4-(((E)-2,4,6-trimethoxystyrylsulfonyl)methyl)benzoic acid | 851799-32-1

• 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: 4-(((E)-2,4,6-trimethoxystyrylsulfonyl)methyl)benzoic acid
• 英文别名: (E)-2,4,6-trimethoxystyryl-4-carboxybenzylsulfone；4-[[(E)-2-(2,4,6-trimethoxyphenyl)ethenyl]sulfonylmethyl]benzoic acid
• CAS: 851799-32-1
• 化学式: C₁₉H₂₀O₇S
• 分子量: 392.43
• InChiKey: KOFZGADJOXHTPZ-CMDGGOBGSA-N

物化性质

• 熔点：
  143-145 °C(Solv: isopropanol (67-63-0))
• 沸点：
  680.8±55.0 °C(Predicted)
• 密度：
  1.322±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  2.5
• 重原子数：
  27
• 可旋转键数：
  8
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.21
• 拓扑面积：
  108
• 氢给体数：
  1
• 氢受体数：
  7

反应信息

• 作为产物：
  描述：

  2,4,6-三甲氧基苯甲醛 、 4-carboxybenzylsulfonylacetic acid 在 苄胺 溶剂黄146 作用下， 以60%的产率得到4-(((E)-2,4,6-trimethoxystyrylsulfonyl)methyl)benzoic acid
  参考文献：
  名称：

  Design, Synthesis, and Biological Evaluation of (E)-Styrylbenzylsulfones as Novel Anticancer Agents

  摘要：

  Cell cycle progression is regulated by cyclins and cyclin-dependent kinases, which are formed at specific stages of the cell cycle and regulate the G1/S and G2/M phase transitions, employing a series of "checkpoints" governed by phosphorylation of their substrates. Tumor development is associated with the loss of these checkpoint controls, and this provides an approach for the development of therapeutic agents that can specifically target tumor cells. Here, we describe the synthesis and SAR of a novel group of cytotoxic molecules that selectively induce growth arrest of normal cells in the G1 phase while inducing a mitotic arrest of tumor cells resulting in selective killing of tumor cell populations with little or no effect on normal cell viability. The broad spectrum of antitumor activity in vitro and xenograft models, lack of in vivo toxicity, and drug resistance suggest potential for use of these agents in cancer therapy.

  DOI：

  10.1021/jm701077b

文献信息

• [EN] PROTECTION OF TISSUES AND CELLS FROM CYTOTOXIC EFFECTS OF IONIZING RADIATION BY ABL INHIBITORS<br/>[FR] PROTECTION DE TISSUS ET DE CELLULES DES EFFETS CYTOTOXIQUES D'UN RAYONNEMENT IONISANT PAR DES INHIBITEURS ABL
  申请人：UNIV TEMPLE

  公开号：WO2005044181A2

  公开（公告）日：2005-05-19

  Pre-treatment with one or more compounds of formula (I), as described herein, protects normal cells from the toxic side effects of ionizing radiation. Administration of one or more radioprotective compounds of formula (I) to a patient prior to anticancer radiotherapy reduces the cytotoxic side effects of the radiation on normal cells. The radioprotective effect of one or more compounds of formula (I) allows for the safe increase the dosage of anticancer radiation. Amelioration of toxicity following inadvertent radiation exposure may also be mitigated with administration of one or more compounds of formula (I).
• [EN] PROTECTION OF TISSUES AND CELLS FROM CYTOTOXIC EFFECTS OF IONIZING RADIATION BY ABL INHIBITORS<br/>[FR] LA PROTECTION DE TISSUS ET DE CELLULES CONTRE LES EFFETS CYTOTOXIQUE D'UN RAYONNEMENT IONISANT PAR DES INHIBITEURS ABL
  申请人：UNIV TEMPLE

  公开号：WO2005065074A2

  公开（公告）日：2005-07-21

  Pre-treatment with one or more compounds of formula (I), as described herein, protects normal cells from the toxic side effects of ionizing radiation. Administration of one or more radioprotective compounds of formula I to a patient prior to anticancer radiotherapy reduces the cytotoxic side effects of the radiation on normal cells. The radioprotective effect of one or more compounds of formula I allows for the safe increase the dosage of anticancer radiation. Amelioration of toxicity following inadvertent radiation exposure may also be mitigated with administration of one or more compounds of formula (I).
• Design, Synthesis, and Biological Evaluation of (<i>E</i>)-Styrylbenzylsulfones as Novel Anticancer Agents
  作者：M. V. Ramana Reddy、Muralidhar R. Mallireddigari、Stephen C. Cosenza、Venkat R. Pallela、Nabisa M. Iqbal、Kimberly A. Robell、Anthony D. Kang、E. Premkumar Reddy

  DOI：10.1021/jm701077b

  日期：2008.1.1

  Cell cycle progression is regulated by cyclins and cyclin-dependent kinases, which are formed at specific stages of the cell cycle and regulate the G1/S and G2/M phase transitions, employing a series of "checkpoints" governed by phosphorylation of their substrates. Tumor development is associated with the loss of these checkpoint controls, and this provides an approach for the development of therapeutic agents that can specifically target tumor cells. Here, we describe the synthesis and SAR of a novel group of cytotoxic molecules that selectively induce growth arrest of normal cells in the G1 phase while inducing a mitotic arrest of tumor cells resulting in selective killing of tumor cell populations with little or no effect on normal cell viability. The broad spectrum of antitumor activity in vitro and xenograft models, lack of in vivo toxicity, and drug resistance suggest potential for use of these agents in cancer therapy.