产品
编 号：F201756
分子式：C25H30N2O2
分子量：390.52
分子式：C25H30N2O2
分子量：390.52
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
1mg
304
In-stock
5mg
612
In-stock
10mg
1020
In-stock
25mg
2108
In-stock
50mg
3400
In-stock
100mg
询价
询价
结构图
CAS No: 168835-82-3
产品详情
生物活性：
SU1498 (AG 1498) is a selective inhibitor of the VEGFR2; inhibits Flk-1 with an IC50 of value of 700 nM.
体外研究：
SU1498 stimulates accumulation of phosphorylated ERKs in human umbilical vein endothelial cells and in human aortic endothelial cells in a manner that is dependent on the functioning of the upstream components of the MAPK pathway, B-Raf, and MEK kinases. The enhanced accumulation of phospho-ERKs is observed only in cells that have been stimulated with sphingosine 1-phosphate or protein growth factors; SU1498 by itself is ineffective. SU1498 blocks signal transduction from VEGFR2 in MS1 VEGF cells.In the presence of SU1498, levels of Ets-1 are decreased, suggesting that VEGF-VEGFR-2 interactions contributed to baseline levels of Ets-1 expression, and interruption of this autocrine interaction with SU1498 led to decreased expression of Ets-1. SU1498 treatment significantly impacts U87 cell proliferation and apoptosis. 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.
SU1498 (AG 1498) is a selective inhibitor of the VEGFR2; inhibits Flk-1 with an IC50 of value of 700 nM.
体外研究：
SU1498 stimulates accumulation of phosphorylated ERKs in human umbilical vein endothelial cells and in human aortic endothelial cells in a manner that is dependent on the functioning of the upstream components of the MAPK pathway, B-Raf, and MEK kinases. The enhanced accumulation of phospho-ERKs is observed only in cells that have been stimulated with sphingosine 1-phosphate or protein growth factors; SU1498 by itself is ineffective. SU1498 blocks signal transduction from VEGFR2 in MS1 VEGF cells.In the presence of SU1498, levels of Ets-1 are decreased, suggesting that VEGF-VEGFR-2 interactions contributed to baseline levels of Ets-1 expression, and interruption of this autocrine interaction with SU1498 led to decreased expression of Ets-1. SU1498 treatment significantly impacts U87 cell proliferation and apoptosis. 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.
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