UCLA Scientists Engineer Antibiotics to Catch up in Race against Drug Resistance

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Led by Professors Gerard Wong and Andrea Kasko, UCLA Scientists have engineered antibiotics that effectively attack persister cells, which are responsible for making bacteria resistant to new drugs.

UCLA Newsroom (By Shaun Mason): We face an urgent global health problem because scientists are not developing new antibiotics as fast as bacteria are developing antibiotic resistance.

But new research from UCLA has made important progress toward solving this problem. An interdisciplinary team of scientists from UCLA’s California NanoSystems Institute has developed a method to re-engineer antibiotics that sharply enhances their activity against certain key bacterial cells, called persisters, that are responsible for making bacteria resistant to new drugs.

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By adding amino acids to the molecule of tobramycin, UCLA researchers created a new antibiotic drug molecule, called Pentobra, which is able to easily punch holes in persister cell membranes and get inside the cells to kill the bacteria.

Persister cells slow down their metabolism and shut down their mechanisms for taking in molecules, preventing normal antibiotics from getting into them, which is necessary for the drug to kill the bug. After the persister cells survive the initial antibiotic treatment, they pass on their genes as the bacteria reproduce.

Led by Gerard Wong, professor in the UCLA Department of Chemistry and Biochemistry and the Department of Bioengineering, and Andrea Kasko, associate professor of bioengineering, the team has developed a method analogous to taking an ordinary car and adding high-performance parts to make a fast and furious street racer.

“We’re in an unsustainable race with bacteria. They become resistant to our antimicrobials too fast,” Wong said. “It takes upwards of $100 million to develop one antibiotic drug, and bacteria develop resistance to it within two years. It’s a race that we can’t win. This reality brought us to the idea of taking an existing antibiotic and renovating it, giving it a new, complementary antimicrobial ability while preserving its original ability to make a better drug overall.”

The study was published Aug. 18 online in the journal ACS Nano.

To read the rest of the story, please visit the UCLA Newsroom.