4-[3-(3-Methylpyridin-2-yl)phenyl]sulfonyl-5-methylsulfanylthiophene-2-carboximidamide | 631903-03-2

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 吡啶及其衍生物
• 英文名称: 4-[3-(3-Methylpyridin-2-yl)phenyl]sulfonyl-5-methylsulfanylthiophene-2-carboximidamide
• CAS: 631903-03-2
• 化学式: C₁₈H₁₇N₃O₂S₃
• 分子量: 403.55
• InChiKey: ZPUIITYLYDYFCH-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.5
• 重原子数：
  26
• 可旋转键数：
  5
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.11
• 拓扑面积：
  159
• 氢给体数：
  2
• 氢受体数：
  6

反应信息

• 作为产物：
  描述：

  4-(3-Bromo-benzenesulfonyl)-5-methylsulfanyl-thiophene-2-carboxamidine 、 zinc,3-methyl-2H-pyridin-2-ide,bromide 在 四(三苯基膦)钯 作用下， 以 四氢呋喃 为溶剂， 反应 1.0h， 生成 4-[3-(3-Methylpyridin-2-yl)phenyl]sulfonyl-5-methylsulfanylthiophene-2-carboximidamide
  参考文献：
  名称：

  Biphenylsulfonyl-thiophene-carboxamidine inhibitors of the complement component C1s

  摘要：

  Complement activation has been implicated in disease states such as hereditary angioedema, ischemia-reperfusion injury, acute respiratory distress syndrome, and acute transplant rejection. Even though the complement cascade provides several protein targets for potential therapeutic intervention only two complement inhibitors have been approved so far for clinical use including anti-C5 antibodies for the treatment of paroxysmal nocturnal hemoglobinuria and purified C1-esterase inhibitor replacement therapy for the control of hereditary angioedema flares. In the present study, optimization of potency and physicochemical properties of a series of thiophene amidine-based C1s inhibitors with potential utility as intravenous agents for the inhibition of the classical pathway of complement is described. (c) 2008 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2008.01.064

文献信息

• Biphenylsulfonyl-thiophene-carboxamidine inhibitors of the complement component C1s
  作者：Jeremy M. Travins、Farah Ali、Hui Huang、Shelley K. Ballentine、Ehab Khalil、Heather R. Hufnagel、Wenxi Pan、Joan Gushue、Kristi Leonard、Roger F. Bone、Richard M. Soll、Renee L. DesJarlais、Carl S. Crysler、Nisha Ninan、Jennifer Kirkpatrick、Maxwell D. Cummings、Norman Huebert、Christopher J. Molloy、Michael Gaul、Bruce E. Tomczuk、Nalin L. Subasinghe

  DOI：10.1016/j.bmcl.2008.01.064

  日期：2008.3

  Complement activation has been implicated in disease states such as hereditary angioedema, ischemia-reperfusion injury, acute respiratory distress syndrome, and acute transplant rejection. Even though the complement cascade provides several protein targets for potential therapeutic intervention only two complement inhibitors have been approved so far for clinical use including anti-C5 antibodies for the treatment of paroxysmal nocturnal hemoglobinuria and purified C1-esterase inhibitor replacement therapy for the control of hereditary angioedema flares. In the present study, optimization of potency and physicochemical properties of a series of thiophene amidine-based C1s inhibitors with potential utility as intravenous agents for the inhibition of the classical pathway of complement is described. (c) 2008 Elsevier Ltd. All rights reserved.