Department of Chemistry, Stanford University, Stanford, California 94305, United States.
Department of Chemical and Systems Biology, Stanford University, Stanford, California 94305, United States.
J Med Chem. 2023 Aug 10;66(15):10226-10237. doi: 10.1021/acs.jmedchem.3c00565. Epub 2023 Jul 21.
Drug resistant bacterial infections have emerged as one of the greatest threats to public health. The discovery and development of new antimicrobials and anti-infective strategies are urgently needed to address this challenge. Vancomycin is one of the most important antibiotics for the treatment of Gram-positive infections. Here, we introduce the vancomycin-arginine conjugate (V-R) as a highly effective antimicrobial against actively growing mycobacteria and difficult-to-treat mycobacterial biofilm populations. Further improvement in efficacy through combination treatment of V-R to inhibit peptidoglycan synthesis and ethambutol to inhibit arabinogalactan synthesis underscores the ability to identify compound synergies to more effectively target the Achilles heel of the cell-wall assembly. Moreover, we introduce mechanistic activity data and a molecular model derived from a d-Ala-d-Ala-bound vancomycin structure that we hypothesize underlies the molecular basis for the antibacterial improvement attributed to the arginine modification that is specific to peptidoglycan chemistry employed by mycobacteria and distinct from Gram-positive pathogens.
耐药细菌感染已成为对公众健康的最大威胁之一。为了应对这一挑战,迫切需要发现和开发新的抗菌药物和抗感染策略。万古霉素是治疗革兰氏阳性感染的最重要的抗生素之一。在这里,我们介绍了万古霉素-精氨酸缀合物(V-R),它是一种对抗生长活跃的分枝杆菌和难以治疗的分枝杆菌生物膜群体的高效抗菌药物。通过将 V-R 与抑制肽聚糖合成的药物联合治疗以及与抑制阿拉伯半乳聚糖合成的乙胺丁醇联合治疗来进一步提高疗效,突出了识别化合物协同作用以更有效地针对细胞壁组装的阿喀琉斯之踵的能力。此外,我们介绍了源自与 D-Ala-D-Ala 结合的万古霉素结构的机制活性数据和分子模型,我们假设该模型是基于对分枝杆菌所采用的肽聚糖化学具有特异性的精氨酸修饰的抗菌改善的分子基础,与革兰氏阳性病原体不同。