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These compounds disarm pathogens of disease-causing toxins without killing them, thereby diminishing survival pressure to develop resistance. Here we show that the small-molecule antivirulence agents F12 and F19 block staphylococcal transcription factor AgrA from binding to its promoter. Consequently, toxin expression is inhibited, thus preventing host cell damage by Gram-positive pathogens. Broad spectrum efficacy against Gram-positive pathogens is due to the existence of AgrA homologs in many Gram-positive bacteria. F12 is more efficacious <jats:italic>in vitro<\/jats:italic> and F19 works better <jats:italic>in vivo<\/jats:italic>. In a murine MRSA bacteremia\/sepsis model, F19 treatment alone resulted in 100% survival while untreated animals had 70% mortality. Furthermore, F19 enhances antibiotic efficacy <jats:italic>in vivo<\/jats:italic>. Notably, in a murine MRSA wound infection model, combination of F19 with antibiotics resulted in bacterial load reduction. 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