| 1621456-26-5

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 喹啉及其衍生物
• CAS: 1621456-26-5
• 化学式: C₁₆H₁₂ClCuN₃O₅
• 分子量: 425.287
• InChiKey: DRAWUGDUALGQNV-DWZOPUQCSA-M

计算性质

• 辛醇/水分配系数(LogP)：
  None
• 重原子数：
  None
• 可旋转键数：
  None
• 环数：
  None
• sp3杂化的碳原子比例：
  None
• 拓扑面积：
  None
• 氢给体数：
  None
• 氢受体数：
  None

反应信息

• 作为产物：
  描述：

  copper(II) nitrate trihydrate 、 4-chloro-2-(quinolin-8-yliminomethyl)phenol 以 水 为溶剂， 反应 48.0h， 以80%的产率得到
  参考文献：
  名称：

  Synthesis, crystal structure, cytotoxicity and cell apoptosis induction of a copper(II)-based Schiff base complex

  摘要：

  A new copper(II) complex, [Cu-II(ClQP)(NO3)(H2O)] (1), bearing with 4-Chloro-2-(quinolin-8-yliminomethyl)- phenol (HClQP) as Schiff base ligand, was synthesized and structurally characterized by IR, elemental analysis, ESI-MS and single crystal X-ray diffraction analysis. The crystal structure revealed that complex 1 was five coordinated by one N, N, O-tridentated ClQP, one H2O and one nitrate anion, respectively, to form a pyramidal coordinating geometry. The antitumor activity of complex 1 against HepG2, BEL-7404, MGC80-3 and NCI-H460 tumor cell lines were screened by MTT assay. The IC50 values were in the range of 6.53-23.62 mu M, in which HepG2 cell line showed the highest sensitivity to complex 1. It is worth noting that complex 1 did not show cytotoxicity to human normal liver cell line HL-7702, suggesting its cytotoxic selectivity on these tumor cell lines. Towards the most sensitive HepG2 cell line, complex 1 significantly induced S phase cell cycle arrest, probably due to its intercalative binding with DNA based on its rigid planar structure as well as the planar aromatic groups of HClQP ligand. Furthermore, the HepG2 cells treated with 1 showed typical cell apoptosis in dose-dependent manner visualized by Hoechst 33258 staining. And the cell apoptosis in the HepG2 cells induced by 1 was further confirmed by the loss of mitochondrial membrane potential visualized by JC-1 staining in cells. The detailed flow cytometric assay revealed that complex 1 could up-regulate the expression of the caspase-3. From these results, it can be concluded that complex 1 induced the mitochondrion-mediated cell apoptosis by caspase- 3 activation, most probably due to the S phase cell cycle arrest in HepG2 cells owing to the DNA binding affinity of 1 via intercalative binding mode. (C) 2014 Elsevier B.V. All rights reserved.

  DOI：

  10.1016/j.ica.2014.05.041