Mitomycin C (1) is a clinically significant antineoplastic antibiotic. In this proposal, a novel hypothesis for the mode of action of this drug is presented. Evidence is cited in support of this pathway. Detailed experiments are proposed to substantiate this mechanism as well as to determine the energetics of key steps. Emphasis has been placed on elucidating the mechanism of the drug-receptor (DNA) interaction. Knowledge of which route is the correct reaction pathway in mitomycin C-mediated processes may provide the molecular basis for subsequent research in cancer chemotherapy and allow future general drug design to proceed on a less empirical basis.
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