Community-associated methicillin-resistant (MRSA) is now a major cause of bacterial infection. Antivirulence therapy does not stimulate evolution of a pathogen toward a resistant phenotype, providing a novel method to treat infectious diseases. Here, we used a cyclic peptide of CP7, an AIP-III variant that specifically inhibited the virulence and biofilm formation of () in a nonbiocidal manner, to conjugate with a broad-spectrum antimicrobial peptide (AMP) via two N-termini to obtain a hybrid AMP called CP7-FP13-2. This peptide not only specifically inhibited the production of virulence of at low micromolar concentrations but also killed , including MRSA, by disrupting the integrity of the bacterial cell membrane. In addition, CP7-FP13-2 inhibited the formation of the biofilm and showed good antimicrobial efficacy against the -infected Kunming mice model. Therefore, this study provides a promising strategy against the resistance and virulence of .
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