2,3-bis(pyridin-2-yl)-6,7-dichloroquinoxaline-5,8-dihydro-5,8-dione | 862801-49-8

• 分子结构分类: 有机化合物 - 有机氧化合物
• 英文名称: 2,3-bis(pyridin-2-yl)-6,7-dichloroquinoxaline-5,8-dihydro-5,8-dione
• CAS: 862801-49-8
• 化学式: C₁₈H₈Cl₂N₄O₂
• 分子量: 383.193
• InChiKey: OPXXAGBZPGYTSE-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.67
• 重原子数：
  26.0
• 可旋转键数：
  2.0
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  85.7
• 氢给体数：
  0.0
• 氢受体数：
  6.0

反应信息

• 作为反应物：
  描述：

  2,3-bis(pyridin-2-yl)-6,7-dichloroquinoxaline-5,8-dihydro-5,8-dione 、 3,4,5-三氟苯胺 以 乙醇 为溶剂， 反应 5.0h， 生成 6-Chloro-2,3-dipyridin-2-yl-7-(3,4,5-trifluoroanilino)quinoxaline-5,8-dione
  参考文献：
  名称：

  Synthesis and biological evaluation of quinoxaline-5,8-diones that inhibit vascular smooth muscle cell proliferation

  摘要：

  A series of 6-arylamino-2,3-bis(pyridin-2-yl)-7-chloro-quinoxaline-5,8-diones were synthesized and evaluated for their inhibitory activity on rat aortic smooth muscle cell (RAoSMC) proliferation. The quinoxaline-5,8-diones exhibited a potent antiproliferative activity. Further mechanistic study revealed that the inhibitory effect of one representative quinoxaline-5,8-dione on SMC proliferation was mediated by modulation of the extracellular signal-regulated kinase 1/2 signaling pathway in the RAoSMCs. (c) 2005 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2005.05.022
• 作为产物：
  描述：

  二(2-吡啶基)乙二酮 在 盐酸 、 硝酸 作用下， 以 水 为溶剂， 反应 1.0h， 生成 2,3-bis(pyridin-2-yl)-6,7-dichloroquinoxaline-5,8-dihydro-5,8-dione
  参考文献：
  名称：

  Synthesis and biological evaluation of quinoxaline-5,8-diones that inhibit vascular smooth muscle cell proliferation

  摘要：

  A series of 6-arylamino-2,3-bis(pyridin-2-yl)-7-chloro-quinoxaline-5,8-diones were synthesized and evaluated for their inhibitory activity on rat aortic smooth muscle cell (RAoSMC) proliferation. The quinoxaline-5,8-diones exhibited a potent antiproliferative activity. Further mechanistic study revealed that the inhibitory effect of one representative quinoxaline-5,8-dione on SMC proliferation was mediated by modulation of the extracellular signal-regulated kinase 1/2 signaling pathway in the RAoSMCs. (c) 2005 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2005.05.022