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10 mM * 1 mL/1 mg/5 mg/10 mg/25 mg/50 mg/100 mg
| 规格： | 10 mM * 1 mL | 产品价格： | ￥1068.0 |
|---|---|---|---|
| 规格： | 1 mg | 产品价格： | ￥380.0 |
| 规格： | 5 mg | 产品价格： | ￥880.0 |
| 规格： | 10 mg | 产品价格： | ￥1320.0 |
| 规格： | 25 mg | 产品价格： | ￥2420.0 |
| 规格： | 50 mg | 产品价格： | ￥3630.0 |
| 规格： | 100 mg | 产品价格： | ￥5390.0 |
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NPS-1034
CAS No. : 1221713-92-3
MCE 国际站：NPS-1034
产品活性：NPS-1034 是 AXL 和 MET 的双重抑制剂，其 IC50 值分别为 10.3 和 48 nM。
研究领域：Protein Tyrosine Kinase/RTK | Apoptosis
作用靶点：TAM Receptor | c-Met/HGFR | Apoptosis
In Vitro: NPS-1034 is a dual inhibitor of AXL and MET with IC50s of 10.3 and 48 nM, respectively.The expression and activity of AXL is significantly increased in HCC827/ER cells, and NPS-1034 treatment effectively inhibits its tyrosine phosphorylation. NPS-1034 inhibits the viability of the MKN45 and SNU638 cell lines, which highly express the MET gene and p-MET (phosphorylated MET), with IC50 values of 112.7 and 190.3 nmol, respectively. In contrast, NPS-1034 inhibits AGS, KATOIII, NCI-N87, MKN1, MKN28, and MKN74 cell viability with IC50 values ranging from 1 μmol to more than 10 μmol. MET phosphorylation is dramatically decreased after treatment with NPS-1034 in the MKN45 cells, but not in the MKN28 cells. NPS-1034 inhibits hepatocyte growth factor (HGF)-stimulated MET autophosphorylation (Y1234/1235) in the AGS and MKN1 cell lines with IC50 values of <10 and <50 nmol, respectively. HGF-induced MET phosphorylation is completely inhibited by 50 nmol NPS-1034.
In Vivo: NPS-1034 inhibits tumor proliferation, which highly expresses p-MET. NPS-1034 treatment induces a clear decrease in the vascularization of the tumors. The expression of alpha-smooth muscle actin (α-SMA) is decreased in the tumor sections of mice treated with NPS-1034. NPS-1034-treated mice show virtually no weight loss, indicating that NPS-1034 is generally well tolerated.
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文献和实验Fluorescence Recovery After Photobleaching (FRAP) with a Focus on F‐actin
in individual stress fibers. Microsc. Res. Tech. 70:1034‐1040. Jacobson, K. and Wojcieszyn, J. 1984. The translational mobility of substances within the cytoplasmic matrix. Proc. Natl
Seu, K.J., Pandey, A.P., Haque, F., Proctor, E.A., Ribbe, A.E., and Hovis, J.S. 2007. Effect of surface treatment on diffusion and domain formation in supported lipid bilayers. Biophysical J. 92:2445‐2450. Soumpasis, D.M. 1983. Theoretical
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