5-(4-chlorophenyl)-1-(3-iodophenyl)-1H-pyrrol-2-yl acetate | 1191053-11-8

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 吡咯
• 英文名称: 5-(4-chlorophenyl)-1-(3-iodophenyl)-1H-pyrrol-2-yl acetate
• 英文别名: [5-(4-Chlorophenyl)-1-(3-iodophenyl)pyrrol-2-yl] acetate
• CAS: 1191053-11-8
• 化学式: C₁₈H₁₃ClINO₂
• 分子量: 437.664
• InChiKey: RGPCIUFDJKLSMZ-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  5.3
• 重原子数：
  23
• 可旋转键数：
  4
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.06
• 拓扑面积：
  31.2
• 氢给体数：
  0
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  5-(4-chlorophenyl)-1-(3-iodophenyl)-1H-pyrrol-2-yl acetate 、 5-(4-溴苯基)-2-呋喃甲醛 在 sodium acetate 、 乙酸酐 作用下， 以 甲醇 为溶剂， 反应 0.33h， 以34%的产率得到(3Z)-3-(4-nitrobenzylidene)-5-(4-chlorophenyl)-1-(3-iodophenyl)-1H-pyrrol-2(3H)-one
  参考文献：
  名称：

  Investigation of N-Aryl-3-alkylidenepyrrolinones as Potential Niemann−Pick Type C Disease Therapeutics

  摘要：

  A five-step synthesis of an array of N-aryl-3-alkylidenepyrrolinones, which are potential Niemann-Pick type C (NPC) disease therapeutics, is described. The synthetic route allows for the production of analogues, including photoaffinity and biotinylated derivatives. Compound 1a increased esterification by acyl-coenzyme A:cholesteryl acyltransferase in NPC1 mutant cells. It also decreased LDL uptake and increased cholesterol efflux in both NPC1-deficient and normal cells.

  DOI：

  10.1021/jm900707n
• 作为产物：
  描述：

  4-(4-chlorophenyl)-N-(3-iodophenyl)-4-oxobutanamide 、 乙酰氯 在 4-二甲氨基吡啶 作用下， 反应 15.0h， 以77%的产率得到5-(4-chlorophenyl)-1-(3-iodophenyl)-1H-pyrrol-2-yl acetate
  参考文献：
  名称：

  Investigation of N-Aryl-3-alkylidenepyrrolinones as Potential Niemann−Pick Type C Disease Therapeutics

  摘要：

  A five-step synthesis of an array of N-aryl-3-alkylidenepyrrolinones, which are potential Niemann-Pick type C (NPC) disease therapeutics, is described. The synthetic route allows for the production of analogues, including photoaffinity and biotinylated derivatives. Compound 1a increased esterification by acyl-coenzyme A:cholesteryl acyltransferase in NPC1 mutant cells. It also decreased LDL uptake and increased cholesterol efflux in both NPC1-deficient and normal cells.

  DOI：

  10.1021/jm900707n