2-(2-bromoethylsulfonyl)selenophene | 1297906-69-4

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 硒吩
• 英文名称: 2-(2-bromoethylsulfonyl)selenophene
• CAS: 1297906-69-4
• 化学式: C₆H₇BrO₂SSe
• 分子量: 302.05
• InChiKey: LPWYIWLGJDUKQX-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  0.91
• 重原子数：
  11
• 可旋转键数：
  3
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.33
• 拓扑面积：
  42.5
• 氢给体数：
  0
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  2-(2-bromoethylsulfonyl)selenophene 在 sodium tetrahydroborate 、 potassium carbonate 作用下， 以 四氢呋喃 、 甲醇 、 N,N-二甲基甲酰胺 为溶剂， 反应 1.0h， 生成 (3R,4R)-methyl 4-(3-hydroxy-3-(6-methoxyquinolin-4-yl)propyl)-1-(2-(selenophen-2-ylsulfonyl)-ethyl)piperidine-3-carboxylate
  参考文献：
  名称：

  Selenophene-Containing Inhibitors of Type IIA Bacterial Topoisomerases

  摘要：

  We investigated compounds related to the previously reported anti-staphyloccocal agent AVE6971 in an effort to attenuate inhibition of hERG potassium channel current that has been noted for this and related antibacterial drug classes. While most modifications of the original thiophene group compromised antibacterial activity, one selenophene analogue displayed (i) improved activity against the primary target enzyme DNA gyrase, (ii) similar activities against a panel of MRSA clinical isolates, and (iii) reduced hERG channel inhibition.

  DOI：

  10.1021/jm2002124
• 作为产物：
  描述：

  (2-bromoethyl)(selenophen-2-yl)sulfane 在 间氯过氧苯甲酸 作用下， 以 二氯甲烷 为溶剂， 反应 1.0h， 以79%的产率得到2-(2-bromoethylsulfonyl)selenophene
  参考文献：
  名称：

  Selenophene-Containing Inhibitors of Type IIA Bacterial Topoisomerases

  摘要：

  We investigated compounds related to the previously reported anti-staphyloccocal agent AVE6971 in an effort to attenuate inhibition of hERG potassium channel current that has been noted for this and related antibacterial drug classes. While most modifications of the original thiophene group compromised antibacterial activity, one selenophene analogue displayed (i) improved activity against the primary target enzyme DNA gyrase, (ii) similar activities against a panel of MRSA clinical isolates, and (iii) reduced hERG channel inhibition.

  DOI：

  10.1021/jm2002124