4-氯-N-(3-甲氧基苯基)-1,3-噻唑-2-胺 | 912969-59-6

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 中文名称: 4-氯-N-(3-甲氧基苯基)-1,3-噻唑-2-胺
• 英文名称: (4-chlorothiazol-2-yl)-3-methoxyphenylamine
• 英文别名: 4-Chloro-N-(3-methoxyphenyl)thiazol-2-amine；4-chloro-N-(3-methoxyphenyl)-1,3-thiazol-2-amine
• CAS: 912969-59-6
• 化学式: C₁₀H₉ClN₂OS
• 分子量: 240.713
• InChiKey: IPVZNNIVNOHRCQ-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.8
• 重原子数：
  15
• 可旋转键数：
  3
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.1
• 拓扑面积：
  62.4
• 氢给体数：
  1
• 氢受体数：
  4

反应信息

• 作为反应物：
  描述：

  4-氯-N-(3-甲氧基苯基)-1,3-噻唑-2-胺 、 2-甲基咪唑 以 N,N-二甲基甲酰胺 为溶剂， 以48%的产率得到N-(3-methoxyphenyl)-4-(2-methylimidazol-1-yl)-1,3-thiazol-2-amine
  参考文献：
  名称：

  [4-(Imidazol-1-yl)thiazol-2-yl]phenylamines. A Novel Class of Highly Potent Colchicine Site Binding Tubulin Inhibitors: Synthesis and Cytotoxic Activity on Selected Human Cancer Cell Lines

  摘要：

  Synthesis and cytotoxic activity in the submicromolar range of a series of [4-(imidazol-l-yl)thiazol-2-yl]-phenylamines are described. Cell cycle dependent cytotoxicity on RKO human colon carcinoma cells with inducible expression of p27(kip1) and the influence on microtubule formation were investigated. Considering the significant correlation between the IC50 values of tubulin polymerization inhibition, [H-3]colchicine competition, and cytotoxicity of the investigated compounds, tubulin is the main cellular target. The inhibition of microtubule formation was shown to be mediated by interference with the colchicine binding site of tubulin. In depth analysis of the investigated compounds allowed the identification of modifications that altered the pharmacological profile of the compounds from a mitosis-inducing phenotype to a G1 cell cycle arresting phenotype.

  DOI：

  10.1021/jm060545p
• 作为产物：
  描述：

  N-benzoyl-N′-(3-methoxyphenyl)thiourea 在 吡啶 、 sodium hydroxide 、 三氯氧磷 作用下， 以 乙醇 为溶剂， 反应 5.0h， 生成 4-氯-N-(3-甲氧基苯基)-1,3-噻唑-2-胺
  参考文献：
  名称：

  [4-(Imidazol-1-yl)thiazol-2-yl]phenylamines. A Novel Class of Highly Potent Colchicine Site Binding Tubulin Inhibitors: Synthesis and Cytotoxic Activity on Selected Human Cancer Cell Lines

  摘要：

  Synthesis and cytotoxic activity in the submicromolar range of a series of [4-(imidazol-l-yl)thiazol-2-yl]-phenylamines are described. Cell cycle dependent cytotoxicity on RKO human colon carcinoma cells with inducible expression of p27(kip1) and the influence on microtubule formation were investigated. Considering the significant correlation between the IC50 values of tubulin polymerization inhibition, [H-3]colchicine competition, and cytotoxicity of the investigated compounds, tubulin is the main cellular target. The inhibition of microtubule formation was shown to be mediated by interference with the colchicine binding site of tubulin. In depth analysis of the investigated compounds allowed the identification of modifications that altered the pharmacological profile of the compounds from a mitosis-inducing phenotype to a G1 cell cycle arresting phenotype.

  DOI：

  10.1021/jm060545p

文献信息

• [4-(Imidazol-1-yl)thiazol-2-yl]phenylamines. A Novel Class of Highly Potent Colchicine Site Binding Tubulin Inhibitors: Synthesis and Cytotoxic Activity on Selected Human Cancer Cell Lines
  作者：Siavosh Mahboobi、Andreas Sellmer、Heymo Höcher、Emerich Eichhorn、Thomas Bär、Mathias Schmidt、Thomas Maier、Josef F. Stadlwieser、Thomas L. Beckers

  DOI：10.1021/jm060545p

  日期：2006.9.1

  Synthesis and cytotoxic activity in the submicromolar range of a series of [4-(imidazol-l-yl)thiazol-2-yl]-phenylamines are described. Cell cycle dependent cytotoxicity on RKO human colon carcinoma cells with inducible expression of p27(kip1) and the influence on microtubule formation were investigated. Considering the significant correlation between the IC50 values of tubulin polymerization inhibition, [H-3]colchicine competition, and cytotoxicity of the investigated compounds, tubulin is the main cellular target. The inhibition of microtubule formation was shown to be mediated by interference with the colchicine binding site of tubulin. In depth analysis of the investigated compounds allowed the identification of modifications that altered the pharmacological profile of the compounds from a mitosis-inducing phenotype to a G1 cell cycle arresting phenotype.