Repositioning Candidate Details
| Candidate ID: | R0371 |
| Source ID: | DB01268 |
| Source Type: | approved; investigational |
| Compound Type: | small molecule |
| Compound Name: | Sunitinib |
| Synonyms: | |
| Molecular Formula: | C22H27FN4O2 |
| SMILES: | CCN(CC)CCNC(=O)C1=C(C)NC(\C=C2/C(=O)NC3=C2C=C(F)C=C3)=C1C |
| Structure: |
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| DrugBank Description: | Sunitinib is a small-molecule multi-targeted receptor tyrosine kinase (RTK) inhibitor. On January 26, 2006, the agent was formally approved by the US FDA for the indications of treating renal cell carcinoma (RCC) and imatinib-resistant gastrointestinal stromal tumor (GIST). For these purposes, sunitinib is generally available as an orally administered formulation. Sunitinib inhibits cellular signaling by targeting multiple RTKs. These include all platelet-derived growth factor receptors (PDGF-R) and vascular endothelial growth factor receptors (VEGF-R). Sunitinib also inhibits KIT (CD117), the RTK that drives the majority of GISTs. In addition, sunitinib inhibits other RTKs including RET, CSF-1R, and flt3. |
| CAS Number: | 557795-19-4 |
| Molecular Weight: | 398.4738 |
| DrugBank Indication: | For the treatment of advanced renal cell carcinoma as well as the treatment of gastrointestinal stromal tumor after disease progression on or intolerance to imatinib mesylate. |
| DrugBank Pharmacology: | Sunitinib is an oral, small-molecule, multi-targeted receptor tyrosine kinase (RTK) inhibitor that was approved by the FDA on January 26, 2006. |
| DrugBank MoA: | 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. |
| Targets: | Platelet-derived growth factor receptor beta; Vascular endothelial growth factor receptor 1; Mast/stem cell growth factor receptor Kit; Vascular endothelial growth factor receptor 2; Vascular endothelial growth factor receptor 3; Receptor-type tyrosine-protein kinase FLT3; Macrophage colony-stimulating factor 1 receptor; Platelet-derived growth factor receptor alpha; Hepatocyte growth factor receptor |
| Inclusion Criteria: |
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