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Santa Cruz discontinued a large number of its polyclonal products as a result of the USDA settlement that was made public May 19th 2016

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Western blot analysis of extracts from HUVE cells serum-starved overnight, untreated (-) or pre-treated with Vandetanib (5 µM, 2 hr; +) and treated with Human Vascular Endothelial Growth Factor-165 (hVEGF165) #8065 (50 ng/ml, 5 min; +) as indicated, using Phospho-VEGF Receptor 2 (Tyr1175) (19A10) Rabbit mAb #2478 (upper) or VEGF Receptor 2 (55B11) Rabbit mAb #2479 (lower).

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Chemical structure of vandetanib.

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Product Usage Information

Vandetanib is supplied as a lyophilized powder. For a 10 mM stock, reconstitute the 5 mg in 1.05 ml DMSO. Working concentrations and length of treatment can vary depending on the desired effect, but it is typically used as a pretreatment at 1-10 µM for 0.5-2 hr prior to treating with a stimulator. It can also be used alone, with varying treatment times lasting up to 24 hr. Soluble in DMSO at 30 mg/ml; soluble in ethanol at 10 mg/ml with warming; very poorly soluble in water with maximum ~10-20 µM.

Storage: Store lyophilized or in solution at -20ºC, desiccated. In lyophilized form, the chemical is stable for 24 months. Once in solution, use within 3 months to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Product Description

Molecular Weight:

475.35 g/mol



Molecular Formula:


Vandetanib, also known as ZD6474, is a selective inhibitor of VEGFR and EGFR tyrosine kinases (1-5). Researchers have shown that vandetanib inhibits VEGFR-2, VEGFR-3, and EGFR in recombinant enzyme assays with IC50 values of 40 nM, 108 nM, and 500 nM, respectively, and had selectivity over a variety of other tyrosine and serine/threonine kinases (2). Vandetanib inhibits VEGF and EGF stimulated proliferation of HUVE cells with an IC50 of 60 nM and 170 nM, respectively (2), and effectively blocks VEGF and EGF induced autophosphorylation (3-5). Inhibition of RET by vandetanib has also been observed (6).

1.  Morabito, A. et al. (2009) Oncologist 14, 378-90.

2.  Wedge, S.R. et al. (2002) Cancer Res 62, 4645-55.

3.  Jane, E.P. et al. (2009) J Pharmacol Exp Ther 331, 327-37.

4.  McCarty, M.F. et al. (2004) Mol Cancer Ther 3, 1041-8.

5.  Ciardiello, F. et al. (2003) Clin Cancer Res 9, 1546-56.

6.  Carlomagno, F. et al. (2002) Cancer Res 62, 7284-90.

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