2-Decylsulfanylacetamide | 294201-39-1

• 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-Decylsulfanylacetamide
• CAS: 294201-39-1
• 化学式: C₁₂H₂₅NOS
• 分子量: 231.403
• InChiKey: UJBLHXFXYXECBB-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.3
• 重原子数：
  15
• 可旋转键数：
  11
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.92
• 拓扑面积：
  68.4
• 氢给体数：
  1
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  2-Decylsulfanylacetamide 在 间氯过氧苯甲酸 作用下， 以 二氯甲烷 为溶剂， 反应 0.75h， 以80%的产率得到2-Decylsulfinylacetamide
  参考文献：
  名称：

  A New Class of Antituberculosis Agents

  摘要：

  Long-chain lipid envelopes are characteristic of mycobacteria such as those that cause tuberculosis and leprosy. Inhibition of fatty acid synthesis or elongation is a strategy demonstrated to be clinically effective against M. tuberculosis. A new class of compounds designed to inhibit the beta-ketoacyl synthase reaction of fatty acid synthesis has been developed. Of >30 compounds described, the most active were acetamides containing alkylsulfonyl substituents. Inhibitory activities were acutely sensitive to net charge, chain length, and degree of unsaturation. The most active compound 5 (alkyl = C-10) contained a single methylene spacer between the sulfone and carboxamide and exhibited an MIC of 0.75-1.5 mu g/mL, comparable to first-line antituberculosis drugs. These compounds are species-specific, exhibiting no significant activity against bacterial species other than M. tuberculosis and closely related strains. The synthesis, biological activity, and specificity of these compounds are described.

  DOI：

  10.1021/jm000149l
• 作为产物：
  描述：

  1-癸硫醇 、 2-溴乙酰胺 在 potassium carbonate 作用下， 以 丙酮 为溶剂， 以100 %的产率得到2-Decylsulfanylacetamide
  参考文献：
  名称：

  重新评估有效抗结核药物 2-(烷基磺酰基)乙酰胺的假定分子靶点

  摘要：

  简单的烷基磺酰乙酰胺具有有效的抗结核活性，并显着降低分枝杆菌中的分枝菌酸水平。尽管这些化合物最初设计用于抑制脂肪酸合酶的酮脂酰合酶结构域，但结构-活性关系和生化证据并不完全支持脂肪酸合酶作为靶标。 2004年，在分枝杆菌中鉴定出一个酶家族，该酶家族参与脂肪酸作为酰基腺苷酸的激活和转移，与通用的乙酰辅酶A载体机制不同。这些由 FadD 家族编码的脂肪酰基-AMP 连接酶 (FAAL) 在分枝菌酸的生物合成以及脂肪酸代谢中发挥着重要作用，并且在此被假设为磺酰乙酰胺的分子靶标。由于与连接酶天然底物的结构相似，人们相信这些化合物通过竞争性抑制这些高效分子靶标发挥作用。本研究的主要目的是合成磺酰乙酰胺衍生物的扩展库，以现有的结构活性关系为基础，借助分子建模验证分子机制，同时尝试探索新的结构电子等排体以用于进一步的药物设计和开发。根据假定的分子靶标对磺酰乙酰胺衍生物进行修饰，从而产生对结核分枝杆菌(H37Rv)

  DOI：

  10.1016/j.ejmech.2023.115983

文献信息

• US7385086B2
  申请人：——

  公开号：US7385086B2

  公开（公告）日：2008-06-10
• A New Class of Antituberculosis Agents
  作者：Paul B. Jones、Nikki M. Parrish、Todd A. Houston、Anthony Stapon、Niharika P. Bansal、James D. Dick、Craig A. Townsend

  DOI：10.1021/jm000149l

  日期：2000.8.1

  Long-chain lipid envelopes are characteristic of mycobacteria such as those that cause tuberculosis and leprosy. Inhibition of fatty acid synthesis or elongation is a strategy demonstrated to be clinically effective against M. tuberculosis. A new class of compounds designed to inhibit the beta-ketoacyl synthase reaction of fatty acid synthesis has been developed. Of >30 compounds described, the most active were acetamides containing alkylsulfonyl substituents. Inhibitory activities were acutely sensitive to net charge, chain length, and degree of unsaturation. The most active compound 5 (alkyl = C-10) contained a single methylene spacer between the sulfone and carboxamide and exhibited an MIC of 0.75-1.5 mu g/mL, comparable to first-line antituberculosis drugs. These compounds are species-specific, exhibiting no significant activity against bacterial species other than M. tuberculosis and closely related strains. The synthesis, biological activity, and specificity of these compounds are described.
• Reassessing the putative molecular Target(s) of potent antitubercular 2-(Alkylsulfonyl)acetamides
  作者：Dylan C. Farr、Thomas Haselhorst、Lendl Tan、Juanelle Furness、Emily Strong、I. Darren Grice、Nicholas P. West、Todd A. Houston

  DOI：10.1016/j.ejmech.2023.115983

  日期：2024.1

  antitubercular activity and significantly decrease mycolic acid levels in mycobacteria. Although these compounds were originally designed to inhibit the ketoacyl synthase domain of fatty acid synthase, structure-activity relationships and biochemical evidence do not fully support fatty acid synthase as the target. In 2004, an enzyme family involved in the activation and transfer of fatty acids as acyl-adenylates

  简单的烷基磺酰乙酰胺具有有效的抗结核活性，并显着降低分枝杆菌中的分枝菌酸水平。尽管这些化合物最初设计用于抑制脂肪酸合酶的酮脂酰合酶结构域，但结构-活性关系和生化证据并不完全支持脂肪酸合酶作为靶标。 2004年，在分枝杆菌中鉴定出一个酶家族，该酶家族参与脂肪酸作为酰基腺苷酸的激活和转移，与通用的乙酰辅酶A载体机制不同。这些由 FadD 家族编码的脂肪酰基-AMP 连接酶 (FAAL) 在分枝菌酸的生物合成以及脂肪酸代谢中发挥着重要作用，并且在此被假设为磺酰乙酰胺的分子靶标。由于与连接酶天然底物的结构相似，人们相信这些化合物通过竞争性抑制这些高效分子靶标发挥作用。本研究的主要目的是合成磺酰乙酰胺衍生物的扩展库，以现有的结构活性关系为基础，借助分子建模验证分子机制，同时尝试探索新的结构电子等排体以用于进一步的药物设计和开发。根据假定的分子靶标对磺酰乙酰胺衍生物进行修饰，从而产生对结核分枝杆菌(H37Rv)