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 |
| 10025 | Th1004 | Denileukin diftitox | >Th1004_Denileukin_diftitox MGADDVVDSSKSFVMENFSSYHGTKPGYVDSIQKGIQKPKSGTQGNYDDDWKGFYSTDNKYDAAGYSVDNENPLSGKAGGVVKVTYPGLTKVLALKVDNAETIKKELGLSLTEPLMEQVGTEEFIKRFGDGASRVVLSLPFAEGSSSVEYINNWEQAKALSVELEINFETRGKRGQDAMYEYMAQACAGNRVRRSVGSSLSCINLDWDVIRDKTKTKIESLKEHGPIKNKMSESPNKTVSEEKAKQYLEEFHQTALEHPELSELKTVTGTNPVFAGANYAAWAVNVAQVIDSETADNLEKTTAALSILPGIGSVMGIADGAVHHNTEEIVAQSIALSSLMVAQAIPLVGELVDIGFAAYNFVESIINLFQVVHNSYNRPAYSPGHKTHAPTSSSTKKTQLQLEHLLLDLQMILNGINNYKNPKLTRMLTFKFYMPKKATELKHLQCLEEELKPLEEVLNLAQSKNFHLRPRDLISNINVIVLELKGSETTFMCEYADETATIVEFLNRWITFCQSIISTLT | 57647.3 | C2560H4042N678O799S17 | 5.45 | -0.301 | NA | 1.16-1.3 hours | A recombinant (using E. coli expression system) DNA-derived cytotoxic protein containing amino acid sequences for diphtheria toxin fragments A and B (Met 1-Thr 387)-His and sequences for interleukin-2 (Ala 1-Thr 133). | Used in the treatment of cutaneous T-cell lymphoma. | Denileukin diftitox (Ontak) uses the cytocidal action of diphtheria toxin on cells which express the IL-2 receptor. The human IL-2 receptor exists in three forms on basis of affinity, low (CD25), intermediate (CD122/CD132) and high (CD25/CD122/CD132). Malignant cells expressing one or more of the subunits of the IL-2 receptor are found in certain leukemias and lymphomas including cutaneous T-cell lymphoma (CTCL). Ontak interacts with the high affinity IL-2 receptor on the cell surface and inhibits cellular protein synthesis, resulting in cell death within hours. | Denileukin diftitox binds to the high-affinity IL-2 receptor. The IL-2 receptor (Tac) subunit is expressed on activated lymphocytes. The diphtheria toxin associated with Ontak selectively kills the IL-2 bearing cells. | NA | NA | NA | 0.06 to 0.09 L/kg | 0.6 - 2.0 mL/min/kg [Lymphoma] | ADP Ribose Transferases, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Bacterial Toxins, Biological Factors, Cancer immunotherapy, CD25-directed Cytotoxin, Cytokines, Enzymes, Enzymes and Coenzymes, Glycosyltransferases, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interleukins, Lymphokines, Narrow Therapeutic Index Drugs, Pentosyltransferases, Peptides, Proteins, Recombinant Proteins, Toxins, Biological, Transferases | NA | NA | NA | Rilonacept decreases effects of toxoids by pharmacodynamic antagonism | Interleukin-2 receptor subunit alpha,Interleukin-2 receptor subunit beta,Cytokine receptor common subunit gamma | Ontak | Eisai Inc. , Hollister-Stier Laboratories LLC , Ligand Pharmaceuticals Inc. | Eisai Inc. , Hollister-Stier Laboratories LLC , Ligand Pharmaceuticals Inc. | Treating leukemia and lymphomas, including cutaneous (of the skin) T-cell lymphoma. | NA | Ontak contains 300 mcg of recombinant denileukin diftitox in a sterile solution of citric acid (20 mM), EDTA (0.05 mM) and polysorbate 20 ( < 1%) in Water for Injection, USP. The solution has a pH range of 6.9-7.2. | Sterile, white, preservative-free, lyophilized powder. | Intravenous (Intravenous) administration | NA | allergic | Common side effects include:headache, dizziness, or nervousness, numbness or tingling, skin itching or rash, runny or stuffy nose; weight gain or loss; mild diarrhea or constipation, or nausea, vomiting, loss of appetite. | Link | NA | NA |
| 10026 | Th1004 | Denileukin diftitox | >Th1004_Denileukin_diftitox MGADDVVDSSKSFVMENFSSYHGTKPGYVDSIQKGIQKPKSGTQGNYDDDWKGFYSTDNKYDAAGYSVDNENPLSGKAGGVVKVTYPGLTKVLALKVDNAETIKKELGLSLTEPLMEQVGTEEFIKRFGDGASRVVLSLPFAEGSSSVEYINNWEQAKALSVELEINFETRGKRGQDAMYEYMAQACAGNRVRRSVGSSLSCINLDWDVIRDKTKTKIESLKEHGPIKNKMSESPNKTVSEEKAKQYLEEFHQTALEHPELSELKTVTGTNPVFAGANYAAWAVNVAQVIDSETADNLEKTTAALSILPGIGSVMGIADGAVHHNTEEIVAQSIALSSLMVAQAIPLVGELVDIGFAAYNFVESIINLFQVVHNSYNRPAYSPGHKTHAPTSSSTKKTQLQLEHLLLDLQMILNGINNYKNPKLTRMLTFKFYMPKKATELKHLQCLEEELKPLEEVLNLAQSKNFHLRPRDLISNINVIVLELKGSETTFMCEYADETATIVEFLNRWITFCQSIISTLT | 57647.3 | C2560H4042N678O799S17 | 5.45 | -0.301 | NA | 1.16-1.3 hours | A recombinant (using E. coli expression system) DNA-derived cytotoxic protein containing amino acid sequences for diphtheria toxin fragments A and B (Met 1-Thr 387)-His and sequences for interleukin-2 (Ala 1-Thr 133). | Used in the treatment of cutaneous T-cell lymphoma. | Denileukin diftitox (Ontak) uses the cytocidal action of diphtheria toxin on cells which express the IL-2 receptor. The human IL-2 receptor exists in three forms on basis of affinity, low (CD25), intermediate (CD122/CD132) and high (CD25/CD122/CD132). Malignant cells expressing one or more of the subunits of the IL-2 receptor are found in certain leukemias and lymphomas including cutaneous T-cell lymphoma (CTCL). Ontak interacts with the high affinity IL-2 receptor on the cell surface and inhibits cellular protein synthesis, resulting in cell death within hours. | Denileukin diftitox binds to the high-affinity IL-2 receptor. The IL-2 receptor (Tac) subunit is expressed on activated lymphocytes. The diphtheria toxin associated with Ontak selectively kills the IL-2 bearing cells. | NA | NA | NA | 0.06 to 0.09 L/kg | 0.6 - 2.0 mL/min/kg [Lymphoma] | ADP Ribose Transferases, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Bacterial Toxins, Biological Factors, Cancer immunotherapy, CD25-directed Cytotoxin, Cytokines, Enzymes, Enzymes and Coenzymes, Glycosyltransferases, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interleukins, Lymphokines, Narrow Therapeutic Index Drugs, Pentosyltransferases, Peptides, Proteins, Recombinant Proteins, Toxins, Biological, Transferases | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10027 | Th1004 | Denileukin diftitox | >Th1004_Denileukin_diftitox MGADDVVDSSKSFVMENFSSYHGTKPGYVDSIQKGIQKPKSGTQGNYDDDWKGFYSTDNKYDAAGYSVDNENPLSGKAGGVVKVTYPGLTKVLALKVDNAETIKKELGLSLTEPLMEQVGTEEFIKRFGDGASRVVLSLPFAEGSSSVEYINNWEQAKALSVELEINFETRGKRGQDAMYEYMAQACAGNRVRRSVGSSLSCINLDWDVIRDKTKTKIESLKEHGPIKNKMSESPNKTVSEEKAKQYLEEFHQTALEHPELSELKTVTGTNPVFAGANYAAWAVNVAQVIDSETADNLEKTTAALSILPGIGSVMGIADGAVHHNTEEIVAQSIALSSLMVAQAIPLVGELVDIGFAAYNFVESIINLFQVVHNSYNRPAYSPGHKTHAPTSSSTKKTQLQLEHLLLDLQMILNGINNYKNPKLTRMLTFKFYMPKKATELKHLQCLEEELKPLEEVLNLAQSKNFHLRPRDLISNINVIVLELKGSETTFMCEYADETATIVEFLNRWITFCQSIISTLT | 57647.3 | C2560H4042N678O799S17 | 5.45 | -0.301 | NA | 1.16-1.3 hours | A recombinant (using E. coli expression system) DNA-derived cytotoxic protein containing amino acid sequences for diphtheria toxin fragments A and B (Met 1-Thr 387)-His and sequences for interleukin-2 (Ala 1-Thr 133). | Used in the treatment of cutaneous T-cell lymphoma. | Denileukin diftitox (Ontak) uses the cytocidal action of diphtheria toxin on cells which express the IL-2 receptor. The human IL-2 receptor exists in three forms on basis of affinity, low (CD25), intermediate (CD122/CD132) and high (CD25/CD122/CD132). Malignant cells expressing one or more of the subunits of the IL-2 receptor are found in certain leukemias and lymphomas including cutaneous T-cell lymphoma (CTCL). Ontak interacts with the high affinity IL-2 receptor on the cell surface and inhibits cellular protein synthesis, resulting in cell death within hours. | Denileukin diftitox binds to the high-affinity IL-2 receptor. The IL-2 receptor (Tac) subunit is expressed on activated lymphocytes. The diphtheria toxin associated with Ontak selectively kills the IL-2 bearing cells. | NA | NA | NA | 0.06 to 0.09 L/kg | 0.6 - 2.0 mL/min/kg [Lymphoma] | ADP Ribose Transferases, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Bacterial Toxins, Biological Factors, Cancer immunotherapy, CD25-directed Cytotoxin, Cytokines, Enzymes, Enzymes and Coenzymes, Glycosyltransferases, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interleukins, Lymphokines, Narrow Therapeutic Index Drugs, Pentosyltransferases, Peptides, Proteins, Recombinant Proteins, Toxins, Biological, Transferases | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | 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 |
| 10049 | Th1008 | Peginterferon alfa-2a | >Th1008_Peginterferon_alfa-2a CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 60000 | NA | 5.99 | NA | 61 | Terminal half life is 164 hours (range 84 to 353 hours). | Human interferon 2a, is a covalent conjugate of recombinant interferon alfa-2a with a single branched bis-mono-methoxy polyethylene glycol (PEG) chain. The PEG moiety is linked at a single site to the interferon alfa moiety via a stable amide bond to lysine. Peginterferon alfa-2a has an approximate molecular weight of 60,000 daltons. Interferon alfa-2a is produced using recombinant DNA technology in which a cloned human leukocyte interferon gene is inserted and expressed in Escherichia coli. The resultant protein is 165 amino acids. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | To treat hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma. | Upregulates the expression of MHC I proteins which increases presentation of peptides derived from viral antigens. Thus enhancing the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and make the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | Peginterferon alfa-2a may manifest neuropsychiatric complications include suicide, suicidal ideation, homicidal ideation, depression, relapse of drug addiction, and drug overdose Label. Hypertension, supraventricular arrhythmias, chest pain, and myocardial infarction have been observed in patients using Peginterferon alfa-2a. | NA | NA | NA | 94 milliliters per hour | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cardiotoxic antineoplastic agents, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatotoxic Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferons, Macromolecular Substances, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | CA2203480 | 30-Jun-2009 | 23-Apr-2017 | Interferon increases the effect and toxicity of theophylline called Aminophylline | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | Pegasys | Hoffman-La Roche Inc | Hoffman-La Roche Inc | Pegasys is used to treat chronic hepatitis B or C (adults), and to treat chronic hepatitis C (children 5 or more years of age). It is mostly used with ribavirin | NA | Each vial of 180 mcg/mL peginterferon alfa-2a (expressed as the amount of interferon alfa-2a) also contains acetic acid (0.05 mg), benzyl alcohol (10 mg), polysorbate 80 (0.05 mg), sodium acetate trihydrate (2.62 mg), and sodium chloride (8 mg) at pH 6 ± | Sterile, preservative-free, colorless to light yellow injectable solution | Subcutaneous Injection | Pegasys is usually given once a week. | Allergic | Nausea, vomiting, loss of appetite; headache, muscle pain, feeling weak or tired; sleep problems (insomnia); temporary hair loss; or itching, redness, dryness, or swelling where the medicine was injected. | Link | NA | NA |
| 10050 | Th1008 | Peginterferon alfa-2a | >Th1008_Peginterferon_alfa-2a CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 60000 | NA | 5.99 | NA | 61 | Terminal half life is 164 hours (range 84 to 353 hours). | Human interferon 2a, is a covalent conjugate of recombinant interferon alfa-2a with a single branched bis-mono-methoxy polyethylene glycol (PEG) chain. The PEG moiety is linked at a single site to the interferon alfa moiety via a stable amide bond to lysine. Peginterferon alfa-2a has an approximate molecular weight of 60,000 daltons. Interferon alfa-2a is produced using recombinant DNA technology in which a cloned human leukocyte interferon gene is inserted and expressed in Escherichia coli. The resultant protein is 165 amino acids. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | To treat hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma. | Upregulates the expression of MHC I proteins which increases presentation of peptides derived from viral antigens. Thus enhancing the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and make the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | Peginterferon alfa-2a may manifest neuropsychiatric complications include suicide, suicidal ideation, homicidal ideation, depression, relapse of drug addiction, and drug overdose Label. Hypertension, supraventricular arrhythmias, chest pain, and myocardial infarction have been observed in patients using Peginterferon alfa-2a. | NA | NA | NA | 94 milliliters per hour | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cardiotoxic antineoplastic agents, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatotoxic Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferons, Macromolecular Substances, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | CA2172664 | 3-Oct-2000 | 26-Mar-2016 | Interferon increases the effect and toxicity of theophylline called Dyphylline | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Having failure or autoimmune hepatitis | NA | Link | NA | NA |
| 10051 | Th1008 | Peginterferon alfa-2a | >Th1008_Peginterferon_alfa-2a CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 60000 | NA | 5.99 | NA | 61 | Terminal half life is 164 hours (range 84 to 353 hours). | Human interferon 2a, is a covalent conjugate of recombinant interferon alfa-2a with a single branched bis-mono-methoxy polyethylene glycol (PEG) chain. The PEG moiety is linked at a single site to the interferon alfa moiety via a stable amide bond to lysine. Peginterferon alfa-2a has an approximate molecular weight of 60,000 daltons. Interferon alfa-2a is produced using recombinant DNA technology in which a cloned human leukocyte interferon gene is inserted and expressed in Escherichia coli. The resultant protein is 165 amino acids. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | To treat hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma. | Upregulates the expression of MHC I proteins which increases presentation of peptides derived from viral antigens. Thus enhancing the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and make the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | Peginterferon alfa-2a may manifest neuropsychiatric complications include suicide, suicidal ideation, homicidal ideation, depression, relapse of drug addiction, and drug overdose Label. Hypertension, supraventricular arrhythmias, chest pain, and myocardial infarction have been observed in patients using Peginterferon alfa-2a. | NA | NA | NA | 94 milliliters per hour | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cardiotoxic antineoplastic agents, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatotoxic Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferons, Macromolecular Substances, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | NA | NA | NA | Etravirine (a CYP2C9 substrate, when used concomitantly with peginterferon alfa-2a, may experience a decrease in serum concentration. It is recommended to monitor effectiveness of etravirine therapy. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Haemoglobin blood cell disorder as sickle cell anemia or thalessimia. | NA | Link | NA | NA |
| 10052 | Th1008 | Peginterferon alfa-2a | >Th1008_Peginterferon_alfa-2a CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 60000 | NA | 5.99 | NA | 61 | Terminal half life is 164 hours (range 84 to 353 hours). | Human interferon 2a, is a covalent conjugate of recombinant interferon alfa-2a with a single branched bis-mono-methoxy polyethylene glycol (PEG) chain. The PEG moiety is linked at a single site to the interferon alfa moiety via a stable amide bond to lysine. Peginterferon alfa-2a has an approximate molecular weight of 60,000 daltons. Interferon alfa-2a is produced using recombinant DNA technology in which a cloned human leukocyte interferon gene is inserted and expressed in Escherichia coli. The resultant protein is 165 amino acids. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | To treat hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma. | Upregulates the expression of MHC I proteins which increases presentation of peptides derived from viral antigens. Thus enhancing the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and make the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | Peginterferon alfa-2a may manifest neuropsychiatric complications include suicide, suicidal ideation, homicidal ideation, depression, relapse of drug addiction, and drug overdose Label. Hypertension, supraventricular arrhythmias, chest pain, and myocardial infarction have been observed in patients using Peginterferon alfa-2a. | NA | NA | NA | 94 milliliters per hour | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cardiotoxic antineoplastic agents, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatotoxic Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferons, Macromolecular Substances, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | NA | NA | NA | Interferon increases the effect and toxicity of theophylline called Oxtriphylline | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10053 | Th1008 | Peginterferon alfa-2a | >Th1008_Peginterferon_alfa-2a CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 60000 | NA | 5.99 | NA | 61 | Terminal half life is 164 hours (range 84 to 353 hours). | Human interferon 2a, is a covalent conjugate of recombinant interferon alfa-2a with a single branched bis-mono-methoxy polyethylene glycol (PEG) chain. The PEG moiety is linked at a single site to the interferon alfa moiety via a stable amide bond to lysine. Peginterferon alfa-2a has an approximate molecular weight of 60,000 daltons. Interferon alfa-2a is produced using recombinant DNA technology in which a cloned human leukocyte interferon gene is inserted and expressed in Escherichia coli. The resultant protein is 165 amino acids. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | To treat hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma. | Upregulates the expression of MHC I proteins which increases presentation of peptides derived from viral antigens. Thus enhancing the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and make the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | Peginterferon alfa-2a may manifest neuropsychiatric complications include suicide, suicidal ideation, homicidal ideation, depression, relapse of drug addiction, and drug overdose Label. Hypertension, supraventricular arrhythmias, chest pain, and myocardial infarction have been observed in patients using Peginterferon alfa-2a. | NA | NA | NA | 94 milliliters per hour | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cardiotoxic antineoplastic agents, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatotoxic Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferons, Macromolecular Substances, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | NA | NA | NA | Interferon increases the effect and toxicity of theophylline | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10054 | Th1008 | Peginterferon alfa-2a | >Th1008_Peginterferon_alfa-2a CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 60000 | NA | 5.99 | NA | 61 | Terminal half life is 164 hours (range 84 to 353 hours). | Human interferon 2a, is a covalent conjugate of recombinant interferon alfa-2a with a single branched bis-mono-methoxy polyethylene glycol (PEG) chain. The PEG moiety is linked at a single site to the interferon alfa moiety via a stable amide bond to lysine. Peginterferon alfa-2a has an approximate molecular weight of 60,000 daltons. Interferon alfa-2a is produced using recombinant DNA technology in which a cloned human leukocyte interferon gene is inserted and expressed in Escherichia coli. The resultant protein is 165 amino acids. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | To treat hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma. | Upregulates the expression of MHC I proteins which increases presentation of peptides derived from viral antigens. Thus enhancing the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and make the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | Peginterferon alfa-2a may manifest neuropsychiatric complications include suicide, suicidal ideation, homicidal ideation, depression, relapse of drug addiction, and drug overdose Label. Hypertension, supraventricular arrhythmias, chest pain, and myocardial infarction have been observed in patients using Peginterferon alfa-2a. | NA | NA | NA | 94 milliliters per hour | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cardiotoxic antineoplastic agents, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatotoxic Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferons, Macromolecular Substances, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | NA | NA | NA | Co-administration of Peginterferon alpha-2a and Telbivudine may increase the risk of serious peripheral neuropathy. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10059 | Th1010 | Interferon alfa-n1 | >Th1010_Interferon_alfa-n1 CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 19241.1 | C860H1353N227O255S9 | 5.99 | -0.336 | 61 | 1.2 hours (mammalian reticulocytes, in vitro) | Purified, natural and glycosylated human interferon alpha proteins of 166 residues. | Used to treat venereal or genital warts caused by the Human Papiloma Virus. | Upregulates the expression of MHC I proteins, allowing increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5-oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors namely IFNAR1 and IFNAR2c which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | NA | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferons, Myelosuppressive Agents, Peptides, Proteins | NA | NA | NA | Interferon increases the effect and toxicity of theophylline | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | Wellferon | GlaxoSmithKline | GlaxoSmithKline | Used for the treatment of patients with hairy cell leukemia, juvenile laryngeal papillomatosis, condylomata acuminata, chronic hepatitis B and chronic hepatitis C infections. | NA | Each vial of clear, colorless solution contains interferon alpha-n1 (lns) [purified human lymphoblastoid interferon] 3, 5 or 10 mega units. 1 mega unit (Mu)=1´10International Units (IU) of lymphoblastoid interferon. Formulated in 1 mL tris-glycine buffere | Solution | Injection | NA | Hypersensitivity | Most side/adverse effects, except the flu-like syndrome, are dose-related . They are usually mild to moderate at systemic doses less than 10 million Units per day }; hematologic and hepatic toxicities tend to be more frequent with doses above 10 million | Link | NA | NA |
| 10060 | Th1010 | Interferon alfa-n1 | >Th1010_Interferon_alfa-n1 CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 19241.1 | C860H1353N227O255S9 | 5.99 | -0.336 | 61 | 20 hours (yeast, in vivo) | Purified, natural and glycosylated human interferon alpha proteins of 166 residues. | Used to treat venereal or genital warts caused by the Human Papiloma Virus. | Upregulates the expression of MHC I proteins, allowing increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5-oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors namely IFNAR1 and IFNAR2c which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | NA | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferons, Myelosuppressive Agents, Peptides, Proteins | NA | NA | NA | Aminophylline | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Reduced blood pressure occurs frequently with systemic use but is rarely symptomatic ; hypotension may occur during administration or up to two days after therapy, and may require supportive therapy including fluid replacement to maintain intravascular v | Link | NA | NA |
| 10061 | Th1010 | Interferon alfa-n1 | >Th1010_Interferon_alfa-n1 CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 19241.1 | C860H1353N227O255S9 | 5.99 | -0.336 | 61 | 10 hours (Escherichia coli, in vivo) | Purified, natural and glycosylated human interferon alpha proteins of 166 residues. | Used to treat venereal or genital warts caused by the Human Papiloma Virus. | Upregulates the expression of MHC I proteins, allowing increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5-oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors namely IFNAR1 and IFNAR2c which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | NA | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferons, Myelosuppressive Agents, Peptides, Proteins | NA | NA | NA | Dyphylline | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Development of neutralizing antibodies has been reported. Relationship of the presence of neutralizing antibodies to loss of antitumor effects is controversial; a possible correlation with titer of neutralizing antibodies has been suggested but not confirmed. | NA | NA | NA |
| 10062 | Th1010 | Interferon alfa-n1 | >Th1010_Interferon_alfa-n1 CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 19241.1 | C860H1353N227O255S9 | 5.99 | -0.336 | 61 | NA | Purified, natural and glycosylated human interferon alpha proteins of 166 residues. | Used to treat venereal or genital warts caused by the Human Papiloma Virus. | Upregulates the expression of MHC I proteins, allowing increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5-oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors namely IFNAR1 and IFNAR2c which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | NA | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferons, Myelosuppressive Agents, Peptides, Proteins | NA | NA | NA | Oxtriphylline | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10063 | Th1010 | Interferon alfa-n1 | >Th1010_Interferon_alfa-n1 CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 19241.1 | C860H1353N227O255S9 | 5.99 | -0.336 | 61 | NA | Purified, natural and glycosylated human interferon alpha proteins of 166 residues. | Used to treat venereal or genital warts caused by the Human Papiloma Virus. | Upregulates the expression of MHC I proteins, allowing increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5-oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors namely IFNAR1 and IFNAR2c which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | NA | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferons, Myelosuppressive Agents, Peptides, Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 |
| 10135 | Th1019 | Peginterferon alfa-2b | >Th1019_Peginterferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 31000 | C130H219N43O42 | 5.99 | NA | 61 | Approximately 40 hours (range 22 to 60 hours) in patients with HCV infection | Peginterferon alfa-2b is a covalent conjugate of recombinant alfa-2b interferon with monomethoxy polyethylene glycol (PEG). The average molecular weight of the PEG portion of the molecule is 12,000 daltons. The average molecular weight of the PEG-Intron molecule is approximately 31,000 daltons. The specific activity of peginterferon alfa-2b is approximately 0.7 x 108 IU/mg protein. Interferon alfa-2b is a water-soluble protein with a molecular weight of 19,271 daltons produced by recombinant DNA techniques. It is obtained from the bacterial fermentation of a strain of Escherichia coli bearing a genetically engineered plasmid containing an interferon gene from human leukocytes. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | Used for the treatment of chronic hepatitis C in patients not previously treated with interferon alpha who have compensated liver disease and are at least 18 years of age. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds to type I interferon receptors IFNAR1 and IFNAR2c which upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | After a single subcutaneous dose of peginterferon alfa-2b, the mean absorption half-life was 4.6 hours. | NA | Oral cl=22 mL/hr/kg [patients with HCV infection], Renal elimination accounts for 30% of the clearance. | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 CYP2C9 Inducers, Cytochrome P-450 CYP2C9 Inducers (weak), Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (weak), Cytochrome P-450 Enzyme Inducers, Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatitis C, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Macromolecular Substances, Myelosuppressive Agents, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | CA1341567 | 19-Feb-2008 | 19-Feb-2025 | Aminophylline. Interferon increases the effect and toxicity of theophylline | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | PEG-Intron | Schering Corp | Schering Corp | Used to treat chronic hepatitis C in adults. Peginterferon alfa-2b is often used in combination with another medication called ribavirin (Rebetol, Ribasphere) to treat hepatitis C in adults and children who are at least 3 years old. It may be used in comb | NA | Provided in both vials and the REDIPEN. Each vial contains either 74 mcg, 118.4 mcg, 177.6 mcg, or 222 mcg of PegIntron as a white to off-white tablet-like solid that is whole/in pieces or as a loose powder, and 1.11 mg dibasic sodium phosphate anhydrous, | Powder | Subcutaneous Injection | 1.5 mcg/kg/week. The volume of PegIntron to be injected depends on the strength of PegIntron and patient's body weight | Allergic or in case of having autoimmune hepatitis, liver failure, severe kidney disease, a hemoglobin blood cell disorder | Vision problems; fast heart rate, feeling like you might pass out; unusual weakness; high fever with severe stomach pain and bloody diarrhea; pain or burning when you urinate; severe pain in your upper stomach spreading to your back, nausea and vomiting and new or worsening liver symptoms. | Link | NA | NA |
| 10136 | Th1019 | Peginterferon alfa-2b | >Th1019_Peginterferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 31000 | C130H219N43O42 | 5.99 | NA | 61 | Approximately 40 hours (range 22 to 60 hours) in patients with HCV infection | Peginterferon alfa-2b is a covalent conjugate of recombinant alfa-2b interferon with monomethoxy polyethylene glycol (PEG). The average molecular weight of the PEG portion of the molecule is 12,000 daltons. The average molecular weight of the PEG-Intron molecule is approximately 31,000 daltons. The specific activity of peginterferon alfa-2b is approximately 0.7 x 108 IU/mg protein. Interferon alfa-2b is a water-soluble protein with a molecular weight of 19,271 daltons produced by recombinant DNA techniques. It is obtained from the bacterial fermentation of a strain of Escherichia coli bearing a genetically engineered plasmid containing an interferon gene from human leukocytes. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | Used for the treatment of chronic hepatitis C in patients not previously treated with interferon alpha who have compensated liver disease and are at least 18 years of age. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds to type I interferon receptors IFNAR1 and IFNAR2c which upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | After a single subcutaneous dose of peginterferon alfa-2b, the mean absorption half-life was 4.6 hours. | NA | Oral cl=22 mL/hr/kg [patients with HCV infection], Renal elimination accounts for 30% of the clearance. | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 CYP2C9 Inducers, Cytochrome P-450 CYP2C9 Inducers (weak), Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (weak), Cytochrome P-450 Enzyme Inducers, Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatitis C, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Macromolecular Substances, Myelosuppressive Agents, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | CA2329474 | 26-Feb-2002 | 31-Oct-2016 | Dyphylline.Interferon increases the effect and toxicity of theophylline | NA | Sylatron | Merck Sharp & Dohme Corp. | Merck Sharp & Dohme Corp. | SYLATRON™ is an alpha interferon indicated for the adjuvant treatment of melanoma with microscopic or gross nodal involvement within 84 days of definitive surgical resection including complete lymphadenect | NA | NA | sterile, white to off-white lyophilized powder | Subcutaneous Injection | The recommended starting dose is 6 mcg/kg/week subcutaneously for 8 doses, followed by 3 mcg/kg/week subcutaneously for up to 5 years. Premedicate with acetaminophen 500 to 1000 mg orally 30 minutes prior to the first dose of SYLATRON and as needed for subsequent doses. The recommended starting doses of SYLATRON in patients with moderate or severe renal impairment or end-stage renal disease (ESRD) are listed in Table 1 [see Use In Specific Populations]. No dose adjustment is needed for patients with a creatinine clearance (CLcr) > 50 mL/min/1.73m². | SYLATRON is contraindicated in patients with: A history of anaphylaxis to peginterferon alfa-2b or interferon alfa-2b autoimmune hepatitis hepatic decompensation (Child-Pugh score >6 [class B and C]) | Headache, joint or muscle pain; nausea, dry mouth, loss of appetite, weight loss; dizziness, sleep problems (insomnia), feeling mildly anxious, depressed, or irritable; or pain, redness, swelling, or irritation where the medicine was injected. | Link | NA | NA |
| 10137 | Th1019 | Peginterferon alfa-2b | >Th1019_Peginterferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 31000 | C130H219N43O42 | 5.99 | NA | 61 | Approximately 40 hours (range 22 to 60 hours) in patients with HCV infection | Peginterferon alfa-2b is a covalent conjugate of recombinant alfa-2b interferon with monomethoxy polyethylene glycol (PEG). The average molecular weight of the PEG portion of the molecule is 12,000 daltons. The average molecular weight of the PEG-Intron molecule is approximately 31,000 daltons. The specific activity of peginterferon alfa-2b is approximately 0.7 x 108 IU/mg protein. Interferon alfa-2b is a water-soluble protein with a molecular weight of 19,271 daltons produced by recombinant DNA techniques. It is obtained from the bacterial fermentation of a strain of Escherichia coli bearing a genetically engineered plasmid containing an interferon gene from human leukocytes. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | Used for the treatment of chronic hepatitis C in patients not previously treated with interferon alpha who have compensated liver disease and are at least 18 years of age. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds to type I interferon receptors IFNAR1 and IFNAR2c which upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | After a single subcutaneous dose of peginterferon alfa-2b, the mean absorption half-life was 4.6 hours. | NA | Oral cl=22 mL/hr/kg [patients with HCV infection], Renal elimination accounts for 30% of the clearance. | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 CYP2C9 Inducers, Cytochrome P-450 CYP2C9 Inducers (weak), Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (weak), Cytochrome P-450 Enzyme Inducers, Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatitis C, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Macromolecular Substances, Myelosuppressive Agents, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | NA | NA | NA | Oxtriphylline. Interferon increases the effect and toxicity of theophylline | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10138 | Th1019 | Peginterferon alfa-2b | >Th1019_Peginterferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 31000 | C130H219N43O42 | 5.99 | NA | 61 | Approximately 40 hours (range 22 to 60 hours) in patients with HCV infection | Peginterferon alfa-2b is a covalent conjugate of recombinant alfa-2b interferon with monomethoxy polyethylene glycol (PEG). The average molecular weight of the PEG portion of the molecule is 12,000 daltons. The average molecular weight of the PEG-Intron molecule is approximately 31,000 daltons. The specific activity of peginterferon alfa-2b is approximately 0.7 x 108 IU/mg protein. Interferon alfa-2b is a water-soluble protein with a molecular weight of 19,271 daltons produced by recombinant DNA techniques. It is obtained from the bacterial fermentation of a strain of Escherichia coli bearing a genetically engineered plasmid containing an interferon gene from human leukocytes. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | Used for the treatment of chronic hepatitis C in patients not previously treated with interferon alpha who have compensated liver disease and are at least 18 years of age. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds to type I interferon receptors IFNAR1 and IFNAR2c which upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | After a single subcutaneous dose of peginterferon alfa-2b, the mean absorption half-life was 4.6 hours. | NA | Oral cl=22 mL/hr/kg [patients with HCV infection], Renal elimination accounts for 30% of the clearance. | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 CYP2C9 Inducers, Cytochrome P-450 CYP2C9 Inducers (weak), Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (weak), Cytochrome P-450 Enzyme Inducers, Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatitis C, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Macromolecular Substances, Myelosuppressive Agents, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | NA | NA | NA | Theophylline. Interferon increases the effect and toxicity of theophylline | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10139 | Th1019 | Peginterferon alfa-2b | >Th1019_Peginterferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 31000 | C130H219N43O42 | 5.99 | NA | 61 | Approximately 40 hours (range 22 to 60 hours) in patients with HCV infection | Peginterferon alfa-2b is a covalent conjugate of recombinant alfa-2b interferon with monomethoxy polyethylene glycol (PEG). The average molecular weight of the PEG portion of the molecule is 12,000 daltons. The average molecular weight of the PEG-Intron molecule is approximately 31,000 daltons. The specific activity of peginterferon alfa-2b is approximately 0.7 x 108 IU/mg protein. Interferon alfa-2b is a water-soluble protein with a molecular weight of 19,271 daltons produced by recombinant DNA techniques. It is obtained from the bacterial fermentation of a strain of Escherichia coli bearing a genetically engineered plasmid containing an interferon gene from human leukocytes. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | Used for the treatment of chronic hepatitis C in patients not previously treated with interferon alpha who have compensated liver disease and are at least 18 years of age. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds to type I interferon receptors IFNAR1 and IFNAR2c which upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | After a single subcutaneous dose of peginterferon alfa-2b, the mean absorption half-life was 4.6 hours. | NA | Oral cl=22 mL/hr/kg [patients with HCV infection], Renal elimination accounts for 30% of the clearance. | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 CYP2C9 Inducers, Cytochrome P-450 CYP2C9 Inducers (weak), Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (weak), Cytochrome P-450 Enzyme Inducers, Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatitis C, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Macromolecular Substances, Myelosuppressive Agents, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | NA | NA | NA | Aldesleukin | NA | Unitron PEG | Merck Ltd. | Merck Ltd. | It is used to treat chronic hepatitis C (a disease of the liver) for people who cannot tolerate or use the antiviral medication, ribavirin. The most effective treatment of chronic hepatitis C is the combination of an interferon and ribavirin. Unitron Peg | NA | NA | Lyophilized powder | Subcutaneous Injection | Its Subcutaneous injection once a week on the same day of the week for 48 weeks. Dosing is based on body weight. Treatment with this medication should be stopped if no response is noticed after 6 months. | Allergic | Abdominal pain or swelling, anemia (paleness, tiredness, shortness of breath), changes in mood (e.g., irritability, depression, anxiety, aggression), confusion, dizziness, eye pain or swelling of the eye, high blood sugar (increased thirst, hunger, weakness, irritability, trouble concentrating, signs of infection (e.g., chills, fever, cough, sore throat, difficulty or painful urination, difficulty breathing), burning sensation in arms or legs, ulcers in mouth or sore throats. | Link | NA | NA |
| 10140 | Th1019 | Peginterferon alfa-2b | >Th1019_Peginterferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 31000 | C130H219N43O42 | 5.99 | NA | 61 | Approximately 40 hours (range 22 to 60 hours) in patients with HCV infection | Peginterferon alfa-2b is a covalent conjugate of recombinant alfa-2b interferon with monomethoxy polyethylene glycol (PEG). The average molecular weight of the PEG portion of the molecule is 12,000 daltons. The average molecular weight of the PEG-Intron molecule is approximately 31,000 daltons. The specific activity of peginterferon alfa-2b is approximately 0.7 x 108 IU/mg protein. Interferon alfa-2b is a water-soluble protein with a molecular weight of 19,271 daltons produced by recombinant DNA techniques. It is obtained from the bacterial fermentation of a strain of Escherichia coli bearing a genetically engineered plasmid containing an interferon gene from human leukocytes. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | Used for the treatment of chronic hepatitis C in patients not previously treated with interferon alpha who have compensated liver disease and are at least 18 years of age. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds to type I interferon receptors IFNAR1 and IFNAR2c which upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | After a single subcutaneous dose of peginterferon alfa-2b, the mean absorption half-life was 4.6 hours. | NA | Oral cl=22 mL/hr/kg [patients with HCV infection], Renal elimination accounts for 30% of the clearance. | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 CYP2C9 Inducers, Cytochrome P-450 CYP2C9 Inducers (weak), Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (weak), Cytochrome P-450 Enzyme Inducers, Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatitis C, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Macromolecular Substances, Myelosuppressive Agents, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | NA | NA | NA | Telbivudine | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Person having decompensated liver disease, epilepsy (seizures), autoimmune diseases (including autoimmune hepatitis), severe psychiatric conditions, severely reduced kidney function and thyroid disease, when medication cannot bring thyroid function in | Signs of infection (e.g., chills, fever, cough, sore throat, difficulty or painful urination, difficulty breathing), tingling or burning sensation in arms or legs, ulcers or sores in the mouth or throat, unusual bruising or bleeding (e.g., bleeding gums, | Link | NA | NA |
| 10141 | Th1019 | Peginterferon alfa-2b | >Th1019_Peginterferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 31000 | C130H219N43O42 | 5.99 | NA | 61 | Approximately 40 hours (range 22 to 60 hours) in patients with HCV infection | Peginterferon alfa-2b is a covalent conjugate of recombinant alfa-2b interferon with monomethoxy polyethylene glycol (PEG). The average molecular weight of the PEG portion of the molecule is 12,000 daltons. The average molecular weight of the PEG-Intron molecule is approximately 31,000 daltons. The specific activity of peginterferon alfa-2b is approximately 0.7 x 108 IU/mg protein. Interferon alfa-2b is a water-soluble protein with a molecular weight of 19,271 daltons produced by recombinant DNA techniques. It is obtained from the bacterial fermentation of a strain of Escherichia coli bearing a genetically engineered plasmid containing an interferon gene from human leukocytes. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | Used for the treatment of chronic hepatitis C in patients not previously treated with interferon alpha who have compensated liver disease and are at least 18 years of age. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds to type I interferon receptors IFNAR1 and IFNAR2c which upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | After a single subcutaneous dose of peginterferon alfa-2b, the mean absorption half-life was 4.6 hours. | NA | Oral cl=22 mL/hr/kg [patients with HCV infection], Renal elimination accounts for 30% of the clearance. | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 CYP2C9 Inducers, Cytochrome P-450 CYP2C9 Inducers (weak), Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (weak), Cytochrome P-450 Enzyme Inducers, Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatitis C, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Macromolecular Substances, Myelosuppressive Agents, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | NA | NA | NA | Theophylline | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Decreased desire for sexual activities, drowsiness, dry mouth, dry skin, flu-like symptoms (unusual tiredness, fever, chills, muscle aches, joint pain and headaches), flushing of the skin, indigestion, loss of appetite, nausea, pain in bones, joints, or muscle stiffness. | Link | NA | NA |
| 10142 | Th1020 | Asparaginase | >Th1020_Asparaginase MEFFKKTALAALVMGFSGAALALPNITILATGGTIAGGGDSATKSNYTVGKVGVENLVNAVPQLKDIANVKGEQVVNIGSQDMNDNVWLTLAKKINTDCDKTDGFVITHGTDTMEETAYFLDLTVKCDKPVVMVGAMRPSTSMSADGPFNLYNAVVTAADKASANRGVLVVMNDTVLDGRDVTKTNTTDVATFKSVNYGPLGYIHNGKIDYQRTPARKHTSDTPFDVSKLNELPKVGIVYNYANASDLPAKALVDAGYDGIVSAGVGNGNLYKSVFDTLATAAKTGTAVVRSSRVPTGATTQDAEVDDAKYGFVASGTLNPQKARVLLQLALTQTKDPQQIQQIFNQY | 31731.9 | C1377H2208N382O442S17 | 4.67 | 0.059 | NA | 8-30 hours | L-asparagine amidohydrolase from E. coli | To treat acute lympocytic leukemia and non-Hodgkins lymphoma | In most patients with acute leukemia, the malignant cells are dependent on an exogenous source of asparagine for survival. Normal cells, however, are able to synthesize asparagine and thus are affected less by the rapid depletion produced by treatment with the enzyme asparaginase. Elspar exploits a metabolic defect in asparagine synthesis of some malignant cells. | Asparaginase converts asparagine to aspartic acid and ammonia. It facilitates production of oxalo-acetate which is needed for general cellular metabolism. Some malignant cells lose the ability to produce asparagine and thus the loss of exogenous sources of asparagine leads to cell death. | NA | NA | NA | Apparent volume of distribution was slightly greater than the plasma volume. Asparaginase levels in cerebrospinal fluid were less than 1% of concurrent plasma levels | NA | Amidohydrolases, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Asparaginase, Asparagine-specific Enzyme, Enzymes, Enzymes and Coenzymes, Hydrolases, Narrow Therapeutic Index Drugs, Thyroxine-binding globulin inhibitors | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | L-asparagine | Elspar | Lundbeck Inc. | Lundbeck Inc. | To treat acute lymphocytic leukemia. It is used along with other cancer medicines. Elspar is an antineoplastic agent that works by decreasing the amount of asparagine in the body, which kills certain leukemia cells | NA | Each vial contains 10,000 International Units of asparaginase and 80 mg of mannitol. | Lyophilized plug or powder | Intravenous or intramuSubcutaneousular. Intravenou | The recommended dose of Elspar is 6,000 International Units/m_ intramuscularly (IM) or intravenously (IV) three times a week. | Allergic | Fever, chills (see flu like symptoms), Nausea and vomiting, Allergic reaction, (sudden onset of wheezing, itching, rash, face swelling, agitation, low blood pressure). You will be monitored closely for this reaction, Poor appetite, Stomach cramping | Link | NA | NA |
| 10143 | Th1020 | Asparaginase | >Th1020_Asparaginase MEFFKKTALAALVMGFSGAALALPNITILATGGTIAGGGDSATKSNYTVGKVGVENLVNAVPQLKDIANVKGEQVVNIGSQDMNDNVWLTLAKKINTDCDKTDGFVITHGTDTMEETAYFLDLTVKCDKPVVMVGAMRPSTSMSADGPFNLYNAVVTAADKASANRGVLVVMNDTVLDGRDVTKTNTTDVATFKSVNYGPLGYIHNGKIDYQRTPARKHTSDTPFDVSKLNELPKVGIVYNYANASDLPAKALVDAGYDGIVSAGVGNGNLYKSVFDTLATAAKTGTAVVRSSRVPTGATTQDAEVDDAKYGFVASGTLNPQKARVLLQLALTQTKDPQQIQQIFNQY | 31731.9 | C1377H2208N382O442S17 | 4.67 | 0.059 | NA | 8-30 hours | L-asparagine amidohydrolase from E. coli | To treat acute lympocytic leukemia and non-Hodgkins lymphoma | In most patients with acute leukemia, the malignant cells are dependent on an exogenous source of asparagine for survival. Normal cells, however, are able to synthesize asparagine and thus are affected less by the rapid depletion produced by treatment with the enzyme asparaginase. Elspar exploits a metabolic defect in asparagine synthesis of some malignant cells. | Asparaginase converts asparagine to aspartic acid and ammonia. It facilitates production of oxalo-acetate which is needed for general cellular metabolism. Some malignant cells lose the ability to produce asparagine and thus the loss of exogenous sources of asparagine leads to cell death. | NA | NA | NA | Apparent volume of distribution was slightly greater than the plasma volume. Asparaginase levels in cerebrospinal fluid were less than 1% of concurrent plasma levels | NA | Amidohydrolases, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Asparaginase, Asparagine-specific Enzyme, Enzymes, Enzymes and Coenzymes, Hydrolases, Narrow Therapeutic Index Drugs, Thyroxine-binding globulin inhibitors | NA | NA | NA | NA | NA | Kidrolase | Jazz Pharmaceuticals France Sas | Jazz Pharmaceuticals France Sas | NA | NA | NA | NA | NA | NA | NA | Mouth sores, Pancreatitis (inflammation of the pancreas) in up to 10% of patients. Mainly noted in blood tests that return to normal after therapy is discontinued. Rarely may be severe causing symptoms. Symptoms of acute pancreatitis include: (pain in the upper abdomen that worsens with eating, swollen and tender abdomen, nausea, vomiting, fever, and rapid pulse). | Link | NA | NA |
| 10144 | Th1020 | Asparaginase | >Th1020_Asparaginase MEFFKKTALAALVMGFSGAALALPNITILATGGTIAGGGDSATKSNYTVGKVGVENLVNAVPQLKDIANVKGEQVVNIGSQDMNDNVWLTLAKKINTDCDKTDGFVITHGTDTMEETAYFLDLTVKCDKPVVMVGAMRPSTSMSADGPFNLYNAVVTAADKASANRGVLVVMNDTVLDGRDVTKTNTTDVATFKSVNYGPLGYIHNGKIDYQRTPARKHTSDTPFDVSKLNELPKVGIVYNYANASDLPAKALVDAGYDGIVSAGVGNGNLYKSVFDTLATAAKTGTAVVRSSRVPTGATTQDAEVDDAKYGFVASGTLNPQKARVLLQLALTQTKDPQQIQQIFNQY | 31731.9 | C1377H2208N382O442S17 | 4.67 | 0.059 | NA | 8-30 hours | L-asparagine amidohydrolase from E. coli | To treat acute lympocytic leukemia and non-Hodgkins lymphoma | In most patients with acute leukemia, the malignant cells are dependent on an exogenous source of asparagine for survival. Normal cells, however, are able to synthesize asparagine and thus are affected less by the rapid depletion produced by treatment with the enzyme asparaginase. Elspar exploits a metabolic defect in asparagine synthesis of some malignant cells. | Asparaginase converts asparagine to aspartic acid and ammonia. It facilitates production of oxalo-acetate which is needed for general cellular metabolism. Some malignant cells lose the ability to produce asparagine and thus the loss of exogenous sources of asparagine leads to cell death. | NA | NA | NA | Apparent volume of distribution was slightly greater than the plasma volume. Asparaginase levels in cerebrospinal fluid were less than 1% of concurrent plasma levels | NA | Amidohydrolases, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Asparaginase, Asparagine-specific Enzyme, Enzymes, Enzymes and Coenzymes, Hydrolases, Narrow Therapeutic Index Drugs, Thyroxine-binding globulin inhibitors | NA | NA | NA | NA | NA | Rylaze, Spectrila | Jazz Pharmaceuticals, Inc., Medac Gesellschaft Fuer Klinische Spezialpraeparate Mb H | Jazz Pharmaceuticals, Inc., Medac Gesellschaft Fuer Klinische Spezialpraeparate Mb H | NA | NA | NA | NA | NA | NA | NA | Central neurotoxicity: excessive sleepiness, depression, hallucinations, agitation, disorientation or seizure, stupor, confusion and/or coma. | Link | NA | NA |
| 10180 | Th1023 | Anakinra | >Th1023_Anakinra MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVVPIEPHALFLGIHGGKMCLSCVKSGDETRLQLEAVNITDLSENRKQDKRFAFIRSDSGPTTSFESAACPGWFLCTAMEADQPVSLTNMPDEGVMVTKFYFQEDE | 17257.6 | C759H1186N208O232S10 | 5.46 | -0.412 | NA | Healthy subjects = 4 - 6 hours | Anakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001. | To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID). | Anakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1. | Anakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption. | Most common adverse reactions (incidence 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used | As a protein-based therapy, anakinra is expected to be metabolized by proteases throughout the body. | When a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once dail | 18.5 L | Clearance is variable and increases with increasing creatinine clearance and body weight. | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Factors, Biologics for Rheumatoid Arthritis Treatment, Cytokines, Disease-modifying Antirheumatic Agents, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interleukin Inhibitors, Interleukin-1 Receptor Antagonist, Peptides, Proteins | CA2141953 | 8-Apr-2008 | 17-Sep-2013 | Canakinumab results in increased immunosuppressive effects; increases the risk of infection. | Interleukin-1 receptor type 1 | Kineret | Amgen Inc | Amgen Inc | To treat the symptoms of moderate to severe rheumatoid arthritis in adults. Anakinra may also help slow the progress of the disease. | NA | The solution may contain trace amounts of small, translucent-to-white amorphous proteinaceous particles. Each prefilled glass syringe contains: 0.67 mL (100 mg) of anakinra in a solution (pH 6.5) containing disodium EDTA (0.12 mg), sodium chloride (5.48 m | Sterile, clear, colorless-to-white, preservative free solution | Subcutaneous (Subcutaneous) administration | 100 mg/day administered daily | Contraindicated in patients with known hypersensitivity to E coli-derived proteins, Kineret, or any components of the product | Nausea, diarrhea, stomach pain; headache; cold symptoms such as stuffy nose, sneezing, sore throat; or redness, bruising, pain, or swelling where the injection was given. | Link | NA | NA |
| 10181 | Th1023 | Anakinra | >Th1023_Anakinra MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVVPIEPHALFLGIHGGKMCLSCVKSGDETRLQLEAVNITDLSENRKQDKRFAFIRSDSGPTTSFESAACPGWFLCTAMEADQPVSLTNMPDEGVMVTKFYFQEDE | 17257.6 | C759H1186N208O232S10 | 5.46 | -0.412 | NA | NOMID patients = 5.7 hours (range of 3.1 - 28.2 hours) | Anakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001. | To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID). | Anakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1. | Anakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption. | Most common adverse reactions (incidence 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used | As a protein-based therapy, anakinra is expected to be metabolized by proteases throughout the body. | When a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once dail | 18.5 L | Clearance is variable and increases with increasing creatinine clearance and body weight. | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Factors, Biologics for Rheumatoid Arthritis Treatment, Cytokines, Disease-modifying Antirheumatic Agents, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interleukin Inhibitors, Interleukin-1 Receptor Antagonist, Peptides, Proteins | CA1341322 | 27-Nov-2001 | 27-Nov-2018 | Certolizumab pegol Co-administration with other TNF-blocking agents may increase the risk of serious infections. Concomitant therapy is not recommended. | NA | NA | BioVitrum AB | BioVitrum AB | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10182 | Th1023 | Anakinra | >Th1023_Anakinra MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVVPIEPHALFLGIHGGKMCLSCVKSGDETRLQLEAVNITDLSENRKQDKRFAFIRSDSGPTTSFESAACPGWFLCTAMEADQPVSLTNMPDEGVMVTKFYFQEDE | 17257.6 | C759H1186N208O232S10 | 5.46 | -0.412 | NA | NA | Anakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001. | To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID). | Anakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1. | Anakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption. | Most common adverse reactions (incidence 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used | As a protein-based therapy, anakinra is expected to be metabolized by proteases throughout the body. | When a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once dail | 18.5 L | Clearance is variable and increases with increasing creatinine clearance and body weight. | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Factors, Biologics for Rheumatoid Arthritis Treatment, Cytokines, Disease-modifying Antirheumatic Agents, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interleukin Inhibitors, Interleukin-1 Receptor Antagonist, Peptides, Proteins | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10183 | Th1023 | Anakinra | >Th1023_Anakinra MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVVPIEPHALFLGIHGGKMCLSCVKSGDETRLQLEAVNITDLSENRKQDKRFAFIRSDSGPTTSFESAACPGWFLCTAMEADQPVSLTNMPDEGVMVTKFYFQEDE | 17257.6 | C759H1186N208O232S10 | 5.46 | -0.412 | NA | NA | Anakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001. | To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID). | Anakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1. | Anakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption. | Most common adverse reactions (incidence 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used | As a protein-based therapy, anakinra is expected to be metabolized by proteases throughout the body. | When a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once dail | 18.5 L | Clearance is variable and increases with increasing creatinine clearance and body weight. | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Factors, Biologics for Rheumatoid Arthritis Treatment, Cytokines, Disease-modifying Antirheumatic Agents, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interleukin Inhibitors, Interleukin-1 Receptor Antagonist, Peptides, Proteins | NA | NA | NA | Golimumab. Avoid combination with anakinra due to the increased chance of serious infection. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10184 | Th1023 | Anakinra | >Th1023_Anakinra MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVVPIEPHALFLGIHGGKMCLSCVKSGDETRLQLEAVNITDLSENRKQDKRFAFIRSDSGPTTSFESAACPGWFLCTAMEADQPVSLTNMPDEGVMVTKFYFQEDE | 17257.6 | C759H1186N208O232S10 | 5.46 | -0.412 | NA | NA | Anakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001. | To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID). | Anakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1. | Anakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption. | Most common adverse reactions (incidence 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used | As a protein-based therapy, anakinra is expected to be metabolized by proteases throughout the body. | When a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once dail | 18.5 L | Clearance is variable and increases with increasing creatinine clearance and body weight. | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Factors, Biologics for Rheumatoid Arthritis Treatment, Cytokines, Disease-modifying Antirheumatic Agents, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interleukin Inhibitors, Interleukin-1 Receptor Antagonist, Peptides, Proteins | NA | NA | NA | Rilonacept results in increased immunosuppressive effects; increases the risk of infection. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10185 | Th1023 | Anakinra | >Th1023_Anakinra MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVVPIEPHALFLGIHGGKMCLSCVKSGDETRLQLEAVNITDLSENRKQDKRFAFIRSDSGPTTSFESAACPGWFLCTAMEADQPVSLTNMPDEGVMVTKFYFQEDE | 17257.6 | C759H1186N208O232S10 | 5.46 | -0.412 | NA | NA | Anakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001. | To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID). | Anakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1. | Anakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption. | Most common adverse reactions (incidence 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used | As a protein-based therapy, anakinra is expected to be metabolized by proteases throughout the body. | When a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once dail | 18.5 L | Clearance is variable and increases with increasing creatinine clearance and body weight. | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Factors, Biologics for Rheumatoid Arthritis Treatment, Cytokines, Disease-modifying Antirheumatic Agents, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interleukin Inhibitors, Interleukin-1 Receptor Antagonist, Peptides, Proteins | NA | NA | NA | Tofacitinib. Avoid combination due to the potential increase in tofacitinib related adverse effects. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10186 | Th1023 | Anakinra | >Th1023_Anakinra MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVVPIEPHALFLGIHGGKMCLSCVKSGDETRLQLEAVNITDLSENRKQDKRFAFIRSDSGPTTSFESAACPGWFLCTAMEADQPVSLTNMPDEGVMVTKFYFQEDE | 17257.6 | C759H1186N208O232S10 | 5.46 | -0.412 | NA | NA | Anakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001. | To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID). | Anakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1. | Anakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption. | Most common adverse reactions (incidence 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used | As a protein-based therapy, anakinra is expected to be metabolized by proteases throughout the body. | When a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once dail | 18.5 L | Clearance is variable and increases with increasing creatinine clearance and body weight. | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Factors, Biologics for Rheumatoid Arthritis Treatment, Cytokines, Disease-modifying Antirheumatic Agents, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interleukin Inhibitors, Interleukin-1 Receptor Antagonist, Peptides, Proteins | NA | NA | NA | Thalidomide may increase the adverse effects of Anakinra. Increased risk of serious infection. Concomitant therapy should be avoided. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10229 | Th1031 | Interferon Alfa-2a, Recombinant | >Th1031_Interferon_Alfa-2a,_Recombinant CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 19241.1 | C860H1353N227O255S9 | 5.99 | -0.336 | NA | IM half-life of interferon alfa-2a is 6 hours to 8 hours | Its a type I interferon consisting of 165 amino acid residues with lysine in position 23. This protein is produced by recombinant DNA technology and resembles interferon secreted by leukocytes. It is used extensively as an antiviral or antineoplastic agent. An oral form is being developed by Amarillo Biosciences. | For the treatment of chronic hepatitis C, hairy cell leukemia, AIDS-related Kaposi's sarcoma, and chronic myelogenous leukemia. Also for the treatment of oral warts arising from HIV infection. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a bbetter target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds directly to the type II interferon gamma receptor IFNGR1, leading to a complex of IFNGR1 and IFNGR2. This activates JAK1 and JAK2 kinases which form a STAT1 docking site. This leads to STAT1 phosphorylation, nuclear translocation and initiation of gene transcription of multiple immune-related genes. | Interferon alfa-2 may cause serious adverse effects such as anemia; autoimmune diseases, including vasculitis, arthritis, hemolytic anemia, and erythematosus syndrome; cardiotoxicity; hepatotoxicity; hyperthyroidism or hypothyroidism; transient ischemic a | NA | Absorption is high (greater than 80%) when administered intramuscularly or subcutaneously. | 0.223 to 0.748 L/kg [healthy people] | 2.14 - 3.62 mL/min/kg [healthy] | Adjuvants, Immunologic, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Myelosuppressive Agents, Peptides, Proteins | CA2172664 | 3-Oct-2000 | 26-Mar-2016 | Interferon increases the effect and toxicity of theophylline | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | Roferon A | Hoffmann-La Roche Inc | Hoffmann-La Roche Inc | To treat chronic hepatitis C and hairy cell leukemia in patients 18 years of age or older. In addition, it is indicated for chronic phase, Philadelphia chromosome (Ph) positive chronic myelogenous leukemia (CML) patients who are minimally pretreated (with | NA | 3 million IU (11.1 mcg/0.5 mL) Roferon-A (interferon alfa-2a, recombinant) per syringe  The solution is colorless and each 0.5 mL contains 3 MIU of Interferon alfa-2a, recombinant, 3.605 mg sodium chloride, 0.1 mg polysorbate 80, 5 mg benzyl alcohol as a | Solution | Subcutaneous Injection | Dosage for the treatment of chronic hepatitis C is 3 MIU three times a week (tiw) administered subcutaneously for 12 months (48-52 weeks). As an alternative, patients may be treated with an induction dose of 6 MIU tiw for the first 3 months (12 weeks) followed by 3 MIU tiw for 9 months (36 weeks). | Hypersensitivity to Roferon-A (interferon alfa-2a, recombinant) or any of its components | Injection site reactions (pain/swelling/redness), headache, tiredness, diarrhea, upset stomach, loss of appetite, back pain, dizziness, dry mouth, taste changes, nausea, or vomiting may occur. Tooth and gum problems may sometimes occur during treatment. | Link | NA | NA |
| 10230 | Th1031 | Interferon Alfa-2a, Recombinant | >Th1031_Interferon_Alfa-2a,_Recombinant CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 19241.1 | C860H1353N227O255S9 | 5.99 | -0.336 | NA | Half-life for IV infusion is 3.7 hours to 8.5 hours (mean 5.1 hours). | Its a type I interferon consisting of 165 amino acid residues with lysine in position 23. This protein is produced by recombinant DNA technology and resembles interferon secreted by leukocytes. It is used extensively as an antiviral or antineoplastic agent. An oral form is being developed by Amarillo Biosciences. | For the treatment of chronic hepatitis C, hairy cell leukemia, AIDS-related Kaposi's sarcoma, and chronic myelogenous leukemia. Also for the treatment of oral warts arising from HIV infection. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a bbetter target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds directly to the type II interferon gamma receptor IFNGR1, leading to a complex of IFNGR1 and IFNGR2. This activates JAK1 and JAK2 kinases which form a STAT1 docking site. This leads to STAT1 phosphorylation, nuclear translocation and initiation of gene transcription of multiple immune-related genes. | Interferon alfa-2 may cause serious adverse effects such as anemia; autoimmune diseases, including vasculitis, arthritis, hemolytic anemia, and erythematosus syndrome; cardiotoxicity; hepatotoxicity; hyperthyroidism or hypothyroidism; transient ischemic a | NA | Absorption is high (greater than 80%) when administered intramuscularly or subcutaneously. | 0.223 to 0.748 L/kg [healthy people] | 2.14 - 3.62 mL/min/kg [healthy] | Adjuvants, Immunologic, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Myelosuppressive Agents, Peptides, Proteins | NA | NA | NA | Aminophylline interferon increases the effect and toxicity of theophylline | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Autoimmune hepatitis or hepatic decompensation (Child-Pugh class B and C) before or during treatment. | NA | Link | NA | NA |
| 10231 | Th1031 | Interferon Alfa-2a, Recombinant | >Th1031_Interferon_Alfa-2a,_Recombinant CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 19241.1 | C860H1353N227O255S9 | 5.99 | -0.336 | NA | NA | Its a type I interferon consisting of 165 amino acid residues with lysine in position 23. This protein is produced by recombinant DNA technology and resembles interferon secreted by leukocytes. It is used extensively as an antiviral or antineoplastic agent. An oral form is being developed by Amarillo Biosciences. | For the treatment of chronic hepatitis C, hairy cell leukemia, AIDS-related Kaposi's sarcoma, and chronic myelogenous leukemia. Also for the treatment of oral warts arising from HIV infection. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a bbetter target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds directly to the type II interferon gamma receptor IFNGR1, leading to a complex of IFNGR1 and IFNGR2. This activates JAK1 and JAK2 kinases which form a STAT1 docking site. This leads to STAT1 phosphorylation, nuclear translocation and initiation of gene transcription of multiple immune-related genes. | Interferon alfa-2 may cause serious adverse effects such as anemia; autoimmune diseases, including vasculitis, arthritis, hemolytic anemia, and erythematosus syndrome; cardiotoxicity; hepatotoxicity; hyperthyroidism or hypothyroidism; transient ischemic a | NA | Absorption is high (greater than 80%) when administered intramuscularly or subcutaneously. | 0.223 to 0.748 L/kg [healthy people] | 2.14 - 3.62 mL/min/kg [healthy] | Adjuvants, Immunologic, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Myelosuppressive Agents, Peptides, Proteins | NA | NA | NA | Dyphylline interferon increases the effect and toxicity of theophylline | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Roferon-A (interferon alfa-2a, recombinant) is contraindicated in neonates and infants because it contains benzyl alcohol. Benzyl alcohol is associated with an increased incidence of neurologic and other complications in neonates and infants, which are sometimes fatal. | NA | Link | NA | NA |
| 10232 | Th1031 | Interferon Alfa-2a, Recombinant | >Th1031_Interferon_Alfa-2a,_Recombinant CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 19241.1 | C860H1353N227O255S9 | 5.99 | -0.336 | NA | NA | Its a type I interferon consisting of 165 amino acid residues with lysine in position 23. This protein is produced by recombinant DNA technology and resembles interferon secreted by leukocytes. It is used extensively as an antiviral or antineoplastic agent. An oral form is being developed by Amarillo Biosciences. | For the treatment of chronic hepatitis C, hairy cell leukemia, AIDS-related Kaposi's sarcoma, and chronic myelogenous leukemia. Also for the treatment of oral warts arising from HIV infection. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a bbetter target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds directly to the type II interferon gamma receptor IFNGR1, leading to a complex of IFNGR1 and IFNGR2. This activates JAK1 and JAK2 kinases which form a STAT1 docking site. This leads to STAT1 phosphorylation, nuclear translocation and initiation of gene transcription of multiple immune-related genes. | Interferon alfa-2 may cause serious adverse effects such as anemia; autoimmune diseases, including vasculitis, arthritis, hemolytic anemia, and erythematosus syndrome; cardiotoxicity; hepatotoxicity; hyperthyroidism or hypothyroidism; transient ischemic a | NA | Absorption is high (greater than 80%) when administered intramuscularly or subcutaneously. | 0.223 to 0.748 L/kg [healthy people] | 2.14 - 3.62 mL/min/kg [healthy] | Adjuvants, Immunologic, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Myelosuppressive Agents, Peptides, Proteins | NA | NA | NA | Oxtriphylline, interferon increases the effect and toxicity of theophylline | NA | Veldona | Amarillo Biosciences | Amarillo Biosciences | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10233 | Th1031 | Interferon Alfa-2a, Recombinant | >Th1031_Interferon_Alfa-2a,_Recombinant CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 19241.1 | C860H1353N227O255S9 | 5.99 | -0.336 | NA | NA | Its a type I interferon consisting of 165 amino acid residues with lysine in position 23. This protein is produced by recombinant DNA technology and resembles interferon secreted by leukocytes. It is used extensively as an antiviral or antineoplastic agent. An oral form is being developed by Amarillo Biosciences. | For the treatment of chronic hepatitis C, hairy cell leukemia, AIDS-related Kaposi's sarcoma, and chronic myelogenous leukemia. Also for the treatment of oral warts arising from HIV infection. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a bbetter target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds directly to the type II interferon gamma receptor IFNGR1, leading to a complex of IFNGR1 and IFNGR2. This activates JAK1 and JAK2 kinases which form a STAT1 docking site. This leads to STAT1 phosphorylation, nuclear translocation and initiation of gene transcription of multiple immune-related genes. | Interferon alfa-2 may cause serious adverse effects such as anemia; autoimmune diseases, including vasculitis, arthritis, hemolytic anemia, and erythematosus syndrome; cardiotoxicity; hepatotoxicity; hyperthyroidism or hypothyroidism; transient ischemic a | NA | Absorption is high (greater than 80%) when administered intramuscularly or subcutaneously. | 0.223 to 0.748 L/kg [healthy people] | 2.14 - 3.62 mL/min/kg [healthy] | Adjuvants, Immunologic, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Myelosuppressive Agents, Peptides, Proteins | NA | NA | NA | Roferon-A (interferon alfa-2a, recombinant) has been reported to reduce the clearance of theophylline. Synergistic toxicity has been observed when Roferon-A (interferon alfa-2a, recombinant) is administered in combination with zidovudine (AZT) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10242 | Th1033 | Oprelvekin | >Th1033_Oprelvekin GPPPGPPRVSPDPRAELDSTVLLTRSLLADTRQLAAQLRDKFPADGDHNLDSLPTLAMSAGALGALQLPGVLTRLRADLLSYLRHVQWLRRAGGSSLKTLEPELGTLQARLDRLLRRLQLLMSRLALPQPPPDPPAPPLAPPSSAWGGIRAAHAILGGLHLTLDWAVRGLLLLKTRL | 19047.2 | C854H1411N253O235S2 | 11.16 | -0.07 | NA | 6.9 ± 1.7 hours | Oprelvekin, the active ingredient in Neumega is recombinant Interleukin eleven, which is produced in Escherichia coli by recombinant DNA technology. The protein has a molecular mass of approximately 19,000 daltons, and is non-glycosylated. The polypeptide is 177 amino acids in length (the natural IL-11 has 178). This alteration has not resulted in measurable differences in bioactivity either in vitro or in vivo. The primary hematopoietic activity of Neumega is stimulation of megakaryocytopoiesis and thrombopoiesis. In mice and nonhuman primate studies Neumega has shown potent thrombopoietic activity in compromised hematopoiesis, including moderately to severely myelosuppressed animals. In these studies, Neumega improved platelet nadirs and accelerated platelet recoveries compared to controls. In animal studies Oprelvekin also has non-hematopoetic activities. This includes the regulation of intestinal epithelium growth (enhanced healing of gastrointestinal lesions), the inhibition of adipogenesis, the induction of acute phase protein synthesis (e.g., fibrinogen), and inhibition of macrophageal released pro-inflammatory cytokines. | Increases reduced platelet levels due to chemotherapy. | Oprelvekin is indicated for the prevention of severe thrombocytopenia and the reduction of the need for platelet transfusions following myelosuppressive chemotherapy in adult patients with nonmyeloid malignancies who are at high risk of severe thrombocytopenia. The primary hematopoietic activity of Oprelvekin is stimulation of megakaryocytopoiesis and thrombopoiesis. Oprelvekin has shown potent thrombopoietic activity in individuals with compromised hematopoiesis | Oprelvekin binds to the interleukin 11 receptor which leads to a cascade of signal transduction events. IL-11 is a thrombopoietic growth factor that directly stimulates the proliferation of hematopoietic stem cells and megakaryocyte progenitor cells and induces megakaryocyte maturation resulting in increased platelet production. | NA | NA | Absolute bioavailability is over 80%. | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Cytokines, Intercellular Signaling Peptides and Proteins, Interleukins, Megakaryocyte Growth Factor, Peptides, Proteins | NA | NA | NA | Dihydrocodeine may increase the serum levels of opioid analgesics. It is recommended to monitor therapy for the signs and symptoms of respiratory depression and enhanced sedation. | Interleukin-11 receptor subunit alpha | Neumega | Wyeth Pharmaceuticals | Wyeth Pharmaceuticals | Prevention of severe reductions in the number of blood clotting cells (platelets) caused by some chemotherapy | NA | Neumega is formulated in single-use vials containing 5 mg of oprelvekin (specific activity approximately 8 x 106 Units/mg) as a sterile, lyophilized powder with 23 mg Glycine, USP, 1.6 mg Dibasic Sodium Phosphate Heptahydrate, USP, and 0.55 mg Monobasic S | Sterile, lyophilized powder | It must be Subcutaneous Injection not in the muSub | The recommended dose of Neumega in adults with severe renal impairment(creatinine clearance<30 mL/min) is 25 µg/kg. An estimate of the patient's creatinine clearance(CLcr) in mL/min is required. CLcr in mL/min may be estimated from a spot serum creatinine determination. | In patients with a history of hypersensitivity to Neumega or any component of the product. | Chills; constipation; cough; diarrhea; dizziness; fever; flushing; hair loss; headache; increased cough; indigestion; inflammation or sores of the mouth or lips; joint pain; loss of appetite; mild swelling of the arms and legs; muscle pain; nausea; nervousness. | Link | NA | NA |
| 10243 | Th1033 | Oprelvekin | >Th1033_Oprelvekin GPPPGPPRVSPDPRAELDSTVLLTRSLLADTRQLAAQLRDKFPADGDHNLDSLPTLAMSAGALGALQLPGVLTRLRADLLSYLRHVQWLRRAGGSSLKTLEPELGTLQARLDRLLRRLQLLMSRLALPQPPPDPPAPPLAPPSSAWGGIRAAHAILGGLHLTLDWAVRGLLLLKTRL | 19047.2 | C854H1411N253O235S2 | 11.16 | -0.07 | NA | 6.9 ± 1.7 hours | Oprelvekin, the active ingredient in Neumega is recombinant Interleukin eleven, which is produced in Escherichia coli by recombinant DNA technology. The protein has a molecular mass of approximately 19,000 daltons, and is non-glycosylated. The polypeptide is 177 amino acids in length (the natural IL-11 has 178). This alteration has not resulted in measurable differences in bioactivity either in vitro or in vivo. The primary hematopoietic activity of Neumega is stimulation of megakaryocytopoiesis and thrombopoiesis. In mice and nonhuman primate studies Neumega has shown potent thrombopoietic activity in compromised hematopoiesis, including moderately to severely myelosuppressed animals. In these studies, Neumega improved platelet nadirs and accelerated platelet recoveries compared to controls. In animal studies Oprelvekin also has non-hematopoetic activities. This includes the regulation of intestinal epithelium growth (enhanced healing of gastrointestinal lesions), the inhibition of adipogenesis, the induction of acute phase protein synthesis (e.g., fibrinogen), and inhibition of macrophageal released pro-inflammatory cytokines. | Increases reduced platelet levels due to chemotherapy. | Oprelvekin is indicated for the prevention of severe thrombocytopenia and the reduction of the need for platelet transfusions following myelosuppressive chemotherapy in adult patients with nonmyeloid malignancies who are at high risk of severe thrombocytopenia. The primary hematopoietic activity of Oprelvekin is stimulation of megakaryocytopoiesis and thrombopoiesis. Oprelvekin has shown potent thrombopoietic activity in individuals with compromised hematopoiesis | Oprelvekin binds to the interleukin 11 receptor which leads to a cascade of signal transduction events. IL-11 is a thrombopoietic growth factor that directly stimulates the proliferation of hematopoietic stem cells and megakaryocyte progenitor cells and induces megakaryocyte maturation resulting in increased platelet production. | NA | NA | Absolute bioavailability is over 80%. | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Cytokines, Intercellular Signaling Peptides and Proteins, Interleukins, Megakaryocyte Growth Factor, Peptides, Proteins | NA | NA | NA | Ifex (ifosfamide) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue; eye infection; eye pain; fainting; heart flutter; irregular or fast heartbeat; pain, redness, or swelling at the injection site; pounding in the chest. | Link | NA | NA |
| 10244 | Th1033 | Oprelvekin | >Th1033_Oprelvekin GPPPGPPRVSPDPRAELDSTVLLTRSLLADTRQLAAQLRDKFPADGDHNLDSLPTLAMSAGALGALQLPGVLTRLRADLLSYLRHVQWLRRAGGSSLKTLEPELGTLQARLDRLLRRLQLLMSRLALPQPPPDPPAPPLAPPSSAWGGIRAAHAILGGLHLTLDWAVRGLLLLKTRL | 19047.2 | C854H1411N253O235S2 | 11.16 | -0.07 | NA | 6.9 ± 1.7 hours | Oprelvekin, the active ingredient in Neumega is recombinant Interleukin eleven, which is produced in Escherichia coli by recombinant DNA technology. The protein has a molecular mass of approximately 19,000 daltons, and is non-glycosylated. The polypeptide is 177 amino acids in length (the natural IL-11 has 178). This alteration has not resulted in measurable differences in bioactivity either in vitro or in vivo. The primary hematopoietic activity of Neumega is stimulation of megakaryocytopoiesis and thrombopoiesis. In mice and nonhuman primate studies Neumega has shown potent thrombopoietic activity in compromised hematopoiesis, including moderately to severely myelosuppressed animals. In these studies, Neumega improved platelet nadirs and accelerated platelet recoveries compared to controls. In animal studies Oprelvekin also has non-hematopoetic activities. This includes the regulation of intestinal epithelium growth (enhanced healing of gastrointestinal lesions), the inhibition of adipogenesis, the induction of acute phase protein synthesis (e.g., fibrinogen), and inhibition of macrophageal released pro-inflammatory cytokines. | Increases reduced platelet levels due to chemotherapy. | Oprelvekin is indicated for the prevention of severe thrombocytopenia and the reduction of the need for platelet transfusions following myelosuppressive chemotherapy in adult patients with nonmyeloid malignancies who are at high risk of severe thrombocytopenia. The primary hematopoietic activity of Oprelvekin is stimulation of megakaryocytopoiesis and thrombopoiesis. Oprelvekin has shown potent thrombopoietic activity in individuals with compromised hematopoiesis | Oprelvekin binds to the interleukin 11 receptor which leads to a cascade of signal transduction events. IL-11 is a thrombopoietic growth factor that directly stimulates the proliferation of hematopoietic stem cells and megakaryocyte progenitor cells and induces megakaryocyte maturation resulting in increased platelet production. | NA | NA | Absolute bioavailability is over 80%. | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Cytokines, Intercellular Signaling Peptides and Proteins, Interleukins, Megakaryocyte Growth Factor, Peptides, Proteins | NA | NA | NA | Ifex / Mesnex (ifosfamide / mesna) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10245 | Th1033 | Oprelvekin | >Th1033_Oprelvekin GPPPGPPRVSPDPRAELDSTVLLTRSLLADTRQLAAQLRDKFPADGDHNLDSLPTLAMSAGALGALQLPGVLTRLRADLLSYLRHVQWLRRAGGSSLKTLEPELGTLQARLDRLLRRLQLLMSRLALPQPPPDPPAPPLAPPSSAWGGIRAAHAILGGLHLTLDWAVRGLLLLKTRL | 19047.2 | C854H1411N253O235S2 | 11.16 | -0.07 | NA | 6.9 ± 1.7 hours | Oprelvekin, the active ingredient in Neumega is recombinant Interleukin eleven, which is produced in Escherichia coli by recombinant DNA technology. The protein has a molecular mass of approximately 19,000 daltons, and is non-glycosylated. The polypeptide is 177 amino acids in length (the natural IL-11 has 178). This alteration has not resulted in measurable differences in bioactivity either in vitro or in vivo. The primary hematopoietic activity of Neumega is stimulation of megakaryocytopoiesis and thrombopoiesis. In mice and nonhuman primate studies Neumega has shown potent thrombopoietic activity in compromised hematopoiesis, including moderately to severely myelosuppressed animals. In these studies, Neumega improved platelet nadirs and accelerated platelet recoveries compared to controls. In animal studies Oprelvekin also has non-hematopoetic activities. This includes the regulation of intestinal epithelium growth (enhanced healing of gastrointestinal lesions), the inhibition of adipogenesis, the induction of acute phase protein synthesis (e.g., fibrinogen), and inhibition of macrophageal released pro-inflammatory cytokines. | Increases reduced platelet levels due to chemotherapy. | Oprelvekin is indicated for the prevention of severe thrombocytopenia and the reduction of the need for platelet transfusions following myelosuppressive chemotherapy in adult patients with nonmyeloid malignancies who are at high risk of severe thrombocytopenia. The primary hematopoietic activity of Oprelvekin is stimulation of megakaryocytopoiesis and thrombopoiesis. Oprelvekin has shown potent thrombopoietic activity in individuals with compromised hematopoiesis | Oprelvekin binds to the interleukin 11 receptor which leads to a cascade of signal transduction events. IL-11 is a thrombopoietic growth factor that directly stimulates the proliferation of hematopoietic stem cells and megakaryocyte progenitor cells and induces megakaryocyte maturation resulting in increased platelet production. | NA | NA | Absolute bioavailability is over 80%. | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Cytokines, Intercellular Signaling Peptides and Proteins, Interleukins, Megakaryocyte Growth Factor, Peptides, Proteins | NA | NA | NA | ifosfamide / mesna | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10246 | Th1034 | Palifermin | >Th1034_Palifermin MSYDYMEGGDIRVRRLFCRTQWYLRIDKRGKVKGTQEMKNNYNIMEIRTVAVGIVAIKGVESEFYLAMNKEGKLYAKKECNEDCNFKELILENHYNTYASAKWTHNGGEMFVALNQKGIPVRGKKTKKEQKTAHFLPMAIT | 16192.7 | C721H1142N202O204S9 | 9.47 | -0.65 | NA | 4.5 hours (range: 3.3-5.7 hours) | Palifermin(140 residues) is a recombinant human keratinocyte growth factor (KGF) produced using E. coli. | For treatment of oral mucositis associated with chemotherapy and radiation therapy. | Used in the prevention or treatment of oral mucoscitis (mouth ulcers arising from chemotherapy), Kepivance binds to the human keratinocyte growth factor (KGF) receptor on buccal cell surfaces. Kepivance acts as both a cell growth and survival factor by stimulating epithelial cell proliferation, differentiation, and migration around the tongue and mouth. The KGF receptor is found on many tissues particularly around the tongue, esophagus, salivary gland and other gastro-intestinal tract organs. | Kepivance binds to the human keratinocyte growth factor (KGF) receptor found on buccal cell surfaces. The binding activates a Ras-MapK (Map kinase) signaling pathway which leads to the transcriptional activation of many proteins important for cell growth and survival. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Factors, Detoxifying Agents for Antineoplastic Treatment, Fibroblast Growth Factors, Increased Epithelial Proliferation, Intercellular Signaling Peptides and Proteins, Mucocutaneous Epithelial Cell Growth Factor, Peptides, Proteins | NA | NA | NA | Increases toxicity of bendamustine. Should not be administered within a 24 hour time period of antineoplastic agent administration. | Fibroblast growth factor receptor 2,Neuropilin-1,Fibroblast growth factor receptor 1,Fibroblast growth factor receptor 4,Fibroblast growth factor receptor 3,Basement membrane-specific heparan sulfate proteoglycan core protein | Kepivance | Amgen Inc, BioVitrum AB | Amgen Inc, BioVitrum AB | Kepivance is used to help prevent or heal mouth sores and ulcers in people being treated with chemotherapy and stem cell treatment. It is used in people receiving chemotherapy to treat blood cancers (Hodgkin's disease, multiple myeloma, leukemia). | NA | NA | Sterile, lyophilized powder | Intravenous infusion | The recommended dose of Kepivance is 60 mcg/kg/day, administered as an intravenous bolus injection for 3 consecutive days before and 3 consecutive days after myelotoxic therapy, for a total of 6 doses. | NA | Fever; swelling or redness of your skin; itching or rash; changes in your sense of taste or sense of touch; unusual or unpleasant sensations in your mouth; numbness in or around your mouth; joint pain; or discolored or thickened tongue. | Link | NA | NA |
| 10247 | Th1034 | Palifermin | >Th1034_Palifermin MSYDYMEGGDIRVRRLFCRTQWYLRIDKRGKVKGTQEMKNNYNIMEIRTVAVGIVAIKGVESEFYLAMNKEGKLYAKKECNEDCNFKELILENHYNTYASAKWTHNGGEMFVALNQKGIPVRGKKTKKEQKTAHFLPMAIT | 16192.7 | C721H1142N202O204S9 | 9.47 | -0.65 | NA | 4.5 hours (range: 3.3-5.7 hours) | Palifermin(140 residues) is a recombinant human keratinocyte growth factor (KGF) produced using E. coli. | For treatment of oral mucositis associated with chemotherapy and radiation therapy. | Used in the prevention or treatment of oral mucoscitis (mouth ulcers arising from chemotherapy), Kepivance binds to the human keratinocyte growth factor (KGF) receptor on buccal cell surfaces. Kepivance acts as both a cell growth and survival factor by stimulating epithelial cell proliferation, differentiation, and migration around the tongue and mouth. The KGF receptor is found on many tissues particularly around the tongue, esophagus, salivary gland and other gastro-intestinal tract organs. | Kepivance binds to the human keratinocyte growth factor (KGF) receptor found on buccal cell surfaces. The binding activates a Ras-MapK (Map kinase) signaling pathway which leads to the transcriptional activation of many proteins important for cell growth and survival. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Factors, Detoxifying Agents for Antineoplastic Treatment, Fibroblast Growth Factors, Increased Epithelial Proliferation, Intercellular Signaling Peptides and Proteins, Mucocutaneous Epithelial Cell Growth Factor, Peptides, Proteins | NA | NA | NA | Increases the toxicity of pralatrexate. Avoid concomitant therapy or do not use palifermin within 24 hours after administration of pralatrexate. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10248 | Th1034 | Palifermin | >Th1034_Palifermin MSYDYMEGGDIRVRRLFCRTQWYLRIDKRGKVKGTQEMKNNYNIMEIRTVAVGIVAIKGVESEFYLAMNKEGKLYAKKECNEDCNFKELILENHYNTYASAKWTHNGGEMFVALNQKGIPVRGKKTKKEQKTAHFLPMAIT | 16192.7 | C721H1142N202O204S9 | 9.47 | -0.65 | NA | 4.5 hours (range: 3.3-5.7 hours) | Palifermin(140 residues) is a recombinant human keratinocyte growth factor (KGF) produced using E. coli. | For treatment of oral mucositis associated with chemotherapy and radiation therapy. | Used in the prevention or treatment of oral mucoscitis (mouth ulcers arising from chemotherapy), Kepivance binds to the human keratinocyte growth factor (KGF) receptor on buccal cell surfaces. Kepivance acts as both a cell growth and survival factor by stimulating epithelial cell proliferation, differentiation, and migration around the tongue and mouth. The KGF receptor is found on many tissues particularly around the tongue, esophagus, salivary gland and other gastro-intestinal tract organs. | Kepivance binds to the human keratinocyte growth factor (KGF) receptor found on buccal cell surfaces. The binding activates a Ras-MapK (Map kinase) signaling pathway which leads to the transcriptional activation of many proteins important for cell growth and survival. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Factors, Detoxifying Agents for Antineoplastic Treatment, Fibroblast Growth Factors, Increased Epithelial Proliferation, Intercellular Signaling Peptides and Proteins, Mucocutaneous Epithelial Cell Growth Factor, Peptides, Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10249 | Th1034 | Palifermin | >Th1034_Palifermin MSYDYMEGGDIRVRRLFCRTQWYLRIDKRGKVKGTQEMKNNYNIMEIRTVAVGIVAIKGVESEFYLAMNKEGKLYAKKECNEDCNFKELILENHYNTYASAKWTHNGGEMFVALNQKGIPVRGKKTKKEQKTAHFLPMAIT | 16192.7 | C721H1142N202O204S9 | 9.47 | -0.65 | NA | 4.5 hours (range: 3.3-5.7 hours) | Palifermin(140 residues) is a recombinant human keratinocyte growth factor (KGF) produced using E. coli. | For treatment of oral mucositis associated with chemotherapy and radiation therapy. | Used in the prevention or treatment of oral mucoscitis (mouth ulcers arising from chemotherapy), Kepivance binds to the human keratinocyte growth factor (KGF) receptor on buccal cell surfaces. Kepivance acts as both a cell growth and survival factor by stimulating epithelial cell proliferation, differentiation, and migration around the tongue and mouth. The KGF receptor is found on many tissues particularly around the tongue, esophagus, salivary gland and other gastro-intestinal tract organs. | Kepivance binds to the human keratinocyte growth factor (KGF) receptor found on buccal cell surfaces. The binding activates a Ras-MapK (Map kinase) signaling pathway which leads to the transcriptional activation of many proteins important for cell growth and survival. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Factors, Detoxifying Agents for Antineoplastic Treatment, Fibroblast Growth Factors, Increased Epithelial Proliferation, Intercellular Signaling Peptides and Proteins, Mucocutaneous Epithelial Cell Growth Factor, Peptides, Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10250 | Th1034 | Palifermin | >Th1034_Palifermin MSYDYMEGGDIRVRRLFCRTQWYLRIDKRGKVKGTQEMKNNYNIMEIRTVAVGIVAIKGVESEFYLAMNKEGKLYAKKECNEDCNFKELILENHYNTYASAKWTHNGGEMFVALNQKGIPVRGKKTKKEQKTAHFLPMAIT | 16192.7 | C721H1142N202O204S9 | 9.47 | -0.65 | NA | 4.5 hours (range: 3.3-5.7 hours) | Palifermin(140 residues) is a recombinant human keratinocyte growth factor (KGF) produced using E. coli. | For treatment of oral mucositis associated with chemotherapy and radiation therapy. | Used in the prevention or treatment of oral mucoscitis (mouth ulcers arising from chemotherapy), Kepivance binds to the human keratinocyte growth factor (KGF) receptor on buccal cell surfaces. Kepivance acts as both a cell growth and survival factor by stimulating epithelial cell proliferation, differentiation, and migration around the tongue and mouth. The KGF receptor is found on many tissues particularly around the tongue, esophagus, salivary gland and other gastro-intestinal tract organs. | Kepivance binds to the human keratinocyte growth factor (KGF) receptor found on buccal cell surfaces. The binding activates a Ras-MapK (Map kinase) signaling pathway which leads to the transcriptional activation of many proteins important for cell growth and survival. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Factors, Detoxifying Agents for Antineoplastic Treatment, Fibroblast Growth Factors, Increased Epithelial Proliferation, Intercellular Signaling Peptides and Proteins, Mucocutaneous Epithelial Cell Growth Factor, Peptides, Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10251 | Th1034 | Palifermin | >Th1034_Palifermin MSYDYMEGGDIRVRRLFCRTQWYLRIDKRGKVKGTQEMKNNYNIMEIRTVAVGIVAIKGVESEFYLAMNKEGKLYAKKECNEDCNFKELILENHYNTYASAKWTHNGGEMFVALNQKGIPVRGKKTKKEQKTAHFLPMAIT | 16192.7 | C721H1142N202O204S9 | 9.47 | -0.65 | NA | 4.5 hours (range: 3.3-5.7 hours) | Palifermin(140 residues) is a recombinant human keratinocyte growth factor (KGF) produced using E. coli. | For treatment of oral mucositis associated with chemotherapy and radiation therapy. | Used in the prevention or treatment of oral mucoscitis (mouth ulcers arising from chemotherapy), Kepivance binds to the human keratinocyte growth factor (KGF) receptor on buccal cell surfaces. Kepivance acts as both a cell growth and survival factor by stimulating epithelial cell proliferation, differentiation, and migration around the tongue and mouth. The KGF receptor is found on many tissues particularly around the tongue, esophagus, salivary gland and other gastro-intestinal tract organs. | Kepivance binds to the human keratinocyte growth factor (KGF) receptor found on buccal cell surfaces. The binding activates a Ras-MapK (Map kinase) signaling pathway which leads to the transcriptional activation of many proteins important for cell growth and survival. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Factors, Detoxifying Agents for Antineoplastic Treatment, Fibroblast Growth Factors, Increased Epithelial Proliferation, Intercellular Signaling Peptides and Proteins, Mucocutaneous Epithelial Cell Growth Factor, Peptides, Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10257 | Th1036 | Aldesleukin | >Th1036_Aldesleukin MPTSSSTKKTQLQLEHLLLDLQMILNGINNYKNPKLTRMLTFKFYMPKKATELKHLQCLEEELKPLEEVLNLAQSKNFHLRPRDLISNINVIVLELKGSETTFMCEYADETATIVEFLNRWITFSQSIISTLT | 15314.8 | C690H1115N177O202S6 | 7.31 | -0.192 | NA | 0.22-1.42 hours | Aldesleukin, a lymphokine, is produced by recombinant DNA technology using a genetically engineered E. coli strain containing an analog of the human interleukin-2 gene. Genetic engineering techniques were used to modify the human IL-2 gene, and the resulting expression clone encodes a modified human interleukin-2. This recombinant form differs from native interleukin-2 in the following ways: a) Aldesleukin is not glycosylated because it is derived from E. coli; b) the molecule has no N-terminal alanine; the codon for this amino acid was deleted during the genetic engineering procedure; c) the molecule has serine substituted for cysteine at amino acid position 125. | For treatment of adults with metastatic renal cell carcinoma. | Aldesleukin is used to treat renal cell carcinoma, it induces the enhancement of lymphocyte mitogenesis and stimulation of long-term growth of human interleukin-2 dependent cell lines, the enhancement of lymphocyte cytotoxicity, the induction of killer cell (lymphokine-activated (LAK) and natural (NK)) activity; and the induction of interferon-gamma production. IL-2 is normally produced by the body, secreted by T cells, and stimulates growth and differentiation of T cell response. It can be used in immunotherapy to treat cancer. It enhances the ability of the immune system to kill tumor cells and may interfere with blood flow to the tumor. | Aldesleukin binds to the IL-2 receptor which leads to heterodimerization of the cytoplasmic domains of the IL-2R beta and gamma chains, activation of the tyrosine kinase Jak3, and phosphorylation of tyrosine residues on the IL-2R beta chain. These events led to the creation of an activated receptor complex, to which various cytoplasmic signaling molecules are recruited and become substrates for regulatory enzymes (especially tyrosine kinases) that are associated with the receptor. These events stimulate growth and differentiation of T cells. | NA | NA | NA | 0.18 l/kg | The pharmacokinetic profile of Proleukin is characterized by high plasma concentrations following a short IV infusion, rapid distribution into the extravascular space and elimination from the body by metabolism in the kidneys with little or no bioactive p | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-HIV Agents, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Biological Factors, Cancer immunotherapy, Cytochrome P-450 CYP2E1 Inhibitors, Cytochrome P-450 CYP2E1 Inhibitors (strength unknown), Cytochrome P-450 CYP3A Inhibitors, Cytochrome P-450 CYP3A4 Inhibitors, Cytochrome P-450 CYP3A4 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drugs that are Mainly Renally Excreted, Hypotensive Agents, Immunosuppressive Agents, Immunotherapy, Increased Lymphocyte Activation, Increased Lymphocyte Cell Production, Intercellular Signaling Peptides and Proteins, Interleukins, Lymphocyte Growth Factor, Lymphokines, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Peptides, Proteins | NA | NA | NA | Corticosteroids such as clobetasol propionate may diminish the antineoplastic effect of aldesleukin. Avoid conccurent use of corticosteroids with aldesleukin. | Interleukin-2 receptor subunit beta,Interleukin-2 receptor subunit alpha,Cytokine receptor common subunit gamma | Proleukin | Bayer Healthcare , Chiron Corp. , Novartis AG , Physicians Total Care Inc. , Prometheus Laboratories Inc. | Bayer Healthcare , Chiron Corp. , Novartis AG , Physicians Total Care Inc. , Prometheus Laboratories Inc. | Treating skin cancer and kidney cancer that has spread to other parts of the body. | desalanyl-1, serine-125 human interleukin-2 | Proleukin is supplied in single-use vials intended for intravenous administration. When reconstituted with 1.2 mL Sterile Water for Injection, USP, each mL contains 18 million International Units (1.1 mg) Proleukin, 50 mg mannitol, and 0.18 mg sodium dod | Sterile, white to off-white, lyophilized cake | Intravenous administration | The recommended Proleukin treatment regimen is administered by a 15 minute Intravenous infusion every 8 hours. 600,000 International Units/kg (0.037 mg/kg) dose administered every 8 hours by a 15 minute Intravenous infusion for a maximum of 14 doses. ollowing 9 days of rest, the schedule is repeated for another 14 doses, for a maximum of 28 doses per course, as tolerated. | Proleukin is contraindicated in patients with a known history of hypersensitivity to interleukin-2 or any component of the Proleukin formulation. | Anxiety; dizziness; general body discomfort; increased cough; infection; loss of appetite; pain; runny nose; weakness. | Link | NA | NA |
| 10258 | Th1036 | Aldesleukin | >Th1036_Aldesleukin MPTSSSTKKTQLQLEHLLLDLQMILNGINNYKNPKLTRMLTFKFYMPKKATELKHLQCLEEELKPLEEVLNLAQSKNFHLRPRDLISNINVIVLELKGSETTFMCEYADETATIVEFLNRWITFSQSIISTLT | 15314.8 | C690H1115N177O202S6 | 7.31 | -0.192 | NA | 0.22-1.42 hours | Aldesleukin, a lymphokine, is produced by recombinant DNA technology using a genetically engineered E. coli strain containing an analog of the human interleukin-2 gene. Genetic engineering techniques were used to modify the human IL-2 gene, and the resulting expression clone encodes a modified human interleukin-2. This recombinant form differs from native interleukin-2 in the following ways: a) Aldesleukin is not glycosylated because it is derived from E. coli; b) the molecule has no N-terminal alanine; the codon for this amino acid was deleted during the genetic engineering procedure; c) the molecule has serine substituted for cysteine at amino acid position 125. | For treatment of adults with metastatic renal cell carcinoma. | Aldesleukin is used to treat renal cell carcinoma, it induces the enhancement of lymphocyte mitogenesis and stimulation of long-term growth of human interleukin-2 dependent cell lines, the enhancement of lymphocyte cytotoxicity, the induction of killer cell (lymphokine-activated (LAK) and natural (NK)) activity; and the induction of interferon-gamma production. IL-2 is normally produced by the body, secreted by T cells, and stimulates growth and differentiation of T cell response. It can be used in immunotherapy to treat cancer. It enhances the ability of the immune system to kill tumor cells and may interfere with blood flow to the tumor. | Aldesleukin binds to the IL-2 receptor which leads to heterodimerization of the cytoplasmic domains of the IL-2R beta and gamma chains, activation of the tyrosine kinase Jak3, and phosphorylation of tyrosine residues on the IL-2R beta chain. These events led to the creation of an activated receptor complex, to which various cytoplasmic signaling molecules are recruited and become substrates for regulatory enzymes (especially tyrosine kinases) that are associated with the receptor. These events stimulate growth and differentiation of T cells. | NA | NA | NA | 0.18 l/kg | The pharmacokinetic profile of Proleukin is characterized by high plasma concentrations following a short IV infusion, rapid distribution into the extravascular space and elimination from the body by metabolism in the kidneys with little or no bioactive p | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-HIV Agents, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Biological Factors, Cancer immunotherapy, Cytochrome P-450 CYP2E1 Inhibitors, Cytochrome P-450 CYP2E1 Inhibitors (strength unknown), Cytochrome P-450 CYP3A Inhibitors, Cytochrome P-450 CYP3A4 Inhibitors, Cytochrome P-450 CYP3A4 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drugs that are Mainly Renally Excreted, Hypotensive Agents, Immunosuppressive Agents, Immunotherapy, Increased Lymphocyte Activation, Increased Lymphocyte Cell Production, Intercellular Signaling Peptides and Proteins, Interleukins, Lymphocyte Growth Factor, Lymphokines, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Peptides, Proteins | NA | NA | NA | Corticosteroids such as clocortolone may diminish the antineoplastic effect of aldesleukin. Avoid conccurent use of corticosteroids with aldesleukin. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Proleukin is contraindicated in patients with an abnormal thallium stress test or abnormal pulmonary function tests and those with organ allografts. Retreatment with Proleukin is contraindicated in patients who have experienced the following drug-related | Rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue; black stools; chest pain; chills; confusion; depression; diarrhea; drowsiness; fainting; fever; heart murmurs or gallops; infrequent urination. | Link | NA | NA |
| 10259 | Th1036 | Aldesleukin | >Th1036_Aldesleukin MPTSSSTKKTQLQLEHLLLDLQMILNGINNYKNPKLTRMLTFKFYMPKKATELKHLQCLEEELKPLEEVLNLAQSKNFHLRPRDLISNINVIVLELKGSETTFMCEYADETATIVEFLNRWITFSQSIISTLT | 15314.8 | C690H1115N177O202S6 | 7.31 | -0.192 | NA | 0.22-1.42 hours | Aldesleukin, a lymphokine, is produced by recombinant DNA technology using a genetically engineered E. coli strain containing an analog of the human interleukin-2 gene. Genetic engineering techniques were used to modify the human IL-2 gene, and the resulting expression clone encodes a modified human interleukin-2. This recombinant form differs from native interleukin-2 in the following ways: a) Aldesleukin is not glycosylated because it is derived from E. coli; b) the molecule has no N-terminal alanine; the codon for this amino acid was deleted during the genetic engineering procedure; c) the molecule has serine substituted for cysteine at amino acid position 125. | For treatment of adults with metastatic renal cell carcinoma. | Aldesleukin is used to treat renal cell carcinoma, it induces the enhancement of lymphocyte mitogenesis and stimulation of long-term growth of human interleukin-2 dependent cell lines, the enhancement of lymphocyte cytotoxicity, the induction of killer cell (lymphokine-activated (LAK) and natural (NK)) activity; and the induction of interferon-gamma production. IL-2 is normally produced by the body, secreted by T cells, and stimulates growth and differentiation of T cell response. It can be used in immunotherapy to treat cancer. It enhances the ability of the immune system to kill tumor cells and may interfere with blood flow to the tumor. | Aldesleukin binds to the IL-2 receptor which leads to heterodimerization of the cytoplasmic domains of the IL-2R beta and gamma chains, activation of the tyrosine kinase Jak3, and phosphorylation of tyrosine residues on the IL-2R beta chain. These events led to the creation of an activated receptor complex, to which various cytoplasmic signaling molecules are recruited and become substrates for regulatory enzymes (especially tyrosine kinases) that are associated with the receptor. These events stimulate growth and differentiation of T cells. | NA | NA | NA | 0.18 l/kg | The pharmacokinetic profile of Proleukin is characterized by high plasma concentrations following a short IV infusion, rapid distribution into the extravascular space and elimination from the body by metabolism in the kidneys with little or no bioactive p | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-HIV Agents, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Biological Factors, Cancer immunotherapy, Cytochrome P-450 CYP2E1 Inhibitors, Cytochrome P-450 CYP2E1 Inhibitors (strength unknown), Cytochrome P-450 CYP3A Inhibitors, Cytochrome P-450 CYP3A4 Inhibitors, Cytochrome P-450 CYP3A4 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drugs that are Mainly Renally Excreted, Hypotensive Agents, Immunosuppressive Agents, Immunotherapy, Increased Lymphocyte Activation, Increased Lymphocyte Cell Production, Intercellular Signaling Peptides and Proteins, Interleukins, Lymphocyte Growth Factor, Lymphokines, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Peptides, Proteins | NA | NA | NA | Corticosteroids such as corticotropin may diminish the antineoplastic effect of Aldesleukin. Avoid conccurent use of corticosteroids with aldesleukin. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10305 | Th1043 | Rasburicase | >Th1043_Rasburicase SAVKAARYGKDNVRVYKVHKDEKTGVQTVYEMTVCVLLEGEIETSYTKADNSVIVATDSIKNTIYITAKQNPVTPPELFGSILGTHFIEKYNHIHAAHVNIVCHRWTRMDIDGKPHPHSFIRDSEEKRNVQVDVVEGKGIDIKSSLSGLTVLKSTNSQFWGFLRDEYTTLKETWDRILSTDVDATWQWKNFSGLQEVRSHVPKFDATWATAREVTLKTFAEDNSASVQATMYKMAEQILARQQLIETVEYSLPNKHYFEIDLSWHKGLQNTGKNAEVFAPQSDPNGLIKCTVGRSSLKSKL | 34109.5 | C1521H2381N417O461S7 | 7.16 | -0.465 | NA | 18 hours | Rasburicase is a recombinant urate-oxidase enzyme produced by a genetically modified Saccharomyces cerevisiae< strain. The cDNA coding for rasburicase was cloned from a strain of Aspergillus flavus. | For treatment of hyperuricemia, reduces elevated plasma uric acid levels (from chemotherapy). | Drugs used to treat lympohoid leukemia, non-Hodgkin's lymphoma and acute myelogenous leukemia often lead to the accumulation of toxic plasma levels of purine metabolites (i.e. uric acid). The injection of rasburicase reduces levels of uric acid and mitigates the toxic effects of chemotherapy induced tumor lysis. | Rasburicase catalyzes enzymatic oxidation of uric acid into an inactive and soluble metabolite (allantoin). | NA | NA | NA | 110 to 127 mL/kg [pediatric patients] | NA | Antigout Preparations, Detoxifying Agents for Antineoplastic Treatment, Enzymes, Enzymes and Coenzymes, Methemoglobinemia Associated Agents, Musculo-Skeletal System, Oxidoreductases, Recombinant Proteins, Uric Acid-specific Enzyme | CA2175971 | 30-Dec-2003 | 7-May-2016 | amyl nitrite / sodium nitrite / sodium thiosulfate | Uric acid | Elitek | Sanofi-Synthelabo Inc | Sanofi-Synthelabo Inc | Used for preventing high blood levels of uric acid from occurring in patients with certain types of cancer (eg, leukemia, lymphoma, solid malignant tumors) who are receiving cancer chemotherapy treatment. | NA | Elitek is supplied in 3 mL and 10 mL colorless, glass vials containing rasburicase at a concentration of 1.5 mg/mL after reconstitution. Elitek 1.5 mg presentation contains 1.5 mg rasburicase, 10.6 mg mannitol, 15.9 mg L-alanine, between 12.6 and 14.3 mg | Sterile, white to off-white, lyophilized powder | Intravenous administration | The recommended dose of Elitek is 0.2 mg/kg as a 30 minute Intravenous infusion daily for up to 5 days. Dosing beyond 5 days or administration of more than one course is not recommended. | Pateints with history of anaphylaxic or severe hypersensitivity | Rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue; blue or gray skin color; chest pain; chills; coughing up blood; dark urine; fever; irregular heartbeat; numbness or tingling of the skin; persistent sore throat; severe dizziness; shortness of breath, trouble breathing, or wheezing; swelling of the hands or feet; weakness; yellowing of the eyes and skin. | Link | NA | NA |
| 10306 | Th1043 | Rasburicase | >Th1043_Rasburicase SAVKAARYGKDNVRVYKVHKDEKTGVQTVYEMTVCVLLEGEIETSYTKADNSVIVATDSIKNTIYITAKQNPVTPPELFGSILGTHFIEKYNHIHAAHVNIVCHRWTRMDIDGKPHPHSFIRDSEEKRNVQVDVVEGKGIDIKSSLSGLTVLKSTNSQFWGFLRDEYTTLKETWDRILSTDVDATWQWKNFSGLQEVRSHVPKFDATWATAREVTLKTFAEDNSASVQATMYKMAEQILARQQLIETVEYSLPNKHYFEIDLSWHKGLQNTGKNAEVFAPQSDPNGLIKCTVGRSSLKSKL | 34109.5 | C1521H2381N417O461S7 | 7.16 | -0.465 | NA | 18 hours | Rasburicase is a recombinant urate-oxidase enzyme produced by a genetically modified Saccharomyces cerevisiae< strain. The cDNA coding for rasburicase was cloned from a strain of Aspergillus flavus. | For treatment of hyperuricemia, reduces elevated plasma uric acid levels (from chemotherapy). | Drugs used to treat lympohoid leukemia, non-Hodgkin's lymphoma and acute myelogenous leukemia often lead to the accumulation of toxic plasma levels of purine metabolites (i.e. uric acid). The injection of rasburicase reduces levels of uric acid and mitigates the toxic effects of chemotherapy induced tumor lysis. | Rasburicase catalyzes enzymatic oxidation of uric acid into an inactive and soluble metabolite (allantoin). | NA | NA | NA | 75.8 to 138 mL/kg [adult patients] | NA | Antigout Preparations, Detoxifying Agents for Antineoplastic Treatment, Enzymes, Enzymes and Coenzymes, Methemoglobinemia Associated Agents, Musculo-Skeletal System, Oxidoreductases, Recombinant Proteins, Uric Acid-specific Enzyme | CA2148537 | 16-Jul-2002 | 3-May-2015 | Citanest Forte (epinephrine / prilocaine) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Individulas deficient in glucose -6-phosphate dehydrogenase. | NA | Link | NA | NA |
| 10307 | Th1043 | Rasburicase | >Th1043_Rasburicase SAVKAARYGKDNVRVYKVHKDEKTGVQTVYEMTVCVLLEGEIETSYTKADNSVIVATDSIKNTIYITAKQNPVTPPELFGSILGTHFIEKYNHIHAAHVNIVCHRWTRMDIDGKPHPHSFIRDSEEKRNVQVDVVEGKGIDIKSSLSGLTVLKSTNSQFWGFLRDEYTTLKETWDRILSTDVDATWQWKNFSGLQEVRSHVPKFDATWATAREVTLKTFAEDNSASVQATMYKMAEQILARQQLIETVEYSLPNKHYFEIDLSWHKGLQNTGKNAEVFAPQSDPNGLIKCTVGRSSLKSKL | 34109.5 | C1521H2381N417O461S7 | 7.16 | -0.465 | NA | 18 hours | Rasburicase is a recombinant urate-oxidase enzyme produced by a genetically modified Saccharomyces cerevisiae< strain. The cDNA coding for rasburicase was cloned from a strain of Aspergillus flavus. | For treatment of hyperuricemia, reduces elevated plasma uric acid levels (from chemotherapy). | Drugs used to treat lympohoid leukemia, non-Hodgkin's lymphoma and acute myelogenous leukemia often lead to the accumulation of toxic plasma levels of purine metabolites (i.e. uric acid). The injection of rasburicase reduces levels of uric acid and mitigates the toxic effects of chemotherapy induced tumor lysis. | Rasburicase catalyzes enzymatic oxidation of uric acid into an inactive and soluble metabolite (allantoin). | NA | NA | NA | NA | NA | Antigout Preparations, Detoxifying Agents for Antineoplastic Treatment, Enzymes, Enzymes and Coenzymes, Methemoglobinemia Associated Agents, Musculo-Skeletal System, Oxidoreductases, Recombinant Proteins, Uric Acid-specific Enzyme | NA | NA | NA | Citanest HCl Plain (prilocaine) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10308 | Th1043 | Rasburicase | >Th1043_Rasburicase SAVKAARYGKDNVRVYKVHKDEKTGVQTVYEMTVCVLLEGEIETSYTKADNSVIVATDSIKNTIYITAKQNPVTPPELFGSILGTHFIEKYNHIHAAHVNIVCHRWTRMDIDGKPHPHSFIRDSEEKRNVQVDVVEGKGIDIKSSLSGLTVLKSTNSQFWGFLRDEYTTLKETWDRILSTDVDATWQWKNFSGLQEVRSHVPKFDATWATAREVTLKTFAEDNSASVQATMYKMAEQILARQQLIETVEYSLPNKHYFEIDLSWHKGLQNTGKNAEVFAPQSDPNGLIKCTVGRSSLKSKL | 34109.5 | C1521H2381N417O461S7 | 7.16 | -0.465 | NA | 18 hours | Rasburicase is a recombinant urate-oxidase enzyme produced by a genetically modified Saccharomyces cerevisiae< strain. The cDNA coding for rasburicase was cloned from a strain of Aspergillus flavus. | For treatment of hyperuricemia, reduces elevated plasma uric acid levels (from chemotherapy). | Drugs used to treat lympohoid leukemia, non-Hodgkin's lymphoma and acute myelogenous leukemia often lead to the accumulation of toxic plasma levels of purine metabolites (i.e. uric acid). The injection of rasburicase reduces levels of uric acid and mitigates the toxic effects of chemotherapy induced tumor lysis. | Rasburicase catalyzes enzymatic oxidation of uric acid into an inactive and soluble metabolite (allantoin). | NA | NA | NA | NA | NA | Antigout Preparations, Detoxifying Agents for Antineoplastic Treatment, Enzymes, Enzymes and Coenzymes, Methemoglobinemia Associated Agents, Musculo-Skeletal System, Oxidoreductases, Recombinant Proteins, Uric Acid-specific Enzyme | NA | NA | NA | Cyanide Antidote Kit (amyl nitrite / sodium nitrite / sodium thiosulfate) | NA | Fasturtec | Sanofi Aventis | Sanofi Aventis | Fasturtec is used to treat and prevent high levels of uric acid in the blood in order to prevent kidney failure. It is used in adults and children with blood cancers who are at risk of a sudden rise in uric acid levels when they start to receive chemother | NA | NA | Powder and solvent that are made upto make solution. | Intravenous administartion | The recommended dose is 0.2 mg per kilogram body weight in both children and adults, given as a daily infusion for up to seven days. The duration of treatment is adjusted depending on the patient’s blood levels of uric acid and the doctor’s judgment. | Hypersensitivity | Rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue; blue or gray skin color; chest pain; chills; coughing up blood; dark urine; fever; irregular heartbeat; numbness or tingling of the skin; persistent sore throat; severe dizziness; shortness of breath, trouble breathing, or wheezing; swelling of the hands or feet; weakness; yellowing of the eyes and skin. | Link | NA | NA |
| 10309 | Th1043 | Rasburicase | >Th1043_Rasburicase SAVKAARYGKDNVRVYKVHKDEKTGVQTVYEMTVCVLLEGEIETSYTKADNSVIVATDSIKNTIYITAKQNPVTPPELFGSILGTHFIEKYNHIHAAHVNIVCHRWTRMDIDGKPHPHSFIRDSEEKRNVQVDVVEGKGIDIKSSLSGLTVLKSTNSQFWGFLRDEYTTLKETWDRILSTDVDATWQWKNFSGLQEVRSHVPKFDATWATAREVTLKTFAEDNSASVQATMYKMAEQILARQQLIETVEYSLPNKHYFEIDLSWHKGLQNTGKNAEVFAPQSDPNGLIKCTVGRSSLKSKL | 34109.5 | C1521H2381N417O461S7 | 7.16 | -0.465 | NA | 18 hours | Rasburicase is a recombinant urate-oxidase enzyme produced by a genetically modified Saccharomyces cerevisiae< strain. The cDNA coding for rasburicase was cloned from a strain of Aspergillus flavus. | For treatment of hyperuricemia, reduces elevated plasma uric acid levels (from chemotherapy). | Drugs used to treat lympohoid leukemia, non-Hodgkin's lymphoma and acute myelogenous leukemia often lead to the accumulation of toxic plasma levels of purine metabolites (i.e. uric acid). The injection of rasburicase reduces levels of uric acid and mitigates the toxic effects of chemotherapy induced tumor lysis. | Rasburicase catalyzes enzymatic oxidation of uric acid into an inactive and soluble metabolite (allantoin). | NA | NA | NA | NA | NA | Antigout Preparations, Detoxifying Agents for Antineoplastic Treatment, Enzymes, Enzymes and Coenzymes, Methemoglobinemia Associated Agents, Musculo-Skeletal System, Oxidoreductases, Recombinant Proteins, Uric Acid-specific Enzyme | NA | NA | NA | Emla (lidocaine / prilocaine topical) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Pateint with a deficiency in glucose-6-phoshphate dehydrogenase or other metabolic disorder known to cause haemolytic anaemia. | NA | Link | NA | NA |
| 10310 | Th1043 | Rasburicase | >Th1043_Rasburicase SAVKAARYGKDNVRVYKVHKDEKTGVQTVYEMTVCVLLEGEIETSYTKADNSVIVATDSIKNTIYITAKQNPVTPPELFGSILGTHFIEKYNHIHAAHVNIVCHRWTRMDIDGKPHPHSFIRDSEEKRNVQVDVVEGKGIDIKSSLSGLTVLKSTNSQFWGFLRDEYTTLKETWDRILSTDVDATWQWKNFSGLQEVRSHVPKFDATWATAREVTLKTFAEDNSASVQATMYKMAEQILARQQLIETVEYSLPNKHYFEIDLSWHKGLQNTGKNAEVFAPQSDPNGLIKCTVGRSSLKSKL | 34109.5 | C1521H2381N417O461S7 | 7.16 | -0.465 | NA | 18 hours | Rasburicase is a recombinant urate-oxidase enzyme produced by a genetically modified Saccharomyces cerevisiae< strain. The cDNA coding for rasburicase was cloned from a strain of Aspergillus flavus. | For treatment of hyperuricemia, reduces elevated plasma uric acid levels (from chemotherapy). | Drugs used to treat lympohoid leukemia, non-Hodgkin's lymphoma and acute myelogenous leukemia often lead to the accumulation of toxic plasma levels of purine metabolites (i.e. uric acid). The injection of rasburicase reduces levels of uric acid and mitigates the toxic effects of chemotherapy induced tumor lysis. | Rasburicase catalyzes enzymatic oxidation of uric acid into an inactive and soluble metabolite (allantoin). | NA | NA | NA | NA | NA | Antigout Preparations, Detoxifying Agents for Antineoplastic Treatment, Enzymes, Enzymes and Coenzymes, Methemoglobinemia Associated Agents, Musculo-Skeletal System, Oxidoreductases, Recombinant Proteins, Uric Acid-specific Enzyme | NA | NA | NA | Emla Anesthetic Disc (lidocaine / prilocaine topical) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10311 | Th1043 | Rasburicase | >Th1043_Rasburicase SAVKAARYGKDNVRVYKVHKDEKTGVQTVYEMTVCVLLEGEIETSYTKADNSVIVATDSIKNTIYITAKQNPVTPPELFGSILGTHFIEKYNHIHAAHVNIVCHRWTRMDIDGKPHPHSFIRDSEEKRNVQVDVVEGKGIDIKSSLSGLTVLKSTNSQFWGFLRDEYTTLKETWDRILSTDVDATWQWKNFSGLQEVRSHVPKFDATWATAREVTLKTFAEDNSASVQATMYKMAEQILARQQLIETVEYSLPNKHYFEIDLSWHKGLQNTGKNAEVFAPQSDPNGLIKCTVGRSSLKSKL | 34109.5 | C1521H2381N417O461S7 | 7.16 | -0.465 | NA | 18 hours | Rasburicase is a recombinant urate-oxidase enzyme produced by a genetically modified Saccharomyces cerevisiae< strain. The cDNA coding for rasburicase was cloned from a strain of Aspergillus flavus. | For treatment of hyperuricemia, reduces elevated plasma uric acid levels (from chemotherapy). | Drugs used to treat lympohoid leukemia, non-Hodgkin's lymphoma and acute myelogenous leukemia often lead to the accumulation of toxic plasma levels of purine metabolites (i.e. uric acid). The injection of rasburicase reduces levels of uric acid and mitigates the toxic effects of chemotherapy induced tumor lysis. | Rasburicase catalyzes enzymatic oxidation of uric acid into an inactive and soluble metabolite (allantoin). | NA | NA | NA | NA | NA | Antigout Preparations, Detoxifying Agents for Antineoplastic Treatment, Enzymes, Enzymes and Coenzymes, Methemoglobinemia Associated Agents, Musculo-Skeletal System, Oxidoreductases, Recombinant Proteins, Uric Acid-specific Enzyme | NA | NA | NA | epinephrine / prilocaine | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10312 | Th1043 | Rasburicase | >Th1043_Rasburicase SAVKAARYGKDNVRVYKVHKDEKTGVQTVYEMTVCVLLEGEIETSYTKADNSVIVATDSIKNTIYITAKQNPVTPPELFGSILGTHFIEKYNHIHAAHVNIVCHRWTRMDIDGKPHPHSFIRDSEEKRNVQVDVVEGKGIDIKSSLSGLTVLKSTNSQFWGFLRDEYTTLKETWDRILSTDVDATWQWKNFSGLQEVRSHVPKFDATWATAREVTLKTFAEDNSASVQATMYKMAEQILARQQLIETVEYSLPNKHYFEIDLSWHKGLQNTGKNAEVFAPQSDPNGLIKCTVGRSSLKSKL | 34109.5 | C1521H2381N417O461S7 | 7.16 | -0.465 | NA | 18 hours | Rasburicase is a recombinant urate-oxidase enzyme produced by a genetically modified Saccharomyces cerevisiae< strain. The cDNA coding for rasburicase was cloned from a strain of Aspergillus flavus. | For treatment of hyperuricemia, reduces elevated plasma uric acid levels (from chemotherapy). | Drugs used to treat lympohoid leukemia, non-Hodgkin's lymphoma and acute myelogenous leukemia often lead to the accumulation of toxic plasma levels of purine metabolites (i.e. uric acid). The injection of rasburicase reduces levels of uric acid and mitigates the toxic effects of chemotherapy induced tumor lysis. | Rasburicase catalyzes enzymatic oxidation of uric acid into an inactive and soluble metabolite (allantoin). | NA | NA | NA | NA | NA | Antigout Preparations, Detoxifying Agents for Antineoplastic Treatment, Enzymes, Enzymes and Coenzymes, Methemoglobinemia Associated Agents, Musculo-Skeletal System, Oxidoreductases, Recombinant Proteins, Uric Acid-specific Enzyme | NA | NA | NA | lidocaine / prilocaine topical | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10313 | Th1043 | Rasburicase | >Th1043_Rasburicase SAVKAARYGKDNVRVYKVHKDEKTGVQTVYEMTVCVLLEGEIETSYTKADNSVIVATDSIKNTIYITAKQNPVTPPELFGSILGTHFIEKYNHIHAAHVNIVCHRWTRMDIDGKPHPHSFIRDSEEKRNVQVDVVEGKGIDIKSSLSGLTVLKSTNSQFWGFLRDEYTTLKETWDRILSTDVDATWQWKNFSGLQEVRSHVPKFDATWATAREVTLKTFAEDNSASVQATMYKMAEQILARQQLIETVEYSLPNKHYFEIDLSWHKGLQNTGKNAEVFAPQSDPNGLIKCTVGRSSLKSKL | 34109.5 | C1521H2381N417O461S7 | 7.16 | -0.465 | NA | 18 hours | Rasburicase is a recombinant urate-oxidase enzyme produced by a genetically modified Saccharomyces cerevisiae< strain. The cDNA coding for rasburicase was cloned from a strain of Aspergillus flavus. | For treatment of hyperuricemia, reduces elevated plasma uric acid levels (from chemotherapy). | Drugs used to treat lympohoid leukemia, non-Hodgkin's lymphoma and acute myelogenous leukemia often lead to the accumulation of toxic plasma levels of purine metabolites (i.e. uric acid). The injection of rasburicase reduces levels of uric acid and mitigates the toxic effects of chemotherapy induced tumor lysis. | Rasburicase catalyzes enzymatic oxidation of uric acid into an inactive and soluble metabolite (allantoin). | NA | NA | NA | NA | NA | Antigout Preparations, Detoxifying Agents for Antineoplastic Treatment, Enzymes, Enzymes and Coenzymes, Methemoglobinemia Associated Agents, Musculo-Skeletal System, Oxidoreductases, Recombinant Proteins, Uric Acid-specific Enzyme | NA | NA | NA | Nithiodote (sodium nitrite / sodium thiosulfate) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10314 | Th1043 | Rasburicase | >Th1043_Rasburicase SAVKAARYGKDNVRVYKVHKDEKTGVQTVYEMTVCVLLEGEIETSYTKADNSVIVATDSIKNTIYITAKQNPVTPPELFGSILGTHFIEKYNHIHAAHVNIVCHRWTRMDIDGKPHPHSFIRDSEEKRNVQVDVVEGKGIDIKSSLSGLTVLKSTNSQFWGFLRDEYTTLKETWDRILSTDVDATWQWKNFSGLQEVRSHVPKFDATWATAREVTLKTFAEDNSASVQATMYKMAEQILARQQLIETVEYSLPNKHYFEIDLSWHKGLQNTGKNAEVFAPQSDPNGLIKCTVGRSSLKSKL | 34109.5 | C1521H2381N417O461S7 | 7.16 | -0.465 | NA | 18 hours | Rasburicase is a recombinant urate-oxidase enzyme produced by a genetically modified Saccharomyces cerevisiae< strain. The cDNA coding for rasburicase was cloned from a strain of Aspergillus flavus. | For treatment of hyperuricemia, reduces elevated plasma uric acid levels (from chemotherapy). | Drugs used to treat lympohoid leukemia, non-Hodgkin's lymphoma and acute myelogenous leukemia often lead to the accumulation of toxic plasma levels of purine metabolites (i.e. uric acid). The injection of rasburicase reduces levels of uric acid and mitigates the toxic effects of chemotherapy induced tumor lysis. | Rasburicase catalyzes enzymatic oxidation of uric acid into an inactive and soluble metabolite (allantoin). | NA | NA | NA | NA | NA | Antigout Preparations, Detoxifying Agents for Antineoplastic Treatment, Enzymes, Enzymes and Coenzymes, Methemoglobinemia Associated Agents, Musculo-Skeletal System, Oxidoreductases, Recombinant Proteins, Uric Acid-specific Enzyme | NA | NA | NA | Oraqix (lidocaine / prilocaine topical) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10315 | Th1043 | Rasburicase | >Th1043_Rasburicase SAVKAARYGKDNVRVYKVHKDEKTGVQTVYEMTVCVLLEGEIETSYTKADNSVIVATDSIKNTIYITAKQNPVTPPELFGSILGTHFIEKYNHIHAAHVNIVCHRWTRMDIDGKPHPHSFIRDSEEKRNVQVDVVEGKGIDIKSSLSGLTVLKSTNSQFWGFLRDEYTTLKETWDRILSTDVDATWQWKNFSGLQEVRSHVPKFDATWATAREVTLKTFAEDNSASVQATMYKMAEQILARQQLIETVEYSLPNKHYFEIDLSWHKGLQNTGKNAEVFAPQSDPNGLIKCTVGRSSLKSKL | 34109.5 | C1521H2381N417O461S7 | 7.16 | -0.465 | NA | 18 hours | Rasburicase is a recombinant urate-oxidase enzyme produced by a genetically modified Saccharomyces cerevisiae< strain. The cDNA coding for rasburicase was cloned from a strain of Aspergillus flavus. | For treatment of hyperuricemia, reduces elevated plasma uric acid levels (from chemotherapy). | Drugs used to treat lympohoid leukemia, non-Hodgkin's lymphoma and acute myelogenous leukemia often lead to the accumulation of toxic plasma levels of purine metabolites (i.e. uric acid). The injection of rasburicase reduces levels of uric acid and mitigates the toxic effects of chemotherapy induced tumor lysis. | Rasburicase catalyzes enzymatic oxidation of uric acid into an inactive and soluble metabolite (allantoin). | NA | NA | NA | NA | NA | Antigout Preparations, Detoxifying Agents for Antineoplastic Treatment, Enzymes, Enzymes and Coenzymes, Methemoglobinemia Associated Agents, Musculo-Skeletal System, Oxidoreductases, Recombinant Proteins, Uric Acid-specific Enzyme | NA | NA | NA | sodium nitrite / sodium thiosulfate | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10316 | Th1044 | Adalimumab | >Th1044_Adalimumab DIQMTQSPSSLSASVGDRVTITCRASQGIRNYLAWYQQKPGKAPKLLIYAASTLQSGVPSRFSGSGSGTDFTLTISSLQPEDVATYYCQRYNRAPYTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | NA | 240-480 hours | Adalimumab(1330 amino acids, molecular weight of approximately 148 kilodaltons) is a human monoclonal antibody against TNF-alpha. It is produced by recombinant DNA technology using a mammalian cell expression system. | For treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease. | Used in the treatment of immune system mediated diseases, adalimumab binds specifically to TNF-alpha and blocks its general cytokine effects, thereby reducing TNF-induced inflammation and halting tissue destruction. | Adalimumab binds to TNF-alpha and blocks its interaction with the p55 and p75 cell surface TNF receptors. Adalimumab also lyses surface TNF expressing cells in vitro in the presence of complement. | Rare side effects include: worsening or initiation of congestive heart failure, a lupus-like syndrome, lymphoma, medically significant cytopenias, and worsening or initiation of multiple sclerosis/neurological diseases. There has been reported pancytopenia and increased liver transaminases with the use of adalimumab, which suggests that laboratory value monitoring blood counts and liver function, at least intermittently, are important | Most likely removed by opsonization via the reticuloendothelial system. | Bioavailability is 64% | 4.7-6.0 L | 12 mL/hr [RA patients with dose 0.25-10 mg/kg] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Disease-modifying Antirheumatic Agents, Globulins, Immunoglobulins, Immunomodulatory Agents, Immunoproteins, Immunosuppressive Agents, Miscellaneous GI Drugs, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | CA2243459 | 17-Sep-2002 | 10-Feb-2017 | Canakinumab and Rilonacept increase immunosuppressive effects and risk of infection. | Tumor necrosis factor,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 gamm | Humira | Abbott Laboratories | Abbott Laboratories | Humira is used to treat rheumatoid arthritis, juvenile idiopathic arthritis, psoriatic arthritis, ankylosing spondylitis, and plaque psoriasis. It is also used to treat Crohn's disease or ulcerative colitis, after other drugs have been tried without succe | NA | It is supplied for a single use. Each prefilled syringe delivers 0.8 mL (40 mg) of drug product. Each 0.8 mL of HUMIRA contains 40 mg adalimumab, 4.93 mg sodium chloride, 0.69 mg monobasic sodium phosphate dihydrate, 1.22 mg dibasic sodium phosphate dihyd | Sterile, preservative-free solution | Subcutaneous administration | The recommended dose of HUMIRA for adult patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), or ankylosing spondylitis (AS) is 40 mg administered every other week. Methotrexate (MTX), other non-biologic DMARDS, glucocorticoids, nonsteroidal anti-inflammatory drugs (NSAIDs), and/or analgesics may be continued during treatment with HUMIRA. | Hypersensitivity | Fever, chills, sore throat, vomiting, diarrhea, flu symptoms, pain or burning when you urinate; signs of tuberculosis - fever with ongoing cough, weight loss (fat or muscle); pale skin, easy bruising or bleeding (nosebleeds, bleeding gums); numbness. | Link | NA | NA |
| 10317 | Th1044 | Adalimumab | >Th1044_Adalimumab DIQMTQSPSSLSASVGDRVTITCRASQGIRNYLAWYQQKPGKAPKLLIYAASTLQSGVPSRFSGSGSGTDFTLTISSLQPEDVATYYCQRYNRAPYTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | NA | 240-480 hours | Adalimumab(1330 amino acids, molecular weight of approximately 148 kilodaltons) is a human monoclonal antibody against TNF-alpha. It is produced by recombinant DNA technology using a mammalian cell expression system. | For treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease. | Used in the treatment of immune system mediated diseases, adalimumab binds specifically to TNF-alpha and blocks its general cytokine effects, thereby reducing TNF-induced inflammation and halting tissue destruction. | Adalimumab binds to TNF-alpha and blocks its interaction with the p55 and p75 cell surface TNF receptors. Adalimumab also lyses surface TNF expressing cells in vitro in the presence of complement. | Rare side effects include: worsening or initiation of congestive heart failure, a lupus-like syndrome, lymphoma, medically significant cytopenias, and worsening or initiation of multiple sclerosis/neurological diseases. There has been reported pancytopenia and increased liver transaminases with the use of adalimumab, which suggests that laboratory value monitoring blood counts and liver function, at least intermittently, are important | Most likely removed by opsonization via the reticuloendothelial system. | Bioavailability is 64% | 4.7-6.0 L | 13 mL/hr [RA patients with dose 0.25-10 mg/kg] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Disease-modifying Antirheumatic Agents, Globulins, Immunoglobulins, Immunomodulatory Agents, Immunoproteins, Immunosuppressive Agents, Miscellaneous GI Drugs, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | NA | Abrilada | Pfizer Canada Ulc | Pfizer Canada Ulc | ABRILADA is indicated for reducing signs and symptoms, inducing major clinical response, inhibiting the progression of structural damage, and improving physical function in adult patients with moderately to severely active rheumatoid arthritis. ABRILADA can be used alone or in combination with methotrexate or other non-biologic disease-modifying anti-rheumatic drugs (DMARDs). | NA | Adalimumab-afzb is a recombinant human IgG1 monoclonal antibody with human derived heavy and light chain variable regions and human IgG1:k constant regions. Adalimumab-afzb is produced by recombinant DNA technology in Chinese hamster ovary cells and is purified by a process that includes specific viral inactivation and removal steps. It consists of 1330 amino acids and has a molecular weight of approximately 148 kilodaltons | sterile, preservative-free solution | Subcutaneous administration | 10 kg (22 lbs) to <15 kg (33 lbs)-10 mg every other week (10 mg prefilled syringe) 15 kg (33 lbs) to <30 kg (66 lbs)-20 mg every other week (20 mg prefilled syringe) ≥30 kg (66 lbs)-40 mg every other week (ABRILADA pen or 40 mg prefilled syringe) | NA | infections (e.g. upper respiratory, sinusitis), injection site reactions, headache, and rash | Link | NA | NA |
| 10318 | Th1044 | Adalimumab | >Th1044_Adalimumab DIQMTQSPSSLSASVGDRVTITCRASQGIRNYLAWYQQKPGKAPKLLIYAASTLQSGVPSRFSGSGSGTDFTLTISSLQPEDVATYYCQRYNRAPYTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | NA | 240-480 hours | Adalimumab(1330 amino acids, molecular weight of approximately 148 kilodaltons) is a human monoclonal antibody against TNF-alpha. It is produced by recombinant DNA technology using a mammalian cell expression system. | For treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease. | Used in the treatment of immune system mediated diseases, adalimumab binds specifically to TNF-alpha and blocks its general cytokine effects, thereby reducing TNF-induced inflammation and halting tissue destruction. | Adalimumab binds to TNF-alpha and blocks its interaction with the p55 and p75 cell surface TNF receptors. Adalimumab also lyses surface TNF expressing cells in vitro in the presence of complement. | Rare side effects include: worsening or initiation of congestive heart failure, a lupus-like syndrome, lymphoma, medically significant cytopenias, and worsening or initiation of multiple sclerosis/neurological diseases. There has been reported pancytopenia and increased liver transaminases with the use of adalimumab, which suggests that laboratory value monitoring blood counts and liver function, at least intermittently, are important | Most likely removed by opsonization via the reticuloendothelial system. | Bioavailability is 64% | 4.7-6.0 L | 14 mL/hr [RA patients with dose 0.25-10 mg/kg] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Disease-modifying Antirheumatic Agents, Globulins, Immunoglobulins, Immunomodulatory Agents, Immunoproteins, Immunosuppressive Agents, Miscellaneous GI Drugs, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | NA | NA | NA | Adalimumab (and other anti-TNF immunosuppressants), when used in combination with tofacitinib, may increase the risk of added immunosuppression. It is recommended to avoid concurrent therapy. | NA | Humira Pen | Abbott Laboratories | Abbott Laboratories | It is used to treat rheumatoid arthritis, juvenile idiopathic arthritis, psoriatic arthritis, ankylosing spondylitis, and plaque psoriasis. It is also used to treat Crohn's disease or ulcerative colitis, after other drugs have been tried without successfu | NA | NA | Sterile, preservative-free solution | Subcutaneous Injection | The recommended dose of HUMIRA for adult patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), or ankylosing spondylitis (AS) is 40 mg administered every other week. Methotrexate (MTX), other non-biologic DMARDS, glucocorticoids,nonsteroidal anti-inflammatory drugs (NSAIDs), and/or analgesics may be continued during treatment with HUMIRA. | Hypersensitivity | Fever, chills, sore throat, vomiting, diarrhea, flu symptoms, pain or burning when you urinate; signs of tuberculosis - fever with ongoing cough, weight loss (fat or muscle); pale skin, easy bruising or bleeding (nosebleeds, bleeding gums); numbness. | Link | NA | NA |
| 10319 | Th1044 | Adalimumab | >Th1044_Adalimumab DIQMTQSPSSLSASVGDRVTITCRASQGIRNYLAWYQQKPGKAPKLLIYAASTLQSGVPSRFSGSGSGTDFTLTISSLQPEDVATYYCQRYNRAPYTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | NA | 240-480 hours | Adalimumab(1330 amino acids, molecular weight of approximately 148 kilodaltons) is a human monoclonal antibody against TNF-alpha. It is produced by recombinant DNA technology using a mammalian cell expression system. | For treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease. | Used in the treatment of immune system mediated diseases, adalimumab binds specifically to TNF-alpha and blocks its general cytokine effects, thereby reducing TNF-induced inflammation and halting tissue destruction. | Adalimumab binds to TNF-alpha and blocks its interaction with the p55 and p75 cell surface TNF receptors. Adalimumab also lyses surface TNF expressing cells in vitro in the presence of complement. | Rare side effects include: worsening or initiation of congestive heart failure, a lupus-like syndrome, lymphoma, medically significant cytopenias, and worsening or initiation of multiple sclerosis/neurological diseases. There has been reported pancytopenia and increased liver transaminases with the use of adalimumab, which suggests that laboratory value monitoring blood counts and liver function, at least intermittently, are important | Most likely removed by opsonization via the reticuloendothelial system. | Bioavailability is 64% | 4.7-6.0 L | 15 mL/hr [RA patients with dose 0.25-10 mg/kg] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Disease-modifying Antirheumatic Agents, Globulins, Immunoglobulins, Immunomodulatory Agents, Immunoproteins, Immunosuppressive Agents, Miscellaneous GI Drugs, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | NA | NA | NA | NA | NA | Amgevita | Amgen Europe B.V. | Amgen Europe B.V. | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10320 | Th1044 | Adalimumab | >Th1044_Adalimumab DIQMTQSPSSLSASVGDRVTITCRASQGIRNYLAWYQQKPGKAPKLLIYAASTLQSGVPSRFSGSGSGTDFTLTISSLQPEDVATYYCQRYNRAPYTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | NA | 240-480 hours | Adalimumab(1330 amino acids, molecular weight of approximately 148 kilodaltons) is a human monoclonal antibody against TNF-alpha. It is produced by recombinant DNA technology using a mammalian cell expression system. | For treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease. | Used in the treatment of immune system mediated diseases, adalimumab binds specifically to TNF-alpha and blocks its general cytokine effects, thereby reducing TNF-induced inflammation and halting tissue destruction. | Adalimumab binds to TNF-alpha and blocks its interaction with the p55 and p75 cell surface TNF receptors. Adalimumab also lyses surface TNF expressing cells in vitro in the presence of complement. | Rare side effects include: worsening or initiation of congestive heart failure, a lupus-like syndrome, lymphoma, medically significant cytopenias, and worsening or initiation of multiple sclerosis/neurological diseases. There has been reported pancytopenia and increased liver transaminases with the use of adalimumab, which suggests that laboratory value monitoring blood counts and liver function, at least intermittently, are important | Most likely removed by opsonization via the reticuloendothelial system. | Bioavailability is 64% | 4.7-6.0 L | 16 mL/hr [RA patients with dose 0.25-10 mg/kg] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Disease-modifying Antirheumatic Agents, Globulins, Immunoglobulins, Immunomodulatory Agents, Immunoproteins, Immunosuppressive Agents, Miscellaneous GI Drugs, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | NA | NA | NA | NA | NA | Amsparity | Pfizer Europe Ma Eeig | Pfizer Europe Ma Eeig | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10321 | Th1044 | Adalimumab | >Th1044_Adalimumab DIQMTQSPSSLSASVGDRVTITCRASQGIRNYLAWYQQKPGKAPKLLIYAASTLQSGVPSRFSGSGSGTDFTLTISSLQPEDVATYYCQRYNRAPYTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | NA | 240-480 hours | Adalimumab(1330 amino acids, molecular weight of approximately 148 kilodaltons) is a human monoclonal antibody against TNF-alpha. It is produced by recombinant DNA technology using a mammalian cell expression system. | For treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease. | Used in the treatment of immune system mediated diseases, adalimumab binds specifically to TNF-alpha and blocks its general cytokine effects, thereby reducing TNF-induced inflammation and halting tissue destruction. | Adalimumab binds to TNF-alpha and blocks its interaction with the p55 and p75 cell surface TNF receptors. Adalimumab also lyses surface TNF expressing cells in vitro in the presence of complement. | Rare side effects include: worsening or initiation of congestive heart failure, a lupus-like syndrome, lymphoma, medically significant cytopenias, and worsening or initiation of multiple sclerosis/neurological diseases. There has been reported pancytopenia and increased liver transaminases with the use of adalimumab, which suggests that laboratory value monitoring blood counts and liver function, at least intermittently, are important | Most likely removed by opsonization via the reticuloendothelial system. | Bioavailability is 64% | 4.7-6.0 L | 17 mL/hr [RA patients with dose 0.25-10 mg/kg] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Disease-modifying Antirheumatic Agents, Globulins, Immunoglobulins, Immunomodulatory Agents, Immunoproteins, Immunosuppressive Agents, Miscellaneous GI Drugs, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | NA | NA | NA | NA | NA | Cyltezo | Boehringer Ingelheim | Boehringer Ingelheim | to treat the symptoms of Rheumatoid Arthritis, Psoriatic Arthritis, Ankylosing Spondylitis, Plaque Psoriasis, Chron Disease and Ulcerative Colitis. Cyltezo may be used alone or with other medications. | NA | Adalimumab-adbm is a recombinant human IgG1 monoclonal antibody specific for human tumor necrosis factor (TNF). Adalimumabadbm is produced by recombinant DNA technology in a mammalian cell expression system and is purified by a process that includes specific viral inactivation and removal steps. It consists of 1330 amino acids and has a molecular weight of approximately 148 kilodaltons. | sterile, preservative-free solution | subcutaneous administration. | The dosage of Cyltezo for rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis is 40 mg every other week. The dosage of Cyltezo for juvenile idiopathic arthritis in children up to 30 kg (66 lbs.) is 40 mg every other week. The initial dose of Cyltezo for adult Crohn's disease and ulcerative colitis is 160 mg on Day 1(four 40 mg injections in one day or two 40 mg injections per day for two consecutive days); second dose two weeks later (Day 15) is 80 mg; two weeks later (Day 29) begin a maintenance dose of 40 mg every other week. The dosage of Cyltezo for plaque psoriasis is an 80 mg initial dose, followed by 40 mg every other week starting one week after initial dose. | NA | infections (e.g. upper respiratory, sinusitis, urinary tract), injection site reactions, headache, rash, flu symptoms, nausea, abdominal pain, high cholesterol, blood in the urine, alkaline phosphatase increased, back pain, and high blood pressure (hypertension). | Link | NA | NA |
| 10322 | Th1044 | Adalimumab | >Th1044_Adalimumab DIQMTQSPSSLSASVGDRVTITCRASQGIRNYLAWYQQKPGKAPKLLIYAASTLQSGVPSRFSGSGSGTDFTLTISSLQPEDVATYYCQRYNRAPYTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | NA | 240-480 hours | Adalimumab(1330 amino acids, molecular weight of approximately 148 kilodaltons) is a human monoclonal antibody against TNF-alpha. It is produced by recombinant DNA technology using a mammalian cell expression system. | For treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease. | Used in the treatment of immune system mediated diseases, adalimumab binds specifically to TNF-alpha and blocks its general cytokine effects, thereby reducing TNF-induced inflammation and halting tissue destruction. | Adalimumab binds to TNF-alpha and blocks its interaction with the p55 and p75 cell surface TNF receptors. Adalimumab also lyses surface TNF expressing cells in vitro in the presence of complement. | Rare side effects include: worsening or initiation of congestive heart failure, a lupus-like syndrome, lymphoma, medically significant cytopenias, and worsening or initiation of multiple sclerosis/neurological diseases. There has been reported pancytopenia and increased liver transaminases with the use of adalimumab, which suggests that laboratory value monitoring blood counts and liver function, at least intermittently, are important | Most likely removed by opsonization via the reticuloendothelial system. | Bioavailability is 64% | 4.7-6.0 L | 18 mL/hr [RA patients with dose 0.25-10 mg/kg] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Disease-modifying Antirheumatic Agents, Globulins, Immunoglobulins, Immunomodulatory Agents, Immunoproteins, Immunosuppressive Agents, Miscellaneous GI Drugs, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | NA | NA | NA | NA | NA | Hadlima Pushtouch | Samsung Bioepis Co., Ltd. | Samsung Bioepis Co., Ltd. | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10323 | Th1044 | Adalimumab | >Th1044_Adalimumab DIQMTQSPSSLSASVGDRVTITCRASQGIRNYLAWYQQKPGKAPKLLIYAASTLQSGVPSRFSGSGSGTDFTLTISSLQPEDVATYYCQRYNRAPYTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | NA | 240-480 hours | Adalimumab(1330 amino acids, molecular weight of approximately 148 kilodaltons) is a human monoclonal antibody against TNF-alpha. It is produced by recombinant DNA technology using a mammalian cell expression system. | For treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease. | Used in the treatment of immune system mediated diseases, adalimumab binds specifically to TNF-alpha and blocks its general cytokine effects, thereby reducing TNF-induced inflammation and halting tissue destruction. | Adalimumab binds to TNF-alpha and blocks its interaction with the p55 and p75 cell surface TNF receptors. Adalimumab also lyses surface TNF expressing cells in vitro in the presence of complement. | Rare side effects include: worsening or initiation of congestive heart failure, a lupus-like syndrome, lymphoma, medically significant cytopenias, and worsening or initiation of multiple sclerosis/neurological diseases. There has been reported pancytopenia and increased liver transaminases with the use of adalimumab, which suggests that laboratory value monitoring blood counts and liver function, at least intermittently, are important | Most likely removed by opsonization via the reticuloendothelial system. | Bioavailability is 64% | 4.7-6.0 L | 19 mL/hr [RA patients with dose 0.25-10 mg/kg] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Disease-modifying Antirheumatic Agents, Globulins, Immunoglobulins, Immunomodulatory Agents, Immunoproteins, Immunosuppressive Agents, Miscellaneous GI Drugs, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | NA | NA | NA | NA | NA | Halimatoz | Sandoz | Sandoz | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10337 | Th1048 | Pegaspargase | >Th1048_Pegaspargase MEFFKKTALAALVMGFSGAALALPNITILATGGTIAGGGDSATKSNYTVGKVGVENLVNAVPQLKDIANVKGEQVVNIGSQDMNDNVWLTLAKKINTDCDKTDGFVITHGTDTMEETAYFLDLTVKCDKPVVMVGAMRPSTSMSADGPFNLYNAVVTAADKASANRGVLVVMNDTVLDGRDVTKTNTTDVATFKSVNYGPLGYIHNGKIDYQRTPARKHTSDTPFDVSKLNELPKVGIVYNYANASDLPAKALVDAGYDGIVSAGVGNGNLYKSVFDTLATAAKTGTAVVRSSRVPTGATTQDAEVDDAKYGFVASGTLNPQKARVLLQLALTQTKDPQQIQQIFNQY | 31731.9 | C1377H2208N382O442S17 | 4.67 | 0.059 | NA | IM: ~6 days | Pegylated L-asparagine amidohydrolase from E. coli. Pegylation substantially (by a factor of 4) extends the protein half life. | For treatment of acute lymphoblastic leukemia. | In a significant number of patients with acute leukemia, the malignant cells are dependent on an exogenous source of asparagine for survival. Normal cells, however, are able to synthesize asparagine and thus are affected less by the rapid depletion produced by treatment with the enzyme asparaginase. Oncaspar exploits a metabolic defect in asparagine synthesis of some malignant cells. | Pegaspargase, more effective than asparaginase, converts asparagine to aspartic acid and ammonia. It facilitates production of oxaloacetate which is needed for general cellular metabolism. Some malignant cells lose the ability to produce asparagine and so the loss of exogenous sources of asparagine leads to cell death. | Adverse effects that occur more than 10% of the time include hepatotoxicity as it is known to increase serum transaminases (ALT, AST). Also known to induce hypersensitivity reactions including anaphylaxis, erythema and bronchospasm. | NA | Onset of Asparagine depletion by IM is within 4 days Time to peak: IM: 3 to 4 days | IV: Adults (asparaginase naive): 2.4 L/m2 Distributes into CSF (reportedly reducing CSF asparagine concentrations to a similar extent as asparaginase | NA | Alcohols, Amidohydrolases, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Asparaginase, Asparagine-specific Enzyme, Compounds used in a research, industrial, or household setting, Delayed-Action Preparations, Enzymes, Enzymes and Coenzymes, Ethylene Glycols, Glycols, Hydrolases, Immunosuppressive Agents, Macromolecular Substances, Pegylated agents, Polymers, Thyroxine-binding globulin inhibitors | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | L-asparagine | Oncaspar | Enzon Inc, Servier Pharmaceuticals LLC, Sigma Tau Pharmaceuticals, Inc., Les Laboratoires Servier, Baxalta US Inc. | Enzon Inc, Servier Pharmaceuticals LLC, Sigma Tau Pharmaceuticals, Inc., Les Laboratoires Servier, Baxalta US Inc. | Oncaspar is indicated as a component of a multi-agent chemotherapeutic regimen for the first line treatment of patients with Acute Lymphoblastic Leukemia (ALL). | NA | Oncaspar is supplied as a clear, colorless, preservative-free, isotonic sterile solution in phosphate-buffered saline, pH 7.3. Each milliliter contains 750 ± 150 International Units of pegaspargase, dibasic sodium phosphate, USP (5.58 mg), monobasic sodiu | Solution | Intravenous or intramuSubcutaneousular administrat | The recommended dose of Oncaspar is 2,500 International Units/m_ intramuscularly or intravenously. Oncaspar should be administered no more frequently than every 14 days. When Oncaspar is administered intramuscularly, the volume at a single injection site should be limited to 2ml. | History of serious allergic reactions to Oncaspar. History of serious thrombosis with prior L-asparaginase therapy. History of pancreatitis with prior L-asparaginase therapy. History of serious hemorrhagic events with prior L-asparaginase therapy. | Hypersensitivity reactions, coagulopathy, hyperglycemia, elevated serum transaminase concentrations, hyperbilirubinemia, pancreatitis, CNS thrombosis.No apparent difference in adverse effects following IV versus IM administration. | Link | NA | NA |
| 10338 | Th1048 | Pegaspargase | >Th1048_Pegaspargase MEFFKKTALAALVMGFSGAALALPNITILATGGTIAGGGDSATKSNYTVGKVGVENLVNAVPQLKDIANVKGEQVVNIGSQDMNDNVWLTLAKKINTDCDKTDGFVITHGTDTMEETAYFLDLTVKCDKPVVMVGAMRPSTSMSADGPFNLYNAVVTAADKASANRGVLVVMNDTVLDGRDVTKTNTTDVATFKSVNYGPLGYIHNGKIDYQRTPARKHTSDTPFDVSKLNELPKVGIVYNYANASDLPAKALVDAGYDGIVSAGVGNGNLYKSVFDTLATAAKTGTAVVRSSRVPTGATTQDAEVDDAKYGFVASGTLNPQKARVLLQLALTQTKDPQQIQQIFNQY | 31731.9 | C1377H2208N382O442S17 | 4.67 | 0.059 | NA | 3 days (range: 1.4 to 5 days) in patients with previous hypersensitivity to native L-asparaginase | Pegylated L-asparagine amidohydrolase from E. coli. Pegylation substantially (by a factor of 4) extends the protein half life. | For treatment of acute lymphoblastic leukemia | In a significant number of patients with acute leukemia, the malignant cells are dependent on an exogenous source of asparagine for survival. Normal cells, however, are able to synthesize asparagine and thus are affected less by the rapid depletion produced by treatment with the enzyme asparaginase. Oncaspar exploits a metabolic defect in asparagine synthesis of some malignant cells. | Pegaspargase, more effective than asparaginase, converts asparagine to aspartic acid and ammonia. It facilitates production of oxaloacetate which is needed for general cellular metabolism. Some malignant cells lose the ability to produce asparagine and so the loss of exogenous sources of asparagine leads to cell death. | Adverse effects that occur more than 10% of the time include hepatotoxicity as it is known to increase serum transaminases (ALT, AST). Also known to induce hypersensitivity reactions including anaphylaxis, erythema and bronchospasm. | NA | Onset of Asparagine depletion by IM is within 4 days Time to peak: IM: 3 to 4 days | IV: Adults (asparaginase naive): 2.4 L/m2 Distributes into CSF (reportedly reducing CSF asparagine concentrations to a similar extent as asparaginase | NA | Alcohols, Amidohydrolases, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Asparaginase, Asparagine-specific Enzyme, Compounds used in a research, industrial, or household setting, Delayed-Action Preparations, Enzymes, Enzymes and Coenzymes, Ethylene Glycols, Glycols, Hydrolases, Immunosuppressive Agents, Macromolecular Substances, Pegylated agents, Polymers, Thyroxine-binding globulin inhibitors | NA | NA | NA | NA | NA | Lyophilized Pegaspargase | Baxalta US Inc., Servier Pharmaceuticals | Baxalta US Inc., Servier Pharmaceuticals | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10339 | Th1048 | Pegaspargase | >Th1048_Pegaspargase MEFFKKTALAALVMGFSGAALALPNITILATGGTIAGGGDSATKSNYTVGKVGVENLVNAVPQLKDIANVKGEQVVNIGSQDMNDNVWLTLAKKINTDCDKTDGFVITHGTDTMEETAYFLDLTVKCDKPVVMVGAMRPSTSMSADGPFNLYNAVVTAADKASANRGVLVVMNDTVLDGRDVTKTNTTDVATFKSVNYGPLGYIHNGKIDYQRTPARKHTSDTPFDVSKLNELPKVGIVYNYANASDLPAKALVDAGYDGIVSAGVGNGNLYKSVFDTLATAAKTGTAVVRSSRVPTGATTQDAEVDDAKYGFVASGTLNPQKARVLLQLALTQTKDPQQIQQIFNQY | 31731.9 | C1377H2208N382O442S17 | 4.67 | 0.059 | NA | Adults (asparaginase naive): 7 days | Pegylated L-asparagine amidohydrolase from E. coli. Pegylation substantially (by a factor of 4) extends the protein half life. | For treatment of acute lymphoblastic leukemia | In a significant number of patients with acute leukemia, the malignant cells are dependent on an exogenous source of asparagine for survival. Normal cells, however, are able to synthesize asparagine and thus are affected less by the rapid depletion produced by treatment with the enzyme asparaginase. Oncaspar exploits a metabolic defect in asparagine synthesis of some malignant cells. | Pegaspargase, more effective than asparaginase, converts asparagine to aspartic acid and ammonia. It facilitates production of oxaloacetate which is needed for general cellular metabolism. Some malignant cells lose the ability to produce asparagine and so the loss of exogenous sources of asparagine leads to cell death. | Adverse effects that occur more than 10% of the time include hepatotoxicity as it is known to increase serum transaminases (ALT, AST). Also known to induce hypersensitivity reactions including anaphylaxis, erythema and bronchospasm. | NA | Onset of Asparagine depletion by IM is within 4 days Time to peak: IM: 3 to 4 days | IV: Adults (asparaginase naive): 2.4 L/m2 Distributes into CSF (reportedly reducing CSF asparagine concentrations to a similar extent as asparaginase | NA | Alcohols, Amidohydrolases, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Asparaginase, Asparagine-specific Enzyme, Compounds used in a research, industrial, or household setting, Delayed-Action Preparations, Enzymes, Enzymes and Coenzymes, Ethylene Glycols, Glycols, Hydrolases, Immunosuppressive Agents, Macromolecular Substances, Pegylated agents, Polymers, Thyroxine-binding globulin inhibitors | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10340 | Th1048 | Pegaspargase | >Th1048_Pegaspargase MEFFKKTALAALVMGFSGAALALPNITILATGGTIAGGGDSATKSNYTVGKVGVENLVNAVPQLKDIANVKGEQVVNIGSQDMNDNVWLTLAKKINTDCDKTDGFVITHGTDTMEETAYFLDLTVKCDKPVVMVGAMRPSTSMSADGPFNLYNAVVTAADKASANRGVLVVMNDTVLDGRDVTKTNTTDVATFKSVNYGPLGYIHNGKIDYQRTPARKHTSDTPFDVSKLNELPKVGIVYNYANASDLPAKALVDAGYDGIVSAGVGNGNLYKSVFDTLATAAKTGTAVVRSSRVPTGATTQDAEVDDAKYGFVASGTLNPQKARVLLQLALTQTKDPQQIQQIFNQY | 31731.9 | C1377H2208N382O442S17 | 4.67 | 0.059 | NA | NA | Pegylated L-asparagine amidohydrolase from E. coli. Pegylation substantially (by a factor of 4) extends the protein half life. | For treatment of acute lymphoblastic leukemia | In a significant number of patients with acute leukemia, the malignant cells are dependent on an exogenous source of asparagine for survival. Normal cells, however, are able to synthesize asparagine and thus are affected less by the rapid depletion produced by treatment with the enzyme asparaginase. Oncaspar exploits a metabolic defect in asparagine synthesis of some malignant cells. | Pegaspargase, more effective than asparaginase, converts asparagine to aspartic acid and ammonia. It facilitates production of oxaloacetate which is needed for general cellular metabolism. Some malignant cells lose the ability to produce asparagine and so the loss of exogenous sources of asparagine leads to cell death. | Adverse effects that occur more than 10% of the time include hepatotoxicity as it is known to increase serum transaminases (ALT, AST). Also known to induce hypersensitivity reactions including anaphylaxis, erythema and bronchospasm. | NA | Onset of Asparagine depletion by IM is within 4 days Time to peak: IM: 3 to 4 days | IV: Adults (asparaginase naive): 2.4 L/m2 Distributes into CSF (reportedly reducing CSF asparagine concentrations to a similar extent as asparaginase | NA | Alcohols, Amidohydrolases, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Asparaginase, Asparagine-specific Enzyme, Compounds used in a research, industrial, or household setting, Delayed-Action Preparations, Enzymes, Enzymes and Coenzymes, Ethylene Glycols, Glycols, Hydrolases, Immunosuppressive Agents, Macromolecular Substances, Pegylated agents, Polymers, Thyroxine-binding globulin inhibitors | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10341 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | CA1341604 | 4-May-2010 | 4-May-2027 | NA | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | Avonex | Biogen Inc | Biogen Inc | Avonex is used to treat relapsing multiple sclerosis (MS). This medication will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | AVONEX is avalible as powder vial, Single used prefillled syringe, single used prefilled autoinjector. Each vial of reconstituted AVONEX contains 30 micrograms of interferon beta-1a; 15 mg Albumin (Human), USP; 5.8 mg Sodium Chloride, USP; 5.7 mg Dibasic | Lyophilized powder vial, Sterile liquid as single used prefilled syringe and also available as single use prefilled autoinjector. | IntramuSubcutaneousular Injection | The recommended dose is 30 micrograms once a week. To reduce the incidence and severity of flu-like symptoms that may occur when initiating AVONEX therapy at a dose of 30 micrograms, AVONEX may be started at a dose of 7.5 micrograms and the dose may beincreased by 7.5 micrograms each week for the next three weeks until the recommended dose of 30 micrograms is achieved. | Hypersensitivity | Stomach pain; headache, drowsiness; or minor irritation where the injection was given. | Link | NA | NA |
| 10342 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10343 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10344 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | Betaferon | Bayer | Bayer | Betaferon is indicated for the treatment of patients with a single demyelinating event with an active inflammatory process, if it is severe enough to warrant treatment with intravenous corticosteroids, if alternative diagnoses have been excluded, and if t | NA | NA | Powder and solvent that are made upto make solution. | Subcutaneous Injection | NA | People with severe depression or thoughts of suicide. People with severe liver disease. Pregnancy. Breastfeeding. | Flu-like symptoms such as fever,chills, painful joints, malaise, sweating, headache or muscular pain. These symptoms may be reduced by taking paracetamol or steroidal anti-inflammatory medicines such as ibuprofen. | Link | NA | NA |
| 10345 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | In injection site reactions, symptoms can include redness, swelling, discolouration, inflammation and pain. These may be reduced by the use of an auto-injector device. | Link | NA | NA |
| 10346 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10347 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | Betaseron | Merck | Merck | Betaseron is used to treat relapsing multiple sclerosis (MS). Betaseron will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | Lyophilized Betaseron is a sterile, white to off-white powder, for subcutaneous injection after reconstitution with the diluent supplied (Sodium Chloride, 0.54% Solution). Albumin (Human) USP and Mannitol, USP (15 mg each/vial) are added as stabilizers. | Sterile, white to off-white powder | Subcutaneous Injection | The recommended starting dose is 0.0625 mg (0.25 mL) subcutaneously every other day, with dose increases over a six week period to the recommended dose of 0.25 mg (1 mL) every other day | Betaseron is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, Albumin (Human). | Depressed mood, anxiety, trouble sleeping, restlessness, or thoughts of suicide or hurting yourself; bruising, swelling, oozing, or skin changes where the injection was given; weight changes, pounding heartbeats, feeling too hot or cold; fever, chills, bo | Link | NA | NA |
| 10348 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Weakness; headache; muscle pain or weakness; sleep problems (insomnia); stomach pain; swelling in your hands or feet; skin rash; or irregular menstrual periods. | Link | NA | NA |
| 10349 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10350 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | Blastoferon | Sidus | Sidus | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10351 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | Extavia | Novartis | Novartis | Extavia is used to treat relapsing multiple sclerosis (MS). This medication will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | Each vial contains 0.3 mg of interferon beta-1b. The unit measurement is derived by comparing the antiviral activity of the product to the World Health Organization (WHO) reference standard of recombinant human interferon beta. Mannitol, USP and Albumin ( | Sterile, white to off-white powder | Subcutaneous Injection | The recommended starting dose is 0.0625 mg (0.25 mL) subcutaneously every other day, with dose increases over a six week period to the recommended dose of 0.25 mg (1 mL) every other day. | Extavia is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, Albumin (Human). | Depressed mood, anxiety, trouble sleeping, restlessness, or thoughts of suicide or hurting yourself; bruising, swelling, oozing, or skin changes where the injection was given; weight changes, pounding heartbeats, feeling too hot or cold; fever, chills, weating, muscle aches and tiredness. | Link | NA | NA |
| 10352 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Weakness; headache; muscle pain or weakness; sleep problems (insomnia); stomach pain; swelling in your hands or feet; skin rash; or irregular menstrual periods. | Link | NA | NA |
| 10353 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10354 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10355 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | Rebif | Merck, EMD Serono, Inc. | Merck, EMD Serono, Inc. | Rebif is used to treat relapsing multiple sclerosis (MS). This medication will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | Each 0.5 mL (0.5 cc) of REBIF contains either 22 mcg or 44 mcg of interferon beta-1a, 2 mg or 4 mg albumin (human), 27.3 mg mannitol, 0.4 mg sodium acetate, and water for injection. Each 0.2 mL (0.2 cc) of REBIF contains 8.8 mcg of interferon beta-1a, 0.8 | Sterile solution in a prefilled syringe or REBIF Rebidose autoinjector | Subcutaneous Injection | The recommended dose of REBIF is either 22 mcg or 44 mcg injected subcutaneously three times per week. REBIF should be administered, if possible, at the same time (preferably in the late afternoon or evening) on the same three days (e.g., Monday, Wednesday, and Friday) at least 48 hours apart each week. | REBIF is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, human albumin | Depressed mood, anxiety, trouble sleeping, restlessness, or thoughts of suicide or hurting yourself; bruising, swelling, oozing, or skin changes where the injection was given; weight changes, pounding heartbeats, feeling too hot or cold; fever, chills. | Link | NA | NA |
| 10356 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Weakness; headache; muscle pain or weakness; sleep problems (insomnia); stomach pain; swelling in your hands or feet; skin rash; or irregular menstrual periods. | Link | NA | NA |
| 10357 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10358 | Th1050 | Pegademase bovine | >Th1050_Pegademase_bovine MAQTPAFNKPKVELHVHLDGAIKPETILYYGRKRGIALPADTPEELQNIIGMDKPLSLPEFLAKFDYYMPAIAGCREAVKRIAYEFVEMKAKDGVVYVEVRYSPHLLANSKVEPIPWNQAEGDLTPDEVVSLVNQGLQEGERDFGVKVRSILCCMRHQPSWSSEVVELCKKYREQTVVAIDLAGDETIEGSSLFPGHVKAYAEAVKSGVHRTVHAGEVGSANVVKEAVDTLKTERLGHGYHTLEDATLYNRLRQENMHFEVCPWSSYLTGAWKPDTEHPVVRFKNDQVNYSLNTDDPLIFKSTLDTDYQMTKNEMGFTEEEFKRLNINAAKSSFLPEDEKKELLDLLYKAYGMPSPASAEQCL | 40788.2 | C1821H2834N484O552S14 | 5.33 | -0.428 | NA | 72-144 hours | Bovine adenosine deaminase derived from bovine intestine that has been extensively pegylated for extended serum half life. | For treatment of adenosine deaminase deficiency | Used to replace deficient or inactive adenosine deaminase which leads to severe combined immunodeficiency disease (SCID). The enzyme is responsible for converting adenosine to inosine. In the absence of adenosine deaminase, the purine substrates adenosine 2-deoxyadenosine and their metabolites are actually toxic to lymphocytes thereby leading to diminished immune function. | Pegademase converts adenosine (toxic) to inosine (less toxic) by deamination. It also converts 2'-deoxyadenosine to 2'-deoxyinosine via deamination. | NA | NA | NA | NA | NA | Adjuvants, Immunologic, Aminohydrolases, Antineoplastic and Immunomodulating Agents, Bovine Intestinal Adenosine Deaminase, Enzymes, Enzymes and Coenzymes, Hydrolases, Nucleoside Deaminases, Pegylated agents, Severe Combined Immunodeficiency | NA | NA | NA | Krystexxa (pegloticase) | Adenosine,Growth factor receptor-bound protein 2 | Adagen | Enzon Inc. | Enzon Inc. | It is used for Treating severe combined immunodeficiency disease (SCID) in certain patients with adenosine deaminase (ADA) deficiency. | (monomethoxypolyethylene glycol succinimidyl) 11-17_ adenosine deaminase | Each ml of ADAGEN injection contains, 250 units of Pegademase bovine, 20 mg of Monobasic sodium phoshphate, USP, 5.58 mg of Dibasic sodium phoshphate, USP, 8.50 mg of Sodiium chloride, USP and q.s. to 0 ml of water for injection. | Isotonic, pyrogen free, Sterile solution, pH 7.2-7.4 | Intramusular Injection | The dosage of ADAGEN (pegademase bovine) Injection should be individualized. The recommended dosing schedule is 10 U/kg for the first dose, 15 U/kg for the second dose, and 20 U/kg for the third dose. The usual maintenance dose is 20 U/kg per week. Further increases of 5 U/kg/week may be necessary, but a maximum single dose of 30 U/kg should not be exceeded. | Allergic | Rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue; dark urine; severe or persistent tiredness or weakness; unusual bruising or bleeding | Link | NA | NA |
| 10359 | Th1050 | Pegademase bovine | >Th1050_Pegademase_bovine MAQTPAFNKPKVELHVHLDGAIKPETILYYGRKRGIALPADTPEELQNIIGMDKPLSLPEFLAKFDYYMPAIAGCREAVKRIAYEFVEMKAKDGVVYVEVRYSPHLLANSKVEPIPWNQAEGDLTPDEVVSLVNQGLQEGERDFGVKVRSILCCMRHQPSWSSEVVELCKKYREQTVVAIDLAGDETIEGSSLFPGHVKAYAEAVKSGVHRTVHAGEVGSANVVKEAVDTLKTERLGHGYHTLEDATLYNRLRQENMHFEVCPWSSYLTGAWKPDTEHPVVRFKNDQVNYSLNTDDPLIFKSTLDTDYQMTKNEMGFTEEEFKRLNINAAKSSFLPEDEKKELLDLLYKAYGMPSPASAEQCL | 40788.2 | C1821H2834N484O552S14 | 5.33 | -0.428 | NA | 72-144 hours | Bovine adenosine deaminase derived from bovine intestine that has been extensively pegylated for extended serum half life. | For treatment of adenosine deaminase deficiency | Used to replace deficient or inactive adenosine deaminase which leads to severe combined immunodeficiency disease (SCID). The enzyme is responsible for converting adenosine to inosine. In the absence of adenosine deaminase, the purine substrates adenosine 2-deoxyadenosine and their metabolites are actually toxic to lymphocytes thereby leading to diminished immune function. | Pegademase converts adenosine (toxic) to inosine (less toxic) by deamination. It also converts 2'-deoxyadenosine to 2'-deoxyinosine via deamination. | NA | NA | NA | NA | NA | Adjuvants, Immunologic, Aminohydrolases, Antineoplastic and Immunomodulating Agents, Bovine Intestinal Adenosine Deaminase, Enzymes, Enzymes and Coenzymes, Hydrolases, Nucleoside Deaminases, Pegylated agents, Severe Combined Immunodeficiency | NA | NA | NA | Pegloticase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Headache; pain or redness at the injection site. | Link | NA | NA |
| 10360 | Th1050 | Pegademase bovine | >Th1050_Pegademase_bovine MAQTPAFNKPKVELHVHLDGAIKPETILYYGRKRGIALPADTPEELQNIIGMDKPLSLPEFLAKFDYYMPAIAGCREAVKRIAYEFVEMKAKDGVVYVEVRYSPHLLANSKVEPIPWNQAEGDLTPDEVVSLVNQGLQEGERDFGVKVRSILCCMRHQPSWSSEVVELCKKYREQTVVAIDLAGDETIEGSSLFPGHVKAYAEAVKSGVHRTVHAGEVGSANVVKEAVDTLKTERLGHGYHTLEDATLYNRLRQENMHFEVCPWSSYLTGAWKPDTEHPVVRFKNDQVNYSLNTDDPLIFKSTLDTDYQMTKNEMGFTEEEFKRLNINAAKSSFLPEDEKKELLDLLYKAYGMPSPASAEQCL | 40788.2 | C1821H2834N484O552S14 | 5.33 | -0.428 | NA | 72-144 hours | Bovine adenosine deaminase derived from bovine intestine that has been extensively pegylated for extended serum half life. | For treatment of adenosine deaminase deficiency | Used to replace deficient or inactive adenosine deaminase which leads to severe combined immunodeficiency disease (SCID). The enzyme is responsible for converting adenosine to inosine. In the absence of adenosine deaminase, the purine substrates adenosine 2-deoxyadenosine and their metabolites are actually toxic to lymphocytes thereby leading to diminished immune function. | Pegademase converts adenosine (toxic) to inosine (less toxic) by deamination. It also converts 2'-deoxyadenosine to 2'-deoxyinosine via deamination. | NA | NA | NA | NA | NA | Adjuvants, Immunologic, Aminohydrolases, Antineoplastic and Immunomodulating Agents, Bovine Intestinal Adenosine Deaminase, Enzymes, Enzymes and Coenzymes, Hydrolases, Nucleoside Deaminases, Pegylated agents, Severe Combined Immunodeficiency | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10368 | Th1054 | Infliximab | NA | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | 71 | 9.5 days | Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion. | To manage the signs and symptoms, as well as to induce and maintain clinical remission in adults with moderate to severe active Crohn's disease or ulcerative colitis. Also used to manage signs and symptoms of rheumatoid arthritis (in conjunction with methotrexate), ankylosing spondylitis, psoriatic arthritis, and juvenile arthritis. | Infliximab is a chimeric human-murine anti-human tumor necrosis factor (TNF) monoclonal antibody. It binds to tumor necrosis factor alpha (TNFa) and inhibits binding of TNFa with its receptors. This reduces production of pro-inflammatory cytokines such as interleukins (IL) 1 and 6. This also limits leukocyte migration and expression of adhesion molecules by endothelial cells and leukocytes. Infliximab also limits the activation of neutrophil and eosinophil functional activity, reduces production of tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Infliximab decreases synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal. | Infliximab neutralizes the biological activity of TNFa by binding with high affinity to the soluble and transmembrane forms of TNFa and inhibits binding of TNFa with its receptors. Infliximab does not neutralize TNFb (lymphotoxin a), a related cytokine that utilizes the same receptors as TNFa. Neutralization of the biological activity of TNFa leads to an overall reduction in inflammation. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production | NA | NA | In patients with Crohn's disease, the total body clearance (CL) of infliximab following single doses of 5 mg/kg and 10 mg/kg was 18.4 mL/h and 14.3 mL/h, respectively. In a maintenance therapy study, multiple infusions of infliximab (at week 0, 2 and 6) at the same dose of 5 mg/kg and 10 mg/kg resulted in CL of 15.2 mL/h and 15.2 mL/h, respectively. | Agents Causing Muscle Toxicity, Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Dermatologicals, Disease-modifying Antirheumatic Agents, Gastrointestinal Agents, Globulins, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | CA2106299 | 6-Feb-2001 | 18-Mar-2012 | Golimumab avoid combination with infliximab due to the potential increased immunosuppression of infliximab | Tumor necrosis factor | REMICADE | Centocor Inc | Centocor Inc | used in crohn disease, Ankylosing pondylitis, Psoriatic Arthritis, Plaque Psoriasis and ulcerative colitis | NA | Each single-use vial contains 100 mg infliximab, 500 mg sucrose, 0.5 mg polysorbate 80, 2.2 mg monobasic sodium phosphate, monohydrate, and 6.1 mg dibasic sodium phosphate, dihydrate. No preservatives are present. | REMICADE is supplied as a Sterile, white, lyophilized powder, Following reconstitution with 10 mL of Sterile Water for Injection, USP, the resulting pH is approximately 7.2. | Intravenous infusion | for crohn disease, Ankylosing pondylitis, Psoriatic Arthritis, Plaque Psoriasis and ulcerative colitis : The recommended dose of REMICADE is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks for rhematoid arthritis: The recommended dose of REMICADE is 3 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks | REMICADE at doses > 5 mg/kg should not be administered to patients with moderate to severe heart failure.; REMICADE should not be re-administered to patients who have experienced a severe hypersensitivity reaction to REMICADE | Hepatotoxicity, Immunogenicity, Nausea, Diarrhea, Dysepsia, Sinusitis, Bronchitis, Phrayngitis, Rash, Fatigue, Fever, urinary tract infections. | Link | NA | NA |
| 10369 | Th1054 | Infliximab | NA | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | 71 | 9.5 days | Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion. | To manage the signs and symptoms, as well as to induce and maintain clinical remission in adults with moderate to severe active Crohn's disease or ulcerative colitis. Also used to manage signs and symptoms of rheumatoid arthritis (in conjunction with methotrexate), ankylosing spondylitis, psoriatic arthritis, and juvenile arthritis. | Infliximab is a chimeric human-murine anti-human tumor necrosis factor (TNF) monoclonal antibody. It binds to tumor necrosis factor alpha (TNFa) and inhibits binding of TNFa with its receptors. This reduces production of pro-inflammatory cytokines such as interleukins (IL) 1 and 6. This also limits leukocyte migration and expression of adhesion molecules by endothelial cells and leukocytes. Infliximab also limits the activation of neutrophil and eosinophil functional activity, reduces production of tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Infliximab decreases synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal. | Infliximab neutralizes the biological activity of TNFa by binding with high affinity to the soluble and transmembrane forms of TNFa and inhibits binding of TNFa with its receptors. Infliximab does not neutralize TNFb (lymphotoxin a), a related cytokine that utilizes the same receptors as TNFa. Neutralization of the biological activity of TNFa leads to an overall reduction in inflammation. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production | NA | NA | In patients with rheumatoid arthritis, the CL of infliximab following a single dose infusion of 5 mg/kg, 10 mg/kg and 20 mg/kg were 11±7.5 mL/h, 11.4±5 mL/h, and 11±8.9 mL/h, respectively. | Agents Causing Muscle Toxicity, Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Dermatologicals, Disease-modifying Antirheumatic Agents, Gastrointestinal Agents, Globulins, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | NA | NA | NA | Rilonacept results in increased immunosuppressive effects; increases the risk of infection | NA | Avsola | AMGEN INC | AMGEN INC | Rheumatoid Arthritis -adults with moderately to severely active rheumatoid arthritis, along with the medicine methotrexate. Crohn's Disease -children 6 years and older and adults with Crohn's disease who have not responded well to other medicines. Ankylosing Spondylitis. Psoriatic Arthritis. Plaque Psoriasis -adult patients with plaque psoriasis that is chronic (does not go away), severe, extensive, and/or disabling. Ulcerative Colitis -children 6 years and older and adults with moderately to severely active ulcerative colitis who have not responded well to other medicines. | NA | Following reconstitution with 10 mL of Sterile Water for Injection, USP, the resulting pH is approximately 7.2. Each single-dose vial contains 100 mg infliximab-axxq, dibasic sodium phosphate, anhydrous (4.9 mg), monobasic sodium phosphate, monohydrate (2.2 mg), polysorbate 80 (0.5 mg), and sucrose (500 mg). | sterile, white to slightly yellow, lyophilized powder | intravenous infusion. | Crohn's Disease The recommended dose of AVSOLA is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 8 weeks thereafter for the treatment of adults with moderately to severely active Crohn's disease or fistulizing Crohn's disease. For adult patients who respond and then lose their response, consideration may be given to treatment with 10 mg/kg. Patients who do not respond by Week 14 are unlikely to respond with continued dosing and consideration should be given to discontinue AVSOLA in these patients. Pediatric Crohn's Disease The recommended dose of AVSOLA for pediatric patients 6 years and older with moderately to severely active Crohn's disease is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 8 weeks. Ulcerative Colitis The recommended dose of AVSOLA is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 8 weeks thereafter for the treatment of adult patients with moderately to severely active ulcerative colitis. Pediatric Ulcerative Colitis The recommended dose of AVSOLA for pediatric patients 6 years and older with moderately to severely active ulcerative colitis is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 8 weeks. Rheumatoid Arthritis The recommended dose of AVSOLA is 3 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 3 mg/kg every 8 weeks thereafter for the treatment of moderately to severely active rheumatoid arthritis. AVSOLA should be given in combination with methotrexate. For patients who have an incomplete response, consideration may be given to adjusting the dose up to 10 mg/kg or treating as often as every 4 weeks bearing in mind that risk of serious infections is increased at higher doses [see ADVERSE REACTIONS]. Ankylosing Spondylitis The recommended dose of AVSOLA is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 6 weeks thereafter for the treatment of active ankylosing spondylitis. Psoriatic Arthritis The recommended dose of AVSOLA is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 8 weeks thereafter for the treatment of psoriatic arthritis. AVSOLA can be used with or without methotrexate. Plaque Psoriasis The recommended dose of AVSOLA is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 8 weeks thereafter for the treatment of chronic severe (i.e., extensive and/or disabling) plaque psoriasis. | AVSOLA at doses >5 mg/kg should not be administered to patients with moderate to severe heart failure. In a randomized study evaluating infliximab in patients with moderate to severe heart failure (New York Heart Association [NYHA] Functional Class III/IV), infliximab treatment at 10 mg/kg was associated with an increased incidence of death and hospitalization due to worsening heart failure. AVSOLA should not be re-administered to patients who have experienced a severe hypersensitivity reaction to infliximab products. Additionally, AVSOLA should not be administered to patients with known hypersensitivity to inactive components of the product or to any murine proteins. | feel unwell tiredness (fatigue) poor appetite fever, skin rash, or joint pain | Link | NA | NA |
| 10370 | Th1054 | Infliximab | NA | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | 71 | 9.5 days | Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion. | To manage the signs and symptoms, as well as to induce and maintain clinical remission in adults with moderate to severe active Crohn's disease or ulcerative colitis. Also used to manage signs and symptoms of rheumatoid arthritis (in conjunction with methotrexate), ankylosing spondylitis, psoriatic arthritis, and juvenile arthritis. | Infliximab is a chimeric human-murine anti-human tumor necrosis factor (TNF) monoclonal antibody. It binds to tumor necrosis factor alpha (TNFa) and inhibits binding of TNFa with its receptors. This reduces production of pro-inflammatory cytokines such as interleukins (IL) 1 and 6. This also limits leukocyte migration and expression of adhesion molecules by endothelial cells and leukocytes. Infliximab also limits the activation of neutrophil and eosinophil functional activity, reduces production of tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Infliximab decreases synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal. | Infliximab neutralizes the biological activity of TNFa by binding with high affinity to the soluble and transmembrane forms of TNFa and inhibits binding of TNFa with its receptors. Infliximab does not neutralize TNFb (lymphotoxin a), a related cytokine that utilizes the same receptors as TNFa. Neutralization of the biological activity of TNFa leads to an overall reduction in inflammation. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production | NA | NA | NA | Agents Causing Muscle Toxicity, Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Dermatologicals, Disease-modifying Antirheumatic Agents, Gastrointestinal Agents, Globulins, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | NA | NA | NA | Tofacitinib avoid combination with infliximab and other anti-TNF drugs due to the potential enhancement of tofacitinib related adverse effects | NA | Flixabi | Samsung Bioepis Nl B.V. | Samsung Bioepis Nl B.V. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10371 | Th1054 | Infliximab | NA | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | 71 | 9.5 days | Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion. | To manage the signs and symptoms, as well as to induce and maintain clinical remission in adults with moderate to severe active Crohn's disease or ulcerative colitis. Also used to manage signs and symptoms of rheumatoid arthritis (in conjunction with methotrexate), ankylosing spondylitis, psoriatic arthritis, and juvenile arthritis. | Infliximab is a chimeric human-murine anti-human tumor necrosis factor (TNF) monoclonal antibody. It binds to tumor necrosis factor alpha (TNFa) and inhibits binding of TNFa with its receptors. This reduces production of pro-inflammatory cytokines such as interleukins (IL) 1 and 6. This also limits leukocyte migration and expression of adhesion molecules by endothelial cells and leukocytes. Infliximab also limits the activation of neutrophil and eosinophil functional activity, reduces production of tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Infliximab decreases synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal. | Infliximab neutralizes the biological activity of TNFa by binding with high affinity to the soluble and transmembrane forms of TNFa and inhibits binding of TNFa with its receptors. Infliximab does not neutralize TNFb (lymphotoxin a), a related cytokine that utilizes the same receptors as TNFa. Neutralization of the biological activity of TNFa leads to an overall reduction in inflammation. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production | NA | NA | NA | Agents Causing Muscle Toxicity, Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Dermatologicals, Disease-modifying Antirheumatic Agents, Gastrointestinal Agents, Globulins, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events | NA | Inflectra | Pfizer Europe Ma Eeig | Pfizer Europe Ma Eeig | Crohn's Disease | NA | Following reconstitution with 10 mL of Sterile Water for Injection, USP, the resulting pH is approximately 7.2. Each single-use vial contains 100 mg infliximab-dyyb, 500 mg sucrose, 0.5 mg polysorbate 80, 2.2 mg sodium dihydrogen phosphate monohydrate, and 6.1 mg di-Sodium hydrogen phosphate dihydrate. No preservatives are present. | sterile, white, lyophilized powder | intravenous Injection | The recommended dose of INFLECTRA is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 8 weeks thereafter for the treatment of adults with moderately to severely active Crohn's disease or fistulizing Crohn's disease. For adult patients who respond and then lose their response, consideration may be given to treatment with 10 mg/kg. Patients who do not respond by Week 14 are unlikely to respond with continued dosing and consideration should be given to discontinue INFLECTRA in these patients. | INFLECTRA at doses >5 mg/kg should not be administered to patients with moderate to severe heart failure. In a randomized study evaluating infliximab in patients with moderate to severe heart failure (New York Heart Association [NYHA] Functional Class III/IV), infliximab treatment at 10 mg/kg was associated with an increased incidence of death and hospitalization due to worsening heart failure. INFLECTRA should not be readministered to patients who have experienced a severe hypersensitivity reaction to infliximab products. Additionally, INFLECTRA should not be administered to patients with known hypersensitivity to inactive components of the product or to any murine proteins. | upper respiratory infections sinus infections runny or stuffy nose sore throat cough bronchitis infusion-related reactions headache abdominal pain nausea diarrhea indigestion rash itching fatigue pain fever oral thrush joint pain urinary tract infection, and high blood pressure (hypertension) | Link | NA | NA |
| 10376 | Th1057 | Interferon beta-1b | >Th1057_Interferon_beta-1b SYNLLGFLQRSSNFQSQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20011 | C908H1408N246O253S6 | 9.02 | -0.447 | NA | 10-20 minutes | Human interferon beta (165 residues), cysteine 17 is substituted with serine. Produced in E. coli, no carbohydrates, MW=18.5kD. | Interferon beta-1b is a drug used for the treatment of relapsing/remitting multiple sclerosis. It has been shown to slow the advance of the disease as well as to decrease the frequency of attacks. | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin, neopterin and protein kinase R. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | 0.25 to 2,88 L/kg | 9.4 - 28.9 mL/min/kg [patients with diseases other than MS receiving single intravenous doses up to 2.0 mg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Myelosuppressive Agents, Peptides, Proteins, Recombinant Human Interferon beta | CA1340861 | 28-Dec-1999 | 28-Dec-2016 | NA | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | Betaseron | Bayer | Bayer | Betaseron is used to treat relapsing multiple sclerosis (MS). Betaseron will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | Each vial contains 0.3 mg of interferon beta-lb. The unit measurement is derived by comparing the antiviral activity of the product to the World Health Organization (WHO) reference standard of recombinant human interferon beta. Mannitol, USP and Albumin (Human), USP (15 mg each/vial) are added as stabilizers. | Sterile, white to off-white powder | Subcutaneous Injection | The recommended starting dose is 0.0625 mg (0.25 mL) subcutaneously every other day, with dose increases over a six week period to the recommended dose of 0.25 mg (1 mL) every other day. | Betaseron is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, Albumin (Human), | serious side effects: depressed mood, anxiety, trouble sleeping, restlessness, or thoughts of suicide or hurting yourself; bruising, swelling, oozing, or skin changes where the injection was given; weight changes, pounding heartbeats, feeling too hot or cold; fever, chills, body aches, flu symptoms; or nausea, stomach pain, low fever, loss of appetite, dark urine, clay-colored stools, jaundice (yellowing of the skin or eyes). | Link | NA | NA |
| 10377 | Th1057 | Interferon beta-1b | >Th1057_Interferon_beta-1b SYNLLGFLQRSSNFQSQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20011 | C908H1408N246O253S7 | 9.02 | -0.447 | NA | 10-20 minutes | Human interferon beta (165 residues), cysteine 17 is substituted with serine. Produced in E. coli, no carbohydrates, MW=18.5kD. | Interferon beta-1b is a drug used for the treatment of relapsing/remitting multiple sclerosis. It has been shown to slow the advance of the disease as well as to decrease the frequency of attacks. | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin, neopterin and protein kinase R. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | 0.25 to 2,88 L/kg | 9.4 - 28.9 mL/min/kg [patients with diseases other than MS receiving single intravenous doses up to 2.0 mg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Myelosuppressive Agents, Peptides, Proteins, Recombinant Human Interferon beta | CA1339707 | 10-Mar-1998 | 10-Mar-2015 | NA | NA | Betaferon | Bayer | Bayer | Betaferon is indicated for the treatment of patients with a single demyelinating event with an active inflammatory process, if it is severe enough to warrant treatment with intravenous corticosteroids, if alternative diagnoses have been excluded, and if they are determined to be at high risk of developing clinically definite multiple sclerosis; patients with relapsing-remitting multiple sclerosis and two or more relapses within the last two years; patients with secondary progressive multiple sclerosis with active disease, evidenced by relapses. | NA | NA | Powder and solvent that are made upto make solution. | Subcutaneous Injection | NA | People with severe depression or thoughts of suicide; People with severe liver disease; Pregnancy; Breastfeeding. | The most frequently observed side-effects are: Flu-like symptoms- such as fever,chills, painful joints, malaise, sweating, headache or muscular pain. These symptoms may be reduced by taking paracetamol or steroidal anti-inflammatory medicines such as ibuprofen. Injection site reactions. - Symptoms can include redness, swelling, discolouration, inflammation and pain. These may be reduced by the use of an auto-injector device. | Link | NA | NA |
| 10378 | Th1057 | Interferon beta-1b | >Th1057_Interferon_beta-1b SYNLLGFLQRSSNFQSQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20011 | C908H1408N246O253S8 | 9.02 | -0.447 | NA | 10-20 minutes | Human interferon beta (165 residues), cysteine 17 is substituted with serine. Produced in E. coli, no carbohydrates, MW=18.5kD. | Interferon beta-1b is a drug used for the treatment of relapsing/remitting multiple sclerosis. It has been shown to slow the advance of the disease as well as to decrease the frequency of attacks. | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin, neopterin and protein kinase R. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | 0.25 to 2,88 L/kg | 9.4 - 28.9 mL/min/kg [patients with diseases other than MS receiving single intravenous doses up to 2.0 mg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Myelosuppressive Agents, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | Extavia | Novartis | Novartis | Extavia is used to treat relapsing multiple sclerosis (MS). This medication will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | Each vial contains 0.3 mg of interferon beta-1b. The unit measurement is derived by comparing the antiviral activity of the product to the World Health Organization (WHO) reference standard of recombinant human interferon beta. Mannitol, USP and Albumin (Human), USP (15 mg each/vial) are added as stabilizers. | Sterile, white to off-white powder | Subcutaneous Injection | The recommended starting dose is 0.0625 mg (0.25 mL) subcutaneously every other day, with dose increases over a six week period to the recommended dose of 0.25 mg (1 mL) every other day. | Extavia is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, Albumin (Human), | serious side effects: depressed mood, anxiety, trouble sleeping, restlessness, or thoughts of suicide or hurting yourself; bruising, swelling, oozing, or skin changes where the injection was given; weight changes, pounding heartbeats, feeling too hot or cold; fever, chills, body aches, flu symptoms; or nausea, stomach pain, low fever, loss of appetite, dark urine, clay-colored stools, jaundice (yellowing of the skin or eyes). | Link | NA | NA |
| 10379 | Th1058 | Interferon alfacon-1 | >Th1058_Interferon_alfacon-1 MCDLPQTHSLGNRRALILLAQMRRISPFSCLKDRHDFGFPQEEFDGNQFQKAQAISVLHEMIQQTFNLFSTKDSSAAWDESLLEKFYTELYQQLNDLEACVIQEVGVEETPLMNVDSILAVKKYFQRITLYLTEKKYSPCAWEVVRAEIMRSFSLSTNLQERLRRKE | 19343 | C860H1353N227O255S9 | 5.99 | -0.336 | 61 | 1.3 hours in golden Syrian hamsters and 3.4 hours in rhesus monkeys. | Recombinant type-I Interferon alpha 2b (human leukocyte clone hif-sn 206 protein moiety reduced), composed of 165 amino acid residues with R at position 23. It resembles leukocyte secreted interferon. Widely used as an antiviral or antineoplastic agent. | For the treatment of hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | There is limited experience with overdosage. Postmarketing surveillance includes reports of patients receiving a single dose as great as 10 times the recommended dose. In general, the primary effects of an overdose are consistent with the effects seen with therapeutic doses of interferon alfa-2b. Hepatic enzyme abnormalities, renal failure, hemorrhage, and myocardial infarction have been reported with single administration overdoses and/or with longer durations of treatment than prescribed. Toxic effects after ingestion of interferon alfa-2b are not expected because interferons are poorly absorbed orally. | NA | Absorption is high (greater than 80%) when administered intramuscularly or subcutaneously. | NA | NA | Adjuvants, Immunologic, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferons, Myelosuppressive Agents, Peptides, Proteins | CA1341567 | 19-Feb-2008 | 19-Feb-2025 | Zidovudine, The interferon increases the effect and toxicity of zidovudine | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | INFERGEN | Kadmon Pharmaceuticals, LLC., Valeant Pharmaceuticals, Inc., Three Rivers Pharmaceuticals Llc | Kadmon Pharmaceuticals, LLC., Valeant Pharmaceuticals, Inc., Three Rivers Pharmaceuticals Llc | INFERGEN (interferon alfacon-1) is indicated for treatment of chronic hepatitis C in patients 18 years of age or older with compensated liver disease. | NA | single-use vials containing 9 mcg and 15 mcg interferon alfacon-1 at a fill volume of 0.3 mL and 0.5 mL, respectively. INFERGEN vials contain 0.03 mg/mL interferon alfacon-1, sodium chloride (5.9 mg/mL), and sodium phosphate (3.8 mg/mL) in Water for Injection, USP. | INFERGEN is a Sterile, clear, colorless, preservative-free liquid | Subcutaneous Injection | The recommended dose of INFERGEN monotherapy for the initial treatment of chronic HCV infection is 9 mcg administered three times a week as a single subcutaneous injection for 24 weeks. | contraindicated in patients with hepatic decompensation; autoimmune hepatitis; known hypersensitivity reactions such as urticaria, angioedema, bronchoconstriction, anaphylaxis to interferon alphas or to any component of the product. | INFERGEN alone or in combination with ribavirin causes a broad range of serious adverse reactions; | Link | NA | NA |
| 10380 | Th1058 | Interferon alfacon-1 | >Th1058_Interferon_alfacon-1 MCDLPQTHSLGNRRALILLAQMRRISPFSCLKDRHDFGFPQEEFDGNQFQKAQAISVLHEMIQQTFNLFSTKDSSAAWDESLLEKFYTELYQQLNDLEACVIQEVGVEETPLMNVDSILAVKKYFQRITLYLTEKKYSPCAWEVVRAEIMRSFSLSTNLQERLRRKE | 19343 | C860H1353N227O255S9 | 5.99 | -0.336 | 61 | 1.3 hours in golden Syrian hamsters and 3.4 hours in rhesus monkeys. | Recombinant type-I Interferon alpha 2b (human leukocyte clone hif-sn 206 protein moiety reduced), composed of 165 amino acid residues with R at position 23. It resembles leukocyte secreted interferon. Widely used as an antiviral or antineoplastic agent. | For the treatment of hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | There is limited experience with overdosage. Postmarketing surveillance includes reports of patients receiving a single dose as great as 10 times the recommended dose. In general, the primary effects of an overdose are consistent with the effects seen with therapeutic doses of interferon alfa-2b. Hepatic enzyme abnormalities, renal failure, hemorrhage, and myocardial infarction have been reported with single administration overdoses and/or with longer durations of treatment than prescribed. Toxic effects after ingestion of interferon alfa-2b are not expected because interferons are poorly absorbed orally. | NA | Absorption is high (greater than 80%) when administered intramuscularly or subcutaneously. | NA | NA | Adjuvants, Immunologic, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferons, Myelosuppressive Agents, Peptides, Proteins | CA2201749 | 15-Jun-1999 | 10-Oct-2015 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 |
| 10389 | Th1062 | Rituximab | >Th1062_Rituximab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143859.7 | C6416H9874N1688O1987S44 | 8.68 | -0.414 | 61 (FAB f | 22 days: , Non-Hodgkin's Lymphoma | Rituxan is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences. Rituximab is composed of two heavy chains of 451 amino acids and two light chains of 213 amino acids. | For treatment of CD20-positive non-Hodgkins lymphoma, chronic lymphocytic leukemia, and rheumatoid arthritis. | Rituximab binds to the CD20 antigen, which is predominantly expressed on mature B cells and 90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. | The Fab regions of rituximab binds to the CD20 antigen on B lymphocytes, while the Fc domain recruits antibodies and complements to mediate cell lysis. | NA | Most likely removed by opsonization via the reticuloendothelial system. | Following the administration of 2 doses of rituximab in patients with rheumatoid arthritis (RA), the mean (± S.D.; % CV) concentrations after the first infusion (Cmax first) and second infusion (Cmax second) were : 157 ( ± 46; 29%) and 183 ( ± 55; 30%) mcg/mL, and 318 ( ± 86; 27%) and 381 ( ± 98; 26%) mcg/mL for the 2 × 500 mg and 2 × 1000 mg doses, respectively | 3.1 L | 0.34 L/day [RA patients] | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antirheumatic Agents, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Cancer immunotherapy, CD20-directed Antibody Interactions, CD20-directed Cytolytic Antibody, Globulins, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | CA2149329 | 15-Jul-2008 | 12-Nov-2013 | Azilsartan medoxomil used in combination with rituximab may lead to hypotension | NA | Rituxan | Biogen Idec Inc., and Genentech USA, Inc | Biogen Idec Inc., and Genentech USA, Inc | used in Non–Hodgkin's Lymphoma (NHL), Chronic Lymphocytic Leukemia (CLL), Rheumatoid Arthritis (RA), Granulomatosis with Polyangiitis (GPA) (Wegener's Granulomatosis) and Microscopic Polyangiitis (MPA) | NA | Rituxan is supplied at a concentration of 10 mg/mL in either 100 mg/10 mL or 500 mg/50 mL single-use vials. The product is formulated in polysorbate 80 (0.7 mg/mL), sodium citrate dihydrate (7.35 mg/mL), sodium chloride (9 mg/mL) and Water for Injection. The pH is 6.5. | Rituxan is a Sterile, clear, colorless, preservative-free liquid concentrate |  Intravenous administration | Initiate infusion at a rate of 50 mg/hr. In the absence of infusion toxicity, increase infusion rate by 50 mg/hr increments every 30 minutes, to a maximum of 400 mg/hr. In NHL the recommended dose is 375 mg/m2 as an Intravenous infusion. In CLL 375 mg/m2 the day prior to the initiation of FC chemotherapy, then 500 mg/m2 on Day 1 of cycles 2–6 (every 28 days). Administer Rituxan as two-1000 mg Intravenous infusions separated by 2 weeks. Administer Rituxan as a 375 mg/m2 Intravenous infusion once weekly for 4 weeks. | none | Infusion reactions, Mucocutaneous reactions, Hepatitis B reactivation with fulminant hepatitis, Progressive multifocal leukoencephalopathy , Tumor lysis syndrome , Infections, Cardiac arrhythmias, Renal toxicity, Bowel obstruction and perforation | Link | NA | NA |
| 10390 | Th1062 | Rituximab | >Th1062_Rituximab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143859.7 | C6416H9874N1688O1987S44 | 8.68 | -0.414 | 61 (FAB f | 18 days: Rheumatoid Arthritis | Rituxan is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences. Rituximab is composed of two heavy chains of 451 amino acids and two light chains of 213 amino acids. | For treatment of CD20-positive non-Hodgkins lymphoma, chronic lymphocytic leukemia, and rheumatoid arthritis. | Rituximab binds to the CD20 antigen, which is predominantly expressed on mature B cells and 90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. | The Fab regions of rituximab binds to the CD20 antigen on B lymphocytes, while the Fc domain recruits antibodies and complements to mediate cell lysis. | NA | Most likely removed by opsonization via the reticuloendothelial system. | Following the administration of 2 doses of rituximab in patients with rheumatoid arthritis (RA), the mean (± S.D.; % CV) concentrations after the first infusion (Cmax first) and second infusion (Cmax second) were : 157 ( ± 46; 29%) and 183 ( ± 55; 30%) mcg/mL, and 318 ( ± 86; 27%) and 381 ( ± 98; 26%) mcg/mL for the 2 × 500 mg and 2 × 1000 mg doses, respectively | 3.1 L | 0.34 L/day [RA patients] | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antirheumatic Agents, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Cancer immunotherapy, CD20-directed Antibody Interactions, CD20-directed Cytolytic Antibody, Globulins, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | CA1336826 | 29-Aug-1995 | 29-Aug-2012 | Betaxolol, Chlorothiazide may enhance the hypotensive effect of rituximab. Consider temporarily withholding antihypertensive medications for 12 hours prior to rituximab infusion to avoid excessive hypotension during or immediately after infusion | Receptor tyrosine-protein kinase erbB-2,Epidermal growth factor receptor,Complement C1r subcomponent,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,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,Low affinity immunoglobulin gamma Fc region receptor III-B,Low affinity immunoglobulin gamma Fc region receptor III-A | Blitzima | Celltrion Healthcare Hungary Kft. | Celltrion Healthcare Hungary Kft. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10391 | Th1062 | Rituximab | >Th1062_Rituximab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143859.7 | C6416H9874N1688O1987S44 | 8.68 | -0.414 | 61 (FAB f | 32 days: Chronic Lymphocytic Leukemia (CLL) | Rituxan is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences. Rituximab is composed of two heavy chains of 451 amino acids and two light chains of 213 amino acids. | For treatment of CD20-positive non-Hodgkins lymphoma, chronic lymphocytic leukemia, and rheumatoid arthritis. | Rituximab binds to the CD20 antigen, which is predominantly expressed on mature B cells and 90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. | The Fab regions of rituximab binds to the CD20 antigen on B lymphocytes, while the Fc domain recruits antibodies and complements to mediate cell lysis. | NA | Most likely removed by opsonization via the reticuloendothelial system. | Following the administration of 2 doses of rituximab in patients with rheumatoid arthritis (RA), the mean (± S.D.; % CV) concentrations after the first infusion (Cmax first) and second infusion (Cmax second) were : 157 ( ± 46; 29%) and 183 ( ± 55; 30%) mcg/mL, and 318 ( ± 86; 27%) and 381 ( ± 98; 26%) mcg/mL for the 2 × 500 mg and 2 × 1000 mg doses, respectively | 3.1 L | 0.34 L/day [RA patients] | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antirheumatic Agents, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Cancer immunotherapy, CD20-directed Antibody Interactions, CD20-directed Cytolytic Antibody, Globulins, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | US5736137 | 7-Apr-1998 | 7-Apr-2015 | Certolizumab pegol Co-administration with trastuzumab may increase the risk of serious infections. Concomitant therapy is not recommended | NA | Mabthera | Roche Registration Gmb H | Roche Registration Gmb H | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10392 | Th1062 | Rituximab | >Th1062_Rituximab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143859.7 | C6416H9874N1688O1987S44 | 8.68 | -0.414 | 61 (FAB f | 23 days: Granulomatosis with Polyangitis and Microscopic Polyangitis | Rituxan is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences. Rituximab is composed of two heavy chains of 451 amino acids and two light chains of 213 amino acids. | For treatment of CD20-positive non-Hodgkins lymphoma, chronic lymphocytic leukemia, and rheumatoid arthritis. | Rituximab binds to the CD20 antigen, which is predominantly expressed on mature B cells and 90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. | The Fab regions of rituximab binds to the CD20 antigen on B lymphocytes, while the Fc domain recruits antibodies and complements to mediate cell lysis. | NA | Most likely removed by opsonization via the reticuloendothelial system. | Following the administration of 2 doses of rituximab in patients with rheumatoid arthritis (RA), the mean (± S.D.; % CV) concentrations after the first infusion (Cmax first) and second infusion (Cmax second) were : 157 ( ± 46; 29%) and 183 ( ± 55; 30%) mcg/mL, and 318 ( ± 86; 27%) and 381 ( ± 98; 26%) mcg/mL for the 2 × 500 mg and 2 × 1000 mg doses, respectively | 3.1 L | 0.34 L/day [RA patients] | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antirheumatic Agents, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Cancer immunotherapy, CD20-directed Antibody Interactions, CD20-directed Cytolytic Antibody, Globulins, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Telmisartan may increase the hypotensive effect of Rituximab. Telmisartan should be withheld prior to and throughout Rituximab administration | NA | Riabni | AMGEN INC | AMGEN INC | RIABNI is a prescription medicine used to treat adults with: Non-Hodgkin’s Lymphoma (NHL): alone or with other chemotherapy medicines. Chronic Lymphocytic Leukemia (CLL): with the chemotherapy medicines fludarabine and cyclophosphamide. Granulomatosis with Polyangiitis (GPA) (Wegener’s Granulomatosis) and Microscopic Polyangiitis (MPA): with glucocorticoids, to treat GPA and MPA. | NA | RIABNI is supplied at a concentration of 10 mg/mL in either 100 mg/10 mL or 500 mg/50 mL single-dose vials. Each mL of solution contains 10 mg rituximabarrx, polysorbate 80 (0.7 mg), sodium chloride (9 mg), sodium citrate dihydrate (7.35 mg), and Water for Injection, USP. Hydrochloric acid is used to adjust the buffer solution pH. The pH is 6.5. | sterile, preservative-free, clear to slightly opalescent, colorless to slightly yellow solution | intravenous infusion. | Initiate at a rate of 20% of the total dose given in the first 30 minutes and the remaining 80% of the total dose given over the next 60 minutes. If the 90-minute infusion is tolerated in Cycle 2, the same rate can be used when administering the remainder of the treatment regimen (through Cycle 6 or 8). | NA | fever cold symptoms, such as runny nose or sore throat that do not go away flu symptoms, such as cough, tiredness, and body aches earache or headache pain during urination cold sores in the mouth or throat cuts, scrapes or incisions that are red, warm, swollen or painful | Link | NA | NA |
| 10393 | Th1062 | Rituximab | >Th1062_Rituximab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143859.7 | C6416H9874N1688O1987S44 | 8.68 | -0.414 | 61 (FAB f | NA | Rituxan is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences. Rituximab is composed of two heavy chains of 451 amino acids and two light chains of 213 amino acids. | For treatment of CD20-positive non-Hodgkins lymphoma, chronic lymphocytic leukemia, and rheumatoid arthritis. | Rituximab binds to the CD20 antigen, which is predominantly expressed on mature B cells and 90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. | The Fab regions of rituximab binds to the CD20 antigen on B lymphocytes, while the Fc domain recruits antibodies and complements to mediate cell lysis. | NA | Most likely removed by opsonization via the reticuloendothelial system. | Following the administration of 2 doses of rituximab in patients with rheumatoid arthritis (RA), the mean (± S.D.; % CV) concentrations after the first infusion (Cmax first) and second infusion (Cmax second) were : 157 ( ± 46; 29%) and 183 ( ± 55; 30%) mcg/mL, and 318 ( ± 86; 27%) and 381 ( ± 98; 26%) mcg/mL for the 2 × 500 mg and 2 × 1000 mg doses, respectively | 3.1 L | 0.34 L/day [RA patients] | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antirheumatic Agents, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Cancer immunotherapy, CD20-directed Antibody Interactions, CD20-directed Cytolytic Antibody, Globulins, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Terazosin, Torasemide, Trichlormethiazide causes additive antihypertensive effects may occur. Increased risk of hypotension. Consider withholding drug for 12 hours prior to administration of Rituximab | NA | Ritemvia | Celltrion Healthcare Hungary Kft. | Celltrion Healthcare Hungary Kft. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10394 | Th1062 | Rituximab | >Th1062_Rituximab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143859.7 | C6416H9874N1688O1987S44 | 8.68 | -0.414 | 61 (FAB f | NA | Rituxan is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences. Rituximab is composed of two heavy chains of 451 amino acids and two light chains of 213 amino acids. | For treatment of CD20-positive non-Hodgkins lymphoma, chronic lymphocytic leukemia, and rheumatoid arthritis. | Rituximab binds to the CD20 antigen, which is predominantly expressed on mature B cells and 90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. | The Fab regions of rituximab binds to the CD20 antigen on B lymphocytes, while the Fc domain recruits antibodies and complements to mediate cell lysis. | NA | Most likely removed by opsonization via the reticuloendothelial system. | Following the administration of 2 doses of rituximab in patients with rheumatoid arthritis (RA), the mean (± S.D.; % CV) concentrations after the first infusion (Cmax first) and second infusion (Cmax second) were : 157 ( ± 46; 29%) and 183 ( ± 55; 30%) mcg/mL, and 318 ( ± 86; 27%) and 381 ( ± 98; 26%) mcg/mL for the 2 × 500 mg and 2 × 1000 mg doses, respectively | 3.1 L | 0.34 L/day [RA patients] | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antirheumatic Agents, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Cancer immunotherapy, CD20-directed Antibody Interactions, CD20-directed Cytolytic Antibody, Globulins, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Tofacitinib avoid combination due to the potential increase in tofacitinib related adverse effects | B-lymphocyte antigen CD20,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 | Rituzena | Celltrion Healthcare Hungary Kft., Sandoz | Celltrion Healthcare Hungary Kft., Sandoz | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10395 | Th1062 | Rituximab | >Th1062_Rituximab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143859.7 | C6416H9874N1688O1987S44 | 8.68 | -0.414 | 61 (FAB f | NA | Rituxan is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences. Rituximab is composed of two heavy chains of 451 amino acids and two light chains of 213 amino acids. | For treatment of CD20-positive non-Hodgkins lymphoma, chronic lymphocytic leukemia, and rheumatoid arthritis. | Rituximab binds to the CD20 antigen, which is predominantly expressed on mature B cells and 90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. | The Fab regions of rituximab binds to the CD20 antigen on B lymphocytes, while the Fc domain recruits antibodies and complements to mediate cell lysis. | NA | Most likely removed by opsonization via the reticuloendothelial system. | Following the administration of 2 doses of rituximab in patients with rheumatoid arthritis (RA), the mean (± S.D.; % CV) concentrations after the first infusion (Cmax first) and second infusion (Cmax second) were : 157 ( ± 46; 29%) and 183 ( ± 55; 30%) mcg/mL, and 318 ( ± 86; 27%) and 381 ( ± 98; 26%) mcg/mL for the 2 × 500 mg and 2 × 1000 mg doses, respectively | 3.1 L | 0.34 L/day [RA patients] | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antirheumatic Agents, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Cancer immunotherapy, CD20-directed Antibody Interactions, CD20-directed Cytolytic Antibody, Globulins, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Tolazamide, Valsartan, Verapamil causes additive hypotensive effects . Consider withholding drug for 12 hours prior to administration of Rituximab | NA | Rixathon | Sandoz | Sandoz | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10396 | Th1062 | Rituximab | >Th1062_Rituximab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143859.7 | C6416H9874N1688O1987S44 | 8.68 | -0.414 | 61 (FAB f | NA | Rituxan is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences. Rituximab is composed of two heavy chains of 451 amino acids and two light chains of 213 amino acids. | For treatment of CD20-positive non-Hodgkins lymphoma, chronic lymphocytic leukemia, and rheumatoid arthritis. | Rituximab binds to the CD20 antigen, which is predominantly expressed on mature B cells and 90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. | The Fab regions of rituximab binds to the CD20 antigen on B lymphocytes, while the Fc domain recruits antibodies and complements to mediate cell lysis. | NA | Most likely removed by opsonization via the reticuloendothelial system. | Following the administration of 2 doses of rituximab in patients with rheumatoid arthritis (RA), the mean (± S.D.; % CV) concentrations after the first infusion (Cmax first) and second infusion (Cmax second) were : 157 ( ± 46; 29%) and 183 ( ± 55; 30%) mcg/mL, and 318 ( ± 86; 27%) and 381 ( ± 98; 26%) mcg/mL for the 2 × 500 mg and 2 × 1000 mg doses, respectively | 3.1 L | 0.34 L/day [RA patients] | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antirheumatic Agents, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Cancer immunotherapy, CD20-directed Antibody Interactions, CD20-directed Cytolytic Antibody, Globulins, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Trandolapril may increase the hypotensive effect of Rituximab | NA | Riximyo | Sandoz | Sandoz | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10397 | Th1062 | Rituximab | >Th1062_Rituximab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143859.7 | C6416H9874N1688O1987S44 | 8.68 | -0.414 | 61 (FAB f | NA | Rituxan is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences. Rituximab is composed of two heavy chains of 451 amino acids and two light chains of 213 amino acids. | For treatment of CD20-positive non-Hodgkins lymphoma, chronic lymphocytic leukemia, and rheumatoid arthritis. | Rituximab binds to the CD20 antigen, which is predominantly expressed on mature B cells and 90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. | The Fab regions of rituximab binds to the CD20 antigen on B lymphocytes, while the Fc domain recruits antibodies and complements to mediate cell lysis. | NA | Most likely removed by opsonization via the reticuloendothelial system. | Following the administration of 2 doses of rituximab in patients with rheumatoid arthritis (RA), the mean (± S.D.; % CV) concentrations after the first infusion (Cmax first) and second infusion (Cmax second) were : 157 ( ± 46; 29%) and 183 ( ± 55; 30%) mcg/mL, and 318 ( ± 86; 27%) and 381 ( ± 98; 26%) mcg/mL for the 2 × 500 mg and 2 × 1000 mg doses, respectively | 3.1 L | 0.34 L/day [RA patients] | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antirheumatic Agents, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Cancer immunotherapy, CD20-directed Antibody Interactions, CD20-directed Cytolytic Antibody, Globulins, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | NA | Ruxience | Pfizer | Pfizer | Non-Hodgkin’s Lymphoma (NHL): alone or with other chemotherapy medicines. Chronic Lymphocytic Leukemia (CLL): with the chemotherapy medicines fludarabine and cyclophosphamide. Granulomatosis with Polyangiitis (GPA) (Wegener's Granulomatosis) and Microscopic Polyangiitis (MPA): with glucocorticoids, to treat GPA and MPA. | NA | RUXIENCE is supplied at a concentration of 10 mg/mL in either 100 mg/10 mL or 500 mg/50 mL single-dose vials. Each mL of solution contains 10 mg rituximab-pvvr, 0.056 mg of edetate disodium dihydrate, 1.2 mg of L-histidine, 2.57 mg of L-histidine hydrochloride monohydrate, 0.2 mg of polysorbate 80, 85 mg of sucrose, and Water for Injection, USP. The pH is 5.8. | sterile, preservative-free, clear to slightly opalescent, colorless to pale brownish-yellow solution | intravenous infusion | First Infusion: Initiate infusion at a rate of 50 mg/hour. In the absence of infusion toxicity, increase infusion rate by 50 mg/hour increments every 30 minutes, to a maximum of 400 mg/hour. Subsequent Infusions: Standard Infusion: Initiate infusion at a rate of 100 mg/hour. In the absence of infusion toxicity, increase rate by 100 mg/hour increments at 30-minute intervals, to a maximum of 400 mg/hour. For Previously Untreated Follicular NHL and DLBCL Patients: If patients did not experience a Grade 3 or 4 infusion-related adverse event during Cycle 1, a 90-minute infusion can be administered in Cycle 2 with a glucocorticoid-containing chemotherapy regimen. Initiate at a rate of 20% of the total dose given in the first 30 minutes and the remaining 80% of the total dose given over the next 60 minutes. If the 90-minute infusion is tolerated in Cycle 2, the same rate can be used when administering the remainder of the treatment regimen (through Cycle 6 or 8). Patients who have clinically significant cardiovascular disease or who have a circulating lymphocyte count ≥5,000/mm³ before Cycle 2 should not be administered the 90-minute infusion | NA | fever cold symptoms, such as runny nose or sore throat that do not go away flu symptoms, such as cough, tiredness, and body aches earache or headache pain during urination cold sores in the mouth or throat cuts, scrapes or incisions that are red, warm, swollen or painful | Link | NA | NA |
| 10398 | Th1063 | Basiliximab | >Th1063_Basiliximab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143801.3 | C6378H9844N1698O1997S48 | 8.68 | -0.473 | 71 | 7.2 ± 3.2 days (adults) | A recombinant chimeric (murine/human) monoclonal antibody (IgG1k) that functions as an immunosuppressive agent, specifically binding to and blocking the interleukin-2 receptor a-chain (IL-2R alpha, also known as CD25 antigen) on the surface of activated T-lymphocytes. It is a 144 kDa glycoprotein obtained from fermentation of an established mouse myeloma cell line genetically engineered to express plasmids containing the human heavy and light chain constant region genes and mouse heavy and light chain variable region genes encoding the RFT5 antibody that binds selectively to the IL-2R alpha. | For prophylactic treatment of kidney transplant rejection | Basiliximab functions as an IL-2 receptor antagonist. Specifically it inhibits IL-2-mediated activation of lymphocytes, a critical pathway in the cellular immune response involved in allograft rejection. | Basiliximab binds with high-affinity to the alpha-subunit (CD25) of the high-affinity IL-2 receptor. This inhibits IL-2 binding, which inhibits T-cell activation and prevents the body from mounting an immune response against the foreign kidney. | NA | Most likely removed by opsonization via the reticuloendothelial system. | NA | 7.8 ± 5.1 L [Pediatric] 4.8 ± 2.1 L [Adult] | 41 ± 19 mL/h [Adult patients undergoing first kidney transplantation] 17 ± 6 mL/h [pediatric patients undergoing renal transplantation] 31 ± 19 mL/h [adolescent patients undergoing renal transplantation] | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic and Immunomodulating Agents, Blood Proteins, Globulins, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Interleukin 2 Receptor-directed Antibody Interactions, Interleukin Inhibitors, Interleukin-2 Receptor Antagonist, Interleukin-2 Receptor Blocking Antibody, Proteins, Serum Globulins | CA2038279 | 9-Mar-1999 | 14-Mar-2011 | Canakinumab, Rilonacept results in increased immunosuppressive effects; increases the risk of infection | Interleukin-2 receptor subunit alpha, Interleukin-2 receptor subunit beta | Simulect | Novartis | Novartis | Simulect (basiliximab) is indicated for the prophylaxis of acute organ rejection in patients receiving renal transplantation when used as part of an immunosuppressive regimen that includes cyclosporine, USP (MODIFIED) and corticosteroids. | NA | Each 10-mg vial contains 10 mg basiliximab, 3.61 mg monobasic potassium phosphate, 0.50 mg disodium hydrogen phosphate (anhydrous), 0.80 mg sodium chloride, 10 mg sucrose, 40 mg mannitol and 20 mg glycine, to be reconstituted in 2.5 mL of Sterile Water for Injection, USP. No preservatives are added. Each 20-mg vial contains 20 mg basiliximab, 7.21 mg monobasic potassium phosphate, 0.99 mg disodium hydrogen phosphate (anhydrous), 1.61 mg sodium chloride, 20 mg sucrose, 80 mg mannitol and 40 mg glycine, to be reconstituted in 5 mL of Sterile Water for Injection, USP. No preservatives are added. | Simulect (basiliximab) , is a sterile lyophilisate which is available in 6 mL colorless glass vials and is available in 10 mg and 20 mg strength powder. | intavenous infusion mainly or bolus (if no allerg | In adult patients, the recommended regimen is two doses of 20 mg each. The first 20-mg dose should be given within 2 hours prior to transplantation surgery. The recommended second 20-mg dose should be given 4 days after transplantation. | Simulect (basiliximab) is contraindicated in patients with known hypersensitivity to basiliximab or any other component of the formulation. | Gastrointestinal System: constipation, nausea, abdominal pain, vomiting, diarrhea, dyspepsia; Body as a Whole-General: pain, peripheral edema, fever, viral infection; Metabolic and Nutritional: hyperkalemia, hypokalemia, hyperglycemia, hypercholesterolemia, hypophosphatemia, hyperuricemia; Urinary System: urinary tract infection;Respiratory System: dyspnea, upper respiratory tract infection; Skin and Appendages: surgical wound complications, acne;Cardiovascular Disorders-General: hypertension; Central and Peripheral Nervous System: headache, tremor; Psychiatric: insomnia; Red Blood Cell: anemia. | Link | NA | NA |
| 10399 | Th1063 | Basiliximab | >Th1063_Basiliximab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143801.3 | C6378H9844N1698O1997S48 | 8.68 | -0.473 | 71 | 7.2 ± 3.2 days (adults) | A recombinant chimeric (murine/human) monoclonal antibody (IgG1k) that functions as an immunosuppressive agent, specifically binding to and blocking the interleukin-2 receptor a-chain (IL-2R alpha, also known as CD25 antigen) on the surface of activated T-lymphocytes. It is a 144 kDa glycoprotein obtained from fermentation of an established mouse myeloma cell line genetically engineered to express plasmids containing the human heavy and light chain constant region genes and mouse heavy and light chain variable region genes encoding the RFT5 antibody that binds selectively to the IL-2R alpha. | For prophylactic treatment of kidney transplant rejection | Basiliximab functions as an IL-2 receptor antagonist. Specifically it inhibits IL-2-mediated activation of lymphocytes, a critical pathway in the cellular immune response involved in allograft rejection. | Basiliximab binds with high-affinity to the alpha-subunit (CD25) of the high-affinity IL-2 receptor. This inhibits IL-2 binding, which inhibits T-cell activation and prevents the body from mounting an immune response against the foreign kidney. | NA | Most likely removed by opsonization via the reticuloendothelial system. | NA | 7.8 ± 5.1 L [Pediatric] 4.8 ± 2.1 L [Adult] | 41 ± 19 mL/h [Adult patients undergoing first kidney transplantation] 17 ± 6 mL/h [pediatric patients undergoing renal transplantation] 31 ± 19 mL/h [adolescent patients undergoing renal transplantation] | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic and Immunomodulating Agents, Blood Proteins, Globulins, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Interleukin 2 Receptor-directed Antibody Interactions, Interleukin Inhibitors, Interleukin-2 Receptor Antagonist, Interleukin-2 Receptor Blocking Antibody, Proteins, Serum Globulins | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10400 | Th1064 | Muromonab | >Th1064_Muromonab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146189.7 | C6460H9946N1720O2043S56 | 8.31 | -0.513 | 71 | 0.8 hours (mammalian reticulocytes, in vitro) | Murine monoclonal antibody specific to CD3 T-cell lymphocyte antigens. More specifically it is a purified murine (mouse) monoclonal antibody, directed against the CD3 (T3) receptor on the surface of human T-cells (T-lymphocytes) cultured using the murine ascites method. Muromonab is 93% monomeric immune globulin G type 2a (IgG2a). | For treatment of organ transplant recipients, prevention of organ rejection | Used in organ transplant prophylaxis, Muromonab or OKT-3 binds specifically to the CD-3 complex, which is involved in antigen recognition and cell stimulation, on the surface of T lymphocytes. Immediately after administration CD-3-positive T lymphocytes are abruptly removed from circulation. It has been effective in reversing corticosteroid-resistant acute rejection in renal, liver, and cardiac transplant recipients. | Muromonab binds to the T-cell surface glycoprotein CD3 epsilon chain. It appears to kill CD-3 positive cells by inducing Fc mediated apoptosis, antibody mediated cytotoxicity and complement-dependent cytotoxicity. | NA | Most likely removed by opsonization via the reticuloendothelial system. | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antineoplastic and Immunomodulating Agents, Blood Proteins, CD3 Blocker Immunosuppressant, CD3 Receptor Antagonists, CD3-directed Antibody Interactions, Decreased Immunologic Activity, Globulins, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Proteins, Selective Immunosuppressants, Serum Globulins | NA | NA | NA | Cyclosporine with Muromonab increases the levels of cyclosporine | T-cell surface glycoprotein CD3 delta chain, T-cell surface glycoprotein CD3 epsilon chain, T-cell surface glycoprotein CD3 gamma chain,T-cell surface glycoprotein CD3 zeta chain, Low affinity immunoglobulin gamma Fc region receptor III-B | ORTHOCLONE OKT3 STERILE SOLUTION | Centocor Ortho Biotech, L.P., Janssen Pharmaceuticals | Centocor Ortho Biotech, L.P., Janssen Pharmaceuticals | ORTHOCLONE OKT3 is indicated for the treatment of acute allograft rejection in renal transplant patients. ORTHOCLONE OKT3 is indicated for the treatment of steroid-resistant acute allograft rejection in cardiac and hepatic transplant patients. | NA | Each 5 mL ampule of ORTHOCLONE OKT3 Sterile Solution contains 5 mg (1 mg/mL) of muromonab-CD3 in a clear colorless solution which may contain a few fine translucent protein particles. Each ampule contains a buffered solution (pH 7.0 ± 0.5) of monobasic sodium phosphate (2.25 mg), dibasic sodium phosphate (9.0 mg), sodium chloride (43 mg), and polysorbate 80 (1.0 mg) in water for injection. | ORTHOCLONE OKT3 (muromonab-CD3)sterile solution is a murine monoclonal antibody to the CD3 antigen of human T cells which functions as an immunosuppressant. | For Intravenous Use Only | The recommended dose of ORTHOCLONE OKT3 for the treatment of acute renal, steroid-resistant cardiac, or steroid-resistant hepatic allograft rejection is 5 mg per day in a single (bolus) Intravenous infusion in less than one minute for 10 to 14 days. | not given to patient which are hypersensitive to this or any other product of murine origin, have anti-mouse antibody titers ≥1:1000; are in (uncompensated) heart failure or in fluid overload, as evidenced by chest X-ray or a greater than 3 percent weight gain within the week prior to planned ORTHOCLONE OKT3 administration; have uncontrolled hypertension; have a history of seizures, or are predisposed to seizures. | RTHOCLONE OKT3 therapy includes adverse effects: Dyspnea(21%), nausea(19%), vomiting (19%), chest pain (14%), diarrhea (14%), tremor (13%), wheezing (13%), headache (11%), tachycardia (10%), rigor (8%), and hypertension (8%), Angina, Cardiac Arrest, Fluctuation in Blood Pressure, Heart Failure, Myocardial Infarction, Shock, Thrombosis, Coma, Encephalopathy, Epilepsy, Hypotonia, Gastrointestinal Hemorrhage, Coagulation Disorder, Lymphadenopathy, Lymphopenia, Anuria, Oliguria, Apnea, Pneumonitis, Conjunctivitis, Hearing Decreases. | Link | NA | NA |
| 10401 | Th1064 | Muromonab | >Th1064_Muromonab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146189.7 | C6460H9946N1720O2043S56 | 8.31 | -0.513 | 71 | 0.8 hours (mammalian reticulocytes, in vitro) | Murine monoclonal antibody specific to CD3 T-cell lymphocyte antigens. More specifically it is a purified murine (mouse) monoclonal antibody, directed against the CD3 (T3) receptor on the surface of human T-cells (T-lymphocytes) cultured using the murine ascites method. Muromonab is 93% monomeric immune globulin G type 2a (IgG2a). | For treatment of organ transplant recipients, prevention of organ rejection | Used in organ transplant prophylaxis, Muromonab or OKT-3 binds specifically to the CD-3 complex, which is involved in antigen recognition and cell stimulation, on the surface of T lymphocytes. Immediately after administration CD-3-positive T lymphocytes are abruptly removed from circulation. It has been effective in reversing corticosteroid-resistant acute rejection in renal, liver, and cardiac transplant recipients. | Muromonab binds to the T-cell surface glycoprotein CD3 epsilon chain. It appears to kill CD-3 positive cells by inducing Fc mediated apoptosis, antibody mediated cytotoxicity and complement-dependent cytotoxicity. | NA | Most likely removed by opsonization via the reticuloendothelial system. | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antineoplastic and Immunomodulating Agents, Blood Proteins, CD3 Blocker Immunosuppressant, CD3 Receptor Antagonists, CD3-directed Antibody Interactions, Decreased Immunologic Activity, Globulins, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Proteins, Selective Immunosuppressants, Serum Globulins | NA | NA | NA | Rilonacept results in increased immunosuppressive effects; increases the risk of infection | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10402 | Th1064 | Muromonab | >Th1064_Muromonab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146189.7 | C6460H9946N1720O2043S56 | 8.31 | -0.513 | 71 | 0.8 hours (mammalian reticulocytes, in vitro) | Murine monoclonal antibody specific to CD3 T-cell lymphocyte antigens. More specifically it is a purified murine (mouse) monoclonal antibody, directed against the CD3 (T3) receptor on the surface of human T-cells (T-lymphocytes) cultured using the murine ascites method. Muromonab is 93% monomeric immune globulin G type 2a (IgG2a). | For treatment of organ transplant recipients, prevention of organ rejection | Used in organ transplant prophylaxis, Muromonab or OKT-3 binds specifically to the CD-3 complex, which is involved in antigen recognition and cell stimulation, on the surface of T lymphocytes. Immediately after administration CD-3-positive T lymphocytes are abruptly removed from circulation. It has been effective in reversing corticosteroid-resistant acute rejection in renal, liver, and cardiac transplant recipients. | Muromonab binds to the T-cell surface glycoprotein CD3 epsilon chain. It appears to kill CD-3 positive cells by inducing Fc mediated apoptosis, antibody mediated cytotoxicity and complement-dependent cytotoxicity. | NA | Most likely removed by opsonization via the reticuloendothelial system. | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antineoplastic and Immunomodulating Agents, Blood Proteins, CD3 Blocker Immunosuppressant, CD3 Receptor Antagonists, CD3-directed Antibody Interactions, Decreased Immunologic Activity, Globulins, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Proteins, Selective Immunosuppressants, Serum Globulins | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10412 | Th1068 | Tositumomab | >Th1068_Tositumomab QAYLQQSGAELVRPGASVKMSCKASGYTFTSYNMHWVKQTPRQGLEWIGAIYPGNGDTSYNQKFKGKATLTVDKSSSTAYMQLSSLTSEDSAVYFCARVVYYSNSYWYFDVWGTGTTVTVSGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143859.7 | C6416H9874N1688O1987S44 | 8.68 | -0.4144 | 71 | 0.8 hours (mammalian reticulocytes, in vitro) | Murine IgG2a lambda monoclonal antibody against CD20 antigen (2 heavy chains of 451 residues, 2 lambda chains of 220 residues). It is produced in an antibiotic-free culture of mammalian cells. It can be covalently linked to Iodine 131 (a radioactive isotope of iodine). | For treatment of non-Hodgkin's lymphoma (CD20 positive, follicular) | Tositumomab binds to the CD20 antigen, which is predominantly expressed on mature B cells and on >90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. | Binds to the CD20 antigen which is found on mature B lymphocytes. The antibody binding appears to induce apoptosis, complement-dependent cytotoxicity and cell death through ionizing radiation. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to B lymphocytes, or by human antimurine antibody production | NA | NA | 68.2 mg/hr [patients with NHL] | Amino Acids, Peptides, and Proteins, Antibodies, Antigens, CD20, Antineoplastic Agents, Blood Proteins, CD20-directed Antibody Interactions, CD20-directed Radiotherapeutic Antibody, Drugs that are Mainly Renally Excreted, Globulins, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Iodine (131I) Compounds, Myelosuppressive Agents, Proteins, Radioimmunotherapy, Radiopharmaceutical Activity, Serum Globulins, Therapeutic Radiopharmaceutical | NA | NA | NA | Natalizumab with immunosuppressant, Tositumomab, may increase the adverse effects. Increased risk of Progressive Multifocal Leukoencephalopathy (PML) and other infections. Concurrent therapy should be avoided | B-lymphocyte antigen CD20,Low affinity immunoglobulin gamma Fc region receptor II-b | Bexxar | Galaxo Smith Kline | Galaxo Smith Kline | The BEXXAR therapeutic regimen (Tositumomab and Iodine I 131 Tositumomab) is indicated for the treatment of patients with CD20 antigen-expressing relapsed or refractory, low grade, follicular, or transformed non-Hodgkin's lymphoma, including patients with Rituximab-refractory non-Hodgkin’s lymphoma. Determination of the effectiveness of the BEXXAR therapeutic regimen is based on overall response rates in patients whose disease is refractory to chemotherapy alone or to chemotherapy and Rituximab. The effects of the BEXXAR therapeutic regimen on survival are not known. | NA | The formulation contains 100 mg/mL maltose, 8.5 mg/mL sodium chloride, 1 mg/mL phosphate, 1 mg/mL potassium hydroxide, and Water for Injection, USP. The pH is approximately 7.2. | Tositumomab is supplied as a Sterile, pyrogen-free, clear to opalescent, colorless to slightly yellow, preservative-free solution | Intravenous (Intravenous) administration | The BEXXAR therapeutic regimen consists of 2 separate components (tositumomab and iodine I 131 tositumomab) administered in 2 separate steps (dosimetric dose and therapeutic dose) separated by 7 to 14 days.Tositumomab 450 mg by Intravenous infusion.I-131 tositumomab (5 mCi I-131 and 35 mg protein) by Intravenous infusion | The BEXXAR therapeutic regimen is contraindicated in patients with known hypersensitivity to murine proteins or any other component of the BEXXAR therapeutic regimen. | Serious Allergic Reactions, Including Anaphylaxis, Prolonged and Severe Cytopenias, Secondary malignancies, Hypothyroidism, neutropenia, thrombocytopenia, anemia, infections (including pneumonia, bacteremia, septicemia, bronchitis, and skin infections), infusion reactions, asthenia, fever, and nausea. | Link | NA | NA |
| 10413 | Th1068 | Tositumomab | >Th1068_Tositumomab QAYLQQSGAELVRPGASVKMSCKASGYTFTSYNMHWVKQTPRQGLEWIGAIYPGNGDTSYNQKFKGKATLTVDKSSSTAYMQLSSLTSEDSAVYFCARVVYYSNSYWYFDVWGTGTTVTVSGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143859.7 | C6416H9874N1688O1987S44 | 8.68 | -0.4144 | 71 | 0.8 hours (mammalian reticulocytes, in vitro) | Murine IgG2a lambda monoclonal antibody against CD20 antigen (2 heavy chains of 451 residues, 2 lambda chains of 220 residues). It is produced in an antibiotic-free culture of mammalian cells. It can be covalently linked to Iodine 131 (a radioactive isotope of iodine). | For treatment of non-Hodgkin's lymphoma (CD20 positive, follicular) | Tositumomab binds to the CD20 antigen, which is predominantly expressed on mature B cells and on >90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. | Binds to the CD20 antigen which is found on mature B lymphocytes. The antibody binding appears to induce apoptosis, complement-dependent cytotoxicity and cell death through ionizing radiation. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to B lymphocytes, or by human antimurine antibody production | NA | NA | 68.2 mg/hr [patients with NHL] | Amino Acids, Peptides, and Proteins, Antibodies, Antigens, CD20, Antineoplastic Agents, Blood Proteins, CD20-directed Antibody Interactions, CD20-directed Radiotherapeutic Antibody, Drugs that are Mainly Renally Excreted, Globulins, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Iodine (131I) Compounds, Myelosuppressive Agents, Proteins, Radioimmunotherapy, Radiopharmaceutical Activity, Serum Globulins, Therapeutic Radiopharmaceutical | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10414 | Th1068 | Tositumomab | >Th1068_Tositumomab QAYLQQSGAELVRPGASVKMSCKASGYTFTSYNMHWVKQTPRQGLEWIGAIYPGNGDTSYNQKFKGKATLTVDKSSSTAYMQLSSLTSEDSAVYFCARVVYYSNSYWYFDVWGTGTTVTVSGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143859.7 | C6416H9874N1688O1987S44 | 8.68 | -0.4144 | 71 | 0.8 hours (mammalian reticulocytes, in vitro) | Murine IgG2a lambda monoclonal antibody against CD20 antigen (2 heavy chains of 451 residues, 2 lambda chains of 220 residues). It is produced in an antibiotic-free culture of mammalian cells. It can be covalently linked to Iodine 131 (a radioactive isotope of iodine). | For treatment of non-Hodgkin's lymphoma (CD20 positive, follicular) | Tositumomab binds to the CD20 antigen, which is predominantly expressed on mature B cells and on >90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. | Binds to the CD20 antigen which is found on mature B lymphocytes. The antibody binding appears to induce apoptosis, complement-dependent cytotoxicity and cell death through ionizing radiation. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to B lymphocytes, or by human antimurine antibody production | NA | NA | 68.2 mg/hr [patients with NHL] | Amino Acids, Peptides, and Proteins, Antibodies, Antigens, CD20, Antineoplastic Agents, Blood Proteins, CD20-directed Antibody Interactions, CD20-directed Radiotherapeutic Antibody, Drugs that are Mainly Renally Excreted, Globulins, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Iodine (131I) Compounds, Myelosuppressive Agents, Proteins, Radioimmunotherapy, Radiopharmaceutical Activity, Serum Globulins, Therapeutic Radiopharmaceutical | NA | NA | NA | NA | Bacterial outer membrane,Lipoteichoic acid synthesis | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10431 | Th1073 | Alemtuzumab | >Th1073_Alemtuzumab QVQLQESGPGLVRPSQTLSLTCTVSGFTFTDFYMNWVRQPPGRGLEWIGFIRDKAKGYTTEYNPSVKGRVTMLVDTSKNQFSLRLSSVTAADTAVYYCAREGHTAAPFDYWGQGSLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145453.8 | C6468H10066N1732O2005S40 | 8.76 | -0.431 | 61 (FAB f | 288 hrs | Humanized monoclonal antibody specific to lymphocyte antigens. It is a recombinant DNA-derived humanized monoclonal antibody (Campath-1H) that is directed against the 21-28 kD cell surface glycoprotein,CD52. The Campath-1H antibody is an IgG1 kappa with human variable framework and constant regions, and complementarity-determining regions from a murine (rat) monoclonal antibody (Campath-1G). Campath is produced in mammalian cell (Chinese hamster ovary) suspension culture in a medium containing neomycin. | Alemtuzumab (Campath) is a monoclonal antibody therapy used for treatment of B-cell chronic lymphocytic leukemia. | Campath is used to treat leukemia by exploiting antibody mediated lysis of CD52 presenting cells. The CD52 antigen is a cell surface protein found on essentially all B and T lymphocytes, a majority of monocytes, macrophages and most granulocytes. The CD52 antigen is not present on erythrocytes or hematopoetic stem cells. In leukemia there is an excess of B and T cells, so Campath permits selective reduction of lymphocyte populations. | Campath binds to the CD52 antigen present on most B and T lymphocytes. This binding leads to antibody-dependent lysis of leukemic cells. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to B or T lymphocytes | NA | 0.18 L/kg | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,CD52-directed Antibody Interactions,CD52-directed Cytolytic Antibody,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Myelosuppressive Agents,Narrow Therapeutic Index Drugs,Proteins,Selective Immunosuppressants,Serum Globulins | CA1339198 | 5-Aug-1997 | 5-Aug-2014 | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | CAMPATH-1 antigen,Low affinity immunoglobulin gamma Fc region receptor III-B,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 | CAMPATH | Genzyme Corporation | Genzyme Corporation | Campath is a CD52-directed cytolytic antibody indicated as a single agent for the treatment of B-cell chronic lymphocytic leukemia (B-CLL) | NA | Each single use vial of Campath contains 30 mg alemtuzumab, 8.0 mg sodium chloride, 1.44 mg dibasic sodium phosphate, 0.2 mg potassium chloride, 0.2 mg monobasic potassium phosphate, 0.1 mg polysorbate 80, and 0.0187 mg disodium edetate dihydrate. No preservatives are added. | Campath is a sterile, clear, colorless, isotonic solution (pH 6.8-7.4) for injection. | Intravenous infusion | Administer as an IV infusion over 2 hours, Escalate to recommended dose of 30 mg/day three times per week for 12 weeks, Premedicate with oral antihistamine and acetaminophen prior to dosing | None | Most common adverse reactions (>=10%): cytopenias, infusion reactions, cytomegalovirus (CMV) and other infections, nausea, emesis, diarrhea, and insomnia. | Link | NA | NA |
| 10432 | Th1073 | Alemtuzumab | >Th1073_Alemtuzumab QVQLQESGPGLVRPSQTLSLTCTVSGFTFTDFYMNWVRQPPGRGLEWIGFIRDKAKGYTTEYNPSVKGRVTMLVDTSKNQFSLRLSSVTAADTAVYYCAREGHTAAPFDYWGQGSLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145453.8 | C6468H10066N1732O2005S40 | 8.76 | -0.431 | 62 (FAB f | 289 hrs | Humanized monoclonal antibody specific to lymphocyte antigens. It is a recombinant DNA-derived humanized monoclonal antibody (Campath-1H) that is directed against the 21-28 kD cell surface glycoprotein,CD52. The Campath-1H antibody is an IgG1 kappa with human variable framework and constant regions, and complementarity-determining regions from a murine (rat) monoclonal antibody (Campath-1G). Campath is produced in mammalian cell (Chinese hamster ovary) suspension culture in a medium containing neomycin. | Alemtuzumab (Campath) is a monoclonal antibody therapy used for treatment of B-cell chronic lymphocytic leukemia. | Campath is used to treat leukemia by exploiting antibody mediated lysis of CD52 presenting cells. The CD52 antigen is a cell surface protein found on essentially all B and T lymphocytes, a majority of monocytes, macrophages and most granulocytes. The CD52 antigen is not present on erythrocytes or hematopoetic stem cells. In leukemia there is an excess of B and T cells, so Campath permits selective reduction of lymphocyte populations. | Campath binds to the CD52 antigen present on most B and T lymphocytes. This binding leads to antibody-dependent lysis of leukemic cells. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to B or T lymphocytes | NA | 0.18 L/kg | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,CD52-directed Antibody Interactions,CD52-directed Cytolytic Antibody,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Myelosuppressive Agents,Narrow Therapeutic Index Drugs,Proteins,Selective Immunosuppressants,Serum Globulins | NA | NA | NA | NA | CAMPATH-1 antigen,Low affinity immunoglobulin gamma Fc region receptor III-B,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 | LEMTRADA | Sanofi Genzyme, a Division of Sanofi Aventis Canada Inc | Sanofi Genzyme, a Division of Sanofi Aventis Canada Inc | LEMTRADA is a CD52-directed cytolytic monoclonal antibody indicated for the treatment of patients with relapsing forms of multiple sclerosis (MS). Because of its safety profile, the use of LEMTRADA should generally be reserved for patients who have had an inadequate response to two or more drugs indicated for the treatment of MS. | NA | Each 1 mL of solution contains alemtuzumab 10 mg, dibasic sodium phosphate (1.15 mg), disodium edetate dihydrate (0.0187 mg), polysorbate 80 (0.1 mg), potassium chloride (0.2 mg), potassium dihydrogen phosphate (0.2 mg), sodium chloride (8 mg), and water for injection. | LEMTRADA is a sterile, clear and colorless to slightly yellow, solution (pH 7.2±0.2) for infusion. | Intravenous infusion | Administer LEMTRADA by Intravenous infusion over 4 hours for 2 treatment courses. First course: 12 mg/day on 5 consecutive days. Second course: 12 mg/day on 3 consecutive days 12 months after first treatment course. | LEMTRADA is contraindicated in patients who are infected with Human Immunodeficiency Virus (HIV) because LEMTRADA causes prolonged reductions of CD4+ lymphocyte counts. | Most common adverse reactions (incidence >= 10% and > interferon beta-1a): rash, headache, pyrexia, nasopharyngitis, nausea, urinary tract infection, fatigue, insomnia, upper respiratory tract infection, herpes viral infection, urticaria, pruritus, thyroid gland disorders, fungal infection, arthralgia, pain in extremity, back pain, diarrhea, sinusitis, oropharyngeal pain, paresthesia, dizziness, abdominal pain, flushing, and vomiting. | Link | NA | NA |
| 10433 | Th1073 | Alemtuzumab | >Th1073_Alemtuzumab QVQLQESGPGLVRPSQTLSLTCTVSGFTFTDFYMNWVRQPPGRGLEWIGFIRDKAKGYTTEYNPSVKGRVTMLVDTSKNQFSLRLSSVTAADTAVYYCAREGHTAAPFDYWGQGSLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145453.8 | C6468H10066N1732O2005S40 | 8.76 | -0.431 | 62 (FAB f | 289 hrs | Humanized monoclonal antibody specific to lymphocyte antigens. It is a recombinant DNA-derived humanized monoclonal antibody (Campath-1H) that is directed against the 21-28 kD cell surface glycoprotein,CD52. The Campath-1H antibody is an IgG1 kappa with human variable framework and constant regions, and complementarity-determining regions from a murine (rat) monoclonal antibody (Campath-1G). Campath is produced in mammalian cell (Chinese hamster ovary) suspension culture in a medium containing neomycin. | Alemtuzumab (Campath) is a monoclonal antibody therapy used for treatment of B-cell chronic lymphocytic leukemia. | Campath is used to treat leukemia by exploiting antibody mediated lysis of CD52 presenting cells. The CD52 antigen is a cell surface protein found on essentially all B and T lymphocytes, a majority of monocytes, macrophages and most granulocytes. The CD52 antigen is not present on erythrocytes or hematopoetic stem cells. In leukemia there is an excess of B and T cells, so Campath permits selective reduction of lymphocyte populations. | Campath binds to the CD52 antigen present on most B and T lymphocytes. This binding leads to antibody-dependent lysis of leukemic cells. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to B or T lymphocytes | NA | 0.18 L/kg | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,CD52-directed Antibody Interactions,CD52-directed Cytolytic Antibody,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Myelosuppressive Agents,Narrow Therapeutic Index Drugs,Proteins,Selective Immunosuppressants,Serum Globulins | NA | NA | NA | NA | CAMPATH-1 antigen,Low affinity immunoglobulin gamma Fc region receptor III-B,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 | Mabcampath | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10443 | Th1078 | Efalizumab | >Th1078_Efalizumab EVQLVESGGGLVQPGGSLRLSCAASGYSFTGHWMNWVRQAPGKGLEWVGIMIHPSDSETRYNQKFKDIRFTISVDKSKNTLYLQMNSLRAEDTAVYYCARIGIYFYGTTYFDYIWGQGTLVTVSS | 150000 | NA | NA | NA | 61 (FAB f | 5 days | Efalizumab is Humanized IgG1 kappa isotype monoclonal antibody that binds to human CD11a. It is produced in a Chinese hamster ovary mammalian cell expression system in a nutrient medium containing the antibiotic gentamicin. | Indcated in treatment of adult patients with moderate to severe chronic plaque psoriasis, who are candidates for phototherapy or systemic therapy. | In psoriatic skin, ICAM-1 cell surface expression is upregulated on endothelium and keratinocytes. Raptiva inhibits the binding of LFA-1 to the intercellular adhesion molecule-1 (ICAM-1), thereby inhibiting the adhesion of leukocytes to other cell types. | Efalizumab binds to CD11a, a subunit of leukocyte function antigen-1 (LFA-1), which is expressed on all leukocytes. As a result efalizumab decreases cell surface expression of CD11a. | NA | NA | Average efalizumab bioavailability following subcutaneous administration was estimated at 30 to 50%. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antigens, CD11,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,CD11a-directed Antibody Interactions,CD11a-directed Humanized IgG1 Antibody,Cell Migration Inhibition,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Proteins,Selective Immunosuppressants,Serum Globulins | NA | NA | NA | Ergonovine is the antiretroviral agent may increase the ergot derivative | Integrin alpha-L,Integrin alpha-X | RAPTIVA | Genentech, Inc. | Genentech, Inc. | RAPTIVA (efalizumab) is indicated for the treatment of adult patients (18 years or older) with chronic moderate to severe plaque psoriasis who are candidates for systemic therapy or phototherapy. | NA | Each single-use vial of RAPTIVA contains 150 mg of efalizumab, 123.2 mg of sucrose, 6.8 mg of L-histidine hydrochloride monohydrate, 4.3 mg of L-histidine and 3 mg of polysorbate 20 and is designed to deliver 125 mg of efalizumab in 1.25 mL. | RAPTIVA (efalizumab) is supplied as a sterile, white to off-white, lyophilized powder in single-use glass vials | Subcutaneous (Subcutaneous) Injection. | The recommended dose of RAPTIVA (efalizumab) is a single 0.7 mg/kg SCconditioning dose followed by weekly SC doses of 1 mg/kg (maximum single dose not to exceed a total of 200 mg). | RAPTIVA (efalizumab) should not be administered to patients with known hypersensitivity to RAPTIVA (efalizumab) or any of its components. | he most serious adverse reactions observed during treatment with RAPTIVA (efalizumab) are serious infections, including PML, malignancies,thrombocytopenia, hemolytic anemia, arthritis events, psoriasis worsening and variants, and neurologic events. The most common adverse reactions associated with RAPTIVA (efalizumab) were a first dose reaction complex that included headache, chills, fever, nausea, and myalgia. | Link | NA | NA |
| 10444 | Th1078 | Efalizumab | >Th1078_Efalizumab EVQLVESGGGLVQPGGSLRLSCAASGYSFTGHWMNWVRQAPGKGLEWVGIMIHPSDSETRYNQKFKDIRFTISVDKSKNTLYLQMNSLRAEDTAVYYCARIGIYFYGTTYFDYIWGQGTLVTVSS | 150000 | NA | NA | NA | 61 (FAB f | 5 days | Efalizumab is Humanized IgG1 kappa isotype monoclonal antibody that binds to human CD11a. It is produced in a Chinese hamster ovary mammalian cell expression system in a nutrient medium containing the antibiotic gentamicin. | Indcated in treatment of adult patients with moderate to severe chronic plaque psoriasis, who are candidates for phototherapy or systemic therapy. | In psoriatic skin, ICAM-1 cell surface expression is upregulated on endothelium and keratinocytes. Raptiva inhibits the binding of LFA-1 to the intercellular adhesion molecule-1 (ICAM-1), thereby inhibiting the adhesion of leukocytes to other cell types. | Efalizumab binds to CD11a, a subunit of leukocyte function antigen-1 (LFA-1), which is expressed on all leukocytes. As a result efalizumab decreases cell surface expression of CD11a. | NA | NA | Average efalizumab bioavailability following subcutaneous administration was estimated at 30 to 50%. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antigens, CD11,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,CD11a-directed Antibody Interactions,CD11a-directed Humanized IgG1 Antibody,Cell Migration Inhibition,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Proteins,Selective Immunosuppressants,Serum Globulins | NA | NA | NA | Rilonacept results in increased immunosuppressive effects; increases the risk of infection. | Integrin alpha-L,Integrin alpha-X | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10445 | Th1078 | Efalizumab | >Th1078_Efalizumab EVQLVESGGGLVQPGGSLRLSCAASGYSFTGHWMNWVRQAPGKGLEWVGIMIHPSDSETRYNQKFKDIRFTISVDKSKNTLYLQMNSLRAEDTAVYYCARIGIYFYGTTYFDYIWGQGTLVTVSS | 150000 | NA | NA | NA | 61 (FAB f | 5 days | Efalizumab is Humanized IgG1 kappa isotype monoclonal antibody that binds to human CD11a. It is produced in a Chinese hamster ovary mammalian cell expression system in a nutrient medium containing the antibiotic gentamicin. | Indcated in treatment of adult patients with moderate to severe chronic plaque psoriasis, who are candidates for phototherapy or systemic therapy. | In psoriatic skin, ICAM-1 cell surface expression is upregulated on endothelium and keratinocytes. Raptiva inhibits the binding of LFA-1 to the intercellular adhesion molecule-1 (ICAM-1), thereby inhibiting the adhesion of leukocytes to other cell types. | Efalizumab binds to CD11a, a subunit of leukocyte function antigen-1 (LFA-1), which is expressed on all leukocytes. As a result efalizumab decreases cell surface expression of CD11a. | NA | NA | Average efalizumab bioavailability following subcutaneous administration was estimated at 30 to 50%. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antigens, CD11,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,CD11a-directed Antibody Interactions,CD11a-directed Humanized IgG1 Antibody,Cell Migration Inhibition,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Proteins,Selective Immunosuppressants,Serum Globulins | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | Integrin alpha-L,Integrin alpha-X | 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 |
| 10482 | Th1090 | Daclizumab | >Th1090_Daclizumab QVQLVQSGAEVKKPGSSVKVSCKASGYTFTSYRMHWVRQAPGQGLEWIGYINPSTGYTEYNQKFKDKATITADESTNTAYMELSSLRSEDTAVYYCARGGGVFDYWGQGTTLTVSSGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 142612.1 | C6332H9808N1678O1989S42 | 8.46 | -0.437 | 61 (FAB fr | 11-38 days | Humanized, recombinant, monoclonal antibody (IgG1k) directed agaisnt the epitope in the A antigenic site of the F protein of respiratory syncytial virus (RSV). Synagis is a composite of human (95%) and murine (5%) antibody sequences. The human heavy chain sequence is derived from the constant domains of human IgG1 and the variable framework regions of the VH genes Cor (1) and Cess (2). The human light chain sequence is derived from the constant domain of Ck and the variable framework regions of the VL gene K104 withJk-4. Palivizumab is expressed from a stable murine myeloma cell line (NS0). Palivizumab is composed of to heavy chains (50.6 kDa each) and two light chains (27.6 kDa each), contains 1-2% carbohydrate by weight and has a molecular weight of 147.7 kDa ± 1 kDa (MALDI-TOF). | Zenapax is a humanized monoclonal antibody used for prevention of renal transplant rejection | Zenapax functions as an IL-2 receptor antagonist. Specifically it inhibits IL-2-mediated activation of lymphocytes, a critical pathway in the cellular immune response involved in allograft rejection. | Zenepax binds with high-affinity to the Tac subunit of the high-affinity IL-2 receptor complex and inhibits IL-2 binding. The IL-2 receptor (Tac) subunit is expressed on activated but not resting lymphocytes. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to lymphocytes. | NA | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Globulins,Immunoglobulins,Immunologic Factors,Immunomodulatory Agents,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Interleukin 2 Receptor-directed Antibody Interactions,Interleukin Inhibitors,Interleukin-2 Receptor Antagonist,Interleukin-2 Receptor Blocking Antibody,Proteins,Serum Globulins | NA | NA | NA | NA | Interleukin-2 receptor subunit alpha,Interleukin-2 receptor subunit beta,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,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 | Zenapax | Roche | Roche | is indicated for the prophylaxis of acute organ rejection in patients receiving renal transplants. It is used as part of an immunosuppressive regimen that includes cyclosporine and corticosteroids. The efficacy of ZENAPAX (daclizumab) for the prophylaxis of acute rejection in recipients of other solid organ allografts has not been demonstrated. | NA | Each milliliter of ZENAPAX contains 5 mg of daclizumab and 3.6 mg sodium phosphate monobasic monohydrate, 11 mg sodium phosphate dibasic heptahydrate, 4.6 mg sodium chloride, 0.2 mg polysorbate 80, and may contain hydrochloric acid or sodium hydroxide to adjust the pH to 6.9. No preservatives are added. | Clear, sterile, colorless concentrate for further dilution and intravenous administration | Intravenous | ZENAPAX (daclizumab) is used as part of an immunosuppressive regimen that includes cyclosporine and corticosteroids. The recommended dose for ZENAPAX (daclizumab) in adult and pediatric patients is 1.0 mg/kg. The calculated volume of ZENAPAX (daclizumab) should be mixed with 50 mL of sterile 0.9% sodium chloride solution and administered via a peripheral or central vein over a 15-minute period. | NA | NA | Link | NA | NA |
| 10483 | Th1090 | Daclizumab | >Th1090_Daclizumab QVQLVQSGAEVKKPGSSVKVSCKASGYTFTSYRMHWVRQAPGQGLEWIGYINPSTGYTEYNQKFKDKATITADESTNTAYMELSSLRSEDTAVYYCARGGGVFDYWGQGTTLTVSSGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 142612.1 | C6332H9808N1678O1989S43 | 8.46 | -0.437 | 62 (FAB fr | 11-38 days | Humanized, recombinant, monoclonal antibody (IgG1k) directed agaisnt the epitope in the A antigenic site of the F protein of respiratory syncytial virus (RSV). Synagis is a composite of human (95%) and murine (5%) antibody sequences. The human heavy chain sequence is derived from the constant domains of human IgG1 and the variable framework regions of the VH genes Cor (1) and Cess (2). The human light chain sequence is derived from the constant domain of Ck and the variable framework regions of the VL gene K104 withJk-4. Palivizumab is expressed from a stable murine myeloma cell line (NS0). Palivizumab is composed of to heavy chains (50.6 kDa each) and two light chains (27.6 kDa each), contains 1-2% carbohydrate by weight and has a molecular weight of 147.7 kDa ± 1 kDa (MALDI-TOF). | Zenapax is a humanized monoclonal antibody used for prevention of renal transplant rejection | Zenapax functions as an IL-2 receptor antagonist. Specifically it inhibits IL-2-mediated activation of lymphocytes, a critical pathway in the cellular immune response involved in allograft rejection. | Zenepax binds with high-affinity to the Tac subunit of the high-affinity IL-2 receptor complex and inhibits IL-2 binding. The IL-2 receptor (Tac) subunit is expressed on activated but not resting lymphocytes. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to lymphocytes. | NA | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Globulins,Immunoglobulins,Immunologic Factors,Immunomodulatory Agents,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Interleukin 2 Receptor-directed Antibody Interactions,Interleukin Inhibitors,Interleukin-2 Receptor Antagonist,Interleukin-2 Receptor Blocking Antibody,Proteins,Serum Globulins | NA | NA | NA | NA | Interleukin-2 receptor subunit alpha,Interleukin-2 receptor subunit beta,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,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 | Zinbryta | 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 |
| 10558 | Th1110 | Thymalfasin | >Th1110_Thymalfasin SDAAVDTSSEITTKDLKEKKEVVEEAEN | 3108.276 | C129H215N33O55 | NA | NA | NA | Approx. 2 hrs | Chemically synthesized version identicle to human acetylated polypeptide , thymosin alpha 1. It is now approved in 35 developing countries for the treatment of Hepatitis B and C and in boosting immunity against other diseases. | Indicated as an adjuvant for influenza vaccine in elderly patients and as an adjuvant for both influenza and hepatitis B vaccines in chronic hemodialysis patients who failed to achieve adequate antibody titers from previous immunization. | Thymalfasin is a 28-amino acid polypeptide produced synthetically but originally isolated from thymosin fraction 5, a bovine thymus extract containing a number of immunologically active peptides. In vitro studies have shown that Thymalfasin can influence T-cell production and maturation, stimulate production of Th1 cytokines such as interferon-gamma and interleukin-2, and activate natural killer cell-mediated cytotoxicity. | The mechanism of action of thymalfasin is not completely understood but is thought to be related to its immunomodulating activities, centered primarily around augmentation of T-cell function. In various in vitro assays, thymosin alpha 1 has been shown to promote T-cell differentiation and maturation; for example, CD4+, CD8+, and CD3+ cells have all been shown to be increased. Thymosin alpha 1 has also been shown to increase production of IFN-g, IL-2, IL-3, and expression of IL-2 receptor following activation by mitogens or antigens, increase NK cell activity, increase production of migratory inhibitory factor (MIF), and increase antibody response to T-cell dependent antigens. Thymosin alpha 1 has also been shown to antagonize dexamethasone-induced apoptosis of thymocytes in vitro. In vivo administration of thymosin alpha 1 to animals immunosuppressed by chemotherapy, tumor burden, or irradiation showed that thymosin alpha 1 protects against cytotoxic damage to bone marrow, tumor progression and opportunistic infections, thereby increasing survival time and number of survivors. Many of the in vitro and in vivo effects of thymosin alpha 1 have been interpreted as influences on either differentiation of pluripotent stem cells to thymocytes or activation of thymocytes into activated T-cells. Thymalfasin also has been shown in vitro to upregulate expression of toll like receptors (TLR) including TLR2 and TLR9 in mouse and human dendritic cells, as well as activate NF-kB and JNK/P38/AP1 pathways. Thymalfasin's activation of dendritic cells provides another possible pathway explaining thymalfasin's immunomodulatory and antiviral effects. | There are no reported instances of deliberate or accidental overdosage in humans. Animal toxicology studies have shown no adverse reactions in single doses up to 20 mg/kg and in repeated doses up to 6 mg/kg/day for 13 weeks, which were the highest doses studied. The highest single dose tested in animals represents 800-times the clinical dose. | NA | Rapidly absorbed with peak serum levels achieved at approximately 2 hours. | NA | NA | Adjuvants, Immunologic,Amino Acids, Peptides, and Proteins,Antineoplastic Agents,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunologic Factors,Peptide Hormones,Peptides,Proteins,Thymus Hormones | NA | NA | NA | NA | NA | Zadaxin | SciClone Pharmaceuticals (SCLN) | SciClone Pharmaceuticals (SCLN) | ZADAXIN thymosin alpha 1 (thymalfasin) is indicated as a monotherapy or combination therapy with interferon for the treatment of chronic hepatitis B. | NA | lyophilized preparation contains 1.6 mg thymosin alpha 1, 50 mg mannitol, and sodium phosphate buffer to adjust the pH to 6.8 | N. A. | Subcutaneous | The recommend-ed dose of ZADAXIN (thymalfasin) for chronic hepatitis B when used as a monotherapy or in combination with interferon (at the labeled dose and schedule for interferon) is 1.6 mg (900 µg/m2) administered subcutaneously twice a week for 6 to 12 months. Patients weighing less than 40 kg should receive a ZADAXIN (thymalfasin) dose of 40 µg/kg. | ZADAXIN (thymalfasin) is contraindicated in patients with a history of hypersensitivity to thymosin alpha 1 or any component of the injection. Because ZADAXIN (thymalfasin) therapy appears to work by enhancing the immune system, it should be considered contraindicated in patients who are being deliberately immunosuppressed, such as organ transplant patients, unless the potential benefits of the therapy clearly outweigh the potential risks. | Adverse experiences have been infrequent and mild, consisting primarily of local discomfort at the injection site, and rare instances of erythema, transient muscle atrophy, polyarthralgia combined with hand edema, and rash. | Link | NA | NA |
| 10576 | Th1117 | Ipilimumab | >Th1117_Ipilimumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSSYTMHWVRQAPGKGLEWVTFISYDGNNKYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAIYYCARTGWLGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | C6572H10126N1734O2080S40 | 6.1-8.5 | NA | 80-90 ºC | 14.7 days | Recombinant, human monoclonal IgG1 kappa immunoglobin. It is an antineoplastic agent developed by Bristol-Myers Squibb and Medarex for the treatment of unresectable or metastatic melanoma in adults. Ipilimumab received FDA approval on March 25, 2011. | Ipilimumab is indicated for the treatment of unresectable or metastatic melanoma in adults. | The pharmacodynamics of Ipilimumab are not completely understood. In melanoma patients receiving Ipilimumab, the mean peripheral blood absolute lymphocyte counts (ALC) increased throughout the induction dosing period. This increase occurred in a dose-dependent fashion in Phase 2 studies. Ipilimumab given with or without gp100 at 3 mg/kg increased ALC throughout the induction dosing period, but no meaningful change in ALC occurred in the control group who received an investigational peptide vaccine alone. Furthermore, ipilimumab binds to CTLA-4 with high affinity (Kd = 5.24 ± 3.62 nM). As a result, ligands CD80 and CD86 are blocked from binding to CTLA-4 with a minimum EC50 value of 0.2 μg/mL. | Ipilimumab is a fully human IgG1K antibody that binds to CTLA-4 (cytotoxic T lymphocyte-associated antigen 4), a molecule on T-cells that is indicated for unresectable or metastatic melanoma. The absence or presence of CTLA-4 can augment or suppress the immune system's T-cell response in fighting disease. Ipilimumab is designed to block the activity of CTLA-4, thereby sustaining an active immune response in its attack on cancer cells. The proposed mechanism of action is indirect, and may be through T-cell - mediated anti-tumor immune responses. | Data regarding ipilumumab overdose is not readily available.[L12126] However, the most common adverse reactions to ipilumumab are fatigue, diarrhea, pruritus, rash, and colitis.[L12126] | The metabolism of ipilimumab does not involve the cytochrome P450 enzyme system.[L12126,L12642] Because ipilimumab is a protein, it is expected to be degraded into small peptides and amino acids by proteolytic enzymes.[A35122] | Cmax was 65.8µg/mL for 2-6 year olds, 70.1µg/mL for 6-<12 year olds, and 73.3µg/mL in patients 12 years and older.[L12126] Data regarding the AUC and Tmax of ipilumumab are not readily available.[A35118,L12126] | The volume of distribution at steady-state of ipilimumab is 7.21L.[A35118] | Ipilimumab has a clearance of 15.3 mL/hr.[A35118] Systemic clearance increases proportionally with body weight.[L12642] | Antineoplastic Agents and Monoclonal antibodies | CA2381770 | 8-Jul-2007 | 8-Aug-2020 | NA | Cytotoxic T-lymphocyte protein 4 | YERVOY | Bristol-Myers Squibb | Bristol-Myers Squibb | YERVOY is a human cytotoxic T-lymphocyte antigen 4 (CTLA-4)-blocking antibody indicated for the treatment of unresectable or metastatic melanoma | NA | It is supplied in single-use vials of 50 mg/10 mL and 200 mg/40 mL. Each milliliter contains 5 mg of ipilimumab and the following inactive ingredients: diethylene triamine pentaacetic acid (DTPA) (0.04 mg), mannitol (10 mg), polysorbate 80 (vegetable origin) (0.1 mg), sodium chloride (5.85 mg), tris hydrochloride (3.15 mg), and Water for Injection, USP at a pH of 7. | Sterile, preservative-free, clear to slightly opalescent, colorless to pale-yellow solution | Intravenous | The recommended dose of YERVOY is 3 mg/kg administered intravenously over 90 minutes every 3 weeks for a total of 4 doses. | Immune-mediated adverse reactions: Permanently discontinue for severe reactions. Less than 7.5 mg prednisone or equivalent per day is administered or systemic high-dose corticosteroids are adminstered for severe, persistent, or recurring immune-mediated reactions. | Most common adverse reactions are fatigue, diarrhea, pruritus, rash, and colitis. | Link | NA | NA |
| 10590 | Th1122 | Rilonacept | >Th1122_Rilonacept SERCDDWGLDTMRQIQVFEDEPARIKCPLFEHFLKFNYSTAHSAGLTLIWYWTRQDRDLEEPINFRLPENRISKEKDVLWFRPTLLNDTGNYTCMLRNTTYCSKVAFPLEVVQKDSCFNSPMKLPVHKLYIEYGIQRITCPNVDGYFPSSVKPTITWYMGCYKIQNFNNVIPEGMNLSFLIALISNNGNYTCVVTYPENGRTFHLTRTLTVKVVGSPKNAVPPVIHSPNDHVVYEKEPGEELLIPCTVYFSFLMDSRNEVWWTIDGKKPDDITIDVTINESISHSRTEDETRTQILSIKKVTSEDLKRSYVCHARSAKGEVAKAAKVKQKVPAPRYTVEKCKEREEKIILVSSANEIDVRPCPLNPNEHKGTITWYKDDSKTPVSTEQASRIHQHKEKLWFVPAKVEDSGHYYCVVRNSSYCLRIKISAKFVENEPNLCYNAQAIFKQKLPVAGDGGLVCPYMEFFKNENNELPKLQWYKDCKPLLLDNIHFSGVKDRLIVMNVAEKHRGNYTCHASYTYLGKQYPITRVIEFITLEENKPTRPVIVSPANETMEVDLGSQIQLICNVTGQLSDIAYWKWNGSVIDEDDPVLGEDYYSVENPANKRRSTLITVLNISEIESRFYKHPFTCFAKNTHGIDAAYIQLIYPVTNSGDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 251000 | C9030H13932N2400O2670S74 | NA | NA | NA | 8.6 days | Dimeric fusion protein consisting of portions of IL-1R and the IL-1R accessory protein, linked to the Fc portion of immunoglobulin G1. It inhibits interleukin 1 and is used in the treatment of cryopyrin-associated periodic syndromes (CAPS), in adults and children overr than 12 of ageold. | Rilonacept is currently used in the treatment of cryopyrin-associated periodic syndrome. In May 2012, an advisory panel for the FDA voted 11-0 against the use of Rilonacept for the treatment of gout. | Treatment with Rilonacept resulted in decreased levels of mean C-Reactive Protein (CRP) and Serum Amyloid A (SAA). Higher levels of CRP and SAA are associated with inflammatory disease activity found in patients with Cryopyrin-Associated Periodic Syndromes. | CAPS refer to rare genetic syndromes generally caused by mutations in the NLRP-3 [Nucleotide-binding domain, leucine rich family (NLR), pyrin domain containing 3] gene (also known as Cold-Induced Auto-inflammatory Syndtrome-1 [CIAS1]). CAPS disorders are inherited in an autosomal dominant pattern with male and female offspring equally affected. Fever, urticaria-like rash, arthralgia, myalgia, fatigue, and conjunctivitis are features common to all disorders. In most cases, inflammation in CAPS is associated with mutations in the NLRP-3 gene which encodes the protein cryopyrin, an important component of the inflammasome. Cryopyrin regulates the protease caspase-1 and controls the activation of interleukin-1 beta (IL-1β). Mutations in NLRP-3 result in an overactive inflammasome resulting in excessive release of activated IL-1β that drives inflammation. Rilonacept blocks IL-1β signaling by acting as a soluble decoy receptor that binds IL-1β and prevents its interaction with cell surface receptors. Rilonacept also binds IL-1α and IL-1 receptor antagonist (IL-1ra) with reduced affinity. By binding IL-1, rilonacept prevents the activation of IL-1 receptors, thus reducing inflammatory responses and other effects related to an excess of IL-1. | NA | NA | NA | NA | NA | Agents reducing cytokine levels,Amino Acids, Peptides, and Proteins,Anti-Inflammatory Agents,Antineoplastic and Immunomodulating Agents,Immunosuppressive Agents,Immunotherapy,Interleukin Inhibitors,Interleukin-1 Receptor Accessory Protein,Proteins,Receptors, Interleukin-1 Type I,Recombinant Proteins | US5844099 | 12-Jan-1998 | 1-Jan-2020 | NA | Interleukin-1 beta,Interleukin-1 alpha,Interleukin-1 receptor antagonist protein | Arcalyst | Regeneron Pharmaceuticals | Regeneron Pharmaceuticals | ARCALYST (rilonacept) is an interleukin-1 blocker indicated for the treatment of Cryopyrin-Associated Periodic Syndromes (CAPS), including Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS) in adults and children 12 and older. | NA | Each vial of ARCALYST (rilonacept) is to be reconstituted with 2.3 mL of Sterile Water for Injection. A volume of up to 2 mL can be withdrawn, which is designed to deliver 160 mg for subcutaneous administration only. The resulting solution is viscous, clear, colorless to pale yellow, and essentially free from particulates. Each vial contains 220 mg rilonacept (80 mg/ 1mL after reconstitution), histidine, arginine, polyethylene glycol 3350, sucrose, and glycine at a pH of 6.5±0.3. No preservatives are present | Sterile, white to off-white, lyophilized powder | Subcutaneous | Adult patients 18 years and older: Treatment should be initiated with a loading dose of 320 mg delivered as two, 2 mL, subcutaneous injections of 160 mgeach given on the same day at two different sites. Dosing should be continued with a once-weekly injection of 160 mg administered as a single, 2-mL, subcutaneous injection. ARCALYST (rilonacept) should not be given more often than once weekly. Dosage modification is not required based on advanced age or gender. Paediatric patients aged 12 to 17 years: Treatment should be initiated with a loading dose of 4.4mg/kg, up to amaximum of 320 mg, delivered as one or two subcutaneous injections with a maximum single-injection volume of 2mL.Dosing should be continued with a once-weekly injection of 2.2 mg/kg, up to a maximum of 160 mg, administered as a single subcutaneous injection, up to 2 mL. If the initial dose is given as two injections, they should be given on the same day at two different sites. ARCALYST (rilonacept) should not be given more often than once weekly. | Certain type of bulging blood vessel (aneurysm), have a heart attack or blood clot in the lung and you also have had recent brain or spinal injury. | Six serious adverse reactions These serious adverse reactions were Mycobacterium intracellular infection; gastrointestinal bleeding and colitis; sinusitis and bronchitis; and Streptococcus pneumoniae meningitis. | Link | NA | NA |
| 10591 | Th1122 | Rilonacept | >Th1122_Rilonacept SERCDDWGLDTMRQIQVFEDEPARIKCPLFEHFLKFNYSTAHSAGLTLIWYWTRQDRDLEEPINFRLPENRISKEKDVLWFRPTLLNDTGNYTCMLRNTTYCSKVAFPLEVVQKDSCFNSPMKLPVHKLYIEYGIQRITCPNVDGYFPSSVKPTITWYMGCYKIQNFNNVIPEGMNLSFLIALISNNGNYTCVVTYPENGRTFHLTRTLTVKVVGSPKNAVPPVIHSPNDHVVYEKEPGEELLIPCTVYFSFLMDSRNEVWWTIDGKKPDDITIDVTINESISHSRTEDETRTQILSIKKVTSEDLKRSYVCHARSAKGEVAKAAKVKQKVPAPRYTVEKCKEREEKIILVSSANEIDVRPCPLNPNEHKGTITWYKDDSKTPVSTEQASRIHQHKEKLWFVPAKVEDSGHYYCVVRNSSYCLRIKISAKFVENEPNLCYNAQAIFKQKLPVAGDGGLVCPYMEFFKNENNELPKLQWYKDCKPLLLDNIHFSGVKDRLIVMNVAEKHRGNYTCHASYTYLGKQYPITRVIEFITLEENKPTRPVIVSPANETMEVDLGSQIQLICNVTGQLSDIAYWKWNGSVIDEDDPVLGEDYYSVENPANKRRSTLITVLNISEIESRFYKHPFTCFAKNTHGIDAAYIQLIYPVTNSGDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 251000 | C9030H13932N2400O2670S74 | NA | NA | NA | 8.6 days | Dimeric fusion protein consisting of portions of IL-1R and the IL-1R accessory protein, linked to the Fc portion of immunoglobulin G1. It inhibits interleukin 1 and is used in the treatment of cryopyrin-associated periodic syndromes (CAPS), in adults and children overr than 12 of ageold. | Rilonacept is currently used in the treatment of cryopyrin-associated periodic syndrome. In May 2012, an advisory panel for the FDA voted 11-0 against the use of Rilonacept for the treatment of gout. | Treatment with Rilonacept resulted in decreased levels of mean C-Reactive Protein (CRP) and Serum Amyloid A (SAA). Higher levels of CRP and SAA are associated with inflammatory disease activity found in patients with Cryopyrin-Associated Periodic Syndromes. | CAPS refer to rare genetic syndromes generally caused by mutations in the NLRP-3 [Nucleotide-binding domain, leucine rich family (NLR), pyrin domain containing 3] gene (also known as Cold-Induced Auto-inflammatory Syndtrome-1 [CIAS1]). CAPS disorders are inherited in an autosomal dominant pattern with male and female offspring equally affected. Fever, urticaria-like rash, arthralgia, myalgia, fatigue, and conjunctivitis are features common to all disorders. In most cases, inflammation in CAPS is associated with mutations in the NLRP-3 gene which encodes the protein cryopyrin, an important component of the inflammasome. Cryopyrin regulates the protease caspase-1 and controls the activation of interleukin-1 beta (IL-1β). Mutations in NLRP-3 result in an overactive inflammasome resulting in excessive release of activated IL-1β that drives inflammation. Rilonacept blocks IL-1β signaling by acting as a soluble decoy receptor that binds IL-1β and prevents its interaction with cell surface receptors. Rilonacept also binds IL-1α and IL-1 receptor antagonist (IL-1ra) with reduced affinity. By binding IL-1, rilonacept prevents the activation of IL-1 receptors, thus reducing inflammatory responses and other effects related to an excess of IL-1. | NA | NA | NA | NA | NA | Agents reducing cytokine levels,Amino Acids, Peptides, and Proteins,Anti-Inflammatory Agents,Antineoplastic and Immunomodulating Agents,Immunosuppressive Agents,Immunotherapy,Interleukin Inhibitors,Interleukin-1 Receptor Accessory Protein,Proteins,Receptors, Interleukin-1 Type I,Recombinant Proteins | US8114394 | 14-02-2012 | 1-Jan-2020 | NA | Interleukin-1 beta,Interleukin-1 alpha,Interleukin-1 receptor antagonist protein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10592 | Th1122 | Rilonacept | >Th1122_Rilonacept SERCDDWGLDTMRQIQVFEDEPARIKCPLFEHFLKFNYSTAHSAGLTLIWYWTRQDRDLEEPINFRLPENRISKEKDVLWFRPTLLNDTGNYTCMLRNTTYCSKVAFPLEVVQKDSCFNSPMKLPVHKLYIEYGIQRITCPNVDGYFPSSVKPTITWYMGCYKIQNFNNVIPEGMNLSFLIALISNNGNYTCVVTYPENGRTFHLTRTLTVKVVGSPKNAVPPVIHSPNDHVVYEKEPGEELLIPCTVYFSFLMDSRNEVWWTIDGKKPDDITIDVTINESISHSRTEDETRTQILSIKKVTSEDLKRSYVCHARSAKGEVAKAAKVKQKVPAPRYTVEKCKEREEKIILVSSANEIDVRPCPLNPNEHKGTITWYKDDSKTPVSTEQASRIHQHKEKLWFVPAKVEDSGHYYCVVRNSSYCLRIKISAKFVENEPNLCYNAQAIFKQKLPVAGDGGLVCPYMEFFKNENNELPKLQWYKDCKPLLLDNIHFSGVKDRLIVMNVAEKHRGNYTCHASYTYLGKQYPITRVIEFITLEENKPTRPVIVSPANETMEVDLGSQIQLICNVTGQLSDIAYWKWNGSVIDEDDPVLGEDYYSVENPANKRRSTLITVLNISEIESRFYKHPFTCFAKNTHGIDAAYIQLIYPVTNSGDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 251000 | C9030H13932N2400O2670S74 | NA | NA | NA | 8.6 days | Dimeric fusion protein consisting of portions of IL-1R and the IL-1R accessory protein, linked to the Fc portion of immunoglobulin G1. It inhibits interleukin 1 and is used in the treatment of cryopyrin-associated periodic syndromes (CAPS), in adults and children overr than 12 of ageold. | Rilonacept is currently used in the treatment of cryopyrin-associated periodic syndrome. In May 2012, an advisory panel for the FDA voted 11-0 against the use of Rilonacept for the treatment of gout. | Treatment with Rilonacept resulted in decreased levels of mean C-Reactive Protein (CRP) and Serum Amyloid A (SAA). Higher levels of CRP and SAA are associated with inflammatory disease activity found in patients with Cryopyrin-Associated Periodic Syndromes. | CAPS refer to rare genetic syndromes generally caused by mutations in the NLRP-3 [Nucleotide-binding domain, leucine rich family (NLR), pyrin domain containing 3] gene (also known as Cold-Induced Auto-inflammatory Syndtrome-1 [CIAS1]). CAPS disorders are inherited in an autosomal dominant pattern with male and female offspring equally affected. Fever, urticaria-like rash, arthralgia, myalgia, fatigue, and conjunctivitis are features common to all disorders. In most cases, inflammation in CAPS is associated with mutations in the NLRP-3 gene which encodes the protein cryopyrin, an important component of the inflammasome. Cryopyrin regulates the protease caspase-1 and controls the activation of interleukin-1 beta (IL-1β). Mutations in NLRP-3 result in an overactive inflammasome resulting in excessive release of activated IL-1β that drives inflammation. Rilonacept blocks IL-1β signaling by acting as a soluble decoy receptor that binds IL-1β and prevents its interaction with cell surface receptors. Rilonacept also binds IL-1α and IL-1 receptor antagonist (IL-1ra) with reduced affinity. By binding IL-1, rilonacept prevents the activation of IL-1 receptors, thus reducing inflammatory responses and other effects related to an excess of IL-1. | NA | NA | NA | NA | NA | Agents reducing cytokine levels,Amino Acids, Peptides, and Proteins,Anti-Inflammatory Agents,Antineoplastic and Immunomodulating Agents,Immunosuppressive Agents,Immunotherapy,Interleukin Inhibitors,Interleukin-1 Receptor Accessory Protein,Proteins,Receptors, Interleukin-1 Type I,Recombinant Proteins | US8080248 | 20-12-2011 | 1-Jan-2020 | NA | Interleukin-1 beta,Interleukin-1 alpha,Interleukin-1 receptor antagonist protein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10593 | Th1122 | Rilonacept | >Th1122_Rilonacept SERCDDWGLDTMRQIQVFEDEPARIKCPLFEHFLKFNYSTAHSAGLTLIWYWTRQDRDLEEPINFRLPENRISKEKDVLWFRPTLLNDTGNYTCMLRNTTYCSKVAFPLEVVQKDSCFNSPMKLPVHKLYIEYGIQRITCPNVDGYFPSSVKPTITWYMGCYKIQNFNNVIPEGMNLSFLIALISNNGNYTCVVTYPENGRTFHLTRTLTVKVVGSPKNAVPPVIHSPNDHVVYEKEPGEELLIPCTVYFSFLMDSRNEVWWTIDGKKPDDITIDVTINESISHSRTEDETRTQILSIKKVTSEDLKRSYVCHARSAKGEVAKAAKVKQKVPAPRYTVEKCKEREEKIILVSSANEIDVRPCPLNPNEHKGTITWYKDDSKTPVSTEQASRIHQHKEKLWFVPAKVEDSGHYYCVVRNSSYCLRIKISAKFVENEPNLCYNAQAIFKQKLPVAGDGGLVCPYMEFFKNENNELPKLQWYKDCKPLLLDNIHFSGVKDRLIVMNVAEKHRGNYTCHASYTYLGKQYPITRVIEFITLEENKPTRPVIVSPANETMEVDLGSQIQLICNVTGQLSDIAYWKWNGSVIDEDDPVLGEDYYSVENPANKRRSTLITVLNISEIESRFYKHPFTCFAKNTHGIDAAYIQLIYPVTNSGDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 251000 | C9030H13932N2400O2670S74 | NA | NA | NA | 8.6 days | Dimeric fusion protein consisting of portions of IL-1R and the IL-1R accessory protein, linked to the Fc portion of immunoglobulin G1. It inhibits interleukin 1 and is used in the treatment of cryopyrin-associated periodic syndromes (CAPS), in adults and children overr than 12 of ageold. | Rilonacept is currently used in the treatment of cryopyrin-associated periodic syndrome. In May 2012, an advisory panel for the FDA voted 11-0 against the use of Rilonacept for the treatment of gout. | Treatment with Rilonacept resulted in decreased levels of mean C-Reactive Protein (CRP) and Serum Amyloid A (SAA). Higher levels of CRP and SAA are associated with inflammatory disease activity found in patients with Cryopyrin-Associated Periodic Syndromes. | CAPS refer to rare genetic syndromes generally caused by mutations in the NLRP-3 [Nucleotide-binding domain, leucine rich family (NLR), pyrin domain containing 3] gene (also known as Cold-Induced Auto-inflammatory Syndtrome-1 [CIAS1]). CAPS disorders are inherited in an autosomal dominant pattern with male and female offspring equally affected. Fever, urticaria-like rash, arthralgia, myalgia, fatigue, and conjunctivitis are features common to all disorders. In most cases, inflammation in CAPS is associated with mutations in the NLRP-3 gene which encodes the protein cryopyrin, an important component of the inflammasome. Cryopyrin regulates the protease caspase-1 and controls the activation of interleukin-1 beta (IL-1β). Mutations in NLRP-3 result in an overactive inflammasome resulting in excessive release of activated IL-1β that drives inflammation. Rilonacept blocks IL-1β signaling by acting as a soluble decoy receptor that binds IL-1β and prevents its interaction with cell surface receptors. Rilonacept also binds IL-1α and IL-1 receptor antagonist (IL-1ra) with reduced affinity. By binding IL-1, rilonacept prevents the activation of IL-1 receptors, thus reducing inflammatory responses and other effects related to an excess of IL-1. | NA | NA | NA | NA | NA | Agents reducing cytokine levels,Amino Acids, Peptides, and Proteins,Anti-Inflammatory Agents,Antineoplastic and Immunomodulating Agents,Immunosuppressive Agents,Immunotherapy,Interleukin Inhibitors,Interleukin-1 Receptor Accessory Protein,Proteins,Receptors, Interleukin-1 Type I,Recombinant Proteins | NA | NA | NA | NA | Interleukin-1 beta,Interleukin-1 alpha,Interleukin-1 receptor antagonist protein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10594 | Th1122 | Rilonacept | >Th1122_Rilonacept SERCDDWGLDTMRQIQVFEDEPARIKCPLFEHFLKFNYSTAHSAGLTLIWYWTRQDRDLEEPINFRLPENRISKEKDVLWFRPTLLNDTGNYTCMLRNTTYCSKVAFPLEVVQKDSCFNSPMKLPVHKLYIEYGIQRITCPNVDGYFPSSVKPTITWYMGCYKIQNFNNVIPEGMNLSFLIALISNNGNYTCVVTYPENGRTFHLTRTLTVKVVGSPKNAVPPVIHSPNDHVVYEKEPGEELLIPCTVYFSFLMDSRNEVWWTIDGKKPDDITIDVTINESISHSRTEDETRTQILSIKKVTSEDLKRSYVCHARSAKGEVAKAAKVKQKVPAPRYTVEKCKEREEKIILVSSANEIDVRPCPLNPNEHKGTITWYKDDSKTPVSTEQASRIHQHKEKLWFVPAKVEDSGHYYCVVRNSSYCLRIKISAKFVENEPNLCYNAQAIFKQKLPVAGDGGLVCPYMEFFKNENNELPKLQWYKDCKPLLLDNIHFSGVKDRLIVMNVAEKHRGNYTCHASYTYLGKQYPITRVIEFITLEENKPTRPVIVSPANETMEVDLGSQIQLICNVTGQLSDIAYWKWNGSVIDEDDPVLGEDYYSVENPANKRRSTLITVLNISEIESRFYKHPFTCFAKNTHGIDAAYIQLIYPVTNSGDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 251000 | C9030H13932N2400O2670S74 | NA | NA | NA | 8.6 days | Dimeric fusion protein consisting of portions of IL-1R and the IL-1R accessory protein, linked to the Fc portion of immunoglobulin G1. It inhibits interleukin 1 and is used in the treatment of cryopyrin-associated periodic syndromes (CAPS), in adults and children overr than 12 of ageold. | Rilonacept is currently used in the treatment of cryopyrin-associated periodic syndrome. In May 2012, an advisory panel for the FDA voted 11-0 against the use of Rilonacept for the treatment of gout. | Treatment with Rilonacept resulted in decreased levels of mean C-Reactive Protein (CRP) and Serum Amyloid A (SAA). Higher levels of CRP and SAA are associated with inflammatory disease activity found in patients with Cryopyrin-Associated Periodic Syndromes. | CAPS refer to rare genetic syndromes generally caused by mutations in the NLRP-3 [Nucleotide-binding domain, leucine rich family (NLR), pyrin domain containing 3] gene (also known as Cold-Induced Auto-inflammatory Syndtrome-1 [CIAS1]). CAPS disorders are inherited in an autosomal dominant pattern with male and female offspring equally affected. Fever, urticaria-like rash, arthralgia, myalgia, fatigue, and conjunctivitis are features common to all disorders. In most cases, inflammation in CAPS is associated with mutations in the NLRP-3 gene which encodes the protein cryopyrin, an important component of the inflammasome. Cryopyrin regulates the protease caspase-1 and controls the activation of interleukin-1 beta (IL-1β). Mutations in NLRP-3 result in an overactive inflammasome resulting in excessive release of activated IL-1β that drives inflammation. Rilonacept blocks IL-1β signaling by acting as a soluble decoy receptor that binds IL-1β and prevents its interaction with cell surface receptors. Rilonacept also binds IL-1α and IL-1 receptor antagonist (IL-1ra) with reduced affinity. By binding IL-1, rilonacept prevents the activation of IL-1 receptors, thus reducing inflammatory responses and other effects related to an excess of IL-1. | NA | NA | NA | NA | NA | Agents reducing cytokine levels,Amino Acids, Peptides, and Proteins,Anti-Inflammatory Agents,Antineoplastic and Immunomodulating Agents,Immunosuppressive Agents,Immunotherapy,Interleukin Inhibitors,Interleukin-1 Receptor Accessory Protein,Proteins,Receptors, Interleukin-1 Type I,Recombinant Proteins | NA | NA | NA | NA | Interleukin-1 beta,Interleukin-1 alpha,Interleukin-1 receptor antagonist protein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10595 | Th1122 | Rilonacept | >Th1122_Rilonacept SERCDDWGLDTMRQIQVFEDEPARIKCPLFEHFLKFNYSTAHSAGLTLIWYWTRQDRDLEEPINFRLPENRISKEKDVLWFRPTLLNDTGNYTCMLRNTTYCSKVAFPLEVVQKDSCFNSPMKLPVHKLYIEYGIQRITCPNVDGYFPSSVKPTITWYMGCYKIQNFNNVIPEGMNLSFLIALISNNGNYTCVVTYPENGRTFHLTRTLTVKVVGSPKNAVPPVIHSPNDHVVYEKEPGEELLIPCTVYFSFLMDSRNEVWWTIDGKKPDDITIDVTINESISHSRTEDETRTQILSIKKVTSEDLKRSYVCHARSAKGEVAKAAKVKQKVPAPRYTVEKCKEREEKIILVSSANEIDVRPCPLNPNEHKGTITWYKDDSKTPVSTEQASRIHQHKEKLWFVPAKVEDSGHYYCVVRNSSYCLRIKISAKFVENEPNLCYNAQAIFKQKLPVAGDGGLVCPYMEFFKNENNELPKLQWYKDCKPLLLDNIHFSGVKDRLIVMNVAEKHRGNYTCHASYTYLGKQYPITRVIEFITLEENKPTRPVIVSPANETMEVDLGSQIQLICNVTGQLSDIAYWKWNGSVIDEDDPVLGEDYYSVENPANKRRSTLITVLNISEIESRFYKHPFTCFAKNTHGIDAAYIQLIYPVTNSGDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 251000 | C9030H13932N2400O2670S74 | NA | NA | NA | 8.6 days | Dimeric fusion protein consisting of portions of IL-1R and the IL-1R accessory protein, linked to the Fc portion of immunoglobulin G1. It inhibits interleukin 1 and is used in the treatment of cryopyrin-associated periodic syndromes (CAPS), in adults and children overr than 12 of ageold. | Rilonacept is currently used in the treatment of cryopyrin-associated periodic syndrome. In May 2012, an advisory panel for the FDA voted 11-0 against the use of Rilonacept for the treatment of gout. | Treatment with Rilonacept resulted in decreased levels of mean C-Reactive Protein (CRP) and Serum Amyloid A (SAA). Higher levels of CRP and SAA are associated with inflammatory disease activity found in patients with Cryopyrin-Associated Periodic Syndromes. | CAPS refer to rare genetic syndromes generally caused by mutations in the NLRP-3 [Nucleotide-binding domain, leucine rich family (NLR), pyrin domain containing 3] gene (also known as Cold-Induced Auto-inflammatory Syndtrome-1 [CIAS1]). CAPS disorders are inherited in an autosomal dominant pattern with male and female offspring equally affected. Fever, urticaria-like rash, arthralgia, myalgia, fatigue, and conjunctivitis are features common to all disorders. In most cases, inflammation in CAPS is associated with mutations in the NLRP-3 gene which encodes the protein cryopyrin, an important component of the inflammasome. Cryopyrin regulates the protease caspase-1 and controls the activation of interleukin-1 beta (IL-1β). Mutations in NLRP-3 result in an overactive inflammasome resulting in excessive release of activated IL-1β that drives inflammation. Rilonacept blocks IL-1β signaling by acting as a soluble decoy receptor that binds IL-1β and prevents its interaction with cell surface receptors. Rilonacept also binds IL-1α and IL-1 receptor antagonist (IL-1ra) with reduced affinity. By binding IL-1, rilonacept prevents the activation of IL-1 receptors, thus reducing inflammatory responses and other effects related to an excess of IL-1. | NA | NA | NA | NA | NA | Agents reducing cytokine levels,Amino Acids, Peptides, and Proteins,Anti-Inflammatory Agents,Antineoplastic and Immunomodulating Agents,Immunosuppressive Agents,Immunotherapy,Interleukin Inhibitors,Interleukin-1 Receptor Accessory Protein,Proteins,Receptors, Interleukin-1 Type I,Recombinant Proteins | NA | NA | NA | NA | Interleukin-1 beta,Interleukin-1 alpha,Interleukin-1 receptor antagonist protein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10596 | Th1122 | Rilonacept | >Th1122_Rilonacept SERCDDWGLDTMRQIQVFEDEPARIKCPLFEHFLKFNYSTAHSAGLTLIWYWTRQDRDLEEPINFRLPENRISKEKDVLWFRPTLLNDTGNYTCMLRNTTYCSKVAFPLEVVQKDSCFNSPMKLPVHKLYIEYGIQRITCPNVDGYFPSSVKPTITWYMGCYKIQNFNNVIPEGMNLSFLIALISNNGNYTCVVTYPENGRTFHLTRTLTVKVVGSPKNAVPPVIHSPNDHVVYEKEPGEELLIPCTVYFSFLMDSRNEVWWTIDGKKPDDITIDVTINESISHSRTEDETRTQILSIKKVTSEDLKRSYVCHARSAKGEVAKAAKVKQKVPAPRYTVEKCKEREEKIILVSSANEIDVRPCPLNPNEHKGTITWYKDDSKTPVSTEQASRIHQHKEKLWFVPAKVEDSGHYYCVVRNSSYCLRIKISAKFVENEPNLCYNAQAIFKQKLPVAGDGGLVCPYMEFFKNENNELPKLQWYKDCKPLLLDNIHFSGVKDRLIVMNVAEKHRGNYTCHASYTYLGKQYPITRVIEFITLEENKPTRPVIVSPANETMEVDLGSQIQLICNVTGQLSDIAYWKWNGSVIDEDDPVLGEDYYSVENPANKRRSTLITVLNISEIESRFYKHPFTCFAKNTHGIDAAYIQLIYPVTNSGDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 251000 | C9030H13932N2400O2670S74 | NA | NA | NA | 8.6 days | Dimeric fusion protein consisting of portions of IL-1R and the IL-1R accessory protein, linked to the Fc portion of immunoglobulin G1. It inhibits interleukin 1 and is used in the treatment of cryopyrin-associated periodic syndromes (CAPS), in adults and children overr than 12 of ageold. | Rilonacept is currently used in the treatment of cryopyrin-associated periodic syndrome. In May 2012, an advisory panel for the FDA voted 11-0 against the use of Rilonacept for the treatment of gout. | Treatment with Rilonacept resulted in decreased levels of mean C-Reactive Protein (CRP) and Serum Amyloid A (SAA). Higher levels of CRP and SAA are associated with inflammatory disease activity found in patients with Cryopyrin-Associated Periodic Syndromes. | CAPS refer to rare genetic syndromes generally caused by mutations in the NLRP-3 [Nucleotide-binding domain, leucine rich family (NLR), pyrin domain containing 3] gene (also known as Cold-Induced Auto-inflammatory Syndtrome-1 [CIAS1]). CAPS disorders are inherited in an autosomal dominant pattern with male and female offspring equally affected. Fever, urticaria-like rash, arthralgia, myalgia, fatigue, and conjunctivitis are features common to all disorders. In most cases, inflammation in CAPS is associated with mutations in the NLRP-3 gene which encodes the protein cryopyrin, an important component of the inflammasome. Cryopyrin regulates the protease caspase-1 and controls the activation of interleukin-1 beta (IL-1β). Mutations in NLRP-3 result in an overactive inflammasome resulting in excessive release of activated IL-1β that drives inflammation. Rilonacept blocks IL-1β signaling by acting as a soluble decoy receptor that binds IL-1β and prevents its interaction with cell surface receptors. Rilonacept also binds IL-1α and IL-1 receptor antagonist (IL-1ra) with reduced affinity. By binding IL-1, rilonacept prevents the activation of IL-1 receptors, thus reducing inflammatory responses and other effects related to an excess of IL-1. | NA | NA | NA | NA | NA | Agents reducing cytokine levels,Amino Acids, Peptides, and Proteins,Anti-Inflammatory Agents,Antineoplastic and Immunomodulating Agents,Immunosuppressive Agents,Immunotherapy,Interleukin Inhibitors,Interleukin-1 Receptor Accessory Protein,Proteins,Receptors, Interleukin-1 Type I,Recombinant Proteins | NA | NA | NA | NA | Interleukin-1 beta,Interleukin-1 alpha,Interleukin-1 receptor antagonist protein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10597 | Th1122 | Rilonacept | >Th1122_Rilonacept SERCDDWGLDTMRQIQVFEDEPARIKCPLFEHFLKFNYSTAHSAGLTLIWYWTRQDRDLEEPINFRLPENRISKEKDVLWFRPTLLNDTGNYTCMLRNTTYCSKVAFPLEVVQKDSCFNSPMKLPVHKLYIEYGIQRITCPNVDGYFPSSVKPTITWYMGCYKIQNFNNVIPEGMNLSFLIALISNNGNYTCVVTYPENGRTFHLTRTLTVKVVGSPKNAVPPVIHSPNDHVVYEKEPGEELLIPCTVYFSFLMDSRNEVWWTIDGKKPDDITIDVTINESISHSRTEDETRTQILSIKKVTSEDLKRSYVCHARSAKGEVAKAAKVKQKVPAPRYTVEKCKEREEKIILVSSANEIDVRPCPLNPNEHKGTITWYKDDSKTPVSTEQASRIHQHKEKLWFVPAKVEDSGHYYCVVRNSSYCLRIKISAKFVENEPNLCYNAQAIFKQKLPVAGDGGLVCPYMEFFKNENNELPKLQWYKDCKPLLLDNIHFSGVKDRLIVMNVAEKHRGNYTCHASYTYLGKQYPITRVIEFITLEENKPTRPVIVSPANETMEVDLGSQIQLICNVTGQLSDIAYWKWNGSVIDEDDPVLGEDYYSVENPANKRRSTLITVLNISEIESRFYKHPFTCFAKNTHGIDAAYIQLIYPVTNSGDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 251000 | C9030H13932N2400O2670S74 | NA | NA | NA | 8.6 days | Dimeric fusion protein consisting of portions of IL-1R and the IL-1R accessory protein, linked to the Fc portion of immunoglobulin G1. It inhibits interleukin 1 and is used in the treatment of cryopyrin-associated periodic syndromes (CAPS), in adults and children overr than 12 of ageold. | Rilonacept is currently used in the treatment of cryopyrin-associated periodic syndrome. In May 2012, an advisory panel for the FDA voted 11-0 against the use of Rilonacept for the treatment of gout. | Treatment with Rilonacept resulted in decreased levels of mean C-Reactive Protein (CRP) and Serum Amyloid A (SAA). Higher levels of CRP and SAA are associated with inflammatory disease activity found in patients with Cryopyrin-Associated Periodic Syndromes. | CAPS refer to rare genetic syndromes generally caused by mutations in the NLRP-3 [Nucleotide-binding domain, leucine rich family (NLR), pyrin domain containing 3] gene (also known as Cold-Induced Auto-inflammatory Syndtrome-1 [CIAS1]). CAPS disorders are inherited in an autosomal dominant pattern with male and female offspring equally affected. Fever, urticaria-like rash, arthralgia, myalgia, fatigue, and conjunctivitis are features common to all disorders. In most cases, inflammation in CAPS is associated with mutations in the NLRP-3 gene which encodes the protein cryopyrin, an important component of the inflammasome. Cryopyrin regulates the protease caspase-1 and controls the activation of interleukin-1 beta (IL-1β). Mutations in NLRP-3 result in an overactive inflammasome resulting in excessive release of activated IL-1β that drives inflammation. Rilonacept blocks IL-1β signaling by acting as a soluble decoy receptor that binds IL-1β and prevents its interaction with cell surface receptors. Rilonacept also binds IL-1α and IL-1 receptor antagonist (IL-1ra) with reduced affinity. By binding IL-1, rilonacept prevents the activation of IL-1 receptors, thus reducing inflammatory responses and other effects related to an excess of IL-1. | NA | NA | NA | NA | NA | Agents reducing cytokine levels,Amino Acids, Peptides, and Proteins,Anti-Inflammatory Agents,Antineoplastic and Immunomodulating Agents,Immunosuppressive Agents,Immunotherapy,Interleukin Inhibitors,Interleukin-1 Receptor Accessory Protein,Proteins,Receptors, Interleukin-1 Type I,Recombinant Proteins | NA | NA | NA | NA | Interleukin-1 beta,Interleukin-1 alpha,Interleukin-1 receptor antagonist protein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 |
| 10649 | Th1134 | Asparaginase erwinia chrysanthemi | >Th1134_Asparaginase_erwinia_chrysanthemi ADKLPNIVILATGGTIAGSAATGTQTTGYKAGALGVDTLINAVPEVKKLANVKGEQFSNMASENMTGDVVLKLSQRVNELLARDDVDGVVITHGTDTVEESAYFLHLTVKSDKPVVFVAAMRPATAISADGPMNLLEAVRVAGDKQSRGRGVMVVLNDRIGSARYITKTNASTLDTFKANEEGYLGVIIGNRIYYQNRIDKLHTTRSVFDVRGLTSLPKVDILYGYQDDPEYLYDAAIQHGVKGIVYAGMGAGSVSVRGIAGMRKAMEKGVVVIRSTRTGNGIVPPDEELPGLVSDSLNPAHARILLMLALTRTSDPKVIQEYFHTY | 140000 | C1546H2510N432O476S9 | NA | NA | NA | 18.2 hours | Erwinaze (asparaginase from Erwiniachryanthemi) is an asparaginase specific enzyme derived from Erwiniachrysanthemi. L-asparaginase is a homo-tetramer with each subnuit having a molecular weight of about 35 kDa. It is an antineoplastic agent and was FDA approved in November 19, 2011. | Asparaginase Erwinia chryanthemi is for the treatment of patients with acute lymphoblastic leukemia (ALL) that have developed a hypersensitivity to Escherichia coli-derivied asparaginase. It is a component of a multi-agent chemotherpeutic regimen for the treatment of the aforementioned disease and is considered second- or third- line treatment in European and American protocols. | NA | Asparaginase Erwinia chrysanthemi catalyzes the deamidation of asparagine to aspartic acid and ammonia, resulting in a reduction in circulating levels of asparagine in the plasma. The mechanism of action of Erwinaze is thought to be based on the inability of leukemic cells to synthesize asparagine due to lack of asparagine synthetase activity, resulting in cytotoxicity specific for leukemic cells that depend on an exogenous source of the amino acid asparagine for their protein metabolism and survival. | There are no known cases of overdose with asparaginase _Erwinia chrysanthemi_.[L149] In clinical trials, the most common adverse effects were hypersensitivity reactions, pancreatic toxicity, blood clots, hemorrhage, and liver toxicity.[L34714] Pancreatitis occurs in 8-14% of pediatric patients, with adolescents at the highest risk for developing this adverse event. Pancreatitis typically occurs after the first few weeks of asparaginase administration, which suggests this complication occurs from an underlying predisposition rather than a cumulative drug effect.[A7464] | Metabolism of asparaginase _Erwinia chrysanthemi_ has not been fully characterized; however, it is suspected to be metabolized into small peptides by catabolic pathways.[L34719] | In patients two to 80 years of age, intramuscular administration of asparaginase _Erwinia chrysanthemi_ 25,000 International Units (IU)/m2 resulted in serum trough asparaginase concentrations = 0.1 IU/mL at either 48-hour (n=35) or 72-hour (n=13) post third dose. 80% of patients evaluted at 48 hours and 38% of patients evaluated at 72 hours had serum asparaginase activity levels > 0.4 IU/mL.[L149] For asparaginase _Erwinia chrysanthemi_ (recombinant)-rywn, the median tmax is 10 hours and the mean absolute bioavailability is 37% in healthy subjects.[L34719] | The volume of distribution of asparaginase _Erwinia chrysanthemi_ can be up to 5 L/m2.[L1448] The geometric mean (%CV) apparent volume of distribution of asparaginase _Erwinia chrysanthemi_ (recombinant)-rywn was 1.48 L/m2 (49%).[L34719] While asparaginases are not detectable in cerebrospinal fluid, asparagine in cerebrospinal fluid is depleted with systemic administration of any formulation of asparaginases.[L1448] | The geometric mean (%CV) apparent clearance of asparaginase _Erwinia chrysanthemi_ (recombinant)-rywn is 0.31 L/hour/m2 (36%).[L34719] | Amidohydrolases,Antineoplastic Agents,Asparaginase,Asparagine-specific Enzyme,Enzymes,Enzymes and Coenzymes,Hepatotoxic Agents,Hydrolases,Narrow Therapeutic Index Drugs,Thyroxine-binding globulin inhibitors | NA | NA | NA | NA | NA | Erwinaze | EUSA Pharma | EUSA Pharma | acute lymphoblastic leukemia | NA | Each vial contains 10,000 International Units of asparaginase Erwinia chrysanthemi, and the following inactive ingredients: glucose monohydrate (5.0 mg), sodium chloride (0.5 mg). | ERWINAZE is supplied as a Sterile, lyophilized, white powder in vials. | Intramuscular | 25,000 International Units/m² | Hypersensitivity reactions to ERWINAZE, including anaphylaxis., pancreatitis with prior L-asparaginase therapy, thrombosis with prior L-asparaginase therapy, hemorrhagic events with prior L-asparaginase therapy. | Hypersensitivity reactions, Pancreatitis, Glucose intolerance, Thrombosis and hemorrhage | Link | NA | NA |
| 10664 | Th1142 | Obinutuzumab | NA | 146100 | C6512H10060N1712O2020S44 | NA | NA | NA | 28.4 days | Humanized monoclonal antibody used along with chlorambucil for the treatment of chronic lymphocytic leukemia. It was approved by the FDA in November 2013 and is marketed under the brand name Gazyva. It carries a black box warning of fatal Hepatitis B Virus (HBV) reactivation and fatal Progressive Multifocal Leukoencephalopathy (PML). | Obinutuzumab is used as a combination treatment with chlorambucil to treat patients with untreated chronic lymphocytic leukemia. | Obinutuzumab is more potent than rituximab in depleting B-cells, antitumor activity, and tumor regression. | In contrast to rituximab, which is a classic type I CD20 antibody, obinutuzumab binds to type II CD20 antibodies. This allows obinutuzumab to have a much higher induction of antibody-dependant cytotoxicity and a higher direct cytotoxic effect than the classic CD20 antibodies. | The most serious toxicities observed with obinutuzumab are Hepatitis B virus (HBV) reactivation and progressive multifocal leukoencephalopathy (PML). HBV reactivation can occur with all anti-CD20 antibodies and can result in hepatic failure, fulminant hepatitis, and death. PML occurs as a result of JC virus infection and can be fatal as well. Other common but less serious adverse reactions include infusion reactions (pre-treat with glucocorticoids, acetaminophen, and anti-histamine to prevent this), neutropenia, thrombocytopenia, and Tumor Lysis Syndrome (TLS) (pre-treat patients, especially with a high lymphocyte count and/or a high tumor burden, with anti-hyperuricemics and hydration). It is also recommended to NOT administer live virus vaccinations prior to or during obinutuzumab treatment. | Obinutuzumab is not metabolized by the liver. | Obinutuzumab is administered intravenously, so its absorption is 100%. | Obinutuzumab has a volume of distribution of about 3.8 L. | The clearance of obinutuzumab is 0.09L/day. | Antineoplastic Agents | NA | NA | NA | NA | B-lymphocyte antigen CD20 | Gazyva | Genentech | Genentech | chronic lymphocytic leukemia (CLL) | NA | GAZYVA is supplied at a concentration of 25 mg/mL in 1000 mg single use vials. The product is formulated in 20 mM L-histidine/L-histidine hydrochloride, 240 mM trehalose, 0.02% poloxamer 188. The pH is 6.0. | GAZYVA is produced by mammalian cell (CHO) suspension culture. GAZYVA is a sterile, clear, colorless to slightly brown, preservative free liquid concentrate for intravenousadministration. | Intravenous infusion | Each dose of GAZYVA is 1000 mg, administered intravenously, with the exception of the first infusions in cycle 1, which are administered on day 1 (100 mg) and day 2 (900 mg). | NA | Hepatitis B reactivation, Progressive multifocal leukoencephalopathy, Infusion reactions, Tumor lysis syndrome, Infections, Neutropenia, Thrombocytopenia. | Link | NA | NA |
| 10672 | Th1147 | Natalizumab | NA | NA | NA | NA | NA | 61 (FAB fr | 11 ± 4 days | Humanized IgG4k monoclonal antibody produced in murine myeloma cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to a4-integrin. Natalizumab was voluntarily withdrawn from U.S. market because of risk of Progressive multifocal leukoencephalopathy (PML). It was returned to market July, 2006. | For treatment of multiple sclerosis. | In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells, and their counter-receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be a secondary result of its blockade of the molecular interaction of a 4b 1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. α4-integrin is required for white blood cells to move into organs, therefore, natalizumab prevents these immune cells from crossing blood vessel walls to reach affected organs thereby decreasing inflamation. | Binds to the α4-subunit of α4b 1 and α4b 7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the α4-mediated adhesion of leukocytes to their counter-receptor(s). | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to leukocytes. | NA | 5.7 ± 1.9 L [Multiple Sclerosis (MS) Patients, 5.2 ± 2.8 L [Crohn's Disease (CD) Patients] | * 16 +/- 5 mL/hour [patients with MS who did not have PML receiving the repeat IV administration of a 300 mg dose] * 22 +/- 22 mL/hour [Patients with Crohn's Disease receiving the repeat IV administration of a 300 mg dose] | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic and Immunomodulating Agents,Blood Proteins,Globulins,Immunoglobulins,Immunologic Factors,Immunomodulatory Agents,Immunoproteins,Immunosuppressive Agents,Integrin Receptor Antagonist,Proteins,Selective Immunosuppressants,Serum Globulins | NA | NA | NA | NA | Integrin alpha-4,Low affinity immunoglobulin gamma Fc region receptor III-B,Intercellular adhesion molecule 1,High affinity immunoglobulin gamma Fc receptor I | Tysabri | Biogen Idec Inc. | Biogen Idec Inc. | It is indicated as monotherapy for the treatment of patients with relapsing forms of multiple sclerosis. Tysabri increases the risk of PML. It is indicated for inducing and maintaining clinical response and remission in adult patients with moderately to severely active Crohn's disease with evidence of inflammation who have had an inadequate response to, or are unable to tolerate, conventional CD therapies and inhibitors of TNF-α. | NA | Each 15 mL dose contains 300 mg natalizumab; 123 mg sodium chloride, USP; 17.0 mg sodium phosphate, monobasic, monohydrate, USP; 7.24 mg sodium phosphate, dibasic, heptahydrate, USP; 3.0 mg polysorbate 80, USP/NF, in water for injection, USP at pH 6.1. | Sterile, colorless, and clear to slightly opalescent concentrate | Intravenous infusion | The recommended dose of Tysabri for multiple sclerosis is 300 mg intravenous infusion over one hour every four weeks. The recommended dose of TysabriI for Crohn's disease is 300 mg intravenous infusion over one hour every four weeks. Tysabri should not be used with concomitant immunosuppressants (e.g., 6-mercaptopurine, azathioprine, cyclosporine, or methotrexate) or concomitant inhibitors of TNF-α. Aminosalicylates may be continued during treatment with Tysabri. | Tysabri is contraindicated in patients who have or have hadprogressive multifocal leukoencephalopathy (PML). It should not be administered to a patient who has had a hypersensitivity reaction to Tysabri. Observed reactions range from urticaria to anaphylaxis | Progressive Multifocal Leukoencephalopathy (PML), Hypersensitivity, Immunosuppression/Infections | Link | NA | NA |
| 10673 | Th1147 | Natalizumab | NA | NA | NA | NA | NA | 61 (FAB fr | 11 ± 4 days | Humanized IgG4k monoclonal antibody produced in murine myeloma cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to a4-integrin. Natalizumab was voluntarily withdrawn from U.S. market because of risk of Progressive multifocal leukoencephalopathy (PML). It was returned to market July, 2006. | For treatment of multiple sclerosis. | In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells, and their counter-receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be a secondary result of its blockade of the molecular interaction of a 4b 1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. α4-integrin is required for white blood cells to move into organs, therefore, natalizumab prevents these immune cells from crossing blood vessel walls to reach affected organs thereby decreasing inflamation. | Binds to the α4-subunit of α4b 1 and α4b 7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the α4-mediated adhesion of leukocytes to their counter-receptor(s). | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to leukocytes. | NA | 5.7 ± 1.9 L [Multiple Sclerosis (MS) Patients, 5.2 ± 2.8 L [Crohn's Disease (CD) Patients] | * 16 +/- 5 mL/hour [patients with MS who did not have PML receiving the repeat IV administration of a 300 mg dose] * 22 +/- 22 mL/hour [Patients with Crohn's Disease receiving the repeat IV administration of a 300 mg dose] | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic and Immunomodulating Agents,Blood Proteins,Globulins,Immunoglobulins,Immunologic Factors,Immunomodulatory Agents,Immunoproteins,Immunosuppressive Agents,Integrin Receptor Antagonist,Proteins,Selective Immunosuppressants,Serum Globulins | NA | NA | NA | NA | Integrin alpha-4,Low affinity immunoglobulin gamma Fc region receptor III-B,Intercellular adhesion molecule 1,High affinity immunoglobulin gamma Fc receptor I | NA | Elan Pharmaceuticals, Inc. | Elan Pharmaceuticals, Inc. | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10674 | Th1147 | Natalizumab | NA | NA | NA | NA | NA | 61 (FAB fr | 11 ± 4 days | Humanized IgG4k monoclonal antibody produced in murine myeloma cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to a4-integrin. Natalizumab was voluntarily withdrawn from U.S. market because of risk of Progressive multifocal leukoencephalopathy (PML). It was returned to market July, 2006. | For treatment of multiple sclerosis. | In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells, and their counter-receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be a secondary result of its blockade of the molecular interaction of a 4b 1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. α4-integrin is required for white blood cells to move into organs, therefore, natalizumab prevents these immune cells from crossing blood vessel walls to reach affected organs thereby decreasing inflamation. | Binds to the α4-subunit of α4b 1 and α4b 7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the α4-mediated adhesion of leukocytes to their counter-receptor(s). | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to leukocytes. | NA | 5.7 ± 1.9 L [Multiple Sclerosis (MS) Patients, 5.2 ± 2.8 L [Crohn's Disease (CD) Patients] | * 16 +/- 5 mL/hour [patients with MS who did not have PML receiving the repeat IV administration of a 300 mg dose] * 22 +/- 22 mL/hour [Patients with Crohn's Disease receiving the repeat IV administration of a 300 mg dose] | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic and Immunomodulating Agents,Blood Proteins,Globulins,Immunoglobulins,Immunologic Factors,Immunomodulatory Agents,Immunoproteins,Immunosuppressive Agents,Integrin Receptor Antagonist,Proteins,Selective Immunosuppressants,Serum Globulins | NA | NA | NA | NA | Integrin alpha-4,Low affinity immunoglobulin gamma Fc region receptor III-B,Intercellular adhesion molecule 1,High affinity immunoglobulin gamma Fc receptor I | NA | Biogen Idec Canada Inc | Biogen Idec Canada Inc | NA | NA | NA | Solution | NA | NA | NA | NA | Link | NA | NA |
| 10675 | Th1147 | Natalizumab | NA | NA | NA | NA | NA | 61 (FAB fr | 11 ± 4 days | Humanized IgG4k monoclonal antibody produced in murine myeloma cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to a4-integrin. Natalizumab was voluntarily withdrawn from U.S. market because of risk of Progressive multifocal leukoencephalopathy (PML). It was returned to market July, 2006. | For treatment of multiple sclerosis. | In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells, and their counter-receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be a secondary result of its blockade of the molecular interaction of a 4b 1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. α4-integrin is required for white blood cells to move into organs, therefore, natalizumab prevents these immune cells from crossing blood vessel walls to reach affected organs thereby decreasing inflamation. | Binds to the α4-subunit of α4b 1 and α4b 7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the α4-mediated adhesion of leukocytes to their counter-receptor(s). | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to leukocytes. | NA | 5.7 ± 1.9 L [Multiple Sclerosis (MS) Patients, 5.2 ± 2.8 L [Crohn's Disease (CD) Patients] | * 16 +/- 5 mL/hour [patients with MS who did not have PML receiving the repeat IV administration of a 300 mg dose] * 22 +/- 22 mL/hour [Patients with Crohn's Disease receiving the repeat IV administration of a 300 mg dose] | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic and Immunomodulating Agents,Blood Proteins,Globulins,Immunoglobulins,Immunologic Factors,Immunomodulatory Agents,Immunoproteins,Immunosuppressive Agents,Integrin Receptor Antagonist,Proteins,Selective Immunosuppressants,Serum Globulins | NA | NA | NA | NA | Integrin alpha-4,Low affinity immunoglobulin gamma Fc region receptor III-B,Intercellular adhesion molecule 1,High affinity immunoglobulin gamma Fc receptor I | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10699 | Th1159 | Gemtuzumab ozogamicin | >Th1159_Gemtuzumab_ozogamicin EVQLVQSGAEVKKPGSSVKVSCKASGYTITDSNIHWVRQAPGQSLEWIGYIYPYNGGTDYNQKFKNRATLTVDNPTNTAYMELSSLRSEDTAFYYCVNGNPWLAYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 151000 to 153000 | NA | NA | NA | 61 (FAB fr | 64±44 h | Recombinant humanized IgG4, kappa antibody conjugated with a cytotoxic antitumor antibiotic, calicheamicin, isolated from fermentation of a bacterium, Micromonospora echinospora ssp. calichensis. The antibody portion of Mylotarg binds specifically to the CD33 antigen, The anti-CD33 hP67.6 antibody is produced by mammalian cell suspension culture using a myeloma NS0 cell line. | For treatment of CD33-positive acute myeloid leukemia in patients 60 and over who are not candidates for other chemotherapy. | Used for the treatment of acute myeloid leukemia (AML), mylotarg binds to the CD33 antigen, which is expressed on the surface of leukemic cells in more than 80% of patients with AML. The CD33 antigen is not expressed on pluripotent hematopoietic stem cells or nonhematopoietic cells. This gives mylotarg the selectivity needed to target leukemic cells. | Mylotarg is directed against the CD33 antigen expressed by hematopoietic cells. Binding of the anti-CD33 antibody portion of Mylotarg with the CD33 antigen results in the formation of a complex that is internalized. Upon internalization, the calicheamicin derivative is released inside the lysosomes of the myeloid cell. The released calicheamicin derivative binds to DNA in the minor groove resulting in DNA double strand breaks and cell death. | The most frequently reported toxicities are myelosuppression and hepatic veno-occlusive disorder. | Metabolic studies indicate hydrolytic release of the calicheamicin derivative from gemtuzumab ozogamicin. The drug is most likely removed by opsonization via the reticuloendothelial system. | In pediatric patients receiving a dose level of 9mg/m^2, the peak plasma concentration (Cmax) was approximately 3.47±1.04 mg/L with the AUC of 136 ±107 mg * h/L [A20377]. | The volume of distribution at steady state (Vss) was approximately 6.5 ± 5.5 L in pediatric patients receiving a dose level of 9mg/m^2 [A20377]. | The mean clearance rate was approximately 0.12±0.15 L/h/m^2 in pediatric patients receiving a dose level of 9mg/m^2 [A20377]. | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Carbohydrates,CD33-directed Antibody Interactions,CD33-directed Cytotoxin,Globulins,Glycosides,Hepatotoxic Agents,Immunoconjugates,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Immunotoxins,Myelosuppressive Agents,Narrow Therapeutic Index Drugs,Noxae,Proteins,Serum Globulins,Toxic Actions | US5585089 | 17-12-1996 | 17-12-2013 | Belizumab, Clozapine, Denosumab, Leflunomide, Natalizumab due to adverse effects of these drugs with Gemtuzumab; Pimecrolimus, Roflumilast, Sipuleucel-T, Tacrolimus, Tofacitinib, Trastuzumab due to adverse effects of above immmunosupressants | Myeloid cell surface antigen CD33,Low affinity immunoglobulin gamma Fc region receptor III-B,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I | Mylotarg | Wyeth pharmaceuticals inc | Wyeth pharmaceuticals inc | Mylotarg (gemtuzumab ozogamicin for injection) is indicated for the treatment of patients with CD33 positive acute myeloid leukemia | NA | 5 mg of drug conjugate (protein equivalent) in an amber vial. The inactive ingredients are: dextran 40; sucrose; sodium chloride; monobasic and dibasic sodium phosphate. | Mylotarg (gemtuzumab ozogamicin for injection) is a sterile, white, preservative-free lyophilized powder | Intravenous infusion | The recommended dose of Mylotarg (gemtuzumab ozogamicin for injection) is 9 mg/m² , infused over a 2-hour period. | Mylotarg (gemtuzumab ozogamicin for injection) is contraindicated in patients with a known hypersensitivity to gemtuzumab ozogamicin or any of its components: anti-CD33 antibody (hP67.6), calicheamicin derivatives, or inactive ingredients. Mylotarg is contraindicated in lactating mothers. | Fever, Nausea, Chills, Vomiting, Headache,Dyspnea, Hypotension, Hypertension, Hypoxia | Link | NA | NA |
| 10700 | Th1159 | Gemtuzumab ozogamicin | >Th1159_Gemtuzumab_ozogamicin EVQLVQSGAEVKKPGSSVKVSCKASGYTITDSNIHWVRQAPGQSLEWIGYIYPYNGGTDYNQKFKNRATLTVDNPTNTAYMELSSLRSEDTAFYYCVNGNPWLAYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 151000 to 153000 | NA | NA | NA | 61 (FAB fr | 64±44 h | NA | NA | NA | NA | The most frequently reported toxicities are myelosuppression and hepatic veno-occlusive disorder. | Metabolic studies indicate hydrolytic release of the calicheamicin derivative from gemtuzumab ozogamicin. The drug is most likely removed by opsonization via the reticuloendothelial system. | In pediatric patients receiving a dose level of 9mg/m^2, the peak plasma concentration (Cmax) was approximately 3.47±1.04 mg/L with the AUC of 136 ±107 mg * h/L [A20377]. | The volume of distribution at steady state (Vss) was approximately 6.5 ± 5.5 L in pediatric patients receiving a dose level of 9mg/m^2 [A20377]. | The mean clearance rate was approximately 0.12±0.15 L/h/m^2 in pediatric patients receiving a dose level of 9mg/m^2 [A20377]. | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Carbohydrates,CD33-directed Antibody Interactions,CD33-directed Cytotoxin,Globulins,Glycosides,Hepatotoxic Agents,Immunoconjugates,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Immunotoxins,Myelosuppressive Agents,Narrow Therapeutic Index Drugs,Noxae,Proteins,Serum Globulins,Toxic Actions | US5773001 | 30-06-1998 | 30-06-2015 | NA | Myeloid cell surface antigen CD33,Low affinity immunoglobulin gamma Fc region receptor III-B,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10736 | Th1170 | Blinatumomab | >Th1170_Blinatumomab DIQLTQSPASLAVSLGQRATISCKASQSVDYDGDSYLNWYQQIPGQPPKLLIYDASNLVSGIPPRFSGSGSGTDFTLNIHPVEKVDAATYHCQQSTEDPWTFGGGTKLEIKGGGGSGGGGSGGGGSQVQLQQSGAELVRPGSSVKISCKASGYAFSSYWMNWVKQRPGQGLEWIGQIWPGDGDTNYNGKFKGKATLTADESSSTAYMQLSSLASEDSAVYFCARRETTTVGRYYYAMDYWGQGTTVTVSSGGGGSDIKLQQSGAELARPGASVKMSCKTSGYTFTRYTMHWVKQRPGQGLEWIGYINPSRGYTNYNQKFKDKATLTTDKSSSTAYMQLSSLTSEDSAVYYCARYYDDHYCLDYWGQGTTLTVSSVEGGSGGSGGSGGSGGVDDIQLTQSPAIMSASPGEKVTMTCRASSSVSYMNWYQQKSGTSPKRWIYDTSKVASGVPYRFSGSGSGTSYSLTISSMEAEDAATYYCQQWSSNPLTFGAGTKLELKHHHHHH | 54100 | C2367H3577N649O772S19 | NA | NA | NA | 2.11 hours, standard deviation 1.42. | Blinatumomab is a BiTE-class (bi-specific T-cell engagers) constructed monoclonal antibody indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). Blinatumomab is manufactured by Amgen Inc. and marketed under the brand Blincyto™. A full treatment regimen consisting of two cycles of four weeks each, is priced at $178 000 USD. Blinatumomab was approved in December 2014 under the FDA’s accelerated approval program, which allows approval of a drug to treat a serious or life-threatening disease based on clinical data showing the drug has an effect on a surrogate endpoint reasonably likely to predict clinical benefit to patients. | Indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). | NA | Blinatumomab is a bispecific CD19-directed CD3 T-cell engager that binds to CD19 expressed on the surface of cells of B-lineage origin and CD3 expressed on the surface of T cells. It activates endogenous T cells by connecting CD3 in the T-cell receptor (TCR) complex with CD19 on benign and malignant B cells. Blinatumomab mediates the formation of a synapse between the T cell and the tumor cell, upregulation of cell adhesion molecules, production of cytolytic proteins, release of inflammatory cytokines, and proliferation of T cells, which result in redirected lysis of CD19+ cells. | - Cytokine Release Syndrome (CRS), which may be life-threatening or fatal, occurred in patients receiving blinatumomab. Interrupt or discontinue blinatumomab as recommended. - Neurological toxicities, which may be severe, life-threatening, or fatal, occurred in patients receiving blinatumomab. Interrupt or discontinue blinatumomab as recommended. - In patients receiving blinatumomab in clinical trials, serious infections such as sepsis, pneumonia, bacteremia, opportunistic infections, and catheter-site infections were observed in approximately 25% of patients, some of which were life-threatening or fatal. - Tumor lysis syndrome (TLS), which may be life-threatening or fatal, has been observed in patients. - Neutropenia and febrile neutropenia, including life-threatening cases, have been observed in patients. - Treatment with blinatumomab was associated with transient elevations in liver enzymes. - Cranial magnetic resonance imaging (MRI) changes showing leukoencephalopathy have been observed in patients receiving blinatumomab, especially in patients with prior treatment with cranial irradiation and antileukemic chemotherapy (including systemic high-dose methotrexate or intrathecal cytarabine). | The metabolic pathway of blinatumomab has not been characterized. Like other protein therapeutics, blinatumomab is expected to be degraded into small peptides and amino acids via catabolic pathways. | NA | 4.52 L, standard deviation 2.89. | 2.92 L/hour, standard deviation 2.83. | Amides,Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antineoplastic Agents,Antineoplastic and Immunomodulating Agents,Bispecific CD19-directed CD3-directed T Cell Engager,Blood Proteins,Cancer immunotherapy,CD19-directed Antibody Interactions,CD3 Receptor Agonists,CD3-directed Antibody Interactions,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Monoterpenes,Myelosuppressive Agents,Narrow Therapeutic Index Drugs,Norbornanes,Proteins,Serum Globulins,Sulfones,Sulfur Compounds,Terpenes | US20120328618 | 27-10-2009 | 27-10-2029 | The risk or severity of adverse effects can be increased when Blinatumomab is combined with Clozapine; The risk or severity of adverse effects can be increased when Denosumab is combined with Blinatumomab; The risk or severity of adverse effects can be increased when Blinatumomab is combined with Leflunomide; The risk or severity of adverse effects can be increased when Metamizole is combined with Blinatumomab; The risk or severity of adverse effects can be increased when Blinatumomab is combined with Natalizumab; The risk or severity of adverse effects can be increased when Pimecrolimus is combined with Blinatumomab; Roflumilast may increase the immunosuppressive activities of Blinatumomab; The therapeutic efficacy of Sipuleucel-T can be decreased when used in combination with Blinatumomab; The risk or severity of adverse effects can be increased when Tacrolimus is combined with Blinatumomab; Blinatumomab may increase the immunosuppressive activities of Tofacitinib. | B-lymphocyte antigen CD19,T-cell surface glycoprotein CD3 delta chain | Blincyto | AMGEN | AMGEN | BLINCYTO is indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). | NA | 12.5 mcg/mL | lyophilized powder for intravenous administration | Intravenous | A single cycle of treatment of BLINCYTO consists of 4 weeks of continuous intravenous infusion followed by a 2-week treatment-free interval. For patients at least 45 kg in weight: In Cycle 1, administer BLINCYTO at 9 mcg/day on Days 1–7 and at 28 mcg/day on Days 8–28. For subsequent cycles, administer BLINCYTO at 28 mcg/day on Days 1–28. Allow for at least 2 weeks treatment-free between cycles of BLINCYTO. A treatment course consists of up to 2 cycles of BLINCYTO for induction followed by 3 additional cycles for consolidation treatment (up to a total of 5 cycles). | BLINCYTO is contraindicated in patients with known hypersensitivity to blinatumomab or to any component of the product formulation. | Cytokine Release Syndrome; Neurological Toxicities; Infections; Tumor Lysis Syndrome; Neutropenia and Febrile Neutropenia; Effects on Ability to Drive and Use Machines; Elevated Liver Enzymes; Leukoencephalopathy; Preparation and Administration Errors. | Link | NA | NA |
| 10737 | Th1170 | Blinatumomab | >Th1170_Blinatumomab DIQLTQSPASLAVSLGQRATISCKASQSVDYDGDSYLNWYQQIPGQPPKLLIYDASNLVSGIPPRFSGSGSGTDFTLNIHPVEKVDAATYHCQQSTEDPWTFGGGTKLEIKGGGGSGGGGSGGGGSQVQLQQSGAELVRPGSSVKISCKASGYAFSSYWMNWVKQRPGQGLEWIGQIWPGDGDTNYNGKFKGKATLTADESSSTAYMQLSSLASEDSAVYFCARRETTTVGRYYYAMDYWGQGTTVTVSSGGGGSDIKLQQSGAELARPGASVKMSCKTSGYTFTRYTMHWVKQRPGQGLEWIGYINPSRGYTNYNQKFKDKATLTTDKSSSTAYMQLSSLTSEDSAVYYCARYYDDHYCLDYWGQGTTLTVSSVEGGSGGSGGSGGSGGVDDIQLTQSPAIMSASPGEKVTMTCRASSSVSYMNWYQQKSGTSPKRWIYDTSKVASGVPYRFSGSGSGTSYSLTISSMEAEDAATYYCQQWSSNPLTFGAGTKLELKHHHHHH | 54101 | C2367H3577N649O772S20 | NA | NA | NA | 2.11 hours, standard deviation 1.42. | Blinatumomab is a BiTE-class (bi-specific T-cell engagers) constructed monoclonal antibody indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). Blinatumomab is manufactured by Amgen Inc. and marketed under the brand Blincyto™. A full treatment regimen consisting of two cycles of four weeks each, is priced at $178 000 USD. Blinatumomab was approved in December 2014 under the FDA’s accelerated approval program, which allows approval of a drug to treat a serious or life-threatening disease based on clinical data showing the drug has an effect on a surrogate endpoint reasonably likely to predict clinical benefit to patients. | Indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). | NA | Blinatumomab is a bispecific CD19-directed CD3 T-cell engager that binds to CD19 expressed on the surface of cells of B-lineage origin and CD3 expressed on the surface of T cells. It activates endogenous T cells by connecting CD3 in the T-cell receptor (TCR) complex with CD19 on benign and malignant B cells. Blinatumomab mediates the formation of a synapse between the T cell and the tumor cell, upregulation of cell adhesion molecules, production of cytolytic proteins, release of inflammatory cytokines, and proliferation of T cells, which result in redirected lysis of CD19+ cells. | - Cytokine Release Syndrome (CRS), which may be life-threatening or fatal, occurred in patients receiving blinatumomab. Interrupt or discontinue blinatumomab as recommended. - Neurological toxicities, which may be severe, life-threatening, or fatal, occurred in patients receiving blinatumomab. Interrupt or discontinue blinatumomab as recommended. - In patients receiving blinatumomab in clinical trials, serious infections such as sepsis, pneumonia, bacteremia, opportunistic infections, and catheter-site infections were observed in approximately 25% of patients, some of which were life-threatening or fatal. - Tumor lysis syndrome (TLS), which may be life-threatening or fatal, has been observed in patients. - Neutropenia and febrile neutropenia, including life-threatening cases, have been observed in patients. - Treatment with blinatumomab was associated with transient elevations in liver enzymes. - Cranial magnetic resonance imaging (MRI) changes showing leukoencephalopathy have been observed in patients receiving blinatumomab, especially in patients with prior treatment with cranial irradiation and antileukemic chemotherapy (including systemic high-dose methotrexate or intrathecal cytarabine). | The metabolic pathway of blinatumomab has not been characterized. Like other protein therapeutics, blinatumomab is expected to be degraded into small peptides and amino acids via catabolic pathways. | NA | 4.52 L, standard deviation 2.89. | 2.92 L/hour, standard deviation 2.83. | Amides,Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antineoplastic Agents,Antineoplastic and Immunomodulating Agents,Bispecific CD19-directed CD3-directed T Cell Engager,Blood Proteins,Cancer immunotherapy,CD19-directed Antibody Interactions,CD3 Receptor Agonists,CD3-directed Antibody Interactions,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Monoterpenes,Myelosuppressive Agents,Narrow Therapeutic Index Drugs,Norbornanes,Proteins,Serum Globulins,Sulfones,Sulfur Compounds,Terpenes | US20130323247 | 11-Jul-2008 | 11-Jul-2028 | The risk or severity of adverse effects can be increased when Blinatumomab is combined with Clozapine; The risk or severity of adverse effects can be increased when Denosumab is combined with Blinatumomab; The risk or severity of adverse effects can be increased when Blinatumomab is combined with Leflunomide; The risk or severity of adverse effects can be increased when Metamizole is combined with Blinatumomab; The risk or severity of adverse effects can be increased when Blinatumomab is combined with Natalizumab; The risk or severity of adverse effects can be increased when Pimecrolimus is combined with Blinatumomab; Roflumilast may increase the immunosuppressive activities of Blinatumomab; The therapeutic efficacy of Sipuleucel-T can be decreased when used in combination with Blinatumomab; The risk or severity of adverse effects can be increased when Tacrolimus is combined with Blinatumomab; Blinatumomab may increase the immunosuppressive activities of Tofacitinib. | B-lymphocyte antigen CD19,T-cell surface glycoprotein CD3 delta chain | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10738 | Th1170 | Blinatumomab | >Th1170_Blinatumomab DIQLTQSPASLAVSLGQRATISCKASQSVDYDGDSYLNWYQQIPGQPPKLLIYDASNLVSGIPPRFSGSGSGTDFTLNIHPVEKVDAATYHCQQSTEDPWTFGGGTKLEIKGGGGSGGGGSGGGGSQVQLQQSGAELVRPGSSVKISCKASGYAFSSYWMNWVKQRPGQGLEWIGQIWPGDGDTNYNGKFKGKATLTADESSSTAYMQLSSLASEDSAVYFCARRETTTVGRYYYAMDYWGQGTTVTVSSGGGGSDIKLQQSGAELARPGASVKMSCKTSGYTFTRYTMHWVKQRPGQGLEWIGYINPSRGYTNYNQKFKDKATLTTDKSSSTAYMQLSSLTSEDSAVYYCARYYDDHYCLDYWGQGTTLTVSSVEGGSGGSGGSGGSGGVDDIQLTQSPAIMSASPGEKVTMTCRASSSVSYMNWYQQKSGTSPKRWIYDTSKVASGVPYRFSGSGSGTSYSLTISSMEAEDAATYYCQQWSSNPLTFGAGTKLELKHHHHHH | 54102 | C2367H3577N649O772S21 | NA | NA | NA | 2.11 hours, standard deviation 1.42. | Blinatumomab is a BiTE-class (bi-specific T-cell engagers) constructed monoclonal antibody indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). Blinatumomab is manufactured by Amgen Inc. and marketed under the brand Blincyto™. A full treatment regimen consisting of two cycles of four weeks each, is priced at $178 000 USD. Blinatumomab was approved in December 2014 under the FDA’s accelerated approval program, which allows approval of a drug to treat a serious or life-threatening disease based on clinical data showing the drug has an effect on a surrogate endpoint reasonably likely to predict clinical benefit to patients. | Indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). | NA | Blinatumomab is a bispecific CD19-directed CD3 T-cell engager that binds to CD19 expressed on the surface of cells of B-lineage origin and CD3 expressed on the surface of T cells. It activates endogenous T cells by connecting CD3 in the T-cell receptor (TCR) complex with CD19 on benign and malignant B cells. Blinatumomab mediates the formation of a synapse between the T cell and the tumor cell, upregulation of cell adhesion molecules, production of cytolytic proteins, release of inflammatory cytokines, and proliferation of T cells, which result in redirected lysis of CD19+ cells. | - Cytokine Release Syndrome (CRS), which may be life-threatening or fatal, occurred in patients receiving blinatumomab. Interrupt or discontinue blinatumomab as recommended. - Neurological toxicities, which may be severe, life-threatening, or fatal, occurred in patients receiving blinatumomab. Interrupt or discontinue blinatumomab as recommended. - In patients receiving blinatumomab in clinical trials, serious infections such as sepsis, pneumonia, bacteremia, opportunistic infections, and catheter-site infections were observed in approximately 25% of patients, some of which were life-threatening or fatal. - Tumor lysis syndrome (TLS), which may be life-threatening or fatal, has been observed in patients. - Neutropenia and febrile neutropenia, including life-threatening cases, have been observed in patients. - Treatment with blinatumomab was associated with transient elevations in liver enzymes. - Cranial magnetic resonance imaging (MRI) changes showing leukoencephalopathy have been observed in patients receiving blinatumomab, especially in patients with prior treatment with cranial irradiation and antileukemic chemotherapy (including systemic high-dose methotrexate or intrathecal cytarabine). | The metabolic pathway of blinatumomab has not been characterized. Like other protein therapeutics, blinatumomab is expected to be degraded into small peptides and amino acids via catabolic pathways. | NA | 4.52 L, standard deviation 2.89. | 2.92 L/hour, standard deviation 2.83. | Amides,Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antineoplastic Agents,Antineoplastic and Immunomodulating Agents,Bispecific CD19-directed CD3-directed T Cell Engager,Blood Proteins,Cancer immunotherapy,CD19-directed Antibody Interactions,CD3 Receptor Agonists,CD3-directed Antibody Interactions,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Monoterpenes,Myelosuppressive Agents,Narrow Therapeutic Index Drugs,Norbornanes,Proteins,Serum Globulins,Sulfones,Sulfur Compounds,Terpenes | US7235641 | 26-06-2007 | 22-12-2023 | The risk or severity of adverse effects can be increased when Blinatumomab is combined with Clozapine; The risk or severity of adverse effects can be increased when Denosumab is combined with Blinatumomab; The risk or severity of adverse effects can be increased when Blinatumomab is combined with Leflunomide; The risk or severity of adverse effects can be increased when Metamizole is combined with Blinatumomab; The risk or severity of adverse effects can be increased when Blinatumomab is combined with Natalizumab; The risk or severity of adverse effects can be increased when Pimecrolimus is combined with Blinatumomab; Roflumilast may increase the immunosuppressive activities of Blinatumomab; The therapeutic efficacy of Sipuleucel-T can be decreased when used in combination with Blinatumomab; The risk or severity of adverse effects can be increased when Tacrolimus is combined with Blinatumomab; Blinatumomab may increase the immunosuppressive activities of Tofacitinib. | B-lymphocyte antigen CD19,T-cell surface glycoprotein CD3 delta chain | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10739 | Th1170 | Blinatumomab | >Th1170_Blinatumomab DIQLTQSPASLAVSLGQRATISCKASQSVDYDGDSYLNWYQQIPGQPPKLLIYDASNLVSGIPPRFSGSGSGTDFTLNIHPVEKVDAATYHCQQSTEDPWTFGGGTKLEIKGGGGSGGGGSGGGGSQVQLQQSGAELVRPGSSVKISCKASGYAFSSYWMNWVKQRPGQGLEWIGQIWPGDGDTNYNGKFKGKATLTADESSSTAYMQLSSLASEDSAVYFCARRETTTVGRYYYAMDYWGQGTTVTVSSGGGGSDIKLQQSGAELARPGASVKMSCKTSGYTFTRYTMHWVKQRPGQGLEWIGYINPSRGYTNYNQKFKDKATLTTDKSSSTAYMQLSSLTSEDSAVYYCARYYDDHYCLDYWGQGTTLTVSSVEGGSGGSGGSGGSGGVDDIQLTQSPAIMSASPGEKVTMTCRASSSVSYMNWYQQKSGTSPKRWIYDTSKVASGVPYRFSGSGSGTSYSLTISSMEAEDAATYYCQQWSSNPLTFGAGTKLELKHHHHHH | 54103 | C2367H3577N649O772S22 | NA | NA | NA | 2.11 hours, standard deviation 1.42. | Blinatumomab is a BiTE-class (bi-specific T-cell engagers) constructed monoclonal antibody indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). Blinatumomab is manufactured by Amgen Inc. and marketed under the brand Blincyto™. A full treatment regimen consisting of two cycles of four weeks each, is priced at $178 000 USD. Blinatumomab was approved in December 2014 under the FDA’s accelerated approval program, which allows approval of a drug to treat a serious or life-threatening disease based on clinical data showing the drug has an effect on a surrogate endpoint reasonably likely to predict clinical benefit to patients. | Indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). | NA | Blinatumomab is a bispecific CD19-directed CD3 T-cell engager that binds to CD19 expressed on the surface of cells of B-lineage origin and CD3 expressed on the surface of T cells. It activates endogenous T cells by connecting CD3 in the T-cell receptor (TCR) complex with CD19 on benign and malignant B cells. Blinatumomab mediates the formation of a synapse between the T cell and the tumor cell, upregulation of cell adhesion molecules, production of cytolytic proteins, release of inflammatory cytokines, and proliferation of T cells, which result in redirected lysis of CD19+ cells. | - Cytokine Release Syndrome (CRS), which may be life-threatening or fatal, occurred in patients receiving blinatumomab. Interrupt or discontinue blinatumomab as recommended. - Neurological toxicities, which may be severe, life-threatening, or fatal, occurred in patients receiving blinatumomab. Interrupt or discontinue blinatumomab as recommended. - In patients receiving blinatumomab in clinical trials, serious infections such as sepsis, pneumonia, bacteremia, opportunistic infections, and catheter-site infections were observed in approximately 25% of patients, some of which were life-threatening or fatal. - Tumor lysis syndrome (TLS), which may be life-threatening or fatal, has been observed in patients. - Neutropenia and febrile neutropenia, including life-threatening cases, have been observed in patients. - Treatment with blinatumomab was associated with transient elevations in liver enzymes. - Cranial magnetic resonance imaging (MRI) changes showing leukoencephalopathy have been observed in patients receiving blinatumomab, especially in patients with prior treatment with cranial irradiation and antileukemic chemotherapy (including systemic high-dose methotrexate or intrathecal cytarabine). | The metabolic pathway of blinatumomab has not been characterized. Like other protein therapeutics, blinatumomab is expected to be degraded into small peptides and amino acids via catabolic pathways. | NA | 4.52 L, standard deviation 2.89. | 2.92 L/hour, standard deviation 2.83. | Amides,Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antineoplastic Agents,Antineoplastic and Immunomodulating Agents,Bispecific CD19-directed CD3-directed T Cell Engager,Blood Proteins,Cancer immunotherapy,CD19-directed Antibody Interactions,CD3 Receptor Agonists,CD3-directed Antibody Interactions,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Monoterpenes,Myelosuppressive Agents,Narrow Therapeutic Index Drugs,Norbornanes,Proteins,Serum Globulins,Sulfones,Sulfur Compounds,Terpenes | US7575923 | 18-08-2009 | 21-04-2018 | The risk or severity of adverse effects can be increased when Blinatumomab is combined with Clozapine; The risk or severity of adverse effects can be increased when Denosumab is combined with Blinatumomab; The risk or severity of adverse effects can be increased when Blinatumomab is combined with Leflunomide; The risk or severity of adverse effects can be increased when Metamizole is combined with Blinatumomab; The risk or severity of adverse effects can be increased when Blinatumomab is combined with Natalizumab; The risk or severity of adverse effects can be increased when Pimecrolimus is combined with Blinatumomab; Roflumilast may increase the immunosuppressive activities of Blinatumomab; The therapeutic efficacy of Sipuleucel-T can be decreased when used in combination with Blinatumomab; The risk or severity of adverse effects can be increased when Tacrolimus is combined with Blinatumomab; Blinatumomab may increase the immunosuppressive activities of Tofacitinib. | B-lymphocyte antigen CD19,T-cell surface glycoprotein CD3 delta chain | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10740 | Th1170 | Blinatumomab | >Th1170_Blinatumomab DIQLTQSPASLAVSLGQRATISCKASQSVDYDGDSYLNWYQQIPGQPPKLLIYDASNLVSGIPPRFSGSGSGTDFTLNIHPVEKVDAATYHCQQSTEDPWTFGGGTKLEIKGGGGSGGGGSGGGGSQVQLQQSGAELVRPGSSVKISCKASGYAFSSYWMNWVKQRPGQGLEWIGQIWPGDGDTNYNGKFKGKATLTADESSSTAYMQLSSLASEDSAVYFCARRETTTVGRYYYAMDYWGQGTTVTVSSGGGGSDIKLQQSGAELARPGASVKMSCKTSGYTFTRYTMHWVKQRPGQGLEWIGYINPSRGYTNYNQKFKDKATLTTDKSSSTAYMQLSSLTSEDSAVYYCARYYDDHYCLDYWGQGTTLTVSSVEGGSGGSGGSGGSGGVDDIQLTQSPAIMSASPGEKVTMTCRASSSVSYMNWYQQKSGTSPKRWIYDTSKVASGVPYRFSGSGSGTSYSLTISSMEAEDAATYYCQQWSSNPLTFGAGTKLELKHHHHHH | 54104 | C2367H3577N649O772S23 | NA | NA | NA | 2.11 hours, standard deviation 1.42. | Blinatumomab is a BiTE-class (bi-specific T-cell engagers) constructed monoclonal antibody indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). Blinatumomab is manufactured by Amgen Inc. and marketed under the brand Blincyto™. A full treatment regimen consisting of two cycles of four weeks each, is priced at $178 000 USD. Blinatumomab was approved in December 2014 under the FDA’s accelerated approval program, which allows approval of a drug to treat a serious or life-threatening disease based on clinical data showing the drug has an effect on a surrogate endpoint reasonably likely to predict clinical benefit to patients. | Indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). | NA | Blinatumomab is a bispecific CD19-directed CD3 T-cell engager that binds to CD19 expressed on the surface of cells of B-lineage origin and CD3 expressed on the surface of T cells. It activates endogenous T cells by connecting CD3 in the T-cell receptor (TCR) complex with CD19 on benign and malignant B cells. Blinatumomab mediates the formation of a synapse between the T cell and the tumor cell, upregulation of cell adhesion molecules, production of cytolytic proteins, release of inflammatory cytokines, and proliferation of T cells, which result in redirected lysis of CD19+ cells. | - Cytokine Release Syndrome (CRS), which may be life-threatening or fatal, occurred in patients receiving blinatumomab. Interrupt or discontinue blinatumomab as recommended. - Neurological toxicities, which may be severe, life-threatening, or fatal, occurred in patients receiving blinatumomab. Interrupt or discontinue blinatumomab as recommended. - In patients receiving blinatumomab in clinical trials, serious infections such as sepsis, pneumonia, bacteremia, opportunistic infections, and catheter-site infections were observed in approximately 25% of patients, some of which were life-threatening or fatal. - Tumor lysis syndrome (TLS), which may be life-threatening or fatal, has been observed in patients. - Neutropenia and febrile neutropenia, including life-threatening cases, have been observed in patients. - Treatment with blinatumomab was associated with transient elevations in liver enzymes. - Cranial magnetic resonance imaging (MRI) changes showing leukoencephalopathy have been observed in patients receiving blinatumomab, especially in patients with prior treatment with cranial irradiation and antileukemic chemotherapy (including systemic high-dose methotrexate or intrathecal cytarabine). | The metabolic pathway of blinatumomab has not been characterized. Like other protein therapeutics, blinatumomab is expected to be degraded into small peptides and amino acids via catabolic pathways. | NA | 4.52 L, standard deviation 2.89. | 2.92 L/hour, standard deviation 2.83. | Amides,Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antineoplastic Agents,Antineoplastic and Immunomodulating Agents,Bispecific CD19-directed CD3-directed T Cell Engager,Blood Proteins,Cancer immunotherapy,CD19-directed Antibody Interactions,CD3 Receptor Agonists,CD3-directed Antibody Interactions,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Monoterpenes,Myelosuppressive Agents,Narrow Therapeutic Index Drugs,Norbornanes,Proteins,Serum Globulins,Sulfones,Sulfur Compounds,Terpenes | US7635472 | 22-12-2009 | 31-05-2023 | The risk or severity of adverse effects can be increased when Blinatumomab is combined with Clozapine; The risk or severity of adverse effects can be increased when Denosumab is combined with Blinatumomab; The risk or severity of adverse effects can be increased when Blinatumomab is combined with Leflunomide; The risk or severity of adverse effects can be increased when Metamizole is combined with Blinatumomab; The risk or severity of adverse effects can be increased when Blinatumomab is combined with Natalizumab; The risk or severity of adverse effects can be increased when Pimecrolimus is combined with Blinatumomab; Roflumilast may increase the immunosuppressive activities of Blinatumomab; The therapeutic efficacy of Sipuleucel-T can be decreased when used in combination with Blinatumomab; The risk or severity of adverse effects can be increased when Tacrolimus is combined with Blinatumomab; Blinatumomab may increase the immunosuppressive activities of Tofacitinib. | B-lymphocyte antigen CD19,T-cell surface glycoprotein CD3 delta chain | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10741 | Th1170 | Blinatumomab | >Th1170_Blinatumomab DIQLTQSPASLAVSLGQRATISCKASQSVDYDGDSYLNWYQQIPGQPPKLLIYDASNLVSGIPPRFSGSGSGTDFTLNIHPVEKVDAATYHCQQSTEDPWTFGGGTKLEIKGGGGSGGGGSGGGGSQVQLQQSGAELVRPGSSVKISCKASGYAFSSYWMNWVKQRPGQGLEWIGQIWPGDGDTNYNGKFKGKATLTADESSSTAYMQLSSLASEDSAVYFCARRETTTVGRYYYAMDYWGQGTTVTVSSGGGGSDIKLQQSGAELARPGASVKMSCKTSGYTFTRYTMHWVKQRPGQGLEWIGYINPSRGYTNYNQKFKDKATLTTDKSSSTAYMQLSSLTSEDSAVYYCARYYDDHYCLDYWGQGTTLTVSSVEGGSGGSGGSGGSGGVDDIQLTQSPAIMSASPGEKVTMTCRASSSVSYMNWYQQKSGTSPKRWIYDTSKVASGVPYRFSGSGSGTSYSLTISSMEAEDAATYYCQQWSSNPLTFGAGTKLELKHHHHHH | 54105 | C2367H3577N649O772S24 | NA | NA | NA | 2.11 hours, standard deviation 1.42. | Blinatumomab is a BiTE-class (bi-specific T-cell engagers) constructed monoclonal antibody indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). Blinatumomab is manufactured by Amgen Inc. and marketed under the brand Blincyto™. A full treatment regimen consisting of two cycles of four weeks each, is priced at $178 000 USD. Blinatumomab was approved in December 2014 under the FDA’s accelerated approval program, which allows approval of a drug to treat a serious or life-threatening disease based on clinical data showing the drug has an effect on a surrogate endpoint reasonably likely to predict clinical benefit to patients. | Indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). | NA | Blinatumomab is a bispecific CD19-directed CD3 T-cell engager that binds to CD19 expressed on the surface of cells of B-lineage origin and CD3 expressed on the surface of T cells. It activates endogenous T cells by connecting CD3 in the T-cell receptor (TCR) complex with CD19 on benign and malignant B cells. Blinatumomab mediates the formation of a synapse between the T cell and the tumor cell, upregulation of cell adhesion molecules, production of cytolytic proteins, release of inflammatory cytokines, and proliferation of T cells, which result in redirected lysis of CD19+ cells. | - Cytokine Release Syndrome (CRS), which may be life-threatening or fatal, occurred in patients receiving blinatumomab. Interrupt or discontinue blinatumomab as recommended. - Neurological toxicities, which may be severe, life-threatening, or fatal, occurred in patients receiving blinatumomab. Interrupt or discontinue blinatumomab as recommended. - In patients receiving blinatumomab in clinical trials, serious infections such as sepsis, pneumonia, bacteremia, opportunistic infections, and catheter-site infections were observed in approximately 25% of patients, some of which were life-threatening or fatal. - Tumor lysis syndrome (TLS), which may be life-threatening or fatal, has been observed in patients. - Neutropenia and febrile neutropenia, including life-threatening cases, have been observed in patients. - Treatment with blinatumomab was associated with transient elevations in liver enzymes. - Cranial magnetic resonance imaging (MRI) changes showing leukoencephalopathy have been observed in patients receiving blinatumomab, especially in patients with prior treatment with cranial irradiation and antileukemic chemotherapy (including systemic high-dose methotrexate or intrathecal cytarabine). | The metabolic pathway of blinatumomab has not been characterized. Like other protein therapeutics, blinatumomab is expected to be degraded into small peptides and amino acids via catabolic pathways. | NA | 4.52 L, standard deviation 2.89. | 2.92 L/hour, standard deviation 2.83. | Amides,Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antineoplastic Agents,Antineoplastic and Immunomodulating Agents,Bispecific CD19-directed CD3-directed T Cell Engager,Blood Proteins,Cancer immunotherapy,CD19-directed Antibody Interactions,CD3 Receptor Agonists,CD3-directed Antibody Interactions,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Monoterpenes,Myelosuppressive Agents,Narrow Therapeutic Index Drugs,Norbornanes,Proteins,Serum Globulins,Sulfones,Sulfur Compounds,Terpenes | US8247194 | 21-08-2012 | 5-May-2024 | The risk or severity of adverse effects can be increased when Blinatumomab is combined with Clozapine; The risk or severity of adverse effects can be increased when Denosumab is combined with Blinatumomab; The risk or severity of adverse effects can be increased when Blinatumomab is combined with Leflunomide; The risk or severity of adverse effects can be increased when Metamizole is combined with Blinatumomab; The risk or severity of adverse effects can be increased when Blinatumomab is combined with Natalizumab; The risk or severity of adverse effects can be increased when Pimecrolimus is combined with Blinatumomab; Roflumilast may increase the immunosuppressive activities of Blinatumomab; The therapeutic efficacy of Sipuleucel-T can be decreased when used in combination with Blinatumomab; The risk or severity of adverse effects can be increased when Tacrolimus is combined with Blinatumomab; Blinatumomab may increase the immunosuppressive activities of Tofacitinib. | B-lymphocyte antigen CD19,T-cell surface glycoprotein CD3 delta chain | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10751 | Th1174 | Daratumumab | >Th1174_Daratumumab EVQLLESGGGLVQPGGSLRLSCAVSGFTFNSFAMSWVRQAPGKGLEWVSAISGSGGGTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCAKDKILWFGEPVFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145391.7 | C6466H9996N1724O2010S42 | NA | NA | NA | Intravenous daratumumab has a terminal half life of 18 ± 9 days.6 Subcutaneous daratumumab has a half life of 20 days | Daratumumab is an anti-cancer drug indicated for multiple myeloma in patients who have received at least 3 prior treatments. It was granted accelerated approval by the FDA in November 2016. Marketed under the brand name Darzalex by Janssen Biotech, daratumumab is the first monoclonal antibody injection approved for this indication and provides another options for patients with multiple myeloma resistant to other therapies. Daratumumab induces apoptosis of cancer cells by targeting the CD38 epitope, which is highly expressed on haematological malignancies. | For the treatment of patients with multiple myeloma who have received at least three prior lines of therapy (a proteasome inhibitor (PI) and an immunomodulatory agent) or who are double-refractory to a PI and an immunomodulatory agent. This indication was approved by accelerated approval based on response rate. | In preclinical trials, daratumumab showed synergistic activity with other multiple myeloma therapies, notably lenalidomide. Daratumumab also causes lysis in other cells that express CD38: myeloid-derived suppressor cells, a subset of regulatory T-cells, and NK cells. Decreases in absolute count and percentage of NK cells were observed during treatment. CD4+ and CD8+ T cell absolute counts as well the percentage of total lymphocytes increased in peripheral blood and bone marrow during daratumumab treatment. | Daratumumab is an immunoglobulin G1 kappa monoclonal antibody against CD38 antigen. CD38 is a transmembrane glycoprotein of many functions, including receptor mediated adhesion, signaling, and modulation of cyclase and hydrolase activity. CD38 is expressed on many cell types and tissues, and highly expressed in haematological malignancies including multiple myeloma tumor cells. By binding CD38, daratumumab causes inhibition of tumor cell growth and induces broad-spectrum apoptosis in multiple ways: by Fc-mediated cross linking, by immune-mediate tumor cell lysis through complement dependent cytotoxicity, antibody dependent cell cytotoxicity, and antibody dependent cellular phagocytosis. | Data regarding overdoses of daratumumab are not readily available.[L13290,L13296] Patients should be treated with symptomatic and supportive measures.[L13290,L13296] | Monoclonal antibodies are expected to be metabolized to smaller proteins and amino acids by proteolytic enzymes.[A19126] | Subcutaneous daratumumab reaches a Cmax of 592µg/mL compared to intravenous daratumumab, which reaches a Cmax of 688µg/mL.[L13296] The AUC of subcutaneous daratumumab is 4017µg/mL | Daratumumab intravenous monotherapy has a volume of distribution of 4.7 ± 1.3L and the combination therapy has a volume of distribution of 4.4 ± 1.5L.[L13290] Subcutaneous daratumumab has a volume of distribution of the central compartment of 5.2L and a volume of distribution of the peripheral compartment of 3.8L.[L13296] | Intravenous daratumumab has a clearance of 171.4 ± 95.3mL/day.[L13290] Subcutaneous daratumumab has a clearance of 119mL/day.[L13296] | Antineoplastic Agents | NA | NA | NA | NA | ADP-ribosyl cyclase 1 | NA | NA | NA | NA | NA | 100 mg/5mL | Solution, concentrate | IV | Injection | NA | NA | Link | NA | NA |
| 10752 | Th1174 | Daratumumab | >Th1174_Daratumumab EVQLLESGGGLVQPGGSLRLSCAVSGFTFNSFAMSWVRQAPGKGLEWVSAISGSGGGTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCAKDKILWFGEPVFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145391.7 | C6466H9996N1724O2010S42 | NA | NA | NA | Intravenous daratumumab has a terminal half life of 18 ± 9 days.6 Subcutaneous daratumumab has a half life of 20 days | Daratumumab is an anti-cancer drug indicated for multiple myeloma in patients who have received at least 3 prior treatments. It was granted accelerated approval by the FDA in November 2016. Marketed under the brand name Darzalex by Janssen Biotech, daratumumab is the first monoclonal antibody injection approved for this indication and provides another options for patients with multiple myeloma resistant to other therapies. Daratumumab induces apoptosis of cancer cells by targeting the CD38 epitope, which is highly expressed on haematological malignancies. | For the treatment of patients with multiple myeloma who have received at least three prior lines of therapy (a proteasome inhibitor (PI) and an immunomodulatory agent) or who are double-refractory to a PI and an immunomodulatory agent. This indication was approved by accelerated approval based on response rate. | In preclinical trials, daratumumab showed synergistic activity with other multiple myeloma therapies, notably lenalidomide. Daratumumab also causes lysis in other cells that express CD38: myeloid-derived suppressor cells, a subset of regulatory T-cells, and NK cells. Decreases in absolute count and percentage of NK cells were observed during treatment. CD4+ and CD8+ T cell absolute counts as well the percentage of total lymphocytes increased in peripheral blood and bone marrow during daratumumab treatment. | Daratumumab is an immunoglobulin G1 kappa monoclonal antibody against CD38 antigen. CD38 is a transmembrane glycoprotein of many functions, including receptor mediated adhesion, signaling, and modulation of cyclase and hydrolase activity. CD38 is expressed on many cell types and tissues, and highly expressed in haematological malignancies including multiple myeloma tumor cells. By binding CD38, daratumumab causes inhibition of tumor cell growth and induces broad-spectrum apoptosis in multiple ways: by Fc-mediated cross linking, by immune-mediate tumor cell lysis through complement dependent cytotoxicity, antibody dependent cell cytotoxicity, and antibody dependent cellular phagocytosis. | Data regarding overdoses of daratumumab are not readily available.[L13290,L13296] Patients should be treated with symptomatic and supportive measures.[L13290,L13296] | Monoclonal antibodies are expected to be metabolized to smaller proteins and amino acids by proteolytic enzymes.[A19126] | Subcutaneous daratumumab reaches a Cmax of 592µg/mL compared to intravenous daratumumab, which reaches a Cmax of 688µg/mL.[L13296] The AUC of subcutaneous daratumumab is 4017µg/mL | Daratumumab intravenous monotherapy has a volume of distribution of 4.7 ± 1.3L and the combination therapy has a volume of distribution of 4.4 ± 1.5L.[L13290] Subcutaneous daratumumab has a volume of distribution of the central compartment of 5.2L and a volume of distribution of the peripheral compartment of 3.8L.[L13296] | Intravenous daratumumab has a clearance of 171.4 ± 95.3mL/day.[L13290] Subcutaneous daratumumab has a clearance of 119mL/day.[L13296] | Antineoplastic Agents | NA | NA | NA | NA | ADP-ribosyl cyclase 1 | Darzalex | Janssen Biotech, Inc. | Janssen Biotech, Inc. | DARZALEX is indicated for the treatment of patients with multiple myeloma who have received at least three prior lines of therapy including a proteasome inhibitor (PI) and an immunomodulatory agent or who are double-refractory to a PI and an immunomodulatory agent. | NA | 100 mg/5mL | Solution, concentrate | IV | The recommended dose of DARZALEX is 16 mg/kg body weight administered as an intravenous infusion according to the following dosing schedule. | The dose of DARZALEX at which severe toxicity occurs is not known. | Infusion reactions | Link | NA | NA |
| 10825 | Th1191 | Vedolizumab | >Th1191_Vedolizumab QVQLVQSGAEVKKPGASVKVSCKGSGYTFTSYWMHWVRQAPGQRLEWIGEIDPSESNTNYNQKFKGRVTLTVDISASTAYMELSSLRSEDTAVYYCARGGYDGWDYAIDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELAGAPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146837 | C6528H10072N1732O2042S42 | 7.6 | NA | NA | 336 to 362 hr. | Vedolizumab is a recombinant humanized IgG1 monoclonal antibody directed against the human lymphocyte α4β7 integrin, a key mediator of gastrointestinal inflammation. It is used in the treatment of moderate to severe active ulcerative colitis and Crohn’s disease for patients who have had an inadequate response with, lost response to, or were intolerant to inhibitors of tumor necrosis factor-alpha (TNF-alpha) or other conventional therapies. By blocking its primary target, α4β7 integrin, vedolizumab reduces inflammation in the gut. | It is indicated for adult patients with moderately to severely active UC or CD who have had an inadequate response with, lost response to, or were intolerant to a tumor necrosis factor (TNF) blocker or immunomodulator; or had an inadequate response with, were intolerant to, or demonstrated dependence on corticosteroids. | Non-clinical studies have shown that the pharmacodynamic effects of vedolizumab are reversible upon removal of the antibody: pharmacologic activity of cells inhibited by vedolizumab could be partially restored within 24 hours after removal, with near complete restoration within 4 days. There are no known drug interactions as vedolizumab is a humanized antibody and does not modulate production of cytokines, which is known to affect drug metabolism | Vedolizumab binds to α4β7 integrin, a key mediator of gastrointestinal inflammation expressed on the surfaces of T and B lymphocytes. By selectively inhibiting the α4β7 integrin, vedolizumab inhibits adhesion of lymphocytes to its natural ligand, mucosal addressin cell adhesion molecule-1 (MAdCAM-1), thereby preventing lymphocytic cells from entering the gut lamina propria and gut-associated lymphoid tissue (GALT). Specifically inhibiting this pathway alleviates GI inflammation without impairing systemic immune responses. | Long-term studies in animals have not been performed to evaluate the carcinogenic potential, mutagenicity, or possible impairments to fertility. Elevated transaminase levels with or without elevated bilirubin has occurred in patients who have received this drug. Progressive multifocal leukoencephalopathy (PML) has not been reported with use of this drug, however it has occurred in patients who have received different integrin receptor antagonists and is therefore considered a risk for this product. Use of vedolizumab may increase risk of developing infections, and one study found that nasopharyngitis occurs more frequently with vedolizumab than with placebo for CD patients (Wang et al, 2014). | The expected consequence of metabolism is proteolytic degradation to small peptides and individual amino acids, and receptor-mediated clearance. | The intended route of administration is intravenous, therefore there is no absorption data and bioavailability is expected to be 100%. | Serum apparent volume of distribution at steady-state has been found to be moderately greater than the serum volume. It is therefore expected to be confined to the systemic circulation, as expected for a high molecular weight protein. | Vedolizumab has a low clearance of 0.180 to 0.266 ml/hr/kg. | Immunosupressive agent, Antineoplastic agent | US2012151248 | 5-Feb-2012 | 5-Feb-2032 | Adalimumab, Belimumab, Certolizumab pegol, Denosumab, Etanercept, Golimumab, Infliximab, Leflunomide, Lenalidomide, Natalizumab, Tacrolimus, Thalidomide, Belimumab, Leflunomide, Natalizumab, Sipuleucel-T, Trastuzumab and Tofacitinib | Integrin alpha-4,Integrin beta-7 | Entyvio | Takeda Pharmaceuticals America, Inc. | Takeda Pharmaceuticals America, Inc. | It is indicated for Adult Ulcerative Colitis and Adult Crohn's Disease | NA | Each single-use vial contains 300 mg vedolizumab, 23 mg L-histidine, 21.4 mg L-histidine monohydrochloride, 131.7 mg L-arginine hydrochloride, 500 mg sucrose and 3 mg polysorbate 80 | Injection, powder, lyophilized, for solution | Intravenous | The recommended dosage of ENTYVIO in adults with ulcerative colitis or Crohn's disease is 300 mg administered by intravenous infusion at zero, two and six weeks and then every eight weeks thereafter | In patients who have had a known serious or severe hypersensitivity reaction to ENTYVIO or any of its excipients (such as dyspnea, bronchospasm, urticaria, flushing, rash and increased heart rate) | The most common adverse reactions were nasopharyngitis, headache, arthralgia, nausea, pyrexia, upper respiratory tract infection, fatigue, cough, bronchitis, influenza, back pain, rash, pruritus, sinusitis, oropharyngeal pain and pain in extremities. | Link | NA | NA |
| 10826 | Th1192 | Ustekinumab | >Th1192_Ustekinumab EVQLVQSGAEVKKPGESLKISCKGSGYSFTTYWLGWVRQMPGKGLDWIGIMSPVDSDIRYSPSFQGQVTMSVDKSITTAYLQWNSLKASDTAMYYCARRRPGQGYFDFWGQGTLVTVSSSSTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTH | 148600 | NA | NA | NA | NA | Following administration of a single subcutaneous dose of 45 mg or 90 mg in patients with psoriasis, the median half-life was 19.8 days and 21.2, respectively. | CNTO 1275 is the experimental name for the human immunosuppressive drug ustekinumab developed by the biotechnology company Centocor. It is a laboratory manufactured, monoclonal antibody directed against interleukins IL-12 and IL-23. | For treatment in psoriasis and psoriatic disorders. | NA | Similar to the immunosuppressive function of Etanercept (Enbrel), CNTO 1275 is designed to interfere with the triggering of the body's inflamatory response through the suppression of certain cytokines. Specifically, CNTO 1275 blocks interleukin IL-12 and IL-23 (via the p40 subunit of IL-12 and IL-23) which help activate certain T-cells. | Signs of dose-limiting toxicity were not observed with intravenous administration of single doses up to 6 mg/kg in clinical trials. Information on overdose of ustekinumab is limited: in the event of overdose, patients should be monitored for any signs and symptoms of drug-related adverse events and appropriate symptomatic treatment should be initiated.[L9383,L9386] | The metabolic pathway of ustekinumab has not been fully characterized; it is expected to undergo nonspecific protein degradation via catabolic pathways in the same manner as endogenous IgG.[L9383,L9386] | The median Tmax following a single subcutaneous dose administration of 45mg and 90mg in adults with psoriasis was 13.5 days and 7 days, respectively. The median Cmax in the same group of patients was 2.4 µg/mL and 5.3 µg/mL at doses of 45mg and 90mg, respectively. The median AUC was 84.9 µg·day/mL and 226.9 µg·day/mL, respectively.[L9491] Following an intravenous induction dose administration, the mean ± SD Cmax was 125.2 ± 33.6 mcg/mL in patients with Crohn’s disease and 129.1 ± 27.6 mcg/mL in patients with ulcerative colitis.[L9386] The systemic exposure of ustekinumab (Cmax and AUC) increases in a linear or dose-proportional manner following a single subcutaneous administration at doses ranging from approximately 24 mg to 240 mg in patients with psoriasis. The estimated absolute bioavailability (F) of ustekinumab following a single subcutaneous dose administration in patients with psoriasis is 57.2%.[L9491] | The total volume of distribution at steady-state was 4.62 L in patients with Crohn’s disease and 4.4 L in patients with ulcerative colitis.[L9386] The median apparent volume of distribution during the terminal phase (Vz/F) ranged from 76 to 161 mL/kg in patients with psoriasis receiving a single subcutaneous dose.[L9491] | The median apparent clearance (CL/F) following a single subcutaneous administration to patients with psoriasis ranged from 2.7 to 5.3 mL/day/kg.[L9491] In patients with Crohn’s disease, the clearance was 0.19 L/day in patients with Crohn’s disease or ulcerative colitis.[L9383,L9386] | Deramtologic agent, Immunosuppressive agent, antineoplastic agent | NA | NA | NA | Belimumab, Denosumab, Infliximab, Leflunomide, Natalizumab, Pimecrolimus, Roflumilast, Sipuleucel-T, Tacrolimus, Tofacitinib, Trastuzumab | Interleukin-12 subunit beta,Interleukin-23 | Stelara | Janssen Biotech, Inc. | Janssen Biotech, Inc. | Psoriasis (Ps) and Psoriatic Arthritis (PsA) | NA | Each 45 mg ustekinumab prefilled syringe also contains: L-histidine and L-histidine monohydrochloride monohydrate (0.5 mg), Polysorbate 80 (0.02 mg), and sucrose (38 mg) to fill to a final volume of 0.5 mL. | solution fro injection | Subcutaneous | In case of psoriasis, for patients weighing ≤ 100 kg (220 lbs), the recommended dose is 45 mg initially and 4 weeks later, followed by 45 mg every 12 weeks. In case of Psoriatic Arthritis ecommended dose is 45 mg initially and 4 weeks later, followed by 45 mg every 12 weeks. | NA | Adverse reactions that occurred at rates less than 1% in the controlled period of Ps STUDIES 1 and 2 through week 12 included: cellulitis, herpes zoster, diverticulitis and certain injection site reaction | Link | NA | NA |
| 10830 | Th1196 | Siltuximab | >Th1196_Siltuximab EVQLVESGGKLLKPGGSLKLSCAASGFTFSSFAMSWFRQSPEKRLEWVAEISSGGSYTYYPDTVTGRFTISRDNAKNTLYLEMSSLRSEDTAMYYCARGLWGYYALDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145000 | C6450H9932N1688O2016S50 | NA | NA | NA | The mean terminal half life after the first intravenous infusion of 11 mg/kg is 20.6 days. | Siltuximab is a chimeric (human-mouse) monoclonal immunoglobulin G1-kappa antibody produced in a Chinese hamster ovary (CHO) cell line by recombinant DNA technology. Siltuximab prevents the binding of IL-6 to soluble and membrane-bound IL-6 receptors by forming high affinity complexes with human interleukin-6 (IL-6). Its use is indicated for the treatment of adult patients with multicentric Castleman’s disease (MCD) who are human immunodeficiency virus (HIV) negative and human herpesvirus-8 (HHV-8) negative. MCD is a rare blood disorder caused by dysregulated IL-6 production, proliferation of lymphocytes, and subsequent enlargement of the lymph nodes. It is administered as a 1 hour intravenous infusion every 3 weeks. | It is indicated for the treatment of patients with multicentric Castleman's disease (MCD) who are human immunodeficiency virus (HIV) negative and human herpesvirus-8 (HHV-8) negative. Siltuximab did not bind to virally produced IL-6 in a nonclinical study and was therefore not studied in patients with MCD who are HIV or HHV-8 positive. | Siltuximab-neutralized antibody-IL-6 complexes interfere with current immunological-based IL-6 quantification methods, therefore measurement of serum or plasma IL-6 concentrations should not be used as a pharmacodynamic marker during treatment. As well, cytochrome P450 enzymes in the liver are down regulated by infection and inflammation stimuli, which includes cytokines such as IL-6. By preventing IL-6 signalling through treatment with siltuximab, CYP450 activity may be increased leading to faster metabolism of drugs that are CYP450 substrates. | Siltuximab complexes with human IL-6 and prevents binding to soluble and membrane-bound IL-6 receptors, thereby inhibiting the proliferation of lymphocytes. | The most common side effects that occurred during siltuximab treatment were pruritis, increased weight, rash, hyperuricemia, and upper respiratory tract infection. Siltuximab should not be administered to patients with severe infections as it may mask signs and symptoms of acute inflammation including suppression of fever and acute phase reactants such as C-reactive protein (CRP). Gastrointestinal perforation has been reported in clinical trials, therefore use with caution in patients who may be at increased risk for GI perforation. | As siltuximab is an antibody, the expected consequence of metabolism is proteolytic degradation to small peptides and individual amino acids, and receptor-mediated clearance. | NA | Based on population pharmacokinetic analysis, the central volume of distribution in a male subject with body weight of 70 kg is 4.5 L. | Body weight was identified as the only statistically significant covariate of siltuximab clearance, therefore body weight based dosing is appropriate. Based on population pharmacokinetic analysis, the clearance of situximab in patients is 0.23 L/day. | Agents reducing cytokine levels,Amino Acids, Peptides, and Proteins,Antibodies,Antineoplastic Agents,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cytochrome P-450 CYP3A Inducers,Cytochrome P-450 CYP3A Inhibitors,Cytochrome P-450 CYP3A4 Inducers,Cytochrome P-450 CYP3A4 Inducers (weak),Cytochrome P-450 CYP3A4 Inhibitors,Cytochrome P-450 CYP3A4 Inhibitors (weak),Cytochrome P-450 Enzyme Inducers,Cytochrome P-450 Enzyme Inhibitors,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Interleukin Inhibitors,Interleukin-6 Antagonist,Proteins,Serum Globulins | US7612182 | 11-Mar-2009 | 8-Jan-2027 | Abiraterone, Alfuzosin, Alprazolam, Aminophylline, Amiodarone, Amlodipine, Apixaban, Apremilast, Aprepitant, Aripiprazole, Armodafinil, Atazanavir, Atorvastatin, Avanafil, Axitinib, Bedaquiline, Belimumab, Benzphetamine, Bisoprolol, Boceprevir, Bortezomib, Bosutinib, Brexpiprazole, Buprenorphine, Buspirone, Cabazitaxel, Cabozantinib, Calcitriol, Carbamazepine, Ceritinib, Chlordiazepoxide, Chloroquine, Cilostazol, Citalopram, Clarithromycin, Clonazepam, Clorazepate, Cobicistat, Cobimetinib, Conivaptan, Crizotinib, Cyclosporine, Cyproterone acetate, Daclatasvir, Dantrolene, Dapsone, Darifenacin, Darunavir, Dasatinib, Delavirdine, Denosumab, Dexamethasone, Diazepam, Dienogest, Diltiazem, Disopyramide, Docetaxel, Doxazosin, Doxorubicin, Dronedarone, Efavirenz, Eliglustat, Elvitegravir, Enzalutamide, Eplerenone, Erlotinib, Erythromycin, Escitalopram, Estradiol, Estrone sulfate, Eszopiclone, Ethosuximide, Etoposide, Etravirine, Everolimus, Exemestane, Felbamate, Felodipine, Fesoterodine, Flibanserin, Flunisolide, Flurazepam, Flutamide, Fosamprenavir, Fosaprepitant, Gefitinib, Guanfacine, Haloperidol, Hydrocodone, Hydroxyprogesterone caproate, Ibrutinib, Idelalisib, Imatinib, Indinavir, Irinotecan, Isavuconazonium, Isosorbide, Isosorbide Dinitrate, Isosorbide Mononitrate, Isradipine, Itraconazole, Ivabradine, Ivacaftor, Ixabepilone, Ixazomib, Ketoconazole, Lansoprazole, Lapatinib, Leflunomide, Levonorgestrel, Lidocaine, Lomitapide, Losartan, Lovastatin, Lurasidone, Macitentan, Maraviroc, Medroxyprogesterone acetate, Mefloquine, Methadone, Midazolam, Mifepristone, Mirtazapine, Modafinil, Naloxegol, Natalizumab, Nateglinide, Nefazodone, Nelfinavir, Nevirapine, Nicardipine, Nifedipine, Nilotinib, Nimodipine, Nisoldipine, Norethisterone, Olaparib, Ondansetron, Ospemifene, Oxycodone, Paclitaxel, Palbociclib, Panobinostat, Pazopanib, Perampanel, Pimecrolimus, Pimozide, Pipotiazine, Praziquantel, Primaquine, Progesterone, Quetiapine, Quinidine, Quinine, Rabeprazole, Ranolazine, Regorafenib, Repaglinide, Rifabutin, Rilpivirine, Riociguat, Ritonavir, Rivaroxaban, Roflumilast, Rolapitant, Ruxolitinib, Saquinavir, Sildenafil, Silodosin, Simeprevir, Simvastatin, Sipuleucel-T, Sirolimus, Solifenacin, Sonidegib, Spiramycin, Stiripentol, Sunitinib, Suvorexant, Tacrolimus, Tamoxifen, Tamsulosin, Tasimelteon, Telaprevir, Telithromycin, Temsirolimus, Teniposide, Tetracycline, Theophylline, Tiagabine, Ticagrelor, Ticlopidine, Tipranavir, Tofacitinib, Tolterodine, Tolvaptan, Toremifene, Trabectedin, Tramadol, Trastuzumab, Trazodone, Triazolam, Trimethoprim, Trimipramine, Ulipristal, Vandetanib, Vemurafenib, Venlafaxine, Verapamil, Vilazodone, Vinblastine, Vincristine, Vinorelbine, Vortioxetine, Zolpidem, Zonisamide, Zopiclone | Interleukin-6 | Sylvant | Janssen Inc | Janssen Inc | NA | NA | 100 mg | Lyophilized powder | Intravenous infusion | SYLVANT 11 mg/kg is given over 1 hour as an intravenous infusion administered every 3 weeks until treatment failure. | Severe hypersensitivity reaction to siltuximab or any of the excipients in SYLVANT. | Concurrent active severe infections; Infusion-related reactions and hypersensitivity | Link | NA | NA |
| 10833 | Th1199 | Ramucirumab | >Th1199_Ramucirumab EVQLVQSGGGLVKPGGSLRLSCAASGFTFSSYSMNWVRQAPGKGLEWVSSISSSSSYIYYADSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCARVTDAFDIWGQGTMVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143600 | C6374H9864N1692O1996S46 | NA | NA | NA | 15 days | Ramucirumab is a human monoclonal antibody (IgG1) against vascular endothelial growth factor receptor 2 (VEGFR2), a type II trans-membrane tyrosine kinase receptor expressed on endothelial cells. By binding to VEGFR2, ramucirumab prevents binding of its ligands (VEGF-A, VEGF-C, and VEGF-D), thereby preventing VEGF-stimulated receptor phosphorylation and downstream ligand-induced proliferation, permeability, and migration of human endothelial cells. VEGFR stimulation also mediates downstream signalling required for angiogenesis and is postulated to be heavily involved in cancer progression, making it a highly likely drug target. In contrast to other agents directed against VEGFR-2, ramucirumab binds a specific epitope on the extracellular domain of VEGFR-2, thereby blocking all VEGF ligands from binding to it. Ramucirumab is indicated for us in advanced gastric or gastro-esophageal junction adenocarcinoma as a single agent or in combination with paclitaxel after prior fluoropyrimidine- or platinum-containing chemotherapy. | For use in advanced gastric or gastro-esophageal junction adenocarcinoma as a single agent or in combination with paclitaxel after prior fluoropyrimidine- or platinum-containing chemotherapy. | Ramucirumab inhibits ligandstimulated activation of VEGF Receptor 2, thereby inhibiting ligand-induced proliferation, and migration of human endothelial cells. Ramucirumab inhibited angiogenesis in an in vivo animal model. | Ramucirumab is a human monoclonal antibody (IgG1) against vascular endothelial growth factor receptor 2 (VEGFR2), a type II trans-membrane tyrosine kinase receptor expressed on endothelial cells. By binding to VEGFR2, ramucirumab prevents binding of its ligands (VEGF-A, VEGF-C, and VEGF-D), thereby preventing VEGF-stimulated receptor phosphorylation and downstream ligand-induced proliferation, permeability, and migration of human endothelial cells. | Ramucirumab packaging includes warnings for arterial thromboembolic events, hypertension, infusion-related reactions, gastrointestinal perforation, clinical deterioration in patients with cirrhosis, and reversible posterior leukoencephalopathy syndrome. The most common reactions observed in single-agent-treated patients at a rate of >10% and >2% higher than placebo were hypertension and diarrhea. The most common adverse reactions observed in patients treated with ramucirumab plus paclitaxel at a rate of of >30% and >2% higher than placebo plus paclitaxel were fatigue, neutropenia, diarrhea, and epistaxis. | NA | NA | 5.5 L | 0.014 L/hour | Antineoplastic and Immunomodulating Agents | US2013067098 | 11-Feb-2011 | 11-Feb-2031 | Belimumab, Pamidronate | Vascular endothelial growth factor receptor 2 | Cyramza | Eli Lilly and Company | Eli Lilly and Company | CYRAMZA®as a single agent, or in combination with paclitaxel, is indicated for the treatment of patients with advanced or metastatic, gastric or gastro-esophageal junction adenocarcinoma with disease progression on or after prior fluoropyrimidine-or platinum-containing chemotherapy. | NA | 10 mg/mL | Solution | Intravenous | Either 8mg/kg or 10 mg/kg every 2 weeks | NA | Hemorrhage; Arterial Thromboembolic Events; Hypertension; Infusion-Related Reactions; Gastrointestinal Perforation; Impaired Wound Healing; Patients with Child-Pugh B or C Cirrhosis; Reversible Posterior Leukoencephalopathy Syndrome; Proteinuria Including Nephrotic Syndrome; Thyroid Dysfunction. | 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 |
| 10841 | Th1204 | Ofatumumab | >Th1204_Ofatumumab EVQLVESGGGLVQPGRSLRLSCAASGFTFNDYAMHWVRQAPGKGLEWVSTISWNSGSIGYADSVKGRFTISRDNAKKSLYLQMNSLRAEDTALYYCAKDIQYGNYYYGMDVWGQGTTVTVSSASTKGPSVFPLAPGSSKSTSGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEP | 146100 | C6480H10022N1742O2020S44 | NA | NA | NA | Approximately 14 days. Range: 2.3 to 61.5 days | Ofatumumab is a human monoclonal antibody for the CD20 protein. Ofatumumab binds specifically to both the small and large extracellular loops of the CD20 molecule. The CD20 molecule is expressed on normal B lymphocytes (pre-B- to mature B-lymphocyte) and on B-cell CLL. The Fab domain of ofatumumab binds to the CD20 molecule and the Fc domain mediates immune effector functions to result in B-cell lysis in vitro. Ofatumumab received FDA approval on April 17, 2014, for use in combination with chlorambucil, for the treatment of previously untreated patients with CLL for whom fludarabine-based therapy is considered inappropriate. Ofatumumab was also approved by Health Canada on August 13th, 2012. | Ofatumumab is indicated for the treatment of patients with chronic lymphocytic leukemia (CLL) refractory to fludarabine and alemtuzumab | In patients with CLL refractory to fludarabine and alemtuzumab, the median decrease in circulating CD19-positive B cells was 91% (n = 50) with the 8th infusion and 85% (n = 32) with the 12th infusion. The time to recovery of lymphocytes, including CD19-positive B cells, to normal levels has not been determined. | Ofatumumab binds specifically to both the small and large extracellular loops of the CD20 molecule. The CD20 molecule is expressed on normal B lymphocytes (pre-B- to mature B-lymphocyte) and on B-cell CLL. The CD20 molecule is not shed from the cell surface and is not internalized following antibody binding. The Fab domain of ofatumumab binds to the CD20 molecule and the Fc domain mediates immune effector functions to result in B-cell lysis in vitro. Data suggest that possible mechanisms of cell lysis include complement-dependent cytotoxicity and antibody-dependent, cell-mediated cytotoxicity. | There is limited information on overdose of ofatumumab. Ofatumumab may cause B-cell depletion in the fetus when administered in pregnant women.[L12612] | Like other monoclonal antibodies, ofatumumab is expected to undergo lysosomal degradation by the reticuloendothelial system and protein catabolism by a target-mediated disposition pathway.[A40006] | In one study consisting of patients with relapsed or refractory chronic lymphocytic leukemia and small lymphocytic lymphoma, the Cmax was 94 µg/mL and the Tmax was 7.3 hours following the first infusion of 300 mg ofatumumab.[A193059] Following subcutaneous injection, ofatumumab is thought to be absorbed primarily into the lymphatic system. Subcutaneous dosing of 20 mg every four weeks resulted in a mean AUCtau of 483 µg | In patients with CLL, the mean volume of distribution at steady-state was 5.8 L.[L12612] Repeated subcutaneous dosing with 20 mg of ofatumumab resulted in a steady-state volume of distribution of 5.42 L.[L15581] | In patients with CLL, the mean clearance at steady-state was 11.6 mL/hour.[L12612] In patients administered ofatumumab subcutaneously in repeated 20 mg injections, the steady-state clearance following B-cell depletion was estimated to be 0.34 L/day.[L15581] | Antineoplastic and Immunomodulating Agents | US8337847 | 25-12-2012 | 25-11-2028 | B-lymphocyte antigen CD20 | B-lymphocyte antigen CD20 | Arzerra | Glaxo Smith Kline Llc | Glaxo Smith Kline Llc | ARZERRA (ofatumumab) is indicated, in combination with chlorambucil, for the treatment of previously untreated patients with chronic lymphocytic leukemia (CLL) for whom fludarabine-based therapy is considered inappropriate | NA | Solution | Liquid | Intravenous | Dilute and administer as an intravenous infusion according to the following schedules. Do not administer as an intravenous push or bolus or as a subcutaneous injection. Pre-medicate before each infusion. For Previously Untreated CLL 300 mg on Day 1 followed 1 week later by 1,000 mg on Day 8 (Cycle 1) followed by 1,000 mg on Day 1 of subsequent 28-day cycles for a minimum of 3 cycles until best response or a maximum of 12 cycles. For Extended Treatment in CLL: 300 mg on Day 1, followed by 1,000 mg 1 week later on Day 8, followed by 1,000 mg 7 weeks later and every 8 weeks thereafter for up to a maximum of 2 years. For Refractory CLL: 300 mg initial dose on Day 1, followed 1 week later by 2,000 mg weekly for 7 doses (Infusions 2 through 8), followed 4 weeks later by 2,000 mg every 4 weeks for 4 doses (Infusions 9 through 12). | NA | Infusion Reactions; Hepatitis B Virus Reactivation; Hepatitis B Virus Infection; Progressive Multifocal Leukoencephalopathy; Tumor Lysis Syndrome; Cytopenias. | Link | NA | NA |
| 10843 | Th1206 | Nivolumab | >Th1206_Nivolumab QVQLVESGGGVVQPGRSLRLDCKASGITFSNSGMHWVRQAPGKGLEWVAVIWYDGSKRYYADSVKGRFTISRDNSKNTLFLQMNSLRAEDTAVYYCATNDDYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 143597.4 | C6362H9862N1712O1995S42 | 6.1-8.5 | NA | 80-90 ºC | 26.7 days | Nivolumab is a fully human IgG4 monoclonal antibody that acts as an immunomodulator by blocking ligand activation of programmed cell death 1 (PD-1) receptor on T cells. It is indicated for use in patients with unresectable (cannot be surgically removed) or metastatic melanoma who no longer respond to other drugs. Nivolumab is administered as an intravenous infusion over 60 minutes every 2 weeks. | Nivolumab is indicated for the treatment of unresectable or metastatic melanoma for patients who no longer respond to treatment with other drugs. It is intended for use in patients who have been previously treated with ipilimumab and is used for melanoma patients after treatment with ipilimumab and a BRAF inhibitor in patients whose tumors express BRAF V600 gene mutations. Historically there have been very few effective treatments for advanced melanoma, which is why this product was approved under an FDA accelerated program to allow earlier patient access. | Combined nivolumab (anti-PD-1) and ipilimumab (anti-CTLA-4) mediated inhibition results in enhanced T-cell function that is greater than the effects of either antibody alone, and results in improved anti-tumor responses in metastatic melanoma. In murine syngeneic tumor models, dual blockade of PD-1 and CTLA-4 resulted in increased anti-tumor activity. | Nivolumab is a human immunoglobulin G4 (IgG4) monoclonal antibody that binds to the programmed cell death 1 (PD-1) receptor and selectively blocks interaction with its programmed death ligands PD-L1 and PD-L2. Upregulation of PD-1 ligands occurs in some tumors and signalling through this pathway can contribute to inhibition of active T-cell immune surveillance of tumour tissue. The inhibitory effect of PD-1 and its ligands occurs through the promotion of apoptosis in antigen specific T cells while simultaneously blocking apoptosis in suppressor T cells. Blocking PD-1 activity has been shown to lead to decreased tumour growth in mouse tumour models. | Data regarding overdoses of nivolumab are not readily available.[L12129] Common adverse effects include Rash, pruritus, cough, upper respiratory tract infection, and peripheral edema.[L12129] | There have not been formal studies regarding the specific metabolism of nivolumab but as a human monoclonal antibody, it has been suggested to be degraded to small peptides and individual amino acids.[L12618] | Pharmacokinetic studies have suggested that nivolumab presents linear pharmacokinetics with a dose-proportional increase in peak concentration and AUC. The time to peak plasma concentration ranges between 1-4 hours.[A35187] The absorption pharmacokinetic properties respective to the administration of a dose of 10 mg/kg are reported to be Cmax, Tmax and AUC of 242 µg/kg, 2.99 hours and 68100 µg | The volume of distribution at steady state when a dose of 10 mg/kg of nivolumab is administered is reported to be 91.1 mL/kg.[A35285] At doses ranging from 0.1 to 20 mg/kg the volume of distribution is reported to be 8L.[A35290] | The estimated clearance rate of nivolumab is 9.4 mL/h.[A35284] The clearance rate seems to be increased according to body weight.[A35290] | Antineoplastic and Immunomodulating Agents | US2013173223 | 13-05-2013 | 13-05-2033 | Belimumab | Programmed cell death protein 1 | Opdivo | E.R. Squibb & Sons, L.L.C. | E.R. Squibb & Sons, L.L.C. | OPDIVO® (nivolumab) as a single agent is indicated for the treatment of patients with BRAF V600 wild-type unresectable or metastatic melanoma; Also for the treatment of patients with BRAF V600 mutation-positive unresectable or metastatic melanoma; approved under accelerated approval based on progression-free survival. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials; and in combination with ipilimumab, is indicated for the treatment of patients with unresectable or metastatic melanoma. | NA | solution | Liquid | Intravenous | The recommended dose of OPDIVO as a single agent is 3 mg/kg administered as an intravenous infusion over 60 minutes every 2 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; Immune-Mediated Rash; Immune-Mediated Encephalitis; Other Immune-Mediated Adverse Reactions; Infusion Reactions; Complications of Allogeneic HSCT after OPDIVO. | Link | NA | NA |
| 10848 | Th1211 | Ixekizumab | >Th1211_Ixekizumab QVQLVQSGAEVKKPGSSVKVSCKASGYSFTDYHIHWVRQAPGQGLEWMGVINPMYGTTDYNQRFKGRVTITADESTSTAYMELSSLRSEDTAVYYCARYDYFTGTGVYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 1,46,158 | C6492H10012N1728O2028S46 | NA | NA | NA | 13 days | Ixekizumab is a humanized immunoglobulin G subclass 4 (IgG4) monoclonal antibody (mAb) with neutralizing activity against IL-17A. Ixekizumab is produced by recombinant DNA technology in a recombinant mammalian cell line and purified using standard technology for bioprocessing. Ixekizumab is comprised of two identical light chain polypeptides of 219 amino acids each and two identical heavy chain polypeptides of 445 amino acids each, and has a molecular weight of 146,158 Daltons for the protein backbone of the molecule. | For the treatment of adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy | No formal pharmacodynamic studies have been conducted with TALTZ. | Ixekizumab is a humanized IgG4 monoclonal antibody that selectively binds with the interleukin 17A (IL-17A) cytokine and inhibits its interaction with the IL-17 receptor. IL-17A is a naturally occurring cytokine that is involved in normal inflammatory and immune responses. Ixekizumab inhibits the release of proinflammatory cytokines and chemokines. | The most common adverse reactions associated with Ixekizumab treatment are injection site reactions, upper respiratory tract infections, nausea, and tinea infections. | The metabolic pathway of ixekizumab has not been characterized. As a humanized IgG4 monoclonal antibody ixekizumab is expected to be degraded into small peptides and amino acids via catabolic pathways in the same manner as endogenous IgG. | Following a single subcutaneous dose of 160 mg in subjects with plaque psoriasis, ixekizumab reached peak mean (±SD) serum concentrations (Cmax) of 16.2 ±6.6 mcg/mL by approximately 4 days post dose. | The mean (geometric CV%) volume of distribution at steady-state was 7.11 L (29%) in subjects with plaque psoriasis. | 0.39 L/day | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic and Immunomodulating Agents,Blood Proteins,Dermatologicals,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Interleukin Inhibitors,Interleukin-17,Interleukin-17A Antagonist,Misc. Skin and Mucous Membrane Agents,Proteins,Serum Globulins | NA | NA | NA | NA | Interleukin-17A | Taltz | Eli lilly | Eli lilly | Taltz is indicated for the treatment of moderate to severe plaque psoriasis in adults who are candidates for systemic therapy or phototherapy. | NA | 80 mg of ixekizumab in a 1 mL single-dose prefilled autoinjector or a single-dose prefilled syringe | Sterile, preservative free, clear and colorless to slightly yellow solution | Subcutaneous | TALTZ is administered by subcutaneous injection. The recommended dose is 160 mg (two 80 mg injections) at Week 0, followed by 80 mg at Weeks 2, 4, 6, 8, 10, and 12, then 80 mg every 4 weeks. | TALTZ is contraindicated in patients with a previous serious hypersensitivity reaction, such as anaphylaxis, to ixekizumab or to any of the excipients | Infections; Hypersensitivity Reactions; Inflammatory Bowel Disease | Link | NA | NA |
| 10858 | Th1220 | Brodalumab | NA | 1,44,000 | C6372H9840N1712O1988S52 | NA | NA | NA | NA | Brodalumab has been used in trials studying the treatment of Asthma, Psoriasis, Crohn's Disease, Psoriatic Arthritis, and Rheumatoid Arthritis. Brodalumab was FDA approved in February, 2017 as Siliq for the treatment of moderate-to-severe plaque psoriasis. | Brodalumab has been approved for the treatment of psoriasis vulgaris, psoriatic arthritis, pustular psoriasis and psoriatic erythroderma. | Increase in the level of IL-17 due to blocking of its receptors. | Brodalumab binds with high affinity to interleukin (IL)-17 receptor A, thereby inhibiting several pro-inflammatory cytokines from the IL-17 family. | NA | NA | NA | 4.62 L. | 0.223 L/day. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | The risk or severity of adverse effects can be increased with combination of drugs like BCG, Denosumab, Fingolimod, G17DT, GI-5005, INGN 201, INGN 225, Leflunomide, Natalizumab, Pimecrolimus. | Interleukin 17 receptor A | Siliq | NA | NA | SILIQ™ is indicated for the treatment of moderate to severe plaque psoriasis in adult patients who are candidates for systemic therapy or phototherapy and have failed to respond or have lost response to other systemic therapies. | NA | Each SILIQ single-dose prefilled syringe delivers 1.5 mL of solution containing 210 mg of brodalumab formulated in glutamate (6.5 mg), polysorbate 20 (0.15 mg), proline (36 mg), and Water for Injection, USP at pH 4.8. | sterile, preservative-free, clear to slightly opalescent, colorless to slightly yellow solution | Subcutaneous | The recommended SILIQ dose is 210 mg administered by subcutaneous injection at Weeks 0, 1, and 2 followed by 210 mg every 2 weeks. | SILIQ is contraindicated in patients with Crohn’s disease because SILIQ may cause worsening of disease | Suicidal Ideation and Behavior, Infection and Crohn’s Disease | Link | NA | NA |
| 10865 | Th1226 | Dinutuximab | NA | 145000 | C6422H9982N1722O2008S48 | NA | NA | NA | The terminal half-life is 10 days | Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. It is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse. | Dinutuximab is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse. | In vitro dinutuximab binds to neuroblastoma tumour cells and mediates the lysis of tumour cells via cell-mediated and complement-mediated cytotoxicity. | Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. | The most common (incidence 15 %) grade 3 or 4 treatment-related adverse events in dinutuximab compared with standard therapy recipients were neuropathic pain (52 vs. 6 %), fever without neutropenia (39 vs. 6 %), any in-fection (39 vs. 22 %), hypokalaemia (35 vs. 2 %), hypersensitivity reactions (25 vs. 1 %), hyponatraemia (23 vs. 4 %), elevation of alanine transferase levels (23 vs. 3 %) and hypotension (18 vs. 0 %). Based on its mechanism of action, dinutuximab may cause fetal harm when administered to a pregnant woman however, there are no studies in pregnant women and no reproductive studies in animals to inform the drug-associated risk. Non-clinical studies suggest that dinutuximab-induced neuropathic pain is mediated by binding of the antibody to the GD2 antigen located on the surface of peripheral nerve fibers and myelin and subsequent induction of cell- and complement-mediated cytotoxicity. In clinical trials, 114 (85%) patients treated in the dinutuximab/RA group experienced pain despite pre-treatment with analgesics including morphine sulfate infusion. Severe (Grade 3) pain occurred in 68 (51%) patients in the dinutuximab/RA group compared to 5 (5%) patients in the RA group. Pain typically occurred during the dinutuximab infusion and was most commonly reported as abdominal pain, generalized pain, extremity pain, back pain, neuralgia, musculoskeletal chest pain, and arthralgia. | NA | NA | The mean volume of distribution at steady state (Vdss) is 5.4 L | The clearance is 0.21 L/day and increases with body size | Antibody, Immunosuppresive agent, Antineoplastic agent | US20140170155 | 18-02-2014 | 18-02-2038 | Severity of adverse effect can be increased while combining Dinutuximab with Acebutolol, Acetazolamide, Acetyldigitoxin, Aldesleukin, Aliskiren, Amifostine, Amiloride, Amiodarone, Amlodipine etc | GD2 disialoganglioside | unituxin | NA | NA | Unituxin (dinutuximab) is indicated, in combination with granulocyte- macrophage colony - stimulating factor (GM- CSF), interleukin- 2 (IL- 2) and 13- cis -retinoic acid (RA ), for the treatment of pediatric patients with high- risk neuroblastoma who achieve at least a partial response to prior first -line multiagent, multimodality therapy. | NA | 1 mL of concentrate contains 3.5 mg of dinutuximab | sterile, preservative-free, clear/colorless to slightly opalescent solution | Intravenous | The recommended dose of Unituxin is 17.5 mg/m2/day administered as an intravenous infusion over 10 to 20 hours for 4 consecutive days for a maximum of 5 cycles. | History of anaphylaxis to dinutuximab. | The most common serious adverse reactions (≥ 5%) are infections, infusion reactions, hypokalemia, hypotension, pain, fever, and capillary leak syndrome. | Link | NA | NA |
| 10872 | Th1232 | Lenograstim | NA | 18668 | C840-H1330-N222-O242-S8 | NA | NA | NA | The pharmacokinetic profile of lenograstim is similar in healthy volunteers and cancer patients with elimination half-life (t½β) values of 2.3 - 3.3 hrs (volunteers); 2.8-7.5 hrs (cancer patients) following sc administration, and 0.8 - 2.1 hrs (volunteers); 1.1 - 4.0 hrs (cancer patients) following iv administration. | Lenograstim is a recombinant granulocyte colony-stimulating factor which functions as an immunostimulator. | The drug is used to reduce the risk of life-threatening infection in patients with neutropenia, particularly after cytotoxic chemotherapy. GRANOCYTE ( Lenograstim) is indicated as a treatment to reduce the duration of neutropenia and the severity of infections in patients with non-myeloid malignancy who have undergone autologous or allogeneic bone marrow transplantation, or treatment with established cytotoxic chemotherapy and in addition to reduce the incidence of infection associated with established cytotoxic chemotherapy. GRANOCYTE is also indicated to mobilise peripheral blood progenitor cells (PBPCs) with GRANOCYTE alone, or after myelosuppressive chemotherapy, in order to accelerate haematopoietic recovery by infusion of such cells, after myelosuppressive or myeloablative therapy. GRANOCYTE is also indicated to accelerate the engraftment of these cells after their reinfusion. GRANOCYTE is also indicated for the treatment of severe chronic neutropenia including congenital agranulocytosis (Kostmann's syndrome). | Lenograstim has been confirmed as a valuable adjunct to minimise the haematological toxicity of myelosuppressive chemotherapy in patients with malignant disease. The drug also enhances neutrophil recovery in patients undergoing stem cell rescue, and assists PBSC mobilisation. | Lenograstim is the glycosylated recombinant form of human granulocyte colony stimulating factor. Lenograstim accelerates neutrophil recovery significantly after chemotherapy, with beneficial effects on clinical end-points such as incidence of laboratory-confirmed infection and length of hospital stay. Chemotherapy dose intensity has also been increased in patients receiving lenograstim, notably those with breast or small cell lung cancer, although improvements in tumour response and survival have not been demonstrated. Lenograstim also assists neutrophil recovery in patients undergoing bone marrow transplantation, and stimulates the production of peripheral blood stem cells (PBSCs) for autologous transfusion after aggressive chemotherapy. | Species observed : Human (Man) Test type: TDLo ( Lowest Published Toxic Dose) Route of exposure: Subcutaneous Dose/Duration: 21428mg/kg/15 Toxic Effect: Skin and appendages: Dermatitis, allergic ( after systemic exposure ) Species observed : Rodent - Rat Test type: LD50 Route of exposure: Oral Dose/Duration: >5mg/kg Toxic Effect: Details of toxic effects not reported other than lethal dose value Species observed : Rodent - Rat Test type: LD50 Route of exposure: Subcutaneous Dose/Duration: >5mg/kg Toxic Effect: Details of toxic effects not reported other than lethal dose value Species observed : Rodent - Rat Test type: LD50 Route of exposure: Intravenous Dose/Duration: >5mg/kg Toxic Effect: Details of toxic effects not reported other than lethal dose value Species observed : Mammal - Dog Test type: LD50 Route of exposure: Intravenous Dose/Duration: >5mg/kg Toxic Effect: Details of toxic effects not reported other than lethal dose value Species observed : Mammal - Dog Test type: LD50 Route of exposure: Subcutaneous Dose/Duration: >5mg/kg Toxic Effect: Details of toxic effects not reported other than lethal dose value | Lenograstim is metabolised to peptides. | During repeated dosing (iv and sc routes), peak serum concentrations (at the end of iv infusion or after sc injection) are proportional to the injected dose. Repeated dosing with lenograstim by the two injection routes results in no evidence of drug accumulation. | Apparent distribution volume (Vd area) is approximately 52 ± 5 mL/kg body weight. | Plasma clearance of lenograstim increased 3-fold (from 50 up to 150 mL/min) during repeated sc dosing. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Granulocyte colony-stimulating factor receptor | Granocyte | NA | NA | Reducing the duration of neutropenia and risk of infection in people treated with chemotherapy for cancer. | L-treonine-colony-stimulating factor | NA | Solid | Subcutaneous or Intravenous | NA | People with malignancies affecting myeloid cell | Decrease in the number of platelets in the blood (thrombocytopenia), Headache, Feeling weak, Bone pain, Back pain, Elevated levels of liver enzymes | 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 |
| 11015 | Th1241 | Asparaginase Escherichia coli | >Th1241_Asparaginase_Escherichia_coli MEFFKKTALAALVMGFSGAALALPNITILATGGTIAGGGDSATKSNYTVGKVGVENLVNAVPQLKDIANVKGEQVVNIGSQDMNDNVWLTLAKKINTDCDKTDGFVITHGTDTMEETAYFLDLTVKCDKPVVMVGAMRPSTSMSADGPFNLYNAVVTAADKASANRGVLVVMNDTVLDGRDVTKTNTTDVATFKSVNYGPLGYIHNGKIDYQRTPARKHTSDTPFDVSKLNELPKVGIVYNYANASDLPAKALVDAGYDGIVSAGVGNGNLYKSVFDTLATAAKTGTAVVRSSRVPTGATTQDAEVDDAKYGFVASGTLNPQKARVLLQLALTQTKDPQQIQQIFNQY | NA | C1377H2208N382O442S17 | 4.67 | 0.059 | NA | Plasma half life of L-asparagine derived from _E. coli_ following intravenous injection was 8-30 hrs [FDA Label]. Plasma half-life was 34 to 49 hours after intramuscular injection [FDA Label]. Half-life (mean ± SD) of native _E. coli_ asparaginase is approximately 1.28 ± 0.35 days [A31999]. | Asparaginase derived from _Escherichia coli_ (L-asparagine amidohydrolase, EC 3.5.1.1) is an enzyme responsible for the metabolism of L-asparagine, by catalyzing L-asparagine into L-aspartic acid and ammonia. It also facilitates the production of oxaloacetate which is needed for general cellular metabolism. Asparaginase from _E. coli_ has clinically shown to exhibit antitumor actions in models of leukaemias [A31996, A31997]. L-asparaginase of _E. coli_ is marketed under several different trade names, including Elspar, for the treatment of acute lymphoblastic leukemia (ALL) as part of a multi-agent chemotherapeutic regimen. It is available as intramuscular or intravenous injections. Therapeutic L-asparaginase from _E. coli_ works by depleting the levels of non-essential amino acid, asparagine, in lymphoblastic leukemic cells thus promoting apoptotic cell death [A31999]. For patients who develop hypersensitivity to _E. coli_-derived formulations of L-asparaginase, the use of PEGylated or non-PEGylated [DB08886] is recommended [A31999]. | Indicated as a component of a multi-agent chemotherapeutic regimen for the treatment of patients with acute lymphoblastic leukemia (ALL) [FDA Label]. | In clinical trials of patients with previously untreated, standard-risk ALL, administration of asparaginase resulted in a decrease of plasma asparagine levels from average of 41 µM to less than 3 µM [FDA Label]. The native asparaginase in whom plasma enzyme activity before treatment was greater than 0.1 International Units/mL [FDA Label]. In this study, cerebrospinal fluid asparagine levels in patients treated with asparaginase decreased from 2.8 µM (pretreatment) to 1.0 µM and 0.3 µM at day 7 and day 28 of induction, respectively [FDA Label]. Native E. coli asparaginase results in asparagine depletion in 14 to 23 days following administration [A31999]. | Asparagine is a non-essential amino acid that maintains DNA, RNA and protein synthesis and promotes cell growth. While healthy and normal cells are capable of obtaining asparagine via dietary intake or synthesizing the asparagine from aspartate via asparagine synthetase activity, lymphoblastic leukemic cells lack the asparagine synthetase enzyme and cannot produce asparagine _de novo_ [A31999]. Thus, leukemic cells rely on exogenous source of asparagine for protein synthesis and cell survival [A31999]. L-asparagine from E. coli serves to deplete plasma levels of asparagine in leukemic cells by converting L-asparagine to L-aspartic acid and ammonia [A31999], leading to reduced reduced DNA, RNA and protein synthesis; inhibition of cell growth; and ultimately the activation of apoptotic cell-death mechanisms [A31999]. Normal cells, however, are able to synthesize asparagine and thus are affected less by the rapid depletion produced by treatment with the enzyme asparaginase [FDA Label]. | No studies assessing the mutagenic or carcinogenic potential of _E. coli_ L-asparagine have been conducted. In the Ames assay, no mutagenic effect was demonstrated when tested against Salmonella typhimurium strains [FDA Label]. No studies have been performed on impairment of fertility [FDA Label]. Following a single, intravenous injection of 12,500 to 50,000 International Units L-asparagine/kg in rabbits, edema and necrosis of pancreatic islets were observed. The clinical relevance of this finding is unclear as it does not indicate pancreatitis [FDA Label]. | NA | In a study in patients with metastatic cancer and leukemia, daily intravenous administration of L-asparaginase derived from _E. coli_ resulted in a cumulative increase in plasma levels. Following intramuscular injection in patients with metastatic cancer and leukemia, peak plasma levels of asparaginase was achieved 14 to 24 hours post-dosing [FDA Label]. Peak asparaginase activity of native _E. coli_ asparaginase can be observed in 24 to 48 hours following administration [A31999]. | Apparent volume of distribution was slightly greater than the plasma volume. Asparaginase levels in cerebrospinal fluid were less than 1% of concurrent plasma levels [A31999]. | NA | Antineoplastic Agents | NA | NA | NA | NA | L-asparagine | Kidrolase | Jazz Pharmaceuticals France Sas | Jazz Pharmaceuticals France Sas | Intramuscular; Intravenous | 10000 unit / vial | NA | Fever, chills (see flu like symptoms) Nausea and vomiting Allergic reaction, (sudden onset of wheezing, itching, rash, face swelling, agitation, low blood pressure). You will be monitored closely for this reaction. Poor appetite Stomach cramping Central neurotoxicity: excessive sleepiness, depression, hallucinations, agitation, disorientation or seizure. Less commonly seen stupor, confusion and/or coma. | Kidrolase is an anti-cancer ("antineoplastic" or "cytotoxic") chemotherapy drug. This medication is classified as an "enzyme." | Acute lymphocytic leukemia (ALL) | NA | NA | Link | Link | NA |
| 11016 | Th1241 | Asparaginase Escherichia coli | >Th1241_Asparaginase_Escherichia_coli MEFFKKTALAALVMGFSGAALALPNITILATGGTIAGGGDSATKSNYTVGKVGVENLVNAVPQLKDIANVKGEQVVNIGSQDMNDNVWLTLAKKINTDCDKTDGFVITHGTDTMEETAYFLDLTVKCDKPVVMVGAMRPSTSMSADGPFNLYNAVVTAADKASANRGVLVVMNDTVLDGRDVTKTNTTDVATFKSVNYGPLGYIHNGKIDYQRTPARKHTSDTPFDVSKLNELPKVGIVYNYANASDLPAKALVDAGYDGIVSAGVGNGNLYKSVFDTLATAAKTGTAVVRSSRVPTGATTQDAEVDDAKYGFVASGTLNPQKARVLLQLALTQTKDPQQIQQIFNQY | NA | C1377H2208N382O442S17 | 4.67 | 0.059 | NA | Plasma half life of L-asparagine derived from _E. coli_ following intravenous injection was 8-30 hrs [FDA Label]. Plasma half-life was 34 to 49 hours after intramuscular injection [FDA Label]. Half-life (mean ± SD) of native _E. coli_ asparaginase is approximately 1.28 ± 0.35 days [A31999]. | Asparaginase derived from _Escherichia coli_ (L-asparagine amidohydrolase, EC 3.5.1.1) is an enzyme responsible for the metabolism of L-asparagine, by catalyzing L-asparagine into L-aspartic acid and ammonia. It also facilitates the production of oxaloacetate which is needed for general cellular metabolism. Asparaginase from _E. coli_ has clinically shown to exhibit antitumor actions in models of leukaemias [A31996, A31997]. L-asparaginase of _E. coli_ is marketed under several different trade names, including Elspar, for the treatment of acute lymphoblastic leukemia (ALL) as part of a multi-agent chemotherapeutic regimen. It is available as intramuscular or intravenous injections. Therapeutic L-asparaginase from _E. coli_ works by depleting the levels of non-essential amino acid, asparagine, in lymphoblastic leukemic cells thus promoting apoptotic cell death [A31999]. For patients who develop hypersensitivity to _E. coli_-derived formulations of L-asparaginase, the use of PEGylated or non-PEGylated [DB08886] is recommended [A31999]. | Indicated as a component of a multi-agent chemotherapeutic regimen for the treatment of patients with acute lymphoblastic leukemia (ALL) [FDA Label]. | In clinical trials of patients with previously untreated, standard-risk ALL, administration of asparaginase resulted in a decrease of plasma asparagine levels from average of 41 µM to less than 3 µM [FDA Label]. The native asparaginase in whom plasma enzyme activity before treatment was greater than 0.1 International Units/mL [FDA Label]. In this study, cerebrospinal fluid asparagine levels in patients treated with asparaginase decreased from 2.8 µM (pretreatment) to 1.0 µM and 0.3 µM at day 7 and day 28 of induction, respectively [FDA Label]. Native E. coli asparaginase results in asparagine depletion in 14 to 23 days following administration [A31999]. | Asparagine is a non-essential amino acid that maintains DNA, RNA and protein synthesis and promotes cell growth. While healthy and normal cells are capable of obtaining asparagine via dietary intake or synthesizing the asparagine from aspartate via asparagine synthetase activity, lymphoblastic leukemic cells lack the asparagine synthetase enzyme and cannot produce asparagine _de novo_ [A31999]. Thus, leukemic cells rely on exogenous source of asparagine for protein synthesis and cell survival [A31999]. L-asparagine from E. coli serves to deplete plasma levels of asparagine in leukemic cells by converting L-asparagine to L-aspartic acid and ammonia [A31999], leading to reduced reduced DNA, RNA and protein synthesis; inhibition of cell growth; and ultimately the activation of apoptotic cell-death mechanisms [A31999]. Normal cells, however, are able to synthesize asparagine and thus are affected less by the rapid depletion produced by treatment with the enzyme asparaginase [FDA Label]. | No studies assessing the mutagenic or carcinogenic potential of _E. coli_ L-asparagine have been conducted. In the Ames assay, no mutagenic effect was demonstrated when tested against Salmonella typhimurium strains [FDA Label]. No studies have been performed on impairment of fertility [FDA Label]. Following a single, intravenous injection of 12,500 to 50,000 International Units L-asparagine/kg in rabbits, edema and necrosis of pancreatic islets were observed. The clinical relevance of this finding is unclear as it does not indicate pancreatitis [FDA Label]. | NA | In a study in patients with metastatic cancer and leukemia, daily intravenous administration of L-asparaginase derived from _E. coli_ resulted in a cumulative increase in plasma levels. Following intramuscular injection in patients with metastatic cancer and leukemia, peak plasma levels of asparaginase was achieved 14 to 24 hours post-dosing [FDA Label]. Peak asparaginase activity of native _E. coli_ asparaginase can be observed in 24 to 48 hours following administration [A31999]. | Apparent volume of distribution was slightly greater than the plasma volume. Asparaginase levels in cerebrospinal fluid were less than 1% of concurrent plasma levels [A31999]. | NA | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | L-asparagine | Rylaze | Jazz Pharmaceuticals, Inc. | Jazz Pharmaceuticals, Inc. | Intramuscular | 20 mg/1mL | RYLAZE is contraindicated in patients with a history of: Serious hypersensitivity reactions to Erwinia asparaginase, including anaphylaxis Serious pancreatitis during previous asparaginase therapy Serious thrombosis during previous asparaginase therapy Serious hemorrhagic events during previous asparaginase therapy | abnormal liver test, nausea, musculoskeletal pain, fatigue, infection, headache, fever, drug hypersensitivity, febrile neutropenia, decreased appetite, sores or inflammation in the mouth, bleeding, high blood sugar (hyperglycemia), abdominal pain, fast heart rate, diarrhea, constipation, dehydration, numbness and tingling of extremities, cough, and insomnia. | Rylaze is a cancer medicine. Erwinaze is used to treat acute lymphoblastic leukemia in adults and children at least 1 year old. Rylaze is used to treat lymphoblastic lymphoma in adults and children at least 1 month old who have become allergic to other forms of asparaginase such as Elspar or Oncaspar.... | Rylaze (asparaginase erwinia chrysanthemi (recombinant) - rywn) is a prescription medicine used to treat the symptoms of Acute Lymphoblastic Leukemia, and Lymphoblastic Lymphoma. Rylaze may be used alone or with other medications. | NA | Asparaginase erwinia chrysanthemi (recombinant)-rywn contains an asparagine specific bacterial enzyme (L-asparaginase). L-asparaginase is a tetrameric enzyme that consists of four identical 35 kDa subunits with a combined molecular weight of 140 kDa. The amino acid sequence is identical to native asparaginase Erwinia chrystanthemi (also known as crisantaspase). The activity of asparaginase erwinia chrysanthemi (recombinant)-rywn is expressed in units, defined as the amount of enzyme that catalyzes the conversion of 1μmol of L-asparagine per reaction minute, per mg of protein. | Link | Link | NA |
| 11374 | Th1245 | Interferon alfa-2a | >Th1245_Interferon_alfa-2a CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 19241.1 | C860H1353N227O255S9 | 5.99 | -0.336 | NA | The IM half-life of interferon alfa-2a is 6 hours to 8 hours; the half-life for IV infusion is 3.7 hours to 8.5 hours (mean 5.1 hours). | Interferon a (human leukocyte protein moiety reduced). A type I interferon consisting of 165 amino acid residues with lysine in position 23. This protein is produced by recombinant DNA technology and resembles interferon secreted by leukocytes. It is used extensively as an antiviral or antineoplastic agent. An oral form is being developed by Amarillo Biosciences. | For the treatment of chronic hepatitis C, hairy cell leukemia, AIDS-related Kaposi's sarcoma, and chronic myelogenous leukemia. Also for the treatment of oral warts arising from HIV infection. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | Interferon alfa-2 may cause serious adverse effects such as anemia; autoimmune diseases, including vasculitis, arthritis, hemolytic anemia, and erythematosus syndrome; cardiotoxicity; hepatotoxicity; hyperthyroidism or hypothyroidism; transient ischemic attacks; leukopenia; neurotoxicity; peripheral neuropathy; and thrombocytopenia. Some lesser side effects that may not need medical attention include blurred vision, change in taste or metallic taste, cold sores or stomatitis, diarrhea, dizziness, dry mouth, dry skin or itching, flu-like syndrome, increased sweating, leg cramps, loss of appetite, nausea or vomiting, skin rash, unusual tiredness, weight loss, and partial loss of hair. | NA | Absorption is high (greater than 80%) when administered intramuscularly or subcutaneously. | * 0.223 to 0.748 L/kg [healthy people] | * 2.14 - 3.62 mL/min/kg [healthy] | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | Roferon A Sterile Pws 3m Unit/vial | Hoffmann La Roche | Hoffmann La Roche | Intramuscular; Subcutaneous | 3000000 unit / vial | Roferon-A (interferon alfa-2a, recombinant) is contraindicated in patients with: Hypersensitivity to Roferon-A (interferon alfa-2a, recombinant) or any of its components Autoimmune hepatitis Hepatic decompensation (Child-Pugh class B and C) before or during treatment Roferon-A (interferon alfa-2a, recombinant) is contraindicated in neonates and infants because it contains benzyl alcohol. Benzyl alcohol is associated with an increased incidence of neurologic and other complications in neonates and infants, which are sometimes fatal. | lu like symptoms such as fatigue (58% to 95%), fever (25% to 92%), myalgia (68% to 71%), headache (44% to 66%), chills (23% to 64%), arthralgia/bone pain (25% to 47%), asthenia (6%), sweating (5%), leg cramps (3%), and malaise (1%). Weight loss (25% to 33%), change in taste or smell (3% to 25%), pain (24%), back pain (16%), night sweats (8%), menstrual irregularity (4%), reversible hearing loss, and tinnitus have also been reported | NA | NA | NA | NA | Link | Link | NA |
| 11557 | Th1250 | Pegademase | >Th1250_Pegademase MAQTPAFNKPKVELHVHLDGAIKPETILYYGRKRGIALPADTPEELQNIIGMDKPLSLPEFLAKFDYYMPAIAGCREAVKRIAYEFVEMKAKDGVVYVEVRYSPHLLANSKVEPIPWNQAEGDLTPDEVVSLVNQGLQEGERDFGVKVRSILCCMRHQPSWSSEVVELCKKYREQTVVAIDLAGDETIEGSSLFPGHVKAYAEAVKSGVHRTVHAGEVGSANVVKEAVDTLKTERLGHGYHTLEDATLYNRLRQENMHFEVCPWSSYLTGAWKPDTEHPVVRFKNDQVNYSLNTDDPLIFKSTLDTDYQMTKNEMGFTEEEFKRLNINAAKSSFLPEDEKKELLDLLYKAYGMPSPASAEQCL | 40788.2 | C1821H2834N484O552S14 | 5.33 | -0.428 | NA | plasma adenosine deaminase elimination half-life is 3 to >6 days | Bovine adenosine deaminase derived from bovine intestine that has been extensively pegylated for extended serum half life. | For treatment of adenosine deaminase deficiency | Used to replace deficient or inactive adenosine deaminase which leads to severe combined immunodeficiency disease (SCID). The enzyme is responsible for converting adenosine to inosine. In the absence of adenosine deaminase, the purine substrates adenosine, 2'-deoxyadenosine and their metabolites are actually toxic to lymphocytes thereby leading to diminished immune function. | Pegademase converts adenosine (toxic) to inosine (less toxic) by deamination. It also converts 2'-deoxyadenosine to 2'-deoxyinosine via deamination. | NA | NA | Time to peak for plasma adenosine deaminase is 2 to 3 days | NA | NA | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Adenosine,Growth factor receptor-bound protein 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11737 | Th1255 | Antithymocyte immunoglobulin (rabbit) | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | 2-3 days, may increase after multiple doses administration | Rabbit anti-thymocyte globulin. Thymoglobulin is a polyclonal antibody that suppresses certain types of immune cells responsible for acute organ rejection in transplant patients. Thymoglobulin is a mixture of antibodies intended to bind to various cell surface antigens. The most common mode of action of Thymoglobulin is via selective depletion of T-cells. | For prevention of renal transplant rejection | Antithymocyte Globulin (ATG) is a concentrated anti-human T-lymphocyte immunoglobulin preparation derived from rabbits after immunization with a T-lympoblast cell line. ATG is an immunosuppressive product for the prevention and treatment of acute rejection following organ transplantation. ATG reduces the host immune response against tissue transplants or organ allografts. | Binds to multiple, T-cell specific antigens leading to T-lymphocyte cell death via complement mediated cytotoxicity or apoptosis. | Not known whether ATG (rabbit) distributes into human milk; however, other immunoglobulins are distributed into human milk. | Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production. | T-cell depletion usually observed within 1 day after initiating therapy. Average 21.5 and 87 mcg/mL 4–8 hours post-infusion after first and last IV doses, respectively, when given for 7–11 days. | NA | NA | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | T-cell surface glycoprotein CD1a,Major histocompatibility complex class I-related gene protein,Integrin alpha-L,T-lymphocyte activation antigen CD86,Low affinity immunoglobulin gamma Fc region receptor II-b,T-cell surface glycoprotein CD4,Integrin beta-1,Integrin alpha-V,Integrin beta-3 | 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 |
| 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 |
| 11902 | Th1266 | Afelimomab | NA | NA | NA | NA | NA | NA | 44.7 hours | Afelimomab (also known as Fab 2 or MAK 195F) is an anti-TNF-a monoclonal antibody. Administration of 195F reduces the concentration of interleukin-6 in patients with sepsis. | Investigated for use/treatment in sepsis and septicemia. | Afelimomab is the F(ab')2 fragment of a murine anti-TNF-alpha antibody, and has been evaluated in clinical trials in septic patients. The results suggest that the drug is well tolerated, and may be of benefit in certain groups of patients with sepsis. Afelimomab is safe, biologically active, and well tolerated in patients with severe sepsis, reduces 28-day all-cause mortality, and attenuates the severity of organ dysfunction in patients with elevated interleukin-6 levels. | NA | NA | NA | NA | NA | NA | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Tumor necrosis factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11916 | Th1267 | Epratuzumab | NA | NA | NA | NA | NA | NA | NA | Epratuzumab is a humanized monoclonal antibody derived from the murine IG2a monoclonal antibody, LL2 (EPB-2). This agent may subsequently be well matched for use in oncology and the treatment of inflammatory autoimmune disorders, such as lupus. | Investigated for use/treatment in leukemia (lymphoid), lymphoma (non-hodgkin's), and systemic lupus erythematosus. | NA | Epratuzumab is a recombinant, humanized monoclonal antibody directed against CD22, a cell surface glycoprotein present on mature B-cells and on many types of malignant B-cells. It binds with high specificity to normal B-cells and B-cell tumors at the third Ig-like domain of CD22. After binding to CD22, epratuzumab's predominant antitumor activity appears to be mediated through antibody-dependent cellular cytotoxicity (ADCC). | NA | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | B-cell receptor CD22 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11917 | Th1267 | Epratuzumab | NA | NA | NA | NA | NA | NA | NA | Epratuzumab is a humanized monoclonal antibody derived from the murine IG2a monoclonal antibody, LL2 (EPB-2). This agent may subsequently be well matched for use in oncology and the treatment of inflammatory autoimmune disorders, such as lupus. | Investigated for use/treatment in leukemia (lymphoid), lymphoma (non-hodgkin's), and systemic lupus erythematosus. | NA | Epratuzumab is a recombinant, humanized monoclonal antibody directed against CD22, a cell surface glycoprotein present on mature B-cells and on many types of malignant B-cells. It binds with high specificity to normal B-cells and B-cell tumors at the third Ig-like domain of CD22. After binding to CD22, epratuzumab's predominant antitumor activity appears to be mediated through antibody-dependent cellular cytotoxicity (ADCC). | NA | NA | NA | NA | NA | Antineoplastic Agents, Immunological | NA | NA | NA | NA | B-cell receptor CD22 | 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 |
| 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 |
| 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 |
| 12093 | Th1285 | Glatiramer | >Th1285_Glatiramer EAYKAAEKAYAAKEAAKEAAKAKAEKKAAYAKAKAAKYEKKAKKAAAEYKKK | 7000 | C254H422N70O72 | NA | NA | NA | NA | Glatiramer acetate consists of the acetate salts of synthetic polypeptides, containing four naturally occurring amino acids: L-glutamic acid, L-alanine, L-tyrosine, and L-lysine with an average molar fraction of 0.141, 0.427, 0.095, and 0.338, respectively. The average molecular weight of glatiramer acetate is 5,000-9,000 daltons. It is an immunomodulator, licensed in much of the world for reduced frequency of relapses in relapsing-remitting multiple sclerosis. | For reduction of the frequency of relapses in patients with Relapsing-Remitting Multiple Sclerosis. | Glatiramer acetate was originally designed to mimic a protein in myelin, called myelin basic protein, with the intention of inducing EAE (an animal model of MS). Quite to the contrary, it was found to suppress the disease and as a result came to be trialed in human MS. There is some evidence that Glatiramer acetate converts the body's immune response from a Th1 type to a Th2 one, promotes suppressor T cells or acts as an altered peptide ligand. Studies in animals and in vitro systems suggest that upon its administration, glatiramer acetate-specific suppressor T-cells are induced and activated in the periphery. Some fraction of the injected material, either intact or partially hydrolyzed, is presumed to enter the lymphatic circulation, enabling it to reach regional lymph nodes, and some may enter the systemic circulation intact. | Glatiramer acetate (GA) exhibits strong and promiscuous binding to MHC molecules (HLA DRB1* variants) and consequent competition with various myelin antigens for their presentation to T cells. A further aspect of its action is potent induction of specific suppressor cells of the T helper 2 (Th2) type that migrate to the brain and lead to in situ bystander suppression. Furthermore, the GA-specific cells in the brain express the anti-inflammatory cytokines IL-10 and transforming growth factor beta, in addition to brain-derived neurotrophic factor, whereas they do not express the inflammatory cytokine IFN-gamma. Recent evidence also suggests that Glatiramer acetate directly inhibits dendritic cells and monocytes - both of which are circulating antigen presenting cells. | Adverse reactions include injection site reactions, vasodilatation, chest pain, asthenia, infection, pain, nausea, arthralgia, anxiety, and hypertonia. | Hydrolyzed by proteases | NA | NA | NA | Antineoplastic and Immunomodulating Agents | 8232250 | 31-07-2012 | 19-08-2030 | NA | HLA class II histocompatibility antigen, DRB1-1 beta chain | Copaxone | Sanofi Aventis | Sanofi Aventis | Subcutaneous | 20 mg/1mL | COPAXONE is contraindicated in patients with known hypersensitivity to glatiramer acetate or mannitol. | injection site reactions (e.g., pain, redness, soreness, itching, swelling, or a hard lump), nausea, vomiting, chills, joint aches, body aches, neck pain, back pain, double vision, headache, increased urge to urinate, weakness, runny nose, swelling in your hands or feet, vaginal itching or discharge, fever, chills, flu symptoms, sore throat, or white patches or sores inside your mouth or on your lips. | Copaxone is a combination of four amino acids (proteins) that affect the immune system. Copaxone injection is used to treat relapsing forms of multiple sclerosis in adults (including clinically isolated syndrome, relapsing-remitting disease, and active secondary progressive disease). Copaxone will not... | Copaxone is a prescription medicine used to treat the symptoms of Multiple Sclerosis. Copaxone may be used alone or with other medications. | NA | Glatiramer acetate, the active ingredient of COPAXONE, consists of the acetate salts of synthetic polypeptides, containing four naturally occurring amino acids: L-glutamic acid, L-alanine, L-tyrosine, and L-lysine with an average molar fraction of 0.141, 0.427, 0.095, and 0.338, respectively. The average molecular weight of glatiramer acetate is 5,000 – 9,000 daltons. Glatiramer acetate is identified by specific antibodies. | Link | Link | NA |
| 12203 | Th1298 | Albinterferon Alfa-2B | >Th1298_Albinterferon_Alfa-2B DAHKSEVAHRFKDLGEENFKALVLIAFAQYLQQCPFEDHVKLVNEVTEFAKTCVADESAENCDKSLHTLFGDKLCTVATLRETYGEMADCCAKQEPERNECFLQHKDDNPNLPRLVRPEVDVMCTAFHDNEETFLKKYLYEIARRHPYFYAPELLFFAKRYKAAFTECCQAADKAACLLPKLDELRDEGKASSAKQRLKCASLQKFGERAFKAWAVARLSQRFPKAEFAEVSKLVTDLTKVHTECCHGDLLECADDRADLAKYICENQDSISSKLKECCEKPLLEKSHCIAEVENDEMPADLPSLAADFVESKDVCKNYAEAKDVFLGMFLYEYARRHPDYSVVLLLRLAKTYETTLEKCCAAADPHECYAKVFDEFKPLVEEPQNLIKQNCELFEQLGEYKFQNALLVRYTKKVPQVSTPTLVEVSRNLGKVGSKCCKHPEAKRMPCAEDYLSVVLNQLCVLHEKTPVSDRVTKCCTESLVNRRPCFSALEVDETYVPKEFNAETFTFHADICTLSEKERQIKKQTALVELVKHKPKATKEQLKAVMDDFAAFVEKCCKADDKETCFAEEGKKLVAASQAALGLCDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 85700 | C3796H5937N1015O1143S50 | NA | NA | NA | NA | Albumin-interferon alpha (Albuferon) is a novel, long-acting form of interferon alpha. Recombinant interferon alpha is approved for the treatment of hepatitis C, hepatitis B, and a broad range of cancers. Human Genome Sciences modified interferon alpha to improve its pharmacological properties by using the company's proprietary albumin fusion technology. Human Genome Sciences is developing Albuferon as a potential treatment for chronic hepatitis C. The drug was under investigation as an alternative to pegylated IFN-a-2a for the treatment of hepatitis C. In response to an FDA ruling, Novartis and Human Genome Sciences announced on October 5, 2010 that they ceased development of the drug. | Investigated for use/treatment in hepatitis (viral, C). | NA | Interferons belong to a family of proteins known as cytokines that occur naturally in the human body. Cytokines control cellular processes, such as cell growth, activation, migration and aging. While the precise mechanism of action for interferon alpha is not known, research has demonstrated direct antiviral activity in patients with diseases like hepatitis C, as well as immune-modulating and direct antitumor effects in certain types of cancer. | NA | NA | NA | NA | NA | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12238 | Th1303 | Briakinumab | >Th1303_Briakinumab MEPLVTWVVPLLFLFLLSRQGAACRTSECCFQDPPYPDADSGSASGPRDLRCYRISSDRYECSWQYEGPTAGVSHFLRCCLSSGRCCYFAAGSATRLQFSDQAGVSVLYTVTLWVESWARNQTEKSPEVTLQLYNSVKYEPPLGDIKVSKLAGQLRMEWETPDNQVGAEVQFRHRTPSSPWKLGDCGPQDDDTESCLCPLEMNVAQEFQLRRRQLGSQGSSWSKWSSPVCVPPENPPQPQVRFSVEQLGQDGRRRLTLKEQPTQLELPEGCQGLAPGTEVTYRLQLHMLSCPCKAKATRTLHLGKMPYLSGAAYNVAVISSNQFGPGLNQTWHIPADTHTEPVALNISVGTNGTTMYWPARAQSMTYCIEWQPVGQDGGLATCSLTAPQDPDPAGMATYSWSRESGAMGQEKCYYITIFASAHPEKLTLWSTVLSTYHFGGNASAAGTPHHVSVKNHSLDSVSVDWAPSLLSTCPGVLKEYVVRCRDEDSKQVSEHPVQPTETQVTLSGLRAGVAYTVQVRADTAWLRGVWSQPQRFSIEVQVSDWLIFFASLGSFLSILLVGVLGYLGLNRAARHLCPPLPTPCASSAIEFPGGKETWQWINPVDFQEEASLQEALVVEMSWDKGERTEPLEKTELPEGAPELALDTELSLEDGDRCKAKM | 146500 | C6376H9874N1722O1992S44 | NA | NA | NA | NA | Briakinumab is a human anti-IL-12 monoclonal antibody being developed for the treatment of a number of T-cell driven autoimmune diseases. It targets and neutralize interleukin-12 and interleukin-23, two proteins associated with inflammation, such as pro-inflammatory interleukins or tumor necrosis factor- alpha. Briakinumab represents a novel approach to treating psoriasis, Multiple Sclerosis, Crohn’s Disease and other autoimmune and inflammatory disorders. As of 2011 drug development for psoriasis has been discontinued in the U.S. and Europe. | Investigated for use/treatment in autoimmune diseases, crohn's disease, multiple sclerosis, psoriasis and psoriatic disorders, and rheumatoid arthritis. | Briakinumab is a human anti-IL-12 monoclonal antibody being developed for the treatment of a number of T-cell driven autoimmune diseases. It targets and neutralizes interleukin-12 and interleukin-23, two proteins associated with inflammation. | Briakinumab targets and neutralizes interleukin-12 and interleukin-23. | NA | NA | NA | NA | NA | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Interleukin-12 subunit beta,Interleukin-23 subunit 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 |
| 12345 | Th1316 | Veltuzumab | >Th1316_Veltuzumab QVQLQQSGAEVKKPGSSVKVSCKASGYTFTSYNMHWVKQAPGQGLEWIGAIYPGNGDTSYNQKFKGKATLTADESTNTAYMELSSLRSEDTAFYYCARSTYYGGDWYFDVWGQGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | C6458H9918N1706O2026S46 | NA | NA | NA | NA | Veltuzumab is a monoclonal antibody which, as of October 2009, is undergoing Phase I/II clinical trials for the treatment of non-Hodgkin's lymphoma. | Investigated for use/treatment in lymphoma (non-hodgkin's). | 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 |
| 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 |
| 12464 | Th1326 | Inotuzumab ozogamicin | NA | NA | NA | NA | NA | NA | The elimination half life at the end of Cycle 4 of administration is approximately 12.3 days in a 2-compartment model [L938]. | Inotuzumab ozogamicin is an antibody-drug conjugate using linker and cytotoxic drug technology similar to that developed for the ground-breaking treatment Mylotarg ([DB00056]), which was approved by the US FDA in 2000 for the treatment of acute myeloid leukaemia. Inotuzumab ozogamicin consists of a recombinant humanised IgG4 kappa CD22-targeting monoclonal antibody covalently attached to calicheamicin derivative, N-acetyl-gamma-calicheamicin dimethylhydrazide, which is a potent DNA-binding cytotoxic agent [A20352]. Developed by Pfizer and UCB, inotuzumab ozogamicin was granted approval by EU in June 2017 followed by FDA on August 17th, 2017 for the treatment of adults with relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). ALL is a rapidly progressing cancer of the bone marrow that is associated with high mortality rates and low therapeutic response from standard chemotherapies in relasping conditions. In a randomized trial, inotuzumab ozogamicin displayed higher percentages of patients undergoing longer periods of complete remission with no evidence of disease in comparison to patients receiving alternative chemotherapy [A20353]. | Indicated as monotherapy for the treatment of adults with relapsed or refractory CD22-positive B cell precursor acute lymphoblastic leukaemia (ALL). | Inotuzumab ozogamicin is an antineoplastic agent that targets CD22 antigen expressed on immature B-cell lymphocytes and blocks further growth of tumor cells. The drug aims to restore normal blood counts and achieve complete remission from the disease. QT interval prolongation was observed in patients receiving inotuzumab ozogamicin. | Inotuzumab ozogamicin is comprised of cytotoxic antibiotic N-acetyl-gamma-calicheamicin dimethylhydrazide attached to a humanized monoclonal IgG4 antibody via 4-(4 acetylphenoxy) butanoic acid (acetyl butyrate) linker. The drug exerts a potent cytotoxic effect against CD22+ B-cell lymphoma when the antibody binds to the CD22 receptor on the surface of B cells . The drug-CD22 complex is rapidly internalized into the cell, forming an endosome which subsequently fuses with lysosomes. N-acetyl-gamma-calicheamicin dimethylhydrazide is then intracellularly released into the acidic environment. N-acetyl-gamma-calicheamicin dimethylhydrazide is a calicheamicin derivative, which is naturally produced by the bacterium Micromonospora echinospora, and is toxic to the body when not bound to the antibody. It mediates apoptosis of the cell by binding to the minor groove of DNA in a sequence-specific manner and undergoing a structural change to generate diradicals [A20354]. These changes abstract hydrogen ions from the phosphodiester bonds of double-stranded DNA, resulting in breaks and cell apoptosis [A3883, A3884, A20352]. | Inotuzumab ozogamicin was shown to be clastogenic *in vivo* in the bone marrow of male mice but was not mutagenic in an* in vitro* bacterial reverse mutation (Ames) assay. In rat toxicity studies, rats developed oval cell hyperplasia, altered hepatocellular foci, and hepatocellular adenomas however the carcinogenic potential of inotuzumab ozogamicin on humans is undetermined. Based on reproductive toxicity studies involving female rats and non-clinical studies, inotuzumab ozogamicin has the potential to impair reproductive function and fertility in men and women [L938]. | N-acetyl-gamma-calicheamicin dimethylhydrazide primarily undergoes nonenzymatic reduction *in vitro*. The metabolism of N-acetyl-gamma-calicheamicin dimethylhydrazide in human serum is not clearly understood as the level of the drug is below the limit of quantification of 50 pg/mL [L938]. The antibody portion of the drug is thought to undergo proteolytic degradation into amino acids then recycled into other proteins [A20351]. | Inotuzumab ozogamicin is intended to be administered in cycles that each run for 3 to 4 weeks. The steady state exposure of the drug is reached by Cycle 4. The mean (SD) maximum serum concentration (Cmax) of inotuzumab ozogamicin was 308 ng/mL (362) with patients receving the recommended dose of 1.8 mg/m^2/cycle [L938]. | The total volume of distribution of inotuzumab ozogamicin is approximately 12L [L938]. | The clearance of inotuzumab ozogamicin at steady state is 0.0333 L/h [L938]. | Antineoplastic Agents | NA | NA | NA | NA | B-cell receptor CD22 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12465 | Th1326 | Inotuzumab ozogamicin | NA | NA | NA | NA | NA | NA | The elimination half life at the end of Cycle 4 of administration is approximately 12.3 days in a 2-compartment model [L938]. | Inotuzumab ozogamicin is an antibody-drug conjugate using linker and cytotoxic drug technology similar to that developed for the ground-breaking treatment Mylotarg ([DB00056]), which was approved by the US FDA in 2000 for the treatment of acute myeloid leukaemia. Inotuzumab ozogamicin consists of a recombinant humanised IgG4 kappa CD22-targeting monoclonal antibody covalently attached to calicheamicin derivative, N-acetyl-gamma-calicheamicin dimethylhydrazide, which is a potent DNA-binding cytotoxic agent [A20352]. Developed by Pfizer and UCB, inotuzumab ozogamicin was granted approval by EU in June 2017 followed by FDA on August 17th, 2017 for the treatment of adults with relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). ALL is a rapidly progressing cancer of the bone marrow that is associated with high mortality rates and low therapeutic response from standard chemotherapies in relasping conditions. In a randomized trial, inotuzumab ozogamicin displayed higher percentages of patients undergoing longer periods of complete remission with no evidence of disease in comparison to patients receiving alternative chemotherapy [A20353]. | Indicated as monotherapy for the treatment of adults with relapsed or refractory CD22-positive B cell precursor acute lymphoblastic leukaemia (ALL). | Inotuzumab ozogamicin is an antineoplastic agent that targets CD22 antigen expressed on immature B-cell lymphocytes and blocks further growth of tumor cells. The drug aims to restore normal blood counts and achieve complete remission from the disease. QT interval prolongation was observed in patients receiving inotuzumab ozogamicin. | Inotuzumab ozogamicin is comprised of cytotoxic antibiotic N-acetyl-gamma-calicheamicin dimethylhydrazide attached to a humanized monoclonal IgG4 antibody via 4-(4 acetylphenoxy) butanoic acid (acetyl butyrate) linker. The drug exerts a potent cytotoxic effect against CD22+ B-cell lymphoma when the antibody binds to the CD22 receptor on the surface of B cells . The drug-CD22 complex is rapidly internalized into the cell, forming an endosome which subsequently fuses with lysosomes. N-acetyl-gamma-calicheamicin dimethylhydrazide is then intracellularly released into the acidic environment. N-acetyl-gamma-calicheamicin dimethylhydrazide is a calicheamicin derivative, which is naturally produced by the bacterium Micromonospora echinospora, and is toxic to the body when not bound to the antibody. It mediates apoptosis of the cell by binding to the minor groove of DNA in a sequence-specific manner and undergoing a structural change to generate diradicals [A20354]. These changes abstract hydrogen ions from the phosphodiester bonds of double-stranded DNA, resulting in breaks and cell apoptosis [A3883, A3884, A20352]. | Inotuzumab ozogamicin was shown to be clastogenic *in vivo* in the bone marrow of male mice but was not mutagenic in an* in vitro* bacterial reverse mutation (Ames) assay. In rat toxicity studies, rats developed oval cell hyperplasia, altered hepatocellular foci, and hepatocellular adenomas however the carcinogenic potential of inotuzumab ozogamicin on humans is undetermined. Based on reproductive toxicity studies involving female rats and non-clinical studies, inotuzumab ozogamicin has the potential to impair reproductive function and fertility in men and women [L938]. | N-acetyl-gamma-calicheamicin dimethylhydrazide primarily undergoes nonenzymatic reduction *in vitro*. The metabolism of N-acetyl-gamma-calicheamicin dimethylhydrazide in human serum is not clearly understood as the level of the drug is below the limit of quantification of 50 pg/mL [L938]. The antibody portion of the drug is thought to undergo proteolytic degradation into amino acids then recycled into other proteins [A20351]. | Inotuzumab ozogamicin is intended to be administered in cycles that each run for 3 to 4 weeks. The steady state exposure of the drug is reached by Cycle 4. The mean (SD) maximum serum concentration (Cmax) of inotuzumab ozogamicin was 308 ng/mL (362) with patients receving the recommended dose of 1.8 mg/m^2/cycle [L938]. | The total volume of distribution of inotuzumab ozogamicin is approximately 12L [L938]. | The clearance of inotuzumab ozogamicin at steady state is 0.0333 L/h [L938]. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | B-cell receptor CD22 | 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 |
| 12535 | Th1331 | Glembatumumab vedotin | >Th1331_Glembatumumab_vedotin QVQLQESGPGLVKPSQTLSLTCTVSGGSISSFNYYWSWIRHHPGKGLEWIGYIYYSGSTYSNPSLKSRVTISVDTSKNQFSLTLSSVTAADTAVYYCARGYNWNYFDYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKCCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | A conjugate of an anti-glycoprotein non-metastatic melanoma protein B mAb and monomethyl auristatin E for the treatment of melanoma and breast cancer. | Investigated for use/treatment in melanoma. | NA | CR011 is a fully-human monoclonal antibody which utilizes antibody-drug conjugation (ADC) technology licensed from Seattle Genetics. The ADC technology links vcMMAE, a potent chemotherapeutic, to the CR011 antibody resulting in the antibody-drug conjugate CR011-vcMMAE. CR011-vcMMAE targets GPNMB, a protein located specifically on the surface of melanoma cells. After CR011-vcMMAE binds to GPNMB, it is transported inside the cancer cell where the chemotherapy payload, Auristatin E, is cleaved from the antibody and activated. | NA | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | Transmembrane glycoprotein NMB | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12536 | Th1331 | Glembatumumab vedotin | >Th1331_Glembatumumab_vedotin QVQLQESGPGLVKPSQTLSLTCTVSGGSISSFNYYWSWIRHHPGKGLEWIGYIYYSGSTYSNPSLKSRVTISVDTSKNQFSLTLSSVTAADTAVYYCARGYNWNYFDYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKCCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | A conjugate of an anti-glycoprotein non-metastatic melanoma protein B mAb and monomethyl auristatin E for the treatment of melanoma and breast cancer. | Investigated for use/treatment in melanoma. | NA | CR011 is a fully-human monoclonal antibody which utilizes antibody-drug conjugation (ADC) technology licensed from Seattle Genetics. The ADC technology links vcMMAE, a potent chemotherapeutic, to the CR011 antibody resulting in the antibody-drug conjugate CR011-vcMMAE. CR011-vcMMAE targets GPNMB, a protein located specifically on the surface of melanoma cells. After CR011-vcMMAE binds to GPNMB, it is transported inside the cancer cell where the chemotherapy payload, Auristatin E, is cleaved from the antibody and activated. | NA | NA | NA | NA | NA | Antineoplastic Agents, Immunological | NA | NA | NA | NA | Transmembrane glycoprotein NMB | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12548 | Th1332 | Olaratumab | >Th1332_Olaratumab QLQLQESGPGLVKPSETLSLTCTVSGGSINSSSYYWGWLRQSPGKGLEWIGSFFYTGSTYYNPSLRSRLTISVDTSKNQFSLMLSSVTAADTAVYYCARQSTYYYGSGNYYGWFDRWDQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 154000 | C6554H10076N1736O2048S40 | NA | NA | NA | Estimated value of 11 days | Olaratumab (IMC-3G3) is a fully human IgG1 monoclonal antibody with antitumor activity that selectively binds the external domain of human platelet-derived growth factor receptor (PDGFR)-a with high affinity and blocks ligand binding. It is composed of two heavy chain molecule fragments and 2 light chain fragments. Studies show that the treatment of olaratumab in combination with doxorubicin resulted in significant reduction of cancer cell proliferation and tumor growth. Olaratumab was granted accelerated approval (as Lartruvo) as initial therapy to treat adults with certain types of soft tissue sarcoma (STS) in October, 2016. | Olaratumab is indicated, in combination with doxorubicin, for the treatment of adult patients with advanced or mestastatic soft tissue sarcoma (STS) with a histologic subtype for which an anthracycline-containing regimen is appropriate and which is not amenable to curative treatment with radiotherapy or surgery. | It exerts an anti-tumor activity in vivo and in vitro against selected sarcoma cells by inhibiting tumor growth by binding to PDGFR-alpha that is present on several types of cancer on transformed cells and in tumor stroma [A18695]. Olaratumab antibody binding leads to inhibition of ligand-dependent signaling in PDGFR(alpha)-expressing tumor cells, as well as stromal cells in the tumor microenviroment that are dependent on PDGFR(alpha) signaling. When used in a combination therapy with doxorubicin, olaratumab improves progression-free survival in patients with advanced soft-tissue sarcoma. | Olaratumab blocks ligand-induced tumor cell proliferation, and inhibits receptor autophosphorylation and ligand-induced phosphorylation of the downstream signaling molecules protein kinase B (Akt) and mitogen-activated protein kinase [A19171]. PDGFR signalling is a type of tyrosine kinase-mediated pathway that normally regulates cell growth, chemotaxis, and mesenchymal stem cell differentiation. It also promotes internalization of PDGFR thus alters the surface levels of PDGFR. | Infusion-related reactions may occur during or after the administration which include bronchospasm, flushing, hypotension, anaphylactic shock, or cardiac arrest. Olaratumab may cause embryo-fetal toxicity based on animal data and its mechanism of action. Other reported adverse effects include neutropenia, leukopenia, anemia, nausea and musculoskeletal pain. | Mainly degraded nonspecifically by proteolytic enzymes | NA | 7.7 L at steady state. | Mean value of 0.56L/day | Antineoplastic Agents | NA | NA | NA | NA | Platelet-derived growth factor receptor alpha | Lartruvo | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Intravenous | 190 mg / 19 mL | None. | nausea, fatigue, musculoskeletal pain, inflammation of the mucous membranes in the digestive tract (mucositis), hair loss, vomiting, diarrhea, decreased appetite, abdominal pain, numbness and tingling, headache, fatigue, infusion-related reactions, anxiety, dry eyes, and lab abnormalities (lymphopenia, neutropenia, thrombocytopenia, hyperglycemia, elevated aPTT, hypokalemia, and hypophosphatemia). | Olaratumab is a recombinant human IgG1 monoclonal blocking antibody that binds specifically to human plateletderived growth factor receptor alpha (PDGFR-α). LARTRUVO has an approximate molecular weight of 154 kDa. LARTRUVO is produced in genetically engineered mammalian NS0 cells. | LARTRUVO™ is indicated, in combination with doxorubicin, for the treatment of adult patients with soft tissue sarcoma (STS) with a histologic subtype for which an anthracycline-containing regimen is appropriate and which is not amenable to curative treatment with radiotherapy or surgery. | NA | NA | Link | Link | NA |
| 12549 | Th1332 | Olaratumab | >Th1332_Olaratumab QLQLQESGPGLVKPSETLSLTCTVSGGSINSSSYYWGWLRQSPGKGLEWIGSFFYTGSTYYNPSLRSRLTISVDTSKNQFSLMLSSVTAADTAVYYCARQSTYYYGSGNYYGWFDRWDQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 154000 | C6554H10076N1736O2048S40 | NA | NA | NA | Estimated value of 11 days | Olaratumab (IMC-3G3) is a fully human IgG1 monoclonal antibody with antitumor activity that selectively binds the external domain of human platelet-derived growth factor receptor (PDGFR)-a with high affinity and blocks ligand binding. It is composed of two heavy chain molecule fragments and 2 light chain fragments. Studies show that the treatment of olaratumab in combination with doxorubicin resulted in significant reduction of cancer cell proliferation and tumor growth. Olaratumab was granted accelerated approval (as Lartruvo) as initial therapy to treat adults with certain types of soft tissue sarcoma (STS) in October, 2016. | Olaratumab is indicated, in combination with doxorubicin, for the treatment of adult patients with advanced or mestastatic soft tissue sarcoma (STS) with a histologic subtype for which an anthracycline-containing regimen is appropriate and which is not amenable to curative treatment with radiotherapy or surgery. | It exerts an anti-tumor activity in vivo and in vitro against selected sarcoma cells by inhibiting tumor growth by binding to PDGFR-alpha that is present on several types of cancer on transformed cells and in tumor stroma [A18695]. Olaratumab antibody binding leads to inhibition of ligand-dependent signaling in PDGFR(alpha)-expressing tumor cells, as well as stromal cells in the tumor microenviroment that are dependent on PDGFR(alpha) signaling. When used in a combination therapy with doxorubicin, olaratumab improves progression-free survival in patients with advanced soft-tissue sarcoma. | Olaratumab blocks ligand-induced tumor cell proliferation, and inhibits receptor autophosphorylation and ligand-induced phosphorylation of the downstream signaling molecules protein kinase B (Akt) and mitogen-activated protein kinase [A19171]. PDGFR signalling is a type of tyrosine kinase-mediated pathway that normally regulates cell growth, chemotaxis, and mesenchymal stem cell differentiation. It also promotes internalization of PDGFR thus alters the surface levels of PDGFR. | Infusion-related reactions may occur during or after the administration which include bronchospasm, flushing, hypotension, anaphylactic shock, or cardiac arrest. Olaratumab may cause embryo-fetal toxicity based on animal data and its mechanism of action. Other reported adverse effects include neutropenia, leukopenia, anemia, nausea and musculoskeletal pain. | Mainly degraded nonspecifically by proteolytic enzymes | NA | 7.7 L at steady state. | Mean value of 0.56L/day | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Platelet-derived growth factor receptor alpha | 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 |
| 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 |
| 12936 | Th1370 | Catumaxomab | NA | 150511 | NA | NA | NA | NA | Catumaxomab has an apparent half life of elimination of 2.5 days [FDA Label]. | Catumaxumab is a trifunctional monoclonal antibody developed for use in cancer treatment. It has affinity for T-cells, accessory immune cells, and cancer cells. Catumaxumab was initially authorized for market by the European Medicines Agency in April 2009 for the treatment of malignant ascites [L1122]. Its market authorization was withdrawn in the EU in June 2017 at the manufacturer's request due to the company's insolvency. Catumaxumab was approved for market in Canada in May 2012 for the same condition [FDA Label]. It is currently available under the brand name Removab. | For use in the management of malignant ascites tumours via intraperitoneal infusion where standard therapy is not available or feasible [FDA Label]. | Catumaxomab brings cancer cells, T cells, and accessory immune cells into close proximity and stimulates activation and of immune cells [FDA Label, A31531]. This facilitates immune system-mediated destruction of the cancer cells. | Catumaxomab contains epitopes for human CD3 and human epithelial cell adehesion molecule. It also has an intact immunoglobulin gamma constant region allowing it to bind to Fc | As a mouse/rat hybrid antibody, Catumaxomab can produce immunogenicity in other species [A31531]. No acute toxicity was found in mice using an analog with an anti-mouse CD3 paratope in place of Catumaxomab's anti-human CD3 paratope. A transient decrease in serum leukocytes has been observed but is attributed to migration of immune cells into EpCAM positive tissues. Data specific to Catumaxomab is extremely limited as its specificity for human protein requires data from human subjects [FDA Label]. | NA | Catumaxomab has an observed bioavailability of 82% [A31533]. This value decreases as the EpCAM positive tumour load and number of immune cells in the peritoneal cavity increases. While some Catumaxomab escapes into systemic circulation, most localizes to EpCAM positive tissues. Tmax is 19 h. | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | Epithelial cell adhesion molecule,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor III-A,Low affinity immunoglobulin gamma Fc region receptor III-B,T-cell surface glycoprotein CD3 epsilon chain,High affinity immunoglobulin gamma Fc receptor I | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12937 | Th1370 | Catumaxomab | NA | 150511 | NA | NA | NA | NA | Catumaxomab has an apparent half life of elimination of 2.5 days [FDA Label]. | Catumaxumab is a trifunctional monoclonal antibody developed for use in cancer treatment. It has affinity for T-cells, accessory immune cells, and cancer cells. Catumaxumab was initially authorized for market by the European Medicines Agency in April 2009 for the treatment of malignant ascites [L1122]. Its market authorization was withdrawn in the EU in June 2017 at the manufacturer's request due to the company's insolvency. Catumaxumab was approved for market in Canada in May 2012 for the same condition [FDA Label]. It is currently available under the brand name Removab. | For use in the management of malignant ascites tumours via intraperitoneal infusion where standard therapy is not available or feasible [FDA Label]. | Catumaxomab brings cancer cells, T cells, and accessory immune cells into close proximity and stimulates activation and of immune cells [FDA Label, A31531]. This facilitates immune system-mediated destruction of the cancer cells. | Catumaxomab contains epitopes for human CD3 and human epithelial cell adehesion molecule. It also has an intact immunoglobulin gamma constant region allowing it to bind to Fc | As a mouse/rat hybrid antibody, Catumaxomab can produce immunogenicity in other species [A31531]. No acute toxicity was found in mice using an analog with an anti-mouse CD3 paratope in place of Catumaxomab's anti-human CD3 paratope. A transient decrease in serum leukocytes has been observed but is attributed to migration of immune cells into EpCAM positive tissues. Data specific to Catumaxomab is extremely limited as its specificity for human protein requires data from human subjects [FDA Label]. | NA | Catumaxomab has an observed bioavailability of 82% [A31533]. This value decreases as the EpCAM positive tumour load and number of immune cells in the peritoneal cavity increases. While some Catumaxomab escapes into systemic circulation, most localizes to EpCAM positive tissues. Tmax is 19 h. | NA | NA | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Epithelial cell adhesion molecule,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor III-A,Low affinity immunoglobulin gamma Fc region receptor III-B,T-cell surface glycoprotein CD3 epsilon chain,High affinity immunoglobulin gamma Fc receptor I | 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 |
| 13093 | Th1380 | Antilymphocyte immunoglobulin (horse) | NA | NA | NA | NA | NA | NA | The half-life of equine immunoglobulin after ATGAM infusion was found to be 5.7 ± 3.0 days in one group of recipients. The range for half-life was 1.5 to 13 days. | Equine anti-thymocyte globulin is composed of purified gamma globulin containing primarily IgG against human thymus lymphocytes. It is formed by inoculating a horse with an antigen (human thymoyctes) which then induces the horse immune system's B-lymphocytes to produce IgG immunoglobulins specific for that antigen. The result is polyclonal IgG that is then purified from the horse's serum to produce a usable drug product that can be used for immunosuppression. Although the exact mechanism of action is unknown, equine anti-thymocyte globulin targets a variety of immune system proteins including lymphocyte surface proteins, granulocytes, platelets, bone marrow cells, and other cell types. Equine ATG is currently indicated for the suppression of the immune system to prevent renal transplant rejection and in the treatment of aplastic anemia. Induction of T cell apoptosis and resulting T-cell lymphopenia found in vivo is credited for its therapeutic effect in these conditions. There are currently various ATG products available, which differ in the source of inoculated animal (rabbit, horse, or pig) and in the type of antigen product used to produce immunoglobulin (thymocytes, peripheral T cells, etc.). | For prevention of renal transplant rejection and for the treatment of aplastic anemia. | NA | NA | The most commonly reported adverse reactions (occurring in greater than 10% of patients) are pyrexia, chills, rash, thrombocytopenia, leukopenia and arthralgia. | NA | NA | During infusion of 10 to 15 mg/kg/day, the mean peak value (n = 27 renal transplant patients) was found to be 727 ± 310 µg/mL. | NA | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | NA | Atgam Sterile Solution IV 50mg/ml | Pharmacia & Upjohn Inc | Pharmacia & Upjohn Inc | Intravenous | 50 mg | Do not administer ATGAM to a patient who has had a systemic reaction (e.g., anaphylactic reaction) during prior administration of ATGAM or any other equine gamma globulin preparation | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, chest pain, back pain, fast heartbeat, trouble breathing, lightheadedness, easy bruising, unusual bleeding (nose, mouth, vagina, or rectum), purple or red pinpoint spots under your skin, coughing up blood, vomit that looks like coffee grounds, seizure, fever, swollen glands, skin sores, rash, itching, muscle or joint pain, weakness, and tiredness | Lymphocyte immune globulin anti-thymocyte (also called equine anti-thymocyte immune globulin), is an immunosuppressant that lowers your body's immune system. The immune system helps your body fight infections. | used to treat or prevent organ rejection after a kidney transplant. | NA | NA | Link | Link | NA |
| 13380 | Th1399 | Ravulizumab | >Th1399_Ravulizumab DIQMTQSPSSLSASVGDRVTITCGASENIYGALNWYQQKPGKAPKLLIYGATNLADGVPSRFSGSGSGTDFTLTISSLQPEDFATYYCQNVLNTPLTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | NA | NA | NA | NA | NA | The mean (SD) terminal elimination half-life of ravulizumab in patients with PNH was recorded as 49.7 (8.9) days [FDA Label]. | Ravulizumab is considered a long-acting complement 5 (C5) inhibitor that has been undergoing clinical trials for the treatment of paroxysmal nocturnal haemoglobinuria (PNH) as of 4 February, 2016. A drug similar to ravulizumab (ALXN1210), called eculizumab, is currently approved for the treatment of PNH in 46 countries under the brand name Soliris®. Ravulizumab is considered by Alexion Pharmaceuticals Inc. to be a "next-generation" eculizumab molecule. Ravulizumab was subsequently approved by the US FDA in December of 2018 for a variety of beneficial characteristics that make it an advanced, next-generation agent in comparison to eculizumab [F2473]. In particular, ravulizumab is currently the first and only long-acting C5 complement inhibitor that can be administered every eight weeks for the treatment of adult patients with PNH whereas eculizumab is a bi-weekly treatment [F2473, FDA Label]. Moreover, virtually all of the phase 3 trial results for ravulizumab have demonstrated the equivalent efficacy and safety established by eculizumab and that patients transition safely and effectively from using eculizumab to ravulizumab [F2473]. Subsequently, whereas PNH patients may have needed to previously plan their lives rather strictly around the bi-weekly infusion administrations of eculizumab, with ravulizumab such patients can find a more relaxed dosing schedule of only six or seven infusions over an entire year [F2473, FDA Label]. Just as the US FDA permitted a timely and expedited approval of ravulizumab ahead of the Prescription Drug User Fee Act (PDUFA) date of February 18, 2019 following the use of a rare disease priority review voucher by Ultomiris (ravulizumab) developer Alexion for many of the aforementioned beneficial treatment reasons, regulatory authorities in the European Union (EU) and Japan have currently accepted and are reviewing applications for the approval of Ultomiris (ravulizumab) as a treatment for adults with PNH as well [F2473]. | Ravulizumab is indicated for the treatment of adult patients with paroxysmal nocturnal hemoglobinuria (PNH) [FDA Label]. | Immediate and complete inhibition of serum-free complement protein C5 (concentration of less than 0.5 mcg/mL) was observed by the end of the first ravulizumab infusion and sustained throughout the entire 26-week treatment period in all patients, both complement-inhibitor naïve and previously treated with eculizumab [FDA Label]. The extent and duration of the pharmacodynamic response in patients with PNH were exposure dependent for ravulizumab [FDA Label]. Free C5 levels of <0.5 mcg/mL were correlated with maximal intravascular hemolysis control and complete terminal complement inhibition [FDA Label]. Complete terminal complement inhibition following initiation of ravulizumab treatment led to normalization of serum LDH by week 4 in complement-inhibitor naïve patients and maintained LDH normalization in patients previously treated with eculizumab [FDA Label]. | Paroxysmal nocturnal hemoglobinuria (PNH) is a chronic, progressive, debilitating and life-threatening ultra-rare blood disorder characterized by hemolysis (destruction of red blood cells) that is mediated by the uncontrolled activation of the complement system, a component of the body’s immune system [L4900]. Ravulizumab is subsequently a terminal complement inhibitor that specifically binds to the particular complement protein C5 with high affinity, thereby inhibiting its cleavage to C5a (the proinflammatory anaphylatoxin) and C5b (the initiating subunit of the terminal complement complex [C5b-9]) and preventing the generation of the terminal complement complex C5b9 [FDA Label]. Ravulizumab inhibits terminal complement-mediated intravascular hemolysis in patients with PNH [FDA Label]. | Although PNH in pregnancy is associated with adverse maternal outcomes, including worsening cytopenias, thrombotic events, infections, bleeding, miscarriages, increased maternal mortality, and adverse fetal outcomes like fetal death and premature delivery, there are no available data on ravulizumab use in pregnant women to inform a drug-associated risk of major birth defects, miscarriage, or adverse maternal or fetal outcomes [FDA Label]. Although there are currently no human reproductive studies, human immunoglobulins like ravulizumab are known to cross the human placental barrier, and thus may potentially cause terminal complement inhibition in the fetal circulation [FDA Label]. There are no data on the presence of ravulizumab in human milk, the effect on the breastfed child, or the effect on milk production [FDA Label]. Since many medicinal products and immunoglobulins are secreted into human milk, and because of the potential for serious adverse reactions in a nursing child, breastfeeding should be discontinued during treatment and for 8 months after the final dose [FDA Label]. The safety and efficacy of ravulizumab in pediatric patients and geriatric use have not yet been established [FDA Label]. Genotoxicity studies have not been conducted with ravulizumab [FDA Label]. Effects of ravulizumab upon fertility have not been studied in animals [FDA Label]. Intravenous injections of male and female mice with a murine anti-C5 antibody at up to 0.8-2.2 times the equivalent of the clinical dose of ravulizumab had no adverse effects on mating or fertility [FDA Label]. | Monoclonal antibody agents like ravulizumab are not expected to generate toxic metabolites as they generally undergo proteolysis to their constituent amino acids [F94]. | It has been demonstrated that mean ravulizumab Cmax and AUC8 increase in a dose-proportional manner and that a single 400 mg intravenous dose of ravulizumab administered to subjects reach or exceed the threshold level of 100 µg/mL [L4915]. | The mean (SD) volume of distribution at steady state was 5.34 (0.92) L [FDA Label]. | The mean (SD) clearance of ravulizumab in patients with PNH was recorded as being 0.08 (0.022) L/day respectively [FDA Label]. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Complement C5 | Ultomiris | Alexion Europe Sas | Alexion Europe Sas | Intravenous | 300 mg | ULTOMIRIS is contraindicated in: Patients with unresolved Neisseria meningitidis infection [see WARNINGS AND PRECAUTIONS]. Patients who are not currently vaccinated against Neisseria meningitidis, unless the risks of delaying ULTOMIRIS treatment outweigh the risks of developing a meningococcal infection [see WARNINGS AND PRECAUTIONS]. | upper respiratory infection, headache, diarrhea, nausea, abdominal pain, fever, pain in extremities, joint pain, and dizziness | Ultomiris is a monoclonal antibody. Monoclonal antibodies are man-made antibodies that fight antigens (harmful substances) in the body. Ultomiris injection is used to treat paroxysmal nocturnal hemoglobinuria (PNH) in adults and children who are at least 1 month old. PNH is a rare genetic disorder in... | Ultomiris is a prescription medicine used to treat the symptoms of Paroxysmal Nocturnal Hemoglobinuria (PNH), and Atypical Hemolytic Uremic Syndrome (aHUS). Ultomiris may be used alone or with other medications. | NA | Ravulizumab-cwvz, a complement inhibitor, is a humanized monoclonal antibody (mAb) produced in Chinese hamster ovary (CHO) cells. Ravulizumab-cwvz consists of 2 identical 448 amino acid heavy chains and 2 identical 214 amino acid light chains and has a molecular weight of approximately 148 kDa. The constant regions of ravulizumabcwvz include the human kappa light chain constant region, and the protein engineered “IgG2/4” heavy chain constant region. | Link | Link | NA |
| 13448 | Th1404 | Tasonermin | >Th1404_Tasonermin VRSSSRTPSDKPVAHVVANPQAEGQLQWLNRRANALLANGVELRDNQLVVPSEGLYLIYSQVLFKGQGCPSTHVLLTHTISRIAVSYQTKVNLLSAIKSPCQRETPEGAEAKPWYEPIYLGGVFQLEKGDRLSAEINRPDYLDFAESGQVYFGIIAL | 17724 | NA | 6.7 | NA | NA | Tasonermin has a terminal half life of 20-30 min at doses of 150 µg/m² [L1339]. This value increases as dosage increases. | Tasonermin is recombinant soluble form tumor necrosis factor α produced via _Escherichia coli_ cell culture. It was approved for use by the European Medicines Agency in April of 1999 for use as an adjunt to surgery for the subsequent removal of the tumor and in palliative care for irresectable soft tissue sarcoma of the limbs as the product Beromun. It is administered with [DB01042] via mild hyperthermic isolated limb perfusion. | For use in adults as an adjunct to surgery for subsequent removal of the tumour so as to prevent or delay amputation, or in palliative care, for irresectable soft tissue sarcoma of the limbs [FDA Label]. Used in combination with melphalan via mild hyperthermic isolated limb perfusion. | Tasonermin is thought to contribute to the destruction of tumor tissue via several direct and indirect effects [FDA Label]. Tasonermin directly inhibits cell proliferation in a variety of cancer cells. It also modifies endothelial cell morphology and reduces their proliferation in tumor microvasculature. Modification of the expression of cell adhesion proteins, proteins affecting coagulation, interleukins, and hematopoietic growth factors favors a procoagulant state resulting in microvascular thrombosis. These changes also increase infiltration of the tumor tissue by leukocytes. Monocytes, macrophages, and granulocytes are activated allowing better adherence to the endothelium and subjecting the tumor cells to phagocytosis and respiratory bursts as well as producing degranulation of immune cells to further enhance inflammatory activity. Active antigen presenting cells are able to activate and induce proliferation of T- and B-lymphocyte cells to allow the adaptive immune system to contribute to tumor cell damage. These changes lead to hemorraghic necrosis of the tumor. | Since tasonermin is recombinant TNF-α, it functions exactly as endogenous TNF-α does. The direct cytotoxic effect of TNF-α is mediated by TNF-α receptor 1 [A31954]. The bound receptor activates the well-reviewed death receptor pathway involving the activation of initiator caspases 8 and 9 then ultimately ending in the activation of effector caspase 3 which begins the process of apoptosis. The effect on tumor vasculature is mediated by the inflammatory signalling pathway of TNF-α, the NFκB pathway [A31954]. This pathway is also activated by TNFR1 when bound to TNFα. The NFκB transcription factor increases expression of proteins in vascular endothelial cells. These proteins include cell adhesion molecules, inflammatory mediators like prostaglandins and interleukins, and growth factors [A31958]. TNF-&alpha also increases the expression of inducible nitric oxide synthase via this pathway which contributes to the generation of reactive nitrogen species [A31956]. These species are able to damage cells in the tumor and microvasculature. The cytokines produced from NFκB activation and TNF-&aplha; itself serve to activate the cells of the immune system which further damage tumor cells with respiratory bursts, phagocytosis and subsequent breakdown of the cell, and release of cytotoxic enzymes. The antigen presenting cells which phagocytose the tumor cells are able to activate lymphocytes and allow the adaptive immune system to further damage the tumor tissue [T116]. | In addition to its intended cytotoxic effects, tasonermin produces secondary adverse effects. Studies in mice, rats, dogs, monkeys, and rabbits observed hematological changes including anemia, increased hematocrit, and changes in leukocyte and platelet counts dependent on species and treatment duration [FDA Label]. Tasonermin also produces decreases in blood pressure. Increases in heart rate and reductions in cardiac contractility have been noted in some studies. Increased liver enzymes suggest altered liver function as a result of tasonermin administration. Changes in kidney function have also been observed including increased water and sodium excretion as well as increased serum urea and creatinine. The only study to determine a no observable adverse effect level found the value to be 0.1 µg/kg in monkeys during a 7-day course of tasonermin. | No metabolism data is available. Tasonermin is assumed to be broken down similarly to other proteins in systemic circulation. | No absorption data is available. No enteral route formulation exists for tasonermin. | The estimated volume of distribution varies with the dose administered with intravenous doses of 35 µg/m² and 150 µg/m² producing values of 55 L and 17 L respectively [L1339]. | Clearance was estimated to be 2 L/min and 0.5 L/min after intravenous doses of 35 µg/m² and 150 µg/m² respectively [L1339]. This value decreases as dosage increases. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 1A,Tumor necrosis factor receptor superfamily member 1B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13488 | Th1408 | Conatumumab | NA | NA | NA | NA | NA | NA | NA | Conatumumab has been used in trials studying the treatment of Sarcoma, Lymphoma, Oncology, Colon Cancer, and Rectal Cancer, among others. | NA | 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 |
| 13489 | Th1408 | Conatumumab | NA | NA | NA | NA | NA | NA | NA | Conatumumab has been used in trials studying the treatment of Sarcoma, Lymphoma, Oncology, Colon Cancer, and Rectal Cancer, among others. | NA | 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 |
| 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 |
| 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 |
| 13583 | Th1417 | Endostar | NA | NA | NA | NA | NA | NA | NA | Endostar is under investigation for the treatment of Nasopharyngeal Carcinoma. Endostar has been investigated for the treatment of Non-small Cell Lung Cancer. | NA | 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 |
| 13623 | Th1420 | Sarilumab | >Th1420_Sarilumab EVQLVESGGGLVQPGRSLRLSCAASRFTFDDYAMHWVRQAPGKGLEWVSGISWNSGRIGYADSVKGRFTISRDNAENSLFLQMNGLRAEDTALYYCAKGRDSFDIWGQGTMVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 150000 | C6388H9918N1718O1998S44 | 6.6 - 7.2 | NA | 69 °C (midpoint transition), 80 °C (whole IgG1) | The half life will depend on the administered concentration. At 200 mg every 2 weeks, half-life is up to 10 days in patients with RA at steady state. At 150 mg every 2 weeks, half-life is up to 8 days in patients with RA at steady state. After the last steady state dose of 150 mg and 200 mg, the time to reach nondetectable concentration is 28 and 43 days, respectively [L1000]. | Sarilumab is a fully human anti-IL-6R monoclonal IgG1 antibody that binds to both membrane bound and soluble interleukin 6 (IL-6) receptor forms, thus blocking the cis- and trans-inflammatory signalling cascades of IL-6 [A27262]. Sarilumab was developped by Sanofi and Regeneron Pharmaceuticals, Inc; it was US FDA-approved in May 2017 and followed by EU approval in June 2017 for the treatment of moderate to severe Rheumatoid Arthritis (RA) in combination with methotrexate [A27265]. RA is a chronic inflammatory disease characterized by polyarthritis and its treatment has been challenged by the different response in every patient [A27264]. Subcutaneous administration of Sarilumab has been shown to decrease acute-phase reactant levels and improve in clinical RA symptoms [A27263]. | Indicated for modere to severe reactive RA in adult patients who are irresponsive, respond inadequately or present intolerance to disease-modifying anti-rheumatic drugs (DMARDs) or tumor necrosis factor (TNF) antagonists. It is indicated to be used in combination with methotrexate (MTX) or as a monotherapy when there is intolerance to MTX or MTX administration is inappropriate. | Single-dose subcutaneous administration of Sarilumab produced a rapid reduction of CRP levels, leading to normal levels after two weeks of treatment. Peak reduction in the absolute neutrophile count was observed after 3 to 4 days of treatment followed by a recovery to baseline levels. It is observed a decrease in fibrinogen and serum amyloid A as well as an increase in hemoglobin and serum albumin. | Sarilumab is a human recombinant IgG1 antibody that binds to both forms of interleukin 6 receptors (IL-6R), thus inhibiting the IL-6-mediated signaling. IL-6 is known to be a pleiotropic cytokine that activates immune cells (T and B cells), as well as hepatocytes for the release of acute phase proteins like CRP, serum amyloid A and fibrinogen which are biomarkers of RA activity. IL-6 is also found in synovial fluid and plays a major role in the pathological inflammation and joint destruction features of RA. Thus, it is used for the treatment of RA due to its ability to inhibit intra-articular and systemic IL-6 signaling [L1000, L1001, FDA file]. | Repeat dose exposure has been shown to produce a partially reversible decrease in neutophil count and a reversible decrease in fibrinogen [L1000]. | The metabolism of Sarilumab has not been characterized. As it is a monoclonal antibody, It is thought to be degraded into small peptides and amino acids [FDA file]. | Sarilumab is shown to be well absorbed in RA patients after single SC administration with a maximum of serum concentration presented after 2 to 4 days. For the 150 mg every two weeks dose regimen, the AUC, Cmin and Cmax of sarilumab were 202 ± 120 mg.day/L, 6.35 ± 7.54 mg/L, and 20.0 ± 9.20 mg/L, respectively. For the 200 mg every two weeks dose regimen, the AUC, Cmin and Cmax of sarilumab were 395 ± 207 mg.day/L, 16.5 ± 14.1 mg/L, and 35.6 ± 15.2 mg/L, respectively [L1001, FDA file]. | In patients with RA, the apparent volume of distribution at steady state was 7.3 L [L1001, FDA file]. | Sarilumab is not eliminated via renal or hepatic pathways. RA patients have shown a trend toward higher clearance in presence of anti-sarilumab antibodies [FDA file]. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Interleukin-6 receptor subunit alpha,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 III-A,Low affinity immunoglobulin gamma Fc region receptor III-B | Kevzara | sanofi-aventis U.S. LLC | sanofi-aventis U.S. LLC | Subcutaneous | 200 mg/1.14mL | KEVZARA is contraindicated in patients with known hypersensitivity to sarilumab or any of the inactive ingredients [see WARNINGS AND PRECAUTIONS and ADVERSE REACTIONS]. | low white blood cell count (neutropenia), increased ALT, injection site redness, upper respiratory infections, nasal congestion, runny nose, sore throat, urinary tract infections, and low platelet counts (thrombocytopenia). | Kevzara reduces the effects of a substance in the body that can cause inflammation. Kevzara is used to treat moderate to severe rheumatoid arthritis in adults. Itis sometimes given together with other arthritis medicines. Kevzara is usually given after other medications have been tried without successful... | Kevzara is a prescription medicine used to treat the symptoms of Rheumatoid Arthritis. Kevzara may be used alone or with other medications. | NA | Sarilumab is a human recombinant monoclonal antibody of the IgG1 subclass that binds to the IL-6 receptor and has an approximate molecular weight of 150 kDa. Sarilumab is produced by recombinant DNA technology in Chinese Hamster Ovary cell suspension culture. | Link | Link | NA |
| 13647 | Th1421 | Tremelimumab | >Th1421_Tremelimumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSSYGMHWVRQAPGKGLEWVAVIWYDGSNKYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARDPRGATLYYYYYGMDVWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKCCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Tremelimumab is under investigation for the treatment of Mesothelioma, Liver Cancer, Liver Neoplasms, Liver Cell Caricinoma, and HepatoCellular Carcinoma. Tremelimumab has been investigated in Part C: Malignant Mesothelioma and Part A and B: Advanced Solid Malignancies. | NA | NA | NA | NA | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | Cytotoxic T-lymphocyte protein 4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13675 | Th1424 | Sirukumab | NA | NA | NA | NA | NA | NA | NA | Sirukumab has been used in trials studying the treatment and basic science of Giant Cell Arteritis and Arthritis, Rheumatoid. | NA | NA | NA | NA | NA | NA | NA | NA | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13699 | Th1426 | Guselkumab | >Th1426_Guselkumab EVQLVQSGAEVKKPGESLKISCKGSGYSFSNYWIGWVRQMPGKGLEWMGIIDPSNSYTRYSPSFQGQVTISADKSISTAYLQWSSLKASDTAMYYCARWYYKPFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143.6 | C6402H9864N1676O1994S42 | NA | NA | NA | Mean half-life of guselkumab is approximately 15 to 18 days in subjects with plaque psoriasis [FDA Label]. | Guselkumab is a human immunoglobulin G1 lambda (IgG1 | Indicated for the treatment of adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy. | Guselkumab is shown to reduce serum levels of IL-17A, IL-17F and IL-22 [FDA Label]. | Guselkumab targets the p19 alpha subunit of IL-23. While IL-23 promotes the normal inflammatory and immune responses, the p19 and p40 subunits of IL-23 are found to be over-expressed in the condition of psoriasis and other autoimmune inflammatory skin diseases [A20357, A20359]. Guselkumab selectively binds to the p19 subunit of IL-23 in dendritic cells and keratinocytes and blocks its interaction with IL-23 receptor, which further prevents the release of other pro-inflammatory cytokines and chemokines via stimulation of immune cells such as Th17 cells [FDA Label]. Thus, guselkumab blocks the abnormally-heightened signalling of inflammatory cascades that promote epidermal abnormalities including keratinocyte hyperproliferation and psoriatic plaque formation [A20358]. | Animal studies to assess the effect of guselkumab on carcinogenesis, mutagenesis and impairment on fertility have not been conducted. When subcutaneously injected into guinea pigs, the doses of guselkumab up to 100mg/kg twice-weekly demonstrated no effects on fertility parameters [FDA Label]. | Like other human IgG monoclonal antibodies, guselkumab is expected to be degraded into small peptides and amino acids via catabolic pathways [FDA Label]. | Following a 100mg subcutaneous administration, the peak plasma concentration (Cmax) of guselkumab is 8.09 ± 3.68 mcg/mL which is reached after approximately 5.5 days [FDA Label]. | The apparent volume of distribution is 13.5 L [FDA Label]. | Apparent clearance in subjects with plaque psoriasis is 0.516 L/day [FDA Label]. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Interleukin-23 subunit alpha | Tremfya | Janssen Cilag International Nv | Janssen Cilag International Nv | Subcutaneous | 100 mg | TREMFYA is contraindicated in patients with a history of serious hypersensitivity reaction to guselkumab or to any of the excipients [see WARNINGS AND PRECAUTIONS]. | upper respiratory infections, headache, injection site reactions, joint pain, diarrhea, gastroenteritis (nausea, vomiting, diarrhea, cramps, and fever), tinea infections (athlete's foot, ringworm, jock itch), and herpes simplex infections | Tremfya is a monoclonal antibody that blocks a certain protein in the body that can cause inflammation and other immune responses. Tremfya is used to treat moderate to severe plaque psoriasis in adults. Tremfya is also used to treat active psoriatic arthritis in adults. Warnings Tremfya can weaken (suppress)... | TREMFYA® is indicated for the treatment of adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy. | NA | NA | Link | Link | NA |
| 13840 | Th1440 | Avelumab | >Th1440_Avelumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYIMMWVRQAPGKGLEWVSSIYPSGGITFYADTVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARIKLGTVTTVDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 142 | C6374H9898N1694O2010S44 | NA | NA | NA | The terminal half-life is approximately 6.1 days in patients receiving 10 mg/kg. | Avelumab is a programmed death ligand-1 (PD-L1) blocking antibody indicated for the treatment of adults and pediatric patients 12 years and older with metastatic Merkel cell carcinoma (MCC). It is a fully human anti-PD immunoglobulin G1 (IgG1) lambda monoclonal antibody with antineoplastic actions. It was granted accelerated approval in March 2017 under the name Bavencio. | Indicated for the treatment of adults and pediatric patients 12 years and older with metastatic Merkel cell carcinoma (MCC). | Avelumab is a whole antibody that binds the immunosuppressive programmed death-ligand 1 and inhibits the interaction between PD-1 and PD-L1. It prevents the formation of a PD-1/PD-L1 receptor/ligand complex that normally leads to inhibition of CD8+ T cells, and therefore inhibition of an immune reaction. Alevumab is an immunotherapeutic and antineoplastic agent that belongs to the group of immune checkpoint blockade cancer therapies. By retaining a native Fc-region, avelumab is thought to engage the innate immune system and may induce antibody-dependent cell-mediated cytotoxicity (ADCC). | PD-L1 may be expressed on tumor cells and tumor-infiltrating immune cells and can contribute to the inhibition of the anti-tumor immune response in the tumor microenvironment. Binding of PD-L1 to the PD-1 and B7.1 receptors found on T cells and antigen presenting cells suppresses cytotoxic T-cell activity, T-cell proliferation and cytokine production. Avelumab binds PD-L1 through the FG loops [A19625] and blocks the interaction between PD-L1 and its receptors PD-1 and B7.1. This interaction releases the inhibitory effects of PD-L1 on the immune response resulting in the restoration of immune responses, including anti-tumor immune responses. Avelumab has also been shown to induce antibody-dependent cell-mediated cytotoxicity (ADCC) in vitro. In syngeneic mouse tumor models, blocking PD-L1 activity resulted in decreased tumor growth. | Avelumab toxicity includes the possibility of experiencing potentially fatal infusion reactions and/or immunogenic reactions like pneumonitis, hepatitis, colitis, adrenal insufficiency, hypo- and hyperthyroidism, diabetes mellitus, and nephritis, among others. Other common adverse effects include fatigue, musculoskeletal pain, diarrhea, nausea, infusion-related reaction, rash, decreased appetite, and peripheral edema. | Avelumab undergoes nonspecific proteolytic degradation. | The exposure of avelumab increased dose-proportionally in the dose range of 10 to 20 mg/kg every 2 weeks. Steady-state concentrations of avelumab were reached after approximately 4 to 6 weeks (2 to 3 cycles) of repeated dosing, and the systemic accumulation was approximately 1.25-fold. | The geometric mean volume of distribution at steady state for a subject receiving 10 mg/kg is 4.72 L. | The total systemic clearance is approximately 0.59 L/day. | 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 |
| 13841 | Th1440 | Avelumab | >Th1440_Avelumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYIMMWVRQAPGKGLEWVSSIYPSGGITFYADTVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARIKLGTVTTVDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 142 | C6374H9898N1694O2010S44 | NA | NA | NA | The terminal half-life is approximately 6.1 days in patients receiving 10 mg/kg. | Avelumab is a programmed death ligand-1 (PD-L1) blocking antibody indicated for the treatment of adults and pediatric patients 12 years and older with metastatic Merkel cell carcinoma (MCC). It is a fully human anti-PD immunoglobulin G1 (IgG1) lambda monoclonal antibody with antineoplastic actions. It was granted accelerated approval in March 2017 under the name Bavencio. | Indicated for the treatment of adults and pediatric patients 12 years and older with metastatic Merkel cell carcinoma (MCC). | Avelumab is a whole antibody that binds the immunosuppressive programmed death-ligand 1 and inhibits the interaction between PD-1 and PD-L1. It prevents the formation of a PD-1/PD-L1 receptor/ligand complex that normally leads to inhibition of CD8+ T cells, and therefore inhibition of an immune reaction. Alevumab is an immunotherapeutic and antineoplastic agent that belongs to the group of immune checkpoint blockade cancer therapies. By retaining a native Fc-region, avelumab is thought to engage the innate immune system and may induce antibody-dependent cell-mediated cytotoxicity (ADCC). | PD-L1 may be expressed on tumor cells and tumor-infiltrating immune cells and can contribute to the inhibition of the anti-tumor immune response in the tumor microenvironment. Binding of PD-L1 to the PD-1 and B7.1 receptors found on T cells and antigen presenting cells suppresses cytotoxic T-cell activity, T-cell proliferation and cytokine production. Avelumab binds PD-L1 through the FG loops [A19625] and blocks the interaction between PD-L1 and its receptors PD-1 and B7.1. This interaction releases the inhibitory effects of PD-L1 on the immune response resulting in the restoration of immune responses, including anti-tumor immune responses. Avelumab has also been shown to induce antibody-dependent cell-mediated cytotoxicity (ADCC) in vitro. In syngeneic mouse tumor models, blocking PD-L1 activity resulted in decreased tumor growth. | Avelumab toxicity includes the possibility of experiencing potentially fatal infusion reactions and/or immunogenic reactions like pneumonitis, hepatitis, colitis, adrenal insufficiency, hypo- and hyperthyroidism, diabetes mellitus, and nephritis, among others. Other common adverse effects include fatigue, musculoskeletal pain, diarrhea, nausea, infusion-related reaction, rash, decreased appetite, and peripheral edema. | Avelumab undergoes nonspecific proteolytic degradation. | The exposure of avelumab increased dose-proportionally in the dose range of 10 to 20 mg/kg every 2 weeks. Steady-state concentrations of avelumab were reached after approximately 4 to 6 weeks (2 to 3 cycles) of repeated dosing, and the systemic accumulation was approximately 1.25-fold. | The geometric mean volume of distribution at steady state for a subject receiving 10 mg/kg is 4.72 L. | The total systemic clearance is approximately 0.59 L/day. | 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 |
| 13876 | Th1443 | Rilotumumab | NA | NA | NA | NA | NA | NA | NA | Rilotumumab has been investigated for the treatment of Cancer, Lung Cancer, Solid Tumors, Gastric Cancer, and Prostate Cancer, among others. | NA | 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 |
| 13877 | Th1443 | Rilotumumab | NA | NA | NA | NA | NA | NA | NA | Rilotumumab has been investigated for the treatment of Cancer, Lung Cancer, Solid Tumors, Gastric Cancer, and Prostate Cancer, among others. | NA | 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 |
| 13897 | Th1445 | Ocrelizumab | NA | 145000 | C6494H9978N1718O2014S46 | NA | NA | NA | The terminal elimination half-life was 26 days [FDA Label]. | Ocrelizumab is a CD20-directed cytolytic antibody indicated for the treatment of patients with relapsing or primary progressive forms of multiple sclerosis. It is a second-generation recombinant humanized monoclonal IgG1 antibody that selectively targets the B lymphocytes that express the CD20 antigen. As a humanized molecule, ocrelizumab is expected to be less immunogenic with repeated infusions which improves the benefit-to-risk profile for patients with relapsing or progressive forms of MS. Multiple sclerosis (MS) is a chronic, inflammatory, autoimmune disease of the central nervous system that leads to neurological disabilities and significantly reduced quality of life [L1199]. Most patients with MS experience episodes of relapses with worsening function, followed by recovery periods, or remissions. Primary progressive multiple sclerosis (PPMS) accounts for 10-15% of the overall population of patients with MS, and involves gradual worsening of neurologic disability from symptom onset, often without early relapses or remissions [A31741]. Developed by Genentech/Roche, ocrelizumab was approved by the FDA in March 2017 under the market name Ocrevustm for intravenous injection. It was later approved by Health Canada (as Ocrevus) in August 2017, making the drug the first available treatment for PPMS in both U.S. and Canada. In clinical trials of patients with relapsing forms of MS, treatment with ocrelizumab resulted in reduced relapse rates and reduced worsening of disability compared to interferon beta-1a [L1199]. In phase 3 clinical trials of patients with PPMS, treatment with ocrelizumab demonstrated lower rates of clinical and MRI progression than placebo [A31741]. | Indicated for the treatment of adult patients with relapsing or primary progressive forms of multiple sclerosis [FDA Label]. | Since ocrelizumab interferes with the CD20 assay, CD19+B-cells were used to assess B-cell counts after ocrelizumab treatment. 14 days following infusion, a reduction in CD19+B-cell counts was observed. In clinical studies, B-cell counts rose to above the lower limit of normal (LLN) or above baseline counts between infusions of ocrelizumab at least one time in 0.3% to 4.1% of patients. In a clinical study involving 51 patients, the time for B-cell counts to return to baseline or LLN was ranged from 27 to 125 weeks, with the median time of 72 weeks, after the last infusion. Within 2.5 years after the last infusion, B-cell counts returned to either baseline or LNN in 90% of the patients [FDA Label]. | B lymphocytes are known to contribute to the pathogenesis of MS through activation of pro-inflammatory T cells and secretion of proinflammatory cytokines. B cells may differentiate into plasma cells that can produce autoantibodies directed against myelin and cause complement-mediated attack on the myelin sheath [A31739]. CD20 is a cell-surface antigen found on pre-B cells, naïve and mature B cells and memory B cells. However, this activated glycosylated phosphoprotein is not expressed on haematopoietic stem cells, pro-B cells (precursors), or differentiated plasma cells [A31739, A31741]. While the exact mechanism of ocrelizumab leading to B-cell depletion is unknown, there are several different proposed mechanisms. Upon cell surface binding to CD20-expressing B lymphocytes, ocrelizumab promotes antibody-dependent cellular cytotoxicity and complement-mediated cell lysis. The capacity for B-cell reconstitution and preexisting humoral immunity is preserved [A31741], such as levels of IgG and IgM antibodies in the blood of cerebrospinal fluid. Ocrelizumab may induce antibody-dependant cellular cytotoxicity involving macrophages, natural killer cells, and cytotoxic T cells that act together to cause cell death [A31739]. Another mechanism is apoptosis, which may result from cross-linking membrane CD20 on the target cell surface [A31739]. | Studies assessing the carcinogenicity and mutagenicity of ocrelizumab have not been conducted [FDA Label]. | As with other antibodies, ocrelizumab is expected to undergo nonspecific catabolism and broken into smaller peptides and amino acids [FDA Label]. | Ocrelizumab displays a two-compartment pharmacokinetic model with time-dependent clearance. The overall exposure at the steady-state (AUC over the 24 week dosing intervals) of ocrelizumab was 3,510 mcg/mL per day. Following intravenous infusion of maintenance doses of 600 mg every 6 months in relapsing MS patients, the mean peak plasma concentration (Cmax) was 212 mcg/mL. Following intravenous infusion of two 300 mg doses separated by 14 days every 6 months in patients with PPMS, Cmax was reported to be 141 mcg/mL. The pharmacokinetics of ocrelizumab was essentially linear and dose proportional between 400 mg and 2000 mg [FDA Label]. | Central volume of distribution was 2.78 L [FDA Label]. | Constant clearance was estimated at 0.17 L/day, and initial time-dependent clearance at 0.05 L/day. Peripheral volume and inter-compartment clearance were estimated at 2.68 L and 0.29 L/day, respectively [FDA Label]. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | B-lymphocyte antigen CD20 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13982 | Th1453 | Trebananib | NA | NA | NA | NA | NA | NA | NA | Trebananib is under investigation for the treatment of Ovarian Cancer, Peritoneal Cancer, and Fallopian Tube Cancer. Trebananib has been investigated for the treatment of Cancer, Oncology, Carcinoma, Metastases, and Colon Cancer, among others. | NA | 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 |
| 14010 | Th1456 | Lorvotuzumab mertansine | >Th1456_Lorvotuzumab_mertansine QVQLVESGGGVVQPGRSLRLSCAASGFTFSSFGMHWVRQAPGKGLEWVAYISSGSFTIYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARMRKGYAMDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Lorvotuzumab mertansine has been used in trials studying the treatment of SCLC, Leukemia, Ovarian Cancer, Multiple Myeloma, and Merkel Cell Carcinoma, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2S)-2-amino-6-[4-[[3-[[(2S)-1-[[(1S,2R,3S,5S,6S,16E,18E,20R,21S)-11-chloro-21-hydroxy-12,20-dimethoxy-2,5,9,16-tetramethyl-8,23-dioxo-4,24-dioxa-9,22-diazatetracyclo[19.3.1.110,14.03,5]hexacosa-10,12,14(26),16,18-pentaen-6-yl]oxy]-1-oxopropan-2-yl]-methylamino]-3-oxopropyl]disulfanyl]pentanoylamino]hexanoic acid | NA | Link | NA | NA |
| 14011 | Th1456 | Lorvotuzumab mertansine | >Th1456_Lorvotuzumab_mertansine QVQLVESGGGVVQPGRSLRLSCAASGFTFSSFGMHWVRQAPGKGLEWVAYISSGSFTIYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARMRKGYAMDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Lorvotuzumab mertansine has been used in trials studying the treatment of SCLC, Leukemia, Ovarian Cancer, Multiple Myeloma, and Merkel Cell Carcinoma, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antineoplastic Agents, Immunological | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2S)-2-amino-6-[4-[[3-[[(2S)-1-[[(1S,2R,3S,5S,6S,16E,18E,20R,21S)-11-chloro-21-hydroxy-12,20-dimethoxy-2,5,9,16-tetramethyl-8,23-dioxo-4,24-dioxa-9,22-diazatetracyclo[19.3.1.110,14.03,5]hexacosa-10,12,14(26),16,18-pentaen-6-yl]oxy]-1-oxopropan-2-yl]-methylamino]-3-oxopropyl]disulfanyl]pentanoylamino]hexanoic acid | NA | Link | NA | NA |
| 14012 | Th1456 | Lorvotuzumab mertansine | >Th1456_Lorvotuzumab_mertansine QVQLVESGGGVVQPGRSLRLSCAASGFTFSSFGMHWVRQAPGKGLEWVAYISSGSFTIYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARMRKGYAMDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Lorvotuzumab mertansine has been used in trials studying the treatment of SCLC, Leukemia, Ovarian Cancer, Multiple Myeloma, and Merkel Cell Carcinoma, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antineoplastic Agents, Phytogenic | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2S)-2-amino-6-[4-[[3-[[(2S)-1-[[(1S,2R,3S,5S,6S,16E,18E,20R,21S)-11-chloro-21-hydroxy-12,20-dimethoxy-2,5,9,16-tetramethyl-8,23-dioxo-4,24-dioxa-9,22-diazatetracyclo[19.3.1.110,14.03,5]hexacosa-10,12,14(26),16,18-pentaen-6-yl]oxy]-1-oxopropan-2-yl]-methylamino]-3-oxopropyl]disulfanyl]pentanoylamino]hexanoic acid | NA | Link | NA | NA |
| 14082 | Th1464 | Duligotuzumab | NA | NA | NA | NA | NA | NA | NA | Duligotuzumab has been used in trials studying the treatment of Neoplasms, Colorectal Cancer, Head and Neck Cancer, and Epithelial Tumors, Malignant. | NA | 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 |
| 14141 | Th1469 | Binetrakin | >Th1469_Binetrakin HKCDITLQEIIKTLNSLTEQKTLCTELTVTDIFAASKNTTEKETFCRAATVLRQFYSHHEKDTRCLGATAQQFHRHKQLIRFLKRLDRNLWGLAGLNSCPVKEANQSTLENFLERLKTIMREKYSKCSS | NA | NA | NA | NA | NA | NA | Binetrakin has been used in trials studying the treatment of HIV Infections, Sarcoma, Kaposi, Non-Hodgkin's Lymphoma (NHL), Myelodysplastic Syndrome (MDS), and Leukemia, Acute Myelogenous (AML), among others. | NA | 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 |
| 14166 | Th1471 | Zalutumumab | >Th1471_Zalutumumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSTYGMHWVRQAPGKGLEWVAVIWDDGSYKYYGDSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARDGITMVRGVMKDYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146641.0546 | C6512H10074N1734O2032S46 | NA | NA | NA | NA | Zalutumumab is a fully human IgG1 monoclonal antibody designed to bind with selectivity to the epidermal growth factor receptor (EGFR). Zalutumumab has been investigated for the treatment of Squamous Cell Cancer and Head and Neck Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14167 | Th1471 | Zalutumumab | >Th1471_Zalutumumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSTYGMHWVRQAPGKGLEWVAVIWDDGSYKYYGDSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARDGITMVRGVMKDYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146641.0546 | C6512H10074N1734O2032S46 | NA | NA | NA | NA | Zalutumumab is a fully human IgG1 monoclonal antibody designed to bind with selectivity to the epidermal growth factor receptor (EGFR). Zalutumumab has been investigated for the treatment of Squamous Cell Cancer and Head and Neck Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antineoplastic Agents, Immunological | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14196 | Th1474 | Polatuzumab vedotin | NA | 149987 | NA | NA | NA | NA | The antibody conjugated monomethyl auristatin E has a terminal half life of 12 days.[Label] | Polatuzumab vedotin is a CD79b specific antibody conjugated to the antineoplastic agent monomethyl auristatin E.[Label] This medication was granted accelerated FDA approval on 10 June 2019.[L6658] | This medication is indicated to treat adults with relapsed or refractory diffuse large B-cell lymphoma in combination with bendamustine and rituximab that has returned of progressed after 2 or more previous therapies.[Label] | The binding of the unconjugated drug to microtubules in B cells leads to a number of immunosuppressant adverse effects including neutropenia and thrombocytopenia.[Label,A179380] The incidence of peripheral neuropathy also increases with increasing doses and time exposed to the drug.[A179374] Polatuzumab vedotin does not prolong the QTc interval. | Polatuzumab vedotin is an antibody targeted to CD79b conjugated to the antineoplastic agent monomethyl auristatin E (MMAE).[Label] The antibody binds to CD79b on the surface of B cells, causing the conjugate to be endocytosed.[Label] Once inside the cell, lysosomal proteases cleave the link between MMAE and the antibody allowing MMAE to bind to microtubules, inhibit cell division, and induce apoptosis.[Label] | Data regarding overdoses and LD50 are not readily available. In animal studies, embryo-fetal morality and birth defects were observed at less than the recommended dose and so the risk to the fetus must be weighed against the benefit to the mother.[Label] There is currently no data for the effects of polatuzumab vedotin on human pregnancies, though women are advised to used contraception while taking this medication.[Label] Women are advised not to breastfeed until 2 months after their last dose due to the potential risk to the infant, however no data is available regarding the effects of polatuzumab vedotin on the child or if it is present in breastmilk.[Label] Studies have not been performed to determine the carcinogenicity of this medication.[Label] Monomethyl auristatine E (MMAE) appears to be genotoxic in in vivo experiments but is not mutagenic in any tests performed.[Label] Based on animal data, polatuzumab vedotin may adversely affect male fertility and it is not known if this effect would be reversible.[Label] | The metabolism of polatuzumab vedotin has not been studied in humans but is likely to be catabolized to small peptides, amino acids, unconjugated monomethyl auristatin E (MMAE), and metabolites of MMAE.[Label] MMAE is metabolized by cytochrome P450 3A4.[Label] | Antibody conjugated monomethyl auristatin E (MMAE) reaches a maximum concentration of 803±233ng/mL while unconjugated MMAE reaches a maximum concentration of 6.82±4.73ng/mL.[Label] The area under the curve for the conjugated medication is 1860±966day | The central volume of distribution is 3.15L.[Label] | 0.9L/day.[Label] | Antineoplastic Agents | NA | NA | NA | NA | B-cell antigen receptor complex-associated protein beta chain | Polivy | Roche Registration Gmb H | Roche Registration Gmb H | Intravenous | 30 mg | None. | low white blood cell count (neutropenia), low platelet count (thrombocytopenia), anemia, numbness and tingling of extremities, fatigue, diarrhea, fever, decreased appetite, pneumonia, vomiting, infusion site reactions, weight loss, and low blood potassium | Polivy is used to treat diffuse large B-cell lymphoma after at least two other cancer treatments did not work or have stopped working. Polivy is given in combination with bendamustine (Bendeka, Treanda) and a medicine that contains rituximab (Rituxan). Polivy may also be used for purposes not listed... | Polivy is a prescription medicine used to treat the symptoms of Diffuse Large B-Cell Lymphoma. Polivy may be used alone or with other medications. | NA | Polatuzumab vedotin-piiq is a CD79b-directed antibody-drug conjugate (ADC) consisting of three components: 1) the humanized immunoglobulin G1 (IgG1) monoclonal antibody specific for human CD79b; 2) the small molecule anti-mitotic agent MMAE; and 3) a protease-cleavable linker maleimidocaproyl-valine-citrulline-p-aminobenzyloxycarbonyl (mc-vc-PAB) that covalently attaches MMAE to the polatuzumab antibody. | Link | Link | NA |
| 14442 | Th1504 | Mogamulizumab | >Th1504_Mogamulizumab EVQLVESGGDLVQPGRSLRLSCAASGFIFSNYGMSWVRQAPGKGLEWVATISSASTYSYYPDSVKGRFTISRDNAKNSLYLQMNSLRVEDTALYYCGRHSDGNFAFGYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | The terminal half-life is 17 days [FDA label]. | Mogamulizumab is a humanized monoclonal antibody (mAb) directed against CC chemokine receptor 4 (CCR4) for the treatment of Mycosis Fungoides (MF) and Sézary Syndrome (SS), the most common subtypes of cutaneous T-cell lymphoma. Cutaneous T-cell lymphomas occur when certain white blood cells, called T cells, become cancerous; these cancers typically affect the skin, causing various types of skin lesions [L4170]. On August 8 2018, the U.S. Food and Drug Administration (FDA) approved mogamulizumab injection (also known as _Poteligeo_) for intravenous use for the treatment of adult patients with relapsed or refractory mycosis fungoides (MF) or Sézary syndrome (SS) after at least one prior systemic therapy [L4168]. Mogamulizumab is derived from Kyowa Hakko Kirin's POTELLIGENT (®) technology, which produces antibodies with enhanced antibody-dependent cell-mediated cytotoxicity (ADCC) activity. Approval in Japan was granted on April 30 2012 by the Japanese Ministry of Health, Labour and Welfare for patients with relapsed or refractory CCR4-positive adult T-cell leukemia-lymphoma [A36741]. | For the intravenous use for the treatment of adult patients with relapsed or refractory mycosis fungoides (MF) or Sézary syndrome (SS) after at least one prior systemic therapy. This approval provides a new treatment option for patients with MF and is the first FDA approval of a drug specifically for Sézary Syndrome [FDA label]. | This drug is a CC chemokine receptor 4 (CCR4) antagonist. It is a monoclonal antibody which blocks T cell proliferation, which leads to malignancy [A36739], [A36758]. CCR4 is a chemokine receptor that is preferentially expressed by Th2 and regulatory T (Treg) cells. In response to its ligands, CCL17 (TARC) and CCL22 (MDC), CCR4 promotes T-cell migration to extranodal sites, including the skin [A36758]. | Mogamulizumab selectively binds to and inhibits the activity of CCR4, which may block CCR4-mediated signal transduction pathways and, so, chemokine-mediated cellular migration and proliferation of T cells, as well as chemokine-mediated angiogenesis. Additionally, this agent may induce antibody-dependent cell-mediated cytotoxicity (ADCC) against CCR4-positive T cells. CCR4, a G-coupled-protein receptor for C-C chemokines such MIP-1, RANTES, TARC and MCP-1, is expressed on the surfaces of some types of T cells, endothelial cells, and certain types of neurons. CCR4, also known as CD194, may be overexpressed on adult T-cell lymphoma (ATL) and peripheral T-cell lymphoma (PTCL) cells [L4175]. In addition to directly targeting malignant T cells expressing CCR4, mogamulizumab depletes Treg cells, an important therapeutic target in many human cancers because of their role in suppressing host antitumor immunity [A36758]. | The most common adverse reactions (reported in =20% of patients randomized to mogamulizumab) were rash (including drug eruption), infusion-related reactions, fatigue, diarrhea, upper respiratory tract infection and musculoskeletal pain [FDA label]. Due to various adverse effects related to this drug, the adverse reactions have been categorized by organ system. Because of the risk of serious/fatal ADRs, patients administered mogamulizumab should be carefully monitored [A36743]. **Upper respiratory tract infection**: This may occur due to decreased immunity following the administration of this drug. Monitor for signs of respiratory infection including fever, cough and shortness of breath [L4171]. **Dermatological**: Patients must contact their healthcare provider immediately if they experience a new or worsening skin rash. Treatment should be temporarily interrupted for moderate or severe skin rashes and permanently discontinued for a life-threatening rash. Fatal and life-threatening skin adverse reactions, including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), have occurred in recipients of mogamulizumab. Rash (drug eruption) is one of the most common adverse reactions associated with mogamulizumab [L4171], [FDA label]. **Infusion Reactions**: Patients must contact their healthcare provider immediately for signs or symptoms of infusion reactions. Treatment should be suspended for any infusion reaction and permanently discontinued for any life-threatening infusion reaction [L4171]. **Infections**: Patients must contact their healthcare provider if they experience fever or other signs of infection. Infections should be monitored and treated promptly [L4171]. **Autoimmune Complications**: Immune-mediated or possibly immune-mediated reactions have included myositis, myocarditis, polymyositis, hepatitis, pneumonitis, and a variant of Guillain- Barré syndrome [FDA label]. Patients must notify their healthcare provider of any history of autoimmune disease. Treatment should be suspended or permanently discontinued as appropriate [L4171]. Fatal and life-threatening immune-mediated complications have been reported in recipients of this drug [FDA label]. **Musculoskeletal pain**: This drug may cause musculoskeletal pain [FDA label] **A note on complications of allogeneic hematopoietic stem cell transplantation**: Patients must be aware of the possible risk of post-transplant complications when taking this agent. Patients should be monitored for severe acute graft-versus-host disease (GVHD) and steroid-refractory GVHD. **Females of Reproductive Potential**: Females who are able to become pregnant should use an effective method of birth control during treatment with Poteligeo and for at least three months after the last dose [L4171]. | NA | Following repeated dosing of the approved recommended dosage, steady-state concentrations were reached after 8 doses (12 weeks), and the systemic accumulation was 1.6-fold. At steady state, the peak concentration (Cmax,ss) is 32 (68%) µg/mL, the trough concentration (Cmin,ss) is 11 (239%) µg/mL, and AUCss is 5577 (125%) µg•hr/mL [FDA label]. | The central volume of distribution is 3.6 L [FDA label]. | Clearance is 12 mL/h [FDA label]. | Antineoplastic Agents | NA | NA | NA | NA | C-C chemokine receptor type 4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14443 | Th1504 | Mogamulizumab | >Th1504_Mogamulizumab EVQLVESGGDLVQPGRSLRLSCAASGFIFSNYGMSWVRQAPGKGLEWVATISSASTYSYYPDSVKGRFTISRDNAKNSLYLQMNSLRVEDTALYYCGRHSDGNFAFGYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | The terminal half-life is 17 days [FDA label]. | Mogamulizumab is a humanized monoclonal antibody (mAb) directed against CC chemokine receptor 4 (CCR4) for the treatment of Mycosis Fungoides (MF) and Sézary Syndrome (SS), the most common subtypes of cutaneous T-cell lymphoma. Cutaneous T-cell lymphomas occur when certain white blood cells, called T cells, become cancerous; these cancers typically affect the skin, causing various types of skin lesions [L4170]. On August 8 2018, the U.S. Food and Drug Administration (FDA) approved mogamulizumab injection (also known as _Poteligeo_) for intravenous use for the treatment of adult patients with relapsed or refractory mycosis fungoides (MF) or Sézary syndrome (SS) after at least one prior systemic therapy [L4168]. Mogamulizumab is derived from Kyowa Hakko Kirin's POTELLIGENT (®) technology, which produces antibodies with enhanced antibody-dependent cell-mediated cytotoxicity (ADCC) activity. Approval in Japan was granted on April 30 2012 by the Japanese Ministry of Health, Labour and Welfare for patients with relapsed or refractory CCR4-positive adult T-cell leukemia-lymphoma [A36741]. | For the intravenous use for the treatment of adult patients with relapsed or refractory mycosis fungoides (MF) or Sézary syndrome (SS) after at least one prior systemic therapy. This approval provides a new treatment option for patients with MF and is the first FDA approval of a drug specifically for Sézary Syndrome [FDA label]. | This drug is a CC chemokine receptor 4 (CCR4) antagonist. It is a monoclonal antibody which blocks T cell proliferation, which leads to malignancy [A36739], [A36758]. CCR4 is a chemokine receptor that is preferentially expressed by Th2 and regulatory T (Treg) cells. In response to its ligands, CCL17 (TARC) and CCL22 (MDC), CCR4 promotes T-cell migration to extranodal sites, including the skin [A36758]. | Mogamulizumab selectively binds to and inhibits the activity of CCR4, which may block CCR4-mediated signal transduction pathways and, so, chemokine-mediated cellular migration and proliferation of T cells, as well as chemokine-mediated angiogenesis. Additionally, this agent may induce antibody-dependent cell-mediated cytotoxicity (ADCC) against CCR4-positive T cells. CCR4, a G-coupled-protein receptor for C-C chemokines such MIP-1, RANTES, TARC and MCP-1, is expressed on the surfaces of some types of T cells, endothelial cells, and certain types of neurons. CCR4, also known as CD194, may be overexpressed on adult T-cell lymphoma (ATL) and peripheral T-cell lymphoma (PTCL) cells [L4175]. In addition to directly targeting malignant T cells expressing CCR4, mogamulizumab depletes Treg cells, an important therapeutic target in many human cancers because of their role in suppressing host antitumor immunity [A36758]. | The most common adverse reactions (reported in =20% of patients randomized to mogamulizumab) were rash (including drug eruption), infusion-related reactions, fatigue, diarrhea, upper respiratory tract infection and musculoskeletal pain [FDA label]. Due to various adverse effects related to this drug, the adverse reactions have been categorized by organ system. Because of the risk of serious/fatal ADRs, patients administered mogamulizumab should be carefully monitored [A36743]. **Upper respiratory tract infection**: This may occur due to decreased immunity following the administration of this drug. Monitor for signs of respiratory infection including fever, cough and shortness of breath [L4171]. **Dermatological**: Patients must contact their healthcare provider immediately if they experience a new or worsening skin rash. Treatment should be temporarily interrupted for moderate or severe skin rashes and permanently discontinued for a life-threatening rash. Fatal and life-threatening skin adverse reactions, including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), have occurred in recipients of mogamulizumab. Rash (drug eruption) is one of the most common adverse reactions associated with mogamulizumab [L4171], [FDA label]. **Infusion Reactions**: Patients must contact their healthcare provider immediately for signs or symptoms of infusion reactions. Treatment should be suspended for any infusion reaction and permanently discontinued for any life-threatening infusion reaction [L4171]. **Infections**: Patients must contact their healthcare provider if they experience fever or other signs of infection. Infections should be monitored and treated promptly [L4171]. **Autoimmune Complications**: Immune-mediated or possibly immune-mediated reactions have included myositis, myocarditis, polymyositis, hepatitis, pneumonitis, and a variant of Guillain- Barré syndrome [FDA label]. Patients must notify their healthcare provider of any history of autoimmune disease. Treatment should be suspended or permanently discontinued as appropriate [L4171]. Fatal and life-threatening immune-mediated complications have been reported in recipients of this drug [FDA label]. **Musculoskeletal pain**: This drug may cause musculoskeletal pain [FDA label] **A note on complications of allogeneic hematopoietic stem cell transplantation**: Patients must be aware of the possible risk of post-transplant complications when taking this agent. Patients should be monitored for severe acute graft-versus-host disease (GVHD) and steroid-refractory GVHD. **Females of Reproductive Potential**: Females who are able to become pregnant should use an effective method of birth control during treatment with Poteligeo and for at least three months after the last dose [L4171]. | NA | Following repeated dosing of the approved recommended dosage, steady-state concentrations were reached after 8 doses (12 weeks), and the systemic accumulation was 1.6-fold. At steady state, the peak concentration (Cmax,ss) is 32 (68%) µg/mL, the trough concentration (Cmin,ss) is 11 (239%) µg/mL, and AUCss is 5577 (125%) µg•hr/mL [FDA label]. | The central volume of distribution is 3.6 L [FDA label]. | Clearance is 12 mL/h [FDA label]. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | C-C chemokine receptor type 4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14467 | Th1506 | Molgramostim | NA | NA | NA | NA | NA | NA | NA | Molgramostim has been used in trials studying the treatment of Bronchiectasis, Cystic Fibrosis, Pulmonary Alveolar Proteinosis, Acute Respiratory Distress Syndrome, and Autoimmune Pulmonary Alveolar Proteinosis. | NA | 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 |
| 14468 | Th1506 | Molgramostim | NA | NA | NA | NA | NA | NA | NA | Molgramostim has been used in trials studying the treatment of Bronchiectasis, Cystic Fibrosis, Pulmonary Alveolar Proteinosis, Acute Respiratory Distress Syndrome, and Autoimmune Pulmonary Alveolar Proteinosis. | NA | NA | NA | NA | NA | NA | NA | NA | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14530 | Th1512 | Dacetuzumab | NA | NA | NA | NA | NA | NA | NA | Dacetuzumab has been used in trials studying the treatment of Multiple Myeloma, Non-Hodgkin Lymphoma, Leukemia, Lymphocytic, Chronic, and Lymphoma, Large B-Cell, Diffuse. It is a humanized anti-CD40 antibody and induces cytotoxicity in human multiple myeloma cells. | Investigated for use/treatment in lymphoma (non-hodgkin's) and multiple myeloma. | NA | NA | NA | NA | NA | NA | NA | Antineoplastic Agents | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14531 | Th1512 | Dacetuzumab | NA | NA | NA | NA | NA | NA | NA | Dacetuzumab has been used in trials studying the treatment of Multiple Myeloma, Non-Hodgkin Lymphoma, Leukemia, Lymphocytic, Chronic, and Lymphoma, Large B-Cell, Diffuse. It is a humanized anti-CD40 antibody and induces cytotoxicity in human multiple myeloma cells. | Investigated for use/treatment in lymphoma (non-hodgkin's) and multiple myeloma. | NA | NA | NA | NA | NA | NA | NA | Antineoplastic Agents, Immunological | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | 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 |
| 14637 | Th1523 | Balugrastim | NA | NA | NA | NA | NA | NA | NA | Balugrastim has been used in trials studying the treatment of Solid Tumors. | NA | NA | NA | NA | NA | NA | NA | NA | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14653 | Th1524 | Intetumumab | NA | NA | NA | NA | NA | NA | NA | Intetumumab has been used in trials studying the treatment of Melanoma. | NA | 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 |
| 14654 | Th1524 | Intetumumab | NA | NA | NA | NA | NA | NA | NA | Intetumumab has been used in trials studying the treatment of Melanoma. | NA | 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 |
| 14730 | Th1532 | Ecromeximab | NA | NA | NA | NA | NA | NA | NA | Ecromeximab has been used in trials studying the treatment of Cutaneous Melanoma and Metastatic Melanoma. | NA | 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 |
| 14731 | Th1532 | Ecromeximab | NA | NA | NA | NA | NA | NA | NA | Ecromeximab has been used in trials studying the treatment of Cutaneous Melanoma and Metastatic Melanoma. | NA | 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 |
| 14751 | Th1534 | Cepeginterferon alfa-2B | NA | NA | NA | NA | NA | NA | NA | Cepeginterferon alfa-2B is under investigation in clinical trial NCT01889433 (An Open-label Comparative Efficacy and Safety Study of Algeron (Cepeginterferon Alfa-2b) in Treatment-naive Patients With Chronic Hepatitis C). | NA | NA | NA | NA | NA | NA | NA | NA | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 |
| 15191 | Th1571 | Lipegfilgrastim | >Th1571_Lipegfilgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 39000 | C866H1372N226O258S9*(C2H4O)n | NA | NA | NA | The average terminal half-life ranged from approximately 32 to 62 hours after a single subcutaneous injection of 6 mg lipegfilgrastim in healthy individuals [L2441]. | Lipegfilgrastim, previously known as XM22, is a pegylated, recombinant granulocyte colony-stimulating factor (G-CSF) that was synthetized using a highly site-specific glycoPEGylation technology [A32665]. It is used as an alternate to [DB00019] for prophylactic use in cancer patients receiving chemotherapy and at risk for developing chemotherapy-induced neutropenia. Since July 2013, lipegfilgrastim is marketed by the EMA as Lonquex for subcutaneously injection, where it is administered once following cytotoxic chemotherapy for each chemotherapy cycle in adult patients being treated with cytotoxic chemotherapy for malignancy. It aims to reduce the duration of neutropenia and the incidence of febrile neutropenia. Neutropenia and febrile neutropenia (FN) are frequent and potentially fatal complications that occur from myelosuppressive anticancer treatments [A32665]. Severe chemotherapy-induced neutropenia and febrile neutropenia significantly increases the risk for life-threatening infection and sepsis. Granulocyte colony-stimulating factors (G-CSFs) were introduced in the 1980's to the clinical setting to stimulate neutrophil proliferation and differentiation, thereby reducing the duration and severity of chemotherapy-induced neutropenia [A32665]. Lipegfilgrastim is a covalent conjugate of [DB00099] with a single methoxy polyethylene glycol (PEG) molecule via a carbohydrate linker consisting of glycine, N-acetylneuraminic acid and N-acetylgalactosamine [L2441]. The average molecular mass of lipegfilgrastim comprises 18,798 Da for [DB00099], 203 Da for GalNAc, 338 Da for glycylsialic acid and approximately 20,000 Da for PEG [L2449]. PEG moiety protects the active molecule from enzyme degradation, which allows longer half-life of drug and less frequent dosing-schedule in addition to acceptable safety and efficacy profile [A32665]. | Indicated for the reduction in the duration of neutropenia and the incidence of febrile neutropenia in adult patients treated with cytotoxic chemotherapy for malignancy (with the exception of chronic myeloid leukaemia and myelodysplastic syndromes) [L2441]. | Mimicking endogenous granulocyte colony-stimulating factors, lipegfilgrastim enhances the number and function of circulating neutrophils by binding to endogenous G-CSF receptors. A small increase in monocyte and/or lymphocyte counts may also be observed [L2441]. Following a single subcutaneous dose administration of 100 µg/kg, lipegfilgrastim resulted in a significant increase in neutrophilic granulocyte and large unstained cell counts [L2449]. G-CSF also increases the antibacterial activities of neutrophils including the phagocytosis [L2441]. Due to structural similarity between lipegfilgrastim and pegfilgrastim, G-CSF receptor binding was equivalent between two molecules [A32665]. However, lipegfilgrastim showed greater time-dependent resistance to neutrophil elastase degradation and greater retention of activity than pegfilgrastim [A32665]. | Endogenous granulocyte colony-stimulating factor (G-CSF) is a glycoprotein that stimulates neutrophil progenitors. It is produced mainly by monocytes, fibroblasts and endothelial cells to promote the development of neutrophils and increase their proliferation and maturation [T28]. Subsequently, G-SCF stimulates the release of matured neutrophils from the bone marrow storage pools into the peripheral blood to enhance their function [L2441, T28]. Via binding to to the human G-CSF receptors, lipegfilgrastim activates the receptor signalling pathway as a growth factor to stimulate proliferation of haematopoietic progenitor cells and their differentiation into mature cells, and promote subsequent release into the peripheral blood [L2441]. This stimulatory effect of lipegfilgrastim may extend to other single lineage and multilineage progenitors and pluripotent haematopoietic stem cells [L2441]. The presence of the PEG moiety in lipegfilgrastim decreases the plasma clearance and extends the drug's terminal elimination half-life, allowing for less frequent dosing [A32664]. | In safety pharmacological studies in rats and dogs, lipegfilgrastim was well tolerated at a single subcutaneous dose of 10 mg/kg. In the renal excretion study in rats, an intravenous dose of 250 µg/kg was well tolerated [L2449]. While mutagenicity and genotoxicity studies have not been conducted with lipegfilgrastim, G-CSF has been reported to stimulate tumour growth and intratumoural vessel density in animal tumour models [L2449]. | Lipegfilgrastim is metabolised via intra- or extracellular degradation by proteolytic enzymes [L2441]. Following binding to the G-CSF receptors, it is proposed to be internalized by neutrophils via a non-linear process, and then undergoes degradation within the cell by endogenous proteolytic enzymes. Alternatively, the linear pathway is likely due to extracellular protein degradation by neutrophil elastase and other plasma proteases [L2441]. | In studies of healthy volunteers receiving a single subcutaneous injection of 6 mg of lipegfilgrastim, the peak plasma concentration of lipegfilgrastim was reached after a median of 30 to 36 hours [L2441]. Based on its molecular weight, lipegfilgrastim is believed to be primarily absorbed via the lymphatic system then drained into the vascular system [L2455]. Peak concentration and area under the curve, indicating full bioavailability, was lower in injection site of the thigh compared to subcutaneous injection in the abdomen and in the upper arm, with differences among the injection sites being the greatest in males compared to female subjects [L2441]. | Lipegfilgrastim has a weight-dependent volume of distribution of 70 mL/kg, indicating minimal distribution beyond the lymphatic or vascular system [L2455]. | In a phase 1, multinational, open-label, single-arm study of paediatric patients with Ewing family of tumors or rhabdomyosarcoma treated with myelosuppressive chemotherapy, the mean apparent clearance (CL/F) was approximately 71 mL/h, 120 mL/h, and 116 mL/h for age groups of 2-6 years, 6-12 years, and 12-18 years, respectively [A32674]. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Granulocyte colony-stimulating factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | 2-[[5-acetamido-6-(1-amino-1-carboxypropan-2-yl)oxy-3,4-dihydroxyoxan-2-yl]methoxy]-4-hydroxy-5-[[2-(2-methoxyethoxycarbonylamino)acetyl]amino]-6-(1,2,3-trihydroxypropyl)oxane-2-carboxylic acid | NA | Link | NA | NA |
| 15216 | Th1573 | Begelomab | NA | NA | NA | NA | NA | NA | NA | 0 | NA | NA | NA | NA | NA | NA | NA | NA | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15232 | Th1575 | Edrecolomab | NA | NA | NA | NA | NA | NA | NA | 0 | NA | 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 |
| 15233 | Th1575 | Edrecolomab | NA | NA | NA | NA | NA | NA | NA | 0 | NA | NA | NA | NA | NA | NA | NA | NA | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15303 | Th1585 | Talimogene laherparepvec | >Th1585_Talimogene_laherparepvec MFSGGGGPLSPGGKSAARAASGFFAPAGPRGASRGPPPCLRQNFYNPYLAPVGTQQKPTGPTQRHTYYSECDEFRFIAPRVLDEDAPPEKRAGVHDGHLKRAPKVYCGGDERDVLRVGSGGFWPRRSRLWGGVDHAPAGFNPTVTVFHVYDILENVEHAYGMRAAQFHARFMDAITPTGTVITLLGLTPEGHRVAVHVYGTRQYFYMNKEEVDRHLQCRAPRDLCERMAAALRESPGASFRGISADHFEAEVVERTDVYYYETRPALFYRVYVRSGRVLSYLCDNFCPAIKKYEGGVDATTRFILDNPGFVTFGWYRLKPGRNNTLAQPAAPMAFGTSSDVEFNCTADNLAIEGGMSDLPAYKLMCFDIECKAGGEDELAFPVAGHPEDLVIQISCLLYDLSTTALEHVLLFSLGSCDLPESHLNELAARGLPTPVVLEFDSEFEMLLAFMTLVKQYGPEFVTGYNIINFDWPFLLAKLTDIYKVPLDGYGRMNGRGVFRVWDIGQSHFQKRSKIKVNGMVNIDMYGIITDKIKLSSYKLNAVAEAVLKDKKKDLSYRDIPAYYAAGPAQRGVIGEYCIQDSLLVGQLFFKFLPHLELSAVARLAGINITRTIYDGQQIRVFTCLLRLADQKGFILPDTQGRFRGAGGEAPKRPAAAREDEERPEEEGEDEDEREEGGGEREPEGARETAGRHVGYQGARVLDPTSGFHVNPVVVFDFASLYPSIIQAHNLCFSTLSLRADAVAHLEAGKDYLEIEVGGRRLFFVKAHVRESLLSILLRDWLAMRKQIRSRIPQSSPEEAVLLDKQQAAIKVVCNSVYGFTGVQHGLLPCLHVAATVTTIGREMLLATREYVHARWAAFEQLLADFPEAADMRAPGPYSMRIIYGDTDSIFVLCRGLTAAGLTAVGDKMASHISRALFLPPIKLECEKTFTKLLLIAKKKYIGVIYGGKMLIKGVDLVRKNNCAFINRTSRALVDLLFYDDTVSGAAAALAERPAEEWLARPLPEGLQAFGAVLVDAHRRITDPERDIQDFVLTAELSRHPRAYTNKRLAHLTVYYKLMARRAQVPSIKDRIPYVIVAQTREVEETVARLAALRELDAAAPGDEPAPPAALPSPAKRPRETPSPADPPGGASKPRKLLVSELAEDPAYAIAHGVALNTDYYFSHLLGAACVTFKALFGNNAKITESLLKRFIPEVWHPPDDVAARLRTAGFGAVGAGATAEETRRMLHRAFDTLA | NA | NA | NA | NA | NA | Readily accessible data regarding the half-life of talimogene laherparepvec is not available, although talimogene laherparepvec DNA has been found in patient subjects' injected tumor through 84 days [FDA Label] and the half-lives of antibody-based therapeutics are often times generally long, on the order of days versus hours with small molecule drugs [T165]. | Talimogene laherparepvec is an oncolytic treatment used in local treatment of unresectable cutaneous, subcutaneous, and nodal lesions in patients with recurrent melanoma. It is a genetically administered herpes simplex virus 1 (HSV-1) that expresses human cytokine granulocyte-macrophage colony stimulating factor (GM-CSF) with antitumor and immune-stimulating activities. It specifically replicates within tumor cells and causes lysis. It was approved by the FDA in 2015 under the market name Imlygic. In general, talimogene laherparepvec has been modified so that it can infect and multiply inside melanoma cells [L2221]. The drug subsequently uses the melanoma cells' own machinery to multiply, eventually overwhelming the melanoma cells and killing them [L2221]. Alternatively, although talimogene laherparepvec also enters healthy cells, it is not designed to multiply inside them [L2221]. | This medication is a genetically modified oncolytic viral therapy indicated for the local treatment of unresectable, cutaneous, subcutaneous, and nodal lesions in patients with melanoma recurrent after initial surgery [FDA Label]. Elsewhere, the EMA notes that the agent is indicated for the treatment of adults with unresectable melanoma that is regionally or distantly metastatic (Stage IIIB, IIIC, and IVM1a) with no bone, brain, lung, or other visceral diseases [L2209]. | Talimogene laherparepvec has been genetically modified to replicate within tumors and to produce the immune stimulatory protein GM-CSF (granulocyte macrophage colony stimulating factor) [FDA Label]. The medication causes lysis of tumors, followed by the release of tumor-derived antigens, which together with virally derived GM-CSF may promote an anti-tumor immune response in the body [FDA Label]. | Talimogene laherparepvec is an oncolytic immunotherapy that is derived from Herpes Simplex Virus type-1 (HSV-1) [L2212]. It has been modified to replicate within tumor cells and to produce the immune response stimulatory protein, human GM-CSF (granulocyte macrophage colony stimulating factor) [L2212]. The medication causes the death of tumor cells and the release of tumor-derived antigens [L2212]. It is believed that together with GM-CSF, talimogene laherparepvec can promote a systemic anti-tumor immune response and an effector T-cell response [L2212]. Mice subjects involved in talimogene laherparepvec treatment studies that had complete regression of their primary tumors following therapy were resistant to subsequent tumor rechallenge [L2212]. The genetic modifications to talimogene laherparepvec from HSV-1 include deletion of the ICP34.5 and ICP47 genes [L2212]. Whereas anti-viral immune responses defend normal cells following infection by talimogene laherparepvec, tumors have been shown to be susceptible to injury and cell death from ICP34.5-deficient HSV-1 derived viruses, including talimogene laherparepvec [L2212]. Moreover, deletion of ICP47 prevents the down-regulation of antigen presentation molecules in the targeted tumor cells and increases the expression of the HSV US11 gene, thereby enhancing the talimogene laherparepvec viral replication in tumor cells and increases chances of tumor cell injury and death [L2212]. Although the talimogene laherparepvec virus is specifically modified to infect and multiply inside melanoma cells and uses melanoma cells' own machinery to multiply, the medication is not designed to multiply inside healthy cells, which it is also capable of entering [L2221]. | There is no clinical experience with overdose with talimogene laherparepvec [FDA Label, L2209]. Doses up to 4 mL at a concentration of 10^8 PFU/mL every 2 weeks have been administered in clinical trials with no evidence of dose-limiting toxicity [FDA Label, L2209]. The maximum dose of talimogene laherparepvec that can be safely administered has not been determined [FDA Label, L2209]. Nevertheless, some adverse reactions that are possible from taking talimogene laherparepvec range from fatigue, chills, pyrexia, nausea, influenza-like illness, injection site pain, to even injection site complications (including cellulitis, systemic bacterial infection, and others), herpetic infection, or plasmacytoma at or near the injection site [FDA Label, L2209]. As a result, healthcare providers and caregivers must observe the necessary safety precautions when administering talimogene laherparepvec to patients as accidental exposure to the agent can lead to exposure to and transmission of talimogene laherparepvec and herpetic infection in individuals who do not need the medication or in whom the medication is not indicated [FDA Label, L2209]. Moreover, in the event of a suspected overdose or inadvertent intravenous administration, the patient should be treated symptomatically, ie. with acyclovir or other anti-viral agents and supportive measures instituted as needed [FDA Label, L2209]. | Talimogene laherparepvec is cleared through general host defense mechanisms like autophagy and adaptive immune responses [L2212]. The agent is ultimately degraded by common endogenous protein and DNA catabolic pathways [L2212]. As with other wild-type HSV-1 (herpes simplex virus type-1) infections, a latent pool of talimogene laherparepvec DNA may persist in neuronal cell bodies innervating the injection sites [L2212]. Consequently, the occurrence of latent infection with talimogene laherparepvec cannot be excluded [L2212]. | Cellular uptake of talimogene laherparepvec occurs through HSV-1 receptors on both tumor and non-tumor cells following local injection into physical tumors [L2212]. After injection, the talimogene laherparepvec subsequently replicates intratumorally, where bioavailability and systemic concentration of the agent are not largely predictive of drug substance activity and therefore such data has not been evaluated to any particular degree [L2212]. | Talimogene laherparepvec is a genetically modified and replication-competent HSV-1 virus [L2212]. Therefore, its pharmacokinetics and biodistribution are driven by the specific site of intralesional injection, tumor-selective replication, and release from tumor tissue [L2212]. As a result, the specific pharmacokinetics of the agent, including distribution may vary depending on particular parameters of each unique administration. | Although readily accessible data regarding the clearance of talimogene laherparepvec is not available, in an ongoing melanoma study, it was determined that the proportion of patients with detectable talimogene laherparepvec DNA in blood and urine was highest during the second cycle of therapy [L2212]. Additionally, even though talimogene laherparepvec DNA was detected in samples from injected lesions in about 90% of patients, only 14% of patients tested positive for infective virus by 50% Tissue Culture Infectious Dose (TCID50) assay, all within 8 days of treatment administration [L2212]. 17% of samples from the exterior occlusive dressing tested positive for talimogene laherparepvec DNA but none tested positive for the presence of infective virus [L2212]. Moreover, only 1 sample had detectable talimogene laherparepvec DNA located on the oral mucosa - but the sample did not test positive for the presence of infective virus [L2212]. | Antineoplastic Agents | NA | NA | NA | NA | Heparan sulfate,DNA polymerase catalytic subunit,DNA polymerase catalytic subunit | Imlygic | AMGEN INC | AMGEN INC | Intralesional | 100000000 [PFU]/1mL | Immunocompromised Patients IMLYGIC is a live, attenuated herpes simplex virus and may cause life-threatening disseminated herpetic infection in patients who are immunocompromised. Do not administer IMLYGIC to immunocompromised patients, including those with a history of primary or acquired immunodeficient states, leukemia, lymphoma, AIDS or other clinical manifestations of infection with human immunodeficiency viruses, and those on immunosuppressive therapy [see Nonclinical Toxicology]. Pregnant Patients Do not administer IMLYGIC to pregnant patients. | fatigue, chills, fever, nausea, influenza-like illness, injection site pain, nausea, vomiting, diarrhea, constipation, abdominal pain, joint pain muscle pain, pain in extremities, headache, dizziness, mouth and throat pain, and weight loss | Imlygic is a cancer medicine that affects the actions of the body's immune system, helping the body produce an "antitumor" response. Imlygic is a genetically modified weak form of type 1 herpes simplex virus (the virus that causes common cold sores). Imlygic is used to treat a type of cancer called melanoma... | Imlygic is a prescription medicine used to treat the symptoms of Melanoma. Imlygic may be used alone or with other medications. | NA | IMLYGIC (talimogene laherparepvec) is a sterile suspension for intralesional injection. IMLYGIC is a live, attenuated HSV-1 that has been genetically modified to express huGM-CSF. The parental virus for IMLYGIC was a primary isolate, which was subsequently altered using recombinant methods to result in gene deletions and insertions. | Link | Link | NA |
| 15304 | Th1585 | Talimogene laherparepvec | >Th1585_Talimogene_laherparepvec MFSGGGGPLSPGGKSAARAASGFFAPAGPRGASRGPPPCLRQNFYNPYLAPVGTQQKPTGPTQRHTYYSECDEFRFIAPRVLDEDAPPEKRAGVHDGHLKRAPKVYCGGDERDVLRVGSGGFWPRRSRLWGGVDHAPAGFNPTVTVFHVYDILENVEHAYGMRAAQFHARFMDAITPTGTVITLLGLTPEGHRVAVHVYGTRQYFYMNKEEVDRHLQCRAPRDLCERMAAALRESPGASFRGISADHFEAEVVERTDVYYYETRPALFYRVYVRSGRVLSYLCDNFCPAIKKYEGGVDATTRFILDNPGFVTFGWYRLKPGRNNTLAQPAAPMAFGTSSDVEFNCTADNLAIEGGMSDLPAYKLMCFDIECKAGGEDELAFPVAGHPEDLVIQISCLLYDLSTTALEHVLLFSLGSCDLPESHLNELAARGLPTPVVLEFDSEFEMLLAFMTLVKQYGPEFVTGYNIINFDWPFLLAKLTDIYKVPLDGYGRMNGRGVFRVWDIGQSHFQKRSKIKVNGMVNIDMYGIITDKIKLSSYKLNAVAEAVLKDKKKDLSYRDIPAYYAAGPAQRGVIGEYCIQDSLLVGQLFFKFLPHLELSAVARLAGINITRTIYDGQQIRVFTCLLRLADQKGFILPDTQGRFRGAGGEAPKRPAAAREDEERPEEEGEDEDEREEGGGEREPEGARETAGRHVGYQGARVLDPTSGFHVNPVVVFDFASLYPSIIQAHNLCFSTLSLRADAVAHLEAGKDYLEIEVGGRRLFFVKAHVRESLLSILLRDWLAMRKQIRSRIPQSSPEEAVLLDKQQAAIKVVCNSVYGFTGVQHGLLPCLHVAATVTTIGREMLLATREYVHARWAAFEQLLADFPEAADMRAPGPYSMRIIYGDTDSIFVLCRGLTAAGLTAVGDKMASHISRALFLPPIKLECEKTFTKLLLIAKKKYIGVIYGGKMLIKGVDLVRKNNCAFINRTSRALVDLLFYDDTVSGAAAALAERPAEEWLARPLPEGLQAFGAVLVDAHRRITDPERDIQDFVLTAELSRHPRAYTNKRLAHLTVYYKLMARRAQVPSIKDRIPYVIVAQTREVEETVARLAALRELDAAAPGDEPAPPAALPSPAKRPRETPSPADPPGGASKPRKLLVSELAEDPAYAIAHGVALNTDYYFSHLLGAACVTFKALFGNNAKITESLLKRFIPEVWHPPDDVAARLRTAGFGAVGAGATAEETRRMLHRAFDTLA | NA | NA | NA | NA | NA | Readily accessible data regarding the half-life of talimogene laherparepvec is not available, although talimogene laherparepvec DNA has been found in patient subjects' injected tumor through 84 days [FDA Label] and the half-lives of antibody-based therapeutics are often times generally long, on the order of days versus hours with small molecule drugs [T165]. | Talimogene laherparepvec is an oncolytic treatment used in local treatment of unresectable cutaneous, subcutaneous, and nodal lesions in patients with recurrent melanoma. It is a genetically administered herpes simplex virus 1 (HSV-1) that expresses human cytokine granulocyte-macrophage colony stimulating factor (GM-CSF) with antitumor and immune-stimulating activities. It specifically replicates within tumor cells and causes lysis. It was approved by the FDA in 2015 under the market name Imlygic. In general, talimogene laherparepvec has been modified so that it can infect and multiply inside melanoma cells [L2221]. The drug subsequently uses the melanoma cells' own machinery to multiply, eventually overwhelming the melanoma cells and killing them [L2221]. Alternatively, although talimogene laherparepvec also enters healthy cells, it is not designed to multiply inside them [L2221]. | This medication is a genetically modified oncolytic viral therapy indicated for the local treatment of unresectable, cutaneous, subcutaneous, and nodal lesions in patients with melanoma recurrent after initial surgery [FDA Label]. Elsewhere, the EMA notes that the agent is indicated for the treatment of adults with unresectable melanoma that is regionally or distantly metastatic (Stage IIIB, IIIC, and IVM1a) with no bone, brain, lung, or other visceral diseases [L2209]. | Talimogene laherparepvec has been genetically modified to replicate within tumors and to produce the immune stimulatory protein GM-CSF (granulocyte macrophage colony stimulating factor) [FDA Label]. The medication causes lysis of tumors, followed by the release of tumor-derived antigens, which together with virally derived GM-CSF may promote an anti-tumor immune response in the body [FDA Label]. | Talimogene laherparepvec is an oncolytic immunotherapy that is derived from Herpes Simplex Virus type-1 (HSV-1) [L2212]. It has been modified to replicate within tumor cells and to produce the immune response stimulatory protein, human GM-CSF (granulocyte macrophage colony stimulating factor) [L2212]. The medication causes the death of tumor cells and the release of tumor-derived antigens [L2212]. It is believed that together with GM-CSF, talimogene laherparepvec can promote a systemic anti-tumor immune response and an effector T-cell response [L2212]. Mice subjects involved in talimogene laherparepvec treatment studies that had complete regression of their primary tumors following therapy were resistant to subsequent tumor rechallenge [L2212]. The genetic modifications to talimogene laherparepvec from HSV-1 include deletion of the ICP34.5 and ICP47 genes [L2212]. Whereas anti-viral immune responses defend normal cells following infection by talimogene laherparepvec, tumors have been shown to be susceptible to injury and cell death from ICP34.5-deficient HSV-1 derived viruses, including talimogene laherparepvec [L2212]. Moreover, deletion of ICP47 prevents the down-regulation of antigen presentation molecules in the targeted tumor cells and increases the expression of the HSV US11 gene, thereby enhancing the talimogene laherparepvec viral replication in tumor cells and increases chances of tumor cell injury and death [L2212]. Although the talimogene laherparepvec virus is specifically modified to infect and multiply inside melanoma cells and uses melanoma cells' own machinery to multiply, the medication is not designed to multiply inside healthy cells, which it is also capable of entering [L2221]. | There is no clinical experience with overdose with talimogene laherparepvec [FDA Label, L2209]. Doses up to 4 mL at a concentration of 10^8 PFU/mL every 2 weeks have been administered in clinical trials with no evidence of dose-limiting toxicity [FDA Label, L2209]. The maximum dose of talimogene laherparepvec that can be safely administered has not been determined [FDA Label, L2209]. Nevertheless, some adverse reactions that are possible from taking talimogene laherparepvec range from fatigue, chills, pyrexia, nausea, influenza-like illness, injection site pain, to even injection site complications (including cellulitis, systemic bacterial infection, and others), herpetic infection, or plasmacytoma at or near the injection site [FDA Label, L2209]. As a result, healthcare providers and caregivers must observe the necessary safety precautions when administering talimogene laherparepvec to patients as accidental exposure to the agent can lead to exposure to and transmission of talimogene laherparepvec and herpetic infection in individuals who do not need the medication or in whom the medication is not indicated [FDA Label, L2209]. Moreover, in the event of a suspected overdose or inadvertent intravenous administration, the patient should be treated symptomatically, ie. with acyclovir or other anti-viral agents and supportive measures instituted as needed [FDA Label, L2209]. | Talimogene laherparepvec is cleared through general host defense mechanisms like autophagy and adaptive immune responses [L2212]. The agent is ultimately degraded by common endogenous protein and DNA catabolic pathways [L2212]. As with other wild-type HSV-1 (herpes simplex virus type-1) infections, a latent pool of talimogene laherparepvec DNA may persist in neuronal cell bodies innervating the injection sites [L2212]. Consequently, the occurrence of latent infection with talimogene laherparepvec cannot be excluded [L2212]. | Cellular uptake of talimogene laherparepvec occurs through HSV-1 receptors on both tumor and non-tumor cells following local injection into physical tumors [L2212]. After injection, the talimogene laherparepvec subsequently replicates intratumorally, where bioavailability and systemic concentration of the agent are not largely predictive of drug substance activity and therefore such data has not been evaluated to any particular degree [L2212]. | Talimogene laherparepvec is a genetically modified and replication-competent HSV-1 virus [L2212]. Therefore, its pharmacokinetics and biodistribution are driven by the specific site of intralesional injection, tumor-selective replication, and release from tumor tissue [L2212]. As a result, the specific pharmacokinetics of the agent, including distribution may vary depending on particular parameters of each unique administration. | Although readily accessible data regarding the clearance of talimogene laherparepvec is not available, in an ongoing melanoma study, it was determined that the proportion of patients with detectable talimogene laherparepvec DNA in blood and urine was highest during the second cycle of therapy [L2212]. Additionally, even though talimogene laherparepvec DNA was detected in samples from injected lesions in about 90% of patients, only 14% of patients tested positive for infective virus by 50% Tissue Culture Infectious Dose (TCID50) assay, all within 8 days of treatment administration [L2212]. 17% of samples from the exterior occlusive dressing tested positive for talimogene laherparepvec DNA but none tested positive for the presence of infective virus [L2212]. Moreover, only 1 sample had detectable talimogene laherparepvec DNA located on the oral mucosa - but the sample did not test positive for the presence of infective virus [L2212]. | Antineoplastic Agents, Immunological | NA | NA | NA | NA | Heparan sulfate,DNA polymerase catalytic subunit,DNA polymerase catalytic subunit | Imylgic | Amgen Europe B.V. | Amgen Europe B.V. | Intralesional | 1000000 PFU/ml | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15305 | Th1585 | Talimogene laherparepvec | >Th1585_Talimogene_laherparepvec MFSGGGGPLSPGGKSAARAASGFFAPAGPRGASRGPPPCLRQNFYNPYLAPVGTQQKPTGPTQRHTYYSECDEFRFIAPRVLDEDAPPEKRAGVHDGHLKRAPKVYCGGDERDVLRVGSGGFWPRRSRLWGGVDHAPAGFNPTVTVFHVYDILENVEHAYGMRAAQFHARFMDAITPTGTVITLLGLTPEGHRVAVHVYGTRQYFYMNKEEVDRHLQCRAPRDLCERMAAALRESPGASFRGISADHFEAEVVERTDVYYYETRPALFYRVYVRSGRVLSYLCDNFCPAIKKYEGGVDATTRFILDNPGFVTFGWYRLKPGRNNTLAQPAAPMAFGTSSDVEFNCTADNLAIEGGMSDLPAYKLMCFDIECKAGGEDELAFPVAGHPEDLVIQISCLLYDLSTTALEHVLLFSLGSCDLPESHLNELAARGLPTPVVLEFDSEFEMLLAFMTLVKQYGPEFVTGYNIINFDWPFLLAKLTDIYKVPLDGYGRMNGRGVFRVWDIGQSHFQKRSKIKVNGMVNIDMYGIITDKIKLSSYKLNAVAEAVLKDKKKDLSYRDIPAYYAAGPAQRGVIGEYCIQDSLLVGQLFFKFLPHLELSAVARLAGINITRTIYDGQQIRVFTCLLRLADQKGFILPDTQGRFRGAGGEAPKRPAAAREDEERPEEEGEDEDEREEGGGEREPEGARETAGRHVGYQGARVLDPTSGFHVNPVVVFDFASLYPSIIQAHNLCFSTLSLRADAVAHLEAGKDYLEIEVGGRRLFFVKAHVRESLLSILLRDWLAMRKQIRSRIPQSSPEEAVLLDKQQAAIKVVCNSVYGFTGVQHGLLPCLHVAATVTTIGREMLLATREYVHARWAAFEQLLADFPEAADMRAPGPYSMRIIYGDTDSIFVLCRGLTAAGLTAVGDKMASHISRALFLPPIKLECEKTFTKLLLIAKKKYIGVIYGGKMLIKGVDLVRKNNCAFINRTSRALVDLLFYDDTVSGAAAALAERPAEEWLARPLPEGLQAFGAVLVDAHRRITDPERDIQDFVLTAELSRHPRAYTNKRLAHLTVYYKLMARRAQVPSIKDRIPYVIVAQTREVEETVARLAALRELDAAAPGDEPAPPAALPSPAKRPRETPSPADPPGGASKPRKLLVSELAEDPAYAIAHGVALNTDYYFSHLLGAACVTFKALFGNNAKITESLLKRFIPEVWHPPDDVAARLRTAGFGAVGAGATAEETRRMLHRAFDTLA | NA | NA | NA | NA | NA | Readily accessible data regarding the half-life of talimogene laherparepvec is not available, although talimogene laherparepvec DNA has been found in patient subjects' injected tumor through 84 days [FDA Label] and the half-lives of antibody-based therapeutics are often times generally long, on the order of days versus hours with small molecule drugs [T165]. | Talimogene laherparepvec is an oncolytic treatment used in local treatment of unresectable cutaneous, subcutaneous, and nodal lesions in patients with recurrent melanoma. It is a genetically administered herpes simplex virus 1 (HSV-1) that expresses human cytokine granulocyte-macrophage colony stimulating factor (GM-CSF) with antitumor and immune-stimulating activities. It specifically replicates within tumor cells and causes lysis. It was approved by the FDA in 2015 under the market name Imlygic. In general, talimogene laherparepvec has been modified so that it can infect and multiply inside melanoma cells [L2221]. The drug subsequently uses the melanoma cells' own machinery to multiply, eventually overwhelming the melanoma cells and killing them [L2221]. Alternatively, although talimogene laherparepvec also enters healthy cells, it is not designed to multiply inside them [L2221]. | This medication is a genetically modified oncolytic viral therapy indicated for the local treatment of unresectable, cutaneous, subcutaneous, and nodal lesions in patients with melanoma recurrent after initial surgery [FDA Label]. Elsewhere, the EMA notes that the agent is indicated for the treatment of adults with unresectable melanoma that is regionally or distantly metastatic (Stage IIIB, IIIC, and IVM1a) with no bone, brain, lung, or other visceral diseases [L2209]. | Talimogene laherparepvec has been genetically modified to replicate within tumors and to produce the immune stimulatory protein GM-CSF (granulocyte macrophage colony stimulating factor) [FDA Label]. The medication causes lysis of tumors, followed by the release of tumor-derived antigens, which together with virally derived GM-CSF may promote an anti-tumor immune response in the body [FDA Label]. | Talimogene laherparepvec is an oncolytic immunotherapy that is derived from Herpes Simplex Virus type-1 (HSV-1) [L2212]. It has been modified to replicate within tumor cells and to produce the immune response stimulatory protein, human GM-CSF (granulocyte macrophage colony stimulating factor) [L2212]. The medication causes the death of tumor cells and the release of tumor-derived antigens [L2212]. It is believed that together with GM-CSF, talimogene laherparepvec can promote a systemic anti-tumor immune response and an effector T-cell response [L2212]. Mice subjects involved in talimogene laherparepvec treatment studies that had complete regression of their primary tumors following therapy were resistant to subsequent tumor rechallenge [L2212]. The genetic modifications to talimogene laherparepvec from HSV-1 include deletion of the ICP34.5 and ICP47 genes [L2212]. Whereas anti-viral immune responses defend normal cells following infection by talimogene laherparepvec, tumors have been shown to be susceptible to injury and cell death from ICP34.5-deficient HSV-1 derived viruses, including talimogene laherparepvec [L2212]. Moreover, deletion of ICP47 prevents the down-regulation of antigen presentation molecules in the targeted tumor cells and increases the expression of the HSV US11 gene, thereby enhancing the talimogene laherparepvec viral replication in tumor cells and increases chances of tumor cell injury and death [L2212]. Although the talimogene laherparepvec virus is specifically modified to infect and multiply inside melanoma cells and uses melanoma cells' own machinery to multiply, the medication is not designed to multiply inside healthy cells, which it is also capable of entering [L2221]. | There is no clinical experience with overdose with talimogene laherparepvec [FDA Label, L2209]. Doses up to 4 mL at a concentration of 10^8 PFU/mL every 2 weeks have been administered in clinical trials with no evidence of dose-limiting toxicity [FDA Label, L2209]. The maximum dose of talimogene laherparepvec that can be safely administered has not been determined [FDA Label, L2209]. Nevertheless, some adverse reactions that are possible from taking talimogene laherparepvec range from fatigue, chills, pyrexia, nausea, influenza-like illness, injection site pain, to even injection site complications (including cellulitis, systemic bacterial infection, and others), herpetic infection, or plasmacytoma at or near the injection site [FDA Label, L2209]. As a result, healthcare providers and caregivers must observe the necessary safety precautions when administering talimogene laherparepvec to patients as accidental exposure to the agent can lead to exposure to and transmission of talimogene laherparepvec and herpetic infection in individuals who do not need the medication or in whom the medication is not indicated [FDA Label, L2209]. Moreover, in the event of a suspected overdose or inadvertent intravenous administration, the patient should be treated symptomatically, ie. with acyclovir or other anti-viral agents and supportive measures instituted as needed [FDA Label, L2209]. | Talimogene laherparepvec is cleared through general host defense mechanisms like autophagy and adaptive immune responses [L2212]. The agent is ultimately degraded by common endogenous protein and DNA catabolic pathways [L2212]. As with other wild-type HSV-1 (herpes simplex virus type-1) infections, a latent pool of talimogene laherparepvec DNA may persist in neuronal cell bodies innervating the injection sites [L2212]. Consequently, the occurrence of latent infection with talimogene laherparepvec cannot be excluded [L2212]. | Cellular uptake of talimogene laherparepvec occurs through HSV-1 receptors on both tumor and non-tumor cells following local injection into physical tumors [L2212]. After injection, the talimogene laherparepvec subsequently replicates intratumorally, where bioavailability and systemic concentration of the agent are not largely predictive of drug substance activity and therefore such data has not been evaluated to any particular degree [L2212]. | Talimogene laherparepvec is a genetically modified and replication-competent HSV-1 virus [L2212]. Therefore, its pharmacokinetics and biodistribution are driven by the specific site of intralesional injection, tumor-selective replication, and release from tumor tissue [L2212]. As a result, the specific pharmacokinetics of the agent, including distribution may vary depending on particular parameters of each unique administration. | Although readily accessible data regarding the clearance of talimogene laherparepvec is not available, in an ongoing melanoma study, it was determined that the proportion of patients with detectable talimogene laherparepvec DNA in blood and urine was highest during the second cycle of therapy [L2212]. Additionally, even though talimogene laherparepvec DNA was detected in samples from injected lesions in about 90% of patients, only 14% of patients tested positive for infective virus by 50% Tissue Culture Infectious Dose (TCID50) assay, all within 8 days of treatment administration [L2212]. 17% of samples from the exterior occlusive dressing tested positive for talimogene laherparepvec DNA but none tested positive for the presence of infective virus [L2212]. Moreover, only 1 sample had detectable talimogene laherparepvec DNA located on the oral mucosa - but the sample did not test positive for the presence of infective virus [L2212]. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Heparan sulfate,DNA polymerase catalytic subunit,DNA polymerase catalytic subunit | Imylgic | Amgen Europe B.V. | Amgen Europe B.V. | Intralesional | 100000000 PFU/ml | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15389 | Th1593 | Tildrakizumab | >Th1593_Tildrakizumab QVQLVQSGAEVKKPGASVKVSCKASGYIFITYWMTWVRQAPGQGLEWMGQIFPASGSADYNEKFEGRVTMTTDTSTSTAYMELRSLRSDDTAVYYCARGGGGFAYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144400 | C6426H9918N1698O2000S46 | NA | NA | NA | The half-life is approximately 23 days (23%) [L1858]. | Tildrakizumab is a high-affinity, humanized, IgG1 | Moderate-severe plaque psoriasis [L1858], [FDA label]. | Tildrakuzimab is a targeted immunomodulator that decreases inflammation by inhibiting the action of various cytokines associated with plaque psoriasis, thus relieving its symptom of scaly plaques [L1869], [FDA label]. | This drug selectively binds interleukin (IL)-23 p19 subunit of cytokine IL-23 and neutralizes its function IL-23 regulates Th17 cells and is a powerful activator of keratinocyte proliferation [A32256]. Targeting IL-23p19 alone has been found to be a promising treatment approach in patients with moderate-to-severe chronic plaque psoriasis. Upon administration, downregulation of Th17 and Th22 cell responses occur [A32255]. IL-23 is a naturally occurring cytokine that is involved in inflammatory and immune responses. Tildrakizumab inhibits the release of proinflammatory cytokines and chemokines [FDA label]. | It is advised to evaluate patients for tuberculosis infection prior to initiating treatment with ILUMYA. This drug may increase the risk of infection [L1858]. It is advisable to perform tests for current tuberculosis status, as this drug may lead to reactivation of latent infection [FDA label]. A common issue for monoclonal antibody drugs is the development of antibodies to the drugs, thus rendering them less effective or completely ineffective [L1861]. A clinical trial was done to assess antibody development to this drug [L1858], [FDA label]. Up until week 64, approximately 6.5% of subjects treated with ILUMYA 100 mg developed antibodies to tildrakizumab. Of the subjects who developed antibodies to tildrakizumab, approximately 40% (2.5% of all patients receiving ILUMYA) had antibodies that were considered neutralizing. The development of neutralizing antibodies to tildrakizumab was associated with lower serum tildrakizumab concentrations and decreased efficacy [FDA label]. Most common (= 1% and at a higher rate than placebo) adverse reactions associated with ILUMYA treatment are upper respiratory infections, injection site reactions, and diarrhea [L1858]. Cases of angioedema and urticaria occurred in ILUMYA treated subjects in various clinical trials. If a hypersensitivity reaction occurs, the drug should be discontinued immediately and appropriate therapy should be initiated [FDA label]. In an embryo-fetal study, subcutaneous doses up to 300 mg/kg tildrakizumab were given to pregnant cynomolgus monkeys once every two weeks during organogenesis to 118 days gestation (22 days from parturition). No maternal or embryo-fetal toxicities were seen at doses up to 300 mg/kg (159 times the MRHD of 100 mg, based on AUC comparison). Tildrakizumab crossed the placenta in monkeys [FDA label]. | The metabolic pathway of tildrakizumab has not been characterized. As a humanized IgG1/k monoclonal antibody, tildrakizumab is expected to be degraded into small peptides and amino acids via catabolic pathways in a manner similar to endogenous IgG [L1858]. The AUCinf of dextromethorphan (CYP2D6 substrate) increased by 20% when used concomitantly with tildrakizumab 200 mg (two times the approved recommended dose) administered subcutaneously at Weeks 0 and 4 in subjects with plaque psoriasis. No clinically significant changes in AUCinf of caffeine (CYP1A2 substrate), warfarin (CYP2C9 substrate), omeprazole (CYP2C19 substrate), and midazolam (CYP3A4 substrate) were observed [FDA label]. | The mean (± SD) steady-state trough concentrations at 16 weeks post initiation of treatment ranged from 1.22 ± 0.94 mcg/mL to 1.47 ± 1.12 mcg/mL. The geometric mean (CV%) steady-state Cmax was 8.1 mcg/mL (34%) [L1858]. The absolute bioavailability of tildrakizumab is estimated to be about 73-80% after subcutaneous administration. The peak concentration (Cmax) is reached by approximately 6 days [FDA label]. | The geometric mean (CV%) volume of distribution is 10.8 L (24%) [L1858]. | The mean (CV%) systemic clearance is 0.32 L/day (38%) [L1858]. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Interleukin-23 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15562 | Th1608 | Cemiplimab | >Th1608_Cemiplimab EVQLLESGGVLVQPGGSLRLSCAASGFTFSNFGMTWVRQAPGKGLEWVSGISGGGRDTYFADSVKGRFTISRDNSKNTLYLQMNSLKGEDTAVYYCVKWGNIYFDYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 146000 | NA | NA | NA | NA | The elimination half-life (CV%) at steady state is 19 days (30%) [FDA label]. | The U.S. Food and Drug Administration (FDA) approved Cemiplimab (_Libtayo_), manufactured by Regeneron Pharmaceuticals, on September 28, 2018. This is the first FDA approval of a drug specifically for the treatment of advanced cutaneous squamous cell carcinoma (CSCC) [A39201, L4615]. | This drug is a programmed death receptor-1 (PD-1) blocking antibody indicated for the treatment of patients with metastatic cutaneous squamous cell carcinoma (CSCC) or locally advanced CSCC who are not candidates for curative surgery or curative radiation [FDA label, A39201]. | Cemiplimab inhibits tumor growth by an immune-mediated mechanism, specifically by the inhibition of the programmed death receptor 1 (PD-1), treating cutaneous squamous cell carcinoma [FDA label], [A39201], [A39204]. | Binding of the programmed death receptor (PD) ligands PD-L1 and PD-L2, to the PD-1 receptor, which is found on T cells, inhibits T-cell proliferation and cytokine production. The upregulation of PD-1 ligands occurs in some tumors and signaling through this pathway may contribute to the inhibition of active T-cell immune surveillance of tumors. Cemiplimab is a recombinant human immunoglobulin G4 (IgG4) monoclonal antibody that binds to the PD-1 receptor and blocks its interaction with PD-L1 and PD-L2 ligands, causing PD-1 pathway-mediated inhibition of the immune response, including the anti-tumor immune response. In mouse tumor models, blocking PD-1 activity resulted in decreased rates of tumor growth [FDA label]. | The most common adverse reactions (incidence = 20%) were fatigue, rash, and diarrhea in clinical studies [FDA label]. Severe and fatal immune-mediated adverse reactions may occur in any organ system or tissue, including the following: immune-mediated pneumonitis, immune-mediated colitis, immune-mediated hepatitis, immune-mediated endocrinopathies, immune-mediated dermatologic adverse reactions, and immune-mediated nephritis and renal dysfunction. Monitor for symptoms and signs of immune-mediated adverse reactions. Regularly perform chemistry panels, including liver and thyroid function, at baseline and periodically during treatment. Withhold or permanently discontinue this drug and administer corticosteroids based on the severity of the reaction. Infusion-related reactions may also occur. Interrupt, decrease the rate of infusion or permanently discontinue based on the severity of the reaction. **A note on fetal toxicity:** This drug can cause fetal harm. Advise females of reproductive potential of the potential risk to a fetus and use of effective contraception [FDA label]. | NA | After a dose of 350 mg cemiplimab administered intravenously every 3 weeks, median steady-state concentrations (CV%) of cemiplimab ranged between a maximum concentration (Cmax,ss) of 166 mcg/mL (28%) and a minimum concentration (Cmin,ss) of 59 mcg/mL (48%). Steady-state exposure was achieved after approximately 4 months [FDA label]. | The volume of distribution of cemiplimab at steady state is 5.3 L (25%) [FDA label]. | Cemiplimab clearance (CV%) after the first dose is 0.32 L/day (39%) and decreases over time by 34%, resulting in a steady-state clearance (CLss) (CV%) of 0.21 L/day (39%) [FDA label]. | Antineoplastic Agents | NA | NA | NA | NA | Programmed cell death protein 1 | Libtayo | Regeneron Pharmaceuticals, Inc. | Regeneron Pharmaceuticals, Inc. | Intravenous | 50 mg/1mL | None. | fatigue, rash, diarrhea, itching, nausea, constipation, fatigue, musculoskeletal pain, and decreased appetite | Libtayo is a medicine used to treat skin cancer by working with your immune system. Libtayo is used to treat a certain type of skin cancer called cutaneous squamous cell carcinoma (CSCC) that has spread to other parts of the body or cannot be treated with radiation or surgery. Libtayo is used to treat... | LIBTAYO is indicated for the treatment of patients with metastatic cutaneous squamous cell carcinoma (mCSCC) or locally advanced CSCC (laCSCC) who are not candidates for curative surgery or curative radiation. | NA | Cemiplimab-rwlc is a human programmed death receptor-1 (PD-1) blocking antibody. Cemiplimab-rwlc is a recombinant human IgG4 monoclonal antibody that binds to PD-1 and blocks its interaction with PD-L1 and PD-L2. Cemiplimab-rwlc is produced by recombinant DNA technology in Chinese hamster ovary (CHO) cell suspension culture. Cemiplimab-rwlc has an approximate molecular weight of 146 kDa. | Link | Link | NA |
| 15563 | Th1608 | Cemiplimab | >Th1608_Cemiplimab EVQLLESGGVLVQPGGSLRLSCAASGFTFSNFGMTWVRQAPGKGLEWVSGISGGGRDTYFADSVKGRFTISRDNSKNTLYLQMNSLKGEDTAVYYCVKWGNIYFDYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 146000 | NA | NA | NA | NA | The elimination half-life (CV%) at steady state is 19 days (30%) [FDA label]. | The U.S. Food and Drug Administration (FDA) approved Cemiplimab (_Libtayo_), manufactured by Regeneron Pharmaceuticals, on September 28, 2018. This is the first FDA approval of a drug specifically for the treatment of advanced cutaneous squamous cell carcinoma (CSCC) [A39201, L4615]. | This drug is a programmed death receptor-1 (PD-1) blocking antibody indicated for the treatment of patients with metastatic cutaneous squamous cell carcinoma (CSCC) or locally advanced CSCC who are not candidates for curative surgery or curative radiation [FDA label, A39201]. | Cemiplimab inhibits tumor growth by an immune-mediated mechanism, specifically by the inhibition of the programmed death receptor 1 (PD-1), treating cutaneous squamous cell carcinoma [FDA label], [A39201], [A39204]. | Binding of the programmed death receptor (PD) ligands PD-L1 and PD-L2, to the PD-1 receptor, which is found on T cells, inhibits T-cell proliferation and cytokine production. The upregulation of PD-1 ligands occurs in some tumors and signaling through this pathway may contribute to the inhibition of active T-cell immune surveillance of tumors. Cemiplimab is a recombinant human immunoglobulin G4 (IgG4) monoclonal antibody that binds to the PD-1 receptor and blocks its interaction with PD-L1 and PD-L2 ligands, causing PD-1 pathway-mediated inhibition of the immune response, including the anti-tumor immune response. In mouse tumor models, blocking PD-1 activity resulted in decreased rates of tumor growth [FDA label]. | The most common adverse reactions (incidence = 20%) were fatigue, rash, and diarrhea in clinical studies [FDA label]. Severe and fatal immune-mediated adverse reactions may occur in any organ system or tissue, including the following: immune-mediated pneumonitis, immune-mediated colitis, immune-mediated hepatitis, immune-mediated endocrinopathies, immune-mediated dermatologic adverse reactions, and immune-mediated nephritis and renal dysfunction. Monitor for symptoms and signs of immune-mediated adverse reactions. Regularly perform chemistry panels, including liver and thyroid function, at baseline and periodically during treatment. Withhold or permanently discontinue this drug and administer corticosteroids based on the severity of the reaction. Infusion-related reactions may also occur. Interrupt, decrease the rate of infusion or permanently discontinue based on the severity of the reaction. **A note on fetal toxicity:** This drug can cause fetal harm. Advise females of reproductive potential of the potential risk to a fetus and use of effective contraception [FDA label]. | NA | After a dose of 350 mg cemiplimab administered intravenously every 3 weeks, median steady-state concentrations (CV%) of cemiplimab ranged between a maximum concentration (Cmax,ss) of 166 mcg/mL (28%) and a minimum concentration (Cmin,ss) of 59 mcg/mL (48%). Steady-state exposure was achieved after approximately 4 months [FDA label]. | The volume of distribution of cemiplimab at steady state is 5.3 L (25%) [FDA label]. | Cemiplimab clearance (CV%) after the first dose is 0.32 L/day (39%) and decreases over time by 34%, resulting in a steady-state clearance (CLss) (CV%) of 0.21 L/day (39%) [FDA label]. | 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 |
| 15564 | Th1608 | Cemiplimab | >Th1608_Cemiplimab EVQLLESGGVLVQPGGSLRLSCAASGFTFSNFGMTWVRQAPGKGLEWVSGISGGGRDTYFADSVKGRFTISRDNSKNTLYLQMNSLKGEDTAVYYCVKWGNIYFDYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 146000 | NA | NA | NA | NA | The elimination half-life (CV%) at steady state is 19 days (30%) [FDA label]. | The U.S. Food and Drug Administration (FDA) approved Cemiplimab (_Libtayo_), manufactured by Regeneron Pharmaceuticals, on September 28, 2018. This is the first FDA approval of a drug specifically for the treatment of advanced cutaneous squamous cell carcinoma (CSCC) [A39201, L4615]. | This drug is a programmed death receptor-1 (PD-1) blocking antibody indicated for the treatment of patients with metastatic cutaneous squamous cell carcinoma (CSCC) or locally advanced CSCC who are not candidates for curative surgery or curative radiation [FDA label, A39201]. | Cemiplimab inhibits tumor growth by an immune-mediated mechanism, specifically by the inhibition of the programmed death receptor 1 (PD-1), treating cutaneous squamous cell carcinoma [FDA label], [A39201], [A39204]. | Binding of the programmed death receptor (PD) ligands PD-L1 and PD-L2, to the PD-1 receptor, which is found on T cells, inhibits T-cell proliferation and cytokine production. The upregulation of PD-1 ligands occurs in some tumors and signaling through this pathway may contribute to the inhibition of active T-cell immune surveillance of tumors. Cemiplimab is a recombinant human immunoglobulin G4 (IgG4) monoclonal antibody that binds to the PD-1 receptor and blocks its interaction with PD-L1 and PD-L2 ligands, causing PD-1 pathway-mediated inhibition of the immune response, including the anti-tumor immune response. In mouse tumor models, blocking PD-1 activity resulted in decreased rates of tumor growth [FDA label]. | The most common adverse reactions (incidence = 20%) were fatigue, rash, and diarrhea in clinical studies [FDA label]. Severe and fatal immune-mediated adverse reactions may occur in any organ system or tissue, including the following: immune-mediated pneumonitis, immune-mediated colitis, immune-mediated hepatitis, immune-mediated endocrinopathies, immune-mediated dermatologic adverse reactions, and immune-mediated nephritis and renal dysfunction. Monitor for symptoms and signs of immune-mediated adverse reactions. Regularly perform chemistry panels, including liver and thyroid function, at baseline and periodically during treatment. Withhold or permanently discontinue this drug and administer corticosteroids based on the severity of the reaction. Infusion-related reactions may also occur. Interrupt, decrease the rate of infusion or permanently discontinue based on the severity of the reaction. **A note on fetal toxicity:** This drug can cause fetal harm. Advise females of reproductive potential of the potential risk to a fetus and use of effective contraception [FDA label]. | NA | After a dose of 350 mg cemiplimab administered intravenously every 3 weeks, median steady-state concentrations (CV%) of cemiplimab ranged between a maximum concentration (Cmax,ss) of 166 mcg/mL (28%) and a minimum concentration (Cmin,ss) of 59 mcg/mL (48%). Steady-state exposure was achieved after approximately 4 months [FDA label]. | The volume of distribution of cemiplimab at steady state is 5.3 L (25%) [FDA label]. | Cemiplimab clearance (CV%) after the first dose is 0.32 L/day (39%) and decreases over time by 34%, resulting in a steady-state clearance (CLss) (CV%) of 0.21 L/day (39%) [FDA label]. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15578 | Th1609 | Elapegademase | >Th1609_Elapegademase AQTPAFNKPKVELHVHLDGAIKPETILYYGRKRGIALPADTPEELQNIIGMDKPLSLPEFLAKFDYYMPAIAGSREAVKRIAYEFVEMKAKDGVVYVEVRYSPHLLANSKVEPIPWNQAEGDLTPDEVVSLVNQGLQEGERDFGVKVRSILCCMRHQPSWSSEVVELCKKYREQTVVAIDLAGDETIEGSSLFPGHVKAYAEAVKSGVHRTVHAGEVGSANVVKEAVDTLKTERLGHGYHTLEDTTLYNRLRQENMHFEVCPWSSYLTGAWKPDTEHPVVRFKNDQVNYSLNTDDPLIFKSTLDTDYQMTKNEMGFTEEEFKRLNINAAKSSFLPEDEKKELLDLLYKAYGMPSPA | 115000 | C1797H2795N477O544S12 | NA | NA | NA | This pharmacokinetic property has not been fully studied. | Elapegademase is a PEGylated recombinant adenosine deaminase. It can be defined molecularly as a genetically modified bovine adenosine deaminase with a modification in cysteine 74 for serine and with about 13 methoxy polyethylene glycol chains bound via carbonyl group in alanine and lysine residues.[F1937] Elapegademase is generated in _E. coli_, developed by Leadiant Biosciences and FDA approved on October 5, 2018.[L4654,F1939] | Elapegademase is approved for the treatment of adenosine deaminase severe combined immune deficiency (ADA-SCID) in pediatric and adult patients.[L4654] This condition was previously treated by the use of bovine pegamedase as part of an enzyme replacement therapy.[L4655] ADA-SCID is a genetically inherited disorder that is very rare and characterized by a deficiency in the adenosine deaminase enzyme. The patients suffering from this disease often present with a compromised immune system. This condition is characterized by very low levels of white blood cells and immunoglobulin levels which results in severe and recurring infections.[L4656] | In clinical trials, elapegademase was shown to increase adenosine deaminase activity while reducing the concentrations of toxic metabolites which are the hallmark of ADA-SCID. As well, it was shown to improve the total lymphocyte count.[F1940] | The ADA-SCID is caused by the presence of mutations in the ADA gene which is responsible for the synthesis of adenosine deaminase. This enzyme is found throughout the body but it is mainly active in lymphocytes. The normal function of adenosine deaminase is to eliminate deoxyadenosine, created when DNA is degraded, by converting it into deoxyinosine. This degradation process is very important as deoxyadenosine is cytotoxic, especially for lymphocytes. Immature lymphocytes are particularly vulnerable as deoxyadenosine kills them before maturation making them unable to produce their immune function.[L4656] Therefore, based on the causes of ADA-SCID, elapegademase works by supplementing the levels of adenosine deaminase. Being a recombinant and an _E. coli_-produced molecule, the use of this drug eliminates the need to source the enzyme from animals, as it was previously.[L4654] | As elapegademase is a therapeutic protein, there is a potential risk of immunogenicity. There are no studies related to overdose but the highest weekly prescribed dose in clinical trials was 0.4 mg/kg. In nonclinical studies, a dosage of 1.8 fold of the clinical dose produced a slight increase in the activated partial thromboplastin time.[FDA label] | Metabolism studies have not been performed but it is thought to be degraded by proteases to small peptides and individual amino acids. | Elapegademase is administered intramuscularly and the reported Tmax, Cmax and AUC are approximately 60 hours, 240 mmol.h/L and 33000 hr.mmol/L as reported during a week.[FDA label] | This pharmacokinetic property has not been fully studied. | This pharmacokinetic property has not been fully studied. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Adenosine | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2S)-2-amino-6-(2-methoxyethoxycarbonylamino)hexanoic acid | NA | Link | NA | NA |
| 15587 | Th1610 | Emapalumab | >Th1610_Emapalumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYAMSWVRQAPGKGLEWVSAISGSGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDGSSGWYVPHWFDPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 154400 | C6430H9898N1718O2038S46 | 6.6 - 7.2 | NA | 78 ºC | Emapalumab elimination half-life is of approximately 22 days in healthy subjects and it ranges between 2.5-18.9 in HLH patients.[FDA label] | Emapalumab, also known as NI-0501, is a fully human monoclonal antibody that targets interferon gamma. Emapalumab development was sponsored by NovImmune SA, further developed by Sobi and FDA approved on November 20, 2018.[A38676, L4840] The approval of emapalumab was followed by the designation of orphan drug, priority review and breakthrough therapy.[L4840] As well, emapalumab was given the status of PRIME by the EMA.[L4845] | Emapalumab is indicated for the treatment of pediatric and adult patients with primary hemophagocytic lymphohistiocytosis (HLH) with refractory, recurrent or progressive disease or intolerance to conventional HLH therapy.[L4840] The HLH condition is a hyperinflammatory status characterized by the overwhelming activation of normal T lymphocytes and macrophages which can lead to disturbances in the hematology profile and even death. As part of the condition profile, there have been reports proving a massive overexpression of interferon-gamma which is thought to drive the immune hyperactivation leading to organ failure.[A38676] This condition is usually developed and present the symptomatic profile within the first months or years of life. These symptoms consist of fever, enlarged liver or spleen and a lower number of blood cells.[L4840] | In phase 2/3 clinical trials, emapalumab administered concomitantly with dexamethasone reported an overall response in 63% of the patients. The overall response was defined as achievement of a complete or partial response or HLH improvement.[L4841] In this trial and as a proof of interferon-gamma neutralization, there was registered a sharp decrease in serum CXCL9 and to avoid QT prolongation in the presence of low doses of emapalumab.[L4846] | Emapalumab acts by binding and neutralizing interferon-gamma.[A38676] The specific interaction between emapalumab and interferon-gamma produces an inhibition in the interaction between interferon-gamma and its cognate receptor on T-cells which produces the neutralizing activity.[L4845] It is important to consider that emapalumab inhibits both free and IFNGR1-bound interferon-gamma as well as the interaction with IFNGR1 and IFNGR2 at the cell surface.[A40061] HLH is an immune dysregulation syndrome in which several cytokines are involved but it has been reported that interferon-gamma plays a pivotal role in the development of this disease as studies have shown a vast increase in the interferon-gamma levels in HLH patients.[A40059] | There are no reported effects in male or female reproductive organs after an 8- or 13-week repeat-dose toxicity study in animals.[FDA label] | Monoclonal antibodies are thought to be internalized in endothelial cells bound to Fc receptor and rescued from metabolism by recycling. Later, they are degraded in the reticuloendothelial system to small peptides and amino acids which can be used for de-novo protein synthesis.[A31470] | In clinical pharmacokinetic studies, a dose of 1 mg/kg of emapalumab was administered which generated a peak concentration at steady state of 44 mcg/ml and a median steady-state concentration of 25 mcg/ml. The serum concentration of emapalumab increases proportionally between a dose of 1-3 mg/kg and the steady-state is attained by the 7th infusion.[FDA label] | The central and peripheral volume of distribution of emapalumab are 4.2 and 5.6 L, respectively.[FDA label] | Emapalumab clearance is reported to be 0.007 L/h in healthy subjects. This clearance rate can vary in HLH patients depending on the production of interferon-gamma.[FDA label] | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Interferon gamma | Gamifant | SWEDISH ORPHAN BIOVITRUM AB (PUBL) | SWEDISH ORPHAN BIOVITRUM AB (PUBL) | Intravenous | 100 mg/20mL | None. | infections, high blood pressure (hypertension), infusion-related reactions (rash, redness, and increased sweating), fever, low blood potassium (hypokalemia), constipation, abdominal pain, cytomegalovirus infection, diarrhea, increased white blood cells, cough, irritability, fast heart rate, and rapid/shallow breathing | Gamifant is used together with a medicine called dexamethasone to treat hemophagocytic lymphohistiocytosis (HLH), a rare disease that is sometimes inherited. HLH causes your immune system to attack healthy blood cells, which can lead to serious or life-threatening side effects on your spleen or liver.... | Gamifant is a prescription medicine used to treat the symptoms of Hemophagocytic Lymphohistiocytosis. Gamifant may be used alone or with other medications. | NA | GAMIFANT (emapalumab-lzsg) injection for intravenous use is a sterile, preservative-free, clear to slightly opalescent, colorless to slightly yellow solution provided in single-dose vials that require dilution prior to intravenous infusion. | Link | Link | NA |
| 15600 | Th1611 | Tagraxofusp | >Th1611_Tagraxofusp MGADDVVDSSKSFVMENFSSYHGTKPGYVDSIQKGIQKPKSGTQGNYDDDWKGFYSTDNKYDAAGYSVDNENPLSGKAGGVVKVTYPGLTKVLALKVDNAETIKKELGLSLTEPLMEQVGTEEFIKRFGDGASRVVLSLPFAEGSSSVEYINNWEQAKALSVELEINFETRGKRGQDAMYEYMAQACAGNRVRRSVGSSLSCINLDWDVIRDKTKTKIESLKEHGPIKNKMSESPNKTVSEEKAKQYLEEFHQTALEHPELSELKTVTGTNPVFAGANYAAWAVNVAQVIDSETADNLEKTTAALSILPGIGSVMGIADGAVHHNTEEIVAQSIALSSLMVAQAIPLVGELVDIGFAAYNFVESIINLFQVVHNSYNRPAYSPGHKTRPHMAPMTQTTSLKTSWVNCSNMIDEIITHLKQPPLPLLDFNNLNGEDQDILMENNLRRPNLEAFNRAVKSLQNASAIESILKNLLPCLPLATAAPTRHPIHIKDGDWNEFRRKLTFYLKTLENAQAQQTTLSLAIF | NA | C2553 H4026 N692 O798 S16 | NA | NA | NA | The reported half-life of tagraxofusp is of around 51 minutes.[L4897] | Tagraxofusp is an IL-3 conjugated truncated diphtheria toxin.[L4895] It is composed by the catalytic and translocation domains of diphtheria toxin fused via Met-His linker to a full-length human IL-3.[L4897, L4898] Tagraxofusp was developed by Stemline Therapeutics Inc and FDA approved on December 21, 2018, as the first therapy for blastic plasmacytoid dendritic cell neoplasm.[L4894] This drug achieved approval after being designated with the title of breakthrough therapy, priority review, and orphan drug status.[L4893] Tagraxofusp has been designated as an orphan drug in the EU since November 2015.[L4898] | Tagraxofusp is indicated for the treatment of blastic plasmacytoid dendritic cell neoplasm (BPDCN) in adults and pediatric patients over 2 years old. This treatment allows an alternative for the previous intense treatment which consisted of intensive chemotherapy followed by bone marrow transplantation.[L4893] BPDCN is a rare hematologic malignancy derived from plasmacytoid dendritic cells. It is characterized by the significantly increased expression of cells expressing CD4/CD56/CD123 and other markers restricted to plasmacytoid dendritic cells and a lack of expression of lymphoid, natural killer or myeloid lineage-associated antigens.[A40274] A key feature of the malignant cells is the overexpression of CD123, also known as interleukin-3 receptor, and the constant requirement of IL-3 for survival.[L4897] | In vitro studies showed that BPDCN blasts are ultrasensitive to tagraxofusp by presenting IC50 values in the femtomolar scale.[L4897] One of the main physiological changes of BPDCN is the presence of elevated interferon alpha and to produce an inflammatory response. In trials with tagraxofusp and following cell depletion, there was observed a significant reduction in the levels of interferon alpha and interleukin 6.[L4896] In clinical trials, tagraxofusp reported complete remission and complete remission with a skin abnormality not indicative of active disease in 54% of the treated patients.[L4893] | Tagraxofusp binds to cells expressing the IL-3 receptor and delivers in them the diphtheria toxin after binding. This is very useful as the malignant cells in BPDCN present a particularly high expression of IL-3 receptor (CD123+ pDC).[L4896] To be more specific, tagraxofusp gets internalized to the IL-3 receptor-expressing cell allowing for diphtheria toxin translocation to the cytosol and followed by the binding to ADP-ribosylation elongation factor 2 which is a key factor for protein translation. Once the protein synthesis is inhibited, the cell goes under a process of apoptosis.[L4895, L4897] As the apoptosis induction requires an active state of protein synthesis, tagraxofusp is not able to perform its apoptotic function in dormant cells.[L4897] | There haven't been analysis observing the carcinogenic, mutagenic potential nor the effect on fertility. However, in studies performed in cynomolgus monkeys at an overdose rate of 1.6 times the recommended dose, it was observed severe kidney tubular degeneration. Similar studies at the recommended dose reported the presence of degeneration and necrosis of choroid plexus in the brain were. This effect seems to be progressive even 3 weeks after therapy withdrawal.[FDA label] | For the metabolism, as tagraxofusp is a fusion protein, it is expected to get processed until small peptides and amino acids by the actions of proteases. | The reported Cmax in clinical trials was of around 23 ng/ml.[L4897] After a 15 min infusion of a dose of 12 mcg/kg the registered AUC and Cmax was 231 mcg.h/L and 162 mcg/L respectively.[FDA label] | In BPDCN patients, the reported volume of distribution is of 5.1 L.[FDA label] | The clearance of tagraxofusp was reported to fit a mono-exponential model.[L4897] The reported clearance rate is reported to be of 7.1 L/h.[FDA label] | Antineoplastic Agents | NA | NA | NA | NA | Interleukin-3 receptor subunit alpha,ADP-ribosylation factor-like protein 2 | Elzonris | Stemline Therapeutics, Inc. | Stemline Therapeutics, Inc. | Intravenous | 1000 ug/1mL | None. | capillary leak syndrome, high or low blood pressure, nausea, fatigue, swelling of extremities, fever, weight gain, constipation, vomiting, diarrhea, chills, headache, dizziness, decreased appetite, back pain, pain in extremities, shortness of breath, cough, nosebleed, sore throat or mouth pain, insomnia, anxiety, confusion, fast heart rate, itching, small red or purple spots on the skin, or blood in the urine. | Elzonris is used to treat blastic plasmacytoid dendritic cell neoplasm, a rare blood and/or bone marrow cancer. Elzonris is for use in adults and children at least 2 years old. Elzonris may also be used for purposes not listed in this medication guide. | ELZONRIS is a CD123-directed cytotoxin for the treatment of blastic plasmacytoid dendritic cell neoplasm (BPDCN) in adults and in pediatric patients 2 years and older. | NA | NA | Link | Link | NA |
| 15601 | Th1611 | Tagraxofusp | >Th1611_Tagraxofusp MGADDVVDSSKSFVMENFSSYHGTKPGYVDSIQKGIQKPKSGTQGNYDDDWKGFYSTDNKYDAAGYSVDNENPLSGKAGGVVKVTYPGLTKVLALKVDNAETIKKELGLSLTEPLMEQVGTEEFIKRFGDGASRVVLSLPFAEGSSSVEYINNWEQAKALSVELEINFETRGKRGQDAMYEYMAQACAGNRVRRSVGSSLSCINLDWDVIRDKTKTKIESLKEHGPIKNKMSESPNKTVSEEKAKQYLEEFHQTALEHPELSELKTVTGTNPVFAGANYAAWAVNVAQVIDSETADNLEKTTAALSILPGIGSVMGIADGAVHHNTEEIVAQSIALSSLMVAQAIPLVGELVDIGFAAYNFVESIINLFQVVHNSYNRPAYSPGHKTRPHMAPMTQTTSLKTSWVNCSNMIDEIITHLKQPPLPLLDFNNLNGEDQDILMENNLRRPNLEAFNRAVKSLQNASAIESILKNLLPCLPLATAAPTRHPIHIKDGDWNEFRRKLTFYLKTLENAQAQQTTLSLAIF | NA | C2553 H4026 N692 O798 S16 | NA | NA | NA | The reported half-life of tagraxofusp is of around 51 minutes.[L4897] | Tagraxofusp is an IL-3 conjugated truncated diphtheria toxin.[L4895] It is composed by the catalytic and translocation domains of diphtheria toxin fused via Met-His linker to a full-length human IL-3.[L4897, L4898] Tagraxofusp was developed by Stemline Therapeutics Inc and FDA approved on December 21, 2018, as the first therapy for blastic plasmacytoid dendritic cell neoplasm.[L4894] This drug achieved approval after being designated with the title of breakthrough therapy, priority review, and orphan drug status.[L4893] Tagraxofusp has been designated as an orphan drug in the EU since November 2015.[L4898] | Tagraxofusp is indicated for the treatment of blastic plasmacytoid dendritic cell neoplasm (BPDCN) in adults and pediatric patients over 2 years old. This treatment allows an alternative for the previous intense treatment which consisted of intensive chemotherapy followed by bone marrow transplantation.[L4893] BPDCN is a rare hematologic malignancy derived from plasmacytoid dendritic cells. It is characterized by the significantly increased expression of cells expressing CD4/CD56/CD123 and other markers restricted to plasmacytoid dendritic cells and a lack of expression of lymphoid, natural killer or myeloid lineage-associated antigens.[A40274] A key feature of the malignant cells is the overexpression of CD123, also known as interleukin-3 receptor, and the constant requirement of IL-3 for survival.[L4897] | In vitro studies showed that BPDCN blasts are ultrasensitive to tagraxofusp by presenting IC50 values in the femtomolar scale.[L4897] One of the main physiological changes of BPDCN is the presence of elevated interferon alpha and to produce an inflammatory response. In trials with tagraxofusp and following cell depletion, there was observed a significant reduction in the levels of interferon alpha and interleukin 6.[L4896] In clinical trials, tagraxofusp reported complete remission and complete remission with a skin abnormality not indicative of active disease in 54% of the treated patients.[L4893] | Tagraxofusp binds to cells expressing the IL-3 receptor and delivers in them the diphtheria toxin after binding. This is very useful as the malignant cells in BPDCN present a particularly high expression of IL-3 receptor (CD123+ pDC).[L4896] To be more specific, tagraxofusp gets internalized to the IL-3 receptor-expressing cell allowing for diphtheria toxin translocation to the cytosol and followed by the binding to ADP-ribosylation elongation factor 2 which is a key factor for protein translation. Once the protein synthesis is inhibited, the cell goes under a process of apoptosis.[L4895, L4897] As the apoptosis induction requires an active state of protein synthesis, tagraxofusp is not able to perform its apoptotic function in dormant cells.[L4897] | There haven't been analysis observing the carcinogenic, mutagenic potential nor the effect on fertility. However, in studies performed in cynomolgus monkeys at an overdose rate of 1.6 times the recommended dose, it was observed severe kidney tubular degeneration. Similar studies at the recommended dose reported the presence of degeneration and necrosis of choroid plexus in the brain were. This effect seems to be progressive even 3 weeks after therapy withdrawal.[FDA label] | For the metabolism, as tagraxofusp is a fusion protein, it is expected to get processed until small peptides and amino acids by the actions of proteases. | The reported Cmax in clinical trials was of around 23 ng/ml.[L4897] After a 15 min infusion of a dose of 12 mcg/kg the registered AUC and Cmax was 231 mcg.h/L and 162 mcg/L respectively.[FDA label] | In BPDCN patients, the reported volume of distribution is of 5.1 L.[FDA label] | The clearance of tagraxofusp was reported to fit a mono-exponential model.[L4897] The reported clearance rate is reported to be of 7.1 L/h.[FDA label] | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Interleukin-3 receptor subunit alpha,ADP-ribosylation factor-like protein 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15636 | Th1615 | Risankizumab | >Th1615_Risankizumab QVQLVQSGAEVKKPGSSVKVSCKASGYTFTDQTIHWMRQAPGQGLEWIGYIYPRDDSPKYNENFKGKVTITADKSTSTAYMELSSLRSEDTAVYYCAIPDRSGYAWFIYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 145600 | C6476H9992N1720O2016S44 | NA | NA | NA | The half-life of risankizumab is about 28 days in patients with plaque psoriasis.[FDA label] | Risankizumab is a fully humanized IgG1 monoclonal antibody (mAb) that is selective for interleukin 23 (IL-23). On April 23, 2019 it was approved by the FDA (as _SKYRIZI_) for the treatment of moderate-to-severe plaque psoriasis in adults who are clinically considered eligible for systemic therapy or phototherapy for psoriasis.[FDA label] This drug has been commercialized through collaboration between the German pharmaceutical company, Boehringer Ingelheim, and Abbvie.[A177601] Psoriasis is a chronic inflammatory disease of the skin most commonly characterized by raised, red plaques covered with silver scales in cases of plaque psoriasis. There are several subtypes of psoriasis, however, plaque psoriasis is most prevalent.[A177604] This disease occurs mainly in adults (with a prevalence ranging from 0.91% to 8.5%). Psoriasis has a peak incidence at two age groups: approximately 30–39 years and approximately 60 years of age.[A177604] Depending on disease severity, psoriasis may have significant effects on quality of life and can lead to embarrassment and negative social consequences.[A177607] Risankizumab is a promising drug for the relief of plaque psoriasis and has been shown to be effective in managing the above unpleasant symptoms.[FDA label] | This drug is for the treatment of moderate-to-severe plaque psoriasis in adults who are eligible to receive systemic therapy or phototherapy based on their disease process.[FDA label] | No formal studies examining pharmacodynamic properties have been completed with risankizumab [FDA label], however, this drug is expected to relieve symptoms of psoriasis by targeting interleukin 23 (IL-23) and preventing the initiation of the inflammatory cascade that is implicated in psoriasis.[A177601] | Risankizumab acts to prevent the release of pro-inflammatory cytokines and chemokines that often lead to inflammatory skin symptoms, such as redness, pain, and plaques. Risankizumab binds with a high affinity to the p19 subunit of human interleukin 23 (IL-23) cytokine [A177601], thereby preventing its action on the IL-23 receptor. IL-23 is a cytokine released in the human body that is involved in inflammatory and immune processes, especially in peripheral tissues.[A177601] IL-23 plays a role in polarized type-1 T cell-mediated inflammatory response. Type-1 T cells are found in very high concentrations in psoriasis-affected skin in addition to the blood of psoriasis patients.[A177601] By promoting the action of interferon (IFN)-gamma [A177616], type-1 T cells increase the expression of many inflammatory genes that induce inflammatory cascades [A177610]. Variants of the gene encoding IL-23 p19 subunit and the IL-23 receptor have been recognized as part of the pathogenesis of plaque psoriasis, rendering IL-23 an ideal target for risankizumab therapy.[A177601] | **Overdosage** In cases of overdose, ensure to monitor the patient for any signs or symptoms of adverse reactions and provide supportive treatment accordingly.[FDA label] **Carcinogenesis and mutagenesis** Currently, no studies examining carcinogenic potential or mutagenic potential have been conducted using this drug.[FDA label] **Use in pregnancy** There are limited data regarding the administration of risankizumab in pregnant women. An associated risk of major birth defects, miscarriage, or adverse effects on the mother or fetus is not yet established [FDA label]. It is important to note, however, that human IgG [A177613] is known to cross the placenta, and this drug may similarly be transmitted to the growing fetus. Risankizumab belongs to an IgG antibody subclass [A177613] and likely shares similar properties [FDA label]. The Canadian monograph for risankizumab indicates that women of childbearing potential should take adequate contraception during therapy and for at least 20 weeks after the final dose.[F4504] **Use during nursing** Currently, there are no available data regarding risankizumab in human milk, its effect on the production of milk, and its effect on a nursing child. Maternal IgG is, however, found to be excreted in human milk. This drug belongs to an IgG subclass, and may share similar properties. [A177613] The benefits of breastfeeding should be considered in addition to the mother's requirement for risankizumab and any possible risks resulting from nursing while taking this drug, which is likely to be present in human milk.[FDA label] | The metabolic pathway of risankizumab has not been characterized. As a humanized IgG1 monoclonal antibody, risankizumab is likely to be catabolized into small peptides and amino acids in the same way as endogenous IgG.[FDA label,A40006] | The absolute bioavailability of risankizumab is estimated at approximately 89% after a dose given by subcutaneous injection. In a clinical study, peak concentration (Cmax) was reached within 3-14 days after beginning risankizumab therapy.[FDA label] In patients diagnosed with psoriasis, estimated risankizumab trough plasma concentrations were found to be 1.72 ± 1.11 at week 16 of treatment and 1.36 ± 0.923 µg/mL at week 52 of treatment, using a predictive pharmacokinetic model.[A178045] The area under the curve (AUC) curve at steady state (study weeks 40–52) was predicted at 344 ± 151 µg/day/mL [A178045]. | The approximate volume of distribution at steady state is 11.2 L (34%) in patients diagnosed with plaque psoriasis, but may vary with increased body weight.[FDA label] | Systemic clearance is estimated at 0.31 L per day (24%).[FDA label] One study found that interindividual clearance for risankizumab varied by 37%.[A178045] Risankizumab clearance is found to decrease with an increase in body weight.[FDA label] Despite this tendency, no dose adjustment is advised in overweight patients.[FDA label] | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Interleukin-23 | Skyrizi | Abb Vie Deutschland Gmb H & Co. Kg | Abb Vie Deutschland Gmb H & Co. Kg | Subcutaneous | 75 mg | SKYRIZI is contraindicated in patients with a history of serious hypersensitivity reaction to risankizumab-rzaa or any of the excipients [see WARNINGS AND PRECAUTIONS]. | upper respiratory infections, headache, fatigue, injection site reactions (bruising, redness, fluid leakage, bleeding, infection, inflammation, irritation, pain, itching, swelling, warmth), and tinea infections (such as ringworm, athlete's foot and jock itch) | Skyrizi is an interleukin-23 antagonist. Interleukin-23 triggers an inflammatory response in the skin. Skyrizi is a prescription medicine used to treat moderate to severe plaque psoriasis in adults who may benefit from taking injections or pills (systemic therapy) or treatment using ultraviolet or UV... | Skyrizi is a prescription medicine used to treat the symptoms of Plaque Psoriasis. Skyrizi may be used alone or with other medications. | NA | SKYRIZI (risankizumab-rzaa) injection is a sterile, preservative-free, colorless to slightly yellow, and clear to slightly opalescent solution for subcutaneous use. | Link | Link | NA |
| 15652 | Th1616 | Isatuximab | >Th1616_Isatuximab QVQLVQSGAEVAKPGTSVKLSCKASGYTFTDYWMQWVKQRPGQGLEWIGTIYPGDGDTGYAQKFQGKATLTADKSSKTVYMHLSSLASEDSAVYYCARGDYYGSNSLDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | NA | Isatuximab (formerly SAR650984) is a humanized, IgG1-derived monoclonal antibody (mAb) produced from a Chinese hamster ovary (CHO) cell line.[L12099,A191799] Structurally, isatuximab is comprised of two identical immunoglobulin kappa light chains and two identical immunoglobulin gamma heavy chains.[L12099] It is a cytolytic antibody targeted against CD38, a glycoprotein found on the surface of some immune cells that is highly expressed by malignant plasma cells in multiple myeloma.[L12099] Along with [daratumumab], another anti-CD38 mAb, isatuximab constitutes a novel treatment modality for patients with difficult-to-treat multiple myeloma. Following three consecutive years on the yearly "Antibodies to watch" list published in "mAb", a peer-reviewed scientific journal dedicated to antibody research,[A38676,A191826,A191829] isatuximab was granted Orphan Drug designation and approved on March 2nd, 2020, for the treatment of multiple myeloma.[L12099,L12102] It is manufactured by Sanofi-Aventis U.S. under the brand name Sarclisa.[L12102] | Isatuximab is indicated in combination with [pomalidomide] and [dexamethasone] for the treatment of multiple myeloma in adults who have received at least two prior therapies including [lenalidomide] and a proteasome inhibitor.[L12099] It is also indicated in combination [carfilzomib] and dexamethasone for the treatment of adult patients with relapsed or refractory multiple myeloma who have received 1 to 3 prior lines of therapy.[L12099] | Isatuximab results in the apoptosis of malignant plasma cells via inhibition of a surface protein key to their survival and proliferation.[L12099] It has a relatively long residence time in the body, taking approximately 2 months to clear following the final dose, and may therefore be infused on a weekly or bimonthly schedule.[L12099] Isatuximab is given in combination with [pomalidomide] due to a synergy that exists between the two - isatuximab can induce a depletion in host NK lymphocytes, yet the ADCC effect of anti-CD38 mAbs has been shown to be superior in patient samples with a high ratio of NK to myleoma cells.[A191808] Pomalidomide, another antineoplastic agent, has the ability to induce and enhance NK lymphocyte activity[A191796,A191808] and thus works synergistically to enhance isatuximab-mediated killing of myeloma cells.[A191799] Isatuximab is formulated as an intravenous infusion and its administration may result in infusion-related reactions characterized most commonly by dyspnea, cough, chills, and nausea.[L12099] All noted reactions started during the first infusion and 98% resolved on the same day. Reactions may be mitigated by pre-medication with acetaminophen, H2 antagonists, diphenyhdramine, and/or dexamethasone.[L12099] Patients with grade 1 or 2 reactions may restart the infusion at a slower rate following resolution of symptoms, but patients experiencing a grade 3 or higher reaction (e.g. hypertension, bronchospasm) should discontinue therapy indefinitely.[L12099] Isatuximab can generate false positive results for indirect antglobulin tests (indirect Coombs tests), immunofixation tests, and serum protein electrophoresis.[L12099] | Multiple myeloma is a blood cancer characterized by an overproduction of malignant plasma cells in the bone marrow. A unique characteristic of myeloma cells is their dense and uniform expression of CD38 surface glycoproteins - these proteins, also expressed in relatively minor quantities on other lymphoid and myeloid cells, have been identified as performing several critical cellular functions, and this, along with their relative abundance on myeloma cells, has made them an attractive target for multiple myeloma treatment. CD38 was first identified as an activation marker, but has subsequently demonstrated roles in adhesion to endothelial CD31 proteins, as an accessory component of the synapse complex, and as an ectoenzyme involved in the metabolism of extracellular NAD+ and cytoplasmic NADP. The products of CD38’s ectoenzymatic activity include the calcium-mobilizing compound adenosine diphosphate ribose (ADPR), which can be further metabolized by CD203a/PC-1 and CD73 to adenosine, an immunosuppressive molecule that may play a role in tumour cell evasion of the immune system.[A191799] Isatuximab is an IgG1-derived monoclonal antibody targeted against CD38 proteins.[L12099] Its activity against CD38 results in a number of downstream effects, including direct apoptosis of the affected cell and activation of immune mechanisms including antibody-dependent cell-mediated cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), and complement dependent cytotoxicity (CDC), all of which result in potent anti-tumour activity.[L12099,A191799] Via allosteric antagonism, isatuximab also inhibits CD38 ectoenzymatic activity, preventing the immunosuppressive effects of its downstream products. Isatuximab may also exert its effects via downstream promotion of lysosome-dependent cell death, upregulation of reactive oxygen species, and restoration of antitumor immune effector cell functions.[A191799] | There is no known antidote for isatuximab, nor does there appear to be any clinical experience with overdose.[L12099] Symptoms of overdosage are likely to be consistent with isatuximab's adverse effect profile and may therefore include significant infusion-site reactions, gastrointestinal disturbances, and may increase the risk of infection. Treatment of overdose should involve careful monitoring of the patient and symptomatic and supportive measures as clinically indicated.[L12099] | Isatuximab metabolism is likely to involve catabolism to smaller proteins and peptides.[L12099] | When administered at the recommended dose and schedule, the steady-state Cmax and AUC were found to be 351 µg/mL and 72,600 µg·h/mL, respectively.[L12099] It takes approximately 8 weeks for isatuximab to reach steady-state. Over a dosage range of 1 mg/kg to 20 mg/kg given every 2 weeks AUC increases in a greater than dose-proportional manner, whereas over a dosage range of 5 mg/kg to 20 mg/kg every 4 weeks (followed by every 2 weeks) AUC was found to increase proportionately with dose. Steady-state AUC is lower in patients with increased body weight, but not to the extent that dose adjustments are required.[L12099] Tmax ranges from approximately 2 to 5 hours, increasing with dose and with repeated dosing.[A191802] | The predicted volume of distribution of isatuximab is 8.13 L.[L12099] | Total clearance decreases with increasing dose and with multiple dosing.[L12099] At steady-state, it takes approximately 2 months to eliminate =99% of isatuximab from plasma following the last dose.[L12099] | Antineoplastic Agents | NA | NA | NA | NA | ADP-ribosyl cyclase 1 | Sarclisa | Sanofi Aventis | Sanofi Aventis | Intravenous | 100 mg / 5 mL | SARCLISA is contraindicated in patients with severe hypersensitivity to isatuximab-irfc or to any of its excipients [see WARNINGS AND PRECAUTIONS]. | low white blood cell count (neutropenia), infusion-related reactions (shortness of breath, high blood pressure, and bronchospasm), pneumonia, upper respiratory tract infection, diarrhea, anemia, low lymphocytes (lymphopenia), and low platelets (thrombocytopenia) | Sarclisa is a prescription medicine used in combination with: the medicines pomalidomide and dexamethasone, to treat adults who have received at least 2 prior therapies including lenalidomide and a proteasome inhibitor to treat multiple myeloma. the medicines carfilzomib and dexamethasone, to treat adults... | SARCLISA is indicated: | NA | SARCLISA (isatuximab-irfc) injection is a sterile, preservative-free, clear to slightly opalescent, colorless to slightly yellow solution, essentially free of visible particles in a single-dose vial for intravenous use. Each vial contains either 100 mg/5 mL or 500 mg/25 mL of isatuximab-irfc at a concentration of 20 mg/mL with a pH of 6.0. Each mL of solution contains 20 mg isatuximabirfc, histidine (1.46 mg), histidine hydrochloride monohydrate (2.22 mg), polysorbate 80 (0.2 mg), sucrose (100 mg), and water for injection. | 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 |
| 15756 | Th1624 | Ropeginterferon alfa-2b | >Th1624_Ropeginterferon_alfa-2b PCDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 60000 | C16H29N3O6(C2H4O)n(C2H4O)n | NA | NA | NA | Ropeginterferon alfa-2b administered to polycythemia vera patients over a dose range of 100-500 µg has a half-life of approximately seven days.[L39170] | Polycythemia vera (PV) is the most common Philadelphia chromosome-negative myeloproliferative neoplasm (MPN), characterized by increased hematocrit and platelet/leukocyte counts, an increased risk for hemorrhage and thromboembolic events, and a long-term propensity for myelofibrosis and leukemia.[A242000, A242005] [Interferon alfa-2b] has been used for decades to treat PV but requires frequent dosing and is not tolerated by all patients.[A242005] Ropeginterferon alfa-2b is a next-generation mono-pegylated type I interferon produced from proline-IFN-a-2b in _Escherichia coli_ that has high tolerability and a long half-life.[A242015, L39170] Ropeginterferon alfa-2b has shown efficacy in PV in _in vitro_ and _in vivo_ models and clinical trials.[A242010, A242015] Ropeginterferon alfa-2b was approved by the FDA on November 12, 2021, and is currently marketed under the trademark BESREMi by PharmaEssentia Corporation.[L39170] | Ropeginterferon alfa-2b is indicated for the treatment of adult patients with polycythemia vera.[L39170] | Ropeginterferon alfa-2b acts through the interferon-alpha/beta receptor to initiate downstream JAK/STAT signalling leading to its therapeutic effects. Like other interferon alfa products, ropeginterferon alfa-2b may cause various toxicities, including endocrine, cardiovascular, pulmonary, ophthalmologic, dental/periodontal, renal, and dermatological toxicity. In addition, interferon alfa has been associated with hepatotoxicity, including increases in serum ALT, AST, GGT, and bilirubin; ropeginterferon alfa-2b is contraindicated in patients with moderate to severe (Child-Pugh B or C) hepatic impairment. Pancreatitis and colitis, including fatal ulcerative/hemorrhagic/ischemic colitis, have occurred in patients treated with interferon alfa. Significant toxicity of any kind may require treatment discontinuation. Interferon alfa treatment has decreased peripheral blood counts, including thrombocytopenia and leukopenia, and altered lipid levels, including hyperlipidemia, hypertriglyceridemia, and dyslipidemia. Hypersensitivity reactions, including anaphylaxis, may occur; ropeginterferon alfa-2b is contraindicated in hypersensitive patients and those with known hypersensitivity to other interferons. Life-threatening or fatal neuropsychiatric reactions may occur, including in patients without prior history; ropeginterferon alfa-2b is contraindicated in patients with a history of severe psychiatric disorders. Finally, ropeginterferon alfa-2b can cause fetal harm and should be used with caution in females of reproductive potential.[L39170] | Polycythemia vera (PV) is the most common Philadelphia chromosome-negative myeloproliferative neoplasm (MPN), which also includes essential thrombocytopenia and myelofibrosis.[A242000, A242005] PV is characterized by increased hematocrit and platelet/leukocyte counts, an increased risk for hemorrhage and thromboembolic events, and a long-term propensity for myelofibrosis and leukemia. The main driver mutation, _JAK2_ V617F, is present in >95% of PV patients and results in constitutive JAK/STAT signalling; other exon 12 mutations in _JAK2_ may also result in PV. PV results in clonal hematopoietic stem cells, such that they form endogenous erythroid colonies (EECs) _in vitro_.[A242000] Interferon alfa-2b has been used for decades in PV despite the lack of formal approval.[A242005] Although the mechanism of action is unclear, interferon alfa-2b is known to bind the interferon-alpha/beta receptor (IFNAR) and activate downstream JAK/STAT signalling.[A242005, L39170] The overall result is a series of anti-proliferative, anti-angiogenic, pro-apoptotic, and immunomodulatory effects, including augmenting T-cell, macrophage, and natural killer cells.[A242005] Interestingly, _in vitro_ studies have revealed that ropeginterferon alfa-2b is specific to some extent for _JAK2_-mutant EECs, a result that is in line with the reduced allelic burden observed in clinical trials.[A242010, A242015] Partial and complete molecular and hematological responses have been achieved with ropeginterferon alfa-2b.[A242015] | Ropeginterferon alfa-2b overdose may present with influenza-like symptoms or other adverse reactions. As there is no known antidote, symptomatic and supportive care should be administered in the result of an overdose. Ropeginterferon alfa-2b is not mutagenic in standard assays but has not been tested for carcinogenic potential.[L39170] | Ropeginterferon alfa-2b is expected to be catabolized by various proteolytic enzymes.[L15811] | In patients with polycythemia vera on a two-week dosing interval, the estimated steady-state Cmin was 1.4-12 ng/mL, Cmax was 4.4-31 ng/mL, and AUC was 1011-7809 ng | Ropeginterferon alfa-2b has an estimated geometric mean apparent volume of distribution (%CV) of 4.8 L (21%) in polycythemia vera patients.[L39170] | Ropeginterferon alfa-2b administered to polycythemia vera patients over a dose range of 100-500 µg has a clearance of 1.7-2.5 L/h.[L39170] | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Interferon alpha/beta receptor (IFNAR) | Besremi | Aop Orphan Pharmaceuticals Gmb H | Aop Orphan Pharmaceuticals Gmb H | Subcutaneous | 500 ?g/0.5ml | BESREMi is contraindicated in patients with: Existence of, or history of severe psychiatric disorders, particularly severe depression, suicidal ideation, or suicide attempt Hypersensitivity to interferons including interferon alfa-2b or any of the inactive ingredients of BESREMi. Moderate (Child-Pugh B) or severe (Child-Pugh C) hepatic impairment History or presence of active serious or untreated autoimmune disease Immunosuppressed transplant recipients | influenza-like illness, joint pain, fatigue, itching, runny or stuffy nose, musculoskeletal pain, headache, diarrhea, increased sweating, nausea, upper respiratory tract infection, local administration site reactions, dizziness, abdominal pain, depression, sleep problems (insomnia, abnormal dreams), low white blood cell count (leukopenia, neutropenia), decreased appetite, hair loss, fluid retention (edema), high blood pressure (hypertension), muscle spasms, rash, transaminase elevations, urinary tract infection (UTI), low blood platelets (thrombocytopenia), and spinning sensation (vertigo). | Besremi is a prescription medicine that is used to treat adults with polycythemia vera. It is not known if this medicine is safe and effective in children. Important information Besremi can cause serious side effects that: may cause death, or may worsen certain serious diseases that you may already have... | Besremi is a prescription medicine used to treat the symptoms of Polycythemia Vera. Besremi may be used alone or with other medications. | (2S)-1-[3,7-bis(2-methoxyethoxycarbonylamino)heptyl]pyrrolidine-2-carboxylic acid | Ropeginterferon alfa-2b-njft, an interferon alfa-2b, is an N-terminal monopegylated covalent conjugate of proline interferon alfa-2b, produced in Escherichia coli cells by recombinant DNA technology, with a methoxy polyethylene glycol (mPEG) moiety. Ropeginterferon alfa-2b-njft has an approximate molecular weight of 60 kDa and the approximate molecular weight of the PEG portion of the molecule is 40 kDa. | Link | Link | NA |
| 15776 | Th1626 | Imlifidase | >Th1626_Imlifidase MDSFSANQEIRYSEVTPYHVTSVWTKGVTPPANFTQGEDVFHAPYVANQGWYDITKTFNGKDDLLCGAATAGNMLHWWFDQNKDQIKRYLEEHPEKQKINFNGEQMFDVKEAIDTKNHQLDSKLFEYFKEKAFPYLSTKHLGVFPDHVIDMFINGYRLSLTNHGPTPVKEGSKDPRGGIFDAVFTRGDQSKLLTSRHDFKEKNLKEISDLIKKELTEGKALGLSHTYANVRINHVINLWGADFDSNGNLKAIYVTDSDSNASIGMKKYFVGVNSAGKVAISAKEIKEDNIGAQVLGLFTLSTGQDSWNQTN | NA | C1575H2400N422O477S6 | NA | NA | NA | The mean distribution half-life of imlifidase is reported to be 1.8 hours, while the mean elimination half-life is reported to be 89 hours.[A225836] | Chronic kidney disease (CKD) is a progressive and irreversible disease that represents a significant burden for both the individual and healthcare system at large.[A225916] Currently available treatments for end-stage renal disease are limited to dialysis and renal transplantation, with the former associated with significant costs and lower quality of life.[A225836,A225916] Patients who have developed human leukocyte antigen (HLA) sensitization from prior exposure to blood products, pregnancy, or any other circumstance which may have resulted in exposure to non-self HLA antigens, face additional barriers to transplantation.[A225836,A225921] Highly sensitized individuals carry high levels of anti-HLA antibodies and are at significant risk for antibody-mediated rejection which occurs mainly through complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC).[A225836] High levels of anti-HLA antibodies also contribute to poor graft survival.[A225836] As a result, highly sensitized individuals experience marked delays on transplant lists due to the challenges associated with procuring an HLA compatible donor graft.[A225836,A225921] Imlifidase is a cysteine protease and eliminates Fc-dependent effector functions such as CDC and ADCC by cleaving the heavy chains of human immunoglobulin G (IgG) antibodies.[L28001] As a result, the risk of antibody-mediated rejection is reduced allowing kidney transplantation in highly sensitized patients to proceed.[A225836,L28001] | Imlifidase is indicated for desensitization of highly sensitized adult kidney transplant patients with a positive crossmatch against an available deceased donor.[L28001] The treatment is reserved for patients unlikely to receive a transplant under the available kidney allocation system including prioritization programs for highly sensitized patients.[L28001] | Imlifidase is highly specific to all four human IgG subclasses and does not cleave any other immunoglobulins (IgM, IgA, IgE, IgD).[A225836,L28041] The inactivation of human IgG antibodies occurs rapidly and efficiently after administration of imlifidase, with the effect lasting for several weeks.[A226045] | Imlifidase is a cysteine protease derived from _Streptococcus pyogenes_ which degrades immunoglobulin G (IgG) in a multistep process.[A226040,L28001] In the first step, imlifidase cleaves one of the two IgG heavy chains at the lower hinge leaving the other intact, resulting in a single cleaved IgG molecule. In the second step, the second heavy chain is cleaved yielding one homodimeric Fc fragment and one F(ab’)2 fragment.[A226040,A226045,L28001] This process removes the ability of the F(ab’)2 fragments to participate in Fc-mediated functions including antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC).[L28001,L28041] Ultimately, by degrading the entire IgG pool, imlifidase reduces donor-specific antibodies (DSA) and allows transplantation to occur.[A225836,L28001] | There is currently no data for imlifidase administered at supra-therapeutic doses; therefore, toxicity information is not readily available.[L28001] In cases of overdose, the patient should be carefully monitored and symptomatic treatment should be initiated as needed.[L28001] Although there is no antidote to imlifidase, administration of intravenous IgG may correct depleted IgG levels.[L28001] | There is currently no imlifidase metabolism data available; however, it is thought to be eliminated via proteolysis.[L28041] | Given that imlifidase is administered intravenously, it is fully absorbed and bioavailable; imlifidase exposure is dose-proportional and predictable.[A225836,L28001] After a dose of 0.25 mg/kg, the mean Cmax of imlifidase was 5.8 (4.2-8.9) ug/mL.[L28001] Tmax occurs once infusion is complete or soon after.[A225836] Food is not expected to impact the effectiveness or absorption of imlifidase.[L28001] | The volume of distribution of imlifidase is reported to be 0.2 L/kg in the elimination phase.[A225836] | The mean clearance value of imlifidase is reported to be 1.8 mL/h/kg.[A225836] | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | IgG heavy chain | Idefirix | Hansa Biopharma Ab | Hansa Biopharma Ab | Intravenous | 11 mg | NA | The most common side effects with Idefirix (which may affect more than 1 in 10 people) are infections, including pneumonia (infection of the lungs), urinary tract infection and sepsis (blood poisoning). Other common side effects (which may affect up to 1 in 10 people) are pain and reactions around the infusion site, increased blood levels of certain liver enzymes, muscle pain, headache and flushing. | Idefirix is for hospital use only and can only be obtained with a prescription. Idefirix treatment should only be prescribed and supervised by a doctor experienced in the use of immunosuppressive medicines (medicines that reduce the activity of the immune system, the body’s natural defences) and in the management of sensitised kidney transplant patients. | Highly sensitised patients have high levels of antibodies (proteins in the blood that fight infections and other foreign cells) against the donor’s tissue, including immunoglobulin G (IgG) antibodies. This makes their body more likely to reject the donor organ. The active substance in Idefirix, imlifidase, is an enzyme (a protein) that breaks down the IgG antibodies, thereby reducing the likelihood of the body rejecting the donor kidney. | NA | NA | Link | Link | 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 |
| 15835 | Th1633 | Edodekin alfa | NA | NA | NA | NA | NA | NA | NA | Edodekin alfa is under investigation in clinical trial NCT01468896 (Cetuximab and Recombinant Interleukin-12 in Treating Patients With Squamous Cell Carcinoma of the Head and Neck That Is Recurrent, Metastatic, or Cannot Be Removed by Surgery). | NA | 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 |
| 15907 | Th1642 | Interferon Gamma | >Th1642_Interferon_Gamma MQDPYVKEAENLKKYFNAGHSDVADNGTLFLGILKNWKEESDRKIMQSQIVSFYFKLFKNFKDDQSIQKSVETIKEDMNVKFFNSNKKKRDDFEKLTNYSVTDLNVQRKAIHELIQVMAELSPAAKTGKRKRSQMLFRGR | NA | NA | NA | NA | NA | NA | Interferon gamma is a Type 1 inflammatory cytokine and the only type II interferon. It has antitumor properties, antiviral activities, and important immunoregulatory functions. The interferon is primarily produced by activated T lymphocytes and natural killer cells. | NA | NA | Interferon gamma signals as an antiparallel homodimeric glycoprotein, acting at the complex of interferon gamma receptor 1 (IFNGR1) and IFNGR2 after direct binding to IFNGR1. It activates the JAK/STAT, MAPK, and PI3-Kinase pathways. In addition, Interferon gamma activates macrophages, mediates antiviral and antibacterial immunity, regulates Th1/Th2 balance, and controls cellular proliferation and apoptosis. It is currently being investigated as an antitumor drug, and a therapy for juvenile rheumatoid arthritis, chemoresistant pulmonary tuberculosis, idiopathic pulmonary fibrosis, and atypical pulmonary mycobacteriosis. This cytokine has been found to have effects such as promotion of host response in antitumor immunity, playing roles in all three phases (elimination, equilibrium, and escape) of cancer immunoediting, directly influencing antiproliferation, apoptosis, and antiangiogenesis on tumor cells, and indirectly influencing antitumor immunity. However, currently there is no approved indication report of using interferon gamma in cancer treatment, indicating that interferon has not yet reached a stage of being a clinically-useful antitumor drug. Interferon gamma, when administered in combination with interferon alpha-2-beta as part of the HerberFERON therapy, is found to have synergistic effects, with the potential for more favorable pharmacodynamics than either alone. This synergy between interferon alpha and gamma include antiproliferative effects on several cancers. | NA | NA | NA | NA | NA | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | NA | 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 |
| 16379 | Th1889 | Abatacept | >Th1889_Abatacept MDPQCTMGLSNILFVMAFLLSGAAPLKIQAYFNETADLPCQFANSQNQSLSELVVFWQDQENLVLNEVYLGKEKFDSVHSKYMGRTSFDSDSWTLRLHNLQIKDKGLYQCIIHHKKPTGMIRIHQMNSELSVLANFSQPEIVPISNITENVYINLTCSSIHGYPEPKKMSVLLRTKNSTIEYDGVMQKSQDNVTELYDVSISLSVSFPDVTSNMTIFCILETDKTRLLSSPFSIELEDPQPPPDHIPWITAVLPTVIICVMVFCLILWKWKKKKRPRNSYKCGTNTMEREESEQTKKREKIHIPERSDEAQRVFKSSKTSSCDKSDTCF | 92300.0 Da | C3498H5458N922O1090S32 | NA | NA | NA | 16.7 (12-23) days in healthy subjects; 13.1 (8-25) days in RA subjects; 14.3 days when subcutaneously administered to adult RA patients. | Abatacept is a disease-modifying antirheumatic drug (DMARD) used in the management of rheumatic conditions, such as rheumatoid or psoriatic arthritis, and for the prophylaxis of acute graft-versus-host disease. | Abatacept is indicated in adult patients for the treatment of moderately-to-severely active rheumatoid arthritis and for the treatment of active psoriatic arthritis.In patients two years of age and older, abatacept is also indicated for the treatment of moderately-to-severely active juvenile idiopathic arthritis. Abatacept is also indicated for the prophylaxis of acute graft-versus-host disease, in combination with methotrexate and a calcineurin inhibitor such as tacrolimus, in patients two years of age and older who are undergoing hematopoietic stem cell transplantation from a matched or 1 allele-mismatched unrelated donor. | Abatacept is the first in a new class of drugs known as Selective Co-stimulation Modulators. Known as a recombinant fusion protein, the drug consists of the extracellular domain of human cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) linked to a modified Fc portion of human immunoglobulin G1 (IgG1. The Fc portion of the drug consists of the hinge region, the CH2 domain, and the CH3 domain of IgG1. Although there are multiple pathways and cell types involved in the pathogenesis of rheumatoid arthritis, evidence suggests that T-cell activation may play an important role in the immunopathology of the disease. | Abatacept is a selective costimulation modulator - like CTLA-4, the drug has shown to inhibit T-cell (T lymphocyte) activation by binding to CD80 and CD86, thereby blocking interaction with CD28. Blockade of this interaction has been shown to inhibit the delivery of the second co-stimulatory signal required for optimal activation of T-cells. This results in the inhibition of autoimmune T-Cell activation that has been implcated in the pathogenesis of rheumatoid arthritis. | Most common adverse events (≥10%) are headache, upper respiratory tract infection, nasopharyngitis, and nausea. Doses up to 50 mg/kg have been administered without apparent toxic effect. | NA | When a single 10 mg/kg intravenous infusion of abatacept is administered in healthy subjects, the peak plasma concentration (Cmax) was 292 mcg/mL. When multiple doses of 10 mg/kg was given to rheumatoid arthritis (RA) patients, the Cmax was 295 mcg/mL. The bioavailability of abatacept following subcutaneous administration relative to intravenous administration is 78.6%. | 0.07 L/kg [RA Patients, IV administration] 0.09 L/kg [Healthy Subjects, IV administration] 0.11 L/kg [RA patients, subcutaneous administration] | 0.23 mL/h/kg [Healthy Subjects after 10 mg/kg Intravenous Infusion] 0.22 mL/h/kg [RA Patients after multiple 10 mg/kg Intravenous Infusions] 0.4 mL/h/kg [juvenile idiopathic arthritis patients]. The mean systemic clearance is 0.28 mL/h/kg when a subcutaneously administered to adult RA patients. The clearance of abatacept increases with increasing body weight. | Agents reducing cytokine levels,Amino Acids, Peptides, and Proteins,Antibodies,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Antirheumatic Agents,Biologics for Rheumatoid Arthritis Treatment,Blood Proteins,CD80-directed Antibody Interactions,CD86-directed Antibody Interactions,Decreased Cytokine Activity,Disease-modifying Antirheumatic Agents,Globulins,Immune Checkpoint Inhibitors,Immunoconjugates,Immunologic Factors,Immunosuppressive Agents,Proteins,Selective Immunosuppressants,Selective T Cell Costimulation Modulator,Serum Globulins | CA2110518 | 2007-05-22 | 2012-06-16 | NA | T-lymphocyte activation antigen CD80, T-lymphocyte activation antigen CD86, Cytotoxic T-lymphocyte protein 4 | Orencia | Bristol Myers Squibb Pharma Eeig | Bristol Myers Squibb Pharma Eeig | Intravenous | 250 mg | None | fever, chills, night sweats, flu symptoms, weight loss, feeling very tired, dry cough, sore throat, warmth, pain or redness of your skin trouble breathing, stabbing chest pain, wheezing, cough with yellow or green mucus, pain or burning when you urinate, and signs of skin infection such as itching, swelling, warmth, redness, or oozing | Orencia belongs to a class of drugs called DMARDs, Immunomodulators; Immunosuppressants. | Orencia is a prescription medicine used to treat the symptoms of Moderate-to-Severe Rheumatoid Arthritis and Psoriatic Arthritis. | NA | ORENCIA for Injection is a lyophilized powder for intravenous infusion. ORENCIA for Injection is supplied as a sterile, white, preservative-free, lyophilized powder for reconstitution and dilution prior to intravenous administration. Following reconstitution of the lyophilized powder with 10 mL of Sterile Water for Injection, USP, the solution of ORENCIA is clear, colorless to pale yellow, with a pH range of 7.2 to 7.8. Each single-use vial of ORENCIA for Injection provides 250 mg abatacept, maltose (500 mg), monobasic sodium phosphate (17.2 mg), and sodium chloride (14.6 mg) for administration. | Link | Link | NA |