N-(4-(benzo[d]oxazol-2-yl)phenyl)-2-(trifluoromethyl)benzenesulfonamide

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 唑类
• 英文名称: N-(4-(benzo[d]oxazol-2-yl)phenyl)-2-(trifluoromethyl)benzenesulfonamide
• 英文别名: N-[4-(1,3-benzoxazol-2-yl)phenyl]-2-(trifluoromethyl)benzenesulfonamide
• 化学式: C₂₀H₁₃F₃N₂O₃S
• 分子量: 418.396
• InChiKey: JESCTCQPDHESJC-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.8
• 重原子数：
  29
• 可旋转键数：
  4
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.05
• 拓扑面积：
  80.6
• 氢给体数：
  1
• 氢受体数：
  8

反应信息

• 作为产物：
  描述：

  4-苯并噁唑-2-苯胺 、 2-三氟甲基苯磺酰氯 在 吡啶 作用下， 以 二氯甲烷 为溶剂， 反应 18.0h， 生成 N-(4-(benzo[d]oxazol-2-yl)phenyl)-2-(trifluoromethyl)benzenesulfonamide
  参考文献：
  名称：

  Dual-targeting GroEL/ES chaperonin and protein tyrosine phosphatase B (PtpB) inhibitors: A polypharmacology strategy for treating Mycobacterium tuberculosis infections

  摘要：

  Current treatments for Mycobacterium tuberculosis infections require long and complicated regimens that can lead to patient non-compliance, increasing incidences of antibiotic-resistant strains, and lack of efficacy against latent stages of disease. Thus, new therapeutics are needed to improve tuberculosis standard of care. One strategy is to target protein homeostasis pathways by inhibiting molecular chaperones such as GroEL/ES (HSP60/10) chaperonin systems. M. tuberculosis has two GroEL homologs: GroEL1 is not essential but is important for cytokine-dependent granuloma formation, while GroEL2 is essential for survival and likely functions as the canonical housekeeping chaperonin for folding proteins. Another strategy is to target the protein tyrosine phosphatase B (PtpB) virulence factor that M. tuberculosis secretes into host cells to help evade immune responses. In the present study, we have identified a series of GroEL/ES inhibitors that inhibit M. tuberculosis growth in liquid culture and biochemical function of PtpB in vitro. With further optimization, such dual-targeting GroEL/ES and PtpB inhibitors could be effective against all stages of tuberculosis - actively replicating bacteria, bacteria evading host cell immune responses, and granuloma formation in latent disease - which would be a significant advance to augment current therapeutics that primarily target actively replicating bacteria.

  DOI：

  10.1016/j.bmcl.2019.04.034