SU1498-AG-1498-DataSheet-生命科學(xué)試劑-MedChemExpress

1、Hotline: 400-820-3792Inhibitors Agonists Screening Librarieswww.MedChemESU1498Cat. No.: HY-19326CAS No.: 168835-82-3Synonyms: AG 1498; Tyrphostin SU 1498分式: CHNO分量: 390.52作靶點(diǎn): VEGFR作通路: Protein Tyrosine Kinase/RTK儲(chǔ)存式: Powder -20C 3 years4C 2 yearsIn solvent -80C 6 months-20C 1 month溶解性數(shù)據(jù)體外實(shí)驗(yàn) DMSO :

2、150 mg/mL (384.10 mM)* means soluble, but saturation unknown.Mass Solvent1 mg 5 mg 10 mg Concentration制備儲(chǔ)備液1 mM 2.5607 mL 12.8034 mL 25.6069 mL5 mM 0.5121 mL 2.5607 mL 5.1214 mL10 mM 0.2561 mL 1.2803 mL 2.5607 mL請(qǐng)根據(jù)產(chǎn)品在不同溶劑中的溶解度，選擇合適的溶劑配制儲(chǔ)備液，并請(qǐng)注意儲(chǔ)備液的保存式和期限。BIOLOGICAL ACTIVITY物活性 SU1498是選擇性的VEGFR2抑制劑；

3、抑制Flk-1的IC50值為700 nM。IC50 & Target Flk-1700 nM (IC50)1/2 Master of Small Molecules 您邊的抑制劑師www.MedChemE體外研究 SU1498 stimulates accumulation of phosphorylated ERKs in human umbilical vein endothelial cells and inhuman aortic endothelial cells in a manner that is dependent on the functioning of the upst

4、ream componentsof the MAPK pathway, B-Raf, and MEK kinases. The enhanced accumulation of phospho-ERKs is observedonly in cells that have been stimulated with sphingosine 1-phosphate or protein growth factors; SU1498 byitself is ineffective 2. SU1498 blocks signal transduction from VEGFR2 in MS1 VEGF

5、 cells.In the presenceof SU1498, levels of Ets-1 are decreased, suggesting that VEGF-VEGFR-2 interactions contributed tobaseline levels of Ets-1 expression, and interruption of this autocrine interaction with SU1498 led todecreased expression of Ets-1 3. SU1498 treatment significantly impacts U87 ce

6、ll proliferation andapoptosis. SU1498 induces a marked increase in lipids and a decrease in glycerophosphocholine.Accordingly, accumulation of lipid droplets is seen in the cytoplasm of SU1498-treated U87 cells 4.PROTOCOLKinase Assay 2 The ERK1 or ERK2 solution is pipetted into tubes (1 L per tube)

7、and mixed with 0-10 L of 50 M SU1498(in kinase buffer without ATP). The blank tube receives buffer only. The volume is adjusted to 11 L with thesame buffer, and the mixtures are incubated for 10 min at 25C. This is followed by the addition of 40 L ofthe Elk1-ATP-buffer solution, and the incubations

8、are continued for 30 min at 30C. The reactions arestopped with 20 L of 4 sample buffer mix and heating at 95C for 10 min. Samples (15 L) are fractionatedby SDS, and phosphorylated Elk1 is detected by immunoblotting with anti-phospho-Elk1 antibody 2.MCE has not independently confirmed the accuracy of

9、 these methods. They are for reference only.Cell Assay 4 For cell proliferation assay, U87 cells are seeded in 24-well plates (30,000 cells/well) and allowed to attachovernight. Cells are then treated for 24 or 72 h with different concentrations of Bevacizumab (from 10 ng/mLto 250 g/mL) or SU1498 (f

10、rom 1 M to 30 M) in triplicate wells. The cell viability is then assessed with theMTT assay 4.MCE has not independently confirmed the accuracy of these methods. They are for reference only.REFERENCES1. Strawn LM, et al. Flk-1 as a target for tumor growth inhibition.Cancer Res. 1996 Aug 1;56(15):3540

11、-5.2. Boguslawski G, et al. SU1498, an inhibitor of vascular endothelial growth factor receptor 2, causes accumulation of phosphorylated ERKkinases and inhibits their activity in vivo and in vitro.J Biol Chem. 2004 Feb 13;279(7):5716-24.3. Arbiser JL, et al. Overexpression of VEGF 121 in immortalize

12、d endothelial cells causes conversion to slowly growing angiosarcoma andhigh level expression of the VEGF receptors VEGFR-1 and VEGFR-2 in vivo.Am J Pathol. 2000 Apr;156(4):1469-76.4. Mesti T, et al. Metabolic impact of anti-angiogenic agents on U87 glioma cells.PLoS One. 2014 Jun 12;9(6):e99198.McePdfHeightCaution: P