1-甲基-5-丙基-1H-吡唑-4-甲酰氯 | 706819-89-8

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 唑类
• 中文名称: 1-甲基-5-丙基-1H-吡唑-4-甲酰氯
• 英文名称: 1-Methyl-5-propyl-1H-pyrazole-4-carbonyl chloride
• 英文别名: 1-methyl-5-propylpyrazole-4-carbonyl chloride
• CAS: 706819-89-8
• 化学式: C₈H₁₁ClN₂O
• 分子量: 186.641
• InChiKey: UMHWOKHANGEIJP-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1.9
• 重原子数：
  12
• 可旋转键数：
  3
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.5
• 拓扑面积：
  34.9
• 氢给体数：
  0
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  1-甲基-5-丙基-1H-吡唑-4-甲酰氯 在 三甲基铝 、 氯化铵 作用下， 以 丙酮 、 甲苯 为溶剂， 反应 9.0h， 生成 4-[4-(1-methyl-5-propyl-1H-pyrazol-4-yl)-thiazol-2-yl]-5-methylsulfanyl-thiophene-2-carboxamidine
  参考文献：
  名称：

  A novel series of potent and selective small molecule inhibitors of the complement component C1s

  摘要：

  Activation of the classical pathway of complement has been implicated in disease states such as hereditary angioedema, ischemia-reperfusion injury and acute transplant rejection. The trypsin-like serine protease C1s represents a pivotal upstream point of control in the classical pathway of complement activation and is therefore likely to be a useful target in the therapeutic intervention of these disease states. A series of thiopheneamidine-based inhibitors of C1s has been optimized to give a 70 nM inhibitor that inhibits the classical pathway of complement activation in vitro. (C) 2004 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2004.04.034
• 作为产物：
  描述：

  1-Methyl-5-propyl-1H-pyrazole-4-carboxylic acid ethyl ester 在 sodium hydroxide 、 草酰氯 、 N,N-二甲基甲酰胺 作用下， 以 甲醇 、 二氯甲烷 为溶剂， 反应 4.0h， 生成 1-甲基-5-丙基-1H-吡唑-4-甲酰氯
  参考文献：
  名称：

  A novel series of potent and selective small molecule inhibitors of the complement component C1s

  摘要：

  Activation of the classical pathway of complement has been implicated in disease states such as hereditary angioedema, ischemia-reperfusion injury and acute transplant rejection. The trypsin-like serine protease C1s represents a pivotal upstream point of control in the classical pathway of complement activation and is therefore likely to be a useful target in the therapeutic intervention of these disease states. A series of thiopheneamidine-based inhibitors of C1s has been optimized to give a 70 nM inhibitor that inhibits the classical pathway of complement activation in vitro. (C) 2004 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2004.04.034

文献信息

• THIADIAZOLE DERIVATIVES FOR THE TREATMENT OF NEURODEGENERATIVE DISEASES
  申请人：GRIFFIOEN Gerard

  公开号：US20090054410A1

  公开（公告）日：2009-02-26

  This invention provides specifically substituted 1,2,4-thiadiazole derivatives for use in the treatment of an α-synucleopathy such as Parkinson's disease, diffuse Lewy body disease, traumatic brain injury, amyotrophic lateral sclerosis, Niemann-Pick disease, Hallervorden-Spatz syndrome, Down syndrome, neuroaxonal dystrophy, multiple system atrophy and Alzheimer's disease. This invention also provides various methods for producing such substituted 1,2,4-thiadiazole derivatives.
• US8541406B2
  申请人：——

  公开号：US8541406B2

  公开（公告）日：2013-09-24
• A novel series of potent and selective small molecule inhibitors of the complement component C1s
  作者：Nalin L. Subasinghe、Farah Ali、Carl R. Illig、M. Jonathan Rudolph、Scott Klein、Ehab Khalil、Richard M. Soll、Roger F. Bone、John C. Spurlino、Renee L. DesJarlais、Carl S. Crysler、Maxwell D. Cummings、Philip E. Morris、John M. Kilpatrick、Y. Sudhakara Babu

  DOI：10.1016/j.bmcl.2004.04.034

  日期：2004.6

  Activation of the classical pathway of complement has been implicated in disease states such as hereditary angioedema, ischemia-reperfusion injury and acute transplant rejection. The trypsin-like serine protease C1s represents a pivotal upstream point of control in the classical pathway of complement activation and is therefore likely to be a useful target in the therapeutic intervention of these disease states. A series of thiopheneamidine-based inhibitors of C1s has been optimized to give a 70 nM inhibitor that inhibits the classical pathway of complement activation in vitro. (C) 2004 Elsevier Ltd. All rights reserved.