1,5-bis-diethylthiophosphinoyl-pentane | 25900-31-6

• 物质功能分类: 有机原料 - 有机膦化合物
• 分子结构分类: 有机化合物 - 有机磷化合物 - 有机硫代磷化合物
• 英文名称: 1,5-bis-diethylthiophosphinoyl-pentane
• 英文别名: Tetra-P-aethyl-P,P'-pentandiyl-bis-phosphinoxid；1,5-Bis-diaethylthiophosphinoyl-pentan；(Pentane-1,5-diyl)bis[diethyl(sulfanylidene)-lambda~5~-phosphane]；5-diethylphosphinothioylpentyl-diethyl-sulfanylidene-λ5-phosphane
• CAS: 25900-31-6
• 化学式: C₁₃H₃₀P₂S₂
• 分子量: 312.461
• InChiKey: WXDJPDPWJQHJQO-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.5
• 重原子数：
  17
• 可旋转键数：
  10
• 环数：
  0.0
• sp3杂化的碳原子比例：
  1.0
• 拓扑面积：
  64.2
• 氢给体数：
  0
• 氢受体数：
  2

反应信息

• 作为产物：
  描述：

  1,5-Pentandiylbis(diethylphosphan) 在 sulfur 、 苯 作用下， 生成 1,5-bis-diethylthiophosphinoyl-pentane
  参考文献：
  名称：

  CD4+ T-Lymphocytes Regulate Airway Remodeling and Hyper-Reactivity in a Mouse Model of Chronic Asthma

  摘要：

  Asthma is an acute-on-chronic inflammatory disease of the airways, characterized by airflow obstruction and hyper-reactivity of the airways to a variety of stimuli. Chronic asthma is associated with remodeling of the airway wall, which may contribute to hyper-reactivity and fixed airflow obstruction. We used an improved mouse model of chronic asthma to investigate the role of CD4(+) T-lymphocytes in airway remodeling and hyper-reactivity. Animals functionally depleted of CD4(+) T-lymphocytes by repeated administration of a monoclonal antibody exhibited markedly decreased airway responsiveness. In addition, these mice had greatly diminished subepithelial fibrosis, epithelial thickening, and mucous cell hyperplasia/metaplasia. Chronic inflammation in the airway wall was moderately reduced, with a marked decrease in the accumulation of immunoglobulin-synthesizing plasma cells. However, intraepithelial accumulation of eosinophils was not significantly inhibited and airway epithelial expression of eotaxin was undiminished. This work provides the first experimental evidence that CD4(+) T-lymphocytes play a crucial role in the pathogenesis of the lesions of chronic asthma and ends support to the notion that functional inhibition of these cells may be an important therapeutic target.

  DOI：

  10.1038/labinvest.3780438