2-cyanotricyclo[3.3.1.1^3,7]decane-1-carboxylic acid | 1581695-79-5

• 分子结构分类: 有机化合物 - 有机酸及其衍生物 - 羧酸及其衍生物
• 英文名称: 2-cyanotricyclo[3.3.1.1^3,7]decane-1-carboxylic acid
• 英文别名: 2-cyanoadamantane-1-carboxylate；2-Cyanoadamantane-1-carboxylic acid
• CAS: 1581695-79-5
• 化学式: C₁₂H₁₅NO₂
• 分子量: 205.257
• InChiKey: PUVRDKAGEWYCNQ-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1.7
• 重原子数：
  15
• 可旋转键数：
  1
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.83
• 拓扑面积：
  61.1
• 氢给体数：
  1
• 氢受体数：
  3

反应信息

• 作为反应物：
  描述：

  2-cyanotricyclo[3.3.1.1^3,7]decane-1-carboxylic acid 在 盐酸 、 platinum(IV) oxide 、 氢气 作用下， 以 乙醇 为溶剂， 25.0 ℃ 、344.75 kPa 条件下， 反应 5.0h， 以100%的产率得到2-aminomethyl-1-tricyclo[3.3.1.1^1,7]decanecarboxylic acid hydrochloride
  参考文献：
  名称：

  Anti-allodynic effect of 2-(aminomethyl)adamantane-1-carboxylic acid in a rat model of neuropathic pain: A mechanism dependent on CaV2.2 channel inhibition

  摘要：

  Neuropathic pain is a serious physical disabling condition resulting from lesion or dysfunction of the peripheral sensory nervous system. Despite the fact that the mechanisms underlying neuropathic pain are poorly understood, the involvement of voltage-gated calcium (Ca-V) channels in its pathophysiology has justified the use of drugs that bind the Ca-V channel alpha(2)delta auxiliary subunit, such as gabapentin (GBP), to attain analgesic and anti-allodynic effects in models involving neuronal sensitization and nerve injury. GBP binding to alpha(2)delta inhibits nerve injury-induced trafficking of the alpha(1) pore forming subunits of Ca-V channels, particularly of the N-type, from the cytoplasm to the plasma membrane of pre-synaptic terminals in dorsal root ganglion neurons and dorsal horn spinal neurons. In the search for alternative forms of treatment, in this study we describe the synthesis and pharmacological profile of a GABA derivative, 2-aminoadamantane-1-carboxylic acid (GZ4), which displays a close structure-activity relationship with GBP. Behavioral assessment using von Frey filament stimuli showed that GZ4 treatment reverted mechanical allodynia/hyperalgesia in an animal model of spinal nerve ligation-induced neuropathic pain. In addition, using the patch clamp technique we show that GZ4 treatment significantly decreased whole-cell currents through N-type Ca-V channels heterologously expressed in HEK-293 cells. Interestingly, the behavioral and electrophysiological time course of GZ4 actions reflects that its mechanism of action is similar but not identical to that of GBP. While GBP actions require at least 24 h and imply uptake of the drug, which suggests that the drug acts mainly intracellularly affecting channels trafficking to the plasma membrane, the faster time course (1-3 h) of GZ4 effects suggests also a direct inhibition of Ca2+ currents acting on cell surface channels. (C) 2014 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmc.2014.02.006
• 作为产物：
  描述：

  ethyl 2-cyanotricyclo[3.3.1.1^3,7]decane-1-carboxylate 在 potassium hydroxide 作用下， 以 乙醇 、 水 为溶剂， 反应 70.0h， 以95%的产率得到2-cyanotricyclo[3.3.1.1^3,7]decane-1-carboxylic acid
  参考文献：
  名称：

  邻苯二甲酰亚胺活化的金刚烷氨基酸的光脱羧

  摘要：

  合成了由邻苯二甲酰亚胺（即 3-6）活化的金刚烷 α-、β-和 δ-氨基酸，并研究了它们的光化学反应性。氨基酸衍生物 3-6 经历了光诱导电子转移 (PET) 和脱羧反应序列，最有可能是通过三重激发态。β-氨基酸衍生物的脱羧通过环化反应成功，提供了具有潜在生物学意义的复杂多环分子。光诱导脱羧产生的金刚烷基自由基可以被烯烃或氧捕获，分别传递加合物或醇。在丙酮敏化条件下（量子产率，Φ = 0.02-0.5），光脱羧过程比直接激发更有效，并且反应性取决于衍生物的电子供体（羧酸盐）和受体（三重激发态的邻苯二甲酰亚胺）之间的链长（分子内距离）。不同自由基的形成，即 1- 或 2-金刚烷基中间体，可能不会影响脱羧的整体速率本报告提供了对光脱羧的更好理解和分子系统的合理设计以进行光诱导脱羧和环化反应。

  DOI：

  10.1002/ejoc.201600491

文献信息

• ADAMANTYL-ACETAMIDE DERIVATIVES AS INHIBITORS OF THE 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE 1 ENZYME
  申请人：ABBOTT LABORATORIES

  公开号：EP1751108A1

  公开（公告）日：2007-02-14
• [EN] ADAMANTYL-ACETAMIDE DERIVATIVES AS INHIBITORS OF THE 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE 1 ENZYME<br/>[FR] DERIVES D'ADAMANTYL-ACETAMIDE EN TANT QU'INHIBITEURS DE L'ENZYME DE TYPE 1 DE LA 11-BETA-HYDROXYSTEROIDE DESHYDROGENASE
  申请人：ABBOTT LAB

  公开号：WO2005108368A1

  公开（公告）日：2005-11-17

  The present invention relates to compounds which are inhibitors of the 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme. The present invention further relates to the use of inhibitors of 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme for the treatment of non-insulin dependent type 2 diabetes, insulin resistance, obesity, lipid disorders, metabolic syndrome, and other diseases and conditions that are mediated by excessive glucocorticoid action.