4-benzyl-1-(3-chloro-2-pyridinyl)piperazine | 87394-58-9

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 二嗪烷类
• 英文名称: 4-benzyl-1-(3-chloro-2-pyridinyl)piperazine
• 英文别名: 1-Benzyl-4-(3-chloro-pyridin-2-yl)-piperazine；1-benzyl-4-(3-chloropyridin-2-yl)piperazine
• CAS: 87394-58-9
• 化学式: C₁₆H₁₈ClN₃
• 分子量: 287.792
• InChiKey: DXBCZLBBXQSAMW-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.2
• 重原子数：
  20
• 可旋转键数：
  3
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.312
• 拓扑面积：
  19.4
• 氢给体数：
  0
• 氢受体数：
  3

反应信息

• 作为产物：
  描述：

  2,3-二氯吡啶 在 三乙胺 作用下， 以 乙腈 、 正丁醇 为溶剂， 反应 78.0h， 生成 4-benzyl-1-(3-chloro-2-pyridinyl)piperazine
  参考文献：
  名称：

  Pyridinylpiperazines, a new class of selective .alpha.2-adrenoceptor antagonists

  摘要：

  A series of 1-(2-pyridinyl)piperazine derivatives was synthesized and evaluated for adrenergic activity. In vitro activity was assessed through the antagonism of clonidine's effect in the rat, isolated, field-stimulated vas deferens and by the displacement of [3H]clonidine from membrane binding sites of calf cerebral cortex. Antagonism of clonidine-induced mydriasis in the rat was used as an in vivo assay. Several members of the series proved to be potent, selective alpha 2-adrenoceptor antagonists. 1-(3-Fluoro-2-pyridinyl)piperazine was more potent than either yohimbine or rauwolscine in displacement of [3H]clonidine and had a higher affinity for this binding site (alpha 2) than for the [3H]prazosin site (alpha 1). In vivo, the 3-F derivative was more potent than the reference standards in reversing clonidine-induced mydriasis. None of the members of this series was more selective or potent than rauwolscine in antagonizing clonidine in the rat vas deferens.

  DOI：

  10.1021/jm00366a007

文献信息

• Pyridinylpiperazines, a new class of selective .alpha.2-adrenoceptor antagonists
  作者：Walfred S. Saari、Wasyl Halczenko、Stella W. King、Joel R. Huff、James P. Guare、Cecilia A. Hunt、William C. Randall、Paul S. Anderson、Victor J. Lotti

  DOI：10.1021/jm00366a007

  日期：1983.12

  A series of 1-(2-pyridinyl)piperazine derivatives was synthesized and evaluated for adrenergic activity. In vitro activity was assessed through the antagonism of clonidine's effect in the rat, isolated, field-stimulated vas deferens and by the displacement of [3H]clonidine from membrane binding sites of calf cerebral cortex. Antagonism of clonidine-induced mydriasis in the rat was used as an in vivo assay. Several members of the series proved to be potent, selective alpha 2-adrenoceptor antagonists. 1-(3-Fluoro-2-pyridinyl)piperazine was more potent than either yohimbine or rauwolscine in displacement of [3H]clonidine and had a higher affinity for this binding site (alpha 2) than for the [3H]prazosin site (alpha 1). In vivo, the 3-F derivative was more potent than the reference standards in reversing clonidine-induced mydriasis. None of the members of this series was more selective or potent than rauwolscine in antagonizing clonidine in the rat vas deferens.