1-(3,5-二氟苯基)-3-(4-甲氧基苯基)-1-丙酮 | 898776-43-7

• 分子结构分类: 有机化合物 - 苯丙烷和聚酮 - 直链 1,3-二芳基丙烷
• 中文名称: 1-(3,5-二氟苯基)-3-(4-甲氧基苯基)-1-丙酮
• 英文名称: 3',5'-Difluoro-3-(4-methoxyphenyl)propiophenone
• 英文别名: 1-(3,5-difluorophenyl)-3-(4-methoxyphenyl)propan-1-one
• CAS: 898776-43-7
• 化学式: C₁₆H₁₄F₂O₂
• 分子量: 276.28
• InChiKey: FOUKUWYGDYKPSM-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.7
• 重原子数：
  20
• 可旋转键数：
  5
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.19
• 拓扑面积：
  26.3
• 氢给体数：
  0
• 氢受体数：
  4

安全信息

• 海关编码：
  2914700090

反应信息

• 作为产物：
  描述：

  (E)-1-(3,5-difluorophenyl)-3-(4-methoxyphenyl)prop-2-en-1-one 在 palladium 10% on activated carbon 、 甲酸铵 作用下， 以 乙醇 为溶剂， 以43 %的产率得到1-(3,5-二氟苯基)-3-(4-甲氧基苯基)-1-丙酮
  参考文献：
  名称：

  通过调节 NF-κB 和 JNK 激活鉴定查耳酮类似物作为抗炎剂

  摘要：

  为了开发具有改进药物特性的新型抗炎剂，设计并合成了一系列查尔酮类似物。通过筛选这些化合物对 RAW264.7 细胞系中 NO 产生的抑制作用来评估这些化合物的体外抗炎活性。通过评估其对细胞因子（如 TNF-α、IL-1β、IL-6 和 PGE2 释放）的剂量依赖性抑制活性，选择最有前途的化合物3h和3l进行进一步研究。进一步研究还表明3h和3l可通过NF-κB/JNK信号通路显着抑制iNOS和COX-2的表达。此外，化合物3h和3l还可以显着抑制炎症相关基因的mRNA表达。同时， 3小时也可以下调ROS的产生。进行对接模拟以将化合物3h和3l定位到 iNOS 结合位点以预测可能的结合模式。总之，通过计算机快速预测获得的这一系列具有合理药物相似性的查耳酮类似物可以用作有前途的先导候选物。

  DOI：

  10.1039/d4md00011k

文献信息

• Discovery of Loureirin analogues with colorectal cancer suppressive activity via regulating cell cycle and Fas death receptor
  作者：Peng Li、Xiangjuan Tian、Die Zhang、Huiping Ou、Qiufeng Huang、Wenbin Jin、Ran Liu

  DOI：10.1186/s40360-024-00758-2

  日期：——

  Chalcones and dihydrochalcones (DHCs) are important bioactive natural products (BNPs) isolated from traditional Chinese medicine. In this study, 13 chalcones were designed with the inspiration of Loureirin, a DHC extracted from Resina Draconis, and synthesized by classical Claisen-Schmidt reactions. Afterwards the reduction reactions were carried out to obtain the corresponding DHCs. Cytotoxicity assay indicated chalcones and DHCs possessed selective cytotoxicity against colorectal cancer (CRC) cells. The preliminary structure-activity relationships (SAR) of these compounds suggested the α, β-unsaturated ketone of the chalcones were crucial for the anticancer activity. Interestingly, compounds 3d and 4c exhibited selective anticancer activity against CRC cell line HCT116 with IC50s of 8.4 and 17.9 μM but not normal cell. Moreover, 4c could also inhibit the migration and invasion of CRC cells. Mechanism investigations showed 4c could induce cell cycle G2/M arrest by regulating cell cycle-associated proteins and could also up-regulate Fas cell surface death receptor. The virtual docking further pointed out that compounds 3d and 4c could nicely bind to the Fas/FADD death domain complex (ID: 3EZQ). Furthermore, silencing of Fas significantly enhanced the proliferation of CRC cells and attenuated the cytotoxicity induced by 4c. These results suggested 4c exerted its anticancer activity possibly regulating cell cycle and Fas death receptor. In summary, this study investigated the anticancer activity and mechanism of Loureirin analogues in CRC, suggesting these compounds may warrant further investigation as promising anticancer drug candidates for the treatment of CRC.