A principal mechanism of action of the clinical antitumor drugs etoposide (1) and teniposide (2) is the inhibition of catalytic activity of type I1 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 a-peltatin (4) including its glucosidic ethylidene and thenylidene cyclic acetals (25 and 26), has ...
![(5S,5aR,8aR,9R)-5-ethylsulfanyl-9-(4-hydroxy-3,5-dimethoxyphenyl)-5a,6,8a,9-tetrahydro-5H-[2]benzofuro[5,6-f][1,3]benzodioxol-8-one Structure](https://image.chemsrc.com/caspic/464/118356-06-2.png)