ELECTRONIC TUNING OF SITE SELECTIVITY

摘要

Site-selective functionalization of Amphotericin B has been achieved by simply modifying the electronic nature of the reagents. A Hammett analysis is consistent with linking of this phenomenon to the Hammond postulate: electronic tuning to a more product- like transition state amplifies site-discriminating interactions between a reagent and its substrate. Electronic tuning of both an acylpyridinium donor and its carboxylate counterion further promoted site-divergent functionalization. A range of modifications to one of the many hydroxyl groups appended to the ion channel-forming natural product amphotericin B was achieved.