product name Apatinib
Description: Apatinib is an orally bioavailable, selective VEGFR2 inhibitor with IC50 of 1 nM. Apatinib is a small-molecule receptor tyrosine kinase inhibitor with potential antiangiogenic and antineoplastic activities. Apatinib selectively binds to and inhibits vascular endothelial growth factor receptor 2, which may inhibit VEGF-stimulated endothelial cell migration and proliferation and decrease tumor microvessel density.
References: Cancer Sci. 2011;102(7):1374-80; Cancer Res. 2010;70(20):7981-91; Biochem Pharmacol. 2012;83(5):586-97.
493.58
Formula
C25H27N5O4S
CAS No.
811803-05-1
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 22 mg/mL (44.57 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
0.5% CMC: 6mg/mL
Synonyms
YN968D1
other peoduct :
| In Vitro |
In vitro activity: Apatinib (YN968D1) is a novel, orally bioavailable, selective inhibitor with potential antiangiogenic and antineoplastic activities. Apatinib selectively binds to and inhibits VEGFR2. Apatinib can also potently suppress the activities of Ret, c-kit and c-src with IC50 of 0.013 μM, 0.429 μM and 0.53 μM, respectively. Apatinib inhibits cellular phosphorylation of VEGFR-2, c-kit and PDGFRβ. Apatinib significantly inhibits proliferation stimulated by 20 ng/mL VEGF (IC50 = 0.17μM). Apatinib effectively inhibits proliferation, migration and tube formation of human umbilical vein endothelial cells induced by FBS, and blocked the budding of rat aortic ring. Apatinib reverses ABCB1- and ABCG2-mediated MDR by inhibiting their transport function, but not by blocking the AKT or ERK1/2 pathway or downregulating ABCB1 or ABCG2 expression. Apatinib significantly potentiates the cytotoxicity of established ABCB1 and ABCG2 substrates and increased the accumulation of DOX and Rho 123 in ABCB1- or ABCG2-overexpressing cells. Furthermore, apatinib significantly inhibited the photoaffinity labeling of both ABCB1 and ABCG2 with [125I]iodoarylazidoprazosin in a concentration-dependent manner. Kinase Assay: Cell Assay: In HUVEC, Apatinib decreases VEGF-stimulated phosphorylation of VEGFR-2 KDR in a concentration-dependent manner. It also completely inhibits VEGFR-2 activation at a concentration of 0.1 μM. Furthermore, Apatinib abrogates the phosphorylation of c-kit and PDGFRb in Mo7e and NIH-3T3 cells stimulated with the relevant ligand, respectively, in a concentration-dependent manner. In addition, Apatinib inhibits proliferation, migration and tube formation of HUVEC in vitro and blocking of rat aortic ring budding. |
|---|---|
| In Vivo | Apatinib inhibits the growth of a broad range of human tumor xenografts in a significant dose-dependent manner. Apatinib reverses ABCB1-mediated MDR in the nude mouse xenograft model. Apatinib significantly enhances the antitumor activity of doxorubicin in nude mice bearing K562/ADR xenografts. |
| Animal model | Nude mice human tumor xenografts |
| Formulation & Dosage | Formulated in 0.5% (w/v) carboxymethyl cellulose; 50, 100, 200 mg/kg; oral gavage |
| References | Cancer Sci. 2011 Jul;102(7):1374-80; Cancer Res. 2010 Oct 15;70(20):7981-91; Biochem Pharmacol. 2012 Mar 1;83(5):586-97. |
