(E)-3-(3-ethoxy-4-hydroxyphenyl)-1-(pyridin-3-yl)prop-2-en-1-one

• 分子结构分类: 有机化合物 - 苯丙烷和聚酮 - 肉桂酸及其衍生物
• 英文名称: (E)-3-(3-ethoxy-4-hydroxyphenyl)-1-(pyridin-3-yl)prop-2-en-1-one
• 英文别名: (E)-3-(3-ethoxy-4-hydroxyphenyl)-1-pyridin-3-ylprop-2-en-1-one
• 化学式: C₁₆H₁₅NO₃
• 分子量: 269.3
• InChiKey: LSVFTMWDQNMBDP-FNORWQNLSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.6
• 重原子数：
  20
• 可旋转键数：
  5
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.12
• 拓扑面积：
  59.4
• 氢给体数：
  1
• 氢受体数：
  4

反应信息

• 作为产物：
  描述：

  3-ethoxy-4-((tetrahydro-2H-pyran-2-yl)oxy)benzaldehyde 在 对甲苯磺酸 、 sodium hydroxide 作用下， 以 甲醇 、 水 为溶剂， 反应 24.0h， 生成 (E)-3-(3-ethoxy-4-hydroxyphenyl)-1-(pyridin-3-yl)prop-2-en-1-one
  参考文献：
  名称：

  Hydroxy-substituted trans -cinnamoyl derivatives as multifunctional tools in the context of Alzheimer's disease

  摘要：

  Alzheimer's disease (AD) is a multifactorial pathology that requires multifaceted agents able to address its peculiar nature. In recent years, a plethora of proteins and biochemical pathways has been proposed as possible targets to counteract neurotoxicity. Although the complex scenario is not completely elucidated, close relationships are emerging among some of these actors. In particular, increasing evidence has shown that aggregation of amyloid beta (A beta), glycogen synthase kinase 3 beta (GSK-3 beta) and oxidative stress are strictly interconnected and their concomitant modulation may have a positive and synergic effect in contrasting AD-related impairments. We designed compound 3 which demonstrated the ability to inhibit both GSK-3 beta (IC50 = 24.36 +/- 0.01 mu M) and A beta(42) self-aggregation (IC50 = 9.0 +/- 1.4 mu M), to chelate copper (II) and to act as exceptionally strong radical scavenger (k(inh) = 6.8 +/- 0.5 . 10(5) M(-1)s(-1)) even in phosphate buffer at pH 7.4 (k(inh) = 3.2 +/- 0.5 . 10(5) M(-1)s(-1)). Importantly, compound 3 showed high predicted blood-brain barrier permeability, did not exert any significant cytotoxic effects in immature cortical neurons up to 50 mu M and showed neuroprotective properties at micromolar concentration against toxic insult induced by glutamate. (C) 2017 Elsevier Masson SAS. All rights reserved.

  DOI：

  10.1016/j.ejmech.2017.07.058

文献信息

• Zamocka; Gregan, Pharmazie, 1993, vol. 48, # 11, p. 857 - 859
  作者：Zamocka、Gregan

  DOI：——

  日期：——
• Hydroxy-substituted trans -cinnamoyl derivatives as multifunctional tools in the context of Alzheimer's disease
  作者：Angela De Simone、Manuela Bartolini、Andrea Baschieri、Kim Y.P. Apperley、Huan Huan Chen、Melissa Guardigni、Serena Montanari、Tereza Kobrlova、Ondrej Soukup、Luca Valgimigli、Vincenza Andrisano、Jeffrey W. Keillor、Manuela Basso、Andrea Milelli

  DOI：10.1016/j.ejmech.2017.07.058

  日期：2017.10

  Alzheimer's disease (AD) is a multifactorial pathology that requires multifaceted agents able to address its peculiar nature. In recent years, a plethora of proteins and biochemical pathways has been proposed as possible targets to counteract neurotoxicity. Although the complex scenario is not completely elucidated, close relationships are emerging among some of these actors. In particular, increasing evidence has shown that aggregation of amyloid beta (A beta), glycogen synthase kinase 3 beta (GSK-3 beta) and oxidative stress are strictly interconnected and their concomitant modulation may have a positive and synergic effect in contrasting AD-related impairments. We designed compound 3 which demonstrated the ability to inhibit both GSK-3 beta (IC50 = 24.36 +/- 0.01 mu M) and A beta(42) self-aggregation (IC50 = 9.0 +/- 1.4 mu M), to chelate copper (II) and to act as exceptionally strong radical scavenger (k(inh) = 6.8 +/- 0.5 . 10(5) M(-1)s(-1)) even in phosphate buffer at pH 7.4 (k(inh) = 3.2 +/- 0.5 . 10(5) M(-1)s(-1)). Importantly, compound 3 showed high predicted blood-brain barrier permeability, did not exert any significant cytotoxic effects in immature cortical neurons up to 50 mu M and showed neuroprotective properties at micromolar concentration against toxic insult induced by glutamate. (C) 2017 Elsevier Masson SAS. All rights reserved.