1-(bispyridin-2-ylmethylamino)-3-chloropropan-2-ol

• 分子结构分类: 有机化合物 - 有机氮化合物
• 英文名称: 1-(bispyridin-2-ylmethylamino)-3-chloropropan-2-ol
• 英文别名: 1-Chloro-3-(dipyridin-2-ylmethylamino)propan-2-ol；1-chloro-3-(dipyridin-2-ylmethylamino)propan-2-ol
• 化学式: C₁₄H₁₆ClN₃O
• 分子量: 277.754
• InChiKey: YAAWYQVGLJYVFG-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  0.9
• 重原子数：
  19
• 可旋转键数：
  6
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.29
• 拓扑面积：
  58
• 氢给体数：
  2
• 氢受体数：
  4

反应信息

• 作为反应物：
  描述：

  iron(III) chloride hexahydrate 、 1-(bispyridin-2-ylmethylamino)-3-chloropropan-2-ol 在 sodium nitrate 作用下， 以 甲醇 为溶剂， 生成
  参考文献：
  名称：

  Highly efficient synthetic iron-dependent nucleases activate both intrinsic and extrinsic apoptotic death pathways in leukemia cancer cells

  摘要：

  The nuclease activity and the cytotoxicity toward human leukemia cancer cells of iron complexes, [Fe(HPClNOL) Cl-2]NO3 (1), [Cl(HPClNOL)Fe(mu-O)Fe(HPClNOL)Cl]Cl-2 center dot 2H(2)O (2), and [(SO4)(HPCINOL)Fe(mu-O)Fe(HPCINOL)(SO4)]center dot 6H(2)O (3) (HPCINOL = 1-(bis-pyridin-2-ylmethyl-amino)-3-chloropropan-2-ol), were investigated. Each complex was able to promote plasmid DNA cleavage and change the supercoiled form of the plasmid to circular and linear ones. Kinetic data revealed that (1), (2) and (3) increase the rate of DNA hydrolysis about 278, 192 and 339 million-fold, respectively. The activity of the complexes was inhibited by distamycin, indicating that they interact with the minor groove of the DNA. The cytotoxic activity of the complexes toward U937, HL-60, Jukart and THP-1 leukemia cancer cells was studied employing 3-(4,5-dimethythiazol-2-y1)-2,5-diphenyl tetrazolium bromide (MTT), fluorescence and electronic transmission microscopies, flow cytometry and a cytochrome C release assay. Compound (2) has the highest activity toward cancer cells and is the least toxic for normal ones (i.e. peripheral blood mononuclear cells (PBMCs)). In contrast, compound (1) is the least active toward cancer cells but displays the highest toxicity toward normal cells. Transmission electronic microscopy indicates that cell death shows features typical of apoptotic cells, which was confirmed using the annexin V-FITC/PI (fluorescein isothiocyanate/propidium iodide) assay. Furthermore, our data demonstrate that at an early stage during the treatment with complex (2) mitochondria lose their transmembrane potential, resulting in cytochrome C release. A quantification of caspases 3,9 (intrinsic apoptosis pathway) and caspase 8 (extrinsic apoptosis pathway) indicated that both the intrinsic (via mitochondria) and extrinsic (via death receptors) pathways are involved in the apoptotic stimuli. (C) 2013 Elsevier Inc. All rights reserved.

  DOI：

  10.1016/j.jinorgbio.2013.07.019