Catalog No.S1017 Synonyms: NSC-732208
Molecular Weight(MW): 450.51
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 in HUVEC cells. Phase 3.
Cited by 17 Publications
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Western blots of EZH2 expression in A549, HCC461, and HCC4006 cells upon treatment with different doses of VEGFR-2-inhibitor AZD2171 (0, 5 and 10 nM). AZD2171 decreased the expression of EZH2 in HCC4006 and HCC461 cells expressing VEGFR-2 in a dose-dependent manner but did not do so in A549 cells lacking expression of VEGFR-2.
Clin Cancer Res 2014 20, 3849-61. Cediranib (AZD2171) purchased from Selleck.
Representative histological tumor sections with CD31 vascular staining (brown) and hematoxylin nuclear counterstain (blue) from the 4 treatment groups(untreated, quinacrine, cediranib, ced+quin). Discrete staining is associated with vascular endothelial cells, whereas more diffuse and variable staining is nonspecific and associated with tumor necrosis. Microvessel examples are marked by arrows.
Neuro Oncol 2013 15, 1673-83. Cediranib (AZD2171) purchased from Selleck.
(A) Representative LC3 Western blots obtained from 4C8 cells grown under normoxic (20% O2) or hypoxic (0.5% O2) conditions for 10 h while untreated or exposed to cediranib (3 uM), quinacrine (0.8 uM), or combined cediranib/quinacrine. (B) RFP-LC3-expressing 4C8 cells were visualized using EVOS fl microscopy, grown under hypoxic conditions for 24 h while untreated or exposed to cediranib (2.5 uM), quinacrine (2.5 uM), or combined cediranib/quinacrine. (C) Representative cleaved caspase-3 Western blots obtained from 4C8 cells grown under normoxic (20% O2) or hypoxic (0.5% O2) conditions for 72 h while untreated or exposed to cediranib (2 uM), quinacrine (2 uM), or combined cediranib/quinacrine.
Neuro Oncol 2013 15, 1673-83. Cediranib (AZD2171) purchased from Selleck.
Inhibition of P-gp and Bcrp by cediranib. Accumulation of [3H]vin-blastine in MDR1-transfected cells and [3H]prazosin in Bcrp1-transfected cells in the presence of increasing concentrations of cediranib ranging from 0 to 40 μM is shown.
J Pharmacol Exp Ther 2012 341, 386-395 . Cediranib (AZD2171) purchased from Selleck.
Ba/F3 cell lines expressing the recombinant TEL/kinase domain fusion protein for FGFR1-4 .Cells were grown in RPMI 1640 containing 10% FBS and 500 ng/mL puromycin. The parental Ba/F3 cell line transduced with an empty vector was grown in 10 ng/mL IL-3 (R & D systems). Cell viability was assessed at 72 hours using the Cell Titer 96 Aqueous One Solution (Promega). Data were plotted as percent viability relative to vehicle-treated cells and are shown as mean (±SD) from 3 experiments.
Dr. Mikhail Menshikov of Cardiology Research Center. Cediranib (AZD2171) purchased from Selleck.
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|Description||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 in HUVEC cells. Phase 3.|
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. 
|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.  Besides, Cediranib causes regression of vascular tissues in human lung tumor xenografts. |
Kinase inhibition:Cediranib is dissolved in DMSO at a concentration of 10 mM. All enzyme assays are run at, or just below, the respective Km for ATP (0.2 - 30 μM). The inhibitory activity of Cediranib is determined against a range of recombinant tyrosine kinases [KDR, Flt-1, Flt-4, c-Kit, PDGFRα, PDGFRβ, CSF-1R, Flt-3, FGFR1, Src, Abl, epidermal growth factor receptor (EGFR), ErbB2, Aurora A, and Aurora B] using ELISA. Selectivity versus CDK2 and CDK4 serine/threonine kinases is examined using scintillation proximity assays with a retinoblastoma substrate and [γ-sup>33P]ATP. Activity of Cediranib is compared to MAPK kinase (MEK), which shows dual specificity. It is determined using a MAPK substrate, [γ-33P]ATP, and paper capture/scintillation counting.
|In vitro||DMSO||90 mg/mL (199.77 mM)|
|In vivo||5% DMSO+50% PEG 300+5% Tween+ddH2O||5mg/mL|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02484404||Recruiting||Lung Cancer|Breast Cancer|Ovarian Cancer|Colorectal Cancer|Prostate Cancer|Triple Negative Breast Cancer||National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC)||June 4, 2015||Phase 1|Phase 2|
|NCT02974621||Not yet recruiting||Recurrent Glioblastoma||National Cancer Institute (NCI)||September 2017||Phase 2|
|NCT02889900||Recruiting||Recurrent Platinum Resistant Ovarian Cancer||AstraZeneca|Myriad Genetic Laboratories, Inc.||January 2017||Phase 2|
|NCT02893917||Suspended||Hormone-Resistant Prostate Cancer|Metastatic Prostate Carcinoma|Prostate Adenocarcinoma With Focal Neuroendocrine Differentiation|Prostate Carcinoma Metastatic in the Bone|Prostate Small Cell Carcinoma|Stage IV Prostate Adenocarcinoma||National Cancer Institute (NCI)||December 2016||Phase 2|
|NCT02899728||Not yet recruiting||Small Cell Lung Carcinoma||National Cancer Institute (NCI)||November 2016||Phase 2|
|NCT02855697||Not yet recruiting||Ovarian Cancer||Anna Thomason|The Christie NHS Foundation Trust||November 2016||Early Phase 1|
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