1-[4-(4-methoxyphenyl)-1,3-thiazol-2-yl]-5-(trifluoromethyl)-1H-pyrazole-4-carboxylic acid

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 唑类
• 英文名称: 1-[4-(4-methoxyphenyl)-1,3-thiazol-2-yl]-5-(trifluoromethyl)-1H-pyrazole-4-carboxylic acid
• 英文别名: 1-[4-(4-methoxyphenyl)-1,3-thiazol-2-yl]-5-(trifluoromethyl)pyrazole-4-carboxylic acid
• 化学式: C₁₅H₁₀F₃N₃O₃S
• 分子量: 369.324
• InChiKey: QKNWCKIISBFDQN-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.3
• 重原子数：
  25
• 可旋转键数：
  4
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.13
• 拓扑面积：
  106
• 氢给体数：
  1
• 氢受体数：
  9

反应信息

• 作为反应物：
  描述：

  1-[4-(4-methoxyphenyl)-1,3-thiazol-2-yl]-5-(trifluoromethyl)-1H-pyrazole-4-carboxylic acid 、 3-二乙胺基丙胺 在 N,N'-羰基二咪唑 作用下， 生成 N-[3-(diethylamino)propyl]-1-[4-(4-methoxyphenyl)-1,3-thiazol-2-yl]-5-(trifluoromethyl)pyrazole-4-carboxamide
  参考文献：
  名称：

  Novel Thiazole-Based Heterocycles as Selective Inhibitors of Fibrinogen-Mediated Platelet Aggregation

  摘要：

  The synthesis and biological activity of novel thiazole-based heterocycles as inhibitors of thrombin-induced human platelet aggregation are described. Further evaluation of selected compounds show they inhibit platelet aggregation as stimulated by a variety of agonists. The more active compounds also were found to inhibit fibrinogen binding to platelets. To further delineate the mechanism of action of these compounds, direct binding studies with the purified glycoprotein (GP) IIb/IIIa receptor were performed. Flow cytometry analyses of 24 and 32 indicate that these compounds block the activation process of the GPIIb/IIIa receptor without denaturing the integrin receptor. On the basis of these studies, 32 exhibited the best profile as a novel nonpeptide inhibitor of fibrinogen-mediated platelet aggregation.

  DOI：

  10.1021/jm00001a008
• 作为产物：
  描述：

  ethyl 1-[4-(4-methoxyphenyl)-1,3-thiazol-2-yl]-5-(trifluoromethyl)-1H-pyrazole-4-carboxylate 在 氢氧化钾 作用下， 以 乙醇 为溶剂， 反应 3.0h， 生成 1-[4-(4-methoxyphenyl)-1,3-thiazol-2-yl]-5-(trifluoromethyl)-1H-pyrazole-4-carboxylic acid
  参考文献：
  名称：

  Novel Thiazole-Based Heterocycles as Selective Inhibitors of Fibrinogen-Mediated Platelet Aggregation

  摘要：

  The synthesis and biological activity of novel thiazole-based heterocycles as inhibitors of thrombin-induced human platelet aggregation are described. Further evaluation of selected compounds show they inhibit platelet aggregation as stimulated by a variety of agonists. The more active compounds also were found to inhibit fibrinogen binding to platelets. To further delineate the mechanism of action of these compounds, direct binding studies with the purified glycoprotein (GP) IIb/IIIa receptor were performed. Flow cytometry analyses of 24 and 32 indicate that these compounds block the activation process of the GPIIb/IIIa receptor without denaturing the integrin receptor. On the basis of these studies, 32 exhibited the best profile as a novel nonpeptide inhibitor of fibrinogen-mediated platelet aggregation.

  DOI：

  10.1021/jm00001a008

文献信息

• Novel Thiazole-Based Heterocycles as Selective Inhibitors of Fibrinogen-Mediated Platelet Aggregation
  作者：Pauline J. Sanfilippo、Patricia Andrade-Gordon、Maud J. Urbanski、Kimberly N. Beers、Annette Eckardt、Robert Falotico、Mark H. Ginsberg、Steve Offord、Jeffrey B. Press

  DOI：10.1021/jm00001a008

  日期：1995.1

  The synthesis and biological activity of novel thiazole-based heterocycles as inhibitors of thrombin-induced human platelet aggregation are described. Further evaluation of selected compounds show they inhibit platelet aggregation as stimulated by a variety of agonists. The more active compounds also were found to inhibit fibrinogen binding to platelets. To further delineate the mechanism of action of these compounds, direct binding studies with the purified glycoprotein (GP) IIb/IIIa receptor were performed. Flow cytometry analyses of 24 and 32 indicate that these compounds block the activation process of the GPIIb/IIIa receptor without denaturing the integrin receptor. On the basis of these studies, 32 exhibited the best profile as a novel nonpeptide inhibitor of fibrinogen-mediated platelet aggregation.