3a-phenyl-1,2,3,3a-tetrahydropyrrolo<2,1-b>-benzothiazol-1-one | 5218-24-6

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 英文名称: 3a-phenyl-1,2,3,3a-tetrahydropyrrolo<2,1-b>-benzothiazol-1-one
• 英文别名: 3a-phenyl-3,3a-dihydro-2H-benzo[d]pyrrolo[2,1-b]thiazol-1-one；3a-Phenyl-2,3-dihydropyrrolo[2,1-b][1,3]benzothiazol-1-one
• CAS: 5218-24-6
• 化学式: C₁₆H₁₃NOS
• 分子量: 267.351
• InChiKey: ZAZNEWXJOHOGBS-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.1
• 重原子数：
  19
• 可旋转键数：
  1
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.19
• 拓扑面积：
  45.6
• 氢给体数：
  0
• 氢受体数：
  2

反应信息

• 作为产物：
  描述：

  2-氨基苯硫醇 、 3-苯丙烯溴酸酯 以47%的产率得到3a-phenyl-1,2,3,3a-tetrahydropyrrolo<2,1-b>-benzothiazol-1-one
  参考文献：
  名称：

  1,2,3,3a-四氢吡咯并[2,1-b]-苯并噻唑-，-噻唑-或-恶唑-1-酮在啮齿动物中的合成及抗惊厥活性。

  摘要：

  为了确定更有效的抗惊厥药，并深入了解确定新型抗惊厥药效能的结构性质，一些3a取代的四氢吡咯并[2,1-b]苯并噻唑-1-酮（1a-d）和噻唑和已合成恶唑类似物（分别为2a-c和3a-c），并测试了其对啮齿动物中异烟肼诱发的癫痫发作的抗惊厥活性。活性更强的化合物2a在小鼠和大鼠中的中位有效剂量（ED50，ip）分别为24.3 mg kg-1和15.9 mg kg-1，经过更广泛的研究，发现其增强了地西epa的作用。在化合物1-3的抗惊厥活性和亲脂性分子之间没有观察到明显的相关性。分子模型研究证明了抗癫痫药物苯巴比妥和化合物1-3之间的结构相似性，并用于推导初步的结构活性关系。结果表明2a作为抗惊厥药是有吸引力的候选药物，值得进一步研究，可能有助于其他抗惊厥药的设计。

  DOI：

  10.1111/j.2042-7158.1996.tb03984.x

文献信息

• Synthesis and anticonvulsant activity of some 1,2,3,3a-tetrahydropyrrolo[2,1-b]benzothiazol-1-ones and pyrrolo[2,1-b]thiazole analogues
  作者：G Trapani、M Franco、A Latrofa、G Genchi、G Siro Brigiani、M Mazzoccoli、M Persichella、M Serra、G Biggio、G Liso

  DOI：10.1016/0223-5234(94)90038-8

  日期：1994.1

  Tetrahydropyrrolo[2,1-b]benzothiazol-1-ones 2a-l and its analogues 3a-d were synthesized and tested as anticonvulsant agents. Some of the compounds were effective against bicuculline-induced seizures in mice. Binding studies with the prepared compounds using [H-3]flunitrazepam as a ligand for the benzodiazepine receptor and [H-3]muscimol for the gamma-aminobutyric acid (GABA) receptor, demonstrate that such compounds have no affinity for these recognition sites. On the contrary, some of these compounds reduced, at very high concentrations, the binding of [S-35]-tert-butylbicyclophosphorothionate ([S-35]TBPS) to recognition sites located at the GABA-coupled chloride channel. However, a lack of correlation between the anticonvulsant activity of these compounds and their capability to displace [S-35]TBPS binding was observed. Furthermore, an in vitro study on the most active compound 2a indicates that this compound may act intact on its target(s) rather than as a hydrolyzed compound 9.