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High Purity Pharmaceutical Raw Material Cediranib / Azd2171 (288383-20-0)

Basic Info

Model No.:  288383-20-0

Product Description

Model NO.: 288383-20-0 Synonyms: Azd2171;Recentin;Cediranib R Appearance: White Crystalline Solid Trademark: shuangbojie Origin: China Name: Cediranib CAS: 288383-20-0 Assay: 99% Specification: ISO9001 HS Code: 29144000 Cediranib Synonyms:AZD2171;4-(4-Fluoro-2-methylindol-5-yloxy)-6-methoxy-7-[3-(pyrrolidin-1-yl)propoxy]quinazoline;Recentin;Cediranib R CAS:288383-20-0 MF:C25H27FN4O3 MW:450.51 Appearance: White crystalline solid Assay:99% Solubility:DMSO (10 mM) Storage Temp.: -20°C Shipping Conditions: RT Handling: Protect from air and moisture Description:Cediranib (AZD2171) s a potent inhibitor of vascular endothelial growth factor (VEGF) receptor tyrosine kinases. Usage:Cediranib (AZD2171) inhibited VEGF-stimulated proliferation and KDR phosphorylation with IC50 of 0.4 and 0.5 nM, respectively. Packing:1g/foil bag   Abstract Using MRI techniques, we show here that normalization of tumor vessels in recurrent glioblastoma patients by daily administration of AZD2171-an oral tyrosine kinase inhibitor of VEGF receptors-has rapid onset, is prolonged but reversible, and has the significant clinical benefit of alleviating edema. Reversal of normalization began by 28 days, though some features persisted for as long as four months. Basic FGF, SDF1alpha, and viable circulating endothelial cells (CECs) increased when tumors escaped treatment, and circulating progenitor cells (CPCs) increased when tumors progressed after drug interruption. Our study provides insight into different mechanisms of action of this class of drugs in recurrent glioblastoma patients and suggests that the timing of combination therapy may be critical for optimizing activity against this tumor.

Application: Cediranib inhibition of bFGF and EGF when an IC50 of 0.5 and 0.11 μM. In the MG63 cell lines, Cediranib inhibiting PDGF-AA, IC50 of 0.04 μM. Cediranib Flt-1 associated kinase inhibition, IC50 of 5 nM, Cediranib inhibition of VEGF-C and VEGF-D receptor Flt-4, IC50 of less than 3 nM. [1] In addition, cediranib inhibition of c-Kit and PDGFR-β tyrosine kinase, IC50 were 2 and 5 nM. In vitro, micromolar concentrations cediranib can directly inhibit the proliferation of tumor cells. Sub nanomolar Cediranib blocking tubules produced, and inhibits VEGF-induced angiogenesis in vivo.  
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