A new antibiotic that works by disrupting two different cellular targets would make it 100 million times more difficult for bacteria to evolve resistance, according to new research from the University of Illinois Chicago. For a new paper in Nature Chemical Biology , researchers probed how a class of synthetic drugs called macrolones disrupt bacterial cell function to fight infectious diseases. Their experiments demonstrate that macrolones can work two different ways – either by interfering with protein production or corrupting DNA structure.
Because bacteria would need to implement defenses to both attacks simultaneously, the researchers calculated that drug resistance is nearly impossible. The beauty of this antibiotic is that it kills through two different targets in bacteria. If the antibiotic hits both targets at the same concentration, then the bacteria lose their ability to become resistant via acquisition of random mutations in any of the two targets.
" Alexander Mankin, distinguished professor of pharmaceutical sciences at UIC Macrolones are synthetic antibiotics that combine the structures of two widely used antibiotics with different mechanisms. Macrolides, such as erythromycin, block the ribosome, the protein manufacturing factories of the cell. Fluoroquinolones, such as ciprofloxacin, target a bacteria-specific enzyme called DNA gyrase.
Two UIC laboratories led by Yury Polikanov, associate professor of biological sciences, and Mankin and Nora Vázquez-Laslop, re.