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Merck
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Key Documents

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SML2850

Sigma-Aldrich

Cediranib

≥98% (HPLC)

Sinónimos:

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

Fórmula empírica (notación de Hill):
C25H27FN4O3
Número de CAS:
288383-20-0
Peso molecular:
450.51
MDL number:
MFCD09954115
UNSPSC Code:
12352200
NACRES:
NA.77

Quality Level

100

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear

storage temp.

2-8°C

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

Biochem/physiol Actions

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.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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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
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
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
Wenhua Jiang et al.
Oncology letters, 13(4), 2623-2630 (2017-04-30)
The aim of the present study was to identify the target genes of cediranib and the associated signaling pathways in alveolar soft part sarcoma (ASPS). A microarray dataset (GSE32569) was obtained from the Gene Expression Omnibus database. The R software
A L R Bordinhão et al.
Oncology reports, 36(6), 3197-3206 (2016-10-18)
Cediranib, a pan-tyrosine kinase inhibitor is showing promising results for the treatment of several solid tumours. In breast cancer, its effects remain unclear, and there are no predictive biomarkers. Several studies have examined the expression profiles of microRNAs (miRNAs) in response
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