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- 详细信息
- 文献和实验
- 技术资料
- 保存条件:
Store at -20℃ for one year(Powder);Store at 2-4℃ for two weeks;Store at -20℃ for six months after dissolution.
- 保质期:
Store at -20℃ for one year(Powder);Store at 2-4℃ for two weeks;Store at -20℃ for six months after dissolution.
- 英文名:
SU1498 ;AG-1498;Tyrphostin SU 1498
- 库存:
12
- 供应商:
爱必信(上海)生物科技有限公司
- CAS号:
168835-82-3
- 规格:
25mg/5mg
| 规格: | 25mg | 产品价格: | ¥3749.0 |
|---|---|---|---|
| 规格: | 5mg | 产品价格: | ¥1048.0 |
| 公告提醒:爱必信所有产品和服务仅用于科学研究,不用于临床应用及其他用途提供产品和服务(也不为任何个人提供产品和服务)!
抑制剂描述: 产品名称:SU1498 产品别名:见爱必信官网 英文别名:SU1498 靶点:VEGFR CAS:168835-82-3 纯度:≥98% 外观:见爱必信官网 保存方法:Store at -20℃ for one year(Powder);Store at 2-4℃ for two weeks;Store at -20℃ for six months after dissolution. 描述: SU1498 is a selective inhibitor of the VEGFR2; inhibits Flk-1 with an IC50 of value of 700 nM. 溶解性:DMSO :78 mg/mL (199.73 mM) 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. 体内研究:
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文献和实验2.Fedorov, O.,Marsden, B.,Pogacic, V., et al. A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases. Proceedings of the National Academy of Sciences of the United States of America 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. American Journal of Pathology 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. The Journal of Biological Chemisty 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).
6.Pan, Z.,Fukuoka, S.,Karagianni, N., et al. Vascular endothelial growth factor promotes anatomical and functional recovery of injured peripheral nerves in the avascular cornea. FEBS Journal 27(7), 2756-2767 (2013).
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