Instead of waiting years to develop new antibiotics, a research team from the University of New York designed an early-stage therapeutic that sabotages ‘the pump of antibiotics’ mechanism used by the staphylococcus aureus bacteria to escape drugs.
S. aureus is a major cause of death among hospitalized patients when infections become severe. ‘Efflux pumps’ represent one mechanism by which S. aureus has evolved resistance to fluoroquinolones, a group of more than 60 approved antibiotics that includes norfloxacin (Noroxin), levofloxacin (Levaquin), and ciprofloxacin (Cipro).
During the study published in the latest issue of the journal Nature Chemical Biology, the team designed efflux pump inhibitors, which will allow people to keep using the currently available antibiotics.
"Instead of trying to find a new antibiotic, we hope to make the most widely used antibiotics over the last few decades, rendered ineffective by bacterial resistance, highly effective again," says Doug Brawley, first study author and professor at the medicine school in the University of New York.
During their study, the team realized that the part of the antibody most deeply embedded in NorA's binding cavity was a segment of protein building blocks of peptide NPI-1.
