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Western blot analysis of extracts from NIH/3T3 cells, serum-starved overnight and untreated or treated with hPDGF-BB #8912 (100 ng/ml, 5 min) either with or without Sunitinib pre-treatment (2 hr) at the indicated concentrations, using Phospho-PDGF Receptor β (Tyr1009) (42F9) Rabbit mAb #3124 (upper) or PDGF Receptor β (28E1) Rabbit mAb #3169 (lower).

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Chemical structure of sunitinib.

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Product Usage Information

Sunitinib is supplied as a lyophilized powder. For a 5 mM stock, reconstitute the 10 mg in 3.76 ml DMSO. Working concentrations and length of treatment can vary depending on the desired effect, but it is typically used at 0.1-10 µM either as a pretreatment for 0.5-2 hr prior to treating with a stimulator or is used alone with varying treatment times lasting up to 24 hr. Sunitinib is soluble in DMSO at 40 mg/ml; poorly soluble in ethanol and water with maximum solubility in water ~10-50 µM.


Storage: Store lyophilized or in solution at -20ºC, desiccated. Protect from light. 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:

532.56 g/mol


Purity:

>99%


Molecular Formula:

C22H27FN4O2•C4H6O5


Sunitinib, also known as SU11248, is a multi-tyrosine kinase inhibitor widely known to target PDGFR, VEGFR, KIT, and FLT3, and therefore has both antitumor and antiangiogenic activities. Cellular phosphorylation assays show that sunitinib effectively inhibits ligand-dependent phosphorylation of these receptor tyrosine kinases in nanomolar concentrations and can also inhibit ligand-dependent cellular proliferation (1-3). Sunitinib displays greater than 10-fold selectively for PDGFRB and VEGFR over numerous other kinases, including EGFR, Cdk2, Met, IGF -1R, Abl, and src (2). Inhibition of CSF-1 (4) and RET (5) by sunitinib has also been observed.


1.  Abrams, T.J. et al. (2003) Mol Cancer Ther 2, 471-8.

2.  Mendel, D.B. et al. (2003) Clin Cancer Res 9, 327-37.

3.  O'Farrell, A.M. et al. (2003) Blood 101, 3597-605.

4.  Guo, J. et al. (2006) Mol Cancer Ther 5, 1007-13.

5.  Broutin, S. et al. (2011) Clin Cancer Res 17, 2044-54.



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