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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Bactericidal activity and target preference of a piperazinyl-cross-linked ciprofloxacin dimer with Staphylococcus aureus and Escherichia coli.

Background: Previous work showed that piperazinyl-cross-linked ciprofloxacin dimer exhibits good bacteriostatic activity with Streptococcus pneumoniae and Staphylococcus aureus; lethal activity was not measured. Subsequently, the dimer failed to kill Mycobacterium smegmatis but blocked growth. Whether the compound is lethal with non-mycobacterial species is not known. METHODS: Bacteriostatic and bactericidal activities were measured with wild-type cells and topoisomerase mutants of S. aureus and Escherichia coli for ciprofloxacin and a dimer of ciprofloxacin. Spontaneous resistance mutants were selected with S. aureus for both compounds, followed by target identification by nucleotide sequence determination of the quinolone-resistance-determining-region of gyrA (gyrase) and parC (topoisomerase IV). RESULTS: The dimer was lethal, in some cases exhibiting more activity than ciprofloxacin (particularly with wild-type cells and a parC mutant of S. aureus). Dimerization affected target preference with S. aureus but not with E. coli. Resistance mutations in either gyrA or parC of S. aureus raised the MIC of the dimer, but only a parC mutation raised the MIC of ciprofloxacin. With S. aureus, the dimer selected spontaneous resistant gyrA mutants, whereas ciprofloxacin selected a parC mutant. With E. coli, a gyrA, but not a parC, mutation raised the MIC of both compounds. CONCLUSION: The dimer readily killed S. aureus and E. coli, representative Gram-positive and Gram-negative bacteria. In both cases the preferred target was DNA gyrase. The switch in target preference may be responsible for the greater lethality of the dimer seen with S. aureus.[1]


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