2,4-Dichloro-6-(2-pyrazol-1-ylethyliminomethyl)phenol | 1227291-68-0

• 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: 2,4-Dichloro-6-(2-pyrazol-1-ylethyliminomethyl)phenol
• CAS: 1227291-68-0
• 化学式: C₁₂H₁₁Cl₂N₃O
• 分子量: 284.145
• InChiKey: ZYEYGCJFMPCHGR-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.3
• 重原子数：
  18
• 可旋转键数：
  4
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.17
• 拓扑面积：
  50.4
• 氢给体数：
  1
• 氢受体数：
  3

反应信息

• 作为反应物：
  描述：

  2,4-Dichloro-6-(2-pyrazol-1-ylethyliminomethyl)phenol 在 sodium tetrahydroborate 作用下， 以 甲醇 为溶剂， 以84%的产率得到2,4-Dichloro-6-[(2-pyrazol-1-ylethylamino)methyl]phenol
  参考文献：
  名称：

  Synthesis, characterization and cytotoxic activity of gallium(III) complexes anchored by tridentate pyrazole-based ligands

  摘要：

  Reactions of GaCl3 with pyrazole-containing ligands of the pyrazole-imine-phenol (HL1-HL3) or pyrazole-amine-phenol (HL4-HL6) types led to the synthesis of well-defined [GaL2](+) homoleptic complexes (1-6). Complexes 1-6 were characterized by elemental analysis, ESI-MS (electrospray ionization-mass spectrometry), IR and NMR spectroscopies, and in the case of Complex 1 also by X-ray diffraction analysis. In complexes 1-3, the pyrazole-imine-phenolate ligands act as monoanionic chelators that coordinate to the metal in a meridional fashion, while 4-6 contain monoanionic and facially coordinated pyrazole-amine-phenolate ligands. Complexes 1-3 have a greater stability in solution compared to 4-6, which have shown a more pronounced tendency to release the respective ancillary ligands. The cytotoxicity of 1-6 and of the respective ligands (HL1-HL6) was evaluated against human prostate cancer cells PC-3 and human breast cancer cells MCF-7. The substituents of the phenolate rings strongly influenced the cytotoxicity of the compounds. Complexes 3 and 6 that contain chloride substituents at the phenolate rings have shown the highest cytotoxicity, including in the cisplatin-resistant PC-3 cell line. The cytotoxic profile of 3 and 6 is very similar to the one displayed by the respective anchor ligands, respectively HL1 and HL6. The cytotoxic activity of 3 and 6 is slightly increased by the presence of transferrin, and both complexes provoke cell death mainly by induction of apoptotic pathways. (C) 2010 Elsevier Inc. All rights reserved.

  DOI：

  10.1016/j.jinorgbio.2010.01.003
• 作为产物：
  描述：

  2-吡唑-1-基乙胺 、 3,5-二氯水杨醛 以 乙醇 为溶剂， 反应 2.0h， 以88%的产率得到2,4-Dichloro-6-(2-pyrazol-1-ylethyliminomethyl)phenol
  参考文献：
  名称：

  Synthesis, characterization and cytotoxic activity of gallium(III) complexes anchored by tridentate pyrazole-based ligands

  摘要：

  Reactions of GaCl3 with pyrazole-containing ligands of the pyrazole-imine-phenol (HL1-HL3) or pyrazole-amine-phenol (HL4-HL6) types led to the synthesis of well-defined [GaL2](+) homoleptic complexes (1-6). Complexes 1-6 were characterized by elemental analysis, ESI-MS (electrospray ionization-mass spectrometry), IR and NMR spectroscopies, and in the case of Complex 1 also by X-ray diffraction analysis. In complexes 1-3, the pyrazole-imine-phenolate ligands act as monoanionic chelators that coordinate to the metal in a meridional fashion, while 4-6 contain monoanionic and facially coordinated pyrazole-amine-phenolate ligands. Complexes 1-3 have a greater stability in solution compared to 4-6, which have shown a more pronounced tendency to release the respective ancillary ligands. The cytotoxicity of 1-6 and of the respective ligands (HL1-HL6) was evaluated against human prostate cancer cells PC-3 and human breast cancer cells MCF-7. The substituents of the phenolate rings strongly influenced the cytotoxicity of the compounds. Complexes 3 and 6 that contain chloride substituents at the phenolate rings have shown the highest cytotoxicity, including in the cisplatin-resistant PC-3 cell line. The cytotoxic profile of 3 and 6 is very similar to the one displayed by the respective anchor ligands, respectively HL1 and HL6. The cytotoxic activity of 3 and 6 is slightly increased by the presence of transferrin, and both complexes provoke cell death mainly by induction of apoptotic pathways. (C) 2010 Elsevier Inc. All rights reserved.

  DOI：

  10.1016/j.jinorgbio.2010.01.003