methyl 2-(cyclohexylcarbamoyl)-6-methyl-3-(2-phenylethyl)-1H-indole-5-carboxylate | 1015464-56-8

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 吲哚及其衍生物
• 英文名称: methyl 2-(cyclohexylcarbamoyl)-6-methyl-3-(2-phenylethyl)-1H-indole-5-carboxylate
• CAS: 1015464-56-8
• 化学式: C₂₆H₃₀N₂O₃
• 分子量: 418.536
• InChiKey: OGRLWZSAUWCART-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  5.9
• 重原子数：
  31
• 可旋转键数：
  7
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.38
• 拓扑面积：
  71.2
• 氢给体数：
  2
• 氢受体数：
  3

反应信息

• 作为反应物：
  描述：

  methyl 2-(cyclohexylcarbamoyl)-6-methyl-3-(2-phenylethyl)-1H-indole-5-carboxylate 在 sodium hydroxide 作用下， 以 1,4-二氧六环 、 甲醇 为溶剂， 反应 4.0h， 生成 2-(cyclohexylcarbamoyl)-6-methyl-3-(2-phenylethyl)-1H-indole-5-carboxylic acid
  参考文献：
  名称：

  Indole-2-amide based biochemical antagonist of Dishevelled PDZ domain interaction down-regulates Dishevelled-driven Tcf transcriptional activity

  摘要：

  We designed and synthesized a series of indole-2-amide-based compounds that antagonize interaction between the Dishevelled (Dvl) PDZ domain and a peptide derived from the natural PDZ ligand Frizzled-7 (Fz7). These compounds inhibit Tcf-mediated transcription activated by exogenous Dvl via the biochemical antagonism. We confirmed tumor cell-selective activation of caspases by these compounds. (C) 2007 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2007.12.039
• 作为产物：
  描述：

  5-(methoxycarbonyl)-6-methyl-3-phenethyl-1H-indole-2-carboxylic acid 、 环己胺 在 O-(1H-benzotriazol-1-yl)-N,N,N',N'-tetramethyluronium hexafluorophosphate 、 N,N-二异丙基乙胺 作用下， 以 N,N-二甲基甲酰胺 为溶剂， 反应 19.0h， 生成 methyl 2-(cyclohexylcarbamoyl)-6-methyl-3-(2-phenylethyl)-1H-indole-5-carboxylate
  参考文献：
  名称：

  Indole-2-amide based biochemical antagonist of Dishevelled PDZ domain interaction down-regulates Dishevelled-driven Tcf transcriptional activity

  摘要：

  We designed and synthesized a series of indole-2-amide-based compounds that antagonize interaction between the Dishevelled (Dvl) PDZ domain and a peptide derived from the natural PDZ ligand Frizzled-7 (Fz7). These compounds inhibit Tcf-mediated transcription activated by exogenous Dvl via the biochemical antagonism. We confirmed tumor cell-selective activation of caspases by these compounds. (C) 2007 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2007.12.039