956905-27-4

• 常用中文名：2-[4-[1-(喹啉-6-甲基)-1H-[1,2,3]三唑并[4,5-B]吡嗪-6-基]-1H-吡唑-1-基]乙醇
• 常用英文名：PF-04217903
• CAS号：956905-27-4
• 分子式：C₁₉H₁₆N₈O
• 分子量：372.383
• 相关类别： 生物化工 抑制剂 蛋白酪氨酸激酶
• 发布时间：2016-07-19 17:45:05
• 更新时间：2026-07-16 13:14:06
• PF-04217903是ATP竞争性c-Met抑制剂,IC50为4.8 nM,对突变型Y1230C无活性。

名称

• 中文名: 2-[4-[1-(喹啉-6-甲基)-1H-[1,2,3]三唑并[4,5-B]吡嗪-6-基]-1H-吡唑-1-基]乙醇
• 英文名: 2-{4-[1-(6-Quinolinylmethyl)-1H-[1,2,3]triazolo[4,5-b]pyrazin-6-yl]-1H-pyrazol-1-yl}ethanol
• 中文别名: 2-[4-[1-(喹啉-6-甲基)-1H-[1,2,3]三唑并[4,5-B]吡嗪-6-基]-1H-吡唑-1-基]乙醇甲磺酸盐; PF-04217903 5mg 试剂; 2-(4-(1-(喹啉-6-基甲基)-1H-[1,2,3]三唑并[4,5-B]吡嗪-6-基)-1H-吡唑-1-基)乙醇; 2-[4-[1-(喹啉-6-基甲基)-1H-[1,2,3]三氮唑并[4,5-B]吡嗪-6-基]-1H-吡唑-1-基]乙醇
• 英文别名: 1H-Pyrazole-1-ethanol, 4-[1-(6-quinolinylmethyl)-1H-1,2,3-triazolo[4,5-b]pyrazin-6-yl]; 2-[4-[1-(Quinolin-6-ylmethyl)-1H-[1,2,3]triazolo[4,5-b]pyrazin-6-yl]-1H-pyrazol-1-yl]ethanol PF; 2-[4-[1-(Quinolin-6-ylmethyl)-1H-[1,2,3]triazolo[4,5-b]pyrazin-6-yl]-1H-pyrazol-1-yl]ethanol; PD04217903; 4-[1-(Quinolin-6-ylmethyl)-1H-1,2,3-triazolo[4,5-b]pyrazin-6-yl]pyrazol-1-ethanol; PF 04217903 2-[4-[1-(Quinolin-6-ylmethyl)-1H-[1,2,3]triazolo[4,5-b]pyrazin-6-yl]-1H-pyrazol-1-yl]ethanol; PF-04217903;PF; PF-04217903, 10 mM in DMSO; 2-(4-(3-(quinolin-6-ylmethyl)-3H-[1,2,3]triazolo[4,5-b]pyrazin-5-yl)-1H-pyrazol-1-yl)ethanol; PF-04217903cas; PD04217903 //BP; PF04217903; 2-{4-[1-(6-Quinolinylmethyl)-1H-[1,2,3]triazolo[4,5-b]pyrazin-6-y l]-1H-pyrazol-1-yl}ethanol; 2-[4-[3-(quinolin-6-ylmethyl)triazolo[4,5-b]pyrazin-5-yl]pyrazol-1-yl]ethanol

物化性质

• 密度: 1.5±0.1 g/cm3
• 沸点: 718.1±60.0 °C at 760 mmHg
• 分子式: C₁₉H₁₆N₈O
• 分子量: 372.383
• 闪点: 388.1±32.9 °C
• 精确质量: 372.144714
• PSA: 107.43000
• LogP: 0.30
• 蒸汽压: 0.0±2.4 mmHg at 25°C
• 折射率: 1.807
• 储存条件: -20°C

生物活性

• 描述: PF-04217903是ATP竞争性c-Met抑制剂,IC50为4.8 nM,对突变型Y1230C无活性。
• 相关类别:
  信号通路 >> 蛋白酪氨酸激酶 >> c-Met的/HGFR
  研究领域 >> 癌症
• 参考文献:

  [1]. Timofeevski SL, et al. Enzymatic characterization of c-Met receptor tyrosine kinase oncogenic mutants and kinetic studies with aminopyridine and triazolopyrazine inhibitors. Biochemistry, 2009, 48(23), 5339-5349.

  [2]. Shojaei F, et al. HGF/c-Met acts as an alternative angiogenic pathway in sunitinib-resistant tumors. Cancer Res, 2010, 70(24), 10090-10100.

  [3]. Krumbach R, et al. Primary resistance to cetuximab in a panel of patient-derived tumour xenograft models: activation of MET as one mechanism for drug resistance. Eur J Cancer, 2011, 47(8), 1231-1243.