4-(4-butyl-phenyl)-[1,2,4]triazolidine-3,5-dione | 117026-11-6

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 唑类
• 英文名称: 4-(4-butyl-phenyl)-[1,2,4]triazolidine-3,5-dione
• 英文别名: 4-(4-Butyl-phenyl)-[1,2,4]triazolidin-3,5-dion；4-(4-Butylphenyl)-1,2,4-triazolidine-3,5-dione
• CAS: 117026-11-6
• 化学式: C₁₂H₁₅N₃O₂
• 分子量: 233.27
• InChiKey: ZMALMWLVFXZKLF-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.6
• 重原子数：
  17
• 可旋转键数：
  4
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.33
• 拓扑面积：
  61.4
• 氢给体数：
  2
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  4-(4-butyl-phenyl)-[1,2,4]triazolidine-3,5-dione 在 硝酸铵 、 aluminum hydrogen sulfate 作用下， 以 二氯甲烷 为溶剂， 反应 1.33h， 以96%的产率得到4-(4-Butyl-phenyl)-[1,2,4]triazole-3,5-dione
  参考文献：
  名称：

  硝酸铵和金属硫酸氢盐催化的脲醛衍生物及其相应的三唑啉二酮的催化高效氧化

  摘要：

  已经在室温下在二氯甲烷中开发了在催化量的硫酸氢铝存在下，通过NH 4 NO 3的组合，将多种脲唑催化氧化为三唑啉二酮的方法。

  DOI：

  10.1002/cjoc.201090206

文献信息

• Treatment of Sepsis Pathogenesis with High Mobility Group Box Protein 1-Regulating Anti-inflammatory Agents
  作者：Wansang Cho、Ja Young Koo、Yeonju Park、Keunhee Oh、Sanghee Lee、Jin-Sook Song、Myung Ae Bae、Donghyun Lim、Dong-Sup Lee、Seung Bum Park

  DOI：10.1021/acs.jmedchem.6b00954

  日期：2017.1.12

  Sepsis is one of the major causes of death worldwide when associated with multiple organ failure. However, there is a critical lack of adequate sepsis therapies because of its diverse patterns of pathogenesis. The pro-inflammatory cytokine cascade mediates sepsis pathogenesis, and high mobility group box proteins (HMGBs) play an important role as late-stage cytokines. We previously reported the small-molecule modulator, inflachromene (1d), which inhibits the release of HMGBs and, thereby, reduces the production of pro-inflammatory cytokines. In this context, we intraperitoneally administered Id to a cecal ligation and puncture (CLP)-induced mouse model of sepsis and confirmed that it successfully ameliorated sepsis pathogenesis. On the basis of a structure activity relationship study, we discovered new candidate compounds, 2j and 21, with improved therapeutic efficacy in vivo. Therefore, our study clearly demonstrates that the regulation of HMGB1 release using small molecules is a promising strategy for the treatment of sepsis.