Sunitinib（CAS# 557795-19-4)

Chemical Property:

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.