4-(3-甲基-4-羟基苯基偶氮)苯磺酸 | 78659-97-9

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 偶氮苯
• 中文名称: 4-(3-甲基-4-羟基苯基偶氮)苯磺酸
• 英文名称: 4-(3-methyl-4-hydroxyphenylazo)benzenesulfonic acid
• 英文别名: 4-(3-methyl-4-hydroxyphenylazo)benzoic acid；4-(4-hydroxy-3-methyl-phenylazo)-benzenesulfonic acid；4-Hydroxy-3-methyl-azobenzol-sulfonsaeure-(4')；4-(4-Hydroxy-3-methyl-phenylazo)-benzolsulfonsaeure；(Benzol-sulfonsaeure-(1))-(4 azo 5)-(2-oxy-toluol)；p-Benzolsulfonsaeure-azo-o-kresol；4-[(4-hydroxy-3-methylphenyl)diazenyl]benzenesulfonic acid
• CAS: 78659-97-9
• 化学式: C₁₃H₁₂N₂O₄S
• 分子量: 292.315
• InChiKey: HVFDEWUPMDGDAM-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.5
• 重原子数：
  20
• 可旋转键数：
  3
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.08
• 拓扑面积：
  108
• 氢给体数：
  2
• 氢受体数：
  6

反应信息

• 作为反应物：
  描述：

  4-(3-甲基-4-羟基苯基偶氮)苯磺酸 反应 0.42h， 以87%的产率得到2-甲基-4-氨基苯酚
  参考文献：
  名称：

  2-甲基-4-氨基苯酚的制备方法、2-甲基-4-(Boc-氨基)-苯酚的制备方法

  摘要：

  本发明属于药物合成技术领域，具体涉及2‑甲基‑4‑氨基苯酚的制备方法、2‑甲基‑4‑(Boc‑氨基)‑苯酚的制备方法。本发明提供的2‑甲基‑4‑氨基苯酚的制备方法，包括以下步骤：将对氨基苯磺酸盐和重氮化剂混合，进行重氮化反应，得到苯磺酸重氮盐；将所述苯磺酸重氮盐、邻甲苯酚和强碱水溶液混合，进行Friedel‑Crafts反应，得到偶氮化合物；将所述偶氮化合物与还原剂混合，进行还原反应，得到2‑甲基‑4‑氨基苯酚。本发明提供的制备方法副产物少、产品纯化容易。

  公开号：

  CN114933538A
• 作为产物：
  描述：

  对氨基苯磺酸 在 sodium carbonate 、 sodium hydroxide 、 sodium nitrite 作用下， 以 水 为溶剂， 反应 5.17h， 生成 4-(3-甲基-4-羟基苯基偶氮)苯磺酸
  参考文献：
  名称：

  2-甲基-4-氨基苯酚的制备方法、2-甲基-4-(Boc-氨基)-苯酚的制备方法

  摘要：

  本发明属于药物合成技术领域，具体涉及2‑甲基‑4‑氨基苯酚的制备方法、2‑甲基‑4‑(Boc‑氨基)‑苯酚的制备方法。本发明提供的2‑甲基‑4‑氨基苯酚的制备方法，包括以下步骤：将对氨基苯磺酸盐和重氮化剂混合，进行重氮化反应，得到苯磺酸重氮盐；将所述苯磺酸重氮盐、邻甲苯酚和强碱水溶液混合，进行Friedel‑Crafts反应，得到偶氮化合物；将所述偶氮化合物与还原剂混合，进行还原反应，得到2‑甲基‑4‑氨基苯酚。本发明提供的制备方法副产物少、产品纯化容易。

  公开号：

  CN114933538A

文献信息

• Noelting; Kohn, Chemische Berichte, 1884, vol. 17, p. 363
  作者：Noelting、Kohn

  DOI：——

  日期：——
• Goldschmidt; Merz, Chemische Berichte, 1897, vol. 30, p. 671,687
  作者：Goldschmidt、Merz

  DOI：——

  日期：——
• Comparative toxicities and analgesic activities of three monomethylated analogs of acetaminophen
  作者：Peter J. Harvison、Anthony J. Forte、Sidney D. Nelson

  DOI：10.1021/jm00159a029

  日期：1986.9

  Three monomethylated derivatives of 4'-hydroxyacetanilide (acetaminophen) were prepared in order to compare their cytotoxic potential and analgesic activity with that of acetaminophen. Only 4'-hydroxy-N-methylacetanilide (N-methylacetaminophen) was devoid of cytotoxic effects to hepatic tissue of mice. Results of comparative tissue distribution studies and metabolism studies both in vivo and in vitro in mice indicate that the disposition of N-methylacetaminophen is similar to that of acetaminophen except that it is not oxidized to a toxic metabolite. In contrast, 3'-methyl-4'-hydroxyacetanilide (3-methylacetaminophen) is as hepatotoxic as acetaminophen in mice while 2'-methyl-4'-hydroxyacetanilide (2-methylacetaminophen) is less hepatotoxic. The analgesic potency of the analogues seems to parallel their hepatotoxic potential, and both activities parallel the oxidation potentials in this series of compounds.
• Fierz-David; Blangey; Streiff, Helvetica Chimica Acta, 1946, vol. 29, p. 1718,1758
  作者：Fierz-David、Blangey、Streiff

  DOI：——

  日期：——
• A Small Molecule Binding to the Coactivator CREB-Binding Protein Blocks Apoptosis in Cardiomyocytes
  作者：Jagat C. Borah、Shiraz Mujtaba、Ioannis Karakikes、Lei Zeng、Michaela Muller、Jigneshkumar Patel、Natasha Moshkina、Keita Morohashi、Weijia Zhang、Guillermo Gerona-Navarro、Roger J. Hajjar、Ming-Ming Zhou

  DOI：10.1016/j.chembiol.2010.12.021

  日期：2011.4

  As a master transcription factor in cellular responses to external stress, tumor suppressor p53 is tightly regulated. Excessive p53 activity during myocardial ischemia causes irreversible cellular injury and cardiomyocyte death. p53 activation is dependent on lysine acetylation by the lysine acetyltransferase and transcriptional coactivator CREB-binding protein (CBP) and on acetylation-directed CBP recruitment for p53 target gene expression. Here, we report a small molecule ischemin, developed with a structure-guided approach to inhibit the acetyl-lysine binding activity of the bromodomain of CBP. We show that ischemin alters post-translational modifications on p53 and histones, inhibits p53 interaction with CBP and transcriptional activity in cells, and prevents apoptosis in ischemic cardiomyocytes. Our study suggests small molecule modulation of acetylation-mediated interactions in gene transcription as a new approach to therapeutic interventions of human disorders such as myocardial ischemia.