SML2850
Cediranib
≥98% (HPLC)
别名:
4-(4-Fluoro-2-methylindol-5-yloxy)-6-methoxy-7-[3-(pyrrolidin-1-yl)propoxy]quinazoline, 4-[(4-Fluoro-2-methyl-1H-indol-5-yl)oxy]-6-methoxy-7-[3-(1-pyrrolidinyl)propoxy]quinazoline, 4-[(4-Fluoro-2-methyl-1H-indol-5-yl)oxy]-6-methoxy-7-[3-(pyrrolidin-1-yl)propoxy]quinazoline, AZD 2171, AZD2171
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About This Item
推荐产品
质量水平
方案
≥98% (HPLC)
表单
powder
颜色
white to beige
溶解性
DMSO: 2 mg/mL, clear
储存温度
2-8°C
SMILES字符串
Fc1c2c([nH]c(c2)C)ccc1Oc3ncnc4c3cc(c(c4)OCCCN5CCCC5)OC
InChI
1S/C25H27FN4O3/c1-16-12-17-19(29-16)6-7-21(24(17)26)33-25-18-13-22(31-2)23(14-20(18)27-15-28-25)32-11-5-10-30-8-3-4-9-30/h6-7,12-15,29H,3-5,8-11H2,1-2H3
InChI key
XXJWYDDUDKYVKI-UHFFFAOYSA-N
生化/生理作用
Cediranib (AZD2171) is an orally active anticancer agent and a highly potent ATP-competitive receptor tyrosine kinase (RTK) inhibitor against VEGFR (IC50 = 5 nM/Flt-1 (VEGFR1), <1 nM/KDR (VEGFR2), ≤3 nM/Flt-4 (VEGFR3), c-Kit (IC50 = 2 nM), PDGFR1/2 (IC50 = 5/36 nM), and FGFR1 (IC50 = 26 nM). Cediranib exhibits reduced activity against CSF-1R, Src, Abl (IC50 = 110, 130, 260 nM, respectively) and little or no potency toward Flt-3, EGFR, ErbB2 (Her-2/neu), CDK2/4, Aurora A/B, and MEK.
Orally active anticancer agent, highly potent ATP-competitive tyrosine kinase inhibitor against VEGFR1/2/3 (Flt-1/KDR/Flt-4), c-Kit, PDGFR1/2 & FGFR1.
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
法规信息
新产品
历史批次信息供参考:
Carolyn Cao et al.
Cancer research, 66(23), 11409-11415 (2006-12-06)
The vascular endothelial growth factor receptor (VEGFR) tyrosine kinases are being explored as targets for antiangiogenic cancer therapy. Radiotherapy also inhibits tumor growth and affects vasculature. We investigated the combination of the potent VEGFR tyrosine kinase inhibitor AZD2171 and ionizing
Stephen R Wedge et al.
Cancer research, 65(10), 4389-4400 (2005-05-19)
Inhibition of vascular endothelial growth factor-A (VEGF) signaling is a promising therapeutic approach that aims to stabilize the progression of solid malignancies by abrogating tumor-induced angiogenesis. This may be accomplished by inhibiting the kinase activity of VEGF receptor-2 (KDR), which
Z Ping Lin et al.
PloS one, 13(11), e0207399-e0207399 (2018-11-18)
PARP inhibitors target BRCA mutations and defective homologous recombination repair (HRR) for the treatment of epithelial ovarian cancer (EOC). However, the treatment of HRR-proficient EOC with PARP inhibitors remains challenging. The objective of this study was to determine whether the
Ji Yeong Kim et al.
Anticancer research, 39(7), 3785-3793 (2019-07-03)
This study investigated drugs able to sensitize P-glycoprotein (P-gp)-overexpressing resistant KBV20C cancer cells to vincristine or eribulin treatment and assessed their associated mechanisms of action. Eight tyrosine kinase inhibitors (lapatinib, gefitinib, imatinib, erlotinib, nilotinib, pazopanib, cediranib, and vandetanib) and one
Kathy D Miller et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 12(1), 281-288 (2006-01-07)
This pilot study combined physiologic imaging, microcomputed tomography, and histologic tumor evaluation with a xenograft model of breast cancer to identify surrogates likely to correlate with response to AZD2171, an inhibitor of the vascular endothelial growth factor (VEGF) receptor tyrosine
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