Cediranib

SKU: orb1305389

Description

Cediranib (AZD2171) is a potent ATP-competitive inhibitor targeting VEGFR-2 (KDR) with sub-nanomolar activity. It also potently inhibits VEGFR-1/3, PDGFRβ, and c-Kit, demonstrating selectivity over related kinases. This inhibitor is widely used in preclinical cancer research, particularly in studies of angiogenesis and tumor growth in both cellular and animal models.

Research Area

Cardiovascular Research, Cell Biology, Signal Transduction

Key Properties

• CAS Number: 288383-20-0
• MW: 450.51
• Purity: 99.94% (May vary between batches)
• Formula: C₂₅H₂₇FN₄O₃
• SMILES: O(C=1C2=C(C=C(OCCCN3CCCC3)C(OC)=C2)N=CN1)C=4C(F)=C5C(=CC4)NC(C)=C5
• Target: VEGFR,Autophagy,FLT,c-Kit,PDGFR
• Solubility: Ethanol:< 1 mg/mL (insoluble or slightly soluble);10% DMSO+40% PEG300+5% Tween 80+45% Saline:3.3 mg/mL (7.33 mM);DMSO:118 mg/mL (261.93 mM);H2O:< 1 mg/mL (insoluble or slightly soluble)

Bioactivity

• Target IC50:
  FLT4:≤3 nM|FLK1:5 nM|KDR:1 nM|c-Kit:2 nM|PDGFRα:36 nM|PDGFRβ:5 nM
• In Vivo:
  In vitro, Cediranib directly inhibits the proliferation of tumor cells and blocks microtubule formation, while also suppressing angiogenesis induced by VEGF in vivo. Cediranib exhibits inhibition against bFGF (IC50: 0.5 μM) and EGF (IC50: 0.11 μM), and in the MG63 cell line, it inhibits PDGF-AA (IC50: 0.04 μM). Furthermore, Cediranib suppresses Flt-1 associated kinases (IC50: 5 nM) and exhibits inhibitory effects on the VEGF-C and VEGF-D receptors, Flt-4 (IC50 < 3 nM), in addition to inhibiting the tyrosine kinases c-Kit (IC50: 2 nM) and PDGFR-β (IC50: 5 nM).
• In Vitro:
  Cediranib exhibits highly effective and dose-dependent activity in human xenograft models. Additionally, Cediranib induces vascular regression in human lung cancer xenografts. It causes excessive skeletal growth, obstructs the production of corpora lutea in the ovaries, and inhibits physiological processes that are dependent on angiogenesis.
• Cell Research:
  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. (Only for Reference)

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

PDGFR, PDGFRβ, VEGFR, Vascular endothelial growth factor receptor, VEGFR3/FLT4, VEGFR2/KDR, VEGFR1/FLT1, Inhibitor, Flt4, Flt1, inhibit, Platelet-derived growth factor receptor, NSC732208, NSC-732208, NSC 732208, c-Kit, cKit, Cediranib, AZD2171, AZD-2171, Autophagy, AZD 2171

Compound Identifiers

PubChem CID

9933475