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 |
| 10028 | Th1005 | Etanercept | >Th1005_Etanercept LPAQVAFTPYAPEPGSTCRLREYYDQTAQMCCSKCSPGQHAKVFCTKTSDTVCDSCEDSTYTQLWNWVPECLSCGSRCSSDQVETQACTREQNRICTCRPGWYCALSKQEGCRLCAPLRKCRPGFGVARPGTETSDVVCKPCAPGTFSNTTSSTDICRPHQICNVVAIPGNASMDAVCTSTSPTRSMAPGAVHLPQPVSTRSQHTQPTPEPSTAPSTSFLLPMGPSPPAEGSTGDEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 51234.9 | C2224H3475N621O698S36 | 7.89 | -0.529 | 71 | 102 hours in RA patients | It is a dimeric fusion protein (934 amino acids) consisting of extracellular ligand-binding portion of the human 75 kilodalton (p75) tumor necrosis factor receptor (TNFR) linked to Fc portion of human IgG1 produced by recombinant DNA technology in a Chinese hamster ovary (CHO) mammalian cell expression system.. The Fc component of etanercept contains the CH2 domain, the CH3 domain and hinge region, but not the CH1 domain of IgG1. | Used to treat severe rheumatoid arthritis in adults, severe juvenile idiopathic arthritis, ankylosing spondylitis, and severe plaque psoriasis. | TNF, a naturally occurring cytokine is involved in normal inflammatory and immune responses. Elevated levels of TNF are found in tissues and fluids of patients suffering from rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis (AS), and plaque psoriasis. Etanercept binds specifically to tumor necrosis factor (TNF) and blocks its interaction with cell surface TNF receptors. | There are two distinct receptors for TNF (TNFRs), a 55 kilodalton (p55) and a 75 kilodalton receptor (p75). The biological activity of TNF is dependent upon binding to either of the cell surface receptors p75 or p55. Etanercept is a dimeric soluble form of the p75 TNF receptor that can bind to two TNF molecules, thereby effectively removing them from circulation. | NA | NA | NA | NA | 160 ± 80 mL/hr [RA patients] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Dermatologicals, Disease-modifying Antirheumatic Agents, Immunoglobulin Constant Regions, Immunoglobulin Fc Fragments, Immunoglobulin Fragments, Immunoglobulin Isotypes, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Membrane Proteins, Peptides, Proteins, Tumor Necrosis Factor Blockers | CA2476934 | 16-Jun-2009 | 27-Feb-2023 | Rilonacept results in increased immunosuppressive effects; increases the risk of infection. | Tumor necrosis factor,Tumor necrosis factor receptor superfamily member 1B,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c,Lymphotoxin-alpha,Low affinity immunoglobulin gamma Fc region receptor III-B | Enbrel | Immunex Corp | Immunex Corp | Used to treat rheumatoid arthritis, psoriatic arthritis, or ankylosing spondylitis, and prevent joint damage caused by these conditions. Enbrel is also used to treat plaque psoriasis in adults and polyarticular juvenile idiopathic arthritis (in children a | NA | Supplied in a multiple-use vial as a sterile, white, preservative-free, lyophilized powder. Reconstitution with 1 mL of the supplied Sterile Bacteriostatic Water for Injection, USP (containing 0.9% benzyl alcohol) yields a multiple-use, clear, and colorle | Lyophilized powder. | Subcutaneous Injection | NA | NA | Signs of infection (fever, chills, sore throat, body aches, confusion, neck stiffness, flu symptoms); shortness of breath with swelling, rapid weight gain; chest pain, ongoing cough, coughing up mucus or blood; signs of skin infection such as itching, sw | Link | NA | NA |
| 10029 | Th1005 | Etanercept | >Th1005_Etanercept LPAQVAFTPYAPEPGSTCRLREYYDQTAQMCCSKCSPGQHAKVFCTKTSDTVCDSCEDSTYTQLWNWVPECLSCGSRCSSDQVETQACTREQNRICTCRPGWYCALSKQEGCRLCAPLRKCRPGFGVARPGTETSDVVCKPCAPGTFSNTTSSTDICRPHQICNVVAIPGNASMDAVCTSTSPTRSMAPGAVHLPQPVSTRSQHTQPTPEPSTAPSTSFLLPMGPSPPAEGSTGDEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 51234.9 | C2224H3475N621O698S36 | 7.89 | -0.529 | 71 | 68 hours in healthy adults | It is a dimeric fusion protein (934 amino acids) consisting of extracellular ligand-binding portion of the human 75 kilodalton (p75) tumor necrosis factor receptor (TNFR) linked to Fc portion of human IgG1 produced by recombinant DNA technology in a Chinese hamster ovary (CHO) mammalian cell expression system.. The Fc component of etanercept contains the CH2 domain, the CH3 domain and hinge region, but not the CH1 domain of IgG1. | Used to treat severe rheumatoid arthritis in adults, severe juvenile idiopathic arthritis, ankylosing spondylitis, and severe plaque psoriasis. | TNF, a naturally occurring cytokine is involved in normal inflammatory and immune responses. Elevated levels of TNF are found in tissues and fluids of patients suffering from rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis (AS), and plaque psoriasis. Etanercept binds specifically to tumor necrosis factor (TNF) and blocks its interaction with cell surface TNF receptors. | There are two distinct receptors for TNF (TNFRs), a 55 kilodalton (p55) and a 75 kilodalton receptor (p75). The biological activity of TNF is dependent upon binding to either of the cell surface receptors p75 or p55. Etanercept is a dimeric soluble form of the p75 TNF receptor that can bind to two TNF molecules, thereby effectively removing them from circulation. | NA | NA | NA | NA | 160 ± 80 mL/hr [RA patients] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Dermatologicals, Disease-modifying Antirheumatic Agents, Immunoglobulin Constant Regions, Immunoglobulin Fc Fragments, Immunoglobulin Fragments, Immunoglobulin Isotypes, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Membrane Proteins, Peptides, Proteins, Tumor Necrosis Factor Blockers | CA2123593 | 14-Mar-2000 | 14-Sep-2013 | Tofacitinib increases the risk of added immunosuppression. It is recommended to avoid concurrent therapy. | NA | Enbrel Sureclick | Amgen Inc. , Boehringer Ingelheim Ltd. | Amgen Inc. , Boehringer Ingelheim Ltd. | NA | NA | NA | Solution | Subcutaneous Injection | NA | Allergy or severe infection as sepsis. | NA | Link | NA | NA |
| 10030 | Th1005 | Etanercept | >Th1005_Etanercept LPAQVAFTPYAPEPGSTCRLREYYDQTAQMCCSKCSPGQHAKVFCTKTSDTVCDSCEDSTYTQLWNWVPECLSCGSRCSSDQVETQACTREQNRICTCRPGWYCALSKQEGCRLCAPLRKCRPGFGVARPGTETSDVVCKPCAPGTFSNTTSSTDICRPHQICNVVAIPGNASMDAVCTSTSPTRSMAPGAVHLPQPVSTRSQHTQPTPEPSTAPSTSFLLPMGPSPPAEGSTGDEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 51234.9 | C2224H3475N621O698S36 | 7.89 | -0.529 | 71 | 70.7-94.8 hours in pediatric JIA patients | It is a dimeric fusion protein (934 amino acids) consisting of extracellular ligand-binding portion of the human 75 kilodalton (p75) tumor necrosis factor receptor (TNFR) linked to Fc portion of human IgG1 produced by recombinant DNA technology in a Chinese hamster ovary (CHO) mammalian cell expression system.. The Fc component of etanercept contains the CH2 domain, the CH3 domain and hinge region, but not the CH1 domain of IgG1. | Used to treat severe rheumatoid arthritis in adults, severe juvenile idiopathic arthritis, ankylosing spondylitis, and severe plaque psoriasis. | TNF, a naturally occurring cytokine is involved in normal inflammatory and immune responses. Elevated levels of TNF are found in tissues and fluids of patients suffering from rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis (AS), and plaque psoriasis. Etanercept binds specifically to tumor necrosis factor (TNF) and blocks its interaction with cell surface TNF receptors. | There are two distinct receptors for TNF (TNFRs), a 55 kilodalton (p55) and a 75 kilodalton receptor (p75). The biological activity of TNF is dependent upon binding to either of the cell surface receptors p75 or p55. Etanercept is a dimeric soluble form of the p75 TNF receptor that can bind to two TNF molecules, thereby effectively removing them from circulation. | NA | NA | NA | NA | 160 ± 80 mL/hr [RA patients] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Dermatologicals, Disease-modifying Antirheumatic Agents, Immunoglobulin Constant Regions, Immunoglobulin Fc Fragments, Immunoglobulin Fragments, Immunoglobulin Isotypes, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Membrane Proteins, Peptides, Proteins, Tumor Necrosis Factor Blockers | US7276477 | 2-Oct-2007 | 18-Nov-2024 | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | NA | Eticovo | Samsung Bioepis Co., Ltd. | Samsung Bioepis Co., Ltd. | rheumatoid arthritis (RA), polyarticular juvenile idiopathic arthritis (JIA) in patients aged 2 years or older, psoriatic arthritis (PsA), ankylosing spondylitis (AS), and plaque psoriasis (PsO) in patients 4 years or older. | NA | 8.18 mg sodium chloride 0.665 mg sodium phosphate dibasic heptahydrate 1.038 mg sodium phosphate monobasic monohydrate 10 mg sucrose Water for Injection, USP | clear to opalescent, colorless to pale yellow, sterile, and preservative-free solution | Injection in the single-dose prefilled syring | Starting Dose: 50 mg twice weekly for 3 months Maintenance Dose: 50 mg once weekly | Eticovo should not be administered to patients with sepsis. | pneumonia, cellulitis, septic arthritis, bronchitis, gastroenteritis, pyelonephritis, sepsis, abscess and osteomyelitis. | Link | NA | NA |
| 10031 | Th1005 | Etanercept | >Th1005_Etanercept LPAQVAFTPYAPEPGSTCRLREYYDQTAQMCCSKCSPGQHAKVFCTKTSDTVCDSCEDSTYTQLWNWVPECLSCGSRCSSDQVETQACTREQNRICTCRPGWYCALSKQEGCRLCAPLRKCRPGFGVARPGTETSDVVCKPCAPGTFSNTTSSTDICRPHQICNVVAIPGNASMDAVCTSTSPTRSMAPGAVHLPQPVSTRSQHTQPTPEPSTAPSTSFLLPMGPSPPAEGSTGDEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 51234.9 | C2224H3475N621O698S36 | 7.89 | -0.529 | 71 | NA | It is a dimeric fusion protein (934 amino acids) consisting of extracellular ligand-binding portion of the human 75 kilodalton (p75) tumor necrosis factor receptor (TNFR) linked to Fc portion of human IgG1 produced by recombinant DNA technology in a Chinese hamster ovary (CHO) mammalian cell expression system.. The Fc component of etanercept contains the CH2 domain, the CH3 domain and hinge region, but not the CH1 domain of IgG1. | Used to treat severe rheumatoid arthritis in adults, severe juvenile idiopathic arthritis, ankylosing spondylitis, and severe plaque psoriasis. | TNF, a naturally occurring cytokine is involved in normal inflammatory and immune responses. Elevated levels of TNF are found in tissues and fluids of patients suffering from rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis (AS), and plaque psoriasis. Etanercept binds specifically to tumor necrosis factor (TNF) and blocks its interaction with cell surface TNF receptors. | There are two distinct receptors for TNF (TNFRs), a 55 kilodalton (p55) and a 75 kilodalton receptor (p75). The biological activity of TNF is dependent upon binding to either of the cell surface receptors p75 or p55. Etanercept is a dimeric soluble form of the p75 TNF receptor that can bind to two TNF molecules, thereby effectively removing them from circulation. | NA | NA | NA | NA | 160 ± 80 mL/hr [RA patients] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Dermatologicals, Disease-modifying Antirheumatic Agents, Immunoglobulin Constant Regions, Immunoglobulin Fc Fragments, Immunoglobulin Fragments, Immunoglobulin Isotypes, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Membrane Proteins, Peptides, Proteins, Tumor Necrosis Factor Blockers | US36755 | 21-10-1862 | 21-10-1879 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10193 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. | Used as replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage taggingor neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | Antibodies in Flebogamma 5% may interfere with the response to live viral vaccines, such as measles, mumps, and rubella. Physicians should be informed of recent therapy with Immune Globulin Intravenous (Human) so that administration of live viral vaccine | High affinity immunoglobulin gamma Fc receptor I,High affinity immunoglobulin gamma Fc receptor IB,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc reg | Civacir | NA | NA | To prevent HCV infection in liver transplant patients; Prevent recurrence of hepatitis C-related liver disease in HCV positive liver transplant recipients or in patients who received an HCV-positive liver; Treat and prevent HCV infection | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10194 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. | Used as replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage taggingor neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Asceniv | Adma Biologics, Inc. | Adma Biologics, Inc. | used to treat the symptoms of Primary Immunodeficiency Syndrome (PI), Immune Thrombocytopenic Purpura (ITP), Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Bone Marrow Transplant, B-cell Chronic Lymphocytic Leukemia, Multifocal Motor Neuropathy, and Dermatomyositis. | NA | The manufacturing process of ASCENIV employs three steps to remove/inactivate adventitious viruses to minimize the risk of virus transmission. The steps are "Precipitation and removal of fraction III" during cold ethanol fractionation, classical "solvent/detergent treatment" and "35 nm virus filtration." In compliance with current guidelines, the steps have been separately validated in a series of in vitro experiments for their capacity to inactivate or remove both enveloped and nonenveloped viruses. | clear to opalescent liquid, which is colorless to pale yellow. | Intravenous | The recommended dose of ASCENIV for replacement therapy in primary humoral immunodeficiency (PI) is 300 to 800 mg/kg body weight administered every 3 to 4 weeks. The dose may be adjusted over time to achieve the desired trough levels and clinical response. | ASCENIV is contraindicated in: patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. IgA-deficiency patients with antibodies to IgA and a history of hypersensitivity. | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, dizziness, nausea, lightheadedness, sweating, headache, pounding in your neck or ears, fever, chills, chest tightness, warmth or redness in your face, pale or yellowed skin, dark colored urine, fever, confusion, weakness, increased thirst or feeling hot, inability to urinate, heavy sweating, hot and dry skin, little or no urination, swelling, rapid weight gain, shortness of breath, chest pain, trouble breathing, blue colored lips, fingers, or toes, fever with severe headache, neck stiffness, eye pain, increased sensitivity to light, shortness of breath, chest pain with deep breathing, rapid heart rate, numbness or weakness on one side of the body, and welling and warmth, or discoloration in an arm or leg | Link | NA | NA |
| 10195 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. | Used as replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage taggingor neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Bivigam | Adma Biologics, Inc. | Adma Biologics, Inc. | BIVIGAM is an Immune Globulin Intravenous (Human), 10% Liquid, indicated for the treatment of patients with primary humoral immunodeficiency (PI). This includes, but is not limited to, the humoral immune defect in common variable immunodeficiency (CVID), X-linked agammaglobulinemia, congenital agammaglobulinemia, Wiskott-Aldrich syndrome, and severe combined immunodeficiencies. | NA | The manufacturing process of BIVIGAM employs three steps to remove/inactivate adventitious viruses to minimize the risk of virus transmission. The steps are “Precipitation and removal of fraction III” during cold ethanol fractionation, classical “Solvent/detergent treatment” and “35 nm virus filtration”. In compliance with current guidelines, the steps have been separately validated in a series of in vitro experiments for their capacity to inactivate or remove both enveloped and non-enveloped viruses. Precipitation and removal of fraction III removes both enveloped and non-enveloped viruses, solvent/detergent treatment represents a virus inactivation step for enveloped viruses, and 35 nm virus filtration removes both enveloped and non-enveloped viruses by size exclusion. In addition to the steps above, low pH during several steps of the production process contributes to virus inactivation. The results of virus validation studies for BIVIGAM are shown in Table 3, expressed as log10 reduction factors. | sterile liquid | Intravenous infusion | The recommended dose of BIVIGAM for replacement therapy in primary humoral immunodeficiency (PI) is 300 to 800 mg/kg body weight administered every 3 to 4 weeks. The dosage may be adjusted over time to achieve the desired trough levels and clinical response. | BIVIGAM is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. BIVIGAM is contraindicated in IgA deficiency patients with antibodies to IgA and a history of hypersensitivity. | headache fatigue infusion site reaction nausea sinus infection increased blood pressure diarrhea dizziness tiredness back pain migraine muscle pain, and sore throat | Link | NA | NA |
| 10196 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. | Used as replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage taggingor neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Flebogamma | Instituto Grifols SA | Instituto Grifols SA | It is indicated for replacement therapy in primary (inherited) humoral immunodeficiency disorders, such as common variable immunodeficiency, x-linked agammaglobulinemia, severe combined immunodeficiency, and Wiskott-Aldrich Syndrome. Flebogamma 5% is espe | NA | Flebogamma 5% contains 50 mg IgG per mL, 50 mg D-sorbitol per mL, and _ 6 mg/mL polyethylene glycol. There is no preservative in the formulation. The pH of the solution ranges from 5 to 6 and the osmolarity from 240 to 350 mOsm/L | Sterile, clear or slightly opalescent and colorless to pale yellow liquid | Intravenous infusion | Normally given as 300 to 600 mg/kg body weight subjects with primary humoral immunodeficiency disease (PID) every 3 or 4 weeks for 12 months. | Flebogamma 5% should not be administered to individuals with a history of severe or anaphylactic reactions to blood or blood-derived products. Individuals with selective IgA deficiency and demonstrable antibodies to IgA should not receive Flebogamma 5%. | Rash; itching; hives; difficulty breathing or swallowing; tightness in the chest; swelling of the mouth, hands, face, lips, eyes, throat, or tongue; bloating; calf pain or tenderness; chest pain; confusion; dark urine; decreased urination; fainting; fast or irregular heartbeat; fever or chills; increased or painful urination; numbness of an arm or a leg; one-sided weakness; red, swollen, blistered, or peeling skin; seizures; severe headache, dizziness, or stomach pain; shortness of breath or trouble breathing; speech problems; sweating; symptoms of kidney problems (eg, decreased urination, lower back or flank pain, swelling or bloating, sudden weight gain); unusual tiredness or weakness; vision problems; yellowing of the skin or eyes. | Link | NA | NA |
| 10197 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. | Used as replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage taggingor neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Cutaquig | Pfizer | Pfizer | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10198 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. | Used as replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage taggingor neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Gamastan | Grifols Therapeutics Llc | Grifols Therapeutics Llc | used to treat the symptoms of Hepatitis A, Measles, Rubella, and Varicella. | NA | In the manufacturing process of GAMASTAN, there are several steps with the capacity for viral inactivation or removal. The main steps of the manufacturing process that contribute to the virus clearance capacity are as follows: Caprylate precipitation/depth filtration Caprylate incubation Depth filtration Column chromatography Nanofiltration Low pH final container incubation | clear or slightly opalescent, and colorless or pale yellow or light brown sterile solution | Intravenous | 0.1 mL/kg 0.2 mL/kg 0.2 mL/kg | GAMASTAN is contraindicated in: Anaphylactic or severe systemic hypersensitivity reactions to immune globulin (human). | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, itching, red, swollen, blistered, or peeling skin with or without fever, wheezing, tightness in the chest or throat, trouble breathing, swallowing, or talking, and unusual hoarseness | Link | NA | NA |
| 10199 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. | Used as replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage taggingor neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Gamunex | Talecris Biotherapeutics | Talecris Biotherapeutics | Gamunex-C is used to treat primary immunodeficiency (PI). This includes, but is not limited to, congenital agammaglobulinemia, common variable immunodeficiency, X-linked agammaglobulinemia, Wiskott-Aldrich syndrome, and severe combined immunodeficiencies. | NA | GAMUNEX (immune globulin intravenous human 10%) consists of 9%–11% protein in 0.16–0.24 M glycine. Not less than 98% of the protein has the electrophoretic mobility of gamma globulin. GAMUNEX (immune globulin intravenous human 10%) contains trace levels o | Sterile solution | Intravenous infusion | Treatment of Primary Humoral Immunodeficiency = The dose of GAMUNEX (immune globulin intravenous (human) 10%) for replacement therapy in primary immune deficiency diseases is 300 to 600 mg/kg body weight (3-6 mL/kg) administered every 3 to 4 weeks. The dosage may be adjusted over time to achieve the desired trough levels and clinical responses. | GAMUNEX (immune globulin intravenous (human) 10%) is contraindicated in individuals with acute severe hypersensitivity reactions to Immune Globulin (Human). GAMUNEX (immune globulin intravenous (human) 10%) contains trace amounts of IgA. It is contraindic in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. | Mild headache; dizziness; tired feeling; back pain, muscle cramps; minor chest pain; or flushing (warmth, redness, or tingly feeling). | Link | NA | NA |
| 10200 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. | Used as replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage taggingor neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Gamimune N | Talecris Biotherapeutics Inc | Talecris Biotherapeutics Inc | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10265 | Th1038 | Omalizumab | >Th1038_Omalizumab EVQLVESGGGLVQPGGSLRLSCAVSGYSITSGYSWNWIRQAPGKGLEWVASITYDGSTNYADSVKGRFTISRDDSKNTFYLQMNSLRAEDTAVYYCARGSHYFGHWHFAVWGQGTLVTVSSGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6450H9916N1714O2023S38 | 6.6 - 7.2 | -0.432 | 61(FAB fra | 624 hours | A recombinant DNA-derived humanized IgG1k monoclonal antibody that selectively binds to human immunoglobulin E. Xolair is produced by a Chinese hamster ovary cell suspension culture in a nutrient medium containing the antibiotic gentamicin. | For treatment of asthma caused by allergies | Xolair inhibits the binding of IgE to the high-affinity IgE receptor (FceRI) on the surface of mast cells and basophils. Reduction in surface-bound IgE on FceRI-bearing cells limits the degree of release of mediators of the allergic response. Xolair is used to treat severe, persisten asthma. | Xolair binds to IgE (a class of antibodies normally secreted in allergic responses), which prevents their binding to mast cells and basophils. | Anaphylaxis may occur rarely with this agent, either after the first dose or multiple doses | Most likely removed by opsonization via the reticuloendothelial system. | bioavailability of 62% | 78 ± 32 mL/kg | Liver elimination of IgG includes degradation in the liver reticuloendothelial system (RES) and endothelial cells. Intact IgG is also excreted in bile. | Agents to Treat Airway Disease, Amino Acids, Peptides, and Proteins, Anti-Allergic Agents, Anti-Asthmatic Agents, Anti-IgE, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Blood Proteins, Decreased IgE Activity, Globulins, IgE-directed Antibody Interactions, Immunoglobulins, Immunoproteins, Proteins, Respiratory Agents, Miscellaneous, Respiratory System Agents, Serum Globulins | CA2113813 | 12-Apr-2005 | 14-Aug-2012 | NA | High affinity immunoglobulin epsilon receptor subunit alpha and beta | Xolair | Genentech Inc, Novartis Europharm Limited | Genentech Inc, Novartis Europharm Limited | Xolair is used to treat moderate to severe asthma that is caused by allergies, and chronic idiopathic urticaria (a form of chronic hives) in adults and children who are at least 12 years old. Xolair is usually given after other asthma medications have bee | NA | Formulated in a single use vial that is reconstituted with sterile water for injection (SWFI), USP, and administered as a subcutaneous (SC) injection. Each 202.5 mg vial of omalizumab also contains L-histidine (1.8 mg), L-histidine hydrochloride monohydra | Sterile, white, preservative free, lyophilized powder | Subcutaneous Injection | Xolair is administered at 150 to 375 mg by subcutaneous injection every 2 or 4 weeks. Determine doses (mg) and dosing frequency by serum total IgE level (IU/mL), measured before the start of treatment, and body weight (kg) as if serum IgE is less than 30-or >700 IU/mL and <66 or >330 lb, respectively) should not be dosed. | Severe hypersensitivity | Wheezing, tightness in your chest, trouble breathing; hives or skin rash; feeling anxious or light-headed, fainting; warmth or tingling under your skin; or swelling of your face, lips, tongue, or throat. | Link | NA | NA |
| 10266 | Th1038 | Omalizumab | >Th1038_Omalizumab EVQLVESGGGLVQPGGSLRLSCAVSGYSITSGYSWNWIRQAPGKGLEWVASITYDGSTNYADSVKGRFTISRDDSKNTFYLQMNSLRAEDTAVYYCARGSHYFGHWHFAVWGQGTLVTVSSGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6450H9916N1714O2023S38 | 6.6 - 7.3 | -0.432 | 61(FAB fra | 624 hours | A recombinant DNA-derived humanized IgG1k monoclonal antibody that selectively binds to human immunoglobulin E. Xolair is produced by a Chinese hamster ovary cell suspension culture in a nutrient medium containing the antibiotic gentamicin. | For treatment of asthma caused by allergies | Xolair inhibits the binding of IgE to the high-affinity IgE receptor (FceRI) on the surface of mast cells and basophils. Reduction in surface-bound IgE on FceRI-bearing cells limits the degree of release of mediators of the allergic response. Xolair is used to treat severe, persisten asthma. | Xolair binds to IgE (a class of antibodies normally secreted in allergic responses), which prevents their binding to mast cells and basophils. | Anaphylaxis may occur rarely with this agent, either after the first dose or multiple doses | Most likely removed by opsonization via the reticuloendothelial system. | bioavailability of 62% | 78 ± 32 mL/kg | Liver elimination of IgG includes degradation in the liver reticuloendothelial system (RES) and endothelial cells. Intact IgG is also excreted in bile. | Agents to Treat Airway Disease, Amino Acids, Peptides, and Proteins, Anti-Allergic Agents, Anti-Asthmatic Agents, Anti-IgE, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Blood Proteins, Decreased IgE Activity, Globulins, IgE-directed Antibody Interactions, Immunoglobulins, Immunoproteins, Proteins, Respiratory Agents, Miscellaneous, Respiratory System Agents, Serum Globulins | CA1340233 | 15-Dec-1998 | 15-Dec-2015 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Pain; headache, tired feeling; joint or muscle pain; dizziness; ear pain; hair loss; mild itching or skin rash; sore throat or cold symptoms; or redness, bruising, warmth, burning, stinging, itching, pain, or swelling of your skin where the injection was given. | Link | NA | NA |
| 10267 | Th1038 | Omalizumab | >Th1038_Omalizumab EVQLVESGGGLVQPGGSLRLSCAVSGYSITSGYSWNWIRQAPGKGLEWVASITYDGSTNYADSVKGRFTISRDDSKNTFYLQMNSLRAEDTAVYYCARGSHYFGHWHFAVWGQGTLVTVSSGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6450H9916N1714O2023S38 | 6.6 - 7.4 | -0.432 | 61(FAB fra | 624 hours | A recombinant DNA-derived humanized IgG1k monoclonal antibody that selectively binds to human immunoglobulin E. Xolair is produced by a Chinese hamster ovary cell suspension culture in a nutrient medium containing the antibiotic gentamicin. | For treatment of asthma caused by allergies | Xolair inhibits the binding of IgE to the high-affinity IgE receptor (FceRI) on the surface of mast cells and basophils. Reduction in surface-bound IgE on FceRI-bearing cells limits the degree of release of mediators of the allergic response. Xolair is used to treat severe, persisten asthma. | Xolair binds to IgE (a class of antibodies normally secreted in allergic responses), which prevents their binding to mast cells and basophils. | Anaphylaxis may occur rarely with this agent, either after the first dose or multiple doses | Most likely removed by opsonization via the reticuloendothelial system. | bioavailability of 62% | 78 ± 32 mL/kg | Liver elimination of IgG includes degradation in the liver reticuloendothelial system (RES) and endothelial cells. Intact IgG is also excreted in bile. | Agents to Treat Airway Disease, Amino Acids, Peptides, and Proteins, Anti-Allergic Agents, Anti-Asthmatic Agents, Anti-IgE, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Blood Proteins, Decreased IgE Activity, Globulins, IgE-directed Antibody Interactions, Immunoglobulins, Immunoproteins, Proteins, Respiratory Agents, Miscellaneous, Respiratory System Agents, Serum Globulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10268 | Th1038 | Omalizumab | >Th1038_Omalizumab EVQLVESGGGLVQPGGSLRLSCAVSGYSITSGYSWNWIRQAPGKGLEWVASITYDGSTNYADSVKGRFTISRDDSKNTFYLQMNSLRAEDTAVYYCARGSHYFGHWHFAVWGQGTLVTVSSGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6450H9916N1714O2023S38 | 6.6 - 7.5 | -0.432 | 61(FAB fra | 624 hours | A recombinant DNA-derived humanized IgG1k monoclonal antibody that selectively binds to human immunoglobulin E. Xolair is produced by a Chinese hamster ovary cell suspension culture in a nutrient medium containing the antibiotic gentamicin. | For treatment of asthma caused by allergies | Xolair inhibits the binding of IgE to the high-affinity IgE receptor (FceRI) on the surface of mast cells and basophils. Reduction in surface-bound IgE on FceRI-bearing cells limits the degree of release of mediators of the allergic response. Xolair is used to treat severe, persisten asthma. | Xolair binds to IgE (a class of antibodies normally secreted in allergic responses), which prevents their binding to mast cells and basophils. | Anaphylaxis may occur rarely with this agent, either after the first dose or multiple doses | Most likely removed by opsonization via the reticuloendothelial system. | bioavailability of 62% | 78 ± 32 mL/kg | Liver elimination of IgG includes degradation in the liver reticuloendothelial system (RES) and endothelial cells. Intact IgG is also excreted in bile. | Agents to Treat Airway Disease, Amino Acids, Peptides, and Proteins, Anti-Allergic Agents, Anti-Asthmatic Agents, Anti-IgE, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Blood Proteins, Decreased IgE Activity, Globulins, IgE-directed Antibody Interactions, Immunoglobulins, Immunoproteins, Proteins, Respiratory Agents, Miscellaneous, Respiratory System Agents, Serum Globulins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | 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 |
| 10327 | Th1046 | Abciximab | >Th1046_Abciximab EVQLQQSGTVLARPGASVKMSCEASGYTFTNYWMHWVKQRPGQGLEWIGAIYPGNSDTSYIQKFKGKAKLTAVTSTTSVYMELSSLTNEDSAVYYCTLYDGYYVFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTH | 145651.1 | C6462H9964N1690O2049S48 | 6.16 | -0.424 | 71 | initial half-life of less than 10 minutes and a second phase half-life of about 30 minutes | Abciximab is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules. It also binds to vitronectin (αvβ3) receptor found on platelets and vessel wall endothelial and smooth muscle cells. | Abciximab is indicated as an adjunct to percutaneous coronary intervention for the prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention and in patients with unstable angina not responding to conventional medical therapy when percutaneous coronary intervention is planned within 24 hours. Abciximab is intended for use with aspirin and heparin and has been studied only in that setting. | Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets. A single intravenous bolus dose from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function. After two hours post-injection with a dose of 0.25 - 0.30 mg/kg, 80% of the GPIIb/IIIa receptors were blocked and platelet aggregation was prevented. GPIIb/IIIa is the major surface receptor involved in the final pathway of platelet aggregation. Bleeding time increases to over 30 minutes at the aforementioned doses. To compare, baseline values were five minutes. | Abciximab binds to the intact platelet GPIIb/IIIa receptor, which is a member of the integrin family of adhesion receptors and the major platelet surface receptor involved in platelet aggregation. This binding is thought to involve steric hindrance and/orconformational alterations which block access of large molecules to the receptor rather than direct interaction with the RGD (arginine-glycine-aspartic acid) binding site of GPIIb/IIIa. By binding to the vitronectin receptor (also known as the αvβ3 integrin), abciximab blocks effects mediated by this integrin which include cell adhesion. Furthermore, abciximab blocks Mac-1 receptor on monocytes and neutrophils thus inhibiting monocyte adhesion. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to platelets, or by human antimurine antibody production. Excreted renally. | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Anticoagulants, Antiplatelet agents, Blood and Blood Forming Organs, Blood Proteins, Globulins, Hematologic Agents, Immunoglobulin Fab Fragments, Immunoglobulin Fragments, Immunoglobulins, Immunoproteins, Miscellaneous Therapeutic Agents, Peptide Fragments, Peptides, Platelet Aggregation Inhibitors Excl. Heparin, Proteins, Serum Globulins | CA1341357 | 7-May-2002 | 7-May-2019 | Additive anticoagulant/antiplatelet effects may increase bleed risk. Concomitant therapy should be avoided with Ginkgo biloba. | Integrin beta-3,Integrin alpha-IIb,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 immuno | ReoPro | Eli Lilly and Company, Janssen Pharmaceuticals, Janssen Biotech, Inc. | Eli Lilly and Company, Janssen Pharmaceuticals, Janssen Biotech, Inc. | ReoPro is used to lessen the chance of heart attack in people who need percutaneous coronary intervention (PCI), a procedure to open blocked arteries of the heart. | NA | Each single use vial contains 2 mg/mL of Abciximab in a buffered solution (pH 7.2) of 0.01 M sodium phosphate, 0.15 M sodium chloride and 0.001% polysorbate 80 in Water for Injection. No preservatives are added. | Clear, colorless, Sterile, non-pyrogenic solution | Intravenous administartion | The recommended dosage of Abciximab in adults is a 0.25 mg/kg intravenous bolus administered 10-60 minutes before the start of PCI, followed by a continuous Intravenous infusion of 0.125 _g/kg/min (to a maximum of 10 _g/min) for 12 hours. | Active internal bleeding, Recent (within six weeks) gastrointestinal (GI) or genitourinary (GU) bleeding of clinical significance, History of cerebrovascular accident (CVA) within two years, or CVA with a significant residual neurological deficit, Bleeding diathesis; Administration of oral anticoagulants within seven days unless prothrombin time is I 1.2 times control; Thrombocytopenia (< 100,000 cells/pL); Recent (within six weeks) major surgery or trauma; Intracranial neoplasm, arteriovenous malformation, or aneurysm; Severe uncontrolled hypertension; Presumed or documented history of vasculitis; Use of intravenous dextran before percutaneous coronary intervention, or intent to use it during an intervention. | Bleeding; blurred vision; confusion; dizziness, faintness, or lightheadedness when getting up from a lying or sitting position suddenly; sweating; unusual tiredness or weakness | Link | NA | NA |
| 10328 | Th1046 | Abciximab | >Th1046_Abciximab EVQLQQSGTVLARPGASVKMSCEASGYTFTNYWMHWVKQRPGQGLEWIGAIYPGNSDTSYIQKFKGKAKLTAVTSTTSVYMELSSLTNEDSAVYYCTLYDGYYVFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTH | 145651.1 | C6462H9964N1690O2049S48 | 6.16 | -0.424 | 71 | initial half-life of less than 10 minutes and a second phase half-life of about 30 minutes | Abciximab is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules. It also binds to vitronectin (αvβ3) receptor found on platelets and vessel wall endothelial and smooth muscle cells. | Abciximab is indicated as an adjunct to percutaneous coronary intervention for the prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention and in patients with unstable angina not responding to conventional medical therapy when percutaneous coronary intervention is planned within 24 hours. Abciximab is intended for use with aspirin and heparin and has been studied only in that setting. | Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets. A single intravenous bolus dose from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function. After two hours post-injection with a dose of 0.25 - 0.30 mg/kg, 80% of the GPIIb/IIIa receptors were blocked and platelet aggregation was prevented. GPIIb/IIIa is the major surface receptor involved in the final pathway of platelet aggregation. Bleeding time increases to over 30 minutes at the aforementioned doses. To compare, baseline values were five minutes. | Abciximab binds to the intact platelet GPIIb/IIIa receptor, which is a member of the integrin family of adhesion receptors and the major platelet surface receptor involved in platelet aggregation. This binding is thought to involve steric hindrance and/orconformational alterations which block access of large molecules to the receptor rather than direct interaction with the RGD (arginine-glycine-aspartic acid) binding site of GPIIb/IIIa. By binding to the vitronectin receptor (also known as the αvβ3 integrin), abciximab blocks effects mediated by this integrin which include cell adhesion. Furthermore, abciximab blocks Mac-1 receptor on monocytes and neutrophils thus inhibiting monocyte adhesion. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to platelets, or by human antimurine antibody production. Excreted renally. | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Anticoagulants, Antiplatelet agents, Blood and Blood Forming Organs, Blood Proteins, Globulins, Hematologic Agents, Immunoglobulin Fab Fragments, Immunoglobulin Fragments, Immunoglobulins, Immunoproteins, Miscellaneous Therapeutic Agents, Peptide Fragments, Peptides, Platelet Aggregation Inhibitors Excl. Heparin, Proteins, Serum Globulins | NA | NA | NA | Tirofiban has additive effects. Concomitant use is contraindicated. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Black, tarry stools; bleeding gums; blood in urine or stools; pinpoint red spots on skin; unusual bleeding or bruising | Link | NA | NA |
| 10329 | Th1046 | Abciximab | >Th1046_Abciximab EVQLQQSGTVLARPGASVKMSCEASGYTFTNYWMHWVKQRPGQGLEWIGAIYPGNSDTSYIQKFKGKAKLTAVTSTTSVYMELSSLTNEDSAVYYCTLYDGYYVFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTH | 145651.1 | C6462H9964N1690O2049S48 | 6.16 | -0.424 | 71 | initial half-life of less than 10 minutes and a second phase half-life of about 30 minutes | Abciximab is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules. It also binds to vitronectin (αvβ3) receptor found on platelets and vessel wall endothelial and smooth muscle cells. | Abciximab is indicated as an adjunct to percutaneous coronary intervention for the prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention and in patients with unstable angina not responding to conventional medical therapy when percutaneous coronary intervention is planned within 24 hours. Abciximab is intended for use with aspirin and heparin and has been studied only in that setting. | Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets. A single intravenous bolus dose from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function. After two hours post-injection with a dose of 0.25 - 0.30 mg/kg, 80% of the GPIIb/IIIa receptors were blocked and platelet aggregation was prevented. GPIIb/IIIa is the major surface receptor involved in the final pathway of platelet aggregation. Bleeding time increases to over 30 minutes at the aforementioned doses. To compare, baseline values were five minutes. | Abciximab binds to the intact platelet GPIIb/IIIa receptor, which is a member of the integrin family of adhesion receptors and the major platelet surface receptor involved in platelet aggregation. This binding is thought to involve steric hindrance and/orconformational alterations which block access of large molecules to the receptor rather than direct interaction with the RGD (arginine-glycine-aspartic acid) binding site of GPIIb/IIIa. By binding to the vitronectin receptor (also known as the αvβ3 integrin), abciximab blocks effects mediated by this integrin which include cell adhesion. Furthermore, abciximab blocks Mac-1 receptor on monocytes and neutrophils thus inhibiting monocyte adhesion. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to platelets, or by human antimurine antibody production. Excreted renally. | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Anticoagulants, Antiplatelet agents, Blood and Blood Forming Organs, Blood Proteins, Globulins, Hematologic Agents, Immunoglobulin Fab Fragments, Immunoglobulin Fragments, Immunoglobulins, Immunoproteins, Miscellaneous Therapeutic Agents, Peptide Fragments, Peptides, Platelet Aggregation Inhibitors Excl. Heparin, Proteins, Serum Globulins | NA | NA | NA | Abciximab may increase the risk of a hypersensitivy reaction to Trastuzumab. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Chest pain or discomfort; chills; cough; eye pain; fever; general feeling of illness; headache; pale skin; rapid weight gain; shortness of breath; slow or irregular heartbeat; sneezing; sore throat; swelling of hands, ankles, feet, or lower legs. | Link | NA | NA |
| 10330 | Th1046 | Abciximab | >Th1046_Abciximab EVQLQQSGTVLARPGASVKMSCEASGYTFTNYWMHWVKQRPGQGLEWIGAIYPGNSDTSYIQKFKGKAKLTAVTSTTSVYMELSSLTNEDSAVYYCTLYDGYYVFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTH | 145651.1 | C6462H9964N1690O2049S48 | 6.16 | -0.424 | 71 | initial half-life of less than 10 minutes and a second phase half-life of about 30 minutes | Abciximab is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules. It also binds to vitronectin (αvβ3) receptor found on platelets and vessel wall endothelial and smooth muscle cells. | Abciximab is indicated as an adjunct to percutaneous coronary intervention for the prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention and in patients with unstable angina not responding to conventional medical therapy when percutaneous coronary intervention is planned within 24 hours. Abciximab is intended for use with aspirin and heparin and has been studied only in that setting. | Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets. A single intravenous bolus dose from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function. After two hours post-injection with a dose of 0.25 - 0.30 mg/kg, 80% of the GPIIb/IIIa receptors were blocked and platelet aggregation was prevented. GPIIb/IIIa is the major surface receptor involved in the final pathway of platelet aggregation. Bleeding time increases to over 30 minutes at the aforementioned doses. To compare, baseline values were five minutes. | Abciximab binds to the intact platelet GPIIb/IIIa receptor, which is a member of the integrin family of adhesion receptors and the major platelet surface receptor involved in platelet aggregation. This binding is thought to involve steric hindrance and/orconformational alterations which block access of large molecules to the receptor rather than direct interaction with the RGD (arginine-glycine-aspartic acid) binding site of GPIIb/IIIa. By binding to the vitronectin receptor (also known as the αvβ3 integrin), abciximab blocks effects mediated by this integrin which include cell adhesion. Furthermore, abciximab blocks Mac-1 receptor on monocytes and neutrophils thus inhibiting monocyte adhesion. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to platelets, or by human antimurine antibody production. Excreted renally. | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Anticoagulants, Antiplatelet agents, Blood and Blood Forming Organs, Blood Proteins, Globulins, Hematologic Agents, Immunoglobulin Fab Fragments, Immunoglobulin Fragments, Immunoglobulins, Immunoproteins, Miscellaneous Therapeutic Agents, Peptide Fragments, Peptides, Platelet Aggregation Inhibitors Excl. Heparin, Proteins, Serum Globulins | NA | NA | NA | The prostacyclin analogue, Treprostinil, increases the risk of bleeding when combined with the antiplatelet agent, Abciximab. Monitor for increased bleeding during concomitant thearpy. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 |
| 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 |
| 10406 | Th1066 | Ibritumomab | >Th1066_Ibritumomab QAYLQQSGAELVRPGASVKMSCKASGYTFTSYNMHWVKQTPRQGLEWIGAIYPGNGDTSYNQKFKGKATLTVDKSSSTAYMQLSSLTSEDSAVYFCARVVYYSNSYWYFDVWGTGTTVTVSAPSVYPLAPVCGDTTGSSVTLGCLVKGYFPEPVTLTWNSGSLSSGVHTFPAVLQSDLYTLSSSVTVTSSTWPSQSITCNVAHPASSTKVDKKIEPRGPTIKPCPPCKCPAPNLLGGPSVFIFPPKIKDVLMISLSPIVTCVVVDVSEDDPDVQISWFVNNVEVHTAQTQTHREDYNSTLRVVSALPIQHQDWMSGKEFKCKVNNKDLPAPIERTISKPKGSVRAPQVYVLPPPEEEMTKKQVTLTCMVTDFMPEDIYVEWTNNGKTELNYKNTEPVLDSDGSYFMYSKLRVEKKNWVERNSYSCSVVHEGLHNHHTTKSFSR | 143375.5 | C6382H9830N1672O1979S54 | 7.91 | -0.359 | 71 | 0.8 hours (mammalian reticulocytes, in vitro) | Indium conjugated murine IgG1 kappa monoclonal antibody directed against the CD20 antigen, which is found on the surface of normal and malignant B lymphocytes. Ibritumomab is produced in Chinese hamster ovary cells and is composed of two murine gamma 1 heavy chains of 445 amino acids each and two kappa light chains of 213 amino acids each. | For treatment of non-Hodgkin's lymphoma | Ibritumomab is a murine monoclonal antibody against CD20 that has been radiolabeled with yttrium-90. | The Fab segment of the antibody targets the CD20 epitope on B-cells, allowing the radioactive yttrium to destroy the cell via production of beta particles. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to B cells, or by human antimurine antibody production | NA | NA | Approximately 7.2% of injected dose of yttrium Y 90 ibritumomab tiuxetan is excreted in urine within 7 days. | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antigens, CD20, Blood Proteins, Cancer immunotherapy, CD20-directed Antibody Interactions, CD20-directed Radiotherapeutic Antibody, Globulins, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Lymphoma, B-Cell, Myelosuppressive Agents, Proteins, Radiopharmaceutical Activity, Serum Globulins, Therapeutic Radiopharmaceuticals, Various Therapeutic Radiopharmaceuticals, Yttrium Radioisotopes | CA2149329 | 15-Jul-2008 | 12-Nov-2013 | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | B-lymphocyte antigen CD20 | Zevalin | Spectrum Pharmaceuticals, Ceft Biopharma S.R.O., Acrotech Biopharma Llc | Spectrum Pharmaceuticals, Ceft Biopharma S.R.O., Acrotech Biopharma Llc | Zevalin is indicated for the treatment of relapsed or refractory, low-grade or follicular B-cell non-Hodgkin's lymphoma (NHL). Zevalin is indicated for the treatment of previously untreated follicular NHL in patients who achieve a partial or complete response to first-line chemotherapy. | NA |  Each single-use vial includes 3.2 mg of ibritumomab tiuxetan in 2 mL of 0.9% Sodium Chloride. | Ibritumomab tiuxetan is a clear, colorless, sterile, pyrogen-free, preservative-free solution that may contain translucent particles. | Intravenous infusion | Day 1: Administer rituximab 250 mg/m2 intravenous ; Day 7,8, or 9: Administer rituximab 250 mg/m2 Intravenous infusion If platelets ≥ 150,000/mm3: Within 4 hours after rituximab infusion, administer 0.4 mCi/kg (14.8 MBq per kg) Y-90 Zevalin intravenous. If platelets ≥ 100,000 but ≤ 149,000/mm3 in relapsed or refractory patients: Within 4 hours after rituximab infusion, administer 0.3 mCi/kg (11.1 MBq per kg) Y-90 Zevalin intravenous. | None. | Serious Infusion Reactions, prolonged and Severe Cytopenias, Severe Cutaneous and Mucocutaneous Reactions, Leukemia and Myelodysplastic Syndrome, Cytopenias, fatigue, nasopharyngitis, nausea, abdominal pain, asthenia, cough, diarrhea, and pyrexia. | Link | NA | NA |
| 10407 | Th1066 | Ibritumomab | >Th1066_Ibritumomab QAYLQQSGAELVRPGASVKMSCKASGYTFTSYNMHWVKQTPRQGLEWIGAIYPGNGDTSYNQKFKGKATLTVDKSSSTAYMQLSSLTSEDSAVYFCARVVYYSNSYWYFDVWGTGTTVTVSAPSVYPLAPVCGDTTGSSVTLGCLVKGYFPEPVTLTWNSGSLSSGVHTFPAVLQSDLYTLSSSVTVTSSTWPSQSITCNVAHPASSTKVDKKIEPRGPTIKPCPPCKCPAPNLLGGPSVFIFPPKIKDVLMISLSPIVTCVVVDVSEDDPDVQISWFVNNVEVHTAQTQTHREDYNSTLRVVSALPIQHQDWMSGKEFKCKVNNKDLPAPIERTISKPKGSVRAPQVYVLPPPEEEMTKKQVTLTCMVTDFMPEDIYVEWTNNGKTELNYKNTEPVLDSDGSYFMYSKLRVEKKNWVERNSYSCSVVHEGLHNHHTTKSFSR | 143375.5 | C6382H9830N1672O1979S54 | 7.91 | -0.359 | 71 | 0.8 hours (mammalian reticulocytes, in vitro) | Indium conjugated murine IgG1 kappa monoclonal antibody directed against the CD20 antigen, which is found on the surface of normal and malignant B lymphocytes. Ibritumomab is produced in Chinese hamster ovary cells and is composed of two murine gamma 1 heavy chains of 445 amino acids each and two kappa light chains of 213 amino acids each. | For treatment of non-Hodgkin's lymphoma | Ibritumomab is a murine monoclonal antibody against CD20 that has been radiolabeled with yttrium-90. | The Fab segment of the antibody targets the CD20 epitope on B-cells, allowing the radioactive yttrium to destroy the cell via production of beta particles. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to B cells, or by human antimurine antibody production | NA | NA | Approximately 7.2% of injected dose of yttrium Y 90 ibritumomab tiuxetan is excreted in urine within 7 days. | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antigens, CD20, Blood Proteins, Cancer immunotherapy, CD20-directed Antibody Interactions, CD20-directed Radiotherapeutic Antibody, Globulins, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Lymphoma, B-Cell, Myelosuppressive Agents, Proteins, Radiopharmaceutical Activity, Serum Globulins, Therapeutic Radiopharmaceuticals, Various Therapeutic Radiopharmaceuticals, Yttrium Radioisotopes | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10408 | Th1066 | Ibritumomab | >Th1066_Ibritumomab QAYLQQSGAELVRPGASVKMSCKASGYTFTSYNMHWVKQTPRQGLEWIGAIYPGNGDTSYNQKFKGKATLTVDKSSSTAYMQLSSLTSEDSAVYFCARVVYYSNSYWYFDVWGTGTTVTVSAPSVYPLAPVCGDTTGSSVTLGCLVKGYFPEPVTLTWNSGSLSSGVHTFPAVLQSDLYTLSSSVTVTSSTWPSQSITCNVAHPASSTKVDKKIEPRGPTIKPCPPCKCPAPNLLGGPSVFIFPPKIKDVLMISLSPIVTCVVVDVSEDDPDVQISWFVNNVEVHTAQTQTHREDYNSTLRVVSALPIQHQDWMSGKEFKCKVNNKDLPAPIERTISKPKGSVRAPQVYVLPPPEEEMTKKQVTLTCMVTDFMPEDIYVEWTNNGKTELNYKNTEPVLDSDGSYFMYSKLRVEKKNWVERNSYSCSVVHEGLHNHHTTKSFSR | 143375.5 | C6382H9830N1672O1979S54 | 7.91 | -0.359 | 71 | 0.8 hours (mammalian reticulocytes, in vitro) | Indium conjugated murine IgG1 kappa monoclonal antibody directed against the CD20 antigen, which is found on the surface of normal and malignant B lymphocytes. Ibritumomab is produced in Chinese hamster ovary cells and is composed of two murine gamma 1 heavy chains of 445 amino acids each and two kappa light chains of 213 amino acids each. | For treatment of non-Hodgkin's lymphoma | Ibritumomab is a murine monoclonal antibody against CD20 that has been radiolabeled with yttrium-90. | The Fab segment of the antibody targets the CD20 epitope on B-cells, allowing the radioactive yttrium to destroy the cell via production of beta particles. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to B cells, or by human antimurine antibody production | NA | NA | Approximately 7.2% of injected dose of yttrium Y 90 ibritumomab tiuxetan is excreted in urine within 7 days. | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antigens, CD20, Blood Proteins, Cancer immunotherapy, CD20-directed Antibody Interactions, CD20-directed Radiotherapeutic Antibody, Globulins, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Lymphoma, B-Cell, Myelosuppressive Agents, Proteins, Radiopharmaceutical Activity, Serum Globulins, Therapeutic Radiopharmaceuticals, Various Therapeutic Radiopharmaceuticals, Yttrium Radioisotopes | NA | NA | NA | NA | Digoxin | 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 |
| 10481 | Th1089 | Palivizumab | >Th1089_Palivizumab QVTLRESGPALVKPTQTLTLTCTFSGFSLSTSGMSVGWIRQPPGKALEWLADIWWDDKKDYNPSLKSRLTISKDTSKNQVVLKVTNMDPADTATYYCARSMITNWYFDVWGAGTTVTVSS | NA | NA | NA | NA | 61 (FAB fr | 18-20 days (in adults) | 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). | For prophylaxis of respiratory diseases casued by respiratory syncytial virus. | Synagis exhibits neutralizing and fusion-inhibitory activity against Respiratory syncytial virus (RSV). These activities inhibit RSV replication or spread. Synagis is given to prevent the development of lower respiratory tract disease in pediatric patients. | Palivizumab binds to the fusion glycoprotein of RSV. This prevents its binding and uptake by host cellular receptors. | NA | Most likely removed by opsonization via the reticuloendothelial system. | NA | NA | NA | Amino Acids, Peptides, and Proteins,Anti-Infective Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antiinfectives for Systemic Use,Antiviral Agents,Blood Proteins,Fusion Protein Inhibitors,Globulins,Immune Sera and Immunoglobulins,Immunoglobulins,Immunoproteins,Proteins,Respiratory Syncytial Virus Anti-F Protein Monoclonal Antibody,Serum Globulins,Specific Immunoglobulins | CA2197684 | 31-Oct-2000 | 9-Aug-2015 | NA | Fusion glycoprotein F0,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-b | Synagis | MedImmune | MedImmune | Palivizumab inhibits the actions of respiratory syncytial virus (RSV) and helps to prevent the disease | NA | 100 mg single-dose vial of Synagis liquid solution contains 100 mg of palivizumab and also contains chloride (0.5 mg), glycine (0.1 mg), and histidine (3.9 mg), in a volume of 1 mL. | Sterile, preservative-free liquid solution | Intramuscular | recommended dose of Synagis is 15 mg per kg of body weight given monthly by intramuscular injection. The first dose of Synagis should be administered prior to commencement of the RSV season and the remaining doses should be administered monthly throughout the RSV season. Children who develop an RSV infection should continue to receive monthly doses throughout the RSV season. In the northern hemisphere, the RSV season typically commences in November and lasts through April, but it may begin earlier or persist later in certain communities. | indicated for the prevention of serious lower respiratory tract disease caused by respiratory syncytial virus (RSV) in children at high risk of RSV disease.The following points should be considered when prescribing Synagis: Safety and efficacy were established in children with bronchopulmonary dysplasia (BPD), infants with a history of premature birth (less than or equal to 35 weeks gestational age), and children with hemodynamically significant congenital heart disease (CHD). | high fever, ear pain or drainage, tugging at the ear; warmth or swelling of the ear; crying or fussiness, especially while lying down; change in sleeping patterns; poor feeding or loss of appetite; easy bruising or bleeding; or trouble breathing. | Link | 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 |
| 10499 | Th1095 | Ranibizumab | >Th1095_Ranibizumab EVQLVESGGGLVQPGGSLRLSCAASGYDFTHYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPYYYGTSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHL | 48349.61 | C2158H3282N562O681S12 | NA | NA | NA | Approximately 9 days. | Recombinant (E.coli derived), humanized IgG1 kappa isotype monoclonal antibody (intraocular use). It binds to and inhibits the biologic activity of human vascular endothelial growth factor A (VEGF-A). Ranibizumab is marketed under the name Lucentis. | For the treatment of patients with macular edema after retinal vein occlusion, age-related macular degeneration (wet), and diabetic macular edema. | Ranibizumab is a recombinant humanized IgG1 kappa isotype monoclonal antibody fragment designed for intraocular use. Ranibizumab is a VEGF-A antagonist that binds to and inhibits the biologic activity of active forms of human VEGF-A, including the cleaved form (VEGF110). VEGF-A has been shown to cause neovascularization (angiogenesis) and an increase in vascular permeability, which is thought to contribute to the progression of the neovascular form of age-related macular degeneration (AMD). | Ranibizumab binds to the receptor binding site of active forms of VEGF-A, including the biologically active, cleaved form of this molecule, (VEGF110). The binding of ranibizumab to VEGF-A prevents the interaction of VEGF-A with its receptors (VEGFR1 and VEGFR2) on the surface of endothelial cells, reducing endothelial cell proliferation, vascular leakage, and new blood vessel formation. | There is no information available regarding the LD50 values of ranibizumab. There is also limited clinical experience of ranibizumab overdose: concentrated doses as high as 2 mg ranibizumab in 0.05 mL have been administered to patients, with no additional unexpected adverse reactions that were observed | The metabolism of ranibizumab has not been studied. Since it is a monoclonal antibody fragment, ranibizumab is expected to undergo catabolism. | Ranibizumab rapidly penetrates through the retina to reach the choroid after intravitreal injection. Following monthly intravitreal administration of 0.5 mg ranibizumab in patients with neovascular (wet) age-related macular degeneration, the mean Cmax (±SD) was 1.7 (± 1.1) ng/mL. Following an implant insertion, the mean (±SD) Cmax of ranibizumab was 0.48 (±0.17) ng/mL and median Tmax was 26 days, with a range of one to 89 days. | The apparent volume of the central compartment (Vd/F) is 2.77 L. Ranibizumab is not shown to accumulate in serum. Due to its small size from lacking the Fc region of an antibody, ranibizumab achieves enhanced diffusion into the retina and choroid | In patients with retinal vein occlusion or diabetic macular edema, the apparent clearance (CL/F) of ranibizumab was 24.8 L/day. | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineovascularisation Agents,Blood Proteins,EENT Drugs, Miscellaneous,Globulins,Growth Inhibitors,Growth Substances,Immunoglobulins,Immunoproteins,Ocular Vascular Disorder Agents,Ophthalmics,Ophthalmologicals,Proteins,Sensory Organs,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors | CA2286330 | 10-Jun-2008 | 3-Apr-2018 | NA | Vascular endothelial growth factor A | Lucentis | Genentech | Genentech | Neovascular (Wet) Age-Related Macular Degeneration (AMD), Macular Edema Following Retinal Vein Occlusion (RVO), Diabetic Macular Edema (DME), Diabetic Retinopathy (Non Proliferative Diabetic Retinopathy (NPDR), Proliferative Diabetic Retinopathy (PDR)) In patients With Diabetic Macular Edema (DME) | NA | supplied as a preservative-free, sterile solution in a single-use glass vial designed to deliver 0.05 mL of 10 mg/mL LUCENTIS (0.5 mg dose vial) or 6 mg/mL LUCENTIS (0.3 mg dose vial) aqueous solution with 10 mM histidine HCl, 10% α,α-trehalose dihydrate, 0.01% polysorbate 20, pH 5.5. | Sterile, colorless to pale yellow solution in a single-use glass vial | Intravitreal Injection ONLY | Neovascular (Wet) Age-Related Macular Degeneration (AMD): LUCENTIS 0.5 mg (0.05 mL of 10 mg/mL LUCENTIS solution) is recommended to be administered by intravitreal injection once a month (approximately 28 days). LUCENTIS 0.5 mg (0.05 mL of 10 mg/mL LUCENTIS solution) is recommended to be administered by intravitreal injection once a month (approximately 28 days). Diabetic Macular Edema (DME): LUCENTIS 0.3 mg (0.05 mL of 6 mg/mL LUCENTIS solution) is recommended to be administered by intravitreal injection once a month (approximately 28 days).; Diabetic Retinopathy In Patients With Diabetic Macular Edema: LUCENTIS 0.3 mg (0.05 mL of 6 mg/mL LUCENTIS solution) is recommended to be administered by intravitreal injection once a month (approximately 28 days). | Ocular Or Periocular Infections LUCENTIS is contraindicated in patients with ocular or periocular infections. Hypersensitivity to ranibizumab or any of the excipients in LUCENTIS. Hypersensitivity reactions may manifest as severe intraocular inflammation. | Endophthalmitis and Retinal Detachments Increases in Intraocular Pressure, Thromboembolic Events, Fatal Events in patients with DME and DR at baseline. | Link | NA | NA |
| 10500 | Th1095 | Ranibizumab | >Th1095_Ranibizumab EVQLVESGGGLVQPGGSLRLSCAASGYDFTHYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPYYYGTSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHL | 48349.61 | C2158H3282N562O681S12 | NA | NA | NA | Approximately 9 days. | Recombinant (E.coli derived), humanized IgG1 kappa isotype monoclonal antibody (intraocular use). It binds to and inhibits the biologic activity of human vascular endothelial growth factor A (VEGF-A). Ranibizumab is marketed under the name Lucentis. | For the treatment of patients with macular edema after retinal vein occlusion, age-related macular degeneration (wet), and diabetic macular edema. | Ranibizumab is a recombinant humanized IgG1 kappa isotype monoclonal antibody fragment designed for intraocular use. Ranibizumab is a VEGF-A antagonist that binds to and inhibits the biologic activity of active forms of human VEGF-A, including the cleaved form (VEGF110). VEGF-A has been shown to cause neovascularization (angiogenesis) and an increase in vascular permeability, which is thought to contribute to the progression of the neovascular form of age-related macular degeneration (AMD). | Ranibizumab binds to the receptor binding site of active forms of VEGF-A, including the biologically active, cleaved form of this molecule, (VEGF110). The binding of ranibizumab to VEGF-A prevents the interaction of VEGF-A with its receptors (VEGFR1 and VEGFR2) on the surface of endothelial cells, reducing endothelial cell proliferation, vascular leakage, and new blood vessel formation. | There is no information available regarding the LD50 values of ranibizumab. There is also limited clinical experience of ranibizumab overdose: concentrated doses as high as 2 mg ranibizumab in 0.05 mL have been administered to patients, with no additional unexpected adverse reactions that were observed | The metabolism of ranibizumab has not been studied. Since it is a monoclonal antibody fragment, ranibizumab is expected to undergo catabolism. | Ranibizumab rapidly penetrates through the retina to reach the choroid after intravitreal injection. Following monthly intravitreal administration of 0.5 mg ranibizumab in patients with neovascular (wet) age-related macular degeneration, the mean Cmax (±SD) was 1.7 (± 1.1) ng/mL. Following an implant insertion, the mean (±SD) Cmax of ranibizumab was 0.48 (±0.17) ng/mL and median Tmax was 26 days, with a range of one to 89 days. | The apparent volume of the central compartment (Vd/F) is 2.77 L. Ranibizumab is not shown to accumulate in serum. Due to its small size from lacking the Fc region of an antibody, ranibizumab achieves enhanced diffusion into the retina and choroid | In patients with retinal vein occlusion or diabetic macular edema, the apparent clearance (CL/F) of ranibizumab was 24.8 L/day. | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineovascularisation Agents,Blood Proteins,EENT Drugs, Miscellaneous,Globulins,Growth Inhibitors,Growth Substances,Immunoglobulins,Immunoproteins,Ocular Vascular Disorder Agents,Ophthalmics,Ophthalmologicals,Proteins,Sensory Organs,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors | CA2286330 | 10-Jun-2008 | 3-Apr-2018 | NA | Vascular endothelial growth factor A | Byooviz | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10501 | Th1095 | Ranibizumab | >Th1095_Ranibizumab EVQLVESGGGLVQPGGSLRLSCAASGYDFTHYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPYYYGTSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHL | 48349.61 | C2158H3282N562O681S12 | NA | NA | NA | Approximately 9 days. | Recombinant (E.coli derived), humanized IgG1 kappa isotype monoclonal antibody (intraocular use). It binds to and inhibits the biologic activity of human vascular endothelial growth factor A (VEGF-A). Ranibizumab is marketed under the name Lucentis. | For the treatment of patients with macular edema after retinal vein occlusion, age-related macular degeneration (wet), and diabetic macular edema. | Ranibizumab is a recombinant humanized IgG1 kappa isotype monoclonal antibody fragment designed for intraocular use. Ranibizumab is a VEGF-A antagonist that binds to and inhibits the biologic activity of active forms of human VEGF-A, including the cleaved form (VEGF110). VEGF-A has been shown to cause neovascularization (angiogenesis) and an increase in vascular permeability, which is thought to contribute to the progression of the neovascular form of age-related macular degeneration (AMD). | Ranibizumab binds to the receptor binding site of active forms of VEGF-A, including the biologically active, cleaved form of this molecule, (VEGF110). The binding of ranibizumab to VEGF-A prevents the interaction of VEGF-A with its receptors (VEGFR1 and VEGFR2) on the surface of endothelial cells, reducing endothelial cell proliferation, vascular leakage, and new blood vessel formation. | There is no information available regarding the LD50 values of ranibizumab. There is also limited clinical experience of ranibizumab overdose: concentrated doses as high as 2 mg ranibizumab in 0.05 mL have been administered to patients, with no additional unexpected adverse reactions that were observed | The metabolism of ranibizumab has not been studied. Since it is a monoclonal antibody fragment, ranibizumab is expected to undergo catabolism. | Ranibizumab rapidly penetrates through the retina to reach the choroid after intravitreal injection. Following monthly intravitreal administration of 0.5 mg ranibizumab in patients with neovascular (wet) age-related macular degeneration, the mean Cmax (±SD) was 1.7 (± 1.1) ng/mL. Following an implant insertion, the mean (±SD) Cmax of ranibizumab was 0.48 (±0.17) ng/mL and median Tmax was 26 days, with a range of one to 89 days. | The apparent volume of the central compartment (Vd/F) is 2.77 L. Ranibizumab is not shown to accumulate in serum. Due to its small size from lacking the Fc region of an antibody, ranibizumab achieves enhanced diffusion into the retina and choroid | In patients with retinal vein occlusion or diabetic macular edema, the apparent clearance (CL/F) of ranibizumab was 24.8 L/day. | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineovascularisation Agents,Blood Proteins,EENT Drugs, Miscellaneous,Globulins,Growth Inhibitors,Growth Substances,Immunoglobulins,Immunoproteins,Ocular Vascular Disorder Agents,Ophthalmics,Ophthalmologicals,Proteins,Sensory Organs,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors | CA2286330 | 10-Jun-2008 | 3-Apr-2018 | NA | Vascular endothelial growth factor A | Susvimo | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10565 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | ILARIS | Novartis Pharmaceuticals | Novartis Pharmaceuticals | Cryopyrin-Associated Periodic Syndromes (CAPS), Familial Cold Autoinflammatory Syndrome (FCAS), Muckle-Wells Syndrome (MWS), Systemic Juvenile Idiopathic Arthritis (SJIA) | NA | Reconstitution with 1 mL of preservative-free Sterile Water for Injection is required prior to subcutaneous administration of the drug. The reconstituted canakinumab is a 150 mg/mL solution essentially free of particulates, clear to slightly opalescent, and is colorless or may have a slightly brownish-yellow tint. A volume of up to 1 mL can be withdrawn for delivery of 150 mg/mL canakinumab for subcutaneous administration. Each reconstituted vial contains 180 mg canakinumab, sucrose, L-histidine, L-histidine HCL monohydrate, polysorbate 80 and Sterile Water for Injection. No preservatives are present. | 180 mg of canakinumab as a white, preservative-free, lyophilized powder | Subcutaneous | Cryopyrin-Associated Periodic Syndromes (CAPS): The recommended dose of ILARIS is 150 mg for CAPS patients with body weight greater than 40 kg. For CAPS patients with body weight greater than or equal to 15 kg and less than or equal to 40 kg, the recommended dose is 2 mg/kg. For children 15 to 40 kg with an inadequate response, the dose can be increased to 3 mg/kg. Systemic Juvenile Idiopathic Arthritis (SJIA): The recommended dose of ILARIS for SJIA patients with a body weight greater than or equal to 7.5 kg is 4mg/kg (with a maximum of 300 mg) administered every four weeks via subcutaneous injection. | Confirmed hypersensitivity to the active substance or to any of the excipients. | ILARIS has been associated with an increased risk of serious infections, Immunosuppression, Hypersensitivity , Live vaccines should not be given concurrently with ILARIS. | Link | NA | NA |
| 10566 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis Pharmaceuticals Corporation | Novartis Pharmaceuticals Corporation | NA | NA | NA | Injection, powder, lyophilized, for solution | Subcutaneous | 150 mg/1mL | NA | NA | NA | NA | NA |
| 10567 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis Pharmaceuticals Corporation | Novartis Pharmaceuticals Corporation | NA | NA | NA | Injection, solution | Subcutaneous | 150 mg/1mL | NA | NA | NA | NA | NA |
| 10568 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis | Novartis | NA | NA | NA | Powder, for solution | Subcutaneous | 150 mg / vial | NA | NA | NA | NA | NA |
| 10569 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis | Novartis | NA | NA | NA | Solution | Subcutaneous | 150 mg / mL | NA | NA | NA | NA | NA |
| 10570 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis Europharm Limited | Novartis Europharm Limited | NA | NA | NA | Injection, powder, for solution | Subcutaneous | 150 mg | NA | NA | NA | NA | NA |
| 10571 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis Europharm Limited | Novartis Europharm Limited | NA | NA | NA | Injection, powder, for solution | Subcutaneous | 150 mg | NA | NA | NA | NA | NA |
| 10572 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis Europharm Limited | Novartis Europharm Limited | NA | NA | NA | Injection, powder, for solution | Subcutaneous | 150 mg | NA | NA | NA | NA | NA |
| 10573 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis Europharm Limited | Novartis Europharm Limited | NA | NA | NA | Injection, solution | Subcutaneous | 150 mg/ml | NA | NA | NA | NA | NA |
| 10574 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10575 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 |
| 10588 | Th1121 | Pertuzumab | >Th1121_Pertuzumab EVQLVESGGGLVQPGGSLRLSCAASGFTFTDYTMDWVRQAPGKGLEWVADVNPNSGGSIYNQRFKGRFTLSVDRSKNTLYLQMNSLRAEDTAVYYCARNLGPSFYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 148000 | NA | NA | NA | NA | 18 days | Recombinant, humanized monoclonal antibody that targets the extracellular dimerization domain (Subdomain II) of the human epidermal growth factor receptor 2 protein (HER2). Two heavy chains and two lights chains are composed of 448 and 214 residues respectively. FDA approved June 8, 2012. | Pertuzumab is indicated for use in combination with trastuzumab and docetaxel for the treatment of patients with HER2-positive metastatic breast cancer who have not received prior anti-HER2 therapy or chemotherapy for metastatic disease. | NA | Pertuzumab is a humanized monoclonal antibody designed to bind to the HER2 receptor and inhibit the ability of HER2 to interact with other HER family members (HER1, HER2, HER3, and HER4) on the surface of cancer cells. The HER signaling pathway plays a role in the formation and growth of numerous cancers, and previous clinical trials of pertuzumab in a single agent setting had suggested clinical activity - including stable disease - in heavily pretreated patients with advanced ovarian and breast cancers. | There are no data regarding overdose of pertuzumab. Single doses higher than 25 mg/kg have not been tested.[L14747] Symptoms of overdose are likely to be consistent with pertuzumab's adverse effect profile, and may therefore involve significant diarrhea, alopecia, neutropenia, nausea, fatigue, rash, and/or peripheral neuropathy.[L14642] Pertuzumab has been associated with the development of left ventricular dysfunction (i.e. cardiotoxicity) that may be exacerbated in instances of overdose.[L14642] | The metabolism of pertuzumab has not been studied directly. Monoclonal antibodies are typically subject to catabolism to smaller peptides and proteins prior to elimination.[L14747] | Intravenously administered pertuzumab, given as a loading dose of 840mg followed by a maintenance dose of 420mg every 3 weeks, reaches steady-state concentration following the first maintenance dose.[L14747] In its subcutaneous formulation, in combination with [hylauronidase], the absolute bioavailability of pertuzumab is approximately 0.7 and the median Tmax is 4 days.[L14531] This subcutaneous formulation leverages the benefits of co-administration with hyaluronidase - this enzyme breaks down hylauronic acid, thereby decreasing the viscosity of the extracellular matrix (ECM) and allowing for greater bioavailability with subcutaneous administration.[L14531] | The average steady-state volume of distribution following intravenous administration is 3.53 - 7.5 L.[L14747] | The median clearance of pertuzumab was determined to be 0.24 L/day based on a population pharmacokinetic analysis.[L14642] | Monoclonal antibodies | CA2376596 | 10-Jun-2009 | 23-06-2020 | NA | Receptor tyrosine-protein kinase erbB-2 | Perjeta | Genentech | Genentech | Neoadjuvant Treatment of Breast Cancer, Metastatic Breast Cancer (MBC), | NA | Each single use vial contains 420 mg of pertuzumab at a concentration of 30 mg/mL in 20 mM L-histidine acetate (pH 6.0), 120 mM sucrose and 0.02% polysorbate 20 | Sterile, clear to slightly opalescent, colorless to pale brown liquid | Intravenous infusion | The initial dose of PERJETA is 840 mg administered as a 60-minute Intravenous infusion, followed every 3 weeks by a dose of 420 mg administered as an Intravenous infusion over 30 to 60 minutes. When administered with PERJETA, the recommended initial dose of trastuzumab is 8 mg/kg administered as a 90-minute Intravenous infusion, followed every 3 weeks by a dose of 6 mg/kg administered as an Intravenous infusion over 30 to 90 minutes.PERJETA, trastuzumab, and docetaxel should be administered sequentially. PERJETA and trastuzumab can be given in any order. Docetaxel should be administered after PERJETA and trastuzumab. An observation period of 30 to 60 minutes is recommended after each PERJETA infusion and before commencement of any subsequent infusion of trastuzumab. | NA | Embryo-Fetal Toxicity , Left Ventricular Dysfunction , Infusion-Related Reactions, Hypersensitivity Reactions. | Link | NA | NA |
| 10589 | Th1121 | Pertuzumab | >Th1121_Pertuzumab EVQLVESGGGLVQPGGSLRLSCAASGFTFTDYTMDWVRQAPGKGLEWVADVNPNSGGSIYNQRFKGRFTLSVDRSKNTLYLQMNSLRAEDTAVYYCARNLGPSFYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | NA | NA | NA | NA | NA | 18 days | Recombinant, humanized monoclonal antibody that targets the extracellular dimerization domain (Subdomain II) of the human epidermal growth factor receptor 2 protein (HER2). Two heavy chains and two lights chains are composed of 448 and 214 residues respectively. FDA approved June 8, 2012. | Pertuzumab is indicated for use in combination with trastuzumab and docetaxel for the treatment of patients with HER2-positive metastatic breast cancer who have not received prior anti-HER2 therapy or chemotherapy for metastatic disease. | NA | Pertuzumab is a humanized monoclonal antibody designed to bind to the HER2 receptor and inhibit the ability of HER2 to interact with other HER family members (HER1, HER2, HER3, and HER4) on the surface of cancer cells. The HER signaling pathway plays a role in the formation and growth of numerous cancers, and previous clinical trials of pertuzumab in a single agent setting had suggested clinical activity - including stable disease - in heavily pretreated patients with advanced ovarian and breast cancers. | There are no data regarding overdose of pertuzumab. Single doses higher than 25 mg/kg have not been tested.[L14747] Symptoms of overdose are likely to be consistent with pertuzumab's adverse effect profile, and may therefore involve significant diarrhea, alopecia, neutropenia, nausea, fatigue, rash, and/or peripheral neuropathy.[L14642] Pertuzumab has been associated with the development of left ventricular dysfunction (i.e. cardiotoxicity) that may be exacerbated in instances of overdose.[L14642] | The metabolism of pertuzumab has not been studied directly. Monoclonal antibodies are typically subject to catabolism to smaller peptides and proteins prior to elimination.[L14747] | Intravenously administered pertuzumab, given as a loading dose of 840mg followed by a maintenance dose of 420mg every 3 weeks, reaches steady-state concentration following the first maintenance dose.[L14747] In its subcutaneous formulation, in combination with [hylauronidase], the absolute bioavailability of pertuzumab is approximately 0.7 and the median Tmax is 4 days.[L14531] This subcutaneous formulation leverages the benefits of co-administration with hyaluronidase - this enzyme breaks down hylauronic acid, thereby decreasing the viscosity of the extracellular matrix (ECM) and allowing for greater bioavailability with subcutaneous administration.[L14531] | The average steady-state volume of distribution following intravenous administration is 3.53 - 7.5 L.[L14747] | The median clearance of pertuzumab was determined to be 0.24 L/day based on a population pharmacokinetic analysis.[L14642] | Monoclonal antibodies | CA2579861 | 18-12-2012 | 19-10-2025 | NA | Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10598 | Th1123 | Denosumab | >Th1123_Denosumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYAMSWVRQAPGKGLEWVSGITGSGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDPGTTVIMSWFDPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144700 | C6404H9912N1724O2004S50 | NA | NA | NA | 25.4 days | Novel, fully human IgG2 monoclonal antibody, specific to receptor activator of nuclear factor kappa-B ligand (RANKL). It suppresses bone resorption markers in patients suffering from metastatic tumors and is being investigated in multiple clinical trials for the prevention and treatment of bone metastases. Each light chain consists of 215 amino acids and the heavy chain consists of 448 amino acids. FDA approved on June 1, 2010. | Prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It reduces the incidence of vertebral, nonvertebral, and hip fractures. Prolia is also indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. It can also be used in men with osteoporosis at high risk for fracture or in men receiving androgen deprivation therapy for nonmetastatic prostate cancer to increase bone mass. Xgeva is indicated for the prevention of skeletal-related events in patients with bone metastases from solid tumors. | In clinical studies, treatment with 60 mg of Prolia resulted in reduction in the bone resorption marker serum type 1 C-telopeptide (CTX) by approximately 85% by 3 days. Consistent with the physiological coupling of bone formation and resorption in skeletal remodeling, subsequent reductions in bone formation markers (i.e. osteocalcin and procollagen type 1 N-terminal peptide [PlNP]) were observed starting 1 month after the first dose of Prolia. | Denosumab is designed to target RANKL (RANK ligand), a protein that acts as the primary signal to promote bone removal/resorption. In many bone loss conditions, RANKL overwhelms the body's natural defense against bone destruction. Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone. | In patients with postmenopausal osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, pain in extremity, hypercholesterolemia, musculoskeletal pain, and cystitis. Pancreatitis has been reported in clinical trials. In male patients with osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, arthralgia, and nasopharyngitis. In patients experiencing bone loss due to hormone ablation for cancer, the most common adverse reactions (= 10% and more common than placebo) were: arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials | NA | When 60 mg of denosumab was subcutaneously administered to healthy subjects after fasting for 12 hours, the pharmacokinetic parameters are as follows: Cmax = 6.75 mcg/mL; Tmax= 10 days (range of 3 to 21 days); AUC (0-16 weeks) = 316 mcg•day/mL. Denosumab does not accumulate following multiple doses once every 6 months. The pharmacokinetics of denosumab were not affected by the formation of antibodies. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Bone Density Conservation Agents,Cancer immunotherapy,Drugs Affecting Bone Structure and Mineralization,Drugs for Treatment of Bone Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Musculo-Skeletal System,Proteins,RANK Ligand Blocking Activity,RANK Ligand Inhibitor,Serum Globulins | CA2257247 | 9-Nov-2012 | 15-04-2018 | NA | Tumor necrosis factor ligand superfamily member 11 | Xgeva | Amgen. | Amgen. | Bone Metastasis From Solid Tumors, Giant Cell Tumor Of Bone, Hypercalcemia Of Malignancy | NA | Each single-use vial of Xgeva contains 120 mg denosumab, acetate (18 mM), sorbitol (4.6%), Water for Injection (USP), and sodium hydroxide to a pH of 5.2 | Sterile, preservative-free, clear, colorless to pale yellow solution | NA | Bone Metastasis From Solid Tumors: The recommended dose of Xgeva is 120 mg administered as a subcutaneous injection every 4 weeks. Administer calcium and vitamin D as necessary to treat or prevent hypocalcemia.; Giant Cell Tumor Of Bone: The recommended dose of Xgeva is 120 mg administered every 4 weeks with additional 120 mg doses on Days 8 and 15 of the first month of therapy. Administer calcium and vitamin D as necessary to treat or prevent hypocalcemia.; Hypercalcemia Of Malignancy: The recommended dose of Xgeva is 120 mg administered every 4 weeks with additional 120 mg doses on Days 8 and 15 of the first month of therapy. | Xgeva is not indicated for the prevention of skeletal-related events in patients with multiple myeloma. | Hypocalcemia, Osteonecrosis of the Jaw. | Link | NA | NA |
| 10599 | Th1123 | Denosumab | >Th1123_Denosumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYAMSWVRQAPGKGLEWVSGITGSGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDPGTTVIMSWFDPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144700 | C6404H9912N1724O2004S50 | NA | NA | NA | 25.4 days | Novel, fully human IgG2 monoclonal antibody, specific to receptor activator of nuclear factor kappa-B ligand (RANKL). It suppresses bone resorption markers in patients suffering from metastatic tumors and is being investigated in multiple clinical trials for the prevention and treatment of bone metastases. Each light chain consists of 215 amino acids and the heavy chain consists of 448 amino acids. FDA approved on June 1, 2010. | Prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It reduces the incidence of vertebral, nonvertebral, and hip fractures. Prolia is also indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. It can also be used in men with osteoporosis at high risk for fracture or in men receiving androgen deprivation therapy for nonmetastatic prostate cancer to increase bone mass. Xgeva is indicated for the prevention of skeletal-related events in patients with bone metastases from solid tumors. | In clinical studies, treatment with 60 mg of Prolia resulted in reduction in the bone resorption marker serum type 1 C-telopeptide (CTX) by approximately 85% by 3 days. Consistent with the physiological coupling of bone formation and resorption in skeletal remodeling, subsequent reductions in bone formation markers (i.e. osteocalcin and procollagen type 1 N-terminal peptide [PlNP]) were observed starting 1 month after the first dose of Prolia. | Denosumab is designed to target RANKL (RANK ligand), a protein that acts as the primary signal to promote bone removal/resorption. In many bone loss conditions, RANKL overwhelms the body's natural defense against bone destruction. Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone. | In patients with postmenopausal osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, pain in extremity, hypercholesterolemia, musculoskeletal pain, and cystitis. Pancreatitis has been reported in clinical trials. In male patients with osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, arthralgia, and nasopharyngitis. In patients experiencing bone loss due to hormone ablation for cancer, the most common adverse reactions (= 10% and more common than placebo) were: arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials | NA | When 60 mg of denosumab was subcutaneously administered to healthy subjects after fasting for 12 hours, the pharmacokinetic parameters are as follows: Cmax = 6.75 mcg/mL; Tmax= 10 days (range of 3 to 21 days); AUC (0-16 weeks) = 316 mcg•day/mL. Denosumab does not accumulate following multiple doses once every 6 months. The pharmacokinetics of denosumab were not affected by the formation of antibodies. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Bone Density Conservation Agents,Cancer immunotherapy,Drugs Affecting Bone Structure and Mineralization,Drugs for Treatment of Bone Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Musculo-Skeletal System,Proteins,RANK Ligand Blocking Activity,RANK Ligand Inhibitor,Serum Globulins | CA2274987 | 24-01-2012 | 22-12-2017 | NA | Tumor necrosis factor ligand superfamily member 11 | Prolia | Amgen. | Amgen. | Treatment Of Postmenopausal Women With Osteoporosis At High Risk For Fracture,Treatment To Increase Bone Mass In Men With Osteoporosis, Treatment Of Bone Loss In Men Receiving Androgen Deprivation Therapy For Prostate Cancer, Treatment Of Bone Loss In Women Receiving Adjuvant Aromatase Inhibitor Therapy For Breast Cancer | NA | Each 1 mL single-use prefilled syringe of Prolia contains 60 mg denosumab (60 mg/mL solution), 4.7% sorbitol, 17 mM acetate, 0.01% polysorbate 20, Water for Injection (USP), and sodium hydroxide to a pH of 5.2. Each 1 mL single-use vial of Prolia contains 60 mg denosumab (60 mg/mL solution), 4.7% sorbitol, 17 mM acetate, Water for Injection (USP), and sodium hydroxide to a pH of 5.2 | Sterile, preservative-free, clear, colorless to pale yellow solution | NA | NA | Hypocalcemia. Pregnancy. Hypersensitivity | Hypocalcemia, Serious Infections, Dermatologic Adverse Reactions, Osteonecrosis of the Jaw, Atypical Subtrochanteric and Diaphyseal Femoral Fractures | Link | NA | NA |
| 10600 | Th1123 | Denosumab | >Th1123_Denosumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYAMSWVRQAPGKGLEWVSGITGSGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDPGTTVIMSWFDPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144700 | C6404H9912N1724O2004S50 | NA | NA | NA | 25.4 days | Novel, fully human IgG2 monoclonal antibody, specific to receptor activator of nuclear factor kappa-B ligand (RANKL). It suppresses bone resorption markers in patients suffering from metastatic tumors and is being investigated in multiple clinical trials for the prevention and treatment of bone metastases. Each light chain consists of 215 amino acids and the heavy chain consists of 448 amino acids. FDA approved on June 1, 2010. | Prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It reduces the incidence of vertebral, nonvertebral, and hip fractures. Prolia is also indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. It can also be used in men with osteoporosis at high risk for fracture or in men receiving androgen deprivation therapy for nonmetastatic prostate cancer to increase bone mass. Xgeva is indicated for the prevention of skeletal-related events in patients with bone metastases from solid tumors. | In clinical studies, treatment with 60 mg of Prolia resulted in reduction in the bone resorption marker serum type 1 C-telopeptide (CTX) by approximately 85% by 3 days. Consistent with the physiological coupling of bone formation and resorption in skeletal remodeling, subsequent reductions in bone formation markers (i.e. osteocalcin and procollagen type 1 N-terminal peptide [PlNP]) were observed starting 1 month after the first dose of Prolia. | Denosumab is designed to target RANKL (RANK ligand), a protein that acts as the primary signal to promote bone removal/resorption. In many bone loss conditions, RANKL overwhelms the body's natural defense against bone destruction. Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone. | In patients with postmenopausal osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, pain in extremity, hypercholesterolemia, musculoskeletal pain, and cystitis. Pancreatitis has been reported in clinical trials. In male patients with osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, arthralgia, and nasopharyngitis. In patients experiencing bone loss due to hormone ablation for cancer, the most common adverse reactions (= 10% and more common than placebo) were: arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials | NA | When 60 mg of denosumab was subcutaneously administered to healthy subjects after fasting for 12 hours, the pharmacokinetic parameters are as follows: Cmax = 6.75 mcg/mL; Tmax= 10 days (range of 3 to 21 days); AUC (0-16 weeks) = 316 mcg•day/mL. Denosumab does not accumulate following multiple doses once every 6 months. The pharmacokinetics of denosumab were not affected by the formation of antibodies. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Bone Density Conservation Agents,Cancer immunotherapy,Drugs Affecting Bone Structure and Mineralization,Drugs for Treatment of Bone Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Musculo-Skeletal System,Proteins,RANK Ligand Blocking Activity,RANK Ligand Inhibitor,Serum Globulins | CA2285746 | 28-09-2010 | 15-04-2018 | NA | Tumor necrosis factor ligand superfamily member 11 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10601 | Th1123 | Denosumab | >Th1123_Denosumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYAMSWVRQAPGKGLEWVSGITGSGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDPGTTVIMSWFDPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144700 | C6404H9912N1724O2004S50 | NA | NA | NA | 25.4 days | Novel, fully human IgG2 monoclonal antibody, specific to receptor activator of nuclear factor kappa-B ligand (RANKL). It suppresses bone resorption markers in patients suffering from metastatic tumors and is being investigated in multiple clinical trials for the prevention and treatment of bone metastases. Each light chain consists of 215 amino acids and the heavy chain consists of 448 amino acids. FDA approved on June 1, 2010. | Prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It reduces the incidence of vertebral, nonvertebral, and hip fractures. Prolia is also indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. It can also be used in men with osteoporosis at high risk for fracture or in men receiving androgen deprivation therapy for nonmetastatic prostate cancer to increase bone mass. Xgeva is indicated for the prevention of skeletal-related events in patients with bone metastases from solid tumors. | In clinical studies, treatment with 60 mg of Prolia resulted in reduction in the bone resorption marker serum type 1 C-telopeptide (CTX) by approximately 85% by 3 days. Consistent with the physiological coupling of bone formation and resorption in skeletal remodeling, subsequent reductions in bone formation markers (i.e. osteocalcin and procollagen type 1 N-terminal peptide [PlNP]) were observed starting 1 month after the first dose of Prolia. | Denosumab is designed to target RANKL (RANK ligand), a protein that acts as the primary signal to promote bone removal/resorption. In many bone loss conditions, RANKL overwhelms the body's natural defense against bone destruction. Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone. | In patients with postmenopausal osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, pain in extremity, hypercholesterolemia, musculoskeletal pain, and cystitis. Pancreatitis has been reported in clinical trials. In male patients with osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, arthralgia, and nasopharyngitis. In patients experiencing bone loss due to hormone ablation for cancer, the most common adverse reactions (= 10% and more common than placebo) were: arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials | NA | When 60 mg of denosumab was subcutaneously administered to healthy subjects after fasting for 12 hours, the pharmacokinetic parameters are as follows: Cmax = 6.75 mcg/mL; Tmax= 10 days (range of 3 to 21 days); AUC (0-16 weeks) = 316 mcg•day/mL. Denosumab does not accumulate following multiple doses once every 6 months. The pharmacokinetics of denosumab were not affected by the formation of antibodies. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Bone Density Conservation Agents,Cancer immunotherapy,Drugs Affecting Bone Structure and Mineralization,Drugs for Treatment of Bone Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Musculo-Skeletal System,Proteins,RANK Ligand Blocking Activity,RANK Ligand Inhibitor,Serum Globulins | CA2400929 | 31-05-2011 | 23-02-2021 | NA | Tumor necrosis factor ligand superfamily member 11 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10602 | Th1123 | Denosumab | >Th1123_Denosumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYAMSWVRQAPGKGLEWVSGITGSGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDPGTTVIMSWFDPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144700 | C6404H9912N1724O2004S50 | NA | NA | NA | 25.4 days | Novel, fully human IgG2 monoclonal antibody, specific to receptor activator of nuclear factor kappa-B ligand (RANKL). It suppresses bone resorption markers in patients suffering from metastatic tumors and is being investigated in multiple clinical trials for the prevention and treatment of bone metastases. Each light chain consists of 215 amino acids and the heavy chain consists of 448 amino acids. FDA approved on June 1, 2010. | Prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It reduces the incidence of vertebral, nonvertebral, and hip fractures. Prolia is also indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. It can also be used in men with osteoporosis at high risk for fracture or in men receiving androgen deprivation therapy for nonmetastatic prostate cancer to increase bone mass. Xgeva is indicated for the prevention of skeletal-related events in patients with bone metastases from solid tumors. | In clinical studies, treatment with 60 mg of Prolia resulted in reduction in the bone resorption marker serum type 1 C-telopeptide (CTX) by approximately 85% by 3 days. Consistent with the physiological coupling of bone formation and resorption in skeletal remodeling, subsequent reductions in bone formation markers (i.e. osteocalcin and procollagen type 1 N-terminal peptide [PlNP]) were observed starting 1 month after the first dose of Prolia. | Denosumab is designed to target RANKL (RANK ligand), a protein that acts as the primary signal to promote bone removal/resorption. In many bone loss conditions, RANKL overwhelms the body's natural defense against bone destruction. Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone. | In patients with postmenopausal osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, pain in extremity, hypercholesterolemia, musculoskeletal pain, and cystitis. Pancreatitis has been reported in clinical trials. In male patients with osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, arthralgia, and nasopharyngitis. In patients experiencing bone loss due to hormone ablation for cancer, the most common adverse reactions (= 10% and more common than placebo) were: arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials | NA | When 60 mg of denosumab was subcutaneously administered to healthy subjects after fasting for 12 hours, the pharmacokinetic parameters are as follows: Cmax = 6.75 mcg/mL; Tmax= 10 days (range of 3 to 21 days); AUC (0-16 weeks) = 316 mcg•day/mL. Denosumab does not accumulate following multiple doses once every 6 months. The pharmacokinetics of denosumab were not affected by the formation of antibodies. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Bone Density Conservation Agents,Cancer immunotherapy,Drugs Affecting Bone Structure and Mineralization,Drugs for Treatment of Bone Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Musculo-Skeletal System,Proteins,RANK Ligand Blocking Activity,RANK Ligand Inhibitor,Serum Globulins | CA2328140 | 13-03-2012 | 13-05-2019 | NA | Tumor necrosis factor ligand superfamily member 11 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10603 | Th1123 | Denosumab | >Th1123_Denosumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYAMSWVRQAPGKGLEWVSGITGSGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDPGTTVIMSWFDPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144700 | C6404H9912N1724O2004S50 | NA | NA | NA | 25.4 days | Novel, fully human IgG2 monoclonal antibody, specific to receptor activator of nuclear factor kappa-B ligand (RANKL). It suppresses bone resorption markers in patients suffering from metastatic tumors and is being investigated in multiple clinical trials for the prevention and treatment of bone metastases. Each light chain consists of 215 amino acids and the heavy chain consists of 448 amino acids. FDA approved on June 1, 2010. | Prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It reduces the incidence of vertebral, nonvertebral, and hip fractures. Prolia is also indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. It can also be used in men with osteoporosis at high risk for fracture or in men receiving androgen deprivation therapy for nonmetastatic prostate cancer to increase bone mass. Xgeva is indicated for the prevention of skeletal-related events in patients with bone metastases from solid tumors. | In clinical studies, treatment with 60 mg of Prolia resulted in reduction in the bone resorption marker serum type 1 C-telopeptide (CTX) by approximately 85% by 3 days. Consistent with the physiological coupling of bone formation and resorption in skeletal remodeling, subsequent reductions in bone formation markers (i.e. osteocalcin and procollagen type 1 N-terminal peptide [PlNP]) were observed starting 1 month after the first dose of Prolia. | Denosumab is designed to target RANKL (RANK ligand), a protein that acts as the primary signal to promote bone removal/resorption. In many bone loss conditions, RANKL overwhelms the body's natural defense against bone destruction. Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone. | In patients with postmenopausal osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, pain in extremity, hypercholesterolemia, musculoskeletal pain, and cystitis. Pancreatitis has been reported in clinical trials. In male patients with osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, arthralgia, and nasopharyngitis. In patients experiencing bone loss due to hormone ablation for cancer, the most common adverse reactions (= 10% and more common than placebo) were: arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials | NA | When 60 mg of denosumab was subcutaneously administered to healthy subjects after fasting for 12 hours, the pharmacokinetic parameters are as follows: Cmax = 6.75 mcg/mL; Tmax= 10 days (range of 3 to 21 days); AUC (0-16 weeks) = 316 mcg•day/mL. Denosumab does not accumulate following multiple doses once every 6 months. The pharmacokinetics of denosumab were not affected by the formation of antibodies. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Bone Density Conservation Agents,Cancer immunotherapy,Drugs Affecting Bone Structure and Mineralization,Drugs for Treatment of Bone Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Musculo-Skeletal System,Proteins,RANK Ligand Blocking Activity,RANK Ligand Inhibitor,Serum Globulins | NA | NA | NA | NA | Tumor necrosis factor ligand superfamily member 11 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10611 | Th1125 | Golimumab | NA | 146943.2 | C6530H10068N1752O2026S44 | NA | NA | NA | About 2 weeks | Human IgG1Ò› monoclonal antibody derived from immunizing genetically engineered mice with human TNFα. It binds and inhibits soluble and transmembrane human TNFα. Increased TNFα is associated with chronic inflammation. Thus golimumab is indicated for use in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. In the U.S. and Canada, golimumab is marketed under the brand name Simponi. The FDA label includes a black box warning of serious infections and malignancy. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | Used in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. | Golimumab inhibits the activity of the cytokine, tumor necrosis factor alpha (TNFα). In areas such as the joints and blood, increased TNFαis associated with chronic inflammation seen in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Thus golimumab decreases the inflammation in these conditions. Concerning ulcerative colitis, the physiological effects of golimumab has yet to be determined. | As a human monoclonal antibody, golimumab binds and inhibits soluble and transmembrane human TNFα. Inhibition of TNFα prevents it binding to its receptors, which prevents both leukocyte infiltration through prevention of cell adhesion proteins such as E-selectin, ICAM-1 and VCAM-1, and pro-inflammatory cytokine secretion such as IL-6, IL-8, G-CSF and GM-CSF in vitro. Consequently, in patients with chronic inflammatory conditions, decreases in ICAM-1 and IL-6 as well as C-reactive protein (CRP), matrix metalloproteinase 3 (MMP-3), and vascular endothelial growth factor (VEGF) were observed. | The FDA label includes a black box warning of serious infections and malignancy. Specifically there have been hospitalizations or death from infections such as bacterial sepsis, tuberculosis (TB), and invasive fungal (histoplasmosis) and other opportunistic infections. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | The metabolism of golimumab has yet to be determined. | After subcutaneous administration, golimumab can achieve maximum serum concentrations in 2 to 6 days and has an approximate bioavailability of 53%. In healthy volunteers, the maximum average concentration reached was 3.2 ± 1.4 µg/mL. | After IV administration, golimumab has a volume of distribution of about 58 to 126 mL/kg. This means that golimumab stays mostly in the circulatory system. | After one IV dose of golimumab, the systemic clearance was about 4.9 to 6.7 mL/day/kg. | Antipsoriatic Agents and Monoclonal antibodies and TNF inhibitor | NA | NA | NA | NA | Tumor necrosis factor | Simponi Injection | NA | NA | Rheumatoid Arthritis, Psoriatic Arthritis, Ankylosing Spondylitis, Ulcerative Colitis | NA | pH of approximately 5.5. SIMPONI is provided in two strengths: 50 mg of the golimumab antibody in 0.5 mL of solution and 100 mg of the golimumab antibody in 1 mL of solution. In the 50 mg strength, 0.5 mL of SIMPONI contains 50 mg of the golimumab antibody, 0.44 mg of L-histidine and L-histidine monohydrochloride monohydrate, 20.5 mg of sorbitol, 0.08 mg of polysorbate 80, and Water for Injection. In the 100 mg strength, 1 mL of SIMPONI contains 100 mg of the golimumab antibody, 0.87 mg of L-histidine and L-histidine monohydrochloride monohydrate, 41.0 mg of sorbitol, 0.15 mg of polysorbate 80, and Water for Injection. | The solution is clear to slightly opalescent, colorless to light yellow | Subcutaneous | 50 mg once a month | NA | sepsis, alanine aminotransferase, aspartate aminotransferase, tuberculosis, anemia | Link | NA | NA |
| 10612 | Th1125 | Golimumab | NA | 146943.2 | C6530H10068N1752O2026S44 | NA | NA | NA | About 2 weeks | Human IgG1Ò› monoclonal antibody derived from immunizing genetically engineered mice with human TNFα. It binds and inhibits soluble and transmembrane human TNFα. Increased TNFα is associated with chronic inflammation. Thus golimumab is indicated for use in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. In the U.S. and Canada, golimumab is marketed under the brand name Simponi. The FDA label includes a black box warning of serious infections and malignancy. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | Used in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. | Golimumab inhibits the activity of the cytokine, tumor necrosis factor alpha (TNFα). In areas such as the joints and blood, increased TNFαis associated with chronic inflammation seen in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Thus golimumab decreases the inflammation in these conditions. Concerning ulcerative colitis, the physiological effects of golimumab has yet to be determined. | As a human monoclonal antibody, golimumab binds and inhibits soluble and transmembrane human TNFα. Inhibition of TNFα prevents it binding to its receptors, which prevents both leukocyte infiltration through prevention of cell adhesion proteins such as E-selectin, ICAM-1 and VCAM-1, and pro-inflammatory cytokine secretion such as IL-6, IL-8, G-CSF and GM-CSF in vitro. Consequently, in patients with chronic inflammatory conditions, decreases in ICAM-1 and IL-6 as well as C-reactive protein (CRP), matrix metalloproteinase 3 (MMP-3), and vascular endothelial growth factor (VEGF) were observed. | The FDA label includes a black box warning of serious infections and malignancy. Specifically there have been hospitalizations or death from infections such as bacterial sepsis, tuberculosis (TB), and invasive fungal (histoplasmosis) and other opportunistic infections. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | The metabolism of golimumab has yet to be determined. | After subcutaneous administration, golimumab can achieve maximum serum concentrations in 2 to 6 days and has an approximate bioavailability of 53%. In healthy volunteers, the maximum average concentration reached was 3.2 ± 1.4 µg/mL. | After IV administration, golimumab has a volume of distribution of about 58 to 126 mL/kg. This means that golimumab stays mostly in the circulatory system. | After one IV dose of golimumab, the systemic clearance was about 4.9 to 6.7 mL/day/kg. | Antipsoriatic Agents and Monoclonal antibodies and TNF inhibitor | NA | NA | NA | NA | Tumor necrosis factor | Simponi Aria | NA | NA | rheumatoid arthritis. | NA | SIMPONI ARIA does not contain preservatives, natural rubber or latex. The solution is colorless to light yellow with a pH of approximately 5.5. Each 4 mL vial of SIMPONI ARIA contains 50 mg golimumab, 9.5 mM histidine, 4.5% (w/v) sorbitol, and 0.015% (w/v) polysorbate 80. | The SIMPONI ARIA drug product is a sterile concentrated solution of the golimumab antibody supplied in a 4 mL glass vial for Intravenous infusion. | Intravenous infusion | 2 mg per kg | NA | sepsis, pneumonia, cellulitis, abscess, opportunistic infections, tuberculosis (TB), and invasive fungal infections, Malignancies, Liver Enzyme Elevations, Autoimmune Disorders And Autoantibodies | Link | NA | NA |
| 10613 | Th1125 | Golimumab | NA | 146943.2 | C6530H10068N1752O2026S44 | NA | NA | NA | About 2 weeks | Human IgG1Ò› monoclonal antibody derived from immunizing genetically engineered mice with human TNFα. It binds and inhibits soluble and transmembrane human TNFα. Increased TNFα is associated with chronic inflammation. Thus golimumab is indicated for use in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. In the U.S. and Canada, golimumab is marketed under the brand name Simponi. The FDA label includes a black box warning of serious infections and malignancy. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | Used in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. | Golimumab inhibits the activity of the cytokine, tumor necrosis factor alpha (TNFα). In areas such as the joints and blood, increased TNFαis associated with chronic inflammation seen in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Thus golimumab decreases the inflammation in these conditions. Concerning ulcerative colitis, the physiological effects of golimumab has yet to be determined. | As a human monoclonal antibody, golimumab binds and inhibits soluble and transmembrane human TNFα. Inhibition of TNFα prevents it binding to its receptors, which prevents both leukocyte infiltration through prevention of cell adhesion proteins such as E-selectin, ICAM-1 and VCAM-1, and pro-inflammatory cytokine secretion such as IL-6, IL-8, G-CSF and GM-CSF in vitro. Consequently, in patients with chronic inflammatory conditions, decreases in ICAM-1 and IL-6 as well as C-reactive protein (CRP), matrix metalloproteinase 3 (MMP-3), and vascular endothelial growth factor (VEGF) were observed. | The FDA label includes a black box warning of serious infections and malignancy. Specifically there have been hospitalizations or death from infections such as bacterial sepsis, tuberculosis (TB), and invasive fungal (histoplasmosis) and other opportunistic infections. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | The metabolism of golimumab has yet to be determined. | After subcutaneous administration, golimumab can achieve maximum serum concentrations in 2 to 6 days and has an approximate bioavailability of 53%. In healthy volunteers, the maximum average concentration reached was 3.2 ± 1.4 µg/mL. | After IV administration, golimumab has a volume of distribution of about 58 to 126 mL/kg. This means that golimumab stays mostly in the circulatory system. | After one IV dose of golimumab, the systemic clearance was about 4.9 to 6.7 mL/day/kg. | Antipsoriatic Agents and Monoclonal antibodies and TNF inhibitor | NA | NA | NA | NA | Tumor necrosis factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10614 | Th1125 | Golimumab | NA | 146943.2 | C6530H10068N1752O2026S44 | NA | NA | NA | About 2 weeks | Human IgG1Ò› monoclonal antibody derived from immunizing genetically engineered mice with human TNFα. It binds and inhibits soluble and transmembrane human TNFα. Increased TNFα is associated with chronic inflammation. Thus golimumab is indicated for use in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. In the U.S. and Canada, golimumab is marketed under the brand name Simponi. The FDA label includes a black box warning of serious infections and malignancy. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | Used in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. | Golimumab inhibits the activity of the cytokine, tumor necrosis factor alpha (TNFα). In areas such as the joints and blood, increased TNFαis associated with chronic inflammation seen in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Thus golimumab decreases the inflammation in these conditions. Concerning ulcerative colitis, the physiological effects of golimumab has yet to be determined. | As a human monoclonal antibody, golimumab binds and inhibits soluble and transmembrane human TNFα. Inhibition of TNFα prevents it binding to its receptors, which prevents both leukocyte infiltration through prevention of cell adhesion proteins such as E-selectin, ICAM-1 and VCAM-1, and pro-inflammatory cytokine secretion such as IL-6, IL-8, G-CSF and GM-CSF in vitro. Consequently, in patients with chronic inflammatory conditions, decreases in ICAM-1 and IL-6 as well as C-reactive protein (CRP), matrix metalloproteinase 3 (MMP-3), and vascular endothelial growth factor (VEGF) were observed. | The FDA label includes a black box warning of serious infections and malignancy. Specifically there have been hospitalizations or death from infections such as bacterial sepsis, tuberculosis (TB), and invasive fungal (histoplasmosis) and other opportunistic infections. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | The metabolism of golimumab has yet to be determined. | After subcutaneous administration, golimumab can achieve maximum serum concentrations in 2 to 6 days and has an approximate bioavailability of 53%. In healthy volunteers, the maximum average concentration reached was 3.2 ± 1.4 µg/mL. | After IV administration, golimumab has a volume of distribution of about 58 to 126 mL/kg. This means that golimumab stays mostly in the circulatory system. | After one IV dose of golimumab, the systemic clearance was about 4.9 to 6.7 mL/day/kg. | Antipsoriatic Agents and Monoclonal antibodies and TNF inhibitor | NA | NA | NA | NA | Tumor necrosis factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10615 | Th1125 | Golimumab | NA | 146943.2 | C6530H10068N1752O2026S44 | NA | NA | NA | About 2 weeks | Human IgG1Ò› monoclonal antibody derived from immunizing genetically engineered mice with human TNFα. It binds and inhibits soluble and transmembrane human TNFα. Increased TNFα is associated with chronic inflammation. Thus golimumab is indicated for use in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. In the U.S. and Canada, golimumab is marketed under the brand name Simponi. The FDA label includes a black box warning of serious infections and malignancy. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | Used in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. | Golimumab inhibits the activity of the cytokine, tumor necrosis factor alpha (TNFα). In areas such as the joints and blood, increased TNFαis associated with chronic inflammation seen in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Thus golimumab decreases the inflammation in these conditions. Concerning ulcerative colitis, the physiological effects of golimumab has yet to be determined. | As a human monoclonal antibody, golimumab binds and inhibits soluble and transmembrane human TNFα. Inhibition of TNFα prevents it binding to its receptors, which prevents both leukocyte infiltration through prevention of cell adhesion proteins such as E-selectin, ICAM-1 and VCAM-1, and pro-inflammatory cytokine secretion such as IL-6, IL-8, G-CSF and GM-CSF in vitro. Consequently, in patients with chronic inflammatory conditions, decreases in ICAM-1 and IL-6 as well as C-reactive protein (CRP), matrix metalloproteinase 3 (MMP-3), and vascular endothelial growth factor (VEGF) were observed. | The FDA label includes a black box warning of serious infections and malignancy. Specifically there have been hospitalizations or death from infections such as bacterial sepsis, tuberculosis (TB), and invasive fungal (histoplasmosis) and other opportunistic infections. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | The metabolism of golimumab has yet to be determined. | After subcutaneous administration, golimumab can achieve maximum serum concentrations in 2 to 6 days and has an approximate bioavailability of 53%. In healthy volunteers, the maximum average concentration reached was 3.2 ± 1.4 µg/mL. | After IV administration, golimumab has a volume of distribution of about 58 to 126 mL/kg. This means that golimumab stays mostly in the circulatory system. | After one IV dose of golimumab, the systemic clearance was about 4.9 to 6.7 mL/day/kg. | Antipsoriatic Agents and Monoclonal antibodies and TNF inhibitor | NA | NA | NA | NA | Tumor necrosis factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10616 | Th1125 | Golimumab | NA | 146943.2 | C6530H10068N1752O2026S44 | NA | NA | NA | About 2 weeks | Human IgG1Ò› monoclonal antibody derived from immunizing genetically engineered mice with human TNFα. It binds and inhibits soluble and transmembrane human TNFα. Increased TNFα is associated with chronic inflammation. Thus golimumab is indicated for use in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. In the U.S. and Canada, golimumab is marketed under the brand name Simponi. The FDA label includes a black box warning of serious infections and malignancy. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | Used in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. | Golimumab inhibits the activity of the cytokine, tumor necrosis factor alpha (TNFα). In areas such as the joints and blood, increased TNFαis associated with chronic inflammation seen in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Thus golimumab decreases the inflammation in these conditions. Concerning ulcerative colitis, the physiological effects of golimumab has yet to be determined. | As a human monoclonal antibody, golimumab binds and inhibits soluble and transmembrane human TNFα. Inhibition of TNFα prevents it binding to its receptors, which prevents both leukocyte infiltration through prevention of cell adhesion proteins such as E-selectin, ICAM-1 and VCAM-1, and pro-inflammatory cytokine secretion such as IL-6, IL-8, G-CSF and GM-CSF in vitro. Consequently, in patients with chronic inflammatory conditions, decreases in ICAM-1 and IL-6 as well as C-reactive protein (CRP), matrix metalloproteinase 3 (MMP-3), and vascular endothelial growth factor (VEGF) were observed. | The FDA label includes a black box warning of serious infections and malignancy. Specifically there have been hospitalizations or death from infections such as bacterial sepsis, tuberculosis (TB), and invasive fungal (histoplasmosis) and other opportunistic infections. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | The metabolism of golimumab has yet to be determined. | After subcutaneous administration, golimumab can achieve maximum serum concentrations in 2 to 6 days and has an approximate bioavailability of 53%. In healthy volunteers, the maximum average concentration reached was 3.2 ± 1.4 µg/mL. | After IV administration, golimumab has a volume of distribution of about 58 to 126 mL/kg. This means that golimumab stays mostly in the circulatory system. | After one IV dose of golimumab, the systemic clearance was about 4.9 to 6.7 mL/day/kg. | Antipsoriatic Agents and Monoclonal antibodies and TNF inhibitor | NA | NA | NA | NA | Tumor necrosis factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10617 | Th1125 | Golimumab | NA | 146943.2 | C6530H10068N1752O2026S44 | NA | NA | NA | About 2 weeks | Human IgG1Ò› monoclonal antibody derived from immunizing genetically engineered mice with human TNFα. It binds and inhibits soluble and transmembrane human TNFα. Increased TNFα is associated with chronic inflammation. Thus golimumab is indicated for use in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. In the U.S. and Canada, golimumab is marketed under the brand name Simponi. The FDA label includes a black box warning of serious infections and malignancy. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | Used in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. | Golimumab inhibits the activity of the cytokine, tumor necrosis factor alpha (TNFα). In areas such as the joints and blood, increased TNFαis associated with chronic inflammation seen in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Thus golimumab decreases the inflammation in these conditions. Concerning ulcerative colitis, the physiological effects of golimumab has yet to be determined. | As a human monoclonal antibody, golimumab binds and inhibits soluble and transmembrane human TNFα. Inhibition of TNFα prevents it binding to its receptors, which prevents both leukocyte infiltration through prevention of cell adhesion proteins such as E-selectin, ICAM-1 and VCAM-1, and pro-inflammatory cytokine secretion such as IL-6, IL-8, G-CSF and GM-CSF in vitro. Consequently, in patients with chronic inflammatory conditions, decreases in ICAM-1 and IL-6 as well as C-reactive protein (CRP), matrix metalloproteinase 3 (MMP-3), and vascular endothelial growth factor (VEGF) were observed. | The FDA label includes a black box warning of serious infections and malignancy. Specifically there have been hospitalizations or death from infections such as bacterial sepsis, tuberculosis (TB), and invasive fungal (histoplasmosis) and other opportunistic infections. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | The metabolism of golimumab has yet to be determined. | After subcutaneous administration, golimumab can achieve maximum serum concentrations in 2 to 6 days and has an approximate bioavailability of 53%. In healthy volunteers, the maximum average concentration reached was 3.2 ± 1.4 µg/mL. | After IV administration, golimumab has a volume of distribution of about 58 to 126 mL/kg. This means that golimumab stays mostly in the circulatory system. | After one IV dose of golimumab, the systemic clearance was about 4.9 to 6.7 mL/day/kg. | Antipsoriatic Agents and Monoclonal antibodies and TNF inhibitor | NA | NA | NA | NA | Tumor necrosis factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10618 | Th1125 | Golimumab | NA | 146943.2 | C6530H10068N1752O2026S44 | NA | NA | NA | About 2 weeks | Human IgG1Ò› monoclonal antibody derived from immunizing genetically engineered mice with human TNFα. It binds and inhibits soluble and transmembrane human TNFα. Increased TNFα is associated with chronic inflammation. Thus golimumab is indicated for use in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. In the U.S. and Canada, golimumab is marketed under the brand name Simponi. The FDA label includes a black box warning of serious infections and malignancy. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | Used in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. | Golimumab inhibits the activity of the cytokine, tumor necrosis factor alpha (TNFα). In areas such as the joints and blood, increased TNFαis associated with chronic inflammation seen in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Thus golimumab decreases the inflammation in these conditions. Concerning ulcerative colitis, the physiological effects of golimumab has yet to be determined. | As a human monoclonal antibody, golimumab binds and inhibits soluble and transmembrane human TNFα. Inhibition of TNFα prevents it binding to its receptors, which prevents both leukocyte infiltration through prevention of cell adhesion proteins such as E-selectin, ICAM-1 and VCAM-1, and pro-inflammatory cytokine secretion such as IL-6, IL-8, G-CSF and GM-CSF in vitro. Consequently, in patients with chronic inflammatory conditions, decreases in ICAM-1 and IL-6 as well as C-reactive protein (CRP), matrix metalloproteinase 3 (MMP-3), and vascular endothelial growth factor (VEGF) were observed. | The FDA label includes a black box warning of serious infections and malignancy. Specifically there have been hospitalizations or death from infections such as bacterial sepsis, tuberculosis (TB), and invasive fungal (histoplasmosis) and other opportunistic infections. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | The metabolism of golimumab has yet to be determined. | After subcutaneous administration, golimumab can achieve maximum serum concentrations in 2 to 6 days and has an approximate bioavailability of 53%. In healthy volunteers, the maximum average concentration reached was 3.2 ± 1.4 µg/mL. | After IV administration, golimumab has a volume of distribution of about 58 to 126 mL/kg. This means that golimumab stays mostly in the circulatory system. | After one IV dose of golimumab, the systemic clearance was about 4.9 to 6.7 mL/day/kg. | Antipsoriatic Agents and Monoclonal antibodies and TNF inhibitor | NA | NA | NA | NA | Tumor necrosis factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10619 | Th1125 | Golimumab | NA | 146943.2 | C6530H10068N1752O2026S44 | NA | NA | NA | About 2 weeks | Human IgG1Ò› monoclonal antibody derived from immunizing genetically engineered mice with human TNFα. It binds and inhibits soluble and transmembrane human TNFα. Increased TNFα is associated with chronic inflammation. Thus golimumab is indicated for use in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. In the U.S. and Canada, golimumab is marketed under the brand name Simponi. The FDA label includes a black box warning of serious infections and malignancy. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | Used in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. | Golimumab inhibits the activity of the cytokine, tumor necrosis factor alpha (TNFα). In areas such as the joints and blood, increased TNFαis associated with chronic inflammation seen in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Thus golimumab decreases the inflammation in these conditions. Concerning ulcerative colitis, the physiological effects of golimumab has yet to be determined. | As a human monoclonal antibody, golimumab binds and inhibits soluble and transmembrane human TNFα. Inhibition of TNFα prevents it binding to its receptors, which prevents both leukocyte infiltration through prevention of cell adhesion proteins such as E-selectin, ICAM-1 and VCAM-1, and pro-inflammatory cytokine secretion such as IL-6, IL-8, G-CSF and GM-CSF in vitro. Consequently, in patients with chronic inflammatory conditions, decreases in ICAM-1 and IL-6 as well as C-reactive protein (CRP), matrix metalloproteinase 3 (MMP-3), and vascular endothelial growth factor (VEGF) were observed. | The FDA label includes a black box warning of serious infections and malignancy. Specifically there have been hospitalizations or death from infections such as bacterial sepsis, tuberculosis (TB), and invasive fungal (histoplasmosis) and other opportunistic infections. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | The metabolism of golimumab has yet to be determined. | After subcutaneous administration, golimumab can achieve maximum serum concentrations in 2 to 6 days and has an approximate bioavailability of 53%. In healthy volunteers, the maximum average concentration reached was 3.2 ± 1.4 µg/mL. | After IV administration, golimumab has a volume of distribution of about 58 to 126 mL/kg. This means that golimumab stays mostly in the circulatory system. | After one IV dose of golimumab, the systemic clearance was about 4.9 to 6.7 mL/day/kg. | Antipsoriatic Agents and Monoclonal antibodies and TNF inhibitor | NA | NA | NA | NA | Tumor necrosis factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10620 | Th1125 | Golimumab | NA | 146943.2 | C6530H10068N1752O2026S44 | NA | NA | NA | About 2 weeks | Human IgG1Ò› monoclonal antibody derived from immunizing genetically engineered mice with human TNFα. It binds and inhibits soluble and transmembrane human TNFα. Increased TNFα is associated with chronic inflammation. Thus golimumab is indicated for use in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. In the U.S. and Canada, golimumab is marketed under the brand name Simponi. The FDA label includes a black box warning of serious infections and malignancy. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | Used in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. | Golimumab inhibits the activity of the cytokine, tumor necrosis factor alpha (TNFα). In areas such as the joints and blood, increased TNFαis associated with chronic inflammation seen in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Thus golimumab decreases the inflammation in these conditions. Concerning ulcerative colitis, the physiological effects of golimumab has yet to be determined. | As a human monoclonal antibody, golimumab binds and inhibits soluble and transmembrane human TNFα. Inhibition of TNFα prevents it binding to its receptors, which prevents both leukocyte infiltration through prevention of cell adhesion proteins such as E-selectin, ICAM-1 and VCAM-1, and pro-inflammatory cytokine secretion such as IL-6, IL-8, G-CSF and GM-CSF in vitro. Consequently, in patients with chronic inflammatory conditions, decreases in ICAM-1 and IL-6 as well as C-reactive protein (CRP), matrix metalloproteinase 3 (MMP-3), and vascular endothelial growth factor (VEGF) were observed. | The FDA label includes a black box warning of serious infections and malignancy. Specifically there have been hospitalizations or death from infections such as bacterial sepsis, tuberculosis (TB), and invasive fungal (histoplasmosis) and other opportunistic infections. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | The metabolism of golimumab has yet to be determined. | After subcutaneous administration, golimumab can achieve maximum serum concentrations in 2 to 6 days and has an approximate bioavailability of 53%. In healthy volunteers, the maximum average concentration reached was 3.2 ± 1.4 µg/mL. | After IV administration, golimumab has a volume of distribution of about 58 to 126 mL/kg. This means that golimumab stays mostly in the circulatory system. | After one IV dose of golimumab, the systemic clearance was about 4.9 to 6.7 mL/day/kg. | Antipsoriatic Agents and Monoclonal antibodies and TNF inhibitor | NA | NA | NA | NA | Tumor necrosis factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10621 | Th1125 | Golimumab | NA | 146943.2 | C6530H10068N1752O2026S44 | NA | NA | NA | About 2 weeks | Human IgG1Ò› monoclonal antibody derived from immunizing genetically engineered mice with human TNFα. It binds and inhibits soluble and transmembrane human TNFα. Increased TNFα is associated with chronic inflammation. Thus golimumab is indicated for use in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. In the U.S. and Canada, golimumab is marketed under the brand name Simponi. The FDA label includes a black box warning of serious infections and malignancy. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | Used in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. | Golimumab inhibits the activity of the cytokine, tumor necrosis factor alpha (TNFα). In areas such as the joints and blood, increased TNFαis associated with chronic inflammation seen in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Thus golimumab decreases the inflammation in these conditions. Concerning ulcerative colitis, the physiological effects of golimumab has yet to be determined. | As a human monoclonal antibody, golimumab binds and inhibits soluble and transmembrane human TNFα. Inhibition of TNFα prevents it binding to its receptors, which prevents both leukocyte infiltration through prevention of cell adhesion proteins such as E-selectin, ICAM-1 and VCAM-1, and pro-inflammatory cytokine secretion such as IL-6, IL-8, G-CSF and GM-CSF in vitro. Consequently, in patients with chronic inflammatory conditions, decreases in ICAM-1 and IL-6 as well as C-reactive protein (CRP), matrix metalloproteinase 3 (MMP-3), and vascular endothelial growth factor (VEGF) were observed. | The FDA label includes a black box warning of serious infections and malignancy. Specifically there have been hospitalizations or death from infections such as bacterial sepsis, tuberculosis (TB), and invasive fungal (histoplasmosis) and other opportunistic infections. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | The metabolism of golimumab has yet to be determined. | After subcutaneous administration, golimumab can achieve maximum serum concentrations in 2 to 6 days and has an approximate bioavailability of 53%. In healthy volunteers, the maximum average concentration reached was 3.2 ± 1.4 µg/mL. | After IV administration, golimumab has a volume of distribution of about 58 to 126 mL/kg. This means that golimumab stays mostly in the circulatory system. | After one IV dose of golimumab, the systemic clearance was about 4.9 to 6.7 mL/day/kg. | Antipsoriatic Agents and Monoclonal antibodies and TNF inhibitor | NA | NA | NA | NA | Tumor necrosis factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10622 | Th1125 | Golimumab | NA | 146943.2 | C6530H10068N1752O2026S44 | NA | NA | NA | About 2 weeks | Human IgG1Ò› monoclonal antibody derived from immunizing genetically engineered mice with human TNFα. It binds and inhibits soluble and transmembrane human TNFα. Increased TNFα is associated with chronic inflammation. Thus golimumab is indicated for use in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. In the U.S. and Canada, golimumab is marketed under the brand name Simponi. The FDA label includes a black box warning of serious infections and malignancy. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | Used in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. | Golimumab inhibits the activity of the cytokine, tumor necrosis factor alpha (TNFα). In areas such as the joints and blood, increased TNFαis associated with chronic inflammation seen in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Thus golimumab decreases the inflammation in these conditions. Concerning ulcerative colitis, the physiological effects of golimumab has yet to be determined. | As a human monoclonal antibody, golimumab binds and inhibits soluble and transmembrane human TNFα. Inhibition of TNFα prevents it binding to its receptors, which prevents both leukocyte infiltration through prevention of cell adhesion proteins such as E-selectin, ICAM-1 and VCAM-1, and pro-inflammatory cytokine secretion such as IL-6, IL-8, G-CSF and GM-CSF in vitro. Consequently, in patients with chronic inflammatory conditions, decreases in ICAM-1 and IL-6 as well as C-reactive protein (CRP), matrix metalloproteinase 3 (MMP-3), and vascular endothelial growth factor (VEGF) were observed. | The FDA label includes a black box warning of serious infections and malignancy. Specifically there have been hospitalizations or death from infections such as bacterial sepsis, tuberculosis (TB), and invasive fungal (histoplasmosis) and other opportunistic infections. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | The metabolism of golimumab has yet to be determined. | After subcutaneous administration, golimumab can achieve maximum serum concentrations in 2 to 6 days and has an approximate bioavailability of 53%. In healthy volunteers, the maximum average concentration reached was 3.2 ± 1.4 µg/mL. | After IV administration, golimumab has a volume of distribution of about 58 to 126 mL/kg. This means that golimumab stays mostly in the circulatory system. | After one IV dose of golimumab, the systemic clearance was about 4.9 to 6.7 mL/day/kg. | Antipsoriatic Agents and Monoclonal antibodies and TNF inhibitor | NA | NA | NA | NA | Tumor necrosis factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10623 | Th1125 | Golimumab | NA | 146943.2 | C6530H10068N1752O2026S44 | NA | NA | NA | About 2 weeks | Human IgG1Ò› monoclonal antibody derived from immunizing genetically engineered mice with human TNFα. It binds and inhibits soluble and transmembrane human TNFα. Increased TNFα is associated with chronic inflammation. Thus golimumab is indicated for use in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. In the U.S. and Canada, golimumab is marketed under the brand name Simponi. The FDA label includes a black box warning of serious infections and malignancy. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | Used in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. | Golimumab inhibits the activity of the cytokine, tumor necrosis factor alpha (TNFα). In areas such as the joints and blood, increased TNFαis associated with chronic inflammation seen in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Thus golimumab decreases the inflammation in these conditions. Concerning ulcerative colitis, the physiological effects of golimumab has yet to be determined. | As a human monoclonal antibody, golimumab binds and inhibits soluble and transmembrane human TNFα. Inhibition of TNFα prevents it binding to its receptors, which prevents both leukocyte infiltration through prevention of cell adhesion proteins such as E-selectin, ICAM-1 and VCAM-1, and pro-inflammatory cytokine secretion such as IL-6, IL-8, G-CSF and GM-CSF in vitro. Consequently, in patients with chronic inflammatory conditions, decreases in ICAM-1 and IL-6 as well as C-reactive protein (CRP), matrix metalloproteinase 3 (MMP-3), and vascular endothelial growth factor (VEGF) were observed. | The FDA label includes a black box warning of serious infections and malignancy. Specifically there have been hospitalizations or death from infections such as bacterial sepsis, tuberculosis (TB), and invasive fungal (histoplasmosis) and other opportunistic infections. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | The metabolism of golimumab has yet to be determined. | After subcutaneous administration, golimumab can achieve maximum serum concentrations in 2 to 6 days and has an approximate bioavailability of 53%. In healthy volunteers, the maximum average concentration reached was 3.2 ± 1.4 µg/mL. | After IV administration, golimumab has a volume of distribution of about 58 to 126 mL/kg. This means that golimumab stays mostly in the circulatory system. | After one IV dose of golimumab, the systemic clearance was about 4.9 to 6.7 mL/day/kg. | Antipsoriatic Agents and Monoclonal antibodies and TNF inhibitor | NA | NA | NA | NA | Tumor necrosis factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10637 | Th1132 | Belimumab | NA | 147000 | C 6358 H 9904 N 1728 O 2010 S 44 | NA | NA | NA | Elimination half life- 19.4 days, Distribution half life- 1.75 days | RAV12 is a monoclonal antibody that is being studied in the treatment of certain cancers.It binds to a carbohydrate molecule found on gastric, colon, pancreatic, prostate, ovarian, breast, and kidney cancer cells. Administering RAV12 along with gemcitabine may kill more tumor cells than either one alone. | Adjunct treatment for auto-antibody-positive active systemic lupus erythematosus. | By the 52nd week of treatment with belimumab, a reduction in CD19+, CD20+, naive and activated B cells, plasma cells, plasmacytoid cells, and SLE B-cell subset can be observed. Reductions in plasma cells and SLE B-cell subset can be seen by the eighth week and these levels were maintained to week 52. Belimumab also reduced levels of IgG and anti-dsDNA. | Belimumab selectively binds to soluble human B lymphocyte stimulator protein (BLyS) so that BLyS is unable to bind to receptors on B lymphocytes. The binding of BLyS to its receptor is essential for the survival of B lymphocytes. Consequently, belimumab reduces B-cell mediated immunity and the autoimmune response. | The most commonly-reported adverse reactions, occurring in =5% of patients in clinical trials were nausea, diarrhea, pyrexia, nasopharyngitis, bronchitis, insomnia, pain in extremity, depression, migraine, and pharyngitis. The most common serious adverse reactions were serious infections. | Because belimumab is a protein, it is expected that it is degraded into peptides and amino acids by proteolytic enzymes. | Cmax, 10 mg/kg, SLE patients = 313 µg/mL; AUC (0-8), 10 mg/kg, SLE patients = 3083. | Vdss, 10 mg/kg, SLE patients = 5.29 L. | Systemic clearance, 10 mg/kg, SLE patients = 215 mL/day. | Monoclonal antibodies | NA | NA | NA | NA | Tumor necrosis factor ligand superfamily member 13B | Benlysta | GlaxoSmithKline | GlaxoSmithKline | NA | NA | Upon reconstitution with Sterile Water for Injection, USP, each single-use vial delivers 80 mg/mL belimumab in 0.16 mg/mL citric acid, 0.4 mg/mL polysorbate 80, 2.7 mg/mL sodium citrate, and 80 mg/mL sucrose, with a pH of 6.5. | BENLYSTA is supplied as a sterile, white to off-white, preservative-free, lyophilized powder for Intravenous infusion | Intravenous infusion | 10 mg/kg at 2-week intervals for the first 3 doses and at 4-week intervals thereafter. Reconstitute, dilute, and administer as an Intravenous infusion only, over a period of 1 hour. | anaphylaxis with belimumab | Mortality, Serious Infections, Malignancy, Hypersensitivity Reactions, Including Anaphylaxis, Infusion Reactions, Depression | Link | NA | NA |
| 10638 | Th1132 | Belimumab | NA | 147000 | C 6358 H 9904 N 1728 O 2010 S 44 | NA | NA | NA | Elimination half life- 19.4 days, Distribution half life- 1.75 days | RAV12 is a monoclonal antibody that is being studied in the treatment of certain cancers.It binds to a carbohydrate molecule found on gastric, colon, pancreatic, prostate, ovarian, breast, and kidney cancer cells. Administering RAV12 along with gemcitabine may kill more tumor cells than either one alone. | Adjunct treatment for auto-antibody-positive active systemic lupus erythematosus. | By the 52nd week of treatment with belimumab, a reduction in CD19+, CD20+, naive and activated B cells, plasma cells, plasmacytoid cells, and SLE B-cell subset can be observed. Reductions in plasma cells and SLE B-cell subset can be seen by the eighth week and these levels were maintained to week 52. Belimumab also reduced levels of IgG and anti-dsDNA. | Belimumab selectively binds to soluble human B lymphocyte stimulator protein (BLyS) so that BLyS is unable to bind to receptors on B lymphocytes. The binding of BLyS to its receptor is essential for the survival of B lymphocytes. Consequently, belimumab reduces B-cell mediated immunity and the autoimmune response. | The most commonly-reported adverse reactions, occurring in =5% of patients in clinical trials were nausea, diarrhea, pyrexia, nasopharyngitis, bronchitis, insomnia, pain in extremity, depression, migraine, and pharyngitis. The most common serious adverse reactions were serious infections. | Because belimumab is a protein, it is expected that it is degraded into peptides and amino acids by proteolytic enzymes. | Cmax, 10 mg/kg, SLE patients = 313 µg/mL; AUC (0-8), 10 mg/kg, SLE patients = 3083. | Vdss, 10 mg/kg, SLE patients = 5.29 L. | Systemic clearance, 10 mg/kg, SLE patients = 215 mL/day. | Monoclonal antibodies | NA | NA | NA | NA | Tumor necrosis factor ligand superfamily member 13B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10639 | Th1132 | Belimumab | NA | 147000 | C 6358 H 9904 N 1728 O 2010 S 44 | NA | NA | NA | Elimination half life- 19.4 days, Distribution half life- 1.75 days | RAV12 is a monoclonal antibody that is being studied in the treatment of certain cancers.It binds to a carbohydrate molecule found on gastric, colon, pancreatic, prostate, ovarian, breast, and kidney cancer cells. Administering RAV12 along with gemcitabine may kill more tumor cells than either one alone. | Adjunct treatment for auto-antibody-positive active systemic lupus erythematosus. | By the 52nd week of treatment with belimumab, a reduction in CD19+, CD20+, naive and activated B cells, plasma cells, plasmacytoid cells, and SLE B-cell subset can be observed. Reductions in plasma cells and SLE B-cell subset can be seen by the eighth week and these levels were maintained to week 52. Belimumab also reduced levels of IgG and anti-dsDNA. | Belimumab selectively binds to soluble human B lymphocyte stimulator protein (BLyS) so that BLyS is unable to bind to receptors on B lymphocytes. The binding of BLyS to its receptor is essential for the survival of B lymphocytes. Consequently, belimumab reduces B-cell mediated immunity and the autoimmune response. | The most commonly-reported adverse reactions, occurring in =5% of patients in clinical trials were nausea, diarrhea, pyrexia, nasopharyngitis, bronchitis, insomnia, pain in extremity, depression, migraine, and pharyngitis. The most common serious adverse reactions were serious infections. | Because belimumab is a protein, it is expected that it is degraded into peptides and amino acids by proteolytic enzymes. | Cmax, 10 mg/kg, SLE patients = 313 µg/mL; AUC (0-8), 10 mg/kg, SLE patients = 3083. | Vdss, 10 mg/kg, SLE patients = 5.29 L. | Systemic clearance, 10 mg/kg, SLE patients = 215 mL/day. | Monoclonal antibodies | NA | NA | NA | NA | Tumor necrosis factor ligand superfamily member 13B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10640 | Th1132 | Belimumab | NA | 147000 | C 6358 H 9904 N 1728 O 2010 S 44 | NA | NA | NA | Elimination half life- 19.4 days, Distribution half life- 1.75 days | RAV12 is a monoclonal antibody that is being studied in the treatment of certain cancers.It binds to a carbohydrate molecule found on gastric, colon, pancreatic, prostate, ovarian, breast, and kidney cancer cells. Administering RAV12 along with gemcitabine may kill more tumor cells than either one alone. | Adjunct treatment for auto-antibody-positive active systemic lupus erythematosus. | By the 52nd week of treatment with belimumab, a reduction in CD19+, CD20+, naive and activated B cells, plasma cells, plasmacytoid cells, and SLE B-cell subset can be observed. Reductions in plasma cells and SLE B-cell subset can be seen by the eighth week and these levels were maintained to week 52. Belimumab also reduced levels of IgG and anti-dsDNA. | Belimumab selectively binds to soluble human B lymphocyte stimulator protein (BLyS) so that BLyS is unable to bind to receptors on B lymphocytes. The binding of BLyS to its receptor is essential for the survival of B lymphocytes. Consequently, belimumab reduces B-cell mediated immunity and the autoimmune response. | The most commonly-reported adverse reactions, occurring in =5% of patients in clinical trials were nausea, diarrhea, pyrexia, nasopharyngitis, bronchitis, insomnia, pain in extremity, depression, migraine, and pharyngitis. The most common serious adverse reactions were serious infections. | Because belimumab is a protein, it is expected that it is degraded into peptides and amino acids by proteolytic enzymes. | Cmax, 10 mg/kg, SLE patients = 313 µg/mL; AUC (0-8), 10 mg/kg, SLE patients = 3083. | Vdss, 10 mg/kg, SLE patients = 5.29 L. | Systemic clearance, 10 mg/kg, SLE patients = 215 mL/day. | Monoclonal antibodies | NA | NA | NA | NA | Tumor necrosis factor ligand superfamily member 13B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10641 | Th1132 | Belimumab | NA | 147000 | C 6358 H 9904 N 1728 O 2010 S 44 | NA | NA | NA | Elimination half life- 19.4 days, Distribution half life- 1.75 days | RAV12 is a monoclonal antibody that is being studied in the treatment of certain cancers.It binds to a carbohydrate molecule found on gastric, colon, pancreatic, prostate, ovarian, breast, and kidney cancer cells. Administering RAV12 along with gemcitabine may kill more tumor cells than either one alone. | Adjunct treatment for auto-antibody-positive active systemic lupus erythematosus. | By the 52nd week of treatment with belimumab, a reduction in CD19+, CD20+, naive and activated B cells, plasma cells, plasmacytoid cells, and SLE B-cell subset can be observed. Reductions in plasma cells and SLE B-cell subset can be seen by the eighth week and these levels were maintained to week 52. Belimumab also reduced levels of IgG and anti-dsDNA. | Belimumab selectively binds to soluble human B lymphocyte stimulator protein (BLyS) so that BLyS is unable to bind to receptors on B lymphocytes. The binding of BLyS to its receptor is essential for the survival of B lymphocytes. Consequently, belimumab reduces B-cell mediated immunity and the autoimmune response. | The most commonly-reported adverse reactions, occurring in =5% of patients in clinical trials were nausea, diarrhea, pyrexia, nasopharyngitis, bronchitis, insomnia, pain in extremity, depression, migraine, and pharyngitis. The most common serious adverse reactions were serious infections. | Because belimumab is a protein, it is expected that it is degraded into peptides and amino acids by proteolytic enzymes. | Cmax, 10 mg/kg, SLE patients = 313 µg/mL; AUC (0-8), 10 mg/kg, SLE patients = 3083. | Vdss, 10 mg/kg, SLE patients = 5.29 L. | Systemic clearance, 10 mg/kg, SLE patients = 215 mL/day. | Monoclonal antibodies | NA | NA | NA | NA | Tumor necrosis factor ligand superfamily member 13B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10642 | Th1132 | Belimumab | NA | 147000 | C 6358 H 9904 N 1728 O 2010 S 44 | NA | NA | NA | Elimination half life- 19.4 days, Distribution half life- 1.75 days | RAV12 is a monoclonal antibody that is being studied in the treatment of certain cancers.It binds to a carbohydrate molecule found on gastric, colon, pancreatic, prostate, ovarian, breast, and kidney cancer cells. Administering RAV12 along with gemcitabine may kill more tumor cells than either one alone. | Adjunct treatment for auto-antibody-positive active systemic lupus erythematosus. | By the 52nd week of treatment with belimumab, a reduction in CD19+, CD20+, naive and activated B cells, plasma cells, plasmacytoid cells, and SLE B-cell subset can be observed. Reductions in plasma cells and SLE B-cell subset can be seen by the eighth week and these levels were maintained to week 52. Belimumab also reduced levels of IgG and anti-dsDNA. | Belimumab selectively binds to soluble human B lymphocyte stimulator protein (BLyS) so that BLyS is unable to bind to receptors on B lymphocytes. The binding of BLyS to its receptor is essential for the survival of B lymphocytes. Consequently, belimumab reduces B-cell mediated immunity and the autoimmune response. | The most commonly-reported adverse reactions, occurring in =5% of patients in clinical trials were nausea, diarrhea, pyrexia, nasopharyngitis, bronchitis, insomnia, pain in extremity, depression, migraine, and pharyngitis. The most common serious adverse reactions were serious infections. | Because belimumab is a protein, it is expected that it is degraded into peptides and amino acids by proteolytic enzymes. | Cmax, 10 mg/kg, SLE patients = 313 µg/mL; AUC (0-8), 10 mg/kg, SLE patients = 3083. | Vdss, 10 mg/kg, SLE patients = 5.29 L. | Systemic clearance, 10 mg/kg, SLE patients = 215 mL/day. | Monoclonal antibodies | NA | NA | NA | NA | Tumor necrosis factor ligand superfamily member 13B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10655 | Th1138 | Raxibacumab | NA | 142844.5 | C6320H9794N1702O1998S42 | 9 | NA | NA | Elimnation half life-IM dose- 15-19 days; IV dose-16-19 days | Recombinant (murine cell line derived), human IgG1 monoclonal antibody that binds the protective antigen (PA) component of B. anthracis toxin. FDA approved on December 14, 2012. | Raxibacumab is indicated for the treatment of adult and pediatric patients with inhalational anthrax due to Bacillus anthracis in combination with appropriate antibacterial drugs, and for prophylaxis of inhalational anthrax when alternative therapies are not available or are not appropriate. | NA | Raxibacumab is a monoclonal antibody that binds free PA with an affinity equilibrium dissociation constant (Kd) of 2.78 ± 0.9 nM. Raxibacumab inhibits the binding of PA to its cellular receptors, preventing the intracellular entry of the anthrax lethal factor and edema factor, the enzymatic toxin components responsible for the pathogenic effects of anthrax toxin. It does not have direct antibacterial activity. | The most frequently reported adverse reactions were rash, pain in extremity, pruritus, and somnolence. | NA | Raxibacumab does not cross the blood-brain-barrier. When a single IV dose of 40 mg/kg was administered to healthy, male and female human subjects, the pharmacokinetic parameters are as follows: Cmax = 1020.3 ± 140.6 mcg/mL; AUCinf = 15845.8 ± 4333.5 mcg·day/mL. Bioavailability is also dependent on site of injection. When administered to the vastus lateralis, the bioavailability is 71-85%. When administered to the gluteus maximus, the bioavailability is 50-54%. | Steady state volume of distribution exceeded plasma volume. This suggests that there is some distribution into the tissues. | Clearance values were much smaller than the glomerular filtration rate indicating that there is virtually no renal clearance of raxibacumab. | Anti-Infective Agents and Monoclonal antibodies | NA | NA | NA | NA | Protective antigen | RAXIBACUMAB | GSK | GSK | Raxibacumab is indicated for the treatment of adult and pediatric patients with inhalational anthrax due to Bacillus anthracis in combination with appropriate antibacterial drugs, and for prophylaxis of inhalational anthrax when alternative therapies are not available or are not appropriate | NA | Single-use vial contains 1700 mg/34 mL (50 mg/mL) raxibacumab solution. | Raxibacumab is supplied as a sterile, liquid formulation in single-dose vials for Intravenous infusion. Each vial contains 50 mg/mL raxibacumab in citric acid (0.13 mg/mL), glycine (18 mg/mL), polysorbate 80 [0.2 mg/mL (w/v)], sodium citrate (2.8 mg/mL), and sucrose (10 mg/mL), with a pH of 6.5. Eac | NA | Premedicate with diphenhydramine. Dilute and administer as an Intravenous infusion over 2 hours and 15 minutes. Adults: 40 mg/kg raxibacumab. Pediatrics greater than 50 kg: 40 mg/kg raxibacumab. Pediatrics greater than 15 kg to 50 kg: 60 mg/kg raxibacumab. Pediatrics 15 kg or less: 80 mg/kg raxibacumab. | There have been no studies of raxibacumab in the pediatric population. Dosing in pediatric patients was derived using a population PK approach. Raxibacumab does not cross the blood-brain barrier and does not prevent or treat meningitis. Raxibacumab should be used in combination with appropriate antibacterial drugs. Nursing Mothers: Caution should be exercised when administered to a nursing woman. Pediatric Use: Safety and effectiveness in children <16 years of age not studied. | Infusion reactions may occur. Premedicate with diphenhydramine. Slow or interrupt infusion and administer treatment based on severity of the reaction. Common adverse reactions in healthy adult subjects (≥1.5%) were: rash, pain in extremity, pruritus, and somnolence. | 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 |
| 10769 | Th1179 | Evolocumab | NA | 141800 | C6242H9648N1668O1996S56 | NA | NA | NA | NA | Evolocumab is a monoclonal antibody designed for the treatment of hyperlipidemia by Amgen. It is a subcutaneous injection approved by the FDA for individuals on maximum statin therapy who still require additional LDL-cholesterol lowering. It is approved for both homozygous and heterozygous familial cholesterolemia as an adjunct to other first-line therapies. Evolocumab is a human IgG2 monoclonal antibody that inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9). PCSK9 is a protein that targets LDL receptors for degradation, therefore reducing the liver’s ability to remove LDL-cholesterol (LDL-C), or “bad†cholesterol, from the blood. Evolocumab is designed to bind to PCSK9 and inhibit PCSK9 from binding to LDL receptors on the liver surface, resulting in more LDL receptors on the surface of the liver to remove LDL-C from the blood. Evolocumab is the second PCSK9 inhibitor on the market, first being alirocumab. | For the treatment of heterozygous/homozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease in patients on maximum tolerated statin therapy requiring additional LDL-cholesterol lowering. | Following single subcutaneous administration of 140 mg or 420 mg of evolocumab, maximum suppression of circulating unbound PCSK9 occurred by 4 hours. Unbound PCSK9 concentrations returned toward baseline when evolocumab concentrations decreased below the limit of quantitation. | Evolocumab is a human IgG monoclonal antibody which targets PCSK9 (proprotein convertase subtilisin/kexin type 9). PCSK9 is a serine protease produced by the liver which binds LDL receptors and creates a complex to be targeted for lysosomal degradation. LDL receptors typically bind LDL-cholesterol (bad cholesterol) for cellular reuptake, therefore the formation of these complexes with PCSK9 inhibits LDL receptor recycling to the cell surface, resulting in decreased cellular reuptake of LDL-C and increased levels of free LDL-C in the plasma. Individuals with familial hypercholesterolemia often may have gain of function mutations in the PCSK9 molecules in their body, resulting in increased LDL-C plasma levels and a consequent cardiovascular risk. Evolocumab is able to bind both the normal PCSK9 and the gain of function mutant, D374Y. The exact mechanism of the binding has not been published, however the precursor molecule, mAb1, is indicative of the interaction. The mAb1 molecule binds on the catalytic site of PCSK9 next to the binding site for the LDL receptor and creates hydrogen bonds and hydrophobic interactions, resulting in the steric inhibition of binding between PCSK9 and the LDL receptor. Because the formation of complexes between LDL receptor and PCSK9 are prevented, the internalized LDL receptors are less likely to be degrated by lysosomes and may recycle to the surface of the cell to serve their function of removing LDL from the blood. | NA | NA | Total bioavailability from subcutaneous injection was 82% in cynomolgus monkeys. | NA | Evolocumab showed non-linear, dose-dependent clearance in healthy volunteers; clearance decreased with increasing dose. | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Anticholesteremic Agents,Antimetabolites,Blood Proteins,Globulins,Hypolipidemic Agents,Hypolipidemic Agents Indicated for Hyperlipidemia,Immunoglobulins,Immunoproteins,Lipid Modifying Agents,Lipid Modifying Agents, Plain,Lipid Regulating Agents,Non-statin Hypolipidemic Agents Indicated for Hyperlipidemia,Noxae,PCSK9 Inhibitor,Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Inhibitors,Proteins,Serum Globulins,Toxic Actions | NA | NA | NA | The risk or severity of adverse effects can be increased when Evolocumab is combined with Belimumab. | Proprotein convertase subtilisin/kexin type 9 | NA | NA | NA | NA | NA | 140 mg/mL; 140 mg | Injection, solution; Injection | Subcutaneous | NA | NA | NA | NA | NA | NA |
| 10770 | Th1179 | Evolocumab | NA | 141800 | C6242H9648N1668O1996S57 | NA | NA | NA | NA | Evolocumab is a monoclonal antibody designed for the treatment of hyperlipidemia by Amgen. It is a subcutaneous injection approved by the FDA for individuals on maximum statin therapy who still require additional LDL-cholesterol lowering. It is approved for both homozygous and heterozygous familial cholesterolemia as an adjunct to other first-line therapies. Evolocumab is a human IgG2 monoclonal antibody that inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9). PCSK9 is a protein that targets LDL receptors for degradation, therefore reducing the liver’s ability to remove LDL-cholesterol (LDL-C), or “bad†cholesterol, from the blood. Evolocumab is designed to bind to PCSK9 and inhibit PCSK9 from binding to LDL receptors on the liver surface, resulting in more LDL receptors on the surface of the liver to remove LDL-C from the blood. Evolocumab is the second PCSK9 inhibitor on the market, first being alirocumab. | For the treatment of heterozygous/homozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease in patients on maximum tolerated statin therapy requiring additional LDL-cholesterol lowering. | Following single subcutaneous administration of 140 mg or 420 mg of evolocumab, maximum suppression of circulating unbound PCSK9 occurred by 4 hours. Unbound PCSK9 concentrations returned toward baseline when evolocumab concentrations decreased below the limit of quantitation. | Evolocumab is a human IgG monoclonal antibody which targets PCSK9 (proprotein convertase subtilisin/kexin type 9). PCSK9 is a serine protease produced by the liver which binds LDL receptors and creates a complex to be targeted for lysosomal degradation. LDL receptors typically bind LDL-cholesterol (bad cholesterol) for cellular reuptake, therefore the formation of these complexes with PCSK9 inhibits LDL receptor recycling to the cell surface, resulting in decreased cellular reuptake of LDL-C and increased levels of free LDL-C in the plasma. Individuals with familial hypercholesterolemia often may have gain of function mutations in the PCSK9 molecules in their body, resulting in increased LDL-C plasma levels and a consequent cardiovascular risk. Evolocumab is able to bind both the normal PCSK9 and the gain of function mutant, D374Y. The exact mechanism of the binding has not been published, however the precursor molecule, mAb1, is indicative of the interaction. The mAb1 molecule binds on the catalytic site of PCSK9 next to the binding site for the LDL receptor and creates hydrogen bonds and hydrophobic interactions, resulting in the steric inhibition of binding between PCSK9 and the LDL receptor. Because the formation of complexes between LDL receptor and PCSK9 are prevented, the internalized LDL receptors are less likely to be degrated by lysosomes and may recycle to the surface of the cell to serve their function of removing LDL from the blood. | NA | NA | Total bioavailability from subcutaneous injection was 82% in cynomolgus monkeys. | NA | Evolocumab showed non-linear, dose-dependent clearance in healthy volunteers; clearance decreased with increasing dose. | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Anticholesteremic Agents,Antimetabolites,Blood Proteins,Globulins,Hypolipidemic Agents,Hypolipidemic Agents Indicated for Hyperlipidemia,Immunoglobulins,Immunoproteins,Lipid Modifying Agents,Lipid Modifying Agents, Plain,Lipid Regulating Agents,Non-statin Hypolipidemic Agents Indicated for Hyperlipidemia,Noxae,PCSK9 Inhibitor,Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Inhibitors,Proteins,Serum Globulins,Toxic Actions | NA | NA | NA | The risk or severity of adverse effects can be increased when Evolocumab is combined with Belimumab. | Proprotein convertase subtilisin/kexin type 9 | Repatha | Amgen Inc | Amgen Inc | REPATHA™ is indicated as an adjunct to diet and maximally tolerated statin therapy for the treatment of adults with heterozygous familial hypercholesterolemia (HeFH) or clinical atherosclerotic cardiovascular disease (CVD), who require additional lowering of low density lipoprotein cholesterol (LDL-C); Also indicated as an adjunct to diet and other LDL-lowering therapies (e.g., statins, ezetimibe, LDL apheresis) for the treatment of patients with homozygous familial hypercholesterolemia (HoFH) who require additional lowering of LDL-C. | NA | 140 mg/mL | injection, solution | Subcutaneous | The recommended subcutaneous dosage of REPATHA in patients with HeFH or patients with primary hyperlipidemia with established clinical atherosclerotic CVD is either 140 mg every 2 weeks OR 420 mg once monthly. When switching dosage regimens, administer the first dose of the new regimen on the next scheduled date of the prior regimen. The recommended subcutaneous dosage of REPATHA in patients with HoFH is 420 mg once monthly. In patients with HoFH, measure LDL-C levels 4 to 8 weeks after starting REPATHA, since response to therapy will depend on the degree of LDL-receptor function. | REPATHA is contraindicated in patients with a history of a serious hypersensitivity reaction to REPATHA | Allergic reactions | Link | NA | NA |
| 10771 | Th1179 | Evolocumab | NA | 141800 | C6242H9648N1668O1996S58 | NA | NA | NA | NA | Evolocumab is a monoclonal antibody designed for the treatment of hyperlipidemia by Amgen. It is a subcutaneous injection approved by the FDA for individuals on maximum statin therapy who still require additional LDL-cholesterol lowering. It is approved for both homozygous and heterozygous familial cholesterolemia as an adjunct to other first-line therapies. Evolocumab is a human IgG2 monoclonal antibody that inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9). PCSK9 is a protein that targets LDL receptors for degradation, therefore reducing the liver’s ability to remove LDL-cholesterol (LDL-C), or “bad†cholesterol, from the blood. Evolocumab is designed to bind to PCSK9 and inhibit PCSK9 from binding to LDL receptors on the liver surface, resulting in more LDL receptors on the surface of the liver to remove LDL-C from the blood. Evolocumab is the second PCSK9 inhibitor on the market, first being alirocumab. | For the treatment of heterozygous/homozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease in patients on maximum tolerated statin therapy requiring additional LDL-cholesterol lowering. | Following single subcutaneous administration of 140 mg or 420 mg of evolocumab, maximum suppression of circulating unbound PCSK9 occurred by 4 hours. Unbound PCSK9 concentrations returned toward baseline when evolocumab concentrations decreased below the limit of quantitation. | Evolocumab is a human IgG monoclonal antibody which targets PCSK9 (proprotein convertase subtilisin/kexin type 9). PCSK9 is a serine protease produced by the liver which binds LDL receptors and creates a complex to be targeted for lysosomal degradation. LDL receptors typically bind LDL-cholesterol (bad cholesterol) for cellular reuptake, therefore the formation of these complexes with PCSK9 inhibits LDL receptor recycling to the cell surface, resulting in decreased cellular reuptake of LDL-C and increased levels of free LDL-C in the plasma. Individuals with familial hypercholesterolemia often may have gain of function mutations in the PCSK9 molecules in their body, resulting in increased LDL-C plasma levels and a consequent cardiovascular risk. Evolocumab is able to bind both the normal PCSK9 and the gain of function mutant, D374Y. The exact mechanism of the binding has not been published, however the precursor molecule, mAb1, is indicative of the interaction. The mAb1 molecule binds on the catalytic site of PCSK9 next to the binding site for the LDL receptor and creates hydrogen bonds and hydrophobic interactions, resulting in the steric inhibition of binding between PCSK9 and the LDL receptor. Because the formation of complexes between LDL receptor and PCSK9 are prevented, the internalized LDL receptors are less likely to be degrated by lysosomes and may recycle to the surface of the cell to serve their function of removing LDL from the blood. | NA | NA | Total bioavailability from subcutaneous injection was 82% in cynomolgus monkeys. | NA | Evolocumab showed non-linear, dose-dependent clearance in healthy volunteers; clearance decreased with increasing dose. | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Anticholesteremic Agents,Antimetabolites,Blood Proteins,Globulins,Hypolipidemic Agents,Hypolipidemic Agents Indicated for Hyperlipidemia,Immunoglobulins,Immunoproteins,Lipid Modifying Agents,Lipid Modifying Agents, Plain,Lipid Regulating Agents,Non-statin Hypolipidemic Agents Indicated for Hyperlipidemia,Noxae,PCSK9 Inhibitor,Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Inhibitors,Proteins,Serum Globulins,Toxic Actions | NA | NA | NA | The risk or severity of adverse effects can be increased when Evolocumab is combined with Belimumab. | Proprotein convertase subtilisin/kexin type 9 | Repatha | Amgen Canada Inc | Amgen Canada Inc | REPATHA™ is indicated as an adjunct to diet and maximally tolerated statin therapy for the treatment of adults with heterozygous familial hypercholesterolemia (HeFH) or clinical atherosclerotic cardiovascular disease (CVD), who require additional lowering of low density lipoprotein cholesterol (LDL-C); Also indicated as an adjunct to diet and other LDL-lowering therapies (e.g., statins, ezetimibe, LDL apheresis) for the treatment of patients with homozygous familial hypercholesterolemia (HoFH) who require additional lowering of LDL-C. | NA | 140 mg | solution | Subcutaneous | The recommended subcutaneous dosage of REPATHA in patients with HeFH or patients with primary hyperlipidemia with established clinical atherosclerotic CVD is either 140 mg every 2 weeks OR 420 mg once monthly. When switching dosage regimens, administer the first dose of the new regimen on the next scheduled date of the prior regimen. The recommended subcutaneous dosage of REPATHA in patients with HoFH is 420 mg once monthly. In patients with HoFH, measure LDL-C levels 4 to 8 weeks after starting REPATHA, since response to therapy will depend on the degree of LDL-receptor function. | REPATHA is contraindicated in patients with a history of a serious hypersensitivity reaction to REPATHA | Allergic reactions | Link | NA | NA |
| 10772 | Th1179 | Evolocumab | NA | 141800 | C6242H9648N1668O1996S59 | NA | NA | NA | NA | Evolocumab is a monoclonal antibody designed for the treatment of hyperlipidemia by Amgen. It is a subcutaneous injection approved by the FDA for individuals on maximum statin therapy who still require additional LDL-cholesterol lowering. It is approved for both homozygous and heterozygous familial cholesterolemia as an adjunct to other first-line therapies. Evolocumab is a human IgG2 monoclonal antibody that inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9). PCSK9 is a protein that targets LDL receptors for degradation, therefore reducing the liver’s ability to remove LDL-cholesterol (LDL-C), or “bad†cholesterol, from the blood. Evolocumab is designed to bind to PCSK9 and inhibit PCSK9 from binding to LDL receptors on the liver surface, resulting in more LDL receptors on the surface of the liver to remove LDL-C from the blood. Evolocumab is the second PCSK9 inhibitor on the market, first being alirocumab. | For the treatment of heterozygous/homozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease in patients on maximum tolerated statin therapy requiring additional LDL-cholesterol lowering. | Following single subcutaneous administration of 140 mg or 420 mg of evolocumab, maximum suppression of circulating unbound PCSK9 occurred by 4 hours. Unbound PCSK9 concentrations returned toward baseline when evolocumab concentrations decreased below the limit of quantitation. | Evolocumab is a human IgG monoclonal antibody which targets PCSK9 (proprotein convertase subtilisin/kexin type 9). PCSK9 is a serine protease produced by the liver which binds LDL receptors and creates a complex to be targeted for lysosomal degradation. LDL receptors typically bind LDL-cholesterol (bad cholesterol) for cellular reuptake, therefore the formation of these complexes with PCSK9 inhibits LDL receptor recycling to the cell surface, resulting in decreased cellular reuptake of LDL-C and increased levels of free LDL-C in the plasma. Individuals with familial hypercholesterolemia often may have gain of function mutations in the PCSK9 molecules in their body, resulting in increased LDL-C plasma levels and a consequent cardiovascular risk. Evolocumab is able to bind both the normal PCSK9 and the gain of function mutant, D374Y. The exact mechanism of the binding has not been published, however the precursor molecule, mAb1, is indicative of the interaction. The mAb1 molecule binds on the catalytic site of PCSK9 next to the binding site for the LDL receptor and creates hydrogen bonds and hydrophobic interactions, resulting in the steric inhibition of binding between PCSK9 and the LDL receptor. Because the formation of complexes between LDL receptor and PCSK9 are prevented, the internalized LDL receptors are less likely to be degrated by lysosomes and may recycle to the surface of the cell to serve their function of removing LDL from the blood. | NA | NA | Total bioavailability from subcutaneous injection was 82% in cynomolgus monkeys. | NA | Evolocumab showed non-linear, dose-dependent clearance in healthy volunteers; clearance decreased with increasing dose. | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Anticholesteremic Agents,Antimetabolites,Blood Proteins,Globulins,Hypolipidemic Agents,Hypolipidemic Agents Indicated for Hyperlipidemia,Immunoglobulins,Immunoproteins,Lipid Modifying Agents,Lipid Modifying Agents, Plain,Lipid Regulating Agents,Non-statin Hypolipidemic Agents Indicated for Hyperlipidemia,Noxae,PCSK9 Inhibitor,Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Inhibitors,Proteins,Serum Globulins,Toxic Actions | NA | NA | NA | The risk or severity of adverse effects can be increased when Evolocumab is combined with Belimumab. | Proprotein convertase subtilisin/kexin type 9 | Repatha | Amgen Inc | Amgen Inc | REPATHA™ is indicated as an adjunct to diet and maximally tolerated statin therapy for the treatment of adults with heterozygous familial hypercholesterolemia (HeFH) or clinical atherosclerotic cardiovascular disease (CVD), who require additional lowering of low density lipoprotein cholesterol (LDL-C); Also indicated as an adjunct to diet and other LDL-lowering therapies (e.g., statins, ezetimibe, LDL apheresis) for the treatment of patients with homozygous familial hypercholesterolemia (HoFH) who require additional lowering of LDL-C. | NA | 140 mg/mL | injection, solution | Subcutaneous | The recommended subcutaneous dosage of REPATHA in patients with HeFH or patients with primary hyperlipidemia with established clinical atherosclerotic CVD is either 140 mg every 2 weeks OR 420 mg once monthly. When switching dosage regimens, administer the first dose of the new regimen on the next scheduled date of the prior regimen. The recommended subcutaneous dosage of REPATHA in patients with HoFH is 420 mg once monthly. In patients with HoFH, measure LDL-C levels 4 to 8 weeks after starting REPATHA, since response to therapy will depend on the degree of LDL-receptor function. | REPATHA is contraindicated in patients with a history of a serious hypersensitivity reaction to REPATHA | Allergic reactions | 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 |
| 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 |
| 10842 | Th1205 | Obiltoxaximab | NA | 148000 | NA | NA | NA | NA | NA | Obiltoxaximab, an affinity-enhanced monoclonal antibody (Mab), is used for prevention and treatment of infection and death caused by anthrax toxin. Obiltoxaximab is a chimeric IgG1 kappa monoclonal antibody (mAb) that binds the PA component of B. anthracis toxin. It has an approximate molecular weight of 148 kDa. | Investigated for use/treatment in anthrax exposure, bacterial infection, crohn's disease, and graft versus host disease. | NA | ETI-204 is an affinity-enhanced, de-immunized antibody, which means that its ability to bind to its target pathogen has been strengthened and that elements that might cause an immune response have been removed. ETI-204 targets and binds to Protective Antigen, which prevents the anthrax toxins from binding to and entering the cells in the body, thereby preventing death. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins,Anthrax Protective Antigen-directed Antibody,Anthrax Protective Antigen-directed Antibody Interactions,Antibodies,Antiinfectives for Systemic Use,Biological Products,Blood,Blood Proteins,Body Fluids,Complex Mixtures,Fluids and Secretions,Globulins,Hemic and Immune Systems,Immune Sera,Immune Sera and Immunoglobulins,Immunoglobulins,Immunoproteins,Proteins,Serum,Serum Globulins,Specific Immunoglobulins | NA | NA | NA | NA | NA | Anthim | Elusys Therapeutics, Inc. | Elusys Therapeutics, Inc. | ANTHIM is indicated in adult and pediatric patients for the treatment of inhalational anthrax due to Bacillus anthracis in combination with appropriate antibacterial drugs.; Also is indicated for prophylaxis of inhalational anthrax due to B. anthracis when alternative therapies are not available or not appropriate. | NA | Solution | Liquid | Intravenous infusion | The recommended dosage of ANTHIM in adult patients is a single dose of 16 mg/kg administered intravenously over 90 minutes (1 hour and 30 minutes); For adult patients weighing less than 40 kg. | NA | Hypersensitivity and Anaphylaxis | Link | NA | NA |
| 10847 | Th1210 | Mepolizumab | NA | 149000 | NA | NA | NA | NA | 16 to 22 days. | Mepolizumab is a humanized IL-5 antagonist monoclonal antibody produced by recombinant DNA technology in Chinese hamster ovary cells. It has a molecular weight of approximately 149 kDa. It was approved by the FDA in November, 2015 for the treatment of asthma under the brand name Nucala (marketed by GlaxoSmithKline). Mepolizumab has been investigated in the treatment of severe nasal polyposis, among numerous other conditions. | Mepolizumab is indicated for add-on maintenance treatment of severe eosinophilic asthma, as identified by blood eosinophils greater than or equal to 150 cells/μl at initiation of treatment or blood eosinophils greater than or equal to 300 cells/μl in the past 12 months, in patients aged 12 years and older. Mepolizumab has been shown to reduce exacerbations of asthma in patients with an exacerbation history | The pharmacodynamic response (blood eosinophil reduction) following repeat doses of mepolizumab administered subcutaneously or intravenously was evaluated in subjects with asthma and blood eosinophil levels greater than 200 cells/mcL. Subjects received 1 of 4 mepolizumab treatments (administered every 28 days for a total of 3 doses): 12.5 mg SC, 125 mg SC, 250 mg SC, or 75 mg IV. Sixty-six (66) of the 70 randomized subjects completed the trial. Compared with baseline levels, blood eosinophils decreased in a dose-dependent manner. A reduction in blood eosinophil levels was observed in all treatment groups by Day 3. On Day 84 (4 weeks post-last dose), the observed geometric mean reduction from baseline in blood eosinophils was 64%, 78%, 84%, and 90% in the 12.5-mg SC, 75-mg IV, 125-mg SC, and 250-mg SC treatment groups, respectively. The model-predicted SC doses providing 50% and 90% of maximal reduction of blood eosinophils at Day 84 were estimated to be 11 and 99 mg, respectively. These results, along with the clinical efficacy data from the dose-ranging exacerbation trial (Trial 1) supported the evaluation of mepolizumab 75 mg IV and 100 mg SC in the confirmatory trials [see Clinical Studies (14)]. Following SC administration of mepolizumab 100 mg every 4 weeks for 32 weeks (Trial 2), blood eosinophils were reduced to a geometric mean count of 40 cells/mcL, which corresponds to a geometric mean reduction of 84% compared with placebo. This magnitude of reduction was observed within 4 weeks of treatment and was maintained throughout the treatment period | Mepolizumab is an interleukin-5 antagonist (IgG1 kappa). IL-5 is the major cytokine responsible for the growth and differentiation, recruitment, activation, and survival of eosinophils. Mepolizumab binds to IL-5 with a dissociation constant of 100 pM, inhibiting the bioactivity of IL-5 by blocking its binding to the alpha chain of the IL-5 receptor complex expressed on the eosinophil cell surface. Inflammation is an important component in the pathogenesis of asthma. Multiple cell types (e.g., mast cells, eosinophils, neutrophils, macrophages, lymphocytes) and mediators (e.g., histamine, eicosanoids, leukotrienes, cytokines) are involved in inflammation. Mepolizumab, by inhibiting IL-5 signaling, reduces the production and survival of eosinophils; however, the mechanism of mepolizumab action in asthma has not been definitively established. | Toxicity information regarding mepolizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as newly established or worsening chronic infections, including those caused by helminths, and generalized immune depression. Symptomatic and supportive measures are recommended.[L16518] | As a monoclonal antibody, mepolizumab is subject to proteolytic degradation at sites distributed throughout the body.[L16518] | Mepolizumab is administered subcutaneously and has a bioavailability of approximately 80% based on a 100 mg dose given to both adult and adolescent subjects with asthma. With the recommended four-week dosing schedule, there is an approximately two-fold accumulation of mepolizumab at steady-state.[L16518] | Mepolizumab has a population central volume of distribution of 3.6 L (for a 70 kg individual) in adult asthma patients.[L16518] | Mepolizumab has an estimated apparent population systemic clearance of 0.28 L/day (for a 70-kg individual) in adult and adolescent subjects.[L16518] | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Drugs for Obstructive Airway Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Interleukin-5 Antagonist,Proteins,Serum Globulins | US2008134721 | NA | NA | NA | Interleukin-5 | Nucala | Glaxosmithkline Inc | Glaxosmithkline Inc | NUCALA® is indicated for the add-on maintenance treatment of patients with severe asthma aged 12 years and older, and with an eosinophilic phenotype. | NA | 100 mg/mL | lyophilized powder | subcutaneous | The recommended dose of NUCALA is 100 mg administered once every 4 weeks by subcutaneous injection into the upper arm, thigh, or abdomen. | NUCALA should not be administered to patients with a history of hypersensitivity to mepolizumab or excipients in the formulation. | Hypersensitivity reactions; Opportunistic infections: herpes zoster | 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 |
| 10860 | Th1222 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant, human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It is expressed in a murine Sp2/0-Ag14 cell line and comprised of two 447- (or 448-) residue heavy chains and two 214-residue light chains, with a molecular mass of 145157 Daltons when deglycosylated. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at asparagine 298 (Asn 298). Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). Canakinumab is marketed under the brand name Ilaris and indicated for patients 4 years of age and older to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS) as well as for patients 2 years of age and older to treat systemic juvenile idiopathic arthritis (SJIA). Clinical trials have established the administration of canakinumab every 2 weeks to be safe and effective, offering a considerable advantage over the existing treatment with the human IL-1 receptor antagonist, anakinra, which must be injected daily and which is often poorly tolerated by patients. | Used in patients 4 years of age and older to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS) as well as for patients 2 years of age and older to treat systemic juvenile idiopathic arthritis (SJIA). | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | * 6.01 L [typical CAPS patient weighing 70 kg] | * 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | The risk or severity of adverse effects can be increased when Canakinumab is combined with Adalimumab, Afelimomab, Anakinra, BCG, Certolizumab pegol, Denosumab, Etanercept, Fingolimod, G17DT, GI-5005 etc | Interleukin-1 beta | Ilaris | Novartis | Novartis | Ilaris is used to treat certain types of periodic fever syndromes, sometimes called auto-inflammatory syndromes. | NA | Each vial of sterile, white, preservative-free, lyophilized powder contains canakinumab 150 mg. Nonmedicinal ingredients: sucrose, L-histidine, L-histidine HCL monohydrate, polysorbate 80. | Lyphilized powder | Subcutaneous | The recommended dose of Ilaris is 150 mg for CAPS patients with body weight greater than 40 kg. For CAPS patients with body weight greater than or equal to 15 kg and less than or equal to 40 kg, the recommended dose is 2 mg/kg. For children 15 to 40 kg with an inadequate response, the dose can be increased to 3 mg | Confirmed hypersensitivity to the active substance or to any of the excipients. | The most common adverse reactionsgreater than 10% reported by patients treated with ILARISare nasopharyngitis, diarrhea, influenza, rhinitis, nausea, headache, bronchitis, gastroenteritis, pharyngitis, weight increased, musculoskeletal pain, and vertigo. | Link | NA | NA |
| 10871 | Th1231 | Ibritumomab tiuxetan | >Th1231_Ibritumomab_tiuxetan QAYLQQSGAELVRPGASVKMSCKASGYTFTSYNMHWVKQTPRQGLEWIGAIYPGNGDTSYNQKFKGKATLTVDKSSSTAYMQLSSLTSEDSAVYFCARVVYYSNSYWYFDVWGTGTTVTVSAPSVYPLAPVCGDTTGSSVTLGCLVKGYFPEPVTLTWNSGSLSSGVHTFPAVLQSDLYTLSSSVTVTSSTWPSQSITCNVAHPASSTKVDKKIEPRGPTIKPCPPCKCPAPNLLGGPSVFIFPPKIKDVLMISLSPIVTCVVVDVSEDDPDVQISWFVNNVEVHTAQTQTHREDYNSTLRVVSALPIQHQDWMSGKEFKCKVNNKDLPAPIERTISKPKGSVRAPQVYVLPPPEEEMTKKQVTLTCMVTDFMPEDIYVEWTNNGKTELNYKNTEPVLDSDGSYFMYSKLRVEKKNWVERNSYSCSVVHEGLHNHHTTKSFSR | 143375.5 | C6382H9830N1672O1979S54 | 7.91 | -0.359 | 61 °C (FAB fragment), 71 °C (whole mAb) | 0.8 hours | Indium or yttrium conjugated murine IgG1 kappa monoclonal antibody directed against the CD20 antigen, which is found on the surface of normal and malignant B lymphocytes. Ibritumomab is produced in Chinese hamster ovary cells and is composed of two murine gamma 1 heavy chains of 445 amino acids each and two kappa light chains of 213 amino acids each. | For treatment of non-Hodgkin's lymphoma | Ibritumomab is a murine monoclonal antibody against CD20 that has been radiolabeled with yttrium-90. | The Fab segment of the antibody targets the CD20 epitope on B-cells, allowing the radioactive yttrium to destroy the cell via production of beta particles. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to B cells, or by human antimurine antibody production | NA | Binding observed on lymphoid cells of the bone marrow, lymph node, thymus, red and white pulp of the spleen, lymphoid follicles of the tonsil, and lymphoid nodules of other organs (e.g., large and small intestines) | Approximately 7.2% of injected dose of yttrium Y 90 ibritumomab tiuxetan is excreted in urine within 7 days. | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antigens, CD20,Blood Proteins,Cancer immunotherapy,CD20-directed Antibody Interactions,CD20-directed Radiotherapeutic Antibody,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Lymphoma, B-Cell,Myelosuppressive Agents,Proteins,Radiopharmaceutical Activity,Serum Globulins,Therapeutic Radiopharmaceuticals,Various Therapeutic Radiopharmaceuticals,Yttrium Radioisotopes | CA2149329 | 15-07-2008 | 11-Dec-2013 | The risk or severity of adverse effects can be increased while combining Ibritumomab tiuxetan with Abciximab, Acenocoumarol, Acetylsalicylic acid, Alprostadil, Anagrelide, Ancrod, Antithrombin III human, Apixaban, Ardeparin, Argatroban. | B-lymphocyte antigen CD20 | Zevalin | Spectrum Pharmaceuticals B.V. | Spectrum Pharmaceuticals B.V. | Zevalin is indicated for the treatment of relapsed or refractory, low-grade or follicular B-cell non-Hodgkin's lymphoma (NHL). | NA | 3.2 mg ibritumomab tiuxetan per 2 mL in a single-use vial. The contents of all vials are sterile, pyrogenfree, contain no preservatives, and are not radioactive. | Colourless Solution | Intravenous | nitiate the Zevalin therapeutic regimen following recovery of platelet counts to ≥ 150,000/mm³ at least 6 weeks, but no more than 12 weeks, following the last dose of first-line chemotherapy | None. | Serious Infusion Reactions, Severe Cutaneous and Mucocutaneous Reactions, Prolonged and Severe Cytopeniasmight occur | Link | NA | NA |
| 11150 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging” or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab')2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,High affinity immunoglobulin gamma Fc receptor IB,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-A,Low affinity immunoglobulin gamma Fc region receptor III-B,Complement C3,Complement C4-A,Complement C4-B,Complement C5 | Bivigam | Kedrion Biopharma, Inc. | Kedrion Biopharma, Inc. | Intravenous | 1 g/10mL | BIVIGAM is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. BIVIGAM is contraindicated in IgA deficiency patients with antibodies to IgA and a history of hypersensitivity. | headache fatigue infusion site reaction nausea sinus infection increased blood pressure diarrhea dizziness tiredness back pain migraine muscle pain, and sore throat | Immune globulin intravenous (IGIV, for injection into a vein) is used to treat primary immunodeficiency. IGIV is also used to increase platelets (blood clotting cells) in people with immune thrombocytopenic purpura. IGIV is also used in to help prevent certain infections in people with B-cell chronic... | Bivigam [Immune Globulin Intravenous (Human), 10% Liquid] is an immune globulin used to treat primary humoral immunodeficiency (PI). | NA | 2. Cayco, A.V., M.A. Perazella, and J.P. Hayslett. Renal insufficiency after intravenous immune globulin therapy: a report of two cases and an analysis of the literature. J Am Soc Nephrol 1997; 8:1788-1794. | Link | Link | NA |
| 11719 | Th1254 | Capromab pendetide | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide [Indium In-111] during imaging to evaluate the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | * 4 ± 2.1 L | * 42 +/- 22 mL/hr | Antibodies | NA | NA | NA | NA | Glutamate carboxypeptidase 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | [(2R,3S,4R,5R)-5-(2-amino-6-oxo-1H-purin-9-yl)-4-hydroxy-2-(phosphonooxymethyl)oxolan-3-yl] dihydrogen phosphate | NA | Link | NA | NA |
| 11735 | 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 | Antibodies | 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 | Thymoglobulin | Sanofi Aventis | Sanofi Aventis | Intravenous | 25 mg / vial | THYMOGLOBULIN is contraindicated in patients with history of allergy or anaphylactic reaction to rabbit proteins or to any product excipients, or who have active acute or chronic infections that contraindicate any additional immunosuppression [see WARNINGS AND PRECAUTIONS; ADVERSE REACTIONS]. | chills low levels of white blood cells (leukopenia) headache abdominal pain high blood pressure (hypertension) nausea shortness of breath high levels of potassium in the blood (hyperkalemia) muscle pain insomnia low blood pressure (hypotension) rash sweating general feeling of being unwell (malaise), and acne | Thymoglobulin is a sterilized solution made of the cells of rabbits that have been injected with white blood cells from humans. Thymoglobulin lowers your body's immune system. The immune system helps your body fight infections. The immune system can also fight or "reject" a transplanted organ such as... | Thymoglobulin is a prescription medicine used as a prophylaxis and to treat the symptoms of Acute Rental Graft Rejection. Thymoglobulin may be used alone or with other medications. | NA | THYMOGLOBULIN® (anti-thymocyte globulin [rabbit]) is a purified, pasteurized, immunoglobulin G, obtained by immunization of rabbits with human thymocytes. This immunosuppressive product contains cytotoxic antibodies directed against antigens expressed on human T-lymphocytes. | Link | Link | NA |
| 11825 | Th1258 | Galiximab | NA | NA | NA | NA | NA | NA | 13 to 24 days | Galiximab is a chimeric monoclonal antibody which is used as an immunosuppressive drug. | Investigated for use/treatment in lymphoma (non-hodgkin's), psoriasis and psoriatic disorders, bone metastases, multiple myeloma, prostate cancer, and rheumatoid arthritis. | Galiximab is a monoclonal antibody that is being studied in the treatment of follicular non-Hodgkin lymphoma. Monoclonal antibodies are made in the laboratory and can locate and bind to cancer cells. Galiximab binds to the protein CD80, which is found on certain normal and cancerous white blood cells. | Galiximab, an IgG(1) anti-CD80 antibody, binds to CD80, a costimulatory molecule involved in T-cell activation. Reduction in lesional, activated T cells induces improvement in psoriatic plaques. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | T-lymphocyte activation antigen CD80 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11871 | Th1264 | Pexelizumab | >Th1264_Pexelizumab MADIQMTQSPSSLSASVGDRVTITCGASENIYGALNWYQRKPGKAPKLLIYGATNLADGVPSRFSGSGSGTDYTLTISSLQPEDFATYYCQNVLNTPLTFGQGTKVEIKRTGGGGSGGGGSGGGGSQVQLVQSGAEVEKPGASVKKVSCKASGYIFSNYWIQWVRQAPGQGLEWMGEILPGSGSTEYAQKFQGRVTMTADTSTSTAYMELSSLRSEDTAVYYCARYFFGSSPNYWYFDVWGQGTLVTVSS | NA | NA | NA | NA | NA | 7.0 hours to 14.5 hours. | Pexelizumab is a humanized monoclonal antibody used as an immunosuppressive drug. It is being investigated by Alexion Pharmaceuticals. | For the treatment of inflammation during cardiac surgery. | Myocardial injury and dysfunction in acute infarction and during cardiac surgery with cardiopulmonary bypass (CPB) are associated with an undesirable systemic inflammatory response, in which the complement cascade plays a major role. In animal models C5 inhibition has been found to significantly reduce myocardial infarct size and decrease cellular necrosis and apoptosis. Pexelizumab is a humanized, monoclonal, single-chain antibody fragment that inhibits C5, thereby blocking its cleavage into active forms. | Although inflammation is a normal response, continued exposure to foreign surfaces, toxic antigens, and tissue injury results in pathologic local and systemic inflammation (SIRS). This response involves multiple humoral and cellular components, including the coagulation (Factor XII, thrombin, Proteins C and S, platelets) and complement systems, cytokines (TNF-alpha, interleukins), leukocytes, monocytes, adhesion molecules (ICAM-1), and endothelial cells, among others. The complement system is a group of glycoproteins, which, when activated, results in the formation of C3-convertase, which converts C3 to C3a and C3b. C3a cleaves C5 to C5a and C5b. C5b, in conjunction with C6, C7, C8, and C9, forms the membrane attack or terminal complement complex (TCC) C5b-9. Both C5a and C5b-9 activate, promote, and amplify inflammatory components, and likely play central roles in the development of SIRS, tissue injury, reperfusion injury, and apoptosis. Pexelizumab, a recombinant humanized single chain monoclonal antibody to C5, blocks the conversion of C5 to C5a and C5b-9. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11872 | Th1264 | Pexelizumab | >Th1264_Pexelizumab MADIQMTQSPSSLSASVGDRVTITCGASENIYGALNWYQRKPGKAPKLLIYGATNLADGVPSRFSGSGSGTDYTLTISSLQPEDFATYYCQNVLNTPLTFGQGTKVEIKRTGGGGSGGGGSGGGGSQVQLVQSGAEVEKPGASVKKVSCKASGYIFSNYWIQWVRQAPGQGLEWMGEILPGSGSTEYAQKFQGRVTMTADTSTSTAYMELSSLRSEDTAVYYCARYFFGSSPNYWYFDVWGQGTLVTVSS | NA | NA | NA | NA | NA | 7.0 hours to 14.5 hours. | Pexelizumab is a humanized monoclonal antibody used as an immunosuppressive drug. It is being investigated by Alexion Pharmaceuticals. | For the treatment of inflammation during cardiac surgery. | Myocardial injury and dysfunction in acute infarction and during cardiac surgery with cardiopulmonary bypass (CPB) are associated with an undesirable systemic inflammatory response, in which the complement cascade plays a major role. In animal models C5 inhibition has been found to significantly reduce myocardial infarct size and decrease cellular necrosis and apoptosis. Pexelizumab is a humanized, monoclonal, single-chain antibody fragment that inhibits C5, thereby blocking its cleavage into active forms. | Although inflammation is a normal response, continued exposure to foreign surfaces, toxic antigens, and tissue injury results in pathologic local and systemic inflammation (SIRS). This response involves multiple humoral and cellular components, including the coagulation (Factor XII, thrombin, Proteins C and S, platelets) and complement systems, cytokines (TNF-alpha, interleukins), leukocytes, monocytes, adhesion molecules (ICAM-1), and endothelial cells, among others. The complement system is a group of glycoproteins, which, when activated, results in the formation of C3-convertase, which converts C3 to C3a and C3b. C3a cleaves C5 to C5a and C5b. C5b, in conjunction with C6, C7, C8, and C9, forms the membrane attack or terminal complement complex (TCC) C5b-9. Both C5a and C5b-9 activate, promote, and amplify inflammatory components, and likely play central roles in the development of SIRS, tissue injury, reperfusion injury, and apoptosis. Pexelizumab, a recombinant humanized single chain monoclonal antibody to C5, blocks the conversion of C5 to C5a and C5b-9. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11873 | Th1264 | Pexelizumab | >Th1264_Pexelizumab MADIQMTQSPSSLSASVGDRVTITCGASENIYGALNWYQRKPGKAPKLLIYGATNLADGVPSRFSGSGSGTDYTLTISSLQPEDFATYYCQNVLNTPLTFGQGTKVEIKRTGGGGSGGGGSGGGGSQVQLVQSGAEVEKPGASVKKVSCKASGYIFSNYWIQWVRQAPGQGLEWMGEILPGSGSTEYAQKFQGRVTMTADTSTSTAYMELSSLRSEDTAVYYCARYFFGSSPNYWYFDVWGQGTLVTVSS | NA | NA | NA | NA | NA | 7.0 hours to 14.5 hours. | Pexelizumab is a humanized monoclonal antibody used as an immunosuppressive drug. It is being investigated by Alexion Pharmaceuticals. | For the treatment of inflammation during cardiac surgery. | Myocardial injury and dysfunction in acute infarction and during cardiac surgery with cardiopulmonary bypass (CPB) are associated with an undesirable systemic inflammatory response, in which the complement cascade plays a major role. In animal models C5 inhibition has been found to significantly reduce myocardial infarct size and decrease cellular necrosis and apoptosis. Pexelizumab is a humanized, monoclonal, single-chain antibody fragment that inhibits C5, thereby blocking its cleavage into active forms. | Although inflammation is a normal response, continued exposure to foreign surfaces, toxic antigens, and tissue injury results in pathologic local and systemic inflammation (SIRS). This response involves multiple humoral and cellular components, including the coagulation (Factor XII, thrombin, Proteins C and S, platelets) and complement systems, cytokines (TNF-alpha, interleukins), leukocytes, monocytes, adhesion molecules (ICAM-1), and endothelial cells, among others. The complement system is a group of glycoproteins, which, when activated, results in the formation of C3-convertase, which converts C3 to C3a and C3b. C3a cleaves C5 to C5a and C5b. C5b, in conjunction with C6, C7, C8, and C9, forms the membrane attack or terminal complement complex (TCC) C5b-9. Both C5a and C5b-9 activate, promote, and amplify inflammatory components, and likely play central roles in the development of SIRS, tissue injury, reperfusion injury, and apoptosis. Pexelizumab, a recombinant humanized single chain monoclonal antibody to C5, blocks the conversion of C5 to C5a and C5b-9. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11901 | 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 | Antibodies | NA | NA | NA | NA | Tumor necrosis factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11913 | 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 | Antibodies | NA | NA | NA | NA | B-cell receptor CD22 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11914 | 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 | Antibodies, Monoclonal | NA | NA | NA | NA | B-cell receptor CD22 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11915 | 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 | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | B-cell receptor CD22 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11925 | Th1268 | Bectumomab | NA | NA | NA | NA | NA | NA | NA | Bectumomab (marketed under the trade name LymphoScan®) is a mouse monoclonal antibody and which it's used to treat non-Hodgkin's lymphoma. It has a radioisotope, technetium (99m TC) which it's added. | Investigated for use/treatment in lymphoma (non-hodgkin's). | NA | Using bectumomab, a mouse-derived monoclonal antibody labeled with technetium-99m (Tc-99m), a widely available, inexpensive radioisotope, medical professionals can determine through nuclear imaging the extent of CD22-expressing lymphomas. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11933 | Th1269 | Oregovomab | NA | NA | NA | NA | NA | NA | NA | Oregovomab is a murine monoclonal antibody that attaches to the tumor-associated antigen CA125. | Investigated for use/treatment in ovarian cancer. | Oregovomab is well tolerated and induces multiple antigen-specific immune responses, maintained during concomitant chemotherapy. A significant survival benefit has been observed in patients mounting a T-cell response to CA125 and/or autologous tumor. Vaccination with oregovomab may stimulate a host cytotoxic immune response against tumor cells that express CA125. | Oregovomab targets the circulating tumour-associated antigen CA 125, which is shed from the surface of human ovarian cancer cells; the antibodies induce broad cellular and humoral immune responses against CA 125 via complex formation. Unlike free CA 125, CA 125-oregovomab complexes can prime dendritic cells, leading to downstream activation of T cells. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Mucin-16 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11958 | Th1273 | IGN311 | NA | NA | NA | NA | NA | NA | NA | IGN311 is a humanized monoclonal antibody (mab) against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. | Intended for the treatment of various forms of cancer. | IGN311 is a fully humanized IgG1 variant 1 of the parent murine IgG3 mab ABL 364. It is an antibody against the Lewis-Y carbohydrate antigen and Igeneon's next-generation antibody, IGN312. | IGN311 is a humanized monoclonal antibody against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. Lewis Y is over-expressed in up to 90% of all epithelial cancers and its expression on adult normal tissues is very restricted; hence IGN311 has the potential to target a broad range of carcinomas. IGN311 is designed to exert clinical effects by destruction of tumor cells by activation of effector functions and by selective growth inhibition via functional receptors. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Epidermal growth factor receptor,Receptor tyrosine-protein kinase erbB-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11966 | Th1274 | Adecatumumab | NA | NA | NA | NA | NA | NA | NA | Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. | Investigated for use/treatment in breast cancer and prostate cancer. | NA | Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11995 | Th1276 | Labetuzumab | NA | NA | NA | NA | NA | NA | NA | Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. | Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from "http://en.wikipedia.org/wiki/Labetuzumab" | NA | labetuzumab could significantly increase the chemosensitivity of human colon and breast cancer cells in vitro to several anticancer drugs. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Carcinoembryonic antigen-related cell adhesion molecule 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11996 | Th1276 | Labetuzumab | NA | NA | NA | NA | NA | NA | NA | Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. | Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from "http://en.wikipedia.org/wiki/Labetuzumab" | NA | labetuzumab could significantly increase the chemosensitivity of human colon and breast cancer cells in vitro to several anticancer drugs. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Carcinoembryonic antigen-related cell adhesion molecule 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11997 | Th1276 | Labetuzumab | NA | NA | NA | NA | NA | NA | NA | Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. | Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from "http://en.wikipedia.org/wiki/Labetuzumab" | NA | labetuzumab could significantly increase the chemosensitivity of human colon and breast cancer cells in vitro to several anticancer drugs. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Carcinoembryonic antigen-related cell adhesion molecule 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12007 | Th1277 | Matuzumab | >Th1277_Matuzumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTSHWMHWVRQAPGQGLEWIGEFNPSNGRTNYNEKFKSKATMTVDTSTNTAYMELSSLRSEDTAVYYCASRDYDYDGRYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKS | NA | NA | NA | NA | NA | 196 hours | Matuzumab (formerly known as the experimental drug, EMD 72000) is a humanized monoclonal antibody used in cancer treatment. It has a high affinity for EGFR (epithelial growth factor receptor), frequently associated with the growth of blood vessels in malignancy, facilitating tumor growth and survival. | Investigated for use/treatment in cervical dysplasia/cancer, colorectal cancer, gastric cancer, and lung cancer. | NA | Matuzumab binds the epidermal growth factor receptor (EGFR) with high affinity, competitively blocking natural ligand binding and blocking receptor-mediated downstream signalling, resulting in impaired tumor cell proliferation. Matuzumab (EMD-72000) is a humanized IgG1 MAb that not only binds with high specificity and affinity to EGFR, but also modulates antibody-dependent cellular cytotoxicity (ADCC). | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12008 | Th1277 | Matuzumab | >Th1277_Matuzumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTSHWMHWVRQAPGQGLEWIGEFNPSNGRTNYNEKFKSKATMTVDTSTNTAYMELSSLRSEDTAVYYCASRDYDYDGRYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKS | NA | NA | NA | NA | NA | 196 hours | Matuzumab (formerly known as the experimental drug, EMD 72000) is a humanized monoclonal antibody used in cancer treatment. It has a high affinity for EGFR (epithelial growth factor receptor), frequently associated with the growth of blood vessels in malignancy, facilitating tumor growth and survival. | Investigated for use/treatment in cervical dysplasia/cancer, colorectal cancer, gastric cancer, and lung cancer. | NA | Matuzumab binds the epidermal growth factor receptor (EGFR) with high affinity, competitively blocking natural ligand binding and blocking receptor-mediated downstream signalling, resulting in impaired tumor cell proliferation. Matuzumab (EMD-72000) is a humanized IgG1 MAb that not only binds with high specificity and affinity to EGFR, but also modulates antibody-dependent cellular cytotoxicity (ADCC). | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12009 | Th1277 | Matuzumab | >Th1277_Matuzumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTSHWMHWVRQAPGQGLEWIGEFNPSNGRTNYNEKFKSKATMTVDTSTNTAYMELSSLRSEDTAVYYCASRDYDYDGRYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKS | NA | NA | NA | NA | NA | 196 hours | Matuzumab (formerly known as the experimental drug, EMD 72000) is a humanized monoclonal antibody used in cancer treatment. It has a high affinity for EGFR (epithelial growth factor receptor), frequently associated with the growth of blood vessels in malignancy, facilitating tumor growth and survival. | Investigated for use/treatment in cervical dysplasia/cancer, colorectal cancer, gastric cancer, and lung cancer. | NA | Matuzumab binds the epidermal growth factor receptor (EGFR) with high affinity, competitively blocking natural ligand binding and blocking receptor-mediated downstream signalling, resulting in impaired tumor cell proliferation. Matuzumab (EMD-72000) is a humanized IgG1 MAb that not only binds with high specificity and affinity to EGFR, but also modulates antibody-dependent cellular cytotoxicity (ADCC). | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12017 | Th1278 | Fontolizumab | NA | NA | NA | NA | NA | NA | NA | Fontolizumab (marketed under the trade name HuZAF™) is a humanized monoclonal antibody which is used as an immunosuppressive drug to treat Crohn's disease. | Investigated for use/treatment in crohn's disease and psoriasis and psoriatic disorders. | NA | Fontolizumab is a humanised antibody directed against recombinant human IFN-{gamma}. The antibody binds to natural human IFN-{gamma} and inhibits expression of IFN-{gamma} regulated genes known to be upregulated in Crohn’s disease. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Interferon gamma | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12018 | Th1278 | Fontolizumab | NA | NA | NA | NA | NA | NA | NA | Fontolizumab (marketed under the trade name HuZAF™) is a humanized monoclonal antibody which is used as an immunosuppressive drug to treat Crohn's disease. | Investigated for use/treatment in crohn's disease and psoriasis and psoriatic disorders. | NA | Fontolizumab is a humanised antibody directed against recombinant human IFN-{gamma}. The antibody binds to natural human IFN-{gamma} and inhibits expression of IFN-{gamma} regulated genes known to be upregulated in Crohn’s disease. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Interferon gamma | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12019 | Th1278 | Fontolizumab | NA | NA | NA | NA | NA | NA | NA | Fontolizumab (marketed under the trade name HuZAF™) is a humanized monoclonal antibody which is used as an immunosuppressive drug to treat Crohn's disease. | Investigated for use/treatment in crohn's disease and psoriasis and psoriatic disorders. | NA | Fontolizumab is a humanised antibody directed against recombinant human IFN-{gamma}. The antibody binds to natural human IFN-{gamma} and inhibits expression of IFN-{gamma} regulated genes known to be upregulated in Crohn’s disease. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Interferon gamma | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12027 | Th1279 | Bavituximab | >Th1279_Bavituximab EVQLQQSGPELEKPGASVKLSCKASGYSFTGYNMNWVKQSHGKSLEWIGHIDPYYGDTSYNQKFRGKATLTVDKSSSTAYMQLKSLTSEDSAVYYCVKGGYYGHWYFDVWGAGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | 30 Hrs | Bavituximab is a chimeric Anti-PS monoclonal antibody analog which is used to potentially treat cancers and viral infections. It binds to phosphatidylserine and other exposed host cell lipids when induced by cellular stress. Additional analogs in the class include 3G4, 2aG4, 9d2 and Hu3g4. | Investigated for use/treatment in breast cancer, cancer/tumors (unspecified), HIV infection, hepatitis (viral, C), and solid tumors. | NA | Bavituximab Anti-Cancer is a monoclonal antibody that binds to a basic component of the cell structure called a phospholipid that is exposed only on the surface of tumor blood vessel cells or on cells infected with certain viruses. Bavituximab binding to the tumor blood vessel cells alerts the body’s immune system to attack the tumor and its blood supply. This has been shown to inhibit tumor growth and development. Because in healthy cells the phospholipids are concealed inside the cell, the bavituximab does not bind to them. This targets the bavituximab to the malignant cells and potentially minimizes unwanted side effects. Bavituximab Anti-Viral represents a unique approach to treating viral diseases by recognizing features found only on infected cells and enveloped viruses. Bavituximab is a monoclonal antibody that binds to a basic component of the cell structure called an aminophospholipid that is exposed on the surface of cells only when they are infected with certain viruses or when they are malignant. After binding to these infected cells, the drug alerts the body’s immune system to attack the infected cells. This makes infected cells particularly susceptible to bavituximab treatment, while potentially sparing healthy cells. Also, bavituximab binds to phospholipids which are derived from the host (human) cell and not the virus, which indicates it may not be susceptible to viral drug resistance. In addition to treating an active illness, bavituximab may also confer long-term immunity. Bavituximab induces a pro-inflammatory cytokine profile, defined as an increase in the ratio of TNF alpha and TGF beta. Stimulating an immune response is a key proposed anti-viral mechanism of action of bavituximab. | Direct clearance of free virus and antibody-dependent cellular cytotoxicity of virus-infected cells appear to be the major mechanisms that contribute to the anti-viral effect of bavituximab | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12037 | Th1280 | CR002 | >Th1280_CR002 MVRHPYSVQTQLSTEAKAIWRSMQQQETNLLANLTTNDARDNSKDFQNSKVGAAATSRDEGCNCPIIGEIVISCYWLFEIPPLISE | NA | NA | NA | NA | NA | NA | CR002 is a novel investigational fully human monoclonal antibody that blocks the activity of excess platelet-derived growth factor-D (PDGF-D), a target shown to play a role in kidney inflammation. This is a novel therapeutic approach to treat kidney inflammation. | Investigated for use/treatment in nephropathy. | NA | CR002 blocks the activity of excess platelet-derived growth factor-D (PDGF-D), a target shown to play a role in kidney inflammation. Diabetic nephropathy, IgA nephropathy, and lupus nephritis are histologically characterized by glomerular mesangial cell proliferation and extracellular matrix accumulation. PDGF-D and its receptors play an important role in the pathogenesis of nephritis, based on their potent induction of mesangial cell proliferation and extracellular matrix accumulation shown both in vitro and in vivo. A fully human monoclonal antibody that neutralizes PDGF-D represents a novel therapeutic approach to block nephritides. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Platelet-derived growth factor D | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12052 | Th1282 | Rozrolimupab | NA | NA | NA | NA | NA | NA | NA | Rozrolimupab is a recombinant polyclonal antibody consisting of 25 different anti-Rhesus D (RhD) antibodies to replace existing anti-RhD hyperimmune immunoglobulins for the treatment of Idiopathic Thrombocytopenic Purpura (ITP) and the prevention of Hemolytic Disease of Newborns (HDN). | Investigated for use/treatment in thrombocytopenia. | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Rhesus blood group D antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12118 | Th1287 | Girentuximab | >Th1287_Girentuximab DVKLVESGGGLVKLGGSLKLSCAASGFTFSNYYMSWVRQTPEKRLELVAAINSDGGITYYLDTVKGRFTISRDNAKNTLYLQMSSLKSEDTALFYCARHRSGYFSMDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Girentuximab is a monoclonal chimeric (mouse/human) antibody directed against carbonic anhydrase IX, an antigen expressed in 95% of clear cell renal cell carcinomas (RCC). | Investigated for use/treatment in gall bladder cancer and renal cell carcinoma. | NA | Mechanism of action of girentuximab is antibody dependent cellular cytotoxicity (ADCC). As a monotherapy in metastatic renal cell carcinomas(RCC), girentuximab demonstrated minimal clinical activity with a 3% partial response rate and a median survival of 16 months. In vitro data suggest that the number of activated ADCC effector cells can be upregulated by low dose interleukin 2 (IL2) administered in a pulsatile fashion. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Carbonic anhydrase 9,Interleukin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12150 | Th1291 | Oportuzumab monatox | >Th1291_Oportuzumab_monatox HHHHHHDIQMTQSPSSLSASVGDRVTITCRSTKSLLHSNGITYLYWYQQKPGKAPKLLIYQMSNLASGVPSRFSSSGSGTDFTLTISSLQPEDFATYYCAQNLEIPRTFGQGTKVELKRATPSHNSHQVPSAGGPTANSGTSGSEVQLVQSGPGLVQPGGSVRISCAASGYTFTNYGMNWVKQAPGKGLEWMGWINTYTGESTYADSFKGRFTFSLDTSASAAYLQINSLRAEDTAVYYCARFAIKGDYWGQGTLLTVSSEFGGAPEFPKPSTPPGSSGLEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAASADVVSLTCPVAAGECAGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTGLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPHHHHHHKDEL | NA | NA | NA | NA | NA | NA | VB4-845 is studied in the treatment of certain types of head and neck cancer. VB4-845 is made by linking a monoclonal antibody fragment to a toxic protein that may kill cancer cells. VB4-845 is a fusion protein containing humanized scFv specific for the epithelial cell adhesion molecule, Ep-CAM, a tumor cell-associated target highly expressed on carcinoma cells of epithelial origin and a truncated portion of Pseudomonas exotoxin A. | Investigated for use/treatment in bladder cancer and head and neck cancer. | NA | VB4-845 binds to EpCAM (a protein on the surface of epithelial cells and some types of cancer cells). Also called anti-EpCAM-Pseudomonas-exotoxin fusion protein and Proxinium. It targets and kills Ep-CAM-positive tumors by apoptosis. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Epithelial cell adhesion molecule | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12151 | Th1291 | Oportuzumab monatox | >Th1291_Oportuzumab_monatox HHHHHHDIQMTQSPSSLSASVGDRVTITCRSTKSLLHSNGITYLYWYQQKPGKAPKLLIYQMSNLASGVPSRFSSSGSGTDFTLTISSLQPEDFATYYCAQNLEIPRTFGQGTKVELKRATPSHNSHQVPSAGGPTANSGTSGSEVQLVQSGPGLVQPGGSVRISCAASGYTFTNYGMNWVKQAPGKGLEWMGWINTYTGESTYADSFKGRFTFSLDTSASAAYLQINSLRAEDTAVYYCARFAIKGDYWGQGTLLTVSSEFGGAPEFPKPSTPPGSSGLEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYLAARLSWNQVDQVIRNALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAASADVVSLTCPVAAGECAGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTGLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTVVIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPHHHHHHKDEL | NA | NA | NA | NA | NA | NA | VB4-845 is studied in the treatment of certain types of head and neck cancer. VB4-845 is made by linking a monoclonal antibody fragment to a toxic protein that may kill cancer cells. VB4-845 is a fusion protein containing humanized scFv specific for the epithelial cell adhesion molecule, Ep-CAM, a tumor cell-associated target highly expressed on carcinoma cells of epithelial origin and a truncated portion of Pseudomonas exotoxin A. | Investigated for use/treatment in bladder cancer and head and neck cancer. | NA | VB4-845 binds to EpCAM (a protein on the surface of epithelial cells and some types of cancer cells). Also called anti-EpCAM-Pseudomonas-exotoxin fusion protein and Proxinium. It targets and kills Ep-CAM-positive tumors by apoptosis. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Epithelial cell adhesion molecule | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12219 | Th1300 | XTL-001 | NA | NA | NA | NA | NA | NA | NA | XTL001 is an investigational monoclonal antibody (MAb) product developed by XTL Biopharmaceuticals to evaluate the safety profile and antiviral activity of the compound in patients chronically infected with hepatitis B virus (HBV). | Investigated for use/treatment in hepatitis (viral, B). | NA | XTL001 is a combination of two high-affinity, fully human monoclonal antibodies that bind to distinct sites on the surface antigen of HBV to neutralize the virus and limit viral escape. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12227 | Th1301 | NAV 1800 | NA | NA | NA | NA | NA | NA | NA | RIGScan CR49, a 125I-labelled CR monoclonal antibody directed against the tumour-associated antigen TAG-72, is undergoing development with Neoprobe for the intraoperative detection of metastatic colorectal cancer. | Investigated for use/treatment in colorectal cancer and solid tumors. | NA | RIGScan CR49 is used to locate cancerous tissue during surgery for patients with metastatic cancer of the colon or rectum (colorectal). In multicenter Phase II and pivotal Phase III clinical trials, RIGScan CR49 located tumor confirmed by pathology tests in 90 percent of evaluable patients who participated in the studies. The product found pathology-confirmed tumor that was missed by the surgeon and by preoperative diagnostic scans in one of five of the evaluable patients. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12237 | 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 | Antibodies | 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 |
| 12250 | Th1305 | Otelixizumab | NA | NA | NA | NA | NA | NA | NA | Otelixizumab is a monoclonal antibody that binds to a receptor found on all T cells called CD3, which is involved in normal T cell signaling. Otelixizumab is believed to inhibit the function of autoreactive T cells, which are important in propagating autoimmune diseases, while inducing regulatory T cell pathways that promote immunological tolerance and inhibit autoreactive disease activity. Tolerx is developing otelixizumab to treat patients with type 1 diabetes, psoriasis and other autoimmune diseases such as rheumatoid arthritis. | Investigated for use/treatment in diabetes mellitus type 1, pediatric indications, and psoriasis and psoriatic disorders. | Otelixizumab is a monoclonal antibody that binds to a receptor found on all T cells called CD3, which is involved in normal T cell signaling. Tolerx is developing otelixizumab to treat patients with type 1 diabetes, psoriasis and other autoimmune diseases such as rheumatoid arthritis. | Otelixizumab is a monoclonal antibody that binds to a receptor found on all T cells called CD3, which is involved in normal T cell signaling. Otelixizumab is believed to inhibit the function of autoreactive T cells, which are important in propagating autoimmune diseases, while inducing regulatory T cell pathways that promote immunological tolerance and inhibit autoreactive disease activity. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12251 | Th1305 | Otelixizumab | NA | NA | NA | NA | NA | NA | NA | Otelixizumab is a monoclonal antibody that binds to a receptor found on all T cells called CD3, which is involved in normal T cell signaling. Otelixizumab is believed to inhibit the function of autoreactive T cells, which are important in propagating autoimmune diseases, while inducing regulatory T cell pathways that promote immunological tolerance and inhibit autoreactive disease activity. Tolerx is developing otelixizumab to treat patients with type 1 diabetes, psoriasis and other autoimmune diseases such as rheumatoid arthritis. | Investigated for use/treatment in diabetes mellitus type 1, pediatric indications, and psoriasis and psoriatic disorders. | Otelixizumab is a monoclonal antibody that binds to a receptor found on all T cells called CD3, which is involved in normal T cell signaling. Tolerx is developing otelixizumab to treat patients with type 1 diabetes, psoriasis and other autoimmune diseases such as rheumatoid arthritis. | Otelixizumab is a monoclonal antibody that binds to a receptor found on all T cells called CD3, which is involved in normal T cell signaling. Otelixizumab is believed to inhibit the function of autoreactive T cells, which are important in propagating autoimmune diseases, while inducing regulatory T cell pathways that promote immunological tolerance and inhibit autoreactive disease activity. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12268 | Th1308 | AMG 108 | NA | NA | NA | NA | NA | NA | NA | AMG 108 was investigated for use as an antirheumatic agent. | Investigated for use/treatment in osteoarthritis and rheumatoid arthritis. | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12277 | Th1309 | Iratumumab | NA | NA | NA | NA | NA | NA | NA | Immunoglobulin G1, anti-(human CD30 (antigen)) (human monoclonal MDX-060 heavy chain), disulfide with human monoclonal MDX-060 light chain, dimer. Molecular weight is approximately 170,000 daltons. In phase I/II clinical trials for treatment of CD30+ lymphomas. | Investigated for use/treatment in lymphoma (unspecified). | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12285 | Th1310 | Enokizumab | NA | NA | NA | NA | NA | NA | NA | A humanized immunoglobulin G1k anti-interleukin-9 mAb. | Investigated for use/treatment in asthma. | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12286 | Th1310 | Enokizumab | NA | NA | NA | NA | NA | NA | NA | A humanized immunoglobulin G1k anti-interleukin-9 mAb. | Investigated for use/treatment in asthma. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12287 | Th1310 | Enokizumab | NA | NA | NA | NA | NA | NA | NA | A humanized immunoglobulin G1k anti-interleukin-9 mAb. | Investigated for use/treatment in asthma. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12312 | Th1312 | Cantuzumab ravtansine | >Th1312_Cantuzumab_ravtansine XVQLVQSGAEVKKPGETVKISCKASDYTFTYYGMNWVKQAPGQGLKWMGWIDTTTGEPTYAQKFQGRIAFSLETSASTAYLQIKSLKSEDTATYFCARRGPYNWYFDVWGQGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | C6570H10130N1726O2018S44(C42H59ClN3O11S2)n | NA | NA | NA | NA | 0 | Investigated for use/treatment in gastric cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12313 | Th1312 | Cantuzumab ravtansine | >Th1312_Cantuzumab_ravtansine XVQLVQSGAEVKKPGETVKISCKASDYTFTYYGMNWVKQAPGQGLKWMGWIDTTTGEPTYAQKFQGRIAFSLETSASTAYLQIKSLKSEDTATYFCARRGPYNWYFDVWGQGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | C6570H10130N1726O2018S44(C42H59ClN3O11S2)n | NA | NA | NA | NA | 0 | Investigated for use/treatment in gastric cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12319 | Th1313 | Farletuzumab | >Th1313_Farletuzumab EVQLVESGGGVVQPGRSLRLSCSASGFTFSGYGLSWVRQAPGKGLEWVAMISSGGSYTYYADSVKGRFAISRDNAKNTLFLQMDSLRPEDTGVYFCARHGDDPAWFAYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Farletuzumab (MORAb-003) is a fully humanized monoclonal antibody against the folate receptor alpha, for the potential treatment of epithelial ovarian cancer. | Investigated for use/treatment in ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Folate receptor alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12320 | Th1313 | Farletuzumab | >Th1313_Farletuzumab EVQLVESGGGVVQPGRSLRLSCSASGFTFSGYGLSWVRQAPGKGLEWVAMISSGGSYTYYADSVKGRFAISRDNAKNTLFLQMDSLRPEDTGVYFCARHGDDPAWFAYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Farletuzumab (MORAb-003) is a fully humanized monoclonal antibody against the folate receptor alpha, for the potential treatment of epithelial ovarian cancer. | Investigated for use/treatment in ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Folate receptor alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12321 | Th1313 | Farletuzumab | >Th1313_Farletuzumab EVQLVESGGGVVQPGRSLRLSCSASGFTFSGYGLSWVRQAPGKGLEWVAMISSGGSYTYYADSVKGRFAISRDNAKNTLFLQMDSLRPEDTGVYFCARHGDDPAWFAYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Farletuzumab (MORAb-003) is a fully humanized monoclonal antibody against the folate receptor alpha, for the potential treatment of epithelial ovarian cancer. | Investigated for use/treatment in ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Folate receptor alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12342 | 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 | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12343 | 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 | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12344 | 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 | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12380 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Antibodies | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | Kadcyla | Genentech, Inc. | Genentech, Inc. | Intravenous | 20 mg/1mL | None. | fatigue, tiredness, nausea, musculoskeletal pain, headache, constipation, low platelet count, liver problems, low levels of red blood cells, nerve problems, and low levels of potassium in the blood. | Kadcyla is a cancer medicine that interferes with the growth and spread of cancer cells in the body. Kadcyla is used to treat HER2-positive breast cancer. Kadcyla is used both for early breast cancer and for breast cancer that has spread to other parts of the body (metastatic). Kadcyla is usually given... | Kadcyla is a prescription medicine used to treat the symptoms of Breast Cancer. Kadcyla may be used alone or with other medications. | NA | KADCYLA (ado-trastuzumab emtansine) is a HER2-targeted antibody-drug conjugate (ADC) which contains the humanized anti-HER2 IgG1, trastuzumab, covalently linked to the microtubule inhibitory drug DM1 (a maytansine derivative) via the stable thioether linker MCC (4-[N-maleimidomethyl] cyclohexane-1-carboxylate). Emtansine refers to the MCC-DM1 complex. | Link | Link | NA |
| 12381 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Antibodies, Monoclonal | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | Kadcyla | Roche Registration Gmb H | Roche Registration Gmb H | Intravenous | 100 mg | None. | fatigue, tiredness, nausea, musculoskeletal pain, headache, constipation, low platelet count, liver problems, low levels of red blood cells, nerve problems, and low levels of potassium in the blood. | Kadcyla is a cancer medicine that interferes with the growth and spread of cancer cells in the body. Kadcyla is used to treat HER2-positive breast cancer. Kadcyla is used both for early breast cancer and for breast cancer that has spread to other parts of the body (metastatic). Kadcyla is usually given... | Kadcyla is a prescription medicine used to treat the symptoms of Breast Cancer. Kadcyla may be used alone or with other medications. | NA | KADCYLA (ado-trastuzumab emtansine) is a HER2-targeted antibody-drug conjugate (ADC) which contains the humanized anti-HER2 IgG1, trastuzumab, covalently linked to the microtubule inhibitory drug DM1 (a maytansine derivative) via the stable thioether linker MCC (4-[N-maleimidomethyl] cyclohexane-1-carboxylate). Emtansine refers to the MCC-DM1 complex. | Link | Link | NA |
| 12382 | Th1320 | Trastuzumab emtansine | NA | NA | NA | NA | NA | NA | Trastuzumab emtansine has a long half life of about 4 days. | Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. | Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis. | Trastuzumab emtansine is a HER2 antibody-drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis. Trastuzumab emtansine binds to the HER2 receptor’s sub-domain IV and goes into the cell by receptor-mediated endocytosis. Lysosomes degrade trastuzumab emtansine and release DM1. DM1 binds to tubulin in microtubules and inhibits microtubule function producing cell arrest and apoptosis. As well, similar to trastuzumab, in vitro studies have shown that both HER2 receptor signalling inhibition and antibody-dependent cytotoxicity are mediated by trastuzumab emtansine. | The FDA label includes a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. | Trastuzumab emtansine undergoes lysosomal degradation to MCC-DM1, Lys-MCC-DM1, and DM1. All of these products are detected at low levels in the plasma. DM1 undergoes further degradation by CYP3A4 and CYP3A5, but DM1 does not induce or inhibit any of the CYP450 enzymes. | The absorption/ bioavailability should be close to 100% since trastuzumab emtansine is administered IV. | The volume of distribution of trastuzumab emtansine is about 3.13 L. | After IV infusion, trastuzumab emtansine has a clearance of 0.68 L/day. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Receptor tyrosine-protein kinase erbB-2 | Kadcyla | Roche Registration Gmb H | Roche Registration Gmb H | Intravenous | 160 mg | None. | fatigue, tiredness, nausea, musculoskeletal pain, headache, constipation, low platelet count, liver problems, low levels of red blood cells, nerve problems, and low levels of potassium in the blood. | Kadcyla is a cancer medicine that interferes with the growth and spread of cancer cells in the body. Kadcyla is used to treat HER2-positive breast cancer. Kadcyla is used both for early breast cancer and for breast cancer that has spread to other parts of the body (metastatic). Kadcyla is usually given... | Kadcyla is a prescription medicine used to treat the symptoms of Breast Cancer. Kadcyla may be used alone or with other medications. | NA | KADCYLA (ado-trastuzumab emtansine) is a HER2-targeted antibody-drug conjugate (ADC) which contains the humanized anti-HER2 IgG1, trastuzumab, covalently linked to the microtubule inhibitory drug DM1 (a maytansine derivative) via the stable thioether linker MCC (4-[N-maleimidomethyl] cyclohexane-1-carboxylate). Emtansine refers to the MCC-DM1 complex. | Link | Link | NA |
| 12461 | 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]. | Antibodies | NA | NA | NA | NA | B-cell receptor CD22 | Besponsa | Pfizer Canada Ulc | Pfizer Canada Ulc | Intravenous | 0.9 mg / vial | None. | low platelet counts (thrombocytopenia), low white blood cell counts (neutropenia, leukopenia), infection, anemia, fatigue, bleeding, fever, nausea, headache, febrile neutropenia, transaminases increased, abdominal pain, diarrhea, constipation, vomiting, swelling and sores inside the mouth, chills, gamma-glutamyltransferase increased, and too much bilirubin in the blood | Besponsa is a antineoplastic biological drug used to treat adults with a type of blood cancer called acute lymphoblastic leukemia (ALL), which is also known as acute lymphocytic leukemia. Besponsa is an antibody-drug conjugate - it uses an antibody to target an anticancer drug to B-cell leukemia cells.... | Besponsa (inotuzumab ozogamicin) for injection is a CD22-directed antibody-drug conjugate (ADC) indicated for the treatment of adults with relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). | NA | NA | Link | Link | NA |
| 12462 | 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]. | Antibodies, Monoclonal | NA | NA | NA | NA | B-cell receptor CD22 | Besponsa | Pfizer Europe Ma Eeig | Pfizer Europe Ma Eeig | Intravenous | 1 mg | None. | low platelet counts (thrombocytopenia), low white blood cell counts (neutropenia, leukopenia), infection, anemia, fatigue, bleeding, fever, nausea, headache, febrile neutropenia, transaminases increased, abdominal pain, diarrhea, constipation, vomiting, swelling and sores inside the mouth, chills, gamma-glutamyltransferase increased, and too much bilirubin in the blood | Besponsa is a antineoplastic biological drug used to treat adults with a type of blood cancer called acute lymphoblastic leukemia (ALL), which is also known as acute lymphocytic leukemia. Besponsa is an antibody-drug conjugate - it uses an antibody to target an anticancer drug to B-cell leukemia cells.... | Besponsa (inotuzumab ozogamicin) for injection is a CD22-directed antibody-drug conjugate (ADC) indicated for the treatment of adults with relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). | NA | NA | Link | Link | NA |
| 12463 | 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]. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | B-cell receptor CD22 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12484 | Th1327 | RI 624 | NA | NA | NA | NA | NA | NA | NA | RI 624 is a novel humanized monoclonal antibody that blocks nerve growth factor (NGF), a key mediator of acute and chronic pain. RI 624 is being developed by Rinat and is currently in Phase I clinical trials. | Investigated for use/treatment in pain (acute or chronic). | NA | RI 624 works very differently from all currently approved drugs for the treatment of pain. Unlike the other pain relievers, RI 624 primarily works to inhibit the production of NGF, rather than COX-2 for instance. NGF is a member of a family of proteins known as neurotrophins that plays a role in the growth of certain sensory neurons, an activity that appears to end at birth or shortly afterward. Pain-causing injury or inflammation induces the synthesis and stimulates the release of NGF in later stages of life. Scientific observation has shown that the up-regulation of NGF is a common component of the inflammatory response that initiates and sustains the pain sensation. NGF therefore appears to have profound direct and indirect stimulatory effects on the primary sensory neurons that mediate pain. RI 624 essentially blocks NGF from binding to its target area and thus impedes an imflammatory response. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Beta-nerve growth factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12485 | Th1327 | RI 624 | NA | NA | NA | NA | NA | NA | NA | RI 624 is a novel humanized monoclonal antibody that blocks nerve growth factor (NGF), a key mediator of acute and chronic pain. RI 624 is being developed by Rinat and is currently in Phase I clinical trials. | Investigated for use/treatment in pain (acute or chronic). | NA | RI 624 works very differently from all currently approved drugs for the treatment of pain. Unlike the other pain relievers, RI 624 primarily works to inhibit the production of NGF, rather than COX-2 for instance. NGF is a member of a family of proteins known as neurotrophins that plays a role in the growth of certain sensory neurons, an activity that appears to end at birth or shortly afterward. Pain-causing injury or inflammation induces the synthesis and stimulates the release of NGF in later stages of life. Scientific observation has shown that the up-regulation of NGF is a common component of the inflammatory response that initiates and sustains the pain sensation. NGF therefore appears to have profound direct and indirect stimulatory effects on the primary sensory neurons that mediate pain. RI 624 essentially blocks NGF from binding to its target area and thus impedes an imflammatory response. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Beta-nerve growth factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12504 | Th1329 | CT-011 | >Th1329_CT-011 MHCLPVLVILLLLIASTPSVDARPKTKDDVPLASFHGADNANRILRTLWNLRGCCEDKTCCFIG | NA | NA | NA | NA | NA | NA | CT-011 is a humanized monoclonal antibody directed against a B7 family-associated protein, in patients with advanced haematological malignancies. It is directed against human PD-1 (programmed cell death 1; PDCD1), with immunomodulating and antitumor activities. | Investigated for use/treatment in cancer/tumors (unspecified). | NA | CT-011 blocks interaction between the receptor PD-1 with its ligands, PD-1 ligand 1 (PD-1L1) and PD-1 ligand 2 (PD-1L2), resulting in the attenuation of apoptotic processes in lymphocytes, primarily effector/memory T cells, and the augmentation of the anti-tumor activities of NK cells. PD-1 is an inhibitory receptor belonging to the B7-receptor family that is expressed on lymphocytes and myeloid cells; its ligands, PD-1L1 and PD-1L2, are expressed not only by hematopoietic cells but also by cells in non-lymphoid tissues. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12517 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Antibodies | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12518 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Antibodies, Monoclonal | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12519 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12520 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Antibodies, Viral | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12523 | Th1330 | Leronlimab | >Th1330_Leronlimab EVQLVESGGGLVKPGGSLRLSCAASGYTFSNYWIGWVRQAPGKGLEWIGDIYPGGNYIRNNEKFKDKTTLSADTSKNTAYLQMNSLKTEDTAVYYCGSSFGSNYVFAWFTYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half life of a 162mg subcutaneous dose is 3.4 days while the half life of a 324mg subcutaneous dose is 3.7 days.[A192846] | Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn.[L12684] It was first described in the literature in 2001.[A3922] This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients.[A192846,A192858,L12684] | Leronlimab is currently being investigated for the treatment of a number of cancers[A192858] and HIV.[A3922] Recently leronlimab has begun a phase II clinical trial in severely ill COVID-19 patients.[L12684] Preliminary data shows a reduction in the 'cytokine storm', particularly IL-6, as well as a normalization of the CD4/CD8 T-cell ratio.[L12684] These results may mitigate immune mediate injury seen in severely ill COVID-19 patients.[L12684] | Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects.[A3922,A192858,L12684] | CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins.[A3922,A192858] When a chemokine binds CCR5, the Gaß | Data regarding overdose of leronlimab is not readily available. | Data regarding the metabolism of leronlimab is not readily available. However, as a monoclonal antibody it is expected to be degraded to smaller proteins and amino acids by proteolytic enzymes. | A 162mg subcutaneous dose reaches a Cmax of 6.1mg/L, with a Tmax of 32 hours, and an AUC of 24.4mg | Data regarding the volume of distribution of leronlimab is not readily available. | Data regarding the clearance of leronlimab is not readily available. | Deltaretrovirus Antibodies | NA | NA | NA | NA | C-C chemokine receptor type 5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12534 | 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 | Antibodies | NA | NA | NA | NA | Transmembrane glycoprotein NMB | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12546 | 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 | Antibodies | NA | NA | NA | NA | Platelet-derived growth factor receptor alpha | Lartruvo | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Intravenous | 500 mg / 50 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 |
| 12547 | 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 | Antibodies, Monoclonal | NA | NA | NA | NA | Platelet-derived growth factor receptor alpha | Lartruvo | Eli Lilly and Company | Eli Lilly and Company | Intravenous | 10 mg/1mL | 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 |
| 12559 | Th1333 | IPH 2101 | NA | NA | NA | NA | NA | NA | NA | IPH-2101 (NN-1975), a fully human monoclonal antibody developed for patients with acute myeloid leukemia. | Investigated for use/treatment in leukemia (myeloid) and multiple myeloma. | NA | The therapeutic principle of IPH 2101 (NN 1975) is based on the activation of Natural Killer (NK) cells by a monoclonal antibody which blocks the NK’s KIR inhibitory receptors, thereby potentiating NK cells anti-cancer action. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12567 | Th1334 | TB-402 | NA | NA | NA | NA | NA | NA | NA | TB-402 is a human antibody binding to Factor VIII, which plays a crucial role in the coagulation of the blood. It is expected to be developed as a potential treatment to prevent blood clot formation in connection with certain types of heart arrhythmia, such as atrial fibrillation. | Investigated for use/treatment in atrial fibrillation and thrombosis. | NA | TB-402 is a human antibody binding to Factor VIII, which plays a crucial role in the coagulation of the blood. The antibody has shown a beneficial partial inhibition of Factor VIII, even when applied in excess dosage. Extensive testing in several animal models has shown that TB-402 strongly reduces the risk of thrombosis without increasing the risk of bleeding. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Coagulation factor VIII | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12575 | Th1335 | Caplacizumab | >Th1335_Caplacizumab EVQLVESGGGLVQPGGSLRLSCAASGRTFSYNPMGWFRQAPGKGRELVAAISRTGGSTYYPDSVEGRFTISRDNAKRMVYLQMNSLRAEDTAVYYCAAAGVRAEDGRVRTLPSEYTFWGQGTQVTVSSAAAEVQLVESGGGLVQPGGSLRLSCAASGRTFSYNPMGWFRQAPGKGRELVAAISRTGGSTYYPDSVEGRFTISRDNAKRMVYLQMNSLRAEDTAVYYCAAAGVRAEDGRVRTLPSEYTFWGQGTQVTVSS | 27880 | C1213H1891N357O380S10 | 6.6 - 7.2 | NA | 61 ºC (Fab fragment) | The reported half-life is reported to be in the range of 16-27 hours.[F3457] | Caplacizumab, firstly called ALX-0081, is a humanized single-variable-domain immunoglobulin consisting of two identical humanized building blocks genetically linked by a three-alanine linker. Caplacizumab was developed by Ablynx, a Sanofi company and FDA approved on February 6, 2019,[L5302] and approved previously by the EU in October 2018 as a combination therapy with plasma exchange and immunosuppression.[A174634] | Capacizumab is approved for the treatment of adults experiencing an episode of acquired thrombotic thrombocytopenic purpura (aTTP) in conjunction with plasma exchange and immunosuppression in patients 18 years or older.[A174634, L5302] aTTP is a rare autoimmune condition presented by a disruption of blood clotting order which is translated into systemic microvascular thrombosis leading to profound thrombocytopenia, hemolytic anemia and organ ischemia. It is caused by the production of autoantibodies against ADAMTS-13 which is the protein in charge of cleaving the von-Wilebrand factor. The lack of this process produces the generation of ultra large von Wilebrand multimers that bind to platelets and form microthrombi and causing thromboembolic complications.[A174649] Previously, capacizumab was under review for the prevention of thrombosis in high-risk patients with acute coronary syndrome undergoing percutaneous coronary intervention but this indication was withdrawn.[A174634] | _In vitro_ studies have shown a caplacizumab-driven complete inhibition of platelet aggregation and in phase II clinical trials, it was shown to reduce the activity of the von Willebrand factor by 20% from treatment day 1 until treatment day 30. The level of von Willebrand factor in the plasma was also significantly reduced due to the clearance of the von Willebrand-caplacizumab complex.[A174634] In phase III clinical trials, more than 50% of the tested individuals reached a platelet normal count. In these trials, it was observed as well a significant reduction in the incidence of aTTP[A174634] as well as a significant reduction in the median time to response of about 39%.[A174652] However, as caplacizumab does not target autoimmune response, relapses were observed after treatment discontinuation.[A174643] The last clinical trial prior approval showed production of a platelet count of more than 150,000 per mcl after the cessation of plasma exchange therapy for 5 days as well as a reduction of patient recurrent thrombotic thrombocytopenic purpura and of disease-related death during treatment.[L5302] | Caplacizumab acts by targetting the A1 domain of the ultra-large von Willebrand factor which in order inhibits the interaction with the glycoprotein Ib-IX-V receptor in the platelets. Caplacizumab binds to von Willebrand factor with an affinity of 8.5 nM, thus it is very target specific.[5305] The blockage of the von Willebrand factor prevents the interaction between the von Willebrand factor and the platelets, hence, preventing platelet aggregation.[A174634] | Cases of overdose are represented by an increased risk of bleeding and in these cases, external administration of von Willebrand factor concentrate should be done.[FDA label] To this point, there have not been performed studies regarding the effect on fertility, genotoxicity, or carcinogenicity | Caplacizumab is degraded in the reticuloendothelial system to small peptides and amino acids which can be used for de-novo protein synthesis.[A31470] | After intravenous administration of caplacizumab, the pharmacokinetic profile is non-linear and to follow a non-compartmental model as the pharmacokinetic profile of this drug is dependent on the expression of von Willebrand factor. After administration, caplacizumab is rapidly absorbed with a dose-dependent behavior. The peak concentration was reached after 6-7 hours[A174634] and it presents a very high bioavailability reaching approximately 90%.[F3457] The subcutaneous administration of a dose of 10 mg of caplacizumab produced a peak concentration of 528 ng/ml and an AUC of 7951 ng.h/ml.[L5314] | The reported volume of distribution of caplacizumab is 6.33 L.[A174634] | As the elimination is highly divided among hepatic, target-driven and renal elimination, the calculation of the clearance rate is not significant for drug description. | Antibodies, Monoclonal | NA | NA | NA | NA | von Willebrand factor | Cablivi | Ablynx Nv | Ablynx Nv | Intravenous; Subcutaneous | 10 mg | CABLIVI is contraindicated in patients with a previous severe hypersensitivity reaction to caplacizumab-yhdp or to any of the excipients. Hypersensitivity reactions have included urticaria | nosebleed, headache, bleeding gums, fatigue, fever, injection site reactions (bleeding, itching), back pain, muscle pain, numbness and tingling, urinary tract infection (UTI), blood in the urine, abnormal vaginal bleeding, shortness of breath, and hives | Cablivi is used to treat acquired thrombotic thrombocytopenic purpura (aTTP) in adults. This medicine is given together with immunosuppressant medication and plasma exchange (transfusion). Cablivi may also be used for purposes not listed in this medication guide. Warnings Cablivi can increase your risk... | Cablivi is a prescription medicine used to treat the symptoms of Acquired Thrombotic Thrombocytopenia Purpura (aTTP). Cablivi may be used alone or with other medications. | NA | Caplacizumab-yhdp is a von Willebrand factor (vWF)-directed antibody fragment that consists of two identical humanized building blocks, linked by a three-alanine linker. Caplacizumab-yhdp is produced in Escherichia coli by recombinant DNA technology and has an approximate molecular weight of 28 kDa. | Link | Link | NA |
| 12576 | Th1335 | Caplacizumab | >Th1335_Caplacizumab EVQLVESGGGLVQPGGSLRLSCAASGRTFSYNPMGWFRQAPGKGRELVAAISRTGGSTYYPDSVEGRFTISRDNAKRMVYLQMNSLRAEDTAVYYCAAAGVRAEDGRVRTLPSEYTFWGQGTQVTVSSAAAEVQLVESGGGLVQPGGSLRLSCAASGRTFSYNPMGWFRQAPGKGRELVAAISRTGGSTYYPDSVEGRFTISRDNAKRMVYLQMNSLRAEDTAVYYCAAAGVRAEDGRVRTLPSEYTFWGQGTQVTVSS | 27880 | C1213H1891N357O380S10 | 6.6 - 7.2 | NA | 61 ºC (Fab fragment) | The reported half-life is reported to be in the range of 16-27 hours.[F3457] | Caplacizumab, firstly called ALX-0081, is a humanized single-variable-domain immunoglobulin consisting of two identical humanized building blocks genetically linked by a three-alanine linker. Caplacizumab was developed by Ablynx, a Sanofi company and FDA approved on February 6, 2019,[L5302] and approved previously by the EU in October 2018 as a combination therapy with plasma exchange and immunosuppression.[A174634] | Capacizumab is approved for the treatment of adults experiencing an episode of acquired thrombotic thrombocytopenic purpura (aTTP) in conjunction with plasma exchange and immunosuppression in patients 18 years or older.[A174634, L5302] aTTP is a rare autoimmune condition presented by a disruption of blood clotting order which is translated into systemic microvascular thrombosis leading to profound thrombocytopenia, hemolytic anemia and organ ischemia. It is caused by the production of autoantibodies against ADAMTS-13 which is the protein in charge of cleaving the von-Wilebrand factor. The lack of this process produces the generation of ultra large von Wilebrand multimers that bind to platelets and form microthrombi and causing thromboembolic complications.[A174649] Previously, capacizumab was under review for the prevention of thrombosis in high-risk patients with acute coronary syndrome undergoing percutaneous coronary intervention but this indication was withdrawn.[A174634] | _In vitro_ studies have shown a caplacizumab-driven complete inhibition of platelet aggregation and in phase II clinical trials, it was shown to reduce the activity of the von Willebrand factor by 20% from treatment day 1 until treatment day 30. The level of von Willebrand factor in the plasma was also significantly reduced due to the clearance of the von Willebrand-caplacizumab complex.[A174634] In phase III clinical trials, more than 50% of the tested individuals reached a platelet normal count. In these trials, it was observed as well a significant reduction in the incidence of aTTP[A174634] as well as a significant reduction in the median time to response of about 39%.[A174652] However, as caplacizumab does not target autoimmune response, relapses were observed after treatment discontinuation.[A174643] The last clinical trial prior approval showed production of a platelet count of more than 150,000 per mcl after the cessation of plasma exchange therapy for 5 days as well as a reduction of patient recurrent thrombotic thrombocytopenic purpura and of disease-related death during treatment.[L5302] | Caplacizumab acts by targetting the A1 domain of the ultra-large von Willebrand factor which in order inhibits the interaction with the glycoprotein Ib-IX-V receptor in the platelets. Caplacizumab binds to von Willebrand factor with an affinity of 8.5 nM, thus it is very target specific.[5305] The blockage of the von Willebrand factor prevents the interaction between the von Willebrand factor and the platelets, hence, preventing platelet aggregation.[A174634] | Cases of overdose are represented by an increased risk of bleeding and in these cases, external administration of von Willebrand factor concentrate should be done.[FDA label] To this point, there have not been performed studies regarding the effect on fertility, genotoxicity, or carcinogenicity | Caplacizumab is degraded in the reticuloendothelial system to small peptides and amino acids which can be used for de-novo protein synthesis.[A31470] | After intravenous administration of caplacizumab, the pharmacokinetic profile is non-linear and to follow a non-compartmental model as the pharmacokinetic profile of this drug is dependent on the expression of von Willebrand factor. After administration, caplacizumab is rapidly absorbed with a dose-dependent behavior. The peak concentration was reached after 6-7 hours[A174634] and it presents a very high bioavailability reaching approximately 90%.[F3457] The subcutaneous administration of a dose of 10 mg of caplacizumab produced a peak concentration of 528 ng/ml and an AUC of 7951 ng.h/ml.[L5314] | The reported volume of distribution of caplacizumab is 6.33 L.[A174634] | As the elimination is highly divided among hepatic, target-driven and renal elimination, the calculation of the clearance rate is not significant for drug description. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | von Willebrand factor | Cablivi | Genzyme Corporation | Genzyme Corporation | Intravenous; Subcutaneous | 11 mg/1mL | CABLIVI is contraindicated in patients with a previous severe hypersensitivity reaction to caplacizumab-yhdp or to any of the excipients. Hypersensitivity reactions have included urticaria | nosebleed, headache, bleeding gums, fatigue, fever, injection site reactions (bleeding, itching), back pain, muscle pain, numbness and tingling, urinary tract infection (UTI), blood in the urine, abnormal vaginal bleeding, shortness of breath, and hives | Cablivi is used to treat acquired thrombotic thrombocytopenic purpura (aTTP) in adults. This medicine is given together with immunosuppressant medication and plasma exchange (transfusion). Cablivi may also be used for purposes not listed in this medication guide. Warnings Cablivi can increase your risk... | Cablivi is a prescription medicine used to treat the symptoms of Acquired Thrombotic Thrombocytopenia Purpura (aTTP). Cablivi may be used alone or with other medications. | NA | Caplacizumab-yhdp is a von Willebrand factor (vWF)-directed antibody fragment that consists of two identical humanized building blocks, linked by a three-alanine linker. Caplacizumab-yhdp is produced in Escherichia coli by recombinant DNA technology and has an approximate molecular weight of 28 kDa. | Link | Link | NA |
| 12600 | Th1337 | Lumiliximab | NA | 47750 | C2115H3252N556O673S16 | NA | NA | NA | NA | Lumiliximab is a chimeric monoclonal antibody which is used as an immunosuppressive drug. It is a primatized anti-CD23 macaque/human chimeric antibody that inhibits the production of the IgE antibody, for the potential treatment of allergic conditions. Lumiliximab was developed by IDEC Pharmaceuticals, which was acquired by Biogen. Clinical trials for CLL were terminated in 2010, and for allergic asthma in 2007. Results published from the CLL clinical trial failed to meet primary endpoints. | Investigated for use/treatment in asthma and leukemia (lymphoid). | NA | Lumiliximab is a chimeric macaque-human monoclonal antibody to CD23, a protein expressed on virtually all chronic lymphocytic leukemia (CLL) cells. CD23, also known as Fc epsilon RII, or FcεRII, is the "low affinity" receptor for IgE, an antibody isotype involved in allergy and resistance to parasites and is important in regulation of IgE levels. Unlike many of the antibody receptors, CD23 is a C-type lectin. It is found on mature B cells, activated macrophages, eosinophils, follicular dendritic cells and platelets. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Low affinity immunoglobulin epsilon Fc receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12608 | Th1338 | Nimotuzumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12609 | Th1338 | Nimotuzumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12610 | Th1338 | Nimotuzumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12620 | Th1339 | Clenoliximab | NA | NA | NA | NA | NA | NA | NA | Clenoliximab is a chimeric monoclonal antibody from _Macaca irus_ against CD4 which acts as an immunomodulator. It has investigated for the treatment of rheumatoid arthritis. | Investigated for use/treatment in rheumatoid arthritis. | NA | Clenoliximab is a macaque-human chimeric monoclonal antibody (immunoglobulin G4)that binds specifically to the CD4 receptor present on T-lympocytes (Helper T lymphocytes). CD-4 lymphocytes are implicated in the pathogenesis of rheumatoid arthritis (RA). Clenoliximab coats the CD4 T-lymphocytes and thus down-modulates the CD4 T-lympocytes in a dose and concentration-dependent manner without decreasing the amount of CD4 T-lympocytes in circulation. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | T-cell surface glycoprotein CD4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12649 | Th1342 | BIIB015 | NA | NA | NA | NA | NA | NA | NA | BIIB015 is a humanized, IgG1 [immunoglobulin G 1], DM4-Conjugated, anti-cripto, monoclonal antibody. It has been investigated for the treatment of subjects with relapsed or refractory solid tumours. | Investigated for use/treatment in solid tumors. | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12659 | Th1343 | Sonepcizumab | NA | NA | NA | NA | NA | NA | NA | A humanized monoclonal antibody directed against sphingosine 1-phosphate (S1P) with potential antiangiogenic and antineoplastic activities. Upon administration, sonepcizumab binds S1P, which may result in the inhibition of tumor angiogenesis. S1P is the extracellular ligand for the G protein-coupled lysophospholipid receptor EDG-1 (endothelial differentiation gene-1). | Investigated for use/treatment in solid tumors. | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12660 | Th1343 | Sonepcizumab | NA | NA | NA | NA | NA | NA | NA | A humanized monoclonal antibody directed against sphingosine 1-phosphate (S1P) with potential antiangiogenic and antineoplastic activities. Upon administration, sonepcizumab binds S1P, which may result in the inhibition of tumor angiogenesis. S1P is the extracellular ligand for the G protein-coupled lysophospholipid receptor EDG-1 (endothelial differentiation gene-1). | Investigated for use/treatment in solid tumors. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12661 | Th1343 | Sonepcizumab | NA | NA | NA | NA | NA | NA | NA | A humanized monoclonal antibody directed against sphingosine 1-phosphate (S1P) with potential antiangiogenic and antineoplastic activities. Upon administration, sonepcizumab binds S1P, which may result in the inhibition of tumor angiogenesis. S1P is the extracellular ligand for the G protein-coupled lysophospholipid receptor EDG-1 (endothelial differentiation gene-1). | Investigated for use/treatment in solid tumors. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12669 | Th1344 | Motavizumab | >Th1344_Motavizumab QVTLRESGPALVKPTQTLTLTCTFSGFSLSTAGMSVGWIRQPPGKALEWLADIWWDDKKHYNPSLKDRLTISKDTSKNQVVLKVTNMDPADTATYYCARDMIFNFYFDVWGQGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in viral infection and pediatric indications. | NA | Motavizumab is a second generation, ultra-potent, affinity-matured, humanized mAb derived from palivizumab that reduces replication of Respiratory Syncytial Virus (RSV), a pathogen which causes lower respiratory tract disease. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12670 | Th1344 | Motavizumab | >Th1344_Motavizumab QVTLRESGPALVKPTQTLTLTCTFSGFSLSTAGMSVGWIRQPPGKALEWLADIWWDDKKHYNPSLKDRLTISKDTSKNQVVLKVTNMDPADTATYYCARDMIFNFYFDVWGQGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in viral infection and pediatric indications. | NA | Motavizumab is a second generation, ultra-potent, affinity-matured, humanized mAb derived from palivizumab that reduces replication of Respiratory Syncytial Virus (RSV), a pathogen which causes lower respiratory tract disease. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12671 | Th1344 | Motavizumab | >Th1344_Motavizumab QVTLRESGPALVKPTQTLTLTCTFSGFSLSTAGMSVGWIRQPPGKALEWLADIWWDDKKHYNPSLKDRLTISKDTSKNQVVLKVTNMDPADTATYYCARDMIFNFYFDVWGQGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in viral infection and pediatric indications. | NA | Motavizumab is a second generation, ultra-potent, affinity-matured, humanized mAb derived from palivizumab that reduces replication of Respiratory Syncytial Virus (RSV), a pathogen which causes lower respiratory tract disease. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12684 | Th1345 | AVE9633 | NA | NA | NA | NA | NA | NA | NA | AVE9633 is an anti-CD33 monoclonal antibody-DM4 conjugate. | Investigated for use/treatment in leukemia (myeloid). | An immunoconjugate consisting of the humanized monoclonal antibody huMy9-6 conjugated to the cytotoxic maytansinoid derivative DM4 with potential antineoplastic activity. The monoclonal antibody portion of anti-CD33 monoclonal antibody-DM4 conjugate AVE9633 specifically binds to the cell surface antigen CD33 expressed on myeloid leukemia cells; upon internalization, the DM4 moiety is released, binds tubulin, and disrupts microtubule assembly/disassembly dynamics, resulting in the inhibition of cell division and cell growth in myeloid leukemia cells that express CD33. CD33 is expressed on normal non-pluripotent hematopoietic stem cells as well as on myeloid leukemia cells. [National Cancer Institute Drug Dictionary] | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Myeloid cell surface antigen CD33 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12685 | Th1345 | AVE9633 | NA | NA | NA | NA | NA | NA | NA | AVE9633 is an anti-CD33 monoclonal antibody-DM4 conjugate. | Investigated for use/treatment in leukemia (myeloid). | An immunoconjugate consisting of the humanized monoclonal antibody huMy9-6 conjugated to the cytotoxic maytansinoid derivative DM4 with potential antineoplastic activity. The monoclonal antibody portion of anti-CD33 monoclonal antibody-DM4 conjugate AVE9633 specifically binds to the cell surface antigen CD33 expressed on myeloid leukemia cells; upon internalization, the DM4 moiety is released, binds tubulin, and disrupts microtubule assembly/disassembly dynamics, resulting in the inhibition of cell division and cell growth in myeloid leukemia cells that express CD33. CD33 is expressed on normal non-pluripotent hematopoietic stem cells as well as on myeloid leukemia cells. [National Cancer Institute Drug Dictionary] | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Myeloid cell surface antigen CD33 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12702 | Th1346 | Carotuximab | >Th1346_Carotuximab EVKLEESGGGLVQPGGSMKLSCAASGFTFSDAWMDWVRQSPEKGLEWVAEIRSKASNHATYYAESVKGRFTISRDDSKSSVYLQMNSLRAEDTGIYYCTRWRRFFDSWGQGTTLTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in solid tumors. | NA | TRC105 is a first-in-class human chimeric monoclonal antibody that inhibits tumor growth by binding to CD105 (endoglin), a receptor over-expressed on proliferating endothelium that is required for angiogenesis (growth of new blood vessels). TRC105 has shown activity, as monotherapy or when combined with chemotherapy, in pre-clinical studies of breast and colorectal cancer. Pre-clinical data also indicate CD105 expression is increased following treatment of human cancer with anti-VEGF therapy. The target of TRC105 shares many features with the VEGF receptor. Most importantly, both the VEGF and CD105 receptors are essential for angiogenesis, in that deletion of either receptor prevents blood vessel formation in utero. [Traecon Pharmaceuticals Press Release] | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Endoglin | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12714 | Th1348 | XmAb 2513 | NA | NA | NA | NA | NA | NA | NA | XmAb 2513 is a humanized monoclonal antibody that targets the antigen CD30, a molecule expressed on the surface of a number of tumor cell types. It has been investigated for the treatment of hodgkin’s lymphoma. | Investigated for use/treatment in lymphoma (unspecified) and lymphoma (non-hodgkin's). | NA | XmAb™2513 is a humanized monoclonal antibody that targets the antigen CD30, a molecule expressed on the surface of a number of tumor cell types. XmAb™2513 has an XmAb™ Fc domain which increases its cytotoxic potency. XmAb™2513 recruits primary human immune cells to kill tumor cells in vitro models and is active in blocking tumor growth in rodent models. [Xencor Website] | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 8 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12715 | Th1348 | XmAb 2513 | NA | NA | NA | NA | NA | NA | NA | XmAb 2513 is a humanized monoclonal antibody that targets the antigen CD30, a molecule expressed on the surface of a number of tumor cell types. It has been investigated for the treatment of hodgkin’s lymphoma. | Investigated for use/treatment in lymphoma (unspecified) and lymphoma (non-hodgkin's). | NA | XmAb™2513 is a humanized monoclonal antibody that targets the antigen CD30, a molecule expressed on the surface of a number of tumor cell types. XmAb™2513 has an XmAb™ Fc domain which increases its cytotoxic potency. XmAb™2513 recruits primary human immune cells to kill tumor cells in vitro models and is active in blocking tumor growth in rodent models. [Xencor Website] | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 8 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12729 | Th1350 | Coltuximab ravtansine | NA | NA | NA | NA | NA | NA | NA | Coltuximab ravtansine (SAR3419) targets CD19 and is being investigated for the treatment of acute lymphoblastic leukemia (ALL). | Investigated for use/treatment in lymphoma (non-hodgkin's). | NA | SAR3419 is an anti-CD19-DM4 immunoconjugate consisting of an anti-CD19 monoclonal antibody conjugated to the maytansinoid DM4, a derivative of the cytotoxic agent maytansine (DM1), with potential antineoplastic activity. SAR3419 targets the cell surface antigen CD19, found on a number of B-cell-derived cancers. Upon antibody/antigen binding and internalization, the immunoconjugate releases DM4, which binds to tubulin and disrupts microtubule assembly/disassembly dynamics, resulting in inhibition of cell division and cell growth of CD19-expressing tumor cells. [National Cancer Institute Drug Dictionary] | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | B-lymphocyte antigen CD19 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12730 | Th1350 | Coltuximab ravtansine | NA | NA | NA | NA | NA | NA | NA | Coltuximab ravtansine (SAR3419) targets CD19 and is being investigated for the treatment of acute lymphoblastic leukemia (ALL). | Investigated for use/treatment in lymphoma (non-hodgkin's). | NA | SAR3419 is an anti-CD19-DM4 immunoconjugate consisting of an anti-CD19 monoclonal antibody conjugated to the maytansinoid DM4, a derivative of the cytotoxic agent maytansine (DM1), with potential antineoplastic activity. SAR3419 targets the cell surface antigen CD19, found on a number of B-cell-derived cancers. Upon antibody/antigen binding and internalization, the immunoconjugate releases DM4, which binds to tubulin and disrupts microtubule assembly/disassembly dynamics, resulting in inhibition of cell division and cell growth of CD19-expressing tumor cells. [National Cancer Institute Drug Dictionary] | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | B-lymphocyte antigen CD19 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12748 | Th1351 | Teprotumumab | >Th1351_Teprotumumab QVELVESGGGVVQPGRSQRLSCAASGFTFSSYGMHWVRQAPGKGLEWVAIIWFDGSSTYYADSVRGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCARELGRRYFDLWGRGTLVSVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The half-life of teprotumumab is 20 ± 5 days.[L11359] | Teprotumumab is a fully human IgG1 monoclonal antibody directed against the human insulin-like growth factor-1 receptor.[L11359] Following a clinical trial in which its efficacy in the treatment of thyroid eye disease (TED) was assessed, it received "breakthrough therapy" designation from the FDA in 2016[A190129] and was approved by the FDA in January 2020 for the treatment of TED.[L11350] Thyroid eye disease is a potentially debilitating complication of Graves' Disease involving inflammation and tissue remodeling behind the eye, and previous treatment options typically involved multiple invasive surgeries - teprotumumab is the first drug ever approved for the treatment of TED and therefore represents a significant step forward in the treatment this disease.[L11350] | Teprotumumab is indicated for the treatment of thyroid eye disease.[L11359] | Teprotumumab inhibits the downstream effects of IGF-1R signaling, namely tissue inflammation and remodeling, which are responsible for the various symptoms of thyroid eye disease.[L11359,A190138] Teprotumumab may cause disease flares in patients with pre-existing inflammatory bowel disease (IBD) - patients experiencing an exacerbation should discontinue therapy with teprotumumab. Significant hyperglycemia has been observed in patients receiving treatment with teprotumumab which may require antihyperglycemic medications. Based on its mechanism of action, it is likely that teprotumumab will cause fetal harm in pregnant woman - for this reason, females of child-bearing age should use effective contraception prior to initiation, during therapy, and for 6 months following the last dose of teprotumumab.[L11359] | Graves’ Disease is an autoimmune syndrome involving the thyroid, orbital connective tissues, and some regions of the skin.[A190138] One manifestation of Graves’ Disease is thyroid-associated ophthalmopathy, or thyroid eye disease, which is characterized by orbital inflammation, tissue remodeling, and fibrosis. As the disease progresses, patients may develop proptosis, strabismus, corneal ulceration, and optic neuropathy.[A189937] It has been demonstrated that insulin-like growth factor-1 receptors (IGF-1R) are overexpressed by orbital fibroblasts in patients with thyroid eye disease, in addition to being overexpressed on T-cells and B-cells in these patients.[A190138] It was found that Graves’ Disease IgG molecules could mimic the principal ligand of IGF-1R, insulin-like growth factor-1 (IGF-1), and their binding of IGF-1R induces the expression of chemokines that play roles in tissue remodeling and inflammation. For these reasons, IGF-1R was sought after as a potential therapeutic target for the treatment of thyroid eye disease.[A190138] Teprotumumab is a fully human IgG1 monoclonal antibody directed against IGF-1R. It binds to and induces internalization and degradation of these receptors,[A189937] thus preventing their downstream effects and alleviating symptoms of thyroid eye disease.[L11359] | Toxicity information, including information regarding overdosage, is currently unavailable.[L11359] Symptoms of teprotumumab overdose are likely to be consistent with its adverse effect profile. | The metabolism of teprotumumab has not been fully characterized. As a protein, its metabolism is expected to involve proteolysis to smaller proteins and peptides.[L11359] | In a population of 40 patients receiving standard dosing in two clinical trials of teprotumumab, utilizing a two-compartment pharmacokinetic model, the AUC and Cmax were estimated to be 138 ± 34 mg•hr/mL and 632 ± 139 mcg/mL, respectively.[L11359] | Following the standard dosing regimen, the mean central and peripheral volumes of distribution are approximately 3.26 ± 0.87 L and 4.32 ± 0.67 L, respectively.[L11359] | The estimated mean clearance of teprotumumab is 0.27 L/day.[L11359] The inter-compartment clearance is 0.74 L/day.[L11359] | Antibodies | NA | NA | NA | NA | Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12757 | Th1352 | Siplizumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in psoriasis and psoriatic disorders, transplant (rejection), graft versus host disease, lymphoma (unspecified), and leukemia (unspecified). | NA | Siplizumab has been shown to cause depletion of T-cells. It is therefore considered to be an immunomodulator in clinical settings where the depletion of T-cells may have clinical benefits, such as certain autoimmune diseases and T-cell cancers. In addition, preclinical studies have also suggested that siplizumab, by binding to the CD2 receptor, may selectively produce cell death and reduce cancerous cells. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | T-cell surface antigen CD2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12758 | Th1352 | Siplizumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in psoriasis and psoriatic disorders, transplant (rejection), graft versus host disease, lymphoma (unspecified), and leukemia (unspecified). | NA | Siplizumab has been shown to cause depletion of T-cells. It is therefore considered to be an immunomodulator in clinical settings where the depletion of T-cells may have clinical benefits, such as certain autoimmune diseases and T-cell cancers. In addition, preclinical studies have also suggested that siplizumab, by binding to the CD2 receptor, may selectively produce cell death and reduce cancerous cells. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | T-cell surface antigen CD2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12759 | Th1352 | Siplizumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in psoriasis and psoriatic disorders, transplant (rejection), graft versus host disease, lymphoma (unspecified), and leukemia (unspecified). | NA | Siplizumab has been shown to cause depletion of T-cells. It is therefore considered to be an immunomodulator in clinical settings where the depletion of T-cells may have clinical benefits, such as certain autoimmune diseases and T-cell cancers. In addition, preclinical studies have also suggested that siplizumab, by binding to the CD2 receptor, may selectively produce cell death and reduce cancerous cells. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | T-cell surface antigen CD2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12822 | Th1357 | Apolizumab | NA | NA | NA | NA | NA | NA | NA | Apolizumab is a humanized monoclonal antibody that is being studied as a treatment for hematologic cancers. | Investigated for use/treatment in lymphoma (non-hodgkin's), leukemia (lymphoid), and solid tumors. | NA | Apolizumab is a humanized monoclonal antibody directed against 1D10, a polymorphic determinant on the HLA-DR beta chain that is expressed on normal and neoplastic B cells. Apolizumab induces complement-mediated cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and apoptosis of 1D10 antigen-positive B cells in vitro. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12823 | Th1357 | Apolizumab | NA | NA | NA | NA | NA | NA | NA | Apolizumab is a humanized monoclonal antibody that is being studied as a treatment for hematologic cancers. | Investigated for use/treatment in lymphoma (non-hodgkin's), leukemia (lymphoid), and solid tumors. | NA | Apolizumab is a humanized monoclonal antibody directed against 1D10, a polymorphic determinant on the HLA-DR beta chain that is expressed on normal and neoplastic B cells. Apolizumab induces complement-mediated cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and apoptosis of 1D10 antigen-positive B cells in vitro. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12824 | Th1357 | Apolizumab | NA | NA | NA | NA | NA | NA | NA | Apolizumab is a humanized monoclonal antibody that is being studied as a treatment for hematologic cancers. | Investigated for use/treatment in lymphoma (non-hodgkin's), leukemia (lymphoid), and solid tumors. | NA | Apolizumab is a humanized monoclonal antibody directed against 1D10, a polymorphic determinant on the HLA-DR beta chain that is expressed on normal and neoplastic B cells. Apolizumab induces complement-mediated cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and apoptosis of 1D10 antigen-positive B cells in vitro. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12832 | Th1358 | Sibrotuzumab | NA | NA | NA | NA | NA | NA | NA | Sibrotuzumab is a humanized monoclonal antibody directed against fibroblast activation protein (FAP). It is used to treat cancer. | Investigated for use/treatment in cancer/tumors (unspecified), colorectal cancer, and lung cancer. | NA | Human FAP is unique in its selective expression by tumor stromal fibroblasts in epithelial carcinomas, but not by epithelial carcinoma cells, normal fibroblasts, or other normal tissues. Therefore, FAP is an attractive target for the study of tumor stromal cell biology and provides valuable insights into the roles of the tumor microenvironment. Sibrotuzumab is a humanized monoclonal antibody designed to attack the cell-surface antigen FAP. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Seprase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12833 | Th1358 | Sibrotuzumab | NA | NA | NA | NA | NA | NA | NA | Sibrotuzumab is a humanized monoclonal antibody directed against fibroblast activation protein (FAP). It is used to treat cancer. | Investigated for use/treatment in cancer/tumors (unspecified), colorectal cancer, and lung cancer. | NA | Human FAP is unique in its selective expression by tumor stromal fibroblasts in epithelial carcinomas, but not by epithelial carcinoma cells, normal fibroblasts, or other normal tissues. Therefore, FAP is an attractive target for the study of tumor stromal cell biology and provides valuable insights into the roles of the tumor microenvironment. Sibrotuzumab is a humanized monoclonal antibody designed to attack the cell-surface antigen FAP. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Seprase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12834 | Th1358 | Sibrotuzumab | NA | NA | NA | NA | NA | NA | NA | Sibrotuzumab is a humanized monoclonal antibody directed against fibroblast activation protein (FAP). It is used to treat cancer. | Investigated for use/treatment in cancer/tumors (unspecified), colorectal cancer, and lung cancer. | NA | Human FAP is unique in its selective expression by tumor stromal fibroblasts in epithelial carcinomas, but not by epithelial carcinoma cells, normal fibroblasts, or other normal tissues. Therefore, FAP is an attractive target for the study of tumor stromal cell biology and provides valuable insights into the roles of the tumor microenvironment. Sibrotuzumab is a humanized monoclonal antibody designed to attack the cell-surface antigen FAP. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Seprase | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12842 | Th1359 | Ruplizumab | NA | NA | NA | NA | NA | NA | NA | Ruplizumab is a humanized monoclonal antibody used as an immunosuppressive drug and is a component of Antova. | Investigated for use/treatment in thrombocytopenia, systemic lupus erythematosus, transplant (rejection), blood (blood forming organ disorders, unspecified), and multiple sclerosis. | NA | Ruplizumab is an anti-CD40L monoclonal antibody. The binding of CD40 to its ligand, CD40L, is a critical element in T cell activation. In systemic lupus erythematosus, CD40L is over-expressed on T cells, B cells, and monocytes. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | CD40 ligand | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12843 | Th1359 | Ruplizumab | NA | NA | NA | NA | NA | NA | NA | Ruplizumab is a humanized monoclonal antibody used as an immunosuppressive drug and is a component of Antova. | Investigated for use/treatment in thrombocytopenia, systemic lupus erythematosus, transplant (rejection), blood (blood forming organ disorders, unspecified), and multiple sclerosis. | NA | Ruplizumab is an anti-CD40L monoclonal antibody. The binding of CD40 to its ligand, CD40L, is a critical element in T cell activation. In systemic lupus erythematosus, CD40L is over-expressed on T cells, B cells, and monocytes. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | CD40 ligand | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12871 | Th1363 | Bivatuzumab | NA | NA | NA | NA | NA | NA | NA | Bivatuzumab (previously BIWA 4) is a humanized monoclonal antibody against CD44 v6. [A31688,A31689] | Investigated for use/treatment in cancer/tumors (unspecified) and head and neck cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | CD44 antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12872 | Th1363 | Bivatuzumab | NA | NA | NA | NA | NA | NA | NA | Bivatuzumab (previously BIWA 4) is a humanized monoclonal antibody against CD44 v6. [A31688,A31689] | Investigated for use/treatment in cancer/tumors (unspecified) and head and neck cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | CD44 antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12873 | Th1363 | Bivatuzumab | NA | NA | NA | NA | NA | NA | NA | Bivatuzumab (previously BIWA 4) is a humanized monoclonal antibody against CD44 v6. [A31688,A31689] | Investigated for use/treatment in cancer/tumors (unspecified) and head and neck cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | CD44 antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12881 | Th1364 | Lerdelimumab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in glaucoma and cataracts. | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12889 | Th1365 | Pascolizumab | NA | NA | NA | NA | NA | NA | NA | Pascolizumab (SB 240683) is a humanized anti-interleukin-4 antibody with therapeutic potential in asthma. | Investigated for use/treatment in asthma. | NA | Pascolizumab is a humanized anti-IL-4 monoclonal antibody that can inhibit upstream and downstream events associated with asthma, including (T(H)2) cell activation and immunoglobulin E production. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Interleukin-4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12890 | Th1365 | Pascolizumab | NA | NA | NA | NA | NA | NA | NA | Pascolizumab (SB 240683) is a humanized anti-interleukin-4 antibody with therapeutic potential in asthma. | Investigated for use/treatment in asthma. | NA | Pascolizumab is a humanized anti-IL-4 monoclonal antibody that can inhibit upstream and downstream events associated with asthma, including (T(H)2) cell activation and immunoglobulin E production. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Interleukin-4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12899 | Th1367 | Lexatumumab | >Th1367_Lexatumumab EVQLVQSGGGVERPGGSLRLSCAASGFTFDDYGMSWVRQAPGKGLEWVSGINWNGGSTGYADSVKGRVTISRDNAKNSLYLQMNSLRAEDTAVYYCAKILGAGRGWYFDLWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Lexatumumab is a fully humanized, high-affinity immunoglobulin G(1 lambda) monoclonal antibody (mAb). | Investigated for use/treatment in cancer/tumors (unspecified). | NA | Lexatumumab agonizes the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAIL-R2), triggering the extrinsic apoptotic pathway. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 10B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12910 | Th1368 | Reslizumab | NA | 147000 | NA | NA | NA | NA | The half-life is approximately 24 days [FDA Label]. | Reslizumab is a humanized interleukin-5 (IL-5) antagonist monoclonal antibody (IgG4 kappa) that is produced by recombinant DNA technology in murine myeloma non-secreting 0 (NS0) cells. IL-5 is a pro-inflammatory cytokine that is responsible for the growth and differentiation, recruitment, activation, and survival of eosinophils [FDA Label]. Elevated levels of eosinophils increase the risk for asthma exacerbations, including both allergic forms and nonallergic forms of asthma where eosinophilia is prominent. By targeting the IL-5 and disrupting its signalling pathways, reslizumab aims to inhibit eosinophil maturation and promote programmed cell death [A31578]. Asthma is a chronic respiratory disease that causes inflammation in the lungs with asthma attacks that lead to severe breathing difficulties. Patients often experience persistent or exacerbating symptoms overtime despite conventional first-line therapies available. Inflammation-predominant asthma, which is chatacterized by eosinophilic infiltration of airway mucosa and elevated levels of eosinophils in the blood, sputum and BAL fluid, is associated with an increased risk for recurrent exacerbation and asthma-related hospitalizations [A31579]. In four double-blind, randomized, placebo-controlled trials in patients with severe asthma on currently available therapies, patients receiving reslizumab had fewer asthma attacks, and a longer time to the first attack compared to patients receiving placebo [FDA Label, A31579]. In addition, a significant improvement in lung function was seen, as measured by the volume of air exhaled by patients in one second [L1133]. Studies demonstrated that reslizumab was not effective in various asthma outcomes in patients without eosinophilia [A31577]. Reslizumab was developed by Teva Pharmaceuticals. Approved by the FDA in March 2016, reslizumab is marketed under the brand name Cinqair for intravenous injection. It is injected once every four weeks via intravenous infusion. Cinqair is indicated as an add-on maintenance therapy for adults with severe asthma with an eosinophilic phenotype. It is approved for patients who have a history of severe asthma attacks (exacerbations) despite receiving their current asthma medicines. Reslizumab is marketed as Cinqaero in Europe. | Indicated for the add-on maintenance treatment of patients with severe asthma aged 18 years and older with an eosinophilic phenotype. | A reduction in blood eosinophil counts was observed in clinical studies following an initial infusion of 3 mg/kg reslizumab and was maintained through 52 weeks of treatment with no signs of tachyphylaxis. Greater reductions of blood eosinophils were observed in subjects with higher reslizumab serum concentrations. This effect was independent of the presence of treatment-emergent anti-reslizumab antibodies [FDA Label]. | Reslizumab an interleukin-5 (IL-5) antagonist (IgG4, kappa) that binds to IL-5 with a dissociation constant of 81 pM. IL-5 is a proinflammatory cytokine responsible for the terminal maturation of eosinophils and increases chemotaxis, endothelial adhesion, activation and survival of eosinophils. Eosinophils are known to play a central role in the pathophysiology of many patients with asthma; upon activation, eosinophils release leukotrienes, platelet activation factor, major basic protein, eosinophil cationic protein, eosinophil peroxidase, eosinophil-derived neurotoxin, and other cytokines that are cytotoxic to the bronchial epithelium and lead to airway inflammation and bronchospasm [A31577]. IL-5 production is increased by upon activation of TH2 lymphocytes after antigen exposure and IL-5 stimulates the production and maturation of eosinophil precursors in the bone marrow [A31577]. IL-5 promotes the growth and differentiation, recruitment, activation, and survival of eosinophils via interacting with the IL-5 receptor expressed on the eosinophil surface [FDA Label]. Increased production and activation of eosinophils is especially prominent in nonallergic forms of asthma [A31577]. Reslizumab is a humanized monoclonal antibody that occupies the region ERRR (glutamic acid, arginine, arginine, arginine) corresponding to amino acids 89–92 on IL-5, which is a region critical for its interaction with the IL-5 receptor on the eosinophil surface [A31577]. By binding to IL-5 and disrupting its binding to the alpha chain of the IL-5 receptor complex, reslizumab inhibits the bioactivity of IL-5 and attenuates IL-5 signaling. Blocking of IL-5 signalling thereby reduces the production and survival of eosinophils and inhibits eosinophilic-driven inflammation. | Single doses of up to 732 mg have been administered intravenously to subjects in clinical trials without evidence of dose-related toxicities. There is no specific treatment for an overdose with reslizumab. If the event of an overdose, the patient should be treated supportively with appropriate monitoring as necessary [FDA Label]. Based on the findings of a 6-month bioassay, reslizumab showed no evidence of carcinogenicity. In a fertility study, administration of reslizumab to parental mice at doses up to 50 mg/kg (approximately 6 times the MRHD on an AUC basis) had no effects on male or female mating or fertility. The malignancy risk of reslizumab in humans with effects on tumor growth is not yet established [FDA Label]. | Like other monoclonal antibodies, reslizumab is assumed to undergo enzymatic proteolysis into smaller peptides and amino acids. As reslizumab bind to the target, it is not expected to undergo a target-mediated clearance [FDA Label]. | The peak serum concentrations of reslizumab were typically observed at the end of the infusion with the serum concentrations gradually declining from the peak in a biphasic manner. Following multiple doses, serum concentrations of reslizumab accumulated approximately 1.5 to 1.9-fold. Interindividual variability in peak and overall exposure across healthy individuals, patients with asthma, and other populations in pharmacokinetic studies was around 20-30% [FDA Label]. Systemic exposure to reslizumab appeared to be unaffected by the presence of treatment-emergent anti-reslizumab antibodies. | The approximate volume of distribution of reslizumab is 5L, suggesting minimal distribution to the extravascular tissues [FDA Label]. | Reslizumab clearance was approximately 7 mL/hour [FDA Label]. | Antibodies | NA | NA | NA | NA | Interleukin-5 | Cinqair | TEVA Canada Limited | TEVA Canada Limited | Intravenous | 10 mg / mL | CINQAIR is contraindicated in patients who have known hypersensitivity to reslizumab or any of its excipients | mouth and throat pain. | Cinqair is a monoclonal antibody that affects the actions of the body's immune system. Reslizumab works by reducing levels of a certain type of white blood cell that may contribute to the symptoms of asthma. Cinqair is a prescription medicin eused together with other medicines to help control severe... | Cinqair is a prescription medicine used to treat the symptoms of Asthma. Cinqair may be used alone or with other medications. | NA | CINQAIR (reslizumab) is a humanized interleukin-5 antagonist monoclonal antibody (IgG4κ). Reslizumab is produced by recombinant DNA technology in murine myeloma non-secreting 0 (NS0) cells. Reslizumab has a molecular weight of approximately 147 kDa. | Link | Link | NA |
| 12911 | Th1368 | Reslizumab | NA | 147000 | NA | NA | NA | NA | The half-life is approximately 24 days [FDA Label]. | Reslizumab is a humanized interleukin-5 (IL-5) antagonist monoclonal antibody (IgG4 kappa) that is produced by recombinant DNA technology in murine myeloma non-secreting 0 (NS0) cells. IL-5 is a pro-inflammatory cytokine that is responsible for the growth and differentiation, recruitment, activation, and survival of eosinophils [FDA Label]. Elevated levels of eosinophils increase the risk for asthma exacerbations, including both allergic forms and nonallergic forms of asthma where eosinophilia is prominent. By targeting the IL-5 and disrupting its signalling pathways, reslizumab aims to inhibit eosinophil maturation and promote programmed cell death [A31578]. Asthma is a chronic respiratory disease that causes inflammation in the lungs with asthma attacks that lead to severe breathing difficulties. Patients often experience persistent or exacerbating symptoms overtime despite conventional first-line therapies available. Inflammation-predominant asthma, which is chatacterized by eosinophilic infiltration of airway mucosa and elevated levels of eosinophils in the blood, sputum and BAL fluid, is associated with an increased risk for recurrent exacerbation and asthma-related hospitalizations [A31579]. In four double-blind, randomized, placebo-controlled trials in patients with severe asthma on currently available therapies, patients receiving reslizumab had fewer asthma attacks, and a longer time to the first attack compared to patients receiving placebo [FDA Label, A31579]. In addition, a significant improvement in lung function was seen, as measured by the volume of air exhaled by patients in one second [L1133]. Studies demonstrated that reslizumab was not effective in various asthma outcomes in patients without eosinophilia [A31577]. Reslizumab was developed by Teva Pharmaceuticals. Approved by the FDA in March 2016, reslizumab is marketed under the brand name Cinqair for intravenous injection. It is injected once every four weeks via intravenous infusion. Cinqair is indicated as an add-on maintenance therapy for adults with severe asthma with an eosinophilic phenotype. It is approved for patients who have a history of severe asthma attacks (exacerbations) despite receiving their current asthma medicines. Reslizumab is marketed as Cinqaero in Europe. | Indicated for the add-on maintenance treatment of patients with severe asthma aged 18 years and older with an eosinophilic phenotype. | A reduction in blood eosinophil counts was observed in clinical studies following an initial infusion of 3 mg/kg reslizumab and was maintained through 52 weeks of treatment with no signs of tachyphylaxis. Greater reductions of blood eosinophils were observed in subjects with higher reslizumab serum concentrations. This effect was independent of the presence of treatment-emergent anti-reslizumab antibodies [FDA Label]. | Reslizumab an interleukin-5 (IL-5) antagonist (IgG4, kappa) that binds to IL-5 with a dissociation constant of 81 pM. IL-5 is a proinflammatory cytokine responsible for the terminal maturation of eosinophils and increases chemotaxis, endothelial adhesion, activation and survival of eosinophils. Eosinophils are known to play a central role in the pathophysiology of many patients with asthma; upon activation, eosinophils release leukotrienes, platelet activation factor, major basic protein, eosinophil cationic protein, eosinophil peroxidase, eosinophil-derived neurotoxin, and other cytokines that are cytotoxic to the bronchial epithelium and lead to airway inflammation and bronchospasm [A31577]. IL-5 production is increased by upon activation of TH2 lymphocytes after antigen exposure and IL-5 stimulates the production and maturation of eosinophil precursors in the bone marrow [A31577]. IL-5 promotes the growth and differentiation, recruitment, activation, and survival of eosinophils via interacting with the IL-5 receptor expressed on the eosinophil surface [FDA Label]. Increased production and activation of eosinophils is especially prominent in nonallergic forms of asthma [A31577]. Reslizumab is a humanized monoclonal antibody that occupies the region ERRR (glutamic acid, arginine, arginine, arginine) corresponding to amino acids 89–92 on IL-5, which is a region critical for its interaction with the IL-5 receptor on the eosinophil surface [A31577]. By binding to IL-5 and disrupting its binding to the alpha chain of the IL-5 receptor complex, reslizumab inhibits the bioactivity of IL-5 and attenuates IL-5 signaling. Blocking of IL-5 signalling thereby reduces the production and survival of eosinophils and inhibits eosinophilic-driven inflammation. | Single doses of up to 732 mg have been administered intravenously to subjects in clinical trials without evidence of dose-related toxicities. There is no specific treatment for an overdose with reslizumab. If the event of an overdose, the patient should be treated supportively with appropriate monitoring as necessary [FDA Label]. Based on the findings of a 6-month bioassay, reslizumab showed no evidence of carcinogenicity. In a fertility study, administration of reslizumab to parental mice at doses up to 50 mg/kg (approximately 6 times the MRHD on an AUC basis) had no effects on male or female mating or fertility. The malignancy risk of reslizumab in humans with effects on tumor growth is not yet established [FDA Label]. | Like other monoclonal antibodies, reslizumab is assumed to undergo enzymatic proteolysis into smaller peptides and amino acids. As reslizumab bind to the target, it is not expected to undergo a target-mediated clearance [FDA Label]. | The peak serum concentrations of reslizumab were typically observed at the end of the infusion with the serum concentrations gradually declining from the peak in a biphasic manner. Following multiple doses, serum concentrations of reslizumab accumulated approximately 1.5 to 1.9-fold. Interindividual variability in peak and overall exposure across healthy individuals, patients with asthma, and other populations in pharmacokinetic studies was around 20-30% [FDA Label]. Systemic exposure to reslizumab appeared to be unaffected by the presence of treatment-emergent anti-reslizumab antibodies. | The approximate volume of distribution of reslizumab is 5L, suggesting minimal distribution to the extravascular tissues [FDA Label]. | Reslizumab clearance was approximately 7 mL/hour [FDA Label]. | Antibodies, Monoclonal | NA | NA | NA | NA | Interleukin-5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12912 | Th1368 | Reslizumab | NA | 147000 | NA | NA | NA | NA | The half-life is approximately 24 days [FDA Label]. | Reslizumab is a humanized interleukin-5 (IL-5) antagonist monoclonal antibody (IgG4 kappa) that is produced by recombinant DNA technology in murine myeloma non-secreting 0 (NS0) cells. IL-5 is a pro-inflammatory cytokine that is responsible for the growth and differentiation, recruitment, activation, and survival of eosinophils [FDA Label]. Elevated levels of eosinophils increase the risk for asthma exacerbations, including both allergic forms and nonallergic forms of asthma where eosinophilia is prominent. By targeting the IL-5 and disrupting its signalling pathways, reslizumab aims to inhibit eosinophil maturation and promote programmed cell death [A31578]. Asthma is a chronic respiratory disease that causes inflammation in the lungs with asthma attacks that lead to severe breathing difficulties. Patients often experience persistent or exacerbating symptoms overtime despite conventional first-line therapies available. Inflammation-predominant asthma, which is chatacterized by eosinophilic infiltration of airway mucosa and elevated levels of eosinophils in the blood, sputum and BAL fluid, is associated with an increased risk for recurrent exacerbation and asthma-related hospitalizations [A31579]. In four double-blind, randomized, placebo-controlled trials in patients with severe asthma on currently available therapies, patients receiving reslizumab had fewer asthma attacks, and a longer time to the first attack compared to patients receiving placebo [FDA Label, A31579]. In addition, a significant improvement in lung function was seen, as measured by the volume of air exhaled by patients in one second [L1133]. Studies demonstrated that reslizumab was not effective in various asthma outcomes in patients without eosinophilia [A31577]. Reslizumab was developed by Teva Pharmaceuticals. Approved by the FDA in March 2016, reslizumab is marketed under the brand name Cinqair for intravenous injection. It is injected once every four weeks via intravenous infusion. Cinqair is indicated as an add-on maintenance therapy for adults with severe asthma with an eosinophilic phenotype. It is approved for patients who have a history of severe asthma attacks (exacerbations) despite receiving their current asthma medicines. Reslizumab is marketed as Cinqaero in Europe. | Indicated for the add-on maintenance treatment of patients with severe asthma aged 18 years and older with an eosinophilic phenotype. | A reduction in blood eosinophil counts was observed in clinical studies following an initial infusion of 3 mg/kg reslizumab and was maintained through 52 weeks of treatment with no signs of tachyphylaxis. Greater reductions of blood eosinophils were observed in subjects with higher reslizumab serum concentrations. This effect was independent of the presence of treatment-emergent anti-reslizumab antibodies [FDA Label]. | Reslizumab an interleukin-5 (IL-5) antagonist (IgG4, kappa) that binds to IL-5 with a dissociation constant of 81 pM. IL-5 is a proinflammatory cytokine responsible for the terminal maturation of eosinophils and increases chemotaxis, endothelial adhesion, activation and survival of eosinophils. Eosinophils are known to play a central role in the pathophysiology of many patients with asthma; upon activation, eosinophils release leukotrienes, platelet activation factor, major basic protein, eosinophil cationic protein, eosinophil peroxidase, eosinophil-derived neurotoxin, and other cytokines that are cytotoxic to the bronchial epithelium and lead to airway inflammation and bronchospasm [A31577]. IL-5 production is increased by upon activation of TH2 lymphocytes after antigen exposure and IL-5 stimulates the production and maturation of eosinophil precursors in the bone marrow [A31577]. IL-5 promotes the growth and differentiation, recruitment, activation, and survival of eosinophils via interacting with the IL-5 receptor expressed on the eosinophil surface [FDA Label]. Increased production and activation of eosinophils is especially prominent in nonallergic forms of asthma [A31577]. Reslizumab is a humanized monoclonal antibody that occupies the region ERRR (glutamic acid, arginine, arginine, arginine) corresponding to amino acids 89–92 on IL-5, which is a region critical for its interaction with the IL-5 receptor on the eosinophil surface [A31577]. By binding to IL-5 and disrupting its binding to the alpha chain of the IL-5 receptor complex, reslizumab inhibits the bioactivity of IL-5 and attenuates IL-5 signaling. Blocking of IL-5 signalling thereby reduces the production and survival of eosinophils and inhibits eosinophilic-driven inflammation. | Single doses of up to 732 mg have been administered intravenously to subjects in clinical trials without evidence of dose-related toxicities. There is no specific treatment for an overdose with reslizumab. If the event of an overdose, the patient should be treated supportively with appropriate monitoring as necessary [FDA Label]. Based on the findings of a 6-month bioassay, reslizumab showed no evidence of carcinogenicity. In a fertility study, administration of reslizumab to parental mice at doses up to 50 mg/kg (approximately 6 times the MRHD on an AUC basis) had no effects on male or female mating or fertility. The malignancy risk of reslizumab in humans with effects on tumor growth is not yet established [FDA Label]. | Like other monoclonal antibodies, reslizumab is assumed to undergo enzymatic proteolysis into smaller peptides and amino acids. As reslizumab bind to the target, it is not expected to undergo a target-mediated clearance [FDA Label]. | The peak serum concentrations of reslizumab were typically observed at the end of the infusion with the serum concentrations gradually declining from the peak in a biphasic manner. Following multiple doses, serum concentrations of reslizumab accumulated approximately 1.5 to 1.9-fold. Interindividual variability in peak and overall exposure across healthy individuals, patients with asthma, and other populations in pharmacokinetic studies was around 20-30% [FDA Label]. Systemic exposure to reslizumab appeared to be unaffected by the presence of treatment-emergent anti-reslizumab antibodies. | The approximate volume of distribution of reslizumab is 5L, suggesting minimal distribution to the extravascular tissues [FDA Label]. | Reslizumab clearance was approximately 7 mL/hour [FDA Label]. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Interleukin-5 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12924 | Th1369 | Teplizumab | >Th1369_Teplizumab QVQLVQSGGGVVQPGRSLRLSCKASGYTFTRYTMHWVRQAPGKGLEWIGYINPSRGYTNYNQKVKDRFTISRDNSKNTAFLQMDSLRPEDTGVYFCARYYDDHYCLDYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin.[A241490] Targeting T cells can be achieved through antibodies against the T cell receptor (TCR) component CD3 e. However, if Fc binding is left intact, severe adverse effects related to cytokine release syndrome (CRS) are observed, and therefore Fc-nonbinding antibodies are the preferred method of choice.[A241480] Anti-CD3 therapy has traditionally been used to prevent graft-versus-host-disease in organ transplantation but more recently has been explored to prolong the onset of (T1D) in high-risk patients.[A241480, A241500] Teplizumab is a humanized IgG1 | Investigated for use/treatment in diabetes mellitus type 1. | NA | Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin. T1D is a progressive disease with three recognizable stages and in which only Stage 3 is associated with clinically apparent symptoms.[A241490] The earliest indication of T1D risk is the presence of at least two autoantibodies against relevant antigens, confirming an important role for B cells in what has traditionally been considered a T cell-dominated condition.[A241490, A241495] Combined with other observations from animal and human studies, it is clear that the T-B axis plays a role in T1D; treatment has focussed on targeting B and T cells independently, as well as their interactions.[A241495] The T cell receptor (TCR) comprises TCR a and ß chains together with six CD3 molecules, including two CD3 e chains. It is responsible for recognizing antigens displayed on the MHC complex of other cells to elicit a response.[A241480] Teplizumab, a humanized IgG1 | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | T-cell surface glycoprotein CD3 epsilon chain | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12925 | Th1369 | Teplizumab | >Th1369_Teplizumab QVQLVQSGGGVVQPGRSLRLSCKASGYTFTRYTMHWVRQAPGKGLEWIGYINPSRGYTNYNQKVKDRFTISRDNSKNTAFLQMDSLRPEDTGVYFCARYYDDHYCLDYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin.[A241490] Targeting T cells can be achieved through antibodies against the T cell receptor (TCR) component CD3 e. However, if Fc binding is left intact, severe adverse effects related to cytokine release syndrome (CRS) are observed, and therefore Fc-nonbinding antibodies are the preferred method of choice.[A241480] Anti-CD3 therapy has traditionally been used to prevent graft-versus-host-disease in organ transplantation but more recently has been explored to prolong the onset of (T1D) in high-risk patients.[A241480, A241500] Teplizumab is a humanized IgG1 | Investigated for use/treatment in diabetes mellitus type 1. | NA | Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin. T1D is a progressive disease with three recognizable stages and in which only Stage 3 is associated with clinically apparent symptoms.[A241490] The earliest indication of T1D risk is the presence of at least two autoantibodies against relevant antigens, confirming an important role for B cells in what has traditionally been considered a T cell-dominated condition.[A241490, A241495] Combined with other observations from animal and human studies, it is clear that the T-B axis plays a role in T1D; treatment has focussed on targeting B and T cells independently, as well as their interactions.[A241495] The T cell receptor (TCR) comprises TCR a and ß chains together with six CD3 molecules, including two CD3 e chains. It is responsible for recognizing antigens displayed on the MHC complex of other cells to elicit a response.[A241480] Teplizumab, a humanized IgG1 | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | T-cell surface glycoprotein CD3 epsilon chain | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12926 | Th1369 | Teplizumab | >Th1369_Teplizumab QVQLVQSGGGVVQPGRSLRLSCKASGYTFTRYTMHWVRQAPGKGLEWIGYINPSRGYTNYNQKVKDRFTISRDNSKNTAFLQMDSLRPEDTGVYFCARYYDDHYCLDYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin.[A241490] Targeting T cells can be achieved through antibodies against the T cell receptor (TCR) component CD3 e. However, if Fc binding is left intact, severe adverse effects related to cytokine release syndrome (CRS) are observed, and therefore Fc-nonbinding antibodies are the preferred method of choice.[A241480] Anti-CD3 therapy has traditionally been used to prevent graft-versus-host-disease in organ transplantation but more recently has been explored to prolong the onset of (T1D) in high-risk patients.[A241480, A241500] Teplizumab is a humanized IgG1 | Investigated for use/treatment in diabetes mellitus type 1. | NA | Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin. T1D is a progressive disease with three recognizable stages and in which only Stage 3 is associated with clinically apparent symptoms.[A241490] The earliest indication of T1D risk is the presence of at least two autoantibodies against relevant antigens, confirming an important role for B cells in what has traditionally been considered a T cell-dominated condition.[A241490, A241495] Combined with other observations from animal and human studies, it is clear that the T-B axis plays a role in T1D; treatment has focussed on targeting B and T cells independently, as well as their interactions.[A241495] The T cell receptor (TCR) comprises TCR a and ß chains together with six CD3 molecules, including two CD3 e chains. It is responsible for recognizing antigens displayed on the MHC complex of other cells to elicit a response.[A241480] Teplizumab, a humanized IgG1 | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | T-cell surface glycoprotein CD3 epsilon chain | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12934 | 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 | Antibodies | 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 | Removab | Neovii Biotech | Neovii Biotech | Intraperitoneal | 10 microgram | NA | Around 90% of patients treated with Removab have side effects. The most common side effects with Removab (seen in more than 1 patient in 10) are lymphopenia (low level of lymphocytes, a type of white blood cell), abdominal (tummy) pain, nausea (feeling sick), vomiting, diarrhoea, pyrexia (fever), fatigue (tiredness), chills and pain. | Removab is a concentrate that is made up into a solution for infusion (a drip). It contains the active substance catumaxomab. | Removab is used to treat malignant ascites, fluid accumulation in the peritoneal cavity (abdominal space) that is caused by a cancer. It is used when standard treatment is not available or is no longer feasible. | NA | NA | Link | Link | NA |
| 12935 | 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 | Antibodies, Monoclonal | 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 | Removab | Neovii Biotech | Neovii Biotech | Intraperitoneal | 50 microgram | NA | Around 90% of patients treated with Removab have side effects. The most common side effects with Removab (seen in more than 1 patient in 10) are lymphopenia (low level of lymphocytes, a type of white blood cell), abdominal (tummy) pain, nausea (feeling sick), vomiting, diarrhoea, pyrexia (fever), fatigue (tiredness), chills and pain. | Removab is a concentrate that is made up into a solution for infusion (a drip). It contains the active substance catumaxomab. | Removab is used to treat malignant ascites, fluid accumulation in the peritoneal cavity (abdominal space) that is caused by a cancer. It is used when standard treatment is not available or is no longer feasible. | NA | NA | Link | Link | NA |
| 12962 | Th1372 | Volociximab | NA | NA | NA | NA | NA | NA | NA | 0 | Investigated for use/treatment in solid tumors, renal cell carcinoma, melanoma, pancreatic cancer, lung cancer, and ovarian cancer. | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13377 | 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]. | Antibodies | NA | NA | NA | NA | Complement C5 | Ultomiris | Alexion Pharmaceuticals Inc. | Alexion Pharmaceuticals Inc. | Intravenous | 300 mg/3mL | 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 |
| 13378 | 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]. | Antibodies, Monoclonal | NA | NA | NA | NA | Complement C5 | Ultomiris | Alexion Pharmaceuticals Inc. | Alexion Pharmaceuticals Inc. | Intravenous | 1100 mg/11mL | 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 |
| 13379 | 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]. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Complement C5 | Ultomiris | Alexion Pharma Gmbh | Alexion Pharma Gmbh | Intravenous | 10 mg / mL | 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 |
| 13487 | 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 | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13497 | Th1409 | Tabalumab | NA | NA | NA | NA | NA | NA | NA | Tabalumab has been used in trials studying the treatment of Autoimmune Disease, Rheumatoid Arthritis, Kidney Failure, Chronic, Connective Tissue Disease, and Systemic Lupus Erythematosus, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13521 | Th1412 | Ficlatuzumab | NA | NA | NA | NA | NA | NA | NA | Ficlatuzumab has been used in trials studying the treatment of Acute Myeloid Leukemia, Non-small Cell Lung Cancer, Mullerian Mixed Tumor of Ovary, Relapsed Acute Myeloid Leukemia, and Refractory Acute Myeloid Leukemia, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13522 | Th1412 | Ficlatuzumab | NA | NA | NA | NA | NA | NA | NA | Ficlatuzumab has been used in trials studying the treatment of Acute Myeloid Leukemia, Non-small Cell Lung Cancer, Mullerian Mixed Tumor of Ovary, Relapsed Acute Myeloid Leukemia, and Refractory Acute Myeloid Leukemia, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13523 | Th1412 | Ficlatuzumab | NA | NA | NA | NA | NA | NA | NA | Ficlatuzumab has been used in trials studying the treatment of Acute Myeloid Leukemia, Non-small Cell Lung Cancer, Mullerian Mixed Tumor of Ovary, Relapsed Acute Myeloid Leukemia, and Refractory Acute Myeloid Leukemia, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13531 | Th1413 | Figitumumab | NA | NA | NA | NA | NA | NA | NA | Figitumumab has been used in trials studying the treatment of Sarcoma, Solid Tumor, Breast Cancer, Lung Neoplasms, and Advanced Cancer, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13550 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Antibodies | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | Imfinzi | AstraZeneca Pharmaceuticals LP | AstraZeneca Pharmaceuticals LP | Intravenous | 120 mg/2.4mL | None. | fatigue, musculoskeletal pain, constipation, decreased appetite, nausea, swelling of extremities, urinary tract infection, abdominal pain, diarrhea/colitis, fever, shortness of breath, cough, and rash. | Imfinzi is a cancer medicine that works with your immune system to interfere with the growth and spread of cancer cells in the body. Imfinzi is used to treat non-small cell lung cancer in patients whose tumors cannot be removed by surgery, and whose cancer has not progressed after treatment with chemotherapy... | Imfinzi is a prescription medicine used to treat the symptoms of Urothelial Carcinoma, Non-small Cell Lung Cancer and Small Cell Lung Cancer. Imfinzi may be used alone or with other medications. | NA | Durvalumab is a programmed cell death ligand 1 (PD-L1) blocking antibody. Durvalumab is a human immunoglobulin G1 kappa (IgG1κ) monoclonal antibody that is produced by recombinant DNA technology in Chinese Hamster Ovary (CHO) cell suspension culture. | Link | Link | NA |
| 13551 | Th1415 | Durvalumab | >Th1415_Durvalumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSRYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCAREGGWFGELAFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146300 | C6502H10018N1742O2024S42 | NA | NA | NA | Based on baseline clearance rate, the geometric mean terminal half-life is 18 days.[L12621,L12627] | Durvalumab is a human immunoglobulin G1 kappa (IgG1 | Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.[L12621] Durvalumab is indicated for the treatment of patients with unresectable Stage III non-small cell lung cancer (NSCLC) whose disease has not progressed following concurrent platinum-based chemotherapy and radiation therapy.[L12621] It is also approved for the treatment of patients with extensive-stage small cell lung cancer (ES-SCLC) in combination with [etoposide] and either [carboplatin] or [cisplatin] as first-line therapy.[L12624] Durvalumab is indicated as monotherapy used for the treatment of locally advanced, unresectable non-small cell lung cancer (NSCLC) in adults whose tumours express PD-L1 on = 1% of tumour cells and whose disease has not progressed following platinum-based chemoradiation therapy.[L12627] | Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells.[L12621] In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner.[A192807] In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC).[L12621] | Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival.[A192798] Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment.[A192789,L12621] PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure.[A192789,A192801] Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.[A193005] The expression of PD-L1 is an adaptive immune response by tumour cells, resulting in over-expression of the molecule in some cancers.[A192801] PD-L1 interacts with PD-1 and CD80, which leads to blocked cytotoxic T cell activation, T cell proliferation, and cytokine production.[L12621] By binding to PD-L1 and preventing its association with PD-1 and CD80, durvalumab activates the immune responses mediated by cytotoxic T cells that attack tumour cells.[L12621] Durvalumab displays selective and high affinity toward PD-L1 but not PD-L2, which is a regulatory ligand expressed in tumour cells to a lesser extent and involved in regulating inflammation and differentiation of T cells.[A192789] | There is limited information about the overdose profile and LD50 of durvalumab. In case of overdose, the patient should be closely monitored for drug-related adverse events, and appropriate symptomatic treatment should be immediately initiated.[L12627] Based on the findings of clinical studies, durvalumab had a risk of causing immune-mediated reactions, such as pneumonitis, hepatitis, and other serious infections. In animal reproductive studies, durvalumab caused fetal harm and this fetal toxicity may be possible in humans.[L12621] | Durvalumab is subject to protein catabolism via reticuloedothelial system or target-mediated disposition.[L12627] | Durvalumab exhibits a dose-proportional pharmacokinetic profile that is non-linear at doses <3 mg/kg and linear at doses =3 mg/kg. Following intravenous administration in patients with solid tumours, the steady-state plasma concentrations were reached at approximately 16 weeks.[L12621] | In patients receiving the dose range of = 10 mg/kg every 2 weeks, the mean steady state volume of distribution (Vss) was 5.64 L.[L12621,L12627] | Clearance of durvalumab decreases over time, resulting in a mean steady-state clearance (CLss) of 8.2 mL/h following 365 days of initial drug administration. However, the decrease in CLss is not considered clinically relevant.[L12621,L12627] | Antibodies, Monoclonal | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | Imfinzi | AstraZeneca Pharmaceuticals LP | AstraZeneca Pharmaceuticals LP | Intravenous | 500 mg/10mL | None. | fatigue, musculoskeletal pain, constipation, decreased appetite, nausea, swelling of extremities, urinary tract infection, abdominal pain, diarrhea/colitis, fever, shortness of breath, cough, and rash. | Imfinzi is a cancer medicine that works with your immune system to interfere with the growth and spread of cancer cells in the body. Imfinzi is used to treat non-small cell lung cancer in patients whose tumors cannot be removed by surgery, and whose cancer has not progressed after treatment with chemotherapy... | Imfinzi is a prescription medicine used to treat the symptoms of Urothelial Carcinoma, Non-small Cell Lung Cancer and Small Cell Lung Cancer. Imfinzi may be used alone or with other medications. | NA | Durvalumab is a programmed cell death ligand 1 (PD-L1) blocking antibody. Durvalumab is a human immunoglobulin G1 kappa (IgG1κ) monoclonal antibody that is produced by recombinant DNA technology in Chinese Hamster Ovary (CHO) cell suspension culture. | Link | Link | NA |
| 13569 | Th1416 | Bapineuzumab | NA | NA | NA | NA | NA | NA | NA | Bapineuzumab has been investigated for the treatment of Alzheimer's Disease. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13570 | Th1416 | Bapineuzumab | NA | NA | NA | NA | NA | NA | NA | Bapineuzumab has been investigated for the treatment of Alzheimer's Disease. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13571 | Th1416 | Bapineuzumab | NA | NA | NA | NA | NA | NA | NA | Bapineuzumab has been investigated for the treatment of Alzheimer's Disease. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13601 | Th1418 | Onartuzumab | NA | NA | NA | NA | NA | NA | NA | Onartuzumab has been used in trials studying the treatment of Neoplasms, Lung Cancer, Glioblastoma, Gastric Cancer, and Colorectal Cancer, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13602 | Th1418 | Onartuzumab | NA | NA | NA | NA | NA | NA | NA | Onartuzumab has been used in trials studying the treatment of Neoplasms, Lung Cancer, Glioblastoma, Gastric Cancer, and Colorectal Cancer, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13603 | Th1418 | Onartuzumab | NA | NA | NA | NA | NA | NA | NA | Onartuzumab has been used in trials studying the treatment of Neoplasms, Lung Cancer, Glioblastoma, Gastric Cancer, and Colorectal Cancer, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13611 | Th1419 | Solanezumab | NA | NA | NA | NA | NA | NA | NA | Solanezumab is under investigation for the treatment of Dementia, Alzheimers Disease, and Alzheimers Disease, Familial. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13612 | Th1419 | Solanezumab | NA | NA | NA | NA | NA | NA | NA | Solanezumab is under investigation for the treatment of Dementia, Alzheimers Disease, and Alzheimers Disease, Familial. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13613 | Th1419 | Solanezumab | NA | NA | NA | NA | NA | NA | NA | Solanezumab is under investigation for the treatment of Dementia, Alzheimers Disease, and Alzheimers Disease, Familial. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13621 | 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]. | Antibodies | 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 | Sanofi Aventis | Subcutaneous | 200 mg / 1.14 mL | 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 |
| 13622 | 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]. | Antibodies, Monoclonal | 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 | 150 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 |
| 13646 | 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 | Antibodies | NA | NA | NA | NA | Cytotoxic T-lymphocyte protein 4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13674 | 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 | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13686 | Th1425 | Lampalizumab | NA | NA | NA | NA | NA | NA | NA | Lampalizumab has been used in trials studying the treatment of Geographic Atrophy. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13687 | Th1425 | Lampalizumab | NA | NA | NA | NA | NA | NA | NA | Lampalizumab has been used in trials studying the treatment of Geographic Atrophy. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13698 | 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]. | Antibodies | NA | NA | NA | NA | Interleukin-23 subunit alpha | Tremfya | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Subcutaneous | 100 mg / 1 mL | 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 |
| 13711 | Th1427 | Dalotuzumab | NA | NA | NA | NA | NA | NA | NA | Dalotuzumab has been investigated for the treatment of Breast Cancer, Non Small Cell Lung Cancer, and Metastatic Colorectal Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13712 | Th1427 | Dalotuzumab | NA | NA | NA | NA | NA | NA | NA | Dalotuzumab has been investigated for the treatment of Breast Cancer, Non Small Cell Lung Cancer, and Metastatic Colorectal Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13713 | Th1427 | Dalotuzumab | NA | NA | NA | NA | NA | NA | NA | Dalotuzumab has been investigated for the treatment of Breast Cancer, Non Small Cell Lung Cancer, and Metastatic Colorectal Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13721 | Th1428 | Emibetuzumab | NA | NA | NA | NA | NA | NA | NA | Emibetuzumab has been used in trials studying the treatment of Advanced Cancer, Renal Cell Carcinoma, Hepatocellular Cancer, Gastric Adenocarcinoma, and Non-Small Cell Lung Cancer, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13722 | Th1428 | Emibetuzumab | NA | NA | NA | NA | NA | NA | NA | Emibetuzumab has been used in trials studying the treatment of Advanced Cancer, Renal Cell Carcinoma, Hepatocellular Cancer, Gastric Adenocarcinoma, and Non-Small Cell Lung Cancer, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13723 | Th1428 | Emibetuzumab | NA | NA | NA | NA | NA | NA | NA | Emibetuzumab has been used in trials studying the treatment of Advanced Cancer, Renal Cell Carcinoma, Hepatocellular Cancer, Gastric Adenocarcinoma, and Non-Small Cell Lung Cancer, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13731 | Th1429 | Ublituximab | NA | NA | NA | NA | NA | NA | NA | Ublituximab has been used in trials studying the treatment of B-cell Lymphoma, Neuromyelitis Optica, Mantle Cell Lymphoma, Non-Hodgkins Lymphoma, and Marginal Zone Lymphoma, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13755 | Th1431 | Ligelizumab | >Th1431_Ligelizumab QVQLVQSGAEVMKPGSSVKVSCKASGYTFSWYWLEWVRQAPGHGLEWMGEIDPGTFTTNYNEKFKARVTFTADTSTSTAYMELSSLRSEDTAVYYCARFSHFSGSNYDYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Ligelizumab is a humanized IgG1k monoclonal antibody targeted against immunoglobulin E (IgE). Similar in mechanism to [omalizumab], another IgE-directed monoclonal antibody, ligelizumab has a distinct binding epitope as compared to its peer (with a small degree of overlap) which appears to confer a greater affinity for free serum IgE and an altered sensitivity to IgE conformation.[A242292] Ligelizumab is currently under investigation for the treatment of chronic spontaneous urticaria (CSU), an autoimmune-driven inflammatory condition. While the precise pathogenesis of CSU is not entirely clear, autoantibodies against IgE receptors, and sometimes against IgE itself, are thought to exist in 30-40% of patients,[A242362,A242367] and the efficacy anti-IgE antibody therapy in the treatment of CSU has been previously established with omalizumab. Initial trials of ligelizumab suggest a greater efficacy over its predecessor for the treatment of CSU.[A242367] | NA | NA | Immunoglobulin E (IgE) is a key driver of hypersensitivity reactions, and has thus become an attractive target in the treatment of immune-mediated hypersensitivity disorders. Immediate hypersensitivity reactions are due to IgE binding with FceRI, which activates allergic effector cells that undergo degranulation to release vasoactive and pro-inflammatory mediators.[A242292] IgE also binds to CD23/FceRII, which appears responsible for antigen presentation, antigen transport across airway/epithelial barriers, and the regulation of IgE synthesis.[A242292] Ligelizumab is a monoclonal antibody directed at IgE, binding specifically to an epitope in the IgE Ce3 domain.[A242292] It neutralizes serum IgE and also appears to inhibit the production of IgE via inhibition of IgE-FceRI binding activity and, to a lesser extent, IgE binding to CD23. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Immunoglobulin heavy constant epsilon | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13756 | Th1431 | Ligelizumab | >Th1431_Ligelizumab QVQLVQSGAEVMKPGSSVKVSCKASGYTFSWYWLEWVRQAPGHGLEWMGEIDPGTFTTNYNEKFKARVTFTADTSTSTAYMELSSLRSEDTAVYYCARFSHFSGSNYDYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Ligelizumab is a humanized IgG1k monoclonal antibody targeted against immunoglobulin E (IgE). Similar in mechanism to [omalizumab], another IgE-directed monoclonal antibody, ligelizumab has a distinct binding epitope as compared to its peer (with a small degree of overlap) which appears to confer a greater affinity for free serum IgE and an altered sensitivity to IgE conformation.[A242292] Ligelizumab is currently under investigation for the treatment of chronic spontaneous urticaria (CSU), an autoimmune-driven inflammatory condition. While the precise pathogenesis of CSU is not entirely clear, autoantibodies against IgE receptors, and sometimes against IgE itself, are thought to exist in 30-40% of patients,[A242362,A242367] and the efficacy anti-IgE antibody therapy in the treatment of CSU has been previously established with omalizumab. Initial trials of ligelizumab suggest a greater efficacy over its predecessor for the treatment of CSU.[A242367] | NA | NA | Immunoglobulin E (IgE) is a key driver of hypersensitivity reactions, and has thus become an attractive target in the treatment of immune-mediated hypersensitivity disorders. Immediate hypersensitivity reactions are due to IgE binding with FceRI, which activates allergic effector cells that undergo degranulation to release vasoactive and pro-inflammatory mediators.[A242292] IgE also binds to CD23/FceRII, which appears responsible for antigen presentation, antigen transport across airway/epithelial barriers, and the regulation of IgE synthesis.[A242292] Ligelizumab is a monoclonal antibody directed at IgE, binding specifically to an epitope in the IgE Ce3 domain.[A242292] It neutralizes serum IgE and also appears to inhibit the production of IgE via inhibition of IgE-FceRI binding activity and, to a lesser extent, IgE binding to CD23. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Immunoglobulin heavy constant epsilon | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13757 | Th1431 | Ligelizumab | >Th1431_Ligelizumab QVQLVQSGAEVMKPGSSVKVSCKASGYTFSWYWLEWVRQAPGHGLEWMGEIDPGTFTTNYNEKFKARVTFTADTSTSTAYMELSSLRSEDTAVYYCARFSHFSGSNYDYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Ligelizumab is a humanized IgG1k monoclonal antibody targeted against immunoglobulin E (IgE). Similar in mechanism to [omalizumab], another IgE-directed monoclonal antibody, ligelizumab has a distinct binding epitope as compared to its peer (with a small degree of overlap) which appears to confer a greater affinity for free serum IgE and an altered sensitivity to IgE conformation.[A242292] Ligelizumab is currently under investigation for the treatment of chronic spontaneous urticaria (CSU), an autoimmune-driven inflammatory condition. While the precise pathogenesis of CSU is not entirely clear, autoantibodies against IgE receptors, and sometimes against IgE itself, are thought to exist in 30-40% of patients,[A242362,A242367] and the efficacy anti-IgE antibody therapy in the treatment of CSU has been previously established with omalizumab. Initial trials of ligelizumab suggest a greater efficacy over its predecessor for the treatment of CSU.[A242367] | NA | NA | Immunoglobulin E (IgE) is a key driver of hypersensitivity reactions, and has thus become an attractive target in the treatment of immune-mediated hypersensitivity disorders. Immediate hypersensitivity reactions are due to IgE binding with FceRI, which activates allergic effector cells that undergo degranulation to release vasoactive and pro-inflammatory mediators.[A242292] IgE also binds to CD23/FceRII, which appears responsible for antigen presentation, antigen transport across airway/epithelial barriers, and the regulation of IgE synthesis.[A242292] Ligelizumab is a monoclonal antibody directed at IgE, binding specifically to an epitope in the IgE Ce3 domain.[A242292] It neutralizes serum IgE and also appears to inhibit the production of IgE via inhibition of IgE-FceRI binding activity and, to a lesser extent, IgE binding to CD23. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Immunoglobulin heavy constant epsilon | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13764 | Th1432 | Seribantumab | NA | NA | NA | NA | NA | NA | NA | Seribantumab has been used in trials studying the treatment of NSCLC, Heregulin, Adenocarcinoma, Colorectal Cancer, and Solid Tumor Cancers, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13772 | Th1433 | Landogrozumab | NA | NA | NA | NA | NA | NA | NA | Landogrozumab has been used in trials studying the treatment of Advanced Cancer, Muscular Atrophy, and Pancreatic Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13773 | Th1433 | Landogrozumab | NA | NA | NA | NA | NA | NA | NA | Landogrozumab has been used in trials studying the treatment of Advanced Cancer, Muscular Atrophy, and Pancreatic Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13774 | Th1433 | Landogrozumab | NA | NA | NA | NA | NA | NA | NA | Landogrozumab has been used in trials studying the treatment of Advanced Cancer, Muscular Atrophy, and Pancreatic Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13782 | Th1434 | Romosozumab | NA | 145805 | NA | NA | NA | NA | 12.8 days[L9554]. | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. | 3.92L[L9554]. | 0.38mL/hr/kg[L9554]. | Antibodies | NA | NA | NA | NA | Sclerostin | Evenity | Amgen | Amgen | Subcutaneous | 105 mg / 1.17 mL | EVENITY is contraindicated in patients with: Hypocalcemia. Pre-existing hypocalcemia must be corrected prior to initiating therapy with EVENITY [see WARNINGS AND PRECAUTIONS, ADVERSE REACTIONS and Use In Specific Populations]. A history of systemic hypersensitivity to romosozumab or to any component of the product formulation. Reactions have included angioedema, erythema multiforme, and urticaria [see WARNINGS AND PRECAUTIONS and ADVERSE REACTIONS]. | joint pain, headache, muscle spasms, swelling of extremities, weakness, neck pain, insomnia, numbness and tingling sensation | Evenity is a sclerostin inhibitor. Sclerostin suppresses bone formation. Evenity is a prescription medicine used to treat osteoporosis in postmenopausal women with a high risk of bone fracture who cannot use other osteoporosis medications (or when other medications did not work). It is not known if Evenity... | Evenity is a prescription medicine used to treat the symptoms of Osteoporosis. Evenity may be used alone or with other medications. | NA | EVENITY (romosozumab-aqqg) injection is supplied as a sterile, preservative-free, clear to opalescent, colorless to light yellow solution for subcutaneous injection in a single-use prefilled syringe. | Link | Link | NA |
| 13783 | Th1434 | Romosozumab | NA | 145805 | NA | NA | NA | NA | 12.8 days[L9554]. | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. | 3.92L[L9554]. | 0.38mL/hr/kg[L9554]. | Antibodies, Monoclonal | NA | NA | NA | NA | Sclerostin | Evenity | AMGEN INC | AMGEN INC | Subcutaneous | 105 mg/1.17mL | EVENITY is contraindicated in patients with: Hypocalcemia. Pre-existing hypocalcemia must be corrected prior to initiating therapy with EVENITY [see WARNINGS AND PRECAUTIONS, ADVERSE REACTIONS and Use In Specific Populations]. A history of systemic hypersensitivity to romosozumab or to any component of the product formulation. Reactions have included angioedema, erythema multiforme, and urticaria [see WARNINGS AND PRECAUTIONS and ADVERSE REACTIONS]. | joint pain, headache, muscle spasms, swelling of extremities, weakness, neck pain, insomnia, numbness and tingling sensation | Evenity is a sclerostin inhibitor. Sclerostin suppresses bone formation. Evenity is a prescription medicine used to treat osteoporosis in postmenopausal women with a high risk of bone fracture who cannot use other osteoporosis medications (or when other medications did not work). It is not known if Evenity... | Evenity is a prescription medicine used to treat the symptoms of Osteoporosis. Evenity may be used alone or with other medications. | NA | EVENITY (romosozumab-aqqg) injection is supplied as a sterile, preservative-free, clear to opalescent, colorless to light yellow solution for subcutaneous injection in a single-use prefilled syringe. | Link | Link | NA |
| 13784 | Th1434 | Romosozumab | NA | 145805 | NA | NA | NA | NA | 12.8 days[L9554]. | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. | 3.92L[L9554]. | 0.38mL/hr/kg[L9554]. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Sclerostin | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13796 | Th1435 | Vadastuximab talirine | NA | NA | NA | NA | NA | NA | NA | Vadastuximab Talirine has been used in trials studying the treatment of Acute myeloid leukemia, Myelodysplastic Syndrome, Acute Myelogenous Leukemia, and Acute Promyelocytic Leukemia. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-3-[(3R)-1-[6-[[(2S)-1-[[(2S)-1-[4-[(6aS)-3-[3-[[(6aS)-2-methoxy-8-(4-methoxyphenyl)-11-oxo-6a,7-dihydropyrrolo[2,1-c][1,4]benzodiazepin-3-yl]oxy]propoxy]-2-methoxy-11-oxo-6a,7-dihydropyrrolo[2,1-c][1,4]benzodiazepin-8-yl]anilino]-1-oxopropan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-6-oxohexyl]-2,5-dioxopyrrolidin-3-yl]sulfanyl-2-aminopropanoic acid | NA | Link | NA | NA |
| 13797 | Th1435 | Vadastuximab talirine | NA | NA | NA | NA | NA | NA | NA | Vadastuximab Talirine has been used in trials studying the treatment of Acute myeloid leukemia, Myelodysplastic Syndrome, Acute Myelogenous Leukemia, and Acute Promyelocytic Leukemia. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-3-[(3R)-1-[6-[[(2S)-1-[[(2S)-1-[4-[(6aS)-3-[3-[[(6aS)-2-methoxy-8-(4-methoxyphenyl)-11-oxo-6a,7-dihydropyrrolo[2,1-c][1,4]benzodiazepin-3-yl]oxy]propoxy]-2-methoxy-11-oxo-6a,7-dihydropyrrolo[2,1-c][1,4]benzodiazepin-8-yl]anilino]-1-oxopropan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-6-oxohexyl]-2,5-dioxopyrrolidin-3-yl]sulfanyl-2-aminopropanoic acid | NA | Link | NA | NA |
| 13812 | Th1437 | Lebrikizumab | >Th1437_Lebrikizumab QVTLRESGPALVKPTQTLTLTCTVSGFSLSAYSVNWIRQPPGKALEWLAMIWGDGKIVYNSALKSRLTISKDTSKNQVVLTMTNMDPVDTATYYCAGDGYYPYAMDNWGQGSLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | NA | Lebrikizumab has been used in trials studying the treatment of Asthma, Allergic Asthma, Atopic Dermatitis, Idiopathic Pulmonary Fibrosis, and COPD, Chronic Obstructive Pulmonary Disease. | NA | NA | Anti-IL-13 humanized monoclonal antibody Lebrikizumab binds to and blocks the activity of IL-13, which may result in the inhibition of Hodkin lympoma cell proliferation. IL-13 cytokine, an important mediator in allergic inflammation, may be an autocrine growth factor for Hodgkin lymphoma cells. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Interleukin-13,IL13 protein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13813 | Th1437 | Lebrikizumab | >Th1437_Lebrikizumab QVTLRESGPALVKPTQTLTLTCTVSGFSLSAYSVNWIRQPPGKALEWLAMIWGDGKIVYNSALKSRLTISKDTSKNQVVLTMTNMDPVDTATYYCAGDGYYPYAMDNWGQGSLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | NA | Lebrikizumab has been used in trials studying the treatment of Asthma, Allergic Asthma, Atopic Dermatitis, Idiopathic Pulmonary Fibrosis, and COPD, Chronic Obstructive Pulmonary Disease. | NA | NA | Anti-IL-13 humanized monoclonal antibody Lebrikizumab binds to and blocks the activity of IL-13, which may result in the inhibition of Hodkin lympoma cell proliferation. IL-13 cytokine, an important mediator in allergic inflammation, may be an autocrine growth factor for Hodgkin lymphoma cells. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Interleukin-13,IL13 protein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13814 | Th1437 | Lebrikizumab | >Th1437_Lebrikizumab QVTLRESGPALVKPTQTLTLTCTVSGFSLSAYSVNWIRQPPGKALEWLAMIWGDGKIVYNSALKSRLTISKDTSKNQVVLTMTNMDPVDTATYYCAGDGYYPYAMDNWGQGSLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | NA | Lebrikizumab has been used in trials studying the treatment of Asthma, Allergic Asthma, Atopic Dermatitis, Idiopathic Pulmonary Fibrosis, and COPD, Chronic Obstructive Pulmonary Disease. | NA | NA | Anti-IL-13 humanized monoclonal antibody Lebrikizumab binds to and blocks the activity of IL-13, which may result in the inhibition of Hodkin lympoma cell proliferation. IL-13 cytokine, an important mediator in allergic inflammation, may be an autocrine growth factor for Hodgkin lymphoma cells. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Interleukin-13,IL13 protein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13830 | Th1439 | Varlilumab | NA | NA | NA | NA | NA | NA | NA | Varlilumab has been used in trials studying the treatment of MELANOMA, Skin Ulcer, Burkett's Lymphoma, Mantle cell lymphoma, and Any T-cell Malignancy, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13838 | 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. | Antibodies | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | Bavencio | Merck Europe B.V. | Merck Europe B.V. | Intravenous | 20 mg/mL | NA | fatigue/lack of energy, musculoskeletal pain (back pain, neck pain, pain in extremities), diarrhea, nausea, infusion-related reactions (chills, fever, back pain, hypersensitivity reactions and low blood pressure), rash and skin redness, decreased appetite, swelling of the extremities, joint pain, constipation, abdominal pain, vomiting, itching, weight loss, cough, shortness of breath, dizziness, headache, and high blood pressure (hypertension). | Bavencio is a cancer medicine that interferes with the growth and spread of cancer cells in the body. Bavencio is used to treat a type of skin cancer called Merkel cell carcinoma in adults and children at least 12 years old, when the cancer has spread to other parts of the body (metastatic). Bavencio... | BAVENCIO (avelumab) is indicated for the treatment of adults and pediatric patients 12 years and older with metastatic Merkel cell carcinoma (MCC). This indication is approved under accelerated approval based on tumor response rate and duration of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials [see Clinical Studies]. | NA | Avelumab is a programmed death ligand1 (PD-L1) blocking antibody. Avelumab- is a human IgG1 lambda monoclonal antibody produced in Chinese hamster ovary cells and has a molecular weight of approximately 147 kDa. | Link | Link | NA |
| 13839 | 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. | Antibodies, Monoclonal | NA | NA | NA | NA | Programmed cell death 1 ligand 1 | Bavencio | EMD Serono, Inc. | EMD Serono, Inc. | Intravenous | 20 mg/1mL | NA | fatigue/lack of energy, musculoskeletal pain (back pain, neck pain, pain in extremities), diarrhea, nausea, infusion-related reactions (chills, fever, back pain, hypersensitivity reactions and low blood pressure), rash and skin redness, decreased appetite, swelling of the extremities, joint pain, constipation, abdominal pain, vomiting, itching, weight loss, cough, shortness of breath, dizziness, headache, and high blood pressure (hypertension). | Bavencio is a cancer medicine that interferes with the growth and spread of cancer cells in the body. Bavencio is used to treat a type of skin cancer called Merkel cell carcinoma in adults and children at least 12 years old, when the cancer has spread to other parts of the body (metastatic). Bavencio... | BAVENCIO (avelumab) is indicated for the treatment of adults and pediatric patients 12 years and older with metastatic Merkel cell carcinoma (MCC). This indication is approved under accelerated approval based on tumor response rate and duration of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials [see Clinical Studies]. | NA | Avelumab is a programmed death ligand1 (PD-L1) blocking antibody. Avelumab- is a human IgG1 lambda monoclonal antibody produced in Chinese hamster ovary cells and has a molecular weight of approximately 147 kDa. | Link | Link | NA |
| 13865 | Th1442 | Crenezumab | >Th1442_Crenezumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSYGMSWVRQAPGKGLELVASINSNGGSTYYPDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCASGDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | NA | NA | NA | NA | NA | NA | Crenezumab has been used in trials studying the treatment of Alzheimer's Disease. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13866 | Th1442 | Crenezumab | >Th1442_Crenezumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSYGMSWVRQAPGKGLELVASINSNGGSTYYPDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCASGDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | NA | NA | NA | NA | NA | NA | Crenezumab has been used in trials studying the treatment of Alzheimer's Disease. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13867 | Th1442 | Crenezumab | >Th1442_Crenezumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSYGMSWVRQAPGKGLELVASINSNGGSTYYPDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCASGDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | NA | NA | NA | NA | NA | NA | Crenezumab has been used in trials studying the treatment of Alzheimer's Disease. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13875 | 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 | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13885 | Th1444 | Anifrolumab | >Th1444_Anifrolumab EVQLVQSGAEVKKPGESLKISCKGSGYIFTNYWIAWVRQMPGKGLESMGIIYPGDSDIRYSPSFQGQVTISADKSITTAYLQWSSLKASDTAMYYCARHDIEGFDYWGRGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The serum elimination half life anifrolumab in a phase 1 trial in patients with scleroderma was 0.84 days for a 0.1 mg/kg single dose, 1.24 days for a 0.3 mg/kg single dose, 2.96 days for a 1.0 mg/kg single dose, 4.07 days for a 3.0 mg/kg single dose, and 7.70 days for a 10.0 mg/kg single dose.[A237044] | Anifrolumab, or MEDI-546, is a type 1 interferon receptor (IFNAR) inhibiting IgG1 | Anifrolumab is indicated in the treatment of adults with moderate to severe systemic lupus erythematosus.[L34929] | Anifrolumab is a type 1 interferon receptor (IFNAR) inhibiting IgG1 | Systemic lupus erythematosus (SLE) is an autoimmune disorder affecting multiple systems in the body.[A237059] SLE may manifest as a rash on the skin, and can progress to life-threatening autoimmune reactions in the kidney or nervous system.[A237069] Type 1 interferon pathway activation has been identified as a mediator of pathogenesis in SLE, and the level of type 1 interferon expression is correlated with severity of SLE.[A237059,A237069,A237084] Activation of the type 1 interferon receptor (INFAR1) by interferons alpha, beta, epsilon, kappa, and omega lead to stimulation of gene transcription.[A237059] Activation of INFAR1 and INFAR2 lead to phosphorylation of STAT1 and STAT2, which are translocated with interferon regulatory factor 9 (IRF9) to the cell nucleus to activate the interferon-stimulated response element (ISRE).[A237069] Activation of ISRE leads to the expression of many proinflammatory and immunomodulatory proteins, as well as the activation of a positive feedback loop that produces more type 1 interferons.[A237069] Interferon alpha stimulates monocytes to mature into myeloid dendritic cells that express self antigens.[A237084] CD4+ and CD8+ T-cells, as well as B cells, that are autoreactive will respond to the self antigens and induce inflammmation and apoptosis in cells.[A237084] This self-reactive immune response damages otherwise healthy tissue throughout the body.[A237084] Anifrolumab is an immunoglobulin gamma 1 kappa (IgG1 | Data regarding overdose is not readily available.[L34929] In a phase 1 clinical trial, patients given a single dose of 20.0 mg/kg experienced upper respiratory tract infections, headache, diarrhea, and nausea.[A237044] 2 patients in the 3.0 mg/kg single dose group experienced osteomyelitis and skin ulcer.[A237044] A single patient in the 1.0 mg/kg/week group developed chronic myelogenous leukemia.[A237044] The frequency and severity of adverse effects does not appear to be closely related to dose.[A237044] In the event of an overdose, treat patients with symptomatic and supportive measures. | Monoclonal antibodies are mainly catabolized to smaller oligopeptides and individual amino acids.[A40006,L34929] | A 300 mg intravenous dose reaches a mean Cmax of 82.4 µg/mL, with a Tmax of 0.03 days, and an AUC of 907 day | The estimated volume of distribution of anifrolumab at steady state is 6.23 L for a 69.1 kg patient.[L34929] | The estimated systemic clearance of anifrolumab is 0.193 L/day.[L34929] | Antibodies | NA | NA | NA | NA | Interferon alpha/beta receptor 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13894 | 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]. | Antibodies | NA | NA | NA | NA | B-lymphocyte antigen CD20 | Ocrevus | Roche Registration Gmb H | Roche Registration Gmb H | Intravenous | 300 mg | OCREVUS is contraindicated in patients with:Active HBV infection [see DOSAGE AND ADMINISTRATION and WARNINGS AND PRECAUTIONS]A history of life-threatening infusion reaction to OCREVUS [see WARNINGS AND PRECAUTIONS] | upper respiratory tract infections, infusion reactions (itching, rash, hives, redness, bronchospasm, swollen and sore throat, mouth pain, shortness of breath, flushing, hypotension, fever, fatigue, headache, dizziness, nausea, and fast heart rate), skin infections, lower respiratory tract infections, depression, back pain, and pain in the extremities. | Ocrevus is a monoclonal antibody that affects the actions of the body's immune system. Monoclonal antibodies are made to target and destroy only certain cells in the body. This may help to protect healthy cells from damage. Ocrevus is used to treat primary progressive multiple sclerosis and relapsing... | OCREVUS is indicated for the treatment of: | NA | OCREVUS (ocrelizumab) Injection for intravenous infusion is a preservative-free, sterile, clear or slightly opalescent, and colorless to pale brown solution supplied in single-dose vials. Each mL of solution contains 30 mg ocrelizumab, glacial acetic acid (0.25 mg), polysorbate 20 (0.2 mg), sodium acetate trihydrate (2.14 mg), and trehalose dihydrate (40 mg) at pH 5.3. | Link | Link | NA |
| 13895 | 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]. | Antibodies, Monoclonal | NA | NA | NA | NA | B-lymphocyte antigen CD20 | Ocrevus | Hoffmann La Roche | Hoffmann La Roche | Intravenous | 30 mg / mL | OCREVUS is contraindicated in patients with:Active HBV infection [see DOSAGE AND ADMINISTRATION and WARNINGS AND PRECAUTIONS]A history of life-threatening infusion reaction to OCREVUS [see WARNINGS AND PRECAUTIONS] | upper respiratory tract infections, infusion reactions (itching, rash, hives, redness, bronchospasm, swollen and sore throat, mouth pain, shortness of breath, flushing, hypotension, fever, fatigue, headache, dizziness, nausea, and fast heart rate), skin infections, lower respiratory tract infections, depression, back pain, and pain in the extremities. | Ocrevus is a monoclonal antibody that affects the actions of the body's immune system. Monoclonal antibodies are made to target and destroy only certain cells in the body. This may help to protect healthy cells from damage. Ocrevus is used to treat primary progressive multiple sclerosis and relapsing... | OCREVUS is indicated for the treatment of: | NA | OCREVUS (ocrelizumab) Injection for intravenous infusion is a preservative-free, sterile, clear or slightly opalescent, and colorless to pale brown solution supplied in single-dose vials. Each mL of solution contains 30 mg ocrelizumab, glacial acetic acid (0.25 mg), polysorbate 20 (0.2 mg), sodium acetate trihydrate (2.14 mg), and trehalose dihydrate (40 mg) at pH 5.3. | Link | Link | NA |
| 13896 | 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]. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | B-lymphocyte antigen CD20 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13926 | Th1448 | Ozoralizumab | NA | NA | NA | NA | NA | NA | NA | Ozoralizumab has been used in trials studying the treatment of Rheumatoid Arthritis and Active Rheumatoid Arthritis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13927 | Th1448 | Ozoralizumab | NA | NA | NA | NA | NA | NA | NA | Ozoralizumab has been used in trials studying the treatment of Rheumatoid Arthritis and Active Rheumatoid Arthritis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13934 | Th1449 | Benralizumab | >Th1449_Benralizumab EVQLVQSGAEVKKPGASVKVSCKASGYTFTSYVIHWVRQRPGQGLAWMGYINPYNDGTKYNERFKGKVTITSDRSTSTVYMELSSLRSEDTAVYLCGREGIRYYGLLGDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146054 | C6492H10060N1724O2028S42 | 6.6 - 7.2 | NA | 69 °C (midpoint transition), 80 °C (whole IgG1) | The half-life of Benralizumab is estimated to be 15-18 days.[A31293] | Benralizumab is a humanized recombinant monoclonal antibody of the isotype IgG1k immunoglobulin that specifically binds to the alpha chain of the interleukin 5 receptor (IL-5R) expressed on eosinophils and basophils.[A31294] It inhibits the binding of IL-5 as well as the hetero-oligomerization of the alpha and beta subunits of the IL-5R, thus blocking, signal transduction. Besides, it is an afucosylated IgG which gives it high affinity for the Fc | Benralizumab is indicated as a maintenance treatment of patients 12 years or older with severe asthma and an eosinophilic phenotype.[L1020] The pathology of severe asthma with eosinophilic phenotype is also denotated as TH2-high phenotype. The patients with this phenotype are characterized by the expression of IL-5 and IL-13, airway hyperresponsiveness, responsiveness to inhaled corticosteroids, high serum IgE and eosinophilia in blood and airway. In the TH2-high phenotype, IL-5 presents a central role as it is responsible for eosinophil differentiation, survival, activation and migration to the lungs.[A31295] | Eosinophils are the key target of inflammatory respiratory diseases and they undergo apoptosis in absence of IL-5. Therefore, benralizumab action on the IL-5 receptor in basophils and eosinophils produces the apoptosis and its significant reduction in the blood.[A31294] On the other hand, Benralizumab binding to natural killer cells Fc | Interleukin-5 (IL-5) induces an eosinophil-mediated inflammatory response by binding to the IL-5 receptor (IL-5R) expressed in eosinophils, basophils and some mast cells. Benralizumab, unlike IL-5 low-affinity binding, binds with high affinity to the domain I of the a-chain of IL-5R and blocks its signaling and the proliferation of IL-5-dependent cell lines. On the other hand, Benralizumab is an afucosylated antibody in the CH2 region which gives it a high affinity for the Fc | There are not reports of long-term studies regarding tumorgenesis or carcinogenesis. Fertility studies performed in aminal trials showed no adverse histopathological findings.[FDA label] | As any monoclonal IgG antibody, Beralizumab is degraded by proteases widely spread in the body. [FDA label] | Subcutaneous administration of Benralizumab presented a dose-proportional pharmacokinetic profile. The administration of 20-200 mg presented an absorption half-life of 3.6 days with a bioavailability of 58%.[FDA label] It is also reported for Benralizumab a Cmax of 82 mcg/ml and AUC of 775 mcg day/ml.[A31293] | Pharmacokinetic reports of Benralizumab showed a volume of distribution in a range of 52-93ml/kg. For a 70kg individual, the central volume of distribution of Benralizumab is 3.2 L while the peripheral volume of distribution is reported to be 2.5 L.[A31297] | For a subject weighting 70kg, the typical systemic clearance is 0.29L/day.[FDA label] | Antibodies | NA | NA | NA | NA | Interleukin-5 receptor subunit alpha,Low affinity immunoglobulin gamma Fc region receptor III-A | Fasenra | Astra Zeneca | Astra Zeneca | Subcutaneous | 30 mg / mL | FASENRA is contraindicated in patients who have known hypersensitivity to benralizumab or any of its excipients | headache, sore throat, fever, hypersensitivity reactions, and injection site reactions (pain, redness, itching, or a small lump) | Fasenra is a monoclonal antibody that affects the actions of the body's immune system. Benralizumab works by reducing levels of eosinophils, a certain type of white blood cell that may contribute to the symptoms of asthma. Fasenra injection is a prescription medicine used together with other asthma medicines... | Fasenra is a prescription medicine used to treat the symptoms of Severe Asthma. Fasenra may be used alone or with other medications. | NA | Benralizumab is a humanized monoclonal antibody (IgG1/κ-class) selective for interleukin-5 receptor alpha subunit (IL5Rα). Benralizumab is produced in Chinese hamster ovary cells by recombinant DNA technology. Benralizumab has a molecular weight of approximately 150 kDa. | Link | Link | NA |
| 13935 | Th1449 | Benralizumab | >Th1449_Benralizumab EVQLVQSGAEVKKPGASVKVSCKASGYTFTSYVIHWVRQRPGQGLAWMGYINPYNDGTKYNERFKGKVTITSDRSTSTVYMELSSLRSEDTAVYLCGREGIRYYGLLGDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146054 | C6492H10060N1724O2028S42 | 6.6 - 7.2 | NA | 69 °C (midpoint transition), 80 °C (whole IgG1) | The half-life of Benralizumab is estimated to be 15-18 days.[A31293] | Benralizumab is a humanized recombinant monoclonal antibody of the isotype IgG1k immunoglobulin that specifically binds to the alpha chain of the interleukin 5 receptor (IL-5R) expressed on eosinophils and basophils.[A31294] It inhibits the binding of IL-5 as well as the hetero-oligomerization of the alpha and beta subunits of the IL-5R, thus blocking, signal transduction. Besides, it is an afucosylated IgG which gives it high affinity for the Fc | Benralizumab is indicated as a maintenance treatment of patients 12 years or older with severe asthma and an eosinophilic phenotype.[L1020] The pathology of severe asthma with eosinophilic phenotype is also denotated as TH2-high phenotype. The patients with this phenotype are characterized by the expression of IL-5 and IL-13, airway hyperresponsiveness, responsiveness to inhaled corticosteroids, high serum IgE and eosinophilia in blood and airway. In the TH2-high phenotype, IL-5 presents a central role as it is responsible for eosinophil differentiation, survival, activation and migration to the lungs.[A31295] | Eosinophils are the key target of inflammatory respiratory diseases and they undergo apoptosis in absence of IL-5. Therefore, benralizumab action on the IL-5 receptor in basophils and eosinophils produces the apoptosis and its significant reduction in the blood.[A31294] On the other hand, Benralizumab binding to natural killer cells Fc | Interleukin-5 (IL-5) induces an eosinophil-mediated inflammatory response by binding to the IL-5 receptor (IL-5R) expressed in eosinophils, basophils and some mast cells. Benralizumab, unlike IL-5 low-affinity binding, binds with high affinity to the domain I of the a-chain of IL-5R and blocks its signaling and the proliferation of IL-5-dependent cell lines. On the other hand, Benralizumab is an afucosylated antibody in the CH2 region which gives it a high affinity for the Fc | There are not reports of long-term studies regarding tumorgenesis or carcinogenesis. Fertility studies performed in aminal trials showed no adverse histopathological findings.[FDA label] | As any monoclonal IgG antibody, Beralizumab is degraded by proteases widely spread in the body. [FDA label] | Subcutaneous administration of Benralizumab presented a dose-proportional pharmacokinetic profile. The administration of 20-200 mg presented an absorption half-life of 3.6 days with a bioavailability of 58%.[FDA label] It is also reported for Benralizumab a Cmax of 82 mcg/ml and AUC of 775 mcg day/ml.[A31293] | Pharmacokinetic reports of Benralizumab showed a volume of distribution in a range of 52-93ml/kg. For a 70kg individual, the central volume of distribution of Benralizumab is 3.2 L while the peripheral volume of distribution is reported to be 2.5 L.[A31297] | For a subject weighting 70kg, the typical systemic clearance is 0.29L/day.[FDA label] | Antibodies, Monoclonal | NA | NA | NA | NA | Interleukin-5 receptor subunit alpha,Low affinity immunoglobulin gamma Fc region receptor III-A | Fasenra Pen | Astra Zeneca | Astra Zeneca | Subcutaneous | 30 mg / mL | FASENRA is contraindicated in patients who have known hypersensitivity to benralizumab or any of its excipients [see WARNINGS AND PRECAUTIONS]. | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, fast heartbeat, fever, skin rash, itching, hoarseness, irritation, joint pain, stiffness, or swelling, redness of the skin, swelling of the eyelids, face, lips, hands, or feet, tightness in the chest, trouble swallowing, cough, dizziness, and unusual tiredness or weakness | Antihemophilic Factor (Human), Monoclate-P®, Factor VIII:C Pasteurized, Monoclonal Antibody Purified, is a sterile, stable, lyophilized concentrate of Factor VIII:C with reduced amounts of VWF:Ag and purified of extraneous plasma-derived protein by use of affinity chromatography. A murine monoclonal antibody to VWF:Ag is used as an affinity ligand to first isolate the Factor VIII Complex. Factor VIII:C is then dissociated from VWF:Ag, recovered, formulated and provided as a sterile lyophilized powder.1,2,3 The concentrate as formulated contains Albumin (Human) as a stabilizer, resulting in a concentrate with a specific activity between 4 and 10 units/mg of total protein. In the absence of this added Albumin (Human) stabilizer, specific activity has been determined to exceed 3000 units/mg of protein.4 Monoclate-P® has been prepared from pooled human plasma and is intended for use in therapy of classical hemophilia (Hemophilia A). | used to treat the symptoms of Hemophilia A. | NA | NA | Link | Link | NA |
| 13936 | Th1449 | Benralizumab | >Th1449_Benralizumab EVQLVQSGAEVKKPGASVKVSCKASGYTFTSYVIHWVRQRPGQGLAWMGYINPYNDGTKYNERFKGKVTITSDRSTSTVYMELSSLRSEDTAVYLCGREGIRYYGLLGDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146054 | C6492H10060N1724O2028S42 | 6.6 - 7.2 | NA | 69 °C (midpoint transition), 80 °C (whole IgG1) | The half-life of Benralizumab is estimated to be 15-18 days.[A31293] | Benralizumab is a humanized recombinant monoclonal antibody of the isotype IgG1k immunoglobulin that specifically binds to the alpha chain of the interleukin 5 receptor (IL-5R) expressed on eosinophils and basophils.[A31294] It inhibits the binding of IL-5 as well as the hetero-oligomerization of the alpha and beta subunits of the IL-5R, thus blocking, signal transduction. Besides, it is an afucosylated IgG which gives it high affinity for the Fc | Benralizumab is indicated as a maintenance treatment of patients 12 years or older with severe asthma and an eosinophilic phenotype.[L1020] The pathology of severe asthma with eosinophilic phenotype is also denotated as TH2-high phenotype. The patients with this phenotype are characterized by the expression of IL-5 and IL-13, airway hyperresponsiveness, responsiveness to inhaled corticosteroids, high serum IgE and eosinophilia in blood and airway. In the TH2-high phenotype, IL-5 presents a central role as it is responsible for eosinophil differentiation, survival, activation and migration to the lungs.[A31295] | Eosinophils are the key target of inflammatory respiratory diseases and they undergo apoptosis in absence of IL-5. Therefore, benralizumab action on the IL-5 receptor in basophils and eosinophils produces the apoptosis and its significant reduction in the blood.[A31294] On the other hand, Benralizumab binding to natural killer cells Fc | Interleukin-5 (IL-5) induces an eosinophil-mediated inflammatory response by binding to the IL-5 receptor (IL-5R) expressed in eosinophils, basophils and some mast cells. Benralizumab, unlike IL-5 low-affinity binding, binds with high affinity to the domain I of the a-chain of IL-5R and blocks its signaling and the proliferation of IL-5-dependent cell lines. On the other hand, Benralizumab is an afucosylated antibody in the CH2 region which gives it a high affinity for the Fc | There are not reports of long-term studies regarding tumorgenesis or carcinogenesis. Fertility studies performed in aminal trials showed no adverse histopathological findings.[FDA label] | As any monoclonal IgG antibody, Beralizumab is degraded by proteases widely spread in the body. [FDA label] | Subcutaneous administration of Benralizumab presented a dose-proportional pharmacokinetic profile. The administration of 20-200 mg presented an absorption half-life of 3.6 days with a bioavailability of 58%.[FDA label] It is also reported for Benralizumab a Cmax of 82 mcg/ml and AUC of 775 mcg day/ml.[A31293] | Pharmacokinetic reports of Benralizumab showed a volume of distribution in a range of 52-93ml/kg. For a 70kg individual, the central volume of distribution of Benralizumab is 3.2 L while the peripheral volume of distribution is reported to be 2.5 L.[A31297] | For a subject weighting 70kg, the typical systemic clearance is 0.29L/day.[FDA label] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Interleukin-5 receptor subunit alpha,Low affinity immunoglobulin gamma Fc region receptor III-A | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13949 | Th1450 | Gantenerumab | NA | NA | NA | NA | NA | NA | NA | Gantenerumab is under investigation for the treatment of Dementia, Alzheimers Disease, and Alzheimers Disease, Familial. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13969 | Th1452 | Visilizumab | NA | NA | NA | NA | NA | NA | NA | Visilizumab has been investigated for the treatment of Ulcerative Colitis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13970 | Th1452 | Visilizumab | NA | NA | NA | NA | NA | NA | NA | Visilizumab has been investigated for the treatment of Ulcerative Colitis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13971 | Th1452 | Visilizumab | NA | NA | NA | NA | NA | NA | NA | Visilizumab has been investigated for the treatment of Ulcerative Colitis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13997 | Th1455 | Urelumab | >Th1455_Urelumab QVQLQQWGAGLLKPSETLSLTCAVYGGSFSGYYWSWIRQSPEKGLEWIGEINHGGYVTYNPSLESRVTISVDTSKNQFSLKLSSVTAADTAVYYCARDYGPGNYDWYFDLWGRGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | NA | Urelumab has been used in trials studying the treatment of Leukemia, Multiple Myeloma, Malignant Tumors, and Cancer - Solid Tumors and B-Cell Non-Hodgkin's Lymphoma. Urelumab is a fully human antibody that targets CD137. The antibody product was developed using Medarex's UltiMAb(R) technology and was the first UltiMAb- derived antibody in clinical development by Bristol-Myers Squibb under the December 2003 agreement with Medarex. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 9 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14007 | 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 | Antibodies | 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 |
| 14008 | 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 | Antibodies, Monoclonal | 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 |
| 14009 | 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 | Antibodies, Monoclonal, Humanized | 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 |
| 14033 | Th1457 | Patritumab | NA | NA | NA | NA | NA | NA | NA | Patritumab has been used in trials studying the treatment of LUNG CANCER, Solid Tumors, Neoplasms by Site, Head and Neck Neoplasms, and Non-small Cell Lung Cancer, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14041 | Th1458 | Fulranumab | NA | NA | NA | NA | NA | NA | NA | Fulranumab has been used in trials studying the treatment of Pain, Cystitis, Neuralgia, Joint Pain, and Arthralgia, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14049 | Th1459 | Tarextumab | NA | NA | NA | NA | NA | NA | NA | Tarextumab has been used in trials studying the treatment of Solid Tumors, Stage IV Pancreatic Cancer, and Stage IV Small Cell Lung Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14064 | Th1461 | Gevokizumab | >Th1461_Gevokizumab QVQLQESGPGLVKPSQTLSLTCSFSGFSLSTSGMGVGWIRQPSGKGLEWLAHIWWDGDESYNPSLKSRLTISKDTSKNQVSLKITSVTAADTAVYFCARNRYDPPWFVDWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVTSSNFGTQTYTCNVDHKPSNTKVDKTVERKCCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGMEVHNAKTKPREEQFNSTFR300VVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | NA | NA | NA | NA | NA | NA | Gevokizumab has been used in trials studying the treatment of Acne Vulgaris, Osteoarthritis, Behcet's Uveitis, Pyoderma Gangrenosum, and Behcet's Disease Uveitis, among others. Gevokizumab acts as a modulator of cytokine imbalance in IL-1 mediated disease states. It has a very high binding affinity of 300fM and blocks the activation of IL-1 receptors. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Interleukin-1 beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14065 | Th1461 | Gevokizumab | >Th1461_Gevokizumab QVQLQESGPGLVKPSQTLSLTCSFSGFSLSTSGMGVGWIRQPSGKGLEWLAHIWWDGDESYNPSLKSRLTISKDTSKNQVSLKITSVTAADTAVYFCARNRYDPPWFVDWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVTSSNFGTQTYTCNVDHKPSNTKVDKTVERKCCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGMEVHNAKTKPREEQFNSTFR300VVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | NA | NA | NA | NA | NA | NA | Gevokizumab has been used in trials studying the treatment of Acne Vulgaris, Osteoarthritis, Behcet's Uveitis, Pyoderma Gangrenosum, and Behcet's Disease Uveitis, among others. Gevokizumab acts as a modulator of cytokine imbalance in IL-1 mediated disease states. It has a very high binding affinity of 300fM and blocks the activation of IL-1 receptors. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Interleukin-1 beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14066 | Th1461 | Gevokizumab | >Th1461_Gevokizumab QVQLQESGPGLVKPSQTLSLTCSFSGFSLSTSGMGVGWIRQPSGKGLEWLAHIWWDGDESYNPSLKSRLTISKDTSKNQVSLKITSVTAADTAVYFCARNRYDPPWFVDWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVTSSNFGTQTYTCNVDHKPSNTKVDKTVERKCCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGMEVHNAKTKPREEQFNSTFR300VVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | NA | NA | NA | NA | NA | NA | Gevokizumab has been used in trials studying the treatment of Acne Vulgaris, Osteoarthritis, Behcet's Uveitis, Pyoderma Gangrenosum, and Behcet's Disease Uveitis, among others. Gevokizumab acts as a modulator of cytokine imbalance in IL-1 mediated disease states. It has a very high binding affinity of 300fM and blocks the activation of IL-1 receptors. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Interleukin-1 beta | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14079 | 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 | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14080 | 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 | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14081 | 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 | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14091 | Th1465 | Simtuzumab | NA | NA | NA | NA | NA | NA | NA | Simtuzumab has been used in trials studying the treatment and basic science of Myelofibrosis, Pancreatic Cancer, Colorectal Cancer, and Idiopathic Pulmonary Fibrosis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14092 | Th1465 | Simtuzumab | NA | NA | NA | NA | NA | NA | NA | Simtuzumab has been used in trials studying the treatment and basic science of Myelofibrosis, Pancreatic Cancer, Colorectal Cancer, and Idiopathic Pulmonary Fibrosis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14093 | Th1465 | Simtuzumab | NA | NA | NA | NA | NA | NA | NA | Simtuzumab has been used in trials studying the treatment and basic science of Myelofibrosis, Pancreatic Cancer, Colorectal Cancer, and Idiopathic Pulmonary Fibrosis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14103 | Th1466 | Fasinumab | >Th1466_Fasinumab QVQLVQSGAEVKKPGASVKVSCKVSGFTLTELSIHWVRQAPGKGLEWMGGFDPEDGETIYAQKFQGRVTMTEDTSTDTAYMELTSLRSEDTAVYYCSTIGVVTNFDNWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | NA | Fasinumab is a human IgG1k monoclonal antibody targeted against nerve growth factor (NGF). It is currently under investigation for the treatment osteoarthritic pain[A241045] and has demonstrated significantly greater pain relief and functional improvement as compared to standard therapy (i.e. NSAIDs and/or opioids) in this patient population.[A241165] NGF was first discovered in the 1950s[A241180] and was the first neurotrophic factor to be identified and biochemically characterized.[A241190] It has since been recognized for its role in nociceptive signaling transduction and has thus become an attractive target in the treatment of chronic pain conditions. | NA | NA | During embryonic development, nerve growth factor (NGF) binds to tropomyosin receptor kinase A receptor (TrkA) and the low-affinity p75 neurotrophin receptor (NTR) on developing neuronal cell surfaces, which activates signaling pathways involved in neuronal growth and survival.[A241180] In adults, the primary role of NGF shifts towards influencing nociceptive signaling transduction by releasing inflammatory mediators and regulating ion channels or receptors.[A241180,A241190] Fasinumab is a human IgG1k monoclonal antibody targeted against NGF,[A241045] interrupting pain signaling pathways and thus alleviating pain and improving function in patients suffering from chronic pain conditions. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Beta-nerve growth factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14104 | Th1466 | Fasinumab | >Th1466_Fasinumab QVQLVQSGAEVKKPGASVKVSCKVSGFTLTELSIHWVRQAPGKGLEWMGGFDPEDGETIYAQKFQGRVTMTEDTSTDTAYMELTSLRSEDTAVYYCSTIGVVTNFDNWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | NA | Fasinumab is a human IgG1k monoclonal antibody targeted against nerve growth factor (NGF). It is currently under investigation for the treatment osteoarthritic pain[A241045] and has demonstrated significantly greater pain relief and functional improvement as compared to standard therapy (i.e. NSAIDs and/or opioids) in this patient population.[A241165] NGF was first discovered in the 1950s[A241180] and was the first neurotrophic factor to be identified and biochemically characterized.[A241190] It has since been recognized for its role in nociceptive signaling transduction and has thus become an attractive target in the treatment of chronic pain conditions. | NA | NA | During embryonic development, nerve growth factor (NGF) binds to tropomyosin receptor kinase A receptor (TrkA) and the low-affinity p75 neurotrophin receptor (NTR) on developing neuronal cell surfaces, which activates signaling pathways involved in neuronal growth and survival.[A241180] In adults, the primary role of NGF shifts towards influencing nociceptive signaling transduction by releasing inflammatory mediators and regulating ion channels or receptors.[A241180,A241190] Fasinumab is a human IgG1k monoclonal antibody targeted against NGF,[A241045] interrupting pain signaling pathways and thus alleviating pain and improving function in patients suffering from chronic pain conditions. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Beta-nerve growth factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14117 | Th1467 | Dupilumab | >Th1467_Dupilumab EVQLVESGGGLEQPGGSLRLSCAGSGFTFRDYAMTWVRQAPGKGLEWVSSISGSGGNTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDRLSITIRPRYYGLDVWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 146896.9522 | C6512H10066N1730O2052S46 | NA | NA | NA | There is limited human data on the half-life of dupilumab.[L7192] In single-dose pharmacokinetic studies, the mean half-life of dupilumab following intravenous or subcutaneous administration ranged from 4.8 to 7 days in rats and 11.7 to 20.5 days in cynomolgus monkeys.[L7369,L7372] In these studies, the mean half-life was comparable was comparable following intravenous and subcutaneous administration.[L7369] | Dupilumab is a fully human monoclonal antibody of the immunoglobulin G4 subclass that binds to the interleukin-4 (IL-4) receptor, inhibiting the receptor signaling pathways.[A180478] As an interleukin-4 receptor alpha antagonist, dupilumab inhibits the signaling of pro-inflammatory cytokines, called interleukins (IL), that induce inflammatory and immunological reactions in several atopic or allergic conditions, such as eczema, allergic reaction, and rhinosinusitis.[A180478] Dupilumab was generated by recombinant DNA technology in Chinese Hamster Ovary cell suspension culture.[L7186] Dupilumab is commonly marketed as Dupixent®, which is available as a formulation for subcutaneous injection. It was first approved by the FDA in 2017 for patients 12 and older with eczema or atopic dermatitis. Dupilumab is also approved by Health Canada for the same indication and the European Commission for use in atopic dermatitis as well as severe asthma with type 2 inflammation.[L7225] It is the first biologic therapy to have been approved for the treatment of adult patients with moderate-to-severe AD in the EU and USA.[A180484] In 2018, FDA approved the use of dupilumab as an add-on maintenance treatment for patients 12 years and older with moderate-to-severe eosinophilic asthma or with oral corticosteroid-dependent asthma. In June 2019, dupilumab was also approved by the FDA as an add-on maintenance treatment for inadequately controlled chronic rhinosinusitis with nasal polyps in adult patients.[L7258] Dupilumab is currently under investigations for potential therapeutic use in diseases driven by allergic reactions or type 2 inflammation, such as pediatric atopic dermatitis, eosinophilic esophagitis, and chronic obstructive pulmonary disease. It is also being studied in combination with another antibody that which targets IL-33.[L7225] | Dupilumab is indicated, as monotherapy or in combination with topical corticosteroids, for the treatment of patients aged 12 years and older with moderate-to-severe atopic dermatitis whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable.[L7186] It is also used as an add-on maintenance treatment in patients with moderate-to-severe asthma aged 12 years and older with an eosinophilic phenotype or with oral corticosteroid dependent asthma. It is not indicated for the relief of acute bronchospasm or status asthmaticus.[L7186] Dupilumab is indicated as an add-on maintenance treatment in adult patients with inadequately controlled chronic rhinosinusitis with nasal polyposis.[L10770] | Dupilumab is an recombinant human IgG4 antibody to the IL-4 receptor that works by inhibiting the activation of certain pro-inflammatory cytokines that are implicated in the pathophysiology of several allergic and atopic conditions, including asthma, chronic rhinosinusitis with nasal polyps, and food and environmental allergies. _In vivo_, dupilumab was shown to reduce the levels of type 2 inflammatory biomarkers associated with atopic dermatitis, such as thymus and activation-regulated chemokine (TARC/CCL17), total serum IgE, allergen-specific IgE, and lactate dehydrogenase (LDH). A decrease in the levels of biomarkers of asthma, such as FeNO, eotaxin-3, IgE, periostin, and eotaxin-3 (CCL26) was also observed.[L7192,L7225] Since dupilumab works to suppress the immune response, it is proposed that it may influence the immune response against some infections, such as helminth infections, by inhibiting IL-4/IL-13 signaling. It is advised that infections are appropriately treated until resolved before initiating dupilumab therapy.[L7192] While findings of some _in vitro_ and _in vivo_ studies suggest that some cytokine modulators may influence the expression and activity of specific cytochrome P450 (CYP450) enzymes, an open-label drug-drug interaction study demonstrated that dupilumab displays no significant effect on the activity of CYP450 enzymes studied (CYP3A, CYP2C19, CYP2C9, CYP1A2, and CYP2D6).[A180712] | Type 2 inflammatory processes in various allergic and atopic conditions, such as asthma and atopic diseases, involve the type 2 helper T-cell (Th2) immunity.[A180709] Upregulation of this Type 2/Th2 pathway is commonly observed in other inflammatory conditions [A180712] and the activation of Th2 cells is linked to the production of Th2-associated cytokines, such as interleukin (IL) 4, IL-5, IL-9, and IL-13.[A180709] IL-4 and IL-13 play a central role in inducing inflammatory conditions such as allergic rhinitis, asthma, and atopic dermatitis,[L7225] by regulating Type 2 inflammation and immune function. These inflammatory cytokines work by modulating gene expression downstream of receptor signalling,[A180712] regulating Th2 cell differentiation, and activating inflammatory cells such as mast cells and macrophages.[A181274] There are two types of receptors for IL-4: the type 1 receptor, which is composed of the IL-4 chain (IL-4Ra) and a | There is limited data on the overdose of dupilumab. As there is no specific treatment for dupilumab, close monitoring of the patient with appropriate symptomatic treatment is advised in case of suspected overdosage.[] | Being a monoclonal antibody, dupilumab is not expected to undergo significant hepatic metabolism.[L7192] While the metabolism of dupilumab has not been characterized, it is speculated that dupilumab undergoes nonspecific degradation into smaller peptides and amino acids, as often observed with endogenous IgG.[A180478] | The Cmax following administration of a single subcutaneous dose of 600 mg or 400 mg of dupilumab were 70.1 ± 24.1 mcg/mL or 41.8 ± 12.4 mcg/mL, respectively. The Tmax ranged from 3 to 7 days following administration of a single subcutaneous dose ranging from 75 to 600 mg.[L7186] Following a subcutaneous dose, the absolute bioavailability of dupilumab ranged between 61% and 64% in patients with atopic dermatitis or asthma.[L7192] In clinical trials, the steady-state concentrations were reached by week 16 following the administration of 600 mg starting dose and 300 mg dose every other week. At these concentrations, the mean trough concentrations ranged from 60.3 ± 35.1 mcg/mL to 79.9 ± 41.4 mcg/mL for 300 mg dose and from 29.2 ± 18.7 to 36.5 ± 22.2 mcg/mL for 200 mg dose administered every other week.[L7186] | The estimated volume of distribution is 4.8 ± 1.3 L.[A180478] | There is limited data on the clearance of dupilumab.[L7192] | Antibodies | NA | NA | NA | NA | Interleukin-4 receptor subunit alpha | Dupixent | Sanofi Aventis Groupe | Sanofi Aventis Groupe | Subcutaneous | 300 mg | DUPIXENT is contraindicated in patients who have known hypersensitivity to dupilumab or any excipients of DUPIXENT[see WARNINGS AND PRECAUTIONS]. | injection site reactions, pink eye (conjunctivitis), swollen or puffy eyelids, oral herpes, inflammation of the cornea (keratitis), eye itching, other herpes simplex virus infection, dry eye, mouth and throat pain, elevated white blood cells (eosinophilia), insomnia, toothache, gastritis, joint pain, and upper respiratory tract infections. | Dupixent is a prescription medicine that works by blocking two proteins that contribute to a type of inflammation that plays a major role in atopic dermatitis, asthma, and chronic rhinosinusitis with nasal polyposis. Dupixent is used to treat moderate-to-severe eczema (atopic dermatitis) that cannot... | Dupixent (dupilumab) injection is aninterleukin-4 receptor alpha-antagonist indicated for the treatment of patients with moderate-to-severe atopic dermatitis whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable; as an add-on maintenance treatment of adult and pediatric patients aged 6 years and older with moderate-to-severe asthma characterized by an eosinophilic phenotype or with oral corticosteroid dependent asthma; as an add-on maintenance treatment in adult patients with inadequately controlled chronic rhinosinusitis with nasal polyposis (CRSwNP), and for the treatment of adult and pediatric patients aged 12 years and older, weighing at least 40 kg, with eosinophilic esophagitis (EoE). | NA | Dupilumab, an interleukin-4 receptor alpha antagonist, is a human monoclonal antibody of the IgG4 subclass that binds to the IL-4Rα subunit and inhibits IL-4 and IL-13 signaling. Dupilumab has an approximate molecular weight of 147 kDa. | Link | Link | NA |
| 14118 | Th1467 | Dupilumab | >Th1467_Dupilumab EVQLVESGGGLEQPGGSLRLSCAGSGFTFRDYAMTWVRQAPGKGLEWVSSISGSGGNTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDRLSITIRPRYYGLDVWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 146896.9522 | C6512H10066N1730O2052S46 | NA | NA | NA | There is limited human data on the half-life of dupilumab.[L7192] In single-dose pharmacokinetic studies, the mean half-life of dupilumab following intravenous or subcutaneous administration ranged from 4.8 to 7 days in rats and 11.7 to 20.5 days in cynomolgus monkeys.[L7369,L7372] In these studies, the mean half-life was comparable was comparable following intravenous and subcutaneous administration.[L7369] | Dupilumab is a fully human monoclonal antibody of the immunoglobulin G4 subclass that binds to the interleukin-4 (IL-4) receptor, inhibiting the receptor signaling pathways.[A180478] As an interleukin-4 receptor alpha antagonist, dupilumab inhibits the signaling of pro-inflammatory cytokines, called interleukins (IL), that induce inflammatory and immunological reactions in several atopic or allergic conditions, such as eczema, allergic reaction, and rhinosinusitis.[A180478] Dupilumab was generated by recombinant DNA technology in Chinese Hamster Ovary cell suspension culture.[L7186] Dupilumab is commonly marketed as Dupixent®, which is available as a formulation for subcutaneous injection. It was first approved by the FDA in 2017 for patients 12 and older with eczema or atopic dermatitis. Dupilumab is also approved by Health Canada for the same indication and the European Commission for use in atopic dermatitis as well as severe asthma with type 2 inflammation.[L7225] It is the first biologic therapy to have been approved for the treatment of adult patients with moderate-to-severe AD in the EU and USA.[A180484] In 2018, FDA approved the use of dupilumab as an add-on maintenance treatment for patients 12 years and older with moderate-to-severe eosinophilic asthma or with oral corticosteroid-dependent asthma. In June 2019, dupilumab was also approved by the FDA as an add-on maintenance treatment for inadequately controlled chronic rhinosinusitis with nasal polyps in adult patients.[L7258] Dupilumab is currently under investigations for potential therapeutic use in diseases driven by allergic reactions or type 2 inflammation, such as pediatric atopic dermatitis, eosinophilic esophagitis, and chronic obstructive pulmonary disease. It is also being studied in combination with another antibody that which targets IL-33.[L7225] | Dupilumab is indicated, as monotherapy or in combination with topical corticosteroids, for the treatment of patients aged 12 years and older with moderate-to-severe atopic dermatitis whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable.[L7186] It is also used as an add-on maintenance treatment in patients with moderate-to-severe asthma aged 12 years and older with an eosinophilic phenotype or with oral corticosteroid dependent asthma. It is not indicated for the relief of acute bronchospasm or status asthmaticus.[L7186] Dupilumab is indicated as an add-on maintenance treatment in adult patients with inadequately controlled chronic rhinosinusitis with nasal polyposis.[L10770] | Dupilumab is an recombinant human IgG4 antibody to the IL-4 receptor that works by inhibiting the activation of certain pro-inflammatory cytokines that are implicated in the pathophysiology of several allergic and atopic conditions, including asthma, chronic rhinosinusitis with nasal polyps, and food and environmental allergies. _In vivo_, dupilumab was shown to reduce the levels of type 2 inflammatory biomarkers associated with atopic dermatitis, such as thymus and activation-regulated chemokine (TARC/CCL17), total serum IgE, allergen-specific IgE, and lactate dehydrogenase (LDH). A decrease in the levels of biomarkers of asthma, such as FeNO, eotaxin-3, IgE, periostin, and eotaxin-3 (CCL26) was also observed.[L7192,L7225] Since dupilumab works to suppress the immune response, it is proposed that it may influence the immune response against some infections, such as helminth infections, by inhibiting IL-4/IL-13 signaling. It is advised that infections are appropriately treated until resolved before initiating dupilumab therapy.[L7192] While findings of some _in vitro_ and _in vivo_ studies suggest that some cytokine modulators may influence the expression and activity of specific cytochrome P450 (CYP450) enzymes, an open-label drug-drug interaction study demonstrated that dupilumab displays no significant effect on the activity of CYP450 enzymes studied (CYP3A, CYP2C19, CYP2C9, CYP1A2, and CYP2D6).[A180712] | Type 2 inflammatory processes in various allergic and atopic conditions, such as asthma and atopic diseases, involve the type 2 helper T-cell (Th2) immunity.[A180709] Upregulation of this Type 2/Th2 pathway is commonly observed in other inflammatory conditions [A180712] and the activation of Th2 cells is linked to the production of Th2-associated cytokines, such as interleukin (IL) 4, IL-5, IL-9, and IL-13.[A180709] IL-4 and IL-13 play a central role in inducing inflammatory conditions such as allergic rhinitis, asthma, and atopic dermatitis,[L7225] by regulating Type 2 inflammation and immune function. These inflammatory cytokines work by modulating gene expression downstream of receptor signalling,[A180712] regulating Th2 cell differentiation, and activating inflammatory cells such as mast cells and macrophages.[A181274] There are two types of receptors for IL-4: the type 1 receptor, which is composed of the IL-4 chain (IL-4Ra) and a | There is limited data on the overdose of dupilumab. As there is no specific treatment for dupilumab, close monitoring of the patient with appropriate symptomatic treatment is advised in case of suspected overdosage.[] | Being a monoclonal antibody, dupilumab is not expected to undergo significant hepatic metabolism.[L7192] While the metabolism of dupilumab has not been characterized, it is speculated that dupilumab undergoes nonspecific degradation into smaller peptides and amino acids, as often observed with endogenous IgG.[A180478] | The Cmax following administration of a single subcutaneous dose of 600 mg or 400 mg of dupilumab were 70.1 ± 24.1 mcg/mL or 41.8 ± 12.4 mcg/mL, respectively. The Tmax ranged from 3 to 7 days following administration of a single subcutaneous dose ranging from 75 to 600 mg.[L7186] Following a subcutaneous dose, the absolute bioavailability of dupilumab ranged between 61% and 64% in patients with atopic dermatitis or asthma.[L7192] In clinical trials, the steady-state concentrations were reached by week 16 following the administration of 600 mg starting dose and 300 mg dose every other week. At these concentrations, the mean trough concentrations ranged from 60.3 ± 35.1 mcg/mL to 79.9 ± 41.4 mcg/mL for 300 mg dose and from 29.2 ± 18.7 to 36.5 ± 22.2 mcg/mL for 200 mg dose administered every other week.[L7186] | The estimated volume of distribution is 4.8 ± 1.3 L.[A180478] | There is limited data on the clearance of dupilumab.[L7192] | Antibodies, Monoclonal | NA | NA | NA | NA | Interleukin-4 receptor subunit alpha | Dupixent | sanofi-aventis U.S. LLC | sanofi-aventis U.S. LLC | Subcutaneous | 200 mg/1.14mL | DUPIXENT is contraindicated in patients who have known hypersensitivity to dupilumab or any excipients of DUPIXENT[see WARNINGS AND PRECAUTIONS]. | injection site reactions, pink eye (conjunctivitis), swollen or puffy eyelids, oral herpes, inflammation of the cornea (keratitis), eye itching, other herpes simplex virus infection, dry eye, mouth and throat pain, elevated white blood cells (eosinophilia), insomnia, toothache, gastritis, joint pain, and upper respiratory tract infections. | Dupixent is a prescription medicine that works by blocking two proteins that contribute to a type of inflammation that plays a major role in atopic dermatitis, asthma, and chronic rhinosinusitis with nasal polyposis. Dupixent is used to treat moderate-to-severe eczema (atopic dermatitis) that cannot... | Dupixent (dupilumab) injection is aninterleukin-4 receptor alpha-antagonist indicated for the treatment of patients with moderate-to-severe atopic dermatitis whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable; as an add-on maintenance treatment of adult and pediatric patients aged 6 years and older with moderate-to-severe asthma characterized by an eosinophilic phenotype or with oral corticosteroid dependent asthma; as an add-on maintenance treatment in adult patients with inadequately controlled chronic rhinosinusitis with nasal polyposis (CRSwNP), and for the treatment of adult and pediatric patients aged 12 years and older, weighing at least 40 kg, with eosinophilic esophagitis (EoE). | NA | Dupilumab, an interleukin-4 receptor alpha antagonist, is a human monoclonal antibody of the IgG4 subclass that binds to the IL-4Rα subunit and inhibits IL-4 and IL-13 signaling. Dupilumab has an approximate molecular weight of 147 kDa. | Link | Link | NA |
| 14131 | Th1468 | Tralokinumab | >Th1468_Tralokinumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTNYGLSWVRQAPGQGLEWMGWISANNGDTNYGQEFQGRVTMTTDTSTSTAYMELRSLRSDDTAVYYCARDSSSSWARWFFDLWGRGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 147000 | C6374H9822N1698O2014S44 | NA | NA | NA | The half-life of tralokinumab is approximately 22 days.[L39287] | Atopic dermatitis (AD) is an inflammatory skin disorder that causes skin inflammation, skin barrier dysfunction, and chronic pruritus.[A242432] It is estimated to affect up to 20% of adults and children worldwide, and is frequently associated with other atopic conditions such as asthma or allergic rhinitis. While AD is a heterogenous condition with a variety of apparent genetic and environmental causes,[A242422] it is primarily driven by the pro-inflammatory cytokine interleukin-13 (IL-13).[A242427] Tralokinumab is a fully human IgG4 monoclonal antibody targeted against IL-13. It neutralizes IL-13 activity by inhibiting its ability to bind with receptors, thus helping to alleviate AD symptoms. Tralokinumab was first approved for the treatment of atopic dermatitis by the EMA in June 2021, under the brand name Adtralza (Leo Pharma), and was subsequently approved in Canada in October 2021.[L39287] | Tralokinumab is indicated in Canada and the EU for the treatment of adult patients with moderate-to-severe atopic dermatitis who are candidates for systemic therapy and are inadequately controlled with topical interventions.[L39282,L39287] | Tralokinumab exerts its therapeutic effects by inhibiting the inflammatory cytokine (IL-13) primarily responsible for the pathogenesis of atopic dermatitis. It is administered subcutaneously with a loading dose of 600mg followed by a maintenance dose of 300mg every two weeks.[L39287] In clinical studies, tralokinumab treatment decreased the concentrations of a number of Th2 and Th22 immunity biomarkers in the blood, including periostin, IL-22, serum IgE. It also reduced epidermal thickness and decreased the expression of Keratin 16 and Ki-67 in skin affected by atopic dermatitis.[L39287] Hypersensitivity reactions, including anaphylaxis, have been reported following the use of tralokinumab.[L39287] Patients experiencing a systemic hypersensitivity reaction should discontinue treatment and initiate immediate therapy as clinically indicated. Tralokinumab should not be used in patients with pre-existing helminth infections, as the influence of tralokinumab on the immune response against helminth infections is unclear.[L39287] Patients with helminth infections should be treated prior to therapy with tralokinumab. Patients becoming infected during the course of therapy may be treated with anti-helminth medications, but should discontinue tralokinumab if the infection fails to resolve.[L39287] | Interleukin-13 (IL-13) is a pro-inflammatory cytokine that has been implicated as the primary driver of atopic dermatitis (AD).[A242427] IL-13 binds with high affinity to both a heterodimeric form of IL-13Ra1 - complexed with IL-4Ra - and to IL-13Ra2, both of which are expressed on keratinocytes and fibroblasts.[A242432] While IL-13Ra2 does not appear to act as a signal mediator, the binding of IL-13 to heterodimeric IL-4Ra and IL-13Ra1 activates downstream Janus kinase 2 (JAK2) and tyrosine kinase 2 (TYK2) pathways which proceed to activate various signal transducer and activator of transcription (STAT) pathways.[A242432] STAT signalling induces the expression of periostin, an extracellular matrix protein which serves a number of physiological functions in addition to its pathogenic role in skin fibrosis and chronic allergic inflammation. IL-13 also appears to contribute to skin barrier dysfunction via an indirect downregulation of filaggrin (FLG), a structural protein essential for correct skin barrier functioning.[A242432] Tralokinumab is a monoclonal antibody targeted against IL-13. It neutralizes the activity of IL-13 by blocking its interaction with both the IL-13Ra1/IL-4Ra receptor complex and IL-13Ra2 receptors.[L39287] | There are no data regarding overdosage with tralokinumab. In clinical trials, intravenous doses up to 30 mg/kg and subcutaneous doses of 600mg every two weeks for 3 months were found to be well-tolerated.[L39282] In the event of a suspected overdose, patients should be administered supportive care as clinically indicated. | As with other therapeutic and endogenous proteins, the metabolism of tralokinumab is likely to occur via catabolism to smaller peptides and amino acids and has not been studied directly.[L39287] | The absolute bioavailability of tralokinumab following subcutaneous administration is 76%, with a median Tmax of 5-8 days.[L39287] In clinical trials, steady-state serum concentrations were achieved by week 16 of treatment, with trough concentrations ranging from 98.0±41.1 mcg/mL to 101.4±42.7 mcg/mL.[L39287] | The volume of distribution of tralokinumab as estimated by population pharmacokinetic analysis was 4.2 L.[L39287] | The clearance of tralokinumab following subcutaneous administration was estimated to be 0.149 L/day.[L39282] | Antibodies | NA | NA | NA | NA | Interleukin-13 | Adtralza | Leo Pharma | Leo Pharma | Subcutaneous | 150 mg / mL | NA | The most common side effects with Adtralza are upper respiratory tract infections (colds and other infections of the nose and throat) which may affect more than 1 in 10 people. Other common side effects include reactions at the injection site and redness and discomfort in the eye (which may affect up to 1 in 10 people). | Adtralza was more effective than a placebo (dummy treatment) at reducing the extent and severity of atopic dermatitis after 16 weeks of treatment in three main studies in patients with moderate to severe disease that had not responded well enough to treatment applied to the skin. The main measures of effectiveness were having clear or almost clear skin, and a reduction in symptom score of at least 75%. | Adtralza is a medicine for treating adults with moderate to severe atopic dermatitis (also known as eczema, when the skin is itchy, red and dry). | NA | NA | Link | Link | NA |
| 14152 | Th1470 | Etrolizumab | NA | NA | NA | NA | NA | NA | NA | Etrolizumab has been used in trials studying the treatment of Crohn Disease and Ulcerative Colitis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14153 | Th1470 | Etrolizumab | NA | NA | NA | NA | NA | NA | NA | Etrolizumab has been used in trials studying the treatment of Crohn Disease and Ulcerative Colitis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14154 | Th1470 | Etrolizumab | NA | NA | NA | NA | NA | NA | NA | Etrolizumab has been used in trials studying the treatment of Crohn Disease and Ulcerative Colitis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14165 | 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 | Antibodies | NA | NA | NA | NA | Epidermal growth factor receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14175 | Th1472 | Ganitumab | NA | NA | NA | NA | NA | NA | NA | Ganitumab has been used in trials studying the treatment of Colon Cancer, Rectal Cancer, Breast Cancer, Breast Tumors, and Breast Neoplasms, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14183 | Th1473 | Etaracizumab | NA | NA | NA | NA | NA | NA | NA | Etaracizumab has been investigated for the treatment of Psoriasis, Renal Cell Carcinoma, Stage IV Renal Cell Cancer, Recurrent Renal Cell Cancer, and Stage III Renal Cell Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14184 | Th1473 | Etaracizumab | NA | NA | NA | NA | NA | NA | NA | Etaracizumab has been investigated for the treatment of Psoriasis, Renal Cell Carcinoma, Stage IV Renal Cell Cancer, Recurrent Renal Cell Cancer, and Stage III Renal Cell Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14185 | Th1473 | Etaracizumab | NA | NA | NA | NA | NA | NA | NA | Etaracizumab has been investigated for the treatment of Psoriasis, Renal Cell Carcinoma, Stage IV Renal Cell Cancer, Recurrent Renal Cell Cancer, and Stage III Renal Cell Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14193 | 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] | Antibodies | NA | NA | NA | NA | B-cell antigen receptor complex-associated protein beta chain | Polivy | Hoffmann La Roche | Hoffmann La Roche | Intravenous | 30 mg / vial | 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 |
| 14194 | 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] | Antibodies, Monoclonal | NA | NA | NA | NA | B-cell antigen receptor complex-associated protein beta chain | Polivy | Hoffmann La Roche | Hoffmann La Roche | Intravenous | 140 mg / vial | 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 |
| 14195 | 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] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | B-cell antigen receptor complex-associated protein beta chain | Polivy | Roche Registration Gmb H | Roche Registration Gmb H | Intravenous | 140 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 |
| 14211 | Th1475 | Inclacumab | NA | NA | NA | NA | NA | NA | NA | Inclacumab has been used in trials studying the treatment and prevention of Myocardial Infarction, Peripheral Arterial Disease (PAD), and Coronary Heart Disease, Graft Occlusion, Vascular. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14226 | Th1477 | Cixutumumab | NA | NA | NA | NA | NA | NA | 148 h (3 mg/kg dose level) 209 h (6mg/kg dose level) | Cixutumumab has been used in trials studying the treatment of Lung Cancer, Malignant Neoplasm, Leukemia, Mast-Cell, Non-Small-Cell Lung Carcinoma, and Adenocarcinoma of the Prostate. Cixutumumab is a highly specific recombinant human monoclonal antibody with high affinity for the insulin-like growth factor-I receptor (IGF-IR). IGF-IR is overexpressed in a variety of tumour types. | NA | NA | Cixutumumab is a fully human monoclonal antibody that specifically targets the type 1 human insulin-like growth factor receptor (IGF-IR). Tumors have receptors for the insulin-like growth factor-1 (IGF-I), and it is thought that the presence of these receptors cause tumors to grow. Cixutumumab attaches to the receptors and may inhibit the growth of cancer cells. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14240 | Th1479 | Ascrinvacumab | NA | NA | NA | NA | NA | NA | NA | Ascrinvacumab has been used in trials studying the treatment and basic science of Neoplasms, Advanced Solid Tumors, Carcinoma, Hepatocellular, and Malignant Pleural Mesothelioma. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14250 | Th1480 | Aducanumab | >Th1480_Aducanumab XVQLVESGGGVVQPGRSLRLSCAASGFAFSSYGMHWVRQAPGKGLEWVAVIWFDGTKKYYTDSVKGRFTISRDNSKNTLYLQMNTLRAEDTAVYYCARDRGIGARRGPYYMDVWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 146000 | NA | NA | NA | NA | The terminal half life of aducanumab is 24.8 days.[L34393] | Aducanumab, or BIIB037, is a monoclonal IgG1 antibody that targets extracellular amyloid-ß plaques in the brain; similar to [gantenerumab], [bapineuzumab] and [solanezumab].[A235668,A235730] Aducanumab is a recombinant antibody derived from patients with slow or absent cognitive decline, and phase 1b clinical trial data has shown patients treated with aducanumab show a reduction in amyloid-ß plaques.[A235668] Based on Mini-Mental State Examination and Clinical Dementia Rating (CDR), patients taking aducanumab showed signs of slowing progression, however these data are controversial.[A235668,A235720] Clinical trials showed a 23% relative difference between the experimental and placebo groups as determined by CDR, however this is equivalent to an absolute difference of 0.4/18.[A235720] Although aducanumab's approval represents the first drug treatment for Alzheimer's disease, the approval is conditional on further results.[L34420] Biogen enrolled patients in phase 3 clinical trials in 2015, but increased the size of the trials from 1350 patients to 1650 patients to maintain statistical power in the face of a high standard deviation.[A235720] Development of aducanumab was discontinued in March 2019 when two phase 3 clinical trials did not pass futility analysis, however Biogen sought FDA approval in October 2019 after reanalysis of the data.[A235720] Aducanumab was granted accelerated FDA approval on 7 June 2021.[L34393] Continued approval will be based on further trials confirming a clinical benefit over currently available therapy.[L34420] | Aducanumab is indicated in the treatment of Alzheimer's disease.[L34393] | Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß, reducing amyloid plaques in the brain.[L34393] It has a long duration of action as it is given once every 4 weeks.[L34393] Patients should be counselled regarding the risk of amyloid related imaging abnormalities, including microhemorrhages, and hypersensitivity reactions.[L34393] | Alzheimer's disease is a neurodegenerative disease.[A235668] Part of the pathology of Alzheimer's disease is the presence of plaques forming extracellularly in the brain.[A235668] These plaques are mostly composed of amyloid-ß, a peptide of varying length formed by the cleavage of the amyloid precursor protein.[A235668] The "amyloid cascade hypothesis" suggests that the accumulation of amyloid-ß oligopeptides in the brain drives the pathogenesis of Alzheimer's disease.[A235730] Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß at amino acids 3-7.[A235668,L34393] The amyloid-ß residues Phe4, His6, Glu3, and Arg5 are responsible for the majority of the contact between amyloid-ß and aducanumab's Fab region.[A235668] Data from studies in mice and humans shows aducanumab treatment reduces amyloid-ß, however human trials show non-significant changes in amyloid-ß40 and amyloid-ß42 across a dose range of 0.3-30 mg/kg and an increase in amyloid-ß40 and amyloid-ß42 at 60 mg/kg.[A235730] Aducanumab treatment is associated with slowing the rate of progression of Alzheimer's disease, based on Mini-Mental State Examination, Clinical Dementia Rating, and levels of p-tau in the cerebrospinal fluid.[A235715] | Patients experiencing dose-limiting toxicity may present with amyloid-related imaging abnormalities including edema or microhemorrhages of the brain.[A235730] Symptoms of dose limiting toxicity were generally transient,[A235730] however patients may need to be treated with symptomatic and supportive measures. | Aducanumab is expected to be broken down into smaller oligopeptides and amino acids.[A40006,L34393] | A 10 mg/kg intravenous dose of aducanumab reached a Cmax of 182.7 µg/mL, with a Tmax of 3.0 hours, and an AUCinf of 31,400 h | The volume of distribution of aducanumab is 9.63 L.[L34393] | A 10 mg/kg intravenous dose of aducanumab has a clearance of 0.39 mL/h/kg.[A235730] | Antibodies | NA | NA | NA | NA | Amyloid beta A4 protein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14251 | Th1480 | Aducanumab | >Th1480_Aducanumab XVQLVESGGGVVQPGRSLRLSCAASGFAFSSYGMHWVRQAPGKGLEWVAVIWFDGTKKYYTDSVKGRFTISRDNSKNTLYLQMNTLRAEDTAVYYCARDRGIGARRGPYYMDVWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 146000 | NA | NA | NA | NA | The terminal half life of aducanumab is 24.8 days.[L34393] | Aducanumab, or BIIB037, is a monoclonal IgG1 antibody that targets extracellular amyloid-ß plaques in the brain; similar to [gantenerumab], [bapineuzumab] and [solanezumab].[A235668,A235730] Aducanumab is a recombinant antibody derived from patients with slow or absent cognitive decline, and phase 1b clinical trial data has shown patients treated with aducanumab show a reduction in amyloid-ß plaques.[A235668] Based on Mini-Mental State Examination and Clinical Dementia Rating (CDR), patients taking aducanumab showed signs of slowing progression, however these data are controversial.[A235668,A235720] Clinical trials showed a 23% relative difference between the experimental and placebo groups as determined by CDR, however this is equivalent to an absolute difference of 0.4/18.[A235720] Although aducanumab's approval represents the first drug treatment for Alzheimer's disease, the approval is conditional on further results.[L34420] Biogen enrolled patients in phase 3 clinical trials in 2015, but increased the size of the trials from 1350 patients to 1650 patients to maintain statistical power in the face of a high standard deviation.[A235720] Development of aducanumab was discontinued in March 2019 when two phase 3 clinical trials did not pass futility analysis, however Biogen sought FDA approval in October 2019 after reanalysis of the data.[A235720] Aducanumab was granted accelerated FDA approval on 7 June 2021.[L34393] Continued approval will be based on further trials confirming a clinical benefit over currently available therapy.[L34420] | Aducanumab is indicated in the treatment of Alzheimer's disease.[L34393] | Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß, reducing amyloid plaques in the brain.[L34393] It has a long duration of action as it is given once every 4 weeks.[L34393] Patients should be counselled regarding the risk of amyloid related imaging abnormalities, including microhemorrhages, and hypersensitivity reactions.[L34393] | Alzheimer's disease is a neurodegenerative disease.[A235668] Part of the pathology of Alzheimer's disease is the presence of plaques forming extracellularly in the brain.[A235668] These plaques are mostly composed of amyloid-ß, a peptide of varying length formed by the cleavage of the amyloid precursor protein.[A235668] The "amyloid cascade hypothesis" suggests that the accumulation of amyloid-ß oligopeptides in the brain drives the pathogenesis of Alzheimer's disease.[A235730] Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß at amino acids 3-7.[A235668,L34393] The amyloid-ß residues Phe4, His6, Glu3, and Arg5 are responsible for the majority of the contact between amyloid-ß and aducanumab's Fab region.[A235668] Data from studies in mice and humans shows aducanumab treatment reduces amyloid-ß, however human trials show non-significant changes in amyloid-ß40 and amyloid-ß42 across a dose range of 0.3-30 mg/kg and an increase in amyloid-ß40 and amyloid-ß42 at 60 mg/kg.[A235730] Aducanumab treatment is associated with slowing the rate of progression of Alzheimer's disease, based on Mini-Mental State Examination, Clinical Dementia Rating, and levels of p-tau in the cerebrospinal fluid.[A235715] | Patients experiencing dose-limiting toxicity may present with amyloid-related imaging abnormalities including edema or microhemorrhages of the brain.[A235730] Symptoms of dose limiting toxicity were generally transient,[A235730] however patients may need to be treated with symptomatic and supportive measures. | Aducanumab is expected to be broken down into smaller oligopeptides and amino acids.[A40006,L34393] | A 10 mg/kg intravenous dose of aducanumab reached a Cmax of 182.7 µg/mL, with a Tmax of 3.0 hours, and an AUCinf of 31,400 h | The volume of distribution of aducanumab is 9.63 L.[L34393] | A 10 mg/kg intravenous dose of aducanumab has a clearance of 0.39 mL/h/kg.[A235730] | Antibodies, Monoclonal | NA | NA | NA | NA | Amyloid beta A4 protein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14272 | Th1482 | Anrukinzumab | NA | NA | NA | NA | NA | NA | NA | Anrukinzumab has been used in trials studying the diagnostic of Asthma. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14273 | Th1482 | Anrukinzumab | NA | NA | NA | NA | NA | NA | NA | Anrukinzumab has been used in trials studying the diagnostic of Asthma. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14279 | Th1483 | GS-5745 | NA | NA | NA | NA | NA | NA | NA | GS-5745 has been used in trials studying the treatment of Tumors, Breast Cancer, Crohn's Disease, Colorectal Cancer, and Pancreatic Cancer, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 1-bromo-2-fluoro-4-methoxy-3-nitrobenzene | NA | Link | NA | NA |
| 14288 | Th1485 | Vanucizumab | NA | NA | NA | NA | NA | NA | NA | Vanucizumab has been used in trials studying the treatment of ColoRectal Cancer and Advanced/Metastatic Solid Tumors. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14289 | Th1485 | Vanucizumab | NA | NA | NA | NA | NA | NA | NA | Vanucizumab has been used in trials studying the treatment of ColoRectal Cancer and Advanced/Metastatic Solid Tumors. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14290 | Th1485 | Vanucizumab | NA | NA | NA | NA | NA | NA | NA | Vanucizumab has been used in trials studying the treatment of ColoRectal Cancer and Advanced/Metastatic Solid Tumors. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14303 | Th1487 | Labetuzumab govitecan | NA | NA | NA | NA | NA | NA | NA | Labetuzumab govitecan has been used in trials studying the treatment of Colon Cancer, Rectal Cancer, and Metastatic Colorectal Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | 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)-5-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-oxopentan-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 |
| 14304 | Th1487 | Labetuzumab govitecan | NA | NA | NA | NA | NA | NA | NA | Labetuzumab govitecan has been used in trials studying the treatment of Colon Cancer, Rectal Cancer, and Metastatic Colorectal Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | 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)-5-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-oxopentan-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 |
| 14313 | Th1488 | Tanezumab | NA | NA | NA | NA | NA | NA | NA | Tanezumab has been investigated for the treatment of Osteoarthritis, Knee and Neuralgia, Postherpetic. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14314 | Th1488 | Tanezumab | NA | NA | NA | NA | NA | NA | NA | Tanezumab has been investigated for the treatment of Osteoarthritis, Knee and Neuralgia, Postherpetic. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14315 | Th1488 | Tanezumab | NA | NA | NA | NA | NA | NA | NA | Tanezumab has been investigated for the treatment of Osteoarthritis, Knee and Neuralgia, Postherpetic. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14327 | Th1489 | Ensituximab | NA | NA | NA | NA | NA | NA | NA | Ensituximab has been used in trials studying the treatment of Pancreatic Cancer, Adult, Metastatic Colorectal Cancer, and Metastatic Pancreatic Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14335 | Th1490 | Fezakinumab | NA | NA | NA | NA | NA | NA | NA | Fezakinumab has been used in trials studying the treatment of Atopic Dermatitis and Rheumatoid Arthritis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14344 | Th1491 | Vatelizumab | NA | NA | NA | NA | NA | NA | NA | Vatelizumab has been used in trials studying the treatment of Ulcerative Colitis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14345 | Th1491 | Vatelizumab | NA | NA | NA | NA | NA | NA | NA | Vatelizumab has been used in trials studying the treatment of Ulcerative Colitis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14358 | Th1493 | Dusigitumab | NA | NA | NA | NA | NA | NA | NA | Dusigitumab has been used in trials studying the treatment of Cancer, Advanced Solid Malignancies, Unresectable or Metastatic Hepatocellular Carcinoma (HCC), and Hormone-sensitive, HER-2 Negative Metastatic Breast Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14374 | Th1497 | Fresolimumab | >Th1497_Fresolimumab QVQLVQSGAEVKKPGSSVKVSCKASGYTFSSNVISWVRQAPGQGLEWMGGVIPIVDIANYAQRFKGRVTITADESTSTTYMELSSLRSEDTAVYYCASTLGLVLDAMDYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | NA | Fresolimumab has been used in trials studying the treatment of Primary Brain Tumors, Metastatic Breast Cancer, Diffuse Systemic Sclerosis, Pleural Malignant Mesothelioma, and Primary Focal Segmental Glomerulosclerosis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14396 | Th1499 | Indusatumab vedotin | NA | NA | NA | NA | NA | NA | NA | Indusatumab vedotin has been used in trials studying the treatment of Pancreatic Adenocarcinoma, Adenocarcinoma of the Stomach, Recurrent Gastric Adenocarcinoma, Metastatic Gastric Adenocarcinoma, and Advanced Gastrointestinal Carcinoma, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14417 | Th1501 | Bococizumab | NA | NA | NA | NA | NA | NA | NA | Bococizumab has been used in trials studying the treatment and prevention of Dyslipidemia, Hyperlipidemia, Hypercholesterolemia, Cardiovascular Disease, and Heterozygous Familial Hypercholesterolemia. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14418 | Th1501 | Bococizumab | NA | NA | NA | NA | NA | NA | NA | Bococizumab has been used in trials studying the treatment and prevention of Dyslipidemia, Hyperlipidemia, Hypercholesterolemia, Cardiovascular Disease, and Heterozygous Familial Hypercholesterolemia. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14419 | Th1501 | Bococizumab | NA | NA | NA | NA | NA | NA | NA | Bococizumab has been used in trials studying the treatment and prevention of Dyslipidemia, Hyperlipidemia, Hypercholesterolemia, Cardiovascular Disease, and Heterozygous Familial Hypercholesterolemia. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14439 | 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]. | Antibodies | NA | NA | NA | NA | C-C chemokine receptor type 4 | Poteligeo | Kyowa Kirin Holdings B.V. | Kyowa Kirin Holdings B.V. | Intravenous | 4 mg/ml | None. | rash, infusion related reactions chills, nausea, fever, fast heart rate, shaking, headache, and vomiting, fatigue, diarrhea, musculoskeletal pain, and upper respiratory tract infection | Poteligeo is used to treat mycosis fungoides or Sézary syndrome in adults. Poteligeo is given after at least one other medication did not work or has stopped working. Poteligeo may also be used for purposes not listed in this medication guide. Warnings Poteligeo can cause serious or life-threatening... | POTELIGEO is a prescription medicine used to treat mycosis fungoides (MF) or Sézary syndrome (SS) in adults when you have tried at least one prior medicine (taken by mouth or injection) and it did not work or the disease has come back. | NA | NA | Link | Link | NA |
| 14440 | 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]. | Antibodies, Monoclonal | NA | NA | NA | NA | C-C chemokine receptor type 4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14441 | 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]. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | C-C chemokine receptor type 4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14456 | Th1505 | Plozalizumab | >Th1505_Plozalizumab EVQLVESGGGLVKPGGSLRLSCAASGFTFSAYAMNWVRQAPGKGLEWVGRIRTKNNNYATYYADSVKDRFTISRDDSKNTLYLQMNSLKTEDTAVYYCTTFYGNGVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELAGAPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Plozalizumab has been investigated for the treatment of Atherosclerosis. Plozalizumab, a novel humanized monoclonal antibody, specifically targets CCR2 chemokine receptors found on the surface of certain white blood cells including macrophages and monocytes. Preclinical studies suggest that CCR2 plays an important role in the trafficking of monocytes and macrophages to sites of inflammation. The recruitment of macrophages to the arterial wall is believed to be a critical step in the development of atherosclerosis. | NA | NA | Preclinical studies suggest that CCR2 plays an important role in the trafficking of monocytes and macrophages to sites of inflammation. The recruitment of macrophages to the arterial wall is believed to be a critical step in the development of atherosclerosis. Plozalizumab targets CCR2 chemokine receptors found on the surface of certain white blood cells including macrophages and monocytes. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | C-C chemokine receptor type 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14457 | Th1505 | Plozalizumab | >Th1505_Plozalizumab EVQLVESGGGLVKPGGSLRLSCAASGFTFSAYAMNWVRQAPGKGLEWVGRIRTKNNNYATYYADSVKDRFTISRDDSKNTLYLQMNSLKTEDTAVYYCTTFYGNGVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELAGAPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Plozalizumab has been investigated for the treatment of Atherosclerosis. Plozalizumab, a novel humanized monoclonal antibody, specifically targets CCR2 chemokine receptors found on the surface of certain white blood cells including macrophages and monocytes. Preclinical studies suggest that CCR2 plays an important role in the trafficking of monocytes and macrophages to sites of inflammation. The recruitment of macrophages to the arterial wall is believed to be a critical step in the development of atherosclerosis. | NA | NA | Preclinical studies suggest that CCR2 plays an important role in the trafficking of monocytes and macrophages to sites of inflammation. The recruitment of macrophages to the arterial wall is believed to be a critical step in the development of atherosclerosis. Plozalizumab targets CCR2 chemokine receptors found on the surface of certain white blood cells including macrophages and monocytes. | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | C-C chemokine receptor type 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14458 | Th1505 | Plozalizumab | >Th1505_Plozalizumab EVQLVESGGGLVKPGGSLRLSCAASGFTFSAYAMNWVRQAPGKGLEWVGRIRTKNNNYATYYADSVKDRFTISRDDSKNTLYLQMNSLKTEDTAVYYCTTFYGNGVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELAGAPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Plozalizumab has been investigated for the treatment of Atherosclerosis. Plozalizumab, a novel humanized monoclonal antibody, specifically targets CCR2 chemokine receptors found on the surface of certain white blood cells including macrophages and monocytes. Preclinical studies suggest that CCR2 plays an important role in the trafficking of monocytes and macrophages to sites of inflammation. The recruitment of macrophages to the arterial wall is believed to be a critical step in the development of atherosclerosis. | NA | NA | Preclinical studies suggest that CCR2 plays an important role in the trafficking of monocytes and macrophages to sites of inflammation. The recruitment of macrophages to the arterial wall is believed to be a critical step in the development of atherosclerosis. Plozalizumab targets CCR2 chemokine receptors found on the surface of certain white blood cells including macrophages and monocytes. | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | C-C chemokine receptor type 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14481 | Th1507 | Inebilizumab | >Th1507_Inebilizumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSSWMNWVRQAPGKGLEWVGRIYPGDGDTNYNVKFKGRFTISRDDSKNSLYLQMNSLKTEDTAVYYCARSGFITTVRDFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | NA | NA | NA | NA | Inebilizumab exhibits biphasic pharmacokinetics with a mean terminal half-life of 18 days.[L14315] The terminal half-life reported in phase I studies varied by dose but was typically close to 18 days, with a range of 6.8 to 18.7 days.[A214298, A214301] | Inappropriate growth of or self-directed antibody production by B-cells is the etiological underpinning of a variety of conditions, including the multiple sclerosis-like neurological condition neuromyelitis optica spectrum disorder (NMOSD).[A214283, A214286] Inebilizumab is a humanized afucosylated monoclonal IgG1 antibody directed against the broadly expressed B-cell surface antigen CD19. Inebilizumab is cytolytic, resulting in B-cell depletion and offering therapeutic benefit to patients suffering from NMOSD. Compared to the anti-CD20 antibody [rituximab], which is also used to treat NMOSD, inebilizumab has broader specificity.[A214280, A214289, A214292, A214295, A214298, A214301] Inebilizumab was granted FDA approval on June 11, 2020, for the treatment of anti-aquaporin 4 positive NMOSD patients.[L14315] Given its mechanism of action and good safety profile, it may prove useful in the treatment of other conditions linked to autoimmune antibody production or B-cell malignancies.[A214280, A214295] | Inebilizumab is indicated for the treatment of aquaporin-4 (AQP4) immunoglobulin-positive (AQP4-IgG) neuromyelitis optica spectrum disorder (NMOSD) in adult patients.[L14315] | Inebilizumab is a CD19-directed monoclonal antibody that results in immunosuppression through B-cell depletion with sufficient efficacy to allow a six-month dosing schedule.[A214280, A214289, A214292, L14315] Due to this mechanism of action, patients undergoing inebilizumab treatment may be at higher risk of infections and should be monitored for active infections and immunoglobulin levels while undergoing treatment; vaccination is not recommended during inebilizumab treatment. Also, there is a risk of severe infusion reactions. Animal data suggests the possibility of fetal harm with inebilizumab and therefore, effective contraception during and for six months following inebilizumab treatment is recommended.[L14315] | Neuromyelitis optica spectrum disorder (NMOSD), formerly referred to as Devic's disease, is an antibody-mediated autoimmune condition resulting in astroglial cell death, demyelination, and central nervous system (CNS) inflammation.[A214283, A214286] The presence of anti-aquaporin 4 immunoglobulin (AQP4-IgG) is the most frequent biomarker, although AQP4-IgG negative, anti-myelin oligodendrocyte glycoprotein (anti-MOG) positive, variants with similar presentation also exist.[A214283, A214286] The theoretical origin of symptoms is through AQP4-IgG-mediated astrocyte cytotoxicity and subsequent infiltration of neutrophils, eosinophils, and macrophages, leading to inflammatory-mediated oligodendrocyte damage and myelin sheath loss.[A214286] In general, this manifests as optic neuritis and transverse myelitis with occasional involvement of the diencephalic, brainstem, and cerebral hemisphere.[A214295] CD19 is a B-cell surface antigen expressed on most B-cells,[A214280] including the expanded population of CD27high CD38high CD180- CD19+ plasmablasts that are the origin of astrocytic AQP4-IgG in most NMOSD patients.[A214283, A214286] Inebilizumab binds to CD19 and, through one of several potential mechanisms, results in cell death.[A214280, A214289, A214292, L14315] Destruction of the specific AQP4-IgG-producing plasmablasts results in lower amounts of AQP4-IgG in the CNS and therefore slows neuronal damage and improves patient outcomes.[A214295] | Toxicity information regarding inebilizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as severe infusion reactions, infections, and arthralgia. Symptomatic and supportive measures are recommended. | Inebilizumab is a monoclonal antibody and is hence likely degraded through proteolysis.[L14315] | Inebilizumab is given intravenously and hence is immediately exposed to the systemic circulation. The mean reported Cmax following second dose 300 mg administration was 108 µg/mL, and the cumulative AUC following 26 weeks of treatment with two IV administrations was 2980 µg | Inebilizumab has an estimated central volume of distribution of 2.95L and a peripheral volume of distribution of 2.57L.[L14315] The steady-state volume of distribution in patients administered with a range of doses between 0.1 and 10.0 mg/kg ranged from 53.7 to 71.7 mL/kg.[A214301] | Inebilizumab has an estimated systemic clearance of 0.19 L/day.[L14315] In phase I studies, the reported clearance varied between 139-180 mL/day in one study,[A214298] and 3.5-6.2 mL/kg/day in another,[A214301] depending on the dose. | Antibodies | NA | NA | NA | NA | B-lymphocyte antigen CD19 | Uplizna | Viela Bio, Inc. | Viela Bio, Inc. | Intravenous | 10 mg/1mL | UPLIZNA is contraindicated in patients with: A history of a life-threatening infusion reaction to UPLIZNA Active hepatitis B infection | urinary tract infection (UTI), joint pain, headache, and back pain | Uplizna is a prescription medicine used to treat adults with neuromyelitis optic spectrum disorder (NMOSD) who are anti-aquaporin-4 (AQP4) antibody positive. It is not known if Uplizna is safe or effective in children. | Uplizna (inebilizumab-cdon) is a CD19-directed cytolytic antibody used to treat neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive. | NA | NA | Link | Link | NA |
| 14482 | Th1507 | Inebilizumab | >Th1507_Inebilizumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSSWMNWVRQAPGKGLEWVGRIYPGDGDTNYNVKFKGRFTISRDDSKNSLYLQMNSLKTEDTAVYYCARSGFITTVRDFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | NA | NA | NA | NA | Inebilizumab exhibits biphasic pharmacokinetics with a mean terminal half-life of 18 days.[L14315] The terminal half-life reported in phase I studies varied by dose but was typically close to 18 days, with a range of 6.8 to 18.7 days.[A214298, A214301] | Inappropriate growth of or self-directed antibody production by B-cells is the etiological underpinning of a variety of conditions, including the multiple sclerosis-like neurological condition neuromyelitis optica spectrum disorder (NMOSD).[A214283, A214286] Inebilizumab is a humanized afucosylated monoclonal IgG1 antibody directed against the broadly expressed B-cell surface antigen CD19. Inebilizumab is cytolytic, resulting in B-cell depletion and offering therapeutic benefit to patients suffering from NMOSD. Compared to the anti-CD20 antibody [rituximab], which is also used to treat NMOSD, inebilizumab has broader specificity.[A214280, A214289, A214292, A214295, A214298, A214301] Inebilizumab was granted FDA approval on June 11, 2020, for the treatment of anti-aquaporin 4 positive NMOSD patients.[L14315] Given its mechanism of action and good safety profile, it may prove useful in the treatment of other conditions linked to autoimmune antibody production or B-cell malignancies.[A214280, A214295] | Inebilizumab is indicated for the treatment of aquaporin-4 (AQP4) immunoglobulin-positive (AQP4-IgG) neuromyelitis optica spectrum disorder (NMOSD) in adult patients.[L14315] | Inebilizumab is a CD19-directed monoclonal antibody that results in immunosuppression through B-cell depletion with sufficient efficacy to allow a six-month dosing schedule.[A214280, A214289, A214292, L14315] Due to this mechanism of action, patients undergoing inebilizumab treatment may be at higher risk of infections and should be monitored for active infections and immunoglobulin levels while undergoing treatment; vaccination is not recommended during inebilizumab treatment. Also, there is a risk of severe infusion reactions. Animal data suggests the possibility of fetal harm with inebilizumab and therefore, effective contraception during and for six months following inebilizumab treatment is recommended.[L14315] | Neuromyelitis optica spectrum disorder (NMOSD), formerly referred to as Devic's disease, is an antibody-mediated autoimmune condition resulting in astroglial cell death, demyelination, and central nervous system (CNS) inflammation.[A214283, A214286] The presence of anti-aquaporin 4 immunoglobulin (AQP4-IgG) is the most frequent biomarker, although AQP4-IgG negative, anti-myelin oligodendrocyte glycoprotein (anti-MOG) positive, variants with similar presentation also exist.[A214283, A214286] The theoretical origin of symptoms is through AQP4-IgG-mediated astrocyte cytotoxicity and subsequent infiltration of neutrophils, eosinophils, and macrophages, leading to inflammatory-mediated oligodendrocyte damage and myelin sheath loss.[A214286] In general, this manifests as optic neuritis and transverse myelitis with occasional involvement of the diencephalic, brainstem, and cerebral hemisphere.[A214295] CD19 is a B-cell surface antigen expressed on most B-cells,[A214280] including the expanded population of CD27high CD38high CD180- CD19+ plasmablasts that are the origin of astrocytic AQP4-IgG in most NMOSD patients.[A214283, A214286] Inebilizumab binds to CD19 and, through one of several potential mechanisms, results in cell death.[A214280, A214289, A214292, L14315] Destruction of the specific AQP4-IgG-producing plasmablasts results in lower amounts of AQP4-IgG in the CNS and therefore slows neuronal damage and improves patient outcomes.[A214295] | Toxicity information regarding inebilizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as severe infusion reactions, infections, and arthralgia. Symptomatic and supportive measures are recommended. | Inebilizumab is a monoclonal antibody and is hence likely degraded through proteolysis.[L14315] | Inebilizumab is given intravenously and hence is immediately exposed to the systemic circulation. The mean reported Cmax following second dose 300 mg administration was 108 µg/mL, and the cumulative AUC following 26 weeks of treatment with two IV administrations was 2980 µg | Inebilizumab has an estimated central volume of distribution of 2.95L and a peripheral volume of distribution of 2.57L.[L14315] The steady-state volume of distribution in patients administered with a range of doses between 0.1 and 10.0 mg/kg ranged from 53.7 to 71.7 mL/kg.[A214301] | Inebilizumab has an estimated systemic clearance of 0.19 L/day.[L14315] In phase I studies, the reported clearance varied between 139-180 mL/day in one study,[A214298] and 3.5-6.2 mL/kg/day in another,[A214301] depending on the dose. | Antibodies, Monoclonal | NA | NA | NA | NA | B-lymphocyte antigen CD19 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14483 | Th1507 | Inebilizumab | >Th1507_Inebilizumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSSWMNWVRQAPGKGLEWVGRIYPGDGDTNYNVKFKGRFTISRDDSKNSLYLQMNSLKTEDTAVYYCARSGFITTVRDFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | NA | NA | NA | NA | Inebilizumab exhibits biphasic pharmacokinetics with a mean terminal half-life of 18 days.[L14315] The terminal half-life reported in phase I studies varied by dose but was typically close to 18 days, with a range of 6.8 to 18.7 days.[A214298, A214301] | Inappropriate growth of or self-directed antibody production by B-cells is the etiological underpinning of a variety of conditions, including the multiple sclerosis-like neurological condition neuromyelitis optica spectrum disorder (NMOSD).[A214283, A214286] Inebilizumab is a humanized afucosylated monoclonal IgG1 antibody directed against the broadly expressed B-cell surface antigen CD19. Inebilizumab is cytolytic, resulting in B-cell depletion and offering therapeutic benefit to patients suffering from NMOSD. Compared to the anti-CD20 antibody [rituximab], which is also used to treat NMOSD, inebilizumab has broader specificity.[A214280, A214289, A214292, A214295, A214298, A214301] Inebilizumab was granted FDA approval on June 11, 2020, for the treatment of anti-aquaporin 4 positive NMOSD patients.[L14315] Given its mechanism of action and good safety profile, it may prove useful in the treatment of other conditions linked to autoimmune antibody production or B-cell malignancies.[A214280, A214295] | Inebilizumab is indicated for the treatment of aquaporin-4 (AQP4) immunoglobulin-positive (AQP4-IgG) neuromyelitis optica spectrum disorder (NMOSD) in adult patients.[L14315] | Inebilizumab is a CD19-directed monoclonal antibody that results in immunosuppression through B-cell depletion with sufficient efficacy to allow a six-month dosing schedule.[A214280, A214289, A214292, L14315] Due to this mechanism of action, patients undergoing inebilizumab treatment may be at higher risk of infections and should be monitored for active infections and immunoglobulin levels while undergoing treatment; vaccination is not recommended during inebilizumab treatment. Also, there is a risk of severe infusion reactions. Animal data suggests the possibility of fetal harm with inebilizumab and therefore, effective contraception during and for six months following inebilizumab treatment is recommended.[L14315] | Neuromyelitis optica spectrum disorder (NMOSD), formerly referred to as Devic's disease, is an antibody-mediated autoimmune condition resulting in astroglial cell death, demyelination, and central nervous system (CNS) inflammation.[A214283, A214286] The presence of anti-aquaporin 4 immunoglobulin (AQP4-IgG) is the most frequent biomarker, although AQP4-IgG negative, anti-myelin oligodendrocyte glycoprotein (anti-MOG) positive, variants with similar presentation also exist.[A214283, A214286] The theoretical origin of symptoms is through AQP4-IgG-mediated astrocyte cytotoxicity and subsequent infiltration of neutrophils, eosinophils, and macrophages, leading to inflammatory-mediated oligodendrocyte damage and myelin sheath loss.[A214286] In general, this manifests as optic neuritis and transverse myelitis with occasional involvement of the diencephalic, brainstem, and cerebral hemisphere.[A214295] CD19 is a B-cell surface antigen expressed on most B-cells,[A214280] including the expanded population of CD27high CD38high CD180- CD19+ plasmablasts that are the origin of astrocytic AQP4-IgG in most NMOSD patients.[A214283, A214286] Inebilizumab binds to CD19 and, through one of several potential mechanisms, results in cell death.[A214280, A214289, A214292, L14315] Destruction of the specific AQP4-IgG-producing plasmablasts results in lower amounts of AQP4-IgG in the CNS and therefore slows neuronal damage and improves patient outcomes.[A214295] | Toxicity information regarding inebilizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as severe infusion reactions, infections, and arthralgia. Symptomatic and supportive measures are recommended. | Inebilizumab is a monoclonal antibody and is hence likely degraded through proteolysis.[L14315] | Inebilizumab is given intravenously and hence is immediately exposed to the systemic circulation. The mean reported Cmax following second dose 300 mg administration was 108 µg/mL, and the cumulative AUC following 26 weeks of treatment with two IV administrations was 2980 µg | Inebilizumab has an estimated central volume of distribution of 2.95L and a peripheral volume of distribution of 2.57L.[L14315] The steady-state volume of distribution in patients administered with a range of doses between 0.1 and 10.0 mg/kg ranged from 53.7 to 71.7 mL/kg.[A214301] | Inebilizumab has an estimated systemic clearance of 0.19 L/day.[L14315] In phase I studies, the reported clearance varied between 139-180 mL/day in one study,[A214298] and 3.5-6.2 mL/kg/day in another,[A214301] depending on the dose. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | B-lymphocyte antigen CD19 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14491 | Th1508 | Mavrilimumab | NA | NA | NA | NA | NA | NA | NA | Mavrilimumab has been investigated for the treatment of Rheumatoid Arthritis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14500 | Th1509 | Blosozumab | NA | NA | NA | NA | NA | NA | NA | Blosozumab has been used in trials studying the basic science and treatment of Osteoporosis and Osteoporosis, Postmenopausal. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14501 | Th1509 | Blosozumab | NA | NA | NA | NA | NA | NA | NA | Blosozumab has been used in trials studying the basic science and treatment of Osteoporosis and Osteoporosis, Postmenopausal. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14502 | Th1509 | Blosozumab | NA | NA | NA | NA | NA | NA | NA | Blosozumab has been used in trials studying the basic science and treatment of Osteoporosis and Osteoporosis, Postmenopausal. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14519 | Th1511 | Bimagrumab | NA | NA | NA | NA | NA | NA | NA | Bimagrumab has been used in trials studying the treatment and supportive care of Sarcopenia, Skeletal Muscle, Mechanical Ventilation, Sporadic Inclusion Body Myositis, and Sporadic Inclusion Body Myositis (sIBM), among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14527 | 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 | Antibodies | 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 |
| 14528 | 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 | Antibodies, Monoclonal | 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 |
| 14529 | 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 | Antibodies, Monoclonal, Humanized | 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 |
| 14539 | Th1513 | Tovetumab | NA | NA | NA | NA | NA | NA | NA | Tovetumab has been used in trials studying the treatment of Cancer, Glioblastoma Multiforme, and Advanced Solid Malignancies. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14540 | Th1513 | Tovetumab | NA | NA | NA | NA | NA | NA | NA | Tovetumab has been used in trials studying the treatment of Cancer, Glioblastoma Multiforme, and Advanced Solid Malignancies. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14560 | Th1516 | Samalizumab | NA | NA | NA | NA | NA | NA | NA | Samalizumab has been used in trials studying the treatment of Multiple Myeloma and B-cell Chronic Lymphocytic Leukemia. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14561 | Th1516 | Samalizumab | NA | NA | NA | NA | NA | NA | NA | Samalizumab has been used in trials studying the treatment of Multiple Myeloma and B-cell Chronic Lymphocytic Leukemia. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14576 | Th1519 | Lumretuzumab | NA | NA | NA | NA | NA | NA | NA | Lumretuzumab has been used in trials studying the treatment of Neoplasms, Breast Cancer, Squamous Non-Small Cell Lung Cancer, and Non-Squamous Non-Small Cell Lung Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14577 | Th1519 | Lumretuzumab | NA | NA | NA | NA | NA | NA | NA | Lumretuzumab has been used in trials studying the treatment of Neoplasms, Breast Cancer, Squamous Non-Small Cell Lung Cancer, and Non-Squamous Non-Small Cell Lung Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14578 | Th1519 | Lumretuzumab | NA | NA | NA | NA | NA | NA | NA | Lumretuzumab has been used in trials studying the treatment of Neoplasms, Breast Cancer, Squamous Non-Small Cell Lung Cancer, and Non-Squamous Non-Small Cell Lung Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14602 | Th1521 | Moxetumomab pasudotox | >Th1521_Moxetumomab_pasudotox MEVQLVESGGGLVKPGGSLKLSCAASGFAFSIYDMSWVRQTPEKCLEWVAYISSGGGTTYYPDTVKGRFTISRDNAKNTLYLQMSSLKSEDTAMYYCARHSGYGTHWGVLFAYWGQGTLVSAKASGGPEGGSLAALTAHQACHLPLETFTRHRQPRGWEQLEQCGYPVQRLVALYIAARLSWNQVDQVIRALASPGSGGDLGEAIREQPEQARLALTLAAAESERFVRQGTGNDEAGAANGPADSGDALLERNYPTGAEFLGDGGDVSFSTRGTQNWTVERLLQAHRQLEERGYVFVGYHGTFLEAAQSIVFGGVRARSQDLDAIWRGFYIAGDPALAYGYAQDQEPDARGRIRNGALLRVYVPRSSLPGFYRTSLTLAAPEAAGEVERLIGHPLPLRLDAITGPEEEGGRLETILGWPLAERTWIPSAIPTDPRNVGGDLDPSSIPDKEQAISALPDYASQPGKPPREDLK | 63500 | C2804H4339N783O870S14 | NA | NA | NA | MxP presents a short half-life, which limits its efficacy against solid tumors.[A38882] The half-life is reported to be of only 1.4 hours.[A38883] | CD22 is a lineage-restricted B-cell antigen that is expressed solely in on B-chronic lymphocytic leukemia, hairy cell leukemia, acute lymphocytic leukemiathe and Burkitt's lymphoma. The predecessor of Moxetumab pasudotox (MxP), named BL22, was first created based on the antibody RFB4 which specifically binds to CD22. This antibody was used to generate a recombinant immunotoxin in which a stabilized Fv segment by a disulfide bond is fused to the _Pseudomonas_ exotoxin A (PE38) which does not have the cell-binding portion.[A38864] MxP appears as an improved form of BL22 by the mutation of the Fv region and the antibody phage-displayed. As well the residues SSY in the heavy chain are mutated to THW.[A38864] It was developed by Astra Zeneca and FDA approved on September 13, 2018, after being granted the status of Fast Track, Priority Review and Orphan Drug designations.[L4568] | MxP is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies including treatment with a purine nucleoside analog. The use of this drug is not recommended in patients with severe renal impairment (CrCl < 29 ml/min).[L4568] HCL is an uncommon type of lymphocytic leukemia that starts in B cells or B lymphocytes. It is characterized by an accumulation of abnormal B lymphocytes. HCL is called "hairy" as it produces hair-like projections in the surface of the cancer cells. A usual symptom in people having HCL is the presence of splenomegaly and less often hepatomegaly.[A38877] | Compared with its predecessor, MxP is even 50-fold more active on lymphoma cell lines and leukemic cells. In phase I clinical trial, MxP showed no dose-limiting toxicity and the overall response rate was of 79%. From pediatric patients with acute lymphoblastic leukemia, the complete response was observed in 12 individuals which is a result that has never been seen before.[A38880] In an open-label clinical trial, MxP showed a complete response, defined as the maintenance of hematologic remission, of more than 180 days in 30% of the patients and 75% of the patients achieved at least partial response.[L4568] Hence, the phase III clinical trial met the primary endpoint of durable complete response.[L4572] | MxP is a CD22-directed cytotoxin. It is stated as an immunotoxin which is defined as the class of agents that combine the selectivity of antibodies towards the target and the potency of toxins to perform the pharmacological anticancer function. CD22 is a B-lymphocyte restricted transmembrane protein with a high density in HCL cells when compared with normal B cells. After binding to CD22, MxP is internalized and processed, which allows the release of the modified toxin. This toxin inhibits protein translation which induces an apoptotic state of the high CD22-expressed cancer cell.[A38879] The toxin included in MxP is the _Pseudomonas_ exotoxin A which, after internalization, undergoes conformational changes and in the cytosol, the ribosylation activity of the domain III of the toxin inactivates the eukaryotic translation elongation factor (eEF-2) by transferring ADP (adenosine di-phosphate-ribose) from NAD to a modified histidine at position 715 in eEF-2. This action produces the inactivation of eEF-2 which leads to protein synthesis inhibition and programmed cell death.[A38881] | No studies have been performed regarding the carcinogenic potential and/or effect on fertility of MxP. It has been observed that the administration of MxP in a dose > 3 times the recommended can produce the degeneration of heart tissue and a dose > 10 times the recommended there are reports of gliosis, axonal degeneration in the spinal cord and body tremors.[FDA label] | The metabolism of MxP has not been well established but due to the nature of the drug, it is thought to be degraded into small peptides and individual amino acids.[A38883] | MxP serum concentration increases in a dose-proportional manner and reaches a mean steady state of 379 ng/ml with a Cmax of 626 ng.h/ml. There are no reports of systemic accumulation.[A38883] | The mean volume of distribution calculated based on population is 6.5 L.[A38883] | The mean systemic clearance is very fast and it is reported to be of 25 L/h. This clearance rate is decreased after subsequent dosing to 4 L/h.[A38883] | Antibodies, Monoclonal | NA | NA | NA | NA | B-cell receptor CD22,Elongation factor 2 | Lumoxiti | Astra Zeneca Ab | Astra Zeneca Ab | Intravenous | 1 mg | None. | infusion related reactions, fluid retention (including facial swelling, abdominal bloating, weight gain, swelling of extremities), nausea, fatigue, headache, fever, constipation, anemia, diarrhea, eye problems (blurred vision, dry eye, cataracts, eye discomfort or pain, eye swelling, conjunctivitis, and tearing) | Lumoxiti is an injection used to treat hairy cell leukemia. Lumoxiti is used in adult patients with hairy cell leukemia that has relapsed. Lumoxiti is also used if the patient has not responded to previous treatments, and has received at least 2 other treatments, including a type of medicine called purine... | LUMOXITI is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies, including treatment with a purine nucleoside analog (PNA). | NA | NA | Link | Link | NA |
| 14616 | Th1522 | Ibalizumab | >Th1522_Ibalizumab QVQLQQSGPEVVKPGASVKMSCKASGYTFTSYVIHWVRQKPGQGLDWIGYINPYNDGTDYDEKFKGKATLTSDTSTSTAYMELSSLRSEDTAVYYCAREKDNYATGAWFAYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half-life of ibalizumab is 3 to 3.5 days on average. The half-life was estimated from a multiple-dose study evaluating weekly ibalizumab 10 mg/kg in 1 study arm and biweekly ibalizumab 25 mg/kg in another study arm, given via intravenous (IV) infusion in adults with HIV [L1555]. In one clinical trial, the elimination half-life increased from 2.7 to 64 hours as the dose increased from 0.3 to 25 mg/kg (0.01 to 0.9 times the approved recommended loading dose based on a 70 kg patient) [FDA label]. | Ibalizumab (also known as _ibalizumab-uiyk_ and formerly known as TNX-355) is a monoclonal antibody that binds to CD4 receptors on the surface of CD4-positive cells, preventing HIV particle entry into the lymphocytes. It is an advanced and current antibody in development for the treatment of HIV/AIDS. It has been developed by Taimed biologics and Theratechnologies [L1558, L1554]. This drug was approved in March 2018 for the management of treatment-resistant HIV [L1554]. | Indicated for the treatment of human immunodeficiency virus type 1 (HIV-1) infection in highly treatment-experienced adults with multidrug-resistant HIV-1 infection failing their current antiretroviral regimen [FDA label]. The approval of Trogarzo was supported by a clinical trial of 40 treatment-experienced adults with MDR HIV-1 infection who persistently had elevated levels of HIV RNA in their blood despite heavy antiretroviral therapy. The majority of study patients had previously been treated with =10 antiretroviral medications [L1554]. | Trogarzo safety and effectiveness have been confirmed in a clinical trial of 40 patients who suffer multidrug-resistant HIV. The majority of these patients experienced a substantial decrease in their HIV-RNA levels within 7 days after receiving the drug. Approximately 43 percent of patients continued to experience HIV-RNA inhibition after 24 weeks of taking Trogarzo [L1554]. Trogarzo inhibits viral entry into cells, effectively managing HIV-1 infection in those who have attempted other therapies to no avail [L1554]. | Ibalizumab is a monoclonal antibody and viral-entry inhibitor that coats CD4-positive cells, the main target of HIV infection. By blocking viral entry into CD4 cells, ibalizumab creates a barrier for HIV, which is a different mechanism from those of entry inhibitors that target viral proteins or chemokine co-receptors. Ibalizumab is a CD4 domain 2-directed post-attachment HIV-1 inhibitor. This binding specificity of ibalizumab-uiyk to domain 2 of CD4 allows ibalizumab-uiyk to prevent viral entry into host cells without causing immunosuppression. Epitope mapping studies confirm that ibalizumab-uiyk binds to a conformational epitope located mainly in domain 2 of the extracellular region of the CD4 receptor. This epitope is located on the surface of CD4 opposite to the site in domain 1 that is essential for CD4 binding of the MHC class II molecules. This drug, therefore, does not interfere with CD4 cell-mediated immune functions. In addition, ibalizumab-uiyk does not interfere with gp120 attachment to CD4 [FDA label]. Ibalizumab’s post-binding conformational effects block the gp120-CD4 complex from interacting with CCR5 or CXCR4 and thus prevents viral entry and fusion [L1555]. CD4 is an integral cell surface glycoprotein that is able to enhance T cell-specific antigen responses when it interacts with its physiological ligand, class II major histocompatibility (MHC) molecules. In addition, CD4 is a specific cell-surface receptor for the human immunodeficiency virus-1 (HIV-1). The entry of human immunodeficiency virus (HIV) into cells requires the sequential binding of the viral exterior envelope glycoprotein, gp120, with the CD4 glycoprotein and a chemokine receptor on the cell surface. In addition, the CD4/gp120 interaction may directly inhibit T cell function [A32076]. In addition to the above mechanism of action, it was found in one study that ibalizumab-uiyk inhibits the replication of CCR5- and CXCR4- receptor laboratory strains and primary isolates of HIV-1 in phytohemagglutinin-stimulated peripheral blood lymphocytes, further confirming its action [L1559]. | Immune reconstitution inflammatory syndrome has been reported in one patient treated with TROGARZO in combination with other antiretrovirals. During the initial phase of combination antiretroviral therapies, patients whose immune systems respond may develop an inflammatory response to indolent or residual opportunistic infections, which may necessitate further evaluation and treatment [FDA label]. | Metabolized by CD4 receptor internalization, ibalizumab has no significant impact on liver or kidney metabolism [L1560]. | NA | 4.8 L [FDA label] | Following single-dose administrations of ibalizumab-uiyk as 0.5 to 1.5-hour infusions, the area under the concentration-time curve increased in a greater than dose-proportional manner, clearance decreased from 9.54 to 0.36 mL/h/kg and elimination half-life increased from 2.7 to 64 hours as the dose increased from 0.3 to 25 mg/kg [FDA label]. | Antibodies | NA | NA | NA | NA | T-cell surface glycoprotein CD4,C-C chemokine receptor type 5,C-X-C chemokine receptor type 4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14617 | Th1522 | Ibalizumab | >Th1522_Ibalizumab QVQLQQSGPEVVKPGASVKMSCKASGYTFTSYVIHWVRQKPGQGLDWIGYINPYNDGTDYDEKFKGKATLTSDTSTSTAYMELSSLRSEDTAVYYCAREKDNYATGAWFAYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half-life of ibalizumab is 3 to 3.5 days on average. The half-life was estimated from a multiple-dose study evaluating weekly ibalizumab 10 mg/kg in 1 study arm and biweekly ibalizumab 25 mg/kg in another study arm, given via intravenous (IV) infusion in adults with HIV [L1555]. In one clinical trial, the elimination half-life increased from 2.7 to 64 hours as the dose increased from 0.3 to 25 mg/kg (0.01 to 0.9 times the approved recommended loading dose based on a 70 kg patient) [FDA label]. | Ibalizumab (also known as _ibalizumab-uiyk_ and formerly known as TNX-355) is a monoclonal antibody that binds to CD4 receptors on the surface of CD4-positive cells, preventing HIV particle entry into the lymphocytes. It is an advanced and current antibody in development for the treatment of HIV/AIDS. It has been developed by Taimed biologics and Theratechnologies [L1558, L1554]. This drug was approved in March 2018 for the management of treatment-resistant HIV [L1554]. | Indicated for the treatment of human immunodeficiency virus type 1 (HIV-1) infection in highly treatment-experienced adults with multidrug-resistant HIV-1 infection failing their current antiretroviral regimen [FDA label]. The approval of Trogarzo was supported by a clinical trial of 40 treatment-experienced adults with MDR HIV-1 infection who persistently had elevated levels of HIV RNA in their blood despite heavy antiretroviral therapy. The majority of study patients had previously been treated with =10 antiretroviral medications [L1554]. | Trogarzo safety and effectiveness have been confirmed in a clinical trial of 40 patients who suffer multidrug-resistant HIV. The majority of these patients experienced a substantial decrease in their HIV-RNA levels within 7 days after receiving the drug. Approximately 43 percent of patients continued to experience HIV-RNA inhibition after 24 weeks of taking Trogarzo [L1554]. Trogarzo inhibits viral entry into cells, effectively managing HIV-1 infection in those who have attempted other therapies to no avail [L1554]. | Ibalizumab is a monoclonal antibody and viral-entry inhibitor that coats CD4-positive cells, the main target of HIV infection. By blocking viral entry into CD4 cells, ibalizumab creates a barrier for HIV, which is a different mechanism from those of entry inhibitors that target viral proteins or chemokine co-receptors. Ibalizumab is a CD4 domain 2-directed post-attachment HIV-1 inhibitor. This binding specificity of ibalizumab-uiyk to domain 2 of CD4 allows ibalizumab-uiyk to prevent viral entry into host cells without causing immunosuppression. Epitope mapping studies confirm that ibalizumab-uiyk binds to a conformational epitope located mainly in domain 2 of the extracellular region of the CD4 receptor. This epitope is located on the surface of CD4 opposite to the site in domain 1 that is essential for CD4 binding of the MHC class II molecules. This drug, therefore, does not interfere with CD4 cell-mediated immune functions. In addition, ibalizumab-uiyk does not interfere with gp120 attachment to CD4 [FDA label]. Ibalizumab’s post-binding conformational effects block the gp120-CD4 complex from interacting with CCR5 or CXCR4 and thus prevents viral entry and fusion [L1555]. CD4 is an integral cell surface glycoprotein that is able to enhance T cell-specific antigen responses when it interacts with its physiological ligand, class II major histocompatibility (MHC) molecules. In addition, CD4 is a specific cell-surface receptor for the human immunodeficiency virus-1 (HIV-1). The entry of human immunodeficiency virus (HIV) into cells requires the sequential binding of the viral exterior envelope glycoprotein, gp120, with the CD4 glycoprotein and a chemokine receptor on the cell surface. In addition, the CD4/gp120 interaction may directly inhibit T cell function [A32076]. In addition to the above mechanism of action, it was found in one study that ibalizumab-uiyk inhibits the replication of CCR5- and CXCR4- receptor laboratory strains and primary isolates of HIV-1 in phytohemagglutinin-stimulated peripheral blood lymphocytes, further confirming its action [L1559]. | Immune reconstitution inflammatory syndrome has been reported in one patient treated with TROGARZO in combination with other antiretrovirals. During the initial phase of combination antiretroviral therapies, patients whose immune systems respond may develop an inflammatory response to indolent or residual opportunistic infections, which may necessitate further evaluation and treatment [FDA label]. | Metabolized by CD4 receptor internalization, ibalizumab has no significant impact on liver or kidney metabolism [L1560]. | NA | 4.8 L [FDA label] | Following single-dose administrations of ibalizumab-uiyk as 0.5 to 1.5-hour infusions, the area under the concentration-time curve increased in a greater than dose-proportional manner, clearance decreased from 9.54 to 0.36 mL/h/kg and elimination half-life increased from 2.7 to 64 hours as the dose increased from 0.3 to 25 mg/kg [FDA label]. | Antibodies, Monoclonal | NA | NA | NA | NA | T-cell surface glycoprotein CD4,C-C chemokine receptor type 5,C-X-C chemokine receptor type 4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14618 | Th1522 | Ibalizumab | >Th1522_Ibalizumab QVQLQQSGPEVVKPGASVKMSCKASGYTFTSYVIHWVRQKPGQGLDWIGYINPYNDGTDYDEKFKGKATLTSDTSTSTAYMELSSLRSEDTAVYYCAREKDNYATGAWFAYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPSCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | NA | NA | NA | NA | NA | The half-life of ibalizumab is 3 to 3.5 days on average. The half-life was estimated from a multiple-dose study evaluating weekly ibalizumab 10 mg/kg in 1 study arm and biweekly ibalizumab 25 mg/kg in another study arm, given via intravenous (IV) infusion in adults with HIV [L1555]. In one clinical trial, the elimination half-life increased from 2.7 to 64 hours as the dose increased from 0.3 to 25 mg/kg (0.01 to 0.9 times the approved recommended loading dose based on a 70 kg patient) [FDA label]. | Ibalizumab (also known as _ibalizumab-uiyk_ and formerly known as TNX-355) is a monoclonal antibody that binds to CD4 receptors on the surface of CD4-positive cells, preventing HIV particle entry into the lymphocytes. It is an advanced and current antibody in development for the treatment of HIV/AIDS. It has been developed by Taimed biologics and Theratechnologies [L1558, L1554]. This drug was approved in March 2018 for the management of treatment-resistant HIV [L1554]. | Indicated for the treatment of human immunodeficiency virus type 1 (HIV-1) infection in highly treatment-experienced adults with multidrug-resistant HIV-1 infection failing their current antiretroviral regimen [FDA label]. The approval of Trogarzo was supported by a clinical trial of 40 treatment-experienced adults with MDR HIV-1 infection who persistently had elevated levels of HIV RNA in their blood despite heavy antiretroviral therapy. The majority of study patients had previously been treated with =10 antiretroviral medications [L1554]. | Trogarzo safety and effectiveness have been confirmed in a clinical trial of 40 patients who suffer multidrug-resistant HIV. The majority of these patients experienced a substantial decrease in their HIV-RNA levels within 7 days after receiving the drug. Approximately 43 percent of patients continued to experience HIV-RNA inhibition after 24 weeks of taking Trogarzo [L1554]. Trogarzo inhibits viral entry into cells, effectively managing HIV-1 infection in those who have attempted other therapies to no avail [L1554]. | Ibalizumab is a monoclonal antibody and viral-entry inhibitor that coats CD4-positive cells, the main target of HIV infection. By blocking viral entry into CD4 cells, ibalizumab creates a barrier for HIV, which is a different mechanism from those of entry inhibitors that target viral proteins or chemokine co-receptors. Ibalizumab is a CD4 domain 2-directed post-attachment HIV-1 inhibitor. This binding specificity of ibalizumab-uiyk to domain 2 of CD4 allows ibalizumab-uiyk to prevent viral entry into host cells without causing immunosuppression. Epitope mapping studies confirm that ibalizumab-uiyk binds to a conformational epitope located mainly in domain 2 of the extracellular region of the CD4 receptor. This epitope is located on the surface of CD4 opposite to the site in domain 1 that is essential for CD4 binding of the MHC class II molecules. This drug, therefore, does not interfere with CD4 cell-mediated immune functions. In addition, ibalizumab-uiyk does not interfere with gp120 attachment to CD4 [FDA label]. Ibalizumab’s post-binding conformational effects block the gp120-CD4 complex from interacting with CCR5 or CXCR4 and thus prevents viral entry and fusion [L1555]. CD4 is an integral cell surface glycoprotein that is able to enhance T cell-specific antigen responses when it interacts with its physiological ligand, class II major histocompatibility (MHC) molecules. In addition, CD4 is a specific cell-surface receptor for the human immunodeficiency virus-1 (HIV-1). The entry of human immunodeficiency virus (HIV) into cells requires the sequential binding of the viral exterior envelope glycoprotein, gp120, with the CD4 glycoprotein and a chemokine receptor on the cell surface. In addition, the CD4/gp120 interaction may directly inhibit T cell function [A32076]. In addition to the above mechanism of action, it was found in one study that ibalizumab-uiyk inhibits the replication of CCR5- and CXCR4- receptor laboratory strains and primary isolates of HIV-1 in phytohemagglutinin-stimulated peripheral blood lymphocytes, further confirming its action [L1559]. | Immune reconstitution inflammatory syndrome has been reported in one patient treated with TROGARZO in combination with other antiretrovirals. During the initial phase of combination antiretroviral therapies, patients whose immune systems respond may develop an inflammatory response to indolent or residual opportunistic infections, which may necessitate further evaluation and treatment [FDA label]. | Metabolized by CD4 receptor internalization, ibalizumab has no significant impact on liver or kidney metabolism [L1560]. | NA | 4.8 L [FDA label] | Following single-dose administrations of ibalizumab-uiyk as 0.5 to 1.5-hour infusions, the area under the concentration-time curve increased in a greater than dose-proportional manner, clearance decreased from 9.54 to 0.36 mL/h/kg and elimination half-life increased from 2.7 to 64 hours as the dose increased from 0.3 to 25 mg/kg [FDA label]. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | T-cell surface glycoprotein CD4,C-C chemokine receptor type 5,C-X-C chemokine receptor type 4 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14652 | 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 | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14662 | Th1525 | Carlumab | NA | NA | NA | NA | NA | NA | NA | Carlumab has been used in trials studying the treatment of Cancer and Prostate Cancer. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14686 | Th1527 | Demcizumab | NA | NA | NA | NA | NA | NA | NA | Demcizumab is under investigation for the treatment of Nonsquamous Nonsmall Cell Neoplasm of Lung. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14687 | Th1527 | Demcizumab | NA | NA | NA | NA | NA | NA | NA | Demcizumab is under investigation for the treatment of Nonsquamous Nonsmall Cell Neoplasm of Lung. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14688 | Th1527 | Demcizumab | NA | NA | NA | NA | NA | NA | NA | Demcizumab is under investigation for the treatment of Nonsquamous Nonsmall Cell Neoplasm of Lung. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14696 | Th1528 | Brontictuzumab | NA | NA | NA | NA | NA | NA | NA | Brontictuzumab has been used in trials studying the treatment of Adenoid Cystic Carcinoma, Relapsed or Refractory Solid Tumors, and Relapsed or Refractory Lymphoid Malignancies. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14697 | Th1528 | Brontictuzumab | NA | NA | NA | NA | NA | NA | NA | Brontictuzumab has been used in trials studying the treatment of Adenoid Cystic Carcinoma, Relapsed or Refractory Solid Tumors, and Relapsed or Refractory Lymphoid Malignancies. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14709 | Th1530 | Sifalimumab | >Th1530_Sifalimumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTSYSISWVRQAPGQGLEWMGWISVYNGNTNYAQKFQGRVTMTTDTSTSTAYLELRSLRSDDTAVYYCARDPIAAGYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Sifalimumab is a fully human monoclonal antibody targeting interferon-alpha. The levels of interferon-alpha are elevated in many patients with active systemic lupus erythematosus (SLE, or lupus) and other autoimmune disorders, and may be associated with disease activity. Sifalimumab may suppress the abnormal immune activity associated with lupus by binding to multiple interferon-alpha subtypes seen in the serum of lupus patients. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Interferon alpha-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14718 | Th1531 | Abituzumab | NA | NA | NA | NA | NA | NA | NA | Abituzumab has been used in trials studying the treatment of Prostate Cancer Metastatic. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14719 | Th1531 | Abituzumab | NA | NA | NA | NA | NA | NA | NA | Abituzumab has been used in trials studying the treatment of Prostate Cancer Metastatic. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14720 | Th1531 | Abituzumab | NA | NA | NA | NA | NA | NA | NA | Abituzumab has been used in trials studying the treatment of Prostate Cancer Metastatic. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14728 | 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 | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14729 | 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 | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14739 | Th1533 | Naptumomab estafenatox | NA | NA | NA | NA | NA | NA | NA | Naptumomab Estafenatox has been used in trials studying the treatment of Pancreatic Cancer, Renal Cell Carcinoma, and Non-Small-Cell Lung Carcinoma. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14760 | Th1535 | Crotedumab | NA | NA | NA | NA | NA | NA | NA | Crotedumab has been used in trials studying the treatment of Diabetes Mellitus, Type 2. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14768 | Th1536 | Concizumab | NA | NA | NA | NA | NA | NA | NA | Concizumab has been used in trials studying the treatment of Haemophilia A and Congenital Bleeding Disorder. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14769 | Th1536 | Concizumab | NA | NA | NA | NA | NA | NA | NA | Concizumab has been used in trials studying the treatment of Haemophilia A and Congenital Bleeding Disorder. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14770 | Th1536 | Concizumab | NA | NA | NA | NA | NA | NA | NA | Concizumab has been used in trials studying the treatment of Haemophilia A and Congenital Bleeding Disorder. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14788 | Th1538 | Monalizumab | NA | NA | NA | NA | NA | NA | NA | Monalizumab has been used in trials studying the treatment of Gynecologic Cancer, Chronic Lymphocytic Leukemia, and Squamous Cell Carcinoma of the Oral Cavity. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14789 | Th1538 | Monalizumab | NA | NA | NA | NA | NA | NA | NA | Monalizumab has been used in trials studying the treatment of Gynecologic Cancer, Chronic Lymphocytic Leukemia, and Squamous Cell Carcinoma of the Oral Cavity. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14795 | Th1539 | Depatuxizumab | >Th1539_Depatuxizumab QVQLQESGPGLVKPSQTLSLTCTVSGYSISSDFAWNWIRQPPGKGLEWMGYISYSGNTRYQPSLKSRITISRDTSKNQFFLKLNSVTAADTATYYCVTAGRGFPYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Depatuxizumab has been used in trials studying the treatment and diagnostic of Adenocarcinoma and Advanced Solid Tumors. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14796 | Th1539 | Depatuxizumab | >Th1539_Depatuxizumab QVQLQESGPGLVKPSQTLSLTCTVSGYSISSDFAWNWIRQPPGKGLEWMGYISYSGNTRYQPSLKSRITISRDTSKNQFFLKLNSVTAADTATYYCVTAGRGFPYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Depatuxizumab has been used in trials studying the treatment and diagnostic of Adenocarcinoma and Advanced Solid Tumors. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14811 | Th1541 | Rontalizumab | NA | NA | NA | NA | NA | NA | NA | Rontalizumab has been used in trials studying the treatment of Systemic Lupus Erythematosus. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14812 | Th1541 | Rontalizumab | NA | NA | NA | NA | NA | NA | NA | Rontalizumab has been used in trials studying the treatment of Systemic Lupus Erythematosus. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14813 | Th1541 | Rontalizumab | NA | NA | NA | NA | NA | NA | NA | Rontalizumab has been used in trials studying the treatment of Systemic Lupus Erythematosus. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14821 | Th1542 | Amatuximab | >Th1542_Amatuximab QVQLQQSGPELEKPGASVKISCKASGYSFTGYTMNWVKQSHGKSLEWIGLITPYNGASSYNQKFRGKATLTVDKSSSTAYMDLLSLTSEDSAVYFCARGGYDGRGFDYWGSGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Amatuximab has been used in trials studying the treatment and basic science of Mesothelioma, Ovarian Cancer, Ovarian Neoplasms, Pancreatic Cancer, and Mesothelioma, Malignant, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Mesothelin | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14829 | Th1543 | Clazakizumab | NA | NA | NA | NA | NA | NA | NA | Clazakizumab has been used in trials studying the treatment of Rheumatoid Arthritis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14830 | Th1543 | Clazakizumab | NA | NA | NA | NA | NA | NA | NA | Clazakizumab has been used in trials studying the treatment of Rheumatoid Arthritis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14831 | Th1543 | Clazakizumab | NA | NA | NA | NA | NA | NA | NA | Clazakizumab has been used in trials studying the treatment of Rheumatoid Arthritis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14855 | Th1547 | Ozanezumab | NA | NA | NA | NA | NA | NA | NA | Ozanezumab has been used in trials studying the treatment of Multiple Sclerosis, Amyotrophic Lateral Sclerosis, and Multiple Sclerosis, Relapsing-Remitting. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14856 | Th1547 | Ozanezumab | NA | NA | NA | NA | NA | NA | NA | Ozanezumab has been used in trials studying the treatment of Multiple Sclerosis, Amyotrophic Lateral Sclerosis, and Multiple Sclerosis, Relapsing-Remitting. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14857 | Th1547 | Ozanezumab | NA | NA | NA | NA | NA | NA | NA | Ozanezumab has been used in trials studying the treatment of Multiple Sclerosis, Amyotrophic Lateral Sclerosis, and Multiple Sclerosis, Relapsing-Remitting. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14866 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Antibodies | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14867 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Antibodies, Monoclonal | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14868 | Th1548 | Sacituzumab govitecan | NA | NA | NA | NA | NA | NA | Sacituzumab govitecan has a mean half-life of 16 hours, while free SN-38 has a mean half-life of 18 hours.[L13002, A193731] | Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents.[A193653] Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment.[A193671] One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38.[L13002, A193674] Sacituzumab govitecan was granted FDA approval on April 22nd, 2020 and is marketed under the brand name Trodelvy™ by Immunomedics, Inc.; it is currently indicated under accelerated approval for the treatment of mTNBC patients who have undergone two or more prior therapies. As a targeted cytotoxic agent, it is hoped to provide similar efficacy with reduced adverse effects.[A193653] In November 2021, sacituzumab govitecan was also approved by the European Commission.[L39372] | Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease.[L13002] Sacituzumab govitecan is also indicated for the treatment of locally advanced or metastatic urothelial cancer in adult patients who have received previous platinum-based therapy and either a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor. This indication has been approved under accelerated approval, and continued approval may be contingent on the demonstration of clinical benefit in confirmatory trials.[L13002] | Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia.[L13002] | Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.[L13002, A193662] The proposed mechanism of action first involves the binding of the RS7 component to TROP-2, which is highly expressed on the cell surface of multiple cancers.[A193671] Binding of RS7 to TROP-2 results in rapid internalization of bound antibody[A193656, A193659], and the likely intracellular release of SN-38 via hydrolysis of the CL2A linker[L13002, A193674]. SN-38 is an active metabolite of the anti-cancer drug [irinotecan], which is thought to work primarily through inhibition of DNA topoisomerase I, leading to DNA damage and eventual cell death.[A193665] In addition, recent work has identified a possible secondary mechanism of action for SN-38 by disrupting the binding of Far Upstream Binding Protein 1 (FUBP1) to the _FUSE_ elements regulating oncogene expression.[A193668] In addition to SN-38-mediated cell death, there is also some evidence that the RS7 component of the conjugate drug possesses antibody-directed cellular toxicity.[A193674, A193662] | Toxicity information regarding sacituzumab govitecan is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as neutropenia, diarrhea, hypersensitivity, nausea/vomiting, and other systemic effects related to cytotoxic drugs. Symptomatic and supportive measures are recommended.[L13002] | The metabolism of sacituzumab govitecan has not been extensively studied. The SN-38 moiety is known to undergo O-glucuronidation by UGT1A1, presumably in the liver, and the SN-38 glucuronide metabolite SN-38G is found in the serum of patients undergoing treatment.[L13002, A193665] | In patients receiving 10 mg/kg sacituzumab govitecan the Cmax of the conjugate was 243,000 ± 45,600 ng/mL while the Cmax of free SN-38 was 127 ± 60 ng/mL. Similarly, the AUC0-168 for the conjugate/free SN-38 was 5,210,000 ± 1,230,000 and 3,900 ± 1,830 ng | Sacituzumab govitecan has a mean volume of distribution of 0.045 L/kg.[L13002] | Sacituzumab govitecan has a clearance rate of 0.002 L/h/kg.[L13002] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Tumor-associated calcium signal transducer 2,DNA topoisomerase 1,Far upstream element-binding protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-2-amino-3-[1-[[4-[[1-[2-[2-[2-[2-[2-[2-[2-[2-[2-[[2-[2-[[(2S)-6-amino-1-[4-[[(19S)-10,19-diethyl-7-hydroxy-14,18-dioxo-17-oxa-3,13-diazapentacyclo[11.8.0.02,11.04,9.015,20]henicosa-1(21),2,4(9),5,7,10,15(20)-heptaen-19-yl]oxycarbonyloxymethyl]anilino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]acetyl]amino]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethyl]triazol-4-yl]methylcarbamoyl]cyclohexyl]methyl]-2,5-dioxopyrrolidin-3-yl]sulfanylpropanoic acid | NA | Link | NA | NA |
| 14899 | Th1550 | Bimekizumab | NA | NA | NA | NA | NA | NA | NA | Bimekizumab has been used in trials studying the treatment of Psoriatic arthritis, Ankylosing Spondylitis, Chronic Plaque Psoriasis, and Mild to Moderate Psoriasis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14900 | Th1550 | Bimekizumab | NA | NA | NA | NA | NA | NA | NA | Bimekizumab has been used in trials studying the treatment of Psoriatic arthritis, Ankylosing Spondylitis, Chronic Plaque Psoriasis, and Mild to Moderate Psoriasis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14901 | Th1550 | Bimekizumab | NA | NA | NA | NA | NA | NA | NA | Bimekizumab has been used in trials studying the treatment of Psoriatic arthritis, Ankylosing Spondylitis, Chronic Plaque Psoriasis, and Mild to Moderate Psoriasis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14909 | Th1551 | Milatuzumab | NA | NA | NA | NA | NA | NA | NA | Milatuzumab has been used in trials studying the treatment of Lupus Nephritis, Multiple Myeloma (MM), GVHD (Acute or Chronic), Myelodysplastic Syndrome, and Chronic Lymphocytic Leukemia, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14910 | Th1551 | Milatuzumab | NA | NA | NA | NA | NA | NA | NA | Milatuzumab has been used in trials studying the treatment of Lupus Nephritis, Multiple Myeloma (MM), GVHD (Acute or Chronic), Myelodysplastic Syndrome, and Chronic Lymphocytic Leukemia, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14911 | Th1551 | Milatuzumab | NA | NA | NA | NA | NA | NA | NA | Milatuzumab has been used in trials studying the treatment of Lupus Nephritis, Multiple Myeloma (MM), GVHD (Acute or Chronic), Myelodysplastic Syndrome, and Chronic Lymphocytic Leukemia, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14932 | Th1553 | Robatumumab | NA | NA | NA | NA | NA | NA | NA | Robatumumab has been used in trials studying the treatment of Osteosarcoma, Sarcoma, Ewing's, and Peripheral Neuroectodermal Tumor. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14940 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | Antibodies, Monoclonal | NA | NA | NA | NA | Nectin-4 | Padcev | Seagen Inc. | Seagen Inc. | Intravenous | 30 mg / vial | None. | fatigue, numbness and tingling in extremities, decreased appetite, rash, hair loss, nausea, changes in taste, diarrhea, dry eye, itching, dry skin, dry eye, and vomiting | Padcev is an anticancer medicine that affects the growth and cell division of cancer cells. Padcev is a prescription medicine used to treat adults with cancer of the bladder or urinary tract (renal pelvis, ureter or urethra). Padcev is used when the cancer is advanced, has spread to other parts of the... | PADCEV® is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer (mUC) who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced or metastatic setting. | NA | These are not all of the possible side effects of PADCEV. | Link | Link | NA |
| 14941 | Th1554 | Enfortumab vedotin | NA | 152000 | NA | NA | NA | NA | The elimination half-lives of enfortumab vedotin and MMAE are 3.4 days and 2.4 days, respectively.[L10836] | Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers.[L10836] It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link.[L10836] It is similar to [brentuximab vedotin], another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. The clinical development of enfortumab vedotin was the result of a collaboration between Astellas Pharma and Seattle Genetics[A188868] and it was first approved for use in the United States in December 2019 under the brand name PadcevTM.[L10836] | Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting.[L10836] | Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate.[L10836] Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment.[L10836] Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl.[L10836] | Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components.[L10836] It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers,[A188865] attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.[L10836] | Toxicity information regarding enfortumab vedotin is not readily available. Patients experiencing an overdose are likely at an increased risk of severe adverse effects such as significant nausea, vomiting, neuropathy, or rash.[L10836] Symptomatic and supportive measures are recommended. | The catabolism of enfortumab vedotin has not been studied in humans.[L10836] Given its structure, it is expected to be catabolized to smaller peptides, amino acids, unconjugated MMAE, and MMAE metabolites. MMAE is released from enfortumab vedotin via proteolytic cleavage by intracellular proteases and is metabolized primarily by CYP3A4 _in vitro_.[L10836] | Following the first treatment cycle, Cmax and AUC0-28d for enfortumab vedotin were 28 µg/mL and 111 µg.d/mL, respectively. The Cmax and AUC0-28d of unconjugated MMAE following the same cycle were 4.8 ng/mL and 69 ng.d/mL, respectively.[L10836] The Tmax of MMAE is 1-3 days following the end of the infusion.[A188865] | The estimated steady-state volume of distribution is 11 L.[L10836] | The mean clearance of enfortumab vedotin and free MMAE was 0.10 L/h and 2.7 L/h, respectively.[L10836] The clearance of MMAE appears to be limited by its rate of release from enfortumab vedotin. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Nectin-4 | Padcev Ejfv | Seagen Inc. | Seagen Inc. | Intravenous | 20 mg/2mL | None. | received an immunotherapy medicine and also received a chemotherapy-containing platinum medicine. | It is given as an infusion (drip) into a vein over 30 minutes. The patient should have an infusion three times over the course of 28 days (on days 1, 8 and 15) and should continue treatment until the disease gets worse or the side effects become intolerable. | The active substance in Padcev, enfortumab vedotin, consists of an antibody (a type of protein) combined with another substance known as MMAE. The antibody first attaches to a protein on the surface of cancer cells to gain entry into the cells. Once the active substance is inside the cells, MMAE disrupts the cells’ internal skeleton, causing cell death and helping to stop the cancer from getting worse or spreading. | NA | NA | Link | Link | NA |
| 14954 | Th1555 | Rovalpituzumab tesirine | NA | NA | NA | NA | NA | NA | NA | Rovalpituzumab Tesirine has been used in trials studying the treatment of GLIOBLASTOMA, Malignant Melanoma, Other Solid Tumors, Small Cell Lung Cancer, and Medullary Thyroid Cancer, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-3-[(3R)-1-[3-[2-[2-[2-[2-[2-[2-[2-[2-[3-[[(2S)-1-[[(2S)-1-[4-[[(6S,6aS)-3-[5-[[(6aS)-2-methoxy-8-methyl-11-oxo-6a,7-dihydropyrrolo[2,1-c][1,4]benzodiazepin-3-yl]oxy]pentoxy]-6-hydroxy-2-methoxy-8-methyl-11-oxo-6a,7-dihydro-6H-pyrrolo[2,1-c][1,4]benzodiazepine-5-carbonyl]oxymethyl]anilino]-1-oxopropan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-3-oxopropoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethylamino]-3-oxopropyl]-2,5-dioxopyrrolidin-3-yl]sulfanyl-2-aminopropanoic acid | NA | Link | NA | NA |
| 14955 | Th1555 | Rovalpituzumab tesirine | NA | NA | NA | NA | NA | NA | NA | Rovalpituzumab Tesirine has been used in trials studying the treatment of GLIOBLASTOMA, Malignant Melanoma, Other Solid Tumors, Small Cell Lung Cancer, and Medullary Thyroid Cancer, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-3-[(3R)-1-[3-[2-[2-[2-[2-[2-[2-[2-[2-[3-[[(2S)-1-[[(2S)-1-[4-[[(6S,6aS)-3-[5-[[(6aS)-2-methoxy-8-methyl-11-oxo-6a,7-dihydropyrrolo[2,1-c][1,4]benzodiazepin-3-yl]oxy]pentoxy]-6-hydroxy-2-methoxy-8-methyl-11-oxo-6a,7-dihydro-6H-pyrrolo[2,1-c][1,4]benzodiazepine-5-carbonyl]oxymethyl]anilino]-1-oxopropan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-3-oxopropoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethylamino]-3-oxopropyl]-2,5-dioxopyrrolidin-3-yl]sulfanyl-2-aminopropanoic acid | NA | Link | NA | NA |
| 14956 | Th1555 | Rovalpituzumab tesirine | NA | NA | NA | NA | NA | NA | NA | Rovalpituzumab Tesirine has been used in trials studying the treatment of GLIOBLASTOMA, Malignant Melanoma, Other Solid Tumors, Small Cell Lung Cancer, and Medullary Thyroid Cancer, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2R)-3-[(3R)-1-[3-[2-[2-[2-[2-[2-[2-[2-[2-[3-[[(2S)-1-[[(2S)-1-[4-[[(6S,6aS)-3-[5-[[(6aS)-2-methoxy-8-methyl-11-oxo-6a,7-dihydropyrrolo[2,1-c][1,4]benzodiazepin-3-yl]oxy]pentoxy]-6-hydroxy-2-methoxy-8-methyl-11-oxo-6a,7-dihydro-6H-pyrrolo[2,1-c][1,4]benzodiazepine-5-carbonyl]oxymethyl]anilino]-1-oxopropan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-3-oxopropoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethoxy]ethylamino]-3-oxopropyl]-2,5-dioxopyrrolidin-3-yl]sulfanyl-2-aminopropanoic acid | NA | Link | NA | NA |
| 14976 | Th1557 | Namilumab | NA | NA | NA | NA | NA | NA | NA | Namilumab has been used in trials studying the treatment of Plaque Psoriasis and Rheumatoid Arthritis. | NA | NA | Namilumab is a human antibody which neutralizes the activity of granulocyte/macrophage colony stimulating factor (GM-CSF), which has potential applications in the treatment of various inflammatory and autoimmune diseases, such as rheumatoid arthritis, psoriasis, or multiple sclerosis. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14984 | Th1558 | Racotumomab | NA | NA | NA | NA | NA | NA | NA | Racotumomab has been used in trials studying the treatment of Glioma, Wilm's Tumor, Neuroblastoma, Retinoblastoma, and Ewing's Sarcoma. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14992 | Th1559 | Tregalizumab | NA | NA | NA | NA | NA | NA | NA | Tregalizumab has been used in trials studying the treatment of Rheumatoid Arthritis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14993 | Th1559 | Tregalizumab | NA | NA | NA | NA | NA | NA | NA | Tregalizumab has been used in trials studying the treatment of Rheumatoid Arthritis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14994 | Th1559 | Tregalizumab | NA | NA | NA | NA | NA | NA | NA | Tregalizumab has been used in trials studying the treatment of Rheumatoid Arthritis. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15006 | Th1561 | Olokizumab | NA | NA | NA | NA | NA | NA | When administered either intravenously or subcutaneously to healthy volunteers, olokizumab has a half-life of 22.7-47.4 days.[A241195] | Interleukin-6 (IL-6) is an important cytokine with roles in immune cell proliferation/differentiation, energy and bone metabolism, and the acute phase response of the innate immune system. IL-6 pathway dysregulation is associated with chronic inflammation and lymphoproliferation, including in autoimmune conditions such as rheumatoid arthritis, Castleman disease, and cytokine release syndrome. Targeting IL-6 function can be achieved directly, or through interrupting the IL-6 receptor or gp130 receptor axes.[A241185, A241175] Olokizumab is a humanized anti-IL-6 IgG4 | NA | NA | Interleukin-6 (IL-6) plays a role in numerous autoimmune diseases by perpetuating tissue damage and inflammation. IL-6 acts as an essential differentiation factor for TH17 cells, which, when activated through dendritic cells displaying antigen-specific signals, induce tissue damage and act pathogenically. IL-6 also functions in B cell differentiation and development, including in the production of pathogenic autoantibodies. Combined with other roles for IL-6 in cell proliferation and differentiation, these mechanisms underly the importance of IL-6 in a variety of autoimmune conditions.[A241185, A241175] IL-6 signalling involves a corresponding IL-6 receptor (IL-6R/gp80/CD126) and a co-receptor gp130 (CD130).[A241185] Complex assembly is thought to involve binding of IL-6 to gp80 at Site 1 followed by binding to gp130 at Site 2 to form a heterotrimer; two heterotrimers then combine through Site 3 on IL-6 binding to domain 1 of gp130. The resulting heterohexameric complex is responsible for signal transduction.[A241175] Curiously, although IL-6R is typically membrane-bound, it can also exist in a soluble form (sIL-6R) through limited proteolysis or alternative splicing. This leads to three distinct signalling paradigms: classic signalling, where IL-6R and gp130 exist within the same cell membrane, _trans_-signalling, where sIL-6R interacts with membrane-bound gp130, and _trans_-presentation, where IL-6R from one cell forms a complex with gp130 on a different cell. It is thought that _trans_-signalling is responsible for the majority of IL-6-associated pathology.[A241185, A241175] Olokizumab is a humanized anti-IL-6 IgG4 | NA | NA | Olokizumab administered as a single escalating subcutaneous dose in healthy volunteers had a Cmax between 2.99 ± 0.271 and 22.3 ± 4.48 µg/mL for doses between 0.3 and 3.0 mg/kg. The maximum concentration was achieved at a median of between 120 and 336 hours. The corresponding AUC0-t and AUC0-8 ranges were 2,704 ± 886 to 24,723 ± 2,145 and 2,988 ± 1,124 to 30,444 ± 4,913 µg | When administered either intravenously or subcutaneously to healthy volunteers, olokizumab has a volume of distribution between 5.59-9.71 L.[A241195] | When administered either intravenously or subcutaneously to healthy volunteers, olokizumab has a clearance of 0.116-0.204 L/day.[A241195] | Antibodies | NA | NA | NA | NA | Interleukin-6 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15007 | Th1561 | Olokizumab | NA | NA | NA | NA | NA | NA | When administered either intravenously or subcutaneously to healthy volunteers, olokizumab has a half-life of 22.7-47.4 days.[A241195] | Interleukin-6 (IL-6) is an important cytokine with roles in immune cell proliferation/differentiation, energy and bone metabolism, and the acute phase response of the innate immune system. IL-6 pathway dysregulation is associated with chronic inflammation and lymphoproliferation, including in autoimmune conditions such as rheumatoid arthritis, Castleman disease, and cytokine release syndrome. Targeting IL-6 function can be achieved directly, or through interrupting the IL-6 receptor or gp130 receptor axes.[A241185, A241175] Olokizumab is a humanized anti-IL-6 IgG4 | NA | NA | Interleukin-6 (IL-6) plays a role in numerous autoimmune diseases by perpetuating tissue damage and inflammation. IL-6 acts as an essential differentiation factor for TH17 cells, which, when activated through dendritic cells displaying antigen-specific signals, induce tissue damage and act pathogenically. IL-6 also functions in B cell differentiation and development, including in the production of pathogenic autoantibodies. Combined with other roles for IL-6 in cell proliferation and differentiation, these mechanisms underly the importance of IL-6 in a variety of autoimmune conditions.[A241185, A241175] IL-6 signalling involves a corresponding IL-6 receptor (IL-6R/gp80/CD126) and a co-receptor gp130 (CD130).[A241185] Complex assembly is thought to involve binding of IL-6 to gp80 at Site 1 followed by binding to gp130 at Site 2 to form a heterotrimer; two heterotrimers then combine through Site 3 on IL-6 binding to domain 1 of gp130. The resulting heterohexameric complex is responsible for signal transduction.[A241175] Curiously, although IL-6R is typically membrane-bound, it can also exist in a soluble form (sIL-6R) through limited proteolysis or alternative splicing. This leads to three distinct signalling paradigms: classic signalling, where IL-6R and gp130 exist within the same cell membrane, _trans_-signalling, where sIL-6R interacts with membrane-bound gp130, and _trans_-presentation, where IL-6R from one cell forms a complex with gp130 on a different cell. It is thought that _trans_-signalling is responsible for the majority of IL-6-associated pathology.[A241185, A241175] Olokizumab is a humanized anti-IL-6 IgG4 | NA | NA | Olokizumab administered as a single escalating subcutaneous dose in healthy volunteers had a Cmax between 2.99 ± 0.271 and 22.3 ± 4.48 µg/mL for doses between 0.3 and 3.0 mg/kg. The maximum concentration was achieved at a median of between 120 and 336 hours. The corresponding AUC0-t and AUC0-8 ranges were 2,704 ± 886 to 24,723 ± 2,145 and 2,988 ± 1,124 to 30,444 ± 4,913 µg | When administered either intravenously or subcutaneously to healthy volunteers, olokizumab has a volume of distribution between 5.59-9.71 L.[A241195] | When administered either intravenously or subcutaneously to healthy volunteers, olokizumab has a clearance of 0.116-0.204 L/day.[A241195] | Antibodies, Monoclonal | NA | NA | NA | NA | Interleukin-6 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15008 | Th1561 | Olokizumab | NA | NA | NA | NA | NA | NA | When administered either intravenously or subcutaneously to healthy volunteers, olokizumab has a half-life of 22.7-47.4 days.[A241195] | Interleukin-6 (IL-6) is an important cytokine with roles in immune cell proliferation/differentiation, energy and bone metabolism, and the acute phase response of the innate immune system. IL-6 pathway dysregulation is associated with chronic inflammation and lymphoproliferation, including in autoimmune conditions such as rheumatoid arthritis, Castleman disease, and cytokine release syndrome. Targeting IL-6 function can be achieved directly, or through interrupting the IL-6 receptor or gp130 receptor axes.[A241185, A241175] Olokizumab is a humanized anti-IL-6 IgG4 | NA | NA | Interleukin-6 (IL-6) plays a role in numerous autoimmune diseases by perpetuating tissue damage and inflammation. IL-6 acts as an essential differentiation factor for TH17 cells, which, when activated through dendritic cells displaying antigen-specific signals, induce tissue damage and act pathogenically. IL-6 also functions in B cell differentiation and development, including in the production of pathogenic autoantibodies. Combined with other roles for IL-6 in cell proliferation and differentiation, these mechanisms underly the importance of IL-6 in a variety of autoimmune conditions.[A241185, A241175] IL-6 signalling involves a corresponding IL-6 receptor (IL-6R/gp80/CD126) and a co-receptor gp130 (CD130).[A241185] Complex assembly is thought to involve binding of IL-6 to gp80 at Site 1 followed by binding to gp130 at Site 2 to form a heterotrimer; two heterotrimers then combine through Site 3 on IL-6 binding to domain 1 of gp130. The resulting heterohexameric complex is responsible for signal transduction.[A241175] Curiously, although IL-6R is typically membrane-bound, it can also exist in a soluble form (sIL-6R) through limited proteolysis or alternative splicing. This leads to three distinct signalling paradigms: classic signalling, where IL-6R and gp130 exist within the same cell membrane, _trans_-signalling, where sIL-6R interacts with membrane-bound gp130, and _trans_-presentation, where IL-6R from one cell forms a complex with gp130 on a different cell. It is thought that _trans_-signalling is responsible for the majority of IL-6-associated pathology.[A241185, A241175] Olokizumab is a humanized anti-IL-6 IgG4 | NA | NA | Olokizumab administered as a single escalating subcutaneous dose in healthy volunteers had a Cmax between 2.99 ± 0.271 and 22.3 ± 4.48 µg/mL for doses between 0.3 and 3.0 mg/kg. The maximum concentration was achieved at a median of between 120 and 336 hours. The corresponding AUC0-t and AUC0-8 ranges were 2,704 ± 886 to 24,723 ± 2,145 and 2,988 ± 1,124 to 30,444 ± 4,913 µg | When administered either intravenously or subcutaneously to healthy volunteers, olokizumab has a volume of distribution between 5.59-9.71 L.[A241195] | When administered either intravenously or subcutaneously to healthy volunteers, olokizumab has a clearance of 0.116-0.204 L/day.[A241195] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Interleukin-6 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15038 | Th1564 | Bezlotoxumab | >Th1564_Bezlotoxumab EVQLVQSGAEVKKSGESLKISCKGSGYSFTSYWIGWVRQMPGKGLEWMGIFYPGDSSTRYSPSFQGQVTISADKSVNTAYLQWSSLKASDTAMYYCARRRNWGNAFDIWGQGTMVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | 19 Days | Bezlotoxumab is a human monoclonal antibody that binds to Clostridium difficile toxin B and neutralizes its effects. Used to reduce the recurrence of Clostridium difficle infection in adults receiving antibiotic therapy to treat C. difficile infection and high risk of recurrence. | Prevents recurrence of Clostridium difficile infection in people 18 years or older who are either currently receiving treatment for C. difficile infection or have a high risk of recurrence. | Bezlotoxumab binds to C.difficile toxin B, a virulence factor common to practically all C.difficile, which prevents the bacteria from infecting host cells. Bezlotoxumab binds two epitopes of toxin B, via two Fab regions, which partially blocks the carbohydrate binding pockets of the toxin resulting in the prevention of toxin B from binding to host cells. | A single molecule of bezlotoxumab neutralizes Toxin B by binding its two Fab regions to two epitopes within the N-terminal half of the Toxin B CROP domain, partially blocking the carbohydrate binding pockets of the toxin and preventing toxin binding to host cells. | No data available on overdosage. | Catabolism | Not absorbed since give IV | 7.33L | 0.317 L/day | Antibodies | NA | NA | NA | NA | Clostridium difficile Toxin B | Zinplava | Merck Sharp & Dohme B.V. | Merck Sharp & Dohme B.V. | Intravenous | 25 mg/ml | None. | nausea, fever, and headache. | Zinplava is a monoclonal antibody. Monoclonal antibodies are made to target only certain cells in the body. Bezlotoxumab works by binding to a specific toxin produced by the Clostridium difficile bacteria, to help neutralize the toxin's effects. Zinplava is used together with antibiotic medicine in adults... | Zinplava is a prescription medicine used to treat the symptoms of Clostridium difficile infection (CDI). Zinplava may be used alone or with other medications. | NA | Bezlotoxumab is a human monoclonal antibody that binds to C. difficile toxin B and neutralizes its effects. Bezlotoxumab is an IgG1 immunoglobulin with an approximate molecular weight of 148.2 kDa. | Link | Link | NA |
| 15039 | Th1564 | Bezlotoxumab | >Th1564_Bezlotoxumab EVQLVQSGAEVKKSGESLKISCKGSGYSFTSYWIGWVRQMPGKGLEWMGIFYPGDSSTRYSPSFQGQVTISADKSVNTAYLQWSSLKASDTAMYYCARRRNWGNAFDIWGQGTMVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | 19 Days | Bezlotoxumab is a human monoclonal antibody that binds to Clostridium difficile toxin B and neutralizes its effects. Used to reduce the recurrence of Clostridium difficle infection in adults receiving antibiotic therapy to treat C. difficile infection and high risk of recurrence. | Prevents recurrence of Clostridium difficile infection in people 18 years or older who are either currently receiving treatment for C. difficile infection or have a high risk of recurrence. | Bezlotoxumab binds to C.difficile toxin B, a virulence factor common to practically all C.difficile, which prevents the bacteria from infecting host cells. Bezlotoxumab binds two epitopes of toxin B, via two Fab regions, which partially blocks the carbohydrate binding pockets of the toxin resulting in the prevention of toxin B from binding to host cells. | A single molecule of bezlotoxumab neutralizes Toxin B by binding its two Fab regions to two epitopes within the N-terminal half of the Toxin B CROP domain, partially blocking the carbohydrate binding pockets of the toxin and preventing toxin binding to host cells. | No data available on overdosage. | Catabolism | Not absorbed since give IV | 7.33L | 0.317 L/day | Antibodies, Monoclonal | NA | NA | NA | NA | Clostridium difficile Toxin B | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15230 | Th1575 | Edrecolomab | NA | NA | NA | NA | NA | NA | NA | 0 | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15231 | Th1575 | Edrecolomab | NA | NA | NA | NA | NA | NA | NA | 0 | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15272 | Th1580 | Human cytomegalovirus immune globulin | NA | NA | NA | NA | NA | NA | IgG1 has a half-life of 23—25 days, whereas, the half-life of IgG3 is only 9 days [L2227]. | Cytomegalovirus immunoglobulin is obtained from pooled adult human plasma selected for high titers of antibody for cytomegalovirus (CMV). It contains purified immunoglobulin G (IgG) antibodies targeting cytomegalovirus (CMV)[FDA label]. Cytomegalovirus, a member of the herpes virus family, is ubiquitous the human population, leading to infections which are followed by life-long dormancy in the host with occasional reactivations and recurrent infections. The seroprevalence of antibodies in adults ranges from 40-100 % with an inverse correlation to socioeconomic status. The transmission of cytomegalovirus infection requires intimate contact with infected excretions such as saliva, urine, cervical and vaginal excretions, semen, breast milk and blood [L2228]. CMV infection can lead to a high fever and severe organ-specific damage with significant morbidity and mortality rates. Cytomegalovirus (CMV) may lead to a wide spectrum of infection in immunocompetent hosts. Sites most often involved include the lung (severe community-acquired viral pneumonia), liver (transaminitis), spleen (splenomegaly), GI tract (colitis), CNS (encephalitis), the hematologic system (cytopenias), and multisystem involvement [L2230]. During the span of an individual's life, the virus may reactivate, resulting in repeated shedding and spread of the virus. Molecular mechanisms have been identified by which show that CMVs interfere with the host immune system. Finally, however, the infection is normally controlled by the host's immune response. As a consequence, CMV disease is restricted to the immunocompromised or immunologically immature host, in which it can lead the devastating result of transplant rejection [A32498], [L2229]. | It is used to prevent cytomegalovirus (CMV) disease after organ transplant [L2225]. Cytomegalovirus Immune Globulin Intravenous (Human) is indicated for the prophylaxis of cytomegalovirus disease associated with transplantation of kidney, lung, liver, pancreas, and heart [FDA label]. In transplants of these organs other than the kidney from CMV seropositive donors into seronegative recipients, prophylactic CMV-IGIV should be considered in combination with ganciclovir [FDA label]. | CytoGam (cytomegalovirus immune globulin) contains IgG antibodies representing those of the large number of normal individuals who have contributed to the plasma pools from which the product was derived. The globulin contains a relatively high concentration of antibodies which are directed against cytomegalovirus (CMV). In the case of persons who may possibly be exposed to CMV, CytoGam can increase the relevant antibodies to levels sufficient to prevent or reduce the incidence of serious CMV disease [FDA label]. | CMV—IGIV mainly consists of immunoglobulin G (IgG), specifically subclasses _IgG1_ and _IgG3_. IgG1 and IgG3 play important roles in viral neutralization in addition to tissue protection and complement activation [L2227]. Immunoglobulins, such as CMV-IGIV, inhibit extracellular viruses from infecting their specific target cells. Viral neutralization decreases the capacity of viruses to spread from an extracellular location to an intracellular location. CMV-IGIV inhibits infection of cells with CMV due to the fact that the virus is prevented from accessing key cell membrane targets, or because of interference with uncoating or entry. Cytogam inhibits these process [L2227]. | CMV-IGIV is made from human plasma and, like other plasma products, carries the possibility for transmission of blood-borne viral agents and possibly, the Creutzfeldt-Jakob disease (CJD) prion. The risk of transmission of recognized blood-borne viruses is considered low due to the viral inactivation and removal properties in the Cohn-Oncley cold ethanol [L2228]. **Renal Failure** Renal dysfunction, acute renal failure (ARF), acute tubular necrosis (ATN), proximal tubular nephropathy, osmotic nephrosis, and death reported in patients receiving IGIV. Increases in blood urea nitrogen (BUN) and serum creatinine have occurred as soon as 1–2 days following IGIV treatment and this has progressed to oliguria or anuria [L2231]. **TRALI (transfusion-associated lung injury)** TRALI is characterized by severe respiratory distress, pulmonary edema, hypoxemia, normal left ventricular function, and fever. It typically occurs within 1-6 hours after transfusion of the immunoglobulin. Patients with TRALI should be managed using oxygen therapy combined with ventilatory support [FDA label]. **Hemolysis** Immune Globulin Intravenous (Human) (IGIV) products may contain blood group antibodies which may act as hemolysins and induce in vivo coating of red blood cells with immunoglobulin, causing a positive direct antiglobulin reaction and, sometimes, hemolysis. Hemolytic anemia may develop after IGIV therapy due to enhanced red blood cell sequestration [FDA label]. ****Thrombotic events **** Patients at risk include those with a history of atherosclerosis, multiple cardiovascular risk factors, advanced age, impaired cardiac output, and/or known or suspected hyperviscosity. The possible risks and benefits of IGIV should be weighed against those of alternative therapies for all patients for whom IGIV administration is being considered. Baseline assessment of blood viscosity are an important consideration for patients at risk for blood hyperviscosity [FDA label]. **Aseptic meningitis syndrome** An aseptic meningitis syndrome (AMS) has been reported to occur infrequently in association with Immune Globulin Intravenous (Human) (IGIV) treatment. The syndrome normally begins within several hours to 2 days after treatment. This syndrome is characterized by symptoms and signs including severe headache, nuchal rigidity, drowsiness, fever, photophobia, painful eye movements, and nausea and vomiting [FDA label]. Cerebrospinal fluid (CSF) studies are frequently positive with pleocytosis up to several thousand cells per cu.mm., predominantly from the granulocytic series, and elevated protein levels up to several hundred mg/dL. Patients experiencing such symptoms and signs must receive a thorough neurological assessment, including CSF studies, to rule out other possible causes of meningitis. This condition may occur more frequently in association with high doses (2 g/kg or greater) of IGIV treatment. Discontinuation of IGIV treatment has been followed by the remission of aseptic meningitis syndrome within several days without long-term sequelae [FDA label]. Cytomegalovirus immune globulin (CMV-IGIV) is categorized in FDA pregnancy risk category C. No well-controlled studies have been completed in pregnant women and it is unknown whether CMV-IGIV may cause female harm or negatively affect the reproductive system. According to the Advisory Committee on Immunization Practices, administration of immune globulin to pregnant women results in no known risk to the fetus [FDA label]. No data are available from the manufacturer regarding the use of cytomegalovirus immune globulin (CMV-IGIV) while breastfeeding and it is unknown whether CMV-IGIV is excreted in breast milk [L2227]. | Cytomegalovirus immune globulin (CMV-IGIV) is administered by the intravenous (IV) route. CMV—IGIV is primarily comprised of immunoglobulin G (IgG), specifically subclasses _IgG1_ and _IgG3_. Immunoglobulin catabolism occurs mainly in the plasma, however, the liver may also play a role [FDA label]. IgG metabolism appears to be a multicompartmental, first-order process. Higher IgG concentrations increase the rate of metabolism and shorten its half-life. IgG metabolism is likely a multicompartmental, first-order process [L2227]. | Protection derived from Cytomegalovirus immune globulin (CMV-IGIV) has a rapid onset, imparting relevant CMV antibody concentrations immediately after infusion. The duration of action of CMV-IGIV is 1—3 months [L2227]. | IgG is distributed from the plasma to various other body compartments [L2227]. | NA | Antibodies | NA | NA | NA | NA | NA | Cytogam | Csl Behring Ag | Csl Behring Ag | Intravenous | 50 mg/1mL | CYTOGAM should not be used in individuals with a history of a prior severe reaction associated with the administration of this or other human immunoglobulin preparations. Persons with selective immunoglobulin A deficiency have the potential for developing antibodies to immunoglobulin A and could have anaphylactic reactions to subsequent administration of blood products that contain immunoglobulin A, including CYTOGAM. | flushing sweating fever chills muscle cramps back/joint pain fever nausea vomiting wheezing and injection site reactions (pain, redness, and swelling) | CMV IG is a sterilized solution made from human plasma. It contains the antibodies to help your body protect itself against infection with cytomegalovirus. CMV IG is used to help prevent infection by cytomegalovirus in people who receive an organ transplant (kidney, heart, liver, lung, or pancreas).... | Cytogam is a prescription medicine used as a prophylaxis to the Cytomegalovirus. Cytogam may be used alone or with other medications. | NA | Liquid Formulation Solvent Detergent Treated | Link | Link | NA |
| 15317 | Th1587 | Emicizumab | >Th1587_Emicizumab QVQLVESGGGLVQPGGSLRLSCAASGFTFSYYDIQWVRQAPGKGLEWVSSISPSGQSTYYRREVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARRTGREYGGGWYFDYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQKEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQEGNVFSCSVMHEALHNRYTQKSLSLSP | 145637 | C6434-H9940-N1724-O2047-S45 | 6.6 - 7.2 | NA | 78ºC | Emcicizumab presents a long half-life ranging from 27.8 to 34.4 days.[FDA label, A31279] | Emicizumab is a humanized recombinant monoclonal antibody that mimics the function of the coagulation Factor VIII and it has the capacity to bind simultaneously to activated Factor IX and Factor X. The ability of Emicizumab to bind to all these three different factors allows it to overcome immunogenicity and unstable hemostatic efficacy produced by previous Factor VII agents. Emicizumab was originated as an improved form of hBS23 and it was approved on November 16, 2017.[A31279, L1016] It was created by Chugai Pharmaceuticals Co. Ltd. and co-developed with Roche and Genentech.[L1015] | The main function of Emicizumab is the prevention of bleeding episodes. Thus, Emicizumab is approved for the routine prophylaxis to prevent or reduce the frequency of bleeding episodes of adult and pediatric patients with hemophilia A with or without Factor VIII inhibitors.[L4657] Hemophilia A is a deficiency of coagulation Factor VIII which causes a serious bleeding disorder. The standard treatment is done with the administration of recombinant or serum-deriver Factor VIII which induces the formation of anti-factor VIII alloantibodies (Factor VIII inhibitors) and renders the standard treatment ineffective.[A31286] | Emicizumab mimics the function of coagulation factor VIII, therefore it binds to the activated form of Factor IX (Factor IXa). This binding forms a complex that will later bind to the X factor of the coagulation factor. [A31288] The ability of Emicizumab to interact with both factors (Factor IXa and Factor X) activates the coagulation cascade that will subsequently lead to the segmentation of fibrinogen into fibrin and the formation of blood clots.[A31287] The effect of Emicizumab is translated into the restoration of the blood coagulation process and, therefore, in the reduction of hemorrhagic episodes.[L1016] The activity of emicizumab can also produce changes in activated clotting time (ACT), activated partial thromboplastin time (aPTT) and one-step Factor VIII activity. [L1018] In addition, the unique bispecific structure of Emicizumab prevents the formation of Factor VIII inhibitors or their effect. [A31286] In the first clinical trials, emicizumab was tried on previously treated adult and pediatric patients of hemophilia A with FVIII inhibitors. In this trials, the annualized bleeding rate requiring treatment with coagulation factors was reduced by 87% when compared to untreated patients.[L4660] Those clinical trials were followed by a second round on previously treated patients of severe hemophilia A without FVIII inhibitors. In this trial, the annualized bleed rate was reduced by 96% when compared to untreated patients.[L4660] | Emicizumab exerts its action by performing the function of the coagulation Factor VIII without presenting a structural homology.[L1017] It presents a dual specificity which allows it to bind to both the Factor IXa and Factor X, performing the required bridging activity for the launch of the coagulation cascade.[A31286] | The administration of Emicizumab has reported cases of microangiopathy and thrombotic events with concomitant use of activated prothrombin complex concentrate at doses higher of 100 U/kg/24 hours. There are also reports of injection site reaction, headaches and arthralgia.[L1018] Genotoxicity and carcinogenicity studies have not been performed as it is not expected that emicizumab can have any interaction with DNA, or chromosomal material.[F1947] | Emicizumab is a monoclonal antibody and thus, it is 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] | Subcutaneous administration of Emicizumab presents a very high bioavailability ranging from 80.4% to 93.1% when administered subcutaneously in a dose of 1 mg/kg.[A39524] In clinical trials, at the same dose, Emicizumab presented a linear exposure which concentration peaked 1-2 weeks after administration and presented a profile framed by a Cmax of 5.92 mcg/ml and an AUC of 304 mcg day/ml.[A31279] After subcutaneous administration, the absorption half-life was 1.7 days and the pharmacokinetic profile seemed to be shared when the medication was administered in the abdomen, upper arm, and thigh.[F1947] | The apparent volume of distribution is 11.4 L when administered subcutaneously and there are reports indicating that this value can increase with increasing body weight.[A39524] When emicizumab is administered intravenously, the volume of distribution at steady state is 106 ml/kg.[F1947] | The apparent clearance is 0.24 L/day when administered in multiple subcutaneous injections and there are reports indicating that this value can increase with increasing body weight.[A39524] | Antibodies | NA | NA | NA | NA | Coagulation factor IX,Coagulation factor X | Hemlibra | Genentech, Inc. | Genentech, Inc. | Subcutaneous | 150 mg/1mL | None. | injection site reactions, headache, joint pain, fever, headache, diarrhea, and muscle pain | Hemlibra is a monoclonal antibody that functions in place of a natural blood-clotting factor that is missing in people with hemophilia A. Emicizumab works as a "bridge" between other clotting factors to replace missing factor VIII. Hemlibra is for adults and children with hemophilia A with or without... | HEMLIBRA is a prescription medicine used for routine prophylaxis to prevent or reduce the frequency of bleeding episodes in adults and children, ages newborn and older, with hemophilia A with or without factor VIII inhibitors. Hemophilia A is a bleeding condition people can be born with where a missing or faulty blood clotting factor (factor VIII) prevents blood from clotting normally. | NA | Each single-dose 105 mg vial contains a 0.7 mL solution of emicizumab-kxwh (105 mg), L-arginine (18.3 mg), L-histidine (2.2 mg), and poloxamer 188 (0.4 mg), adjusted to pH 6.0 with L-aspartic acid. | Link | Link | NA |
| 15318 | Th1587 | Emicizumab | >Th1587_Emicizumab QVQLVESGGGLVQPGGSLRLSCAASGFTFSYYDIQWVRQAPGKGLEWVSSISPSGQSTYYRREVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARRTGREYGGGWYFDYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQKEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQEGNVFSCSVMHEALHNRYTQKSLSLSP | 145637 | C6434-H9940-N1724-O2047-S45 | 6.6 - 7.2 | NA | 78ºC | Emcicizumab presents a long half-life ranging from 27.8 to 34.4 days.[FDA label, A31279] | Emicizumab is a humanized recombinant monoclonal antibody that mimics the function of the coagulation Factor VIII and it has the capacity to bind simultaneously to activated Factor IX and Factor X. The ability of Emicizumab to bind to all these three different factors allows it to overcome immunogenicity and unstable hemostatic efficacy produced by previous Factor VII agents. Emicizumab was originated as an improved form of hBS23 and it was approved on November 16, 2017.[A31279, L1016] It was created by Chugai Pharmaceuticals Co. Ltd. and co-developed with Roche and Genentech.[L1015] | The main function of Emicizumab is the prevention of bleeding episodes. Thus, Emicizumab is approved for the routine prophylaxis to prevent or reduce the frequency of bleeding episodes of adult and pediatric patients with hemophilia A with or without Factor VIII inhibitors.[L4657] Hemophilia A is a deficiency of coagulation Factor VIII which causes a serious bleeding disorder. The standard treatment is done with the administration of recombinant or serum-deriver Factor VIII which induces the formation of anti-factor VIII alloantibodies (Factor VIII inhibitors) and renders the standard treatment ineffective.[A31286] | Emicizumab mimics the function of coagulation factor VIII, therefore it binds to the activated form of Factor IX (Factor IXa). This binding forms a complex that will later bind to the X factor of the coagulation factor. [A31288] The ability of Emicizumab to interact with both factors (Factor IXa and Factor X) activates the coagulation cascade that will subsequently lead to the segmentation of fibrinogen into fibrin and the formation of blood clots.[A31287] The effect of Emicizumab is translated into the restoration of the blood coagulation process and, therefore, in the reduction of hemorrhagic episodes.[L1016] The activity of emicizumab can also produce changes in activated clotting time (ACT), activated partial thromboplastin time (aPTT) and one-step Factor VIII activity. [L1018] In addition, the unique bispecific structure of Emicizumab prevents the formation of Factor VIII inhibitors or their effect. [A31286] In the first clinical trials, emicizumab was tried on previously treated adult and pediatric patients of hemophilia A with FVIII inhibitors. In this trials, the annualized bleeding rate requiring treatment with coagulation factors was reduced by 87% when compared to untreated patients.[L4660] Those clinical trials were followed by a second round on previously treated patients of severe hemophilia A without FVIII inhibitors. In this trial, the annualized bleed rate was reduced by 96% when compared to untreated patients.[L4660] | Emicizumab exerts its action by performing the function of the coagulation Factor VIII without presenting a structural homology.[L1017] It presents a dual specificity which allows it to bind to both the Factor IXa and Factor X, performing the required bridging activity for the launch of the coagulation cascade.[A31286] | The administration of Emicizumab has reported cases of microangiopathy and thrombotic events with concomitant use of activated prothrombin complex concentrate at doses higher of 100 U/kg/24 hours. There are also reports of injection site reaction, headaches and arthralgia.[L1018] Genotoxicity and carcinogenicity studies have not been performed as it is not expected that emicizumab can have any interaction with DNA, or chromosomal material.[F1947] | Emicizumab is a monoclonal antibody and thus, it is 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] | Subcutaneous administration of Emicizumab presents a very high bioavailability ranging from 80.4% to 93.1% when administered subcutaneously in a dose of 1 mg/kg.[A39524] In clinical trials, at the same dose, Emicizumab presented a linear exposure which concentration peaked 1-2 weeks after administration and presented a profile framed by a Cmax of 5.92 mcg/ml and an AUC of 304 mcg day/ml.[A31279] After subcutaneous administration, the absorption half-life was 1.7 days and the pharmacokinetic profile seemed to be shared when the medication was administered in the abdomen, upper arm, and thigh.[F1947] | The apparent volume of distribution is 11.4 L when administered subcutaneously and there are reports indicating that this value can increase with increasing body weight.[A39524] When emicizumab is administered intravenously, the volume of distribution at steady state is 106 ml/kg.[F1947] | The apparent clearance is 0.24 L/day when administered in multiple subcutaneous injections and there are reports indicating that this value can increase with increasing body weight.[A39524] | Antibodies, Monoclonal | NA | NA | NA | NA | Coagulation factor IX,Coagulation factor X | Hemlibra | Hoffmann La Roche | Hoffmann La Roche | Subcutaneous | 30 mg / 1 mL | None. | injection site reactions, headache, joint pain, fever, headache, diarrhea, and muscle pain | Hemlibra is a monoclonal antibody that functions in place of a natural blood-clotting factor that is missing in people with hemophilia A. Emicizumab works as a "bridge" between other clotting factors to replace missing factor VIII. Hemlibra is for adults and children with hemophilia A with or without... | HEMLIBRA is a prescription medicine used for routine prophylaxis to prevent or reduce the frequency of bleeding episodes in adults and children, ages newborn and older, with hemophilia A with or without factor VIII inhibitors. Hemophilia A is a bleeding condition people can be born with where a missing or faulty blood clotting factor (factor VIII) prevents blood from clotting normally. | NA | Each single-dose 105 mg vial contains a 0.7 mL solution of emicizumab-kxwh (105 mg), L-arginine (18.3 mg), L-histidine (2.2 mg), and poloxamer 188 (0.4 mg), adjusted to pH 6.0 with L-aspartic acid. | Link | Link | NA |
| 15319 | Th1587 | Emicizumab | >Th1587_Emicizumab QVQLVESGGGLVQPGGSLRLSCAASGFTFSYYDIQWVRQAPGKGLEWVSSISPSGQSTYYRREVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARRTGREYGGGWYFDYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQKEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQEGNVFSCSVMHEALHNRYTQKSLSLSP | 145637 | C6434-H9940-N1724-O2047-S45 | 6.6 - 7.2 | NA | 78ºC | Emcicizumab presents a long half-life ranging from 27.8 to 34.4 days.[FDA label, A31279] | Emicizumab is a humanized recombinant monoclonal antibody that mimics the function of the coagulation Factor VIII and it has the capacity to bind simultaneously to activated Factor IX and Factor X. The ability of Emicizumab to bind to all these three different factors allows it to overcome immunogenicity and unstable hemostatic efficacy produced by previous Factor VII agents. Emicizumab was originated as an improved form of hBS23 and it was approved on November 16, 2017.[A31279, L1016] It was created by Chugai Pharmaceuticals Co. Ltd. and co-developed with Roche and Genentech.[L1015] | The main function of Emicizumab is the prevention of bleeding episodes. Thus, Emicizumab is approved for the routine prophylaxis to prevent or reduce the frequency of bleeding episodes of adult and pediatric patients with hemophilia A with or without Factor VIII inhibitors.[L4657] Hemophilia A is a deficiency of coagulation Factor VIII which causes a serious bleeding disorder. The standard treatment is done with the administration of recombinant or serum-deriver Factor VIII which induces the formation of anti-factor VIII alloantibodies (Factor VIII inhibitors) and renders the standard treatment ineffective.[A31286] | Emicizumab mimics the function of coagulation factor VIII, therefore it binds to the activated form of Factor IX (Factor IXa). This binding forms a complex that will later bind to the X factor of the coagulation factor. [A31288] The ability of Emicizumab to interact with both factors (Factor IXa and Factor X) activates the coagulation cascade that will subsequently lead to the segmentation of fibrinogen into fibrin and the formation of blood clots.[A31287] The effect of Emicizumab is translated into the restoration of the blood coagulation process and, therefore, in the reduction of hemorrhagic episodes.[L1016] The activity of emicizumab can also produce changes in activated clotting time (ACT), activated partial thromboplastin time (aPTT) and one-step Factor VIII activity. [L1018] In addition, the unique bispecific structure of Emicizumab prevents the formation of Factor VIII inhibitors or their effect. [A31286] In the first clinical trials, emicizumab was tried on previously treated adult and pediatric patients of hemophilia A with FVIII inhibitors. In this trials, the annualized bleeding rate requiring treatment with coagulation factors was reduced by 87% when compared to untreated patients.[L4660] Those clinical trials were followed by a second round on previously treated patients of severe hemophilia A without FVIII inhibitors. In this trial, the annualized bleed rate was reduced by 96% when compared to untreated patients.[L4660] | Emicizumab exerts its action by performing the function of the coagulation Factor VIII without presenting a structural homology.[L1017] It presents a dual specificity which allows it to bind to both the Factor IXa and Factor X, performing the required bridging activity for the launch of the coagulation cascade.[A31286] | The administration of Emicizumab has reported cases of microangiopathy and thrombotic events with concomitant use of activated prothrombin complex concentrate at doses higher of 100 U/kg/24 hours. There are also reports of injection site reaction, headaches and arthralgia.[L1018] Genotoxicity and carcinogenicity studies have not been performed as it is not expected that emicizumab can have any interaction with DNA, or chromosomal material.[F1947] | Emicizumab is a monoclonal antibody and thus, it is 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] | Subcutaneous administration of Emicizumab presents a very high bioavailability ranging from 80.4% to 93.1% when administered subcutaneously in a dose of 1 mg/kg.[A39524] In clinical trials, at the same dose, Emicizumab presented a linear exposure which concentration peaked 1-2 weeks after administration and presented a profile framed by a Cmax of 5.92 mcg/ml and an AUC of 304 mcg day/ml.[A31279] After subcutaneous administration, the absorption half-life was 1.7 days and the pharmacokinetic profile seemed to be shared when the medication was administered in the abdomen, upper arm, and thigh.[F1947] | The apparent volume of distribution is 11.4 L when administered subcutaneously and there are reports indicating that this value can increase with increasing body weight.[A39524] When emicizumab is administered intravenously, the volume of distribution at steady state is 106 ml/kg.[F1947] | The apparent clearance is 0.24 L/day when administered in multiple subcutaneous injections and there are reports indicating that this value can increase with increasing body weight.[A39524] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Coagulation factor IX,Coagulation factor X | Hemlibra | Hoffmann La Roche | Hoffmann La Roche | Subcutaneous | 60 mg / 0.4 mL | None. | injection site reactions, headache, joint pain, fever, headache, diarrhea, and muscle pain | Hemlibra is a monoclonal antibody that functions in place of a natural blood-clotting factor that is missing in people with hemophilia A. Emicizumab works as a "bridge" between other clotting factors to replace missing factor VIII. Hemlibra is for adults and children with hemophilia A with or without... | HEMLIBRA is a prescription medicine used for routine prophylaxis to prevent or reduce the frequency of bleeding episodes in adults and children, ages newborn and older, with hemophilia A with or without factor VIII inhibitors. Hemophilia A is a bleeding condition people can be born with where a missing or faulty blood clotting factor (factor VIII) prevents blood from clotting normally. | NA | Each single-dose 105 mg vial contains a 0.7 mL solution of emicizumab-kxwh (105 mg), L-arginine (18.3 mg), L-histidine (2.2 mg), and poloxamer 188 (0.4 mg), adjusted to pH 6.0 with L-aspartic acid. | Link | Link | NA |
| 15348 | Th1590 | Sulesomab | NA | NA | NA | NA | NA | NA | NA | Market product is Tc99m-labeled murine antibody fragment for nuclear imaging of activated granulocytes. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15349 | Th1590 | Sulesomab | NA | NA | NA | NA | NA | NA | NA | Market product is Tc99m-labeled murine antibody fragment for nuclear imaging of activated granulocytes. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15360 | Th1591 | Besilesomab | NA | NA | NA | NA | NA | NA | Whole blood concentration-time radioactivity curves show a two-phase course, which can be subdivided into an early phase (0-2 h) and a late phase (5-24 h) [FDA Label]. After correcting for the decay of radionuclide, the calculated half-life of the early phase is approximately 0.5 h while the late phase demonstrates a calculated half-life of 16 h [FDA Label]. The terminal half-life in man is estimated to be approximately 23 h [L1623]. | Besilesomab is a mouse monoclonal antibody labelled with the radioactive isotope technetium-99m for determining the location of inflammation/infection in peripheral bone in adults with suspected osteomyelitis [FDA Label]. Utilised only as a diagnostic agent, besilesomab is currently approved by the EMEA for marketing and use in various European countries like Italy, France, Germany, Spain, Portugal, Norway, Sweden, the Netherlands, and the United Kingdom [L1564]. | Besilesomab is radiolabelled with sodium pertechnetate (Tc99m) solution to develop technetium (Tc99m) besilesomab solution. This solution is indicated in adults for scintigraphic imaging - in conjunction with other appropriate imaging modalities, when possible - in determining the location of inflammation/infection in peripheral bone in adults with suspected osteomyelitis [FDA Label]. When utilized as such, this medicinal product is for diagnostic use only [FDA Label]. | In a study employing cryo-preserved human tissues using an indirect alkaline phosphatase anti-alkaline phosphatase technique, besilesomab antibody from hybridoma supernatants demonstrated staining to cytoplasmic, membranous, and interstitial areas of primary colon carcinoma tissue, to single granulocytic cells in normal human liver and lung and to a large proportion of granulocytic cells in normal human bone marrow but not to blood vessels or connective tissue [L1623]. Additionally, the antibody also shows binding to the granulocytic cells of breast, kidney, parotid gland, pituitary, lymph nodes, and spleen tissues, as well as colonic, pancreatic, and some lung and breast carcinomas [L1623]. The purified besilesomab antibody and the prepared kit subsequently bound similarly to granulocytes in normal bone marrow, lung, liver, spleen, and colorectal carcinomas. Furthermore, the prepared kit also produced some staining in some connective tissue fibres in normal lung, some muscle fibres in normal colon, and in liver parenchymal cells [L1623]. In general however, besilesomab does not bind significantly to blood vessels and connective tissue [L1623]. | Nonspecific cross-reacting antigens (NCA) is the name of a collection of highly glycosylated bacterial binding receptors expressed on human granulocytes and other tissues [A32084]. In particular, these glycoprotein receptors are members of the immunoglobulin supergene family and are related structurally to carcinoembryonic antigen (CEA) [A32084]. CEA is found naturally in the human body and its expression may be increased in both cancer and non-cancerous (benign) circumstances. Besilesomab is subsequently a murine immunoglobulin monoclonal antibody of IgG1 isotype designed to recognise and bind specifically to NCA-95, or nonspecific cross-reacting antigen 95, an epitope found expressed on the cell membranes of granulocytes and granulocyte precursors [FDA Label]. When radiolabelled with sodium pertechnetate (Tc99m) solution to develop technetium (Tc99m) besilesomab solution, this radiolabelled medicine is injected into patients where the monoclonal antibody carries it to target CEA on target granulocytes [FDA Label]. When large numbers of CEA expressing granulocytes gather to the site of an infection, the radioactive monoclonal antibodies will also accumulate at such sites, where it can be detected by diagnostic scanning [FDA Label]. The resultant images show where the radioactive besilesomab has accumulated, locating areas affected by osteomyelitis, infection, or inflammation [FDA Label]. Furthermore, it is believed that the besilesomab accumulation is predominantly passive (via increased vascular permeability) and only partially active (via migration of human granulocytes carrying besilesomab to the infection/inflammation location) since only 10% to 20% of the injected radio-diagnostic agent binds in vivo to human circulating granulocytes [L1623]. Specific binding of besilesomab to activated granulocytes that have already migrated to sites of infection/inflammation might be the primary part of the detection signal [L1623]. | The most commonly reported adverse reaction associated with the use of besilesomab is the development of Human Anti-Mouse Antibodies (HAMA) after a single administration [FDA Label]. Patients who have developed HAMA may potentially have a higher risk for hypersensitivity reactions. Screening for possible previous exposure to murine monoclonal antibodies and tests for the presence of HAMA in prospective patients should be made prior to administrating besilesomab [FDA Label]. Moreover, because the incidence of developing HAMA appears to be dose related with besilesomab, the recommended dosage is restricted to no more than 250 micrograms of antibody per injection [T132]. Patients who are HAMA positive are consequently contraindicated from using besilesomab [FDA Label]. Hypersensitivity to besilesomab or to any other murine antibodies or to any of the excipients associated with the active besilesomab radio-diagnostic agent is subsequently a contraindication [FDA Label]. Some patients have also reported hypotension as a common adverse reaction [FDA Label]. As exposure to ionizing radiation is linked with cancer induction and a potential for developing hereditary defects, the use of radio-diagnostic besilesomab in pregnant women is considered a formal contraindication [FDA Label]. If in doubt about a woman's potential pregnancy, alternative techniques to not using ionizing radiation should be considered and/or offered instead to the patient [FDA Label]. Moreover, although it is not known if besilesomab is excreted in human milk, the potential risk to a breast-fed child cannot be excluded [FDA Label]. Furthermore, while consideration should be given to the possibility of perhaps delaying the administration of radionuclide agents until the mother has ceased breastfeeding or perhaps certainly choosing alternative radoopharmaceuticals with more appropriate secretion activity, if the use of besilesomab is absolutely necessary then the mother's breastfeeding should be stopped for three days and any expressed feeds during that time discarded [FDA Label]. The time period of three days corresponds to 10 half-lives of technetium (Tc99m)(60 hours) [FDA Label]. At that time, the remaining activity represents about 1/1000 of the initial activity in the body [FDA Label]. In general, close contact with infants and pregnant women should be restricted for patients who have been administered besilesomab during the first 12 hours after the injection [FDA Label]. Since besilesomab contains sorbitol, patients having any rare hereditary conditions of fructose intolerance should not be administered this medicine [FDA Label]. Because no sufficient data regarding the safety and efficacy of using besilesomab in children below the age of 18 years exists, the use of besilesomab in this patient population is not recommended [L1711]. Even though data regarding the repeated dosing of besilesomab is extremely limited, the use of besilesomab should only be used once in a patient's lifetime [FDA Label]. Other medicines that can inhibit inflammation or affect the hematopoietic system (like antibiotics and corticosteroids) can lead to false negative results. Such agents should therefore not be administered together with, or a short time before the injection of besilesomab [FDA Label]. Preclinical data obtained with the non-radioactive compound revealed no special hazard for humans based on conventional studies of safety pharmacology, single-dose and repeated dose toxicity, although antimurine antibodies were found in all dose groups (including controls) in a repeated-dose study in monkeys [FDA Label]. Genotoxicity studies conducted to test for potentially genotoxic impurities were also negative. Long-term carcinogenicity studies and toxicity to reproduction have not yet been carried out [FDA Label]. | The besilesomab antibody is mainly metabolized via hepatic clearance into amino acids [L1623]. Nevertheless, liver uptake of radioactivity was observed to be minimal under trial conditions and liver impairment is considered unlikely to affect besilesomab metabolism and elimination in any clinically significant manner [L1623]. The total blood radioactivity occurring from the administration of besilesomab is generally the result of the contribution of radioactive intact labelled antibody and other radioactive moieties like metabolized antibody fragments, smaller radiometabolites, and free technetium (Tc99m) [L1623]. | As the diagnostic agent is administered intravenously, it is expected that the bioavailability is 100% [L1623]. Approximately six hours after injection, about 1.5% of the whole body radioactivity is detected in the liver while about 3.0% is found in the spleen [FDA Label]. Observations twenty-four hours after injection demonstrate percentages of radioactivity of 1.6% in the liver and 2.3% in the spleen [FDA Label]. However, non pathological, unusual accumulations of the radioactive agent can be detected in the spleen (up to 6% of patients), in the bowel (up to 4% of patients), in the liver and bone marrow (up to 3% of patients), and in the thyroid and kidneys (up to 2% of patients) [FDA Label]. | In the besilesomab clinical trial Study 7D-101SZ-A, volumes of distribution were determined as approximately 4L - which was close to the plasma volume - in the central compartment, whether calculated from plasma radioactivity or from intact monoclonal antibody concentrations; the peripheral compartment was somewhat greater, at about 6L for both methods [L1623]. | Once administered into the body, prepared technetium (Tc99m) besilesomab can be metabolized into free amino acids, smaller radioactive fragments, or even free pertechnetate (Tc99m) [L1623]. The besilesomab clinical study 7D-101SZ-A consequently reports separate estimated clearance rates of 0.322 L/h and 0.242 L/h that were calculated using monitored plasma radioactivity and from monitored intact monoclonal antibody concentrations, respectively [L1623]. | Antibodies | NA | NA | NA | NA | Carcinoembryonic antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15361 | Th1591 | Besilesomab | NA | NA | NA | NA | NA | NA | Whole blood concentration-time radioactivity curves show a two-phase course, which can be subdivided into an early phase (0-2 h) and a late phase (5-24 h) [FDA Label]. After correcting for the decay of radionuclide, the calculated half-life of the early phase is approximately 0.5 h while the late phase demonstrates a calculated half-life of 16 h [FDA Label]. The terminal half-life in man is estimated to be approximately 23 h [L1623]. | Besilesomab is a mouse monoclonal antibody labelled with the radioactive isotope technetium-99m for determining the location of inflammation/infection in peripheral bone in adults with suspected osteomyelitis [FDA Label]. Utilised only as a diagnostic agent, besilesomab is currently approved by the EMEA for marketing and use in various European countries like Italy, France, Germany, Spain, Portugal, Norway, Sweden, the Netherlands, and the United Kingdom [L1564]. | Besilesomab is radiolabelled with sodium pertechnetate (Tc99m) solution to develop technetium (Tc99m) besilesomab solution. This solution is indicated in adults for scintigraphic imaging - in conjunction with other appropriate imaging modalities, when possible - in determining the location of inflammation/infection in peripheral bone in adults with suspected osteomyelitis [FDA Label]. When utilized as such, this medicinal product is for diagnostic use only [FDA Label]. | In a study employing cryo-preserved human tissues using an indirect alkaline phosphatase anti-alkaline phosphatase technique, besilesomab antibody from hybridoma supernatants demonstrated staining to cytoplasmic, membranous, and interstitial areas of primary colon carcinoma tissue, to single granulocytic cells in normal human liver and lung and to a large proportion of granulocytic cells in normal human bone marrow but not to blood vessels or connective tissue [L1623]. Additionally, the antibody also shows binding to the granulocytic cells of breast, kidney, parotid gland, pituitary, lymph nodes, and spleen tissues, as well as colonic, pancreatic, and some lung and breast carcinomas [L1623]. The purified besilesomab antibody and the prepared kit subsequently bound similarly to granulocytes in normal bone marrow, lung, liver, spleen, and colorectal carcinomas. Furthermore, the prepared kit also produced some staining in some connective tissue fibres in normal lung, some muscle fibres in normal colon, and in liver parenchymal cells [L1623]. In general however, besilesomab does not bind significantly to blood vessels and connective tissue [L1623]. | Nonspecific cross-reacting antigens (NCA) is the name of a collection of highly glycosylated bacterial binding receptors expressed on human granulocytes and other tissues [A32084]. In particular, these glycoprotein receptors are members of the immunoglobulin supergene family and are related structurally to carcinoembryonic antigen (CEA) [A32084]. CEA is found naturally in the human body and its expression may be increased in both cancer and non-cancerous (benign) circumstances. Besilesomab is subsequently a murine immunoglobulin monoclonal antibody of IgG1 isotype designed to recognise and bind specifically to NCA-95, or nonspecific cross-reacting antigen 95, an epitope found expressed on the cell membranes of granulocytes and granulocyte precursors [FDA Label]. When radiolabelled with sodium pertechnetate (Tc99m) solution to develop technetium (Tc99m) besilesomab solution, this radiolabelled medicine is injected into patients where the monoclonal antibody carries it to target CEA on target granulocytes [FDA Label]. When large numbers of CEA expressing granulocytes gather to the site of an infection, the radioactive monoclonal antibodies will also accumulate at such sites, where it can be detected by diagnostic scanning [FDA Label]. The resultant images show where the radioactive besilesomab has accumulated, locating areas affected by osteomyelitis, infection, or inflammation [FDA Label]. Furthermore, it is believed that the besilesomab accumulation is predominantly passive (via increased vascular permeability) and only partially active (via migration of human granulocytes carrying besilesomab to the infection/inflammation location) since only 10% to 20% of the injected radio-diagnostic agent binds in vivo to human circulating granulocytes [L1623]. Specific binding of besilesomab to activated granulocytes that have already migrated to sites of infection/inflammation might be the primary part of the detection signal [L1623]. | The most commonly reported adverse reaction associated with the use of besilesomab is the development of Human Anti-Mouse Antibodies (HAMA) after a single administration [FDA Label]. Patients who have developed HAMA may potentially have a higher risk for hypersensitivity reactions. Screening for possible previous exposure to murine monoclonal antibodies and tests for the presence of HAMA in prospective patients should be made prior to administrating besilesomab [FDA Label]. Moreover, because the incidence of developing HAMA appears to be dose related with besilesomab, the recommended dosage is restricted to no more than 250 micrograms of antibody per injection [T132]. Patients who are HAMA positive are consequently contraindicated from using besilesomab [FDA Label]. Hypersensitivity to besilesomab or to any other murine antibodies or to any of the excipients associated with the active besilesomab radio-diagnostic agent is subsequently a contraindication [FDA Label]. Some patients have also reported hypotension as a common adverse reaction [FDA Label]. As exposure to ionizing radiation is linked with cancer induction and a potential for developing hereditary defects, the use of radio-diagnostic besilesomab in pregnant women is considered a formal contraindication [FDA Label]. If in doubt about a woman's potential pregnancy, alternative techniques to not using ionizing radiation should be considered and/or offered instead to the patient [FDA Label]. Moreover, although it is not known if besilesomab is excreted in human milk, the potential risk to a breast-fed child cannot be excluded [FDA Label]. Furthermore, while consideration should be given to the possibility of perhaps delaying the administration of radionuclide agents until the mother has ceased breastfeeding or perhaps certainly choosing alternative radoopharmaceuticals with more appropriate secretion activity, if the use of besilesomab is absolutely necessary then the mother's breastfeeding should be stopped for three days and any expressed feeds during that time discarded [FDA Label]. The time period of three days corresponds to 10 half-lives of technetium (Tc99m)(60 hours) [FDA Label]. At that time, the remaining activity represents about 1/1000 of the initial activity in the body [FDA Label]. In general, close contact with infants and pregnant women should be restricted for patients who have been administered besilesomab during the first 12 hours after the injection [FDA Label]. Since besilesomab contains sorbitol, patients having any rare hereditary conditions of fructose intolerance should not be administered this medicine [FDA Label]. Because no sufficient data regarding the safety and efficacy of using besilesomab in children below the age of 18 years exists, the use of besilesomab in this patient population is not recommended [L1711]. Even though data regarding the repeated dosing of besilesomab is extremely limited, the use of besilesomab should only be used once in a patient's lifetime [FDA Label]. Other medicines that can inhibit inflammation or affect the hematopoietic system (like antibiotics and corticosteroids) can lead to false negative results. Such agents should therefore not be administered together with, or a short time before the injection of besilesomab [FDA Label]. Preclinical data obtained with the non-radioactive compound revealed no special hazard for humans based on conventional studies of safety pharmacology, single-dose and repeated dose toxicity, although antimurine antibodies were found in all dose groups (including controls) in a repeated-dose study in monkeys [FDA Label]. Genotoxicity studies conducted to test for potentially genotoxic impurities were also negative. Long-term carcinogenicity studies and toxicity to reproduction have not yet been carried out [FDA Label]. | The besilesomab antibody is mainly metabolized via hepatic clearance into amino acids [L1623]. Nevertheless, liver uptake of radioactivity was observed to be minimal under trial conditions and liver impairment is considered unlikely to affect besilesomab metabolism and elimination in any clinically significant manner [L1623]. The total blood radioactivity occurring from the administration of besilesomab is generally the result of the contribution of radioactive intact labelled antibody and other radioactive moieties like metabolized antibody fragments, smaller radiometabolites, and free technetium (Tc99m) [L1623]. | As the diagnostic agent is administered intravenously, it is expected that the bioavailability is 100% [L1623]. Approximately six hours after injection, about 1.5% of the whole body radioactivity is detected in the liver while about 3.0% is found in the spleen [FDA Label]. Observations twenty-four hours after injection demonstrate percentages of radioactivity of 1.6% in the liver and 2.3% in the spleen [FDA Label]. However, non pathological, unusual accumulations of the radioactive agent can be detected in the spleen (up to 6% of patients), in the bowel (up to 4% of patients), in the liver and bone marrow (up to 3% of patients), and in the thyroid and kidneys (up to 2% of patients) [FDA Label]. | In the besilesomab clinical trial Study 7D-101SZ-A, volumes of distribution were determined as approximately 4L - which was close to the plasma volume - in the central compartment, whether calculated from plasma radioactivity or from intact monoclonal antibody concentrations; the peripheral compartment was somewhat greater, at about 6L for both methods [L1623]. | Once administered into the body, prepared technetium (Tc99m) besilesomab can be metabolized into free amino acids, smaller radioactive fragments, or even free pertechnetate (Tc99m) [L1623]. The besilesomab clinical study 7D-101SZ-A consequently reports separate estimated clearance rates of 0.322 L/h and 0.242 L/h that were calculated using monitored plasma radioactivity and from monitored intact monoclonal antibody concentrations, respectively [L1623]. | Antibodies, Monoclonal | NA | NA | NA | NA | Carcinoembryonic antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15386 | 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]. | Antibodies | NA | NA | NA | NA | Interleukin-23 | Ilumya | Sun Pharmaceutical Industries, Inc. | Sun Pharmaceutical Industries, Inc. | Subcutaneous | 100 mg/1mL | ILUMYA is contraindicated in patients with a previous serious hypersensitivity reaction to tildrakizumab or to any of the excipients [see WARNINGS AND PRECAUTIONS]. | upper respiratory infections, injection site reactions (hives, itching, pain, redness, inflammation, swelling, bruising, hematoma, and bleeding), and diarrhea | Ilumya reduces the effects of a substance in the body that can cause inflammation. Ilumya injection is a prescription medicine used to treat moderate to severe psoriasis in adults who may benefit from receiving injections, pills, or treatment using ultraviolet or UV light phototherapy). Ilumya may also... | Ilumya is a prescription medicine used to treat the symptoms of moderate to severe Plaque Psoriasis. Ilumya may be used alone or with other medications. | NA | Tildrakizumab-asmn is a humanized IgG1/k antibody that specifically binds to the p19 subunit of interleukin-23 (IL-23). | Link | Link | NA |
| 15387 | 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]. | Antibodies, Monoclonal | NA | NA | NA | NA | Interleukin-23 | Ilumya | Sun Pharma Global FZE | Sun Pharma Global FZE | Subcutaneous | 100 mg / 1 mL | ILUMYA is contraindicated in patients with a previous serious hypersensitivity reaction to tildrakizumab or to any of the excipients [see WARNINGS AND PRECAUTIONS]. | upper respiratory infections, injection site reactions (hives, itching, pain, redness, inflammation, swelling, bruising, hematoma, and bleeding), and diarrhea | Ilumya reduces the effects of a substance in the body that can cause inflammation. Ilumya injection is a prescription medicine used to treat moderate to severe psoriasis in adults who may benefit from receiving injections, pills, or treatment using ultraviolet or UV light phototherapy). Ilumya may also... | Ilumya is a prescription medicine used to treat the symptoms of moderate to severe Plaque Psoriasis. Ilumya may be used alone or with other medications. | NA | Tildrakizumab-asmn is a humanized IgG1/k antibody that specifically binds to the p19 subunit of interleukin-23 (IL-23). | Link | Link | NA |
| 15388 | 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]. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Interleukin-23 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15400 | Th1594 | Burosumab | >Th1594_Burosumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTNHYMHWVRQAPGQGLEWMGIINPISGSTSNAQKFQGRVTMTRDTSTSTVYMELSSLRSEDTAVYYCARDIVDAFDFWGQGTMVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144100 | C6388H9904N1700O2006S46 | NA | NA | NA | About 19 days [L2347]. | Burosumab (KRN23) is an entirely human monoclonal IgG1 antibody that binds excess fibroblast growth factor 23 (FGF23) and has been successfully tested in clinical trials in children with X-linked hypophosphatemic rickets [A32593]. The U.S. Food and Drug Administration approved Crysvita (burosumab) in April 2018. This is the first drug approved to treat adults and children ages 1 year and older with X-linked hypophosphatemia (XLH), which is a rare, inherited form of rickets. X-linked hypophosphatemia causes low circulating levels of phosphorus in the blood. It causes impaired bone growth and development in children and adolescents and issues with bone mineralization throughout a patient’s life [L2346]. XLH is a serious disease which affects about 3,000 children and 12,000 adults in the United States. Most children with XLH suffer from bowed or bent legs, short stature, bone pain and severe dental pain. Some adults with this condition suffer from persistent, unrelenting discomfort and complications, such as joint pain, impaired mobility, tooth abscesses and hearing loss [L2346]. | This drug is indicated for the treatment of X-linked hypophosphatemia with radiological evidence of bone disease in children of 1 year of age and older and adolescents with growing skeletons [L2347]. | This drug has the ability to reduce the loss of phosphate, to improve pathologically low serum phosphate concentrations and other metabolic changes, as well as to reduce the severity of rickets as seen radiographically [L2348]. In summary, this drug works to support of bone mineralization [L2347]. | Burosumab is a recombinant human monoclonal antibody (IgG1) that both binds to and inhibits the actions of fibroblast growth factor 23 (FGF23). By inhibiting this growth factor, burosumab increases the tubular reabsorption of phosphate from the kidney and thus increases serum concentration of 1, 25 dihydroxy-Vitamin D [L2347]. This form of vitamin D enhances intestinal absorption of phosphate and calcium, supporting bone mineralization [L2351]. | The toxicity of Crysvita can be classified into several categories [L2347]: **Ectopic mineralisation**: Clinically manifested by nephrocalcinosis, has been seen in patients with XLH treated with oral phosphorous and vitamin D analogues. These drugs should be stopped at least 1 week before starting burosumab treatment [L2347]. Monitoring for signs and symptoms of nephrocalcinosis, e.g. by renal ultrasonography, is recommended at the beginning of treatment and at intervals of every 6 months for the first 12 months of treatment, and yearly thereafter. Regular monitoring of plasma alkaline phosphatases, Calcium, PTH, and creatinine is advised at 6 months intervals(every 3 months for children 1- 2 years) or as indicated [L2347]. Monitoring of urine calcium and phosphate is suggested every 3 months. **Hyperphosphatemia** Fasting serum phosphate level must be followed due to the risk of hyperphosphatemia while taking this drug. To decrease the risk for ectopic mineralization, it is advised that fasting serum phosphate is aimed to be in the lower end of the normal reference range for any given age. Dose interruption and/or dose reduction may be required. Regular measurement of postprandial serum phosphate is advised [L2347]. **Serum parathyroid hormone increases** Increases in serum parathyroid hormone have been measured in some XLH patients while undergoing treatment with burosumab. Regular measurement of serum parathyroid hormone is recommended [L2347]. **Injection site reactions** Administration of burosumab, like other injections, can lead to local injection site reactions. Administration of this drug should cease in any patient experiencing severe injection site reactions and appropriate medical therapy administered [L2347]. **Hypersensitivity** Burosumab should be discontinued if serious hypersensitivity reactions occur and appropriate medical treatment should be provided [L2347]. **Reproductive toxicity/pregnancy** There are no or limited amount of data available from the use of burosumab in pregnant women. Studies in animals have demonstrated reproductive toxicity. Burosumab use is not advised during pregnancy and in women of childbearing potential/age currently not using contraception [L2347]. | Burosumab is composed solely of amino acids and carbohydrates as a native immunoglobulin and is unlikely to be eliminated via hepatic metabolic mechanisms. Its metabolism and elimination are expected to follow the immunoglobulin clearance pathways, resulting in degradation to small peptides and individual amino acids [L2347]. | Burosumab absorption after subcutaneous injection sites into to the blood circulation is nearly complete. Following the subcutaneous route of administration, the time to reach maximum serum concentrations (Tmax) of burosumab is estimated at 5-10 days. The peak serum concentration (Cmax) and area under the concentration-time curve (AUC) of serum burosumab is proportional to the dose, over the dose range of 0.1-2.0 mg/kg [L2347]. | Burosumab is comprised solely of amino acids and carbohydrates as a native immunoglobulin and is not likeluy to be eliminated by hepatic metabolic mechanisms. The metabolism of burosumab and elimination are expected to follow the immunoglobulin clearance pathways, which results in its degradation to smaller peptides and amino acids [L2347]. | The clearance of burosumab depends on weight and is estimated to be 0.290 L/day and 0.136 L/day in a typical adult (70 kg) and pediatric (30 kg) XLH patient, respectively [L2347]. | Antibodies | NA | NA | NA | NA | Fibroblast growth factor 23 | Crysvita | Kyowa Kirin Holdings B.V. | Kyowa Kirin Holdings B.V. | Subcutaneous | 20 mg/ml | CRYSVITA is contraindicated:In concomitant use with oral phosphate and/or active vitamin D analogs (e.g. calcitriol, paricalcitol, doxercalciferol, calcifediol) due to the risk of hyperphosphatemia [see WARNINGS AND PRECAUTIONS and DRUG INTERACTIONS].When serum phosphorus is within or above the normal range for age [see WARNINGS AND PRECAUTIONS].In patients with severe renal impairment or end stage renal disease because these conditions are associated with abnormal mineral metabolism [see Use In Specific Population]. | headache, injection site reaction, vomiting, fever, pain in extremities, decreased vitamin D levels, back pain, tooth infection, restless leg syndrome, dizziness, constipation, and increased blood phosphorus | Crysvita is a monoclonal antibody that targets and blocks the activity of a blood protein called FGF23. In a genetic condition called X-linked hypophosphatemia (HYE-poe-fos-fa-TEEM-ee-a), low phosphate levels in blood are caused by abnormally high levels of FGF23 protein, which causes the kidneys to... | Crysvita is a prescription medicine used to treat the symptoms of X-Linked Hypophosphatemia and Tumor-Induced Osteomalacia. Crysvita may be used alone or with other medications. | NA | Burosumab-twza is a human immunoglobulin G subclass 1 (IgG1), anti-human fibroblast growth factor 23 (FGF23) antibody produced by recombinant DNA technology using Chinese hamster ovary cells. Burosumab-twza is composed of two heavy chain (γ1-chain) molecules and two light chain (τ-chain) molecules. Each heavy chain has an N-linked carbohydrate moiety at asparagine 297 (Asn297). The molecular weight of burosumab-twza determined by mass spectrometry is approximately 147,000. | Link | Link | NA |
| 15401 | Th1594 | Burosumab | >Th1594_Burosumab QVQLVQSGAEVKKPGASVKVSCKASGYTFTNHYMHWVRQAPGQGLEWMGIINPISGSTSNAQKFQGRVTMTRDTSTSTVYMELSSLRSEDTAVYYCARDIVDAFDFWGQGTMVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144100 | C6388H9904N1700O2006S46 | NA | NA | NA | About 19 days [L2347]. | Burosumab (KRN23) is an entirely human monoclonal IgG1 antibody that binds excess fibroblast growth factor 23 (FGF23) and has been successfully tested in clinical trials in children with X-linked hypophosphatemic rickets [A32593]. The U.S. Food and Drug Administration approved Crysvita (burosumab) in April 2018. This is the first drug approved to treat adults and children ages 1 year and older with X-linked hypophosphatemia (XLH), which is a rare, inherited form of rickets. X-linked hypophosphatemia causes low circulating levels of phosphorus in the blood. It causes impaired bone growth and development in children and adolescents and issues with bone mineralization throughout a patient’s life [L2346]. XLH is a serious disease which affects about 3,000 children and 12,000 adults in the United States. Most children with XLH suffer from bowed or bent legs, short stature, bone pain and severe dental pain. Some adults with this condition suffer from persistent, unrelenting discomfort and complications, such as joint pain, impaired mobility, tooth abscesses and hearing loss [L2346]. | This drug is indicated for the treatment of X-linked hypophosphatemia with radiological evidence of bone disease in children of 1 year of age and older and adolescents with growing skeletons [L2347]. | This drug has the ability to reduce the loss of phosphate, to improve pathologically low serum phosphate concentrations and other metabolic changes, as well as to reduce the severity of rickets as seen radiographically [L2348]. In summary, this drug works to support of bone mineralization [L2347]. | Burosumab is a recombinant human monoclonal antibody (IgG1) that both binds to and inhibits the actions of fibroblast growth factor 23 (FGF23). By inhibiting this growth factor, burosumab increases the tubular reabsorption of phosphate from the kidney and thus increases serum concentration of 1, 25 dihydroxy-Vitamin D [L2347]. This form of vitamin D enhances intestinal absorption of phosphate and calcium, supporting bone mineralization [L2351]. | The toxicity of Crysvita can be classified into several categories [L2347]: **Ectopic mineralisation**: Clinically manifested by nephrocalcinosis, has been seen in patients with XLH treated with oral phosphorous and vitamin D analogues. These drugs should be stopped at least 1 week before starting burosumab treatment [L2347]. Monitoring for signs and symptoms of nephrocalcinosis, e.g. by renal ultrasonography, is recommended at the beginning of treatment and at intervals of every 6 months for the first 12 months of treatment, and yearly thereafter. Regular monitoring of plasma alkaline phosphatases, Calcium, PTH, and creatinine is advised at 6 months intervals(every 3 months for children 1- 2 years) or as indicated [L2347]. Monitoring of urine calcium and phosphate is suggested every 3 months. **Hyperphosphatemia** Fasting serum phosphate level must be followed due to the risk of hyperphosphatemia while taking this drug. To decrease the risk for ectopic mineralization, it is advised that fasting serum phosphate is aimed to be in the lower end of the normal reference range for any given age. Dose interruption and/or dose reduction may be required. Regular measurement of postprandial serum phosphate is advised [L2347]. **Serum parathyroid hormone increases** Increases in serum parathyroid hormone have been measured in some XLH patients while undergoing treatment with burosumab. Regular measurement of serum parathyroid hormone is recommended [L2347]. **Injection site reactions** Administration of burosumab, like other injections, can lead to local injection site reactions. Administration of this drug should cease in any patient experiencing severe injection site reactions and appropriate medical therapy administered [L2347]. **Hypersensitivity** Burosumab should be discontinued if serious hypersensitivity reactions occur and appropriate medical treatment should be provided [L2347]. **Reproductive toxicity/pregnancy** There are no or limited amount of data available from the use of burosumab in pregnant women. Studies in animals have demonstrated reproductive toxicity. Burosumab use is not advised during pregnancy and in women of childbearing potential/age currently not using contraception [L2347]. | Burosumab is composed solely of amino acids and carbohydrates as a native immunoglobulin and is unlikely to be eliminated via hepatic metabolic mechanisms. Its metabolism and elimination are expected to follow the immunoglobulin clearance pathways, resulting in degradation to small peptides and individual amino acids [L2347]. | Burosumab absorption after subcutaneous injection sites into to the blood circulation is nearly complete. Following the subcutaneous route of administration, the time to reach maximum serum concentrations (Tmax) of burosumab is estimated at 5-10 days. The peak serum concentration (Cmax) and area under the concentration-time curve (AUC) of serum burosumab is proportional to the dose, over the dose range of 0.1-2.0 mg/kg [L2347]. | Burosumab is comprised solely of amino acids and carbohydrates as a native immunoglobulin and is not likeluy to be eliminated by hepatic metabolic mechanisms. The metabolism of burosumab and elimination are expected to follow the immunoglobulin clearance pathways, which results in its degradation to smaller peptides and amino acids [L2347]. | The clearance of burosumab depends on weight and is estimated to be 0.290 L/day and 0.136 L/day in a typical adult (70 kg) and pediatric (30 kg) XLH patient, respectively [L2347]. | Antibodies, Monoclonal | NA | NA | NA | NA | Fibroblast growth factor 23 | Crysvita | Kyowa Kirin Holdings B.V. | Kyowa Kirin Holdings B.V. | Subcutaneous | 30 mg/ml | CRYSVITA is contraindicated:In concomitant use with oral phosphate and/or active vitamin D analogs (e.g. calcitriol, paricalcitol, doxercalciferol, calcifediol) due to the risk of hyperphosphatemia [see WARNINGS AND PRECAUTIONS and DRUG INTERACTIONS].When serum phosphorus is within or above the normal range for age [see WARNINGS AND PRECAUTIONS].In patients with severe renal impairment or end stage renal disease because these conditions are associated with abnormal mineral metabolism [see Use In Specific Population]. | headache, injection site reaction, vomiting, fever, pain in extremities, decreased vitamin D levels, back pain, tooth infection, restless leg syndrome, dizziness, constipation, and increased blood phosphorus | Crysvita is a monoclonal antibody that targets and blocks the activity of a blood protein called FGF23. In a genetic condition called X-linked hypophosphatemia (HYE-poe-fos-fa-TEEM-ee-a), low phosphate levels in blood are caused by abnormally high levels of FGF23 protein, which causes the kidneys to... | Crysvita is a prescription medicine used to treat the symptoms of X-Linked Hypophosphatemia and Tumor-Induced Osteomalacia. Crysvita may be used alone or with other medications. | NA | Burosumab-twza is a human immunoglobulin G subclass 1 (IgG1), anti-human fibroblast growth factor 23 (FGF23) antibody produced by recombinant DNA technology using Chinese hamster ovary cells. Burosumab-twza is composed of two heavy chain (γ1-chain) molecules and two light chain (τ-chain) molecules. Each heavy chain has an N-linked carbohydrate moiety at asparagine 297 (Asn297). The molecular weight of burosumab-twza determined by mass spectrometry is approximately 147,000. | Link | Link | NA |
| 15413 | Th1595 | Erenumab | >Th1595_Erenumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSSFGMHWVRQAPGKGLEWVAVISFDGSIKYSVDSVKGRFTISRDNSKNTLFLQMNSLRAEDTAVYYCARDRLNYYDSSGYYHYKYYGMAVWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKCCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | C6472H9964N1728O2018S50 | NA | NA | NA | Erenumab exhibits non-linear kinetics as a result of binding to the CGRP receptor [FDA Label]. Lower than 2-fold accumulation was recorded in trough serum concentrations (Cmin) for episodic and chronic migraine patients following subcutaneous administration of 70 mg once-monthly and 140 mg once-monthly doses [FDA Label]. Serum trough concentrations approached steady state by 3 months of dosing [FDA Label]. The effective half-life of erenumab was observed to be 28 days [FDA Label]. | Erenumab (AMG-334) (INN; trade name Aimovig) is a human monoclonal antibody designed specifically to bind and antagonize the calcitonin gene-related peptide receptor (CGRPR) as a means to prevent migraines. Aimovig, as released and marketed by Novartis and Amgen, is in fact a novel therapeutic approach as the first and only FDA approved treatment specifically developed to prevent migraine by blocking the CGRP receptor, which is believed to play a critical role in migraine [L2823]. In particular, erenumab-aooe is a human immunoglobulin G2 monoclonal antibody that has high affinity binding to the CGRP receptor [FDA Label]. The antibody is produced utlilizing recombinant DNA technology in Chinese hamster ovary cells [FDA Label]. It is composed of 2 heavy chains, each containing 456 amino acids, and 2 light chains of the lambda subclass, each containing 216 amino acids, with an approximate molecular weight of 150 kDa [FDA Label]. | Erenumab is indicated for the preventative treatment of migraine in adults [FDA Label]. | As a human monoclonal antibody designed to specifically bind with and antagonize the calcitonin gene-related peptide (CGRP) receptor, there is the possibility that erenumab could interfere with natural activities of CGRP that may not be immediately or directly associated with migraines. For example, at peripheral synapses, CGRP released from trigeminal terminals results in vasodilation by way of CGRP receptor on smooth muscle cells of meningeal and cerebral blood vessels, making CGRP a potent general arterial vasodilator [A33090]. Antagonism of CGRP receptors responsible for such vasodilation could theoretically result in vasoconstriction and raises in blood pressure. In a randomised, double-blind, placebo-controlled study in healthy volunteers, concomitant administration of erenumab (140 mg intravenous, single dose) with sumatriptan (12 mg subcutaneous, given as two 6 mg doses separated by one hour) had no effect on resting blood pressure compared with sumatriptan alone, however [FDA Label]. Please note that erenumab is indicated for subcutaneous use only, though [FDA Label]. | Erenumab is a human monoclonal antibody that has been designed to bind specifically to the calcitonin gene-related peptide (CGRP) receptor and antagonize the CGRP receptor function [FDA Label]. Studies since 1985 have demonstrated that CGRP levels increase during acute migraine attacks in migraine-suffering patients but normalize after efficacious sumatriptan therapy [A33090]. Moreover, research has also shown that intravenous administration of CGRP can induce migraine-like attacks in migraine-suffering patients [A33090]. For all these reasons, the binding and antagonism of CGRP receptors was designed to be mechanism of action for erenumab to take advantage of in reversing the migraine-inducing activity of natural CGRP. CGRP and its receptor are expressed in both the peripheral and the central nervous system [A33091]. In addition to playing a role in cranial nociception, CGRP is also a potent general arterial vasodilator [A33091]. At peripheral synapses, CGRP released from trigeminal terminals results in vasodilation via CGRP receptors on the smooth muscle cells of meningeal and cerebral blood vessels [A33090]. | The most common side effects of erenumab include pain, redness, or swelling at the injection site, and constipation. Information regarding overdosage is not available [FDA Label]. | Erenumab CGRP antibodies demonstrate a low risk for drug-drug interactions and hepatotoxicity since they are predominantly metabolized by degradation into peptides and single amino acids [A33090]. | Following a single subcutaneous dose of 70 mg or 140 mg erenumab administered to healthy adults, the median peak serum concentrations were attained in about 6 days, and the estimated absolute bioavailability was approximately 82% [FDA Label]. | After a single 140 mg intravenous dose, the mean (SD) volume of distribution during the terminal phase (Vz) was estimated to be approximately 3.86 (0.77) L [FDA Label]. | Certain studies show that the population estimate of linear clearance is independent of erenumab concentrations and stays approximately constant at 0.214 L/day (95% CI: 0.191–0.243) [A33091]. In contrast, the nonlinear clearance is dependent on the target receptor density and the amount of erenumab bound to the receptors [A33091]. Nevertheless, the maximal nonlinear clearance was observed to be about 1.84L/day [A33091]. | Antibodies | NA | NA | NA | NA | Calcitonin gene-related peptide type 1 receptor | Aimovig | Novartis | Novartis | Subcutaneous | 70 mg / mL | AIMOVIG is contraindicated in patients with serious hypersensitivity to erenumab-aooe or to any of the excipients. Reactions have included anaphylaxis and angioedema [see WARNINGS AND PRECAUTIONS]. | injection site reactions (pain or redness), constipation, and muscle spasms or cramps | Aimovig is a monoclonal antibody that blocks the activation of a certain protein that can produce a migraine attack. This protein, called calcitonin gene- related peptide (CGRP), can cause blood vessels to dilate and cause inflammation and migraine headache pain. Aimovig is a prescription medicine used... | Aimovig (erenumab-aooe) Injection is a calcitonin gene-related peptide receptor antagonist indicated for the preventive treatment of migraine in adults. | NA | NA | Link | Link | NA |
| 15414 | Th1595 | Erenumab | >Th1595_Erenumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSSFGMHWVRQAPGKGLEWVAVISFDGSIKYSVDSVKGRFTISRDNSKNTLFLQMNSLRAEDTAVYYCARDRLNYYDSSGYYHYKYYGMAVWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKCCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | C6472H9964N1728O2018S50 | NA | NA | NA | Erenumab exhibits non-linear kinetics as a result of binding to the CGRP receptor [FDA Label]. Lower than 2-fold accumulation was recorded in trough serum concentrations (Cmin) for episodic and chronic migraine patients following subcutaneous administration of 70 mg once-monthly and 140 mg once-monthly doses [FDA Label]. Serum trough concentrations approached steady state by 3 months of dosing [FDA Label]. The effective half-life of erenumab was observed to be 28 days [FDA Label]. | Erenumab (AMG-334) (INN; trade name Aimovig) is a human monoclonal antibody designed specifically to bind and antagonize the calcitonin gene-related peptide receptor (CGRPR) as a means to prevent migraines. Aimovig, as released and marketed by Novartis and Amgen, is in fact a novel therapeutic approach as the first and only FDA approved treatment specifically developed to prevent migraine by blocking the CGRP receptor, which is believed to play a critical role in migraine [L2823]. In particular, erenumab-aooe is a human immunoglobulin G2 monoclonal antibody that has high affinity binding to the CGRP receptor [FDA Label]. The antibody is produced utlilizing recombinant DNA technology in Chinese hamster ovary cells [FDA Label]. It is composed of 2 heavy chains, each containing 456 amino acids, and 2 light chains of the lambda subclass, each containing 216 amino acids, with an approximate molecular weight of 150 kDa [FDA Label]. | Erenumab is indicated for the preventative treatment of migraine in adults [FDA Label]. | As a human monoclonal antibody designed to specifically bind with and antagonize the calcitonin gene-related peptide (CGRP) receptor, there is the possibility that erenumab could interfere with natural activities of CGRP that may not be immediately or directly associated with migraines. For example, at peripheral synapses, CGRP released from trigeminal terminals results in vasodilation by way of CGRP receptor on smooth muscle cells of meningeal and cerebral blood vessels, making CGRP a potent general arterial vasodilator [A33090]. Antagonism of CGRP receptors responsible for such vasodilation could theoretically result in vasoconstriction and raises in blood pressure. In a randomised, double-blind, placebo-controlled study in healthy volunteers, concomitant administration of erenumab (140 mg intravenous, single dose) with sumatriptan (12 mg subcutaneous, given as two 6 mg doses separated by one hour) had no effect on resting blood pressure compared with sumatriptan alone, however [FDA Label]. Please note that erenumab is indicated for subcutaneous use only, though [FDA Label]. | Erenumab is a human monoclonal antibody that has been designed to bind specifically to the calcitonin gene-related peptide (CGRP) receptor and antagonize the CGRP receptor function [FDA Label]. Studies since 1985 have demonstrated that CGRP levels increase during acute migraine attacks in migraine-suffering patients but normalize after efficacious sumatriptan therapy [A33090]. Moreover, research has also shown that intravenous administration of CGRP can induce migraine-like attacks in migraine-suffering patients [A33090]. For all these reasons, the binding and antagonism of CGRP receptors was designed to be mechanism of action for erenumab to take advantage of in reversing the migraine-inducing activity of natural CGRP. CGRP and its receptor are expressed in both the peripheral and the central nervous system [A33091]. In addition to playing a role in cranial nociception, CGRP is also a potent general arterial vasodilator [A33091]. At peripheral synapses, CGRP released from trigeminal terminals results in vasodilation via CGRP receptors on the smooth muscle cells of meningeal and cerebral blood vessels [A33090]. | The most common side effects of erenumab include pain, redness, or swelling at the injection site, and constipation. Information regarding overdosage is not available [FDA Label]. | Erenumab CGRP antibodies demonstrate a low risk for drug-drug interactions and hepatotoxicity since they are predominantly metabolized by degradation into peptides and single amino acids [A33090]. | Following a single subcutaneous dose of 70 mg or 140 mg erenumab administered to healthy adults, the median peak serum concentrations were attained in about 6 days, and the estimated absolute bioavailability was approximately 82% [FDA Label]. | After a single 140 mg intravenous dose, the mean (SD) volume of distribution during the terminal phase (Vz) was estimated to be approximately 3.86 (0.77) L [FDA Label]. | Certain studies show that the population estimate of linear clearance is independent of erenumab concentrations and stays approximately constant at 0.214 L/day (95% CI: 0.191–0.243) [A33091]. In contrast, the nonlinear clearance is dependent on the target receptor density and the amount of erenumab bound to the receptors [A33091]. Nevertheless, the maximal nonlinear clearance was observed to be about 1.84L/day [A33091]. | Antibodies, Monoclonal | NA | NA | NA | NA | Calcitonin gene-related peptide type 1 receptor | Aimovig | AMGEN INC | AMGEN INC | Subcutaneous | 70 mg/1mL | AIMOVIG is contraindicated in patients with serious hypersensitivity to erenumab-aooe or to any of the excipients. Reactions have included anaphylaxis and angioedema [see WARNINGS AND PRECAUTIONS]. | injection site reactions (pain or redness), constipation, and muscle spasms or cramps | Aimovig is a monoclonal antibody that blocks the activation of a certain protein that can produce a migraine attack. This protein, called calcitonin gene- related peptide (CGRP), can cause blood vessels to dilate and cause inflammation and migraine headache pain. Aimovig is a prescription medicine used... | Aimovig (erenumab-aooe) Injection is a calcitonin gene-related peptide receptor antagonist indicated for the preventive treatment of migraine in adults. | NA | NA | Link | Link | NA |
| 15429 | Th1596 | Eptinezumab | >Th1596_Eptinezumab EVQLVESGGGLVQPGGSLRLSCAVSGIDLSGYYMNWVRQAPGKGLEWVGVIGINGATYYASWAKGRFTISRDNSKTTVYLQMNSLRAEDTAVYFCARGDIWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDARVEPKSCDKTHTCPPCPAPELLGGPSVTLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYASTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143000 | NA | NA | NA | NA | The plasma half-life after an intravenous infusion is approximately 27 days.[L12318] | Eptinezumab is a fully-humanized IgG1 antibody manufactured using yeast (_Pichia pastoris_) and developed by Lundbeck Seattle Biopharmaceuticals.[L12318] Eptinezumab has been specifically designed to bind to both alpha and beta forms of the human calcitonin gene-related peptide (CGRP).[F94,A33105,A33106,A33108] It was approved by the FDA in February 2020 for the preventive treatment of migraine headaches in adults.[L12318] | Eptinezumab is indicated for the preventive treatment of migraine in adults.[L12318] | Eptinezumab is experimentally administered as an intravenous infusion and/or subcutaneous injection [A33105, A33108]. During Phase 3 clinical trials, it was noted that patients with episodic migraine who on average had 8.6 days of migraine per month demonstrated significant reductions in migraine frequency over weeks 1-12, associated with the 300mg dose arm.[L2825] Additionally, 29.7% of patients achieved a 75% or greater reduction in migraine days from baseline, compared to 16.2% for placebo (p<0.0007).[L2825] Moreover, a post hoc analysis revealed that those patients achieving a 75% or greater response rate had over an eight-fold increase in days between migraines.[L2825] | Eptinezumab is a fully-humanized IgG1 antibody manufactured and designed specifically to bind both alpha and beta forms of the human calcitonin gene-related peptide (CGRP).[F94,A33105,A33106,A33108,A33114] Studies since 1985 have demonstrated that CGRP levels increase during acute migraine attacks in migraine-suffering patients but normalize after efficacious sumatriptan therapy.[A33090] Moreover, research has also shown that intravenous administration of CGRP can induce migraine-like attacks in migraine-suffering patients.[A33090] For all these reasons, the binding of CGRP to interfere with its activity was specifically designed to be the form and mechanism of action for eptinezumab. The binding of eptinezumab to natural endogenous CGRP subsequently interferes with its activities, such as its binding to CGRP receptors, for example. | The most frequent adverse events associated with eptinezumab use include upper respiratory tract infection, urinary tract infection, fatigue, back pain, arthralgia, and nausea and vomiting [A33108]. No data regarding overdosage has been reported yet. | Monoclonal antibody agents like eptinezumab are not expected to generate toxic metabolites as they generally undergo proteolysis to their constituent amino acids.[F94] | Eptinezumab is the only potent and selective and anti-calcitonin gene-related peptide (CGRP) monoclonal antibody administered by quarterly infusion for migraine prevention delivering 100% bioavailability by way of the intravenous route of administration to immediately inhibit CGRP .[L2825] With an intravenous dose of eptinezumab 1000 mg, the mean maximum concentration of 336.4 ug/mL (SD 79.9) occurred after 4.8 hours after the start of the 1 hour infusion [A33108]. The mean exposure to free eptinezumab, as characterized by area under the plasma concentration-time curve from time zero to the time of the last quantifiable concentration and from time zero to infinity were 8245 days per ug per mL (SD 2619) and 8722 days per ug per mL (SD 2522), respectively [A33108]. | The central volume of distribution for eptinezumab is approximately 3.7 L.[L12318] | The apparent clearance of eptinezumab is 0.006 L/h.[L12318] | Antibodies | NA | NA | NA | NA | Calcitonin gene-related peptide 1,Calcitonin gene-related peptide 2 | Vyepti | Lundbeck Inc. | Lundbeck Inc. | Intravenous | 100 mg / mL | VYEPTI is contraindicated in patients with serious hypersensitivity to eptinezumab-jjmr or to any of the excipients in VYEPTI. Reactions have included angioedema [see WARNINGS AND PRECAUTIONS]. | runny or stuffy nose and hypersensitivity reactions (itching, flushing) | Vyepti is a prescription medicine used for the preventive treatment of migraine in adults. It is not known if this medicine is safe and effective in children. | VYEPTI is indicated for the preventive treatment of migraine in adults. | NA | NA | Link | Link | NA |
| 15430 | Th1596 | Eptinezumab | >Th1596_Eptinezumab EVQLVESGGGLVQPGGSLRLSCAVSGIDLSGYYMNWVRQAPGKGLEWVGVIGINGATYYASWAKGRFTISRDNSKTTVYLQMNSLRAEDTAVYFCARGDIWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDARVEPKSCDKTHTCPPCPAPELLGGPSVTLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYASTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143000 | NA | NA | NA | NA | The plasma half-life after an intravenous infusion is approximately 27 days.[L12318] | Eptinezumab is a fully-humanized IgG1 antibody manufactured using yeast (_Pichia pastoris_) and developed by Lundbeck Seattle Biopharmaceuticals.[L12318] Eptinezumab has been specifically designed to bind to both alpha and beta forms of the human calcitonin gene-related peptide (CGRP).[F94,A33105,A33106,A33108] It was approved by the FDA in February 2020 for the preventive treatment of migraine headaches in adults.[L12318] | Eptinezumab is indicated for the preventive treatment of migraine in adults.[L12318] | Eptinezumab is experimentally administered as an intravenous infusion and/or subcutaneous injection [A33105, A33108]. During Phase 3 clinical trials, it was noted that patients with episodic migraine who on average had 8.6 days of migraine per month demonstrated significant reductions in migraine frequency over weeks 1-12, associated with the 300mg dose arm.[L2825] Additionally, 29.7% of patients achieved a 75% or greater reduction in migraine days from baseline, compared to 16.2% for placebo (p<0.0007).[L2825] Moreover, a post hoc analysis revealed that those patients achieving a 75% or greater response rate had over an eight-fold increase in days between migraines.[L2825] | Eptinezumab is a fully-humanized IgG1 antibody manufactured and designed specifically to bind both alpha and beta forms of the human calcitonin gene-related peptide (CGRP).[F94,A33105,A33106,A33108,A33114] Studies since 1985 have demonstrated that CGRP levels increase during acute migraine attacks in migraine-suffering patients but normalize after efficacious sumatriptan therapy.[A33090] Moreover, research has also shown that intravenous administration of CGRP can induce migraine-like attacks in migraine-suffering patients.[A33090] For all these reasons, the binding of CGRP to interfere with its activity was specifically designed to be the form and mechanism of action for eptinezumab. The binding of eptinezumab to natural endogenous CGRP subsequently interferes with its activities, such as its binding to CGRP receptors, for example. | The most frequent adverse events associated with eptinezumab use include upper respiratory tract infection, urinary tract infection, fatigue, back pain, arthralgia, and nausea and vomiting [A33108]. No data regarding overdosage has been reported yet. | Monoclonal antibody agents like eptinezumab are not expected to generate toxic metabolites as they generally undergo proteolysis to their constituent amino acids.[F94] | Eptinezumab is the only potent and selective and anti-calcitonin gene-related peptide (CGRP) monoclonal antibody administered by quarterly infusion for migraine prevention delivering 100% bioavailability by way of the intravenous route of administration to immediately inhibit CGRP .[L2825] With an intravenous dose of eptinezumab 1000 mg, the mean maximum concentration of 336.4 ug/mL (SD 79.9) occurred after 4.8 hours after the start of the 1 hour infusion [A33108]. The mean exposure to free eptinezumab, as characterized by area under the plasma concentration-time curve from time zero to the time of the last quantifiable concentration and from time zero to infinity were 8245 days per ug per mL (SD 2619) and 8722 days per ug per mL (SD 2522), respectively [A33108]. | The central volume of distribution for eptinezumab is approximately 3.7 L.[L12318] | The apparent clearance of eptinezumab is 0.006 L/h.[L12318] | Antibodies, Monoclonal | NA | NA | NA | NA | Calcitonin gene-related peptide 1,Calcitonin gene-related peptide 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15431 | Th1596 | Eptinezumab | >Th1596_Eptinezumab EVQLVESGGGLVQPGGSLRLSCAVSGIDLSGYYMNWVRQAPGKGLEWVGVIGINGATYYASWAKGRFTISRDNSKTTVYLQMNSLRAEDTAVYFCARGDIWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDARVEPKSCDKTHTCPPCPAPELLGGPSVTLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYASTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143000 | NA | NA | NA | NA | The plasma half-life after an intravenous infusion is approximately 27 days.[L12318] | Eptinezumab is a fully-humanized IgG1 antibody manufactured using yeast (_Pichia pastoris_) and developed by Lundbeck Seattle Biopharmaceuticals.[L12318] Eptinezumab has been specifically designed to bind to both alpha and beta forms of the human calcitonin gene-related peptide (CGRP).[F94,A33105,A33106,A33108] It was approved by the FDA in February 2020 for the preventive treatment of migraine headaches in adults.[L12318] | Eptinezumab is indicated for the preventive treatment of migraine in adults.[L12318] | Eptinezumab is experimentally administered as an intravenous infusion and/or subcutaneous injection [A33105, A33108]. During Phase 3 clinical trials, it was noted that patients with episodic migraine who on average had 8.6 days of migraine per month demonstrated significant reductions in migraine frequency over weeks 1-12, associated with the 300mg dose arm.[L2825] Additionally, 29.7% of patients achieved a 75% or greater reduction in migraine days from baseline, compared to 16.2% for placebo (p<0.0007).[L2825] Moreover, a post hoc analysis revealed that those patients achieving a 75% or greater response rate had over an eight-fold increase in days between migraines.[L2825] | Eptinezumab is a fully-humanized IgG1 antibody manufactured and designed specifically to bind both alpha and beta forms of the human calcitonin gene-related peptide (CGRP).[F94,A33105,A33106,A33108,A33114] Studies since 1985 have demonstrated that CGRP levels increase during acute migraine attacks in migraine-suffering patients but normalize after efficacious sumatriptan therapy.[A33090] Moreover, research has also shown that intravenous administration of CGRP can induce migraine-like attacks in migraine-suffering patients.[A33090] For all these reasons, the binding of CGRP to interfere with its activity was specifically designed to be the form and mechanism of action for eptinezumab. The binding of eptinezumab to natural endogenous CGRP subsequently interferes with its activities, such as its binding to CGRP receptors, for example. | The most frequent adverse events associated with eptinezumab use include upper respiratory tract infection, urinary tract infection, fatigue, back pain, arthralgia, and nausea and vomiting [A33108]. No data regarding overdosage has been reported yet. | Monoclonal antibody agents like eptinezumab are not expected to generate toxic metabolites as they generally undergo proteolysis to their constituent amino acids.[F94] | Eptinezumab is the only potent and selective and anti-calcitonin gene-related peptide (CGRP) monoclonal antibody administered by quarterly infusion for migraine prevention delivering 100% bioavailability by way of the intravenous route of administration to immediately inhibit CGRP .[L2825] With an intravenous dose of eptinezumab 1000 mg, the mean maximum concentration of 336.4 ug/mL (SD 79.9) occurred after 4.8 hours after the start of the 1 hour infusion [A33108]. The mean exposure to free eptinezumab, as characterized by area under the plasma concentration-time curve from time zero to the time of the last quantifiable concentration and from time zero to infinity were 8245 days per ug per mL (SD 2619) and 8722 days per ug per mL (SD 2522), respectively [A33108]. | The central volume of distribution for eptinezumab is approximately 3.7 L.[L12318] | The apparent clearance of eptinezumab is 0.006 L/h.[L12318] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Calcitonin gene-related peptide 1,Calcitonin gene-related peptide 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15443 | Th1597 | Fremanezumab | >Th1597_Fremanezumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSNYWISWVRQAPGKGLEWVAEIRSESDASATHYAEAVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCLAYFDYGLAIQNYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKCCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPSSIEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The mean half-life recorded for fremanezumab was similar across doses for Japanese and Caucasian study subjects and was estimated to be approximately 31-39 days.[A33125,L11749] | Fremanezumab is a humanized monoclonal antibody targeted against human calcitonin gene-related peptide (CGRP) for the prevention of migraine headaches.[L11749] It was developed by Teva Pharmaceuticals USA and approved by the FDA in September 2018.[L11779] Along with other recently approved anti-CGRP therapies such as [galcanezumab], [erenumab], and the oral CGRP antagonist [ubrogepant], fremanezumab represents an important step forward in the treatment and prevention of migraine headaches. | Fremanezumab is indicated for the preventative treatment of migraine in adults.[L11749] | Fremanezumab is a subcutaneous injection that targets the calcitonin gene-related peptide (CGRP) ligand, preventing its binding to the CGRP receptor.[A33114,L11749] It possesses a long duration of action requiring only monthly or quarterly administration and appears well-tolerated in clinical trials.[L11749] | Studies dating back to 1985 have demonstrated that CGRP levels increase during acute migraine attacks in migraine-suffering patients but normalize after administration of antimigraine therapy such as [sumatriptan].[A33090] Moreover, research has shown that intravenous administration of CGRP can induce migraine-like attacks in migraine-suffering patients.[A33090] For these reasons, and despite the fact that their role in migraine headaches has not been entirely elucidated, CGRP and its receptors have become desirable targets for antimigraine therapies. Fremanezumab is a humanized monoclonal antibody directed against endogenous CGRP - it interferes with the activity of CGRP, preventing its downstream effects and ultimately mitigating the development of migraine headaches.[L11749] | Information regarding overdose of fremanezumab is not readily available. The most common adverse events that led to discontinuation of fremanezumab therapy were injection site reactions including erythema, induration, and pain.[L11749] | Like other monoclonal antibodies, fremanezumab is expected to undergo enzymatic proteolysis into smaller peptides and amino acids.[L11749] | Geometric mean ratios (GMRs) for Cmax for Japanese and Caucasian study subjects were 0.91, 1.04, and 1.14 for 225 mg, 675 mg, and 900 mg doses of fremanezumab [A33125]. GMRs for AUC (0-inf) were 0.96, 1.09, and 0.98, respectively [A33125]. Mean Tmax in a range of 5 to 11 days were similar across doses for both ethnicities as well [A33125]. | Fremanezumab has an apparent volume of distribution of approximately 6 liters which indicates very little distribution into tissue.[L11749] | The apparent clearance of fremanezumab is 0.141 L/day.[L11749] | Antibodies | NA | NA | NA | NA | Calcitonin gene-related peptide 1,Calcitonin gene-related peptide 2 | Ajovy | TEVA Canada Limited | TEVA Canada Limited | Subcutaneous | 225 mg / 1.5 mL | AJOVY is contraindicated in patients with serious hypersensitivity to fremanezumab-vfrm or to any of the excipients. Reactions have included anaphylaxis and angioedema [see WARNINGS AND PRECAUTIONS]. | injection site reactions (pain, swelling, and redness) | Ajovy is an injectable prescription medicine used to prevent migraine headaches in adults. Ajovy works by blocking the activity of calcitonin gene-related peptide (CGRP). Ajovy may also be used for purposes not listed in this medication guide. Warnings Follow all directions on your medicine label and... | Ajovy is a prescription medicine used as a preventative treatment of the symptoms of Migraine. Ajovy may be used alone or with other medications. | NA | AJOVY (fremanezumab-vfrm) injection is a sterile, preservative-free, clear to opalescent, colorless to slightly yellow solution for subcutaneous injection, supplied in a single-dose 225 mg/1.5 mL prefilled syringe. | Link | Link | NA |
| 15444 | Th1597 | Fremanezumab | >Th1597_Fremanezumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSNYWISWVRQAPGKGLEWVAEIRSESDASATHYAEAVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCLAYFDYGLAIQNYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKCCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPSSIEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The mean half-life recorded for fremanezumab was similar across doses for Japanese and Caucasian study subjects and was estimated to be approximately 31-39 days.[A33125,L11749] | Fremanezumab is a humanized monoclonal antibody targeted against human calcitonin gene-related peptide (CGRP) for the prevention of migraine headaches.[L11749] It was developed by Teva Pharmaceuticals USA and approved by the FDA in September 2018.[L11779] Along with other recently approved anti-CGRP therapies such as [galcanezumab], [erenumab], and the oral CGRP antagonist [ubrogepant], fremanezumab represents an important step forward in the treatment and prevention of migraine headaches. | Fremanezumab is indicated for the preventative treatment of migraine in adults.[L11749] | Fremanezumab is a subcutaneous injection that targets the calcitonin gene-related peptide (CGRP) ligand, preventing its binding to the CGRP receptor.[A33114,L11749] It possesses a long duration of action requiring only monthly or quarterly administration and appears well-tolerated in clinical trials.[L11749] | Studies dating back to 1985 have demonstrated that CGRP levels increase during acute migraine attacks in migraine-suffering patients but normalize after administration of antimigraine therapy such as [sumatriptan].[A33090] Moreover, research has shown that intravenous administration of CGRP can induce migraine-like attacks in migraine-suffering patients.[A33090] For these reasons, and despite the fact that their role in migraine headaches has not been entirely elucidated, CGRP and its receptors have become desirable targets for antimigraine therapies. Fremanezumab is a humanized monoclonal antibody directed against endogenous CGRP - it interferes with the activity of CGRP, preventing its downstream effects and ultimately mitigating the development of migraine headaches.[L11749] | Information regarding overdose of fremanezumab is not readily available. The most common adverse events that led to discontinuation of fremanezumab therapy were injection site reactions including erythema, induration, and pain.[L11749] | Like other monoclonal antibodies, fremanezumab is expected to undergo enzymatic proteolysis into smaller peptides and amino acids.[L11749] | Geometric mean ratios (GMRs) for Cmax for Japanese and Caucasian study subjects were 0.91, 1.04, and 1.14 for 225 mg, 675 mg, and 900 mg doses of fremanezumab [A33125]. GMRs for AUC (0-inf) were 0.96, 1.09, and 0.98, respectively [A33125]. Mean Tmax in a range of 5 to 11 days were similar across doses for both ethnicities as well [A33125]. | Fremanezumab has an apparent volume of distribution of approximately 6 liters which indicates very little distribution into tissue.[L11749] | The apparent clearance of fremanezumab is 0.141 L/day.[L11749] | Antibodies, Monoclonal | NA | NA | NA | NA | Calcitonin gene-related peptide 1,Calcitonin gene-related peptide 2 | Ajovy Filled Pen | Teva | Teva | Subcutaneous | 225 mg | AJOVY is contraindicated in patients with serious hypersensitivity to fremanezumab-vfrm or to any of the excipients. Reactions have included anaphylaxis and angioedema [see WARNINGS AND PRECAUTIONS]. | The most common side effects with Ajovy (which may affect more than 1 in 10 people) are reactions at the site of injection: pain, hardening (induration) and reddening of the skin (erythema). | A chemical messenger called CGRP contributes to the development of migraine. Ajovy is a monoclonal antibody (a type of protein) designed to attach to CGRP and prevent it from binding to its target on the body’s cells thereby helping to prevent migraines from occurring. | used to prevent migraine in adults who have migraines at least 4 days a month. | NA | NA | Link | Link | NA |
| 15445 | Th1597 | Fremanezumab | >Th1597_Fremanezumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSNYWISWVRQAPGKGLEWVAEIRSESDASATHYAEAVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCLAYFDYGLAIQNYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKCCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPSSIEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The mean half-life recorded for fremanezumab was similar across doses for Japanese and Caucasian study subjects and was estimated to be approximately 31-39 days.[A33125,L11749] | Fremanezumab is a humanized monoclonal antibody targeted against human calcitonin gene-related peptide (CGRP) for the prevention of migraine headaches.[L11749] It was developed by Teva Pharmaceuticals USA and approved by the FDA in September 2018.[L11779] Along with other recently approved anti-CGRP therapies such as [galcanezumab], [erenumab], and the oral CGRP antagonist [ubrogepant], fremanezumab represents an important step forward in the treatment and prevention of migraine headaches. | Fremanezumab is indicated for the preventative treatment of migraine in adults.[L11749] | Fremanezumab is a subcutaneous injection that targets the calcitonin gene-related peptide (CGRP) ligand, preventing its binding to the CGRP receptor.[A33114,L11749] It possesses a long duration of action requiring only monthly or quarterly administration and appears well-tolerated in clinical trials.[L11749] | Studies dating back to 1985 have demonstrated that CGRP levels increase during acute migraine attacks in migraine-suffering patients but normalize after administration of antimigraine therapy such as [sumatriptan].[A33090] Moreover, research has shown that intravenous administration of CGRP can induce migraine-like attacks in migraine-suffering patients.[A33090] For these reasons, and despite the fact that their role in migraine headaches has not been entirely elucidated, CGRP and its receptors have become desirable targets for antimigraine therapies. Fremanezumab is a humanized monoclonal antibody directed against endogenous CGRP - it interferes with the activity of CGRP, preventing its downstream effects and ultimately mitigating the development of migraine headaches.[L11749] | Information regarding overdose of fremanezumab is not readily available. The most common adverse events that led to discontinuation of fremanezumab therapy were injection site reactions including erythema, induration, and pain.[L11749] | Like other monoclonal antibodies, fremanezumab is expected to undergo enzymatic proteolysis into smaller peptides and amino acids.[L11749] | Geometric mean ratios (GMRs) for Cmax for Japanese and Caucasian study subjects were 0.91, 1.04, and 1.14 for 225 mg, 675 mg, and 900 mg doses of fremanezumab [A33125]. GMRs for AUC (0-inf) were 0.96, 1.09, and 0.98, respectively [A33125]. Mean Tmax in a range of 5 to 11 days were similar across doses for both ethnicities as well [A33125]. | Fremanezumab has an apparent volume of distribution of approximately 6 liters which indicates very little distribution into tissue.[L11749] | The apparent clearance of fremanezumab is 0.141 L/day.[L11749] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Calcitonin gene-related peptide 1,Calcitonin gene-related peptide 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15458 | Th1598 | Galcanezumab | >Th1598_Galcanezumab QVQLVQSGAEVKKPGSSVKVSCKASGYTFGNYWMQWVRQAPGQGLEWMGAIYEGTGKTVYIQKFADRVTITADKSTSTAYMELSSLRSEDTAVYYCARLSDYVSGFGYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 147000 | NA | NA | NA | NA | The mean serum half-life of galcanezumab is similar at all dose levels at about 25-30 days.[A33112] The elimination half-life of galcanezumab was ultimately approximately 27 days.[L4894] | LY2951742/galcanezumab is a fully humanized monoclonal antibody against human calcitonin gene-related peptide (CGRP) that is developed by ELi Lilly and Company.[A33105] This therapy is given as a single subcutaneous injection twice a month and ongoing clinical trials for the agent are for episodic and chronic migraine as well as cluster headaches.[A33114] Although various small-molecule CGRP receptor antagonists have also been developed, humanized monoclonal antibodies like galcanezumab are specifically designed to potently and selectively bind to the CGRP entities directly.[A33112] Given this target specificity, lack of off-target toxicity, and characteristic proteolysis profile of immunoglobulin antibodies to not undergo metabolism by liver enzymes, galcanezumab possesses favourable and promising safety and tolerability.[A33112] Galcanezumab was given FDA approval on 27 September 2018.[L4894] | Galcanezumab is a humanized monoclonal antibody that is indicated for migraine prophylaxis and treatment of episodic cluster headaches in adults by binding endogenous human calcitonin gene-related peptide (CGRP).[A33112,L4894] | Galcanezumab is administered as a subcutaneous injection.[A33112,A33114,L4894] During clinical trials, it was noted that galcanezumab therapy resulted in a significant reduction in the mean number of migraine headache days and a good tolerability profile.[A33105] Additionally, post hoc efficacy analyses showed that 32% in the galcanezumab group versus 18% in the placebo group were complete responders.[A33105] Finally, the most commonly reported adverse events associated with galcanezumab use are headache, nasopharyngitis, hematuria, dermatitis, diarrhea, toothache, and increased alanine aminotransferase (ALT).[A33112] | Galcanezumab is a fully humanized monoclonal antibody designed and manufactured specifically against calcitonin gene-related peptide (CGRP).[A33105,L4894] It binds avidly to human CGRP, with a binding affinity (Kd) of 31 pM (4.5 ng/mL). Studies since 1985 have demonstrated that CGRP levels increase during acute migraine attacks in migraine-suffering patients but normalize after efficacious sumatriptan therapy.[A33090] Moreover, research has also shown that intravenous administration of CGRP can induce migraine-like attacks in migraine-suffering patients.[A33090] For all these reasons, the binding of CGRP to interfere with its activity was specifically designed to be the mechanism of action for galcanezumab to take advantage of in reversing the migraine-inducing activity of natural CGRP. The binding of galcanezumab to natural endogenous CGRP subsequently interferes with its activities, such as its binding to CGRP receptors, for example. Studies have also shown that humanized monoclonal antibodies against CGRP have proven successful in reducing the frequency of migraine headaches in early clinical trials as a preventative therapeutic.[A33112] | Overdose and LD50 date are not readily available.[L4894] The most common adverse effects associated with galcanezumab during clinical trials include headache, nasopharyngitis, hematuria, and contact dermatitis.[A33112] However, with the exception of hematuria which was not present in placebo treatment arms, the frequencies of these events were similar to placebo.[A33112] Additional frequently reported adverse effects in subjects receiving galcanezumab were diarrhea, toothache, and increased alanine aminotransferase (ALT).[A33112] The pharmacokinetics of galcanezumab were not affected by age, sex, race, or subtypes of migraine spectrum (episodic or chronic migraine), based on a population pharmacokinetic analysis.[L4894] Body weight has no clinically relevant effect on the pharmacokinetics of galcanezumab.[L4894] Renal and hepatic impairment are not expected to affect the pharmacokinetics of galcanezumab.[L4894] Population pharmacokinetic analysis of integrated data from the galcanezumab clinical studies revealed that creatinine clearance did not affect the pharmacokinetics of galcanezumab in patients with mild or moderate renal impairment.[L4894] Patients with severe renal impairment (creatinine clearance <30 mL/min) have not been studied.[L4894] Based on a population PK analysis, bilirubin concentration did not significantly influence the CL/F of galcanezumab.[L4894] Studies regarding the carcinogenic potential and genetic toxicology of galcanezumab have not yet been conducted.[L4894] When galcanezumab (0, 30, or 250 mg/kg) was administered to male rats by subcutaneous injection prior to and during mating, no adverse effects on fertility was observed.[L4894] The higher dose tested was associated with a plasma exposure (Cave, ss) 8 times that in humans at the recommended human dose (RHD) of 120 mg.[L4894] When galcanezumab was administered to female rats by subcutaneous injection in two studies (0, 30, or 100 mg/kg; 0 or 250 mg/kg) prior to and during mating and continuing throughout organogenesis, no adverse effects on fertility were observed.[L4894] The highest dose tested (250 mg/kg) was associated with a plasma Cave, ss 38 times that in humans at the RHD.[L4894] | Monoclonal antibody agents like galcanezumab are not expected to generate toxic metabolites as they generally undergo proteolysis to their constituent amino acids.[F94] In particular, after administration galcanezumab is specifically expected to be degraded into small peptides and amino acids via catabolic pathways in the same manner as endogenous immunoglobulins.[L4894] Galcanezumab is also not believed to be metabolized by liver enzymes - making drug-drug interactions relatively unlikely.[L4894] | Following single dose subcutaneous administration, the time to maximum concentration was recorded as 5 days.[L4894] The injection site location did not appear to significantly influence the absorption of galcanezumab.[L4894] The Cmax and the area under the concentration-time curve from dosing to infinity (AUC (0-8)) are generally considered to be dose proportional over a dose range.[A33112] | The apparent volume of distribution of galcanezumab is documented to be 7.3 L, with 34% inter-individual variability.[L4894] | It is noted that the clearance of galcanezumab is by proteolysis.[A33112] The apparent clearance of galcanezumab was recorded as 0.008 L/h.[L4894] | Antibodies | NA | NA | NA | NA | Calcitonin gene-related peptide 1,Calcitonin gene-related peptide 2 | Emgality | Eli Lilly and Company | Eli Lilly and Company | Subcutaneous | 120 mg/1mL | EMGALITY is contraindicated in patients with serious hypersensitivity to galcanezumab-gnlm or to any of the excipients [see WARNINGS AND PRECAUTIONS]. | injection site reactions such as pain, redness, and itching | Emgality is a calcitonin-gene related peptide antagonist. Emgality is a prescription medicine used to prevent migraine headaches in adults. Emgality is also used to treat cluster headache episodes in adults. It is not known if Emgality is safe and effective in children. Warnings Follow all directions... | Emgality (galcanezumab-gnlm) is a calcitonin-gene related peptide antagonist indicated for the preventive treatment of migraine in adults. | NA | NA | Link | Link | NA |
| 15459 | Th1598 | Galcanezumab | >Th1598_Galcanezumab QVQLVQSGAEVKKPGSSVKVSCKASGYTFGNYWMQWVRQAPGQGLEWMGAIYEGTGKTVYIQKFADRVTITADKSTSTAYMELSSLRSEDTAVYYCARLSDYVSGFGYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 147000 | NA | NA | NA | NA | The mean serum half-life of galcanezumab is similar at all dose levels at about 25-30 days.[A33112] The elimination half-life of galcanezumab was ultimately approximately 27 days.[L4894] | LY2951742/galcanezumab is a fully humanized monoclonal antibody against human calcitonin gene-related peptide (CGRP) that is developed by ELi Lilly and Company.[A33105] This therapy is given as a single subcutaneous injection twice a month and ongoing clinical trials for the agent are for episodic and chronic migraine as well as cluster headaches.[A33114] Although various small-molecule CGRP receptor antagonists have also been developed, humanized monoclonal antibodies like galcanezumab are specifically designed to potently and selectively bind to the CGRP entities directly.[A33112] Given this target specificity, lack of off-target toxicity, and characteristic proteolysis profile of immunoglobulin antibodies to not undergo metabolism by liver enzymes, galcanezumab possesses favourable and promising safety and tolerability.[A33112] Galcanezumab was given FDA approval on 27 September 2018.[L4894] | Galcanezumab is a humanized monoclonal antibody that is indicated for migraine prophylaxis and treatment of episodic cluster headaches in adults by binding endogenous human calcitonin gene-related peptide (CGRP).[A33112,L4894] | Galcanezumab is administered as a subcutaneous injection.[A33112,A33114,L4894] During clinical trials, it was noted that galcanezumab therapy resulted in a significant reduction in the mean number of migraine headache days and a good tolerability profile.[A33105] Additionally, post hoc efficacy analyses showed that 32% in the galcanezumab group versus 18% in the placebo group were complete responders.[A33105] Finally, the most commonly reported adverse events associated with galcanezumab use are headache, nasopharyngitis, hematuria, dermatitis, diarrhea, toothache, and increased alanine aminotransferase (ALT).[A33112] | Galcanezumab is a fully humanized monoclonal antibody designed and manufactured specifically against calcitonin gene-related peptide (CGRP).[A33105,L4894] It binds avidly to human CGRP, with a binding affinity (Kd) of 31 pM (4.5 ng/mL). Studies since 1985 have demonstrated that CGRP levels increase during acute migraine attacks in migraine-suffering patients but normalize after efficacious sumatriptan therapy.[A33090] Moreover, research has also shown that intravenous administration of CGRP can induce migraine-like attacks in migraine-suffering patients.[A33090] For all these reasons, the binding of CGRP to interfere with its activity was specifically designed to be the mechanism of action for galcanezumab to take advantage of in reversing the migraine-inducing activity of natural CGRP. The binding of galcanezumab to natural endogenous CGRP subsequently interferes with its activities, such as its binding to CGRP receptors, for example. Studies have also shown that humanized monoclonal antibodies against CGRP have proven successful in reducing the frequency of migraine headaches in early clinical trials as a preventative therapeutic.[A33112] | Overdose and LD50 date are not readily available.[L4894] The most common adverse effects associated with galcanezumab during clinical trials include headache, nasopharyngitis, hematuria, and contact dermatitis.[A33112] However, with the exception of hematuria which was not present in placebo treatment arms, the frequencies of these events were similar to placebo.[A33112] Additional frequently reported adverse effects in subjects receiving galcanezumab were diarrhea, toothache, and increased alanine aminotransferase (ALT).[A33112] The pharmacokinetics of galcanezumab were not affected by age, sex, race, or subtypes of migraine spectrum (episodic or chronic migraine), based on a population pharmacokinetic analysis.[L4894] Body weight has no clinically relevant effect on the pharmacokinetics of galcanezumab.[L4894] Renal and hepatic impairment are not expected to affect the pharmacokinetics of galcanezumab.[L4894] Population pharmacokinetic analysis of integrated data from the galcanezumab clinical studies revealed that creatinine clearance did not affect the pharmacokinetics of galcanezumab in patients with mild or moderate renal impairment.[L4894] Patients with severe renal impairment (creatinine clearance <30 mL/min) have not been studied.[L4894] Based on a population PK analysis, bilirubin concentration did not significantly influence the CL/F of galcanezumab.[L4894] Studies regarding the carcinogenic potential and genetic toxicology of galcanezumab have not yet been conducted.[L4894] When galcanezumab (0, 30, or 250 mg/kg) was administered to male rats by subcutaneous injection prior to and during mating, no adverse effects on fertility was observed.[L4894] The higher dose tested was associated with a plasma exposure (Cave, ss) 8 times that in humans at the recommended human dose (RHD) of 120 mg.[L4894] When galcanezumab was administered to female rats by subcutaneous injection in two studies (0, 30, or 100 mg/kg; 0 or 250 mg/kg) prior to and during mating and continuing throughout organogenesis, no adverse effects on fertility were observed.[L4894] The highest dose tested (250 mg/kg) was associated with a plasma Cave, ss 38 times that in humans at the RHD.[L4894] | Monoclonal antibody agents like galcanezumab are not expected to generate toxic metabolites as they generally undergo proteolysis to their constituent amino acids.[F94] In particular, after administration galcanezumab is specifically expected to be degraded into small peptides and amino acids via catabolic pathways in the same manner as endogenous immunoglobulins.[L4894] Galcanezumab is also not believed to be metabolized by liver enzymes - making drug-drug interactions relatively unlikely.[L4894] | Following single dose subcutaneous administration, the time to maximum concentration was recorded as 5 days.[L4894] The injection site location did not appear to significantly influence the absorption of galcanezumab.[L4894] The Cmax and the area under the concentration-time curve from dosing to infinity (AUC (0-8)) are generally considered to be dose proportional over a dose range.[A33112] | The apparent volume of distribution of galcanezumab is documented to be 7.3 L, with 34% inter-individual variability.[L4894] | It is noted that the clearance of galcanezumab is by proteolysis.[A33112] The apparent clearance of galcanezumab was recorded as 0.008 L/h.[L4894] | Antibodies, Monoclonal | NA | NA | NA | NA | Calcitonin gene-related peptide 1,Calcitonin gene-related peptide 2 | Emgality | Eli Lilly Nederland B.V. | Eli Lilly Nederland B.V. | Subcutaneous | 120 mg | EMGALITY is contraindicated in patients with serious hypersensitivity to galcanezumab-gnlm or to any of the excipients [see WARNINGS AND PRECAUTIONS]. | injection site reactions such as pain, redness, and itching | Emgality is a calcitonin-gene related peptide antagonist. Emgality is a prescription medicine used to prevent migraine headaches in adults. Emgality is also used to treat cluster headache episodes in adults. It is not known if Emgality is safe and effective in children. Warnings Follow all directions... | Emgality (galcanezumab-gnlm) is a calcitonin-gene related peptide antagonist indicated for the preventive treatment of migraine in adults. | NA | NA | Link | Link | NA |
| 15460 | Th1598 | Galcanezumab | >Th1598_Galcanezumab QVQLVQSGAEVKKPGSSVKVSCKASGYTFGNYWMQWVRQAPGQGLEWMGAIYEGTGKTVYIQKFADRVTITADKSTSTAYMELSSLRSEDTAVYYCARLSDYVSGFGYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 147000 | NA | NA | NA | NA | The mean serum half-life of galcanezumab is similar at all dose levels at about 25-30 days.[A33112] The elimination half-life of galcanezumab was ultimately approximately 27 days.[L4894] | LY2951742/galcanezumab is a fully humanized monoclonal antibody against human calcitonin gene-related peptide (CGRP) that is developed by ELi Lilly and Company.[A33105] This therapy is given as a single subcutaneous injection twice a month and ongoing clinical trials for the agent are for episodic and chronic migraine as well as cluster headaches.[A33114] Although various small-molecule CGRP receptor antagonists have also been developed, humanized monoclonal antibodies like galcanezumab are specifically designed to potently and selectively bind to the CGRP entities directly.[A33112] Given this target specificity, lack of off-target toxicity, and characteristic proteolysis profile of immunoglobulin antibodies to not undergo metabolism by liver enzymes, galcanezumab possesses favourable and promising safety and tolerability.[A33112] Galcanezumab was given FDA approval on 27 September 2018.[L4894] | Galcanezumab is a humanized monoclonal antibody that is indicated for migraine prophylaxis and treatment of episodic cluster headaches in adults by binding endogenous human calcitonin gene-related peptide (CGRP).[A33112,L4894] | Galcanezumab is administered as a subcutaneous injection.[A33112,A33114,L4894] During clinical trials, it was noted that galcanezumab therapy resulted in a significant reduction in the mean number of migraine headache days and a good tolerability profile.[A33105] Additionally, post hoc efficacy analyses showed that 32% in the galcanezumab group versus 18% in the placebo group were complete responders.[A33105] Finally, the most commonly reported adverse events associated with galcanezumab use are headache, nasopharyngitis, hematuria, dermatitis, diarrhea, toothache, and increased alanine aminotransferase (ALT).[A33112] | Galcanezumab is a fully humanized monoclonal antibody designed and manufactured specifically against calcitonin gene-related peptide (CGRP).[A33105,L4894] It binds avidly to human CGRP, with a binding affinity (Kd) of 31 pM (4.5 ng/mL). Studies since 1985 have demonstrated that CGRP levels increase during acute migraine attacks in migraine-suffering patients but normalize after efficacious sumatriptan therapy.[A33090] Moreover, research has also shown that intravenous administration of CGRP can induce migraine-like attacks in migraine-suffering patients.[A33090] For all these reasons, the binding of CGRP to interfere with its activity was specifically designed to be the mechanism of action for galcanezumab to take advantage of in reversing the migraine-inducing activity of natural CGRP. The binding of galcanezumab to natural endogenous CGRP subsequently interferes with its activities, such as its binding to CGRP receptors, for example. Studies have also shown that humanized monoclonal antibodies against CGRP have proven successful in reducing the frequency of migraine headaches in early clinical trials as a preventative therapeutic.[A33112] | Overdose and LD50 date are not readily available.[L4894] The most common adverse effects associated with galcanezumab during clinical trials include headache, nasopharyngitis, hematuria, and contact dermatitis.[A33112] However, with the exception of hematuria which was not present in placebo treatment arms, the frequencies of these events were similar to placebo.[A33112] Additional frequently reported adverse effects in subjects receiving galcanezumab were diarrhea, toothache, and increased alanine aminotransferase (ALT).[A33112] The pharmacokinetics of galcanezumab were not affected by age, sex, race, or subtypes of migraine spectrum (episodic or chronic migraine), based on a population pharmacokinetic analysis.[L4894] Body weight has no clinically relevant effect on the pharmacokinetics of galcanezumab.[L4894] Renal and hepatic impairment are not expected to affect the pharmacokinetics of galcanezumab.[L4894] Population pharmacokinetic analysis of integrated data from the galcanezumab clinical studies revealed that creatinine clearance did not affect the pharmacokinetics of galcanezumab in patients with mild or moderate renal impairment.[L4894] Patients with severe renal impairment (creatinine clearance <30 mL/min) have not been studied.[L4894] Based on a population PK analysis, bilirubin concentration did not significantly influence the CL/F of galcanezumab.[L4894] Studies regarding the carcinogenic potential and genetic toxicology of galcanezumab have not yet been conducted.[L4894] When galcanezumab (0, 30, or 250 mg/kg) was administered to male rats by subcutaneous injection prior to and during mating, no adverse effects on fertility was observed.[L4894] The higher dose tested was associated with a plasma exposure (Cave, ss) 8 times that in humans at the recommended human dose (RHD) of 120 mg.[L4894] When galcanezumab was administered to female rats by subcutaneous injection in two studies (0, 30, or 100 mg/kg; 0 or 250 mg/kg) prior to and during mating and continuing throughout organogenesis, no adverse effects on fertility were observed.[L4894] The highest dose tested (250 mg/kg) was associated with a plasma Cave, ss 38 times that in humans at the RHD.[L4894] | Monoclonal antibody agents like galcanezumab are not expected to generate toxic metabolites as they generally undergo proteolysis to their constituent amino acids.[F94] In particular, after administration galcanezumab is specifically expected to be degraded into small peptides and amino acids via catabolic pathways in the same manner as endogenous immunoglobulins.[L4894] Galcanezumab is also not believed to be metabolized by liver enzymes - making drug-drug interactions relatively unlikely.[L4894] | Following single dose subcutaneous administration, the time to maximum concentration was recorded as 5 days.[L4894] The injection site location did not appear to significantly influence the absorption of galcanezumab.[L4894] The Cmax and the area under the concentration-time curve from dosing to infinity (AUC (0-8)) are generally considered to be dose proportional over a dose range.[A33112] | The apparent volume of distribution of galcanezumab is documented to be 7.3 L, with 34% inter-individual variability.[L4894] | It is noted that the clearance of galcanezumab is by proteolysis.[A33112] The apparent clearance of galcanezumab was recorded as 0.008 L/h.[L4894] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Calcitonin gene-related peptide 1,Calcitonin gene-related peptide 2 | Emgality | Eli Lilly and Company | Eli Lilly and Company | Subcutaneous | 100 mg/1mL | EMGALITY is contraindicated in patients with serious hypersensitivity to galcanezumab-gnlm or to any of the excipients [see WARNINGS AND PRECAUTIONS]. | injection site reactions such as pain, redness, and itching | Emgality is a calcitonin-gene related peptide antagonist. Emgality is a prescription medicine used to prevent migraine headaches in adults. Emgality is also used to treat cluster headache episodes in adults. It is not known if Emgality is safe and effective in children. Warnings Follow all directions... | Emgality (galcanezumab-gnlm) is a calcitonin-gene related peptide antagonist indicated for the preventive treatment of migraine in adults. | NA | NA | Link | Link | NA |
| 15485 | Th1601 | Fanolesomab | NA | NA | NA | NA | NA | NA | NA | 0 | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15522 | Th1605 | Lecanemab | NA | NA | NA | NA | NA | NA | NA | Lecanemab is an experimental drug that is currently in clinical trials for the treament of Alzheimer's disease. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15523 | Th1605 | Lecanemab | NA | NA | NA | NA | NA | NA | NA | Lecanemab is an experimental drug that is currently in clinical trials for the treament of Alzheimer's disease. | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15531 | Th1606 | Lanadelumab | >Th1606_Lanadelumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSHYIMMWVRQAPGKGLEWVSGIYSSGGITVYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAYRRIGVPRRDEFDIWGQGTMVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 146000 | C6468H10016N1728O2012S47 | 6.1-8.5 | NA | 80-90 ºC (based on IgG properties) | Lanadelumab has a prolonged half-life which is typical of a human monoclonal antibody and it ranged from 13.8 to 15 days.[A38677] | Lanadelumab, also known as DX-2930, is a human IgG1 monoclonal antibody designed for subcutaneous self-injection.[L4538] It is a fully human immunoglobulin, k-light-chain made in recombinant Chinese Hamster Ovary cells.[L4537] The FDA and EU granted the designation of priority review, breakthrough therapy and orphan drug for rare diseases based on the results of the reported clinical trials.[A38676] Lanadelumab was developed by Shire and FDA approved on August 28, 2018.[L4537] | Lanadelumab is indicated for the prophylaxis treatment to prevent attacks in patients 12 years and older with hereditary angioedema.[L4537] The hereditary angioedema (HEA) is an autosomal dominant disorder resulted from the presence of C1 deficiency. Some reports have indicated a high prevalence of cases that result from spontaneous mutations which can be inherited. This condition is manifested by attacks of subcutaneous or submucosal edema in the face, larynx, GI tract, limbs or genitalia. From all the types of attacks, the most serious is the laryngeal as it can compromise the airway. The rest of the attacks are accompanied by pain and considerable dysfunction.[A38679] | In phase 1 studies, the level of kininogen, the substrate of kallikrein, was studied as a marker of kallikrein activity. In patients with C1 deficiency, the level of cleaved kininogen is 4-fold higher when compared with C1-normal individuals. When lanadelumab was administered, the levels of cleaved kininogen were significantly reduced with a dose of 300 and 400 mg of lanadelumab with a maximum reduction at day 22 corresponding with time for maximum concentration. This maximum reduction corresponded with the normal levels of cleaved kininogen. Similarly, the decreases of cleaved kininogen corresponded as well with reductions in the levels of the activated factor XII.[A38677] Clinically, the attacks of angioedema completely vanished in the patients receiving a dose of 300 mg of lanadelumab. In other doses such as 400 mg and combo 300/400 mg the attack reduction reached 90%.[A38677] In phase 3 clinical trials (HELP study, lanadelumab showed an attack rate reduction of over 70% for all three different dose regimes.[A38676] | Lanadelumab is a plasma kallikrein inhibitor. This enzyme works by cleaving high molecular weight kininogen to generate the pro-inflammatory peptide bradykinin which is a potent vasodilator. The activity of plasma kallikrein is regulated by the activity of C1-inhibitor and thus, the patients that are deficient in C1 are known to be correlated to excessive production of bradykinin which will further lead to fatal angioedema.[A19127] Hence, lanadelumab occludes the proteolytic active site of plasma kallikrein, preventing the cleavage of kininogen to bradykinin. It is a selective inhibitor as it has been reported that lanadelumab does not bind to prekallikrein or to inhibit any other serine proteases.[A38679] The activity of lanadelumab works as an additional checkpoint for the patients suffering from C1 deficiency. | In clinical trials, the apparition of antidrug antibodies was nos significant and from those who expressed it, none were neutralizing.[A38677] No significant toxicities related to the administration of lanadelumab have been reported.[A38679] Studies regarding the carcinogenic potential or overdosage effect have not been performed. Fertility studies show no effect on reproductive organs.[FDA label] | Because lanadelumab is a protein, it is expected to be degraded into small peptides and amino acids by proteolytic enzymes. | The drug levels of lanadelumab are dose-dependent and thus, the maximum plasma concentration increased correspondingly with an increased dosage. The Cmax and AUC ranged from 3800 to 45000 ng/ml and from 64000 to 762000 ng.day/ml respectively for concentrations from 30 to 400 mg. As well, sustained quantifiable drug concentration was observed through day 120.[A38677] The bioavailability of lanadelumab is of approximately 66% with a time to reach peak drug concentration of approximately 7 days.[A38679] | The reported volume of distribution of lanadelumab is in the range of 12 to 16 L which variates according to the dose administered.[A38679] | The apparent total plasma clearance after extravascular administration ranges between 18 and 25 ml/h.[A38677] | Antibodies | NA | NA | NA | NA | Plasma kallikrein | Takhzyro | Takeda | Takeda | Subcutaneous | 300 mg / 2 mL | None. | injection site reactions: pain, redness, bruising, bleeding, itching, a hard lump, numbness and tingling, warmth, swelling, and rash) upper respiratory infections, headache, rash, muscle pain, dizziness, and diarrhea | Takhzyro is a monoclonal antibody that works by reducing the activity of an enzyme that is uncontrolled in people with hereditary angioedema (a rare genetic immune system disorder). Takhzyro is used to prevent attacks of hereditary angioedema (HAE) in people who are at least 12 years old. Warnings Follow... | Takhzyro is a prescription medicine used to treat the symptoms of Hereditary Angioedema. Takhzyro may be used alone or with other medications. | NA | Lanadelumab-flyo is non-plasma derived, recombinant, fully human, monoclonal antibody (IgG1/κ-light chain) produced in Chinese Hamster Ovary (CHO) cells. Based on the amino acid sequence, the molecular weight of the non-glycosylated lanadelumab-flyo is 146 kDa. The calculated molecular mass of the fully reduced light chain is 23 kDa. The calculated molecular mass of the fully reduced and non-glycosylated heavy chain is 49 kDa. | Link | Link | NA |
| 15532 | Th1606 | Lanadelumab | >Th1606_Lanadelumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSHYIMMWVRQAPGKGLEWVSGIYSSGGITVYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAYRRIGVPRRDEFDIWGQGTMVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 146000 | C6468H10016N1728O2012S47 | 6.1-8.5 | NA | 80-90 ºC (based on IgG properties) | Lanadelumab has a prolonged half-life which is typical of a human monoclonal antibody and it ranged from 13.8 to 15 days.[A38677] | Lanadelumab, also known as DX-2930, is a human IgG1 monoclonal antibody designed for subcutaneous self-injection.[L4538] It is a fully human immunoglobulin, k-light-chain made in recombinant Chinese Hamster Ovary cells.[L4537] The FDA and EU granted the designation of priority review, breakthrough therapy and orphan drug for rare diseases based on the results of the reported clinical trials.[A38676] Lanadelumab was developed by Shire and FDA approved on August 28, 2018.[L4537] | Lanadelumab is indicated for the prophylaxis treatment to prevent attacks in patients 12 years and older with hereditary angioedema.[L4537] The hereditary angioedema (HEA) is an autosomal dominant disorder resulted from the presence of C1 deficiency. Some reports have indicated a high prevalence of cases that result from spontaneous mutations which can be inherited. This condition is manifested by attacks of subcutaneous or submucosal edema in the face, larynx, GI tract, limbs or genitalia. From all the types of attacks, the most serious is the laryngeal as it can compromise the airway. The rest of the attacks are accompanied by pain and considerable dysfunction.[A38679] | In phase 1 studies, the level of kininogen, the substrate of kallikrein, was studied as a marker of kallikrein activity. In patients with C1 deficiency, the level of cleaved kininogen is 4-fold higher when compared with C1-normal individuals. When lanadelumab was administered, the levels of cleaved kininogen were significantly reduced with a dose of 300 and 400 mg of lanadelumab with a maximum reduction at day 22 corresponding with time for maximum concentration. This maximum reduction corresponded with the normal levels of cleaved kininogen. Similarly, the decreases of cleaved kininogen corresponded as well with reductions in the levels of the activated factor XII.[A38677] Clinically, the attacks of angioedema completely vanished in the patients receiving a dose of 300 mg of lanadelumab. In other doses such as 400 mg and combo 300/400 mg the attack reduction reached 90%.[A38677] In phase 3 clinical trials (HELP study, lanadelumab showed an attack rate reduction of over 70% for all three different dose regimes.[A38676] | Lanadelumab is a plasma kallikrein inhibitor. This enzyme works by cleaving high molecular weight kininogen to generate the pro-inflammatory peptide bradykinin which is a potent vasodilator. The activity of plasma kallikrein is regulated by the activity of C1-inhibitor and thus, the patients that are deficient in C1 are known to be correlated to excessive production of bradykinin which will further lead to fatal angioedema.[A19127] Hence, lanadelumab occludes the proteolytic active site of plasma kallikrein, preventing the cleavage of kininogen to bradykinin. It is a selective inhibitor as it has been reported that lanadelumab does not bind to prekallikrein or to inhibit any other serine proteases.[A38679] The activity of lanadelumab works as an additional checkpoint for the patients suffering from C1 deficiency. | In clinical trials, the apparition of antidrug antibodies was nos significant and from those who expressed it, none were neutralizing.[A38677] No significant toxicities related to the administration of lanadelumab have been reported.[A38679] Studies regarding the carcinogenic potential or overdosage effect have not been performed. Fertility studies show no effect on reproductive organs.[FDA label] | Because lanadelumab is a protein, it is expected to be degraded into small peptides and amino acids by proteolytic enzymes. | The drug levels of lanadelumab are dose-dependent and thus, the maximum plasma concentration increased correspondingly with an increased dosage. The Cmax and AUC ranged from 3800 to 45000 ng/ml and from 64000 to 762000 ng.day/ml respectively for concentrations from 30 to 400 mg. As well, sustained quantifiable drug concentration was observed through day 120.[A38677] The bioavailability of lanadelumab is of approximately 66% with a time to reach peak drug concentration of approximately 7 days.[A38679] | The reported volume of distribution of lanadelumab is in the range of 12 to 16 L which variates according to the dose administered.[A38679] | The apparent total plasma clearance after extravascular administration ranges between 18 and 25 ml/h.[A38677] | Antibodies, Monoclonal | NA | NA | NA | NA | Plasma kallikrein | Takhzyro | Takeda Pharmaceuticals America, Inc. | Takeda Pharmaceuticals America, Inc. | Subcutaneous | 300 mg/2mL | None. | injection site reactions: pain, redness, bruising, bleeding, itching, a hard lump, numbness and tingling, warmth, swelling, and rash) upper respiratory infections, headache, rash, muscle pain, dizziness, and diarrhea | Takhzyro is a monoclonal antibody that works by reducing the activity of an enzyme that is uncontrolled in people with hereditary angioedema (a rare genetic immune system disorder). Takhzyro is used to prevent attacks of hereditary angioedema (HAE) in people who are at least 12 years old. Warnings Follow... | Takhzyro is a prescription medicine used to treat the symptoms of Hereditary Angioedema. Takhzyro may be used alone or with other medications. | NA | Lanadelumab-flyo is non-plasma derived, recombinant, fully human, monoclonal antibody (IgG1/κ-light chain) produced in Chinese Hamster Ovary (CHO) cells. Based on the amino acid sequence, the molecular weight of the non-glycosylated lanadelumab-flyo is 146 kDa. The calculated molecular mass of the fully reduced light chain is 23 kDa. The calculated molecular mass of the fully reduced and non-glycosylated heavy chain is 49 kDa. | Link | Link | NA |
| 15533 | Th1606 | Lanadelumab | >Th1606_Lanadelumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSHYIMMWVRQAPGKGLEWVSGIYSSGGITVYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAYRRIGVPRRDEFDIWGQGTMVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 146000 | C6468H10016N1728O2012S47 | 6.1-8.5 | NA | 80-90 ºC (based on IgG properties) | Lanadelumab has a prolonged half-life which is typical of a human monoclonal antibody and it ranged from 13.8 to 15 days.[A38677] | Lanadelumab, also known as DX-2930, is a human IgG1 monoclonal antibody designed for subcutaneous self-injection.[L4538] It is a fully human immunoglobulin, k-light-chain made in recombinant Chinese Hamster Ovary cells.[L4537] The FDA and EU granted the designation of priority review, breakthrough therapy and orphan drug for rare diseases based on the results of the reported clinical trials.[A38676] Lanadelumab was developed by Shire and FDA approved on August 28, 2018.[L4537] | Lanadelumab is indicated for the prophylaxis treatment to prevent attacks in patients 12 years and older with hereditary angioedema.[L4537] The hereditary angioedema (HEA) is an autosomal dominant disorder resulted from the presence of C1 deficiency. Some reports have indicated a high prevalence of cases that result from spontaneous mutations which can be inherited. This condition is manifested by attacks of subcutaneous or submucosal edema in the face, larynx, GI tract, limbs or genitalia. From all the types of attacks, the most serious is the laryngeal as it can compromise the airway. The rest of the attacks are accompanied by pain and considerable dysfunction.[A38679] | In phase 1 studies, the level of kininogen, the substrate of kallikrein, was studied as a marker of kallikrein activity. In patients with C1 deficiency, the level of cleaved kininogen is 4-fold higher when compared with C1-normal individuals. When lanadelumab was administered, the levels of cleaved kininogen were significantly reduced with a dose of 300 and 400 mg of lanadelumab with a maximum reduction at day 22 corresponding with time for maximum concentration. This maximum reduction corresponded with the normal levels of cleaved kininogen. Similarly, the decreases of cleaved kininogen corresponded as well with reductions in the levels of the activated factor XII.[A38677] Clinically, the attacks of angioedema completely vanished in the patients receiving a dose of 300 mg of lanadelumab. In other doses such as 400 mg and combo 300/400 mg the attack reduction reached 90%.[A38677] In phase 3 clinical trials (HELP study, lanadelumab showed an attack rate reduction of over 70% for all three different dose regimes.[A38676] | Lanadelumab is a plasma kallikrein inhibitor. This enzyme works by cleaving high molecular weight kininogen to generate the pro-inflammatory peptide bradykinin which is a potent vasodilator. The activity of plasma kallikrein is regulated by the activity of C1-inhibitor and thus, the patients that are deficient in C1 are known to be correlated to excessive production of bradykinin which will further lead to fatal angioedema.[A19127] Hence, lanadelumab occludes the proteolytic active site of plasma kallikrein, preventing the cleavage of kininogen to bradykinin. It is a selective inhibitor as it has been reported that lanadelumab does not bind to prekallikrein or to inhibit any other serine proteases.[A38679] The activity of lanadelumab works as an additional checkpoint for the patients suffering from C1 deficiency. | In clinical trials, the apparition of antidrug antibodies was nos significant and from those who expressed it, none were neutralizing.[A38677] No significant toxicities related to the administration of lanadelumab have been reported.[A38679] Studies regarding the carcinogenic potential or overdosage effect have not been performed. Fertility studies show no effect on reproductive organs.[FDA label] | Because lanadelumab is a protein, it is expected to be degraded into small peptides and amino acids by proteolytic enzymes. | The drug levels of lanadelumab are dose-dependent and thus, the maximum plasma concentration increased correspondingly with an increased dosage. The Cmax and AUC ranged from 3800 to 45000 ng/ml and from 64000 to 762000 ng.day/ml respectively for concentrations from 30 to 400 mg. As well, sustained quantifiable drug concentration was observed through day 120.[A38677] The bioavailability of lanadelumab is of approximately 66% with a time to reach peak drug concentration of approximately 7 days.[A38679] | The reported volume of distribution of lanadelumab is in the range of 12 to 16 L which variates according to the dose administered.[A38679] | The apparent total plasma clearance after extravascular administration ranges between 18 and 25 ml/h.[A38677] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Plasma kallikrein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15560 | 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]. | Antibodies | NA | NA | NA | NA | Programmed cell death protein 1 | Libtayo | Sanofi Aventis | Sanofi Aventis | Intravenous | 350 mg / 7 mL | 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 |
| 15561 | 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]. | Antibodies, Monoclonal | NA | NA | NA | NA | Programmed cell death protein 1 | Libtayo | Regeneron Ireland Designated Activity Company (Dac) | Regeneron Ireland Designated Activity Company (Dac) | Intravenous | 350 mg | 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 |
| 15585 | 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] | Antibodies | NA | NA | NA | NA | Interferon gamma | Gamifant | NovImmune SA | NovImmune SA | Intravenous | 10 mg/2mL | 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 |
| 15586 | 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] | Antibodies, Monoclonal | NA | NA | NA | NA | Interferon gamma | Gamifant | NovImmune SA | NovImmune SA | Intravenous | 50 mg/10mL | 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 |
| 15633 | 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] | Antibodies | NA | NA | NA | NA | Interleukin-23 | Skyrizi | AbbVie Inc. | AbbVie Inc. | Subcutaneous | 150 mg/1mL | 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 |
| 15634 | 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] | Antibodies, Monoclonal | NA | NA | NA | NA | Interleukin-23 | Skyrizi | Abbvie | Abbvie | Subcutaneous | 90 mg / 1 mL | 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 |
| 15635 | 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] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Interleukin-23 | Skyrizi | Abbvie | Abbvie | Subcutaneous | 150 mg / 1 mL | 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 |
| 15650 | 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] | Antibodies | NA | NA | NA | NA | ADP-ribosyl cyclase 1 | Sarclisa | sanof-aventis U.S. LLC | sanof-aventis U.S. LLC | Intravenous | 500 mg/25mL | 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 |
| 15651 | 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] | Antibodies, Monoclonal | NA | NA | NA | NA | ADP-ribosyl cyclase 1 | Sarclisa | Sanofi Aventis Groupe | Sanofi Aventis Groupe | Intravenous | 20 mg/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 |
| 15667 | Th1617 | Brolucizumab | >Th1617_Brolucizumab MEIVMTQSPSTLSASVGDRVIITCQASEIIHSWLAWYQQKPGKAPKLLIYLASTLASGVPSRFSGSGSGAEFTLTISSLQPDDFATYYCQNVYLASTNGANFGQGTKLTVLGGGGGSGGGGSGGGGSGGGGSEVQLVESGGGLVQPGGSLRLSCTASGFSLTDYYYMTWVRQAPGKGLEWVGFIDPDDDPYYATWAKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAGGDHNSGWGLDIWGQGTLVTVSS | 26000 | NA | NA | NA | NA | The systemic half life of bolucizumab is 4.4±2.0 days.[L9089] The elimination half life is 108h for a 3mg dose and 103h for a 6mg dose.[L9104] | Brolucizumab, also known as RTH258 or ESBA1008,[A187211] is a monoclonal antibody indicated to treat neovascular age related macular degeneration.[L9089] Brolucizumab was granted FDA approval in October 2019.[L9089] | Brolucizumab is a monoclonal antibody indicated to treat neovascular age related macular degeneration.[A187208,L9089] | Brolucizumab is a vascular endothelial growth factor (VEGF) inhibitor which reduces proliferation of endothelial cells, vascularization of the tissue, and permeability of the vasculature.[L9089] It has a long duration of action as it is given monthly.[L9089] Patients should be counselled regarding the risk of endophthalmitis, retinal detachment, and arterial thromboembolic events following administration of this medication.[L9089] | Brolucizumab is a vascular endothelial growth factor (VEGF) inhibitor which targets the major VEGF-A isoforms: VEGF110, VEGF121, and VEGF165.[A187196,A187208,L9089] Inhibition of these VEGF-A isoforms reduce proliferation of endothelial cells, vascularization of the tissue, and permeability of the vasculature.[L9089] | Data regarding the toxicity of brolucizumab is not readily available.[L9089] | Monoclonal antibodies are expected to undergo proteolysis to smaller peptides and amino acids.[A31470] | A 3mg dose of brolucizumab reaches a Cmax of 20.7ng/mL with a Tmax of 20.3h and an AUC of 2480ng | Data regarding the volume of distribution is not readily available.[L9089] | Data regarding the clearance of brolucizumab is not readily available.[L9089] | Antibodies | NA | NA | NA | NA | Vascular endothelial growth factor A | Beovu | Novartis Europharm Limited | Novartis Europharm Limited | Intravitreal | 120 mg/ml | Ocular Or Periocular Infections BEOVU is contraindicated in patients with ocular or periocular infections. Active Intraocular Inflammation BEOVU is contraindicated in patients with active intraocular inflammation. Hypersensitivity BEOVU is contraindicated in patients with known hypersensitivity to brolucizumab or any of the excipients in BEOVU. Hypersensitivity reactions may manifest as rash, pruritus, urticaria, erythema, or severe intraocular inflammation. | blurred vision, cataracts, bleeding in the eye, eye pain, and eye "floaters" | Beovu (brolucizumab-dbll) injection is a biological drug that is used to treat two chronic eye conditions. One is called neovascular (wet) age-related macular degeneration (AMD) and it is a leading cause of vision loss in people 50 years of age and over. The other is called diabetic macular edema (DME).... | Beovu is a prescription medicine used to treat the symptoms of Macular Degeneration. Beovu may be used alone or with other medications. | NA | Brolucizumab-dbll is a recombinant human vascular endothelial growth factor inhibitor. Brolucizumab-dbll is a humanized monoclonal single-chain Fv (scFv) antibody fragment. Brolucizumab-dbll has a molecular weight of ~26 kilodaltons and is produced in Escherichia coli cells by recombinant DNA technology. | Link | Link | NA |
| 15668 | Th1617 | Brolucizumab | >Th1617_Brolucizumab MEIVMTQSPSTLSASVGDRVIITCQASEIIHSWLAWYQQKPGKAPKLLIYLASTLASGVPSRFSGSGSGAEFTLTISSLQPDDFATYYCQNVYLASTNGANFGQGTKLTVLGGGGGSGGGGSGGGGSGGGGSEVQLVESGGGLVQPGGSLRLSCTASGFSLTDYYYMTWVRQAPGKGLEWVGFIDPDDDPYYATWAKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAGGDHNSGWGLDIWGQGTLVTVSS | 26000 | NA | NA | NA | NA | The systemic half life of bolucizumab is 4.4±2.0 days.[L9089] The elimination half life is 108h for a 3mg dose and 103h for a 6mg dose.[L9104] | Brolucizumab, also known as RTH258 or ESBA1008,[A187211] is a monoclonal antibody indicated to treat neovascular age related macular degeneration.[L9089] Brolucizumab was granted FDA approval in October 2019.[L9089] | Brolucizumab is a monoclonal antibody indicated to treat neovascular age related macular degeneration.[A187208,L9089] | Brolucizumab is a vascular endothelial growth factor (VEGF) inhibitor which reduces proliferation of endothelial cells, vascularization of the tissue, and permeability of the vasculature.[L9089] It has a long duration of action as it is given monthly.[L9089] Patients should be counselled regarding the risk of endophthalmitis, retinal detachment, and arterial thromboembolic events following administration of this medication.[L9089] | Brolucizumab is a vascular endothelial growth factor (VEGF) inhibitor which targets the major VEGF-A isoforms: VEGF110, VEGF121, and VEGF165.[A187196,A187208,L9089] Inhibition of these VEGF-A isoforms reduce proliferation of endothelial cells, vascularization of the tissue, and permeability of the vasculature.[L9089] | Data regarding the toxicity of brolucizumab is not readily available.[L9089] | Monoclonal antibodies are expected to undergo proteolysis to smaller peptides and amino acids.[A31470] | A 3mg dose of brolucizumab reaches a Cmax of 20.7ng/mL with a Tmax of 20.3h and an AUC of 2480ng | Data regarding the volume of distribution is not readily available.[L9089] | Data regarding the clearance of brolucizumab is not readily available.[L9089] | Antibodies, Monoclonal | NA | NA | NA | NA | Vascular endothelial growth factor A | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15669 | Th1617 | Brolucizumab | >Th1617_Brolucizumab MEIVMTQSPSTLSASVGDRVIITCQASEIIHSWLAWYQQKPGKAPKLLIYLASTLASGVPSRFSGSGSGAEFTLTISSLQPDDFATYYCQNVYLASTNGANFGQGTKLTVLGGGGGSGGGGSGGGGSGGGGSEVQLVESGGGLVQPGGSLRLSCTASGFSLTDYYYMTWVRQAPGKGLEWVGFIDPDDDPYYATWAKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAGGDHNSGWGLDIWGQGTLVTVSS | 26000 | NA | NA | NA | NA | The systemic half life of bolucizumab is 4.4±2.0 days.[L9089] The elimination half life is 108h for a 3mg dose and 103h for a 6mg dose.[L9104] | Brolucizumab, also known as RTH258 or ESBA1008,[A187211] is a monoclonal antibody indicated to treat neovascular age related macular degeneration.[L9089] Brolucizumab was granted FDA approval in October 2019.[L9089] | Brolucizumab is a monoclonal antibody indicated to treat neovascular age related macular degeneration.[A187208,L9089] | Brolucizumab is a vascular endothelial growth factor (VEGF) inhibitor which reduces proliferation of endothelial cells, vascularization of the tissue, and permeability of the vasculature.[L9089] It has a long duration of action as it is given monthly.[L9089] Patients should be counselled regarding the risk of endophthalmitis, retinal detachment, and arterial thromboembolic events following administration of this medication.[L9089] | Brolucizumab is a vascular endothelial growth factor (VEGF) inhibitor which targets the major VEGF-A isoforms: VEGF110, VEGF121, and VEGF165.[A187196,A187208,L9089] Inhibition of these VEGF-A isoforms reduce proliferation of endothelial cells, vascularization of the tissue, and permeability of the vasculature.[L9089] | Data regarding the toxicity of brolucizumab is not readily available.[L9089] | Monoclonal antibodies are expected to undergo proteolysis to smaller peptides and amino acids.[A31470] | A 3mg dose of brolucizumab reaches a Cmax of 20.7ng/mL with a Tmax of 20.3h and an AUC of 2480ng | Data regarding the volume of distribution is not readily available.[L9089] | Data regarding the clearance of brolucizumab is not readily available.[L9089] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Vascular endothelial growth factor A | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15688 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Antibodies | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | Enhertu | Astra Zeneca | Astra Zeneca | Intravenous | 100 mg / vial | None. | nausea, vomiting, fatigue, hair loss, constipation, decreased appetite, anemia, low white blood cell count (neutropenia, leukopenia), diarrhea, cough, and low platelets (thrombocytopenia), abdominal pain, inflammation of the mouth and lips, indigestion/heartburn, rash, low potassium (hypokalemia), shortness of breath, nosebleed, interstitial lung disease, headache, dizziness, upper respiratory tract infection, increased aspartate aminotransferase, alanine aminotransferase, and dry eye | Enhertu is a medicine used in adults to treat HER2-positive cancers which includes specific types of breast cancers and stomach cancers. Enhertu is made up of two cancer-fighting medicines, a targeted cancer therapy and a chemotherapy drug. Enhertu is usually given as an infusion into a vein every... | ENHERTU is indicated for the treatment of adult patients with unresectable or metastatic HER2-positive breast cancer who have received two or more prior anti-HER2-based regimens in the metastatic setting. | NA | Fam-trastuzumab deruxtecan-nxki is a HER2-directed antibody and topoisomerase inhibitor conjugate. Fam-trastuzumab deruxtecan-nxki is an antibody-drug conjugate (ADC) composed of three components: 1) a humanized anti-HER2 IgG1 monoclonal antibody (mAb), covalently linked to 2) a topoisomerase inhibitor, via 3) a tetrapeptide-based cleavable linker. Deruxtecan is composed of a protease-cleavable maleimide tetrapeptide linker and the topoisomerase inhibitor, DXd, which is an exatecan derivative. | Link | Link | NA |
| 15689 | Th1619 | Trastuzumab deruxtecan | NA | NA | NA | NA | NA | NA | In a pharmacokinetic study, the median elimination half-life of trastuzumab deruxtecan was about 5.8 days.[L10842] | Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer.[L10842] It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class.[A188988] Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments.[L10842] Promising results from a clinical trial prompted accelerated FDA approval for this indication on December 20, 2019.[L10845] Trastuzumab deruxtecan was developed by Daiichi Sankyo in collaboration with AstraZeneca. The continued approval of this drug will depend on the confirmation of its beneficial effects in ongoing clinical trials.[L10842] | Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic.[L10842] Continued approval will depend on the results of clinical trial results confirming its clinical benefit.[L10842] | Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy.[A188982,L10842,L10845] By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.[A188988] The FDA label warns of a potential risk for neutropenia, interstitial lung disease/pneumonitis, and left ventricular dysfunction following the use of this drug.[L10842] | Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor.[A188976,L10842] It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.[A188988,L10842] Normally, drugs in this class (antibody-drug conjugates) present a challenge. The monoclonal antibody accurately targets cancer cells, however exert limited killing action. The addition of a cytotoxic agent (a topoisomerase I inhibitor in this case) effectively kills dividing cancer cells, including those in the healthy tissues, leading to various adverse effects. The peptide linker used to formulate this drug is cleavable, which is unique to other antibody-drug conjugates, allowing for increased efficacy and reduced drug resistance to topoisomerase.[A188988] | LD50 and overdose information are not currently available, but effects of an overdose are likely to impact the lungs, heart, and circulatory system, leading to significant toxicity.[L10842] | Trastuzumab deruxtecan is likely broken down into small peptides and amino acids through catabolism, just as the metabolism of endogenous IgG.[A189009,L10842] Cathepsin B and L enzymes are thought to be involved in the cleavage of the peptide linker that joins the topoisomerase I inhibitor and the antibody.[A188988] In vitro, DXd, the topoisomerase inhibitor portion of the drug, is found to be metabolized by CYP3A4.[L10842] | The Cmax of trastuzumab deruxtecan at normal therapeutic doses was 122 µg/mL (20%). The AUC of trastuzumab deruxtecan was 735 µg·day/mL (31%).[L10842] | The estimated volume of distribution of trastuzumab deruxtecan in the central compartment is 2.77 L, according to a population based pharmacokinetic study.[L10842] Pharmacokinetic studies found that the unchanged drug is distributed in the blood and is not significantly retained in tissues.[A188979] | Trastuzumab deruxtecan is rapidly cleared from systemic circulation.[A188979] Estimated systemic clearance of trastuzumab deruxtecan is 0.42 L/day, according to a population pharmacokinetic analysis. DXd showed a systemic clearance of about 19.2 L/h.[L10842] | Antibodies, Monoclonal | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,DNA topoisomerase 1 | Enhertu | Daiichi Sankyo Europe, Gmb H | Daiichi Sankyo Europe, Gmb H | Intravenous | 100 mg | None. | nausea, vomiting, fatigue, hair loss, constipation, decreased appetite, anemia, low white blood cell count (neutropenia, leukopenia), diarrhea, cough, and low platelets (thrombocytopenia), abdominal pain, inflammation of the mouth and lips, indigestion/heartburn, rash, low potassium (hypokalemia), shortness of breath, nosebleed, interstitial lung disease, headache, dizziness, upper respiratory tract infection, increased aspartate aminotransferase, alanine aminotransferase, and dry eye | Enhertu is a medicine used in adults to treat HER2-positive cancers which includes specific types of breast cancers and stomach cancers. Enhertu is made up of two cancer-fighting medicines, a targeted cancer therapy and a chemotherapy drug. Enhertu is usually given as an infusion into a vein every... | ENHERTU is indicated for the treatment of adult patients with unresectable or metastatic HER2-positive breast cancer who have received two or more prior anti-HER2-based regimens in the metastatic setting. | NA | Fam-trastuzumab deruxtecan-nxki is a HER2-directed antibody and topoisomerase inhibitor conjugate. Fam-trastuzumab deruxtecan-nxki is an antibody-drug conjugate (ADC) composed of three components: 1) a humanized anti-HER2 IgG1 monoclonal antibody (mAb), covalently linked to 2) a topoisomerase inhibitor, via 3) a tetrapeptide-based cleavable linker. Deruxtecan is composed of a protease-cleavable maleimide tetrapeptide linker and the topoisomerase inhibitor, DXd, which is an exatecan derivative. | Link | Link | NA |
| 15720 | Th1621 | Tafasitamab | >Th1621_Tafasitamab EVQLVESGGGLVKPGGSLKLSCAASGYTFTSYVMHWVRQAPGKGLEWIGYINPYNDGTKYNEKFQGRVTISSDKSISTAYMELSSLRSEDTAMYYCARGTYYYGTRVFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPDVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKALPAPEEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 150000 | NA | NA | NA | NA | The terminal elimination half-life of tafasitamab is approximately 17 days.[L15292] | Tafasitamab is a humanized, CD19-directed cytolytic monoclonal antibody intended for the treatment of B-cell malignancies.[L15302] It is produced using recombinant DNA technology in Chinese hamster ovary cells, and contains an IgG1/2 hybrid Fc-domain which has been modified with 2 amino acid substitutions to enhance its cytotoxicity relative to non-engineered anti-CD19 antibodies.[L15292,A191829] The CD19 surface protein is highly expressed on the surface of B-cells, where it appears to play a role in enhancing B-cell receptor signaling.[L15302] Its relative ubiquity across different stages of B-cell development, including pre-B and mature B-lymphocytes,[L15292] as well as its presence in several B-cell malignancies (e.g. chronic lymphocytic leukemia (CLL), small lymphocytic lymphoma (SLL), diffuse large B-cell lymphoma (DLBCL))[L15302] has made it a desirable target in the treatment these B-cell malignancies. Tafasatimab is designed to bind to and block the activity of the CD19 surface antigen, which ultimately results in the lysis of B-cells (both healthy and malignant).[L15292] Having previously received Breakthrough Therapy, Fast Track, and Orphan designations from the FDA,[A191829] tafasatimab-cxix (Monjuvi®) received an accelerated approval on July 31st, 2020, for the treatment of relapsed or refractory DLBCL in adult patients who cannot receive autologous stem cell transplants.[L15307] It must be used in combination with [lenalidomide], as this combination results in greater efficacy as compared to either agent alone.[L15292] | Tafasitamab is indicated, in combination with [lenalidomide], for the treatment of adult patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL) not otherwise specified whom are ineligible for autologous stem cell transplant (ASCT).[L15292] | Tafasitamab induces a reduction in circulating B-cell counts by binding to a surface antigen, CD19, which is important for their survival.[L15302] Patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL) experienced a 97% reduction in peripheral blood B-cell counts following 8 days of treatment, with a 100% reduction reached within 16 weeks of treatment.[L15292] Tafasitamab can cause infusion-related reactions, particularly during the initial cycles of therapy. Symptoms may include chills, flushing, dyspnea, and hypertension. Patients may be administered premedications (such as [acetaminophen], antihistamines, or glucocorticoids) 0.5 - 2 hours prior to infusion to minimize infusion-related reactions.[L15292] Tafasitamab may also cause significant myelosuppression, and subsequent infection, due to its mechanism of action - patients should undergo monitoring throughout therapy for signs of myelosuppression and/or infection.[L15292] | The CD19 surface antigen is a protein expressed on the surface of pre-B and mature B-lymphocytes[L15292] that appears to play a role in enhancing B-cell receptor signaling and is considered integral to their survival.[L15302] These surface proteins are also highly expressed on several B-cell malignancies, such as chronic lymphocytic leukemia (CLL), small lymphocytic lymphoma (SLL), and diffuse large B-cell lymphoma (DLBCL).[L15302] Tafasitamab is a CD19-directed cytolytic monoclonal antibody that, upon binding and blocking the activity of CD19, causes lysis of B-cells. This process is mediated through both direct apoptosis and immune-mediated effector mechanisms, such as antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP).[L15292] | Data regarding overdose of tafasitamab are unavailable. Symptoms of overdosage are likely to be consistent with its adverse effect profile, and may therefore involve significant infusion-related reactions and/or myelosuppression.[L15292] | The biotransformation of tafasitamab has not been elucidated. Most monoclonal antibodies undergo intracellular catabolism via lysosomal degradation to smaller amino acids and peptides.[A19126,A216712] | Following intravenous administration of tafasitamab 12 mg/kg on Days 1, 8, 15, and 22 in cycle(s) 1-3 (with an additional dose on Day 4 of cycle 1), mean trough concentrations were 179 (± 53) µg/mL. From cycle 4 onwards, which involve the administration of tafasitamab 12 mg/kg on Days 1 and 15, mean trough concentrations were 153 (± 68) µg/mL.[L15292] The overall maximum tafasitamab serum concentrations reached were 483 (± 109) µg/mL.[L15292] | The total volume of distribution of tafasitamab following intravenous injection is approximately 9.3 L.[L15292] | The clearance of tafasitamab is approximately 0.41 L/day.[L15292] | Antibodies | NA | NA | NA | NA | B-lymphocyte antigen CD19 | Minjuvi | Incyte Corporation | Incyte Corporation | Intravenous | 200 mg / vial | NA | The most common side effects with Minjuvi (which may affect more than 1 in 10 people) are infections, neutropenia (low white blood cell count), anaemia (low red blood cell count), thrombocytopaenia (low blood platelet count), diarrhoea, weakness, cough, peripheral oedema (swelling especially of the ankles and feet), fever and decreased appetite. | Minjuvi can only be obtained with a prescription and must be given by a healthcare professional experienced in cancer treatment. The medicine is available as a powder to be made into a solution for infusion (drip) into a vein. | Minjuvi is a cancer medicine used first in combination with another medicine called lenalidomide, and then on its own, to treat adults with diffuse large B-cell lymphoma (DLBCL) whose cancer has returned or has stopped responding to other treatments and who cannot have an autologous stem cell transplantation (a transplant where the stem cells are collected from the patients themselves). | NA | NA | Link | Link | NA |
| 15721 | Th1621 | Tafasitamab | >Th1621_Tafasitamab EVQLVESGGGLVKPGGSLKLSCAASGYTFTSYVMHWVRQAPGKGLEWIGYINPYNDGTKYNEKFQGRVTISSDKSISTAYMELSSLRSEDTAMYYCARGTYYYGTRVFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPDVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKALPAPEEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 150000 | NA | NA | NA | NA | The terminal elimination half-life of tafasitamab is approximately 17 days.[L15292] | Tafasitamab is a humanized, CD19-directed cytolytic monoclonal antibody intended for the treatment of B-cell malignancies.[L15302] It is produced using recombinant DNA technology in Chinese hamster ovary cells, and contains an IgG1/2 hybrid Fc-domain which has been modified with 2 amino acid substitutions to enhance its cytotoxicity relative to non-engineered anti-CD19 antibodies.[L15292,A191829] The CD19 surface protein is highly expressed on the surface of B-cells, where it appears to play a role in enhancing B-cell receptor signaling.[L15302] Its relative ubiquity across different stages of B-cell development, including pre-B and mature B-lymphocytes,[L15292] as well as its presence in several B-cell malignancies (e.g. chronic lymphocytic leukemia (CLL), small lymphocytic lymphoma (SLL), diffuse large B-cell lymphoma (DLBCL))[L15302] has made it a desirable target in the treatment these B-cell malignancies. Tafasatimab is designed to bind to and block the activity of the CD19 surface antigen, which ultimately results in the lysis of B-cells (both healthy and malignant).[L15292] Having previously received Breakthrough Therapy, Fast Track, and Orphan designations from the FDA,[A191829] tafasatimab-cxix (Monjuvi®) received an accelerated approval on July 31st, 2020, for the treatment of relapsed or refractory DLBCL in adult patients who cannot receive autologous stem cell transplants.[L15307] It must be used in combination with [lenalidomide], as this combination results in greater efficacy as compared to either agent alone.[L15292] | Tafasitamab is indicated, in combination with [lenalidomide], for the treatment of adult patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL) not otherwise specified whom are ineligible for autologous stem cell transplant (ASCT).[L15292] | Tafasitamab induces a reduction in circulating B-cell counts by binding to a surface antigen, CD19, which is important for their survival.[L15302] Patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL) experienced a 97% reduction in peripheral blood B-cell counts following 8 days of treatment, with a 100% reduction reached within 16 weeks of treatment.[L15292] Tafasitamab can cause infusion-related reactions, particularly during the initial cycles of therapy. Symptoms may include chills, flushing, dyspnea, and hypertension. Patients may be administered premedications (such as [acetaminophen], antihistamines, or glucocorticoids) 0.5 - 2 hours prior to infusion to minimize infusion-related reactions.[L15292] Tafasitamab may also cause significant myelosuppression, and subsequent infection, due to its mechanism of action - patients should undergo monitoring throughout therapy for signs of myelosuppression and/or infection.[L15292] | The CD19 surface antigen is a protein expressed on the surface of pre-B and mature B-lymphocytes[L15292] that appears to play a role in enhancing B-cell receptor signaling and is considered integral to their survival.[L15302] These surface proteins are also highly expressed on several B-cell malignancies, such as chronic lymphocytic leukemia (CLL), small lymphocytic lymphoma (SLL), and diffuse large B-cell lymphoma (DLBCL).[L15302] Tafasitamab is a CD19-directed cytolytic monoclonal antibody that, upon binding and blocking the activity of CD19, causes lysis of B-cells. This process is mediated through both direct apoptosis and immune-mediated effector mechanisms, such as antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP).[L15292] | Data regarding overdose of tafasitamab are unavailable. Symptoms of overdosage are likely to be consistent with its adverse effect profile, and may therefore involve significant infusion-related reactions and/or myelosuppression.[L15292] | The biotransformation of tafasitamab has not been elucidated. Most monoclonal antibodies undergo intracellular catabolism via lysosomal degradation to smaller amino acids and peptides.[A19126,A216712] | Following intravenous administration of tafasitamab 12 mg/kg on Days 1, 8, 15, and 22 in cycle(s) 1-3 (with an additional dose on Day 4 of cycle 1), mean trough concentrations were 179 (± 53) µg/mL. From cycle 4 onwards, which involve the administration of tafasitamab 12 mg/kg on Days 1 and 15, mean trough concentrations were 153 (± 68) µg/mL.[L15292] The overall maximum tafasitamab serum concentrations reached were 483 (± 109) µg/mL.[L15292] | The total volume of distribution of tafasitamab following intravenous injection is approximately 9.3 L.[L15292] | The clearance of tafasitamab is approximately 0.41 L/day.[L15292] | Antibodies, Monoclonal | NA | NA | NA | NA | B-lymphocyte antigen CD19 | Monjuvi | MorphoSys US Inc. | MorphoSys US Inc. | Intravenous | 200 mg/5mL | None. | low white blood cells (neutropenia), fatigue, anemia, diarrhea, low blood platelets (thrombocytopenia), cough, fever, swelling of extremities, respiratory tract infection, decreased appetite, constipation, nausea, vomiting, shortness of breath, bronchitis, low blood potassium (hypokalemia), back pain, and muscle spasms | Monjuvi is an antibody that targets the CD19 antigen. Monjuvi is used in combination with lenalidomide to treat diffuse large B-cell lymphoma in adults who cannot receive a stem cell transplant. Monjuvi is given after other cancer treatments did not work or have stopped working. Monjuvi was approved... | MONJUVI, in combination with lenalidomide, is indicated for the treatment of adult patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL) not otherwise specified, including DLBCL arising from low grade lymphoma, and who are not eligible for autologous stem cell transplant (ASCT). | NA | MONJUVI (tafasitamab-cxix) for injection is supplied as a sterile, preservative-free, white to slightly yellowish lyophilized powder in a single-dose vial for intravenous use after reconstitution and further dilution. After reconstitution with 5 mL of Sterile Water for Injection, USP, the resulting concentration is 40 mg/mL with a pH of 6.0. Each single-dose vial contains 200 mg tafasitamab-cxix, citric acid monohydrate (3.7 mg), polysorbate 20 (1 mg), sodium citrate dihydrate (31.6 mg ) and trehalose dihydrate (378.3 mg). | Link | Link | NA |
| 15722 | Th1621 | Tafasitamab | >Th1621_Tafasitamab EVQLVESGGGLVKPGGSLKLSCAASGYTFTSYVMHWVRQAPGKGLEWIGYINPYNDGTKYNEKFQGRVTISSDKSISTAYMELSSLRSEDTAMYYCARGTYYYGTRVFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPDVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKALPAPEEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 150000 | NA | NA | NA | NA | The terminal elimination half-life of tafasitamab is approximately 17 days.[L15292] | Tafasitamab is a humanized, CD19-directed cytolytic monoclonal antibody intended for the treatment of B-cell malignancies.[L15302] It is produced using recombinant DNA technology in Chinese hamster ovary cells, and contains an IgG1/2 hybrid Fc-domain which has been modified with 2 amino acid substitutions to enhance its cytotoxicity relative to non-engineered anti-CD19 antibodies.[L15292,A191829] The CD19 surface protein is highly expressed on the surface of B-cells, where it appears to play a role in enhancing B-cell receptor signaling.[L15302] Its relative ubiquity across different stages of B-cell development, including pre-B and mature B-lymphocytes,[L15292] as well as its presence in several B-cell malignancies (e.g. chronic lymphocytic leukemia (CLL), small lymphocytic lymphoma (SLL), diffuse large B-cell lymphoma (DLBCL))[L15302] has made it a desirable target in the treatment these B-cell malignancies. Tafasatimab is designed to bind to and block the activity of the CD19 surface antigen, which ultimately results in the lysis of B-cells (both healthy and malignant).[L15292] Having previously received Breakthrough Therapy, Fast Track, and Orphan designations from the FDA,[A191829] tafasatimab-cxix (Monjuvi®) received an accelerated approval on July 31st, 2020, for the treatment of relapsed or refractory DLBCL in adult patients who cannot receive autologous stem cell transplants.[L15307] It must be used in combination with [lenalidomide], as this combination results in greater efficacy as compared to either agent alone.[L15292] | Tafasitamab is indicated, in combination with [lenalidomide], for the treatment of adult patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL) not otherwise specified whom are ineligible for autologous stem cell transplant (ASCT).[L15292] | Tafasitamab induces a reduction in circulating B-cell counts by binding to a surface antigen, CD19, which is important for their survival.[L15302] Patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL) experienced a 97% reduction in peripheral blood B-cell counts following 8 days of treatment, with a 100% reduction reached within 16 weeks of treatment.[L15292] Tafasitamab can cause infusion-related reactions, particularly during the initial cycles of therapy. Symptoms may include chills, flushing, dyspnea, and hypertension. Patients may be administered premedications (such as [acetaminophen], antihistamines, or glucocorticoids) 0.5 - 2 hours prior to infusion to minimize infusion-related reactions.[L15292] Tafasitamab may also cause significant myelosuppression, and subsequent infection, due to its mechanism of action - patients should undergo monitoring throughout therapy for signs of myelosuppression and/or infection.[L15292] | The CD19 surface antigen is a protein expressed on the surface of pre-B and mature B-lymphocytes[L15292] that appears to play a role in enhancing B-cell receptor signaling and is considered integral to their survival.[L15302] These surface proteins are also highly expressed on several B-cell malignancies, such as chronic lymphocytic leukemia (CLL), small lymphocytic lymphoma (SLL), and diffuse large B-cell lymphoma (DLBCL).[L15302] Tafasitamab is a CD19-directed cytolytic monoclonal antibody that, upon binding and blocking the activity of CD19, causes lysis of B-cells. This process is mediated through both direct apoptosis and immune-mediated effector mechanisms, such as antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP).[L15292] | Data regarding overdose of tafasitamab are unavailable. Symptoms of overdosage are likely to be consistent with its adverse effect profile, and may therefore involve significant infusion-related reactions and/or myelosuppression.[L15292] | The biotransformation of tafasitamab has not been elucidated. Most monoclonal antibodies undergo intracellular catabolism via lysosomal degradation to smaller amino acids and peptides.[A19126,A216712] | Following intravenous administration of tafasitamab 12 mg/kg on Days 1, 8, 15, and 22 in cycle(s) 1-3 (with an additional dose on Day 4 of cycle 1), mean trough concentrations were 179 (± 53) µg/mL. From cycle 4 onwards, which involve the administration of tafasitamab 12 mg/kg on Days 1 and 15, mean trough concentrations were 153 (± 68) µg/mL.[L15292] The overall maximum tafasitamab serum concentrations reached were 483 (± 109) µg/mL.[L15292] | The total volume of distribution of tafasitamab following intravenous injection is approximately 9.3 L.[L15292] | The clearance of tafasitamab is approximately 0.41 L/day.[L15292] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | B-lymphocyte antigen CD19 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15748 | Th1623 | Cusatuzumab | NA | NA | NA | NA | NA | NA | NA | CD70 is a ligand expressed on the surface of activated lymphocytes and mature dendritic cells that, in its binding to CD27 receptors, plays an important role in cell proliferation and survival. An overexpression of CD70 can result in the proliferation of malignant cells and has been documented in a variety of solid and hematological malignancies.[A241975] Cusatuzumab is a humanized IgG1 antibody targeted against CD70.[A241045] It is currently being investigated in the Phase 2 CULMINATE trial, in combination with [azacitidine], for the treatment of newly-diagnosed acute myeloid leukemia (AML) and high-risk myelodysplastic syndrome (MDS) in patients unsuitable for chemotherapy.[A241045,L39120] | NA | NA | CD70 is transiently expressed on activated lymphocytes and mature dendritic cells, where it serves as a ligand for the CD27 receptor.[A241975] The CD70-CD27 interaction results in the downstream activation of the NF- | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | CD70 antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15749 | Th1623 | Cusatuzumab | NA | NA | NA | NA | NA | NA | NA | CD70 is a ligand expressed on the surface of activated lymphocytes and mature dendritic cells that, in its binding to CD27 receptors, plays an important role in cell proliferation and survival. An overexpression of CD70 can result in the proliferation of malignant cells and has been documented in a variety of solid and hematological malignancies.[A241975] Cusatuzumab is a humanized IgG1 antibody targeted against CD70.[A241045] It is currently being investigated in the Phase 2 CULMINATE trial, in combination with [azacitidine], for the treatment of newly-diagnosed acute myeloid leukemia (AML) and high-risk myelodysplastic syndrome (MDS) in patients unsuitable for chemotherapy.[A241045,L39120] | NA | NA | CD70 is transiently expressed on activated lymphocytes and mature dendritic cells, where it serves as a ligand for the CD27 receptor.[A241975] The CD70-CD27 interaction results in the downstream activation of the NF- | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | CD70 antigen | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15784 | Th1628 | Crizanlizumab | >Th1628_Crizanlizumab QVQLVQSGAEVKKPGASVKVSCKVSGYTFTSYDINWVRQAPGKGLEWMGWIYPGDGSIKYNEKFKGRVTMTVDKSTDTAYMELSSLRSEDTAVYYCARRGEYGNYEGAMDYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVTSSNFGTQTYTCNVDHKPSNTKVDKTVERKCCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGMEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCAVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146000 | NA | NA | NA | NA | Given a 5mg/kg dose of crizanlizumab, the mean terminal elimination half life of crizanlizumab is 10.6 days in healthy subjects and 7.6 days in patients with sickle cell disease.[L10097] | Crizanlizumab is a humanized IgG2 monoclonal antibody used to reduce the frequency of vaso-occlusive crises in patients with sickle cell disease.[L10097] Sickle cell disease is a genetically inherited condition prevalent in the Middle East, Africa, and certain parts of India. The genetic mutation associated with this disease leads to the formation of abnormal, sickle shaped red blood cells that aggregate and block blood vessels throughout the body, causing vaso-occlusive crises. Sickle cell disease can lead to excruciating pain, stroke, infection, and various other complications arising from the blockage of blood vessels.[T734] Currently, patients are prescribed [hydroxyurea] to raise levels of fetal hemoglobin as a method of reducing morbidity and mortality.[A187904] Though hydroxyurea has been shown to reduce the frequency of vaso-occlusive crises, adherence to this therapy is difficult due to adverse effects and the high variability of response to the drug between patients.[A187907] Crizanlizumab, or SEG101, is given once every 4 weeks and may improve patient adherence. It was developed by Novartis and was granted FDA approval on November 15, 2019.[L10097] | Crizanlizumab is indicated to reduce the frequency of vaso-occlusive crisis in patients with sickle cell diseases who are =16 years old.[L10097] | Crizanlizumab is a P-selectin inhibitor that prevents interactions between endothelial cells, platelets, red blood cells, and leukocytes.[L10097] It has a long duration of action as it is given every 4 weeks.[L10097] Patients should be counselled regarding the risk of infusion reactions as well as crizanlizumab's interference with platelet counts using EDTA tubes.[L10097] | Crizanlizumab binds to P-selectin on endothelial cells and platelets, preventing their interaction with P-selectin glycoprotein ligand 1 on endothelial cells, platelets, red blood cells, and leukocytes.[A187910,L10097] By preventing this interaction, components of the blood are less likely to come together, causing a vaso-occlusive crisis in patients with sickle cell diseases.[A187910,L10097] The median per year incidence of vaso-occlusive crises was 1.04 in the high-dose crizanlizumab group, 2.00 in the low-dose crizanlizumab group, and 2.08 in the placebo group.[A187901] | Data regarding the toxicity of crizanlizumab is not readily available.[L10097] | Crizanlizumab is expected to be metabolized into smaller peptides and amino acids.[L10097] | Crizanlizumab reaches a Cmax of 0.16mg/mL with an AUC of 34.6mg | The volume of distribution of crizanlizumab is 4.26L.[L10097] | Given a 5mg/kg dose of crizanlizumab, the clearance rate is 11.7ml/hr in healthy subjects.[L10097] | Antibodies, Monoclonal | NA | NA | NA | NA | P-selectin | Adakveo | Novartis Pharmaceuticals Corporation | Novartis Pharmaceuticals Corporation | Intravenous | 10 mg/1mL | None. | nausea, joint pain, back pain, and fever | Adakveo is used: in people 16 years of age and older who have sickle cell disease to help reduce how often certain episodes (crises) happen. It is not known if Adakveo is safe and effective in children under 16 years of age. Warnings Adakveo may cause serious side effects, including: Infusion reactions.... | Adakveo is a prescription medicine used to treat the symptoms of Sickle Cell Disease. Adakveo may be used alone or with other medications. | NA | Crizanlizumab-tmca is a selectin blocker humanized IgG2 kappa monoclonal antibody that binds to P-selectin. Crizanlizumab-tmca is produced using recombinant DNA technology in Chinese hamster ovary (CHO) cells. It is composed of 2 heavy chains, each containing 448 amino acids, and 2 light chains each containing 218 amino acids, with a theoretical molecular weight of approximately 146 kDa. | Link | Link | NA |
| 15785 | Th1628 | Crizanlizumab | >Th1628_Crizanlizumab QVQLVQSGAEVKKPGASVKVSCKVSGYTFTSYDINWVRQAPGKGLEWMGWIYPGDGSIKYNEKFKGRVTMTVDKSTDTAYMELSSLRSEDTAVYYCARRGEYGNYEGAMDYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVTSSNFGTQTYTCNVDHKPSNTKVDKTVERKCCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVQFNWYVDGMEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCAVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146000 | NA | NA | NA | NA | Given a 5mg/kg dose of crizanlizumab, the mean terminal elimination half life of crizanlizumab is 10.6 days in healthy subjects and 7.6 days in patients with sickle cell disease.[L10097] | Crizanlizumab is a humanized IgG2 monoclonal antibody used to reduce the frequency of vaso-occlusive crises in patients with sickle cell disease.[L10097] Sickle cell disease is a genetically inherited condition prevalent in the Middle East, Africa, and certain parts of India. The genetic mutation associated with this disease leads to the formation of abnormal, sickle shaped red blood cells that aggregate and block blood vessels throughout the body, causing vaso-occlusive crises. Sickle cell disease can lead to excruciating pain, stroke, infection, and various other complications arising from the blockage of blood vessels.[T734] Currently, patients are prescribed [hydroxyurea] to raise levels of fetal hemoglobin as a method of reducing morbidity and mortality.[A187904] Though hydroxyurea has been shown to reduce the frequency of vaso-occlusive crises, adherence to this therapy is difficult due to adverse effects and the high variability of response to the drug between patients.[A187907] Crizanlizumab, or SEG101, is given once every 4 weeks and may improve patient adherence. It was developed by Novartis and was granted FDA approval on November 15, 2019.[L10097] | Crizanlizumab is indicated to reduce the frequency of vaso-occlusive crisis in patients with sickle cell diseases who are =16 years old.[L10097] | Crizanlizumab is a P-selectin inhibitor that prevents interactions between endothelial cells, platelets, red blood cells, and leukocytes.[L10097] It has a long duration of action as it is given every 4 weeks.[L10097] Patients should be counselled regarding the risk of infusion reactions as well as crizanlizumab's interference with platelet counts using EDTA tubes.[L10097] | Crizanlizumab binds to P-selectin on endothelial cells and platelets, preventing their interaction with P-selectin glycoprotein ligand 1 on endothelial cells, platelets, red blood cells, and leukocytes.[A187910,L10097] By preventing this interaction, components of the blood are less likely to come together, causing a vaso-occlusive crisis in patients with sickle cell diseases.[A187910,L10097] The median per year incidence of vaso-occlusive crises was 1.04 in the high-dose crizanlizumab group, 2.00 in the low-dose crizanlizumab group, and 2.08 in the placebo group.[A187901] | Data regarding the toxicity of crizanlizumab is not readily available.[L10097] | Crizanlizumab is expected to be metabolized into smaller peptides and amino acids.[L10097] | Crizanlizumab reaches a Cmax of 0.16mg/mL with an AUC of 34.6mg | The volume of distribution of crizanlizumab is 4.26L.[L10097] | Given a 5mg/kg dose of crizanlizumab, the clearance rate is 11.7ml/hr in healthy subjects.[L10097] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | P-selectin | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15793 | Th1629 | Faricimab | >Th1629_Faricimab QVQLVQSGAEVAKPGTSVKLSCKASGYTFTDYWMQWVKQRPGQGLEWIGTIYPGDGDTGYAQKFQGKATLTADKSSKTVYMHLSSLASEDSAVYYCARGDYYGSNSLDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Retinal vascular diseases (RVDs) such as diabetic macular edema (DME), age-related macular degeneration (AMD), and retinal vein occlusion (RVO) are typically caused by retinal ischemia and subsequent neovascularization (NV).[A225985, A225990, A225995] Vascular endothelial growth factor A (VEGF-A) is a well-known mediator of retinal NV, and many currently approved RVD therapies such as [aflibercept] and [ranibizumab] solely target VEGF-A. However, another set of factors, the Tie/Ang axis, comprising the transmembrane Tie-2 receptor and its soluble ligands Ang-1 and Ang-2, has been shown to play critical roles in mediating VEGF-A-induced NV.[A225985, A225990, A225995] Faricimab is an IgG1-derived bispecific antibody capable of simultaneously binding to and depleting VEGF-A and Ang-2, which has been developed to improve therapeutic efficacy, especially in patients that respond poorly to anti-VEGF-A monotherapy.[A225985, A225990, A225995, A226000, A226005, A226010] Faricimab is under investigation in clinical trial NCT03823287 (A Study to Evaluate the Efficacy and Safety of Faricimab in Participants With Neovascular Age-Related Macular Degeneration (TENAYA)). | NA | NA | The retina is largely avascular to facilitate effective photoreceptor function; rather, the retina is fed by both retinal and choroidal capillary networks, pathologies of which result in retinal and choroidal vascular diseases such as diabetic macular edema (DME), age-related macular degeneration (AMD), and retinal vein occlusion (RVO).[A225985, A225990, A225995] One of the underlying causes of retinal vascular diseases (RVDs) is retinal neovascularization (NV), the aberrant growth of new vasculature, usually due to sustained retinal ischemia and mediated primarily by vascular endothelial growth factor A (VEGF-A).[A225985, A225990, A225995] VEGF-A is a VEGF family member, which also includes VEGF-B, -C, and -D, whose members signal through the VEGF receptors (VEGFRs) VEGFR-1, -2, and -3 to mediate endothelial and lymphatic growth.[A225990] Extensive work in animal models of RVD has demonstrated that VEGF-A is necessary but not sufficient in many cases to mediate NV, suggesting that additional factors may be required in deep retinal capillary beds.[A225985] One such factor has been identified as the angiopoietins Ang-1 and Ang-2 and their cellular receptor Tie-2; Ang-1 is a full Tie-2 agonist whose binding results in Tie-2 phosphorylation and downstream signalling, whereas Ang-2 is a Tie-2 partial agonist/antagonist that inhibits Tie-2 phosphorylation. Ang-1 generally has a protective effect, making endothelial cells less responsive to VEGF-A, while Ang-2 increases VEGF-A-dependent NV and stimulates pericyte apoptosis and breakdown of both the blood-brain and blood-retinal barriers; Ang-2 is upregulated in retinal vascular development and retinal ischemia.[A225985, A225990, A225995, A226000] Faricimab is a bispecific antibody (bsAb) based on human IgG1 comprising two different heavy and two different light chains capable of simultaneously binding to both VEGF-A and Ang-2 produced using the "CrossMab" platform.[A225995, A226005, A226010] Faricimab binds VEGF-A and Ang-2 with binding affinities (KD) of approximately 3 and 22 nM, respectively; importantly, faricimab does not detectably bind Ang-1.[A225995] Also, the faricimab Fc region has been modified to reduce binding to Fc | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Vascular endothelial growth factor A,Angiopoietin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15794 | Th1629 | Faricimab | >Th1629_Faricimab QVQLVQSGAEVAKPGTSVKLSCKASGYTFTDYWMQWVKQRPGQGLEWIGTIYPGDGDTGYAQKFQGKATLTADKSSKTVYMHLSSLASEDSAVYYCARGDYYGSNSLDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Retinal vascular diseases (RVDs) such as diabetic macular edema (DME), age-related macular degeneration (AMD), and retinal vein occlusion (RVO) are typically caused by retinal ischemia and subsequent neovascularization (NV).[A225985, A225990, A225995] Vascular endothelial growth factor A (VEGF-A) is a well-known mediator of retinal NV, and many currently approved RVD therapies such as [aflibercept] and [ranibizumab] solely target VEGF-A. However, another set of factors, the Tie/Ang axis, comprising the transmembrane Tie-2 receptor and its soluble ligands Ang-1 and Ang-2, has been shown to play critical roles in mediating VEGF-A-induced NV.[A225985, A225990, A225995] Faricimab is an IgG1-derived bispecific antibody capable of simultaneously binding to and depleting VEGF-A and Ang-2, which has been developed to improve therapeutic efficacy, especially in patients that respond poorly to anti-VEGF-A monotherapy.[A225985, A225990, A225995, A226000, A226005, A226010] Faricimab is under investigation in clinical trial NCT03823287 (A Study to Evaluate the Efficacy and Safety of Faricimab in Participants With Neovascular Age-Related Macular Degeneration (TENAYA)). | NA | NA | The retina is largely avascular to facilitate effective photoreceptor function; rather, the retina is fed by both retinal and choroidal capillary networks, pathologies of which result in retinal and choroidal vascular diseases such as diabetic macular edema (DME), age-related macular degeneration (AMD), and retinal vein occlusion (RVO).[A225985, A225990, A225995] One of the underlying causes of retinal vascular diseases (RVDs) is retinal neovascularization (NV), the aberrant growth of new vasculature, usually due to sustained retinal ischemia and mediated primarily by vascular endothelial growth factor A (VEGF-A).[A225985, A225990, A225995] VEGF-A is a VEGF family member, which also includes VEGF-B, -C, and -D, whose members signal through the VEGF receptors (VEGFRs) VEGFR-1, -2, and -3 to mediate endothelial and lymphatic growth.[A225990] Extensive work in animal models of RVD has demonstrated that VEGF-A is necessary but not sufficient in many cases to mediate NV, suggesting that additional factors may be required in deep retinal capillary beds.[A225985] One such factor has been identified as the angiopoietins Ang-1 and Ang-2 and their cellular receptor Tie-2; Ang-1 is a full Tie-2 agonist whose binding results in Tie-2 phosphorylation and downstream signalling, whereas Ang-2 is a Tie-2 partial agonist/antagonist that inhibits Tie-2 phosphorylation. Ang-1 generally has a protective effect, making endothelial cells less responsive to VEGF-A, while Ang-2 increases VEGF-A-dependent NV and stimulates pericyte apoptosis and breakdown of both the blood-brain and blood-retinal barriers; Ang-2 is upregulated in retinal vascular development and retinal ischemia.[A225985, A225990, A225995, A226000] Faricimab is a bispecific antibody (bsAb) based on human IgG1 comprising two different heavy and two different light chains capable of simultaneously binding to both VEGF-A and Ang-2 produced using the "CrossMab" platform.[A225995, A226005, A226010] Faricimab binds VEGF-A and Ang-2 with binding affinities (KD) of approximately 3 and 22 nM, respectively; importantly, faricimab does not detectably bind Ang-1.[A225995] Also, the faricimab Fc region has been modified to reduce binding to Fc | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Vascular endothelial growth factor A,Angiopoietin-2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15802 | Th1630 | Evinacumab | >Th1630_Evinacumab EVQLVESGGGVIQPGGSLRLSCAASGFTFDDYAMNWVRQGPGKGLEWVSAISGDGGSTYYADSVKGRFTISRDNSKNSLYLQMNSLRAEDTAFFYCAKDLRNTIFGVVIPDAFDIWGQGTMVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 146000 | NA | NA | NA | NA | The elimination half-life of evinacumab is a function of its serum concentration and is therefore variable.[L31833] This is because evinacumab is eliminated by two parallel pathways: at higher concentrations it is eliminated primarily through a non-saturable proteolytic pathway, while at lower concentrations its elimination occurs primarily via a saturable target-mediated pathway.[L31833] | Evinacumab is a recombinant human IgG4 monoclonal antibody targeted against angiopoietin-like protein 3 (ANGPTL3) and the first drug of its kind. The ANGPTL family of proteins serve a number of physiologic functions - including involvement in the regulation of lipid metabolism - which have made them desirable therapeutic targets in recent years.[A229273] Loss-of-function mutations in _ANGPTL3_ have been noted to result in hypolipidemia and subsequent reductions in cardiovascular risk, whereas increases in function appear to be associated with cardiovascular risk, and it was these observations that provided a rationale for the development of a therapy targeted against ANGPTL3.[A229278] In February 2021, evinacumab became the first-and-only inhibitor of ANGPTL3 to receive FDA approval after it was granted approval for the adjunctive treatment of homozygous familial hypercholesterolemia (HoFH) under the brand name "Evkeeza".[L31838] Evinacumab is novel in its mechanism of action compared with other lipid-lowering therapies and therefore provides a unique and synergistic therapeutic option in the treatment of HoFH. | Evinacumab is indicated, as an adjunct with other lipid-lowering therapies, for the treatment of familial homozygous hypercholesterolemia (HoFH) in patients 12 years of age and older.[L31833] | Evinacumab exerts its hypolipidemic and antiatherogenic effects via decreasing circulating levels of triglycerides, HDL-C, and LDL-C, apolipoprotein B, and total cholesterol.[L31833] It is has a relatively long duration of action that allows for its administration via intravenous injection once-monthly.[L31833] Animal studies have demonstrated embryo-fetal toxicity - administration to pregnant rabbits during organogenesis resulted in increases in fetal malformations at concentrations lower than those used in humans. For this reason, patients receiving therapy with evinacumab should obtain a pregnancy test prior to beginning therapy and use effective contraception throughout the duration of therapy and for 5 months following the administration of the last dose.[L31833] | Angiopoetin-like proteins (ANGPTL) are a diverse group of proteins involved in a number of physiological processes, including the regulation of lipoprotein metabolism. Loss-of-function mutations in _ANGPTL3_ and _ANGPTL4_ have been shown to result in hypolipidemia and a reduced risk of coronary artery disease, while increased levels of these proteins appear to be associated with cardiovascular risk.[A229273,A229318] While these observations have made ANGPTLs as a class a desirable target in the treatment of hyperlipidemic disorders,[A229273] ANGPTL3 is the first to be pharmacologically targeted for the purposes of lipid-lowering therapy.[A229318] ANGPTL3 is expressed primarily in the liver and acts as an endogenous inhibitor of lipoprotein lipase (LPL) and endothelial lipase (EL) which are responsible, in part, for metabolizing triglycerides (TG) and HDL-C, respectively.[L31833] Evinacumab is monoclonal antibody that binds to and inhibits ANGPTL3, with the resulting disinhibition of LPL and EL reducing the levels of circulating TG and HDL-C. While the mechanism through which evinacumab reduces LDL-C is not entirely clear, this effect is independent of LDL receptor density and is therefore most likely due to the promotion of VLDL processing and upstream clearance of LDL formation.[L31833] | There are no data regarding overdosage with evinacumab. Symptoms of overdose are likely to be consistent with evinacumab's adverse effect profile and may therefore include significant infusion reactions or dizziness.[L31833] Patients experiencing an overdose should be treated with symptomatic and supportive measures. | The biotransformation of evinacumab has not been characterized.[L31833] Monoclonal antibodies as a class are typically degraded via catabolic pathways into smaller peptides and amino acids.[A216712] | Following the recommended dosing regimen (15 mg/kg intravenously every 4 weeks), steady-state concentrations are reached after four doses. According to population pharmacokinetic modeling, the mean steady-state trough concentration is approximately 241 mg/L and the Cmax at the end of infusion is approximately 689 mg/L.[L31833] | The volume of distribution of evinacumab was estimated to be 4.8 L via population pharmacokinetic analysis.[L31833] | NA | Antibodies | NA | NA | NA | NA | Angiopoietin-related protein 3 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15809 | Th1631 | Dostarlimab | >Th1631_Dostarlimab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYDMSWVRQAPGKGLEWVSTISGGGSYTYYQDSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCASPYYAMDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 144000 | C6420H9832N1680O2014S44 | NA | NA | NA | The mean terminal elimination half-life of dostarlimab is 25.4 days.[L33320] | Dostarlimab is an IgG4 humanized monoclonal antibody targeted against the human programmed death receptor-1 (PD-1).[L33320] PD-1 receptors are found on T-cells and, when activated, serve to inhibit immune responses - some cancers leverage this system by overexpressing PD-1 ligands, thereby effectively inhibiting the anti-tumor immune response that would typically attempt to destroy the cancerous cells.[A234379] Agents acting on the PD-1 pathway, such as [nivolumab] and [pembrolizumab], facilitate endogenous immune-mediated anti-tumor activity and may therefore be used to treat a wide variety of cancers, including those of the skin, lung, kidneys, and liver. In April 2021, dostarlimab was granted an accelerated approval by the FDA - as GlaxoSmithKline's dostarlimab-gxly (Jemperli) - for the treatment of adult patients with recurrent or advanced mismatch repair deficient (dMMR) endometrial cancer experiencing disease progression despite treatment with platinum-containing chemotherapy regimens.[L33340] As this accelerated approval was granted only for the treatment of dMMR endometrial cancers, it was approved alongside a companion diagnostic device - the VENTANA MMR RxDx Panel - for use in selecting appropriate patients for treatment.[L33340] | Dostarlimab-gxly is indicated for the treatment of adult patients with mismatch repair deficient (dMMR) recurrent or advanced endometrial cancer that has progressed despite ongoing or prior treatment with a platinum-containing chemotherapy regimen.[L33320] | Dostarlimab is an immunotherapy that facilitates the body's endogenous anti-tumor immune response in the treatment cancer.[L33320] It is administered over a span of 30 minutes via intravenous infusion every three to six weeks depending on the cycle.[L33320] Agents that interfere with the PD-1/PD-L1 pathway, including dostarlimab, remove an important immune system inhibitory response and may therefore induce immune-mediated adverse reactions which can be severe or fatal. These reactions can occur in any organ system and can occur at any time after starting therapy, and while they most often manifest during therapy they may also appear after discontinuing the causative agent. Patients receiving therapy with dostarlimab should be monitored closely for evidence of an underlying immune-mediated reaction and evaluated and treated promptly if an immune-mediated reaction is suspected.[L33320] | Approximately 13-30% of recurrent endometrial cancers involve microsatellite instability (MSI) or mismatch repair deficiency (dMMR).[A234379,A234389] The mutations resulting in dMMR endometrial cancers are primarily somatic in nature (~90%), although 5-10% of cases involve germline mutations.[A234389] Cancers that have mutations resulting in dMMR can upregulate the expression of programmed death receptor-1 (PD-1) ligands 1 and 2 (PD-L1 and -L2) - PD-1 is found on T-cells and, when activated, inhibits their proliferation and the production of cytokines.[L33320] The binding of these ligands to PD-1 thereby functions as an immune checkpoint that downregulates the anti-tumor immune response.[A234379] Dostarlimab is a monoclonal antibody targeted against PD-1 - it binds to the receptor and prevents interactions with PD-L1 and PD-L2, thus allowing the anti-tumor immune response to proceed unimpeded.[L33320] | There are no data regarding overdose with dostarlimab. Symptoms of overdosage are likely to be consistent with the adverse effect profile of dostarlimab and may therefore involve significant immune-mediated reactions.[L33320] | The metabolism of dostarlimab has not been characterized, but it is expected to be degraded via catabolic pathways into smaller peptides and amino acids.[L33320,A216712] | During the first cycle, and administered at 500mg intravenously every 3 weeks, the mean Cmax and AUC0-tau of dostarlimab-gxly are 171 mcg/mL and 35,730 mcg.h/mL, respectively. When administered at 1000mg every 6 weeks, the mean Cmax and AUC0-tau are 309 mcg/mL and 95,820 mcg.h/mL, respectively.[L33320] | At steady-state, the mean volume of distribution of dostarlimab is 5.3L.[L33320] | At steady-state, the mean clearance of dostarlimab is 0.007 L/h.[L33320] | Antibodies, Monoclonal | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15810 | Th1631 | Dostarlimab | >Th1631_Dostarlimab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYDMSWVRQAPGKGLEWVSTISGGGSYTYYQDSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCASPYYAMDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 144000 | C6420H9832N1680O2014S44 | NA | NA | NA | The mean terminal elimination half-life of dostarlimab is 25.4 days.[L33320] | Dostarlimab is an IgG4 humanized monoclonal antibody targeted against the human programmed death receptor-1 (PD-1).[L33320] PD-1 receptors are found on T-cells and, when activated, serve to inhibit immune responses - some cancers leverage this system by overexpressing PD-1 ligands, thereby effectively inhibiting the anti-tumor immune response that would typically attempt to destroy the cancerous cells.[A234379] Agents acting on the PD-1 pathway, such as [nivolumab] and [pembrolizumab], facilitate endogenous immune-mediated anti-tumor activity and may therefore be used to treat a wide variety of cancers, including those of the skin, lung, kidneys, and liver. In April 2021, dostarlimab was granted an accelerated approval by the FDA - as GlaxoSmithKline's dostarlimab-gxly (Jemperli) - for the treatment of adult patients with recurrent or advanced mismatch repair deficient (dMMR) endometrial cancer experiencing disease progression despite treatment with platinum-containing chemotherapy regimens.[L33340] As this accelerated approval was granted only for the treatment of dMMR endometrial cancers, it was approved alongside a companion diagnostic device - the VENTANA MMR RxDx Panel - for use in selecting appropriate patients for treatment.[L33340] | Dostarlimab-gxly is indicated for the treatment of adult patients with mismatch repair deficient (dMMR) recurrent or advanced endometrial cancer that has progressed despite ongoing or prior treatment with a platinum-containing chemotherapy regimen.[L33320] | Dostarlimab is an immunotherapy that facilitates the body's endogenous anti-tumor immune response in the treatment cancer.[L33320] It is administered over a span of 30 minutes via intravenous infusion every three to six weeks depending on the cycle.[L33320] Agents that interfere with the PD-1/PD-L1 pathway, including dostarlimab, remove an important immune system inhibitory response and may therefore induce immune-mediated adverse reactions which can be severe or fatal. These reactions can occur in any organ system and can occur at any time after starting therapy, and while they most often manifest during therapy they may also appear after discontinuing the causative agent. Patients receiving therapy with dostarlimab should be monitored closely for evidence of an underlying immune-mediated reaction and evaluated and treated promptly if an immune-mediated reaction is suspected.[L33320] | Approximately 13-30% of recurrent endometrial cancers involve microsatellite instability (MSI) or mismatch repair deficiency (dMMR).[A234379,A234389] The mutations resulting in dMMR endometrial cancers are primarily somatic in nature (~90%), although 5-10% of cases involve germline mutations.[A234389] Cancers that have mutations resulting in dMMR can upregulate the expression of programmed death receptor-1 (PD-1) ligands 1 and 2 (PD-L1 and -L2) - PD-1 is found on T-cells and, when activated, inhibits their proliferation and the production of cytokines.[L33320] The binding of these ligands to PD-1 thereby functions as an immune checkpoint that downregulates the anti-tumor immune response.[A234379] Dostarlimab is a monoclonal antibody targeted against PD-1 - it binds to the receptor and prevents interactions with PD-L1 and PD-L2, thus allowing the anti-tumor immune response to proceed unimpeded.[L33320] | There are no data regarding overdose with dostarlimab. Symptoms of overdosage are likely to be consistent with the adverse effect profile of dostarlimab and may therefore involve significant immune-mediated reactions.[L33320] | The metabolism of dostarlimab has not been characterized, but it is expected to be degraded via catabolic pathways into smaller peptides and amino acids.[L33320,A216712] | During the first cycle, and administered at 500mg intravenously every 3 weeks, the mean Cmax and AUC0-tau of dostarlimab-gxly are 171 mcg/mL and 35,730 mcg.h/mL, respectively. When administered at 1000mg every 6 weeks, the mean Cmax and AUC0-tau are 309 mcg/mL and 95,820 mcg.h/mL, respectively.[L33320] | At steady-state, the mean volume of distribution of dostarlimab is 5.3L.[L33320] | At steady-state, the mean clearance of dostarlimab is 0.007 L/h.[L33320] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Programmed cell death protein 1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15820 | Th1632 | Inolimomab | NA | NA | NA | NA | NA | NA | NA | Inolimomab is under investigation as an agent to treat steroid-resistant graft vs host disease. It has thus far offered similar efficacy to other monoclonal antibody options, though it may carry a higher risk of infections.[A241385] | NA | NA | Inolimomab is a murine monoclonal antibody targeting CD-25, also known as the alpha subunit of the interleukin-2 receptor. [L39010] The binding of this antibody to CD-25 blocks the signaling of interleukin-2, preventing clonal expansion of T-cells. The resulting immunosuppressive effect appears to provide a similar benefit in patients with steroid-resistant graft vs host disease to anti-thymocyte globulin.[A241380] | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Interleukin-2 receptor subunit alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15848 | Th1635 | Theralizumab | NA | NA | NA | NA | NA | NA | NA | Theralizumab is a humanized anti-CD28 monoclonal antibody designed for treating autoimmune diseases and cancer. After the first human trial, it was withdrawn due to severe toxicity (likely due to lymphopenia and human cytokine release).[A216527,A216532] | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15849 | Th1635 | Theralizumab | NA | NA | NA | NA | NA | NA | NA | Theralizumab is a humanized anti-CD28 monoclonal antibody designed for treating autoimmune diseases and cancer. After the first human trial, it was withdrawn due to severe toxicity (likely due to lymphopenia and human cytokine release).[A216527,A216532] | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15857 | Th1636 | Bamlanivimab | >Th1636_Bamlanivimab QVQLVQSGAEVKKPGSSVKVSCKASGGTFSNYAISWVRQAPGQGLEWMGRIIPILGIANYAQKFQGRVTITADKSTSTAYMELSSLRSEDTAVYYCARGYYEARHYYYYYAMDVWGQGTAVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146000 | C6498H10068N1732O2032S46 | NA | NA | NA | NA | Bamlanivimab (LY-CoV555, also known as LY3819253), is a synthetic monoclonal antibody (mAb) derived from one of the first blood samples in the United States from a patient who recovered from COVID-19.[A224039, L15311, L15316] Bamlanivimab is a neutralizing IgG1 | Bamlanivimab is not currently approved for any indication by the FDA.[L20974] Bamlanivimab is authorized under an Emergency Use Authorization (EUA) for the treatment of mild to moderate COVID-19 in patients aged 12 years and older weighing at least 40 kg who are at high risk for progressing to severe COVID-19 and/or hospitalization due to COVID-19. Patients should have confirmed COVID-19, with identification of SARS-CoV-2 viral load by an approved test.[L20974, L20979] Under this EUA, bamlanivimab is not authorized in patients who are hospitalized due to COVID-19, who require oxygen due to COVID-19, or in patients on oxygen therapy for a non-COVID-19-related comorbidity who require an increased oxygen flow rate due to COVID-19.[L20974, L20979] | Bamlanivimab is a recombinant human IgG1 | Bamlanivimab is a neutralizing recombinant human IgG1 | Bamlanivimab has been administered at doses of 7000 mg (ten times the authorized dose) during phase 2 clinical trials without any observed dose-limiting toxicity. In the event of an overdose, the recommended treatment is symptomatic and supportive measures; there is no antidote for bamlanivimab overdose.[L20979] | As a monoclonal antibody, it is expected that bamlanivimab will be degraded by proteases in various locations throughout the body. Bamlanivimab is not metabolized by cytochrome P450 enzymes, making drug interactions unlikely.[L20979] | NA | NA | NA | Antibodies | NA | NA | NA | NA | Spike glycoprotein | Bamlanivimab | Eli Lilly and Company | Eli Lilly and Company | Intravenous | 35 mg/1mL | NA | throat irritation, swelling in your face or throat; dizziness, a light-headed feeling (like you might pass out); chest pain, wheezing, shortness of breath; fever, chills, sweating, nausea; fast or slow heartbeats, headache, pounding in your neck or ears; weakness, tiredness; a rash or itching; or muscle pain. | NA | NA | NA | NA | Link | Link | NA |
| 15858 | Th1636 | Bamlanivimab | >Th1636_Bamlanivimab QVQLVQSGAEVKKPGSSVKVSCKASGGTFSNYAISWVRQAPGQGLEWMGRIIPILGIANYAQKFQGRVTITADKSTSTAYMELSSLRSEDTAVYYCARGYYEARHYYYYYAMDVWGQGTAVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146000 | C6498H10068N1732O2032S46 | NA | NA | NA | NA | Bamlanivimab (LY-CoV555, also known as LY3819253), is a synthetic monoclonal antibody (mAb) derived from one of the first blood samples in the United States from a patient who recovered from COVID-19.[A224039, L15311, L15316] Bamlanivimab is a neutralizing IgG1 | Bamlanivimab is not currently approved for any indication by the FDA.[L20974] Bamlanivimab is authorized under an Emergency Use Authorization (EUA) for the treatment of mild to moderate COVID-19 in patients aged 12 years and older weighing at least 40 kg who are at high risk for progressing to severe COVID-19 and/or hospitalization due to COVID-19. Patients should have confirmed COVID-19, with identification of SARS-CoV-2 viral load by an approved test.[L20974, L20979] Under this EUA, bamlanivimab is not authorized in patients who are hospitalized due to COVID-19, who require oxygen due to COVID-19, or in patients on oxygen therapy for a non-COVID-19-related comorbidity who require an increased oxygen flow rate due to COVID-19.[L20974, L20979] | Bamlanivimab is a recombinant human IgG1 | Bamlanivimab is a neutralizing recombinant human IgG1 | Bamlanivimab has been administered at doses of 7000 mg (ten times the authorized dose) during phase 2 clinical trials without any observed dose-limiting toxicity. In the event of an overdose, the recommended treatment is symptomatic and supportive measures; there is no antidote for bamlanivimab overdose.[L20979] | As a monoclonal antibody, it is expected that bamlanivimab will be degraded by proteases in various locations throughout the body. Bamlanivimab is not metabolized by cytochrome P450 enzymes, making drug interactions unlikely.[L20979] | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Spike glycoprotein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15859 | Th1636 | Bamlanivimab | >Th1636_Bamlanivimab QVQLVQSGAEVKKPGSSVKVSCKASGGTFSNYAISWVRQAPGQGLEWMGRIIPILGIANYAQKFQGRVTITADKSTSTAYMELSSLRSEDTAVYYCARGYYEARHYYYYYAMDVWGQGTAVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146000 | C6498H10068N1732O2032S46 | NA | NA | NA | NA | Bamlanivimab (LY-CoV555, also known as LY3819253), is a synthetic monoclonal antibody (mAb) derived from one of the first blood samples in the United States from a patient who recovered from COVID-19.[A224039, L15311, L15316] Bamlanivimab is a neutralizing IgG1 | Bamlanivimab is not currently approved for any indication by the FDA.[L20974] Bamlanivimab is authorized under an Emergency Use Authorization (EUA) for the treatment of mild to moderate COVID-19 in patients aged 12 years and older weighing at least 40 kg who are at high risk for progressing to severe COVID-19 and/or hospitalization due to COVID-19. Patients should have confirmed COVID-19, with identification of SARS-CoV-2 viral load by an approved test.[L20974, L20979] Under this EUA, bamlanivimab is not authorized in patients who are hospitalized due to COVID-19, who require oxygen due to COVID-19, or in patients on oxygen therapy for a non-COVID-19-related comorbidity who require an increased oxygen flow rate due to COVID-19.[L20974, L20979] | Bamlanivimab is a recombinant human IgG1 | Bamlanivimab is a neutralizing recombinant human IgG1 | Bamlanivimab has been administered at doses of 7000 mg (ten times the authorized dose) during phase 2 clinical trials without any observed dose-limiting toxicity. In the event of an overdose, the recommended treatment is symptomatic and supportive measures; there is no antidote for bamlanivimab overdose.[L20979] | As a monoclonal antibody, it is expected that bamlanivimab will be degraded by proteases in various locations throughout the body. Bamlanivimab is not metabolized by cytochrome P450 enzymes, making drug interactions unlikely.[L20979] | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Spike glycoprotein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15866 | Th1637 | Belantamab mafodotin | >Th1637_Belantamab_mafodotin QVQLVQSGAEVKKPGSSVKVSCKASGGTFSNYWMHWVRQAPGQGLEWMGATYRGHSDTYYNQKFKGRVTITADKSTSTAYMELSSLRSEDTAVYYCARGAIYDGYDVLDNWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | The terminal half life of belantamab mafodotin was 12 days after the first dose and 14 days at steady state.[L15326] | Belantamab mafodotin, or GSK2857916, is an afucosylated monoclonal antibody that targets B cell maturation antigen conjugated to the microtubule distrupter monomethyl auristatin-F (MMAF).[A216756] Belantamab mafodotin was granted FDA approval on 5 August 2020.[L15326] | Belantamab mafodotin is indicated in the treatment of adults with relapsed or refractory multiple myeloma who have received at least 4 prior therapies including an anti-CD38 monoclonal antibody, a proteasome inhibitor, and an immunomodulatory agent.[L15326] | Belantamab mafodotin treats multiple myeloma through antibody dependant cell mediated cytotoxicity as well as G2/M cell cycle arrest.[A216771] It has a narrow therapeutic index due to the incidence of adverse effects, and a long duration of action as it is given every 3 weeks.[L15326] Patients should be counselled regarding the risk of keratopathy.[L15326] | Belantamab mafodotin, or GSK2857916, is an afucosylated monoclonal antibody that targets B cell maturation antigen (BCMA) conjugated to the microtubule distrupter monomethyl auristatin-F (MMAF).[A216756] Afucosylation of the Fc region of monoclonal antibodies enhances binding to the Fc region, which enhances antibody dependant cell mediated cytoxicity.[A216771] BCMA is uniquely expressed on CD138-positive myeloma cells.[A216756] Targeting BCMA allows belantamab mafodotin to be highly selective in its delivery of MMAF to multiple myeloma cells.[A216756] Belantamab mafodotin binds to BCMA, is internalised into cells, and releases MMAF.[A216756] The MMAF payload binds to tubulin, stopping the cell cycle at the DNA damage checkpoint between the G2 and M phases, resulting in apoptosis.[A216771] | Data regarding overdose is not readily available.[L15326] However, keratopathy was seen in 71% of patients.[A216756,A216761,A216766,L15326] | Monoclonal antibodies are expected to be metabolized to smaller peptides and amino acids.[L15326] MMAF is expected to be metabolized by oxidation and demethylation, however further data is not readily available.[A216781,A216776] | Belantamab mafodotin at a dose of 2.5mg/kg reaches a Cmax of 42 µg/mL, with a Tmax of 0.78 hours, and an AUC of 4666 µg | The mean steady state volume of distribution of belantamab mafodotin was 11 L.[L15326] | The clearance of belantamab mafodotin was 0.9 L/day after the first dose and 0.7 L/day at steady state.[L15326] | Antibodies | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 17 | Blenrep | Glaxo Smith Kline (Ireland) Limited | Glaxo Smith Kline (Ireland) Limited | Intravenous | 100 mg | None. | keratopathy (corneal epithelium changes on eye exam), decreased visual acuity, nausea, blurred vision, fever, fatigue, infusion-related reactions, decreased platelets, decreased lymphocytes, decreased hemoglobin, decreased neutrophils, increased creatinine, increased gamma-glutamyl transferase, dry eyes, constipation, diarrhea, joint pain, back pain, decreased appetite, and upper respiratory tract infection | Blenrep is an antibody targeting B-cell maturation antigens (BCMA). Blenrep is used to treat multiple myeloma in adults. This medicine is given after at least 4 other treatments did not work or have stopped working. Blenrep was approved by the US Food and Drug Administration (FDA) on an "accelerated"... | BLENREP is indicated for the treatment of adults with relapsed or refractory multiple myeloma who have received at least 4 prior therapies, including an anti-CD38 monoclonal antibody, a proteasome inhibitor, and an immunomodulatory agent. | NA | NA | Link | Link | NA |
| 15867 | Th1637 | Belantamab mafodotin | >Th1637_Belantamab_mafodotin QVQLVQSGAEVKKPGSSVKVSCKASGGTFSNYWMHWVRQAPGQGLEWMGATYRGHSDTYYNQKFKGRVTITADKSTSTAYMELSSLRSEDTAVYYCARGAIYDGYDVLDNWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | The terminal half life of belantamab mafodotin was 12 days after the first dose and 14 days at steady state.[L15326] | Belantamab mafodotin, or GSK2857916, is an afucosylated monoclonal antibody that targets B cell maturation antigen conjugated to the microtubule distrupter monomethyl auristatin-F (MMAF).[A216756] Belantamab mafodotin was granted FDA approval on 5 August 2020.[L15326] | Belantamab mafodotin is indicated in the treatment of adults with relapsed or refractory multiple myeloma who have received at least 4 prior therapies including an anti-CD38 monoclonal antibody, a proteasome inhibitor, and an immunomodulatory agent.[L15326] | Belantamab mafodotin treats multiple myeloma through antibody dependant cell mediated cytotoxicity as well as G2/M cell cycle arrest.[A216771] It has a narrow therapeutic index due to the incidence of adverse effects, and a long duration of action as it is given every 3 weeks.[L15326] Patients should be counselled regarding the risk of keratopathy.[L15326] | Belantamab mafodotin, or GSK2857916, is an afucosylated monoclonal antibody that targets B cell maturation antigen (BCMA) conjugated to the microtubule distrupter monomethyl auristatin-F (MMAF).[A216756] Afucosylation of the Fc region of monoclonal antibodies enhances binding to the Fc region, which enhances antibody dependant cell mediated cytoxicity.[A216771] BCMA is uniquely expressed on CD138-positive myeloma cells.[A216756] Targeting BCMA allows belantamab mafodotin to be highly selective in its delivery of MMAF to multiple myeloma cells.[A216756] Belantamab mafodotin binds to BCMA, is internalised into cells, and releases MMAF.[A216756] The MMAF payload binds to tubulin, stopping the cell cycle at the DNA damage checkpoint between the G2 and M phases, resulting in apoptosis.[A216771] | Data regarding overdose is not readily available.[L15326] However, keratopathy was seen in 71% of patients.[A216756,A216761,A216766,L15326] | Monoclonal antibodies are expected to be metabolized to smaller peptides and amino acids.[L15326] MMAF is expected to be metabolized by oxidation and demethylation, however further data is not readily available.[A216781,A216776] | Belantamab mafodotin at a dose of 2.5mg/kg reaches a Cmax of 42 µg/mL, with a Tmax of 0.78 hours, and an AUC of 4666 µg | The mean steady state volume of distribution of belantamab mafodotin was 11 L.[L15326] | The clearance of belantamab mafodotin was 0.9 L/day after the first dose and 0.7 L/day at steady state.[L15326] | Antibodies, Monoclonal | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 17 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15868 | Th1637 | Belantamab mafodotin | >Th1637_Belantamab_mafodotin QVQLVQSGAEVKKPGSSVKVSCKASGGTFSNYWMHWVRQAPGQGLEWMGATYRGHSDTYYNQKFKGRVTITADKSTSTAYMELSSLRSEDTAVYYCARGAIYDGYDVLDNWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | The terminal half life of belantamab mafodotin was 12 days after the first dose and 14 days at steady state.[L15326] | Belantamab mafodotin, or GSK2857916, is an afucosylated monoclonal antibody that targets B cell maturation antigen conjugated to the microtubule distrupter monomethyl auristatin-F (MMAF).[A216756] Belantamab mafodotin was granted FDA approval on 5 August 2020.[L15326] | Belantamab mafodotin is indicated in the treatment of adults with relapsed or refractory multiple myeloma who have received at least 4 prior therapies including an anti-CD38 monoclonal antibody, a proteasome inhibitor, and an immunomodulatory agent.[L15326] | Belantamab mafodotin treats multiple myeloma through antibody dependant cell mediated cytotoxicity as well as G2/M cell cycle arrest.[A216771] It has a narrow therapeutic index due to the incidence of adverse effects, and a long duration of action as it is given every 3 weeks.[L15326] Patients should be counselled regarding the risk of keratopathy.[L15326] | Belantamab mafodotin, or GSK2857916, is an afucosylated monoclonal antibody that targets B cell maturation antigen (BCMA) conjugated to the microtubule distrupter monomethyl auristatin-F (MMAF).[A216756] Afucosylation of the Fc region of monoclonal antibodies enhances binding to the Fc region, which enhances antibody dependant cell mediated cytoxicity.[A216771] BCMA is uniquely expressed on CD138-positive myeloma cells.[A216756] Targeting BCMA allows belantamab mafodotin to be highly selective in its delivery of MMAF to multiple myeloma cells.[A216756] Belantamab mafodotin binds to BCMA, is internalised into cells, and releases MMAF.[A216756] The MMAF payload binds to tubulin, stopping the cell cycle at the DNA damage checkpoint between the G2 and M phases, resulting in apoptosis.[A216771] | Data regarding overdose is not readily available.[L15326] However, keratopathy was seen in 71% of patients.[A216756,A216761,A216766,L15326] | Monoclonal antibodies are expected to be metabolized to smaller peptides and amino acids.[L15326] MMAF is expected to be metabolized by oxidation and demethylation, however further data is not readily available.[A216781,A216776] | Belantamab mafodotin at a dose of 2.5mg/kg reaches a Cmax of 42 µg/mL, with a Tmax of 0.78 hours, and an AUC of 4666 µg | The mean steady state volume of distribution of belantamab mafodotin was 11 L.[L15326] | The clearance of belantamab mafodotin was 0.9 L/day after the first dose and 0.7 L/day at steady state.[L15326] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 17 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15910 | Th1643 | Satralizumab | >Th1643_Satralizumab QVQLQESGPGLVKPSETLSLTCAVSGHSISHDHAWSWVRQPPGEGLEWIGFISYSGITNYNPSLQGRVTISRDNSKNTLYLQMNSLRAEDTAVYYCARSLARTTAMDYWGEGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKSCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQEGNVFSCSVMHEALHAHYTQKSLSLSP | 143000 | NA | NA | NA | NA | The terminal half-life of satralizumab is approximately 30 days (range 22-37 days).[L15536] | Satralizumab is a recombinant humanized monoclonal antibody targeted against human interleukin-6 (IL-6) receptors, similar to [tocilizumab], which is produced in Chinese hamster ovary cells and based on an IgG2 framework.[L15536] Satralizumab is used in the treatment of neuromyelitis optica spectrum disorder (NMOSD), a rare autoimmune inflammatory disorder of the central nervous system (CNS) involving demyelinating lesions in the optic nerve, spinal cord, brainstem, and cerebrum.[A218551] Some of the pro-inflammatory mechanisms involved in NMOSD are thought to be mediated, at least in part, by IL-6, including increased production of anti-aquaporin-4 (AQP4) autoantibodies and increased permeability of the blood-brain barrier, which allows for the passage of pro-inflammatory mediators into the CNS.[A218546,A218551] Satralizumab is thought to exert its therapeutic benefits by blocking IL-6 receptors and, subsequently, these inflammatory responses. Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] is uniquely formulated with "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner[A218551] - this allows satralizumab to bind an IL-6 receptor until it reaches an endosome, after which the drug may dissociate from the receptor and move back into the plasma to act again. This novel mechanism effectively increases the duration of action of satralizumab, as it allows for single drug molecules to interact with multiple endogenous IL-6 receptors prior to elimination. Satralizumab was first approved for use in Canada in June 2020 for the treatment of AQP4 antibody-positive patients with NMOSD.[A218551] It received subsequent approvals in Switzerland and Japan,[A218551] and was approved for use by the FDA in August 2020,[L15566] becoming the 3rd treatment to receive FDA approval for NMOSD (after [eculizumab] in June 2019 and [inebilizumab] in June 2020). | Satralizumab is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive.[L15536] In Canada, it is also used in adolescent patients for the same indication.[L15546] | Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] utilizes a novel "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner.[A218551] Satralizumab-bound IL-6 receptors are taken up into cells and transported into endosomes, a relatively acidic environment in comparison to plasma (pH 5.5-6.0 vs. pH 7.4) - this decrease in pH allows satralizumab to dissociate from the IL-6 receptor and be recycled back into the plasma, where it can bind to another IL-6 receptor and repeat the process.[A218551] Satralizumab has been associated with an increased risk of infection, including serious and potentially fatal infections. It should not be administered to patients with active infections, including localized infections, until the infection resolves, and is contraindicated for use in patients with active hepatitis B or tuberculosis.[L15536] | Interleukin-6 (IL-6) is a pro-inflammatory cytokine[A218546] which has been implicated in the pathogenesis of NMOSD.[A218551] The inflammatory cascade triggered by IL-6 signaling is thought to result in the differentiation of T-cells into pro-inflammatory TH17 cells[A218551] and the differentiation of B-cells into plasmablasts producing AQP4 autoantibodies.[A218551,A218546] IL-6 may also play a role in increasing the permeability of the blood-brain barrier, thereby allowing penetration of autoantibodies and pro-inflammatory mediators into the central nervous system.[A218551,A218546] Satralizumab is a humanized monoclonal antibody targeted against human IL-6 receptors.[L15536] It binds to soluble and membrane-bound IL-6 receptors and prevents the signaling cascade, and subsequent pro-inflammatory effects, associated with its binding to endogenous IL-6. | There is no data regarding overdose of satralizumab. No serious adverse effects were noted in healthy adults receiving a single dose of 240mg subcutaneously in clinical trials.[L15546] Patients experiencing a suspected overdose should be treated with symptomatic and supportive measures as clinically indicated. | While the metabolism of satralizumab has not been studied directly,[L15536] monoclonal antibodies as a class are principally cleared by catabolism.[L15536,A216712] | The Cmax and AUC at steady-state, achieved after an 8-week loading period, were approximately 31.5 mcg/mL and 737 mcg.mL/day, respectively.[L15536] Average Ctrough concentrations were approximately 19 mcg/mL.[L15546] The bioavailability of satralizumab following subcutaneous injection has been reported to be between 78.5% and 85%.[L15536,L15546] | Satralizumab is subject to biphasic distribution - the estimated volume of distribution for the central and peripheral compartments are 3.46 L and 2.07 L, respectively.[L15546] | The total clearance of satralizumab is concentration-dependent and is estimated to be 0.0601-0.0679 L/day.[L15536,L15546] The inter-compartmental clearance was 0.336 L/day.[L15536] | Antibodies, Monoclonal | NA | NA | NA | NA | Interleukin-6 receptor subunit alpha | Enspryng | Roche Registration Gmb H | Roche Registration Gmb H | Subcutaneous | 120 mg | ENSPRYNG is contraindicated in patients with: A known hypersensitivity to satralizumab or any of the inactive ingredients [see WARNINGS AND PRECAUTIONS] Active Hepatitis B infection [see WARNINGS AND PRECAUTIONS] Active or untreated latent tuberculosis [see WARNINGS AND PRECAUTIONS] | runny or stuffy nose, headache, upper respiratory tract infection, gastritis, rash, joint pain, extremity pain, fatigue, and nausea | Enspryng is a recombinant humanized monoclonal antibody targeting human interleukin-6 (IL-6) receptors. Enspryng is a prescription medicine used to treat adults with neuromyelitis optica spectrum disorder (NMOSD). NMOSD is a rare, chronic autoimmune disease that causes inflammation in the central nervous... | ENSPRYNG is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive. | NA | NA | Link | Link | NA |
| 15911 | Th1643 | Satralizumab | >Th1643_Satralizumab QVQLQESGPGLVKPSETLSLTCAVSGHSISHDHAWSWVRQPPGEGLEWIGFISYSGITNYNPSLQGRVTISRDNSKNTLYLQMNSLRAEDTAVYYCARSLARTTAMDYWGEGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKSCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQEGNVFSCSVMHEALHAHYTQKSLSLSP | 143000 | NA | NA | NA | NA | The terminal half-life of satralizumab is approximately 30 days (range 22-37 days).[L15536] | Satralizumab is a recombinant humanized monoclonal antibody targeted against human interleukin-6 (IL-6) receptors, similar to [tocilizumab], which is produced in Chinese hamster ovary cells and based on an IgG2 framework.[L15536] Satralizumab is used in the treatment of neuromyelitis optica spectrum disorder (NMOSD), a rare autoimmune inflammatory disorder of the central nervous system (CNS) involving demyelinating lesions in the optic nerve, spinal cord, brainstem, and cerebrum.[A218551] Some of the pro-inflammatory mechanisms involved in NMOSD are thought to be mediated, at least in part, by IL-6, including increased production of anti-aquaporin-4 (AQP4) autoantibodies and increased permeability of the blood-brain barrier, which allows for the passage of pro-inflammatory mediators into the CNS.[A218546,A218551] Satralizumab is thought to exert its therapeutic benefits by blocking IL-6 receptors and, subsequently, these inflammatory responses. Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] is uniquely formulated with "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner[A218551] - this allows satralizumab to bind an IL-6 receptor until it reaches an endosome, after which the drug may dissociate from the receptor and move back into the plasma to act again. This novel mechanism effectively increases the duration of action of satralizumab, as it allows for single drug molecules to interact with multiple endogenous IL-6 receptors prior to elimination. Satralizumab was first approved for use in Canada in June 2020 for the treatment of AQP4 antibody-positive patients with NMOSD.[A218551] It received subsequent approvals in Switzerland and Japan,[A218551] and was approved for use by the FDA in August 2020,[L15566] becoming the 3rd treatment to receive FDA approval for NMOSD (after [eculizumab] in June 2019 and [inebilizumab] in June 2020). | Satralizumab is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive.[L15536] In Canada, it is also used in adolescent patients for the same indication.[L15546] | Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] utilizes a novel "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner.[A218551] Satralizumab-bound IL-6 receptors are taken up into cells and transported into endosomes, a relatively acidic environment in comparison to plasma (pH 5.5-6.0 vs. pH 7.4) - this decrease in pH allows satralizumab to dissociate from the IL-6 receptor and be recycled back into the plasma, where it can bind to another IL-6 receptor and repeat the process.[A218551] Satralizumab has been associated with an increased risk of infection, including serious and potentially fatal infections. It should not be administered to patients with active infections, including localized infections, until the infection resolves, and is contraindicated for use in patients with active hepatitis B or tuberculosis.[L15536] | Interleukin-6 (IL-6) is a pro-inflammatory cytokine[A218546] which has been implicated in the pathogenesis of NMOSD.[A218551] The inflammatory cascade triggered by IL-6 signaling is thought to result in the differentiation of T-cells into pro-inflammatory TH17 cells[A218551] and the differentiation of B-cells into plasmablasts producing AQP4 autoantibodies.[A218551,A218546] IL-6 may also play a role in increasing the permeability of the blood-brain barrier, thereby allowing penetration of autoantibodies and pro-inflammatory mediators into the central nervous system.[A218551,A218546] Satralizumab is a humanized monoclonal antibody targeted against human IL-6 receptors.[L15536] It binds to soluble and membrane-bound IL-6 receptors and prevents the signaling cascade, and subsequent pro-inflammatory effects, associated with its binding to endogenous IL-6. | There is no data regarding overdose of satralizumab. No serious adverse effects were noted in healthy adults receiving a single dose of 240mg subcutaneously in clinical trials.[L15546] Patients experiencing a suspected overdose should be treated with symptomatic and supportive measures as clinically indicated. | While the metabolism of satralizumab has not been studied directly,[L15536] monoclonal antibodies as a class are principally cleared by catabolism.[L15536,A216712] | The Cmax and AUC at steady-state, achieved after an 8-week loading period, were approximately 31.5 mcg/mL and 737 mcg.mL/day, respectively.[L15536] Average Ctrough concentrations were approximately 19 mcg/mL.[L15546] The bioavailability of satralizumab following subcutaneous injection has been reported to be between 78.5% and 85%.[L15536,L15546] | Satralizumab is subject to biphasic distribution - the estimated volume of distribution for the central and peripheral compartments are 3.46 L and 2.07 L, respectively.[L15546] | The total clearance of satralizumab is concentration-dependent and is estimated to be 0.0601-0.0679 L/day.[L15536,L15546] The inter-compartmental clearance was 0.336 L/day.[L15536] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Interleukin-6 receptor subunit alpha | Enspryng | Genentech Inc. | Genentech Inc. | Subcutaneous | 120 mg/1mL | ENSPRYNG is contraindicated in patients with: A known hypersensitivity to satralizumab or any of the inactive ingredients [see WARNINGS AND PRECAUTIONS] Active Hepatitis B infection [see WARNINGS AND PRECAUTIONS] Active or untreated latent tuberculosis [see WARNINGS AND PRECAUTIONS] | runny or stuffy nose, headache, upper respiratory tract infection, gastritis, rash, joint pain, extremity pain, fatigue, and nausea | Enspryng is a recombinant humanized monoclonal antibody targeting human interleukin-6 (IL-6) receptors. Enspryng is a prescription medicine used to treat adults with neuromyelitis optica spectrum disorder (NMOSD). NMOSD is a rare, chronic autoimmune disease that causes inflammation in the central nervous... | ENSPRYNG is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive. | NA | NA | Link | Link | NA |
| 15927 | Th1652 | Pentaglobin | NA | NA | NA | NA | NA | NA | NA | Pentaglobin, also known as IgM-enriched immunoglobulin, falls under a group of polyclonal immunoglobulin preparations.[A220173] It is comprised of [immunoglobulin G (IgG)](https://www.drugbank.ca/drugs/DB00028) and immunoglobulin A (IgA) while also being enriched by immunoglobulin M (IgM).[L16353] | NA | NA | Pentaglobin has potential antibacterial and immunomodulatory properties where, compared to immunoglobulin treatments without IgM, pentaglobin may have an increased ability to eliminate infectious pathogens . The IgM in the preparation plays a role in complement activation and neutralization of bacterial endo- and exotoxins.[L16353] Pentaglobin is used as an adjuvant in treatment of severe bacterial infections while it is also investigated against peritonitis, sepsis, and COVID-19.[A220178] | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15949 | Th1655 | Atoltivimab | >Th1655_Atoltivimab QVQLVESGGGVVQPGRSLRLSCAASGFTFNNYGMHWVRQAPGMGLEWVAVIWHDGSDKYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARNWNLFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145097.54 | C6448H9954N1726O2002S44 | NA | NA | NA | Atoltivimab administered to healthy subjects at 50 mg/kg has a mean elimination half-life of 21.2 ± 3.36 days.[L17320] | Ebola virus (EBOV) remains an important human pathogen within the _Ebolavirus_ genus, having been responsible for at least 17 known outbreaks with an average case fatality rate of 43.92%.[A221825] Immune therapy using monoclonal antibodies (mAbs) is becoming an increasingly attractive therapeutic method to combat infectious diseases due to its rapid development, low toxicity, and high specificity.[A222078] The chief surface target of EBOV particles is the GP1,2 glycoprotein, which also appears on the surface of EBOV-infected cells, offering opportunities for both neutralizing and cytotoxic (i.e. through Fc-mediated immune effector function) antibody effects to play a role in combatting EBOV infection.[A221825, A221830] A recent large-scale study elucidated that both neutralizing and Fc-mediated functions of antibodies were important for therapeutic benefit in animal models of EBOV infection.[A222078] INMAZEB™, formerly referred to as REGN-EB3, combines the three humanized IgG1 | Atoltivimab is indicated in combination with [Odesivimab] and [Maftivimab] for the treatment of _Zaire ebolavirus_ infection in adult and pediatric patients, including neonates born to a mother who has been confirmed positive by RT-PCR for _Zaire ebolavirus_ infection. This combination has not been established as efficacious for any other species within either the _Ebolavirus_ or _Marburgvirus_ genera; special care should be taken to evaluate the susceptibility of circulating _Zaire ebolavirus_ strains before beginning treatment, and the possible emergence of resistance should be monitored.[L17320] | Atoltivimab is a fully-humanized IgG1 | Ebola virus (EBOV) is one of several viruses within the _Ebolavirus_ genus known to infect humans with an average case fatality rate of 43.92%.[A221825] EBOV particles expose the GP1,2 glycoprotein on their surface, which comprises a trimer of GP1 and GP2 subunit heterodimers, with the subunits connected by a disulfide bond. GP1,2 plays an important role in both cell surface attachment/entry and eventual lysosomal escape through binding to the NPC intracellular cholesterol transporter 1/Niemann-Pick C1 protein (NPC1). In this manner, GP1,2 is integral to the pathogenic cycle of EBOV.[A221825, A221830] Atoltivimab is a fully-humanized IgG1 | NA | NA | Atoltivimab administered to healthy subjects at 50 mg/kg produced a mean Cmax of 1220 ± 101 mg/L and a mean AUC0-8 of 17,100 ± 4480 mg | Atoltivimab administered to healthy subjects at 50 mg/kg produced a mean steady-state volume of distribution of 58.2 ± 2.66 mL/kg.[L17320] | Atoltivimab administered to healthy subjects at 50 mg/kg has a mean clearance of 3.08 ± 0.719 mL/day/kg.[L17320] | Antibodies, Monoclonal | NA | NA | NA | NA | Envelope glycoprotein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15950 | Th1655 | Atoltivimab | >Th1655_Atoltivimab QVQLVESGGGVVQPGRSLRLSCAASGFTFNNYGMHWVRQAPGMGLEWVAVIWHDGSDKYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCARNWNLFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145097.54 | C6448H9954N1726O2002S44 | NA | NA | NA | Atoltivimab administered to healthy subjects at 50 mg/kg has a mean elimination half-life of 21.2 ± 3.36 days.[L17320] | Ebola virus (EBOV) remains an important human pathogen within the _Ebolavirus_ genus, having been responsible for at least 17 known outbreaks with an average case fatality rate of 43.92%.[A221825] Immune therapy using monoclonal antibodies (mAbs) is becoming an increasingly attractive therapeutic method to combat infectious diseases due to its rapid development, low toxicity, and high specificity.[A222078] The chief surface target of EBOV particles is the GP1,2 glycoprotein, which also appears on the surface of EBOV-infected cells, offering opportunities for both neutralizing and cytotoxic (i.e. through Fc-mediated immune effector function) antibody effects to play a role in combatting EBOV infection.[A221825, A221830] A recent large-scale study elucidated that both neutralizing and Fc-mediated functions of antibodies were important for therapeutic benefit in animal models of EBOV infection.[A222078] INMAZEB™, formerly referred to as REGN-EB3, combines the three humanized IgG1 | Atoltivimab is indicated in combination with [Odesivimab] and [Maftivimab] for the treatment of _Zaire ebolavirus_ infection in adult and pediatric patients, including neonates born to a mother who has been confirmed positive by RT-PCR for _Zaire ebolavirus_ infection. This combination has not been established as efficacious for any other species within either the _Ebolavirus_ or _Marburgvirus_ genera; special care should be taken to evaluate the susceptibility of circulating _Zaire ebolavirus_ strains before beginning treatment, and the possible emergence of resistance should be monitored.[L17320] | Atoltivimab is a fully-humanized IgG1 | Ebola virus (EBOV) is one of several viruses within the _Ebolavirus_ genus known to infect humans with an average case fatality rate of 43.92%.[A221825] EBOV particles expose the GP1,2 glycoprotein on their surface, which comprises a trimer of GP1 and GP2 subunit heterodimers, with the subunits connected by a disulfide bond. GP1,2 plays an important role in both cell surface attachment/entry and eventual lysosomal escape through binding to the NPC intracellular cholesterol transporter 1/Niemann-Pick C1 protein (NPC1). In this manner, GP1,2 is integral to the pathogenic cycle of EBOV.[A221825, A221830] Atoltivimab is a fully-humanized IgG1 | NA | NA | Atoltivimab administered to healthy subjects at 50 mg/kg produced a mean Cmax of 1220 ± 101 mg/L and a mean AUC0-8 of 17,100 ± 4480 mg | Atoltivimab administered to healthy subjects at 50 mg/kg produced a mean steady-state volume of distribution of 58.2 ± 2.66 mL/kg.[L17320] | Atoltivimab administered to healthy subjects at 50 mg/kg has a mean clearance of 3.08 ± 0.719 mL/day/kg.[L17320] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Envelope glycoprotein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15957 | Th1656 | Maftivimab | >Th1656_Maftivimab EVQLVESGGGLVQPGGSLRLSCAASGFTSSSYAMNWVRQAPGKGLEWVSTISGMGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKRGYPHSFDIWGQGTMVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143948.11 | C6368H9886N1706O2008S46 | NA | NA | NA | Maftivimab administered to healthy subjects at 50 mg/kg has a mean elimination half-life of 22.3 ± 3.09 days.[L17320] | Ebola virus (EBOV) remains an important human pathogen within the _Ebolavirus_ genus, having been responsible for at least 17 known outbreaks with an average case fatality rate of 43.92%.[A221825] Immune therapy using monoclonal antibodies (mAbs) is becoming an increasingly attractive therapeutic method to combat infectious diseases due to its rapid development, low toxicity, and high specificity.[A222078] The chief surface target of EBOV particles is the GP1,2 glycoprotein, which also appears on the surface of EBOV-infected cells, offering opportunities for both neutralizing and cytotoxic (i.e. through Fc-mediated immune effector function) antibody effects to play a role in combatting EBOV infection.[A221825, A221830] A recent large-scale study elucidated that both neutralizing and Fc-mediated functions of antibodies were important for therapeutic benefit in animal models of EBOV infection.[A222078] INMAZEB™, formerly referred to as REGN-EB3, combines the three humanized IgG1 | Maftivimab is indicated in combination with [Odesivimab] and [Atoltivimab] for the treatment of _Zaire ebolavirus_ infection in adult and pediatric patients, including neonates born to a mother who has been confirmed positive by RT-PCR for _Zaire ebolavirus_ infection. This combination has not been established as efficacious for any other species within either the _Ebolavirus_ or _Marburgvirus_ genera; special care should be taken to evaluate the susceptibility of circulating _Zaire ebolavirus_ strains before beginning treatment, and the possible emergence of resistance should be monitored.[L17320] | Maftivimab is a fully-humanized IgG1 | Ebola virus (EBOV) is one of several viruses within the _Ebolavirus_ genus known to infect humans with an average case fatality rate of 43.92%.[A221825] EBOV particles expose the GP1,2 glycoprotein on their surface, which comprises a trimer of GP1 and GP2 subunit heterodimers, with the subunits connected by a disulfide bond. GP1,2 plays an important role in both cell surface attachment/entry and eventual lysosomal escape through binding to the NPC intracellular cholesterol transporter 1/Niemann-Pick C1 protein (NPC1). In this manner, GP1,2 is integral to the pathogenic cycle of EBOV.[A221825, A221830] Maftivimab is a fully-humanized IgG1 | NA | NA | Maftivimab administered to healthy subjects at 50 mg/kg produced a mean Cmax of 1280 ± 68.0 mg/L and a mean AUC0-8 of 18,700 ± 4100 mg | Maftivimab administered to healthy subjects at 50 mg/kg produced a mean steady-state volume of distribution of 57.6 ± 3.89 mL/kg.[L17320] | Maftivimab administered to healthy subjects at 50 mg/kg has a mean clearance of 2.78 ± 0.558 mL/day/kg.[L17320] | Antibodies, Monoclonal | NA | NA | NA | NA | Envelope glycoprotein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15958 | Th1656 | Maftivimab | >Th1656_Maftivimab EVQLVESGGGLVQPGGSLRLSCAASGFTSSSYAMNWVRQAPGKGLEWVSTISGMGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKRGYPHSFDIWGQGTMVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143948.11 | C6368H9886N1706O2008S46 | NA | NA | NA | Maftivimab administered to healthy subjects at 50 mg/kg has a mean elimination half-life of 22.3 ± 3.09 days.[L17320] | Ebola virus (EBOV) remains an important human pathogen within the _Ebolavirus_ genus, having been responsible for at least 17 known outbreaks with an average case fatality rate of 43.92%.[A221825] Immune therapy using monoclonal antibodies (mAbs) is becoming an increasingly attractive therapeutic method to combat infectious diseases due to its rapid development, low toxicity, and high specificity.[A222078] The chief surface target of EBOV particles is the GP1,2 glycoprotein, which also appears on the surface of EBOV-infected cells, offering opportunities for both neutralizing and cytotoxic (i.e. through Fc-mediated immune effector function) antibody effects to play a role in combatting EBOV infection.[A221825, A221830] A recent large-scale study elucidated that both neutralizing and Fc-mediated functions of antibodies were important for therapeutic benefit in animal models of EBOV infection.[A222078] INMAZEB™, formerly referred to as REGN-EB3, combines the three humanized IgG1 | Maftivimab is indicated in combination with [Odesivimab] and [Atoltivimab] for the treatment of _Zaire ebolavirus_ infection in adult and pediatric patients, including neonates born to a mother who has been confirmed positive by RT-PCR for _Zaire ebolavirus_ infection. This combination has not been established as efficacious for any other species within either the _Ebolavirus_ or _Marburgvirus_ genera; special care should be taken to evaluate the susceptibility of circulating _Zaire ebolavirus_ strains before beginning treatment, and the possible emergence of resistance should be monitored.[L17320] | Maftivimab is a fully-humanized IgG1 | Ebola virus (EBOV) is one of several viruses within the _Ebolavirus_ genus known to infect humans with an average case fatality rate of 43.92%.[A221825] EBOV particles expose the GP1,2 glycoprotein on their surface, which comprises a trimer of GP1 and GP2 subunit heterodimers, with the subunits connected by a disulfide bond. GP1,2 plays an important role in both cell surface attachment/entry and eventual lysosomal escape through binding to the NPC intracellular cholesterol transporter 1/Niemann-Pick C1 protein (NPC1). In this manner, GP1,2 is integral to the pathogenic cycle of EBOV.[A221825, A221830] Maftivimab is a fully-humanized IgG1 | NA | NA | Maftivimab administered to healthy subjects at 50 mg/kg produced a mean Cmax of 1280 ± 68.0 mg/L and a mean AUC0-8 of 18,700 ± 4100 mg | Maftivimab administered to healthy subjects at 50 mg/kg produced a mean steady-state volume of distribution of 57.6 ± 3.89 mL/kg.[L17320] | Maftivimab administered to healthy subjects at 50 mg/kg has a mean clearance of 2.78 ± 0.558 mL/day/kg.[L17320] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Envelope glycoprotein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15965 | Th1657 | Odesivimab | >Th1657_Odesivimab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSYDMHWVRQATGKGLEWVSAIGTAGDTYYPGSVKGRFTISRENAKNSLYLQMNSLRAGDTAVYYCARTWFGELYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146164.54 | C6506H10024N1720O2030S42 | NA | NA | NA | Odesivimab administered to healthy subjects at 50 mg/kg has a mean elimination half-life of 25.3 ± 3.86 days.[L17320] | Ebola virus (EBOV) remains an important human pathogen within the _Ebolavirus_ genus, having been responsible for at least 17 known outbreaks with an average case fatality rate of 43.92%.[A221825] Immune therapy using monoclonal antibodies (mAbs) is becoming an increasingly attractive therapeutic method to combat infectious diseases due to its rapid development, low toxicity, and high specificity.[A222078] The chief surface target of EBOV particles is the GP1,2 glycoprotein, which also appears on the surface of EBOV-infected cells, offering opportunities for both neutralizing and cytotoxic (i.e. through Fc-mediated immune effector function) antibody effects to play a role in combatting EBOV infection.[A221825, A221830] A recent large-scale study elucidated that both neutralizing and Fc-mediated functions of antibodies were important for therapeutic benefit in animal models of EBOV infection.[A222078] INMAZEB™, formerly referred to as REGN-EB3, combines the three humanized IgG1 | Odesivimab is indicated in combination with [Maftivimab] and [Atoltivimab] for the treatment of _Zaire ebolavirus_ infection in adult and pediatric patients, including neonates born to a mother who has been confirmed positive by RT-PCR for _Zaire ebolavirus_ infection. This combination has not been established as efficacious for any other species within either the _Ebolavirus_ or _Marburgvirus_ genera; special care should be taken to evaluate the susceptibility of circulating _Zaire ebolavirus_ strains before beginning treatment, and the possible emergence of resistance should be monitored.[L17320] | Odesivimab is a fully-humanized IgG1 | Ebola virus (EBOV) is one of several viruses within the _Ebolavirus_ genus known to infect humans with an average case fatality rate of 43.92%.[A221825] EBOV particles expose the GP1,2 glycoprotein on their surface, which comprises a trimer of GP1 and GP2 subunit heterodimers, with the subunits connected by a disulfide bond. GP1,2 plays an important role in both cell surface attachment/entry and eventual lysosomal escape through binding to the NPC intracellular cholesterol transporter 1/Niemann-Pick C1 protein (NPC1). In this manner, GP1,2 is integral to the pathogenic cycle of EBOV.[A221825, A221830] Odesivimab is a fully-humanized IgG1 | NA | NA | Odesivimab administered to healthy subjects at 50 mg/kg produced a mean Cmax of 1260 ± 81.2 mg/L and a mean AUC0-8 of 25,600 ± 5040 mg | Odesivimab administered to healthy subjects at 50 mg/kg produced a mean steady-state volume of distribution of 56.0 ± 3.16 mL/kg.[L17320] | Odesivimab administered to healthy subjects at 50 mg/kg has a mean clearance of 2.02 ± 0.374 mL/day/kg.[L17320] | Antibodies, Monoclonal | NA | NA | NA | NA | Envelope glycoprotein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15966 | Th1657 | Odesivimab | >Th1657_Odesivimab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSYDMHWVRQATGKGLEWVSAIGTAGDTYYPGSVKGRFTISRENAKNSLYLQMNSLRAGDTAVYYCARTWFGELYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146164.54 | C6506H10024N1720O2030S42 | NA | NA | NA | Odesivimab administered to healthy subjects at 50 mg/kg has a mean elimination half-life of 25.3 ± 3.86 days.[L17320] | Ebola virus (EBOV) remains an important human pathogen within the _Ebolavirus_ genus, having been responsible for at least 17 known outbreaks with an average case fatality rate of 43.92%.[A221825] Immune therapy using monoclonal antibodies (mAbs) is becoming an increasingly attractive therapeutic method to combat infectious diseases due to its rapid development, low toxicity, and high specificity.[A222078] The chief surface target of EBOV particles is the GP1,2 glycoprotein, which also appears on the surface of EBOV-infected cells, offering opportunities for both neutralizing and cytotoxic (i.e. through Fc-mediated immune effector function) antibody effects to play a role in combatting EBOV infection.[A221825, A221830] A recent large-scale study elucidated that both neutralizing and Fc-mediated functions of antibodies were important for therapeutic benefit in animal models of EBOV infection.[A222078] INMAZEB™, formerly referred to as REGN-EB3, combines the three humanized IgG1 | Odesivimab is indicated in combination with [Maftivimab] and [Atoltivimab] for the treatment of _Zaire ebolavirus_ infection in adult and pediatric patients, including neonates born to a mother who has been confirmed positive by RT-PCR for _Zaire ebolavirus_ infection. This combination has not been established as efficacious for any other species within either the _Ebolavirus_ or _Marburgvirus_ genera; special care should be taken to evaluate the susceptibility of circulating _Zaire ebolavirus_ strains before beginning treatment, and the possible emergence of resistance should be monitored.[L17320] | Odesivimab is a fully-humanized IgG1 | Ebola virus (EBOV) is one of several viruses within the _Ebolavirus_ genus known to infect humans with an average case fatality rate of 43.92%.[A221825] EBOV particles expose the GP1,2 glycoprotein on their surface, which comprises a trimer of GP1 and GP2 subunit heterodimers, with the subunits connected by a disulfide bond. GP1,2 plays an important role in both cell surface attachment/entry and eventual lysosomal escape through binding to the NPC intracellular cholesterol transporter 1/Niemann-Pick C1 protein (NPC1). In this manner, GP1,2 is integral to the pathogenic cycle of EBOV.[A221825, A221830] Odesivimab is a fully-humanized IgG1 | NA | NA | Odesivimab administered to healthy subjects at 50 mg/kg produced a mean Cmax of 1260 ± 81.2 mg/L and a mean AUC0-8 of 25,600 ± 5040 mg | Odesivimab administered to healthy subjects at 50 mg/kg produced a mean steady-state volume of distribution of 56.0 ± 3.16 mL/kg.[L17320] | Odesivimab administered to healthy subjects at 50 mg/kg has a mean clearance of 2.02 ± 0.374 mL/day/kg.[L17320] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Envelope glycoprotein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15973 | Th1658 | Imdevimab | >Th1658_Imdevimab QVQLVESGGGVVQPGRSLRLSCAASGFTFSNYAMYWVRQAPGKGLEWVAVISYDGSNKYYADSVKGRFTISRDNSKNTLYLQMNSLRTEDTAVYYCASGSDYGDYLLVYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Imdevimab is a monoclonal antibody combined with [casirivimab] in Regeneron's antibody cocktail known as REGEN-COV2 for the treatment of COVID-19.[L23539] This drug is a combination of antibodies derived from humanized VelocImmune® mice in addition to blood samples from patients who have recovered from COVID-19.[A224429] These antibodies have been formulated to bind to multiple locations on the SARS-COV-2 spike protein, preventing viral escape.[A221495] On November 21, 2020, the FDA authorized emergency approval of REGN-COV2 to treat mild to moderate COVID-19 in patients aged 12 years and older. Casirivimab and imdevimab are investigational recombinant human IgG1 monoclonal antibodies that, at this time, are not officially approved by the FDA. They are reserved for Emergency Use Authorization (EUA) only.[L23524] In November 2021, the same indication was approved by the EMA.[L39130,L39135] Full safety and efficacy data on imdevimab are not yet available, and further evaluation of this investigational therapy will continue.[L23529,L23539,L14303] | According to the Emergency Use Authorization (EUA) by the FDA and EMA, indevimab is used only with casirivimab to prevent COVID-19 and treat mild to moderate COVID-19 from laboratory-confirmed SARS-CoV-2 infection in patients aged 12 years of age and older who weigh at least 40 kg. Treatment is reserved for patients who are at high risk for progressing to require hospitalization or severe COVID-19.[L23524,L23534,L39135] This combination may only be administered by intravenous infusion in healthcare settings with immediate access to treatment for infusion reactions and anaphylaxis, and the ability to activate the emergency medical system (EMS), as required.[L23534,L23539] **Limitations of use** Imdevimab and casirivimab are not for use in patients currently hospitalized due to COVID-19, patients requiring oxygen therapy due to COVID-19, patients requiring increases in baseline oxygen flow rate from COVID-19, or patients on oxygen therapy for non-COVID-19 related morbidity.[L23524,L23534] | Casirivimab and imdevimab work to neutralize the spike protein of SARS-CoV-2.[L23524] In a clinical trial, casirivimab and imdevimab, when given together, reduced COVID-19-related hospitalization or emergency room visits in patients diagnosed with COVID-19 who were at high risk for disease progression within 28 days after treatment. No benefit has been shown in patients already hospitalized due to COVID-19 receiving this combination.[L23539] | Imdevimab is a recombinant human IgG1 monoclonal antibody targeting the receptor binding domain of the spike protein of SARS-CoV-2; a protein playing an important role in viral attachment, fusion, and entry into the target cell by binding to the ACE2 receptor.[A224424,A224434,L23529] Together with casirivimab, imdevimab neutralizes the spike protein of SARS-CoV-2.[L23529] | There is limited information on overdose. Up to 4000 mg, which is approximately seven times the recommended dose of the drug, was administered in clinical trials. There is no known specific antidote for imdevimab overdose so treatment of overdose should involve general supportive measures.[L39135] | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Spike glycoprotein | Casirivimab With Imdevimab | Regeneron Pharmaceuticals, Inc. | Regeneron Pharmaceuticals, Inc. | Intravenous | NA | NA | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, severe dizziness, rash, and itching | Regen-Cov is a prescription medicine used to treat the symptoms of COVID-19 (EUA). Regen-Cov may be used alone or with other medications. | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, severe dizziness, rash, and itching | NA | NA | Link | Link | NA |
| 15974 | Th1658 | Imdevimab | >Th1658_Imdevimab QVQLVESGGGVVQPGRSLRLSCAASGFTFSNYAMYWVRQAPGKGLEWVAVISYDGSNKYYADSVKGRFTISRDNSKNTLYLQMNSLRTEDTAVYYCASGSDYGDYLLVYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Imdevimab is a monoclonal antibody combined with [casirivimab] in Regeneron's antibody cocktail known as REGEN-COV2 for the treatment of COVID-19.[L23539] This drug is a combination of antibodies derived from humanized VelocImmune® mice in addition to blood samples from patients who have recovered from COVID-19.[A224429] These antibodies have been formulated to bind to multiple locations on the SARS-COV-2 spike protein, preventing viral escape.[A221495] On November 21, 2020, the FDA authorized emergency approval of REGN-COV2 to treat mild to moderate COVID-19 in patients aged 12 years and older. Casirivimab and imdevimab are investigational recombinant human IgG1 monoclonal antibodies that, at this time, are not officially approved by the FDA. They are reserved for Emergency Use Authorization (EUA) only.[L23524] In November 2021, the same indication was approved by the EMA.[L39130,L39135] Full safety and efficacy data on imdevimab are not yet available, and further evaluation of this investigational therapy will continue.[L23529,L23539,L14303] | According to the Emergency Use Authorization (EUA) by the FDA and EMA, indevimab is used only with casirivimab to prevent COVID-19 and treat mild to moderate COVID-19 from laboratory-confirmed SARS-CoV-2 infection in patients aged 12 years of age and older who weigh at least 40 kg. Treatment is reserved for patients who are at high risk for progressing to require hospitalization or severe COVID-19.[L23524,L23534,L39135] This combination may only be administered by intravenous infusion in healthcare settings with immediate access to treatment for infusion reactions and anaphylaxis, and the ability to activate the emergency medical system (EMS), as required.[L23534,L23539] **Limitations of use** Imdevimab and casirivimab are not for use in patients currently hospitalized due to COVID-19, patients requiring oxygen therapy due to COVID-19, patients requiring increases in baseline oxygen flow rate from COVID-19, or patients on oxygen therapy for non-COVID-19 related morbidity.[L23524,L23534] | Casirivimab and imdevimab work to neutralize the spike protein of SARS-CoV-2.[L23524] In a clinical trial, casirivimab and imdevimab, when given together, reduced COVID-19-related hospitalization or emergency room visits in patients diagnosed with COVID-19 who were at high risk for disease progression within 28 days after treatment. No benefit has been shown in patients already hospitalized due to COVID-19 receiving this combination.[L23539] | Imdevimab is a recombinant human IgG1 monoclonal antibody targeting the receptor binding domain of the spike protein of SARS-CoV-2; a protein playing an important role in viral attachment, fusion, and entry into the target cell by binding to the ACE2 receptor.[A224424,A224434,L23529] Together with casirivimab, imdevimab neutralizes the spike protein of SARS-CoV-2.[L23529] | There is limited information on overdose. Up to 4000 mg, which is approximately seven times the recommended dose of the drug, was administered in clinical trials. There is no known specific antidote for imdevimab overdose so treatment of overdose should involve general supportive measures.[L39135] | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Spike glycoprotein | Imdevimab | Regeneron Pharmaceuticals, Inc. | Regeneron Pharmaceuticals, Inc. | Intravenous | 300 mg/2.5mL | NA | use in treating conditions caused by coronavirus. | Imdevimab is an experimental medicine being studied for use in treating conditions caused by coronavirus. It is not yet known if imdevimab is a safe and effective treatment for any condition. | throat irritation, swelling in your face or throat; dizziness, a light-headed feeling (like you might pass out); chest pain, wheezing, shortness of breath; fever, chills, sweating, nausea, flushing (sudden warmth, redness, or tingly feeling); fast or slow heartbeats, headache, pounding in your neck or ears; weakness, tiredness; rash, itching; or muscle pain. | NA | NA | Link | Link | NA |
| 15982 | Th1659 | Casirivimab | >Th1659_Casirivimab QVQLVESGGGLVKPGGSLRLSCAASGFTFSDYYMSWIRQAPGKGLEWVSYITYSGSTIYYADSVKGRFTISRDNAKSSLYLQMNSLRAEDTAVYYCARDRGTTMVPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Casirivimab is a monoclonal antibody combined with [Imdevimab] in Regeneron's antibody cocktail known as REGN-COV2 for the treatment of COVID-19.[L23539] This drug is a combination of antibodies derived from humanized VelocImmune® mice in addition to blood samples from patients who have recovered from COVID-19.[A224429] These antibodies have been formulated to bind to multiple locations on the SARS-COV-2 spike protein, preventing viral escape.[A221495] On November 21 2020, the FDA authorized emergency approval of REGEN-COV2 to treat mild to moderate COVID-19 in patients aged 12 years and older. Casirivimab and imdevimab are investigational recombinant human IgG1 monoclonal antibodies that, at this time, are not officially approved by the FDA. They are reserved for Emergency Use Authorization (EUA) only.[L23524] In November 2021, the same indication was approved by the EMA.[L39130,L39135] Full safety and efficacy data are not yet available, and further evaluation of this investigational therapy will continue.[L23539,L23529,L14303] | According to the Emergency Use Authorization (EUA) by the FDA and EMA, indevimab is used only with casirivimab to prevent COVID-19 and treat mild to moderate COVID-19 from laboratory-confirmed SARS-CoV-2 infection in patients aged 12 years of age and older who weigh at least 40 kg. Treatment is reserved for patients who are at high risk for progressing to require hospitalization or severe COVID-19.[L23524,L23534,L39135] This combination may only be administered by intravenous infusion in healthcare settings with immediate access to treatment for infusion reactions and anaphylaxis, and the ability to activate the emergency medical system (EMS), as required.[L23539,L23534] **Limitations of use** Imdevimab and casirivimab are not for use in patients currently hospitalized due to COVID-19, patients requiring oxygen therapy due to COVID-19, patients requiring increases in baseline oxygen flow rate from COVID-19, or patients on oxygen therapy for non-COVID-19 related morbidity.[L23524,L23534] | Casirivimab and imdevimab work to neutralize the spike protein of SARS-CoV-2.[L23524] In a clinical trial, casirivimab and imdevimab, when given together, reduced COVID-19-related hospitalization or emergency room visits in patients diagnosed with COVID-19 who were at high risk for disease progression within 28 days after treatment. No benefit has been shown in patients already hospitalized due to COVID-19 receiving this combination.[L23539] | Casirivimab is a recombinant human IgG1 monoclonal antibody targeting the receptor binding domain of the spike protein of SARS-CoV-2; a protein playing an important role in viral attachment, fusion, and entry into the cell.[A224434,L23529] Together with imdevimab, casirivimab neutralizes the spike protein of SARS-CoV-2.[L23529] | There is limited information on overdose. Up to 4000 mg, which is approximately seven times the recommended dose of the drug, was administered in clinical trials. There is no known specific antidote for casirivimab overdose so treatment of overdose should involve general supportive measures.[L39135] | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | Spike glycoprotein | Casirivimab | Regeneron Pharmaceuticals, Inc. | Regeneron Pharmaceuticals, Inc. | Intravenous | 1332 mg/11.1mL | NA | pain, bleeding, bruising of the skin, soreness, swelling, or infection at injection site | On January 24, 2022, FDA reissued the emergency use authorization (EUA) for casirivimab and imdevimab stating that the combination regimen is not authorized for treatment of mild to moderate COVID-19 in geographic regions where infection is likely to have been caused by a non-susceptible SARS-CoV-2 variant based on available information including variant susceptibility to these drugs and regional variant frequency. Given the prevalence of the Omicron variant in the United States, casirivimab and imdevimab is not recommended for use anywhere for mild to moderate disease at the present time. | to treat mild to moderate symptoms of COVID-19. to prevent COVID-19 in those who are not fully vaccinated against COVID-19 or who are vaccinated, but have a weakened immune system, or are taking a medication that affects the immune system and who have had close contact or are at high risk of close contact to someone who is infected with the SARS-CoV-2 virus (for example, nursing homes, prisons). | NA | NA | Link | Link | NA |
| 15983 | Th1659 | Casirivimab | >Th1659_Casirivimab QVQLVESGGGLVKPGGSLRLSCAASGFTFSDYYMSWIRQAPGKGLEWVSYITYSGSTIYYADSVKGRFTISRDNAKSSLYLQMNSLRAEDTAVYYCARDRGTTMVPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | NA | NA | NA | NA | NA | NA | Casirivimab is a monoclonal antibody combined with [Imdevimab] in Regeneron's antibody cocktail known as REGN-COV2 for the treatment of COVID-19.[L23539] This drug is a combination of antibodies derived from humanized VelocImmune® mice in addition to blood samples from patients who have recovered from COVID-19.[A224429] These antibodies have been formulated to bind to multiple locations on the SARS-COV-2 spike protein, preventing viral escape.[A221495] On November 21 2020, the FDA authorized emergency approval of REGEN-COV2 to treat mild to moderate COVID-19 in patients aged 12 years and older. Casirivimab and imdevimab are investigational recombinant human IgG1 monoclonal antibodies that, at this time, are not officially approved by the FDA. They are reserved for Emergency Use Authorization (EUA) only.[L23524] In November 2021, the same indication was approved by the EMA.[L39130,L39135] Full safety and efficacy data are not yet available, and further evaluation of this investigational therapy will continue.[L23539,L23529,L14303] | According to the Emergency Use Authorization (EUA) by the FDA and EMA, indevimab is used only with casirivimab to prevent COVID-19 and treat mild to moderate COVID-19 from laboratory-confirmed SARS-CoV-2 infection in patients aged 12 years of age and older who weigh at least 40 kg. Treatment is reserved for patients who are at high risk for progressing to require hospitalization or severe COVID-19.[L23524,L23534,L39135] This combination may only be administered by intravenous infusion in healthcare settings with immediate access to treatment for infusion reactions and anaphylaxis, and the ability to activate the emergency medical system (EMS), as required.[L23539,L23534] **Limitations of use** Imdevimab and casirivimab are not for use in patients currently hospitalized due to COVID-19, patients requiring oxygen therapy due to COVID-19, patients requiring increases in baseline oxygen flow rate from COVID-19, or patients on oxygen therapy for non-COVID-19 related morbidity.[L23524,L23534] | Casirivimab and imdevimab work to neutralize the spike protein of SARS-CoV-2.[L23524] In a clinical trial, casirivimab and imdevimab, when given together, reduced COVID-19-related hospitalization or emergency room visits in patients diagnosed with COVID-19 who were at high risk for disease progression within 28 days after treatment. No benefit has been shown in patients already hospitalized due to COVID-19 receiving this combination.[L23539] | Casirivimab is a recombinant human IgG1 monoclonal antibody targeting the receptor binding domain of the spike protein of SARS-CoV-2; a protein playing an important role in viral attachment, fusion, and entry into the cell.[A224434,L23529] Together with imdevimab, casirivimab neutralizes the spike protein of SARS-CoV-2.[L23529] | There is limited information on overdose. Up to 4000 mg, which is approximately seven times the recommended dose of the drug, was administered in clinical trials. There is no known specific antidote for casirivimab overdose so treatment of overdose should involve general supportive measures.[L39135] | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Spike glycoprotein | Casirivimab and Imdevimab | Hoffmann La Roche | Hoffmann La Roche | Intravenous | NA | NA | pain, bleeding, bruising of the skin, soreness, swelling, or infection at injection site | On January 24, 2022, FDA reissued the emergency use authorization (EUA) for casirivimab and imdevimab stating that the combination regimen is not authorized for treatment of mild to moderate COVID-19 in geographic regions where infection is likely to have been caused by a non-susceptible SARS-CoV-2 variant based on available information including variant susceptibility to these drugs and regional variant frequency. Given the prevalence of the Omicron variant in the United States, casirivimab and imdevimab is not recommended for use anywhere for mild to moderate disease at the present time. | to treat mild to moderate symptoms of COVID-19. to prevent COVID-19 in those who are not fully vaccinated against COVID-19 or who are vaccinated, but have a weakened immune system, or are taking a medication that affects the immune system and who have had close contact or are at high risk of close contact to someone who is infected with the SARS-CoV-2 virus (for example, nursing homes, prisons). | NA | NA | Link | Link | NA |
| 15992 | Th1660 | Naxitamab | NA | 144000 | NA | NA | NA | NA | The mean terminal half-life of naxitamab is 8.2 days.[L24454] | Naxitamab (humanized 3F8, hu3F8) is an IgG1 monoclonal antibody directed against the oncofetal differentiation antigen GD2 disialoganglioside.[L24454,A224604] Normally expressed during fetal development and in mature neurons, pain fibers, and skin cells, GD2 constitutes a highly efficient target in the treatment of neuroblastoma - it is widely expressed across and within neuroblastomas (and other neuroectodermal tumors),[A224609] and is rarely subject to antigen loss.[A224604] The first anti-GD2-monoclonal IgG antibody to be approved by the FDA for the treatment of neuroblastoma was [dinutuximab] under the brand name Unituxin in 2015.[A224474] One stark disadvantage of this therapy is the requirement for concurrent use of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA).[L24929] Naxitamab-gqgk (Danyelza) was granted accelerated approval by the FDA in November 2020 for the treatment of high-risk relapsed/refractory neuroblastoma of the bone or bone marrow.[L24454] This approval requires naxitamab to be co-administered only with GM-CSF, a factor known to enhance the granulocyte-mediated antibody-dependent cytotoxicity of anti-GD2 therapies,[A224604] making the administration of naxitamab therapy markedly simpler than that of its predecessor. | Naxitamab-gqgk is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), for the treatment of patients 1 year of age and older with relapsed or refractory high-risk neuroblastoma in the bone or bone marrow who have demonstrated a partial response, minor response, or stable disease to prior therapy.[L24454] | In targeting cell surface glycoproteins (GD2) that occur on the surface of neuroendocrine tumors, naxitamab directs the immune system towards these cancerous cells and induces the activation of both complement-dependent and antibody-dependent cytotoxicity.[L24454] Naxitamab can cause serious infusion reactions - including hypotension, hypoxia, anaphylaxis, and cardiac arrest - that necessitate careful monitoring during therapy. All patients should be pre-medicated with intravenous corticosteroids (e.g. [methylprednisolone]) as well as an antihistamine, H2 receptor antagonist, acetaminophen, and an antiemetic prior to therapy to mitigate the risk and severity of infusion-related reactions. Naxitamab may also cause severe neurotoxicity, including significant neuropathic pain, transverse myelitis, reversible posterior leukoencephalopathy syndrome (RPLS), and ocular toxicities. Pain management should be implemented prior to and during therapy - patients should take a 12-day course of neuropathic pain prophylaxis (e.g. gabapentin) starting 4 days prior to infusion, and should receive oral opioids 45-60 minutes prior to infusion and intravenous opioids and/or ketamine as needed thereafter.[L24454] | Neuroblastomas are neuroendocrine tumors occurring in immature and developing cells of the nervous system and are the most common malignancy diagnosed in children <1 year of age.[A224604] The GD2 disialoganglioside is a glycolipid found highly expressed on the surface of neuroectodermal tumors,[A224609] including neuroblastomas. GD2 exhibits high density and homogeneity across neuroblastomas and a rare occurrence of antigen loss,[A224604] making it a desirable target in the treatment of these cancers. Naxitamab is an IgG1 monoclonal antibody directed against GD2 disialogangliosides - it binds to GD2 on the surface of neuroblastoma cells and induces both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC),[L24454] the latter of which is enhanced by co-administration with GM-CSF.[A224604] | Data regarding overdose of naxitamab are unavailable. In the event of an overdose, patients should be treated with symptomatic and supportive measures. | While the metabolism of naxitamab has not been studied directly,[L24454] monoclonal antibodies as a class are principally metabolized to smaller peptides via catabolic processes.[L24454,A216712] | The mean plasma concentration of naxitamab following an intravenous infusion of 3 mg/kg over 30 minutes was 57.4 µg/mL.[L24454] The AUC of naxitamab appears to correlate with body size.[A224474] | NA | The clearance of naxitamab appears to be correlated inversely with body weight.[L24454] | Antibodies, Monoclonal | NA | NA | NA | NA | GD2 disialoganglioside | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15993 | Th1660 | Naxitamab | NA | 144000 | NA | NA | NA | NA | The mean terminal half-life of naxitamab is 8.2 days.[L24454] | Naxitamab (humanized 3F8, hu3F8) is an IgG1 monoclonal antibody directed against the oncofetal differentiation antigen GD2 disialoganglioside.[L24454,A224604] Normally expressed during fetal development and in mature neurons, pain fibers, and skin cells, GD2 constitutes a highly efficient target in the treatment of neuroblastoma - it is widely expressed across and within neuroblastomas (and other neuroectodermal tumors),[A224609] and is rarely subject to antigen loss.[A224604] The first anti-GD2-monoclonal IgG antibody to be approved by the FDA for the treatment of neuroblastoma was [dinutuximab] under the brand name Unituxin in 2015.[A224474] One stark disadvantage of this therapy is the requirement for concurrent use of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA).[L24929] Naxitamab-gqgk (Danyelza) was granted accelerated approval by the FDA in November 2020 for the treatment of high-risk relapsed/refractory neuroblastoma of the bone or bone marrow.[L24454] This approval requires naxitamab to be co-administered only with GM-CSF, a factor known to enhance the granulocyte-mediated antibody-dependent cytotoxicity of anti-GD2 therapies,[A224604] making the administration of naxitamab therapy markedly simpler than that of its predecessor. | Naxitamab-gqgk is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), for the treatment of patients 1 year of age and older with relapsed or refractory high-risk neuroblastoma in the bone or bone marrow who have demonstrated a partial response, minor response, or stable disease to prior therapy.[L24454] | In targeting cell surface glycoproteins (GD2) that occur on the surface of neuroendocrine tumors, naxitamab directs the immune system towards these cancerous cells and induces the activation of both complement-dependent and antibody-dependent cytotoxicity.[L24454] Naxitamab can cause serious infusion reactions - including hypotension, hypoxia, anaphylaxis, and cardiac arrest - that necessitate careful monitoring during therapy. All patients should be pre-medicated with intravenous corticosteroids (e.g. [methylprednisolone]) as well as an antihistamine, H2 receptor antagonist, acetaminophen, and an antiemetic prior to therapy to mitigate the risk and severity of infusion-related reactions. Naxitamab may also cause severe neurotoxicity, including significant neuropathic pain, transverse myelitis, reversible posterior leukoencephalopathy syndrome (RPLS), and ocular toxicities. Pain management should be implemented prior to and during therapy - patients should take a 12-day course of neuropathic pain prophylaxis (e.g. gabapentin) starting 4 days prior to infusion, and should receive oral opioids 45-60 minutes prior to infusion and intravenous opioids and/or ketamine as needed thereafter.[L24454] | Neuroblastomas are neuroendocrine tumors occurring in immature and developing cells of the nervous system and are the most common malignancy diagnosed in children <1 year of age.[A224604] The GD2 disialoganglioside is a glycolipid found highly expressed on the surface of neuroectodermal tumors,[A224609] including neuroblastomas. GD2 exhibits high density and homogeneity across neuroblastomas and a rare occurrence of antigen loss,[A224604] making it a desirable target in the treatment of these cancers. Naxitamab is an IgG1 monoclonal antibody directed against GD2 disialogangliosides - it binds to GD2 on the surface of neuroblastoma cells and induces both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC),[L24454] the latter of which is enhanced by co-administration with GM-CSF.[A224604] | Data regarding overdose of naxitamab are unavailable. In the event of an overdose, patients should be treated with symptomatic and supportive measures. | While the metabolism of naxitamab has not been studied directly,[L24454] monoclonal antibodies as a class are principally metabolized to smaller peptides via catabolic processes.[L24454,A216712] | The mean plasma concentration of naxitamab following an intravenous infusion of 3 mg/kg over 30 minutes was 57.4 µg/mL.[L24454] The AUC of naxitamab appears to correlate with body size.[A224474] | NA | The clearance of naxitamab appears to be correlated inversely with body weight.[L24454] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | GD2 disialoganglioside | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16010 | Th1663 | Sotrovimab | >Th1663_Sotrovimab QVQLVQSGAEVKKPGASVKVSCKASGYPFTSYGISWVRQAPGQGLEWMGWISTYQGNTNYAQKFQGRVTMTTDTSTTTGYMELRRLRSDDTAVYYCARDYTRGAWFGESLIGGFDNWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVLHEALHSHYTQKSLSLSPGK | 149000 | NA | NA | NA | NA | This antibody has undergone modifications for a potentially extended half-life and enhanced lung bioavailability.[L27296] The half-life of sotrovimab is longer than Fc-unmodified IgG due to the LS modification, however, specific values are not available in the literature.[L34430] | Sotrovimab (VIR-7831), also known as GSK4182136, is a monoclonal antibody with the ability to neutralize the SARS-CoV-2 virus.[L34440] On May 26, 2021 the FDA granted GlaxoSmithKline and Vir Biotechnology emergency use authorization for sotrovimab in the treatment of mild-to-moderate COVID-19. This authorization was based on interim results from a clinical trial, demonstrating that treatment with sotrovimab resulted in an 85% reduction in the risk of death or hospitalization in high-risk adults with COVID-19 in the outpatient setting.[L34425,L34440] A fact sheet for healthcare providers is currently available.[L34430] | Sotrovimab is authorized for use under FDA's Emergency Use Authorization (EUA) for the treatment of mild-to-moderate coronavirus disease 2019 (COVID-19) in adults and pediatric patients (12 years of age and older weighing at least 40 kg) with positive results of direct SARSCoV-2 viral testing, and who are at high risk for progression to severe COVID-19, including hospitalization or death.[L34425] | Sotrovimab is a monoclonal antibody that treats mild-to-moderate COVID-19 by binding to and neutralizing the spike protein of SARS-CoV-2.[A235835,L34440] | Sotrovimab is a recombinant human IgG1 | There are currently no data available regarding an overdose with sotrovimab, and LD50 information is not available. If an overdose occurs, provide symptomatic and supportive treatment as required.[L34430] | NA | A non-compartmental analysis determined that the mean Cmax after a 1 hour IV infusion of sotrovimab was 137 µg/mL and the mean Day 29 concentration was 34 µg/mL.[L34430] | Sotrovimab is an Fc-enhanced human immunoglobulin G (IgG), and therefore has the potential for placental transfer.[L34430] | NA | Antibodies, Monoclonal | NA | NA | NA | NA | Spike glycoprotein | Sotrovimab for Injection | Glaxosmithkline Inc | Glaxosmithkline Inc | Intravenous | 500 mg / 8 mL | NA | mild or moderate (grade 1 or 2) rash (2%) and diarrhea (1%). | NA | NA | NA | NA | Link | Link | NA |
| 16017 | Th1664 | Anti-SARS-CoV-2 immunoglobulin | NA | NA | NA | NA | NA | NA | NA | Hyperimmune immunoglobulin to SARS-CoV-2 (hIVIG) is obtained from the plasma of patients who recover from COVID-19 and develop neutralizing antibodies.[L27521] Anti-coronavirus immunoglobulin is derived from [COVID-19 convalescent plasma](https://go.drugbank.com/drugs/DB15692) but contains more SARS-CoV-2 neutralizing antibodies than found in [convalescent plasma](https://go.drugbank.com/drugs/DB15692) as the antibodies are highly purified and concentrated.[L27521, L27526] | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16020 | Th1664 | Anti-SARS-CoV-2 immunoglobulin | NA | NA | NA | NA | NA | NA | NA | Hyperimmune immunoglobulin to SARS-CoV-2 (hIVIG) is obtained from the plasma of patients who recover from COVID-19 and develop neutralizing antibodies.[L27521] Anti-coronavirus immunoglobulin is derived from [COVID-19 convalescent plasma](https://go.drugbank.com/drugs/DB15692) but contains more SARS-CoV-2 neutralizing antibodies than found in [convalescent plasma](https://go.drugbank.com/drugs/DB15692) as the antibodies are highly purified and concentrated.[L27521, L27526] | NA | NA | NA | NA | NA | NA | NA | NA | HIV Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16028 | Th1665 | Actoxumab | NA | NA | NA | NA | NA | NA | NA | Actoxumab is under investigation in clinical trial NCT01241552 (A Study of MK-3415, MK-6072, and MK-3415A in Participants Receiving Antibiotic Therapy for Clostridium Difficile Infection (MK-3415A-001)). | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16036 | Th1666 | Tefibazumab | NA | NA | NA | NA | NA | NA | NA | Tefibazumab is under investigation in clinical trial NCT00198289 (Aurexis® in Cystic Fibrosis Subjects Chronically Colonized With Staphylococcus Aureus in Their Lungs). | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16037 | Th1666 | Tefibazumab | NA | NA | NA | NA | NA | NA | NA | Tefibazumab is under investigation in clinical trial NCT00198289 (Aurexis® in Cystic Fibrosis Subjects Chronically Colonized With Staphylococcus Aureus in Their Lungs). | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16043 | Th1667 | Toralizumab | NA | NA | NA | NA | NA | NA | NA | Toralizumab is under investigation in clinical trial NCT03605927 (CD40-L Blockade for Prevention of Acute Graft-versus-host Disease). | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16044 | Th1667 | Toralizumab | NA | NA | NA | NA | NA | NA | NA | Toralizumab is under investigation in clinical trial NCT03605927 (CD40-L Blockade for Prevention of Acute Graft-versus-host Disease). | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16045 | Th1667 | Toralizumab | NA | NA | NA | NA | NA | NA | NA | Toralizumab is under investigation in clinical trial NCT03605927 (CD40-L Blockade for Prevention of Acute Graft-versus-host Disease). | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16054 | Th1669 | Cilgavimab | >Th1669_Cilgavimab EVQLVESGGGLVKPGGSLRLSCAASGFTFRDVWMSWVRQAPGKGLEWVGRIKSKIDGGTTDYAAPVKGRFTISRDDSKNTLYLQMNSLKTEDTAVYYCTTAGSYYYDTVGPGLPEGKFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPEFEGGPSVFLFPPKPKDTLYITREPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPASIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 152000 | C6626H10218N1750O2078S44 | NA | NA | NA | Cilgavimab has a half-life of 82.9 ± 12.3 days.[L39411] | SARS-CoV-2, the causative agent of COVID-19, enters cells via the interaction between the trimeric spike (S) glycoprotein and host cell angiotensin-converting enzyme 2 (ACE2). Blocking the interaction between the receptor-binding domain (RBD) of the S1 subunit and ACE2 inhibits viral host cell entry; animal studies indicate that antibodies capable of blocking this interaction reduce viral load and improve clinical symptoms of infection.[A243356, A243361] Cilgavimab (formerly AZD1061) is a recombinant monoclonal antibody produced in Chinese hamster ovary (CHO) cells derived from a neutralizing antibody isolated from a patient with a natural history of SARS-CoV-2 infection and modified through targeted amino acid substitutions to exhibit an extended (~85-day) half-life.[A243351, A243356, L39411] As the RBD binding site of cilgavimab does not overlap with that of [tixagevimab], the two can be administered to synergistically impair SARS-CoV-2 infection in individuals who may be exposed to the virus.[A243351, A243361, L39411] Cilgavimab is not approved for any indication by the FDA. Cilgavimab, in combination with [tixagevimab], was issued an FDA emergency use authorization (EUA) on December 9, 2021, for the pre-exposure prophylaxis of COVID-19 in individuals at increased risk for whom vaccination is not recommended. The combination is co-packaged and available under the name EVUSHELD (formerly AZD7442).[L39411] | Cilgavimab has been issued an emergency use authorization (EUA) by the FDA, in combination with [tixagevimab], for the pre-exposure prophylaxis of COVID-19 in adult and pediatric patients aged 12 years and older weighing at least 40 kg. Furthermore, patients must not be currently infected with SARS-CoV-2 or have had known exposure to an individual infected with SARS-CoV-2 and must either be immunocompromised due to a medical condition, medication, or treatment or be otherwise ineligible for vaccination with any eligible COVID-19 vaccine due to a history of severe adverse reactions.[L39411] The combination of cilgavimab and [tixagevimab] is not authorized for the treatment or post-exposure prophylaxis of COVID-19 and is not a substitute for COVID-19 vaccination. Individuals receiving therapy following COVID-19 vaccination should wait at least two weeks.[L39411] | Cilgavimab is an extended half-life recombinant human IgG1 | SARS-CoV-2, the causative agent of COVID-19, enters cells via the interaction between the trimeric spike (S) glycoprotein and host cell angiotensin-converting enzyme 2 (ACE2). Of the two subunits comprising the trimeric S glycoprotein, the S1 subunit binds ACE2 via its receptor-binding domain (RBD) while the central S2 subunit mediates fusion following S1 shedding.[A243351, A243356] Large-scale screens suggest that the most potently neutralizing antibodies recovered from the B cells of those convalescing following natural infection with SARS-CoV-2 bind to the RBD of S1 and are capable of disrupting the interaction between the RBD and human ACE2.[A243356] Cilgavimab (AZD1061) is a recombinant human IgG1 | Toxicity information regarding cilgavimab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects. Symptomatic and supportive measures are recommended.[L39411] | As a monoclonal antibody, cilgavimab is expected to undergo proteolytic degradation.[L39411] | A single 150 mg intramuscular dose of cilgavimab, given concurrently with 150 mg of [tixagevimab], resulted in a Cmax geometric mean (%CV) of 15.3 (38.5) µg/mL in a median Tmax of 14.0 (range 3.1-60) days. The observed geometric mean (%CV) one, 150, or 210 days following dosing was 3.9 (94.4), 5.5 (35.2), and 3.9 (37.1) µg/mL. This single dose resulted in an AUC0-8 of 2133 (31.7) µg | Cilgavimab has an apparent volume of distribution of 8.7 ± 2.73 L.[L39411] | Cilgavimab has an apparent clearance of 0.074 ± 0.028 L/day.[L39411] | Antibodies, Monoclonal | NA | NA | NA | NA | Spike glycoprotein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16063 | Th1670 | Tixagevimab | NA | 149000 | C6488H10034N1746O2038S50 | NA | NA | NA | Tixagevimab has a half-life of 87.9 ± 13.9 days.[L39411] | SARS-CoV-2, the causative agent of COVID-19, enters cells via the interaction between the trimeric spike (S) glycoprotein and host cell angiotensin-converting enzyme 2 (ACE2). Blocking the interaction between the receptor-binding domain (RBD) of the S1 subunit and ACE2 inhibits viral host cell entry; animal studies indicate that antibodies capable of blocking this interaction reduce viral load and improve clinical symptoms of infection.[A243356, A243361] Tixagevimab (formerly AZD8895) is a recombinant monoclonal antibody produced in Chinese hamster ovary (CHO) cells derived from a neutralizing antibody isolated from a patient with a natural history of SARS-CoV-2 infection and modified through targeted amino acid substitutions to exhibit an extended (~85-day) half-life.[A243351, A243356, L39411] As the RBD binding site of tixagevimab does not overlap with that of [cilgavimab], the two can be administered to synergistically impair SARS-CoV-2 infection in individuals who may be exposed to the virus.[A243351, A243361, L39411] Tixagevimab is not approved for any indication by the FDA. Tixagevimab, in combination with [cilgavimab], was issued an FDA emergency use authorization (EUA) on December 9, 2021, for the pre-exposure prophylaxis of COVID-19 in individuals at increased risk for whom vaccination is not recommended. The combination is co-packaged and available under the name EVUSHELD (formerly AZD7442).[L39411] | Tixagevimab has been issued an emergency use authorization (EUA) by the FDA, in combination with [cilgavimab], for the pre-exposure prophylaxis of COVID-19 in adult and pediatric patients aged 12 years and older weighing at least 40 kg. Furthermore, patients must not be currently infected with SARS-CoV-2 or have had known exposure to an individual infected with SARS-CoV-2 and must either be immunocompromised due to a medical condition, medication, or treatment or be otherwise ineligible for vaccination with any eligible COVID-19 vaccine due to a history of severe adverse reactions.[L39411] The combination of tixagevimab and [cilgavimab] is not authorized for the treatment or post-exposure prophylaxis of COVID-19 and is not a substitute for COVID-19 vaccination. Individuals receiving therapy following COVID-19 vaccination should wait at least two weeks.[L39411] | Tixagevimab is an extended half-life recombinant human IgG1 | SARS-CoV-2, the causative agent of COVID-19, enters cells via the interaction between the trimeric spike (S) glycoprotein and host cell angiotensin-converting enzyme 2 (ACE2). Of the two subunits comprising the trimeric S glycoprotein, the S1 subunit binds ACE2 via its receptor-binding domain (RBD) while the central S2 subunit mediates fusion following S1 shedding.[A243351, A243356] Large-scale screens suggest that the most potently neutralizing antibodies recovered from the B cells of those convalescing following natural infection with SARS-CoV-2 bind to the RBD of S1 and are capable of disrupting the interaction between the RBD and human ACE2.[A243356] Tixagevimab (AZD8895)is a recombinant human IgG1 | Toxicity information regarding tixagevimab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects. Symptomatic and supportive measures are recommended.[L39411] | As a monoclonal antibody, tixagevimab is expected to undergo proteolytic degradation.[L39411] | A single 150 mg intramuscular dose of tixagevimab, given concurrently with 150 mg of [cilgavimab], resulted in a Cmax geometric mean (%CV) of 16.5 (35.6) µg/mL in a median Tmax of 14.0 (range 3.1-30) days. The observed geometric mean (%CV) one, 150, or 210 days following dosing was 4.4 (92.2), 6.6 (25.6), and 4.0 (31.6) µg/mL. This single dose resulted in an AUC0-8 of 2529 (30.2) µg | Tixagevimab has an apparent volume of distribution of 7.7 ± 1.97 L.[L39411] | Tixagevimab has an apparent clearance of 0.062 ± 0.019 L/day.[L39411] | Antibodies, Monoclonal | NA | NA | NA | NA | Spike glycoprotein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16073 | Th1672 | Regdanvimab | >Th1672_Regdanvimab ELVLTQPPSVSAAPGQKVTISCSGSSSNIGNNYVSWYQQLPGTAPKLLIYDNNKRPSGIPDRFSGSKSGTSATLGITGLQTGDEADYYCGTWDSSLSAGVFGGGTELTVLGQPKAAPSVTLFPPSSEELQANKATLVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECS | NA | NA | NA | NA | NA | The mean terminal half-life of regdanvimab following intravenous administration of 40 mg/kg to patients with COVID-19 was 17 days.[L39140] | Regdanvimab (CT-P59) is a recombinant human IgG1 monoclonal antibody directed at the receptor binding domain (RBD) of the SARS-CoV-2 spike protein.[L39140] It blocks the interaction between viral spike proteins and angiotensin-converting enzyme 2 (ACE2) that allows for viral entry into the cell, thereby inhibiting the virus' ability to replicate. Trials investigating the use of regdanvimab as a therapeutic candidate for the treatment of COVID-19 began in mid-2020.[A235830,A241995] It received its first full approval in South Korea in September 2021,[A241995] followed by the EU in November 2021.[L39130] | Regdanvimab is indicated in the EU for the treatment of adult patients with COVID-19 who do not require supplemental oxygen and who are at risk of progressing to severe COVID-19.[L39140] | Regdanvimab exerts its antiviral activity by blocking the viral entry of SARS-CoV-2.[L39140] It should be given within seven days of the onset of COVID-19 symptoms, and is administered as a single intravenous infusion. Hypersensitivity reactions, including infusion-related reactions and anaphylaxis, have been reported during and after the intravenous administration of regdanvimab - patients should be observed during administration and for one hour after its completion to monitor for symptoms of infusion-related reactions such as fever, difficulty breathing, arrhythmia, and chills.[L39140] | Regdanvimab is a recombinant human IgG1 monoclonal antibody that is targeted at the receptor binding domain (RBD) of the SARS-CoV-2 spike protein.[L39140,L39145] The interaction between viral spike proteins and angiotensin-converting enzyme 2 (ACE2) receptors facilitates viral entry into host cells - in blocking this interaction, regdanvimab neutralizes SARS-CoV-2 by preventing cellular entry and subsequent viral replication. The binding interaction between regdanvimab and the spike protein RBD is different as compared to most other neutralizing antibodies, as it appears regdanvimab binds to the RBD protein trimer exclusively in its "up" conformation and in an orientation distinct from most other ACE2-blocking antibodies.[A241990] | Single doses of up to 8000mg of ragdanvimab have been administered to patients in clinical trials without evidence of dose-limiting toxicities.[L39140] In the event of a suspected overdose, employ general supportive measures as clinically indicated. | As regdanvimab is a recombinant IgG1 antibody, it is likely to be degraded into smaller peptides and amino acids in the same way as endogenous IgG1.[L39140] | The mean Cmax and AUC0-infof regdanvimab following intravenous administration of 40 mg/kg to patients with COVID-19 were 1017 µg/mL and 182095 µg·h/ml, respectively.[L39140,L39155] | The steady-state apparent volume of distribution following intravenous administration of regdanvimab 40 mg/kg in patients with COVID-19 was 83 mL/kg.[L39140] | The mean clearance of regdanvimab following intravenous administration of 40 mg/kg to patients with COVID-19 was 0.20 mL/hr/kg.[L39140] | Antibodies, Monoclonal | NA | NA | NA | NA | Spike glycoprotein | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16080 | Th1673 | Birtamimab | NA | NA | NA | NA | NA | NA | NA | Birtamimab is under investigation in clinical trial NCT02312206 (The VITAL Amyloidosis Study, a Global Phase 3, Efficacy and Safety Study of NEOD001 in Patients With AL Amyloidosis). | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16081 | Th1673 | Birtamimab | NA | NA | NA | NA | NA | NA | NA | Birtamimab is under investigation in clinical trial NCT02312206 (The VITAL Amyloidosis Study, a Global Phase 3, Efficacy and Safety Study of NEOD001 in Patients With AL Amyloidosis). | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16089 | Th1674 | Volagidemab | NA | NA | NA | NA | NA | NA | NA | Volagidemab is under investigation in clinical trial NCT03117998 (Multiple Dose Study to Evaluate the Efficacy, Safety and Pharmacodynamics of REMD-477 in Subjects With Type 1 Diabetes Mellitus). | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16112 | Th1680 | Bentracimab | NA | NA | NA | NA | NA | NA | NA | Bentracimab is under investigation in clinical trial NCT04286438 (Bentracimab (PB2452) in Ticagrelor-treated Patients With Uncontrolled Major or Life-threatening Bleeding or Requiring Urgent Surgery or Invasive Procedure). | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16128 | Th1681 | Ravagalimab | NA | NA | NA | NA | NA | NA | NA | Ravagalimab is under investigation in clinical trial NCT03695185 (A Study to Investigate How Well Ravagalimab (ABBV-323) Works and How Safe It Is in Participants With Moderate to Severe Ulcerative Colitis Who Failed Prior Therapy). | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16129 | Th1681 | Ravagalimab | NA | NA | NA | NA | NA | NA | NA | Ravagalimab is under investigation in clinical trial NCT03695185 (A Study to Investigate How Well Ravagalimab (ABBV-323) Works and How Safe It Is in Participants With Moderate to Severe Ulcerative Colitis Who Failed Prior Therapy). | NA | NA | NA | NA | NA | NA | NA | NA | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16147 | Th1683 | Amivantamab | >Th1683_Amivantamab QVQLVQSGAEVAKPGTSVKLSCKASGYTFTDYWMQWVKQRPGQGLEWIGTIYPGDGDTGYAQKFQGKATLTADKSSKTVYMHLSSLASEDSAVYYCARGDYYGSNSLDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The terminal half life of amivantamab-vmjw is 11.3 ± 4.53 days.[L34193] | Amivantamab, also known as JNJ-61186372, is an anti-EGFR-MET bispecific antibody, derived from Chinese hamster ovary cells, approved for the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, as detected by an FDA-approved test, whose disease has progressed on or after platinum-based chemotherapy.[A235103,L34193] Patients with NSCLC often develop resistance to drugs that target EGFR and MET individually, so amivantamab was developed to attack both targets, reducing the chance of resistance developing.[A235103,A235118] Amivantamab was found to be more effective than the EGFR inhibitor [erlotinib] or the MET inhibitor [crizotinib] _in vivo_.[A235103,A235123] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and were generally treated with platinum-based therapy.[A235133] Amivantamab was granted FDA approval on 21 May 2021.[L34193] | Amivantamab is indicated in the treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertion mutations, whose disease has progressed on or after platinum-based chemotherapy.[L34193] | Amivantamab is an EGF and MET receptor targeted antibody indicated in the treatment of non-small cell lung cancer with an EGFR 20 exon insertion mutation.[L34193] It has a long duration of action, as activity can be detected up to 8 weeks after treatment.[A235103] Patients should be counselled regarding the risk of infusion-related reactions, interstitial lung disease and pneumonitis, skin reactions, ocular toxicity, and paronychia.[L34193] Patients should not take amivantamab if they are pregnant or breastfeeding.[L34193] | Mesenchymal-epithelial transition factor (MET) is a receptor with tyrosine kinase activity expressed on epithelial cells that, upon signalling, dimerizes and activates downstream pathways that signal cell division.[A235103,A235128] The Epidermal Growth Factor Receptor (EGFR) is a transmembrane protein with tyrosine kinase activity that can further activate downstream pathways that signal cell division, survival, and angiogenesis.[A235103,A235128] Patients with NSCLC with exon 20 insertion mutations in EGFR do not respond to tyrosine kinase inhibitors, and are generally treated with platinum-based therapy.[A235133] Exon 20 insertion mutations in EGFR also lead to conformational changes that activate EGFR.[A235138] Amivantamab targets both EGFR and MET, preventing ligands from binding to the receptors, blocking signalling, marking the cancerous cells for antibody-dependant cellular cytotoxicity by natural killer cells, and allowing macrophages to perform trogocytosis.[L34193] Amivantamab's binding to the EGFR H epitope shares some of the same amino acids that [cetuximab] binds to.[A235103] Amivantamab's binding to the alpha chain of MET stabilizes the Sema domain loop 1 to 2 in a position 6 Angstroms away from the position it would be in under normal binding, preventing its interaction with the hepatocyte growth factor's (HGF) beta chain.[A235103] Another smaller conformational change in the MET Sema domain loop 1 to 3 also contributes to preventing the interaction of the MET Sema domain with HGF's beta chain.[A235103] HGF is no longer able to bind to MET, preventing downstream signalling.[A235103] Amivantamab's Fc portion contains 90% less fucose than normal antibodies, allowing for increased binding to the Fc | Data regarding overdoses of amivantamab are not readily available.[L34193] Patients experiencing an overdose should be treated with symptomatic and supportive measures. | Antibodies are expected to be metabolized to oligopeptides and amino acids.[A40006] | NA | The mean volume of distribution of amivantamab-vmjw is 5.13 ±1.78 L.[L34193] | The mean clearance of amivantamab-vmjw is 360 ± 144 mL/day.[L34193] | Antibodies | NA | NA | NA | NA | Epidermal growth factor receptor,Hepatocyte growth factor receptor,Low affinity immunoglobulin gamma Fc region receptor III-A | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 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 |
| 16380 | Th1890 | Bebtelovimab | >Th1890_Bebtelovimab QITLKESGPTLVKPTQTLTLTCTFSGFSLSISGVGVGWLRQPPGKALEWLALIYWDDDKRYSPSLKSRLTISKDTSKNQVVLKMTNIDPVDTATYYCAHHSISTIFDHWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144000.0 Da | NA | NA | NA | NA | Following a single intravenous dose of 175mg, the mean elimination half-life of bebtelovimab was 11.5 days | Bebtelovimab (LY-COV1404, LY-3853113) is a human monoclonal antibody approved for emergency use in the treatment of COVID-19. It binds to a portion of the SARS-CoV-2 spike (S) protein's receptor-binding domain, thereby preventing spike protein interaction with ACE2 and subsequent viral entry into host cells. Bebtelovimab is notable in that the epitope to which it binds appears infrequently mutated, making it a viable candidate for use in resistant SARS-CoV-2 strains (i.e. variants of concern, VOCs), including the B.1.617.2 (Delta) and B.1.1.529 (Omicron) variants.1 This is in contrast to previously developed COVID-19 monoclonal antibody treatments - including bamlanivimab, etesevimab, casirivimab, and imdevimab - which have been found ineffective in the treatment of COVID-19 caused by the Omicron variant. | The FDA has issued an emergency use authorization (EUA) for the use of bebtelovimab for the treatment of mild-to-moderate COVID-19 in adult and pediatric patients (≥12 years old and ≥40 kg) who are positive for SARS-CoV-2 infection, are at a high risk of progression to severe COVID-19, and for whom alternative treatment options are not accessible or clinically appropriate. | Bebtelovimab binds the SARS-CoV-2 spike protein with a dissocation constant KD = 0.046 - 0.075 nM and blocks spike protein attachment to the human ACE2 receptor with an IC50 value of 0.39 nM. | Bebtelovimab is a neutralizing human IgG1κ monoclonal antibody targeted against the spike (S) protein of SARS-CoV-2,2 which is responsible for facilitating viral entry into host cells. More specifically, bebtelovimab binds to an epitope of the S protein receptor-binding domain (RBD) which overlaps the ACE2-interacting site, effectively inhibiting the interaction between ACE2 and the S protein required for viral entry. | Single doses of up to 1750mg of bebtelovimab (10 times the authorized dose) have been administered in clinical trials without evidence of dose-limited toxicity. Treatment of bebtelovimab overdose should consist of general supportive measures. | As with other therapeutic proteins, bebtelovimab is likely degraded via catabolic processes into smaller peptides and amino acids. | Following a single intravenous dose of 175mg, the mean Cmax and AUCinf of bebtelovimab were 59.8 mcg/mL and 522 mcg.day/mL, respectively. | At steady-state, the volume of distribution of bebtelovimab is 4.61 L. | Following a single intravenous dose of 175mg, the mean clearance of bebtelovimab was 0.335 L/day. | Amino Acids, Peptides, and Proteins,Antibodies,Approved Treatments for COVID-19,Blood Proteins,Globulins,Immunoglobulins,Immunoproteins,Proteins,Serum Globulins | NA | NA | NA | NA | Spike glycoprotein | Bebtelovimab | Eli Lilly and Company | Eli Lilly and Company | Injection, solution | 87.5 mg/1mL | NA | fever difficulty breathing low oxygen level in your blood chills tiredness fast or slow heart rate chest discomfort or pain weakness confusion nausea headache shortness of breath low or high blood pressure wheezing swelling of your lips, face, or throat rash including hives itching muscle aches dizziness feeling faint, and sweating. | Bebtelovimab has not undergone the same type of review as an FDA-approved product. In issuing an EUA under the COVID-19 public health emergency, the FDA has determined, among other things, that based on the total amount of scientific evidence available, including data from adequate and well-controlled clinical trials, it is reasonable to believe that the product may be effective for diagnosing, treating, or preventing COVID-19, or a serious or life-threatening disease or condition caused by COVID-19; that the known and potential benefits of the product, when used to diagnose, treat, or prevent such disease or condition, outweigh the known and potential risks of such product; and that there are no adequate, approved and available alternatives. | Bebtelovimab is an investigational medicine used under Emergency Use Authorization (EUA) for the treatment of mild-to-moderate coronavirus disease 2019 (COVID-19) in adults and children (12 years of age and older weighing at least 88 pounds [40 kg]) | NA | NA | Link | Link | NA |
| 16383 | Th1893 | Sutimlimab | >Th1893_Sutimlimab EVQLVESGGGLVKPGGSLRLSCAASGFTFSNYAMSWVRQAPGKGLEWVATISSGGSHTYYLDSVKGRFTISRDNSKNTLYLQMNSLRAEDTALYYCARLFTGYAMDYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 147000.0 Da | C6436H9934O2012N1700S46 | NA | NA | NA | ,At the approved recommended dosage, the terminal elimination half-life of sutimlimab is 21 days. | Cold agglutinin disease (CAD) is a type of autoimmune hemolytic anemia (AIHA) in which autoantibodies directed against red blood cell surface antigens cause hemolysis at low (3-4°C) temperatures.2,5 This cold subtype accounts for approximately 15-25% of all AIHA and is more common in the elderly.3,5 In approximately 90% of cases, patients develop immunoglobulin M (IgM) autoantibodies towards the I antigen on erythrocytes - these antibodies react optimally at 4°C and are therefore referred to as "cold agglutinin".1 Hemolysis in patients with CAD is driven by complement activation, which initiates a cascade that ultimately leads to both intra- and extravascular hemolysis.3 The most common presenting symptoms in patients with CAD are chronic anemia, acrocyanosis, and Raynaud phenomenon. | Sutimlimab is indicated to decrease the need for red blood cell transfusion due to hemolysis in adult patients with cold agglutinin disease. | Following a single sutimlimab injection, >90% inhibition of the complement pathway was observed, and this inhibition was sustained when concentrations of sutimlimab were ≥100 mcg/mL. As sutimlimab can impair the complement-mediated immune response, patients requiring therapy should receive all appropriate vaccinations against encapsulated bacteria at least 2 weeks prior to its initiation.4 Patients undergoing treatment with sutimlimab are at a higher risk of serious infections, especially those caused by encapsulated bacteria such as Neisseria meningitides or Streptococcus pneumoniae, and should be monitored closely throughout therapy for evidence of developing or ongoing infections. | Hemolysis associated with cold agglutinin disease is driven by the activation of the complement system. Cold agglutinins transiently bind erythrocytes as they circulate through cooler parts of the body (e.g. the extremities) - as they circulate back to warmer areas, C1q esterase activates C4 and C2, which generates C3 convertase, an enzyme which cleaves C3 into C3a and C3b.3 At this stage, the erythrocytes tagged with C3b can be sequestered by macrophages in the reticuloendothelial system, ultimately leading to extravascular hemolysis.Alternatively, C3b may be further cleaved into C3c and C3d - if complement activation continues past the C3 step, the membrane attack complex with C5b-C9 may form, which causes intravascular hemolysis. | Not Available | As with other therapeutic proteins, sutimlimab likely undergoes catabolism to smaller peptides and amino acids. | When administered at the approved weight-based recommended dosage, the exposure to sutimlimab increases proportionately with increasing dosage.4 Steady-state concentrations are achieved by week 7 of therapy. | At steady-state, the volume of distribution of sutimlimab in patients with cold agglutinin disease was approximately 5.8 L. | At the approved recommended dosage, the clearance of sutimlimab is 0.14 L/day.4 The clearance of sutimlimab varies at different doses due to target-mediated drug disposition at lower concentrations | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Blood Proteins,Classical Complement Pathway Inhibitor,Globulins,Immunoglobulins,Immunoproteins,Proteins,Serum Globulins | NA | NA | NA | NA | Complement C1s subcomponent | Enjaymo | Bioverativ U.S. LLC. | Bioverativ U.S. LLC. | Intravenous | 50 mg/1mL | ENJAYMO is contraindicated in patients with known hypersensitivity to sutimlimab-jome or any of the inactive ingredients | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, muscle aches, flu-like symptoms, severe swelling, pain and redness around the injection site or a wound, joint pain or swelling, fever, shortness of breath, rapid heartbeat, and rash | Sutimlimab-jome, a classical complement inhibitor, is a humanized monoclonal antibody expressed by recombinant in Chinese hamster ovary (CHO) cells and produced in vitro using standard mammalian cell culture methods. Sutimlimab-jome is composed of two heterodimers. Each heterodimer is composed of a heavy and a light polypeptide chain. Each heavy chain (H-chain) is composed of 445 amino acids and each light chain (L-chain) contains 216 amino acids. Sutimlimab-jome has a molecular weight of approximately 147 kDa. | Enjaymo is a prescription medicine used to treat the symptoms of Cold Agglutinin Disease. | NA | ENJAYMO (sutimlimab-jome) injection is a sterile, clear to slightly opalescent, colorless to slightly yellow, preservative-free solution for intravenous use. Each single-dose vial contains 1,100 mg sutimlimab-jome at a concentration of 50 mg/mL with a pH of 6.1. Each mL contains 50 mg of sutimlimab-jome and also contains polysorbate 80 (0.2 mg), sodium chloride (8.18 mg), sodium phosphate dibasic heptahydrate (0.48 mg), sodium phosphate monobasic monohydrate (1.13 mg), and Water for Injection, USP. | Link | Link | NA |