5-(chloromethyl)-2-(3,4-dimethoxyphenyl)-1H-imidazole | 160511-31-9

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 唑类
• 英文名称: 5-(chloromethyl)-2-(3,4-dimethoxyphenyl)-1H-imidazole
• CAS: 160511-31-9
• 化学式: C₁₂H₁₃ClN₂O₂
• 分子量: 252.7
• InChiKey: YTSRBXOBYQJAFQ-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.1
• 重原子数：
  17
• 可旋转键数：
  4
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.25
• 拓扑面积：
  47.1
• 氢给体数：
  1
• 氢受体数：
  3

反应信息

• 作为反应物：
  描述：

  5-(chloromethyl)-2-(3,4-dimethoxyphenyl)-1H-imidazole 在 氢溴酸 、 sodium ethanolate 作用下， 反应 76.25h， 生成 2-Amino-3-[2-(3,4-dihydroxy-phenyl)-1H-imidazol-4-yl]-propionic acid; hydrobromide
  参考文献：
  名称：

  Synthesis and preliminary evaluation of hydroquinone-substituted histidine derivatives as putative histaminergic neurotoxins

  摘要：

  A series of hydroquinone-substituted histidine derivatives were synthesized as potential histaminergic neurotoxins. The compounds undergo autoxidation at physiologic pH as exemplified by 2-amino-3-[2-4,5,-trihydroxyphenyl)imidazo-4-yl]propionic acid 11. One of the synthesized histidine derivatives, namely 2-amino-3-[2-(2,3-dihydroxyphenyl)imidazo-4-yl]propionic acid 8, was tested for its degenerating effect on histaminergic, dopaminergic and serotonergic neurons in rat brain. After 4 d of an unilateral injection of 1 mu l 3 mM 8 in 0.1 M phosphate buffer (pH 7.4) into the posterior hypothalamus, a decrease in immunoreactivity in the presumable histaminergic neurons was observed whilst dopaminergic and serotonergic neuronal elements were little affected. A possible mechanism of action is discussed.

  DOI：

  10.1016/0223-5234(94)90142-2
• 作为产物：
  描述：

  2-(3,4-dimethoxyphenyl)-1H-imidazole-4-methanol 在 氯化亚砜 作用下， 反应 0.17h， 生成 5-(chloromethyl)-2-(3,4-dimethoxyphenyl)-1H-imidazole
  参考文献：
  名称：

  2-Phenyl-4-(aminomethyl)imidazoles as Potential Antipsychotic Agents. Synthesis and Dopamine D2 Receptor Binding

  摘要：

  A series of 2-phenyl-4-(aminomethyl)imidazoles were designed as conformationally restricted analogs of the dopamine D-2 selective benzamide antipsychotics. The title compounds were synthesized and tested for blockade of[H-3]YM-09151 binding in cloned African green monkey dopamine D-2 receptor preparations. The binding affinity data thus obtained were compared against that of the benzamides and a previously described series of 2-phenyl-5-(aminomethyl)-pyrroles.

  DOI：

  10.1021/jm00012a026

文献信息

• 2-Phenyl-4-(aminomethyl)imidazoles as Potential Antipsychotic Agents. Synthesis and Dopamine D2 Receptor Binding
  作者：Andrew Thurkauf、Alan Hutchison、John Peterson、Linda Cornfield、Robin Meade、Kevin Huston、Kristine Harris、Philip C. Ross、Karen Gerber、T. V. Ramabhadran

  DOI：10.1021/jm00012a026

  日期：1995.6

  A series of 2-phenyl-4-(aminomethyl)imidazoles were designed as conformationally restricted analogs of the dopamine D-2 selective benzamide antipsychotics. The title compounds were synthesized and tested for blockade of[H-3]YM-09151 binding in cloned African green monkey dopamine D-2 receptor preparations. The binding affinity data thus obtained were compared against that of the benzamides and a previously described series of 2-phenyl-5-(aminomethyl)-pyrroles.
• Synthesis and preliminary evaluation of hydroquinone-substituted histidine derivatives as putative histaminergic neurotoxins
  作者：MQ Zhang、HWM Steinbusch、PJ Kooij、H Timmerman

  DOI：10.1016/0223-5234(94)90142-2

  日期：1994.1

  A series of hydroquinone-substituted histidine derivatives were synthesized as potential histaminergic neurotoxins. The compounds undergo autoxidation at physiologic pH as exemplified by 2-amino-3-[2-4,5,-trihydroxyphenyl)imidazo-4-yl]propionic acid 11. One of the synthesized histidine derivatives, namely 2-amino-3-[2-(2,3-dihydroxyphenyl)imidazo-4-yl]propionic acid 8, was tested for its degenerating effect on histaminergic, dopaminergic and serotonergic neurons in rat brain. After 4 d of an unilateral injection of 1 mu l 3 mM 8 in 0.1 M phosphate buffer (pH 7.4) into the posterior hypothalamus, a decrease in immunoreactivity in the presumable histaminergic neurons was observed whilst dopaminergic and serotonergic neuronal elements were little affected. A possible mechanism of action is discussed.