2-pentoxycinnamaldehyde | 1190299-35-4

• 分子结构分类: 有机化合物 - 苯丙烷和聚酮 - 肉桂醛
• 英文名称: 2-pentoxycinnamaldehyde
• CAS: 1190299-35-4
• 化学式: C₁₄H₁₈O₂
• 分子量: 218.296
• InChiKey: BOOYYDPHVCOQNE-VQHVLOKHSA-N

反应信息

• 作为产物：
  描述：

  methyl 3-(2-(pentoxy)phenyl)acrylate 在 吗啉 、 红铝 作用下， 以 甲苯 为溶剂， 反应 2.0h， 以22%的产率得到2-pentoxycinnamaldehyde
  参考文献：
  名称：

  Cinnamaldehydes inhibit thioredoxin reductase and induce Nrf2: potential candidates for cancer therapy and chemoprevention

  摘要：

  Trans-cinnamaldehyde (CA) and its analogs 2-hydroxycinnamaldehyde and 2-benzoyloxycinnamaldehyde have been reported to possess antitumor activity. CA is also a known Nrf2 activator. In this study a series of, ortho-substituted cinnamaldehyde analogs was synthesized and screened for antiproliferative and thioredoxin reductase (TrxR)-inhibitory activities. Whereas CA was weakly cytotoxic and TrxR inhibiting, hydroxy and benzoyloxy substitutions resulted in analogs with enhanced antiproliferative activity paralleling increased potency in TrxR inactivation. A novel analog, 5-fluoro-2-hydroxycinnamaldehyde, was identified as exhibiting the strongest antitumor effect (GI(50) 1.6 mu M in HCT 116 cells) and TrxR inhibition (IC50 7 mu M, 1 h incubation with recombinant TrxR). CA and its 2-hydroxy- and 2-benzoyloxy-substituted analogs possessed dual TrxR-inhibitory and Nrf2-inducing effects, both attributed to an active Michael acceptor pharmacophore. At lethal concentrations. TrxR-inhibitory potencies correlated with the compounds antiproliferative activities. The penultimate C-terminal selenocysteine residue was shown to be a possible target. Conversely, at sublethal concentrations, these agents induced an adaptive antioxidant response through Nrf2-mediated upregulation of phase II enzymes, including TrxR induction. We conclude from the results obtained that TrxR inactivation contributes at least partly to cinnamaldehyde cytotoxicity. These Michael acceptor molecules can potentially be exploited for use in different concentrations in chemotherapeutic and chemopreventive strategies. (C) 2009 Elsevier Inc. All rights reserved.

  DOI：

  10.1016/j.freeradbiomed.2009.10.028