2-methoxy-4-(5-methoxy-1H-benzimidazol-2-yl)phenol | 1441800-35-6

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 苯并咪唑类
• 英文名称: 2-methoxy-4-(5-methoxy-1H-benzimidazol-2-yl)phenol
• 英文别名: 5-methoxy-2-(3’-methoxy-4’-hydroxyphenyl)-1H-benzimidazole；2-methoxy-4-(6-methoxy-1H-benzimidazol-2-yl)phenol
• CAS: 1441800-35-6
• 化学式: C₁₅H₁₄N₂O₃
• 分子量: 270.288
• InChiKey: RHYCRTYAPUVOEN-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.7
• 重原子数：
  20
• 可旋转键数：
  3
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.13
• 拓扑面积：
  67.4
• 氢给体数：
  2
• 氢受体数：
  4

反应信息

• 作为反应物：
  描述：

  2-氯-1-吗琳乙-1-酮 、 2-methoxy-4-(5-methoxy-1H-benzimidazol-2-yl)phenol 在 potassium carbonate 作用下， 以 N,N-二甲基甲酰胺 为溶剂， 以89 %的产率得到2-(2-methoxy-4-{5-methoxy-1H-benzoimidazol-2-yl}phenoxy)-1-morpholinoethan-1-one
  参考文献：
  名称：

  作为微管蛋白聚合抑制剂的苯并咪唑衍生物：设计、合成和体外细胞毒性研究

  摘要：

  本研究设计并合成了一类新的苯并咪唑衍生物作为微管蛋白聚合抑制剂。在选定的人类癌细胞上对所开发的分子的体外抗癌特性进行了研究。化合物7n和7u具有最高的细胞毒性， IC 50值范围为 2.55 至 17.89 µM，对 SK-Mel-28 细胞具有特异性。它们对正常大鼠肾上皮 NRK52E 细胞的细胞毒性降低了 5 倍，这意味着它们对正常健康细胞无害。应用 AO/EB、DCFDA 和 DAPI 等细胞染色程序来理解细胞凋亡的内在机制，显示细胞核和形态学的改变。进行膜联蛋白 V 结合和 JC-1 研究以评估 SK-Mel-28 细胞系中细胞凋亡的程度和线粒体跨膜电位的下降。化合物7n剂量依赖性地阻止细胞周期的 G2/M 期，基于目标的结果表明7n抑制微管蛋白聚合（IC 50为 5.05±0.13 μM）。还对微管蛋白（PDB ID：3E22）进行了计算研究，以研究化合物7n和7u分别与微管蛋白的稳定结合相互作用。

  DOI：

  10.1016/j.bmcl.2023.129494
• 作为产物：
  描述：

  香草醛 、 2-硝基-4-甲氧基苯胺 在 sodium dithionite 作用下， 以 甲醇 为溶剂， 反应 0.6h， 以82%的产率得到2-methoxy-4-(5-methoxy-1H-benzimidazol-2-yl)phenol
  参考文献：
  名称：

  Synthesis, antioxidant, and antimicrobial evaluation of some 2-arylbenzimidazole derivatives

  摘要：

  A series of 2-arylbenzimidazole derivatives (3a-3p and 4a-4i) were synthesized and evaluated as potential antioxidant and antimicrobial agents. Their antioxidant properties were evaluated by various in vitro assays including hydroxyl radical (HO center dot) scavenging, superoxide radical anion (O-2(center dot)) scavenging, 1,1-diphenyl- 2-picrylhydrazyl (DPPH) radical scavenging, and ferric reducing antioxidant power. Results demonstrated that compounds with hydroxyl group at the 5-position of benzimidazole ring had a comparable or better antioxidant activity in comparison to standard antioxidant tert-butylhydroquinone (TBHQ). Markedly, compound 4h that showed the highest HO center dot scavenging activity (EC50 = 46 mu M) in vitro had a significant reduction of 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH)-induced intracellular oxidative stress and H2O2-induced cell death. In addition, these compounds showed moderate to good inhibitory activity against Staphylococcus aureus selectively at noncytotoxic concentrations. (C) 2013 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2013.05.004

文献信息

• A novel synthesis of 2-arylbenzimidazoles in molecular sieves-MeOH system and their antitubercular activity
  作者：Amit K. Chaturvedi、Amit Kumar Verma、Jay Prakash Thakur、Sudeep Roy、Shashi Bhushan Tripathi、Balagani Sathish Kumar、Sadiya Khwaja、Naresh K. Sachan、Ashok Sharma、Debabrata Chanda、Karuna Shanker、Dharmendra Saikia、Arvind S. Negi

  DOI：10.1016/j.bmc.2018.07.049

  日期：2018.8

  Arylbenzimidazoles have been synthesized as antimycobacterial agents. An efficient synthesis has been developed for 2-arylbenzimidazoles from o-phenylenediamines and aromatic aldehydes in molecular sieves-methanol system. The methodology is straightforward to get 2-arylbenzimidazoles (3a-3z) in excellent yields with high chemoselectivity over 2-aryl-1-benzylbenzimidazoles (4a-4z). All these benzimidazole analogues were evaluated against M. tuberculosis in BACTEC radiometric assay. The compounds 4y and 4z exhibited potential antitubercular activity against M. tuberculosis H (37)Rv, MIC at 16 mu M and 24 mu M respectively. The best compound of the series i.e. compound 4y was well tolerated by Swiss-albino mice in acute oral toxicity. Compound 4y possessing a diarylbenzimidazole core, can further be optimized for better activity.
• Synthesis, antioxidant, and antimicrobial evaluation of some 2-arylbenzimidazole derivatives
  作者：Binhua Zhou、Baojian Li、Wei Yi、Xianzhang Bu、Lin Ma

  DOI：10.1016/j.bmcl.2013.05.004

  日期：2013.7

  A series of 2-arylbenzimidazole derivatives (3a-3p and 4a-4i) were synthesized and evaluated as potential antioxidant and antimicrobial agents. Their antioxidant properties were evaluated by various in vitro assays including hydroxyl radical (HO center dot) scavenging, superoxide radical anion (O-2(center dot)) scavenging, 1,1-diphenyl- 2-picrylhydrazyl (DPPH) radical scavenging, and ferric reducing antioxidant power. Results demonstrated that compounds with hydroxyl group at the 5-position of benzimidazole ring had a comparable or better antioxidant activity in comparison to standard antioxidant tert-butylhydroquinone (TBHQ). Markedly, compound 4h that showed the highest HO center dot scavenging activity (EC50 = 46 mu M) in vitro had a significant reduction of 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH)-induced intracellular oxidative stress and H2O2-induced cell death. In addition, these compounds showed moderate to good inhibitory activity against Staphylococcus aureus selectively at noncytotoxic concentrations. (C) 2013 Elsevier Ltd. All rights reserved.
• Benzimidazole derivatives as tubulin polymerization inhibitors: Design, synthesis and in vitro cytotoxicity studies
  作者：Kritika Laxmikeshav、Ziaur Rahman、Ashutosh Mahale、Durgesh Gurukkala Valapil、Pravesh Sharma、Joel George、Regur Phanindranath、Manoj P. Dandekar、Onkar P. Kulkarni、Narayana Nagesh、Nagula Shankaraiah

  DOI：10.1016/j.bmcl.2023.129494

  日期：2023.11

  A new class of benzimidazole derivatives as tubulin polymerization inhibitors has been designed and synthesized in this study. The in vitro anticancer profile of the developed molecules was reconnoitred on selected human cancer cells. The highest cytotoxicity was illustrated by compounds 7n and 7u with IC50 values ranging from 2.55 to 17.89 µM with specificity toward SK-Mel-28 cells. They displayed

  本研究设计并合成了一类新的苯并咪唑衍生物作为微管蛋白聚合抑制剂。在选定的人类癌细胞上对所开发的分子的体外抗癌特性进行了研究。化合物7n和7u具有最高的细胞毒性， IC 50值范围为 2.55 至 17.89 µM，对 SK-Mel-28 细胞具有特异性。它们对正常大鼠肾上皮 NRK52E 细胞的细胞毒性降低了 5 倍，这意味着它们对正常健康细胞无害。应用 AO/EB、DCFDA 和 DAPI 等细胞染色程序来理解细胞凋亡的内在机制，显示细胞核和形态学的改变。进行膜联蛋白 V 结合和 JC-1 研究以评估 SK-Mel-28 细胞系中细胞凋亡的程度和线粒体跨膜电位的下降。化合物7n剂量依赖性地阻止细胞周期的 G2/M 期，基于目标的结果表明7n抑制微管蛋白聚合（IC 50为 5.05±0.13 μM）。还对微管蛋白（PDB ID：3E22）进行了计算研究，以研究化合物7n和7u分别与微管蛋白的稳定结合相互作用。