Department of Chemistry, McGill University, 801 Sherbrooke Street West, Montréal, Québec, Canada H3A 2K6.
ACS Chem Biol. 2012 Mar 16;7(3):470-5. doi: 10.1021/cb200366u. Epub 2012 Jan 18.
The most common mechanism of resistance to aminoglycoside antibiotics entails bacterial expression of drug-metabolizing enzymes, such as the clinically widespread aminoglycoside N-6'-acetyltransferase (AAC(6')). Aminoglycoside-CoA bisubstrates are highly potent AAC(6') inhibitors; however, their inability to penetrate cells precludes in vivo studies. Some truncated bisubstrates are known to cross cell membranes, yet their activities against AAC(6') are in the micromolar range at best. We report here the synthesis and biological activity of aminoglycoside-pantetheine derivatives that, although devoid of AAC(6') inhibitory activity, can potentiate the antibacterial activity of kanamycin A against an aminoglycoside-resistant strain of Enterococcus faecium. Biological studies demonstrate that these molecules are potentially extended to their corresponding full-length bisubstrates by enzymes of the coenzyme A biosynthetic pathway. This work provides a proof-of-concept for the utility of prodrug compounds activated by enzymes of the coenzyme A biosynthetic pathway, to resensitize resistant strains of bacteria to aminoglycoside antibiotics.
最常见的氨基糖苷类抗生素耐药机制涉及细菌表达药物代谢酶,如临床上广泛存在的氨基糖苷类 N-6'-乙酰转移酶(AAC(6'))。氨基糖苷类-CoA 双底物是高度有效的 AAC(6')抑制剂;然而,它们不能穿透细胞,因此无法进行体内研究。一些截断的双底物已知可以穿过细胞膜,但它们对 AAC(6')的活性最高也只有微摩尔级。我们在这里报告了氨基糖苷类 - 泛酰巯基乙胺衍生物的合成和生物学活性,尽管这些衍生物缺乏 AAC(6')抑制活性,但可以增强卡那霉素 A 对氨基糖苷类耐药粪肠球菌菌株的抗菌活性。生物研究表明,这些分子可以通过辅酶 A 生物合成途径的酶进一步延伸为相应的全长双底物。这项工作为通过辅酶 A 生物合成途径的酶激活前药化合物使耐药菌对氨基糖苷类抗生素重新敏感的实用性提供了概念验证。