4'-demethylepipodophyllotoxin 4-propionate | 118356-08-4

• 分子结构分类: 有机化合物 - 木脂素、新木脂素和相关化合物 - 木脂素内酯
• 英文名称: 4'-demethylepipodophyllotoxin 4-propionate
• 英文别名: [(5S,5aR,8aR,9R)-9-(4-hydroxy-3,5-dimethoxyphenyl)-8-oxo-5a,6,8a,9-tetrahydro-5H-[2]benzofuro[5,6-f][1,3]benzodioxol-5-yl] propanoate
• CAS: 118356-08-4
• 化学式: C₂₄H₂₄O₉
• 分子量: 456.449
• InChiKey: LRSOZMPPKIRBTD-QJXZSUBDSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.7
• 重原子数：
  33
• 可旋转键数：
  6
• 环数：
  5.0
• sp3杂化的碳原子比例：
  0.42
• 拓扑面积：
  110
• 氢给体数：
  1
• 氢受体数：
  9

反应信息

• 作为产物：
  描述：

  鬼臼毒素 在 吡啶 、 咪唑 、 四丁基氟化铵 、 水 、 氢溴酸 、 barium carbonate 作用下， 以 四氢呋喃 为溶剂， 反应 46.25h， 生成 4'-demethylepipodophyllotoxin 4-propionate
  参考文献：
  名称：

  Antitumor agents. 100. Inhibition of human DNA topoisomerase II by cytotoxic ether and ester derivatives of podophyllotoxin and .alpha.-peltatin

  摘要：

  A principal mechanism of action of the clinical antitumor drugs etoposide (1) and teniposide (2) is the inhibition of catalytic activity of type II DNA topoisomerase and concurrent enzyme-mediated production of lethal DNA strand breaks. Substitution of the glycosidic moiety of 1 or 2 by ester and ethers, as well as the esterification and etherification of alpha-peltatin (4) including its glucosidic ethylidene and thenylidene cyclic acetals (25 and 26), has afforded compounds of much less activity than that of 1. The in vitro cytotoxicity (KB) appears to have no correlation with the inhibitory activity of the human DNA topoisomerase II.

  DOI：

  10.1021/jm00123a016

文献信息

• THURSTON, LEE S.;IMAKURA, YASUHIRO;HARUNA, MITSUMASA;LI, DE-HUA;LIU, ZONG+, J. MED. CHEM., 32,(1989) N, C. 604-608
  作者：THURSTON, LEE S.、IMAKURA, YASUHIRO、HARUNA, MITSUMASA、LI, DE-HUA、LIU, ZONG+

  DOI：——

  日期：——
• Antitumor agents. 100. Inhibition of human DNA topoisomerase II by cytotoxic ether and ester derivatives of podophyllotoxin and .alpha.-peltatin
  作者：Lee S. Thurston、Yasuhiro Imakura、Mitsumasa Haruna、De Hua Li、Zong Chao Liu、Su Ying Liu、Yung Chi Cheng、Kuo Hsiung Lee

  DOI：10.1021/jm00123a016

  日期：1989.3

  A principal mechanism of action of the clinical antitumor drugs etoposide (1) and teniposide (2) is the inhibition of catalytic activity of type II DNA topoisomerase and concurrent enzyme-mediated production of lethal DNA strand breaks. Substitution of the glycosidic moiety of 1 or 2 by ester and ethers, as well as the esterification and etherification of alpha-peltatin (4) including its glucosidic ethylidene and thenylidene cyclic acetals (25 and 26), has afforded compounds of much less activity than that of 1. The in vitro cytotoxicity (KB) appears to have no correlation with the inhibitory activity of the human DNA topoisomerase II.