1. Protein Tyrosine Kinase/RTK
  2. VEGFR
  3. Vandetanib trifluoroacetate

Vandetanib trifluoroacetate (Synonyms: ZD6474 trifluoroacetate)

Cat. No.: HY-10260A
Handling Instructions

Vandetanib trifluoroacetate is a potent inhibitor of VEGFR2 with IC50 of 40 nM.

For research use only. We do not sell to patients.

Vandetanib trifluoroacetate Chemical Structure

Vandetanib trifluoroacetate Chemical Structure

CAS No. : 338992-53-3

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Top Publications Citing Use of Products

    Vandetanib trifluoroacetate purchased from MCE. Usage Cited in: Oncotarget. 2014 May 15;5(9):2688-702.

    The Ret expression level is investigated by Western blot in MYCN/KI AlkR1279Q and MYCN/KI AlkF1178L treated tumors and controls using the anti-Ret antibody EPR2871. Actin is used as a standard for quantification.

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    Vandetanib trifluoroacetate is a potent inhibitor of VEGFR2 with IC50 of 40 nM.

    IC50 & Target[1]


    40 nM (IC50)

    In Vitro

    Vandetanib inhibits VEGFR3 and EGFR with IC50 of 110 nM and 500 nM, respectively. Vandetanib is not sensitive to PDGFRβ, Flt1, Tie-2 and FGFR1 with IC50 of 1.1-3.6 μM, while almost has no activity against MEK, CDK2, c-Kit, erbB2, FAK, PDK1, Akt and IGF-1R with IC50 above 10 μM. Vandetanib inhibits VEGF-, EGF- and bFGF-stimulated HUVEC proliferation with IC50 of 60 nM, 170 nM and 800 nM, with no effect on basal endothelial cell growth. Vandetanib inhibits tumor cell growth with IC50 of 2.7 μM (A549) to 13.5 μM (Calu-6)[1]. Odanacatib is a weak inhibitor of antigen presentation, measured in a mouse B cell line (IC50=1.5±0.4 μM), compared to the Cat S inhibitor LHVS (IC50=0.001 μM) in the same assay. Odanacatib also shows weak inhibition of the processing of the MHC II invariant chain protein Iip10 in mouse splenocytes compared to LHVS (minimum inhibitory concentration 1-10 μM versus 0.01 μM, respectively)[2]. Vandetanib suppresses phosphorylation of VEGFR-2 in HUVECs and EGFR in hepatoma cells and inhibits cell proliferation[4].

    In Vivo

    Vandetanib (15 mg/kg, p.o.) has a superior anti-tumor effect than gefitinib in the H1650 xenograft model, and suppresses tumor growth with IC50 of 3.5±1.2 μM[3]. In tumor-bearing mice, vandetanib (50 or 75 mg/kg) suppresses phosphorylation of VEGFR-2 and EGFR in tumor tissues, significantly reduces tumor vessel density, enhances tumor cell apoptosis, suppresses tumor growth, improves survival, reduces number of intrahepatic metastases, and upregulates VEGF, TGF-α, and EGF in tumor tissues[4].

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    Please store the product under the recommended conditions in the Certificate of Analysis.

    Cell Assay

    Growth inhibition is measured by a modified MTT assay. Briefly, the cells are plated on 96-well plates at a density of 2000 cells per well and exposed to each gefitinib or vandetanib for 72 h. Each assay is performed in triplicate. The 50% inhibitory concentration (IC50) of each drug is determined as the mean±standard deviation (SD).

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration

    One million H1650 cells or H1650/PTEN cells (H1650 cells with a transfected PTEN gene) are injected subcutaneously into the backs of each mouse. On 10th day after injection, mice are randomLy assigned to three groups, which receive either vehicle, vandetanib (15 mg/kg/day), or gefitinib (15 mg/kg/day). Vehicle, vandetanib, and gefitinib are administered once per day p.o., five times per week. Tumor volume (width×width×length/2) and body weight are determined periodically. Tumor volumes are expressed as mean±SD. Differences in tumor volume are evaluated using Student's t-test.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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