(Z)-3-(2,5-dimethoxyphenyl)-2-phenylprop-2-enoic acid | 33769-67-4

• 分子结构分类: 有机化合物 - 苯丙烷和聚酮 - 二苯乙烯类
• 英文名称: (Z)-3-(2,5-dimethoxyphenyl)-2-phenylprop-2-enoic acid
• 英文别名: 3-(2,5-dimethoxy-phenyl)-2-phenyl-acrylic acid；2'.5'-Dimethoxy-stilben-α-carbonsaeure；3-(2,5-Dimethoxy-phenyl)-2-phenyl-acrylsaeure；2.5-Dimethoxy-α-phenyl-zimtsaeure；2,5-Dimethoxy-α-phenyl-cis-zimtsaeure
• CAS: 33769-67-4
• 化学式: C₁₇H₁₆O₄
• 分子量: 284.312
• InChiKey: ATVLNLGWMLJJQC-PTNGSMBKSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.5
• 重原子数：
  21
• 可旋转键数：
  5
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.12
• 拓扑面积：
  55.8
• 氢给体数：
  1
• 氢受体数：
  4

反应信息

• 作为产物：
  描述：

  sodium phenylacetate 、 2,5-二甲氧基苯甲醛 在 乙酸酐 作用下， 生成 (Z)-3-(2,5-dimethoxyphenyl)-2-phenylprop-2-enoic acid
  参考文献：
  名称：

  血管紧张素转换酶的抑制作用可保护内皮细胞免受缺氧/复氧损伤。

  摘要：

  血管紧张素转换酶（ACE）抑制剂可预防缺血/再灌注中的心血管组织损伤。但是，尚未详细评估内皮细胞的机制。培养的人主动脉内皮细胞（HAEC）在有或没有复氧的情况下暴露于缺氧状态。缺氧增强了细胞凋亡以及caspase-3的激活。复氧增加了乳酸脱氢酶的释放时间，并伴随着细胞内氧自由基的增加。ACE抑制剂奎那普利拉和缓激肽可显着减少细胞凋亡和乳酸脱氢酶的释放，而激肽B2受体拮抗剂和一氧化氮合酶抑制剂可降低这些作用。总之，缺氧通过增强caspase-3活性激活了自杀途径，导致HAEC凋亡，而随后的复氧通过增强氧自由基的产生而引起坏死。奎那普利拉可以通过增加缓激肽而上调组成型内皮型一氧化氮合酶，从而改善细胞凋亡和坏死，从而增加一氧化氮。

  DOI：

  10.1002/biof.5520110404

文献信息

• Synthesis of combretastatin analogs: evaluation of in vitro anticancer activity and molecular docking studies
  作者：Sunil Kumar、Sameer Sapra、Raj Kumar、Manish Kumar Gupta、Surrinder Koul、Tandeep Kour、Ajit Kumar Saxena、Om Prakash Suri、Kanahya Lal Dhar

  DOI：10.1007/s00044-011-9887-7

  日期：2012.11

  This study is based on the synthesis of a series of combretastatin analogs with different substitutions on one aryl moiety and a carboxylic group in connecting chain. Cis-configuration with respect to aryl groups was established by X-ray crystal analysis. All the synthesized compounds were evaluated for anticancer activity against a panel of cell lines. Six compounds 1a, 1b, 1c, 1k, 1n, and 1p showed marked anticancer activity against human colon (colo-205), lung (A549), ovary (IGROV-1), prostrate (PC-3), CNS (SF-295), leukemia (THP-1), and breast (MCF-7) cell lines. Out of these, 1b showed remarkable inhibitory activity comparable to paclitaxel against lung cancer cell line with IC50 3.9 mu M. Importance of carboxylic group in the synthesized compounds was studied by flexible docking study of 1b which showed the importance of carboxylic group interactions with colchicine-binding site of alpha beta-tubulin.A series of combretastatin analogs have been synthesized by condensation of phenyl acetic acid and different substituted aldehydes. All the synthesized compounds were evaluated for anticancer activity against a panel of cell lines. Six compounds 1a, 1b, 1c, 1k, 1n, and 1p showed better anticancer activity against human colon (colo-205), lung (A549), ovary (IGROV-1), prostrate (PC-3), CNS (SF-295), leukemia (THP-1), and breast (MCF-7) cell lines. Out of these, 1b showed marked inhibitory activity against lung cancer cell line with IC50 3.9 mu M.
• Royer,R. et al., Bulletin de la Societe Chimique de France, 1971, p. 2929 - 2933
  作者：Royer,R. et al.

  DOI：——

  日期：——
• Inhibition of angiotensin-converting enzyme protects endothelial cell against hypoxia/reoxygenation injury
  作者：Noriko Fujita、Hiroki Manabe、Norimasa Yoshida、Naohito Matsumoto、Jun Ochiai、Yasuharu Masui、Manabu Uemura、Yuji Naito、Toshikazu Yoshikawa

  DOI：10.1002/biof.5520110404

  日期：——

  suicide pathway leading to apoptosis of HAEC by enhancing caspase-3 activity, while subsequent reoxygenation induced necrosis by enhancing oxygen radical production. Quinaprilat could ameliorate both apoptosis and necrosis through the upregulation of constitutive endothelial nitric oxide synthase via an increase of bradykinin, with the resulting increase of nitric oxide.

  血管紧张素转换酶（ACE）抑制剂可预防缺血/再灌注中的心血管组织损伤。但是，尚未详细评估内皮细胞的机制。培养的人主动脉内皮细胞（HAEC）在有或没有复氧的情况下暴露于缺氧状态。缺氧增强了细胞凋亡以及caspase-3的激活。复氧增加了乳酸脱氢酶的释放时间，并伴随着细胞内氧自由基的增加。ACE抑制剂奎那普利拉和缓激肽可显着减少细胞凋亡和乳酸脱氢酶的释放，而激肽B2受体拮抗剂和一氧化氮合酶抑制剂可降低这些作用。总之，缺氧通过增强caspase-3活性激活了自杀途径，导致HAEC凋亡，而随后的复氧通过增强氧自由基的产生而引起坏死。奎那普利拉可以通过增加缓激肽而上调组成型内皮型一氧化氮合酶，从而改善细胞凋亡和坏死，从而增加一氧化氮。