1-Cyano-3-(2,3-dihydro-1,4-benzodioxin-6-yl)thiourea | 1195966-27-8

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 苯并二恶烷
• 英文名称: 1-Cyano-3-(2,3-dihydro-1,4-benzodioxin-6-yl)thiourea
• CAS: 1195966-27-8
• 化学式: C₁₀H₉N₃O₂S
• 分子量: 235.266
• InChiKey: AQWJKPUPDFTSBO-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1.8
• 重原子数：
  16
• 可旋转键数：
  1
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.2
• 拓扑面积：
  98.4
• 氢给体数：
  2
• 氢受体数：
  4

反应信息

• 作为反应物：
  描述：

  1-(3-氨基丙基)咪唑 、 1-Cyano-3-(2,3-dihydro-1,4-benzodioxin-6-yl)thiourea 在 盐酸-N-乙基-Nˊ-(3-二甲氨基丙基)碳二亚胺 作用下， 以 乙醇 为溶剂， 反应 3.0h， 以0.13 g的产率得到(3-(1H-Imidazol-1-yl)propyl)-2-cyano-3-(2,3-dihydrobenzo[b][1,4]dioxin-7-yl)guanidine
  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
• 作为产物：
  描述：

  sodium cyanamide 、 2,3-二氢-1,4-苯并二氧-6-基异硫氰酸酯 以 乙醇 为溶剂， 反应 3.0h， 生成 1-Cyano-3-(2,3-dihydro-1,4-benzodioxin-6-yl)thiourea
  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