1-(4-Methoxy-phenyl)-7-(2,3,4-trimethoxy-phenyl)-heptan-3-one | 74882-24-9

• 分子结构分类: 有机化合物 - 脂质和类脂质分子 - 脂肪酰基
• 英文名称: 1-(4-Methoxy-phenyl)-7-(2,3,4-trimethoxy-phenyl)-heptan-3-one
• CAS: 74882-24-9
• 化学式: C₂₃H₃₀O₅
• 分子量: 386.488
• InChiKey: DNTRFRKCHFEQRM-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.64
• 重原子数：
  28.0
• 可旋转键数：
  12.0
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.43
• 拓扑面积：
  53.99
• 氢给体数：
  0.0
• 氢受体数：
  5.0

反应信息

• 作为反应物：
  描述：

  1-(4-Methoxy-phenyl)-7-(2,3,4-trimethoxy-phenyl)-heptan-3-one 在 碘 、 silver trifluoroacetate 作用下， 以 二氯甲烷 为溶剂， 反应 20.0h， 生成 1-(3-iodo-4-methoxyphenyl)-7-(5-iodo-2,3,4-trimethoxyphenyl)heptan-3-one
  参考文献：
  名称：

  Whiting, Donald A.; Wood, Andrew F., Journal of the Chemical Society. Perkin transactions I, 1980, p. 623 - 628

  摘要：

  DOI：
• 作为产物：
  描述：

  3-(4-甲氧苯基)-1-丙醇 在 magnesium 、 pyridinium chlorochromate 作用下， 以 四氢呋喃 、 二氯甲烷 为溶剂， 反应 4.5h， 生成 1-(4-Methoxy-phenyl)-7-(2,3,4-trimethoxy-phenyl)-heptan-3-one
  参考文献：
  名称：

  Henley-Smith, Peter; Whiting, Donald A.; Wood, Andrew F., Journal of the Chemical Society. Perkin transactions I, 1980, p. 614 - 622

  摘要：

  DOI：

文献信息

• New synthesized polyoxygenated diarylheptanoids suppress lipopolysaccharide-induced neuroinflammation
  作者：Anna Santarsiero、Antonella Bochicchio、Maria Funicello、Paolo Lupattelli、Sabine Choppin、Françoise Colobert、Gilles Hanquet、Lucie Schiavo、Paolo Convertini、Lucia Chiummiento、Vittoria Infantino

  DOI：10.1016/j.bbrc.2020.06.122

  日期：2020.9

  In neurodegenerative diseases, such as Alzheimer's disease, Huntington's disease, Parkinson's disease and multiple sclerosis, neuroinflammation induced by the microglial activation plays a crucial role. In effort to develop effective anti-neuroinflammatory compounds, different new linear polyoxygenated diarylheptanoids were synthesized. In LPS-triggered BV-2 microglial cells their ability to reduce the concentration of IL-6 and TNF-alpha pro-inflammatory cytokines was evaluated. Moreover, their effect on NF-kappa B and ATP citrate lyase (ACLY), a recently emerged target of metabolic reprogramming in inflammation, was assessed. Finally, we turned our attention to inflammatory mediators derived from the cleavage of citrate catalyzed by ACLY: prostaglandin E-2, nitric oxide and reactive oxygen species. All compounds showed null or minimal cytotoxicity; most of them had a great anti-neuroinflammatory activity. Diarylheptanoids 6b and 6c, bearing a halide atom and benzyl ether protective groups, exhibited the best effect since they blocked the secretion of all inflammatory mediators analyzed and reduced NF-kB and ACLY protein levels. (c) 2020 Elsevier Inc. All rights reserved.