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HY-10228

CAS:453562-69-1

 (Synonyms  AMG 706; AMG-706)
453562-69-1  Technical Data: Price and Availability of  Cas No:453562-69-1

Cas : 453562-69-1 M.Wt: 373.4509
Cas : 453562-69-1 Formula: C22H23N5O
Cas : 453562-69-1 Purity: >98 %
Cas : 453562-69-1 Storage: at 20℃ 2 years
Cas : 453562-69-1 Solubility: DMSO: ≥ 30 mg/mL
Cas : 453562-69-1 Name: Motesanib
USD
10mg/$50 In-stock
50mg/$160 In-stock
100mg/$280 In-stock
200mg/$360 In-stock
500mg/$810 In-stock
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453562-69-1  Data Sheet:
 
Introduction of 453562-69-1 :
Motesanib is a potent ATP-competitive inhibitor of VEGFR1/2/3 with IC50s of 2 nM/3 nM/6 nM, respectively, and has similar activity against Kit, and is appr 10-fold more selective for VEGFR than PDGFR and Ret. IC50 & Target: IC50: 2 nM (VEGFR1), 3 nM (VEGFR2), 6 nM (VEGFR3) In Vitro: Motesanib has broad activity against the human VEGFR family, and displays > 1000 selectivity against EGFR, Src, and p38 kinase. Motesanib significantly inhibits VEGF-induced cellular proliferation of HUVECs with an IC50 of 10 nM, while displaying little effect at bFGF-induced proliferation with an IC50 of >3,000 nM. Motesanib also potently inhibits PDGF-induced proliferation and SCF-induced c-kit phosphorylation with IC50 of 207 nM and 37 nM, respectively, but not effective against the EGF-induced EGFR phosphorylation and cell viability of A431 cells[1]. Althouth displaying little antiproliferative activity on cell growth of HUVECs alone, Motesanib treatment significantly sensitizes the cells to fractionated radiation[2]. In Vivo: Motesanib (100 mg/kg) significantly inhibits VEGF-induced vascular permeability in a time-dependent manner. Oral administration of Motesanib twice daily or once daily potently inhibits, in a dose-dependent manner, VEGF-induced angiogenesis using the rat corneal model with ED50 of 2.1 mg/kg and 4.9 mg/kg, respectively. Motesanib induces a dose-dependent tumor regression of established A431 xenografts by selectively targeting neovascularization in tumor cells[1]. Motesanib in combination with radiation displays significant anti-tumor activity in head and neck squamous cell carcinoma (HNSCC) xenograft models[2]. Motesanib treatment also induces significant dose-dependent reductions in tumor growth and blood vessel density of MCF-7, MDA-MB-231, or Cal-51 xenografts, which can be markedly enhanced when combined with docetaxel or tamoxifen[3].
 
References on 453562-69-1 :
 

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