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Multikinase inhibitor including VEGF and PDGF receptor tyrosine kinases some of which are implicated in tumor growth angiogenesis and metastasis. 13 NONCLINICAL TOXICOLOGY Sections or subsections omitted from the full prescribing information are not.
Because sunitinib inhibits angiogenesis a critical component of fetal development adverse effects on pregnancy would be expected.
Sunitinib mechanism of action. Sunitinib is an indolinone derivative and tyrosine kinase inhibitor with potential antineoplastic activity. Sunitinib blocks the tyrosine kinase activities of vascular endothelial growth factor receptor 2 VEGFR2 platelet-derived growth factor receptor b PDGFRb and c-kit thereby inhibiting angiogenesis and cell proliferation. This agent also inhibits the phosphorylation of Fms-related.
121 Mechanism of Action Sunitinib is a small molecule that inhibits multiple receptor tyrosine kinases RTKs some of which are implicated in tumor growth pathologic angiogenesis and metastatic progression of cancer. Sunitinib inhibits the phosphorylation of multiple receptor tyrosine kinases RTKs. It is a potent inhibitor of platelet - derived growth factor receptors PDGFRα and PDGFRβ vascular endothelial growth factor receptors VEGFR1.
The mechanisms by which sunitinib affects thyroid function remain unclear but may include antiangiogenic effects 29 30 iodine uptake inhibition 31 destructive thyroiditis 32 inhibition of thyroid peroxidase activity 33 and reduction of vascularity 34 by. Sunitinib is an oral small-molecule multi-targeted receptor tyrosine kinase RTK inhibitor that was approved by the FDA on January 26 2006. Sunitinib is a small molecule that inhibits multiple RTKs some of which are implicated in tumor growth pathologic angiogenesis and metastatic progression of cancer.
Multikinase inhibitor including VEGF and PDGF receptor tyrosine kinases some of which are implicated in tumor growth angiogenesis and metastasis. Steady-state concentrations of sunitinib and its primary active metabolite are achieved within 10-14. Sunitinib is an orally administered multitargeted tyrosine kinase inhibitor approved multinationally for the first- and second-line treatment of metastatic renal cell carcinoma mRCC.
The recommended dose of sunitinib is 50 mg per day for 4 weeks followed by 2. In contrast sunitinib malates mechanism of action inhibits multiple intracellular tyrosine kinases RTKs ultimately producing an inhibitory effect on VEGFR-1 -2 and -3 Figure 2. Mechanism of Action 123.
13 NONCLINICAL TOXICOLOGY. 131 Carcinogenesis Mutagenesis Impairment of Fertility. 14 CLINICAL STUDIES.
Gastrointestinal Stromal Tumor 142. Renal Cell Carcinoma 143. Pancreatic Neuroendocrine Tumors.
16 HOW SUPPLIEDSTORAGE AND HANDLING. Mechanism of action Sunitinib inhibits multiple RTKs in biochemical and cell-based assays and exerts potent antiangiogenesis and antitumor effects in animal experiments. In vivo sunitinib downregulates myeloid-derived suppressor cells MDSC which are thought to contribute to the antitumor effects also.
Sunitinib is an oral multi-targeted and small-molecule inhibitor of receptor tyrosine kinase RTK 1. Sunitinib is a RTK inhibitor against vascular endothelial growth factor receptors VEGFR1-3 platelet-derived growth factor receptors PDGFRα and PDGFRβ stem cell factor receptor c-kit glial cell-line derived neurotrophic factor receptorRET. Mechanism Of Action.
Sunitinib is a small molecule that inhibits multiple receptor tyrosine kinases RTKs some of which are implicated in tumor growth pathologic angiogenesis and metastatic progression of cancer. Sunitinib was evaluated for its inhibitory activity against a variety of kinases 80 kinases and was identified as an inhibitor. Our studies indicate that sunitinib inhibits ccRCC growth primarily through an anti-angiogenic mechanism and not through direct targeting of ccRCC tumor cells.
Higher microvessel density was found in sunitinib-resistant tumors which indicated that an escape from anti-angiogenesis occurred in these tumors. Based on data from animal reproduction studies and its mechanism of action in utero exposure to sunitinib may cause fetal harm. Because sunitinib inhibits angiogenesis a critical component of fetal development adverse effects on pregnancy would be expected.
What is this drug used for. It is used to treat cancer. Sunitinib Malate is the orally bioavailable malate salt of an indolinone-based tyrosine kinase inhibitor with potential antineoplastic activity.
Sunitinib blocks the tyrosine kinase activities of vascular endothelial growth factor receptor 2 VEGFR2 platelet-derived growth factor receptor b PDGFRb and c-kit thereby inhibiting angiogenesis and cell proliferation. L cancer models sunitinib exerts significant antiangiogenesis and antitumor effects. In phase I studies using intermittent dosing schedules oral administration of doses up to 50 mgday were reasonably well tolerated and resulted in plasma concentrations in the range of targeted levels needed for sustained kinase inhibition.
Biomarker and functional imaging studies showed modulation of. 121 Mechanism of Action 173 Other Common Events. 123 Pharmacokinetics 174 Concomitant Medications.
124 Cardiac Electrophysiology 175 FDA-Approved Patient Labeling. 13 NONCLINICAL TOXICOLOGY Sections or subsections omitted from the full prescribing information are not. 131 Carcinogenesis Mutagenesis Impairment of Fertility listed.