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SU 1498 (CAS 168835-82-3) LS-H126

VEGFR2 inhibitor
LS-H126-500 / 500 µg / $185
LS-H126-1000 / 1000 µg / $195
LS-H126-5000 / 5000 µg / $255
USA Shipment Only
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Description: SU 1498 is a selective inhibitor of the receptor tyrosine kinase VEGF receptor 2 (VEGFR2, aka FLK1; IC50 = 700 nM), having negligible activity at several other serine/threonine and tyrosine kinases. It effectively blocks signaling through VEGFR2 both in vitro and in vivo. SU 1498 is used to study the role of VEGFR2 signaling in diverse processes, including angiogenesis, tumor growth, neural progenitor cell survival, and neuroregeneration. H126_ChemicalStructureImage.png
biochemical, chemical, inhibitor
A crystalline solid
Shipped Ambient, store at -20°C, ≥ 2 years shelf life.
This product is for research use only. Not for administration to humans, or for human or veterinary diagnostic or therapeutic use.
Data Sheet DataSheet    SDS SDS
Related Products: KDR / VEGFR2 / FLK1 related products

Usage Information

SU 1498 is supplied as a crystalline solid. A stock solution may be made by dissolving the SU 1498 in the solvent of choice. SU 1498 is soluble in organic solvents such as ethanol, DMSO, and dimethyl formamide (DMF), which should be purged with an inert gas. The solubility of SU 1498 in these solvents is approximately 10, 20, and 50 mg/ml, respectively. SU 1498 is sparingly soluble in aqueous buffers. For maximum solubility in aqueous buffers, SU 1498 should first be dissolved in DMF and then diluted with the aqueous buffer of choice. SU 1498 has a solubility of approximately 0.3 mg/ml in a 1:2 solution of DMF:PBS (pH 7.2) using this method. We do not recommend storing the aqueous solution for more than one day.

  1. Strawn, L.M., McMahon, G., App, H., et al. Flk-1 as a target for tumor growth inhibition. Cancer Res. 56(15), 3540-3545 (1996).
  2. Fedorov, O., Marsden, B., Pogacic, V., et al. A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases. Proc. Natl. Acad. Sci. USA 104(51), 20523-20528 (2007).
  3. Arbiser, J.L., Larsson, H., Claesson-Welsh, L., et al. Overexpression of VEGF 121 in immortalized endothelial cells causes conversion to slowly growing angiosarcoma and high level expression of the VEGF receptors VEGFR-1 and VEGFR-2 in vivo. Am. J. Pathol. 156(4), 1469-1476 (2000).
  4. Francescone, R., Scully, S., Bentley, B., et al. Glioblastoma-derived tumor cells induce vasculogenic mimicry through Flk-1 protein activation. J. Biol. Chem. 287(29), 24821-24831 (2012).
  5. Harms, K.M., Li, L., and Cunningam, L.A. Murine neural stem/progenitor cells protect neurons against ischemia by HIF-1α-regulated VEGF signaling. PLoS One 5(3), 1-12 (2010).

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