4-Hydroxy-3,5-di-tert.-butyl-zimtaldehyd | 789-89-9

• 分子结构分类: 有机化合物 - 苯丙烷和聚酮 - 肉桂醛
• 英文名称: 4-Hydroxy-3,5-di-tert.-butyl-zimtaldehyd
• 英文别名: Zimtaldehyd；3-(3,5-Ditert-butyl-4-hydroxyphenyl)prop-2-enal
• CAS: 789-89-9
• 化学式: C₁₇H₂₄O₂
• 分子量: 260.376
• InChiKey: PEJOWYPEAWNWJV-UHFFFAOYSA-N

物化性质

• 熔点：
  116-117 °C
• 沸点：
  352.1±37.0 °C(Predicted)
• 密度：
  1.003±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  4.8
• 重原子数：
  19
• 可旋转键数：
  4
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.47
• 拓扑面积：
  37.3
• 氢给体数：
  1
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  4-Hydroxy-3,5-di-tert.-butyl-zimtaldehyd 在 sodium tetrahydroborate 作用下， 以 乙酸乙酯 为溶剂， 反应 2.0h， 以90%的产率得到2,6-Ditert-butyl-4-(3-hydroxyprop-1-enyl)phenol
  参考文献：
  名称：

  Discovery of a Negative Allosteric Modulator of GABA_B Receptors

  摘要：

  Initialized from the scaffold of CGP7930, an allosteric agonist of GABA(B) receptors, a series of non-competitive antagonists were discovered. Among these compounds, compounds 3, 6, and 14 decreased agonist GABA-induced maximal effect of IP3 production in HEK293 cells overexpressing GABA(B) receptors and Gq(j9) proteins without changing the EC50. Compounds 3, 6, and 14 not only inhibited agonist baclofen-induced ERK1/2 phosphorylation but also blocked CGP7930-induced ERK1/2 phosphorylation in HEK293 cells overexpressing GABA(B) receptors. The results suggested that compounds 3, 6, and 14 are negative allosteric modulators of GABA(B) receptors. The representative compound 14 decreased GABA-induced IP3 production with IC50 of 37.9 mu M and had no effect on other GPCR Class C members such as mGluR1, mGluR2, and mGluRS. Finally, we showed that compound 14 did not bind to the orthosteric binding sites of GABA(B) receptors, demonstrating that compound 14 negatively modulated GABA(B) receptors activity as a negative allosteric modulator.

  DOI：

  10.1021/ml500162z
• 作为产物：
  描述：

  甲酰甲撑基三苯基磷 、 3,5-二叔丁基-4-羟基苯甲醛 以 甲苯 为溶剂， 以17%的产率得到4-Hydroxy-3,5-di-tert.-butyl-zimtaldehyd
  参考文献：
  名称：

  Discovery of a Negative Allosteric Modulator of GABA_B Receptors

  摘要：

  Initialized from the scaffold of CGP7930, an allosteric agonist of GABA(B) receptors, a series of non-competitive antagonists were discovered. Among these compounds, compounds 3, 6, and 14 decreased agonist GABA-induced maximal effect of IP3 production in HEK293 cells overexpressing GABA(B) receptors and Gq(j9) proteins without changing the EC50. Compounds 3, 6, and 14 not only inhibited agonist baclofen-induced ERK1/2 phosphorylation but also blocked CGP7930-induced ERK1/2 phosphorylation in HEK293 cells overexpressing GABA(B) receptors. The results suggested that compounds 3, 6, and 14 are negative allosteric modulators of GABA(B) receptors. The representative compound 14 decreased GABA-induced IP3 production with IC50 of 37.9 mu M and had no effect on other GPCR Class C members such as mGluR1, mGluR2, and mGluRS. Finally, we showed that compound 14 did not bind to the orthosteric binding sites of GABA(B) receptors, demonstrating that compound 14 negatively modulated GABA(B) receptors activity as a negative allosteric modulator.

  DOI：

  10.1021/ml500162z

文献信息

• Discovery of a Negative Allosteric Modulator of GABA_B Receptors
  作者：Lin-Hai Chen、Bing Sun、Yang Zhang、Tong-Jie Xu、Zhi-Xiong Xia、Jian-Feng Liu、Fa-Jun Nan

  DOI：10.1021/ml500162z

  日期：2014.7.10

  Initialized from the scaffold of CGP7930, an allosteric agonist of GABA(B) receptors, a series of non-competitive antagonists were discovered. Among these compounds, compounds 3, 6, and 14 decreased agonist GABA-induced maximal effect of IP3 production in HEK293 cells overexpressing GABA(B) receptors and Gq(j9) proteins without changing the EC50. Compounds 3, 6, and 14 not only inhibited agonist baclofen-induced ERK1/2 phosphorylation but also blocked CGP7930-induced ERK1/2 phosphorylation in HEK293 cells overexpressing GABA(B) receptors. The results suggested that compounds 3, 6, and 14 are negative allosteric modulators of GABA(B) receptors. The representative compound 14 decreased GABA-induced IP3 production with IC50 of 37.9 mu M and had no effect on other GPCR Class C members such as mGluR1, mGluR2, and mGluRS. Finally, we showed that compound 14 did not bind to the orthosteric binding sites of GABA(B) receptors, demonstrating that compound 14 negatively modulated GABA(B) receptors activity as a negative allosteric modulator.