| 货号 | 规格 | 价格 | 上海 | 北京 | 珠海 | 重庆 | 武汉 | 购买数量 |
|---|---|---|---|---|---|---|---|---|
S80869-5mg买3赠1 |
99.30% | ￥480.00 |
2 | - | - | - | - |
|
S80869-10mg买3赠1 |
99.30% | ￥830.00 |
4 | - | - | - | - |
|
S80869-25mg买3赠1 |
99.30% | ￥1610.00 |
5 | - | - | - | - |
|
S80869-100mg |
≥98% | ￥4260.00 |
货期：2-3天 | - | - | - | - |
|
| 产品描述： | SU11274(IC50=10 nM) is a specific Met inhibitor. It shows no significant effects on PGDFRβ, EGFR or Tie2. | ||||||||||||||||||||
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| 靶点： | Apoptosis;Autophagy;CDK;c-Met/HGFR;FGFR;VEGFR;Apoptosis;VEGFR;FGFR;c-Met/HGFR;CDK;Autophagy | ||||||||||||||||||||
| 体外研究： | SU11274 exhibits greater than 50-fold selectivity for Met versus Flk and more than 500 times selectivity versus other tyrosine kinases such as FGFR-1, c-src, PDGFbR, and EGFR. SU11274 inhibits the phosphorylation of key regulators of the PI3K pathway, including AKT, FKHR, or GSK3β. SU11274 treatment inhibits the growth of TPR-MET-transformed BaF3 cells in a dose-dependent manner with IC50 of < 3 μM in the absence of interleukin 3, without growth inhibition of BaF3 cells transformed by other oncogenic tyrosine kinases, including BCR-ABL, TEL-JAK2, TEL-ABL, and TEL-PDGFβR. In addition to cell growth, SU11274 treatment significantly inhibits the migration of BaF3. TPR-MET cells by 44.8% and 80% at 1 μM and 5 μM, respectively. SU11274 inhibits HGF-dependent phosphorylation of Met as well as HGF-dependent cell proliferation and motility with an IC50 of 1-1.5 μM. In H69 and H345 cells which have functional Met receptor, SU11274 inhibits the HGF-induced cell growth with IC50 of 3.4 μM and 6.5 μM, respectively. SU11274 induces G1 cell cycle arrest with cells in G1 phase increased from 42.4% to 70.6% at 5 μM, and induces caspase-dependent apoptosis by 24% at 1 μM. SU11274 inhibits cell viability in c-Met-expressing non-small cell lung cancer (NSCLC) cells with IC50 values of 0.8-4.4 μM, and abrogates hepatocyte growth factor-induced phosphorylation of c-Met and its downstream signaling. | ||||||||||||||||||||
| 体内研究： | SU11274抑制PI3K通路关键调节器的磷酸化, 包括AKT, FKHR,或GSK3β。SU11274抑制HGF依赖的Met磷酸化,及HGF依赖的细胞增殖和活动,IC50为1-1.5 μM。在TPR-MET转化的BaF3细胞中,白细胞介素- 3存在时,用SU11274处理细胞,以剂量依赖的方式抑制细胞生长。SU11274（IC50<3 μM）则不会抑制其他致癌酪氨酸激酶转化的BaF3细胞生长,包括BCR-ABL, TEL-JAK2, TEL-ABL,和TEL-PDGFβR。在BaF3.TPR-MET细胞中,经SU11274处理,也显著抑制细胞迁移,按1 μM 和5 μM处理,抑制分别为44.8% 和 80%。在具有功能性Met受体的H69和H345细胞中,SU11274抑制 HGF诱导的细胞生长,IC50分别为3.4 μM 和 6.5 μM。表达c-Met的非小细胞肺癌(NSCLC)细胞中,SU1127抑制细胞活力,IC50为0.8-4.4 μM,同时去除肝脏生长因子诱导的c-Met 及其下游信号磷酸化 | ||||||||||||||||||||
| 细胞实验： | Cells are exposed to various concentrations of SU11274 in the presence or absence of HGF for 24, 48, and 72 hours. The number of viable cells is determined using the MTT assay or trypan blue exclusion. Cell Cycle and apoptosis are measured by fluorescence-activated cell sorter analysis via propidium iodide staining and Annexin V-positive staining, respectively. (Only for Reference) | ||||||||||||||||||||
| 参考文献： | 1. Wang X, et al. Potent and selective inhibitors of the Met [hepatocyte growth factor/scatter factor (HGF/SF) receptor] tyrosine kinase block HGF/SF-induced tumor cell growth and invasion. Mol Cancer Ther, 2003, 2(11):1085-1092. 2. Sattler M, et al. A novel small molecule met inhibitor induces apoptosis in cells transformed by the oncogenic TPR-MET tyrosine kinase. Cancer Res, 2003, 63(17), 5462-5469. 3. Ma PC, et al. Functional expression and mutations of c-Met and its therapeutic inhibition with SU11274 and small interfering RNA in non-small cell lung cancer. Cancer Res, 2005, 65(4), 1479-1488. |
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| 溶解性： | Soluble in DMSO、Ethanol | ||||||||||||||||||||
| 保存条件： | -20℃ | ||||||||||||||||||||
| 配置溶液浓度参考： |
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| 注意： | 部分产品我司仅能提供部分信息，我司不保证所提供信息的权威性，仅供客户参考交流研究之用。 |
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营业执照(三证合一)
北京