5,5'-diallyl-2′-((tert-butyldimethylsilyl)oxy)-[1,1′-biphenyl]-2-ol

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 英文名称: 5,5'-diallyl-2′-((tert-butyldimethylsilyl)oxy)-[1,1′-biphenyl]-2-ol
• 英文别名: 5,5'-Diallyl-2'-((tert-butyldimethylsilyl)oxy)-[1,1'-biphenyl]-2-ol；2-[2-[tert-butyl(dimethyl)silyl]oxy-5-prop-2-enylphenyl]-4-prop-2-enylphenol
• 化学式: C₂₄H₃₂O₂Si
• 分子量: 380.602
• InChiKey: OZLVJWBXNJOORJ-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  6.9
• 重原子数：
  27
• 可旋转键数：
  8
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.33
• 拓扑面积：
  29.5
• 氢给体数：
  1
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  5,5'-diallyl-2′-((tert-butyldimethylsilyl)oxy)-[1,1′-biphenyl]-2-ol 在 四丁基氟化铵 、 sodium hydride 作用下， 以 四氢呋喃 、 mineral oil 为溶剂， 反应 4.19h， 生成 2-(4-((2-((5,5′-diallyl-2′-hydroxy-[1,1′-biphenyl]-2-yl)oxy)ethyl)thio)butyl)isoindoline-1,3-dione
  参考文献：
  名称：

  CT2-3, a novel magnolol analogue suppresses NSCLC cells through triggering cell cycle arrest and apoptosis

  摘要：

  Magnolol, a major bioactive component found in Magnolia officinalis with anti-inflammation and anti-oxidation activities as well as minimized cytotoxic effects. Although magnolol has a wide range of clinical applications, the anti-tumor activity of magnolol is not efficient. Herein, we reported the synthesis and anti-cancer activities of three novel magnolol analogues CT2-1, CT2-2, CT2-3, among which CT2-3 revealed more efficient anti-non-small cell lung cancer (NSCLC) activity than magnolol. Our data showed that CT2-3 could significantly inhibit the proliferation of human NSCLC cells in a dose-dependent manner. In addition, we revealed CT2-3 could induce cell cycle arrest through down-regulating mRNA expression of CDK4, CDK6 and cyclin D1. Moreover, we verified that CT2-3 could cause ROS generation, leading to apoptosis of human NSCLC cells. Further more, we also provided strong evidences that CT2-3 down-regulates the expression of c-Myc and topoisomerases, and contributes to the apoptosis of human NSCLC cells. Taken together, the current study is the first to report a promising new chemotherapeutic drug candidate CT2-3 that can efficiently eliminate human NSCLC cells through triggering cell cycle arrest as well as ROS-mediated and c-Myc/topoisomerases-mediated apoptosis.

  DOI：

  10.1016/j.bmc.2020.115352
• 作为产物：
  描述：

  厚朴酚 、 叔丁基二甲基氯硅烷 在 咪唑 作用下， 以 二氯甲烷 为溶剂， 反应 1.0h， 以98%的产率得到5,5'-diallyl-2′-((tert-butyldimethylsilyl)oxy)-[1,1′-biphenyl]-2-ol
  参考文献：
  名称：

  八角茴香来源的Sesquineolignan Simonsol C的全合成

  摘要：

  通过将作为关键步骤的碘代芳烃系环己烯22参与分子内Heck反应，以合成化合物23，从而合成了标题天然产物1的外消旋形式。该角取代的四氢二苯并[ b，d ]呋喃经另外五个步骤精制为靶标（±）-1。

  DOI：

  10.1021/acs.orglett.6b01799

文献信息

• Total Synthesis of the <i>Illicium</i>-Derived Sesquineolignan Simonsol C
  作者：Jeremy Nugent、Martin G. Banwell、Brett D. Schwartz

  DOI：10.1021/acs.orglett.6b01799

  日期：2016.8.5

  The racemic form of the title natural product 1 has been synthesized by engaging, as a key step, the iodoarene-tethered cyclohexene 22 in an intramolecular Heck reaction to give compound 23. This angularly substituted tetrahydrodibenzo[b,d]furan was elaborated over a further five steps into target (±)-1.

  通过将作为关键步骤的碘代芳烃系环己烯22参与分子内Heck反应，以合成化合物23，从而合成了标题天然产物1的外消旋形式。该角取代的四氢二苯并[ b，d ]呋喃经另外五个步骤精制为靶标（±）-1。
• CT2-3, a novel magnolol analogue suppresses NSCLC cells through triggering cell cycle arrest and apoptosis
  作者：Jian Chen、Cheng Tao、Xiaofei Huang、Zide Chen、Li Wang、Xinping Li、Min Ma、Zhengzhi Wu

  DOI：10.1016/j.bmc.2020.115352

  日期：2020.3

  Magnolol, a major bioactive component found in Magnolia officinalis with anti-inflammation and anti-oxidation activities as well as minimized cytotoxic effects. Although magnolol has a wide range of clinical applications, the anti-tumor activity of magnolol is not efficient. Herein, we reported the synthesis and anti-cancer activities of three novel magnolol analogues CT2-1, CT2-2, CT2-3, among which CT2-3 revealed more efficient anti-non-small cell lung cancer (NSCLC) activity than magnolol. Our data showed that CT2-3 could significantly inhibit the proliferation of human NSCLC cells in a dose-dependent manner. In addition, we revealed CT2-3 could induce cell cycle arrest through down-regulating mRNA expression of CDK4, CDK6 and cyclin D1. Moreover, we verified that CT2-3 could cause ROS generation, leading to apoptosis of human NSCLC cells. Further more, we also provided strong evidences that CT2-3 down-regulates the expression of c-Myc and topoisomerases, and contributes to the apoptosis of human NSCLC cells. Taken together, the current study is the first to report a promising new chemotherapeutic drug candidate CT2-3 that can efficiently eliminate human NSCLC cells through triggering cell cycle arrest as well as ROS-mediated and c-Myc/topoisomerases-mediated apoptosis.