2-(5-(benzyloxy)-1H-indol-3-yl)-N-(4-hydroxyphenethyl)acetamide | 1173289-36-5

• 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: 2-(5-(benzyloxy)-1H-indol-3-yl)-N-(4-hydroxyphenethyl)acetamide
• 英文别名: N-[2-(4-hydroxyphenyl)ethyl]-2-(5-phenylmethoxy-1H-indol-3-yl)acetamide
• CAS: 1173289-36-5
• 化学式: C₂₅H₂₄N₂O₃
• 分子量: 400.477
• InChiKey: BORGBWPZDHQNBM-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.3
• 重原子数：
  30
• 可旋转键数：
  8
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.16
• 拓扑面积：
  74.4
• 氢给体数：
  3
• 氢受体数：
  3

反应信息

• 作为产物：
  描述：

  对羟基苯乙胺 、 5-苄氧基吲哚-3-乙酸 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 24.5h， 生成 2-(5-(benzyloxy)-1H-indol-3-yl)-N-(4-hydroxyphenethyl)acetamide
  参考文献：
  名称：

  Structure−Activity Relationships and Cancer-Cell Selective Toxicity of Novel Inhibitors of Glioma-Associated Oncogene Homologue 1 (Gli1) Mediated Transcription

  摘要：

  We report novel inhibitors of Gli1-mediated transcription as potential anticancer agents. Focused chemical libraries were designed and assessed for inhibition of functional cell-based Gli1-mediated transcription and selective toxicity toward cancer cells. The SAR was revealed, and the selectivity of the lead compounds' inhibition of Gli1-mediated transcription over that of Gli2 was determined. Compound 63 (NMDA298-1), which inhibited Gli1-mediated transcription in C3H10T1/2 cells with all IC50 of 6.9 mu M, showed 3-fold selectivity for inhibiting transcription mediated by Gli1 over that by Gli2. Cell-viability assays were performed to evaluate the chemical library in a normal cell line and a panel of cancer cell lines with or without up-regulated expression of the Gli1 gene. These compounds decreased the viability of several cancer cell lines but were less active in the noncancerous BJ-hTERT cells.

  DOI：

  10.1021/jm900106f

文献信息

• Structure−Activity Relationships and Cancer-Cell Selective Toxicity of Novel Inhibitors of Glioma-Associated Oncogene Homologue 1 (Gli1) Mediated Transcription
  作者：Neeraj Mahindroo、Michele C. Connelly、Chandanamali Punchihewa、Hiromichi Kimura、Matthew P. Smeltzer、Song Wu、Naoaki Fujii

  DOI：10.1021/jm900106f

  日期：2009.7.23

  We report novel inhibitors of Gli1-mediated transcription as potential anticancer agents. Focused chemical libraries were designed and assessed for inhibition of functional cell-based Gli1-mediated transcription and selective toxicity toward cancer cells. The SAR was revealed, and the selectivity of the lead compounds' inhibition of Gli1-mediated transcription over that of Gli2 was determined. Compound 63 (NMDA298-1), which inhibited Gli1-mediated transcription in C3H10T1/2 cells with all IC50 of 6.9 mu M, showed 3-fold selectivity for inhibiting transcription mediated by Gli1 over that by Gli2. Cell-viability assays were performed to evaluate the chemical library in a normal cell line and a panel of cancer cell lines with or without up-regulated expression of the Gli1 gene. These compounds decreased the viability of several cancer cell lines but were less active in the noncancerous BJ-hTERT cells.