGFILHNIGTSAVVDIYICVEQGGEQNCKTKAGSFTILGGETEMPFHFDRLYKFDITSALHKLGVPLDGHGFDIKVDVRAVNGSHLDQHILNEPSLLFVPGERKNIYYDGLSQHNLVRKEVSSLTTLEKHFLRKALKNMQADDSPDGYQAIASFHALPPLCPSPSAAHRHACCLHGMATFPQWHRLYTVQFEDSLKRHGSIVGLPYWDWLKPQSALPDLVTQETYEHLFSHKTFPNPFLKANIEFEGEGVTTERDVDAEHLFAKGNLVYNNWFCNQALYALEQENYCDFEIQFEILHNGIHSWVGGSKTHSIGHLHYASYDPLFYIHHSQTDRIWAIWQALQEHRGLSGKEAHCALEQMKDPLKPFSFGSPYNLNKRTQEFSKPEDTFDYHRFGYEYDSLEFVGMSVSSLHNYIKQQQEADRVFAGFLLKGFGQSASVSFDICRPDQSCQEAGYFSVLGGSSEMPWQFDRLYKYDITKTLKDMKLRYDDTFTIKVHIKDIAGAELDSDLIPTPSVLLEEGKHGINVRHVGRNRIRMELSELTERDLASLKSAMRSLQADDGVNGYQAIASFHGLPASCHDDEGHEIACCIHGMPVFPHWHRLYTLQMDMALLSHGSAVAIPYWDWTKPISKLPDLFTSPEYYDPWRDAVVNNPFAKGYIKSEDAYTVRDPQDILYHLQDETGTSVLLDQTLLALEQTDFCDFEVQFEVVHNAIHYLVGGRQVYALSSQHYASYDPAFFIHHSFVDKIWAVWQALQKKRKRPYHKADCALNMMTKPMRPFAHDFNHNGFTKMHAVPNTLFDFQDLFYTYDNLEIAGMNVNQLEAEINRRKSQTRVFAGFLLHGIGRSADVRFWICKTADDCHASGMIFILGGSKEMHWAYDRNFKYDITQALKAQSIHPEDVFDTDAPFFIKVEVHGVNKTALPSSAIPAPTIIYSAGEGHTDDHGSDHIAGSGVRKDVTSLTASEIENLRHALQSVMDDDGPNGFQAIAAYHGSPPMCHMXDGRDVACCTHGMASFPHWHRLFVKQMEDALAAHGAHIGIPYWDWTSAFSHLPALVTDHEHNPFHHGHIAHRNVDTSRSPRDMLFNDPEHGSESFFYRQVLLALEQTDFCQFEVQFEITHNAIHSWTGGHTPYGMSSLEYTAYDPLFYLHHSNTDRIWAIWQALQKYRGFQYNAAHCDIQVLKQPLKPFSESRNPNPVTRANSRAVDSFDYERLNYQYDTLTFHGHSISELDAMLQERKKEERTFAAFLLHGFGASADVSFDVCTPDGHCAFAGTFAVLGGELEMPWSFERLFRYDITKVLKQMNLHYDSEFHFELKIVGTDGTELPSDRIKSPTIEHHGGDHHGGDTSGHDHSERHDGFFRKEVGSLSLDEANDLKNALYKLQNDQGPNGYESIAGYHGYPFLCPEHGEDQYACCVHGMPVFPHWHRLHTIQFERALKEHGSHLGIPYWDWTKSMIALPAFFADSSNSNPFYKYHIMKAGHDTARSPSDLLFNQPQLHGYDYLYYLALSTLEEDNYCDFEVHYEILHNAVHLWLGGTETYSMSSLAFSAYDPVFMILHSGLDRLWIIWQELQKLRKKPYNAAKCAGHMMDEPLHPFNYESANHDSFTRANAKPSTVFDSHKFNYHYDNPDVRGNSIQEISAIIHDLRNQPRVFAGFVLSGIYTSANVKIYLVREGHDDENVGSFVVLGGPKEMPWAYERIFKYDITEVANRLNMHHDDTFNFRLEVQSYTGEMVTHHLPEPLIIYRPAKQEYDVLVIPLGSGHKLPPKVIVKRGTRIMFHPVDDTVNRPVVDLGSHTALYNCVVPPFTYNGYELDHAYSLRDGHYYIAGPTKDLCTSGNVRIHIHIEDE | NA | NA | NA | NA | NA | NA | Keyhole limpet hemocyanin is an immune modulator, given as a vaccine to help the body respond to cancer. A natural protein isolated from the marine mollusc keyhole limpet. Keyhole limpet hemocyanin is an immunogenic carrier protein that, in vivo, increases antigenic immune responses to haptens and other weak antigens such as idiotype proteins. | Investigated for use/treatment in bladder cancer and solid tumors. | NA | Keyhole Limpet Hemocyanin (KLH) is generally a very efficient coupling agent. It is the most common carrier protein used in the preparation of hapten conjugates. KLH is composed of five subunits. It is lysine rich with a large number of available primary amines to facilitate conjugation, antibody production and promote peptide attachment after dissociation. | NA | NA | NA | NA | NA | Arthropod Proteins | NA | NA | NA | NA | Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12110 | Th1286 | Keyhole limpet hemocyanin | >Th1286_Keyhole_limpet_hemocyanin MWTILALLTATLLFEGAFSVDTVVRKNVDSLSSDEVLALEKALDDLQQDDSNQGYQAIAGYHGVPTMCVDKHEKNVACCLHGMPSFPLWHRLYVVQLERALIRKKATISIPYWDWTSELTHLPELVSHPLFVGTEGGKAHDNSWYRADITFLNKKTSRAVDDRLFEKVQPGHHTRLMEGILDALEQDEFCKFEIQFELAHNAIHYLVGGRHTYSMSHLEYTSYDPLFFLHHSNTDRIFAIWQRLQQLRGKDPNSADCAHNLIHTPMEPFDRDTNPLDLTREHAKPADSFDYGRLGYQYDDLSLNGMSPEELNVYLGERAAKERTFASFILSGFGGSANVVVYVCRPAHDEISDDQCIKAGDFFLLGGPTEMKWGFYRAYHFDVTDSVASIDDDGHGHYYVKSELFSVNGSALSNDILRQPTLVHRPAKGHFDKPPVPVAQANLAVRKNINDLTAEETYSLRKAMERFQNDKSVDGYQATVEFHALPARCPRPDAKDRFACCVHGMATFPHWHRLFVTQVEDALLRRGSTIGLPNWDWTMPMDHLPELATSETYLDPVTGETKNNPFHHAQVAFENGVTSRNPDAKLFMKPTYGDHTYLFDSMIYAFEQEDFCDFEVQYELTHNAIHAWVGGSEKYSMSSLHYTAFDPIFYLHHSNVDRLWAIWQALQIRRGKSYKAHCASSQEREPLKPFAFSSPLNNNEKTYHNSVPTNVYDYVGVLHYRYDDLQFGGMTMSELEEYIHKQTQHDRTFAGFFLSYIGTSASVDIFINREGHDKYKVGSFVVLGGSKEMKWGFDRMYKYEITEALKTLNVAVDDGFSITVEITDVDGSPPSADLIPPPAIIFERADAKDFGHSRKIRKAVDSLTVEEQTSLRRAMADLQDDKTSGGFQQIAAFHGEPKWCPSPEAEKKFACCVHGMAVFPHWHRLLTVQGENALRKHGFTGGLPYWDWTRSMSALPHFVADPTYNDAISSQEEDNPWHHGHIDSVGHDTTRDVRDDLYQSPGFGHYTDIAKQVLLAFEQDDFCDFEVQFEIAHNFIHALVGGNEPYSMSSLRYTTYDPIFFLHRSNTDRLWAIWQALQKYRGKPYNTANCAIASMRKPLQPFGLDSVINPDDETREHSVPFRVFDYKNNFDYEYESLAFNGLSIAQLDRELQRRKSHDRVFAGFLLHEIGQSALVKFYVCKHNVSDCDHYAGEFYILGDEAEMPWRYDRVYKYEITQQLHDLDLHVGDNFFLKYEAFDLNGGSLGGSIFSQPSVIFEPAAGSHQADEYREAVTSASHIRKNIRDLSEGEIESIRSAFLQIQKEGIYENIAKFHGKPGLCEHDGHPVACCVHGMPTFPHWHRLYVLQVENALLERGSAVAVPYWDWTEKADSLPSLINDATYFNSRSQTFDPNPFFRGHIAFENAVTSRDPQPELWDNKDFYENVMLALEQDNFCDFEIQLELIHNALHSRLGGRAKYSLSSLDYTAFDPVFFLHHANVDRIWAIWQDLQRYRKKPYNEADCAVNEMRKPLQPFNNPELNSDSMTLKHNLPQDSFDYQNRFRYQYDNLQFNHFSIQKLDQTIQARKQHDRVFAGFILHNIGTSAVVDIYICVEQGGEQNCKTKAGSFTILGGETEMPFHFDRLYKFDITSALHKLGVPLDGHGFDIKVDVRAVNGSHLDQHILNEPSLLFVPGERKNIYYDGLSQHNLVRKEVSSLTTLEKHFLRKALKNMQADDSPDGYQAIASFHALPPLCPSPSAAHRHACCLHGMATFPQWHRLYTVQFEDSLKRHGSIVGLPYWDWLKPQSALPDLVTQETYEHLFSHKTFPNPFLKANIEFEGEGVTTERDVDAEHLFAKGNLVYNNWFCNQALYALEQENYCDFEIQFEILHNGIHSWVGGSKTHSIGHLHYASYDPLFYIHHSQTDRIWAIWQALQEHRGLSGKEAHCALEQMKDPLKPFSFGSPYNLNKRTQEFSKPEDTFDYHRFGYEYDSLEFVGMSVSSLHNYIKQQQEADRVFAGFLLKGFGQSASVSFDICRPDQSCQEAGYFSVLGGSSEMPWQFDRLYKYDITKTLKDMKLRYDDTFTIKVHIKDIAGAELDSDLIPTPSVLLEEGKHGINVRHVGRNRIRMELSELTERDLASLKSAMRSLQADDGVNGYQAIASFHGLPASCHDDEGHEIACCIHGMPVFPHWHRLYTLQMDMALLSHGSAVAIPYWDWTKPISKLPDLFTSPEYYDPWRDAVVNNPFAKGYIKSEDAYTVRDPQDILYHLQDETGTSVLLDQTLLALEQTDFCDFEVQFEVVHNAIHYLVGGRQVYALSSQHYASYDPAFFIHHSFVDKIWAVWQALQKKRKRPYHKADCALNMMTKPMRPFAHDFNHNGFTKMHAVPNTLFDFQDLFYTYDNLEIAGMNVNQLEAEINRRKSQTRVFAGFLLHGIGRSADVRFWICKTADDCHASGMIFILGGSKEMHWAYDRNFKYDITQALKAQSIHPEDVFDTDAPFFIKVEVHGVNKTALPSSAIPAPTIIYSAGEGHTDDHGSDHIAGSGVRKDVTSLTASEIENLRHALQSVMDDDGPNGFQAIAAYHGSPPMCHMXDGRDVACCTHGMASFPHWHRLFVKQMEDALAAHGAHIGIPYWDWTSAFSHLPALVTDHEHNPFHHGHIAHRNVDTSRSPRDMLFNDPEHGSESFFYRQVLLALEQTDFCQFEVQFEITHNAIHSWTGGHTPYGMSSLEYTAYDPLFYLHHSNTDRIWAIWQALQKYRGFQYNAAHCDIQVLKQPLKPFSESRNPNPVTRANSRAVDSFDYERLNYQYDTLTFHGHSISELDAMLQERKKEERTFAAFLLHGFGASADVSFDVCTPDGHCAFAGTFAVLGGELEMPWSFERLFRYDITKVLKQMNLHYDSEFHFELKIVGTDGTELPSDRIKSPTIEHHGGDHHGGDTSGHDHSERHDGFFRKEVGSLSLDEANDLKNALYKLQNDQGPNGYESIAGYHGYPFLCPEHGEDQYACCVHGMPVFPHWHRLHTIQFERALKEHGSHLGIPYWDWTKSMIALPAFFADSSNSNPFYKYHIMKAGHDTARSPSDLLFNQPQLHGYDYLYYLALSTLEEDNYCDFEVHYEILHNAVHLWLGGTETYSMSSLAFSAYDPVFMILHSGLDRLWIIWQELQKLRKKPYNAAKCAGHMMDEPLHPFNYESANHDSFTRANAKPSTVFDSHKFNYHYDNPDVRGNSIQEISAIIHDLRNQPRVFAGFVLSGIYTSANVKIYLVREGHDDENVGSFVVLGGPKEMPWAYERIFKYDITEVANRLNMHHDDTFNFRLEVQSYTGEMVTHHLPEPLIIYRPAKQEYDVLVIPLGSGHKLPPKVIVKRGTRIMFHPVDDTVNRPVVDLGSHTALYNCVVPPFTYNGYELDHAYSLRDGHYYIAGPTKDLCTSGNVRIHIHIEDE | NA | NA | NA | NA | NA | NA | Keyhole limpet hemocyanin is an immune modulator, given as a vaccine to help the body respond to cancer. A natural protein isolated from the marine mollusc keyhole limpet. Keyhole limpet hemocyanin is an immunogenic carrier protein that, in vivo, increases antigenic immune responses to haptens and other weak antigens such as idiotype proteins. | Investigated for use/treatment in bladder cancer and solid tumors. | NA | Keyhole Limpet Hemocyanin (KLH) is generally a very efficient coupling agent. It is the most common carrier protein used in the preparation of hapten conjugates. KLH is composed of five subunits. It is lysine rich with a large number of available primary amines to facilitate conjugation, antibody production and promote peptide attachment after dissociation. | NA | NA | NA | NA | NA | Biological Factors | NA | NA | NA | NA | Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12111 | Th1286 | Keyhole limpet hemocyanin | >Th1286_Keyhole_limpet_hemocyanin MWTILALLTATLLFEGAFSVDTVVRKNVDSLSSDEVLALEKALDDLQQDDSNQGYQAIAGYHGVPTMCVDKHEKNVACCLHGMPSFPLWHRLYVVQLERALIRKKATISIPYWDWTSELTHLPELVSHPLFVGTEGGKAHDNSWYRADITFLNKKTSRAVDDRLFEKVQPGHHTRLMEGILDALEQDEFCKFEIQFELAHNAIHYLVGGRHTYSMSHLEYTSYDPLFFLHHSNTDRIFAIWQRLQQLRGKDPNSADCAHNLIHTPMEPFDRDTNPLDLTREHAKPADSFDYGRLGYQYDDLSLNGMSPEELNVYLGERAAKERTFASFILSGFGGSANVVVYVCRPAHDEISDDQCIKAGDFFLLGGPTEMKWGFYRAYHFDVTDSVASIDDDGHGHYYVKSELFSVNGSALSNDILRQPTLVHRPAKGHFDKPPVPVAQANLAVRKNINDLTAEETYSLRKAMERFQNDKSVDGYQATVEFHALPARCPRPDAKDRFACCVHGMATFPHWHRLFVTQVEDALLRRGSTIGLPNWDWTMPMDHLPELATSETYLDPVTGETKNNPFHHAQVAFENGVTSRNPDAKLFMKPTYGDHTYLFDSMIYAFEQEDFCDFEVQYELTHNAIHAWVGGSEKYSMSSLHYTAFDPIFYLHHSNVDRLWAIWQALQIRRGKSYKAHCASSQEREPLKPFAFSSPLNNNEKTYHNSVPTNVYDYVGVLHYRYDDLQFGGMTMSELEEYIHKQTQHDRTFAGFFLSYIGTSASVDIFINREGHDKYKVGSFVVLGGSKEMKWGFDRMYKYEITEALKTLNVAVDDGFSITVEITDVDGSPPSADLIPPPAIIFERADAKDFGHSRKIRKAVDSLTVEEQTSLRRAMADLQDDKTSGGFQQIAAFHGEPKWCPSPEAEKKFACCVHGMAVFPHWHRLLTVQGENALRKHGFTGGLPYWDWTRSMSALPHFVADPTYNDAISSQEEDNPWHHGHIDSVGHDTTRDVRDDLYQSPGFGHYTDIAKQVLLAFEQDDFCDFEVQFEIAHNFIHALVGGNEPYSMSSLRYTTYDPIFFLHRSNTDRLWAIWQALQKYRGKPYNTANCAIASMRKPLQPFGLDSVINPDDETREHSVPFRVFDYKNNFDYEYESLAFNGLSIAQLDRELQRRKSHDRVFAGFLLHEIGQSALVKFYVCKHNVSDCDHYAGEFYILGDEAEMPWRYDRVYKYEITQQLHDLDLHVGDNFFLKYEAFDLNGGSLGGSIFSQPSVIFEPAAGSHQADEYREAVTSASHIRKNIRDLSEGEIESIRSAFLQIQKEGIYENIAKFHGKPGLCEHDGHPVACCVHGMPTFPHWHRLYVLQVENALLERGSAVAVPYWDWTEKADSLPSLINDATYFNSRSQTFDPNPFFRGHIAFENAVTSRDPQPELWDNKDFYENVMLALEQDNFCDFEIQLELIHNALHSRLGGRAKYSLSSLDYTAFDPVFFLHHANVDRIWAIWQDLQRYRKKPYNEADCAVNEMRKPLQPFNNPELNSDSMTLKHNLPQDSFDYQNRFRYQYDNLQFNHFSIQKLDQTIQARKQHDRVFAGFILHNIGTSAVVDIYICVEQGGEQNCKTKAGSFTILGGETEMPFHFDRLYKFDITSALHKLGVPLDGHGFDIKVDVRAVNGSHLDQHILNEPSLLFVPGERKNIYYDGLSQHNLVRKEVSSLTTLEKHFLRKALKNMQADDSPDGYQAIASFHALPPLCPSPSAAHRHACCLHGMATFPQWHRLYTVQFEDSLKRHGSIVGLPYWDWLKPQSALPDLVTQETYEHLFSHKTFPNPFLKANIEFEGEGVTTERDVDAEHLFAKGNLVYNNWFCNQALYALEQENYCDFEIQFEILHNGIHSWVGGSKTHSIGHLHYASYDPLFYIHHSQTDRIWAIWQALQEHRGLSGKEAHCALEQMKDPLKPFSFGSPYNLNKRTQEFSKPEDTFDYHRFGYEYDSLEFVGMSVSSLHNYIKQQQEADRVFAGFLLKGFGQSASVSFDICRPDQSCQEAGYFSVLGGSSEMPWQFDRLYKYDITKTLKDMKLRYDDTFTIKVHIKDIAGAELDSDLIPTPSVLLEEGKHGINVRHVGRNRIRMELSELTERDLASLKSAMRSLQADDGVNGYQAIASFHGLPASCHDDEGHEIACCIHGMPVFPHWHRLYTLQMDMALLSHGSAVAIPYWDWTKPISKLPDLFTSPEYYDPWRDAVVNNPFAKGYIKSEDAYTVRDPQDILYHLQDETGTSVLLDQTLLALEQTDFCDFEVQFEVVHNAIHYLVGGRQVYALSSQHYASYDPAFFIHHSFVDKIWAVWQALQKKRKRPYHKADCALNMMTKPMRPFAHDFNHNGFTKMHAVPNTLFDFQDLFYTYDNLEIAGMNVNQLEAEINRRKSQTRVFAGFLLHGIGRSADVRFWICKTADDCHASGMIFILGGSKEMHWAYDRNFKYDITQALKAQSIHPEDVFDTDAPFFIKVEVHGVNKTALPSSAIPAPTIIYSAGEGHTDDHGSDHIAGSGVRKDVTSLTASEIENLRHALQSVMDDDGPNGFQAIAAYHGSPPMCHMXDGRDVACCTHGMASFPHWHRLFVKQMEDALAAHGAHIGIPYWDWTSAFSHLPALVTDHEHNPFHHGHIAHRNVDTSRSPRDMLFNDPEHGSESFFYRQVLLALEQTDFCQFEVQFEITHNAIHSWTGGHTPYGMSSLEYTAYDPLFYLHHSNTDRIWAIWQALQKYRGFQYNAAHCDIQVLKQPLKPFSESRNPNPVTRANSRAVDSFDYERLNYQYDTLTFHGHSISELDAMLQERKKEERTFAAFLLHGFGASADVSFDVCTPDGHCAFAGTFAVLGGELEMPWSFERLFRYDITKVLKQMNLHYDSEFHFELKIVGTDGTELPSDRIKSPTIEHHGGDHHGGDTSGHDHSERHDGFFRKEVGSLSLDEANDLKNALYKLQNDQGPNGYESIAGYHGYPFLCPEHGEDQYACCVHGMPVFPHWHRLHTIQFERALKEHGSHLGIPYWDWTKSMIALPAFFADSSNSNPFYKYHIMKAGHDTARSPSDLLFNQPQLHGYDYLYYLALSTLEEDNYCDFEVHYEILHNAVHLWLGGTETYSMSSLAFSAYDPVFMILHSGLDRLWIIWQELQKLRKKPYNAAKCAGHMMDEPLHPFNYESANHDSFTRANAKPSTVFDSHKFNYHYDNPDVRGNSIQEISAIIHDLRNQPRVFAGFVLSGIYTSANVKIYLVREGHDDENVGSFVVLGGPKEMPWAYERIFKYDITEVANRLNMHHDDTFNFRLEVQSYTGEMVTHHLPEPLIIYRPAKQEYDVLVIPLGSGHKLPPKVIVKRGTRIMFHPVDDTVNRPVVDLGSHTALYNCVVPPFTYNGYELDHAYSLRDGHYYIAGPTKDLCTSGNVRIHIHIEDE | NA | NA | NA | NA | NA | NA | Keyhole limpet hemocyanin is an immune modulator, given as a vaccine to help the body respond to cancer. A natural protein isolated from the marine mollusc keyhole limpet. Keyhole limpet hemocyanin is an immunogenic carrier protein that, in vivo, increases antigenic immune responses to haptens and other weak antigens such as idiotype proteins. | Investigated for use/treatment in bladder cancer and solid tumors. | NA | Keyhole Limpet Hemocyanin (KLH) is generally a very efficient coupling agent. It is the most common carrier protein used in the preparation of hapten conjugates. KLH is composed of five subunits. It is lysine rich with a large number of available primary amines to facilitate conjugation, antibody production and promote peptide attachment after dissociation. | NA | NA | NA | NA | NA | Haptens | NA | NA | NA | NA | Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12112 | Th1286 | Keyhole limpet hemocyanin | >Th1286_Keyhole_limpet_hemocyanin MWTILALLTATLLFEGAFSVDTVVRKNVDSLSSDEVLALEKALDDLQQDDSNQGYQAIAGYHGVPTMCVDKHEKNVACCLHGMPSFPLWHRLYVVQLERALIRKKATISIPYWDWTSELTHLPELVSHPLFVGTEGGKAHDNSWYRADITFLNKKTSRAVDDRLFEKVQPGHHTRLMEGILDALEQDEFCKFEIQFELAHNAIHYLVGGRHTYSMSHLEYTSYDPLFFLHHSNTDRIFAIWQRLQQLRGKDPNSADCAHNLIHTPMEPFDRDTNPLDLTREHAKPADSFDYGRLGYQYDDLSLNGMSPEELNVYLGERAAKERTFASFILSGFGGSANVVVYVCRPAHDEISDDQCIKAGDFFLLGGPTEMKWGFYRAYHFDVTDSVASIDDDGHGHYYVKSELFSVNGSALSNDILRQPTLVHRPAKGHFDKPPVPVAQANLAVRKNINDLTAEETYSLRKAMERFQNDKSVDGYQATVEFHALPARCPRPDAKDRFACCVHGMATFPHWHRLFVTQVEDALLRRGSTIGLPNWDWTMPMDHLPELATSETYLDPVTGETKNNPFHHAQVAFENGVTSRNPDAKLFMKPTYGDHTYLFDSMIYAFEQEDFCDFEVQYELTHNAIHAWVGGSEKYSMSSLHYTAFDPIFYLHHSNVDRLWAIWQALQIRRGKSYKAHCASSQEREPLKPFAFSSPLNNNEKTYHNSVPTNVYDYVGVLHYRYDDLQFGGMTMSELEEYIHKQTQHDRTFAGFFLSYIGTSASVDIFINREGHDKYKVGSFVVLGGSKEMKWGFDRMYKYEITEALKTLNVAVDDGFSITVEITDVDGSPPSADLIPPPAIIFERADAKDFGHSRKIRKAVDSLTVEEQTSLRRAMADLQDDKTSGGFQQIAAFHGEPKWCPSPEAEKKFACCVHGMAVFPHWHRLLTVQGENALRKHGFTGGLPYWDWTRSMSALPHFVADPTYNDAISSQEEDNPWHHGHIDSVGHDTTRDVRDDLYQSPGFGHYTDIAKQVLLAFEQDDFCDFEVQFEIAHNFIHALVGGNEPYSMSSLRYTTYDPIFFLHRSNTDRLWAIWQALQKYRGKPYNTANCAIASMRKPLQPFGLDSVINPDDETREHSVPFRVFDYKNNFDYEYESLAFNGLSIAQLDRELQRRKSHDRVFAGFLLHEIGQSALVKFYVCKHNVSDCDHYAGEFYILGDEAEMPWRYDRVYKYEITQQLHDLDLHVGDNFFLKYEAFDLNGGSLGGSIFSQPSVIFEPAAGSHQADEYREAVTSASHIRKNIRDLSEGEIESIRSAFLQIQKEGIYENIAKFHGKPGLCEHDGHPVACCVHGMPTFPHWHRLYVLQVENALLERGSAVAVPYWDWTEKADSLPSLINDATYFNSRSQTFDPNPFFRGHIAFENAVTSRDPQPELWDNKDFYENVMLALEQDNFCDFEIQLELIHNALHSRLGGRAKYSLSSLDYTAFDPVFFLHHANVDRIWAIWQDLQRYRKKPYNEADCAVNEMRKPLQPFNNPELNSDSMTLKHNLPQDSFDYQNRFRYQYDNLQFNHFSIQKLDQTIQARKQHDRVFAGFILHNIGTSAVVDIYICVEQGGEQNCKTKAGSFTILGGETEMPFHFDRLYKFDITSALHKLGVPLDGHGFDIKVDVRAVNGSHLDQHILNEPSLLFVPGERKNIYYDGLSQHNLVRKEVSSLTTLEKHFLRKALKNMQADDSPDGYQAIASFHALPPLCPSPSAAHRHACCLHGMATFPQWHRLYTVQFEDSLKRHGSIVGLPYWDWLKPQSALPDLVTQETYEHLFSHKTFPNPFLKANIEFEGEGVTTERDVDAEHLFAKGNLVYNNWFCNQALYALEQENYCDFEIQFEILHNGIHSWVGGSKTHSIGHLHYASYDPLFYIHHSQTDRIWAIWQALQEHRGLSGKEAHCALEQMKDPLKPFSFGSPYNLNKRTQEFSKPEDTFDYHRFGYEYDSLEFVGMSVSSLHNYIKQQQEADRVFAGFLLKGFGQSASVSFDICRPDQSCQEAGYFSVLGGSSEMPWQFDRLYKYDITKTLKDMKLRYDDTFTIKVHIKDIAGAELDSDLIPTPSVLLEEGKHGINVRHVGRNRIRMELSELTERDLASLKSAMRSLQADDGVNGYQAIASFHGLPASCHDDEGHEIACCIHGMPVFPHWHRLYTLQMDMALLSHGSAVAIPYWDWTKPISKLPDLFTSPEYYDPWRDAVVNNPFAKGYIKSEDAYTVRDPQDILYHLQDETGTSVLLDQTLLALEQTDFCDFEVQFEVVHNAIHYLVGGRQVYALSSQHYASYDPAFFIHHSFVDKIWAVWQALQKKRKRPYHKADCALNMMTKPMRPFAHDFNHNGFTKMHAVPNTLFDFQDLFYTYDNLEIAGMNVNQLEAEINRRKSQTRVFAGFLLHGIGRSADVRFWICKTADDCHASGMIFILGGSKEMHWAYDRNFKYDITQALKAQSIHPEDVFDTDAPFFIKVEVHGVNKTALPSSAIPAPTIIYSAGEGHTDDHGSDHIAGSGVRKDVTSLTASEIENLRHALQSVMDDDGPNGFQAIAAYHGSPPMCHMXDGRDVACCTHGMASFPHWHRLFVKQMEDALAAHGAHIGIPYWDWTSAFSHLPALVTDHEHNPFHHGHIAHRNVDTSRSPRDMLFNDPEHGSESFFYRQVLLALEQTDFCQFEVQFEITHNAIHSWTGGHTPYGMSSLEYTAYDPLFYLHHSNTDRIWAIWQALQKYRGFQYNAAHCDIQVLKQPLKPFSESRNPNPVTRANSRAVDSFDYERLNYQYDTLTFHGHSISELDAMLQERKKEERTFAAFLLHGFGASADVSFDVCTPDGHCAFAGTFAVLGGELEMPWSFERLFRYDITKVLKQMNLHYDSEFHFELKIVGTDGTELPSDRIKSPTIEHHGGDHHGGDTSGHDHSERHDGFFRKEVGSLSLDEANDLKNALYKLQNDQGPNGYESIAGYHGYPFLCPEHGEDQYACCVHGMPVFPHWHRLHTIQFERALKEHGSHLGIPYWDWTKSMIALPAFFADSSNSNPFYKYHIMKAGHDTARSPSDLLFNQPQLHGYDYLYYLALSTLEEDNYCDFEVHYEILHNAVHLWLGGTETYSMSSLAFSAYDPVFMILHSGLDRLWIIWQELQKLRKKPYNAAKCAGHMMDEPLHPFNYESANHDSFTRANAKPSTVFDSHKFNYHYDNPDVRGNSIQEISAIIHDLRNQPRVFAGFVLSGIYTSANVKIYLVREGHDDENVGSFVVLGGPKEMPWAYERIFKYDITEVANRLNMHHDDTFNFRLEVQSYTGEMVTHHLPEPLIIYRPAKQEYDVLVIPLGSGHKLPPKVIVKRGTRIMFHPVDDTVNRPVVDLGSHTALYNCVVPPFTYNGYELDHAYSLRDGHYYIAGPTKDLCTSGNVRIHIHIEDE | NA | NA | NA | NA | NA | NA | Keyhole limpet hemocyanin is an immune modulator, given as a vaccine to help the body respond to cancer. A natural protein isolated from the marine mollusc keyhole limpet. Keyhole limpet hemocyanin is an immunogenic carrier protein that, in vivo, increases antigenic immune responses to haptens and other weak antigens such as idiotype proteins. | Investigated for use/treatment in bladder cancer and solid tumors. | NA | Keyhole Limpet Hemocyanin (KLH) is generally a very efficient coupling agent. It is the most common carrier protein used in the preparation of hapten conjugates. KLH is composed of five subunits. It is lysine rich with a large number of available primary amines to facilitate conjugation, antibody production and promote peptide attachment after dissociation. | NA | NA | NA | NA | NA | Immunologic Factors | NA | NA | NA | NA | Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12113 | Th1286 | Keyhole limpet hemocyanin | >Th1286_Keyhole_limpet_hemocyanin MWTILALLTATLLFEGAFSVDTVVRKNVDSLSSDEVLALEKALDDLQQDDSNQGYQAIAGYHGVPTMCVDKHEKNVACCLHGMPSFPLWHRLYVVQLERALIRKKATISIPYWDWTSELTHLPELVSHPLFVGTEGGKAHDNSWYRADITFLNKKTSRAVDDRLFEKVQPGHHTRLMEGILDALEQDEFCKFEIQFELAHNAIHYLVGGRHTYSMSHLEYTSYDPLFFLHHSNTDRIFAIWQRLQQLRGKDPNSADCAHNLIHTPMEPFDRDTNPLDLTREHAKPADSFDYGRLGYQYDDLSLNGMSPEELNVYLGERAAKERTFASFILSGFGGSANVVVYVCRPAHDEISDDQCIKAGDFFLLGGPTEMKWGFYRAYHFDVTDSVASIDDDGHGHYYVKSELFSVNGSALSNDILRQPTLVHRPAKGHFDKPPVPVAQANLAVRKNINDLTAEETYSLRKAMERFQNDKSVDGYQATVEFHALPARCPRPDAKDRFACCVHGMATFPHWHRLFVTQVEDALLRRGSTIGLPNWDWTMPMDHLPELATSETYLDPVTGETKNNPFHHAQVAFENGVTSRNPDAKLFMKPTYGDHTYLFDSMIYAFEQEDFCDFEVQYELTHNAIHAWVGGSEKYSMSSLHYTAFDPIFYLHHSNVDRLWAIWQALQIRRGKSYKAHCASSQEREPLKPFAFSSPLNNNEKTYHNSVPTNVYDYVGVLHYRYDDLQFGGMTMSELEEYIHKQTQHDRTFAGFFLSYIGTSASVDIFINREGHDKYKVGSFVVLGGSKEMKWGFDRMYKYEITEALKTLNVAVDDGFSITVEITDVDGSPPSADLIPPPAIIFERADAKDFGHSRKIRKAVDSLTVEEQTSLRRAMADLQDDKTSGGFQQIAAFHGEPKWCPSPEAEKKFACCVHGMAVFPHWHRLLTVQGENALRKHGFTGGLPYWDWTRSMSALPHFVADPTYNDAISSQEEDNPWHHGHIDSVGHDTTRDVRDDLYQSPGFGHYTDIAKQVLLAFEQDDFCDFEVQFEIAHNFIHALVGGNEPYSMSSLRYTTYDPIFFLHRSNTDRLWAIWQALQKYRGKPYNTANCAIASMRKPLQPFGLDSVINPDDETREHSVPFRVFDYKNNFDYEYESLAFNGLSIAQLDRELQRRKSHDRVFAGFLLHEIGQSALVKFYVCKHNVSDCDHYAGEFYILGDEAEMPWRYDRVYKYEITQQLHDLDLHVGDNFFLKYEAFDLNGGSLGGSIFSQPSVIFEPAAGSHQADEYREAVTSASHIRKNIRDLSEGEIESIRSAFLQIQKEGIYENIAKFHGKPGLCEHDGHPVACCVHGMPTFPHWHRLYVLQVENALLERGSAVAVPYWDWTEKADSLPSLINDATYFNSRSQTFDPNPFFRGHIAFENAVTSRDPQPELWDNKDFYENVMLALEQDNFCDFEIQLELIHNALHSRLGGRAKYSLSSLDYTAFDPVFFLHHANVDRIWAIWQDLQRYRKKPYNEADCAVNEMRKPLQPFNNPELNSDSMTLKHNLPQDSFDYQNRFRYQYDNLQFNHFSIQKLDQTIQARKQHDRVFAGFILHNIGTSAVVDIYICVEQGGEQNCKTKAGSFTILGGETEMPFHFDRLYKFDITSALHKLGVPLDGHGFDIKVDVRAVNGSHLDQHILNEPSLLFVPGERKNIYYDGLSQHNLVRKEVSSLTTLEKHFLRKALKNMQADDSPDGYQAIASFHALPPLCPSPSAAHRHACCLHGMATFPQWHRLYTVQFEDSLKRHGSIVGLPYWDWLKPQSALPDLVTQETYEHLFSHKTFPNPFLKANIEFEGEGVTTERDVDAEHLFAKGNLVYNNWFCNQALYALEQENYCDFEIQFEILHNGIHSWVGGSKTHSIGHLHYASYDPLFYIHHSQTDRIWAIWQALQEHRGLSGKEAHCALEQMKDPLKPFSFGSPYNLNKRTQEFSKPEDTFDYHRFGYEYDSLEFVGMSVSSLHNYIKQQQEADRVFAGFLLKGFGQSASVSFDICRPDQSCQEAGYFSVLGGSSEMPWQFDRLYKYDITKTLKDMKLRYDDTFTIKVHIKDIAGAELDSDLIPTPSVLLEEGKHGINVRHVGRNRIRMELSELTERDLASLKSAMRSLQADDGVNGYQAIASFHGLPASCHDDEGHEIACCIHGMPVFPHWHRLYTLQMDMALLSHGSAVAIPYWDWTKPISKLPDLFTSPEYYDPWRDAVVNNPFAKGYIKSEDAYTVRDPQDILYHLQDETGTSVLLDQTLLALEQTDFCDFEVQFEVVHNAIHYLVGGRQVYALSSQHYASYDPAFFIHHSFVDKIWAVWQALQKKRKRPYHKADCALNMMTKPMRPFAHDFNHNGFTKMHAVPNTLFDFQDLFYTYDNLEIAGMNVNQLEAEINRRKSQTRVFAGFLLHGIGRSADVRFWICKTADDCHASGMIFILGGSKEMHWAYDRNFKYDITQALKAQSIHPEDVFDTDAPFFIKVEVHGVNKTALPSSAIPAPTIIYSAGEGHTDDHGSDHIAGSGVRKDVTSLTASEIENLRHALQSVMDDDGPNGFQAIAAYHGSPPMCHMXDGRDVACCTHGMASFPHWHRLFVKQMEDALAAHGAHIGIPYWDWTSAFSHLPALVTDHEHNPFHHGHIAHRNVDTSRSPRDMLFNDPEHGSESFFYRQVLLALEQTDFCQFEVQFEITHNAIHSWTGGHTPYGMSSLEYTAYDPLFYLHHSNTDRIWAIWQALQKYRGFQYNAAHCDIQVLKQPLKPFSESRNPNPVTRANSRAVDSFDYERLNYQYDTLTFHGHSISELDAMLQERKKEERTFAAFLLHGFGASADVSFDVCTPDGHCAFAGTFAVLGGELEMPWSFERLFRYDITKVLKQMNLHYDSEFHFELKIVGTDGTELPSDRIKSPTIEHHGGDHHGGDTSGHDHSERHDGFFRKEVGSLSLDEANDLKNALYKLQNDQGPNGYESIAGYHGYPFLCPEHGEDQYACCVHGMPVFPHWHRLHTIQFERALKEHGSHLGIPYWDWTKSMIALPAFFADSSNSNPFYKYHIMKAGHDTARSPSDLLFNQPQLHGYDYLYYLALSTLEEDNYCDFEVHYEILHNAVHLWLGGTETYSMSSLAFSAYDPVFMILHSGLDRLWIIWQELQKLRKKPYNAAKCAGHMMDEPLHPFNYESANHDSFTRANAKPSTVFDSHKFNYHYDNPDVRGNSIQEISAIIHDLRNQPRVFAGFVLSGIYTSANVKIYLVREGHDDENVGSFVVLGGPKEMPWAYERIFKYDITEVANRLNMHHDDTFNFRLEVQSYTGEMVTHHLPEPLIIYRPAKQEYDVLVIPLGSGHKLPPKVIVKRGTRIMFHPVDDTVNRPVVDLGSHTALYNCVVPPFTYNGYELDHAYSLRDGHYYIAGPTKDLCTSGNVRIHIHIEDE | NA | NA | NA | NA | NA | NA | Keyhole limpet hemocyanin is an immune modulator, given as a vaccine to help the body respond to cancer. A natural protein isolated from the marine mollusc keyhole limpet. Keyhole limpet hemocyanin is an immunogenic carrier protein that, in vivo, increases antigenic immune responses to haptens and other weak antigens such as idiotype proteins. | Investigated for use/treatment in bladder cancer and solid tumors. | NA | Keyhole Limpet Hemocyanin (KLH) is generally a very efficient coupling agent. It is the most common carrier protein used in the preparation of hapten conjugates. KLH is composed of five subunits. It is lysine rich with a large number of available primary amines to facilitate conjugation, antibody production and promote peptide attachment after dissociation. | NA | NA | NA | NA | NA | Metalloproteins | NA | NA | NA | NA | Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12114 | Th1286 | Keyhole limpet hemocyanin | >Th1286_Keyhole_limpet_hemocyanin MWTILALLTATLLFEGAFSVDTVVRKNVDSLSSDEVLALEKALDDLQQDDSNQGYQAIAGYHGVPTMCVDKHEKNVACCLHGMPSFPLWHRLYVVQLERALIRKKATISIPYWDWTSELTHLPELVSHPLFVGTEGGKAHDNSWYRADITFLNKKTSRAVDDRLFEKVQPGHHTRLMEGILDALEQDEFCKFEIQFELAHNAIHYLVGGRHTYSMSHLEYTSYDPLFFLHHSNTDRIFAIWQRLQQLRGKDPNSADCAHNLIHTPMEPFDRDTNPLDLTREHAKPADSFDYGRLGYQYDDLSLNGMSPEELNVYLGERAAKERTFASFILSGFGGSANVVVYVCRPAHDEISDDQCIKAGDFFLLGGPTEMKWGFYRAYHFDVTDSVASIDDDGHGHYYVKSELFSVNGSALSNDILRQPTLVHRPAKGHFDKPPVPVAQANLAVRKNINDLTAEETYSLRKAMERFQNDKSVDGYQATVEFHALPARCPRPDAKDRFACCVHGMATFPHWHRLFVTQVEDALLRRGSTIGLPNWDWTMPMDHLPELATSETYLDPVTGETKNNPFHHAQVAFENGVTSRNPDAKLFMKPTYGDHTYLFDSMIYAFEQEDFCDFEVQYELTHNAIHAWVGGSEKYSMSSLHYTAFDPIFYLHHSNVDRLWAIWQALQIRRGKSYKAHCASSQEREPLKPFAFSSPLNNNEKTYHNSVPTNVYDYVGVLHYRYDDLQFGGMTMSELEEYIHKQTQHDRTFAGFFLSYIGTSASVDIFINREGHDKYKVGSFVVLGGSKEMKWGFDRMYKYEITEALKTLNVAVDDGFSITVEITDVDGSPPSADLIPPPAIIFERADAKDFGHSRKIRKAVDSLTVEEQTSLRRAMADLQDDKTSGGFQQIAAFHGEPKWCPSPEAEKKFACCVHGMAVFPHWHRLLTVQGENALRKHGFTGGLPYWDWTRSMSALPHFVADPTYNDAISSQEEDNPWHHGHIDSVGHDTTRDVRDDLYQSPGFGHYTDIAKQVLLAFEQDDFCDFEVQFEIAHNFIHALVGGNEPYSMSSLRYTTYDPIFFLHRSNTDRLWAIWQALQKYRGKPYNTANCAIASMRKPLQPFGLDSVINPDDETREHSVPFRVFDYKNNFDYEYESLAFNGLSIAQLDRELQRRKSHDRVFAGFLLHEIGQSALVKFYVCKHNVSDCDHYAGEFYILGDEAEMPWRYDRVYKYEITQQLHDLDLHVGDNFFLKYEAFDLNGGSLGGSIFSQPSVIFEPAAGSHQADEYREAVTSASHIRKNIRDLSEGEIESIRSAFLQIQKEGIYENIAKFHGKPGLCEHDGHPVACCVHGMPTFPHWHRLYVLQVENALLERGSAVAVPYWDWTEKADSLPSLINDATYFNSRSQTFDPNPFFRGHIAFENAVTSRDPQPELWDNKDFYENVMLALEQDNFCDFEIQLELIHNALHSRLGGRAKYSLSSLDYTAFDPVFFLHHANVDRIWAIWQDLQRYRKKPYNEADCAVNEMRKPLQPFNNPELNSDSMTLKHNLPQDSFDYQNRFRYQYDNLQFNHFSIQKLDQTIQARKQHDRVFAGFILHNIGTSAVVDIYICVEQGGEQNCKTKAGSFTILGGETEMPFHFDRLYKFDITSALHKLGVPLDGHGFDIKVDVRAVNGSHLDQHILNEPSLLFVPGERKNIYYDGLSQHNLVRKEVSSLTTLEKHFLRKALKNMQADDSPDGYQAIASFHALPPLCPSPSAAHRHACCLHGMATFPQWHRLYTVQFEDSLKRHGSIVGLPYWDWLKPQSALPDLVTQETYEHLFSHKTFPNPFLKANIEFEGEGVTTERDVDAEHLFAKGNLVYNNWFCNQALYALEQENYCDFEIQFEILHNGIHSWVGGSKTHSIGHLHYASYDPLFYIHHSQTDRIWAIWQALQEHRGLSGKEAHCALEQMKDPLKPFSFGSPYNLNKRTQEFSKPEDTFDYHRFGYEYDSLEFVGMSVSSLHNYIKQQQEADRVFAGFLLKGFGQSASVSFDICRPDQSCQEAGYFSVLGGSSEMPWQFDRLYKYDITKTLKDMKLRYDDTFTIKVHIKDIAGAELDSDLIPTPSVLLEEGKHGINVRHVGRNRIRMELSELTERDLASLKSAMRSLQADDGVNGYQAIASFHGLPASCHDDEGHEIACCIHGMPVFPHWHRLYTLQMDMALLSHGSAVAIPYWDWTKPISKLPDLFTSPEYYDPWRDAVVNNPFAKGYIKSEDAYTVRDPQDILYHLQDETGTSVLLDQTLLALEQTDFCDFEVQFEVVHNAIHYLVGGRQVYALSSQHYASYDPAFFIHHSFVDKIWAVWQALQKKRKRPYHKADCALNMMTKPMRPFAHDFNHNGFTKMHAVPNTLFDFQDLFYTYDNLEIAGMNVNQLEAEINRRKSQTRVFAGFLLHGIGRSADVRFWICKTADDCHASGMIFILGGSKEMHWAYDRNFKYDITQALKAQSIHPEDVFDTDAPFFIKVEVHGVNKTALPSSAIPAPTIIYSAGEGHTDDHGSDHIAGSGVRKDVTSLTASEIENLRHALQSVMDDDGPNGFQAIAAYHGSPPMCHMXDGRDVACCTHGMASFPHWHRLFVKQMEDALAAHGAHIGIPYWDWTSAFSHLPALVTDHEHNPFHHGHIAHRNVDTSRSPRDMLFNDPEHGSESFFYRQVLLALEQTDFCQFEVQFEITHNAIHSWTGGHTPYGMSSLEYTAYDPLFYLHHSNTDRIWAIWQALQKYRGFQYNAAHCDIQVLKQPLKPFSESRNPNPVTRANSRAVDSFDYERLNYQYDTLTFHGHSISELDAMLQERKKEERTFAAFLLHGFGASADVSFDVCTPDGHCAFAGTFAVLGGELEMPWSFERLFRYDITKVLKQMNLHYDSEFHFELKIVGTDGTELPSDRIKSPTIEHHGGDHHGGDTSGHDHSERHDGFFRKEVGSLSLDEANDLKNALYKLQNDQGPNGYESIAGYHGYPFLCPEHGEDQYACCVHGMPVFPHWHRLHTIQFERALKEHGSHLGIPYWDWTKSMIALPAFFADSSNSNPFYKYHIMKAGHDTARSPSDLLFNQPQLHGYDYLYYLALSTLEEDNYCDFEVHYEILHNAVHLWLGGTETYSMSSLAFSAYDPVFMILHSGLDRLWIIWQELQKLRKKPYNAAKCAGHMMDEPLHPFNYESANHDSFTRANAKPSTVFDSHKFNYHYDNPDVRGNSIQEISAIIHDLRNQPRVFAGFVLSGIYTSANVKIYLVREGHDDENVGSFVVLGGPKEMPWAYERIFKYDITEVANRLNMHHDDTFNFRLEVQSYTGEMVTHHLPEPLIIYRPAKQEYDVLVIPLGSGHKLPPKVIVKRGTRIMFHPVDDTVNRPVVDLGSHTALYNCVVPPFTYNGYELDHAYSLRDGHYYIAGPTKDLCTSGNVRIHIHIEDE | NA | NA | NA | NA | NA | NA | Keyhole limpet hemocyanin is an immune modulator, given as a vaccine to help the body respond to cancer. A natural protein isolated from the marine mollusc keyhole limpet. Keyhole limpet hemocyanin is an immunogenic carrier protein that, in vivo, increases antigenic immune responses to haptens and other weak antigens such as idiotype proteins. | Investigated for use/treatment in bladder cancer and solid tumors. | NA | Keyhole Limpet Hemocyanin (KLH) is generally a very efficient coupling agent. It is the most common carrier protein used in the preparation of hapten conjugates. KLH is composed of five subunits. It is lysine rich with a large number of available primary amines to facilitate conjugation, antibody production and promote peptide attachment after dissociation. | NA | NA | NA | NA | NA | Mollusca | NA | NA | NA | NA | Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12115 | Th1286 | Keyhole limpet hemocyanin | >Th1286_Keyhole_limpet_hemocyanin MWTILALLTATLLFEGAFSVDTVVRKNVDSLSSDEVLALEKALDDLQQDDSNQGYQAIAGYHGVPTMCVDKHEKNVACCLHGMPSFPLWHRLYVVQLERALIRKKATISIPYWDWTSELTHLPELVSHPLFVGTEGGKAHDNSWYRADITFLNKKTSRAVDDRLFEKVQPGHHTRLMEGILDALEQDEFCKFEIQFELAHNAIHYLVGGRHTYSMSHLEYTSYDPLFFLHHSNTDRIFAIWQRLQQLRGKDPNSADCAHNLIHTPMEPFDRDTNPLDLTREHAKPADSFDYGRLGYQYDDLSLNGMSPEELNVYLGERAAKERTFASFILSGFGGSANVVVYVCRPAHDEISDDQCIKAGDFFLLGGPTEMKWGFYRAYHFDVTDSVASIDDDGHGHYYVKSELFSVNGSALSNDILRQPTLVHRPAKGHFDKPPVPVAQANLAVRKNINDLTAEETYSLRKAMERFQNDKSVDGYQATVEFHALPARCPRPDAKDRFACCVHGMATFPHWHRLFVTQVEDALLRRGSTIGLPNWDWTMPMDHLPELATSETYLDPVTGETKNNPFHHAQVAFENGVTSRNPDAKLFMKPTYGDHTYLFDSMIYAFEQEDFCDFEVQYELTHNAIHAWVGGSEKYSMSSLHYTAFDPIFYLHHSNVDRLWAIWQALQIRRGKSYKAHCASSQEREPLKPFAFSSPLNNNEKTYHNSVPTNVYDYVGVLHYRYDDLQFGGMTMSELEEYIHKQTQHDRTFAGFFLSYIGTSASVDIFINREGHDKYKVGSFVVLGGSKEMKWGFDRMYKYEITEALKTLNVAVDDGFSITVEITDVDGSPPSADLIPPPAIIFERADAKDFGHSRKIRKAVDSLTVEEQTSLRRAMADLQDDKTSGGFQQIAAFHGEPKWCPSPEAEKKFACCVHGMAVFPHWHRLLTVQGENALRKHGFTGGLPYWDWTRSMSALPHFVADPTYNDAISSQEEDNPWHHGHIDSVGHDTTRDVRDDLYQSPGFGHYTDIAKQVLLAFEQDDFCDFEVQFEIAHNFIHALVGGNEPYSMSSLRYTTYDPIFFLHRSNTDRLWAIWQALQKYRGKPYNTANCAIASMRKPLQPFGLDSVINPDDETREHSVPFRVFDYKNNFDYEYESLAFNGLSIAQLDRELQRRKSHDRVFAGFLLHEIGQSALVKFYVCKHNVSDCDHYAGEFYILGDEAEMPWRYDRVYKYEITQQLHDLDLHVGDNFFLKYEAFDLNGGSLGGSIFSQPSVIFEPAAGSHQADEYREAVTSASHIRKNIRDLSEGEIESIRSAFLQIQKEGIYENIAKFHGKPGLCEHDGHPVACCVHGMPTFPHWHRLYVLQVENALLERGSAVAVPYWDWTEKADSLPSLINDATYFNSRSQTFDPNPFFRGHIAFENAVTSRDPQPELWDNKDFYENVMLALEQDNFCDFEIQLELIHNALHSRLGGRAKYSLSSLDYTAFDPVFFLHHANVDRIWAIWQDLQRYRKKPYNEADCAVNEMRKPLQPFNNPELNSDSMTLKHNLPQDSFDYQNRFRYQYDNLQFNHFSIQKLDQTIQARKQHDRVFAGFILHNIGTSAVVDIYICVEQGGEQNCKTKAGSFTILGGETEMPFHFDRLYKFDITSALHKLGVPLDGHGFDIKVDVRAVNGSHLDQHILNEPSLLFVPGERKNIYYDGLSQHNLVRKEVSSLTTLEKHFLRKALKNMQADDSPDGYQAIASFHALPPLCPSPSAAHRHACCLHGMATFPQWHRLYTVQFEDSLKRHGSIVGLPYWDWLKPQSALPDLVTQETYEHLFSHKTFPNPFLKANIEFEGEGVTTERDVDAEHLFAKGNLVYNNWFCNQALYALEQENYCDFEIQFEILHNGIHSWVGGSKTHSIGHLHYASYDPLFYIHHSQTDRIWAIWQALQEHRGLSGKEAHCALEQMKDPLKPFSFGSPYNLNKRTQEFSKPEDTFDYHRFGYEYDSLEFVGMSVSSLHNYIKQQQEADRVFAGFLLKGFGQSASVSFDICRPDQSCQEAGYFSVLGGSSEMPWQFDRLYKYDITKTLKDMKLRYDDTFTIKVHIKDIAGAELDSDLIPTPSVLLEEGKHGINVRHVGRNRIRMELSELTERDLASLKSAMRSLQADDGVNGYQAIASFHGLPASCHDDEGHEIACCIHGMPVFPHWHRLYTLQMDMALLSHGSAVAIPYWDWTKPISKLPDLFTSPEYYDPWRDAVVNNPFAKGYIKSEDAYTVRDPQDILYHLQDETGTSVLLDQTLLALEQTDFCDFEVQFEVVHNAIHYLVGGRQVYALSSQHYASYDPAFFIHHSFVDKIWAVWQALQKKRKRPYHKADCALNMMTKPMRPFAHDFNHNGFTKMHAVPNTLFDFQDLFYTYDNLEIAGMNVNQLEAEINRRKSQTRVFAGFLLHGIGRSADVRFWICKTADDCHASGMIFILGGSKEMHWAYDRNFKYDITQALKAQSIHPEDVFDTDAPFFIKVEVHGVNKTALPSSAIPAPTIIYSAGEGHTDDHGSDHIAGSGVRKDVTSLTASEIENLRHALQSVMDDDGPNGFQAIAAYHGSPPMCHMXDGRDVACCTHGMASFPHWHRLFVKQMEDALAAHGAHIGIPYWDWTSAFSHLPALVTDHEHNPFHHGHIAHRNVDTSRSPRDMLFNDPEHGSESFFYRQVLLALEQTDFCQFEVQFEITHNAIHSWTGGHTPYGMSSLEYTAYDPLFYLHHSNTDRIWAIWQALQKYRGFQYNAAHCDIQVLKQPLKPFSESRNPNPVTRANSRAVDSFDYERLNYQYDTLTFHGHSISELDAMLQERKKEERTFAAFLLHGFGASADVSFDVCTPDGHCAFAGTFAVLGGELEMPWSFERLFRYDITKVLKQMNLHYDSEFHFELKIVGTDGTELPSDRIKSPTIEHHGGDHHGGDTSGHDHSERHDGFFRKEVGSLSLDEANDLKNALYKLQNDQGPNGYESIAGYHGYPFLCPEHGEDQYACCVHGMPVFPHWHRLHTIQFERALKEHGSHLGIPYWDWTKSMIALPAFFADSSNSNPFYKYHIMKAGHDTARSPSDLLFNQPQLHGYDYLYYLALSTLEEDNYCDFEVHYEILHNAVHLWLGGTETYSMSSLAFSAYDPVFMILHSGLDRLWIIWQELQKLRKKPYNAAKCAGHMMDEPLHPFNYESANHDSFTRANAKPSTVFDSHKFNYHYDNPDVRGNSIQEISAIIHDLRNQPRVFAGFVLSGIYTSANVKIYLVREGHDDENVGSFVVLGGPKEMPWAYERIFKYDITEVANRLNMHHDDTFNFRLEVQSYTGEMVTHHLPEPLIIYRPAKQEYDVLVIPLGSGHKLPPKVIVKRGTRIMFHPVDDTVNRPVVDLGSHTALYNCVVPPFTYNGYELDHAYSLRDGHYYIAGPTKDLCTSGNVRIHIHIEDE | NA | NA | NA | NA | NA | NA | Keyhole limpet hemocyanin is an immune modulator, given as a vaccine to help the body respond to cancer. A natural protein isolated from the marine mollusc keyhole limpet. Keyhole limpet hemocyanin is an immunogenic carrier protein that, in vivo, increases antigenic immune responses to haptens and other weak antigens such as idiotype proteins. | Investigated for use/treatment in bladder cancer and solid tumors. | NA | Keyhole Limpet Hemocyanin (KLH) is generally a very efficient coupling agent. It is the most common carrier protein used in the preparation of hapten conjugates. KLH is composed of five subunits. It is lysine rich with a large number of available primary amines to facilitate conjugation, antibody production and promote peptide attachment after dissociation. | NA | NA | NA | NA | NA | Pigments, Biological | NA | NA | NA | NA | Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12116 | Th1286 | Keyhole limpet hemocyanin | >Th1286_Keyhole_limpet_hemocyanin MWTILALLTATLLFEGAFSVDTVVRKNVDSLSSDEVLALEKALDDLQQDDSNQGYQAIAGYHGVPTMCVDKHEKNVACCLHGMPSFPLWHRLYVVQLERALIRKKATISIPYWDWTSELTHLPELVSHPLFVGTEGGKAHDNSWYRADITFLNKKTSRAVDDRLFEKVQPGHHTRLMEGILDALEQDEFCKFEIQFELAHNAIHYLVGGRHTYSMSHLEYTSYDPLFFLHHSNTDRIFAIWQRLQQLRGKDPNSADCAHNLIHTPMEPFDRDTNPLDLTREHAKPADSFDYGRLGYQYDDLSLNGMSPEELNVYLGERAAKERTFASFILSGFGGSANVVVYVCRPAHDEISDDQCIKAGDFFLLGGPTEMKWGFYRAYHFDVTDSVASIDDDGHGHYYVKSELFSVNGSALSNDILRQPTLVHRPAKGHFDKPPVPVAQANLAVRKNINDLTAEETYSLRKAMERFQNDKSVDGYQATVEFHALPARCPRPDAKDRFACCVHGMATFPHWHRLFVTQVEDALLRRGSTIGLPNWDWTMPMDHLPELATSETYLDPVTGETKNNPFHHAQVAFENGVTSRNPDAKLFMKPTYGDHTYLFDSMIYAFEQEDFCDFEVQYELTHNAIHAWVGGSEKYSMSSLHYTAFDPIFYLHHSNVDRLWAIWQALQIRRGKSYKAHCASSQEREPLKPFAFSSPLNNNEKTYHNSVPTNVYDYVGVLHYRYDDLQFGGMTMSELEEYIHKQTQHDRTFAGFFLSYIGTSASVDIFINREGHDKYKVGSFVVLGGSKEMKWGFDRMYKYEITEALKTLNVAVDDGFSITVEITDVDGSPPSADLIPPPAIIFERADAKDFGHSRKIRKAVDSLTVEEQTSLRRAMADLQDDKTSGGFQQIAAFHGEPKWCPSPEAEKKFACCVHGMAVFPHWHRLLTVQGENALRKHGFTGGLPYWDWTRSMSALPHFVADPTYNDAISSQEEDNPWHHGHIDSVGHDTTRDVRDDLYQSPGFGHYTDIAKQVLLAFEQDDFCDFEVQFEIAHNFIHALVGGNEPYSMSSLRYTTYDPIFFLHRSNTDRLWAIWQALQKYRGKPYNTANCAIASMRKPLQPFGLDSVINPDDETREHSVPFRVFDYKNNFDYEYESLAFNGLSIAQLDRELQRRKSHDRVFAGFLLHEIGQSALVKFYVCKHNVSDCDHYAGEFYILGDEAEMPWRYDRVYKYEITQQLHDLDLHVGDNFFLKYEAFDLNGGSLGGSIFSQPSVIFEPAAGSHQADEYREAVTSASHIRKNIRDLSEGEIESIRSAFLQIQKEGIYENIAKFHGKPGLCEHDGHPVACCVHGMPTFPHWHRLYVLQVENALLERGSAVAVPYWDWTEKADSLPSLINDATYFNSRSQTFDPNPFFRGHIAFENAVTSRDPQPELWDNKDFYENVMLALEQDNFCDFEIQLELIHNALHSRLGGRAKYSLSSLDYTAFDPVFFLHHANVDRIWAIWQDLQRYRKKPYNEADCAVNEMRKPLQPFNNPELNSDSMTLKHNLPQDSFDYQNRFRYQYDNLQFNHFSIQKLDQTIQARKQHDRVFAGFILHNIGTSAVVDIYICVEQGGEQNCKTKAGSFTILGGETEMPFHFDRLYKFDITSALHKLGVPLDGHGFDIKVDVRAVNGSHLDQHILNEPSLLFVPGERKNIYYDGLSQHNLVRKEVSSLTTLEKHFLRKALKNMQADDSPDGYQAIASFHALPPLCPSPSAAHRHACCLHGMATFPQWHRLYTVQFEDSLKRHGSIVGLPYWDWLKPQSALPDLVTQETYEHLFSHKTFPNPFLKANIEFEGEGVTTERDVDAEHLFAKGNLVYNNWFCNQALYALEQENYCDFEIQFEILHNGIHSWVGGSKTHSIGHLHYASYDPLFYIHHSQTDRIWAIWQALQEHRGLSGKEAHCALEQMKDPLKPFSFGSPYNLNKRTQEFSKPEDTFDYHRFGYEYDSLEFVGMSVSSLHNYIKQQQEADRVFAGFLLKGFGQSASVSFDICRPDQSCQEAGYFSVLGGSSEMPWQFDRLYKYDITKTLKDMKLRYDDTFTIKVHIKDIAGAELDSDLIPTPSVLLEEGKHGINVRHVGRNRIRMELSELTERDLASLKSAMRSLQADDGVNGYQAIASFHGLPASCHDDEGHEIACCIHGMPVFPHWHRLYTLQMDMALLSHGSAVAIPYWDWTKPISKLPDLFTSPEYYDPWRDAVVNNPFAKGYIKSEDAYTVRDPQDILYHLQDETGTSVLLDQTLLALEQTDFCDFEVQFEVVHNAIHYLVGGRQVYALSSQHYASYDPAFFIHHSFVDKIWAVWQALQKKRKRPYHKADCALNMMTKPMRPFAHDFNHNGFTKMHAVPNTLFDFQDLFYTYDNLEIAGMNVNQLEAEINRRKSQTRVFAGFLLHGIGRSADVRFWICKTADDCHASGMIFILGGSKEMHWAYDRNFKYDITQALKAQSIHPEDVFDTDAPFFIKVEVHGVNKTALPSSAIPAPTIIYSAGEGHTDDHGSDHIAGSGVRKDVTSLTASEIENLRHALQSVMDDDGPNGFQAIAAYHGSPPMCHMXDGRDVACCTHGMASFPHWHRLFVKQMEDALAAHGAHIGIPYWDWTSAFSHLPALVTDHEHNPFHHGHIAHRNVDTSRSPRDMLFNDPEHGSESFFYRQVLLALEQTDFCQFEVQFEITHNAIHSWTGGHTPYGMSSLEYTAYDPLFYLHHSNTDRIWAIWQALQKYRGFQYNAAHCDIQVLKQPLKPFSESRNPNPVTRANSRAVDSFDYERLNYQYDTLTFHGHSISELDAMLQERKKEERTFAAFLLHGFGASADVSFDVCTPDGHCAFAGTFAVLGGELEMPWSFERLFRYDITKVLKQMNLHYDSEFHFELKIVGTDGTELPSDRIKSPTIEHHGGDHHGGDTSGHDHSERHDGFFRKEVGSLSLDEANDLKNALYKLQNDQGPNGYESIAGYHGYPFLCPEHGEDQYACCVHGMPVFPHWHRLHTIQFERALKEHGSHLGIPYWDWTKSMIALPAFFADSSNSNPFYKYHIMKAGHDTARSPSDLLFNQPQLHGYDYLYYLALSTLEEDNYCDFEVHYEILHNAVHLWLGGTETYSMSSLAFSAYDPVFMILHSGLDRLWIIWQELQKLRKKPYNAAKCAGHMMDEPLHPFNYESANHDSFTRANAKPSTVFDSHKFNYHYDNPDVRGNSIQEISAIIHDLRNQPRVFAGFVLSGIYTSANVKIYLVREGHDDENVGSFVVLGGPKEMPWAYERIFKYDITEVANRLNMHHDDTFNFRLEVQSYTGEMVTHHLPEPLIIYRPAKQEYDVLVIPLGSGHKLPPKVIVKRGTRIMFHPVDDTVNRPVVDLGSHTALYNCVVPPFTYNGYELDHAYSLRDGHYYIAGPTKDLCTSGNVRIHIHIEDE | NA | NA | NA | NA | NA | NA | Keyhole limpet hemocyanin is an immune modulator, given as a vaccine to help the body respond to cancer. A natural protein isolated from the marine mollusc keyhole limpet. Keyhole limpet hemocyanin is an immunogenic carrier protein that, in vivo, increases antigenic immune responses to haptens and other weak antigens such as idiotype proteins. | Investigated for use/treatment in bladder cancer and solid tumors. | NA | Keyhole Limpet Hemocyanin (KLH) is generally a very efficient coupling agent. It is the most common carrier protein used in the preparation of hapten conjugates. KLH is composed of five subunits. It is lysine rich with a large number of available primary amines to facilitate conjugation, antibody production and promote peptide attachment after dissociation. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12117 | Th1287 | Girentuximab | >Th1287_Girentuximab DVKLVESGGGLVKLGGSLKLSCAASGFTFSNYYMSWVRQTPEKRLELVAAINSDGGITYYLDTVKGRFTISRDNAKNTLYLQMSSLKSEDTALFYCARHRSGYFSMDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Girentuximab is a monoclonal chimeric (mouse/human) antibody directed against carbonic anhydrase IX, an antigen expressed in 95% of clear cell renal cell carcinomas (RCC). | Investigated for use/treatment in gall bladder cancer and renal cell carcinoma. | NA | Mechanism of action of girentuximab is antibody dependent cellular cytotoxicity (ADCC). As a monotherapy in metastatic renal cell carcinomas(RCC), girentuximab demonstrated minimal clinical activity with a 3% partial response rate and a median survival of 16 months. In vitro data suggest that the number of activated ADCC effector cells can be upregulated by low dose interleukin 2 (IL2) administered in a pulsatile fashion. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Carbonic anhydrase 9,Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12118 | Th1287 | Girentuximab | >Th1287_Girentuximab DVKLVESGGGLVKLGGSLKLSCAASGFTFSNYYMSWVRQTPEKRLELVAAINSDGGITYYLDTVKGRFTISRDNAKNTLYLQMSSLKSEDTALFYCARHRSGYFSMDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Girentuximab is a monoclonal chimeric (mouse/human) antibody directed against carbonic anhydrase IX, an antigen expressed in 95% of clear cell renal cell carcinomas (RCC). | Investigated for use/treatment in gall bladder cancer and renal cell carcinoma. | NA | Mechanism of action of girentuximab is antibody dependent cellular cytotoxicity (ADCC). As a monotherapy in metastatic renal cell carcinomas(RCC), girentuximab demonstrated minimal clinical activity with a 3% partial response rate and a median survival of 16 months. In vitro data suggest that the number of activated ADCC effector cells can be upregulated by low dose interleukin 2 (IL2) administered in a pulsatile fashion. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Carbonic anhydrase 9,Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12119 | Th1287 | Girentuximab | >Th1287_Girentuximab DVKLVESGGGLVKLGGSLKLSCAASGFTFSNYYMSWVRQTPEKRLELVAAINSDGGITYYLDTVKGRFTISRDNAKNTLYLQMSSLKSEDTALFYCARHRSGYFSMDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Girentuximab is a monoclonal chimeric (mouse/human) antibody directed against carbonic anhydrase IX, an antigen expressed in 95% of clear cell renal cell carcinomas (RCC). | Investigated for use/treatment in gall bladder cancer and renal cell carcinoma. | NA | Mechanism of action of girentuximab is antibody dependent cellular cytotoxicity (ADCC). As a monotherapy in metastatic renal cell carcinomas(RCC), girentuximab demonstrated minimal clinical activity with a 3% partial response rate and a median survival of 16 months. In vitro data suggest that the number of activated ADCC effector cells can be upregulated by low dose interleukin 2 (IL2) administered in a pulsatile fashion. | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | Carbonic anhydrase 9,Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12120 | Th1287 | Girentuximab | >Th1287_Girentuximab DVKLVESGGGLVKLGGSLKLSCAASGFTFSNYYMSWVRQTPEKRLELVAAINSDGGITYYLDTVKGRFTISRDNAKNTLYLQMSSLKSEDTALFYCARHRSGYFSMDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Girentuximab is a monoclonal chimeric (mouse/human) antibody directed against carbonic anhydrase IX, an antigen expressed in 95% of clear cell renal cell carcinomas (RCC). | Investigated for use/treatment in gall bladder cancer and renal cell carcinoma. | NA | Mechanism of action of girentuximab is antibody dependent cellular cytotoxicity (ADCC). As a monotherapy in metastatic renal cell carcinomas(RCC), girentuximab demonstrated minimal clinical activity with a 3% partial response rate and a median survival of 16 months. In vitro data suggest that the number of activated ADCC effector cells can be upregulated by low dose interleukin 2 (IL2) administered in a pulsatile fashion. | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | Carbonic anhydrase 9,Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12121 | Th1287 | Girentuximab | >Th1287_Girentuximab DVKLVESGGGLVKLGGSLKLSCAASGFTFSNYYMSWVRQTPEKRLELVAAINSDGGITYYLDTVKGRFTISRDNAKNTLYLQMSSLKSEDTALFYCARHRSGYFSMDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Girentuximab is a monoclonal chimeric (mouse/human) antibody directed against carbonic anhydrase IX, an antigen expressed in 95% of clear cell renal cell carcinomas (RCC). | Investigated for use/treatment in gall bladder cancer and renal cell carcinoma. | NA | Mechanism of action of girentuximab is antibody dependent cellular cytotoxicity (ADCC). As a monotherapy in metastatic renal cell carcinomas(RCC), girentuximab demonstrated minimal clinical activity with a 3% partial response rate and a median survival of 16 months. In vitro data suggest that the number of activated ADCC effector cells can be upregulated by low dose interleukin 2 (IL2) administered in a pulsatile fashion. | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | Carbonic anhydrase 9,Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12122 | Th1287 | Girentuximab | >Th1287_Girentuximab DVKLVESGGGLVKLGGSLKLSCAASGFTFSNYYMSWVRQTPEKRLELVAAINSDGGITYYLDTVKGRFTISRDNAKNTLYLQMSSLKSEDTALFYCARHRSGYFSMDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Girentuximab is a monoclonal chimeric (mouse/human) antibody directed against carbonic anhydrase IX, an antigen expressed in 95% of clear cell renal cell carcinomas (RCC). | Investigated for use/treatment in gall bladder cancer and renal cell carcinoma. | NA | Mechanism of action of girentuximab is antibody dependent cellular cytotoxicity (ADCC). As a monotherapy in metastatic renal cell carcinomas(RCC), girentuximab demonstrated minimal clinical activity with a 3% partial response rate and a median survival of 16 months. In vitro data suggest that the number of activated ADCC effector cells can be upregulated by low dose interleukin 2 (IL2) administered in a pulsatile fashion. | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | Carbonic anhydrase 9,Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12123 | Th1287 | Girentuximab | >Th1287_Girentuximab DVKLVESGGGLVKLGGSLKLSCAASGFTFSNYYMSWVRQTPEKRLELVAAINSDGGITYYLDTVKGRFTISRDNAKNTLYLQMSSLKSEDTALFYCARHRSGYFSMDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Girentuximab is a monoclonal chimeric (mouse/human) antibody directed against carbonic anhydrase IX, an antigen expressed in 95% of clear cell renal cell carcinomas (RCC). | Investigated for use/treatment in gall bladder cancer and renal cell carcinoma. | NA | Mechanism of action of girentuximab is antibody dependent cellular cytotoxicity (ADCC). As a monotherapy in metastatic renal cell carcinomas(RCC), girentuximab demonstrated minimal clinical activity with a 3% partial response rate and a median survival of 16 months. In vitro data suggest that the number of activated ADCC effector cells can be upregulated by low dose interleukin 2 (IL2) administered in a pulsatile fashion. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | Carbonic anhydrase 9,Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12124 | Th1287 | Girentuximab | >Th1287_Girentuximab DVKLVESGGGLVKLGGSLKLSCAASGFTFSNYYMSWVRQTPEKRLELVAAINSDGGITYYLDTVKGRFTISRDNAKNTLYLQMSSLKSEDTALFYCARHRSGYFSMDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Girentuximab is a monoclonal chimeric (mouse/human) antibody directed against carbonic anhydrase IX, an antigen expressed in 95% of clear cell renal cell carcinomas (RCC). | Investigated for use/treatment in gall bladder cancer and renal cell carcinoma. | NA | Mechanism of action of girentuximab is antibody dependent cellular cytotoxicity (ADCC). As a monotherapy in metastatic renal cell carcinomas(RCC), girentuximab demonstrated minimal clinical activity with a 3% partial response rate and a median survival of 16 months. In vitro data suggest that the number of activated ADCC effector cells can be upregulated by low dose interleukin 2 (IL2) administered in a pulsatile fashion. | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | Carbonic anhydrase 9,Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12125 | Th1288 | Cintredekin besudotox | >Th1288_Cintredekin_besudotox MHSPGPVPPSTALRELIEELVNITQNQKAPLCNGSMVWSINLTAGMYCAALESLINVSGCSAIEKTQRMLSGFCPHKVSAGQFSSLHVRDTKIEVAQFVKDLLLHLKKLFREGRFNKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDQEQAISALPDYASQPGQPPREDLR | NA | NA | NA | NA | NA | NA | Cintredekin besudotox has been developed as a specific tumor-targeting agent, which is administered by positive-pressure convection-enhanced delivery (CED) directly to brain tissue at risk for residual infiltrating glioblastoma multiforme (GBM) after tumor resection. Cintredekin besudotox is made from a human protein, Interleukin 13 (IL13), linked to a bacterial toxin, _Pseudomonas exotoxin_ (PE). The IL13 portion binds to receptors on the tumor. | Investigated for use/treatment in brain cancer. | NA | A recombinant chimeric protein with potent antitumor activity. Cintredekin besudotox is composed of interleukin-13 (IL13), a pleiotropic immunoregulatory cytokine, linked to a mutated form of pseudomonas exotoxin A; this agent targets and kills tumor cells that express the IL13 receptor (IL13R). The IL13 moiety attaches to the IL13R on the tumor cell membrane, facilitating the entry of the exotoxin. The exotoxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Interleukin-13 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12126 | Th1288 | Cintredekin besudotox | >Th1288_Cintredekin_besudotox MHSPGPVPPSTALRELIEELVNITQNQKAPLCNGSMVWSINLTAGMYCAALESLINVSGCSAIEKTQRMLSGFCPHKVSAGQFSSLHVRDTKIEVAQFVKDLLLHLKKLFREGRFNKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDQEQAISALPDYASQPGQPPREDLR | NA | NA | NA | NA | NA | NA | Cintredekin besudotox has been developed as a specific tumor-targeting agent, which is administered by positive-pressure convection-enhanced delivery (CED) directly to brain tissue at risk for residual infiltrating glioblastoma multiforme (GBM) after tumor resection. Cintredekin besudotox is made from a human protein, Interleukin 13 (IL13), linked to a bacterial toxin, _Pseudomonas exotoxin_ (PE). The IL13 portion binds to receptors on the tumor. | Investigated for use/treatment in brain cancer. | NA | A recombinant chimeric protein with potent antitumor activity. Cintredekin besudotox is composed of interleukin-13 (IL13), a pleiotropic immunoregulatory cytokine, linked to a mutated form of pseudomonas exotoxin A; this agent targets and kills tumor cells that express the IL13 receptor (IL13R). The IL13 moiety attaches to the IL13R on the tumor cell membrane, facilitating the entry of the exotoxin. The exotoxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis. | NA | NA | NA | NA | NA | Biological Factors | NA | NA | NA | NA | Interleukin-13 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12127 | Th1288 | Cintredekin besudotox | >Th1288_Cintredekin_besudotox MHSPGPVPPSTALRELIEELVNITQNQKAPLCNGSMVWSINLTAGMYCAALESLINVSGCSAIEKTQRMLSGFCPHKVSAGQFSSLHVRDTKIEVAQFVKDLLLHLKKLFREGRFNKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDQEQAISALPDYASQPGQPPREDLR | NA | NA | NA | NA | NA | NA | Cintredekin besudotox has been developed as a specific tumor-targeting agent, which is administered by positive-pressure convection-enhanced delivery (CED) directly to brain tissue at risk for residual infiltrating glioblastoma multiforme (GBM) after tumor resection. Cintredekin besudotox is made from a human protein, Interleukin 13 (IL13), linked to a bacterial toxin, _Pseudomonas exotoxin_ (PE). The IL13 portion binds to receptors on the tumor. | Investigated for use/treatment in brain cancer. | NA | A recombinant chimeric protein with potent antitumor activity. Cintredekin besudotox is composed of interleukin-13 (IL13), a pleiotropic immunoregulatory cytokine, linked to a mutated form of pseudomonas exotoxin A; this agent targets and kills tumor cells that express the IL13 receptor (IL13R). The IL13 moiety attaches to the IL13R on the tumor cell membrane, facilitating the entry of the exotoxin. The exotoxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis. | NA | NA | NA | NA | NA | Cytokines | NA | NA | NA | NA | Interleukin-13 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12128 | Th1288 | Cintredekin besudotox | >Th1288_Cintredekin_besudotox MHSPGPVPPSTALRELIEELVNITQNQKAPLCNGSMVWSINLTAGMYCAALESLINVSGCSAIEKTQRMLSGFCPHKVSAGQFSSLHVRDTKIEVAQFVKDLLLHLKKLFREGRFNKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDQEQAISALPDYASQPGQPPREDLR | NA | NA | NA | NA | NA | NA | Cintredekin besudotox has been developed as a specific tumor-targeting agent, which is administered by positive-pressure convection-enhanced delivery (CED) directly to brain tissue at risk for residual infiltrating glioblastoma multiforme (GBM) after tumor resection. Cintredekin besudotox is made from a human protein, Interleukin 13 (IL13), linked to a bacterial toxin, _Pseudomonas exotoxin_ (PE). The IL13 portion binds to receptors on the tumor. | Investigated for use/treatment in brain cancer. | NA | A recombinant chimeric protein with potent antitumor activity. Cintredekin besudotox is composed of interleukin-13 (IL13), a pleiotropic immunoregulatory cytokine, linked to a mutated form of pseudomonas exotoxin A; this agent targets and kills tumor cells that express the IL13 receptor (IL13R). The IL13 moiety attaches to the IL13R on the tumor cell membrane, facilitating the entry of the exotoxin. The exotoxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis. | NA | NA | NA | NA | NA | Intercellular Signaling Peptides and Proteins | NA | NA | NA | NA | Interleukin-13 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12129 | Th1288 | Cintredekin besudotox | >Th1288_Cintredekin_besudotox MHSPGPVPPSTALRELIEELVNITQNQKAPLCNGSMVWSINLTAGMYCAALESLINVSGCSAIEKTQRMLSGFCPHKVSAGQFSSLHVRDTKIEVAQFVKDLLLHLKKLFREGRFNKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDQEQAISALPDYASQPGQPPREDLR | NA | NA | NA | NA | NA | NA | Cintredekin besudotox has been developed as a specific tumor-targeting agent, which is administered by positive-pressure convection-enhanced delivery (CED) directly to brain tissue at risk for residual infiltrating glioblastoma multiforme (GBM) after tumor resection. Cintredekin besudotox is made from a human protein, Interleukin 13 (IL13), linked to a bacterial toxin, _Pseudomonas exotoxin_ (PE). The IL13 portion binds to receptors on the tumor. | Investigated for use/treatment in brain cancer. | NA | A recombinant chimeric protein with potent antitumor activity. Cintredekin besudotox is composed of interleukin-13 (IL13), a pleiotropic immunoregulatory cytokine, linked to a mutated form of pseudomonas exotoxin A; this agent targets and kills tumor cells that express the IL13 receptor (IL13R). The IL13 moiety attaches to the IL13R on the tumor cell membrane, facilitating the entry of the exotoxin. The exotoxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis. | NA | NA | NA | NA | NA | Interleukins | NA | NA | NA | NA | Interleukin-13 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12130 | Th1288 | Cintredekin besudotox | >Th1288_Cintredekin_besudotox MHSPGPVPPSTALRELIEELVNITQNQKAPLCNGSMVWSINLTAGMYCAALESLINVSGCSAIEKTQRMLSGFCPHKVSAGQFSSLHVRDTKIEVAQFVKDLLLHLKKLFREGRFNKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDQEQAISALPDYASQPGQPPREDLR | NA | NA | NA | NA | NA | NA | Cintredekin besudotox has been developed as a specific tumor-targeting agent, which is administered by positive-pressure convection-enhanced delivery (CED) directly to brain tissue at risk for residual infiltrating glioblastoma multiforme (GBM) after tumor resection. Cintredekin besudotox is made from a human protein, Interleukin 13 (IL13), linked to a bacterial toxin, _Pseudomonas exotoxin_ (PE). The IL13 portion binds to receptors on the tumor. | Investigated for use/treatment in brain cancer. | NA | A recombinant chimeric protein with potent antitumor activity. Cintredekin besudotox is composed of interleukin-13 (IL13), a pleiotropic immunoregulatory cytokine, linked to a mutated form of pseudomonas exotoxin A; this agent targets and kills tumor cells that express the IL13 receptor (IL13R). The IL13 moiety attaches to the IL13R on the tumor cell membrane, facilitating the entry of the exotoxin. The exotoxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis. | NA | NA | NA | NA | NA | Peptides | NA | NA | NA | NA | Interleukin-13 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12131 | Th1288 | Cintredekin besudotox | >Th1288_Cintredekin_besudotox MHSPGPVPPSTALRELIEELVNITQNQKAPLCNGSMVWSINLTAGMYCAALESLINVSGCSAIEKTQRMLSGFCPHKVSAGQFSSLHVRDTKIEVAQFVKDLLLHLKKLFREGRFNKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDQEQAISALPDYASQPGQPPREDLR | NA | NA | NA | NA | NA | NA | Cintredekin besudotox has been developed as a specific tumor-targeting agent, which is administered by positive-pressure convection-enhanced delivery (CED) directly to brain tissue at risk for residual infiltrating glioblastoma multiforme (GBM) after tumor resection. Cintredekin besudotox is made from a human protein, Interleukin 13 (IL13), linked to a bacterial toxin, _Pseudomonas exotoxin_ (PE). The IL13 portion binds to receptors on the tumor. | Investigated for use/treatment in brain cancer. | NA | A recombinant chimeric protein with potent antitumor activity. Cintredekin besudotox is composed of interleukin-13 (IL13), a pleiotropic immunoregulatory cytokine, linked to a mutated form of pseudomonas exotoxin A; this agent targets and kills tumor cells that express the IL13 receptor (IL13R). The IL13 moiety attaches to the IL13R on the tumor cell membrane, facilitating the entry of the exotoxin. The exotoxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | Interleukin-13 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12132 | Th1288 | Cintredekin besudotox | >Th1288_Cintredekin_besudotox MHSPGPVPPSTALRELIEELVNITQNQKAPLCNGSMVWSINLTAGMYCAALESLINVSGCSAIEKTQRMLSGFCPHKVSAGQFSSLHVRDTKIEVAQFVKDLLLHLKKLFREGRFNKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDQEQAISALPDYASQPGQPPREDLR | NA | NA | NA | NA | NA | NA | Cintredekin besudotox has been developed as a specific tumor-targeting agent, which is administered by positive-pressure convection-enhanced delivery (CED) directly to brain tissue at risk for residual infiltrating glioblastoma multiforme (GBM) after tumor resection. Cintredekin besudotox is made from a human protein, Interleukin 13 (IL13), linked to a bacterial toxin, _Pseudomonas exotoxin_ (PE). The IL13 portion binds to receptors on the tumor. | Investigated for use/treatment in brain cancer. | NA | A recombinant chimeric protein with potent antitumor activity. Cintredekin besudotox is composed of interleukin-13 (IL13), a pleiotropic immunoregulatory cytokine, linked to a mutated form of pseudomonas exotoxin A; this agent targets and kills tumor cells that express the IL13 receptor (IL13R). The IL13 moiety attaches to the IL13R on the tumor cell membrane, facilitating the entry of the exotoxin. The exotoxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis. | NA | NA | NA | NA | NA | Recombinant Proteins | NA | NA | NA | NA | Interleukin-13 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12133 | Th1288 | Cintredekin besudotox | >Th1288_Cintredekin_besudotox MHSPGPVPPSTALRELIEELVNITQNQKAPLCNGSMVWSINLTAGMYCAALESLINVSGCSAIEKTQRMLSGFCPHKVSAGQFSSLHVRDTKIEVAQFVKDLLLHLKKLFREGRFNKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDQEQAISALPDYASQPGQPPREDLR | NA | NA | NA | NA | NA | NA | Cintredekin besudotox has been developed as a specific tumor-targeting agent, which is administered by positive-pressure convection-enhanced delivery (CED) directly to brain tissue at risk for residual infiltrating glioblastoma multiforme (GBM) after tumor resection. Cintredekin besudotox is made from a human protein, Interleukin 13 (IL13), linked to a bacterial toxin, _Pseudomonas exotoxin_ (PE). The IL13 portion binds to receptors on the tumor. | Investigated for use/treatment in brain cancer. | NA | A recombinant chimeric protein with potent antitumor activity. Cintredekin besudotox is composed of interleukin-13 (IL13), a pleiotropic immunoregulatory cytokine, linked to a mutated form of pseudomonas exotoxin A; this agent targets and kills tumor cells that express the IL13 receptor (IL13R). The IL13 moiety attaches to the IL13R on the tumor cell membrane, facilitating the entry of the exotoxin. The exotoxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis. | NA | NA | NA | NA | NA | Toxins, Biological | NA | NA | NA | NA | Interleukin-13 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12149 | Th1291 | Oportuzumab monatox | >Th1291_Oportuzumab_monatox HHHHHHDIQMTQSPSSLSASVGDRVTITCRSTKSLLHSNGITYLYWYQQKPGKAPKLLIYQMSNLASGVPSRFSSSGSGTDFTLTISSLQPEDFATYYCAQNLEIPRTFGQGTKVELKRATPSHNSHQVPSAGGPTANSGTSGSEVQLVQSGPGLVQPGGSVRISCAASGYTFTNYGMNWVKQAPGKGLEWMGWINTYTGESTYADSFKGRFTFSLDTSASAAYLQINSLRAEDTAVYYCARFAIKGDYWGQGTLLTVSSEFGGAPEFPKPSTPPGSSGLEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAASADVVSLTCPVAAGECAGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTGLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPHHHHHHKDEL | NA | NA | NA | NA | NA | NA | VB4-845 is studied in the treatment of certain types of head and neck cancer. VB4-845 is made by linking a monoclonal antibody fragment to a toxic protein that may kill cancer cells. VB4-845 is a fusion protein containing humanized scFv specific for the epithelial cell adhesion molecule, Ep-CAM, a tumor cell-associated target highly expressed on carcinoma cells of epithelial origin and a truncated portion of Pseudomonas exotoxin A. | Investigated for use/treatment in bladder cancer and head and neck cancer. | NA | VB4-845 binds to EpCAM (a protein on the surface of epithelial cells and some types of cancer cells). Also called anti-EpCAM-Pseudomonas-exotoxin fusion protein and Proxinium. It targets and kills Ep-CAM-positive tumors by apoptosis. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Epithelial cell adhesion molecule | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12150 | Th1291 | Oportuzumab monatox | >Th1291_Oportuzumab_monatox HHHHHHDIQMTQSPSSLSASVGDRVTITCRSTKSLLHSNGITYLYWYQQKPGKAPKLLIYQMSNLASGVPSRFSSSGSGTDFTLTISSLQPEDFATYYCAQNLEIPRTFGQGTKVELKRATPSHNSHQVPSAGGPTANSGTSGSEVQLVQSGPGLVQPGGSVRISCAASGYTFTNYGMNWVKQAPGKGLEWMGWINTYTGESTYADSFKGRFTFSLDTSASAAYLQINSLRAEDTAVYYCARFAIKGDYWGQGTLLTVSSEFGGAPEFPKPSTPPGSSGLEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAASADVVSLTCPVAAGECAGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTGLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPHHHHHHKDEL | NA | NA | NA | NA | NA | NA | VB4-845 is studied in the treatment of certain types of head and neck cancer. VB4-845 is made by linking a monoclonal antibody fragment to a toxic protein that may kill cancer cells. VB4-845 is a fusion protein containing humanized scFv specific for the epithelial cell adhesion molecule, Ep-CAM, a tumor cell-associated target highly expressed on carcinoma cells of epithelial origin and a truncated portion of Pseudomonas exotoxin A. | Investigated for use/treatment in bladder cancer and head and neck cancer. | NA | VB4-845 binds to EpCAM (a protein on the surface of epithelial cells and some types of cancer cells). Also called anti-EpCAM-Pseudomonas-exotoxin fusion protein and Proxinium. It targets and kills Ep-CAM-positive tumors by apoptosis. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Epithelial cell adhesion molecule | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12151 | Th1291 | Oportuzumab monatox | >Th1291_Oportuzumab_monatox HHHHHHDIQMTQSPSSLSASVGDRVTITCRSTKSLLHSNGITYLYWYQQKPGKAPKLLIYQMSNLASGVPSRFSSSGSGTDFTLTISSLQPEDFATYYCAQNLEIPRTFGQGTKVELKRATPSHNSHQVPSAGGPTANSGTSGSEVQLVQSGPGLVQPGGSVRISCAASGYTFTNYGMNWVKQAPGKGLEWMGWINTYTGESTYADSFKGRFTFSLDTSASAAYLQINSLRAEDTAVYYCARFAIKGDYWGQGTLLTVSSEFGGAPEFPKPSTPPGSSGLEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAASADVVSLTCPVAAGECAGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTGLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPHHHHHHKDEL | NA | NA | NA | NA | NA | NA | VB4-845 is studied in the treatment of certain types of head and neck cancer. VB4-845 is made by linking a monoclonal antibody fragment to a toxic protein that may kill cancer cells. VB4-845 is a fusion protein containing humanized scFv specific for the epithelial cell adhesion molecule, Ep-CAM, a tumor cell-associated target highly expressed on carcinoma cells of epithelial origin and a truncated portion of Pseudomonas exotoxin A. | Investigated for use/treatment in bladder cancer and head and neck cancer. | NA | VB4-845 binds to EpCAM (a protein on the surface of epithelial cells and some types of cancer cells). Also called anti-EpCAM-Pseudomonas-exotoxin fusion protein and Proxinium. It targets and kills Ep-CAM-positive tumors by apoptosis. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Epithelial cell adhesion molecule | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12152 | Th1291 | Oportuzumab monatox | >Th1291_Oportuzumab_monatox HHHHHHDIQMTQSPSSLSASVGDRVTITCRSTKSLLHSNGITYLYWYQQKPGKAPKLLIYQMSNLASGVPSRFSSSGSGTDFTLTISSLQPEDFATYYCAQNLEIPRTFGQGTKVELKRATPSHNSHQVPSAGGPTANSGTSGSEVQLVQSGPGLVQPGGSVRISCAASGYTFTNYGMNWVKQAPGKGLEWMGWINTYTGESTYADSFKGRFTFSLDTSASAAYLQINSLRAEDTAVYYCARFAIKGDYWGQGTLLTVSSEFGGAPEFPKPSTPPGSSGLEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAASADVVSLTCPVAAGECAGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTGLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPHHHHHHKDEL | NA | NA | NA | NA | NA | NA | VB4-845 is studied in the treatment of certain types of head and neck cancer. VB4-845 is made by linking a monoclonal antibody fragment to a toxic protein that may kill cancer cells. VB4-845 is a fusion protein containing humanized scFv specific for the epithelial cell adhesion molecule, Ep-CAM, a tumor cell-associated target highly expressed on carcinoma cells of epithelial origin and a truncated portion of Pseudomonas exotoxin A. | Investigated for use/treatment in bladder cancer and head and neck cancer. | NA | VB4-845 binds to EpCAM (a protein on the surface of epithelial cells and some types of cancer cells). Also called anti-EpCAM-Pseudomonas-exotoxin fusion protein and Proxinium. It targets and kills Ep-CAM-positive tumors by apoptosis. | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | Epithelial cell adhesion molecule | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12153 | Th1291 | Oportuzumab monatox | >Th1291_Oportuzumab_monatox HHHHHHDIQMTQSPSSLSASVGDRVTITCRSTKSLLHSNGITYLYWYQQKPGKAPKLLIYQMSNLASGVPSRFSSSGSGTDFTLTISSLQPEDFATYYCAQNLEIPRTFGQGTKVELKRATPSHNSHQVPSAGGPTANSGTSGSEVQLVQSGPGLVQPGGSVRISCAASGYTFTNYGMNWVKQAPGKGLEWMGWINTYTGESTYADSFKGRFTFSLDTSASAAYLQINSLRAEDTAVYYCARFAIKGDYWGQGTLLTVSSEFGGAPEFPKPSTPPGSSGLEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAASADVVSLTCPVAAGECAGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTGLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPHHHHHHKDEL | NA | NA | NA | NA | NA | NA | VB4-845 is studied in the treatment of certain types of head and neck cancer. VB4-845 is made by linking a monoclonal antibody fragment to a toxic protein that may kill cancer cells. VB4-845 is a fusion protein containing humanized scFv specific for the epithelial cell adhesion molecule, Ep-CAM, a tumor cell-associated target highly expressed on carcinoma cells of epithelial origin and a truncated portion of Pseudomonas exotoxin A. | Investigated for use/treatment in bladder cancer and head and neck cancer. | NA | VB4-845 binds to EpCAM (a protein on the surface of epithelial cells and some types of cancer cells). Also called anti-EpCAM-Pseudomonas-exotoxin fusion protein and Proxinium. It targets and kills Ep-CAM-positive tumors by apoptosis. | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | Epithelial cell adhesion molecule | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12154 | Th1291 | Oportuzumab monatox | >Th1291_Oportuzumab_monatox HHHHHHDIQMTQSPSSLSASVGDRVTITCRSTKSLLHSNGITYLYWYQQKPGKAPKLLIYQMSNLASGVPSRFSSSGSGTDFTLTISSLQPEDFATYYCAQNLEIPRTFGQGTKVELKRATPSHNSHQVPSAGGPTANSGTSGSEVQLVQSGPGLVQPGGSVRISCAASGYTFTNYGMNWVKQAPGKGLEWMGWINTYTGESTYADSFKGRFTFSLDTSASAAYLQINSLRAEDTAVYYCARFAIKGDYWGQGTLLTVSSEFGGAPEFPKPSTPPGSSGLEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAASADVVSLTCPVAAGECAGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTGLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPHHHHHHKDEL | NA | NA | NA | NA | NA | NA | VB4-845 is studied in the treatment of certain types of head and neck cancer. VB4-845 is made by linking a monoclonal antibody fragment to a toxic protein that may kill cancer cells. VB4-845 is a fusion protein containing humanized scFv specific for the epithelial cell adhesion molecule, Ep-CAM, a tumor cell-associated target highly expressed on carcinoma cells of epithelial origin and a truncated portion of Pseudomonas exotoxin A. | Investigated for use/treatment in bladder cancer and head and neck cancer. | NA | VB4-845 binds to EpCAM (a protein on the surface of epithelial cells and some types of cancer cells). Also called anti-EpCAM-Pseudomonas-exotoxin fusion protein and Proxinium. It targets and kills Ep-CAM-positive tumors by apoptosis. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | Epithelial cell adhesion molecule | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12155 | Th1291 | Oportuzumab monatox | >Th1291_Oportuzumab_monatox HHHHHHDIQMTQSPSSLSASVGDRVTITCRSTKSLLHSNGITYLYWYQQKPGKAPKLLIYQMSNLASGVPSRFSSSGSGTDFTLTISSLQPEDFATYYCAQNLEIPRTFGQGTKVELKRATPSHNSHQVPSAGGPTANSGTSGSEVQLVQSGPGLVQPGGSVRISCAASGYTFTNYGMNWVKQAPGKGLEWMGWINTYTGESTYADSFKGRFTFSLDTSASAAYLQINSLRAEDTAVYYCARFAIKGDYWGQGTLLTVSSEFGGAPEFPKPSTPPGSSGLEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAASADVVSLTCPVAAGECAGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTGLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPHHHHHHKDEL | NA | NA | NA | NA | NA | NA | VB4-845 is studied in the treatment of certain types of head and neck cancer. VB4-845 is made by linking a monoclonal antibody fragment to a toxic protein that may kill cancer cells. VB4-845 is a fusion protein containing humanized scFv specific for the epithelial cell adhesion molecule, Ep-CAM, a tumor cell-associated target highly expressed on carcinoma cells of epithelial origin and a truncated portion of Pseudomonas exotoxin A. | Investigated for use/treatment in bladder cancer and head and neck cancer. | NA | VB4-845 binds to EpCAM (a protein on the surface of epithelial cells and some types of cancer cells). Also called anti-EpCAM-Pseudomonas-exotoxin fusion protein and Proxinium. It targets and kills Ep-CAM-positive tumors by apoptosis. | NA | NA | NA | NA | NA | Recombinant Proteins | NA | NA | NA | NA | Epithelial cell adhesion molecule | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12156 | Th1291 | Oportuzumab monatox | >Th1291_Oportuzumab_monatox HHHHHHDIQMTQSPSSLSASVGDRVTITCRSTKSLLHSNGITYLYWYQQKPGKAPKLLIYQMSNLASGVPSRFSSSGSGTDFTLTISSLQPEDFATYYCAQNLEIPRTFGQGTKVELKRATPSHNSHQVPSAGGPTANSGTSGSEVQLVQSGPGLVQPGGSVRISCAASGYTFTNYGMNWVKQAPGKGLEWMGWINTYTGESTYADSFKGRFTFSLDTSASAAYLQINSLRAEDTAVYYCARFAIKGDYWGQGTLLTVSSEFGGAPEFPKPSTPPGSSGLEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAASADVVSLTCPVAAGECAGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTGLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPHHHHHHKDEL | NA | NA | NA | NA | NA | NA | VB4-845 is studied in the treatment of certain types of head and neck cancer. VB4-845 is made by linking a monoclonal antibody fragment to a toxic protein that may kill cancer cells. VB4-845 is a fusion protein containing humanized scFv specific for the epithelial cell adhesion molecule, Ep-CAM, a tumor cell-associated target highly expressed on carcinoma cells of epithelial origin and a truncated portion of Pseudomonas exotoxin A. | Investigated for use/treatment in bladder cancer and head and neck cancer. | NA | VB4-845 binds to EpCAM (a protein on the surface of epithelial cells and some types of cancer cells). Also called anti-EpCAM-Pseudomonas-exotoxin fusion protein and Proxinium. It targets and kills Ep-CAM-positive tumors by apoptosis. | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | Epithelial cell adhesion molecule | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12168 | Th1293 | INGN 201 | NA | NA | NA | NA | NA | NA | NA | INGN 201(Advexin) is a replication-impaired adenoviral vector that carries the p53 gene, has been evaluated in both preclinical and clinical trials. Advexin is a well-tolerated and efficacious treatment for numerous cancers, both as monotherapy and in combination with radiation and/or chemotherapy agents. | Investigated for use/treatment in bladder cancer, brain cancer, breast cancer, esophageal cancer, head and neck cancer, lung cancer, oral cavity cancer, ovarian cancer, and prostate cancer. | NA | Advexin® is a vaccine that contains very high concentrations of the p53 protein. Advexin® is administered into or near the site of cancer and has demonstrated the ability to make cancer cells more sensitive to the killing effects of chemotherapy. The p53 gene makes protein that is responsible for stopping uncontrolled growth of a cell. One of its roles is to stop growth of a cell and initiate repair of any detected mutations or damage within the DNA of the cell. In addition, the p53 gene will direct the cell to destroy itself if a mutation or damage is detected that is beyond repair. | NA | NA | NA | NA | NA | Biological Products | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12169 | Th1293 | INGN 201 | NA | NA | NA | NA | NA | NA | NA | INGN 201(Advexin) is a replication-impaired adenoviral vector that carries the p53 gene, has been evaluated in both preclinical and clinical trials. Advexin is a well-tolerated and efficacious treatment for numerous cancers, both as monotherapy and in combination with radiation and/or chemotherapy agents. | Investigated for use/treatment in bladder cancer, brain cancer, breast cancer, esophageal cancer, head and neck cancer, lung cancer, oral cavity cancer, ovarian cancer, and prostate cancer. | NA | Advexin® is a vaccine that contains very high concentrations of the p53 protein. Advexin® is administered into or near the site of cancer and has demonstrated the ability to make cancer cells more sensitive to the killing effects of chemotherapy. The p53 gene makes protein that is responsible for stopping uncontrolled growth of a cell. One of its roles is to stop growth of a cell and initiate repair of any detected mutations or damage within the DNA of the cell. In addition, the p53 gene will direct the cell to destroy itself if a mutation or damage is detected that is beyond repair. | NA | NA | NA | NA | NA | Complex Mixtures | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12170 | Th1293 | INGN 201 | NA | NA | NA | NA | NA | NA | NA | INGN 201(Advexin) is a replication-impaired adenoviral vector that carries the p53 gene, has been evaluated in both preclinical and clinical trials. Advexin is a well-tolerated and efficacious treatment for numerous cancers, both as monotherapy and in combination with radiation and/or chemotherapy agents. | Investigated for use/treatment in bladder cancer, brain cancer, breast cancer, esophageal cancer, head and neck cancer, lung cancer, oral cavity cancer, ovarian cancer, and prostate cancer. | NA | Advexin® is a vaccine that contains very high concentrations of the p53 protein. Advexin® is administered into or near the site of cancer and has demonstrated the ability to make cancer cells more sensitive to the killing effects of chemotherapy. The p53 gene makes protein that is responsible for stopping uncontrolled growth of a cell. One of its roles is to stop growth of a cell and initiate repair of any detected mutations or damage within the DNA of the cell. In addition, the p53 gene will direct the cell to destroy itself if a mutation or damage is detected that is beyond repair. | NA | NA | NA | NA | NA | Gene Transfer Techniques | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12171 | Th1293 | INGN 201 | NA | NA | NA | NA | NA | NA | NA | INGN 201(Advexin) is a replication-impaired adenoviral vector that carries the p53 gene, has been evaluated in both preclinical and clinical trials. Advexin is a well-tolerated and efficacious treatment for numerous cancers, both as monotherapy and in combination with radiation and/or chemotherapy agents. | Investigated for use/treatment in bladder cancer, brain cancer, breast cancer, esophageal cancer, head and neck cancer, lung cancer, oral cavity cancer, ovarian cancer, and prostate cancer. | NA | Advexin® is a vaccine that contains very high concentrations of the p53 protein. Advexin® is administered into or near the site of cancer and has demonstrated the ability to make cancer cells more sensitive to the killing effects of chemotherapy. The p53 gene makes protein that is responsible for stopping uncontrolled growth of a cell. One of its roles is to stop growth of a cell and initiate repair of any detected mutations or damage within the DNA of the cell. In addition, the p53 gene will direct the cell to destroy itself if a mutation or damage is detected that is beyond repair. | NA | NA | NA | NA | NA | Genes, p53 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12172 | Th1294 | INGN 225 | NA | NA | NA | NA | NA | NA | NA | INGN 225 is a therapeutic consisting of a cancer patient's own immune cells treated with an adenovector carrying the human p53 gene, Ad-p53. INGN 225 is currently in Phase 1/2 trials in patients with small cell lung cancer and breast cancer. | Investigated for use/treatment in breast cancer, head and neck cancer, and lung cancer. | INGN 225 uses the p53 tumor suppressor in a different manner than ADVEXIN to create a molecular immunotherapy for cancer that stimulates a particular type of immune system cell known as a dendritic cell. Testing has shown that the human immune system can recognize and kill tumors after treatment with dendritic cells stimulated by the p53 tumor suppressor, which suggests this therapy could have broad utility as a treatment for solid tumors. INGN 225 may also sensitize tumors to the effects of platinum and taxane chemotherapies. | NA | NA | NA | NA | NA | NA | Biological Products | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12173 | Th1294 | INGN 225 | NA | NA | NA | NA | NA | NA | NA | INGN 225 is a therapeutic consisting of a cancer patient's own immune cells treated with an adenovector carrying the human p53 gene, Ad-p53. INGN 225 is currently in Phase 1/2 trials in patients with small cell lung cancer and breast cancer. | Investigated for use/treatment in breast cancer, head and neck cancer, and lung cancer. | INGN 225 uses the p53 tumor suppressor in a different manner than ADVEXIN to create a molecular immunotherapy for cancer that stimulates a particular type of immune system cell known as a dendritic cell. Testing has shown that the human immune system can recognize and kill tumors after treatment with dendritic cells stimulated by the p53 tumor suppressor, which suggests this therapy could have broad utility as a treatment for solid tumors. INGN 225 may also sensitize tumors to the effects of platinum and taxane chemotherapies. | NA | NA | NA | NA | NA | NA | Complex Mixtures | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12174 | Th1294 | INGN 225 | NA | NA | NA | NA | NA | NA | NA | INGN 225 is a therapeutic consisting of a cancer patient's own immune cells treated with an adenovector carrying the human p53 gene, Ad-p53. INGN 225 is currently in Phase 1/2 trials in patients with small cell lung cancer and breast cancer. | Investigated for use/treatment in breast cancer, head and neck cancer, and lung cancer. | INGN 225 uses the p53 tumor suppressor in a different manner than ADVEXIN to create a molecular immunotherapy for cancer that stimulates a particular type of immune system cell known as a dendritic cell. Testing has shown that the human immune system can recognize and kill tumors after treatment with dendritic cells stimulated by the p53 tumor suppressor, which suggests this therapy could have broad utility as a treatment for solid tumors. INGN 225 may also sensitize tumors to the effects of platinum and taxane chemotherapies. | NA | NA | NA | NA | NA | NA | Vaccines | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12226 | Th1301 | NAV 1800 | NA | NA | NA | NA | NA | NA | NA | RIGScan CR49, a 125I-labelled CR monoclonal antibody directed against the tumour-associated antigen TAG-72, is undergoing development with Neoprobe for the intraoperative detection of metastatic colorectal cancer. | Investigated for use/treatment in colorectal cancer and solid tumors. | NA | RIGScan CR49 is used to locate cancerous tissue during surgery for patients with metastatic cancer of the colon or rectum (colorectal). In multicenter Phase II and pivotal Phase III clinical trials, RIGScan CR49 located tumor confirmed by pathology tests in 90 percent of evaluable patients who participated in the studies. The product found pathology-confirmed tumor that was missed by the surgeon and by preoperative diagnostic scans in one of five of the evaluable patients. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12227 | Th1301 | NAV 1800 | NA | NA | NA | NA | NA | NA | NA | RIGScan CR49, a 125I-labelled CR monoclonal antibody directed against the tumour-associated antigen TAG-72, is undergoing development with Neoprobe for the intraoperative detection of metastatic colorectal cancer. | Investigated for use/treatment in colorectal cancer and solid tumors. | NA | RIGScan CR49 is used to locate cancerous tissue during surgery for patients with metastatic cancer of the colon or rectum (colorectal). In multicenter Phase II and pivotal Phase III clinical trials, RIGScan CR49 located tumor confirmed by pathology tests in 90 percent of evaluable patients who participated in the studies. The product found pathology-confirmed tumor that was missed by the surgeon and by preoperative diagnostic scans in one of five of the evaluable patients. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12228 | Th1301 | NAV 1800 | NA | NA | NA | NA | NA | NA | NA | RIGScan CR49, a 125I-labelled CR monoclonal antibody directed against the tumour-associated antigen TAG-72, is undergoing development with Neoprobe for the intraoperative detection of metastatic colorectal cancer. | Investigated for use/treatment in colorectal cancer and solid tumors. | NA | RIGScan CR49 is used to locate cancerous tissue during surgery for patients with metastatic cancer of the colon or rectum (colorectal). In multicenter Phase II and pivotal Phase III clinical trials, RIGScan CR49 located tumor confirmed by pathology tests in 90 percent of evaluable patients who participated in the studies. The product found pathology-confirmed tumor that was missed by the surgeon and by preoperative diagnostic scans in one of five of the evaluable patients. | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12229 | Th1301 | NAV 1800 | NA | NA | NA | NA | NA | NA | NA | RIGScan CR49, a 125I-labelled CR monoclonal antibody directed against the tumour-associated antigen TAG-72, is undergoing development with Neoprobe for the intraoperative detection of metastatic colorectal cancer. | Investigated for use/treatment in colorectal cancer and solid tumors. | NA | RIGScan CR49 is used to locate cancerous tissue during surgery for patients with metastatic cancer of the colon or rectum (colorectal). In multicenter Phase II and pivotal Phase III clinical trials, RIGScan CR49 located tumor confirmed by pathology tests in 90 percent of evaluable patients who participated in the studies. The product found pathology-confirmed tumor that was missed by the surgeon and by preoperative diagnostic scans in one of five of the evaluable patients. | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12230 | Th1301 | NAV 1800 | NA | NA | NA | NA | NA | NA | NA | RIGScan CR49, a 125I-labelled CR monoclonal antibody directed against the tumour-associated antigen TAG-72, is undergoing development with Neoprobe for the intraoperative detection of metastatic colorectal cancer. | Investigated for use/treatment in colorectal cancer and solid tumors. | NA | RIGScan CR49 is used to locate cancerous tissue during surgery for patients with metastatic cancer of the colon or rectum (colorectal). In multicenter Phase II and pivotal Phase III clinical trials, RIGScan CR49 located tumor confirmed by pathology tests in 90 percent of evaluable patients who participated in the studies. The product found pathology-confirmed tumor that was missed by the surgeon and by preoperative diagnostic scans in one of five of the evaluable patients. | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12231 | Th1301 | NAV 1800 | NA | NA | NA | NA | NA | NA | NA | RIGScan CR49, a 125I-labelled CR monoclonal antibody directed against the tumour-associated antigen TAG-72, is undergoing development with Neoprobe for the intraoperative detection of metastatic colorectal cancer. | Investigated for use/treatment in colorectal cancer and solid tumors. | NA | RIGScan CR49 is used to locate cancerous tissue during surgery for patients with metastatic cancer of the colon or rectum (colorectal). In multicenter Phase II and pivotal Phase III clinical trials, RIGScan CR49 located tumor confirmed by pathology tests in 90 percent of evaluable patients who participated in the studies. The product found pathology-confirmed tumor that was missed by the surgeon and by preoperative diagnostic scans in one of five of the evaluable patients. | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12232 | Th1301 | NAV 1800 | NA | NA | NA | NA | NA | NA | NA | RIGScan CR49, a 125I-labelled CR monoclonal antibody directed against the tumour-associated antigen TAG-72, is undergoing development with Neoprobe for the intraoperative detection of metastatic colorectal cancer. | Investigated for use/treatment in colorectal cancer and solid tumors. | NA | RIGScan CR49 is used to locate cancerous tissue during surgery for patients with metastatic cancer of the colon or rectum (colorectal). In multicenter Phase II and pivotal Phase III clinical trials, RIGScan CR49 located tumor confirmed by pathology tests in 90 percent of evaluable patients who participated in the studies. The product found pathology-confirmed tumor that was missed by the surgeon and by preoperative diagnostic scans in one of five of the evaluable patients. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12233 | Th1301 | NAV 1800 | NA | NA | NA | NA | NA | NA | NA | RIGScan CR49, a 125I-labelled CR monoclonal antibody directed against the tumour-associated antigen TAG-72, is undergoing development with Neoprobe for the intraoperative detection of metastatic colorectal cancer. | Investigated for use/treatment in colorectal cancer and solid tumors. | NA | RIGScan CR49 is used to locate cancerous tissue during surgery for patients with metastatic cancer of the colon or rectum (colorectal). In multicenter Phase II and pivotal Phase III clinical trials, RIGScan CR49 located tumor confirmed by pathology tests in 90 percent of evaluable patients who participated in the studies. The product found pathology-confirmed tumor that was missed by the surgeon and by preoperative diagnostic scans in one of five of the evaluable patients. | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12258 | Th1306 | AVN-944 | >Th1306_AVN-944 MWESKFVKEGLTFDDVLLVPAKSDVLPREVSVKTVLSESLQLNIPLISAGMDTVTEADMAIAMARQGGLGIIHKNMSIEQQAEQVDKVKRSESGVISDPFFLTPEHQVYDAEHLMGKYRISGVPVVNNLDERKLVGIITNRDMRFIQDYSIKISDVMTKEQLITAPVGTTLDEAEKILQKYKIEKLPLVDNNGVLQGLITIKDIEKVIEFPNSAKDKQGRLLVGAAVGVTADAMTRIDALVKASVDAIVLDTAHGHSQGVIDKVKEVRAKYPSLNIIAGNVATAEATGALIEAGANVVKVGIGPGSICTTRVVAGVGVPQLTAVYDCATEARKHGIPVIADGGIKYSGDMVKALAAGAHVVMLGSMFAGVAESPGETEIYQGRQFKVYRGMGSVGAMEKGSKDRYFQEGNKKLVPEGIEGRVPYKGPLADTVHQLVGGLRAGMGYCGAQDLEFLRENAQFVRMSGAGLLESHPHHVQITKEAPTTHYNVLYINRRRFYISVYFFLIMLE | NA | NA | NA | NA | NA | NA | AVN944 is a biotech drug that demonstrated a statistically meaningful impact on IMPDH and other proteins that are critical to activities in cancer cells, including nucleotide biosynthesis, energy and metabolism, DNA replication, apoptosis and cell cycle control. AVN944 has been associated with cancer cell death in clinical trials. It is being investigated for the treatment of patients with advanced hematologic malignancies. | Investigated for use/treatment in cancer/tumors (unspecified), leukemia (unspecified), lymphoma (unspecified), multiple myeloma, and pancreatic cancer. | IMPDH is highly upregulated in most hematological cancers and in many solid tumors. AVN944 is a biotech drug that demonstrated a statistically meaningful impact in inhibiting IMPDH and other proteins that are critical to activities in cancer cells, including nucleotide biosynthesis, energy and metabolism, DNA replication, apoptosis and cell cycle control. AVN944 has been associated with cancer cell death in clinical trials. It is being investigated for the treatment of patients with advanced hematologic malignancies. | AVN944 inhibits IMPDH and appears to induce apoptosis. Specifically, it was found that the gene HspA1A, a marker of stress response found to correlate with depleted GTP pools in cancer cell lines, is induced within hours upon the first treatment of the drug in patients, even at the trial's lowest doses. Following continued dosing of AVN944, this marker of disease cell stress was elevated even in the absence of circulating levels of the drug between doses. | NA | NA | NA | NA | NA | Acids, Acyclic | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12259 | Th1306 | AVN-944 | >Th1306_AVN-944 MWESKFVKEGLTFDDVLLVPAKSDVLPREVSVKTVLSESLQLNIPLISAGMDTVTEADMAIAMARQGGLGIIHKNMSIEQQAEQVDKVKRSESGVISDPFFLTPEHQVYDAEHLMGKYRISGVPVVNNLDERKLVGIITNRDMRFIQDYSIKISDVMTKEQLITAPVGTTLDEAEKILQKYKIEKLPLVDNNGVLQGLITIKDIEKVIEFPNSAKDKQGRLLVGAAVGVTADAMTRIDALVKASVDAIVLDTAHGHSQGVIDKVKEVRAKYPSLNIIAGNVATAEATGALIEAGANVVKVGIGPGSICTTRVVAGVGVPQLTAVYDCATEARKHGIPVIADGGIKYSGDMVKALAAGAHVVMLGSMFAGVAESPGETEIYQGRQFKVYRGMGSVGAMEKGSKDRYFQEGNKKLVPEGIEGRVPYKGPLADTVHQLVGGLRAGMGYCGAQDLEFLRENAQFVRMSGAGLLESHPHHVQITKEAPTTHYNVLYINRRRFYISVYFFLIMLE | NA | NA | NA | NA | NA | NA | AVN944 is a biotech drug that demonstrated a statistically meaningful impact on IMPDH and other proteins that are critical to activities in cancer cells, including nucleotide biosynthesis, energy and metabolism, DNA replication, apoptosis and cell cycle control. AVN944 has been associated with cancer cell death in clinical trials. It is being investigated for the treatment of patients with advanced hematologic malignancies. | Investigated for use/treatment in cancer/tumors (unspecified), leukemia (unspecified), lymphoma (unspecified), multiple myeloma, and pancreatic cancer. | IMPDH is highly upregulated in most hematological cancers and in many solid tumors. AVN944 is a biotech drug that demonstrated a statistically meaningful impact in inhibiting IMPDH and other proteins that are critical to activities in cancer cells, including nucleotide biosynthesis, energy and metabolism, DNA replication, apoptosis and cell cycle control. AVN944 has been associated with cancer cell death in clinical trials. It is being investigated for the treatment of patients with advanced hematologic malignancies. | AVN944 inhibits IMPDH and appears to induce apoptosis. Specifically, it was found that the gene HspA1A, a marker of stress response found to correlate with depleted GTP pools in cancer cell lines, is induced within hours upon the first treatment of the drug in patients, even at the trial's lowest doses. Following continued dosing of AVN944, this marker of disease cell stress was elevated even in the absence of circulating levels of the drug between doses. | NA | NA | NA | NA | NA | Benzene Derivatives | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12260 | Th1306 | AVN-944 | >Th1306_AVN-944 MWESKFVKEGLTFDDVLLVPAKSDVLPREVSVKTVLSESLQLNIPLISAGMDTVTEADMAIAMARQGGLGIIHKNMSIEQQAEQVDKVKRSESGVISDPFFLTPEHQVYDAEHLMGKYRISGVPVVNNLDERKLVGIITNRDMRFIQDYSIKISDVMTKEQLITAPVGTTLDEAEKILQKYKIEKLPLVDNNGVLQGLITIKDIEKVIEFPNSAKDKQGRLLVGAAVGVTADAMTRIDALVKASVDAIVLDTAHGHSQGVIDKVKEVRAKYPSLNIIAGNVATAEATGALIEAGANVVKVGIGPGSICTTRVVAGVGVPQLTAVYDCATEARKHGIPVIADGGIKYSGDMVKALAAGAHVVMLGSMFAGVAESPGETEIYQGRQFKVYRGMGSVGAMEKGSKDRYFQEGNKKLVPEGIEGRVPYKGPLADTVHQLVGGLRAGMGYCGAQDLEFLRENAQFVRMSGAGLLESHPHHVQITKEAPTTHYNVLYINRRRFYISVYFFLIMLE | NA | NA | NA | NA | NA | NA | AVN944 is a biotech drug that demonstrated a statistically meaningful impact on IMPDH and other proteins that are critical to activities in cancer cells, including nucleotide biosynthesis, energy and metabolism, DNA replication, apoptosis and cell cycle control. AVN944 has been associated with cancer cell death in clinical trials. It is being investigated for the treatment of patients with advanced hematologic malignancies. | Investigated for use/treatment in cancer/tumors (unspecified), leukemia (unspecified), lymphoma (unspecified), multiple myeloma, and pancreatic cancer. | IMPDH is highly upregulated in most hematological cancers and in many solid tumors. AVN944 is a biotech drug that demonstrated a statistically meaningful impact in inhibiting IMPDH and other proteins that are critical to activities in cancer cells, including nucleotide biosynthesis, energy and metabolism, DNA replication, apoptosis and cell cycle control. AVN944 has been associated with cancer cell death in clinical trials. It is being investigated for the treatment of patients with advanced hematologic malignancies. | AVN944 inhibits IMPDH and appears to induce apoptosis. Specifically, it was found that the gene HspA1A, a marker of stress response found to correlate with depleted GTP pools in cancer cell lines, is induced within hours upon the first treatment of the drug in patients, even at the trial's lowest doses. Following continued dosing of AVN944, this marker of disease cell stress was elevated even in the absence of circulating levels of the drug between doses. | NA | NA | NA | NA | NA | IMP Dehydrogenase, antagonists & inhibitors | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12311 | Th1312 | Cantuzumab ravtansine | >Th1312_Cantuzumab_ravtansine XVQLVQSGAEVKKPGETVKISCKASDYTFTYYGMNWVKQAPGQGLKWMGWIDTTTGEPTYAQKFQGRIAFSLETSASTAYLQIKSLKSEDTATYFCARRGPYNWYFDVWGQGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | C6570H10130N1726O2018S44(C42H59ClN3O11S2)n | NA | NA | NA | NA | 0 | Investigated for use/treatment in gastric cancer. | NA | NA | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12312 | Th1312 | Cantuzumab ravtansine | >Th1312_Cantuzumab_ravtansine XVQLVQSGAEVKKPGETVKISCKASDYTFTYYGMNWVKQAPGQGLKWMGWIDTTTGEPTYAQKFQGRIAFSLETSASTAYLQIKSLKSEDTATYFCARRGPYNWYFDVWGQGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | C6570H10130N1726O2018S44(C42H59ClN3O11S2)n | NA | NA | NA | NA | 0 | Investigated for use/treatment in gastric cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12313 | Th1312 | Cantuzumab ravtansine | >Th1312_Cantuzumab_ravtansine XVQLVQSGAEVKKPGETVKISCKASDYTFTYYGMNWVKQAPGQGLKWMGWIDTTTGEPTYAQKFQGRIAFSLETSASTAYLQIKSLKSEDTATYFCARRGPYNWYFDVWGQGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | C6570H10130N1726O2018S44(C42H59ClN3O11S2)n | NA | NA | NA | NA | 0 | Investigated for use/treatment in gastric cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12314 | Th1312 | Cantuzumab ravtansine | >Th1312_Cantuzumab_ravtansine XVQLVQSGAEVKKPGETVKISCKASDYTFTYYGMNWVKQAPGQGLKWMGWIDTTTGEPTYAQKFQGRIAFSLETSASTAYLQIKSLKSEDTATYFCARRGPYNWYFDVWGQGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | C6570H10130N1726O2018S44(C42H59ClN3O11S2)n | NA | NA | NA | NA | 0 | Investigated for use/treatment in gastric cancer. | NA | NA | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12315 | Th1312 | Cantuzumab ravtansine | >Th1312_Cantuzumab_ravtansine XVQLVQSGAEVKKPGETVKISCKASDYTFTYYGMNWVKQAPGQGLKWMGWIDTTTGEPTYAQKFQGRIAFSLETSASTAYLQIKSLKSEDTATYFCARRGPYNWYFDVWGQGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | C6570H10130N1726O2018S44(C42H59ClN3O11S2)n | NA | NA | NA | NA | 0 | Investigated for use/treatment in gastric cancer. | NA | NA | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12316 | Th1312 | Cantuzumab ravtansine | >Th1312_Cantuzumab_ravtansine XVQLVQSGAEVKKPGETVKISCKASDYTFTYYGMNWVKQAPGQGLKWMGWIDTTTGEPTYAQKFQGRIAFSLETSASTAYLQIKSLKSEDTATYFCARRGPYNWYFDVWGQGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | C6570H10130N1726O2018S44(C42H59ClN3O11S2)n | NA | NA | NA | NA | 0 | Investigated for use/treatment in gastric cancer. | NA | NA | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12317 | Th1312 | Cantuzumab ravtansine | >Th1312_Cantuzumab_ravtansine XVQLVQSGAEVKKPGETVKISCKASDYTFTYYGMNWVKQAPGQGLKWMGWIDTTTGEPTYAQKFQGRIAFSLETSASTAYLQIKSLKSEDTATYFCARRGPYNWYFDVWGQGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | C6570H10130N1726O2018S44(C42H59ClN3O11S2)n | NA | NA | NA | NA | 0 | Investigated for use/treatment in gastric cancer. | NA | NA | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12318 | Th1313 | Farletuzumab | >Th1313_Farletuzumab EVQLVESGGGVVQPGRSLRLSCSASGFTFSGYGLSWVRQAPGKGLEWVAMISSGGSYTYYADSVKGRFAISRDNAKNTLFLQMDSLRPEDTGVYFCARHGDDPAWFAYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Farletuzumab (MORAb-003) is a fully humanized monoclonal antibody against the folate receptor alpha, for the potential treatment of epithelial ovarian cancer. | Investigated for use/treatment in ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Folate receptor alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12319 | Th1313 | Farletuzumab | >Th1313_Farletuzumab EVQLVESGGGVVQPGRSLRLSCSASGFTFSGYGLSWVRQAPGKGLEWVAMISSGGSYTYYADSVKGRFAISRDNAKNTLFLQMDSLRPEDTGVYFCARHGDDPAWFAYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Farletuzumab (MORAb-003) is a fully humanized monoclonal antibody against the folate receptor alpha, for the potential treatment of epithelial ovarian cancer. | Investigated for use/treatment in ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Folate receptor alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12320 | Th1313 | Farletuzumab | >Th1313_Farletuzumab EVQLVESGGGVVQPGRSLRLSCSASGFTFSGYGLSWVRQAPGKGLEWVAMISSGGSYTYYADSVKGRFAISRDNAKNTLFLQMDSLRPEDTGVYFCARHGDDPAWFAYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Farletuzumab (MORAb-003) is a fully humanized monoclonal antibody against the folate receptor alpha, for the potential treatment of epithelial ovarian cancer. | Investigated for use/treatment in ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Folate receptor alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12321 | Th1313 | Farletuzumab | >Th1313_Farletuzumab EVQLVESGGGVVQPGRSLRLSCSASGFTFSGYGLSWVRQAPGKGLEWVAMISSGGSYTYYADSVKGRFAISRDNAKNTLFLQMDSLRPEDTGVYFCARHGDDPAWFAYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Farletuzumab (MORAb-003) is a fully humanized monoclonal antibody against the folate receptor alpha, for the potential treatment of epithelial ovarian cancer. | Investigated for use/treatment in ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Folate receptor alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12322 | Th1313 | Farletuzumab | >Th1313_Farletuzumab EVQLVESGGGVVQPGRSLRLSCSASGFTFSGYGLSWVRQAPGKGLEWVAMISSGGSYTYYADSVKGRFAISRDNAKNTLFLQMDSLRPEDTGVYFCARHGDDPAWFAYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Farletuzumab (MORAb-003) is a fully humanized monoclonal antibody against the folate receptor alpha, for the potential treatment of epithelial ovarian cancer. | Investigated for use/treatment in ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | Folate receptor alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12323 | Th1313 | Farletuzumab | >Th1313_Farletuzumab EVQLVESGGGVVQPGRSLRLSCSASGFTFSGYGLSWVRQAPGKGLEWVAMISSGGSYTYYADSVKGRFAISRDNAKNTLFLQMDSLRPEDTGVYFCARHGDDPAWFAYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Farletuzumab (MORAb-003) is a fully humanized monoclonal antibody against the folate receptor alpha, for the potential treatment of epithelial ovarian cancer. | Investigated for use/treatment in ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | Folate receptor alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12324 | Th1313 | Farletuzumab | >Th1313_Farletuzumab EVQLVESGGGVVQPGRSLRLSCSASGFTFSGYGLSWVRQAPGKGLEWVAMISSGGSYTYYADSVKGRFAISRDNAKNTLFLQMDSLRPEDTGVYFCARHGDDPAWFAYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Farletuzumab (MORAb-003) is a fully humanized monoclonal antibody against the folate receptor alpha, for the potential treatment of epithelial ovarian cancer. | Investigated for use/treatment in ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | Folate receptor alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12325 | Th1313 | Farletuzumab | >Th1313_Farletuzumab EVQLVESGGGVVQPGRSLRLSCSASGFTFSGYGLSWVRQAPGKGLEWVAMISSGGSYTYYADSVKGRFAISRDNAKNTLFLQMDSLRPEDTGVYFCARHGDDPAWFAYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Farletuzumab (MORAb-003) is a fully humanized monoclonal antibody against the folate receptor alpha, for the potential treatment of epithelial ovarian cancer. | Investigated for use/treatment in ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | Folate receptor alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12326 | Th1313 | Farletuzumab | >Th1313_Farletuzumab EVQLVESGGGVVQPGRSLRLSCSASGFTFSGYGLSWVRQAPGKGLEWVAMISSGGSYTYYADSVKGRFAISRDNAKNTLFLQMDSLRPEDTGVYFCARHGDDPAWFAYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Farletuzumab (MORAb-003) is a fully humanized monoclonal antibody against the folate receptor alpha, for the potential treatment of epithelial ovarian cancer. | Investigated for use/treatment in ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | Folate receptor alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12327 | Th1313 | Farletuzumab | >Th1313_Farletuzumab EVQLVESGGGVVQPGRSLRLSCSASGFTFSGYGLSWVRQAPGKGLEWVAMISSGGSYTYYADSVKGRFAISRDNAKNTLFLQMDSLRPEDTGVYFCARHGDDPAWFAYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Farletuzumab (MORAb-003) is a fully humanized monoclonal antibody against the folate receptor alpha, for the potential treatment of epithelial ovarian cancer. | Investigated for use/treatment in ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | Folate receptor alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12328 | Th1313 | Farletuzumab | >Th1313_Farletuzumab EVQLVESGGGVVQPGRSLRLSCSASGFTFSGYGLSWVRQAPGKGLEWVAMISSGGSYTYYADSVKGRFAISRDNAKNTLFLQMDSLRPEDTGVYFCARHGDDPAWFAYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Farletuzumab (MORAb-003) is a fully humanized monoclonal antibody against the folate receptor alpha, for the potential treatment of epithelial ovarian cancer. | Investigated for use/treatment in ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | Folate receptor alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12336 | Th1315 | IRX-2 | >Th1315_IRX-2 MSYPQGYLYQAPGSLALYSCPAYGASALAAPRSEELARSASGSAFSPYPGSAAFTAQAATGFGSPLQYSADAAAAAAGFPSYMGAPYDAHTTGMTGAISYHPYGSAAYPYQLNDPAYRKNATRDATATLKAWLNEHRKNPYPTKGEKIMLAIITKMTLTQVSTWFANARRRLKKENKMTWAPRNKSEDEDEDEGDATRSKDESPDKAQEGTETSAEDEGISLHVDSLTDHSCSAESDGEKLPCRAGDPLCESGSECKDKYDDLEDDEDDDEEGERGLAPPKPVTSSPLTGLEAPLLSPPPEAAPRGGRKTPQGSRTSPGAPPPASKPKLWSLAEIATSDLKQPSLGPGCGPPGLPAAAAPASTGAPPGGSPYPASPLLGRPLYYTSPFYGNYTNYGNLNAALQGQGLLRYNSAAAAPGEALHTAPKAASDAGKAGAHPLESHYRSPGGGYEPKKDASEGCTVVGGGVQPYL | NA | NA | NA | NA | NA | NA | IRX-2 contains multiple human cytokines that are being investigated to promote or enhance an anti-cancer immune response. | Investigated for use/treatment in cancer/tumors (unspecified), head and neck cancer, and solid tumors. | NA | NA | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12337 | Th1315 | IRX-2 | >Th1315_IRX-2 MSYPQGYLYQAPGSLALYSCPAYGASALAAPRSEELARSASGSAFSPYPGSAAFTAQAATGFGSPLQYSADAAAAAAGFPSYMGAPYDAHTTGMTGAISYHPYGSAAYPYQLNDPAYRKNATRDATATLKAWLNEHRKNPYPTKGEKIMLAIITKMTLTQVSTWFANARRRLKKENKMTWAPRNKSEDEDEDEGDATRSKDESPDKAQEGTETSAEDEGISLHVDSLTDHSCSAESDGEKLPCRAGDPLCESGSECKDKYDDLEDDEDDDEEGERGLAPPKPVTSSPLTGLEAPLLSPPPEAAPRGGRKTPQGSRTSPGAPPPASKPKLWSLAEIATSDLKQPSLGPGCGPPGLPAAAAPASTGAPPGGSPYPASPLLGRPLYYTSPFYGNYTNYGNLNAALQGQGLLRYNSAAAAPGEALHTAPKAASDAGKAGAHPLESHYRSPGGGYEPKKDASEGCTVVGGGVQPYL | NA | NA | NA | NA | NA | NA | IRX-2 contains multiple human cytokines that are being investigated to promote or enhance an anti-cancer immune response. | Investigated for use/treatment in cancer/tumors (unspecified), head and neck cancer, and solid tumors. | NA | NA | NA | NA | NA | NA | NA | Biological Factors | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12338 | Th1315 | IRX-2 | >Th1315_IRX-2 MSYPQGYLYQAPGSLALYSCPAYGASALAAPRSEELARSASGSAFSPYPGSAAFTAQAATGFGSPLQYSADAAAAAAGFPSYMGAPYDAHTTGMTGAISYHPYGSAAYPYQLNDPAYRKNATRDATATLKAWLNEHRKNPYPTKGEKIMLAIITKMTLTQVSTWFANARRRLKKENKMTWAPRNKSEDEDEDEGDATRSKDESPDKAQEGTETSAEDEGISLHVDSLTDHSCSAESDGEKLPCRAGDPLCESGSECKDKYDDLEDDEDDDEEGERGLAPPKPVTSSPLTGLEAPLLSPPPEAAPRGGRKTPQGSRTSPGAPPPASKPKLWSLAEIATSDLKQPSLGPGCGPPGLPAAAAPASTGAPPGGSPYPASPLLGRPLYYTSPFYGNYTNYGNLNAALQGQGLLRYNSAAAAPGEALHTAPKAASDAGKAGAHPLESHYRSPGGGYEPKKDASEGCTVVGGGVQPYL | NA | NA | NA | NA | NA | NA | IRX-2 contains multiple human cytokines that are being investigated to promote or enhance an anti-cancer immune response. | Investigated for use/treatment in cancer/tumors (unspecified), head and neck cancer, and solid tumors. | NA | NA | NA | NA | NA | NA | NA | Intercellular Signaling Peptides and Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12339 | Th1315 | IRX-2 | >Th1315_IRX-2 MSYPQGYLYQAPGSLALYSCPAYGASALAAPRSEELARSASGSAFSPYPGSAAFTAQAATGFGSPLQYSADAAAAAAGFPSYMGAPYDAHTTGMTGAISYHPYGSAAYPYQLNDPAYRKNATRDATATLKAWLNEHRKNPYPTKGEKIMLAIITKMTLTQVSTWFANARRRLKKENKMTWAPRNKSEDEDEDEGDATRSKDESPDKAQEGTETSAEDEGISLHVDSLTDHSCSAESDGEKLPCRAGDPLCESGSECKDKYDDLEDDEDDDEEGERGLAPPKPVTSSPLTGLEAPLLSPPPEAAPRGGRKTPQGSRTSPGAPPPASKPKLWSLAEIATSDLKQPSLGPGCGPPGLPAAAAPASTGAPPGGSPYPASPLLGRPLYYTSPFYGNYTNYGNLNAALQGQGLLRYNSAAAAPGEALHTAPKAASDAGKAGAHPLESHYRSPGGGYEPKKDASEGCTVVGGGVQPYL | NA | NA | NA | NA | NA | NA | IRX-2 contains multiple human cytokines that are being investigated to promote or enhance an anti-cancer immune response. | Investigated for use/treatment in cancer/tumors (unspecified), head and neck cancer, and solid tumors. | NA | NA | NA | NA | NA | NA | NA | Peptides | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12340 | Th1315 | IRX-2 | >Th1315_IRX-2 MSYPQGYLYQAPGSLALYSCPAYGASALAAPRSEELARSASGSAFSPYPGSAAFTAQAATGFGSPLQYSADAAAAAAGFPSYMGAPYDAHTTGMTGAISYHPYGSAAYPYQLNDPAYRKNATRDATATLKAWLNEHRKNPYPTKGEKIMLAIITKMTLTQVSTWFANARRRLKKENKMTWAPRNKSEDEDEDEGDATRSKDESPDKAQEGTETSAEDEGISLHVDSLTDHSCSAESDGEKLPCRAGDPLCESGSECKDKYDDLEDDEDDDEEGERGLAPPKPVTSSPLTGLEAPLLSPPPEAAPRGGRKTPQGSRTSPGAPPPASKPKLWSLAEIATSDLKQPSLGPGCGPPGLPAAAAPASTGAPPGGSPYPASPLLGRPLYYTSPFYGNYTNYGNLNAALQGQGLLRYNSAAAAPGEALHTAPKAASDAGKAGAHPLESHYRSPGGGYEPKKDASEGCTVVGGGVQPYL | NA | NA | NA | NA | NA | NA | IRX-2 contains multiple human cytokines that are being investigated to promote or enhance an anti-cancer immune response. | Investigated for use/treatment in cancer/tumors (unspecified), head and neck cancer, and solid tumors. | NA | NA | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12378 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Amides | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | Kadcyla | Hoffmann La Roche | Hoffmann La Roche | Intravenous | 160 mg / vial | None. | fatigue, tiredness, nausea, musculoskeletal pain, headache, constipation, low platelet count, liver problems, low levels of red blood cells, nerve problems, and low levels of potassium in the blood. | Kadcyla is a cancer medicine that interferes with the growth and spread of cancer cells in the body. Kadcyla is used to treat HER2-positive breast cancer. Kadcyla is used both for early breast cancer and for breast cancer that has spread to other parts of the body (metastatic). Kadcyla is usually given... | Kadcyla is a prescription medicine used to treat the symptoms of Breast Cancer. Kadcyla may be used alone or with other medications. | NA | KADCYLA (ado-trastuzumab emtansine) is a HER2-targeted antibody-drug conjugate (ADC) which contains the humanized anti-HER2 IgG1, trastuzumab, covalently linked to the microtubule inhibitory drug DM1 (a maytansine derivative) via the stable thioether linker MCC (4-[N-maleimidomethyl] cyclohexane-1-carboxylate). Emtansine refers to the MCC-DM1 complex. | Link | Link | NA |
| 12379 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | Kadcyla | Hoffmann La Roche | Hoffmann La Roche | Intravenous | 100 mg / vial | None. | fatigue, tiredness, nausea, musculoskeletal pain, headache, constipation, low platelet count, liver problems, low levels of red blood cells, nerve problems, and low levels of potassium in the blood. | Kadcyla is a cancer medicine that interferes with the growth and spread of cancer cells in the body. Kadcyla is used to treat HER2-positive breast cancer. Kadcyla is used both for early breast cancer and for breast cancer that has spread to other parts of the body (metastatic). Kadcyla is usually given... | Kadcyla is a prescription medicine used to treat the symptoms of Breast Cancer. Kadcyla may be used alone or with other medications. | NA | KADCYLA (ado-trastuzumab emtansine) is a HER2-targeted antibody-drug conjugate (ADC) which contains the humanized anti-HER2 IgG1, trastuzumab, covalently linked to the microtubule inhibitory drug DM1 (a maytansine derivative) via the stable thioether linker MCC (4-[N-maleimidomethyl] cyclohexane-1-carboxylate). Emtansine refers to the MCC-DM1 complex. | Link | Link | NA |
| 12380 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Antibodies | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | Kadcyla | Genentech, Inc. | Genentech, Inc. | Intravenous | 20 mg/1mL | None. | fatigue, tiredness, nausea, musculoskeletal pain, headache, constipation, low platelet count, liver problems, low levels of red blood cells, nerve problems, and low levels of potassium in the blood. | Kadcyla is a cancer medicine that interferes with the growth and spread of cancer cells in the body. Kadcyla is used to treat HER2-positive breast cancer. Kadcyla is used both for early breast cancer and for breast cancer that has spread to other parts of the body (metastatic). Kadcyla is usually given... | Kadcyla is a prescription medicine used to treat the symptoms of Breast Cancer. Kadcyla may be used alone or with other medications. | NA | KADCYLA (ado-trastuzumab emtansine) is a HER2-targeted antibody-drug conjugate (ADC) which contains the humanized anti-HER2 IgG1, trastuzumab, covalently linked to the microtubule inhibitory drug DM1 (a maytansine derivative) via the stable thioether linker MCC (4-[N-maleimidomethyl] cyclohexane-1-carboxylate). Emtansine refers to the MCC-DM1 complex. | Link | Link | NA |
| 12381 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Antibodies, Monoclonal | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | Kadcyla | Roche Registration Gmb H | Roche Registration Gmb H | Intravenous | 100 mg | None. | fatigue, tiredness, nausea, musculoskeletal pain, headache, constipation, low platelet count, liver problems, low levels of red blood cells, nerve problems, and low levels of potassium in the blood. | Kadcyla is a cancer medicine that interferes with the growth and spread of cancer cells in the body. Kadcyla is used to treat HER2-positive breast cancer. Kadcyla is used both for early breast cancer and for breast cancer that has spread to other parts of the body (metastatic). Kadcyla is usually given... | Kadcyla is a prescription medicine used to treat the symptoms of Breast Cancer. Kadcyla may be used alone or with other medications. | NA | KADCYLA (ado-trastuzumab emtansine) is a HER2-targeted antibody-drug conjugate (ADC) which contains the humanized anti-HER2 IgG1, trastuzumab, covalently linked to the microtubule inhibitory drug DM1 (a maytansine derivative) via the stable thioether linker MCC (4-[N-maleimidomethyl] cyclohexane-1-carboxylate). Emtansine refers to the MCC-DM1 complex. | Link | Link | NA |
| 12382 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | Kadcyla | Roche Registration Gmb H | Roche Registration Gmb H | Intravenous | 160 mg | None. | fatigue, tiredness, nausea, musculoskeletal pain, headache, constipation, low platelet count, liver problems, low levels of red blood cells, nerve problems, and low levels of potassium in the blood. | Kadcyla is a cancer medicine that interferes with the growth and spread of cancer cells in the body. Kadcyla is used to treat HER2-positive breast cancer. Kadcyla is used both for early breast cancer and for breast cancer that has spread to other parts of the body (metastatic). Kadcyla is usually given... | Kadcyla is a prescription medicine used to treat the symptoms of Breast Cancer. Kadcyla may be used alone or with other medications. | NA | KADCYLA (ado-trastuzumab emtansine) is a HER2-targeted antibody-drug conjugate (ADC) which contains the humanized anti-HER2 IgG1, trastuzumab, covalently linked to the microtubule inhibitory drug DM1 (a maytansine derivative) via the stable thioether linker MCC (4-[N-maleimidomethyl] cyclohexane-1-carboxylate). Emtansine refers to the MCC-DM1 complex. | Link | Link | NA |
| 12383 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Antimitotic Agents | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12384 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Antineoplastic Agents | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12385 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Antineoplastic Agents, Immunological | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12386 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12387 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Blood Proteins | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12388 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Cancer immunotherapy | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12389 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Cytochrome P-450 CYP3A Substrates | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12390 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Cytochrome P-450 CYP3A4 Substrates | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12391 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Cytochrome P-450 CYP3A4 Substrates with a Narrow Therapeutic Index | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12392 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Cytochrome P-450 CYP3A5 Substrates | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12393 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Cytochrome P-450 CYP3A5 Substrates with a Narrow Therapeutic Index | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12394 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Cytochrome P-450 Substrates | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12395 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Globulins | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12396 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Hepatotoxic Agents | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12397 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | HER2 Receptor Antagonist | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12398 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Immunoglobulins | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12399 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Immunoproteins | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12400 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Immunosuppressive Agents | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12401 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Immunotherapy | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12402 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Lactams | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12403 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Lactams, Macrocyclic | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12404 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Lactones | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12405 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Microtubule Inhibitors | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12406 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Mitosis Modulators | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12407 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Myelosuppressive Agents | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12408 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Narrow Therapeutic Index Drugs | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12409 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | P-glycoprotein substrates | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12410 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | P-glycoprotein substrates with a Narrow Therapeutic Index | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12411 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Polyketides | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12412 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Proteins | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12413 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Serum Globulins | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12414 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Tubulin Modulators | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12503 | Th1329 | CT-011 | >Th1329_CT-011 MHCLPVLVILLLLIASTPSVDARPKTKDDVPLASFHGADNANRILRTLWNLRGCCEDKTCCFIG | NA | NA | NA | NA | NA | NA | CT-011 is a humanized monoclonal antibody directed against a B7 family-associated protein, in patients with advanced haematological malignancies. It is directed against human PD-1 (programmed cell death 1; PDCD1), with immunomodulating and antitumor activities. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | CT-011 blocks interaction between the receptor PD-1 with its ligands, PD-1 ligand 1 (PD-1L1) and PD-1 ligand 2 (PD-1L2), resulting in the attenuation of apoptotic processes in lymphocytes, primarily effector/memory T cells, and the augmentation of the anti-tumor activities of NK cells. PD-1 is an inhibitory receptor belonging to the B7-receptor family that is expressed on lymphocytes and myeloid cells; its ligands, PD-1L1 and PD-1L2, are expressed not only by hematopoietic cells but also by cells in non-lymphoid tissues. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12504 | Th1329 | CT-011 | >Th1329_CT-011 MHCLPVLVILLLLIASTPSVDARPKTKDDVPLASFHGADNANRILRTLWNLRGCCEDKTCCFIG | NA | NA | NA | NA | NA | NA | CT-011 is a humanized monoclonal antibody directed against a B7 family-associated protein, in patients with advanced haematological malignancies. It is directed against human PD-1 (programmed cell death 1; PDCD1), with immunomodulating and antitumor activities. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | CT-011 blocks interaction between the receptor PD-1 with its ligands, PD-1 ligand 1 (PD-1L1) and PD-1 ligand 2 (PD-1L2), resulting in the attenuation of apoptotic processes in lymphocytes, primarily effector/memory T cells, and the augmentation of the anti-tumor activities of NK cells. PD-1 is an inhibitory receptor belonging to the B7-receptor family that is expressed on lymphocytes and myeloid cells; its ligands, PD-1L1 and PD-1L2, are expressed not only by hematopoietic cells but also by cells in non-lymphoid tissues. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12505 | Th1329 | CT-011 | >Th1329_CT-011 MHCLPVLVILLLLIASTPSVDARPKTKDDVPLASFHGADNANRILRTLWNLRGCCEDKTCCFIG | NA | NA | NA | NA | NA | NA | CT-011 is a humanized monoclonal antibody directed against a B7 family-associated protein, in patients with advanced haematological malignancies. It is directed against human PD-1 (programmed cell death 1; PDCD1), with immunomodulating and antitumor activities. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | CT-011 blocks interaction between the receptor PD-1 with its ligands, PD-1 ligand 1 (PD-1L1) and PD-1 ligand 2 (PD-1L2), resulting in the attenuation of apoptotic processes in lymphocytes, primarily effector/memory T cells, and the augmentation of the anti-tumor activities of NK cells. PD-1 is an inhibitory receptor belonging to the B7-receptor family that is expressed on lymphocytes and myeloid cells; its ligands, PD-1L1 and PD-1L2, are expressed not only by hematopoietic cells but also by cells in non-lymphoid tissues. | NA | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12506 | Th1329 | CT-011 | >Th1329_CT-011 MHCLPVLVILLLLIASTPSVDARPKTKDDVPLASFHGADNANRILRTLWNLRGCCEDKTCCFIG | NA | NA | NA | NA | NA | NA | CT-011 is a humanized monoclonal antibody directed against a B7 family-associated protein, in patients with advanced haematological malignancies. It is directed against human PD-1 (programmed cell death 1; PDCD1), with immunomodulating and antitumor activities. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | CT-011 blocks interaction between the receptor PD-1 with its ligands, PD-1 ligand 1 (PD-1L1) and PD-1 ligand 2 (PD-1L2), resulting in the attenuation of apoptotic processes in lymphocytes, primarily effector/memory T cells, and the augmentation of the anti-tumor activities of NK cells. PD-1 is an inhibitory receptor belonging to the B7-receptor family that is expressed on lymphocytes and myeloid cells; its ligands, PD-1L1 and PD-1L2, are expressed not only by hematopoietic cells but also by cells in non-lymphoid tissues. | NA | NA | NA | NA | NA | Antineoplastic Agents, Immunological | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12507 | Th1329 | CT-011 | >Th1329_CT-011 MHCLPVLVILLLLIASTPSVDARPKTKDDVPLASFHGADNANRILRTLWNLRGCCEDKTCCFIG | NA | NA | NA | NA | NA | NA | CT-011 is a humanized monoclonal antibody directed against a B7 family-associated protein, in patients with advanced haematological malignancies. It is directed against human PD-1 (programmed cell death 1; PDCD1), with immunomodulating and antitumor activities. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | CT-011 blocks interaction between the receptor PD-1 with its ligands, PD-1 ligand 1 (PD-1L1) and PD-1 ligand 2 (PD-1L2), resulting in the attenuation of apoptotic processes in lymphocytes, primarily effector/memory T cells, and the augmentation of the anti-tumor activities of NK cells. PD-1 is an inhibitory receptor belonging to the B7-receptor family that is expressed on lymphocytes and myeloid cells; its ligands, PD-1L1 and PD-1L2, are expressed not only by hematopoietic cells but also by cells in non-lymphoid tissues. | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12508 | Th1329 | CT-011 | >Th1329_CT-011 MHCLPVLVILLLLIASTPSVDARPKTKDDVPLASFHGADNANRILRTLWNLRGCCEDKTCCFIG | NA | NA | NA | NA | NA | NA | CT-011 is a humanized monoclonal antibody directed against a B7 family-associated protein, in patients with advanced haematological malignancies. It is directed against human PD-1 (programmed cell death 1; PDCD1), with immunomodulating and antitumor activities. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | CT-011 blocks interaction between the receptor PD-1 with its ligands, PD-1 ligand 1 (PD-1L1) and PD-1 ligand 2 (PD-1L2), resulting in the attenuation of apoptotic processes in lymphocytes, primarily effector/memory T cells, and the augmentation of the anti-tumor activities of NK cells. PD-1 is an inhibitory receptor belonging to the B7-receptor family that is expressed on lymphocytes and myeloid cells; its ligands, PD-1L1 and PD-1L2, are expressed not only by hematopoietic cells but also by cells in non-lymphoid tissues. | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12509 | Th1329 | CT-011 | >Th1329_CT-011 MHCLPVLVILLLLIASTPSVDARPKTKDDVPLASFHGADNANRILRTLWNLRGCCEDKTCCFIG | NA | NA | NA | NA | NA | NA | CT-011 is a humanized monoclonal antibody directed against a B7 family-associated protein, in patients with advanced haematological malignancies. It is directed against human PD-1 (programmed cell death 1; PDCD1), with immunomodulating and antitumor activities. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | CT-011 blocks interaction between the receptor PD-1 with its ligands, PD-1 ligand 1 (PD-1L1) and PD-1 ligand 2 (PD-1L2), resulting in the attenuation of apoptotic processes in lymphocytes, primarily effector/memory T cells, and the augmentation of the anti-tumor activities of NK cells. PD-1 is an inhibitory receptor belonging to the B7-receptor family that is expressed on lymphocytes and myeloid cells; its ligands, PD-1L1 and PD-1L2, are expressed not only by hematopoietic cells but also by cells in non-lymphoid tissues. | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12510 | Th1329 | CT-011 | >Th1329_CT-011 MHCLPVLVILLLLIASTPSVDARPKTKDDVPLASFHGADNANRILRTLWNLRGCCEDKTCCFIG | NA | NA | NA | NA | NA | NA | CT-011 is a humanized monoclonal antibody directed against a B7 family-associated protein, in patients with advanced haematological malignancies. It is directed against human PD-1 (programmed cell death 1; PDCD1), with immunomodulating and antitumor activities. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | CT-011 blocks interaction between the receptor PD-1 with its ligands, PD-1 ligand 1 (PD-1L1) and PD-1 ligand 2 (PD-1L2), resulting in the attenuation of apoptotic processes in lymphocytes, primarily effector/memory T cells, and the augmentation of the anti-tumor activities of NK cells. PD-1 is an inhibitory receptor belonging to the B7-receptor family that is expressed on lymphocytes and myeloid cells; its ligands, PD-1L1 and PD-1L2, are expressed not only by hematopoietic cells but also by cells in non-lymphoid tissues. | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12511 | Th1329 | CT-011 | >Th1329_CT-011 MHCLPVLVILLLLIASTPSVDARPKTKDDVPLASFHGADNANRILRTLWNLRGCCEDKTCCFIG | NA | NA | NA | NA | NA | NA | CT-011 is a humanized monoclonal antibody directed against a B7 family-associated protein, in patients with advanced haematological malignancies. It is directed against human PD-1 (programmed cell death 1; PDCD1), with immunomodulating and antitumor activities. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | CT-011 blocks interaction between the receptor PD-1 with its ligands, PD-1 ligand 1 (PD-1L1) and PD-1 ligand 2 (PD-1L2), resulting in the attenuation of apoptotic processes in lymphocytes, primarily effector/memory T cells, and the augmentation of the anti-tumor activities of NK cells. PD-1 is an inhibitory receptor belonging to the B7-receptor family that is expressed on lymphocytes and myeloid cells; its ligands, PD-1L1 and PD-1L2, are expressed not only by hematopoietic cells but also by cells in non-lymphoid tissues. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12512 | Th1329 | CT-011 | >Th1329_CT-011 MHCLPVLVILLLLIASTPSVDARPKTKDDVPLASFHGADNANRILRTLWNLRGCCEDKTCCFIG | NA | NA | NA | NA | NA | NA | CT-011 is a humanized monoclonal antibody directed against a B7 family-associated protein, in patients with advanced haematological malignancies. It is directed against human PD-1 (programmed cell death 1; PDCD1), with immunomodulating and antitumor activities. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | CT-011 blocks interaction between the receptor PD-1 with its ligands, PD-1 ligand 1 (PD-1L1) and PD-1 ligand 2 (PD-1L2), resulting in the attenuation of apoptotic processes in lymphocytes, primarily effector/memory T cells, and the augmentation of the anti-tumor activities of NK cells. PD-1 is an inhibitory receptor belonging to the B7-receptor family that is expressed on lymphocytes and myeloid cells; its ligands, PD-1L1 and PD-1L2, are expressed not only by hematopoietic cells but also by cells in non-lymphoid tissues. | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12513 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12514 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Anti-HIV Agents | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12515 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Anti-Infective Agents | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12516 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Anti-Retroviral Agents | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12517 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Antibodies | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12518 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Antibodies, Monoclonal | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12519 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12520 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Antibodies, Viral | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12521 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Antiviral Agents | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12522 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Blood Proteins | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12523 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Deltaretrovirus Antibodies | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12524 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Experimental Unapproved Treatments for COVID-19 | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12525 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Globulins | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12526 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | HIV Fusion Inhibitors | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12527 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Immunoglobulins | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12528 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Immunoproteins | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12529 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Proteins | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12530 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Receptors, CCR5 | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12531 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Serum Globulins | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12532 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Viral Fusion Protein Inhibitors | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12592 | Th1336 | IMC-1C11 | NA | NA | NA | NA | NA | NA | NA | IMC-1C11 is an anti-angiogenesis agent. It is a chimeric anti-kinase insert domain-containing receptor (KDR) antibody that blocks VEGFR-KDR interaction and inhibits VEGFR-induced endothelial cell proliferation. IMC-1C11 is used for treatment of patients with liver metastases from colorectal carcinoma. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | IMC-1C11 is a chimerized antibody that targets the KDR receptor (also referred to as VEGFr) on vascular endothelial cells by inhibiting binding of the essential ligand, vascular endothelial growth factor (VEGF), to its receptor. KDR is a key receptor associated with tumor angiogenesis. As solid tumors cannot grow efficiently without new blood supply, use of IMC-1C11 results in the inhibition of tumor growth and death of tumor cells by apoptosis. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Vascular endothelial growth factor receptor 1,Vascular endothelial growth factor receptor 2,Vascular endothelial growth factor receptor 3 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12593 | Th1336 | IMC-1C11 | NA | NA | NA | NA | NA | NA | NA | IMC-1C11 is an anti-angiogenesis agent. It is a chimeric anti-kinase insert domain-containing receptor (KDR) antibody that blocks VEGFR-KDR interaction and inhibits VEGFR-induced endothelial cell proliferation. IMC-1C11 is used for treatment of patients with liver metastases from colorectal carcinoma. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | IMC-1C11 is a chimerized antibody that targets the KDR receptor (also referred to as VEGFr) on vascular endothelial cells by inhibiting binding of the essential ligand, vascular endothelial growth factor (VEGF), to its receptor. KDR is a key receptor associated with tumor angiogenesis. As solid tumors cannot grow efficiently without new blood supply, use of IMC-1C11 results in the inhibition of tumor growth and death of tumor cells by apoptosis. | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | Vascular endothelial growth factor receptor 1,Vascular endothelial growth factor receptor 2,Vascular endothelial growth factor receptor 3 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12594 | Th1336 | IMC-1C11 | NA | NA | NA | NA | NA | NA | NA | IMC-1C11 is an anti-angiogenesis agent. It is a chimeric anti-kinase insert domain-containing receptor (KDR) antibody that blocks VEGFR-KDR interaction and inhibits VEGFR-induced endothelial cell proliferation. IMC-1C11 is used for treatment of patients with liver metastases from colorectal carcinoma. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | IMC-1C11 is a chimerized antibody that targets the KDR receptor (also referred to as VEGFr) on vascular endothelial cells by inhibiting binding of the essential ligand, vascular endothelial growth factor (VEGF), to its receptor. KDR is a key receptor associated with tumor angiogenesis. As solid tumors cannot grow efficiently without new blood supply, use of IMC-1C11 results in the inhibition of tumor growth and death of tumor cells by apoptosis. | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | Vascular endothelial growth factor receptor 1,Vascular endothelial growth factor receptor 2,Vascular endothelial growth factor receptor 3 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12595 | Th1336 | IMC-1C11 | NA | NA | NA | NA | NA | NA | NA | IMC-1C11 is an anti-angiogenesis agent. It is a chimeric anti-kinase insert domain-containing receptor (KDR) antibody that blocks VEGFR-KDR interaction and inhibits VEGFR-induced endothelial cell proliferation. IMC-1C11 is used for treatment of patients with liver metastases from colorectal carcinoma. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | IMC-1C11 is a chimerized antibody that targets the KDR receptor (also referred to as VEGFr) on vascular endothelial cells by inhibiting binding of the essential ligand, vascular endothelial growth factor (VEGF), to its receptor. KDR is a key receptor associated with tumor angiogenesis. As solid tumors cannot grow efficiently without new blood supply, use of IMC-1C11 results in the inhibition of tumor growth and death of tumor cells by apoptosis. | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | Vascular endothelial growth factor receptor 1,Vascular endothelial growth factor receptor 2,Vascular endothelial growth factor receptor 3 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12596 | Th1336 | IMC-1C11 | NA | NA | NA | NA | NA | NA | NA | IMC-1C11 is an anti-angiogenesis agent. It is a chimeric anti-kinase insert domain-containing receptor (KDR) antibody that blocks VEGFR-KDR interaction and inhibits VEGFR-induced endothelial cell proliferation. IMC-1C11 is used for treatment of patients with liver metastases from colorectal carcinoma. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | IMC-1C11 is a chimerized antibody that targets the KDR receptor (also referred to as VEGFr) on vascular endothelial cells by inhibiting binding of the essential ligand, vascular endothelial growth factor (VEGF), to its receptor. KDR is a key receptor associated with tumor angiogenesis. As solid tumors cannot grow efficiently without new blood supply, use of IMC-1C11 results in the inhibition of tumor growth and death of tumor cells by apoptosis. | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | Vascular endothelial growth factor receptor 1,Vascular endothelial growth factor receptor 2,Vascular endothelial growth factor receptor 3 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12597 | Th1336 | IMC-1C11 | NA | NA | NA | NA | NA | NA | NA | IMC-1C11 is an anti-angiogenesis agent. It is a chimeric anti-kinase insert domain-containing receptor (KDR) antibody that blocks VEGFR-KDR interaction and inhibits VEGFR-induced endothelial cell proliferation. IMC-1C11 is used for treatment of patients with liver metastases from colorectal carcinoma. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | IMC-1C11 is a chimerized antibody that targets the KDR receptor (also referred to as VEGFr) on vascular endothelial cells by inhibiting binding of the essential ligand, vascular endothelial growth factor (VEGF), to its receptor. KDR is a key receptor associated with tumor angiogenesis. As solid tumors cannot grow efficiently without new blood supply, use of IMC-1C11 results in the inhibition of tumor growth and death of tumor cells by apoptosis. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | Vascular endothelial growth factor receptor 1,Vascular endothelial growth factor receptor 2,Vascular endothelial growth factor receptor 3 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12598 | Th1336 | IMC-1C11 | NA | NA | NA | NA | NA | NA | NA | IMC-1C11 is an anti-angiogenesis agent. It is a chimeric anti-kinase insert domain-containing receptor (KDR) antibody that blocks VEGFR-KDR interaction and inhibits VEGFR-induced endothelial cell proliferation. IMC-1C11 is used for treatment of patients with liver metastases from colorectal carcinoma. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | IMC-1C11 is a chimerized antibody that targets the KDR receptor (also referred to as VEGFr) on vascular endothelial cells by inhibiting binding of the essential ligand, vascular endothelial growth factor (VEGF), to its receptor. KDR is a key receptor associated with tumor angiogenesis. As solid tumors cannot grow efficiently without new blood supply, use of IMC-1C11 results in the inhibition of tumor growth and death of tumor cells by apoptosis. | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | Vascular endothelial growth factor receptor 1,Vascular endothelial growth factor receptor 2,Vascular endothelial growth factor receptor 3 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12607 | Th1338 | Nimotuzumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer. | NA | NA | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12608 | Th1338 | Nimotuzumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12609 | Th1338 | Nimotuzumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12610 | Th1338 | Nimotuzumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12611 | Th1338 | Nimotuzumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer. | NA | NA | NA | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12612 | Th1338 | Nimotuzumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer. | NA | NA | NA | NA | NA | NA | NA | Antineoplastic Agents, Immunological | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12613 | Th1338 | Nimotuzumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer. | NA | NA | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12614 | Th1338 | Nimotuzumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer. | NA | NA | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12615 | Th1338 | Nimotuzumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer. | NA | NA | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12616 | Th1338 | Nimotuzumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer. | NA | NA | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12617 | Th1338 | Nimotuzumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer. | NA | NA | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12618 | Th1338 | Nimotuzumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer. | NA | NA | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12800 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12801 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Angiogenesis Inhibitors | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12802 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Angiogenesis Modulating Agents | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12803 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Angiogenic Proteins | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12804 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Angiostatic Proteins | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12805 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12806 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Biological Factors | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12807 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Biopolymers | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12808 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Collagen | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12809 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Collagen Type XVIII | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12810 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Compounds used in a research, industrial, or household setting | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12811 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Extracellular Matrix Proteins | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12812 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Growth Inhibitors | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12813 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Growth Substances | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12814 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Intercellular Signaling Peptides and Proteins | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12815 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Macromolecular Substances | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12816 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Non-Fibrillar Collagens | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12817 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Peptides | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12818 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Polymers | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12819 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12820 | Th1356 | Endostatin | >Th1356_Endostatin QPVLHLVALNTPLSGGMRGIRGADFQCFQQARAVGLSGTFRAFLSSRLQDLYSIVRRADRGSVPIVNLKDEVLSPSWDSLFSGSQGQLQPGARIFSFDGRDVLRHPAWPQKSVWHGSDPSGRRLMESYCETWRTETTGATGQASSLLSGRLLEQKAASCHNSYIVLCIENSF | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. | NA | Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. | NA | NA | NA | NA | NA | Scleroproteins | NA | NA | NA | NA | 72 kDa type IV collagenase,Matrix metalloproteinase-9,Collagenase 3,Focal adhesion kinase 1,E-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | N-methyl-N-phenacylnitrous amide | NA | Link | NA | NA |
| 12831 | Th1358 | Sibrotuzumab | NA | NA | NA | NA | NA | NA | NA | Sibrotuzumab is a humanized monoclonal antibody directed against fibroblast activation protein (FAP). It is used to treat cancer. | Investigated for use/treatment in cancer/tumors (unspecified), colorectal cancer, and lung cancer. | NA | Human FAP is unique in its selective expression by tumor stromal fibroblasts in epithelial carcinomas, but not by epithelial carcinoma cells, normal fibroblasts, or other normal tissues. Therefore, FAP is an attractive target for the study of tumor stromal cell biology and provides valuable insights into the roles of the tumor microenvironment. Sibrotuzumab is a humanized monoclonal antibody designed to attack the cell-surface antigen FAP. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Seprase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12832 | Th1358 | Sibrotuzumab | NA | NA | NA | NA | NA | NA | NA | Sibrotuzumab is a humanized monoclonal antibody directed against fibroblast activation protein (FAP). It is used to treat cancer. | Investigated for use/treatment in cancer/tumors (unspecified), colorectal cancer, and lung cancer. | NA | Human FAP is unique in its selective expression by tumor stromal fibroblasts in epithelial carcinomas, but not by epithelial carcinoma cells, normal fibroblasts, or other normal tissues. Therefore, FAP is an attractive target for the study of tumor stromal cell biology and provides valuable insights into the roles of the tumor microenvironment. Sibrotuzumab is a humanized monoclonal antibody designed to attack the cell-surface antigen FAP. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Seprase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12833 | Th1358 | Sibrotuzumab | NA | NA | NA | NA | NA | NA | NA | Sibrotuzumab is a humanized monoclonal antibody directed against fibroblast activation protein (FAP). It is used to treat cancer. | Investigated for use/treatment in cancer/tumors (unspecified), colorectal cancer, and lung cancer. | NA | Human FAP is unique in its selective expression by tumor stromal fibroblasts in epithelial carcinomas, but not by epithelial carcinoma cells, normal fibroblasts, or other normal tissues. Therefore, FAP is an attractive target for the study of tumor stromal cell biology and provides valuable insights into the roles of the tumor microenvironment. Sibrotuzumab is a humanized monoclonal antibody designed to attack the cell-surface antigen FAP. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Seprase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12834 | Th1358 | Sibrotuzumab | NA | NA | NA | NA | NA | NA | NA | Sibrotuzumab is a humanized monoclonal antibody directed against fibroblast activation protein (FAP). It is used to treat cancer. | Investigated for use/treatment in cancer/tumors (unspecified), colorectal cancer, and lung cancer. | NA | Human FAP is unique in its selective expression by tumor stromal fibroblasts in epithelial carcinomas, but not by epithelial carcinoma cells, normal fibroblasts, or other normal tissues. Therefore, FAP is an attractive target for the study of tumor stromal cell biology and provides valuable insights into the roles of the tumor microenvironment. Sibrotuzumab is a humanized monoclonal antibody designed to attack the cell-surface antigen FAP. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Seprase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12835 | Th1358 | Sibrotuzumab | NA | NA | NA | NA | NA | NA | NA | Sibrotuzumab is a humanized monoclonal antibody directed against fibroblast activation protein (FAP). It is used to treat cancer. | Investigated for use/treatment in cancer/tumors (unspecified), colorectal cancer, and lung cancer. | NA | Human FAP is unique in its selective expression by tumor stromal fibroblasts in epithelial carcinomas, but not by epithelial carcinoma cells, normal fibroblasts, or other normal tissues. Therefore, FAP is an attractive target for the study of tumor stromal cell biology and provides valuable insights into the roles of the tumor microenvironment. Sibrotuzumab is a humanized monoclonal antibody designed to attack the cell-surface antigen FAP. | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | Seprase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12836 | Th1358 | Sibrotuzumab | NA | NA | NA | NA | NA | NA | NA | Sibrotuzumab is a humanized monoclonal antibody directed against fibroblast activation protein (FAP). It is used to treat cancer. | Investigated for use/treatment in cancer/tumors (unspecified), colorectal cancer, and lung cancer. | NA | Human FAP is unique in its selective expression by tumor stromal fibroblasts in epithelial carcinomas, but not by epithelial carcinoma cells, normal fibroblasts, or other normal tissues. Therefore, FAP is an attractive target for the study of tumor stromal cell biology and provides valuable insights into the roles of the tumor microenvironment. Sibrotuzumab is a humanized monoclonal antibody designed to attack the cell-surface antigen FAP. | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | Seprase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12837 | Th1358 | Sibrotuzumab | NA | NA | NA | NA | NA | NA | NA | Sibrotuzumab is a humanized monoclonal antibody directed against fibroblast activation protein (FAP). It is used to treat cancer. | Investigated for use/treatment in cancer/tumors (unspecified), colorectal cancer, and lung cancer. | NA | Human FAP is unique in its selective expression by tumor stromal fibroblasts in epithelial carcinomas, but not by epithelial carcinoma cells, normal fibroblasts, or other normal tissues. Therefore, FAP is an attractive target for the study of tumor stromal cell biology and provides valuable insights into the roles of the tumor microenvironment. Sibrotuzumab is a humanized monoclonal antibody designed to attack the cell-surface antigen FAP. | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | Seprase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12838 | Th1358 | Sibrotuzumab | NA | NA | NA | NA | NA | NA | NA | Sibrotuzumab is a humanized monoclonal antibody directed against fibroblast activation protein (FAP). It is used to treat cancer. | Investigated for use/treatment in cancer/tumors (unspecified), colorectal cancer, and lung cancer. | NA | Human FAP is unique in its selective expression by tumor stromal fibroblasts in epithelial carcinomas, but not by epithelial carcinoma cells, normal fibroblasts, or other normal tissues. Therefore, FAP is an attractive target for the study of tumor stromal cell biology and provides valuable insights into the roles of the tumor microenvironment. Sibrotuzumab is a humanized monoclonal antibody designed to attack the cell-surface antigen FAP. | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | Seprase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12839 | Th1358 | Sibrotuzumab | NA | NA | NA | NA | NA | NA | NA | Sibrotuzumab is a humanized monoclonal antibody directed against fibroblast activation protein (FAP). It is used to treat cancer. | Investigated for use/treatment in cancer/tumors (unspecified), colorectal cancer, and lung cancer. | NA | Human FAP is unique in its selective expression by tumor stromal fibroblasts in epithelial carcinomas, but not by epithelial carcinoma cells, normal fibroblasts, or other normal tissues. Therefore, FAP is an attractive target for the study of tumor stromal cell biology and provides valuable insights into the roles of the tumor microenvironment. Sibrotuzumab is a humanized monoclonal antibody designed to attack the cell-surface antigen FAP. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | Seprase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12840 | Th1358 | Sibrotuzumab | NA | NA | NA | NA | NA | NA | NA | Sibrotuzumab is a humanized monoclonal antibody directed against fibroblast activation protein (FAP). It is used to treat cancer. | Investigated for use/treatment in cancer/tumors (unspecified), colorectal cancer, and lung cancer. | NA | Human FAP is unique in its selective expression by tumor stromal fibroblasts in epithelial carcinomas, but not by epithelial carcinoma cells, normal fibroblasts, or other normal tissues. Therefore, FAP is an attractive target for the study of tumor stromal cell biology and provides valuable insights into the roles of the tumor microenvironment. Sibrotuzumab is a humanized monoclonal antibody designed to attack the cell-surface antigen FAP. | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | Seprase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12870 | Th1363 | Bivatuzumab | NA | NA | NA | NA | NA | NA | NA | Bivatuzumab (previously BIWA 4) is a humanized monoclonal antibody against CD44 v6. [A31688,A31689] | Investigated for use/treatment in cancer/tumors (unspecified) and head and neck cancer. | NA | NA | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | CD44 antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12871 | Th1363 | Bivatuzumab | NA | NA | NA | NA | NA | NA | NA | Bivatuzumab (previously BIWA 4) is a humanized monoclonal antibody against CD44 v6. [A31688,A31689] | Investigated for use/treatment in cancer/tumors (unspecified) and head and neck cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | CD44 antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12872 | Th1363 | Bivatuzumab | NA | NA | NA | NA | NA | NA | NA | Bivatuzumab (previously BIWA 4) is a humanized monoclonal antibody against CD44 v6. [A31688,A31689] | Investigated for use/treatment in cancer/tumors (unspecified) and head and neck cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | CD44 antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12873 | Th1363 | Bivatuzumab | NA | NA | NA | NA | NA | NA | NA | Bivatuzumab (previously BIWA 4) is a humanized monoclonal antibody against CD44 v6. [A31688,A31689] | Investigated for use/treatment in cancer/tumors (unspecified) and head and neck cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | CD44 antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12874 | Th1363 | Bivatuzumab | NA | NA | NA | NA | NA | NA | NA | Bivatuzumab (previously BIWA 4) is a humanized monoclonal antibody against CD44 v6. [A31688,A31689] | Investigated for use/treatment in cancer/tumors (unspecified) and head and neck cancer. | NA | NA | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | CD44 antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12875 | Th1363 | Bivatuzumab | NA | NA | NA | NA | NA | NA | NA | Bivatuzumab (previously BIWA 4) is a humanized monoclonal antibody against CD44 v6. [A31688,A31689] | Investigated for use/treatment in cancer/tumors (unspecified) and head and neck cancer. | NA | NA | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | CD44 antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12876 | Th1363 | Bivatuzumab | NA | NA | NA | NA | NA | NA | NA | Bivatuzumab (previously BIWA 4) is a humanized monoclonal antibody against CD44 v6. [A31688,A31689] | Investigated for use/treatment in cancer/tumors (unspecified) and head and neck cancer. | NA | NA | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | CD44 antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12877 | Th1363 | Bivatuzumab | NA | NA | NA | NA | NA | NA | NA | Bivatuzumab (previously BIWA 4) is a humanized monoclonal antibody against CD44 v6. [A31688,A31689] | Investigated for use/treatment in cancer/tumors (unspecified) and head and neck cancer. | NA | NA | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | CD44 antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12878 | Th1363 | Bivatuzumab | NA | NA | NA | NA | NA | NA | NA | Bivatuzumab (previously BIWA 4) is a humanized monoclonal antibody against CD44 v6. [A31688,A31689] | Investigated for use/treatment in cancer/tumors (unspecified) and head and neck cancer. | NA | NA | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | CD44 antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12879 | Th1363 | Bivatuzumab | NA | NA | NA | NA | NA | NA | NA | Bivatuzumab (previously BIWA 4) is a humanized monoclonal antibody against CD44 v6. [A31688,A31689] | Investigated for use/treatment in cancer/tumors (unspecified) and head and neck cancer. | NA | NA | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | CD44 antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12898 | Th1367 | Lexatumumab | >Th1367_Lexatumumab EVQLVQSGGGVERPGGSLRLSCAASGFTFDDYGMSWVRQAPGKGLEWVSGINWNGGSTGYADSVKGRVTISRDNAKNSLYLQMNSLRAEDTAVYYCAKILGAGRGWYFDLWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Lexatumumab is a fully humanized, high-affinity immunoglobulin G(1 lambda) monoclonal antibody (mAb). | Investigated for use/treatment in cancer/tumors (unspecified). | NA | Lexatumumab agonizes the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAIL-R2), triggering the extrinsic apoptotic pathway. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 10B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12899 | Th1367 | Lexatumumab | >Th1367_Lexatumumab EVQLVQSGGGVERPGGSLRLSCAASGFTFDDYGMSWVRQAPGKGLEWVSGINWNGGSTGYADSVKGRVTISRDNAKNSLYLQMNSLRAEDTAVYYCAKILGAGRGWYFDLWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Lexatumumab is a fully humanized, high-affinity immunoglobulin G(1 lambda) monoclonal antibody (mAb). | Investigated for use/treatment in cancer/tumors (unspecified). | NA | Lexatumumab agonizes the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAIL-R2), triggering the extrinsic apoptotic pathway. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 10B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12900 | Th1367 | Lexatumumab | >Th1367_Lexatumumab EVQLVQSGGGVERPGGSLRLSCAASGFTFDDYGMSWVRQAPGKGLEWVSGINWNGGSTGYADSVKGRVTISRDNAKNSLYLQMNSLRAEDTAVYYCAKILGAGRGWYFDLWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Lexatumumab is a fully humanized, high-affinity immunoglobulin G(1 lambda) monoclonal antibody (mAb). | Investigated for use/treatment in cancer/tumors (unspecified). | NA | Lexatumumab agonizes the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAIL-R2), triggering the extrinsic apoptotic pathway. | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 10B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12901 | Th1367 | Lexatumumab | >Th1367_Lexatumumab EVQLVQSGGGVERPGGSLRLSCAASGFTFDDYGMSWVRQAPGKGLEWVSGINWNGGSTGYADSVKGRVTISRDNAKNSLYLQMNSLRAEDTAVYYCAKILGAGRGWYFDLWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Lexatumumab is a fully humanized, high-affinity immunoglobulin G(1 lambda) monoclonal antibody (mAb). | Investigated for use/treatment in cancer/tumors (unspecified). | NA | Lexatumumab agonizes the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAIL-R2), triggering the extrinsic apoptotic pathway. | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 10B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12902 | Th1367 | Lexatumumab | >Th1367_Lexatumumab EVQLVQSGGGVERPGGSLRLSCAASGFTFDDYGMSWVRQAPGKGLEWVSGINWNGGSTGYADSVKGRVTISRDNAKNSLYLQMNSLRAEDTAVYYCAKILGAGRGWYFDLWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Lexatumumab is a fully humanized, high-affinity immunoglobulin G(1 lambda) monoclonal antibody (mAb). | Investigated for use/treatment in cancer/tumors (unspecified). | NA | Lexatumumab agonizes the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAIL-R2), triggering the extrinsic apoptotic pathway. | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 10B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12903 | Th1367 | Lexatumumab | >Th1367_Lexatumumab EVQLVQSGGGVERPGGSLRLSCAASGFTFDDYGMSWVRQAPGKGLEWVSGINWNGGSTGYADSVKGRVTISRDNAKNSLYLQMNSLRAEDTAVYYCAKILGAGRGWYFDLWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Lexatumumab is a fully humanized, high-affinity immunoglobulin G(1 lambda) monoclonal antibody (mAb). | Investigated for use/treatment in cancer/tumors (unspecified). | NA | Lexatumumab agonizes the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAIL-R2), triggering the extrinsic apoptotic pathway. | NA | NA | NA | NA | NA | Immunologic Factors | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 10B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12904 | Th1367 | Lexatumumab | >Th1367_Lexatumumab EVQLVQSGGGVERPGGSLRLSCAASGFTFDDYGMSWVRQAPGKGLEWVSGINWNGGSTGYADSVKGRVTISRDNAKNSLYLQMNSLRAEDTAVYYCAKILGAGRGWYFDLWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Lexatumumab is a fully humanized, high-affinity immunoglobulin G(1 lambda) monoclonal antibody (mAb). | Investigated for use/treatment in cancer/tumors (unspecified). | NA | Lexatumumab agonizes the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAIL-R2), triggering the extrinsic apoptotic pathway. | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 10B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12905 | Th1367 | Lexatumumab | >Th1367_Lexatumumab EVQLVQSGGGVERPGGSLRLSCAASGFTFDDYGMSWVRQAPGKGLEWVSGINWNGGSTGYADSVKGRVTISRDNAKNSLYLQMNSLRAEDTAVYYCAKILGAGRGWYFDLWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Lexatumumab is a fully humanized, high-affinity immunoglobulin G(1 lambda) monoclonal antibody (mAb). | Investigated for use/treatment in cancer/tumors (unspecified). | NA | Lexatumumab agonizes the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAIL-R2), triggering the extrinsic apoptotic pathway. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 10B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12906 | Th1367 | Lexatumumab | >Th1367_Lexatumumab EVQLVQSGGGVERPGGSLRLSCAASGFTFDDYGMSWVRQAPGKGLEWVSGINWNGGSTGYADSVKGRVTISRDNAKNSLYLQMNSLRAEDTAVYYCAKILGAGRGWYFDLWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Lexatumumab is a fully humanized, high-affinity immunoglobulin G(1 lambda) monoclonal antibody (mAb). | Investigated for use/treatment in cancer/tumors (unspecified). | NA | Lexatumumab agonizes the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAIL-R2), triggering the extrinsic apoptotic pathway. | NA | NA | NA | NA | NA | Receptors, TNF-Related Apoptosis-Inducing Ligand | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 10B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12907 | Th1367 | Lexatumumab | >Th1367_Lexatumumab EVQLVQSGGGVERPGGSLRLSCAASGFTFDDYGMSWVRQAPGKGLEWVSGINWNGGSTGYADSVKGRVTISRDNAKNSLYLQMNSLRAEDTAVYYCAKILGAGRGWYFDLWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Lexatumumab is a fully humanized, high-affinity immunoglobulin G(1 lambda) monoclonal antibody (mAb). | Investigated for use/treatment in cancer/tumors (unspecified). | NA | Lexatumumab agonizes the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAIL-R2), triggering the extrinsic apoptotic pathway. | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 10B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12959 | Th1372 | Volociximab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in solid tumors, renal cell carcinoma, melanoma, pancreatic cancer, lung cancer, and ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12960 | Th1372 | Volociximab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in solid tumors, renal cell carcinoma, melanoma, pancreatic cancer, lung cancer, and ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Angiogenesis Inhibitors | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12961 | Th1372 | Volociximab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in solid tumors, renal cell carcinoma, melanoma, pancreatic cancer, lung cancer, and ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Angiogenesis Modulating Agents | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12962 | Th1372 | Volociximab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in solid tumors, renal cell carcinoma, melanoma, pancreatic cancer, lung cancer, and ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12963 | Th1372 | Volociximab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in solid tumors, renal cell carcinoma, melanoma, pancreatic cancer, lung cancer, and ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12964 | Th1372 | Volociximab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in solid tumors, renal cell carcinoma, melanoma, pancreatic cancer, lung cancer, and ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12965 | Th1372 | Volociximab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in solid tumors, renal cell carcinoma, melanoma, pancreatic cancer, lung cancer, and ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12966 | Th1372 | Volociximab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in solid tumors, renal cell carcinoma, melanoma, pancreatic cancer, lung cancer, and ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Growth Inhibitors | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12967 | Th1372 | Volociximab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in solid tumors, renal cell carcinoma, melanoma, pancreatic cancer, lung cancer, and ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Growth Substances | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12968 | Th1372 | Volociximab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in solid tumors, renal cell carcinoma, melanoma, pancreatic cancer, lung cancer, and ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12969 | Th1372 | Volociximab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in solid tumors, renal cell carcinoma, melanoma, pancreatic cancer, lung cancer, and ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12970 | Th1372 | Volociximab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in solid tumors, renal cell carcinoma, melanoma, pancreatic cancer, lung cancer, and ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12971 | Th1372 | Volociximab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in solid tumors, renal cell carcinoma, melanoma, pancreatic cancer, lung cancer, and ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13548 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | Imfinzi | Astra Zeneca Ab | Astra Zeneca Ab | Intravenous | 50 mg/ml | None. | fatigue, musculoskeletal pain, constipation, decreased appetite, nausea, swelling of extremities, urinary tract infection, abdominal pain, diarrhea/colitis, fever, shortness of breath, cough, and rash. | Imfinzi is a cancer medicine that works with your immune system to interfere with the growth and spread of cancer cells in the body. Imfinzi is used to treat non-small cell lung cancer in patients whose tumors cannot be removed by surgery, and whose cancer has not progressed after treatment with chemotherapy... | Imfinzi is a prescription medicine used to treat the symptoms of Urothelial Carcinoma, Non-small Cell Lung Cancer and Small Cell Lung Cancer. Imfinzi may be used alone or with other medications. | NA | Durvalumab is a programmed cell death ligand 1 (PD-L1) blocking antibody. Durvalumab is a human immunoglobulin G1 kappa (IgG1κ) monoclonal antibody that is produced by recombinant DNA technology in Chinese Hamster Ovary (CHO) cell suspension culture. | Link | Link | NA |
| 13549 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Antibiotics, Antineoplastic | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | Imfinzi | Astra Zeneca | Astra Zeneca | Intravenous | 50 mg / mL | None. | fatigue, musculoskeletal pain, constipation, decreased appetite, nausea, swelling of extremities, urinary tract infection, abdominal pain, diarrhea/colitis, fever, shortness of breath, cough, and rash. | Imfinzi is a cancer medicine that works with your immune system to interfere with the growth and spread of cancer cells in the body. Imfinzi is used to treat non-small cell lung cancer in patients whose tumors cannot be removed by surgery, and whose cancer has not progressed after treatment with chemotherapy... | Imfinzi is a prescription medicine used to treat the symptoms of Urothelial Carcinoma, Non-small Cell Lung Cancer and Small Cell Lung Cancer. Imfinzi may be used alone or with other medications. | NA | Durvalumab is a programmed cell death ligand 1 (PD-L1) blocking antibody. Durvalumab is a human immunoglobulin G1 kappa (IgG1κ) monoclonal antibody that is produced by recombinant DNA technology in Chinese Hamster Ovary (CHO) cell suspension culture. | Link | Link | NA |
| 13550 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Antibodies | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | Imfinzi | AstraZeneca Pharmaceuticals LP | AstraZeneca Pharmaceuticals LP | Intravenous | 120 mg/2.4mL | None. | fatigue, musculoskeletal pain, constipation, decreased appetite, nausea, swelling of extremities, urinary tract infection, abdominal pain, diarrhea/colitis, fever, shortness of breath, cough, and rash. | Imfinzi is a cancer medicine that works with your immune system to interfere with the growth and spread of cancer cells in the body. Imfinzi is used to treat non-small cell lung cancer in patients whose tumors cannot be removed by surgery, and whose cancer has not progressed after treatment with chemotherapy... | Imfinzi is a prescription medicine used to treat the symptoms of Urothelial Carcinoma, Non-small Cell Lung Cancer and Small Cell Lung Cancer. Imfinzi may be used alone or with other medications. | NA | Durvalumab is a programmed cell death ligand 1 (PD-L1) blocking antibody. Durvalumab is a human immunoglobulin G1 kappa (IgG1κ) monoclonal antibody that is produced by recombinant DNA technology in Chinese Hamster Ovary (CHO) cell suspension culture. | Link | Link | NA |
| 13551 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Antibodies, Monoclonal | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | Imfinzi | AstraZeneca Pharmaceuticals LP | AstraZeneca Pharmaceuticals LP | Intravenous | 500 mg/10mL | None. | fatigue, musculoskeletal pain, constipation, decreased appetite, nausea, swelling of extremities, urinary tract infection, abdominal pain, diarrhea/colitis, fever, shortness of breath, cough, and rash. | Imfinzi is a cancer medicine that works with your immune system to interfere with the growth and spread of cancer cells in the body. Imfinzi is used to treat non-small cell lung cancer in patients whose tumors cannot be removed by surgery, and whose cancer has not progressed after treatment with chemotherapy... | Imfinzi is a prescription medicine used to treat the symptoms of Urothelial Carcinoma, Non-small Cell Lung Cancer and Small Cell Lung Cancer. Imfinzi may be used alone or with other medications. | NA | Durvalumab is a programmed cell death ligand 1 (PD-L1) blocking antibody. Durvalumab is a human immunoglobulin G1 kappa (IgG1κ) monoclonal antibody that is produced by recombinant DNA technology in Chinese Hamster Ovary (CHO) cell suspension culture. | Link | Link | NA |
| 13552 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Antineoplastic Agents | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13553 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Antineoplastic Agents, Immunological | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13554 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13555 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Blood Proteins | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13556 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Cancer immunotherapy | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13557 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Globulins | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13558 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Immune Checkpoint Inhibitors | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13559 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Immunoglobulins | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13560 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Immunoproteins | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13561 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Immunotherapy | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13562 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Narrow Therapeutic Index Drugs | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13563 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Programmed Death Ligand-1 Antagonists | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13564 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Programmed Death Ligand-1 Blocker | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13565 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Programmed Death Ligand-1-directed Antibody Interactions | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13566 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Proteins | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13567 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Serum Globulins | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14218 | Th1476 | Stem bromelain | >Th1476_Stem_bromelain AVPQSIDWRDYGAVTSVKNQNPCGACWAFAAIATVESIYKIKKGILEPLSEQQVLDCAKGYGCKGGWEFRAFEFIISNKGVASGAIYPYKAAKGTCKTDGVPNSAYITGYARVPRNNESSMMYAVSKQPITVAVDANANFQYYKSGVFNGPCGTSLNHAVTAIGYGQDSIIYPKKWGAKWGEAGYIRMARDVSSSSGICGIAIDPLYPTLEE | NA | NA | NA | NA | NA | The estimated plasma half-life of stem bromelain is 6-9 hours [A32644]. | The primary therapeutic use for which stem bromelain is currently and formally indicated is as a burn wound eschar debridement agent that has been approved by the EMA since 2012 and marketed under the brand name Nexobrid [FDA Label]. Bromelain itself belongs to a category of protein-digesting enzymes that are obtained commercially from the fruit or stem of pineapples [A27198]. Although both fruit and stem bromelain are prepared differently and contain different enzymatic compositions, the general term bromelain typically refers to stem bromelain [A27198]. Bromelain is consequently a composite mixture of several different endopeptidases that can facilitate many different reactions with many different substrates. This action allows bromelain to demonstrate a wide range of therapeutic benefits ranging from cardiovascular to anticancer therapy - but the specific mechanisms of action by which it can elicit these effects are currently not properly understood. | The primary medical purpose for which stem bromelain (SB) is currently indicated for is the removal of eschar in adults with deep partial- and full-thickness thermal burns [FDA Label]. Besides this official indication, however, it is also believed that SB may be used as a treatment for several other purposes as well, including cardiovascular health, osteoarthritis, autoimmunity, blood clotting, diarrhea, cancer, surgery, and debridement - although the specific mechanisms of action for these indications remain to be elucidated [A27198]. | Stem bromelain is ultimately a mixture of various different thiol endopeptidases [A27198] that are capable of catalyzing a range of reactions on a number of different substrates, which is perhaps why stem bromelain can evidently be used as some manner of treatment in a range of therapeutic contexts. This notion is facilitated by the fact that various topical and oral administration stem bromelain preparations exist as well, further diversifying the ways in which the medication can be used. Perhaps the most important aspect of stem bromelain, however, is its ability to undergo intestinal absorption undegraded in a functionally intact form, ultimately preserving its proteolytic actions in the plasma [A27198, A32644]. This kind of pharmacodynamic characteristic is another element that perhaps allows stem bromelain to remain active within the body and elicit a number of actions at several major body systems. | Stem bromelain is ultimately a mixture of a number of thiol endopeptidases and other elements including phosphatases, glucosidase, peroxidases, cellulases, glycoproteins, carbohydrates, and various protease inhibitors [A27198]. The many different substrates and reactions that these varied enzymes can catalyze results in a number of different and possible mechanisms of action. Stem bromelain is currently principally used as a topical agent for debridement of necrotic tissue from wounds or second to third-degree burns [FDA Label, A27198]. As bromelain can contain escharase as one of its component enzymes, it is thought that various stem bromelain creams or gels can accelerate the healing process of wounds by facilitating the rapid removal of necrotic layers of dermis while preserving unburned/unharmed tissues [A27198] and/or perhaps by accelerating the recovery of blood perfusion in wound tissue, control the expression of TNF-alpha, and raise the expression of TGT-beta, as demonstrated in the pig animal model [A27198]. This kind of enzymatic debridement is ultimately preferred to surgical debridement as physical, surgical procedures are naturally painful, non-selective, and involve the possibility of repeat or excessive anesthesia and/or bleeding [A27198]. With regards to cardiovascular health, certain studies suggest that stem bromelain is capable of breaking down cholesterol plaques, eliciting a strong fibrinolytic activity, and inhibiting blood platelet aggregation - all of which protect against ischemia/reperfusion injury in skeletal muscle and minimize the risk of arterial thrombosis and embolism [A27198]. Additionally, stem bromelain has also been shown to attenuate allergic airway disease by altering CD4+ and CD8+ T lymphocyte populations - an action that may be beneficial in treating human asthma or hypersensitivity disorders [A27198]. Finally, stem bromelain has also been used to induce cardioprotection against ischemia-reperfusion injury via the Akt/Foxo pathway in rat model myocardium [A27198]. In the treatment of osteoarthritis, it is believed that stem bromelain has analgesic properties which are thought to be the result of direct influence on pain mediators such as bradykinin [A27198]. In addition, various trials suggest that the medication could be useful in reducing swelling, bruising, and pain in women having surgery like episiotomy [A27198]. Moreover, stem bromelain may also be used for treating acute inflammation and sports injuries [A27198]. Furthermore, stem bromelain has also been studied as an adjuvant therapy for chronic inflammatory, malignant, and autoimmune diseases [A27198]. Certain in vitro experiments have demonstrated that stem bromelain can modulate surface adhesion molecules on T cells, macrophages, and natural killer cells and also cause the secretion of IL-1B, IL-6, and Tumor Necrosis Factor-alpha (TNF-alpha) via peripheral blood mononuclear cells [A27198]. The agent has also been able to block the Raf-1/extracellular-regulated-kinase-2 (ERK-2) pathways by preventing T cell signal transduction [A27198]. In particular however, treating cells with stem bromelain decreases the activation of CD4(+) T cells and reduces the expression of CD25 [A27198]. Additionally, there is also evidence to suggest that oral therapy with stem bromelain produces certain analgesic and anti-inflammatory effects in patients with rheumatoid arthritis, which is a particularly common autoimmune disease [A27198]. Stem bromelain also affects blood coagulation by increasing the serum fibrinolytic ability and by preventing the synthesis of fibrin, a protein involved in blood clotting [A27198]. In the rat animal model, the reduction of serum fibrinogen level seems to be dose-dependent when both prothrombin time and activated partial thromboplastin time become markedly prolonged at higher concentrations of administered stem bromelain [A27198]. In vitro and in vivo studies also suggest stem bromelain can act as an effective fibrinolytic agent since it stimulates the conversion of plasminogen to plasmin, causing an increased fibrinolysis by degrading fibrin [A27198]. In terms of potential antimicrobial effects of stem bromelain, there are varying observations regarding its specific mechanism of action [A27198]. When counteracting the effects of some intestinal pathogens like Vibrio cholera or Escherichia coli (whose enterotoxin causes diarrhea in animals), some studies suggest that stem bromelain interacts with intestinal secretory signaling pathways like adenosine 3':5'-cyclic monophosphatase, guanosine 3':5'-cyclic monophosphatase, and/or calcium-dependent signaling cascades [A27198]. Conversely, other studies propose that stem bromelain supplementation can lead to antiadhesion effects which prevent E. coli bacteria from attaching to particular glycoprotein receptors on the intestinal mucosa by proteolytically modifying those receptor attachment sites [A27198]. Additionally, various studies have shown that stem bromelain also possesses anticancer activity. In particular, the agent has been found to increase the expression of p53 and Bax in mouse skin, both of which are well-known apoptosis activators [A27198]. Stem bromelain can also evidently decrease the activity of cell survival regulators like Akt and Erk, therefore inducing apoptotic tumor cell death [A27198]. Finally, stem bromelain has also been observed to downregulate NF-kB and Cox-2 expression in mouse papillomas and in models of skin tumorigenesis [A27198]. It has also demonstrated the capability to inhibit bacterial endotoxin (LPS)-induced NF-kB activity as well as the expression of PGE2 and Cox-2 in human monocytic leukemia and murine microglial cell lines [A27198]. | The human body can seemingly absorb significant amounts of bromelain - about 12 grams/day of bromelain may be consumed without the appearance of any major adverse effects [A27198]. Another study suggests that after giving bromelain (3000 FIP unit/day) to human over a period of ten days discovered no significant changes in blood coagulation parameters [A27198]. Finally, stem bromelain has a relatively low toxicity with an LD50 greater than 10 g/kg in mice, rats, and rabbits [A27198]. | Given its protein structure, it is assumed that stem bromelain, when administered would experience hydrolysis in the gut or eventually in the bloodstream after absorption [A32644]. Regardless, radiolabelled, intact stem bromelain has been found circulating in the plasma after administration [A27198, A32644]. | It appears that stem bromelain can be absorbed from the human gastrointestinal tract to a small but significant extent while remaining undegraded or functionally intact [A27198, A32644]. In a study involving 19 healthy men, daily oral administration of 3g/day of bromelain resulted in a mean plasma concentration of approximately 5000 pg/ml by 48 hours, although the maximum peak blood concentration of bromelain varied between 2000 to 10,000 pg/ml between subjects [A32644]. The average blood concentration of bromelain in the period range of 3 to 51 hours was 10.28 ug [A32644]. | No readily accessible data regarding the volume of distribution of stem bromelain is available. | No readily accessible data regarding the clearance of stem bromelain is available. | Cysteine Endopeptidases | NA | NA | NA | NA | NA | Nexobrid | Medi Wound Germany Gmb H | Medi Wound Germany Gmb H | Cutaneous | 2 g | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14219 | Th1476 | Stem bromelain | >Th1476_Stem_bromelain AVPQSIDWRDYGAVTSVKNQNPCGACWAFAAIATVESIYKIKKGILEPLSEQQVLDCAKGYGCKGGWEFRAFEFIISNKGVASGAIYPYKAAKGTCKTDGVPNSAYITGYARVPRNNESSMMYAVSKQPITVAVDANANFQYYKSGVFNGPCGTSLNHAVTAIGYGQDSIIYPKKWGAKWGEAGYIRMARDVSSSSGICGIAIDPLYPTLEE | NA | NA | NA | NA | NA | The estimated plasma half-life of stem bromelain is 6-9 hours [A32644]. | The primary therapeutic use for which stem bromelain is currently and formally indicated is as a burn wound eschar debridement agent that has been approved by the EMA since 2012 and marketed under the brand name Nexobrid [FDA Label]. Bromelain itself belongs to a category of protein-digesting enzymes that are obtained commercially from the fruit or stem of pineapples [A27198]. Although both fruit and stem bromelain are prepared differently and contain different enzymatic compositions, the general term bromelain typically refers to stem bromelain [A27198]. Bromelain is consequently a composite mixture of several different endopeptidases that can facilitate many different reactions with many different substrates. This action allows bromelain to demonstrate a wide range of therapeutic benefits ranging from cardiovascular to anticancer therapy - but the specific mechanisms of action by which it can elicit these effects are currently not properly understood. | The primary medical purpose for which stem bromelain (SB) is currently indicated for is the removal of eschar in adults with deep partial- and full-thickness thermal burns [FDA Label]. Besides this official indication, however, it is also believed that SB may be used as a treatment for several other purposes as well, including cardiovascular health, osteoarthritis, autoimmunity, blood clotting, diarrhea, cancer, surgery, and debridement - although the specific mechanisms of action for these indications remain to be elucidated [A27198]. | Stem bromelain is ultimately a mixture of various different thiol endopeptidases [A27198] that are capable of catalyzing a range of reactions on a number of different substrates, which is perhaps why stem bromelain can evidently be used as some manner of treatment in a range of therapeutic contexts. This notion is facilitated by the fact that various topical and oral administration stem bromelain preparations exist as well, further diversifying the ways in which the medication can be used. Perhaps the most important aspect of stem bromelain, however, is its ability to undergo intestinal absorption undegraded in a functionally intact form, ultimately preserving its proteolytic actions in the plasma [A27198, A32644]. This kind of pharmacodynamic characteristic is another element that perhaps allows stem bromelain to remain active within the body and elicit a number of actions at several major body systems. | Stem bromelain is ultimately a mixture of a number of thiol endopeptidases and other elements including phosphatases, glucosidase, peroxidases, cellulases, glycoproteins, carbohydrates, and various protease inhibitors [A27198]. The many different substrates and reactions that these varied enzymes can catalyze results in a number of different and possible mechanisms of action. Stem bromelain is currently principally used as a topical agent for debridement of necrotic tissue from wounds or second to third-degree burns [FDA Label, A27198]. As bromelain can contain escharase as one of its component enzymes, it is thought that various stem bromelain creams or gels can accelerate the healing process of wounds by facilitating the rapid removal of necrotic layers of dermis while preserving unburned/unharmed tissues [A27198] and/or perhaps by accelerating the recovery of blood perfusion in wound tissue, control the expression of TNF-alpha, and raise the expression of TGT-beta, as demonstrated in the pig animal model [A27198]. This kind of enzymatic debridement is ultimately preferred to surgical debridement as physical, surgical procedures are naturally painful, non-selective, and involve the possibility of repeat or excessive anesthesia and/or bleeding [A27198]. With regards to cardiovascular health, certain studies suggest that stem bromelain is capable of breaking down cholesterol plaques, eliciting a strong fibrinolytic activity, and inhibiting blood platelet aggregation - all of which protect against ischemia/reperfusion injury in skeletal muscle and minimize the risk of arterial thrombosis and embolism [A27198]. Additionally, stem bromelain has also been shown to attenuate allergic airway disease by altering CD4+ and CD8+ T lymphocyte populations - an action that may be beneficial in treating human asthma or hypersensitivity disorders [A27198]. Finally, stem bromelain has also been used to induce cardioprotection against ischemia-reperfusion injury via the Akt/Foxo pathway in rat model myocardium [A27198]. In the treatment of osteoarthritis, it is believed that stem bromelain has analgesic properties which are thought to be the result of direct influence on pain mediators such as bradykinin [A27198]. In addition, various trials suggest that the medication could be useful in reducing swelling, bruising, and pain in women having surgery like episiotomy [A27198]. Moreover, stem bromelain may also be used for treating acute inflammation and sports injuries [A27198]. Furthermore, stem bromelain has also been studied as an adjuvant therapy for chronic inflammatory, malignant, and autoimmune diseases [A27198]. Certain in vitro experiments have demonstrated that stem bromelain can modulate surface adhesion molecules on T cells, macrophages, and natural killer cells and also cause the secretion of IL-1B, IL-6, and Tumor Necrosis Factor-alpha (TNF-alpha) via peripheral blood mononuclear cells [A27198]. The agent has also been able to block the Raf-1/extracellular-regulated-kinase-2 (ERK-2) pathways by preventing T cell signal transduction [A27198]. In particular however, treating cells with stem bromelain decreases the activation of CD4(+) T cells and reduces the expression of CD25 [A27198]. Additionally, there is also evidence to suggest that oral therapy with stem bromelain produces certain analgesic and anti-inflammatory effects in patients with rheumatoid arthritis, which is a particularly common autoimmune disease [A27198]. Stem bromelain also affects blood coagulation by increasing the serum fibrinolytic ability and by preventing the synthesis of fibrin, a protein involved in blood clotting [A27198]. In the rat animal model, the reduction of serum fibrinogen level seems to be dose-dependent when both prothrombin time and activated partial thromboplastin time become markedly prolonged at higher concentrations of administered stem bromelain [A27198]. In vitro and in vivo studies also suggest stem bromelain can act as an effective fibrinolytic agent since it stimulates the conversion of plasminogen to plasmin, causing an increased fibrinolysis by degrading fibrin [A27198]. In terms of potential antimicrobial effects of stem bromelain, there are varying observations regarding its specific mechanism of action [A27198]. When counteracting the effects of some intestinal pathogens like Vibrio cholera or Escherichia coli (whose enterotoxin causes diarrhea in animals), some studies suggest that stem bromelain interacts with intestinal secretory signaling pathways like adenosine 3':5'-cyclic monophosphatase, guanosine 3':5'-cyclic monophosphatase, and/or calcium-dependent signaling cascades [A27198]. Conversely, other studies propose that stem bromelain supplementation can lead to antiadhesion effects which prevent E. coli bacteria from attaching to particular glycoprotein receptors on the intestinal mucosa by proteolytically modifying those receptor attachment sites [A27198]. Additionally, various studies have shown that stem bromelain also possesses anticancer activity. In particular, the agent has been found to increase the expression of p53 and Bax in mouse skin, both of which are well-known apoptosis activators [A27198]. Stem bromelain can also evidently decrease the activity of cell survival regulators like Akt and Erk, therefore inducing apoptotic tumor cell death [A27198]. Finally, stem bromelain has also been observed to downregulate NF-kB and Cox-2 expression in mouse papillomas and in models of skin tumorigenesis [A27198]. It has also demonstrated the capability to inhibit bacterial endotoxin (LPS)-induced NF-kB activity as well as the expression of PGE2 and Cox-2 in human monocytic leukemia and murine microglial cell lines [A27198]. | The human body can seemingly absorb significant amounts of bromelain - about 12 grams/day of bromelain may be consumed without the appearance of any major adverse effects [A27198]. Another study suggests that after giving bromelain (3000 FIP unit/day) to human over a period of ten days discovered no significant changes in blood coagulation parameters [A27198]. Finally, stem bromelain has a relatively low toxicity with an LD50 greater than 10 g/kg in mice, rats, and rabbits [A27198]. | Given its protein structure, it is assumed that stem bromelain, when administered would experience hydrolysis in the gut or eventually in the bloodstream after absorption [A32644]. Regardless, radiolabelled, intact stem bromelain has been found circulating in the plasma after administration [A27198, A32644]. | It appears that stem bromelain can be absorbed from the human gastrointestinal tract to a small but significant extent while remaining undegraded or functionally intact [A27198, A32644]. In a study involving 19 healthy men, daily oral administration of 3g/day of bromelain resulted in a mean plasma concentration of approximately 5000 pg/ml by 48 hours, although the maximum peak blood concentration of bromelain varied between 2000 to 10,000 pg/ml between subjects [A32644]. The average blood concentration of bromelain in the period range of 3 to 51 hours was 10.28 ug [A32644]. | No readily accessible data regarding the volume of distribution of stem bromelain is available. | No readily accessible data regarding the clearance of stem bromelain is available. | Cysteine Proteases | NA | NA | NA | NA | NA | Nexobrid | Medi Wound Germany Gmb H | Medi Wound Germany Gmb H | Cutaneous | 5 g | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14220 | Th1476 | Stem bromelain | >Th1476_Stem_bromelain AVPQSIDWRDYGAVTSVKNQNPCGACWAFAAIATVESIYKIKKGILEPLSEQQVLDCAKGYGCKGGWEFRAFEFIISNKGVASGAIYPYKAAKGTCKTDGVPNSAYITGYARVPRNNESSMMYAVSKQPITVAVDANANFQYYKSGVFNGPCGTSLNHAVTAIGYGQDSIIYPKKWGAKWGEAGYIRMARDVSSSSGICGIAIDPLYPTLEE | NA | NA | NA | NA | NA | The estimated plasma half-life of stem bromelain is 6-9 hours [A32644]. | The primary therapeutic use for which stem bromelain is currently and formally indicated is as a burn wound eschar debridement agent that has been approved by the EMA since 2012 and marketed under the brand name Nexobrid [FDA Label]. Bromelain itself belongs to a category of protein-digesting enzymes that are obtained commercially from the fruit or stem of pineapples [A27198]. Although both fruit and stem bromelain are prepared differently and contain different enzymatic compositions, the general term bromelain typically refers to stem bromelain [A27198]. Bromelain is consequently a composite mixture of several different endopeptidases that can facilitate many different reactions with many different substrates. This action allows bromelain to demonstrate a wide range of therapeutic benefits ranging from cardiovascular to anticancer therapy - but the specific mechanisms of action by which it can elicit these effects are currently not properly understood. | The primary medical purpose for which stem bromelain (SB) is currently indicated for is the removal of eschar in adults with deep partial- and full-thickness thermal burns [FDA Label]. Besides this official indication, however, it is also believed that SB may be used as a treatment for several other purposes as well, including cardiovascular health, osteoarthritis, autoimmunity, blood clotting, diarrhea, cancer, surgery, and debridement - although the specific mechanisms of action for these indications remain to be elucidated [A27198]. | Stem bromelain is ultimately a mixture of various different thiol endopeptidases [A27198] that are capable of catalyzing a range of reactions on a number of different substrates, which is perhaps why stem bromelain can evidently be used as some manner of treatment in a range of therapeutic contexts. This notion is facilitated by the fact that various topical and oral administration stem bromelain preparations exist as well, further diversifying the ways in which the medication can be used. Perhaps the most important aspect of stem bromelain, however, is its ability to undergo intestinal absorption undegraded in a functionally intact form, ultimately preserving its proteolytic actions in the plasma [A27198, A32644]. This kind of pharmacodynamic characteristic is another element that perhaps allows stem bromelain to remain active within the body and elicit a number of actions at several major body systems. | Stem bromelain is ultimately a mixture of a number of thiol endopeptidases and other elements including phosphatases, glucosidase, peroxidases, cellulases, glycoproteins, carbohydrates, and various protease inhibitors [A27198]. The many different substrates and reactions that these varied enzymes can catalyze results in a number of different and possible mechanisms of action. Stem bromelain is currently principally used as a topical agent for debridement of necrotic tissue from wounds or second to third-degree burns [FDA Label, A27198]. As bromelain can contain escharase as one of its component enzymes, it is thought that various stem bromelain creams or gels can accelerate the healing process of wounds by facilitating the rapid removal of necrotic layers of dermis while preserving unburned/unharmed tissues [A27198] and/or perhaps by accelerating the recovery of blood perfusion in wound tissue, control the expression of TNF-alpha, and raise the expression of TGT-beta, as demonstrated in the pig animal model [A27198]. This kind of enzymatic debridement is ultimately preferred to surgical debridement as physical, surgical procedures are naturally painful, non-selective, and involve the possibility of repeat or excessive anesthesia and/or bleeding [A27198]. With regards to cardiovascular health, certain studies suggest that stem bromelain is capable of breaking down cholesterol plaques, eliciting a strong fibrinolytic activity, and inhibiting blood platelet aggregation - all of which protect against ischemia/reperfusion injury in skeletal muscle and minimize the risk of arterial thrombosis and embolism [A27198]. Additionally, stem bromelain has also been shown to attenuate allergic airway disease by altering CD4+ and CD8+ T lymphocyte populations - an action that may be beneficial in treating human asthma or hypersensitivity disorders [A27198]. Finally, stem bromelain has also been used to induce cardioprotection against ischemia-reperfusion injury via the Akt/Foxo pathway in rat model myocardium [A27198]. In the treatment of osteoarthritis, it is believed that stem bromelain has analgesic properties which are thought to be the result of direct influence on pain mediators such as bradykinin [A27198]. In addition, various trials suggest that the medication could be useful in reducing swelling, bruising, and pain in women having surgery like episiotomy [A27198]. Moreover, stem bromelain may also be used for treating acute inflammation and sports injuries [A27198]. Furthermore, stem bromelain has also been studied as an adjuvant therapy for chronic inflammatory, malignant, and autoimmune diseases [A27198]. Certain in vitro experiments have demonstrated that stem bromelain can modulate surface adhesion molecules on T cells, macrophages, and natural killer cells and also cause the secretion of IL-1B, IL-6, and Tumor Necrosis Factor-alpha (TNF-alpha) via peripheral blood mononuclear cells [A27198]. The agent has also been able to block the Raf-1/extracellular-regulated-kinase-2 (ERK-2) pathways by preventing T cell signal transduction [A27198]. In particular however, treating cells with stem bromelain decreases the activation of CD4(+) T cells and reduces the expression of CD25 [A27198]. Additionally, there is also evidence to suggest that oral therapy with stem bromelain produces certain analgesic and anti-inflammatory effects in patients with rheumatoid arthritis, which is a particularly common autoimmune disease [A27198]. Stem bromelain also affects blood coagulation by increasing the serum fibrinolytic ability and by preventing the synthesis of fibrin, a protein involved in blood clotting [A27198]. In the rat animal model, the reduction of serum fibrinogen level seems to be dose-dependent when both prothrombin time and activated partial thromboplastin time become markedly prolonged at higher concentrations of administered stem bromelain [A27198]. In vitro and in vivo studies also suggest stem bromelain can act as an effective fibrinolytic agent since it stimulates the conversion of plasminogen to plasmin, causing an increased fibrinolysis by degrading fibrin [A27198]. In terms of potential antimicrobial effects of stem bromelain, there are varying observations regarding its specific mechanism of action [A27198]. When counteracting the effects of some intestinal pathogens like Vibrio cholera or Escherichia coli (whose enterotoxin causes diarrhea in animals), some studies suggest that stem bromelain interacts with intestinal secretory signaling pathways like adenosine 3':5'-cyclic monophosphatase, guanosine 3':5'-cyclic monophosphatase, and/or calcium-dependent signaling cascades [A27198]. Conversely, other studies propose that stem bromelain supplementation can lead to antiadhesion effects which prevent E. coli bacteria from attaching to particular glycoprotein receptors on the intestinal mucosa by proteolytically modifying those receptor attachment sites [A27198]. Additionally, various studies have shown that stem bromelain also possesses anticancer activity. In particular, the agent has been found to increase the expression of p53 and Bax in mouse skin, both of which are well-known apoptosis activators [A27198]. Stem bromelain can also evidently decrease the activity of cell survival regulators like Akt and Erk, therefore inducing apoptotic tumor cell death [A27198]. Finally, stem bromelain has also been observed to downregulate NF-kB and Cox-2 expression in mouse papillomas and in models of skin tumorigenesis [A27198]. It has also demonstrated the capability to inhibit bacterial endotoxin (LPS)-induced NF-kB activity as well as the expression of PGE2 and Cox-2 in human monocytic leukemia and murine microglial cell lines [A27198]. | The human body can seemingly absorb significant amounts of bromelain - about 12 grams/day of bromelain may be consumed without the appearance of any major adverse effects [A27198]. Another study suggests that after giving bromelain (3000 FIP unit/day) to human over a period of ten days discovered no significant changes in blood coagulation parameters [A27198]. Finally, stem bromelain has a relatively low toxicity with an LD50 greater than 10 g/kg in mice, rats, and rabbits [A27198]. | Given its protein structure, it is assumed that stem bromelain, when administered would experience hydrolysis in the gut or eventually in the bloodstream after absorption [A32644]. Regardless, radiolabelled, intact stem bromelain has been found circulating in the plasma after administration [A27198, A32644]. | It appears that stem bromelain can be absorbed from the human gastrointestinal tract to a small but significant extent while remaining undegraded or functionally intact [A27198, A32644]. In a study involving 19 healthy men, daily oral administration of 3g/day of bromelain resulted in a mean plasma concentration of approximately 5000 pg/ml by 48 hours, although the maximum peak blood concentration of bromelain varied between 2000 to 10,000 pg/ml between subjects [A32644]. The average blood concentration of bromelain in the period range of 3 to 51 hours was 10.28 ug [A32644]. | No readily accessible data regarding the volume of distribution of stem bromelain is available. | No readily accessible data regarding the clearance of stem bromelain is available. | Endopeptidases | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14221 | Th1476 | Stem bromelain | >Th1476_Stem_bromelain AVPQSIDWRDYGAVTSVKNQNPCGACWAFAAIATVESIYKIKKGILEPLSEQQVLDCAKGYGCKGGWEFRAFEFIISNKGVASGAIYPYKAAKGTCKTDGVPNSAYITGYARVPRNNESSMMYAVSKQPITVAVDANANFQYYKSGVFNGPCGTSLNHAVTAIGYGQDSIIYPKKWGAKWGEAGYIRMARDVSSSSGICGIAIDPLYPTLEE | NA | NA | NA | NA | NA | The estimated plasma half-life of stem bromelain is 6-9 hours [A32644]. | The primary therapeutic use for which stem bromelain is currently and formally indicated is as a burn wound eschar debridement agent that has been approved by the EMA since 2012 and marketed under the brand name Nexobrid [FDA Label]. Bromelain itself belongs to a category of protein-digesting enzymes that are obtained commercially from the fruit or stem of pineapples [A27198]. Although both fruit and stem bromelain are prepared differently and contain different enzymatic compositions, the general term bromelain typically refers to stem bromelain [A27198]. Bromelain is consequently a composite mixture of several different endopeptidases that can facilitate many different reactions with many different substrates. This action allows bromelain to demonstrate a wide range of therapeutic benefits ranging from cardiovascular to anticancer therapy - but the specific mechanisms of action by which it can elicit these effects are currently not properly understood. | The primary medical purpose for which stem bromelain (SB) is currently indicated for is the removal of eschar in adults with deep partial- and full-thickness thermal burns [FDA Label]. Besides this official indication, however, it is also believed that SB may be used as a treatment for several other purposes as well, including cardiovascular health, osteoarthritis, autoimmunity, blood clotting, diarrhea, cancer, surgery, and debridement - although the specific mechanisms of action for these indications remain to be elucidated [A27198]. | Stem bromelain is ultimately a mixture of various different thiol endopeptidases [A27198] that are capable of catalyzing a range of reactions on a number of different substrates, which is perhaps why stem bromelain can evidently be used as some manner of treatment in a range of therapeutic contexts. This notion is facilitated by the fact that various topical and oral administration stem bromelain preparations exist as well, further diversifying the ways in which the medication can be used. Perhaps the most important aspect of stem bromelain, however, is its ability to undergo intestinal absorption undegraded in a functionally intact form, ultimately preserving its proteolytic actions in the plasma [A27198, A32644]. This kind of pharmacodynamic characteristic is another element that perhaps allows stem bromelain to remain active within the body and elicit a number of actions at several major body systems. | Stem bromelain is ultimately a mixture of a number of thiol endopeptidases and other elements including phosphatases, glucosidase, peroxidases, cellulases, glycoproteins, carbohydrates, and various protease inhibitors [A27198]. The many different substrates and reactions that these varied enzymes can catalyze results in a number of different and possible mechanisms of action. Stem bromelain is currently principally used as a topical agent for debridement of necrotic tissue from wounds or second to third-degree burns [FDA Label, A27198]. As bromelain can contain escharase as one of its component enzymes, it is thought that various stem bromelain creams or gels can accelerate the healing process of wounds by facilitating the rapid removal of necrotic layers of dermis while preserving unburned/unharmed tissues [A27198] and/or perhaps by accelerating the recovery of blood perfusion in wound tissue, control the expression of TNF-alpha, and raise the expression of TGT-beta, as demonstrated in the pig animal model [A27198]. This kind of enzymatic debridement is ultimately preferred to surgical debridement as physical, surgical procedures are naturally painful, non-selective, and involve the possibility of repeat or excessive anesthesia and/or bleeding [A27198]. With regards to cardiovascular health, certain studies suggest that stem bromelain is capable of breaking down cholesterol plaques, eliciting a strong fibrinolytic activity, and inhibiting blood platelet aggregation - all of which protect against ischemia/reperfusion injury in skeletal muscle and minimize the risk of arterial thrombosis and embolism [A27198]. Additionally, stem bromelain has also been shown to attenuate allergic airway disease by altering CD4+ and CD8+ T lymphocyte populations - an action that may be beneficial in treating human asthma or hypersensitivity disorders [A27198]. Finally, stem bromelain has also been used to induce cardioprotection against ischemia-reperfusion injury via the Akt/Foxo pathway in rat model myocardium [A27198]. In the treatment of osteoarthritis, it is believed that stem bromelain has analgesic properties which are thought to be the result of direct influence on pain mediators such as bradykinin [A27198]. In addition, various trials suggest that the medication could be useful in reducing swelling, bruising, and pain in women having surgery like episiotomy [A27198]. Moreover, stem bromelain may also be used for treating acute inflammation and sports injuries [A27198]. Furthermore, stem bromelain has also been studied as an adjuvant therapy for chronic inflammatory, malignant, and autoimmune diseases [A27198]. Certain in vitro experiments have demonstrated that stem bromelain can modulate surface adhesion molecules on T cells, macrophages, and natural killer cells and also cause the secretion of IL-1B, IL-6, and Tumor Necrosis Factor-alpha (TNF-alpha) via peripheral blood mononuclear cells [A27198]. The agent has also been able to block the Raf-1/extracellular-regulated-kinase-2 (ERK-2) pathways by preventing T cell signal transduction [A27198]. In particular however, treating cells with stem bromelain decreases the activation of CD4(+) T cells and reduces the expression of CD25 [A27198]. Additionally, there is also evidence to suggest that oral therapy with stem bromelain produces certain analgesic and anti-inflammatory effects in patients with rheumatoid arthritis, which is a particularly common autoimmune disease [A27198]. Stem bromelain also affects blood coagulation by increasing the serum fibrinolytic ability and by preventing the synthesis of fibrin, a protein involved in blood clotting [A27198]. In the rat animal model, the reduction of serum fibrinogen level seems to be dose-dependent when both prothrombin time and activated partial thromboplastin time become markedly prolonged at higher concentrations of administered stem bromelain [A27198]. In vitro and in vivo studies also suggest stem bromelain can act as an effective fibrinolytic agent since it stimulates the conversion of plasminogen to plasmin, causing an increased fibrinolysis by degrading fibrin [A27198]. In terms of potential antimicrobial effects of stem bromelain, there are varying observations regarding its specific mechanism of action [A27198]. When counteracting the effects of some intestinal pathogens like Vibrio cholera or Escherichia coli (whose enterotoxin causes diarrhea in animals), some studies suggest that stem bromelain interacts with intestinal secretory signaling pathways like adenosine 3':5'-cyclic monophosphatase, guanosine 3':5'-cyclic monophosphatase, and/or calcium-dependent signaling cascades [A27198]. Conversely, other studies propose that stem bromelain supplementation can lead to antiadhesion effects which prevent E. coli bacteria from attaching to particular glycoprotein receptors on the intestinal mucosa by proteolytically modifying those receptor attachment sites [A27198]. Additionally, various studies have shown that stem bromelain also possesses anticancer activity. In particular, the agent has been found to increase the expression of p53 and Bax in mouse skin, both of which are well-known apoptosis activators [A27198]. Stem bromelain can also evidently decrease the activity of cell survival regulators like Akt and Erk, therefore inducing apoptotic tumor cell death [A27198]. Finally, stem bromelain has also been observed to downregulate NF-kB and Cox-2 expression in mouse papillomas and in models of skin tumorigenesis [A27198]. It has also demonstrated the capability to inhibit bacterial endotoxin (LPS)-induced NF-kB activity as well as the expression of PGE2 and Cox-2 in human monocytic leukemia and murine microglial cell lines [A27198]. | The human body can seemingly absorb significant amounts of bromelain - about 12 grams/day of bromelain may be consumed without the appearance of any major adverse effects [A27198]. Another study suggests that after giving bromelain (3000 FIP unit/day) to human over a period of ten days discovered no significant changes in blood coagulation parameters [A27198]. Finally, stem bromelain has a relatively low toxicity with an LD50 greater than 10 g/kg in mice, rats, and rabbits [A27198]. | Given its protein structure, it is assumed that stem bromelain, when administered would experience hydrolysis in the gut or eventually in the bloodstream after absorption [A32644]. Regardless, radiolabelled, intact stem bromelain has been found circulating in the plasma after administration [A27198, A32644]. | It appears that stem bromelain can be absorbed from the human gastrointestinal tract to a small but significant extent while remaining undegraded or functionally intact [A27198, A32644]. In a study involving 19 healthy men, daily oral administration of 3g/day of bromelain resulted in a mean plasma concentration of approximately 5000 pg/ml by 48 hours, although the maximum peak blood concentration of bromelain varied between 2000 to 10,000 pg/ml between subjects [A32644]. The average blood concentration of bromelain in the period range of 3 to 51 hours was 10.28 ug [A32644]. | No readily accessible data regarding the volume of distribution of stem bromelain is available. | No readily accessible data regarding the clearance of stem bromelain is available. | Enzymes | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14222 | Th1476 | Stem bromelain | >Th1476_Stem_bromelain AVPQSIDWRDYGAVTSVKNQNPCGACWAFAAIATVESIYKIKKGILEPLSEQQVLDCAKGYGCKGGWEFRAFEFIISNKGVASGAIYPYKAAKGTCKTDGVPNSAYITGYARVPRNNESSMMYAVSKQPITVAVDANANFQYYKSGVFNGPCGTSLNHAVTAIGYGQDSIIYPKKWGAKWGEAGYIRMARDVSSSSGICGIAIDPLYPTLEE | NA | NA | NA | NA | NA | The estimated plasma half-life of stem bromelain is 6-9 hours [A32644]. | The primary therapeutic use for which stem bromelain is currently and formally indicated is as a burn wound eschar debridement agent that has been approved by the EMA since 2012 and marketed under the brand name Nexobrid [FDA Label]. Bromelain itself belongs to a category of protein-digesting enzymes that are obtained commercially from the fruit or stem of pineapples [A27198]. Although both fruit and stem bromelain are prepared differently and contain different enzymatic compositions, the general term bromelain typically refers to stem bromelain [A27198]. Bromelain is consequently a composite mixture of several different endopeptidases that can facilitate many different reactions with many different substrates. This action allows bromelain to demonstrate a wide range of therapeutic benefits ranging from cardiovascular to anticancer therapy - but the specific mechanisms of action by which it can elicit these effects are currently not properly understood. | The primary medical purpose for which stem bromelain (SB) is currently indicated for is the removal of eschar in adults with deep partial- and full-thickness thermal burns [FDA Label]. Besides this official indication, however, it is also believed that SB may be used as a treatment for several other purposes as well, including cardiovascular health, osteoarthritis, autoimmunity, blood clotting, diarrhea, cancer, surgery, and debridement - although the specific mechanisms of action for these indications remain to be elucidated [A27198]. | Stem bromelain is ultimately a mixture of various different thiol endopeptidases [A27198] that are capable of catalyzing a range of reactions on a number of different substrates, which is perhaps why stem bromelain can evidently be used as some manner of treatment in a range of therapeutic contexts. This notion is facilitated by the fact that various topical and oral administration stem bromelain preparations exist as well, further diversifying the ways in which the medication can be used. Perhaps the most important aspect of stem bromelain, however, is its ability to undergo intestinal absorption undegraded in a functionally intact form, ultimately preserving its proteolytic actions in the plasma [A27198, A32644]. This kind of pharmacodynamic characteristic is another element that perhaps allows stem bromelain to remain active within the body and elicit a number of actions at several major body systems. | Stem bromelain is ultimately a mixture of a number of thiol endopeptidases and other elements including phosphatases, glucosidase, peroxidases, cellulases, glycoproteins, carbohydrates, and various protease inhibitors [A27198]. The many different substrates and reactions that these varied enzymes can catalyze results in a number of different and possible mechanisms of action. Stem bromelain is currently principally used as a topical agent for debridement of necrotic tissue from wounds or second to third-degree burns [FDA Label, A27198]. As bromelain can contain escharase as one of its component enzymes, it is thought that various stem bromelain creams or gels can accelerate the healing process of wounds by facilitating the rapid removal of necrotic layers of dermis while preserving unburned/unharmed tissues [A27198] and/or perhaps by accelerating the recovery of blood perfusion in wound tissue, control the expression of TNF-alpha, and raise the expression of TGT-beta, as demonstrated in the pig animal model [A27198]. This kind of enzymatic debridement is ultimately preferred to surgical debridement as physical, surgical procedures are naturally painful, non-selective, and involve the possibility of repeat or excessive anesthesia and/or bleeding [A27198]. With regards to cardiovascular health, certain studies suggest that stem bromelain is capable of breaking down cholesterol plaques, eliciting a strong fibrinolytic activity, and inhibiting blood platelet aggregation - all of which protect against ischemia/reperfusion injury in skeletal muscle and minimize the risk of arterial thrombosis and embolism [A27198]. Additionally, stem bromelain has also been shown to attenuate allergic airway disease by altering CD4+ and CD8+ T lymphocyte populations - an action that may be beneficial in treating human asthma or hypersensitivity disorders [A27198]. Finally, stem bromelain has also been used to induce cardioprotection against ischemia-reperfusion injury via the Akt/Foxo pathway in rat model myocardium [A27198]. In the treatment of osteoarthritis, it is believed that stem bromelain has analgesic properties which are thought to be the result of direct influence on pain mediators such as bradykinin [A27198]. In addition, various trials suggest that the medication could be useful in reducing swelling, bruising, and pain in women having surgery like episiotomy [A27198]. Moreover, stem bromelain may also be used for treating acute inflammation and sports injuries [A27198]. Furthermore, stem bromelain has also been studied as an adjuvant therapy for chronic inflammatory, malignant, and autoimmune diseases [A27198]. Certain in vitro experiments have demonstrated that stem bromelain can modulate surface adhesion molecules on T cells, macrophages, and natural killer cells and also cause the secretion of IL-1B, IL-6, and Tumor Necrosis Factor-alpha (TNF-alpha) via peripheral blood mononuclear cells [A27198]. The agent has also been able to block the Raf-1/extracellular-regulated-kinase-2 (ERK-2) pathways by preventing T cell signal transduction [A27198]. In particular however, treating cells with stem bromelain decreases the activation of CD4(+) T cells and reduces the expression of CD25 [A27198]. Additionally, there is also evidence to suggest that oral therapy with stem bromelain produces certain analgesic and anti-inflammatory effects in patients with rheumatoid arthritis, which is a particularly common autoimmune disease [A27198]. Stem bromelain also affects blood coagulation by increasing the serum fibrinolytic ability and by preventing the synthesis of fibrin, a protein involved in blood clotting [A27198]. In the rat animal model, the reduction of serum fibrinogen level seems to be dose-dependent when both prothrombin time and activated partial thromboplastin time become markedly prolonged at higher concentrations of administered stem bromelain [A27198]. In vitro and in vivo studies also suggest stem bromelain can act as an effective fibrinolytic agent since it stimulates the conversion of plasminogen to plasmin, causing an increased fibrinolysis by degrading fibrin [A27198]. In terms of potential antimicrobial effects of stem bromelain, there are varying observations regarding its specific mechanism of action [A27198]. When counteracting the effects of some intestinal pathogens like Vibrio cholera or Escherichia coli (whose enterotoxin causes diarrhea in animals), some studies suggest that stem bromelain interacts with intestinal secretory signaling pathways like adenosine 3':5'-cyclic monophosphatase, guanosine 3':5'-cyclic monophosphatase, and/or calcium-dependent signaling cascades [A27198]. Conversely, other studies propose that stem bromelain supplementation can lead to antiadhesion effects which prevent E. coli bacteria from attaching to particular glycoprotein receptors on the intestinal mucosa by proteolytically modifying those receptor attachment sites [A27198]. Additionally, various studies have shown that stem bromelain also possesses anticancer activity. In particular, the agent has been found to increase the expression of p53 and Bax in mouse skin, both of which are well-known apoptosis activators [A27198]. Stem bromelain can also evidently decrease the activity of cell survival regulators like Akt and Erk, therefore inducing apoptotic tumor cell death [A27198]. Finally, stem bromelain has also been observed to downregulate NF-kB and Cox-2 expression in mouse papillomas and in models of skin tumorigenesis [A27198]. It has also demonstrated the capability to inhibit bacterial endotoxin (LPS)-induced NF-kB activity as well as the expression of PGE2 and Cox-2 in human monocytic leukemia and murine microglial cell lines [A27198]. | The human body can seemingly absorb significant amounts of bromelain - about 12 grams/day of bromelain may be consumed without the appearance of any major adverse effects [A27198]. Another study suggests that after giving bromelain (3000 FIP unit/day) to human over a period of ten days discovered no significant changes in blood coagulation parameters [A27198]. Finally, stem bromelain has a relatively low toxicity with an LD50 greater than 10 g/kg in mice, rats, and rabbits [A27198]. | Given its protein structure, it is assumed that stem bromelain, when administered would experience hydrolysis in the gut or eventually in the bloodstream after absorption [A32644]. Regardless, radiolabelled, intact stem bromelain has been found circulating in the plasma after administration [A27198, A32644]. | It appears that stem bromelain can be absorbed from the human gastrointestinal tract to a small but significant extent while remaining undegraded or functionally intact [A27198, A32644]. In a study involving 19 healthy men, daily oral administration of 3g/day of bromelain resulted in a mean plasma concentration of approximately 5000 pg/ml by 48 hours, although the maximum peak blood concentration of bromelain varied between 2000 to 10,000 pg/ml between subjects [A32644]. The average blood concentration of bromelain in the period range of 3 to 51 hours was 10.28 ug [A32644]. | No readily accessible data regarding the volume of distribution of stem bromelain is available. | No readily accessible data regarding the clearance of stem bromelain is available. | Enzymes and Coenzymes | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14223 | Th1476 | Stem bromelain | >Th1476_Stem_bromelain AVPQSIDWRDYGAVTSVKNQNPCGACWAFAAIATVESIYKIKKGILEPLSEQQVLDCAKGYGCKGGWEFRAFEFIISNKGVASGAIYPYKAAKGTCKTDGVPNSAYITGYARVPRNNESSMMYAVSKQPITVAVDANANFQYYKSGVFNGPCGTSLNHAVTAIGYGQDSIIYPKKWGAKWGEAGYIRMARDVSSSSGICGIAIDPLYPTLEE | NA | NA | NA | NA | NA | The estimated plasma half-life of stem bromelain is 6-9 hours [A32644]. | The primary therapeutic use for which stem bromelain is currently and formally indicated is as a burn wound eschar debridement agent that has been approved by the EMA since 2012 and marketed under the brand name Nexobrid [FDA Label]. Bromelain itself belongs to a category of protein-digesting enzymes that are obtained commercially from the fruit or stem of pineapples [A27198]. Although both fruit and stem bromelain are prepared differently and contain different enzymatic compositions, the general term bromelain typically refers to stem bromelain [A27198]. Bromelain is consequently a composite mixture of several different endopeptidases that can facilitate many different reactions with many different substrates. This action allows bromelain to demonstrate a wide range of therapeutic benefits ranging from cardiovascular to anticancer therapy - but the specific mechanisms of action by which it can elicit these effects are currently not properly understood. | The primary medical purpose for which stem bromelain (SB) is currently indicated for is the removal of eschar in adults with deep partial- and full-thickness thermal burns [FDA Label]. Besides this official indication, however, it is also believed that SB may be used as a treatment for several other purposes as well, including cardiovascular health, osteoarthritis, autoimmunity, blood clotting, diarrhea, cancer, surgery, and debridement - although the specific mechanisms of action for these indications remain to be elucidated [A27198]. | Stem bromelain is ultimately a mixture of various different thiol endopeptidases [A27198] that are capable of catalyzing a range of reactions on a number of different substrates, which is perhaps why stem bromelain can evidently be used as some manner of treatment in a range of therapeutic contexts. This notion is facilitated by the fact that various topical and oral administration stem bromelain preparations exist as well, further diversifying the ways in which the medication can be used. Perhaps the most important aspect of stem bromelain, however, is its ability to undergo intestinal absorption undegraded in a functionally intact form, ultimately preserving its proteolytic actions in the plasma [A27198, A32644]. This kind of pharmacodynamic characteristic is another element that perhaps allows stem bromelain to remain active within the body and elicit a number of actions at several major body systems. | Stem bromelain is ultimately a mixture of a number of thiol endopeptidases and other elements including phosphatases, glucosidase, peroxidases, cellulases, glycoproteins, carbohydrates, and various protease inhibitors [A27198]. The many different substrates and reactions that these varied enzymes can catalyze results in a number of different and possible mechanisms of action. Stem bromelain is currently principally used as a topical agent for debridement of necrotic tissue from wounds or second to third-degree burns [FDA Label, A27198]. As bromelain can contain escharase as one of its component enzymes, it is thought that various stem bromelain creams or gels can accelerate the healing process of wounds by facilitating the rapid removal of necrotic layers of dermis while preserving unburned/unharmed tissues [A27198] and/or perhaps by accelerating the recovery of blood perfusion in wound tissue, control the expression of TNF-alpha, and raise the expression of TGT-beta, as demonstrated in the pig animal model [A27198]. This kind of enzymatic debridement is ultimately preferred to surgical debridement as physical, surgical procedures are naturally painful, non-selective, and involve the possibility of repeat or excessive anesthesia and/or bleeding [A27198]. With regards to cardiovascular health, certain studies suggest that stem bromelain is capable of breaking down cholesterol plaques, eliciting a strong fibrinolytic activity, and inhibiting blood platelet aggregation - all of which protect against ischemia/reperfusion injury in skeletal muscle and minimize the risk of arterial thrombosis and embolism [A27198]. Additionally, stem bromelain has also been shown to attenuate allergic airway disease by altering CD4+ and CD8+ T lymphocyte populations - an action that may be beneficial in treating human asthma or hypersensitivity disorders [A27198]. Finally, stem bromelain has also been used to induce cardioprotection against ischemia-reperfusion injury via the Akt/Foxo pathway in rat model myocardium [A27198]. In the treatment of osteoarthritis, it is believed that stem bromelain has analgesic properties which are thought to be the result of direct influence on pain mediators such as bradykinin [A27198]. In addition, various trials suggest that the medication could be useful in reducing swelling, bruising, and pain in women having surgery like episiotomy [A27198]. Moreover, stem bromelain may also be used for treating acute inflammation and sports injuries [A27198]. Furthermore, stem bromelain has also been studied as an adjuvant therapy for chronic inflammatory, malignant, and autoimmune diseases [A27198]. Certain in vitro experiments have demonstrated that stem bromelain can modulate surface adhesion molecules on T cells, macrophages, and natural killer cells and also cause the secretion of IL-1B, IL-6, and Tumor Necrosis Factor-alpha (TNF-alpha) via peripheral blood mononuclear cells [A27198]. The agent has also been able to block the Raf-1/extracellular-regulated-kinase-2 (ERK-2) pathways by preventing T cell signal transduction [A27198]. In particular however, treating cells with stem bromelain decreases the activation of CD4(+) T cells and reduces the expression of CD25 [A27198]. Additionally, there is also evidence to suggest that oral therapy with stem bromelain produces certain analgesic and anti-inflammatory effects in patients with rheumatoid arthritis, which is a particularly common autoimmune disease [A27198]. Stem bromelain also affects blood coagulation by increasing the serum fibrinolytic ability and by preventing the synthesis of fibrin, a protein involved in blood clotting [A27198]. In the rat animal model, the reduction of serum fibrinogen level seems to be dose-dependent when both prothrombin time and activated partial thromboplastin time become markedly prolonged at higher concentrations of administered stem bromelain [A27198]. In vitro and in vivo studies also suggest stem bromelain can act as an effective fibrinolytic agent since it stimulates the conversion of plasminogen to plasmin, causing an increased fibrinolysis by degrading fibrin [A27198]. In terms of potential antimicrobial effects of stem bromelain, there are varying observations regarding its specific mechanism of action [A27198]. When counteracting the effects of some intestinal pathogens like Vibrio cholera or Escherichia coli (whose enterotoxin causes diarrhea in animals), some studies suggest that stem bromelain interacts with intestinal secretory signaling pathways like adenosine 3':5'-cyclic monophosphatase, guanosine 3':5'-cyclic monophosphatase, and/or calcium-dependent signaling cascades [A27198]. Conversely, other studies propose that stem bromelain supplementation can lead to antiadhesion effects which prevent E. coli bacteria from attaching to particular glycoprotein receptors on the intestinal mucosa by proteolytically modifying those receptor attachment sites [A27198]. Additionally, various studies have shown that stem bromelain also possesses anticancer activity. In particular, the agent has been found to increase the expression of p53 and Bax in mouse skin, both of which are well-known apoptosis activators [A27198]. Stem bromelain can also evidently decrease the activity of cell survival regulators like Akt and Erk, therefore inducing apoptotic tumor cell death [A27198]. Finally, stem bromelain has also been observed to downregulate NF-kB and Cox-2 expression in mouse papillomas and in models of skin tumorigenesis [A27198]. It has also demonstrated the capability to inhibit bacterial endotoxin (LPS)-induced NF-kB activity as well as the expression of PGE2 and Cox-2 in human monocytic leukemia and murine microglial cell lines [A27198]. | The human body can seemingly absorb significant amounts of bromelain - about 12 grams/day of bromelain may be consumed without the appearance of any major adverse effects [A27198]. Another study suggests that after giving bromelain (3000 FIP unit/day) to human over a period of ten days discovered no significant changes in blood coagulation parameters [A27198]. Finally, stem bromelain has a relatively low toxicity with an LD50 greater than 10 g/kg in mice, rats, and rabbits [A27198]. | Given its protein structure, it is assumed that stem bromelain, when administered would experience hydrolysis in the gut or eventually in the bloodstream after absorption [A32644]. Regardless, radiolabelled, intact stem bromelain has been found circulating in the plasma after administration [A27198, A32644]. | It appears that stem bromelain can be absorbed from the human gastrointestinal tract to a small but significant extent while remaining undegraded or functionally intact [A27198, A32644]. In a study involving 19 healthy men, daily oral administration of 3g/day of bromelain resulted in a mean plasma concentration of approximately 5000 pg/ml by 48 hours, although the maximum peak blood concentration of bromelain varied between 2000 to 10,000 pg/ml between subjects [A32644]. The average blood concentration of bromelain in the period range of 3 to 51 hours was 10.28 ug [A32644]. | No readily accessible data regarding the volume of distribution of stem bromelain is available. | No readily accessible data regarding the clearance of stem bromelain is available. | Hydrolases | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14224 | Th1476 | Stem bromelain | >Th1476_Stem_bromelain AVPQSIDWRDYGAVTSVKNQNPCGACWAFAAIATVESIYKIKKGILEPLSEQQVLDCAKGYGCKGGWEFRAFEFIISNKGVASGAIYPYKAAKGTCKTDGVPNSAYITGYARVPRNNESSMMYAVSKQPITVAVDANANFQYYKSGVFNGPCGTSLNHAVTAIGYGQDSIIYPKKWGAKWGEAGYIRMARDVSSSSGICGIAIDPLYPTLEE | NA | NA | NA | NA | NA | The estimated plasma half-life of stem bromelain is 6-9 hours [A32644]. | The primary therapeutic use for which stem bromelain is currently and formally indicated is as a burn wound eschar debridement agent that has been approved by the EMA since 2012 and marketed under the brand name Nexobrid [FDA Label]. Bromelain itself belongs to a category of protein-digesting enzymes that are obtained commercially from the fruit or stem of pineapples [A27198]. Although both fruit and stem bromelain are prepared differently and contain different enzymatic compositions, the general term bromelain typically refers to stem bromelain [A27198]. Bromelain is consequently a composite mixture of several different endopeptidases that can facilitate many different reactions with many different substrates. This action allows bromelain to demonstrate a wide range of therapeutic benefits ranging from cardiovascular to anticancer therapy - but the specific mechanisms of action by which it can elicit these effects are currently not properly understood. | The primary medical purpose for which stem bromelain (SB) is currently indicated for is the removal of eschar in adults with deep partial- and full-thickness thermal burns [FDA Label]. Besides this official indication, however, it is also believed that SB may be used as a treatment for several other purposes as well, including cardiovascular health, osteoarthritis, autoimmunity, blood clotting, diarrhea, cancer, surgery, and debridement - although the specific mechanisms of action for these indications remain to be elucidated [A27198]. | Stem bromelain is ultimately a mixture of various different thiol endopeptidases [A27198] that are capable of catalyzing a range of reactions on a number of different substrates, which is perhaps why stem bromelain can evidently be used as some manner of treatment in a range of therapeutic contexts. This notion is facilitated by the fact that various topical and oral administration stem bromelain preparations exist as well, further diversifying the ways in which the medication can be used. Perhaps the most important aspect of stem bromelain, however, is its ability to undergo intestinal absorption undegraded in a functionally intact form, ultimately preserving its proteolytic actions in the plasma [A27198, A32644]. This kind of pharmacodynamic characteristic is another element that perhaps allows stem bromelain to remain active within the body and elicit a number of actions at several major body systems. | Stem bromelain is ultimately a mixture of a number of thiol endopeptidases and other elements including phosphatases, glucosidase, peroxidases, cellulases, glycoproteins, carbohydrates, and various protease inhibitors [A27198]. The many different substrates and reactions that these varied enzymes can catalyze results in a number of different and possible mechanisms of action. Stem bromelain is currently principally used as a topical agent for debridement of necrotic tissue from wounds or second to third-degree burns [FDA Label, A27198]. As bromelain can contain escharase as one of its component enzymes, it is thought that various stem bromelain creams or gels can accelerate the healing process of wounds by facilitating the rapid removal of necrotic layers of dermis while preserving unburned/unharmed tissues [A27198] and/or perhaps by accelerating the recovery of blood perfusion in wound tissue, control the expression of TNF-alpha, and raise the expression of TGT-beta, as demonstrated in the pig animal model [A27198]. This kind of enzymatic debridement is ultimately preferred to surgical debridement as physical, surgical procedures are naturally painful, non-selective, and involve the possibility of repeat or excessive anesthesia and/or bleeding [A27198]. With regards to cardiovascular health, certain studies suggest that stem bromelain is capable of breaking down cholesterol plaques, eliciting a strong fibrinolytic activity, and inhibiting blood platelet aggregation - all of which protect against ischemia/reperfusion injury in skeletal muscle and minimize the risk of arterial thrombosis and embolism [A27198]. Additionally, stem bromelain has also been shown to attenuate allergic airway disease by altering CD4+ and CD8+ T lymphocyte populations - an action that may be beneficial in treating human asthma or hypersensitivity disorders [A27198]. Finally, stem bromelain has also been used to induce cardioprotection against ischemia-reperfusion injury via the Akt/Foxo pathway in rat model myocardium [A27198]. In the treatment of osteoarthritis, it is believed that stem bromelain has analgesic properties which are thought to be the result of direct influence on pain mediators such as bradykinin [A27198]. In addition, various trials suggest that the medication could be useful in reducing swelling, bruising, and pain in women having surgery like episiotomy [A27198]. Moreover, stem bromelain may also be used for treating acute inflammation and sports injuries [A27198]. Furthermore, stem bromelain has also been studied as an adjuvant therapy for chronic inflammatory, malignant, and autoimmune diseases [A27198]. Certain in vitro experiments have demonstrated that stem bromelain can modulate surface adhesion molecules on T cells, macrophages, and natural killer cells and also cause the secretion of IL-1B, IL-6, and Tumor Necrosis Factor-alpha (TNF-alpha) via peripheral blood mononuclear cells [A27198]. The agent has also been able to block the Raf-1/extracellular-regulated-kinase-2 (ERK-2) pathways by preventing T cell signal transduction [A27198]. In particular however, treating cells with stem bromelain decreases the activation of CD4(+) T cells and reduces the expression of CD25 [A27198]. Additionally, there is also evidence to suggest that oral therapy with stem bromelain produces certain analgesic and anti-inflammatory effects in patients with rheumatoid arthritis, which is a particularly common autoimmune disease [A27198]. Stem bromelain also affects blood coagulation by increasing the serum fibrinolytic ability and by preventing the synthesis of fibrin, a protein involved in blood clotting [A27198]. In the rat animal model, the reduction of serum fibrinogen level seems to be dose-dependent when both prothrombin time and activated partial thromboplastin time become markedly prolonged at higher concentrations of administered stem bromelain [A27198]. In vitro and in vivo studies also suggest stem bromelain can act as an effective fibrinolytic agent since it stimulates the conversion of plasminogen to plasmin, causing an increased fibrinolysis by degrading fibrin [A27198]. In terms of potential antimicrobial effects of stem bromelain, there are varying observations regarding its specific mechanism of action [A27198]. When counteracting the effects of some intestinal pathogens like Vibrio cholera or Escherichia coli (whose enterotoxin causes diarrhea in animals), some studies suggest that stem bromelain interacts with intestinal secretory signaling pathways like adenosine 3':5'-cyclic monophosphatase, guanosine 3':5'-cyclic monophosphatase, and/or calcium-dependent signaling cascades [A27198]. Conversely, other studies propose that stem bromelain supplementation can lead to antiadhesion effects which prevent E. coli bacteria from attaching to particular glycoprotein receptors on the intestinal mucosa by proteolytically modifying those receptor attachment sites [A27198]. Additionally, various studies have shown that stem bromelain also possesses anticancer activity. In particular, the agent has been found to increase the expression of p53 and Bax in mouse skin, both of which are well-known apoptosis activators [A27198]. Stem bromelain can also evidently decrease the activity of cell survival regulators like Akt and Erk, therefore inducing apoptotic tumor cell death [A27198]. Finally, stem bromelain has also been observed to downregulate NF-kB and Cox-2 expression in mouse papillomas and in models of skin tumorigenesis [A27198]. It has also demonstrated the capability to inhibit bacterial endotoxin (LPS)-induced NF-kB activity as well as the expression of PGE2 and Cox-2 in human monocytic leukemia and murine microglial cell lines [A27198]. | The human body can seemingly absorb significant amounts of bromelain - about 12 grams/day of bromelain may be consumed without the appearance of any major adverse effects [A27198]. Another study suggests that after giving bromelain (3000 FIP unit/day) to human over a period of ten days discovered no significant changes in blood coagulation parameters [A27198]. Finally, stem bromelain has a relatively low toxicity with an LD50 greater than 10 g/kg in mice, rats, and rabbits [A27198]. | Given its protein structure, it is assumed that stem bromelain, when administered would experience hydrolysis in the gut or eventually in the bloodstream after absorption [A32644]. Regardless, radiolabelled, intact stem bromelain has been found circulating in the plasma after administration [A27198, A32644]. | It appears that stem bromelain can be absorbed from the human gastrointestinal tract to a small but significant extent while remaining undegraded or functionally intact [A27198, A32644]. In a study involving 19 healthy men, daily oral administration of 3g/day of bromelain resulted in a mean plasma concentration of approximately 5000 pg/ml by 48 hours, although the maximum peak blood concentration of bromelain varied between 2000 to 10,000 pg/ml between subjects [A32644]. The average blood concentration of bromelain in the period range of 3 to 51 hours was 10.28 ug [A32644]. | No readily accessible data regarding the volume of distribution of stem bromelain is available. | No readily accessible data regarding the clearance of stem bromelain is available. | Peptide Hydrolases | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14601 | Th1521 | Moxetumomab pasudotox | >Th1521_Moxetumomab_pasudotox MEVQLVESGGGLVKPGGSLKLSCAASGFAFSIYDMSWVRQTPEKCLEWVAYISSGGGTTYYPDTVKGRFTISRDNAKNTLYLQMSSLKSEDTAMYYCARHSGYGTHWGVLFAYWGQGTLVSAKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYIAARLSWNQVDQVIRALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTWIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPREDLK | 63500 | C2804H4339N783O870S14 | NA | NA | NA | MxP presents a short half-life, which limits its efficacy against solid tumors.[A38882] The half-life is reported to be of only 1.4 hours.[A38883] | CD22 is a lineage-restricted B-cell antigen that is expressed solely in on B-chronic lymphocytic leukemia, hairy cell leukemia, acute lymphocytic leukemiathe and Burkitt's lymphoma. The predecessor of Moxetumab pasudotox (MxP), named BL22, was first created based on the antibody RFB4 which specifically binds to CD22. This antibody was used to generate a recombinant immunotoxin in which a stabilized Fv segment by a disulfide bond is fused to the _Pseudomonas_ exotoxin A (PE38) which does not have the cell-binding portion.[A38864] MxP appears as an improved form of BL22 by the mutation of the Fv region and the antibody phage-displayed. As well the residues SSY in the heavy chain are mutated to THW.[A38864] It was developed by Astra Zeneca and FDA approved on September 13, 2018, after being granted the status of Fast Track, Priority Review and Orphan Drug designations.[L4568] | MxP is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies including treatment with a purine nucleoside analog. The use of this drug is not recommended in patients with severe renal impairment (CrCl < 29 ml/min).[L4568] HCL is an uncommon type of lymphocytic leukemia that starts in B cells or B lymphocytes. It is characterized by an accumulation of abnormal B lymphocytes. HCL is called "hairy" as it produces hair-like projections in the surface of the cancer cells. A usual symptom in people having HCL is the presence of splenomegaly and less often hepatomegaly.[A38877] | Compared with its predecessor, MxP is even 50-fold more active on lymphoma cell lines and leukemic cells. In phase I clinical trial, MxP showed no dose-limiting toxicity and the overall response rate was of 79%. From pediatric patients with acute lymphoblastic leukemia, the complete response was observed in 12 individuals which is a result that has never been seen before.[A38880] In an open-label clinical trial, MxP showed a complete response, defined as the maintenance of hematologic remission, of more than 180 days in 30% of the patients and 75% of the patients achieved at least partial response.[L4568] Hence, the phase III clinical trial met the primary endpoint of durable complete response.[L4572] | MxP is a CD22-directed cytotoxin. It is stated as an immunotoxin which is defined as the class of agents that combine the selectivity of antibodies towards the target and the potency of toxins to perform the pharmacological anticancer function. CD22 is a B-lymphocyte restricted transmembrane protein with a high density in HCL cells when compared with normal B cells. After binding to CD22, MxP is internalized and processed, which allows the release of the modified toxin. This toxin inhibits protein translation which induces an apoptotic state of the high CD22-expressed cancer cell.[A38879] The toxin included in MxP is the _Pseudomonas_ exotoxin A which, after internalization, undergoes conformational changes and in the cytosol, the ribosylation activity of the domain III of the toxin inactivates the eukaryotic translation elongation factor (eEF-2) by transferring ADP (adenosine di-phosphate-ribose) from NAD to a modified histidine at position 715 in eEF-2. This action produces the inactivation of eEF-2 which leads to protein synthesis inhibition and programmed cell death.[A38881] | No studies have been performed regarding the carcinogenic potential and/or effect on fertility of MxP. It has been observed that the administration of MxP in a dose > 3 times the recommended can produce the degeneration of heart tissue and a dose > 10 times the recommended there are reports of gliosis, axonal degeneration in the spinal cord and body tremors.[FDA label] | The metabolism of MxP has not been well established but due to the nature of the drug, it is thought to be degraded into small peptides and individual amino acids.[A38883] | MxP serum concentration increases in a dose-proportional manner and reaches a mean steady state of 379 ng/ml with a Cmax of 626 ng.h/ml. There are no reports of systemic accumulation.[A38883] | The mean volume of distribution calculated based on population is 6.5 L.[A38883] | The mean systemic clearance is very fast and it is reported to be of 25 L/h. This clearance rate is decreased after subsequent dosing to 4 L/h.[A38883] | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | B-cell receptor CD22,Elongation factor 2 | Lumoxiti | AstraZeneca Pharmaceuticals LP | AstraZeneca Pharmaceuticals LP | Intravenous | 1 mg/1mL | None. | infusion related reactions, fluid retention (including facial swelling, abdominal bloating, weight gain, swelling of extremities), nausea, fatigue, headache, fever, constipation, anemia, diarrhea, eye problems (blurred vision, dry eye, cataracts, eye discomfort or pain, eye swelling, conjunctivitis, and tearing) | Lumoxiti is an injection used to treat hairy cell leukemia. Lumoxiti is used in adult patients with hairy cell leukemia that has relapsed. Lumoxiti is also used if the patient has not responded to previous treatments, and has received at least 2 other treatments, including a type of medicine called purine... | LUMOXITI is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies, including treatment with a purine nucleoside analog (PNA). | NA | NA | Link | Link | NA |
| 14602 | Th1521 | Moxetumomab pasudotox | >Th1521_Moxetumomab_pasudotox MEVQLVESGGGLVKPGGSLKLSCAASGFAFSIYDMSWVRQTPEKCLEWVAYISSGGGTTYYPDTVKGRFTISRDNAKNTLYLQMSSLKSEDTAMYYCARHSGYGTHWGVLFAYWGQGTLVSAKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYIAARLSWNQVDQVIRALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTWIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPREDLK | 63500 | C2804H4339N783O870S14 | NA | NA | NA | MxP presents a short half-life, which limits its efficacy against solid tumors.[A38882] The half-life is reported to be of only 1.4 hours.[A38883] | CD22 is a lineage-restricted B-cell antigen that is expressed solely in on B-chronic lymphocytic leukemia, hairy cell leukemia, acute lymphocytic leukemiathe and Burkitt's lymphoma. The predecessor of Moxetumab pasudotox (MxP), named BL22, was first created based on the antibody RFB4 which specifically binds to CD22. This antibody was used to generate a recombinant immunotoxin in which a stabilized Fv segment by a disulfide bond is fused to the _Pseudomonas_ exotoxin A (PE38) which does not have the cell-binding portion.[A38864] MxP appears as an improved form of BL22 by the mutation of the Fv region and the antibody phage-displayed. As well the residues SSY in the heavy chain are mutated to THW.[A38864] It was developed by Astra Zeneca and FDA approved on September 13, 2018, after being granted the status of Fast Track, Priority Review and Orphan Drug designations.[L4568] | MxP is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies including treatment with a purine nucleoside analog. The use of this drug is not recommended in patients with severe renal impairment (CrCl < 29 ml/min).[L4568] HCL is an uncommon type of lymphocytic leukemia that starts in B cells or B lymphocytes. It is characterized by an accumulation of abnormal B lymphocytes. HCL is called "hairy" as it produces hair-like projections in the surface of the cancer cells. A usual symptom in people having HCL is the presence of splenomegaly and less often hepatomegaly.[A38877] | Compared with its predecessor, MxP is even 50-fold more active on lymphoma cell lines and leukemic cells. In phase I clinical trial, MxP showed no dose-limiting toxicity and the overall response rate was of 79%. From pediatric patients with acute lymphoblastic leukemia, the complete response was observed in 12 individuals which is a result that has never been seen before.[A38880] In an open-label clinical trial, MxP showed a complete response, defined as the maintenance of hematologic remission, of more than 180 days in 30% of the patients and 75% of the patients achieved at least partial response.[L4568] Hence, the phase III clinical trial met the primary endpoint of durable complete response.[L4572] | MxP is a CD22-directed cytotoxin. It is stated as an immunotoxin which is defined as the class of agents that combine the selectivity of antibodies towards the target and the potency of toxins to perform the pharmacological anticancer function. CD22 is a B-lymphocyte restricted transmembrane protein with a high density in HCL cells when compared with normal B cells. After binding to CD22, MxP is internalized and processed, which allows the release of the modified toxin. This toxin inhibits protein translation which induces an apoptotic state of the high CD22-expressed cancer cell.[A38879] The toxin included in MxP is the _Pseudomonas_ exotoxin A which, after internalization, undergoes conformational changes and in the cytosol, the ribosylation activity of the domain III of the toxin inactivates the eukaryotic translation elongation factor (eEF-2) by transferring ADP (adenosine di-phosphate-ribose) from NAD to a modified histidine at position 715 in eEF-2. This action produces the inactivation of eEF-2 which leads to protein synthesis inhibition and programmed cell death.[A38881] | No studies have been performed regarding the carcinogenic potential and/or effect on fertility of MxP. It has been observed that the administration of MxP in a dose > 3 times the recommended can produce the degeneration of heart tissue and a dose > 10 times the recommended there are reports of gliosis, axonal degeneration in the spinal cord and body tremors.[FDA label] | The metabolism of MxP has not been well established but due to the nature of the drug, it is thought to be degraded into small peptides and individual amino acids.[A38883] | MxP serum concentration increases in a dose-proportional manner and reaches a mean steady state of 379 ng/ml with a Cmax of 626 ng.h/ml. There are no reports of systemic accumulation.[A38883] | The mean volume of distribution calculated based on population is 6.5 L.[A38883] | The mean systemic clearance is very fast and it is reported to be of 25 L/h. This clearance rate is decreased after subsequent dosing to 4 L/h.[A38883] | Antibodies, Monoclonal | NA | NA | NA | NA | B-cell receptor CD22,Elongation factor 2 | Lumoxiti | Astra Zeneca Ab | Astra Zeneca Ab | Intravenous | 1 mg | None. | infusion related reactions, fluid retention (including facial swelling, abdominal bloating, weight gain, swelling of extremities), nausea, fatigue, headache, fever, constipation, anemia, diarrhea, eye problems (blurred vision, dry eye, cataracts, eye discomfort or pain, eye swelling, conjunctivitis, and tearing) | Lumoxiti is an injection used to treat hairy cell leukemia. Lumoxiti is used in adult patients with hairy cell leukemia that has relapsed. Lumoxiti is also used if the patient has not responded to previous treatments, and has received at least 2 other treatments, including a type of medicine called purine... | LUMOXITI is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies, including treatment with a purine nucleoside analog (PNA). | NA | NA | Link | Link | NA |
| 14603 | Th1521 | Moxetumomab pasudotox | >Th1521_Moxetumomab_pasudotox MEVQLVESGGGLVKPGGSLKLSCAASGFAFSIYDMSWVRQTPEKCLEWVAYISSGGGTTYYPDTVKGRFTISRDNAKNTLYLQMSSLKSEDTAMYYCARHSGYGTHWGVLFAYWGQGTLVSAKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYIAARLSWNQVDQVIRALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTWIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPREDLK | 63500 | C2804H4339N783O870S14 | NA | NA | NA | MxP presents a short half-life, which limits its efficacy against solid tumors.[A38882] The half-life is reported to be of only 1.4 hours.[A38883] | CD22 is a lineage-restricted B-cell antigen that is expressed solely in on B-chronic lymphocytic leukemia, hairy cell leukemia, acute lymphocytic leukemiathe and Burkitt's lymphoma. The predecessor of Moxetumab pasudotox (MxP), named BL22, was first created based on the antibody RFB4 which specifically binds to CD22. This antibody was used to generate a recombinant immunotoxin in which a stabilized Fv segment by a disulfide bond is fused to the _Pseudomonas_ exotoxin A (PE38) which does not have the cell-binding portion.[A38864] MxP appears as an improved form of BL22 by the mutation of the Fv region and the antibody phage-displayed. As well the residues SSY in the heavy chain are mutated to THW.[A38864] It was developed by Astra Zeneca and FDA approved on September 13, 2018, after being granted the status of Fast Track, Priority Review and Orphan Drug designations.[L4568] | MxP is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies including treatment with a purine nucleoside analog. The use of this drug is not recommended in patients with severe renal impairment (CrCl < 29 ml/min).[L4568] HCL is an uncommon type of lymphocytic leukemia that starts in B cells or B lymphocytes. It is characterized by an accumulation of abnormal B lymphocytes. HCL is called "hairy" as it produces hair-like projections in the surface of the cancer cells. A usual symptom in people having HCL is the presence of splenomegaly and less often hepatomegaly.[A38877] | Compared with its predecessor, MxP is even 50-fold more active on lymphoma cell lines and leukemic cells. In phase I clinical trial, MxP showed no dose-limiting toxicity and the overall response rate was of 79%. From pediatric patients with acute lymphoblastic leukemia, the complete response was observed in 12 individuals which is a result that has never been seen before.[A38880] In an open-label clinical trial, MxP showed a complete response, defined as the maintenance of hematologic remission, of more than 180 days in 30% of the patients and 75% of the patients achieved at least partial response.[L4568] Hence, the phase III clinical trial met the primary endpoint of durable complete response.[L4572] | MxP is a CD22-directed cytotoxin. It is stated as an immunotoxin which is defined as the class of agents that combine the selectivity of antibodies towards the target and the potency of toxins to perform the pharmacological anticancer function. CD22 is a B-lymphocyte restricted transmembrane protein with a high density in HCL cells when compared with normal B cells. After binding to CD22, MxP is internalized and processed, which allows the release of the modified toxin. This toxin inhibits protein translation which induces an apoptotic state of the high CD22-expressed cancer cell.[A38879] The toxin included in MxP is the _Pseudomonas_ exotoxin A which, after internalization, undergoes conformational changes and in the cytosol, the ribosylation activity of the domain III of the toxin inactivates the eukaryotic translation elongation factor (eEF-2) by transferring ADP (adenosine di-phosphate-ribose) from NAD to a modified histidine at position 715 in eEF-2. This action produces the inactivation of eEF-2 which leads to protein synthesis inhibition and programmed cell death.[A38881] | No studies have been performed regarding the carcinogenic potential and/or effect on fertility of MxP. It has been observed that the administration of MxP in a dose > 3 times the recommended can produce the degeneration of heart tissue and a dose > 10 times the recommended there are reports of gliosis, axonal degeneration in the spinal cord and body tremors.[FDA label] | The metabolism of MxP has not been well established but due to the nature of the drug, it is thought to be degraded into small peptides and individual amino acids.[A38883] | MxP serum concentration increases in a dose-proportional manner and reaches a mean steady state of 379 ng/ml with a Cmax of 626 ng.h/ml. There are no reports of systemic accumulation.[A38883] | The mean volume of distribution calculated based on population is 6.5 L.[A38883] | The mean systemic clearance is very fast and it is reported to be of 25 L/h. This clearance rate is decreased after subsequent dosing to 4 L/h.[A38883] | Antineoplastic Agents | NA | NA | NA | NA | B-cell receptor CD22,Elongation factor 2 | Lumoxiti | Innate Pharma, Inc. | Innate Pharma, Inc. | Intravenous | 1 mg/1mL | None. | infusion related reactions, fluid retention (including facial swelling, abdominal bloating, weight gain, swelling of extremities), nausea, fatigue, headache, fever, constipation, anemia, diarrhea, eye problems (blurred vision, dry eye, cataracts, eye discomfort or pain, eye swelling, conjunctivitis, and tearing) | Lumoxiti is an injection used to treat hairy cell leukemia. Lumoxiti is used in adult patients with hairy cell leukemia that has relapsed. Lumoxiti is also used if the patient has not responded to previous treatments, and has received at least 2 other treatments, including a type of medicine called purine... | LUMOXITI is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies, including treatment with a purine nucleoside analog (PNA). | NA | NA | Link | Link | NA |
| 14604 | Th1521 | Moxetumomab pasudotox | >Th1521_Moxetumomab_pasudotox MEVQLVESGGGLVKPGGSLKLSCAASGFAFSIYDMSWVRQTPEKCLEWVAYISSGGGTTYYPDTVKGRFTISRDNAKNTLYLQMSSLKSEDTAMYYCARHSGYGTHWGVLFAYWGQGTLVSAKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYIAARLSWNQVDQVIRALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTWIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPREDLK | 63500 | C2804H4339N783O870S14 | NA | NA | NA | MxP presents a short half-life, which limits its efficacy against solid tumors.[A38882] The half-life is reported to be of only 1.4 hours.[A38883] | CD22 is a lineage-restricted B-cell antigen that is expressed solely in on B-chronic lymphocytic leukemia, hairy cell leukemia, acute lymphocytic leukemiathe and Burkitt's lymphoma. The predecessor of Moxetumab pasudotox (MxP), named BL22, was first created based on the antibody RFB4 which specifically binds to CD22. This antibody was used to generate a recombinant immunotoxin in which a stabilized Fv segment by a disulfide bond is fused to the _Pseudomonas_ exotoxin A (PE38) which does not have the cell-binding portion.[A38864] MxP appears as an improved form of BL22 by the mutation of the Fv region and the antibody phage-displayed. As well the residues SSY in the heavy chain are mutated to THW.[A38864] It was developed by Astra Zeneca and FDA approved on September 13, 2018, after being granted the status of Fast Track, Priority Review and Orphan Drug designations.[L4568] | MxP is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies including treatment with a purine nucleoside analog. The use of this drug is not recommended in patients with severe renal impairment (CrCl < 29 ml/min).[L4568] HCL is an uncommon type of lymphocytic leukemia that starts in B cells or B lymphocytes. It is characterized by an accumulation of abnormal B lymphocytes. HCL is called "hairy" as it produces hair-like projections in the surface of the cancer cells. A usual symptom in people having HCL is the presence of splenomegaly and less often hepatomegaly.[A38877] | Compared with its predecessor, MxP is even 50-fold more active on lymphoma cell lines and leukemic cells. In phase I clinical trial, MxP showed no dose-limiting toxicity and the overall response rate was of 79%. From pediatric patients with acute lymphoblastic leukemia, the complete response was observed in 12 individuals which is a result that has never been seen before.[A38880] In an open-label clinical trial, MxP showed a complete response, defined as the maintenance of hematologic remission, of more than 180 days in 30% of the patients and 75% of the patients achieved at least partial response.[L4568] Hence, the phase III clinical trial met the primary endpoint of durable complete response.[L4572] | MxP is a CD22-directed cytotoxin. It is stated as an immunotoxin which is defined as the class of agents that combine the selectivity of antibodies towards the target and the potency of toxins to perform the pharmacological anticancer function. CD22 is a B-lymphocyte restricted transmembrane protein with a high density in HCL cells when compared with normal B cells. After binding to CD22, MxP is internalized and processed, which allows the release of the modified toxin. This toxin inhibits protein translation which induces an apoptotic state of the high CD22-expressed cancer cell.[A38879] The toxin included in MxP is the _Pseudomonas_ exotoxin A which, after internalization, undergoes conformational changes and in the cytosol, the ribosylation activity of the domain III of the toxin inactivates the eukaryotic translation elongation factor (eEF-2) by transferring ADP (adenosine di-phosphate-ribose) from NAD to a modified histidine at position 715 in eEF-2. This action produces the inactivation of eEF-2 which leads to protein synthesis inhibition and programmed cell death.[A38881] | No studies have been performed regarding the carcinogenic potential and/or effect on fertility of MxP. It has been observed that the administration of MxP in a dose > 3 times the recommended can produce the degeneration of heart tissue and a dose > 10 times the recommended there are reports of gliosis, axonal degeneration in the spinal cord and body tremors.[FDA label] | The metabolism of MxP has not been well established but due to the nature of the drug, it is thought to be degraded into small peptides and individual amino acids.[A38883] | MxP serum concentration increases in a dose-proportional manner and reaches a mean steady state of 379 ng/ml with a Cmax of 626 ng.h/ml. There are no reports of systemic accumulation.[A38883] | The mean volume of distribution calculated based on population is 6.5 L.[A38883] | The mean systemic clearance is very fast and it is reported to be of 25 L/h. This clearance rate is decreased after subsequent dosing to 4 L/h.[A38883] | Blood Proteins | NA | NA | NA | NA | B-cell receptor CD22,Elongation factor 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14605 | Th1521 | Moxetumomab pasudotox | >Th1521_Moxetumomab_pasudotox MEVQLVESGGGLVKPGGSLKLSCAASGFAFSIYDMSWVRQTPEKCLEWVAYISSGGGTTYYPDTVKGRFTISRDNAKNTLYLQMSSLKSEDTAMYYCARHSGYGTHWGVLFAYWGQGTLVSAKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYIAARLSWNQVDQVIRALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTWIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPREDLK | 63500 | C2804H4339N783O870S14 | NA | NA | NA | MxP presents a short half-life, which limits its efficacy against solid tumors.[A38882] The half-life is reported to be of only 1.4 hours.[A38883] | CD22 is a lineage-restricted B-cell antigen that is expressed solely in on B-chronic lymphocytic leukemia, hairy cell leukemia, acute lymphocytic leukemiathe and Burkitt's lymphoma. The predecessor of Moxetumab pasudotox (MxP), named BL22, was first created based on the antibody RFB4 which specifically binds to CD22. This antibody was used to generate a recombinant immunotoxin in which a stabilized Fv segment by a disulfide bond is fused to the _Pseudomonas_ exotoxin A (PE38) which does not have the cell-binding portion.[A38864] MxP appears as an improved form of BL22 by the mutation of the Fv region and the antibody phage-displayed. As well the residues SSY in the heavy chain are mutated to THW.[A38864] It was developed by Astra Zeneca and FDA approved on September 13, 2018, after being granted the status of Fast Track, Priority Review and Orphan Drug designations.[L4568] | MxP is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies including treatment with a purine nucleoside analog. The use of this drug is not recommended in patients with severe renal impairment (CrCl < 29 ml/min).[L4568] HCL is an uncommon type of lymphocytic leukemia that starts in B cells or B lymphocytes. It is characterized by an accumulation of abnormal B lymphocytes. HCL is called "hairy" as it produces hair-like projections in the surface of the cancer cells. A usual symptom in people having HCL is the presence of splenomegaly and less often hepatomegaly.[A38877] | Compared with its predecessor, MxP is even 50-fold more active on lymphoma cell lines and leukemic cells. In phase I clinical trial, MxP showed no dose-limiting toxicity and the overall response rate was of 79%. From pediatric patients with acute lymphoblastic leukemia, the complete response was observed in 12 individuals which is a result that has never been seen before.[A38880] In an open-label clinical trial, MxP showed a complete response, defined as the maintenance of hematologic remission, of more than 180 days in 30% of the patients and 75% of the patients achieved at least partial response.[L4568] Hence, the phase III clinical trial met the primary endpoint of durable complete response.[L4572] | MxP is a CD22-directed cytotoxin. It is stated as an immunotoxin which is defined as the class of agents that combine the selectivity of antibodies towards the target and the potency of toxins to perform the pharmacological anticancer function. CD22 is a B-lymphocyte restricted transmembrane protein with a high density in HCL cells when compared with normal B cells. After binding to CD22, MxP is internalized and processed, which allows the release of the modified toxin. This toxin inhibits protein translation which induces an apoptotic state of the high CD22-expressed cancer cell.[A38879] The toxin included in MxP is the _Pseudomonas_ exotoxin A which, after internalization, undergoes conformational changes and in the cytosol, the ribosylation activity of the domain III of the toxin inactivates the eukaryotic translation elongation factor (eEF-2) by transferring ADP (adenosine di-phosphate-ribose) from NAD to a modified histidine at position 715 in eEF-2. This action produces the inactivation of eEF-2 which leads to protein synthesis inhibition and programmed cell death.[A38881] | No studies have been performed regarding the carcinogenic potential and/or effect on fertility of MxP. It has been observed that the administration of MxP in a dose > 3 times the recommended can produce the degeneration of heart tissue and a dose > 10 times the recommended there are reports of gliosis, axonal degeneration in the spinal cord and body tremors.[FDA label] | The metabolism of MxP has not been well established but due to the nature of the drug, it is thought to be degraded into small peptides and individual amino acids.[A38883] | MxP serum concentration increases in a dose-proportional manner and reaches a mean steady state of 379 ng/ml with a Cmax of 626 ng.h/ml. There are no reports of systemic accumulation.[A38883] | The mean volume of distribution calculated based on population is 6.5 L.[A38883] | The mean systemic clearance is very fast and it is reported to be of 25 L/h. This clearance rate is decreased after subsequent dosing to 4 L/h.[A38883] | Cancer immunotherapy | NA | NA | NA | NA | B-cell receptor CD22,Elongation factor 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14606 | Th1521 | Moxetumomab pasudotox | >Th1521_Moxetumomab_pasudotox MEVQLVESGGGLVKPGGSLKLSCAASGFAFSIYDMSWVRQTPEKCLEWVAYISSGGGTTYYPDTVKGRFTISRDNAKNTLYLQMSSLKSEDTAMYYCARHSGYGTHWGVLFAYWGQGTLVSAKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYIAARLSWNQVDQVIRALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTWIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPREDLK | 63500 | C2804H4339N783O870S14 | NA | NA | NA | MxP presents a short half-life, which limits its efficacy against solid tumors.[A38882] The half-life is reported to be of only 1.4 hours.[A38883] | CD22 is a lineage-restricted B-cell antigen that is expressed solely in on B-chronic lymphocytic leukemia, hairy cell leukemia, acute lymphocytic leukemiathe and Burkitt's lymphoma. The predecessor of Moxetumab pasudotox (MxP), named BL22, was first created based on the antibody RFB4 which specifically binds to CD22. This antibody was used to generate a recombinant immunotoxin in which a stabilized Fv segment by a disulfide bond is fused to the _Pseudomonas_ exotoxin A (PE38) which does not have the cell-binding portion.[A38864] MxP appears as an improved form of BL22 by the mutation of the Fv region and the antibody phage-displayed. As well the residues SSY in the heavy chain are mutated to THW.[A38864] It was developed by Astra Zeneca and FDA approved on September 13, 2018, after being granted the status of Fast Track, Priority Review and Orphan Drug designations.[L4568] | MxP is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies including treatment with a purine nucleoside analog. The use of this drug is not recommended in patients with severe renal impairment (CrCl < 29 ml/min).[L4568] HCL is an uncommon type of lymphocytic leukemia that starts in B cells or B lymphocytes. It is characterized by an accumulation of abnormal B lymphocytes. HCL is called "hairy" as it produces hair-like projections in the surface of the cancer cells. A usual symptom in people having HCL is the presence of splenomegaly and less often hepatomegaly.[A38877] | Compared with its predecessor, MxP is even 50-fold more active on lymphoma cell lines and leukemic cells. In phase I clinical trial, MxP showed no dose-limiting toxicity and the overall response rate was of 79%. From pediatric patients with acute lymphoblastic leukemia, the complete response was observed in 12 individuals which is a result that has never been seen before.[A38880] In an open-label clinical trial, MxP showed a complete response, defined as the maintenance of hematologic remission, of more than 180 days in 30% of the patients and 75% of the patients achieved at least partial response.[L4568] Hence, the phase III clinical trial met the primary endpoint of durable complete response.[L4572] | MxP is a CD22-directed cytotoxin. It is stated as an immunotoxin which is defined as the class of agents that combine the selectivity of antibodies towards the target and the potency of toxins to perform the pharmacological anticancer function. CD22 is a B-lymphocyte restricted transmembrane protein with a high density in HCL cells when compared with normal B cells. After binding to CD22, MxP is internalized and processed, which allows the release of the modified toxin. This toxin inhibits protein translation which induces an apoptotic state of the high CD22-expressed cancer cell.[A38879] The toxin included in MxP is the _Pseudomonas_ exotoxin A which, after internalization, undergoes conformational changes and in the cytosol, the ribosylation activity of the domain III of the toxin inactivates the eukaryotic translation elongation factor (eEF-2) by transferring ADP (adenosine di-phosphate-ribose) from NAD to a modified histidine at position 715 in eEF-2. This action produces the inactivation of eEF-2 which leads to protein synthesis inhibition and programmed cell death.[A38881] | No studies have been performed regarding the carcinogenic potential and/or effect on fertility of MxP. It has been observed that the administration of MxP in a dose > 3 times the recommended can produce the degeneration of heart tissue and a dose > 10 times the recommended there are reports of gliosis, axonal degeneration in the spinal cord and body tremors.[FDA label] | The metabolism of MxP has not been well established but due to the nature of the drug, it is thought to be degraded into small peptides and individual amino acids.[A38883] | MxP serum concentration increases in a dose-proportional manner and reaches a mean steady state of 379 ng/ml with a Cmax of 626 ng.h/ml. There are no reports of systemic accumulation.[A38883] | The mean volume of distribution calculated based on population is 6.5 L.[A38883] | The mean systemic clearance is very fast and it is reported to be of 25 L/h. This clearance rate is decreased after subsequent dosing to 4 L/h.[A38883] | Immunoglobulins | NA | NA | NA | NA | B-cell receptor CD22,Elongation factor 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14607 | Th1521 | Moxetumomab pasudotox | >Th1521_Moxetumomab_pasudotox MEVQLVESGGGLVKPGGSLKLSCAASGFAFSIYDMSWVRQTPEKCLEWVAYISSGGGTTYYPDTVKGRFTISRDNAKNTLYLQMSSLKSEDTAMYYCARHSGYGTHWGVLFAYWGQGTLVSAKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYIAARLSWNQVDQVIRALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTWIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPREDLK | 63500 | C2804H4339N783O870S14 | NA | NA | NA | MxP presents a short half-life, which limits its efficacy against solid tumors.[A38882] The half-life is reported to be of only 1.4 hours.[A38883] | CD22 is a lineage-restricted B-cell antigen that is expressed solely in on B-chronic lymphocytic leukemia, hairy cell leukemia, acute lymphocytic leukemiathe and Burkitt's lymphoma. The predecessor of Moxetumab pasudotox (MxP), named BL22, was first created based on the antibody RFB4 which specifically binds to CD22. This antibody was used to generate a recombinant immunotoxin in which a stabilized Fv segment by a disulfide bond is fused to the _Pseudomonas_ exotoxin A (PE38) which does not have the cell-binding portion.[A38864] MxP appears as an improved form of BL22 by the mutation of the Fv region and the antibody phage-displayed. As well the residues SSY in the heavy chain are mutated to THW.[A38864] It was developed by Astra Zeneca and FDA approved on September 13, 2018, after being granted the status of Fast Track, Priority Review and Orphan Drug designations.[L4568] | MxP is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies including treatment with a purine nucleoside analog. The use of this drug is not recommended in patients with severe renal impairment (CrCl < 29 ml/min).[L4568] HCL is an uncommon type of lymphocytic leukemia that starts in B cells or B lymphocytes. It is characterized by an accumulation of abnormal B lymphocytes. HCL is called "hairy" as it produces hair-like projections in the surface of the cancer cells. A usual symptom in people having HCL is the presence of splenomegaly and less often hepatomegaly.[A38877] | Compared with its predecessor, MxP is even 50-fold more active on lymphoma cell lines and leukemic cells. In phase I clinical trial, MxP showed no dose-limiting toxicity and the overall response rate was of 79%. From pediatric patients with acute lymphoblastic leukemia, the complete response was observed in 12 individuals which is a result that has never been seen before.[A38880] In an open-label clinical trial, MxP showed a complete response, defined as the maintenance of hematologic remission, of more than 180 days in 30% of the patients and 75% of the patients achieved at least partial response.[L4568] Hence, the phase III clinical trial met the primary endpoint of durable complete response.[L4572] | MxP is a CD22-directed cytotoxin. It is stated as an immunotoxin which is defined as the class of agents that combine the selectivity of antibodies towards the target and the potency of toxins to perform the pharmacological anticancer function. CD22 is a B-lymphocyte restricted transmembrane protein with a high density in HCL cells when compared with normal B cells. After binding to CD22, MxP is internalized and processed, which allows the release of the modified toxin. This toxin inhibits protein translation which induces an apoptotic state of the high CD22-expressed cancer cell.[A38879] The toxin included in MxP is the _Pseudomonas_ exotoxin A which, after internalization, undergoes conformational changes and in the cytosol, the ribosylation activity of the domain III of the toxin inactivates the eukaryotic translation elongation factor (eEF-2) by transferring ADP (adenosine di-phosphate-ribose) from NAD to a modified histidine at position 715 in eEF-2. This action produces the inactivation of eEF-2 which leads to protein synthesis inhibition and programmed cell death.[A38881] | No studies have been performed regarding the carcinogenic potential and/or effect on fertility of MxP. It has been observed that the administration of MxP in a dose > 3 times the recommended can produce the degeneration of heart tissue and a dose > 10 times the recommended there are reports of gliosis, axonal degeneration in the spinal cord and body tremors.[FDA label] | The metabolism of MxP has not been well established but due to the nature of the drug, it is thought to be degraded into small peptides and individual amino acids.[A38883] | MxP serum concentration increases in a dose-proportional manner and reaches a mean steady state of 379 ng/ml with a Cmax of 626 ng.h/ml. There are no reports of systemic accumulation.[A38883] | The mean volume of distribution calculated based on population is 6.5 L.[A38883] | The mean systemic clearance is very fast and it is reported to be of 25 L/h. This clearance rate is decreased after subsequent dosing to 4 L/h.[A38883] | Immunotherapy | NA | NA | NA | NA | B-cell receptor CD22,Elongation factor 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14608 | Th1521 | Moxetumomab pasudotox | >Th1521_Moxetumomab_pasudotox MEVQLVESGGGLVKPGGSLKLSCAASGFAFSIYDMSWVRQTPEKCLEWVAYISSGGGTTYYPDTVKGRFTISRDNAKNTLYLQMSSLKSEDTAMYYCARHSGYGTHWGVLFAYWGQGTLVSAKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYIAARLSWNQVDQVIRALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTWIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPREDLK | 63500 | C2804H4339N783O870S14 | NA | NA | NA | MxP presents a short half-life, which limits its efficacy against solid tumors.[A38882] The half-life is reported to be of only 1.4 hours.[A38883] | CD22 is a lineage-restricted B-cell antigen that is expressed solely in on B-chronic lymphocytic leukemia, hairy cell leukemia, acute lymphocytic leukemiathe and Burkitt's lymphoma. The predecessor of Moxetumab pasudotox (MxP), named BL22, was first created based on the antibody RFB4 which specifically binds to CD22. This antibody was used to generate a recombinant immunotoxin in which a stabilized Fv segment by a disulfide bond is fused to the _Pseudomonas_ exotoxin A (PE38) which does not have the cell-binding portion.[A38864] MxP appears as an improved form of BL22 by the mutation of the Fv region and the antibody phage-displayed. As well the residues SSY in the heavy chain are mutated to THW.[A38864] It was developed by Astra Zeneca and FDA approved on September 13, 2018, after being granted the status of Fast Track, Priority Review and Orphan Drug designations.[L4568] | MxP is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies including treatment with a purine nucleoside analog. The use of this drug is not recommended in patients with severe renal impairment (CrCl < 29 ml/min).[L4568] HCL is an uncommon type of lymphocytic leukemia that starts in B cells or B lymphocytes. It is characterized by an accumulation of abnormal B lymphocytes. HCL is called "hairy" as it produces hair-like projections in the surface of the cancer cells. A usual symptom in people having HCL is the presence of splenomegaly and less often hepatomegaly.[A38877] | Compared with its predecessor, MxP is even 50-fold more active on lymphoma cell lines and leukemic cells. In phase I clinical trial, MxP showed no dose-limiting toxicity and the overall response rate was of 79%. From pediatric patients with acute lymphoblastic leukemia, the complete response was observed in 12 individuals which is a result that has never been seen before.[A38880] In an open-label clinical trial, MxP showed a complete response, defined as the maintenance of hematologic remission, of more than 180 days in 30% of the patients and 75% of the patients achieved at least partial response.[L4568] Hence, the phase III clinical trial met the primary endpoint of durable complete response.[L4572] | MxP is a CD22-directed cytotoxin. It is stated as an immunotoxin which is defined as the class of agents that combine the selectivity of antibodies towards the target and the potency of toxins to perform the pharmacological anticancer function. CD22 is a B-lymphocyte restricted transmembrane protein with a high density in HCL cells when compared with normal B cells. After binding to CD22, MxP is internalized and processed, which allows the release of the modified toxin. This toxin inhibits protein translation which induces an apoptotic state of the high CD22-expressed cancer cell.[A38879] The toxin included in MxP is the _Pseudomonas_ exotoxin A which, after internalization, undergoes conformational changes and in the cytosol, the ribosylation activity of the domain III of the toxin inactivates the eukaryotic translation elongation factor (eEF-2) by transferring ADP (adenosine di-phosphate-ribose) from NAD to a modified histidine at position 715 in eEF-2. This action produces the inactivation of eEF-2 which leads to protein synthesis inhibition and programmed cell death.[A38881] | No studies have been performed regarding the carcinogenic potential and/or effect on fertility of MxP. It has been observed that the administration of MxP in a dose > 3 times the recommended can produce the degeneration of heart tissue and a dose > 10 times the recommended there are reports of gliosis, axonal degeneration in the spinal cord and body tremors.[FDA label] | The metabolism of MxP has not been well established but due to the nature of the drug, it is thought to be degraded into small peptides and individual amino acids.[A38883] | MxP serum concentration increases in a dose-proportional manner and reaches a mean steady state of 379 ng/ml with a Cmax of 626 ng.h/ml. There are no reports of systemic accumulation.[A38883] | The mean volume of distribution calculated based on population is 6.5 L.[A38883] | The mean systemic clearance is very fast and it is reported to be of 25 L/h. This clearance rate is decreased after subsequent dosing to 4 L/h.[A38883] | Immunotoxins | NA | NA | NA | NA | B-cell receptor CD22,Elongation factor 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14609 | Th1521 | Moxetumomab pasudotox | >Th1521_Moxetumomab_pasudotox MEVQLVESGGGLVKPGGSLKLSCAASGFAFSIYDMSWVRQTPEKCLEWVAYISSGGGTTYYPDTVKGRFTISRDNAKNTLYLQMSSLKSEDTAMYYCARHSGYGTHWGVLFAYWGQGTLVSAKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYIAARLSWNQVDQVIRALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTWIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPREDLK | 63500 | C2804H4339N783O870S14 | NA | NA | NA | MxP presents a short half-life, which limits its efficacy against solid tumors.[A38882] The half-life is reported to be of only 1.4 hours.[A38883] | CD22 is a lineage-restricted B-cell antigen that is expressed solely in on B-chronic lymphocytic leukemia, hairy cell leukemia, acute lymphocytic leukemiathe and Burkitt's lymphoma. The predecessor of Moxetumab pasudotox (MxP), named BL22, was first created based on the antibody RFB4 which specifically binds to CD22. This antibody was used to generate a recombinant immunotoxin in which a stabilized Fv segment by a disulfide bond is fused to the _Pseudomonas_ exotoxin A (PE38) which does not have the cell-binding portion.[A38864] MxP appears as an improved form of BL22 by the mutation of the Fv region and the antibody phage-displayed. As well the residues SSY in the heavy chain are mutated to THW.[A38864] It was developed by Astra Zeneca and FDA approved on September 13, 2018, after being granted the status of Fast Track, Priority Review and Orphan Drug designations.[L4568] | MxP is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies including treatment with a purine nucleoside analog. The use of this drug is not recommended in patients with severe renal impairment (CrCl < 29 ml/min).[L4568] HCL is an uncommon type of lymphocytic leukemia that starts in B cells or B lymphocytes. It is characterized by an accumulation of abnormal B lymphocytes. HCL is called "hairy" as it produces hair-like projections in the surface of the cancer cells. A usual symptom in people having HCL is the presence of splenomegaly and less often hepatomegaly.[A38877] | Compared with its predecessor, MxP is even 50-fold more active on lymphoma cell lines and leukemic cells. In phase I clinical trial, MxP showed no dose-limiting toxicity and the overall response rate was of 79%. From pediatric patients with acute lymphoblastic leukemia, the complete response was observed in 12 individuals which is a result that has never been seen before.[A38880] In an open-label clinical trial, MxP showed a complete response, defined as the maintenance of hematologic remission, of more than 180 days in 30% of the patients and 75% of the patients achieved at least partial response.[L4568] Hence, the phase III clinical trial met the primary endpoint of durable complete response.[L4572] | MxP is a CD22-directed cytotoxin. It is stated as an immunotoxin which is defined as the class of agents that combine the selectivity of antibodies towards the target and the potency of toxins to perform the pharmacological anticancer function. CD22 is a B-lymphocyte restricted transmembrane protein with a high density in HCL cells when compared with normal B cells. After binding to CD22, MxP is internalized and processed, which allows the release of the modified toxin. This toxin inhibits protein translation which induces an apoptotic state of the high CD22-expressed cancer cell.[A38879] The toxin included in MxP is the _Pseudomonas_ exotoxin A which, after internalization, undergoes conformational changes and in the cytosol, the ribosylation activity of the domain III of the toxin inactivates the eukaryotic translation elongation factor (eEF-2) by transferring ADP (adenosine di-phosphate-ribose) from NAD to a modified histidine at position 715 in eEF-2. This action produces the inactivation of eEF-2 which leads to protein synthesis inhibition and programmed cell death.[A38881] | No studies have been performed regarding the carcinogenic potential and/or effect on fertility of MxP. It has been observed that the administration of MxP in a dose > 3 times the recommended can produce the degeneration of heart tissue and a dose > 10 times the recommended there are reports of gliosis, axonal degeneration in the spinal cord and body tremors.[FDA label] | The metabolism of MxP has not been well established but due to the nature of the drug, it is thought to be degraded into small peptides and individual amino acids.[A38883] | MxP serum concentration increases in a dose-proportional manner and reaches a mean steady state of 379 ng/ml with a Cmax of 626 ng.h/ml. There are no reports of systemic accumulation.[A38883] | The mean volume of distribution calculated based on population is 6.5 L.[A38883] | The mean systemic clearance is very fast and it is reported to be of 25 L/h. This clearance rate is decreased after subsequent dosing to 4 L/h.[A38883] | Narrow Therapeutic Index Drugs | NA | NA | NA | NA | B-cell receptor CD22,Elongation factor 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14610 | Th1521 | Moxetumomab pasudotox | >Th1521_Moxetumomab_pasudotox MEVQLVESGGGLVKPGGSLKLSCAASGFAFSIYDMSWVRQTPEKCLEWVAYISSGGGTTYYPDTVKGRFTISRDNAKNTLYLQMSSLKSEDTAMYYCARHSGYGTHWGVLFAYWGQGTLVSAKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYIAARLSWNQVDQVIRALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTWIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPREDLK | 63500 | C2804H4339N783O870S14 | NA | NA | NA | MxP presents a short half-life, which limits its efficacy against solid tumors.[A38882] The half-life is reported to be of only 1.4 hours.[A38883] | CD22 is a lineage-restricted B-cell antigen that is expressed solely in on B-chronic lymphocytic leukemia, hairy cell leukemia, acute lymphocytic leukemiathe and Burkitt's lymphoma. The predecessor of Moxetumab pasudotox (MxP), named BL22, was first created based on the antibody RFB4 which specifically binds to CD22. This antibody was used to generate a recombinant immunotoxin in which a stabilized Fv segment by a disulfide bond is fused to the _Pseudomonas_ exotoxin A (PE38) which does not have the cell-binding portion.[A38864] MxP appears as an improved form of BL22 by the mutation of the Fv region and the antibody phage-displayed. As well the residues SSY in the heavy chain are mutated to THW.[A38864] It was developed by Astra Zeneca and FDA approved on September 13, 2018, after being granted the status of Fast Track, Priority Review and Orphan Drug designations.[L4568] | MxP is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies including treatment with a purine nucleoside analog. The use of this drug is not recommended in patients with severe renal impairment (CrCl < 29 ml/min).[L4568] HCL is an uncommon type of lymphocytic leukemia that starts in B cells or B lymphocytes. It is characterized by an accumulation of abnormal B lymphocytes. HCL is called "hairy" as it produces hair-like projections in the surface of the cancer cells. A usual symptom in people having HCL is the presence of splenomegaly and less often hepatomegaly.[A38877] | Compared with its predecessor, MxP is even 50-fold more active on lymphoma cell lines and leukemic cells. In phase I clinical trial, MxP showed no dose-limiting toxicity and the overall response rate was of 79%. From pediatric patients with acute lymphoblastic leukemia, the complete response was observed in 12 individuals which is a result that has never been seen before.[A38880] In an open-label clinical trial, MxP showed a complete response, defined as the maintenance of hematologic remission, of more than 180 days in 30% of the patients and 75% of the patients achieved at least partial response.[L4568] Hence, the phase III clinical trial met the primary endpoint of durable complete response.[L4572] | MxP is a CD22-directed cytotoxin. It is stated as an immunotoxin which is defined as the class of agents that combine the selectivity of antibodies towards the target and the potency of toxins to perform the pharmacological anticancer function. CD22 is a B-lymphocyte restricted transmembrane protein with a high density in HCL cells when compared with normal B cells. After binding to CD22, MxP is internalized and processed, which allows the release of the modified toxin. This toxin inhibits protein translation which induces an apoptotic state of the high CD22-expressed cancer cell.[A38879] The toxin included in MxP is the _Pseudomonas_ exotoxin A which, after internalization, undergoes conformational changes and in the cytosol, the ribosylation activity of the domain III of the toxin inactivates the eukaryotic translation elongation factor (eEF-2) by transferring ADP (adenosine di-phosphate-ribose) from NAD to a modified histidine at position 715 in eEF-2. This action produces the inactivation of eEF-2 which leads to protein synthesis inhibition and programmed cell death.[A38881] | No studies have been performed regarding the carcinogenic potential and/or effect on fertility of MxP. It has been observed that the administration of MxP in a dose > 3 times the recommended can produce the degeneration of heart tissue and a dose > 10 times the recommended there are reports of gliosis, axonal degeneration in the spinal cord and body tremors.[FDA label] | The metabolism of MxP has not been well established but due to the nature of the drug, it is thought to be degraded into small peptides and individual amino acids.[A38883] | MxP serum concentration increases in a dose-proportional manner and reaches a mean steady state of 379 ng/ml with a Cmax of 626 ng.h/ml. There are no reports of systemic accumulation.[A38883] | The mean volume of distribution calculated based on population is 6.5 L.[A38883] | The mean systemic clearance is very fast and it is reported to be of 25 L/h. This clearance rate is decreased after subsequent dosing to 4 L/h.[A38883] | Proteins | NA | NA | NA | NA | B-cell receptor CD22,Elongation factor 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14611 | Th1521 | Moxetumomab pasudotox | >Th1521_Moxetumomab_pasudotox MEVQLVESGGGLVKPGGSLKLSCAASGFAFSIYDMSWVRQTPEKCLEWVAYISSGGGTTYYPDTVKGRFTISRDNAKNTLYLQMSSLKSEDTAMYYCARHSGYGTHWGVLFAYWGQGTLVSAKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYIAARLSWNQVDQVIRALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTWIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPREDLK | 63500 | C2804H4339N783O870S14 | NA | NA | NA | MxP presents a short half-life, which limits its efficacy against solid tumors.[A38882] The half-life is reported to be of only 1.4 hours.[A38883] | CD22 is a lineage-restricted B-cell antigen that is expressed solely in on B-chronic lymphocytic leukemia, hairy cell leukemia, acute lymphocytic leukemiathe and Burkitt's lymphoma. The predecessor of Moxetumab pasudotox (MxP), named BL22, was first created based on the antibody RFB4 which specifically binds to CD22. This antibody was used to generate a recombinant immunotoxin in which a stabilized Fv segment by a disulfide bond is fused to the _Pseudomonas_ exotoxin A (PE38) which does not have the cell-binding portion.[A38864] MxP appears as an improved form of BL22 by the mutation of the Fv region and the antibody phage-displayed. As well the residues SSY in the heavy chain are mutated to THW.[A38864] It was developed by Astra Zeneca and FDA approved on September 13, 2018, after being granted the status of Fast Track, Priority Review and Orphan Drug designations.[L4568] | MxP is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies including treatment with a purine nucleoside analog. The use of this drug is not recommended in patients with severe renal impairment (CrCl < 29 ml/min).[L4568] HCL is an uncommon type of lymphocytic leukemia that starts in B cells or B lymphocytes. It is characterized by an accumulation of abnormal B lymphocytes. HCL is called "hairy" as it produces hair-like projections in the surface of the cancer cells. A usual symptom in people having HCL is the presence of splenomegaly and less often hepatomegaly.[A38877] | Compared with its predecessor, MxP is even 50-fold more active on lymphoma cell lines and leukemic cells. In phase I clinical trial, MxP showed no dose-limiting toxicity and the overall response rate was of 79%. From pediatric patients with acute lymphoblastic leukemia, the complete response was observed in 12 individuals which is a result that has never been seen before.[A38880] In an open-label clinical trial, MxP showed a complete response, defined as the maintenance of hematologic remission, of more than 180 days in 30% of the patients and 75% of the patients achieved at least partial response.[L4568] Hence, the phase III clinical trial met the primary endpoint of durable complete response.[L4572] | MxP is a CD22-directed cytotoxin. It is stated as an immunotoxin which is defined as the class of agents that combine the selectivity of antibodies towards the target and the potency of toxins to perform the pharmacological anticancer function. CD22 is a B-lymphocyte restricted transmembrane protein with a high density in HCL cells when compared with normal B cells. After binding to CD22, MxP is internalized and processed, which allows the release of the modified toxin. This toxin inhibits protein translation which induces an apoptotic state of the high CD22-expressed cancer cell.[A38879] The toxin included in MxP is the _Pseudomonas_ exotoxin A which, after internalization, undergoes conformational changes and in the cytosol, the ribosylation activity of the domain III of the toxin inactivates the eukaryotic translation elongation factor (eEF-2) by transferring ADP (adenosine di-phosphate-ribose) from NAD to a modified histidine at position 715 in eEF-2. This action produces the inactivation of eEF-2 which leads to protein synthesis inhibition and programmed cell death.[A38881] | No studies have been performed regarding the carcinogenic potential and/or effect on fertility of MxP. It has been observed that the administration of MxP in a dose > 3 times the recommended can produce the degeneration of heart tissue and a dose > 10 times the recommended there are reports of gliosis, axonal degeneration in the spinal cord and body tremors.[FDA label] | The metabolism of MxP has not been well established but due to the nature of the drug, it is thought to be degraded into small peptides and individual amino acids.[A38883] | MxP serum concentration increases in a dose-proportional manner and reaches a mean steady state of 379 ng/ml with a Cmax of 626 ng.h/ml. There are no reports of systemic accumulation.[A38883] | The mean volume of distribution calculated based on population is 6.5 L.[A38883] | The mean systemic clearance is very fast and it is reported to be of 25 L/h. This clearance rate is decreased after subsequent dosing to 4 L/h.[A38883] | Serum Globulins | NA | NA | NA | NA | B-cell receptor CD22,Elongation factor 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14864 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Alkaloids | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | Trodelvy | Gilead Sciences | Gilead Sciences | Intravenous | 180 mg/1 | TRODELVY is contraindicated in patients who have experienced a severe hypersensitivity reaction to TRODELVY | nausea, low white blood cell count (neutropenia), diarrhea, fatigue, anemia, vomiting, hair loss, constipation, rash, decreased appetite, and abdominal pain | Trodelvy is a prescription medicine used to treat adults with: a type of breast cancer that is estrogen and progesterone hormone receptor (HR) negative, and human epidermal growth factor receptor 2 (HER2) negative (also called triple-negative breast cancer). Trodelvy may be used: when your breast cancer... | TRODELVY is indicated for the treatment of adult patients with unresectable locally advanced or metastatic triple-negative breast cancer (mTNBC) who have received two or more prior systemic therapies, at least one of them for metastatic disease. | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | Sacituzumab govitecan-hziy is a Trop-2 directed antibody and topoisomerase inhibitor conjugate, composed of the following three components: | Link | Link | NA |
| 14865 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | Trodelvy | Gilead Sciences | Gilead Sciences | Intravenous | 180 mg / vial | TRODELVY is contraindicated in patients who have experienced a severe hypersensitivity reaction to TRODELVY | nausea, low white blood cell count (neutropenia), diarrhea, fatigue, anemia, vomiting, hair loss, constipation, rash, decreased appetite, and abdominal pain | Trodelvy is a prescription medicine used to treat adults with: a type of breast cancer that is estrogen and progesterone hormone receptor (HR) negative, and human epidermal growth factor receptor 2 (HER2) negative (also called triple-negative breast cancer). Trodelvy may be used: when your breast cancer... | TRODELVY is indicated for the treatment of adult patients with unresectable locally advanced or metastatic triple-negative breast cancer (mTNBC) who have received two or more prior systemic therapies, at least one of them for metastatic disease. | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | Sacituzumab govitecan-hziy is a Trop-2 directed antibody and topoisomerase inhibitor conjugate, composed of the following three components: | Link | Link | NA |
| 14866 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Antibodies | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14867 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Antibodies, Monoclonal | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14868 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14869 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Antineoplastic Agents | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14870 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Blood Proteins | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14871 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Cancer immunotherapy | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14872 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Globulins | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14873 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Immunoglobulins | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14874 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Immunoproteins | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14875 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Immunotherapy | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14876 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Noxae | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14877 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Proteins | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14878 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Serum Globulins | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14879 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Topoisomerase Inhibitors | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14880 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Toxic Actions | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14881 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | UGT1A1 Substrates | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14939 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Nectin-4 | Padcev | Seagen Inc. | Seagen Inc. | Intravenous | 20 mg / vial | None. | fatigue, numbness and tingling in extremities, decreased appetite, rash, hair loss, nausea, changes in taste, diarrhea, dry eye, itching, dry skin, dry eye, and vomiting | Padcev is an anticancer medicine that affects the growth and cell division of cancer cells. Padcev is a prescription medicine used to treat adults with cancer of the bladder or urinary tract (renal pelvis, ureter or urethra). Padcev is used when the cancer is advanced, has spread to other parts of the... | PADCEV® is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer (mUC) who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced or metastatic setting. | NA | These are not all of the possible side effects of PADCEV. | Link | Link | NA |
| 14940 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | Antibodies, Monoclonal | NA | NA | NA | NA | Nectin-4 | Padcev | Seagen Inc. | Seagen Inc. | Intravenous | 30 mg / vial | None. | fatigue, numbness and tingling in extremities, decreased appetite, rash, hair loss, nausea, changes in taste, diarrhea, dry eye, itching, dry skin, dry eye, and vomiting | Padcev is an anticancer medicine that affects the growth and cell division of cancer cells. Padcev is a prescription medicine used to treat adults with cancer of the bladder or urinary tract (renal pelvis, ureter or urethra). Padcev is used when the cancer is advanced, has spread to other parts of the... | PADCEV® is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer (mUC) who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced or metastatic setting. | NA | These are not all of the possible side effects of PADCEV. | Link | Link | NA |
| 14941 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Nectin-4 | Padcev Ejfv | Seagen Inc. | Seagen Inc. | Intravenous | 20 mg/2mL | None. | received an immunotherapy medicine and also received a chemotherapy-containing platinum medicine. | It is given as an infusion (drip) into a vein over 30 minutes. The patient should have an infusion three times over the course of 28 days (on days 1, 8 and 15) and should continue treatment until the disease gets worse or the side effects become intolerable. | The active substance in Padcev, enfortumab vedotin, consists of an antibody (a type of protein) combined with another substance known as MMAE. The antibody first attaches to a protein on the surface of cancer cells to gain entry into the cells. Once the active substance is inside the cells, MMAE disrupts the cells’ internal skeleton, causing cell death and helping to stop the cancer from getting worse or spreading. | NA | NA | Link | Link | NA |
| 14942 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | Blood Proteins | NA | NA | NA | NA | Nectin-4 | Padcev Ejfv | Seagen Inc. | Seagen Inc. | Intravenous | 30 mg/3mL | None. | received an immunotherapy medicine and also received a chemotherapy-containing platinum medicine. | It is given as an infusion (drip) into a vein over 30 minutes. The patient should have an infusion three times over the course of 28 days (on days 1, 8 and 15) and should continue treatment until the disease gets worse or the side effects become intolerable. | The active substance in Padcev, enfortumab vedotin, consists of an antibody (a type of protein) combined with another substance known as MMAE. The antibody first attaches to a protein on the surface of cancer cells to gain entry into the cells. Once the active substance is inside the cells, MMAE disrupts the cells’ internal skeleton, causing cell death and helping to stop the cancer from getting worse or spreading. | NA | NA | Link | Link | NA |
| 14943 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | Cancer immunotherapy | NA | NA | NA | NA | Nectin-4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14944 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | Cytochrome P-450 CYP3A Substrates | NA | NA | NA | NA | Nectin-4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14945 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | Cytochrome P-450 CYP3A4 Substrates | NA | NA | NA | NA | Nectin-4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14946 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | Cytochrome P-450 Substrates | NA | NA | NA | NA | Nectin-4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14947 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | Immunoglobulins | NA | NA | NA | NA | Nectin-4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14948 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | Immunotherapy | NA | NA | NA | NA | Nectin-4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14949 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | Microtubule Inhibitors | NA | NA | NA | NA | Nectin-4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14950 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | P-glycoprotein substrates | NA | NA | NA | NA | Nectin-4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14951 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | Proteins | NA | NA | NA | NA | Nectin-4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14952 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | Serum Globulins | NA | NA | NA | NA | Nectin-4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15687 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | Enhertu | Daiichi Sankyo, Inc. | Daiichi Sankyo, Inc. | Intravenous | 100 mg/5mL | None. | nausea, vomiting, fatigue, hair loss, constipation, decreased appetite, anemia, low white blood cell count (neutropenia, leukopenia), diarrhea, cough, and low platelets (thrombocytopenia), abdominal pain, inflammation of the mouth and lips, indigestion/heartburn, rash, low potassium (hypokalemia), shortness of breath, nosebleed, interstitial lung disease, headache, dizziness, upper respiratory tract infection, increased aspartate aminotransferase, alanine aminotransferase, and dry eye | Enhertu is a medicine used in adults to treat HER2-positive cancers which includes specific types of breast cancers and stomach cancers. Enhertu is made up of two cancer-fighting medicines, a targeted cancer therapy and a chemotherapy drug. Enhertu is usually given as an infusion into a vein every... | ENHERTU is indicated for the treatment of adult patients with unresectable or metastatic HER2-positive breast cancer who have received two or more prior anti-HER2-based regimens in the metastatic setting. | NA | Fam-trastuzumab deruxtecan-nxki is a HER2-directed antibody and topoisomerase inhibitor conjugate. Fam-trastuzumab deruxtecan-nxki is an antibody-drug conjugate (ADC) composed of three components: 1) a humanized anti-HER2 IgG1 monoclonal antibody (mAb), covalently linked to 2) a topoisomerase inhibitor, via 3) a tetrapeptide-based cleavable linker. Deruxtecan is composed of a protease-cleavable maleimide tetrapeptide linker and the topoisomerase inhibitor, DXd, which is an exatecan derivative. | Link | Link | NA |
| 15688 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Antibodies | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | Enhertu | Astra Zeneca | Astra Zeneca | Intravenous | 100 mg / vial | None. | nausea, vomiting, fatigue, hair loss, constipation, decreased appetite, anemia, low white blood cell count (neutropenia, leukopenia), diarrhea, cough, and low platelets (thrombocytopenia), abdominal pain, inflammation of the mouth and lips, indigestion/heartburn, rash, low potassium (hypokalemia), shortness of breath, nosebleed, interstitial lung disease, headache, dizziness, upper respiratory tract infection, increased aspartate aminotransferase, alanine aminotransferase, and dry eye | Enhertu is a medicine used in adults to treat HER2-positive cancers which includes specific types of breast cancers and stomach cancers. Enhertu is made up of two cancer-fighting medicines, a targeted cancer therapy and a chemotherapy drug. Enhertu is usually given as an infusion into a vein every... | ENHERTU is indicated for the treatment of adult patients with unresectable or metastatic HER2-positive breast cancer who have received two or more prior anti-HER2-based regimens in the metastatic setting. | NA | Fam-trastuzumab deruxtecan-nxki is a HER2-directed antibody and topoisomerase inhibitor conjugate. Fam-trastuzumab deruxtecan-nxki is an antibody-drug conjugate (ADC) composed of three components: 1) a humanized anti-HER2 IgG1 monoclonal antibody (mAb), covalently linked to 2) a topoisomerase inhibitor, via 3) a tetrapeptide-based cleavable linker. Deruxtecan is composed of a protease-cleavable maleimide tetrapeptide linker and the topoisomerase inhibitor, DXd, which is an exatecan derivative. | Link | Link | NA |
| 15689 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Antibodies, Monoclonal | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | Enhertu | Daiichi Sankyo Europe, Gmb H | Daiichi Sankyo Europe, Gmb H | Intravenous | 100 mg | None. | nausea, vomiting, fatigue, hair loss, constipation, decreased appetite, anemia, low white blood cell count (neutropenia, leukopenia), diarrhea, cough, and low platelets (thrombocytopenia), abdominal pain, inflammation of the mouth and lips, indigestion/heartburn, rash, low potassium (hypokalemia), shortness of breath, nosebleed, interstitial lung disease, headache, dizziness, upper respiratory tract infection, increased aspartate aminotransferase, alanine aminotransferase, and dry eye | Enhertu is a medicine used in adults to treat HER2-positive cancers which includes specific types of breast cancers and stomach cancers. Enhertu is made up of two cancer-fighting medicines, a targeted cancer therapy and a chemotherapy drug. Enhertu is usually given as an infusion into a vein every... | ENHERTU is indicated for the treatment of adult patients with unresectable or metastatic HER2-positive breast cancer who have received two or more prior anti-HER2-based regimens in the metastatic setting. | NA | Fam-trastuzumab deruxtecan-nxki is a HER2-directed antibody and topoisomerase inhibitor conjugate. Fam-trastuzumab deruxtecan-nxki is an antibody-drug conjugate (ADC) composed of three components: 1) a humanized anti-HER2 IgG1 monoclonal antibody (mAb), covalently linked to 2) a topoisomerase inhibitor, via 3) a tetrapeptide-based cleavable linker. Deruxtecan is composed of a protease-cleavable maleimide tetrapeptide linker and the topoisomerase inhibitor, DXd, which is an exatecan derivative. | Link | Link | NA |
| 15690 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Antineoplastic Agents | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15691 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | BCRP/ABCG2 Substrates | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15692 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Blood Proteins | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15693 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Cancer immunotherapy | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15694 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Cytochrome P-450 CYP3A Substrates | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15695 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Cytochrome P-450 CYP3A4 Substrates | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15696 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Cytochrome P-450 Substrates | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15697 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Globulins | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15698 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Immunoglobulins | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15699 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Immunoproteins | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15700 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Immunotherapy | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15701 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | MATE 2 Substrates | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15702 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | MATE substrates | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15703 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Noxae | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15704 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | OATP1B3 substrates | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15705 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | P-glycoprotein substrates | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15706 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Proteins | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15707 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Serum Globulins | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15708 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Toxic Actions | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15808 | Th1631 | Dostarlimab | >Th1631_Dostarlimab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYDMSWVRQAPGKGLEWVSTISGGGSYTYYQDSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCASPYYAMDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 144000 | C6420H9832N1680O2014S44 | NA | NA | NA | The mean terminal elimination half-life of dostarlimab is 25.4 days.[L33320] | Dostarlimab is an IgG4 humanized monoclonal antibody targeted against the human programmed death receptor-1 (PD-1).[L33320] PD-1 receptors are found on T-cells and, when activated, serve to inhibit immune responses - some cancers leverage this system by overexpressing PD-1 ligands, thereby effectively inhibiting the anti-tumor immune response that would typically attempt to destroy the cancerous cells.[A234379] Agents acting on the PD-1 pathway, such as [nivolumab] and [pembrolizumab], facilitate endogenous immune-mediated anti-tumor activity and may therefore be used to treat a wide variety of cancers, including those of the skin, lung, kidneys, and liver. In April 2021, dostarlimab was granted an accelerated approval by the FDA - as GlaxoSmithKline's dostarlimab-gxly (Jemperli) - for the treatment of adult patients with recurrent or advanced mismatch repair deficient (dMMR) endometrial cancer experiencing disease progression despite treatment with platinum-containing chemotherapy regimens.[L33340] As this accelerated approval was granted only for the treatment of dMMR endometrial cancers, it was approved alongside a companion diagnostic device - the VENTANA MMR RxDx Panel - for use in selecting appropriate patients for treatment.[L33340] | Dostarlimab-gxly is indicated for the treatment of adult patients with mismatch repair deficient (dMMR) recurrent or advanced endometrial cancer that has progressed despite ongoing or prior treatment with a platinum-containing chemotherapy regimen.[L33320] | Dostarlimab is an immunotherapy that facilitates the body's endogenous anti-tumor immune response in the treatment cancer.[L33320] It is administered over a span of 30 minutes via intravenous infusion every three to six weeks depending on the cycle.[L33320] Agents that interfere with the PD-1/PD-L1 pathway, including dostarlimab, remove an important immune system inhibitory response and may therefore induce immune-mediated adverse reactions which can be severe or fatal. These reactions can occur in any organ system and can occur at any time after starting therapy, and while they most often manifest during therapy they may also appear after discontinuing the causative agent. Patients receiving therapy with dostarlimab should be monitored closely for evidence of an underlying immune-mediated reaction and evaluated and treated promptly if an immune-mediated reaction is suspected.[L33320] | Approximately 13-30% of recurrent endometrial cancers involve microsatellite instability (MSI) or mismatch repair deficiency (dMMR).[A234379,A234389] The mutations resulting in dMMR endometrial cancers are primarily somatic in nature (~90%), although 5-10% of cases involve germline mutations.[A234389] Cancers that have mutations resulting in dMMR can upregulate the expression of programmed death receptor-1 (PD-1) ligands 1 and 2 (PD-L1 and -L2) - PD-1 is found on T-cells and, when activated, inhibits their proliferation and the production of cytokines.[L33320] The binding of these ligands to PD-1 thereby functions as an immune checkpoint that downregulates the anti-tumor immune response.[A234379] Dostarlimab is a monoclonal antibody targeted against PD-1 - it binds to the receptor and prevents interactions with PD-L1 and PD-L2, thus allowing the anti-tumor immune response to proceed unimpeded.[L33320] | There are no data regarding overdose with dostarlimab. Symptoms of overdosage are likely to be consistent with the adverse effect profile of dostarlimab and may therefore involve significant immune-mediated reactions.[L33320] | The metabolism of dostarlimab has not been characterized, but it is expected to be degraded via catabolic pathways into smaller peptides and amino acids.[L33320,A216712] | During the first cycle, and administered at 500mg intravenously every 3 weeks, the mean Cmax and AUC0-tau of dostarlimab-gxly are 171 mcg/mL and 35,730 mcg.h/mL, respectively. When administered at 1000mg every 6 weeks, the mean Cmax and AUC0-tau are 309 mcg/mL and 95,820 mcg.h/mL, respectively.[L33320] | At steady-state, the mean volume of distribution of dostarlimab is 5.3L.[L33320] | At steady-state, the mean clearance of dostarlimab is 0.007 L/h.[L33320] | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Programmed cell death protein 1 | Jemperli | GlaxoSmithKline LLC | GlaxoSmithKline LLC | Intravenous | 50 mg/1mL | NA | fatigue, weakness, nausea, diarrhea, anemia, constipation, vomiting, urinary tract infection (UTI), decreased appetite, muscle pain, cough, and itching | Jemperli is a prescription medicine used to treat adults with certain cancers that have been shown by a laboratory test to be mismatch repair deficient (dMMR), and your cancer has returned, or it has spread or cannot be removed by surgery (advanced cancer). Jemperli may be used when: you have a kind... | JEMPERLI is a prescription medicine used to treat adults with a kind of uterine cancer called endometrial cancer. JEMPERLI may be used when: | NA | NA | Link | Link | NA |
| 15809 | Th1631 | Dostarlimab | >Th1631_Dostarlimab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYDMSWVRQAPGKGLEWVSTISGGGSYTYYQDSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCASPYYAMDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 144000 | C6420H9832N1680O2014S44 | NA | NA | NA | The mean terminal elimination half-life of dostarlimab is 25.4 days.[L33320] | Dostarlimab is an IgG4 humanized monoclonal antibody targeted against the human programmed death receptor-1 (PD-1).[L33320] PD-1 receptors are found on T-cells and, when activated, serve to inhibit immune responses - some cancers leverage this system by overexpressing PD-1 ligands, thereby effectively inhibiting the anti-tumor immune response that would typically attempt to destroy the cancerous cells.[A234379] Agents acting on the PD-1 pathway, such as [nivolumab] and [pembrolizumab], facilitate endogenous immune-mediated anti-tumor activity and may therefore be used to treat a wide variety of cancers, including those of the skin, lung, kidneys, and liver. In April 2021, dostarlimab was granted an accelerated approval by the FDA - as GlaxoSmithKline's dostarlimab-gxly (Jemperli) - for the treatment of adult patients with recurrent or advanced mismatch repair deficient (dMMR) endometrial cancer experiencing disease progression despite treatment with platinum-containing chemotherapy regimens.[L33340] As this accelerated approval was granted only for the treatment of dMMR endometrial cancers, it was approved alongside a companion diagnostic device - the VENTANA MMR RxDx Panel - for use in selecting appropriate patients for treatment.[L33340] | Dostarlimab-gxly is indicated for the treatment of adult patients with mismatch repair deficient (dMMR) recurrent or advanced endometrial cancer that has progressed despite ongoing or prior treatment with a platinum-containing chemotherapy regimen.[L33320] | Dostarlimab is an immunotherapy that facilitates the body's endogenous anti-tumor immune response in the treatment cancer.[L33320] It is administered over a span of 30 minutes via intravenous infusion every three to six weeks depending on the cycle.[L33320] Agents that interfere with the PD-1/PD-L1 pathway, including dostarlimab, remove an important immune system inhibitory response and may therefore induce immune-mediated adverse reactions which can be severe or fatal. These reactions can occur in any organ system and can occur at any time after starting therapy, and while they most often manifest during therapy they may also appear after discontinuing the causative agent. Patients receiving therapy with dostarlimab should be monitored closely for evidence of an underlying immune-mediated reaction and evaluated and treated promptly if an immune-mediated reaction is suspected.[L33320] | Approximately 13-30% of recurrent endometrial cancers involve microsatellite instability (MSI) or mismatch repair deficiency (dMMR).[A234379,A234389] The mutations resulting in dMMR endometrial cancers are primarily somatic in nature (~90%), although 5-10% of cases involve germline mutations.[A234389] Cancers that have mutations resulting in dMMR can upregulate the expression of programmed death receptor-1 (PD-1) ligands 1 and 2 (PD-L1 and -L2) - PD-1 is found on T-cells and, when activated, inhibits their proliferation and the production of cytokines.[L33320] The binding of these ligands to PD-1 thereby functions as an immune checkpoint that downregulates the anti-tumor immune response.[A234379] Dostarlimab is a monoclonal antibody targeted against PD-1 - it binds to the receptor and prevents interactions with PD-L1 and PD-L2, thus allowing the anti-tumor immune response to proceed unimpeded.[L33320] | There are no data regarding overdose with dostarlimab. Symptoms of overdosage are likely to be consistent with the adverse effect profile of dostarlimab and may therefore involve significant immune-mediated reactions.[L33320] | The metabolism of dostarlimab has not been characterized, but it is expected to be degraded via catabolic pathways into smaller peptides and amino acids.[L33320,A216712] | During the first cycle, and administered at 500mg intravenously every 3 weeks, the mean Cmax and AUC0-tau of dostarlimab-gxly are 171 mcg/mL and 35,730 mcg.h/mL, respectively. When administered at 1000mg every 6 weeks, the mean Cmax and AUC0-tau are 309 mcg/mL and 95,820 mcg.h/mL, respectively.[L33320] | At steady-state, the mean volume of distribution of dostarlimab is 5.3L.[L33320] | At steady-state, the mean clearance of dostarlimab is 0.007 L/h.[L33320] | Antibodies, Monoclonal | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15810 | Th1631 | Dostarlimab | >Th1631_Dostarlimab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYDMSWVRQAPGKGLEWVSTISGGGSYTYYQDSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCASPYYAMDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 144000 | C6420H9832N1680O2014S44 | NA | NA | NA | The mean terminal elimination half-life of dostarlimab is 25.4 days.[L33320] | Dostarlimab is an IgG4 humanized monoclonal antibody targeted against the human programmed death receptor-1 (PD-1).[L33320] PD-1 receptors are found on T-cells and, when activated, serve to inhibit immune responses - some cancers leverage this system by overexpressing PD-1 ligands, thereby effectively inhibiting the anti-tumor immune response that would typically attempt to destroy the cancerous cells.[A234379] Agents acting on the PD-1 pathway, such as [nivolumab] and [pembrolizumab], facilitate endogenous immune-mediated anti-tumor activity and may therefore be used to treat a wide variety of cancers, including those of the skin, lung, kidneys, and liver. In April 2021, dostarlimab was granted an accelerated approval by the FDA - as GlaxoSmithKline's dostarlimab-gxly (Jemperli) - for the treatment of adult patients with recurrent or advanced mismatch repair deficient (dMMR) endometrial cancer experiencing disease progression despite treatment with platinum-containing chemotherapy regimens.[L33340] As this accelerated approval was granted only for the treatment of dMMR endometrial cancers, it was approved alongside a companion diagnostic device - the VENTANA MMR RxDx Panel - for use in selecting appropriate patients for treatment.[L33340] | Dostarlimab-gxly is indicated for the treatment of adult patients with mismatch repair deficient (dMMR) recurrent or advanced endometrial cancer that has progressed despite ongoing or prior treatment with a platinum-containing chemotherapy regimen.[L33320] | Dostarlimab is an immunotherapy that facilitates the body's endogenous anti-tumor immune response in the treatment cancer.[L33320] It is administered over a span of 30 minutes via intravenous infusion every three to six weeks depending on the cycle.[L33320] Agents that interfere with the PD-1/PD-L1 pathway, including dostarlimab, remove an important immune system inhibitory response and may therefore induce immune-mediated adverse reactions which can be severe or fatal. These reactions can occur in any organ system and can occur at any time after starting therapy, and while they most often manifest during therapy they may also appear after discontinuing the causative agent. Patients receiving therapy with dostarlimab should be monitored closely for evidence of an underlying immune-mediated reaction and evaluated and treated promptly if an immune-mediated reaction is suspected.[L33320] | Approximately 13-30% of recurrent endometrial cancers involve microsatellite instability (MSI) or mismatch repair deficiency (dMMR).[A234379,A234389] The mutations resulting in dMMR endometrial cancers are primarily somatic in nature (~90%), although 5-10% of cases involve germline mutations.[A234389] Cancers that have mutations resulting in dMMR can upregulate the expression of programmed death receptor-1 (PD-1) ligands 1 and 2 (PD-L1 and -L2) - PD-1 is found on T-cells and, when activated, inhibits their proliferation and the production of cytokines.[L33320] The binding of these ligands to PD-1 thereby functions as an immune checkpoint that downregulates the anti-tumor immune response.[A234379] Dostarlimab is a monoclonal antibody targeted against PD-1 - it binds to the receptor and prevents interactions with PD-L1 and PD-L2, thus allowing the anti-tumor immune response to proceed unimpeded.[L33320] | There are no data regarding overdose with dostarlimab. Symptoms of overdosage are likely to be consistent with the adverse effect profile of dostarlimab and may therefore involve significant immune-mediated reactions.[L33320] | The metabolism of dostarlimab has not been characterized, but it is expected to be degraded via catabolic pathways into smaller peptides and amino acids.[L33320,A216712] | During the first cycle, and administered at 500mg intravenously every 3 weeks, the mean Cmax and AUC0-tau of dostarlimab-gxly are 171 mcg/mL and 35,730 mcg.h/mL, respectively. When administered at 1000mg every 6 weeks, the mean Cmax and AUC0-tau are 309 mcg/mL and 95,820 mcg.h/mL, respectively.[L33320] | At steady-state, the mean volume of distribution of dostarlimab is 5.3L.[L33320] | At steady-state, the mean clearance of dostarlimab is 0.007 L/h.[L33320] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15811 | Th1631 | Dostarlimab | >Th1631_Dostarlimab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYDMSWVRQAPGKGLEWVSTISGGGSYTYYQDSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCASPYYAMDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 144000 | C6420H9832N1680O2014S44 | NA | NA | NA | The mean terminal elimination half-life of dostarlimab is 25.4 days.[L33320] | Dostarlimab is an IgG4 humanized monoclonal antibody targeted against the human programmed death receptor-1 (PD-1).[L33320] PD-1 receptors are found on T-cells and, when activated, serve to inhibit immune responses - some cancers leverage this system by overexpressing PD-1 ligands, thereby effectively inhibiting the anti-tumor immune response that would typically attempt to destroy the cancerous cells.[A234379] Agents acting on the PD-1 pathway, such as [nivolumab] and [pembrolizumab], facilitate endogenous immune-mediated anti-tumor activity and may therefore be used to treat a wide variety of cancers, including those of the skin, lung, kidneys, and liver. In April 2021, dostarlimab was granted an accelerated approval by the FDA - as GlaxoSmithKline's dostarlimab-gxly (Jemperli) - for the treatment of adult patients with recurrent or advanced mismatch repair deficient (dMMR) endometrial cancer experiencing disease progression despite treatment with platinum-containing chemotherapy regimens.[L33340] As this accelerated approval was granted only for the treatment of dMMR endometrial cancers, it was approved alongside a companion diagnostic device - the VENTANA MMR RxDx Panel - for use in selecting appropriate patients for treatment.[L33340] | Dostarlimab-gxly is indicated for the treatment of adult patients with mismatch repair deficient (dMMR) recurrent or advanced endometrial cancer that has progressed despite ongoing or prior treatment with a platinum-containing chemotherapy regimen.[L33320] | Dostarlimab is an immunotherapy that facilitates the body's endogenous anti-tumor immune response in the treatment cancer.[L33320] It is administered over a span of 30 minutes via intravenous infusion every three to six weeks depending on the cycle.[L33320] Agents that interfere with the PD-1/PD-L1 pathway, including dostarlimab, remove an important immune system inhibitory response and may therefore induce immune-mediated adverse reactions which can be severe or fatal. These reactions can occur in any organ system and can occur at any time after starting therapy, and while they most often manifest during therapy they may also appear after discontinuing the causative agent. Patients receiving therapy with dostarlimab should be monitored closely for evidence of an underlying immune-mediated reaction and evaluated and treated promptly if an immune-mediated reaction is suspected.[L33320] | Approximately 13-30% of recurrent endometrial cancers involve microsatellite instability (MSI) or mismatch repair deficiency (dMMR).[A234379,A234389] The mutations resulting in dMMR endometrial cancers are primarily somatic in nature (~90%), although 5-10% of cases involve germline mutations.[A234389] Cancers that have mutations resulting in dMMR can upregulate the expression of programmed death receptor-1 (PD-1) ligands 1 and 2 (PD-L1 and -L2) - PD-1 is found on T-cells and, when activated, inhibits their proliferation and the production of cytokines.[L33320] The binding of these ligands to PD-1 thereby functions as an immune checkpoint that downregulates the anti-tumor immune response.[A234379] Dostarlimab is a monoclonal antibody targeted against PD-1 - it binds to the receptor and prevents interactions with PD-L1 and PD-L2, thus allowing the anti-tumor immune response to proceed unimpeded.[L33320] | There are no data regarding overdose with dostarlimab. Symptoms of overdosage are likely to be consistent with the adverse effect profile of dostarlimab and may therefore involve significant immune-mediated reactions.[L33320] | The metabolism of dostarlimab has not been characterized, but it is expected to be degraded via catabolic pathways into smaller peptides and amino acids.[L33320,A216712] | During the first cycle, and administered at 500mg intravenously every 3 weeks, the mean Cmax and AUC0-tau of dostarlimab-gxly are 171 mcg/mL and 35,730 mcg.h/mL, respectively. When administered at 1000mg every 6 weeks, the mean Cmax and AUC0-tau are 309 mcg/mL and 95,820 mcg.h/mL, respectively.[L33320] | At steady-state, the mean volume of distribution of dostarlimab is 5.3L.[L33320] | At steady-state, the mean clearance of dostarlimab is 0.007 L/h.[L33320] | Antineoplastic Agents | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15812 | Th1631 | Dostarlimab | >Th1631_Dostarlimab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYDMSWVRQAPGKGLEWVSTISGGGSYTYYQDSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCASPYYAMDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 144000 | C6420H9832N1680O2014S44 | NA | NA | NA | The mean terminal elimination half-life of dostarlimab is 25.4 days.[L33320] | Dostarlimab is an IgG4 humanized monoclonal antibody targeted against the human programmed death receptor-1 (PD-1).[L33320] PD-1 receptors are found on T-cells and, when activated, serve to inhibit immune responses - some cancers leverage this system by overexpressing PD-1 ligands, thereby effectively inhibiting the anti-tumor immune response that would typically attempt to destroy the cancerous cells.[A234379] Agents acting on the PD-1 pathway, such as [nivolumab] and [pembrolizumab], facilitate endogenous immune-mediated anti-tumor activity and may therefore be used to treat a wide variety of cancers, including those of the skin, lung, kidneys, and liver. In April 2021, dostarlimab was granted an accelerated approval by the FDA - as GlaxoSmithKline's dostarlimab-gxly (Jemperli) - for the treatment of adult patients with recurrent or advanced mismatch repair deficient (dMMR) endometrial cancer experiencing disease progression despite treatment with platinum-containing chemotherapy regimens.[L33340] As this accelerated approval was granted only for the treatment of dMMR endometrial cancers, it was approved alongside a companion diagnostic device - the VENTANA MMR RxDx Panel - for use in selecting appropriate patients for treatment.[L33340] | Dostarlimab-gxly is indicated for the treatment of adult patients with mismatch repair deficient (dMMR) recurrent or advanced endometrial cancer that has progressed despite ongoing or prior treatment with a platinum-containing chemotherapy regimen.[L33320] | Dostarlimab is an immunotherapy that facilitates the body's endogenous anti-tumor immune response in the treatment cancer.[L33320] It is administered over a span of 30 minutes via intravenous infusion every three to six weeks depending on the cycle.[L33320] Agents that interfere with the PD-1/PD-L1 pathway, including dostarlimab, remove an important immune system inhibitory response and may therefore induce immune-mediated adverse reactions which can be severe or fatal. These reactions can occur in any organ system and can occur at any time after starting therapy, and while they most often manifest during therapy they may also appear after discontinuing the causative agent. Patients receiving therapy with dostarlimab should be monitored closely for evidence of an underlying immune-mediated reaction and evaluated and treated promptly if an immune-mediated reaction is suspected.[L33320] | Approximately 13-30% of recurrent endometrial cancers involve microsatellite instability (MSI) or mismatch repair deficiency (dMMR).[A234379,A234389] The mutations resulting in dMMR endometrial cancers are primarily somatic in nature (~90%), although 5-10% of cases involve germline mutations.[A234389] Cancers that have mutations resulting in dMMR can upregulate the expression of programmed death receptor-1 (PD-1) ligands 1 and 2 (PD-L1 and -L2) - PD-1 is found on T-cells and, when activated, inhibits their proliferation and the production of cytokines.[L33320] The binding of these ligands to PD-1 thereby functions as an immune checkpoint that downregulates the anti-tumor immune response.[A234379] Dostarlimab is a monoclonal antibody targeted against PD-1 - it binds to the receptor and prevents interactions with PD-L1 and PD-L2, thus allowing the anti-tumor immune response to proceed unimpeded.[L33320] | There are no data regarding overdose with dostarlimab. Symptoms of overdosage are likely to be consistent with the adverse effect profile of dostarlimab and may therefore involve significant immune-mediated reactions.[L33320] | The metabolism of dostarlimab has not been characterized, but it is expected to be degraded via catabolic pathways into smaller peptides and amino acids.[L33320,A216712] | During the first cycle, and administered at 500mg intravenously every 3 weeks, the mean Cmax and AUC0-tau of dostarlimab-gxly are 171 mcg/mL and 35,730 mcg.h/mL, respectively. When administered at 1000mg every 6 weeks, the mean Cmax and AUC0-tau are 309 mcg/mL and 95,820 mcg.h/mL, respectively.[L33320] | At steady-state, the mean volume of distribution of dostarlimab is 5.3L.[L33320] | At steady-state, the mean clearance of dostarlimab is 0.007 L/h.[L33320] | Blood Proteins | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15813 | Th1631 | Dostarlimab | >Th1631_Dostarlimab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYDMSWVRQAPGKGLEWVSTISGGGSYTYYQDSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCASPYYAMDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 144000 | C6420H9832N1680O2014S44 | NA | NA | NA | The mean terminal elimination half-life of dostarlimab is 25.4 days.[L33320] | Dostarlimab is an IgG4 humanized monoclonal antibody targeted against the human programmed death receptor-1 (PD-1).[L33320] PD-1 receptors are found on T-cells and, when activated, serve to inhibit immune responses - some cancers leverage this system by overexpressing PD-1 ligands, thereby effectively inhibiting the anti-tumor immune response that would typically attempt to destroy the cancerous cells.[A234379] Agents acting on the PD-1 pathway, such as [nivolumab] and [pembrolizumab], facilitate endogenous immune-mediated anti-tumor activity and may therefore be used to treat a wide variety of cancers, including those of the skin, lung, kidneys, and liver. In April 2021, dostarlimab was granted an accelerated approval by the FDA - as GlaxoSmithKline's dostarlimab-gxly (Jemperli) - for the treatment of adult patients with recurrent or advanced mismatch repair deficient (dMMR) endometrial cancer experiencing disease progression despite treatment with platinum-containing chemotherapy regimens.[L33340] As this accelerated approval was granted only for the treatment of dMMR endometrial cancers, it was approved alongside a companion diagnostic device - the VENTANA MMR RxDx Panel - for use in selecting appropriate patients for treatment.[L33340] | Dostarlimab-gxly is indicated for the treatment of adult patients with mismatch repair deficient (dMMR) recurrent or advanced endometrial cancer that has progressed despite ongoing or prior treatment with a platinum-containing chemotherapy regimen.[L33320] | Dostarlimab is an immunotherapy that facilitates the body's endogenous anti-tumor immune response in the treatment cancer.[L33320] It is administered over a span of 30 minutes via intravenous infusion every three to six weeks depending on the cycle.[L33320] Agents that interfere with the PD-1/PD-L1 pathway, including dostarlimab, remove an important immune system inhibitory response and may therefore induce immune-mediated adverse reactions which can be severe or fatal. These reactions can occur in any organ system and can occur at any time after starting therapy, and while they most often manifest during therapy they may also appear after discontinuing the causative agent. Patients receiving therapy with dostarlimab should be monitored closely for evidence of an underlying immune-mediated reaction and evaluated and treated promptly if an immune-mediated reaction is suspected.[L33320] | Approximately 13-30% of recurrent endometrial cancers involve microsatellite instability (MSI) or mismatch repair deficiency (dMMR).[A234379,A234389] The mutations resulting in dMMR endometrial cancers are primarily somatic in nature (~90%), although 5-10% of cases involve germline mutations.[A234389] Cancers that have mutations resulting in dMMR can upregulate the expression of programmed death receptor-1 (PD-1) ligands 1 and 2 (PD-L1 and -L2) - PD-1 is found on T-cells and, when activated, inhibits their proliferation and the production of cytokines.[L33320] The binding of these ligands to PD-1 thereby functions as an immune checkpoint that downregulates the anti-tumor immune response.[A234379] Dostarlimab is a monoclonal antibody targeted against PD-1 - it binds to the receptor and prevents interactions with PD-L1 and PD-L2, thus allowing the anti-tumor immune response to proceed unimpeded.[L33320] | There are no data regarding overdose with dostarlimab. Symptoms of overdosage are likely to be consistent with the adverse effect profile of dostarlimab and may therefore involve significant immune-mediated reactions.[L33320] | The metabolism of dostarlimab has not been characterized, but it is expected to be degraded via catabolic pathways into smaller peptides and amino acids.[L33320,A216712] | During the first cycle, and administered at 500mg intravenously every 3 weeks, the mean Cmax and AUC0-tau of dostarlimab-gxly are 171 mcg/mL and 35,730 mcg.h/mL, respectively. When administered at 1000mg every 6 weeks, the mean Cmax and AUC0-tau are 309 mcg/mL and 95,820 mcg.h/mL, respectively.[L33320] | At steady-state, the mean volume of distribution of dostarlimab is 5.3L.[L33320] | At steady-state, the mean clearance of dostarlimab is 0.007 L/h.[L33320] | Immune Checkpoint Inhibitors | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15814 | Th1631 | Dostarlimab | >Th1631_Dostarlimab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYDMSWVRQAPGKGLEWVSTISGGGSYTYYQDSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCASPYYAMDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 144000 | C6420H9832N1680O2014S44 | NA | NA | NA | The mean terminal elimination half-life of dostarlimab is 25.4 days.[L33320] | Dostarlimab is an IgG4 humanized monoclonal antibody targeted against the human programmed death receptor-1 (PD-1).[L33320] PD-1 receptors are found on T-cells and, when activated, serve to inhibit immune responses - some cancers leverage this system by overexpressing PD-1 ligands, thereby effectively inhibiting the anti-tumor immune response that would typically attempt to destroy the cancerous cells.[A234379] Agents acting on the PD-1 pathway, such as [nivolumab] and [pembrolizumab], facilitate endogenous immune-mediated anti-tumor activity and may therefore be used to treat a wide variety of cancers, including those of the skin, lung, kidneys, and liver. In April 2021, dostarlimab was granted an accelerated approval by the FDA - as GlaxoSmithKline's dostarlimab-gxly (Jemperli) - for the treatment of adult patients with recurrent or advanced mismatch repair deficient (dMMR) endometrial cancer experiencing disease progression despite treatment with platinum-containing chemotherapy regimens.[L33340] As this accelerated approval was granted only for the treatment of dMMR endometrial cancers, it was approved alongside a companion diagnostic device - the VENTANA MMR RxDx Panel - for use in selecting appropriate patients for treatment.[L33340] | Dostarlimab-gxly is indicated for the treatment of adult patients with mismatch repair deficient (dMMR) recurrent or advanced endometrial cancer that has progressed despite ongoing or prior treatment with a platinum-containing chemotherapy regimen.[L33320] | Dostarlimab is an immunotherapy that facilitates the body's endogenous anti-tumor immune response in the treatment cancer.[L33320] It is administered over a span of 30 minutes via intravenous infusion every three to six weeks depending on the cycle.[L33320] Agents that interfere with the PD-1/PD-L1 pathway, including dostarlimab, remove an important immune system inhibitory response and may therefore induce immune-mediated adverse reactions which can be severe or fatal. These reactions can occur in any organ system and can occur at any time after starting therapy, and while they most often manifest during therapy they may also appear after discontinuing the causative agent. Patients receiving therapy with dostarlimab should be monitored closely for evidence of an underlying immune-mediated reaction and evaluated and treated promptly if an immune-mediated reaction is suspected.[L33320] | Approximately 13-30% of recurrent endometrial cancers involve microsatellite instability (MSI) or mismatch repair deficiency (dMMR).[A234379,A234389] The mutations resulting in dMMR endometrial cancers are primarily somatic in nature (~90%), although 5-10% of cases involve germline mutations.[A234389] Cancers that have mutations resulting in dMMR can upregulate the expression of programmed death receptor-1 (PD-1) ligands 1 and 2 (PD-L1 and -L2) - PD-1 is found on T-cells and, when activated, inhibits their proliferation and the production of cytokines.[L33320] The binding of these ligands to PD-1 thereby functions as an immune checkpoint that downregulates the anti-tumor immune response.[A234379] Dostarlimab is a monoclonal antibody targeted against PD-1 - it binds to the receptor and prevents interactions with PD-L1 and PD-L2, thus allowing the anti-tumor immune response to proceed unimpeded.[L33320] | There are no data regarding overdose with dostarlimab. Symptoms of overdosage are likely to be consistent with the adverse effect profile of dostarlimab and may therefore involve significant immune-mediated reactions.[L33320] | The metabolism of dostarlimab has not been characterized, but it is expected to be degraded via catabolic pathways into smaller peptides and amino acids.[L33320,A216712] | During the first cycle, and administered at 500mg intravenously every 3 weeks, the mean Cmax and AUC0-tau of dostarlimab-gxly are 171 mcg/mL and 35,730 mcg.h/mL, respectively. When administered at 1000mg every 6 weeks, the mean Cmax and AUC0-tau are 309 mcg/mL and 95,820 mcg.h/mL, respectively.[L33320] | At steady-state, the mean volume of distribution of dostarlimab is 5.3L.[L33320] | At steady-state, the mean clearance of dostarlimab is 0.007 L/h.[L33320] | Immunoglobulins | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15815 | Th1631 | Dostarlimab | >Th1631_Dostarlimab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYDMSWVRQAPGKGLEWVSTISGGGSYTYYQDSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCASPYYAMDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 144000 | C6420H9832N1680O2014S44 | NA | NA | NA | The mean terminal elimination half-life of dostarlimab is 25.4 days.[L33320] | Dostarlimab is an IgG4 humanized monoclonal antibody targeted against the human programmed death receptor-1 (PD-1).[L33320] PD-1 receptors are found on T-cells and, when activated, serve to inhibit immune responses - some cancers leverage this system by overexpressing PD-1 ligands, thereby effectively inhibiting the anti-tumor immune response that would typically attempt to destroy the cancerous cells.[A234379] Agents acting on the PD-1 pathway, such as [nivolumab] and [pembrolizumab], facilitate endogenous immune-mediated anti-tumor activity and may therefore be used to treat a wide variety of cancers, including those of the skin, lung, kidneys, and liver. In April 2021, dostarlimab was granted an accelerated approval by the FDA - as GlaxoSmithKline's dostarlimab-gxly (Jemperli) - for the treatment of adult patients with recurrent or advanced mismatch repair deficient (dMMR) endometrial cancer experiencing disease progression despite treatment with platinum-containing chemotherapy regimens.[L33340] As this accelerated approval was granted only for the treatment of dMMR endometrial cancers, it was approved alongside a companion diagnostic device - the VENTANA MMR RxDx Panel - for use in selecting appropriate patients for treatment.[L33340] | Dostarlimab-gxly is indicated for the treatment of adult patients with mismatch repair deficient (dMMR) recurrent or advanced endometrial cancer that has progressed despite ongoing or prior treatment with a platinum-containing chemotherapy regimen.[L33320] | Dostarlimab is an immunotherapy that facilitates the body's endogenous anti-tumor immune response in the treatment cancer.[L33320] It is administered over a span of 30 minutes via intravenous infusion every three to six weeks depending on the cycle.[L33320] Agents that interfere with the PD-1/PD-L1 pathway, including dostarlimab, remove an important immune system inhibitory response and may therefore induce immune-mediated adverse reactions which can be severe or fatal. These reactions can occur in any organ system and can occur at any time after starting therapy, and while they most often manifest during therapy they may also appear after discontinuing the causative agent. Patients receiving therapy with dostarlimab should be monitored closely for evidence of an underlying immune-mediated reaction and evaluated and treated promptly if an immune-mediated reaction is suspected.[L33320] | Approximately 13-30% of recurrent endometrial cancers involve microsatellite instability (MSI) or mismatch repair deficiency (dMMR).[A234379,A234389] The mutations resulting in dMMR endometrial cancers are primarily somatic in nature (~90%), although 5-10% of cases involve germline mutations.[A234389] Cancers that have mutations resulting in dMMR can upregulate the expression of programmed death receptor-1 (PD-1) ligands 1 and 2 (PD-L1 and -L2) - PD-1 is found on T-cells and, when activated, inhibits their proliferation and the production of cytokines.[L33320] The binding of these ligands to PD-1 thereby functions as an immune checkpoint that downregulates the anti-tumor immune response.[A234379] Dostarlimab is a monoclonal antibody targeted against PD-1 - it binds to the receptor and prevents interactions with PD-L1 and PD-L2, thus allowing the anti-tumor immune response to proceed unimpeded.[L33320] | There are no data regarding overdose with dostarlimab. Symptoms of overdosage are likely to be consistent with the adverse effect profile of dostarlimab and may therefore involve significant immune-mediated reactions.[L33320] | The metabolism of dostarlimab has not been characterized, but it is expected to be degraded via catabolic pathways into smaller peptides and amino acids.[L33320,A216712] | During the first cycle, and administered at 500mg intravenously every 3 weeks, the mean Cmax and AUC0-tau of dostarlimab-gxly are 171 mcg/mL and 35,730 mcg.h/mL, respectively. When administered at 1000mg every 6 weeks, the mean Cmax and AUC0-tau are 309 mcg/mL and 95,820 mcg.h/mL, respectively.[L33320] | At steady-state, the mean volume of distribution of dostarlimab is 5.3L.[L33320] | At steady-state, the mean clearance of dostarlimab is 0.007 L/h.[L33320] | Programmed Death Receptor-1 Blocking Antibody | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15816 | Th1631 | Dostarlimab | >Th1631_Dostarlimab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYDMSWVRQAPGKGLEWVSTISGGGSYTYYQDSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCASPYYAMDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 144000 | C6420H9832N1680O2014S44 | NA | NA | NA | The mean terminal elimination half-life of dostarlimab is 25.4 days.[L33320] | Dostarlimab is an IgG4 humanized monoclonal antibody targeted against the human programmed death receptor-1 (PD-1).[L33320] PD-1 receptors are found on T-cells and, when activated, serve to inhibit immune responses - some cancers leverage this system by overexpressing PD-1 ligands, thereby effectively inhibiting the anti-tumor immune response that would typically attempt to destroy the cancerous cells.[A234379] Agents acting on the PD-1 pathway, such as [nivolumab] and [pembrolizumab], facilitate endogenous immune-mediated anti-tumor activity and may therefore be used to treat a wide variety of cancers, including those of the skin, lung, kidneys, and liver. In April 2021, dostarlimab was granted an accelerated approval by the FDA - as GlaxoSmithKline's dostarlimab-gxly (Jemperli) - for the treatment of adult patients with recurrent or advanced mismatch repair deficient (dMMR) endometrial cancer experiencing disease progression despite treatment with platinum-containing chemotherapy regimens.[L33340] As this accelerated approval was granted only for the treatment of dMMR endometrial cancers, it was approved alongside a companion diagnostic device - the VENTANA MMR RxDx Panel - for use in selecting appropriate patients for treatment.[L33340] | Dostarlimab-gxly is indicated for the treatment of adult patients with mismatch repair deficient (dMMR) recurrent or advanced endometrial cancer that has progressed despite ongoing or prior treatment with a platinum-containing chemotherapy regimen.[L33320] | Dostarlimab is an immunotherapy that facilitates the body's endogenous anti-tumor immune response in the treatment cancer.[L33320] It is administered over a span of 30 minutes via intravenous infusion every three to six weeks depending on the cycle.[L33320] Agents that interfere with the PD-1/PD-L1 pathway, including dostarlimab, remove an important immune system inhibitory response and may therefore induce immune-mediated adverse reactions which can be severe or fatal. These reactions can occur in any organ system and can occur at any time after starting therapy, and while they most often manifest during therapy they may also appear after discontinuing the causative agent. Patients receiving therapy with dostarlimab should be monitored closely for evidence of an underlying immune-mediated reaction and evaluated and treated promptly if an immune-mediated reaction is suspected.[L33320] | Approximately 13-30% of recurrent endometrial cancers involve microsatellite instability (MSI) or mismatch repair deficiency (dMMR).[A234379,A234389] The mutations resulting in dMMR endometrial cancers are primarily somatic in nature (~90%), although 5-10% of cases involve germline mutations.[A234389] Cancers that have mutations resulting in dMMR can upregulate the expression of programmed death receptor-1 (PD-1) ligands 1 and 2 (PD-L1 and -L2) - PD-1 is found on T-cells and, when activated, inhibits their proliferation and the production of cytokines.[L33320] The binding of these ligands to PD-1 thereby functions as an immune checkpoint that downregulates the anti-tumor immune response.[A234379] Dostarlimab is a monoclonal antibody targeted against PD-1 - it binds to the receptor and prevents interactions with PD-L1 and PD-L2, thus allowing the anti-tumor immune response to proceed unimpeded.[L33320] | There are no data regarding overdose with dostarlimab. Symptoms of overdosage are likely to be consistent with the adverse effect profile of dostarlimab and may therefore involve significant immune-mediated reactions.[L33320] | The metabolism of dostarlimab has not been characterized, but it is expected to be degraded via catabolic pathways into smaller peptides and amino acids.[L33320,A216712] | During the first cycle, and administered at 500mg intravenously every 3 weeks, the mean Cmax and AUC0-tau of dostarlimab-gxly are 171 mcg/mL and 35,730 mcg.h/mL, respectively. When administered at 1000mg every 6 weeks, the mean Cmax and AUC0-tau are 309 mcg/mL and 95,820 mcg.h/mL, respectively.[L33320] | At steady-state, the mean volume of distribution of dostarlimab is 5.3L.[L33320] | At steady-state, the mean clearance of dostarlimab is 0.007 L/h.[L33320] | Programmed Death Receptor-1-directed Antibody Interactions | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15817 | Th1631 | Dostarlimab | >Th1631_Dostarlimab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYDMSWVRQAPGKGLEWVSTISGGGSYTYYQDSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCASPYYAMDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 144000 | C6420H9832N1680O2014S44 | NA | NA | NA | The mean terminal elimination half-life of dostarlimab is 25.4 days.[L33320] | Dostarlimab is an IgG4 humanized monoclonal antibody targeted against the human programmed death receptor-1 (PD-1).[L33320] PD-1 receptors are found on T-cells and, when activated, serve to inhibit immune responses - some cancers leverage this system by overexpressing PD-1 ligands, thereby effectively inhibiting the anti-tumor immune response that would typically attempt to destroy the cancerous cells.[A234379] Agents acting on the PD-1 pathway, such as [nivolumab] and [pembrolizumab], facilitate endogenous immune-mediated anti-tumor activity and may therefore be used to treat a wide variety of cancers, including those of the skin, lung, kidneys, and liver. In April 2021, dostarlimab was granted an accelerated approval by the FDA - as GlaxoSmithKline's dostarlimab-gxly (Jemperli) - for the treatment of adult patients with recurrent or advanced mismatch repair deficient (dMMR) endometrial cancer experiencing disease progression despite treatment with platinum-containing chemotherapy regimens.[L33340] As this accelerated approval was granted only for the treatment of dMMR endometrial cancers, it was approved alongside a companion diagnostic device - the VENTANA MMR RxDx Panel - for use in selecting appropriate patients for treatment.[L33340] | Dostarlimab-gxly is indicated for the treatment of adult patients with mismatch repair deficient (dMMR) recurrent or advanced endometrial cancer that has progressed despite ongoing or prior treatment with a platinum-containing chemotherapy regimen.[L33320] | Dostarlimab is an immunotherapy that facilitates the body's endogenous anti-tumor immune response in the treatment cancer.[L33320] It is administered over a span of 30 minutes via intravenous infusion every three to six weeks depending on the cycle.[L33320] Agents that interfere with the PD-1/PD-L1 pathway, including dostarlimab, remove an important immune system inhibitory response and may therefore induce immune-mediated adverse reactions which can be severe or fatal. These reactions can occur in any organ system and can occur at any time after starting therapy, and while they most often manifest during therapy they may also appear after discontinuing the causative agent. Patients receiving therapy with dostarlimab should be monitored closely for evidence of an underlying immune-mediated reaction and evaluated and treated promptly if an immune-mediated reaction is suspected.[L33320] | Approximately 13-30% of recurrent endometrial cancers involve microsatellite instability (MSI) or mismatch repair deficiency (dMMR).[A234379,A234389] The mutations resulting in dMMR endometrial cancers are primarily somatic in nature (~90%), although 5-10% of cases involve germline mutations.[A234389] Cancers that have mutations resulting in dMMR can upregulate the expression of programmed death receptor-1 (PD-1) ligands 1 and 2 (PD-L1 and -L2) - PD-1 is found on T-cells and, when activated, inhibits their proliferation and the production of cytokines.[L33320] The binding of these ligands to PD-1 thereby functions as an immune checkpoint that downregulates the anti-tumor immune response.[A234379] Dostarlimab is a monoclonal antibody targeted against PD-1 - it binds to the receptor and prevents interactions with PD-L1 and PD-L2, thus allowing the anti-tumor immune response to proceed unimpeded.[L33320] | There are no data regarding overdose with dostarlimab. Symptoms of overdosage are likely to be consistent with the adverse effect profile of dostarlimab and may therefore involve significant immune-mediated reactions.[L33320] | The metabolism of dostarlimab has not been characterized, but it is expected to be degraded via catabolic pathways into smaller peptides and amino acids.[L33320,A216712] | During the first cycle, and administered at 500mg intravenously every 3 weeks, the mean Cmax and AUC0-tau of dostarlimab-gxly are 171 mcg/mL and 35,730 mcg.h/mL, respectively. When administered at 1000mg every 6 weeks, the mean Cmax and AUC0-tau are 309 mcg/mL and 95,820 mcg.h/mL, respectively.[L33320] | At steady-state, the mean volume of distribution of dostarlimab is 5.3L.[L33320] | At steady-state, the mean clearance of dostarlimab is 0.007 L/h.[L33320] | Proteins | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15818 | Th1631 | Dostarlimab | >Th1631_Dostarlimab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYDMSWVRQAPGKGLEWVSTISGGGSYTYYQDSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCASPYYAMDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 144000 | C6420H9832N1680O2014S44 | NA | NA | NA | The mean terminal elimination half-life of dostarlimab is 25.4 days.[L33320] | Dostarlimab is an IgG4 humanized monoclonal antibody targeted against the human programmed death receptor-1 (PD-1).[L33320] PD-1 receptors are found on T-cells and, when activated, serve to inhibit immune responses - some cancers leverage this system by overexpressing PD-1 ligands, thereby effectively inhibiting the anti-tumor immune response that would typically attempt to destroy the cancerous cells.[A234379] Agents acting on the PD-1 pathway, such as [nivolumab] and [pembrolizumab], facilitate endogenous immune-mediated anti-tumor activity and may therefore be used to treat a wide variety of cancers, including those of the skin, lung, kidneys, and liver. In April 2021, dostarlimab was granted an accelerated approval by the FDA - as GlaxoSmithKline's dostarlimab-gxly (Jemperli) - for the treatment of adult patients with recurrent or advanced mismatch repair deficient (dMMR) endometrial cancer experiencing disease progression despite treatment with platinum-containing chemotherapy regimens.[L33340] As this accelerated approval was granted only for the treatment of dMMR endometrial cancers, it was approved alongside a companion diagnostic device - the VENTANA MMR RxDx Panel - for use in selecting appropriate patients for treatment.[L33340] | Dostarlimab-gxly is indicated for the treatment of adult patients with mismatch repair deficient (dMMR) recurrent or advanced endometrial cancer that has progressed despite ongoing or prior treatment with a platinum-containing chemotherapy regimen.[L33320] | Dostarlimab is an immunotherapy that facilitates the body's endogenous anti-tumor immune response in the treatment cancer.[L33320] It is administered over a span of 30 minutes via intravenous infusion every three to six weeks depending on the cycle.[L33320] Agents that interfere with the PD-1/PD-L1 pathway, including dostarlimab, remove an important immune system inhibitory response and may therefore induce immune-mediated adverse reactions which can be severe or fatal. These reactions can occur in any organ system and can occur at any time after starting therapy, and while they most often manifest during therapy they may also appear after discontinuing the causative agent. Patients receiving therapy with dostarlimab should be monitored closely for evidence of an underlying immune-mediated reaction and evaluated and treated promptly if an immune-mediated reaction is suspected.[L33320] | Approximately 13-30% of recurrent endometrial cancers involve microsatellite instability (MSI) or mismatch repair deficiency (dMMR).[A234379,A234389] The mutations resulting in dMMR endometrial cancers are primarily somatic in nature (~90%), although 5-10% of cases involve germline mutations.[A234389] Cancers that have mutations resulting in dMMR can upregulate the expression of programmed death receptor-1 (PD-1) ligands 1 and 2 (PD-L1 and -L2) - PD-1 is found on T-cells and, when activated, inhibits their proliferation and the production of cytokines.[L33320] The binding of these ligands to PD-1 thereby functions as an immune checkpoint that downregulates the anti-tumor immune response.[A234379] Dostarlimab is a monoclonal antibody targeted against PD-1 - it binds to the receptor and prevents interactions with PD-L1 and PD-L2, thus allowing the anti-tumor immune response to proceed unimpeded.[L33320] | There are no data regarding overdose with dostarlimab. Symptoms of overdosage are likely to be consistent with the adverse effect profile of dostarlimab and may therefore involve significant immune-mediated reactions.[L33320] | The metabolism of dostarlimab has not been characterized, but it is expected to be degraded via catabolic pathways into smaller peptides and amino acids.[L33320,A216712] | During the first cycle, and administered at 500mg intravenously every 3 weeks, the mean Cmax and AUC0-tau of dostarlimab-gxly are 171 mcg/mL and 35,730 mcg.h/mL, respectively. When administered at 1000mg every 6 weeks, the mean Cmax and AUC0-tau are 309 mcg/mL and 95,820 mcg.h/mL, respectively.[L33320] | At steady-state, the mean volume of distribution of dostarlimab is 5.3L.[L33320] | At steady-state, the mean clearance of dostarlimab is 0.007 L/h.[L33320] | Serum Globulins | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16146 | Th1683 | Amivantamab | >Th1683_Amivantamab QVQLVQSGAEVAKPGTSVKLSCKASGYTFTDYWMQWVKQRPGQGLEWIGTIYPGDGDTGYAQKFQGKATLTADKSSKTVYMHLSSLASEDSAVYYCARGDYYGSNSLDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The terminal half life of amivantamab-vmjw is 11.3 ± 4.53 days.[L34193] | Amivantamab, also known as JNJ-61186372, is an anti-EGFR-MET bispecific antibody, derived from Chinese hamster ovary cells, approved for the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, as detected by an FDA-approved test, whose disease has progressed on or after platinum-based chemotherapy.[A235103,L34193] Patients with NSCLC often develop resistance to drugs that target EGFR and MET individually, so amivantamab was developed to attack both targets, reducing the chance of resistance developing.[A235103,A235118] Amivantamab was found to be more effective than the EGFR inhibitor [erlotinib] or the MET inhibitor [crizotinib] _in vivo_.[A235103,A235123] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and were generally treated with platinum-based therapy.[A235133] Amivantamab was granted FDA approval on 21 May 2021.[L34193] | Amivantamab is indicated in the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, whose disease has progressed on or after platinum-based chemotherapy.[L34193] | Amivantamab is an EGF and MET receptor targeted antibody indicated in the treatment of non-small cell lung cancer with an EGFR 20 exon insertion mutation.[L34193] It has a long duration of action, as activity can be detected up to 8 weeks after treatment.[A235103] Patients should be counselled regarding the risk of infusion-related reactions, interstitial lung disease and pneumonitis, skin reactions, ocular toxicity, and paronychia.[L34193] Patients should not take amivantamab if they are pregnant or breastfeeding.[L34193] | Mesenchymal-epithelial transition factor (MET) is a receptor with tyrosine kinase activity expressed on epithelial cells that, upon signalling, dimerizes and activates downstream pathways that signal cell division.[A235103,A235128] The Epidermal Growth Factor Receptor (EGFR) is a transmembrane protein with tyrosine kinase activity that can further activate downstream pathways that signal cell division, survival, and angiogenesis.[A235103,A235128] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and are generally treated with platinum-based therapy.[A235133] Exon 20 insertion mutations in EGFR also lead to conformational changes that activate EGFR.[A235138] Amivantamab targets both EGFR and MET, preventing ligands from binding to the receptors, blocking signalling, marking the cancerous cells for antibody-dependant cellular cytotoxicity by natural killer cells, and allowing macrophages to perform trogocytosis.[L34193] Amivantamab's binding to the EGFR H epitope shares some of the same amino acids that [cetuximab] binds to.[A235103] Amivantamab's binding to the alpha chain of MET stabilizes the Sema domain loop 1 to 2 in a position 6 Angstroms away from the position it would be in under normal binding, preventing its interaction with the hepatocyte growth factor's (HGF) beta chain.[A235103] Another smaller conformational change in the MET Sema domain loop 1 to 3 also contributes to preventing the interaction of the MET Sema domain with HGF's beta chain.[A235103] HGF is no longer able to bind to MET, preventing downstream signalling.[A235103] Amivantamab's Fc portion contains 90% less fucose than normal antibodies, allowing for increased binding to the Fc | Data regarding overdoses of amivantamab are not readily available.[L34193] Patients experiencing an overdose should be treated with symptomatic and supportive measures. | Antibodies are expected to be metabolized to oligopeptides and amino acids.[A40006] | NA | The mean volume of distribution of amivantamab-vmjw is 5.13 ±1.78 L.[L34193] | The mean clearance of amivantamab-vmjw is 360 ± 144 mL/day.[L34193] | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Epidermal growth factor receptor,Hepatocyte growth factor receptor,Low affinity immunoglobulin gamma Fc region receptor III-A | Rybrevant | Janssen Biotech, Inc. | Janssen Biotech, Inc. | Intravenous | 350 mg/1 | None. | rash, infusion related reactions, Infection of the skin surrounding the fingernails or toenails, musculoskeletal pain, shortness of breath, nausea, fatigue, fluid retention (edema), inflammation of the mouth and lips, cough, constipation, vomiting, decreased white blood cells, decreased albumin, decreased phosphate, decreased potassium, increased alkaline phosphatase, increased glucose, increased gamma-glutamyl transferase, and decreased sodium. | Rybrevant is a prescription medicine used to treat adults with non-small cell lung cancer (NSCLC) that: has spread to other parts of the body (metastatic) or cannot be removed by surgery, and has a certain abnormal epidermal growth factor receptor “EGFR” gene(s) and whose disease has worsened while... | RYBREVANT is indicated for the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, as detected by an FDA-approved test [see DOSAGE AND ADMINISTRATION], whose disease has progressed on or after platinum-based chemotherapy. | NA | These are not all of the possible side effects of RYBREVANT. | Link | Link | NA |
| 16147 | Th1683 | Amivantamab | >Th1683_Amivantamab QVQLVQSGAEVAKPGTSVKLSCKASGYTFTDYWMQWVKQRPGQGLEWIGTIYPGDGDTGYAQKFQGKATLTADKSSKTVYMHLSSLASEDSAVYYCARGDYYGSNSLDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The terminal half life of amivantamab-vmjw is 11.3 ± 4.53 days.[L34193] | Amivantamab, also known as JNJ-61186372, is an anti-EGFR-MET bispecific antibody, derived from Chinese hamster ovary cells, approved for the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, as detected by an FDA-approved test, whose disease has progressed on or after platinum-based chemotherapy.[A235103,L34193] Patients with NSCLC often develop resistance to drugs that target EGFR and MET individually, so amivantamab was developed to attack both targets, reducing the chance of resistance developing.[A235103,A235118] Amivantamab was found to be more effective than the EGFR inhibitor [erlotinib] or the MET inhibitor [crizotinib] _in vivo_.[A235103,A235123] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and were generally treated with platinum-based therapy.[A235133] Amivantamab was granted FDA approval on 21 May 2021.[L34193] | Amivantamab is indicated in the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, whose disease has progressed on or after platinum-based chemotherapy.[L34193] | Amivantamab is an EGF and MET receptor targeted antibody indicated in the treatment of non-small cell lung cancer with an EGFR 20 exon insertion mutation.[L34193] It has a long duration of action, as activity can be detected up to 8 weeks after treatment.[A235103] Patients should be counselled regarding the risk of infusion-related reactions, interstitial lung disease and pneumonitis, skin reactions, ocular toxicity, and paronychia.[L34193] Patients should not take amivantamab if they are pregnant or breastfeeding.[L34193] | Mesenchymal-epithelial transition factor (MET) is a receptor with tyrosine kinase activity expressed on epithelial cells that, upon signalling, dimerizes and activates downstream pathways that signal cell division.[A235103,A235128] The Epidermal Growth Factor Receptor (EGFR) is a transmembrane protein with tyrosine kinase activity that can further activate downstream pathways that signal cell division, survival, and angiogenesis.[A235103,A235128] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and are generally treated with platinum-based therapy.[A235133] Exon 20 insertion mutations in EGFR also lead to conformational changes that activate EGFR.[A235138] Amivantamab targets both EGFR and MET, preventing ligands from binding to the receptors, blocking signalling, marking the cancerous cells for antibody-dependant cellular cytotoxicity by natural killer cells, and allowing macrophages to perform trogocytosis.[L34193] Amivantamab's binding to the EGFR H epitope shares some of the same amino acids that [cetuximab] binds to.[A235103] Amivantamab's binding to the alpha chain of MET stabilizes the Sema domain loop 1 to 2 in a position 6 Angstroms away from the position it would be in under normal binding, preventing its interaction with the hepatocyte growth factor's (HGF) beta chain.[A235103] Another smaller conformational change in the MET Sema domain loop 1 to 3 also contributes to preventing the interaction of the MET Sema domain with HGF's beta chain.[A235103] HGF is no longer able to bind to MET, preventing downstream signalling.[A235103] Amivantamab's Fc portion contains 90% less fucose than normal antibodies, allowing for increased binding to the Fc | Data regarding overdoses of amivantamab are not readily available.[L34193] Patients experiencing an overdose should be treated with symptomatic and supportive measures. | Antibodies are expected to be metabolized to oligopeptides and amino acids.[A40006] | NA | The mean volume of distribution of amivantamab-vmjw is 5.13 ±1.78 L.[L34193] | The mean clearance of amivantamab-vmjw is 360 ± 144 mL/day.[L34193] | Antibodies | NA | NA | NA | NA | Epidermal growth factor receptor,Hepatocyte growth factor receptor,Low affinity immunoglobulin gamma Fc region receptor III-A | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16148 | Th1683 | Amivantamab | >Th1683_Amivantamab QVQLVQSGAEVAKPGTSVKLSCKASGYTFTDYWMQWVKQRPGQGLEWIGTIYPGDGDTGYAQKFQGKATLTADKSSKTVYMHLSSLASEDSAVYYCARGDYYGSNSLDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The terminal half life of amivantamab-vmjw is 11.3 ± 4.53 days.[L34193] | Amivantamab, also known as JNJ-61186372, is an anti-EGFR-MET bispecific antibody, derived from Chinese hamster ovary cells, approved for the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, as detected by an FDA-approved test, whose disease has progressed on or after platinum-based chemotherapy.[A235103,L34193] Patients with NSCLC often develop resistance to drugs that target EGFR and MET individually, so amivantamab was developed to attack both targets, reducing the chance of resistance developing.[A235103,A235118] Amivantamab was found to be more effective than the EGFR inhibitor [erlotinib] or the MET inhibitor [crizotinib] _in vivo_.[A235103,A235123] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and were generally treated with platinum-based therapy.[A235133] Amivantamab was granted FDA approval on 21 May 2021.[L34193] | Amivantamab is indicated in the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, whose disease has progressed on or after platinum-based chemotherapy.[L34193] | Amivantamab is an EGF and MET receptor targeted antibody indicated in the treatment of non-small cell lung cancer with an EGFR 20 exon insertion mutation.[L34193] It has a long duration of action, as activity can be detected up to 8 weeks after treatment.[A235103] Patients should be counselled regarding the risk of infusion-related reactions, interstitial lung disease and pneumonitis, skin reactions, ocular toxicity, and paronychia.[L34193] Patients should not take amivantamab if they are pregnant or breastfeeding.[L34193] | Mesenchymal-epithelial transition factor (MET) is a receptor with tyrosine kinase activity expressed on epithelial cells that, upon signalling, dimerizes and activates downstream pathways that signal cell division.[A235103,A235128] The Epidermal Growth Factor Receptor (EGFR) is a transmembrane protein with tyrosine kinase activity that can further activate downstream pathways that signal cell division, survival, and angiogenesis.[A235103,A235128] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and are generally treated with platinum-based therapy.[A235133] Exon 20 insertion mutations in EGFR also lead to conformational changes that activate EGFR.[A235138] Amivantamab targets both EGFR and MET, preventing ligands from binding to the receptors, blocking signalling, marking the cancerous cells for antibody-dependant cellular cytotoxicity by natural killer cells, and allowing macrophages to perform trogocytosis.[L34193] Amivantamab's binding to the EGFR H epitope shares some of the same amino acids that [cetuximab] binds to.[A235103] Amivantamab's binding to the alpha chain of MET stabilizes the Sema domain loop 1 to 2 in a position 6 Angstroms away from the position it would be in under normal binding, preventing its interaction with the hepatocyte growth factor's (HGF) beta chain.[A235103] Another smaller conformational change in the MET Sema domain loop 1 to 3 also contributes to preventing the interaction of the MET Sema domain with HGF's beta chain.[A235103] HGF is no longer able to bind to MET, preventing downstream signalling.[A235103] Amivantamab's Fc portion contains 90% less fucose than normal antibodies, allowing for increased binding to the Fc | Data regarding overdoses of amivantamab are not readily available.[L34193] Patients experiencing an overdose should be treated with symptomatic and supportive measures. | Antibodies are expected to be metabolized to oligopeptides and amino acids.[A40006] | NA | The mean volume of distribution of amivantamab-vmjw is 5.13 ±1.78 L.[L34193] | The mean clearance of amivantamab-vmjw is 360 ± 144 mL/day.[L34193] | Blood Proteins | NA | NA | NA | NA | Epidermal growth factor receptor,Hepatocyte growth factor receptor,Low affinity immunoglobulin gamma Fc region receptor III-A | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16149 | Th1683 | Amivantamab | >Th1683_Amivantamab QVQLVQSGAEVAKPGTSVKLSCKASGYTFTDYWMQWVKQRPGQGLEWIGTIYPGDGDTGYAQKFQGKATLTADKSSKTVYMHLSSLASEDSAVYYCARGDYYGSNSLDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The terminal half life of amivantamab-vmjw is 11.3 ± 4.53 days.[L34193] | Amivantamab, also known as JNJ-61186372, is an anti-EGFR-MET bispecific antibody, derived from Chinese hamster ovary cells, approved for the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, as detected by an FDA-approved test, whose disease has progressed on or after platinum-based chemotherapy.[A235103,L34193] Patients with NSCLC often develop resistance to drugs that target EGFR and MET individually, so amivantamab was developed to attack both targets, reducing the chance of resistance developing.[A235103,A235118] Amivantamab was found to be more effective than the EGFR inhibitor [erlotinib] or the MET inhibitor [crizotinib] _in vivo_.[A235103,A235123] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and were generally treated with platinum-based therapy.[A235133] Amivantamab was granted FDA approval on 21 May 2021.[L34193] | Amivantamab is indicated in the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, whose disease has progressed on or after platinum-based chemotherapy.[L34193] | Amivantamab is an EGF and MET receptor targeted antibody indicated in the treatment of non-small cell lung cancer with an EGFR 20 exon insertion mutation.[L34193] It has a long duration of action, as activity can be detected up to 8 weeks after treatment.[A235103] Patients should be counselled regarding the risk of infusion-related reactions, interstitial lung disease and pneumonitis, skin reactions, ocular toxicity, and paronychia.[L34193] Patients should not take amivantamab if they are pregnant or breastfeeding.[L34193] | Mesenchymal-epithelial transition factor (MET) is a receptor with tyrosine kinase activity expressed on epithelial cells that, upon signalling, dimerizes and activates downstream pathways that signal cell division.[A235103,A235128] The Epidermal Growth Factor Receptor (EGFR) is a transmembrane protein with tyrosine kinase activity that can further activate downstream pathways that signal cell division, survival, and angiogenesis.[A235103,A235128] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and are generally treated with platinum-based therapy.[A235133] Exon 20 insertion mutations in EGFR also lead to conformational changes that activate EGFR.[A235138] Amivantamab targets both EGFR and MET, preventing ligands from binding to the receptors, blocking signalling, marking the cancerous cells for antibody-dependant cellular cytotoxicity by natural killer cells, and allowing macrophages to perform trogocytosis.[L34193] Amivantamab's binding to the EGFR H epitope shares some of the same amino acids that [cetuximab] binds to.[A235103] Amivantamab's binding to the alpha chain of MET stabilizes the Sema domain loop 1 to 2 in a position 6 Angstroms away from the position it would be in under normal binding, preventing its interaction with the hepatocyte growth factor's (HGF) beta chain.[A235103] Another smaller conformational change in the MET Sema domain loop 1 to 3 also contributes to preventing the interaction of the MET Sema domain with HGF's beta chain.[A235103] HGF is no longer able to bind to MET, preventing downstream signalling.[A235103] Amivantamab's Fc portion contains 90% less fucose than normal antibodies, allowing for increased binding to the Fc | Data regarding overdoses of amivantamab are not readily available.[L34193] Patients experiencing an overdose should be treated with symptomatic and supportive measures. | Antibodies are expected to be metabolized to oligopeptides and amino acids.[A40006] | NA | The mean volume of distribution of amivantamab-vmjw is 5.13 ±1.78 L.[L34193] | The mean clearance of amivantamab-vmjw is 360 ± 144 mL/day.[L34193] | Globulins | NA | NA | NA | NA | Epidermal growth factor receptor,Hepatocyte growth factor receptor,Low affinity immunoglobulin gamma Fc region receptor III-A | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16150 | Th1683 | Amivantamab | >Th1683_Amivantamab QVQLVQSGAEVAKPGTSVKLSCKASGYTFTDYWMQWVKQRPGQGLEWIGTIYPGDGDTGYAQKFQGKATLTADKSSKTVYMHLSSLASEDSAVYYCARGDYYGSNSLDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The terminal half life of amivantamab-vmjw is 11.3 ± 4.53 days.[L34193] | Amivantamab, also known as JNJ-61186372, is an anti-EGFR-MET bispecific antibody, derived from Chinese hamster ovary cells, approved for the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, as detected by an FDA-approved test, whose disease has progressed on or after platinum-based chemotherapy.[A235103,L34193] Patients with NSCLC often develop resistance to drugs that target EGFR and MET individually, so amivantamab was developed to attack both targets, reducing the chance of resistance developing.[A235103,A235118] Amivantamab was found to be more effective than the EGFR inhibitor [erlotinib] or the MET inhibitor [crizotinib] _in vivo_.[A235103,A235123] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and were generally treated with platinum-based therapy.[A235133] Amivantamab was granted FDA approval on 21 May 2021.[L34193] | Amivantamab is indicated in the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, whose disease has progressed on or after platinum-based chemotherapy.[L34193] | Amivantamab is an EGF and MET receptor targeted antibody indicated in the treatment of non-small cell lung cancer with an EGFR 20 exon insertion mutation.[L34193] It has a long duration of action, as activity can be detected up to 8 weeks after treatment.[A235103] Patients should be counselled regarding the risk of infusion-related reactions, interstitial lung disease and pneumonitis, skin reactions, ocular toxicity, and paronychia.[L34193] Patients should not take amivantamab if they are pregnant or breastfeeding.[L34193] | Mesenchymal-epithelial transition factor (MET) is a receptor with tyrosine kinase activity expressed on epithelial cells that, upon signalling, dimerizes and activates downstream pathways that signal cell division.[A235103,A235128] The Epidermal Growth Factor Receptor (EGFR) is a transmembrane protein with tyrosine kinase activity that can further activate downstream pathways that signal cell division, survival, and angiogenesis.[A235103,A235128] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and are generally treated with platinum-based therapy.[A235133] Exon 20 insertion mutations in EGFR also lead to conformational changes that activate EGFR.[A235138] Amivantamab targets both EGFR and MET, preventing ligands from binding to the receptors, blocking signalling, marking the cancerous cells for antibody-dependant cellular cytotoxicity by natural killer cells, and allowing macrophages to perform trogocytosis.[L34193] Amivantamab's binding to the EGFR H epitope shares some of the same amino acids that [cetuximab] binds to.[A235103] Amivantamab's binding to the alpha chain of MET stabilizes the Sema domain loop 1 to 2 in a position 6 Angstroms away from the position it would be in under normal binding, preventing its interaction with the hepatocyte growth factor's (HGF) beta chain.[A235103] Another smaller conformational change in the MET Sema domain loop 1 to 3 also contributes to preventing the interaction of the MET Sema domain with HGF's beta chain.[A235103] HGF is no longer able to bind to MET, preventing downstream signalling.[A235103] Amivantamab's Fc portion contains 90% less fucose than normal antibodies, allowing for increased binding to the Fc | Data regarding overdoses of amivantamab are not readily available.[L34193] Patients experiencing an overdose should be treated with symptomatic and supportive measures. | Antibodies are expected to be metabolized to oligopeptides and amino acids.[A40006] | NA | The mean volume of distribution of amivantamab-vmjw is 5.13 ±1.78 L.[L34193] | The mean clearance of amivantamab-vmjw is 360 ± 144 mL/day.[L34193] | Immunoglobulins | NA | NA | NA | NA | Epidermal growth factor receptor,Hepatocyte growth factor receptor,Low affinity immunoglobulin gamma Fc region receptor III-A | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16151 | Th1683 | Amivantamab | >Th1683_Amivantamab QVQLVQSGAEVAKPGTSVKLSCKASGYTFTDYWMQWVKQRPGQGLEWIGTIYPGDGDTGYAQKFQGKATLTADKSSKTVYMHLSSLASEDSAVYYCARGDYYGSNSLDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The terminal half life of amivantamab-vmjw is 11.3 ± 4.53 days.[L34193] | Amivantamab, also known as JNJ-61186372, is an anti-EGFR-MET bispecific antibody, derived from Chinese hamster ovary cells, approved for the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, as detected by an FDA-approved test, whose disease has progressed on or after platinum-based chemotherapy.[A235103,L34193] Patients with NSCLC often develop resistance to drugs that target EGFR and MET individually, so amivantamab was developed to attack both targets, reducing the chance of resistance developing.[A235103,A235118] Amivantamab was found to be more effective than the EGFR inhibitor [erlotinib] or the MET inhibitor [crizotinib] _in vivo_.[A235103,A235123] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and were generally treated with platinum-based therapy.[A235133] Amivantamab was granted FDA approval on 21 May 2021.[L34193] | Amivantamab is indicated in the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, whose disease has progressed on or after platinum-based chemotherapy.[L34193] | Amivantamab is an EGF and MET receptor targeted antibody indicated in the treatment of non-small cell lung cancer with an EGFR 20 exon insertion mutation.[L34193] It has a long duration of action, as activity can be detected up to 8 weeks after treatment.[A235103] Patients should be counselled regarding the risk of infusion-related reactions, interstitial lung disease and pneumonitis, skin reactions, ocular toxicity, and paronychia.[L34193] Patients should not take amivantamab if they are pregnant or breastfeeding.[L34193] | Mesenchymal-epithelial transition factor (MET) is a receptor with tyrosine kinase activity expressed on epithelial cells that, upon signalling, dimerizes and activates downstream pathways that signal cell division.[A235103,A235128] The Epidermal Growth Factor Receptor (EGFR) is a transmembrane protein with tyrosine kinase activity that can further activate downstream pathways that signal cell division, survival, and angiogenesis.[A235103,A235128] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and are generally treated with platinum-based therapy.[A235133] Exon 20 insertion mutations in EGFR also lead to conformational changes that activate EGFR.[A235138] Amivantamab targets both EGFR and MET, preventing ligands from binding to the receptors, blocking signalling, marking the cancerous cells for antibody-dependant cellular cytotoxicity by natural killer cells, and allowing macrophages to perform trogocytosis.[L34193] Amivantamab's binding to the EGFR H epitope shares some of the same amino acids that [cetuximab] binds to.[A235103] Amivantamab's binding to the alpha chain of MET stabilizes the Sema domain loop 1 to 2 in a position 6 Angstroms away from the position it would be in under normal binding, preventing its interaction with the hepatocyte growth factor's (HGF) beta chain.[A235103] Another smaller conformational change in the MET Sema domain loop 1 to 3 also contributes to preventing the interaction of the MET Sema domain with HGF's beta chain.[A235103] HGF is no longer able to bind to MET, preventing downstream signalling.[A235103] Amivantamab's Fc portion contains 90% less fucose than normal antibodies, allowing for increased binding to the Fc | Data regarding overdoses of amivantamab are not readily available.[L34193] Patients experiencing an overdose should be treated with symptomatic and supportive measures. | Antibodies are expected to be metabolized to oligopeptides and amino acids.[A40006] | NA | The mean volume of distribution of amivantamab-vmjw is 5.13 ±1.78 L.[L34193] | The mean clearance of amivantamab-vmjw is 360 ± 144 mL/day.[L34193] | Immunoproteins | NA | NA | NA | NA | Epidermal growth factor receptor,Hepatocyte growth factor receptor,Low affinity immunoglobulin gamma Fc region receptor III-A | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16152 | Th1683 | Amivantamab | >Th1683_Amivantamab QVQLVQSGAEVAKPGTSVKLSCKASGYTFTDYWMQWVKQRPGQGLEWIGTIYPGDGDTGYAQKFQGKATLTADKSSKTVYMHLSSLASEDSAVYYCARGDYYGSNSLDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The terminal half life of amivantamab-vmjw is 11.3 ± 4.53 days.[L34193] | Amivantamab, also known as JNJ-61186372, is an anti-EGFR-MET bispecific antibody, derived from Chinese hamster ovary cells, approved for the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, as detected by an FDA-approved test, whose disease has progressed on or after platinum-based chemotherapy.[A235103,L34193] Patients with NSCLC often develop resistance to drugs that target EGFR and MET individually, so amivantamab was developed to attack both targets, reducing the chance of resistance developing.[A235103,A235118] Amivantamab was found to be more effective than the EGFR inhibitor [erlotinib] or the MET inhibitor [crizotinib] _in vivo_.[A235103,A235123] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and were generally treated with platinum-based therapy.[A235133] Amivantamab was granted FDA approval on 21 May 2021.[L34193] | Amivantamab is indicated in the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, whose disease has progressed on or after platinum-based chemotherapy.[L34193] | Amivantamab is an EGF and MET receptor targeted antibody indicated in the treatment of non-small cell lung cancer with an EGFR 20 exon insertion mutation.[L34193] It has a long duration of action, as activity can be detected up to 8 weeks after treatment.[A235103] Patients should be counselled regarding the risk of infusion-related reactions, interstitial lung disease and pneumonitis, skin reactions, ocular toxicity, and paronychia.[L34193] Patients should not take amivantamab if they are pregnant or breastfeeding.[L34193] | Mesenchymal-epithelial transition factor (MET) is a receptor with tyrosine kinase activity expressed on epithelial cells that, upon signalling, dimerizes and activates downstream pathways that signal cell division.[A235103,A235128] The Epidermal Growth Factor Receptor (EGFR) is a transmembrane protein with tyrosine kinase activity that can further activate downstream pathways that signal cell division, survival, and angiogenesis.[A235103,A235128] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and are generally treated with platinum-based therapy.[A235133] Exon 20 insertion mutations in EGFR also lead to conformational changes that activate EGFR.[A235138] Amivantamab targets both EGFR and MET, preventing ligands from binding to the receptors, blocking signalling, marking the cancerous cells for antibody-dependant cellular cytotoxicity by natural killer cells, and allowing macrophages to perform trogocytosis.[L34193] Amivantamab's binding to the EGFR H epitope shares some of the same amino acids that [cetuximab] binds to.[A235103] Amivantamab's binding to the alpha chain of MET stabilizes the Sema domain loop 1 to 2 in a position 6 Angstroms away from the position it would be in under normal binding, preventing its interaction with the hepatocyte growth factor's (HGF) beta chain.[A235103] Another smaller conformational change in the MET Sema domain loop 1 to 3 also contributes to preventing the interaction of the MET Sema domain with HGF's beta chain.[A235103] HGF is no longer able to bind to MET, preventing downstream signalling.[A235103] Amivantamab's Fc portion contains 90% less fucose than normal antibodies, allowing for increased binding to the Fc | Data regarding overdoses of amivantamab are not readily available.[L34193] Patients experiencing an overdose should be treated with symptomatic and supportive measures. | Antibodies are expected to be metabolized to oligopeptides and amino acids.[A40006] | NA | The mean volume of distribution of amivantamab-vmjw is 5.13 ±1.78 L.[L34193] | The mean clearance of amivantamab-vmjw is 360 ± 144 mL/day.[L34193] | Proteins | NA | NA | NA | NA | Epidermal growth factor receptor,Hepatocyte growth factor receptor,Low affinity immunoglobulin gamma Fc region receptor III-A | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16153 | Th1683 | Amivantamab | >Th1683_Amivantamab QVQLVQSGAEVAKPGTSVKLSCKASGYTFTDYWMQWVKQRPGQGLEWIGTIYPGDGDTGYAQKFQGKATLTADKSSKTVYMHLSSLASEDSAVYYCARGDYYGSNSLDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The terminal half life of amivantamab-vmjw is 11.3 ± 4.53 days.[L34193] | Amivantamab, also known as JNJ-61186372, is an anti-EGFR-MET bispecific antibody, derived from Chinese hamster ovary cells, approved for the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, as detected by an FDA-approved test, whose disease has progressed on or after platinum-based chemotherapy.[A235103,L34193] Patients with NSCLC often develop resistance to drugs that target EGFR and MET individually, so amivantamab was developed to attack both targets, reducing the chance of resistance developing.[A235103,A235118] Amivantamab was found to be more effective than the EGFR inhibitor [erlotinib] or the MET inhibitor [crizotinib] _in vivo_.[A235103,A235123] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and were generally treated with platinum-based therapy.[A235133] Amivantamab was granted FDA approval on 21 May 2021.[L34193] | Amivantamab is indicated in the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, whose disease has progressed on or after platinum-based chemotherapy.[L34193] | Amivantamab is an EGF and MET receptor targeted antibody indicated in the treatment of non-small cell lung cancer with an EGFR 20 exon insertion mutation.[L34193] It has a long duration of action, as activity can be detected up to 8 weeks after treatment.[A235103] Patients should be counselled regarding the risk of infusion-related reactions, interstitial lung disease and pneumonitis, skin reactions, ocular toxicity, and paronychia.[L34193] Patients should not take amivantamab if they are pregnant or breastfeeding.[L34193] | Mesenchymal-epithelial transition factor (MET) is a receptor with tyrosine kinase activity expressed on epithelial cells that, upon signalling, dimerizes and activates downstream pathways that signal cell division.[A235103,A235128] The Epidermal Growth Factor Receptor (EGFR) is a transmembrane protein with tyrosine kinase activity that can further activate downstream pathways that signal cell division, survival, and angiogenesis.[A235103,A235128] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and are generally treated with platinum-based therapy.[A235133] Exon 20 insertion mutations in EGFR also lead to conformational changes that activate EGFR.[A235138] Amivantamab targets both EGFR and MET, preventing ligands from binding to the receptors, blocking signalling, marking the cancerous cells for antibody-dependant cellular cytotoxicity by natural killer cells, and allowing macrophages to perform trogocytosis.[L34193] Amivantamab's binding to the EGFR H epitope shares some of the same amino acids that [cetuximab] binds to.[A235103] Amivantamab's binding to the alpha chain of MET stabilizes the Sema domain loop 1 to 2 in a position 6 Angstroms away from the position it would be in under normal binding, preventing its interaction with the hepatocyte growth factor's (HGF) beta chain.[A235103] Another smaller conformational change in the MET Sema domain loop 1 to 3 also contributes to preventing the interaction of the MET Sema domain with HGF's beta chain.[A235103] HGF is no longer able to bind to MET, preventing downstream signalling.[A235103] Amivantamab's Fc portion contains 90% less fucose than normal antibodies, allowing for increased binding to the Fc | Data regarding overdoses of amivantamab are not readily available.[L34193] Patients experiencing an overdose should be treated with symptomatic and supportive measures. | Antibodies are expected to be metabolized to oligopeptides and amino acids.[A40006] | NA | The mean volume of distribution of amivantamab-vmjw is 5.13 ±1.78 L.[L34193] | The mean clearance of amivantamab-vmjw is 360 ± 144 mL/day.[L34193] | Serum Globulins | NA | NA | NA | NA | Epidermal growth factor receptor,Hepatocyte growth factor receptor,Low affinity immunoglobulin gamma Fc region receptor III-A | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16168 | Th1686 | Tisotumab vedotin | NA | 153000 | NA | NA | NA | NA | The median terminal half-life of tisotumab vedotin-tftv and unconjugated MMAE is 4.04 (range: 2.26-7.25) days and 2.56 (range: 1.81-4.10) days, respectively.[L38424] | Tisotumab vedotin is a tissue factor-directed antibody-drug conjugate (ADC) comprised of an anti-tissue factor (TF) human IgG1-kappa antibody conjugated to monomethyl auristatin E (MMAE), a microtubule-disrupting agent, via a protease-cleavable valine-citrulline linker. Each monoclonal antibody molecule carries an average of four MMAE molecules. Tisotumab vedotin is the first TF-directed ADC [A238914] that works by binding to TFs expressed on solid tumours. TF is a primary initiator of the extrinsic blood coagulation cascade [L38424] and plays a key role in tumor-associated angiogenesis, progression, and metastasis for tumor survival. TF is a novel target for cancers, as it is often overexpressed on solid tumours, including cervical cancer, and it is associated with poor clinical outcomes. Tisotumab vedotin targets TF-expressing cells to deliver MMAE to induce direct cytotoxicity and bystander killing of neighboring cells.[A238914] On September 20, 2021, the FDA granted accelerated approval to tisotumab vedotin-tftv for the treatment of recurrent or metastatic cervical cancer in adults in whom the disease progressed during or after chemotherapy. This is the first and only approved antibody-drug conjugate for this therapeutic indication. The approval was based on tumour response and the durability of the response as demonstrated in InnovaTV 204 (NCT03438396): in this trial, the objective response rate was 24% and the median response duration was 8.3 months.[L38429] Tisotumab vedotin-tftv is marketed under the trade name Tivdak as an intravenous injection. Tisotumab vedotin is currently under investigation as a treatment for other solid tumors, including ovarian, lung, colorectal, pancreatic, and head and neck cancers. It is also being investigated for the combination use with other chemotherapeutic agents for recurrent or metastatic cervical cancer.[A238924] | Tisotumab vedotin is indicated for the treatment of adult patients with recurrent or metastatic cervical cancer with disease progression on or after chemotherapy.[L38424] | Tisotumab vedotin is an anticancer antibody-drug conjugate that is made up of an antibody and monomethyl auristatin E (MMAE), a cytotoxic component of the drug. It works by binding to tissue factors expressed on cervical tumours and releasing MMAE upon cell entry to mediate its cytotoxic activity. Apart from directly killing tumour cells, tisotumab vedotin may exert a bystander effect by killing neighbouring cells [A238914] and promote immunogenic cell death pathways, including antibody-dependent cellular cytotoxicity and antibody-dependent cellular phagocytosis.[L38424] | Tisotumab vedotin is a tissue factor (TF)-directed antibody-drug conjugate (ADC) anti-TF IgG1-kappa antibody conjugated to the microtubule-disrupting agent MMAE via a protease-cleavable vc (valine-citrulline) linker. It may exhibit multiple mechanisms of action; however, it primarily works by inducing cytotoxic effects on TF-expressing tumours. Tisotumab vedotin binds to TFs expressed on cervical tumours, which leads to the internalization of the antibody-drug conjugate-TF complex. Once internalized, MMAE from the drug-target complex is released via proteolytic cleavage. MMAE is a microtubule-disrupting agent that disrupts the microtubule network of actively dividing cells, leading to cell cycle arrest and apoptotic cell death.[L38424] Tisotumab vedotin may also promote bystander killing of neighbouring cells. According to _in vitro_ studies, tisotumab vedotin induces immunogenic cell death and promotes tumour cell death through Fc | There is no information on the LD50 values and overdose profile of tisotumab vedotin. Tisotumab vedotin is associated with a risk for ocular toxicity. In clinical trials, ocular adverse reactions occurred in 60% of patients with cervical cancer. The most common reactions were conjunctival adverse reactions (40%), dry eye (29%), corneal adverse reactions (21%), and blepharitis (8%). More severe reactions included ulcerative keratitis, ulcerative keratitis with perforation requiring corneal transplantation, and symblepharon in patients with other tumor types.[L38424] | Tisotumab vedotin-tftv most likely undergoes catabolism to form small peptides, amino acids, unconjugated MMAE, and unconjugated MMAE-related catabolites. Via proteolytic cleavage, tisotumab vedotin-tftv releases unconjugated MMAE, which is primarily metabolized by CYP3A4 _in vitro_.[L38424] | Following administration of one 3-week cycle of tisotumab vedotin-tftv 2 mg/kg, the peak concentrations reached near the end of the infusion, while unconjugated MMAE concentrations peaked approximately two to three days after tisotumab vedotin-tftv dosing. The mean (± SD) Cmax of tisotumab vedotin-tftv was 40.8 (8.12) µg/mL and the mean (± SD) AUC was 57.5 (13.4) day x µg/mL. The mean (± SD) Cmax of unconjugated MMAE was 5.91 (4.2) ng/mL and the mean (± SD) AUC was 50 (35.8) day x ng/mL. The Cmax of tisotumab vedotin-tftv increased proportionally and there was no drug accumulation. Steady-state concentrations of tisotumab vedotin-tftv and unconjugated MMAE were reached after one treatment cycle.[L38424] | The tisotumab vedotin-tftv steady-state volume of distribution is 7.83 (%CV: 19.1) L.[L38424] | The linear clearance of tisotumab vedotin-tftv and unconjugated MMAE was 1.54 (%CV: 28.8) L/day and 45.9 (%CV: 61.1) L/day, respectively. Elimination of MMAE appeared to be limited by its rate of release from tisotumab vedotin-tftv.[L38424] | Antineoplastic Agents | NA | NA | NA | NA | Tissue factor | Tivdak | Seagen Inc. | Seagen Inc. | Intravenous | 40 mg/4mL | None. | decreased hemoglobin, fatigue, decreased lymphocytes, nausea, numbness and tingling of extremities, hair loss, nosebleed, adverse eye reactions, hemorrhage, decreased leukocytes, increased creatinine, dry eye, increased prothrombin international normalized ratio, prolonged activated partial thromboplastin time, diarrhea, and rash | Tivdak is a prescription medicine used to treat adults with cervical cancer: that has returned or has spread to other parts of the body, and who have received chemotherapy that did not work or is no longer working. It is not known if this medicine is safe and effective in children. Important information... | Tivdak is a prescription medicine used to treat the symptoms of Cervical Cancer. Tivdak may be used alone or with other medications. | NA | Tisotumab vedotin-tftv is a Tissue Factor (TF) directed antibody drug conjugate (ADC) comprised of a human anti-TF IgG1-kappa antibody conjugated to the microtubule-disrupting agent monomethyl auristatin E (MMAE) via a protease-cleavable vc (valine-citrulline) linker. The monoclonal antibody is produced in a mammalian cell cline (Chinese hamster ovary). MMAE and the linker are produced by chemical synthesis. Each monoclonal antibody molecule carries an average of 4 MMAE molecules. Tisotumab vedotin-tftv has an approximate molecular weight of 153 kDa. The chemical structure is as follows: | Link | Link | NA |
| 16169 | Th1686 | Tisotumab vedotin | NA | 153000 | NA | NA | NA | NA | The median terminal half-life of tisotumab vedotin-tftv and unconjugated MMAE is 4.04 (range: 2.26-7.25) days and 2.56 (range: 1.81-4.10) days, respectively.[L38424] | Tisotumab vedotin is a tissue factor-directed antibody-drug conjugate (ADC) comprised of an anti-tissue factor (TF) human IgG1-kappa antibody conjugated to monomethyl auristatin E (MMAE), a microtubule-disrupting agent, via a protease-cleavable valine-citrulline linker. Each monoclonal antibody molecule carries an average of four MMAE molecules. Tisotumab vedotin is the first TF-directed ADC [A238914] that works by binding to TFs expressed on solid tumours. TF is a primary initiator of the extrinsic blood coagulation cascade [L38424] and plays a key role in tumor-associated angiogenesis, progression, and metastasis for tumor survival. TF is a novel target for cancers, as it is often overexpressed on solid tumours, including cervical cancer, and it is associated with poor clinical outcomes. Tisotumab vedotin targets TF-expressing cells to deliver MMAE to induce direct cytotoxicity and bystander killing of neighboring cells.[A238914] On September 20, 2021, the FDA granted accelerated approval to tisotumab vedotin-tftv for the treatment of recurrent or metastatic cervical cancer in adults in whom the disease progressed during or after chemotherapy. This is the first and only approved antibody-drug conjugate for this therapeutic indication. The approval was based on tumour response and the durability of the response as demonstrated in InnovaTV 204 (NCT03438396): in this trial, the objective response rate was 24% and the median response duration was 8.3 months.[L38429] Tisotumab vedotin-tftv is marketed under the trade name Tivdak as an intravenous injection. Tisotumab vedotin is currently under investigation as a treatment for other solid tumors, including ovarian, lung, colorectal, pancreatic, and head and neck cancers. It is also being investigated for the combination use with other chemotherapeutic agents for recurrent or metastatic cervical cancer.[A238924] | Tisotumab vedotin is indicated for the treatment of adult patients with recurrent or metastatic cervical cancer with disease progression on or after chemotherapy.[L38424] | Tisotumab vedotin is an anticancer antibody-drug conjugate that is made up of an antibody and monomethyl auristatin E (MMAE), a cytotoxic component of the drug. It works by binding to tissue factors expressed on cervical tumours and releasing MMAE upon cell entry to mediate its cytotoxic activity. Apart from directly killing tumour cells, tisotumab vedotin may exert a bystander effect by killing neighbouring cells [A238914] and promote immunogenic cell death pathways, including antibody-dependent cellular cytotoxicity and antibody-dependent cellular phagocytosis.[L38424] | Tisotumab vedotin is a tissue factor (TF)-directed antibody-drug conjugate (ADC) anti-TF IgG1-kappa antibody conjugated to the microtubule-disrupting agent MMAE via a protease-cleavable vc (valine-citrulline) linker. It may exhibit multiple mechanisms of action; however, it primarily works by inducing cytotoxic effects on TF-expressing tumours. Tisotumab vedotin binds to TFs expressed on cervical tumours, which leads to the internalization of the antibody-drug conjugate-TF complex. Once internalized, MMAE from the drug-target complex is released via proteolytic cleavage. MMAE is a microtubule-disrupting agent that disrupts the microtubule network of actively dividing cells, leading to cell cycle arrest and apoptotic cell death.[L38424] Tisotumab vedotin may also promote bystander killing of neighbouring cells. According to _in vitro_ studies, tisotumab vedotin induces immunogenic cell death and promotes tumour cell death through Fc | There is no information on the LD50 values and overdose profile of tisotumab vedotin. Tisotumab vedotin is associated with a risk for ocular toxicity. In clinical trials, ocular adverse reactions occurred in 60% of patients with cervical cancer. The most common reactions were conjunctival adverse reactions (40%), dry eye (29%), corneal adverse reactions (21%), and blepharitis (8%). More severe reactions included ulcerative keratitis, ulcerative keratitis with perforation requiring corneal transplantation, and symblepharon in patients with other tumor types.[L38424] | Tisotumab vedotin-tftv most likely undergoes catabolism to form small peptides, amino acids, unconjugated MMAE, and unconjugated MMAE-related catabolites. Via proteolytic cleavage, tisotumab vedotin-tftv releases unconjugated MMAE, which is primarily metabolized by CYP3A4 _in vitro_.[L38424] | Following administration of one 3-week cycle of tisotumab vedotin-tftv 2 mg/kg, the peak concentrations reached near the end of the infusion, while unconjugated MMAE concentrations peaked approximately two to three days after tisotumab vedotin-tftv dosing. The mean (± SD) Cmax of tisotumab vedotin-tftv was 40.8 (8.12) µg/mL and the mean (± SD) AUC was 57.5 (13.4) day x µg/mL. The mean (± SD) Cmax of unconjugated MMAE was 5.91 (4.2) ng/mL and the mean (± SD) AUC was 50 (35.8) day x ng/mL. The Cmax of tisotumab vedotin-tftv increased proportionally and there was no drug accumulation. Steady-state concentrations of tisotumab vedotin-tftv and unconjugated MMAE were reached after one treatment cycle.[L38424] | The tisotumab vedotin-tftv steady-state volume of distribution is 7.83 (%CV: 19.1) L.[L38424] | The linear clearance of tisotumab vedotin-tftv and unconjugated MMAE was 1.54 (%CV: 28.8) L/day and 45.9 (%CV: 61.1) L/day, respectively. Elimination of MMAE appeared to be limited by its rate of release from tisotumab vedotin-tftv.[L38424] | Antineoplastic Agents, Immunological | NA | NA | NA | NA | Tissue factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16170 | Th1686 | Tisotumab vedotin | NA | 153000 | NA | NA | NA | NA | The median terminal half-life of tisotumab vedotin-tftv and unconjugated MMAE is 4.04 (range: 2.26-7.25) days and 2.56 (range: 1.81-4.10) days, respectively.[L38424] | Tisotumab vedotin is a tissue factor-directed antibody-drug conjugate (ADC) comprised of an anti-tissue factor (TF) human IgG1-kappa antibody conjugated to monomethyl auristatin E (MMAE), a microtubule-disrupting agent, via a protease-cleavable valine-citrulline linker. Each monoclonal antibody molecule carries an average of four MMAE molecules. Tisotumab vedotin is the first TF-directed ADC [A238914] that works by binding to TFs expressed on solid tumours. TF is a primary initiator of the extrinsic blood coagulation cascade [L38424] and plays a key role in tumor-associated angiogenesis, progression, and metastasis for tumor survival. TF is a novel target for cancers, as it is often overexpressed on solid tumours, including cervical cancer, and it is associated with poor clinical outcomes. Tisotumab vedotin targets TF-expressing cells to deliver MMAE to induce direct cytotoxicity and bystander killing of neighboring cells.[A238914] On September 20, 2021, the FDA granted accelerated approval to tisotumab vedotin-tftv for the treatment of recurrent or metastatic cervical cancer in adults in whom the disease progressed during or after chemotherapy. This is the first and only approved antibody-drug conjugate for this therapeutic indication. The approval was based on tumour response and the durability of the response as demonstrated in InnovaTV 204 (NCT03438396): in this trial, the objective response rate was 24% and the median response duration was 8.3 months.[L38429] Tisotumab vedotin-tftv is marketed under the trade name Tivdak as an intravenous injection. Tisotumab vedotin is currently under investigation as a treatment for other solid tumors, including ovarian, lung, colorectal, pancreatic, and head and neck cancers. It is also being investigated for the combination use with other chemotherapeutic agents for recurrent or metastatic cervical cancer.[A238924] | Tisotumab vedotin is indicated for the treatment of adult patients with recurrent or metastatic cervical cancer with disease progression on or after chemotherapy.[L38424] | Tisotumab vedotin is an anticancer antibody-drug conjugate that is made up of an antibody and monomethyl auristatin E (MMAE), a cytotoxic component of the drug. It works by binding to tissue factors expressed on cervical tumours and releasing MMAE upon cell entry to mediate its cytotoxic activity. Apart from directly killing tumour cells, tisotumab vedotin may exert a bystander effect by killing neighbouring cells [A238914] and promote immunogenic cell death pathways, including antibody-dependent cellular cytotoxicity and antibody-dependent cellular phagocytosis.[L38424] | Tisotumab vedotin is a tissue factor (TF)-directed antibody-drug conjugate (ADC) anti-TF IgG1-kappa antibody conjugated to the microtubule-disrupting agent MMAE via a protease-cleavable vc (valine-citrulline) linker. It may exhibit multiple mechanisms of action; however, it primarily works by inducing cytotoxic effects on TF-expressing tumours. Tisotumab vedotin binds to TFs expressed on cervical tumours, which leads to the internalization of the antibody-drug conjugate-TF complex. Once internalized, MMAE from the drug-target complex is released via proteolytic cleavage. MMAE is a microtubule-disrupting agent that disrupts the microtubule network of actively dividing cells, leading to cell cycle arrest and apoptotic cell death.[L38424] Tisotumab vedotin may also promote bystander killing of neighbouring cells. According to _in vitro_ studies, tisotumab vedotin induces immunogenic cell death and promotes tumour cell death through Fc | There is no information on the LD50 values and overdose profile of tisotumab vedotin. Tisotumab vedotin is associated with a risk for ocular toxicity. In clinical trials, ocular adverse reactions occurred in 60% of patients with cervical cancer. The most common reactions were conjunctival adverse reactions (40%), dry eye (29%), corneal adverse reactions (21%), and blepharitis (8%). More severe reactions included ulcerative keratitis, ulcerative keratitis with perforation requiring corneal transplantation, and symblepharon in patients with other tumor types.[L38424] | Tisotumab vedotin-tftv most likely undergoes catabolism to form small peptides, amino acids, unconjugated MMAE, and unconjugated MMAE-related catabolites. Via proteolytic cleavage, tisotumab vedotin-tftv releases unconjugated MMAE, which is primarily metabolized by CYP3A4 _in vitro_.[L38424] | Following administration of one 3-week cycle of tisotumab vedotin-tftv 2 mg/kg, the peak concentrations reached near the end of the infusion, while unconjugated MMAE concentrations peaked approximately two to three days after tisotumab vedotin-tftv dosing. The mean (± SD) Cmax of tisotumab vedotin-tftv was 40.8 (8.12) µg/mL and the mean (± SD) AUC was 57.5 (13.4) day x µg/mL. The mean (± SD) Cmax of unconjugated MMAE was 5.91 (4.2) ng/mL and the mean (± SD) AUC was 50 (35.8) day x ng/mL. The Cmax of tisotumab vedotin-tftv increased proportionally and there was no drug accumulation. Steady-state concentrations of tisotumab vedotin-tftv and unconjugated MMAE were reached after one treatment cycle.[L38424] | The tisotumab vedotin-tftv steady-state volume of distribution is 7.83 (%CV: 19.1) L.[L38424] | The linear clearance of tisotumab vedotin-tftv and unconjugated MMAE was 1.54 (%CV: 28.8) L/day and 45.9 (%CV: 61.1) L/day, respectively. Elimination of MMAE appeared to be limited by its rate of release from tisotumab vedotin-tftv.[L38424] | Cytochrome P-450 CYP3A Substrates | NA | NA | NA | NA | Tissue factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16171 | Th1686 | Tisotumab vedotin | NA | 153000 | NA | NA | NA | NA | The median terminal half-life of tisotumab vedotin-tftv and unconjugated MMAE is 4.04 (range: 2.26-7.25) days and 2.56 (range: 1.81-4.10) days, respectively.[L38424] | Tisotumab vedotin is a tissue factor-directed antibody-drug conjugate (ADC) comprised of an anti-tissue factor (TF) human IgG1-kappa antibody conjugated to monomethyl auristatin E (MMAE), a microtubule-disrupting agent, via a protease-cleavable valine-citrulline linker. Each monoclonal antibody molecule carries an average of four MMAE molecules. Tisotumab vedotin is the first TF-directed ADC [A238914] that works by binding to TFs expressed on solid tumours. TF is a primary initiator of the extrinsic blood coagulation cascade [L38424] and plays a key role in tumor-associated angiogenesis, progression, and metastasis for tumor survival. TF is a novel target for cancers, as it is often overexpressed on solid tumours, including cervical cancer, and it is associated with poor clinical outcomes. Tisotumab vedotin targets TF-expressing cells to deliver MMAE to induce direct cytotoxicity and bystander killing of neighboring cells.[A238914] On September 20, 2021, the FDA granted accelerated approval to tisotumab vedotin-tftv for the treatment of recurrent or metastatic cervical cancer in adults in whom the disease progressed during or after chemotherapy. This is the first and only approved antibody-drug conjugate for this therapeutic indication. The approval was based on tumour response and the durability of the response as demonstrated in InnovaTV 204 (NCT03438396): in this trial, the objective response rate was 24% and the median response duration was 8.3 months.[L38429] Tisotumab vedotin-tftv is marketed under the trade name Tivdak as an intravenous injection. Tisotumab vedotin is currently under investigation as a treatment for other solid tumors, including ovarian, lung, colorectal, pancreatic, and head and neck cancers. It is also being investigated for the combination use with other chemotherapeutic agents for recurrent or metastatic cervical cancer.[A238924] | Tisotumab vedotin is indicated for the treatment of adult patients with recurrent or metastatic cervical cancer with disease progression on or after chemotherapy.[L38424] | Tisotumab vedotin is an anticancer antibody-drug conjugate that is made up of an antibody and monomethyl auristatin E (MMAE), a cytotoxic component of the drug. It works by binding to tissue factors expressed on cervical tumours and releasing MMAE upon cell entry to mediate its cytotoxic activity. Apart from directly killing tumour cells, tisotumab vedotin may exert a bystander effect by killing neighbouring cells [A238914] and promote immunogenic cell death pathways, including antibody-dependent cellular cytotoxicity and antibody-dependent cellular phagocytosis.[L38424] | Tisotumab vedotin is a tissue factor (TF)-directed antibody-drug conjugate (ADC) anti-TF IgG1-kappa antibody conjugated to the microtubule-disrupting agent MMAE via a protease-cleavable vc (valine-citrulline) linker. It may exhibit multiple mechanisms of action; however, it primarily works by inducing cytotoxic effects on TF-expressing tumours. Tisotumab vedotin binds to TFs expressed on cervical tumours, which leads to the internalization of the antibody-drug conjugate-TF complex. Once internalized, MMAE from the drug-target complex is released via proteolytic cleavage. MMAE is a microtubule-disrupting agent that disrupts the microtubule network of actively dividing cells, leading to cell cycle arrest and apoptotic cell death.[L38424] Tisotumab vedotin may also promote bystander killing of neighbouring cells. According to _in vitro_ studies, tisotumab vedotin induces immunogenic cell death and promotes tumour cell death through Fc | There is no information on the LD50 values and overdose profile of tisotumab vedotin. Tisotumab vedotin is associated with a risk for ocular toxicity. In clinical trials, ocular adverse reactions occurred in 60% of patients with cervical cancer. The most common reactions were conjunctival adverse reactions (40%), dry eye (29%), corneal adverse reactions (21%), and blepharitis (8%). More severe reactions included ulcerative keratitis, ulcerative keratitis with perforation requiring corneal transplantation, and symblepharon in patients with other tumor types.[L38424] | Tisotumab vedotin-tftv most likely undergoes catabolism to form small peptides, amino acids, unconjugated MMAE, and unconjugated MMAE-related catabolites. Via proteolytic cleavage, tisotumab vedotin-tftv releases unconjugated MMAE, which is primarily metabolized by CYP3A4 _in vitro_.[L38424] | Following administration of one 3-week cycle of tisotumab vedotin-tftv 2 mg/kg, the peak concentrations reached near the end of the infusion, while unconjugated MMAE concentrations peaked approximately two to three days after tisotumab vedotin-tftv dosing. The mean (± SD) Cmax of tisotumab vedotin-tftv was 40.8 (8.12) µg/mL and the mean (± SD) AUC was 57.5 (13.4) day x µg/mL. The mean (± SD) Cmax of unconjugated MMAE was 5.91 (4.2) ng/mL and the mean (± SD) AUC was 50 (35.8) day x ng/mL. The Cmax of tisotumab vedotin-tftv increased proportionally and there was no drug accumulation. Steady-state concentrations of tisotumab vedotin-tftv and unconjugated MMAE were reached after one treatment cycle.[L38424] | The tisotumab vedotin-tftv steady-state volume of distribution is 7.83 (%CV: 19.1) L.[L38424] | The linear clearance of tisotumab vedotin-tftv and unconjugated MMAE was 1.54 (%CV: 28.8) L/day and 45.9 (%CV: 61.1) L/day, respectively. Elimination of MMAE appeared to be limited by its rate of release from tisotumab vedotin-tftv.[L38424] | Cytochrome P-450 CYP3A4 Substrates | NA | NA | NA | NA | Tissue factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16172 | Th1686 | Tisotumab vedotin | NA | 153000 | NA | NA | NA | NA | The median terminal half-life of tisotumab vedotin-tftv and unconjugated MMAE is 4.04 (range: 2.26-7.25) days and 2.56 (range: 1.81-4.10) days, respectively.[L38424] | Tisotumab vedotin is a tissue factor-directed antibody-drug conjugate (ADC) comprised of an anti-tissue factor (TF) human IgG1-kappa antibody conjugated to monomethyl auristatin E (MMAE), a microtubule-disrupting agent, via a protease-cleavable valine-citrulline linker. Each monoclonal antibody molecule carries an average of four MMAE molecules. Tisotumab vedotin is the first TF-directed ADC [A238914] that works by binding to TFs expressed on solid tumours. TF is a primary initiator of the extrinsic blood coagulation cascade [L38424] and plays a key role in tumor-associated angiogenesis, progression, and metastasis for tumor survival. TF is a novel target for cancers, as it is often overexpressed on solid tumours, including cervical cancer, and it is associated with poor clinical outcomes. Tisotumab vedotin targets TF-expressing cells to deliver MMAE to induce direct cytotoxicity and bystander killing of neighboring cells.[A238914] On September 20, 2021, the FDA granted accelerated approval to tisotumab vedotin-tftv for the treatment of recurrent or metastatic cervical cancer in adults in whom the disease progressed during or after chemotherapy. This is the first and only approved antibody-drug conjugate for this therapeutic indication. The approval was based on tumour response and the durability of the response as demonstrated in InnovaTV 204 (NCT03438396): in this trial, the objective response rate was 24% and the median response duration was 8.3 months.[L38429] Tisotumab vedotin-tftv is marketed under the trade name Tivdak as an intravenous injection. Tisotumab vedotin is currently under investigation as a treatment for other solid tumors, including ovarian, lung, colorectal, pancreatic, and head and neck cancers. It is also being investigated for the combination use with other chemotherapeutic agents for recurrent or metastatic cervical cancer.[A238924] | Tisotumab vedotin is indicated for the treatment of adult patients with recurrent or metastatic cervical cancer with disease progression on or after chemotherapy.[L38424] | Tisotumab vedotin is an anticancer antibody-drug conjugate that is made up of an antibody and monomethyl auristatin E (MMAE), a cytotoxic component of the drug. It works by binding to tissue factors expressed on cervical tumours and releasing MMAE upon cell entry to mediate its cytotoxic activity. Apart from directly killing tumour cells, tisotumab vedotin may exert a bystander effect by killing neighbouring cells [A238914] and promote immunogenic cell death pathways, including antibody-dependent cellular cytotoxicity and antibody-dependent cellular phagocytosis.[L38424] | Tisotumab vedotin is a tissue factor (TF)-directed antibody-drug conjugate (ADC) anti-TF IgG1-kappa antibody conjugated to the microtubule-disrupting agent MMAE via a protease-cleavable vc (valine-citrulline) linker. It may exhibit multiple mechanisms of action; however, it primarily works by inducing cytotoxic effects on TF-expressing tumours. Tisotumab vedotin binds to TFs expressed on cervical tumours, which leads to the internalization of the antibody-drug conjugate-TF complex. Once internalized, MMAE from the drug-target complex is released via proteolytic cleavage. MMAE is a microtubule-disrupting agent that disrupts the microtubule network of actively dividing cells, leading to cell cycle arrest and apoptotic cell death.[L38424] Tisotumab vedotin may also promote bystander killing of neighbouring cells. According to _in vitro_ studies, tisotumab vedotin induces immunogenic cell death and promotes tumour cell death through Fc | There is no information on the LD50 values and overdose profile of tisotumab vedotin. Tisotumab vedotin is associated with a risk for ocular toxicity. In clinical trials, ocular adverse reactions occurred in 60% of patients with cervical cancer. The most common reactions were conjunctival adverse reactions (40%), dry eye (29%), corneal adverse reactions (21%), and blepharitis (8%). More severe reactions included ulcerative keratitis, ulcerative keratitis with perforation requiring corneal transplantation, and symblepharon in patients with other tumor types.[L38424] | Tisotumab vedotin-tftv most likely undergoes catabolism to form small peptides, amino acids, unconjugated MMAE, and unconjugated MMAE-related catabolites. Via proteolytic cleavage, tisotumab vedotin-tftv releases unconjugated MMAE, which is primarily metabolized by CYP3A4 _in vitro_.[L38424] | Following administration of one 3-week cycle of tisotumab vedotin-tftv 2 mg/kg, the peak concentrations reached near the end of the infusion, while unconjugated MMAE concentrations peaked approximately two to three days after tisotumab vedotin-tftv dosing. The mean (± SD) Cmax of tisotumab vedotin-tftv was 40.8 (8.12) µg/mL and the mean (± SD) AUC was 57.5 (13.4) day x µg/mL. The mean (± SD) Cmax of unconjugated MMAE was 5.91 (4.2) ng/mL and the mean (± SD) AUC was 50 (35.8) day x ng/mL. The Cmax of tisotumab vedotin-tftv increased proportionally and there was no drug accumulation. Steady-state concentrations of tisotumab vedotin-tftv and unconjugated MMAE were reached after one treatment cycle.[L38424] | The tisotumab vedotin-tftv steady-state volume of distribution is 7.83 (%CV: 19.1) L.[L38424] | The linear clearance of tisotumab vedotin-tftv and unconjugated MMAE was 1.54 (%CV: 28.8) L/day and 45.9 (%CV: 61.1) L/day, respectively. Elimination of MMAE appeared to be limited by its rate of release from tisotumab vedotin-tftv.[L38424] | Cytochrome P-450 Substrates | NA | NA | NA | NA | Tissue factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16173 | Th1686 | Tisotumab vedotin | NA | 153000 | NA | NA | NA | NA | The median terminal half-life of tisotumab vedotin-tftv and unconjugated MMAE is 4.04 (range: 2.26-7.25) days and 2.56 (range: 1.81-4.10) days, respectively.[L38424] | Tisotumab vedotin is a tissue factor-directed antibody-drug conjugate (ADC) comprised of an anti-tissue factor (TF) human IgG1-kappa antibody conjugated to monomethyl auristatin E (MMAE), a microtubule-disrupting agent, via a protease-cleavable valine-citrulline linker. Each monoclonal antibody molecule carries an average of four MMAE molecules. Tisotumab vedotin is the first TF-directed ADC [A238914] that works by binding to TFs expressed on solid tumours. TF is a primary initiator of the extrinsic blood coagulation cascade [L38424] and plays a key role in tumor-associated angiogenesis, progression, and metastasis for tumor survival. TF is a novel target for cancers, as it is often overexpressed on solid tumours, including cervical cancer, and it is associated with poor clinical outcomes. Tisotumab vedotin targets TF-expressing cells to deliver MMAE to induce direct cytotoxicity and bystander killing of neighboring cells.[A238914] On September 20, 2021, the FDA granted accelerated approval to tisotumab vedotin-tftv for the treatment of recurrent or metastatic cervical cancer in adults in whom the disease progressed during or after chemotherapy. This is the first and only approved antibody-drug conjugate for this therapeutic indication. The approval was based on tumour response and the durability of the response as demonstrated in InnovaTV 204 (NCT03438396): in this trial, the objective response rate was 24% and the median response duration was 8.3 months.[L38429] Tisotumab vedotin-tftv is marketed under the trade name Tivdak as an intravenous injection. Tisotumab vedotin is currently under investigation as a treatment for other solid tumors, including ovarian, lung, colorectal, pancreatic, and head and neck cancers. It is also being investigated for the combination use with other chemotherapeutic agents for recurrent or metastatic cervical cancer.[A238924] | Tisotumab vedotin is indicated for the treatment of adult patients with recurrent or metastatic cervical cancer with disease progression on or after chemotherapy.[L38424] | Tisotumab vedotin is an anticancer antibody-drug conjugate that is made up of an antibody and monomethyl auristatin E (MMAE), a cytotoxic component of the drug. It works by binding to tissue factors expressed on cervical tumours and releasing MMAE upon cell entry to mediate its cytotoxic activity. Apart from directly killing tumour cells, tisotumab vedotin may exert a bystander effect by killing neighbouring cells [A238914] and promote immunogenic cell death pathways, including antibody-dependent cellular cytotoxicity and antibody-dependent cellular phagocytosis.[L38424] | Tisotumab vedotin is a tissue factor (TF)-directed antibody-drug conjugate (ADC) anti-TF IgG1-kappa antibody conjugated to the microtubule-disrupting agent MMAE via a protease-cleavable vc (valine-citrulline) linker. It may exhibit multiple mechanisms of action; however, it primarily works by inducing cytotoxic effects on TF-expressing tumours. Tisotumab vedotin binds to TFs expressed on cervical tumours, which leads to the internalization of the antibody-drug conjugate-TF complex. Once internalized, MMAE from the drug-target complex is released via proteolytic cleavage. MMAE is a microtubule-disrupting agent that disrupts the microtubule network of actively dividing cells, leading to cell cycle arrest and apoptotic cell death.[L38424] Tisotumab vedotin may also promote bystander killing of neighbouring cells. According to _in vitro_ studies, tisotumab vedotin induces immunogenic cell death and promotes tumour cell death through Fc | There is no information on the LD50 values and overdose profile of tisotumab vedotin. Tisotumab vedotin is associated with a risk for ocular toxicity. In clinical trials, ocular adverse reactions occurred in 60% of patients with cervical cancer. The most common reactions were conjunctival adverse reactions (40%), dry eye (29%), corneal adverse reactions (21%), and blepharitis (8%). More severe reactions included ulcerative keratitis, ulcerative keratitis with perforation requiring corneal transplantation, and symblepharon in patients with other tumor types.[L38424] | Tisotumab vedotin-tftv most likely undergoes catabolism to form small peptides, amino acids, unconjugated MMAE, and unconjugated MMAE-related catabolites. Via proteolytic cleavage, tisotumab vedotin-tftv releases unconjugated MMAE, which is primarily metabolized by CYP3A4 _in vitro_.[L38424] | Following administration of one 3-week cycle of tisotumab vedotin-tftv 2 mg/kg, the peak concentrations reached near the end of the infusion, while unconjugated MMAE concentrations peaked approximately two to three days after tisotumab vedotin-tftv dosing. The mean (± SD) Cmax of tisotumab vedotin-tftv was 40.8 (8.12) µg/mL and the mean (± SD) AUC was 57.5 (13.4) day x µg/mL. The mean (± SD) Cmax of unconjugated MMAE was 5.91 (4.2) ng/mL and the mean (± SD) AUC was 50 (35.8) day x ng/mL. The Cmax of tisotumab vedotin-tftv increased proportionally and there was no drug accumulation. Steady-state concentrations of tisotumab vedotin-tftv and unconjugated MMAE were reached after one treatment cycle.[L38424] | The tisotumab vedotin-tftv steady-state volume of distribution is 7.83 (%CV: 19.1) L.[L38424] | The linear clearance of tisotumab vedotin-tftv and unconjugated MMAE was 1.54 (%CV: 28.8) L/day and 45.9 (%CV: 61.1) L/day, respectively. Elimination of MMAE appeared to be limited by its rate of release from tisotumab vedotin-tftv.[L38424] | P-glycoprotein substrates | NA | NA | NA | NA | Tissue factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16176 | Th1689 | NV1020 | NA | NA | NA | NA | NA | NA | NA | NV1020, a genetically engineered herpes simplex virus, is a novel anticancer therapeutic. | Intended for the treatment of various forms of cancer. | NA | Cancer-killing viruses, so-called oncolytic viruses are specific herpes simplex viruses, or HSVs, generally known as the cause of cold sores. These viruses are used, however, in a modified and "disarmed" form in order to make them utilizable as a therapeutic agent in humans. This is achieved by switching off certain genes that normally enable the virus to multiply in healthy cells, which would destroy these cells. As a result of this genetic modification, the HSVs are able to reproduce in tumor cells solely, since only these offer an environment that compensates for the loss of the removed viral genes. Consequently, the virus is able to replicate in the tumor cells, selectively destroying them without harming healthy tissue. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16178 | Th1691 | CG7870 | >Th1691_CG7870 MWTCLCQLCFYLLSTLAVAALSIAALVLYKTKPYPNIKRHKDEETFLDPHTIKTVTFPSLEDSPSLELSVIVPAYNEEQRLPSMLDECLAFLEQKSAGTPNFTYEVIVVSDGSQDATVSVALGYSKKHGAEKVRVLELIENRGKGGAVRMGMLSARGRNLLFADADGATKFPDYDKLEVALKQLAPEWRDDGIAIGSRAHLENDAIATRSFFRTILMHGFHFLVWLFAVRSIRDTQCGFKLFTRTTARKLFTSLHVERWAFDVELLYLAENLKLPMSEVAVRWTEIDGSKLTPFWSWLQMGRDLFMIWVRYLVGAWRIASIQKKEK | NA | NA | NA | NA | NA | NA | CG7870 is an oncolytic virus therapy for prostate cancer. It is a replication-selective, prostate-specific antigen-targeted oncolytic adenovirus, for the treatment of hormone-refractory, metastatic prostate cancer. | Intended for the treatment of various forms of cancer. | NA | CG7870 is genetically engineered to replicate preferentially in prostate tissue, ignoring healthy cells. In this manner, the virus is able to selectively attack and kill tumorous cells. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16179 | Th1692 | ZYC300 | NA | NA | NA | NA | NA | NA | NA | ZYC300 is a plasmid DNA of CYP1B1 encapsulated in biodegradable poly-DL-lactide-coglycolide microparticles. It is designed as a vaccine, intended to increase immune system sensitivity to CYP1B1, an enzyme highly prevalent in tumor cells. | For the treatment of various forms of cancer. | NA | CYP1B1 is a unique extra-hepatic member of the cytochrome P450 family of monooxygenases. The CYP1B1 protein is over-expressed in all primary human tumors with minimal expression in critical normal tissues making this an attractive target for immunotherapy. CYP1B1-specific human T lymphocytes lyse tumor cells but not normal cells. To explore the potential clinical utility of elevated CYP1B1 immune responses, a pDNA-based immunogen was developed (ZYC300). The ZYC300 formulation is comprised of PLG microparticles containing a plasmid DNA with a CMV promoter that drives expression of mutated CYP1B1 protein. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16185 | Th1698 | VPM4001 | NA | NA | NA | NA | NA | NA | NA | VPM4001 is an allogeneic vaccine for treatment of prostate carcinoma. It consists of irradiated human LNCaP cells that have been genetically modified to permanently secrete interferon- | Investigated for use/treatment in prostate cancer. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16188 | Th1701 | IGN301 | NA | NA | NA | NA | NA | NA | NA | IGN301 is a cancer vaccine based on an anti-idiotypic antibody which provokes an immune response to Lewis Y. Lewis Y is a carbohydrate molecule expressed on the surface of tumor cells of epithelial origin (e.g. lung, intestinal, breast, prostate or ovarian cancers). | Investigated for use/treatment in cancer/tumors (unspecified). | NA | IGN301 is based on an anti-idiotype antibody designed to trigger an immune response to Lewis Y, a carbohydrate molecule frequently overexpressed in tumor cells of epithelial origin such as lung, colon, breast, prostate or ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16189 | Th1702 | 1D09C3 | NA | NA | NA | NA | NA | NA | NA | 1D09C3, a monoclonal antibody against lymphoid cancers, is an anti-MHC (major histocompatibility complex) class II monoclonal antibody. The antibody was isolated in collaboration with MorphoSys from its HuCAL(R) library of human antibodies. 1D09C3 binds to certain cell surface receptors, selectively killing activated, proliferating MHC class II-positive tumor cells, which include those in B-cell and T-cell lymphomas. 1D09C3 has been shown to induce programmed cell death and does not require a functioning immune system for its cell-killing effect. | Intended for the treatment of various forms of cancer. | NA | 1D09C3 binds specifically to the MHC (major histocompatibility complex) class II molecule, which is found mainly on the surface of blood cells and certain tumor cells. It selectively kills activated, proliferating MHC class II-positive tumor cells, which include those in B-cell and T-cell lymphomas. 1D09C3 has been shown to kill these tumor cells by inducing programmed cell death. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | HLA-DR | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16201 | Th1714 | SOT-107 | NA | NA | NA | NA | NA | NA | NA | SOT-107 is a drug that is a combination of a protein called transferrin and a poison called diphtheria toxin. This drug treat for a type of brain cancer called a high grade glioma brain tumour. About half of all brain tumours are gliomas. | Investigated for use/treatment in brain cancer. | NA | Its mechanism of action involves transferrin-mediated delivery of a modified diphtheria toxin that is capable of selectively killing cancer cells. The agent is administered directly into the glioma using convection enhanced delivery to circumvent the blood-brain barrier and achieve high local concentrations of the drug. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Glioma pathogenesis-related protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16202 | Th1715 | VB2-011 | NA | NA | NA | NA | NA | NA | NA | VB2-011 is an antibody developed as an anti-cancer treatment. According to some preclinical studies, it has a potential to inhibit tumour growth in various cancers including lymphoma and melanoma. This drug includes the parent IgM (H11 IgM) and a recombinant IgG version (H11 IgG). | Investigated for use/treatment in cancer/tumors (unspecified). | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16205 | Th1718 | IDD-1 | >Th1718_IDD-1 MVPKADSGAFLLLFLLVLTVTEPLRPELRCNPGQFACRSGTIQCIPLPWQCDGWATCEDESDEANCPEVTGEVRPHHGKEAVDPRQGRARGGDPSHFHAVNVAQPVRFSSFLGKCPTGWHHYEGTASCYRVYLSGENYWDAAQTCQRLNGSLATFSTDQELRFVLAQEWDQPERSFGWKDQRKLWVGYQYVITGRNRSLEGRWEVAFKGSSEVFLPPDPIFASAMSENDNVFCAQLQCFHFPTLRHHDLHSWHAESCYEKSSFLCKRSQTCVDIKDNVVDEGFYFTPKGDDPCLSCTCHGGEPEMCVAALCERPQGCQQYRKDPKECCKFMCLDPDGNSLFDSMASGMRLVVSCISSFLILSLLLFMVHRLRQRRRERIESLIGANLHHFNLGRRIPGFDYGPDGFGTGLTPLHLSDDGEGGTFHFHDPPPPYTAYKYPDIGQPDDPPPPYEASIHPDSVFYDPADDDAFEPVEVSLPAPGDGGSEGALLRRLEQPLPTAGASLADLEDSADSSSALLVPPDPAQSGSTPAAEALPGGGRHSRSSLNTVV | NA | NA | NA | NA | NA | NA | Lipids promote the fusion of liposomes to cells. Eladem (IDD-1) is a therapeutic vaccine consisting of dendritophages that are loaded in vitro with tumor antigens and then reinjected into the subject. As with other monoclonal antibodies, this process stimulates an immune response to a particular disease-related antigen. | Investigated for use/treatment in prostate cancer. | IDD-1 specifically targets cancer cells by simulating a natural immune response. IDD-1 is produced by coupling dendritophages with tumor antigens obtained from the individual patient. The resulting vaccine is then reinjected into the subject. | The lipid promotes fusion of liposomes to cells. Specifically, IDD-1 targets tumor cells by coupling dendritophages with tumor antigens obtained from the patient. | MoABs have been reported to have low toxicity, as they successfully target the tumor cells. | NA | 3 doses x 3 cycles [each dose divided in 1 i.v.,4 s.c. and 1 i.d. injection] | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16207 | Th1720 | SGN-30 | NA | NA | NA | NA | NA | NA | NA | SGN-30 is an engineered monoclonal antibody (mAb) that reacts with significant affinity to the CD30 antigen, which is highly expressed on a variety of hematologic malignancies as compared to on normal cells. SGN-30 has been shown to induce direct anti-cancer activity towards tumor cells expressing CD30 and is undergoing phase II trials for cancer therapy. SGN-30 has demonstrated objective antitumor responses as a single agent in phase II clinical trials. We are collaborating with the National Cancer Institute (NCI) on three clinical trials of SGN-30 in combination with chemotherapy for the treatment of relapsed Hodgkin lymphoma, front-line ALCL and pediatric ALCL. SGN-30 received orphan drug designation from the FDA in July 2003 for Hodgkin lymphoma and in February 2004 for T-cell lymphomas. | Investigated for use/treatment in autoimmune diseases, cancer/tumors (unspecified), lymphoma (non-hodgkin's), and lymphoma (unspecified). | SGN-30, a monoclonal antibody with activity against CD30+ malignancies. Through investigation of the mechanisms underlying SGN-30's antitumor activity, SGN-30 treatment was found to activate NF-kappaB and modulation of several messages including the growth regulator p21WAF1/CIP1 (p21) and cellular adhesion marker ICAM-1. p21 protein level changes are believed to be associated with arresting cell growth. In addition to directly killing cancerous cells, SGN-30 affects growth arrest and drug sensitization through growth regulating and proapoptotic machinery. SGN-30 could therefore be used to increase the efficacy of standard chemotherapies used to treat patients with CD30+ malignancies. | Through investigation of the mechanisms underlying SGN-30's antitumor activity, SGN-30 treatment was found to activate NF-kappaB and modulation of several messages including the growth regulator p21WAF1/CIP1 (p21) and cellular adhesion marker ICAM-1. p21 protein level changes are believed to be associated with arresting cell growth. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Nuclear factor NF-kappa-B p105 subunit,Nuclear factor NF-kappa-B p100 subunit | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16209 | Th1722 | ADH-1 | >Th1722_ADH-1 GLKAADNDPTAPPYDSLLVFDYEGSGSTAGSLSSLNSSSSGGDQDYDYLNDWGPRFKKLADMYGGGDD | NA | NA | NA | NA | NA | NA | Adherex's biotechnology compound, ADH-1, targets N-cadherin, a protein present on certain tumor cells and established tumor blood vessels. ADH-1 is currently in clinical development in a combination program with a range of chemotherapeutic agents to investigate the synergistic effects noted in our preclinical models. At the end of 2006, the Company also completed patient enrollment in our single-agent Phase Ib/II and Phase II trials of ADH-1. Cadherins are cell adhesion and cell signaling molecules crucial to the development of tissues, organs and organisms. Agents that target and inhibit cadherin function have the potential to attack the progression of cancer at two distinct points: * Direct targeting of cadherins expressed on cancer cells may disturb cadherin-mediated signaling, leading to apoptosis (death) of cancer cells. * Cadherin inhibitors may exploit the inherent structural weaknesses of the tumor vasculature, causing angiolysis (disruption of blood vessels) and tumor damage. As many tumors become more aggressive, invasive, and malignant, researchers have found that N-cadherin is expressed in greater amounts, making it an important target for developing anti-cancer treatments. Poorly differentiated, highly invasive carcinomas are characterized by over-expression of N-cadherin (as opposed to E-cadherin). This change in primary cadherin expression causes the epithelial cells to lose their tightly adherent, polarized and well-defined shape and become loosely adherent, flattened and migratory. Such cadherin switching promotes properties such as dedifferentiation, local invasion and metastasis, leading to poor prognosis. ADH-1 may have utility in a wide variety of cancers as N-cadherin is overexpressed in a variety of tumors. As tumors progress to become higher grade, invasive and more metastatic, the frequency of N-cadherin expression generally rises. | Investigated for use/treatment in breast cancer, cancer/tumors (unspecified), melanoma, ovarian cancer, and solid tumors. | ADH-1 is a biotech compounds that targets N-cadherin, a protein present on certain tumor cells and established tumor blood vessels. Cadherins are cell adhesion and cell signaling molecules crucial to the development of tissues, organs and organisms. Agents that target and inhibit cadherin function have the potential to attack the progression of cancer at two distinct points: * Direct targeting of cadherins expressed on cancer cells may disturb cadherin-mediated signaling, leading to apoptosis (death) of cancer cells. * Cadherin inhibitors may exploit the inherent structural weaknesses of the tumor vasculature, causing angiolysis (disruption of blood vessels) and tumor damage. The compound is indicated for treatment of a variety of invasive carcinomas and ADH-1 has been shown to be synergistic with taxane-based chemotherapy in the systemic treatment of ovarian cancer xenografts. | While ADH-1 has a single molecular target, N-cadherin, we believe its anti-cancer effect results from two distinct mechanisms of action - apoptosis and tumor vessel angiolysis. N-cadherin appears to act as a tumor cell survival factor. In cell culture studies, inhibition of N-cadherin binding between tumor cells has been shown to cause apoptosis of tumor cells, we believe as a result of disrupting the cadherin-regulated cell survival signals. ADH-1 also appears to disrupt the blood vessels needed for cancerous tumors to grow and flourish, with hemorrhaging having been noted in both our clinical and preclinical studies. We believe the mechanism for this disruption is either a competitive inhibition of the binding of cadherins between the endothelial cells of the tumor blood wall or apoptosis in tumor cells that form a part of the blood vessel wall, each leading to leakage and rupture of these vessels. The latter involves the phenomenon of tumor "mosaicism," in which tumor cells form a portion of the vascular wall (along with the endothelial cells). Induction of cell death of these tumor cells would result in tumor vascular disruption. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4R,7S,10S,13S,16R)-16-acetamido-13-(1H-imidazol-5-ylmethyl)-10-methyl-6,9,12,15-tetraoxo-7-propan-2-yl-1,2-dithia-5,8,11,14-tetrazacycloheptadecane-4-carboxamide | NA | Link | NA | NA |
| 16219 | Th1732 | LM-609 | NA | NA | NA | NA | NA | NA | NA | LM-609 (Vitaxin) is an artificial antibody that targets a protein on the surface of newly forming blood vessels, as well as on certain tumors. In addition to cancer, the protein has been implicated in bone destruction in rheumatoid arthritis and the inflammatory process in psoriasis. | Investigated for use/treatment in colorectal cancer, melanoma, prostate cancer, psoriasis and psoriatic disorders, rheumatoid arthritis, and solid tumors. | NA | LM-609 targets the alpha-v beta-3 integrin, which is a protein complex expressed on the surface of newly forming blood vessels, certain tumor types, and on a number of other cell types, including macrophages and osteoclasts. As such, alpha-v beta-3 integrin is implicated in a number of disease processes, including the growth and metastasis of tumors, the bone destruction in RA and the inflammatory process in psoriasis. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Integrin beta-3 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16221 | Th1734 | TA-CIN | NA | NA | NA | NA | NA | NA | NA | TA-CIN is a subunit vaccine comprising L2/E6/E7 proteins from Human Papillomavirus (HPV16), designed to generate a strong cellular immune response against HPV-infected cells. | Investigated for use/treatment in cervical dysplasia/cancer. | NA | TA-CIN is targeted at patients with cervical dysplasia (pre-invasive cervical disease), thus potentially preventing the onset of invasive cervical cancer. The initial product candidate for clinical trials is a genetically engineered fusion of three proteins from HPV 16 known to play a role in the progression of cervical disease. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16223 | Th1736 | GnRH pharmaccine | NA | 1212.3143 | C60H73N15O13 | NA | NA | NA | NA | The GnRH pharmaccine consists of synthetic peptides (constructed to "look like" GnRH), which are bound chemically to a carrier and suspended in a proprietary "delivery vehicle". The pharmaccine is administered intramuscularly to the patient by injection and induces an immune response or production of antibodies in the patient, which neutralize GnRH thus removing it from circulation. | Investigated for use/treatment in prostate cancer. | NA | The immunological neutralization of Gonadotropin Releasing Hormone (GnRH) by the antibodies induced by GnRH pharmaccine shuts down the production of testosterone in the testes. Testosterone fuels prostate cancer, both early stage, primary cancer and metastatic (spreading) cancer. Like physical castration, hormonal, or biological blockage of testosterone has been shown to be efficacious in humans for the treatment of both early and late state prostate cancer. Aphton's GnRH pharmaccine, which is expected to be reversible based on the mechanism of action (in contrast to surgical castration), induces hormonal, or biological blockage of testosterone. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16224 | Th1737 | SGN-15 | NA | NA | NA | NA | NA | NA | NA | SGN-15 is studied in the treatment of cancer. It combines a monoclonal antibody with the anticancer drug doxorubicin. Monoclonal antibodies are substances that are made in the laboratory and that can locate and bind to cancer cells. Doxorubicin is a type of anthracycline antitumor antibiotic. When it is combined with a monoclonal antibody, it forms a type of drug conjugate. Also called cBR96-doxorubicin immunoconjugate. | Investigated for use/treatment in breast cancer, colorectal cancer, and lung cancer. | NA | SGN-15 is a first-generation product composed of the chimeric BR96 antibody chemically joined by an acid-labile hydrazone linker to the chemotherapeutic drug doxorubicin. The antibody component binds to a Lewisy—related carbohydrate antigen that is highly expressed on many solid tumors; it internalizes rapidly and then releases the drug payload at the low pH present with the tumor cells. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16226 | Th1739 | G207 | NA | NA | NA | NA | NA | NA | NA | G207 is cancer-killing viruses, so-called oncolytic viruses, for the treatment of various forms of cancer developed by MediGene AG. These viruses are specific herpes simplex viruses, or HSVs, generally known as the cause of cold sores. MediGene uses these viruses, however, in a modified and "disarmed" form in order to make them utilizable as a therapeutic agent in humans. | Investigated for use/treatment in brain cancer. | NA | G207, Cancer killing viruses are modified to make them utilizable as a therapeutic agent in human by switching off certain genes that normally enable the virus to multiply in healthy cells, which would destroy these cells. As a result of this genetic modification, the HSVs are able to reproduce in tumor cells solely, since only this offer an environment that compensates for the loss of the removed viral genes. Consequently, the virus is able to replicate in the tumor cells, selectively destroying them without harming healthy tissue. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4-butylphenyl)-[4-[(4-propoxyphenyl)diazenyl]phenyl]diazene | NA | Link | NA | NA |
| 16233 | Th1746 | 99mTc-14 F7 Mab | NA | NA | NA | NA | NA | NA | NA | 99mTc 14F7 Mab has strong anti tumor activity against myeloma cells in vivo. Growth inhibition and prolonged survival of the myeloma tumor were obtained as evidences of anti tumor effect after treatment with 99mTc 14F7 Mab. | Investigated for use/treatment in breast cancer. | NA | The 99mTc 14F7 Mab has shown to bind specifically to GM3 (NeuGc) and that it also reacts with human breast and melanoma tumors in contrast with its low reactivity in normal tissues. N-Glycolyl GM3 is considered a heterophilic antigen since is not present in all species, humans are normally lacking them. The discovery of the presence of this molecule in significant amounts in breast tumors allowed considering it as an advantageous target for cancer immunotherapy. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Lactosylceramide alpha-2,3-sialyltransferase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16234 | Th1747 | anti-alpha5Beta1-integrin antibody | NA | NA | NA | NA | NA | NA | NA | Integrins are important adhesion molecules that regulate tumor and endothelial cell survival, proliferation and migration. The integrin alpha5beta1 has been shown to play a critical role during angiogenesis. anti-alpha5beta1 integrin antibody inhibits angiogenesis, including vessel formation induced by vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), as well as other pro-angiogenic growth factors. | Investigated for use/treatment in colorectal cancer, pancreatic cancer, and solid tumors. | NA | Anti-alpha5Beta1-integrin antibody is an anti-angiogenic antibody which targets the endothelium of tumor neovasculature and is being developed as a treatment for solid tumors. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16244 | Th1757 | TRC093 | NA | NA | NA | NA | NA | NA | NA | TRC093 is a recombinant humanized IgG1k monoclonal antibody. | Investigated for use/treatment in solid tumors and cancer/tumors (unspecified). | NA | TRC093 (MT293) is a recombinant humanized IgG1 monoclonal antibody that inhibits angiogenesis, tumor cell growth and metastasis by binding cleaved collagen, which is predominantly produced in the extracellular matrix of tumors. TRC093 targets collagen found in the basement membrane of tumor blood vessels. Collagen is a essential triple helix of polypeptide chains found in the extracellular matrix which is involved with many cellular processs including cell proliferation, adhesion, migration, and angiogenesis (neovascularization - growth of new blood vessels). Matrix metalloproteinase enzymes (MMPs) remodel and denature collagen during angiogenesis, causing changes in bioactive sites which results in altered proliferation, adhesion and migration of cells. TRC093 specifically binds to mice breast cancer blood vessel tumors, inhibiting tumor growth. It is proposed that TRC093 binds to hydroxyproline residues of GPO sequences (the major platelet-activating motif within collagen and essential for collagen folding) when they are exposed by thermal denaturation or partially proteolytically degraded by MMPs. TRC093 may target many different types of cancer as a critical component of the TRC093 epitope is a GPOG sequence which are present in high numbers in many different types of collagen. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Collagen alpha-4(IV) chain | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16246 | Th1759 | Mitumomab | NA | NA | NA | NA | NA | NA | NA | Mitumomab, an anti-BEC-2 monoclonal antibody derived from mice, was previously studied to treat small cell lung carcinoma in combination with BCG vaccination. | Investigated for use/treatment in lung cancer and melanoma. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16251 | Th1764 | rNAPc2 | NA | NA | NA | NA | NA | NA | Over 50 hours | Recombinant nematode anticoagulant protein c2 (rNAPc2) is a specific inhibitor of tissue factor (TF)/factor VIIa complex with novel antithrombotic activity. [A175642] | Investigated for use/treatment in thrombosis (deep vein), angina, coronary artery disease, and colorectal cancer. | NA | Recombinant Nematode Anticoagulant Protein c2 (rNAPc2) is a potent (K(i) =10 pM), inhibitor of the factor VIIa/tissue factor (fVIIa/TF) complex that requires the prerequisite binding to zymogen or activated factor X (fX). This has been shown to attenuate the activation of coagulation and to prevent death in a primate model of sepsis caused by gram-negative bacteria. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Coagulation factor VII,Tissue factor,Coagulation factor X | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |