sunitinib brands

Molecular formula: C22H27FN4O2

Sunitinib is a small molecule that inhibits multiple 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 of platelet-derived growth factor receptors (PDGFRa and PDGFRb), vascular endothelial growth factor receptors (VEGFR1, VEGFR2 and VEGFR3), stem cell factor receptor (KIT), Fms-like tyrosine kinase-3 (FLT3), colony stimulating factor receptor Type 1 (CSF-1R), and the glial cell-line derived neurotrophic factor receptor (RET). Sunitinib inhibition of the activity of these RTKs has been demonstrated in biochemical and cellular assays, and inhibition of function has been demonstrated in cell proliferation assays. The primary metabolite exhibits similar potency compared to sunitinib in biochemical and cellular assays. Sunitinib malate, an inhibitor of multiple receptor tyrosine kinases, is an antineoplastic agent. Receptor tyrosine kinases (RTKs) are involved in the initiation of various cascades of intracellular signaling events that lead to cell proliferation and/or influence processes critical to cell survival and tumor progression (eg, angiogenesis, metastasis, inhibition of apoptosis), based on the respective kinase. Although the exact mechanism of antineoplastic activity of sunitinib has not been fully elucidated, data from biochemical and cellular assays indicate that sunitinib may inhibit signal transduction pathways involving multiple receptor (ie, cell surface) tyrosine kinases, including platelet-derived growth factor receptors (ie, PDGFR-alpha, PDGFR-beta), vascular endothelial growth factor receptors (ie, VEGFR-1, VEGFR-2, VEGFR-3), stem cell factor receptor (ie, c-Kit), fms-like tyrosine kinase 3 (Flt-3), colony stimulating factor receptor type 1 (CSF-1R), and the glial cell line-derived neurotrophic factor receptor (RET). Sunitinib-induced inhibition of signal transduction pathways involving PDGFR-beta, VEGFR-2, and c-Kit has been confirmed in tumor xenografts expressing receptor tyrosine kinase targets in vivo. Sunitinib has been shown to inhibit growth of tumor cells expressing dysregulated target receptor tyrosine kinases (ie, PDGFR, RET, c-Kit) in vitro; the drug also has been shown to inhibit PDGFR-beta- and VEGFR-2-dependent tumor angiogenesis in vivo. Sunitinib inhibited the phosphorylation of multiple RTKs (PDGFR-beta, VEGFR2, KIT) in tumor xenografts expressing RTK targets in vivo and demonstrated inhibition of tumor growth or tumor regression and/or inhibited metastases in some experimental models of cancer. Sunitinib demonstrated the ability to inhibit growth of tumor cells expressing dysregulated target RTKs (PDGFR, RET, or KIT) in vitro and to inhibit PDGFR-beta- and VEGFR2-dependent tumor angiogenesis in vivo. ... Sunitinib malate is an oral, multitargeted kinase inhibitor with antiangiogenic and antitumor activity due to inhibition of vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor alpha (PDGFR-alpha), and the tyrosine kinases c-KIT and FLT3. Sunitinib has antitumor activity in various cancers, including imatinib-resistant gastrointestinal stromal tumors, metastatic breast cancer, neuroendocrine tumors, and renal-cell carcinoma. ... Sunitinib, which is a multitargeted tyrosine-kinase inhibitor, exhibits antiangiogenic and antitumor activity, and extends survival of patients with metastatic renal-cell carcinoma (mRCC) and gastrointestinal stromal tumors (GIST). This molecule has also been reported to be associated with cardiotoxicity at a high frequency, but the mechanism is still unknown. In the present study, /investigators/ observed that Sunitinib showed high anti-proliferative effect on H9c2 cardiac muscle cells measured by PI staining and the MTT assay. But apoptotic markers (PARP cleavage, caspase 3 cleavage and chromatin condensation) were uniformly negative i

Source: PubChem (NCBI) · compound 5329102