N-(2-phenyl-1,3-benzoxazol-5-yl)cyclohexanecarboxamide

• 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-(2-phenyl-1,3-benzoxazol-5-yl)cyclohexanecarboxamide
• 化学式: C₂₀H₂₀N₂O₂
• mdl: MFCD01893064
• 分子量: 320.391
• InChiKey: YLWKHQQOOUABQB-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.7
• 重原子数：
  24
• 可旋转键数：
  3
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.3
• 拓扑面积：
  55.1
• 氢给体数：
  1
• 氢受体数：
  3

反应信息

• 作为产物：
  描述：

  2,4-diaminophenol dihydrochloride 在 碳酸氢钠 作用下， 以 乙醚 为溶剂， 反应 2.5h， 生成 N-(2-phenyl-1,3-benzoxazol-5-yl)cyclohexanecarboxamide
  参考文献：
  名称：

  Synthesis and microbiological activity of some novel N-[2-(p-substitutedphenyl)-5-benzoxazolyl]-cyclohexyl carboxamide, -cyclohexyl acetamide and -cyclohexyl propionamide derivatives

  摘要：

  The synthesis and microbiological activity of a new series of N-[2-(p-substitutedphenyl)-5-benzoxazolyl]-cyclohexyl carboxamide, -cyclohexyl acetamide and -cyclohexyl propionamide derivatives (4-11) is described. The in vitro microbiological activity of the compounds was determined against gram-positive, gram-negative bacteria and the yeast Candida albicans in comparison with standard drugs. Microbiological results indicated that the synthesized compounds possessed a broad spectrum of activity against the tested microorganisms.

  DOI：

  10.1016/s0014-827x(02)01278-8

文献信息

• Benzoxazole-derivatives enhance progranulin expression and reverse the aberrant lysosomal proteome caused by GRN haploinsufficiency
  作者：Rachel Tesla、Charlotte Guhl、Gordon C. Werthmann、Danielle Dixon、Basar Cenik、Yesu Addepalli、Jue Liang、Daniel M. Fass、Zachary Rosenthal、Stephen J. Haggarty、Noelle S. Williams、Bruce A. Posner、Joseph M. Ready、Joachim Herz

  DOI：10.1038/s41467-024-50076-8

  日期：——

  Heterozygous loss-of-function mutations in the GRN gene are a major cause of hereditary frontotemporal dementia. The mechanisms linking frontotemporal dementia pathogenesis to progranulin deficiency are not well understood, and there is currently no treatment. Our strategy to prevent the onset and progression of frontotemporal dementia in patients with GRN mutations is to utilize small molecule positive regulators of GRN expression to boost progranulin levels from the remaining functional GRN allele, thus restoring progranulin levels back to normal within the brain. This work describes a series of blood-brain-barrier-penetrant small molecules which significantly increase progranulin protein levels in human cellular models, correct progranulin protein deficiency in Grn+/− mouse brains, and reverse lysosomal proteome aberrations, a phenotypic hallmark of frontotemporal dementia, more efficiently than the previously described small molecule suberoylanilide hydroxamic acid. These molecules will allow further elucidation of the cellular functions of progranulin and its role in frontotemporal dementia and will also serve as lead structures for further drug development.