N-(1-(3-(5-methyl-1H-imidazol-1-yl)propylamino)-2-nitrovinyl)-4-chlorobenzenamine | 1072452-21-1

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 英文名称: N-(1-(3-(5-methyl-1H-imidazol-1-yl)propylamino)-2-nitrovinyl)-4-chlorobenzenamine
• 英文别名: 1-N'-(4-chlorophenyl)-1-N-[3-(5-methylimidazol-1-yl)propyl]-2-nitroethene-1,1-diamine
• CAS: 1072452-21-1
• 化学式: C₁₅H₁₈ClN₅O₂
• 分子量: 335.793
• InChiKey: IQWGGJDJNCSIRV-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.7
• 重原子数：
  23
• 可旋转键数：
  7
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.27
• 拓扑面积：
  87.7
• 氢给体数：
  2
• 氢受体数：
  5

反应信息

• 作为产物：
  描述：

  3-(5-methyl-1H-imidazol-1-yl)propan-1-amine 、 1-(p-Chloranilino)-1-methylmercapto-2-nitroaethen 以 乙醇 为溶剂， 反应 24.0h， 以0.31 g的产率得到N-(1-(3-(5-methyl-1H-imidazol-1-yl)propylamino)-2-nitrovinyl)-4-chlorobenzenamine
  参考文献：
  名称：

  Inhibitors for Human Glutaminyl Cyclase by Structure Based Design and Bioisosteric Replacement

  摘要：

  The inhibition of human glutaminyl cyclase (hQC) has come into focus as a new potential approach for the treatment of Alzheimer's disease. The hallmark of this principle is the prevention of the formation of A beta(3,11(pE)-40,42), as these A beta-species were shown to be of elevated neurotoxicity and likely to act as a seeding core leading to an accelerated formation of A beta-oligomers and fibrils. Starting from 1-(3-(1H-imidazol-1-yl)propyl)-3-(3,4-dimethoxyphenyl)thiourea, bioisosteric replacements led to the development of new classes of inhibitors. The optimization of the metal-binding group was achieved by homology modeling and afforded a first insight into the probable binding mode of the inhibitors in the hQC active site. The efficacy assessment of the hQC inhibitors was performed in cell culture, directly monitoring the inhibition of A beta(3,11(pE)-40,42) formation.

  DOI：

  10.1021/jm900969p

文献信息

• Inhibitors for Human Glutaminyl Cyclase by Structure Based Design and Bioisosteric Replacement
  作者：Mirko Buchholz、Antje Hamann、Susanne Aust、Wolfgang Brandt、Livia Böhme、Torsten Hoffmann、Stephan Schilling、Hans-Ulrich Demuth、Ulrich Heiser

  DOI：10.1021/jm900969p

  日期：2009.11.26

  The inhibition of human glutaminyl cyclase (hQC) has come into focus as a new potential approach for the treatment of Alzheimer's disease. The hallmark of this principle is the prevention of the formation of A beta(3,11(pE)-40,42), as these A beta-species were shown to be of elevated neurotoxicity and likely to act as a seeding core leading to an accelerated formation of A beta-oligomers and fibrils. Starting from 1-(3-(1H-imidazol-1-yl)propyl)-3-(3,4-dimethoxyphenyl)thiourea, bioisosteric replacements led to the development of new classes of inhibitors. The optimization of the metal-binding group was achieved by homology modeling and afforded a first insight into the probable binding mode of the inhibitors in the hQC active site. The efficacy assessment of the hQC inhibitors was performed in cell culture, directly monitoring the inhibition of A beta(3,11(pE)-40,42) formation.