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Shuttling drugs away from their intended targets can transform compounds that might otherwise be too toxic for people into good antimicrobials, according to researchers at the University of Toronto. Shana O. Kelley and Mark P. Pereira attached a mitochondria-targeting peptide to the cancer drug methotrexate and demonstrated the drug’s antimicrobial abilities (J. Am. Chem. Soc., DOI: 10.1021/ja110246u). The researchers show that the conjugate accumulates in mitochondria in human cells, where it can’t reach its enzyme target, but in the cytoplasm in bacteria. In cell culture, the conjugate killed a broad range of bacteria, including methicillin-resistant Staphylococcus aureus, a microbe resistant to most drugs. Kelley’s group is starting to study animals to see whether the drug retains its activity and reduced toxicity. The approach could be general for other drugs, provided they have a convenient “synthetic handle to tinker with,” Kelley says. The demonstration with methotrexate “opens the door to using similar strategies to revisit or repurpose old molecules that may have been discarded at early stages of antibiotic development,” says infectious disease expert Gerard D. Wright of McMaster University, in Hamilton, Ontario.
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