1-[4-(4-chlorobutoxy)phenyl]-5-methyl-1H-pyridin-2-one | 1415087-96-5

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯酚醚
• 英文名称: 1-[4-(4-chlorobutoxy)phenyl]-5-methyl-1H-pyridin-2-one
• 英文别名: 1-[4-(4-Chlorobutoxy)phenyl]-5-methylpyridin-2-one
• CAS: 1415087-96-5
• 化学式: C₁₆H₁₈ClNO₂
• 分子量: 291.777
• InChiKey: GHRTTWMWQILXIX-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.54
• 重原子数：
  20.0
• 可旋转键数：
  6.0
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.31
• 拓扑面积：
  31.23
• 氢给体数：
  0.0
• 氢受体数：
  3.0

反应信息

• 作为反应物：
  描述：

  四氢吡咯 、 1-[4-(4-chlorobutoxy)phenyl]-5-methyl-1H-pyridin-2-one 在 potassium carbonate 、 sodium iodide 作用下， 以 N,N-二甲基甲酰胺 为溶剂， 反应 72.0h， 以77%的产率得到5-methyl-1-[4-(4-pyrrolidin-1-ylbutoxy)phenyl]-1H-pyridin-2-one
  参考文献：
  名称：

  Synthesis and biological evaluation of the pirfenidone derivatives as antifibrotic agents

  摘要：

  A total of 24 pirfenidone derivatives were designed, synthesized and evaluated for their inhibitory activity against the human lung fibroblast cell line MRC-5. These compounds showed the remarkable proliferation inhibition against MRC-5 compared to pirfenidone as the positive control. The possible mechanism of this kind of derivatives as antifibrotic agents was explored. The molecular docking and p38 binding affinity assays demonstrated that the antifibrotic potential of the pirfenidone derivatives was possibly through the inhibition of p38 MAPK signaling pathway. The data from this study suggested that p38 might be a potential therapeutic target for the new generation antifibrotics. All the pirfenidone derivatives are reported here for the first time. (C) 2013 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2013.11.038
• 作为产物：
  描述：

  2-羟基-5-甲基嘧啶 在 copper(l) iodide 、 5%-palladium/activated carbon 、 氢气 、 potassium carbonate 作用下， 以 四氢呋喃 、 N,N-二甲基甲酰胺 、 丙酮 为溶剂， 反应 82.0h， 生成 1-[4-(4-chlorobutoxy)phenyl]-5-methyl-1H-pyridin-2-one
  参考文献：
  名称：

  Synthesis and biological evaluation of the pirfenidone derivatives as antifibrotic agents

  摘要：

  A total of 24 pirfenidone derivatives were designed, synthesized and evaluated for their inhibitory activity against the human lung fibroblast cell line MRC-5. These compounds showed the remarkable proliferation inhibition against MRC-5 compared to pirfenidone as the positive control. The possible mechanism of this kind of derivatives as antifibrotic agents was explored. The molecular docking and p38 binding affinity assays demonstrated that the antifibrotic potential of the pirfenidone derivatives was possibly through the inhibition of p38 MAPK signaling pathway. The data from this study suggested that p38 might be a potential therapeutic target for the new generation antifibrotics. All the pirfenidone derivatives are reported here for the first time. (C) 2013 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2013.11.038