Sunitinib
Sunitinib
CAS: 557795-19-4
Molecular Formula: C22H27FN4O2
Sunitinib - Names and Identifiers
Sunitinib - Physico-chemical Properties
| Molecular Formula | C22H27FN4O2 |
| Molar Mass | 398.47 |
| Density | 1.2 |
| Melting Point | 189-191°C |
| Boling Point | 572.1±50.0 °C(Predicted) |
| Flash Point | 299.8℃ |
| Solubility | 25°C: DMSO |
| Vapor Presure | 3.13E-23mmHg at 25°C |
| Appearance | Crystalline powder |
| Color | Yellow to Dark Orange |
| pKa | 8.5(at 25℃) |
| Storage Condition | 2-8°C |
| MDL | MFCD08273555 |
| In vitro study | Sunitinib is effective in inhibiting Kit and FLT-3. Sunitinib is an effective ATP competitive inhibitor of VEGFR2 (Flk1) and PDGFRβ, K I is 9 nM and 8 nM respectively, acting on VEGFR2 and PDGFR is more effective than FGFR-1,EGFR,Cdk2,Met,IGFR-1,Abl, and src selectivities were more than 10 times higher. In serum-starved NIH-3T3 cells expressing VEGFR2 or PDGFRβ, Sunitinib inhibited VEGF-dependent VEGFR2 phosphorylation and PDGF-dependent PDGFRβ phosphorylation with an IC50 of 10 nM and 10 nM, respectively. For NIH-3T3 cells overexpressing PDGFRβ or PDGFRα, Sunitinib inhibited the proliferation induced by VEGF with an IC50 of 39 nM and 69 nM, respectively. Sunitinib inhibited wild-type FLT3,FLT3-ITD, and FLT3-Asp835 phosphorylation with IC50 of 250 nM,50 nM, and 30 nM, respectively. Sunitinib inhibited the proliferation of MV4;11 and OC1-AML5 cells with IC50 of 8 nM and 14 nM, respectively, and induced apoptosis in a dose-dependent manner. |
| In vivo study | Consistent with substantial, selective inhibition of phosphorylation and signaling of VEGFR2 or PDGFR in vivo, Sunitinib (20-80 mg/kg/day) has been shown to be responsible for various tumor xenograft models, including HT-29,A431,Colo205, h-460, SF763T,C6,A375, or MDA-MB-435 exhibited broadly potent dose-dependent antitumor activity. Sunitinib at a dose of 80 mg/kg/day for 21 days resulted in complete tumor regression in 6 of 8 mice, and at the end of treatment, tumors did not regenerate during the 110-day observation period. The second round of treatment with Sunitinib was still effective against tumors, but did not fully recover from the first round of treatment. Sunitinib treatment resulted in a significant decrease in tumor MVD, which was reduced by ~ 40% in SF763T gliomas. SU11248 treatment resulted in complete inhibition of additional tumor growth of luciferase-expressing PC-3M xenografts, although there was no reduction in tumor size. In a FLT3-ITD bone marrow transplantation model, Sunitinib treatment (20 mg/kg/day) significantly inhibited the growth of subcutaneous MV4;11 (FLT3-ITD) xenografts and prolonged survival. |
Sunitinib - Risk and Safety
| Safety Description | 24/25 - Avoid contact with skin and eyes. |
| HS Code | 29337900 |
Sunitinib - Reference
| Reference Show more | 1. Chen Aiying, Cheng Min, Miao Yunping, Ye younger brother, Tian Xuejun, Zheng Gaoli. Pharmacokinetics and distribution of sunitinib in brain and kidney [J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2020,25(10):1105-1110. |
Sunitinib - Introduction
Sunitinib is a multi-targeted RTK inhibitor targeting VEGFR2 (Flk-1) and PDGFRβ with IC50 of 80 nM and 2 nM, and also inhibits c-Kit.
Last Update：2022-10-16 17:26:22
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