Catalog Number: 3768
Alternate Names: SU 11248
Chemical Name: N-[2-(Diethylamino)ethyl]-5-[(Z)-(5-fluoro-1,2-dihydro-2-oxo-3H-indol-3-ylidine)methyl]-2,4-dimethyl-1H-pyrrole-3-carboxamide (2S)-2-hydroxybutanedioate salt
Biological Activity
Potent, ATP-competitive VEGFR, PDGFRβ and KIT inhibitor (Ki values are 2, 9, 17, 8 and 4 nM for VEGFR -1, -2, -3, PDGFRβ and KIT respectively). Also inhibits cellular receptor phosphorylation of FLT3, RET and CSF-1R. Exhibits antiangiogenic and antitumor activity in multiple xenograft models.
Technical Data
  • M.Wt:
  • Formula:
  • Solubility:
    Soluble to 25 mM in DMSO
  • Purity:
  • Storage:
    Store at +4°C
  • CAS No:
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis. All Tocris products are intended for laboratory research use only.
Additional Information
Licensing Caveats:
Sold for research purposes under agreement from Pfizer Inc.
Background References
  1. Molecular basis for sunitinib efficacy and future clinical development
    Faivre et al.
    Nat.Rev.Drug Discov., 2007;6:734
  2. In vivo antitumor activity of SU11248, a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor and platelet-derived growth factor receptors: determination of a pharmacokinetic/pharmacodynamic relationship.
    Mendel et al.
    Clin.Cancer Res., 2003;9:327
  3. SU11248 is a novel FLT3 tyrosine kinase inhibitor with potent activity in vitro and in vivo.
    O'Farrell et al.
    Blood, 2003;101:3597
  4. Sunitinib: a VEGF and PDGF receptor protein kinase and angiogenesis inhibitor.
    Biochem.Biophys.Res.Comm., 2007;356:323

The citations listed below are publications that use Tocris products. Selected citations for Sunitinib malate include:

Showing Results 1 - 2 of 2

  1. Feedback circuitry between miR-218 repression and RTK activation in glioblastoma.
    Authors: Mathew Et al.
    Cell Death Differ
  2. Gleevec/imatinib, an ABL2 kinase inhibitor, protects tumor and endothelial cells from semaphorin-induced cytoskeleton collapse and loss of cell motility.
    Authors: Procaccia Et al.
    Biochem Biophys Res Commun
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