2,7-bis(8-aminooctyl)benzo[lmn][3,8]phenanthroline-1,3,6,8(2H,7H)-tetraone | 1191059-00-3

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 吡啶及其衍生物
• 英文名称: 2,7-bis(8-aminooctyl)benzo[lmn][3,8]phenanthroline-1,3,6,8(2H,7H)-tetraone
• 英文别名: 6,13-Bis(8-aminooctyl)-6,13-diazatetracyclo[6.6.2.04,16.011,15]hexadeca-1(15),2,4(16),8,10-pentaene-5,7,12,14-tetrone
• CAS: 1191059-00-3
• 化学式: C₃₀H₄₀N₄O₄
• 分子量: 520.672
• InChiKey: BDURQTRFLVTBRV-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.3
• 重原子数：
  38
• 可旋转键数：
  16
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.53
• 拓扑面积：
  127
• 氢给体数：
  2
• 氢受体数：
  6

反应信息

• 作为反应物：
  描述：

  2,7-bis(8-aminooctyl)benzo[lmn][3,8]phenanthroline-1,3,6,8(2H,7H)-tetraone 、 邻甲氧基苯甲醛 以 甲苯 为溶剂， 反应 3.0h， 生成
  参考文献：
  名称：

  Design, Synthesis, and Biological Evaluation of Substituted Naphthalene Imides and Diimides as Anticancer Agent

  摘要：

  Naphthalimmide (NI) and 1,4,5,8-naphthalenetetracarboxylic diimide (NDI) derivatives were synthesized and evaluated for their antiproliferative activity. NDI derivatives 1-9 were more cytotoxic than the corresponding NI derivatives 10-18. The molecular mechanisms of 1 and 2 were investigated in comparison to mitonafide. They interacted with DNA, were not topoisomerase II alpha poisons, triggered caspase activation, caused p53 protein accumulation, and down-regulated AKT survival. Furthermore, 1 and 2 caused a decrease of ERK1/2 and, unlike mitonafide, inhibited ERKs phosphorylation.

  DOI：

  10.1021/jm901131m
• 作为产物：
  描述：

  1,8-辛二胺 、 1,4,5,8-萘四甲酸酐 以 乙醇 、 甲苯 为溶剂， 反应 24.0h， 生成 2,7-bis(8-aminooctyl)benzo[lmn][3,8]phenanthroline-1,3,6,8(2H,7H)-tetraone
  参考文献：
  名称：

  Design, Synthesis, and Biological Evaluation of Substituted Naphthalene Imides and Diimides as Anticancer Agent

  摘要：

  Naphthalimmide (NI) and 1,4,5,8-naphthalenetetracarboxylic diimide (NDI) derivatives were synthesized and evaluated for their antiproliferative activity. NDI derivatives 1-9 were more cytotoxic than the corresponding NI derivatives 10-18. The molecular mechanisms of 1 and 2 were investigated in comparison to mitonafide. They interacted with DNA, were not topoisomerase II alpha poisons, triggered caspase activation, caused p53 protein accumulation, and down-regulated AKT survival. Furthermore, 1 and 2 caused a decrease of ERK1/2 and, unlike mitonafide, inhibited ERKs phosphorylation.

  DOI：

  10.1021/jm901131m

文献信息

• Naphthalene diimides with improved solubility for visible light photoredox catalysis
  作者：Barbara Reiß、Hans-Achim Wagenknecht

  DOI：10.3762/bjoc.15.201

  日期：——

  Five core-substituted naphthalene diimides bearing two dialkylamino groups were synthesized as potential visible light photoredox catalysts and characterized by methods of optical spectroscopy and electrochemistry in comparison with one unsubstituted naphthalene diimide as reference. The core-substituted naphthalene diimides differ by the alkyl groups at the imide nitrogens and at the nitrogens of

  合成了五种带有两个二烷基氨基的核取代萘二酰亚胺作为潜在的可见光光氧化还原催化剂，并通过光谱和电化学方法对其进行了表征，并与一种未取代的萘二酰亚胺作为参考进行比较。核取代的萘二酰亚胺的不同之处在于酰亚胺氮上的烷基和核上两个取代基的氮上的烷基不同，以增强它们在DMF中的溶解度，从而增强它们的光氧化还原催化潜力。1-乙基丙基作为酰亚胺氮上相当短且支化的烷基取代基，而正丙基作为核心胺处的短且非支化的烷基取代基产生了最好的溶解度。给电子二氨基烷基取代基与萘二酰亚胺的缺电子芳香核一起增加了其光激发态的电荷转移特性，从而将其吸收转移到可见光（500-650 nm）。激发态还原电位估计约为+1.0 V（相对于SCE），足以光催化典型的有机反应。以1-辛醛的α-烷基化反应为基准反应，测试了可见光范围内的光氧化还原催化活性。使用 LED 在 520 nm 至 640 nm 之间的可见光范围内进行照射。可见光照
• Design, Synthesis, and Biological Evaluation of Substituted Naphthalene Imides and Diimides as Anticancer Agent
  作者：Vincenzo Tumiatti、Andrea Milelli、Anna Minarini、Marialuisa Micco、Anna Gasperi Campani、Laura Roncuzzi、Daniela Baiocchi、Jessica Marinello、Giovanni Capranico、Maddalena Zini、Claudio Stefanelli、Carlo Melchiorre

  DOI：10.1021/jm901131m

  日期：2009.12.10

  Naphthalimmide (NI) and 1,4,5,8-naphthalenetetracarboxylic diimide (NDI) derivatives were synthesized and evaluated for their antiproliferative activity. NDI derivatives 1-9 were more cytotoxic than the corresponding NI derivatives 10-18. The molecular mechanisms of 1 and 2 were investigated in comparison to mitonafide. They interacted with DNA, were not topoisomerase II alpha poisons, triggered caspase activation, caused p53 protein accumulation, and down-regulated AKT survival. Furthermore, 1 and 2 caused a decrease of ERK1/2 and, unlike mitonafide, inhibited ERKs phosphorylation.