2-(trimethylsilyl)ethyl 2-(4-isobutylphenyl)propanoate | 1224508-97-7

• 分子结构分类: 有机化合物 - 脂质和类脂质分子 - 异戊烯醇脂质
• 英文名称: 2-(trimethylsilyl)ethyl 2-(4-isobutylphenyl)propanoate
• 英文别名: 2-trimethylsilylethyl 2-[4-(2-methylpropyl)phenyl]propanoate
• CAS: 1224508-97-7
• 化学式: C₁₈H₃₀O₂Si
• 分子量: 306.521
• InChiKey: RPLWYFHASHPJRJ-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.87
• 重原子数：
  21
• 可旋转键数：
  8
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.61
• 拓扑面积：
  26.3
• 氢给体数：
  0
• 氢受体数：
  2

反应信息

• 作为产物：
  描述：

  2-(三甲硅基)乙醇 、 布洛芬 在 4-二甲氨基吡啶 、 盐酸-N-乙基-Nˊ-(3-二甲氨基丙基)碳二亚胺 作用下， 以 二氯甲烷 为溶剂， 以65%的产率得到2-(trimethylsilyl)ethyl 2-(4-isobutylphenyl)propanoate
  参考文献：
  名称：

  Peripheral site acetylcholinesterase inhibitors targeting both inflammation and cholinergic dysfunction

  摘要：

  The design and study of two classes of noncompetitive acetylcholinesterase inhibitors (AChEIs) which also function as NSAID prodrugs are reported. The most potent AChEIs disclosed contain an aromatic alkyl-aryl linker between an NSAID and a lipophilic choline mimic and they inhibit acetylcholinesterase (AChE) in the submicromolar range. These agents have the therapeutic potential to dually target inflammation by releasing an NSAID in vivo and activating the cholinergic anti-inflammatory pathway via cholinergic up-regulation. (C) 2010 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2010.02.102

文献信息

• Peripheral site acetylcholinesterase inhibitors targeting both inflammation and cholinergic dysfunction
  作者：Sherri Young、Karine Fabio、Christophe Guillon、Pramod Mohanta、Timothy A. Halton、Diane E. Heck、Robert A. Flowers、Jeffrey D. Laskin、Ned D. Heindel

  DOI：10.1016/j.bmcl.2010.02.102

  日期：2010.5

  The design and study of two classes of noncompetitive acetylcholinesterase inhibitors (AChEIs) which also function as NSAID prodrugs are reported. The most potent AChEIs disclosed contain an aromatic alkyl-aryl linker between an NSAID and a lipophilic choline mimic and they inhibit acetylcholinesterase (AChE) in the submicromolar range. These agents have the therapeutic potential to dually target inflammation by releasing an NSAID in vivo and activating the cholinergic anti-inflammatory pathway via cholinergic up-regulation. (C) 2010 Elsevier Ltd. All rights reserved.