phenyl(1-(4-(p-tolyl)butyl)piperidin-4-yl)methanone | 1190882-56-4

• 英文名称: phenyl(1-(4-(p-tolyl)butyl)piperidin-4-yl)methanone
• CAS: 1190882-56-4
• 化学式: C₂₃H₂₉NO
• 分子量: 335.489
• InChiKey: YKORQZWRDWEONG-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.91
• 重原子数：
  25.0
• 可旋转键数：
  7.0
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.43
• 拓扑面积：
  20.31
• 氢给体数：
  0.0
• 氢受体数：
  2.0

反应信息

• 作为反应物：
  描述：

  phenyl(1-(4-(p-tolyl)butyl)piperidin-4-yl)methanone 在 sodium tetrahydroborate 作用下， 以 甲醇 、 二氯甲烷 为溶剂， 以12%的产率得到phenyl-[1-(4-p-tolyl-butyl)-piperidin-4-yl]-methanol
  参考文献：
  名称：

  Structural determinants for histamine H1 affinity, hERG affinity and QTc prolongation in a series of terfenadine analogs

  摘要：

  In the late 1980's reports linking the non-sedating antihistamines terfenadine and astemizole with torsades de pointes, a form of ventricular tachyarrhythmia that can degenerate into ventricular fibrillation and sudden death, appeared in the clinical literature. A substantial body of evidence demonstrates that the arrhythmogenic effect of these cardiotoxic antihistamines, as well as a number of structurally related compounds, results from prolongation of the QT interval due to suppression of specific delayed rectifier ventricular K+ currents via blockade of the hERG-IKr channel. In order to better understand the structural requirements for hERG and H-1 binding for terfenadine, a series of analogs of terfenadine has been prepared and studied in both in vitro and in vivo hERG and H-1 assays. (C) 2009 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2009.07.047
• 作为产物：
  描述：

  4-苯甲酰基哌啶盐酸盐 、 1-(4-bromobutyl)-4-methylbenzene 在 potassium carbonate 、 N,N-二异丙基乙胺 作用下， 以 乙腈 为溶剂， 反应 6.5h， 以43%的产率得到phenyl(1-(4-(p-tolyl)butyl)piperidin-4-yl)methanone
  参考文献：
  名称：

  Structural determinants for histamine H1 affinity, hERG affinity and QTc prolongation in a series of terfenadine analogs

  摘要：

  In the late 1980's reports linking the non-sedating antihistamines terfenadine and astemizole with torsades de pointes, a form of ventricular tachyarrhythmia that can degenerate into ventricular fibrillation and sudden death, appeared in the clinical literature. A substantial body of evidence demonstrates that the arrhythmogenic effect of these cardiotoxic antihistamines, as well as a number of structurally related compounds, results from prolongation of the QT interval due to suppression of specific delayed rectifier ventricular K+ currents via blockade of the hERG-IKr channel. In order to better understand the structural requirements for hERG and H-1 binding for terfenadine, a series of analogs of terfenadine has been prepared and studied in both in vitro and in vivo hERG and H-1 assays. (C) 2009 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2009.07.047