CCediranib, Free Base **
產品名稱：CCediranib, Free Base
產品貨號：LC C-4300
產品規格：10 MG
Cediranib is a highly potent inhibitor of recombinant KDR tyrosine kinase activity in vitro (IC50 < 1 nM). Inhibitory activity was also observed against the kinase associated with Flt-1 (IC50 = 5 nM), the VEGF-C and VEGF-D receptor Flt-4 (IC50 ≤ 3 nM), recombinant PDGFR-related kinase c-Kit (IC50 = 2 nM), and PDGFRβ tyrosine kinase (IC50 = 5 nM). In HUVEC, it inhibited VEGF-stimulated phosphorylation of KDR, c-Kit, PDGFR-α, PDGFR-β in a dose-dependent manner with IC50 values of 0.5, 1, 5, and 8 nM, respectively. It inhibited VEGF-stimulated HUVEC proliferation potently with an IC50 value of 0.4 nM. Consistent with potent activity against VEGF signaling, cediranib inhibited vessel branching, length, and area in vitro with IC50 values of 0.1, 0.1, and 0.2 nM, respectively. It also completely abolished VEGF-induced angiogenesis in vivo. However, it inhibited tumor cell proliferation in vitro only at comparatively high concentrations, showing IC50 values of 3.0 µM for SKOV-3 cells, 3.8 µM for MDA-MB-231 cells, 5.8 µM for PC-3 cells, 6.4 µM for Calu-6 cells, and 7.4 µM for SW620 cells. It also inhibited the growth of these five tumor models in nude mice. Furthermore, cediranib induced vascular regression in human lung tumor xenografts. Wedge, S.R., et al. "AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer." Cancer Res. 65: 4389-4400 (2005).
Cediranib significantly increased survival of mice wth glioblastoma by decreasing tumor vessel permeability, normalizing perivascular cell coverage, and thinning of the basement membrane, thus controlling edema. Kamoun, W.S., et al. "Edema control by cediranib, a vascular endothelial growth factor receptor-targeted kinase inhibitor, prolongs survival despite persistent brain tumor growth in mice." J. Clin. Oncol. 27: 2542-2552 (2009).
Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO. Disposal: A
