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It's a story 30-odd years in the making. The tale begins in the 1990s, when Roche had an anti-infectives unit. Back then, plenty of pharmaceutical companies had scientists working on novel antibiotics, inspired financially by the 50 years of successful antimicrobial development that had preceded them and morally by the rise of drug-resistant bacteria. Roche scientists had the idea to create a systemic β-lactam antibiotic for methicillin-resistant Staphylococcus aureus , better known as MRSA. It was the early days of antimicrobial resistance—or at least the appreciation of it—and MRSA appeared to be the greatest threat among drug-resistant bacteria. β-lactams work by binding to penicillin- binding proteins (PBPs), enzymes that are crucial to bacteria's ability to form cell walls. Binding PBPs stops those walls from coming together. But MRSA was near impossible to drug with a β-lactam because MRSA has a gene called mecA . That gene produces a specific kind
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Rowan Walrath (2024) studied this question.
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