Mechanistic studies of DNA damage induced by antitumor acylfulvene

TOXI 15

Jiachang Gong, gongx013@umn.edu, V. G. Vaidyanathan, and Shana J. Sturla. University of Minnesota, Minneapolis, MN 55455
Natural products and their derivatives have contributed significantly to the successful treatment of many cancers. Major limitations arise from low selectivity and high toxicity, leading to severe side affects. A mechanistic understanding of how antitumor agents selectively kill cancer cells may serve as a basis for the design of more selective agents and therapeutic strategies. Semi-synthetic acylfulvenes (AFs) are a family of antitumor agents derivatized from illudin S, with one analogue in clinical trials. Data indicate that acylfulvenes are bioactivated by NADPH-dependent alkenal/one oxidoreductase (AOR), generating intermediates with the capacity to alkylate cellular targets, and macromolecular alkylation is believed to initiate apoptosis. We will discuss the chemical mechanisms of DNA damage induced by acylfulvenes in the presence and absence of metabolic enzyme. The influence of stereochemistry on enzyme-mediated bioactivation and DNA alkylation, and how these processes correlate with cell sensitivity, will be presented.