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    Cediranib (NSC-732208; AZD-2171)
    Cediranib (NSC-732208; AZD-2171)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V0517
    CAS #: 288383-20-0 Purity ≥98%

    Description: Cediranib (also called NSC732208; AZD2171, tentative trade name Recenti), an indole ether quinazoline derivative, is a potent and oral VEGFR (vascular endothelial growth factor receptors) inhibitor with potential antitumor activity. It inhibits VEGFR with an IC50 of<1 nM, and shows >1000-fold selectivity for inhibiting VEGFR over PDGFR-α, CSF-1R and Flt3 in HUVEC cells. Cediranib is being developed clinically by AstraZeneca as an oral therapy for the treatment of cancers such as non-small cell lung cancer, kidney cancer, and colorectal cancer. 

    References: Cancer Res. 2005 May 15;65(10):4389-400; Pediatr Blood Cancer. 2012 Apr;58(4):566-71.

    Related CAS: 857036-77-2 (maleate)
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    Molecular Weight (MW)450.51
    FormulaC25H27FN4O3
    CAS No.288383-20-0 (free base); 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 90 mg/mL (199.8 mM)
    Water: <1 mg/mL
    Ethanol:<1 mg/mL
    Solubility (In vivo)5% DMSO+50% PEG 300+5% Tween+ddH2O: 5 mg/kg
    SynonymsBrand name: Recentin; AZD2171; NSC 732208; NSC732208; AZD 2171; NSC-732208; AZD-2171; 

    Chemical Name: 4-(4-fluoro-2-methyl-1H-indol-5-yloxy)-6-methoxy-7-(3-(pyrrolidin-1-yl)propoxy)quinazoline

    InChi Key: XXJWYDDUDKYVKI-UHFFFAOYSA-N

    InChi Code: 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

    SMILES Code: COC1=CC2=C(OC3=C(F)C4=C(NC(C)=C4)C=C3)N=CN=C2C=C1OCCCN5CCCC5


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    In Vitro

    In vitro activity: Cediranib (also called AZD2171, an indole ether quinazoline derivative) is a highly potent VEGFR (KDR) inhibitor with IC50 of<1nM, >1000-fold selective more for VEGFR than PDGFR-α, CSF-1R and Flt3 in HUVEC cells. 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. By competing with adenosine triphosphate, cediranib binds to and inhibits all three vascular endothelial growth factor receptor (VEGF-1,-2,-3) tyrosine kinases, thereby blocking VEGF-signaling, angiogenesis, and tumor cell growth. Cediranib is being developed clinically as a once-daily oral therapy for the treatment of cancer. Cediranib (also called AZD2171, an indole ether quinazoline derivative) is a highly potent VEGFR (KDR) inhibitor with IC50 of<1 4='' 5='' it='' also='' inhibits='' with='' ic50='' of='' nm='' and='' shows='' similar='' activity='' against='' c-kit='' 110-fold=''>1000-fold selective more for VEGFR than PDGFR-α, CSF-1R and Flt3 in HUVEC cells. 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. By competing with adenosine triphosphate, cediranib binds to and inhibits all three vascular endothelial growth factor receptor (VEGF-1,-2,-3) tyrosine kinases, thereby blocking VEGF-signaling, angiogenesis, and tumor cell growth. Cediranib is being developed clinically as a once-daily oral therapy for the treatment of cancer. 


    Kinase Assay: 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.


    Cell Assay: The proliferation of the HUVEC cell line is evaluated in the presence and absence of growth factors by measuring 3H-thymidine incorporation following a 4-day incubation period. Proliferation of MG63 osteosarcoma cells is induced by PDGF-AA, which selectively activates signaling of the PDGFRα homodimer. HUVEC and MG63 osteosarcoma cells are cultured in DMEM without phenol red containing 1% charcoal stripped FCS, 2 mM glutamine, and 1% nonessential amino acids for 24 hours. Cediranib or vehicle is added with PDGF-AA ligand (50 ng/mL) and plates incubated for another 72 hours. Cellular proliferation is determined using bromodeoxyuridine ELISA.

    In VivoCediranib 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.
    Animal modelfemale nude (nu/nu genotype) mice bearing PC-3, Calu-6, SKOV-3, MDA-MB-231, and SW620 tumors
    Formulation & DosageSuspended in 1% (w/v) aqueous polysorbate 80; 0.75-6 mg/kg; p.o.
    ReferencesCancer Res. 2005 May 15;65(10):4389-400; Pediatr Blood Cancer. 2012 Apr;58(4):566-71.


    These protocols are for reference only. InvivoChem does not independently validate these methods.

    Cediranib (AZD2171)

    AZD2171 inhibits VEGF-stimulated KDR phosphorylation in human endothelial cells.  2005 May 15;65(10):4389-400.

    Cediranib (AZD2171)

    AZD2171 inhibits tubule growth in vitro. HUVECs and human fibroblasts were obtained as commercial cocultures (AngioKit, TCS Cellworks).  2005 May 15;65(10):4389-400.

    Cediranib (AZD2171)

    AZD2171 inhibits VEGF-induced angiogenesis in vivo.  2005 May 15;65(10):4389-400.

    Cediranib (AZD2171)

    Consequences of inhibiting VEGF signaling and physiologic angiogenesis in vivo: effect of AZD2171 on bone morphogenesis and ovarian cycling in young female rats.  2005 May 15;65(10):4389-400.

    Cediranib (AZD2171)

    AZD2171 inhibits human tumor xenograft growth at doses that are well tolerated.  2005 May 15;65(10):4389-400.

    Cediranib (AZD2171)

    AZD2171 causes vascular regression in Calu-6 lung tumor xenografts.  2005 May 15;65(10):4389-400.


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