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NEW DELHI — A newly discovered antibiotic that disrupts two distinct biological targets will make it 100 million times harder for bacteria to evolve resistance, according to a study.
The study from the University of Illinois at Chicago (UIC), in the US, reveals that this antibiotic disrupts two different cellular targets, significantly complicating bacteria's ability to evolve resistance, a dangerous, unwanted side effect.
The study, published in the journal Nature Chemical Biology, focuses on a class of synthetic drugs known as macrolones. These drugs combat bacterial infections by either interfering with protein production or corrupting DNA structure, making it challenging for bacteria to develop resistance to both mechanisms simultaneously.
"The beauty of this antibiotic is that it kills through two different targets in bacteria," said Alexander Mankin, a professor of pharmaceutical sciences at the University of Illinois, Chicago.
"If the antibiotic hits both targets at the same concentration, then the bacteria lose their ability to become resistant via the acquisition of random mutations in any of the two targets," he added.
Macrolones combine features of macrolides, like erythromycin, which block protein synthesis, and fluoroquinolones, such as ciprofloxacin, which target the bacterial enzyme DNA gyrase.
Researchers Yury Polikanov and Nora Vazquez-Laslop at UIC demonstrated that these drugs bind more tightly to ribosomes than traditional antibiotics and are effective even against macrolide-resistant bacterial strains. "By basically hitting two targets at the same concentration, the advantage is that you make it almost impossible for the bacteria to easily come up with a simple genetic defence," Polikanov said.
This discovery underscores the importance of the integration across various scientific fields that fosters significant advancements like this one.