bicyclopentyl-1,1'-dicarboxylic acid | 107153-69-5

• 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: bicyclopentyl-1,1'-dicarboxylic acid
• 英文别名: Bicyclopentyl-1,1'-dicarbonsaeure；1-(1-Carboxycyclopentyl)cyclopentane-1-carboxylic acid
• CAS: 107153-69-5
• 化学式: C₁₂H₁₈O₄
• 分子量: 226.273
• InChiKey: JBFGDGLLTJAJAT-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.1
• 重原子数：
  16
• 可旋转键数：
  3
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.83
• 拓扑面积：
  74.6
• 氢给体数：
  2
• 氢受体数：
  4

反应信息

• 作为反应物：
  描述：

  bicyclopentyl-1,1'-dicarboxylic acid 在 乙酸酐 作用下， 生成 bicyclopentyl-1,1'-dicarboxylic acid-anhydride
  参考文献：
  名称：

  AZO COMPOUNDS. XVII.¹ SYNTHESIS OF UNSYMMETRICAL SPIROANHYDRIDES

  摘要：

  DOI：

  10.1021/jo01364a018
• 作为产物：
  描述：

  1,1'-dicyanobicyclopentyl 在 硫酸 作用下， 生成 bicyclopentyl-1,1'-dicarboxylic acid
  参考文献：
  名称：

  AZO COMPOUNDS. XVII.¹ SYNTHESIS OF UNSYMMETRICAL SPIROANHYDRIDES

  摘要：

  DOI：

  10.1021/jo01364a018

文献信息

• Oxidative coupling of carboxylic acid dianions
  作者：J.L. Belletire、E.G. Spletzer、A.R. Pinhas

  DOI：10.1016/s0040-4039(01)81735-4

  日期：1984.1

  The conditions, scope, and stereochemical consequences of a versatile approach to succinic acid derivatives are described.

  描述了一种通用方法制备琥珀酸衍生物的条件，范围和立体化学结果。
• [EN] BICYCLO[1.1.1]PENTANE INHIBITORS OF DUAL LEUCINE ZIPPER (DLK) KINASE FOR THE TREATMENT OF DISEASE<br/>[FR] INHIBITEURS BICYCLO[1.1.1]PENTANE DE LA DOUBLE FERMETURE À GLISSIÈRE DE LEUCINE KINASE (DLK) DESTINÉS AU TRAITEMENT DE MALADIE
  申请人：UNIV TEXAS

  公开号：WO2021081074A1

  公开（公告）日：2021-04-29

  Disclosed herein are compounds which inhibit the kinase activity of dual leucine zipper (DLK) kinase (MAP3K12), pharmaceutical compositions, and methods of treatment of DLK-mediated diseases, such as neurological diseases that result from traumatic injury to central nervous system and peripheral nervous system neurons (e.g. stroke, traumatic brain injury, spinal cord injury), or that result from a chronic neurodegenerative condition (e.g. Alzheimer's disease, frontotemporal dementia, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, spinocerebellar ataxia, progressive supranuclear palsy, Lewy body disease, Kennedy's disease, and other related conditions), from neuropathies resulting from neurological damage (chemotherapy-induced peripheral neuropathy, diabetic neuropathy, and related conditions) and from cognitive disorders caused by pharmacological intervention (e.g. chemotherapy induced cognitive disorder, also known as chemobrain).

  本文披露了一种抑制双亮氨酸拉链（DLK）激酶（MAP3K12）激酶活性的化合物，以及用于治疗DLK介导的疾病的药物组合物和方法，例如由中枢神经系统和外周神经系统神经元的创伤性损伤导致的神经疾病（例如中风、创伤性脑损伤、脊髓损伤），或由慢性神经退行性疾病导致的疾病（例如阿尔茨海默病、额颞叶痴呆、帕金森病、亨廷顿病、肌萎缩性侧索硬化、脊髓小脑共济失调、进行性上视神经麻痹、Lewy小体病、肯尼迪病和其他相关疾病），以及由神经损伤引起的神经病（化疗引起的周围神经病、糖尿病性神经病和相关疾病）和由药物干预引起的认知障碍（例如化疗引起的认知障碍，也称为化疗脑）。
• BICYCLO[1.1.1]PENTANE INHIBITORS OF DUAL LEUCINE ZIPPER (DLK) KINASE FOR THE TREATMENT OF DISEASE
  申请人：Board of Regents, The University of Texas System

  公开号：US20210115010A1

  公开（公告）日：2021-04-22

  Disclosed herein are compounds which inhibit the kinase activity of dual leucine zipper (DLK) kinase (MAP3K12), pharmaceutical compositions, and methods of treatment of DLK-mediated diseases, such as neurological diseases that result from traumatic injury to central nervous system and peripheral nervous system neurons (e.g. stroke, traumatic brain injury, spinal cord injury), or that result from a chronic neurodegenerative condition (e.g. Alzheimer's disease, frontotemporal dementia, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, spinocerebellar ataxia, progressive supranuclear palsy, Lewy body disease, Kennedy's disease, and other related conditions), from neuropathies resulting from neurological damage (chemotherapy-induced peripheral neuropathy, diabetic neuropathy, and related conditions) and from cognitive disorders caused by pharmacological intervention (e.g. chemotherapy induced cognitive disorder, also known as chemobrain).

  本公开的是抑制双亮氨酸拉链（DLK）激酶（MAP3K12）激酶活性的化合物，以及治疗DLK介导的疾病的药物组合物和方法，如由中枢神经系统和外周神经系统神经元遭受创伤性损伤导致的神经系统疾病（例如中风、创伤性脑损伤、脊髓损伤），或由慢性神经退行性病变引起的神经系统疾病（例如阿尔茨海默病、额颞叶痴呆症、帕金森病、亨廷顿病、肌萎缩侧索硬化、脊髓小脑共济失调、进行性上行性麻痹、Lewy小体病、肯尼迪病等及其他相关疾病），以及由神经损伤引起的神经病（化疗诱导的周围神经病、糖尿病神经病变等）和由药物干预引起的认知障碍（例如化疗诱导的认知障碍，也称为化疗脑）。
• Conformational Effects and Hydrogen Bonding in 1,4-Diols
  作者：Lester P. Kuhn、Paul. Von R. Schleyer、William F. Baitinger、Lennart. Eberson

  DOI：10.1021/ja01058a022

  日期：1964.2
• Benzodiazepines and anterior pituitary function
  作者：E. Arvat、R. Giordano、S. Grottoli、E. Ghigo

  DOI：10.1007/bf03345110

  日期：2002.9

  Benzodiazepines (BDZ) are one of the most prescribed classes of drugs because of their marked anxiolytic, anticonvulsant, muscle relaxant and hypnotic effects. The pharmacological actions of BDZ depend on the activation of 2 specific receptors. The central BDZ receptor, present in several areas of the central nervous system (CNS), is a component of the GABA-A receptor, the activation of which increases GABAergic neurotransmission and is followed by remarkable neuroendocrine effects. The peripheral benzodiazepine receptors (PBR), structurally and functionally different from the GABA-A receptor, have been shown in peripheral tissues but also in the CNS, in both neurones and glial cells, and in the pituitary gland. BDZ receptors bind to a family of natural peptides called endozepines, firstly isolated from neurons and glial cells in the brain and then in several peripheral tissues as well. Endozelpines modulate several central and peripheral biological activities, including some neuroendocrine functions and synthetic BDZ are likely to mimic them, at least partially. BZD, especially alprazolam (AL), possess a clear inhibitory influence on the activity of the HPA axis in both animals and humans. This effect seems to be mediated at the hypothalamic and/or suprahypothalamic level via suppression of CRH. The strong negative influence of AL on hypothalamic-pituitary-adrenal (HPA) axis agrees with its peculiar efficacy in the treatment of panic disorders and depression. BZD have also been shown to increase GH secretion via mechanisms mediated at the hypothalamic or supra-hypothalamic level, though a pituitary action cannot be ruled out. Besides the impact on HPA and somatotrope function, BDZ also significantly affect the secretion of other pituitary hormones, such as gonadotropins and. PRL, probably acting through GABAergic mediation in the hypothalamus and/or in the pituitary gland. In all, BDZ are likely to represent a useful tool to investigate GABAergic activity and clarify its role in the neuroendocrine control of anterior pituitary function; their usefulness probably overrides what had been supposed before.