Cediranib Cediranib;4-(4-Fluoro-2-methylindol-5-yloxy)-6-methoxy-7-[3-(pyrrolidin-1-yl)propoxy]quinazoline;Cadiranib (AZD2171);Cediranib(AZD2171);AZD2171;Recentin;Cadiranib;Cediranib R 288383-20-0
Cediranib (AZD2171) is a highly potent VEGFR(KDR) inhibitor with IC50 of <1 nM, also inhibits Flt1/4 with IC50 of 5 nM/≤3 nM, similar activity against c-Kit and PDGFRβ, 36-, 110-fold and >1000-fold selective more for VEGFR than PDGFR-α, CSF-1R and Flt3.
IC50 value: 0.5 nM (VEGFR2); 5 nM/≤3 nM(Flt1/4) [1]
Target: VEGFR2; Flt1/4
in vitro: Cediranib inhibits VEGF-stimulated proliferation with IC50 of 0.4 nM. Cediranib suppresses PDGF-AA with IC50 of 0.04 μM in MG63 cell lines. Cediranib has been shown to block Flt1-associated kinase with IC50 of 5 nM and VEGF-C and VEGF-D receptor Flt-4 with IC50 less than 3 nM. In addition, the IC50 values for inhibition of c-Kit and PDGFRβ tyrosine kinase are 2 nM and 5 nM respectively. Furthermore, no inhibition of enzyme activity is observed when 10 μM Cediranib is assayed with 100 μM ATP against AMPK, Chk1 Akt/PKB and others. Micromolar concentrations of Cediranib are needed to prevent tumor cell proliferation in vitro [1].
in vivo: Cediranib even suppresses tubule sprouting at subnanomolar concentrations and inhibits VEGF-induced angiogenesis. Cediranib causes hypertrophy in bone growth plate and prevents luteal development in ovary. These are physiological processes that are dependent upon angiogenesis. Cediranib shows broad spectrum activity in human tumor models at doses that are well tolerated [1]. Besides, Cediranib causes regression of vascular tissues in human lung tumor xenografts [2].
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