Blaskovich Mark A T, Hansford Karl A, Gong Yujing, Butler Mark S, Muldoon Craig, Huang Johnny X, Ramu Soumya, Silva Alberto B, Cheng Mu, Kavanagh Angela M, Ziora Zyta, Premraj Rajaratnam, Lindahl Fredrik, Bradford Tanya A, Lee June C, Karoli Tomislav, Pelingon Ruby, Edwards David J, Amado Maite, Elliott Alysha G, Phetsang Wanida, Daud Noor Huda, Deecke Johan E, Sidjabat Hanna E, Ramaologa Sefetogi, Zuegg Johannes, Betley Jason R, Beevers Andrew P G, Smith Richard A G, Roberts Jason A, Paterson David L, Cooper Matthew A
Institute for Molecular Bioscience, The University of Queensland, St. Lucia, QLD, 4072, Australia.
AC Immune SA, EPFL Innovation Park, CH-1015, Lausanne, Switzerland.
Nat Commun. 2018 Jan 2;9(1):22. doi: 10.1038/s41467-017-02123-w.
The public health threat posed by a looming 'post-antibiotic' era necessitates new approaches to antibiotic discovery. Drug development has typically avoided exploitation of membrane-binding properties, in contrast to nature's control of biological pathways via modulation of membrane-associated proteins and membrane lipid composition. Here, we describe the rejuvenation of the glycopeptide antibiotic vancomycin via selective targeting of bacterial membranes. Peptide libraries based on positively charged electrostatic effector sequences are ligated to N-terminal lipophilic membrane-insertive elements and then conjugated to vancomycin. These modified lipoglycopeptides, the 'vancapticins', possess enhanced membrane affinity and activity against methicillin-resistant Staphylococcus aureus (MRSA) and other Gram-positive bacteria, and retain activity against glycopeptide-resistant strains. Optimised antibiotics show in vivo efficacy in multiple models of bacterial infection. This membrane-targeting strategy has potential to 'revitalise' antibiotics that have lost effectiveness against recalcitrant bacteria, or enhance the activity of other intravenous-administered drugs that target membrane-associated receptors.
即将到来的“后抗生素”时代所带来的公共卫生威胁,使得抗生素发现需要新的方法。与自然界通过调节膜相关蛋白和膜脂质组成来控制生物途径不同,药物开发通常避免利用膜结合特性。在此,我们描述了通过选择性靶向细菌膜来使糖肽抗生素万古霉素恢复活力的方法。基于带正电荷的静电效应序列的肽库与N端亲脂性膜插入元件连接,然后与万古霉素偶联。这些修饰的脂糖肽,即“万古结合素”,对耐甲氧西林金黄色葡萄球菌(MRSA)和其他革兰氏阳性菌具有增强的膜亲和力和活性,并对耐糖肽菌株保持活性。优化后的抗生素在多种细菌感染模型中显示出体内疗效。这种膜靶向策略有可能“重振”对顽固细菌失去效力的抗生素,或增强其他靶向膜相关受体的静脉给药药物的活性。