4-(4-methyl-cyclohexyl)-butyric acid

• 分子结构分类: 有机化合物 - 脂质和类脂质分子 - 脂肪酰基
• 英文名称: 4-(4-methyl-cyclohexyl)-butyric acid
• 英文别名: 4-(4-Methyl-cyclohexyl)-buttersaeure；4-(4-methylcyclohexyl)butanoic Acid
• 化学式: C₁₁H₂₀O₂
• 分子量: 184.279
• InChiKey: BDRQJJVKWXGAKS-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.6
• 重原子数：
  13
• 可旋转键数：
  4
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.91
• 拓扑面积：
  37.3
• 氢给体数：
  1
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  α,α-二苯基-4-哌啶甲醇 、 4-(4-methyl-cyclohexyl)-butyric acid 在 苯甲酰三氟丙酮 、 2-二乙氨基氯乙烷盐酸盐 作用下， 以 二氯甲烷 为溶剂， 以3.22 g的产率得到
  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-对甲苯基丁酸 在 铂 作用下， 生成 4-(4-methyl-cyclohexyl)-butyric acid
  参考文献：
  名称：

  Fieser et al., Journal of the American Chemical Society, 1948, vol. 70, p. 3177

  摘要：

  DOI：

文献信息

• Fieser et al., Journal of the American Chemical Society, 1948, vol. 70, p. 3177
  作者：Fieser et al.

  DOI：——

  日期：——
• Structural determinants for histamine H1 affinity, hERG affinity and QTc prolongation in a series of terfenadine analogs
  作者：Robert Aslanian、John J. Piwinski、Xiaohong Zhu、Tony Priestley、Steve Sorota、Xiao-Yi Du、Xue-Song Zhang、Robbie L. McLeod、Robert E. West、Shirley M. Williams、John A. Hey

  DOI：10.1016/j.bmcl.2009.07.047

  日期：2009.9

  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.