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A New Strategy to Stop the TB Bacterium

September 18, 2013
“Extremely gratifying results”

Graduate student Corey Compton, left, and Jason Sello synthesized 14 β-lactones. Four of them killed a close relative of the TB bacterium. β-lactone 7 was the most potent.

To stay ahead in the race against drug-resistant infections, scientists constantly search for and exploit vulnerabilities in deadly bacteria. Now, researchers from Brown, including doctoral Chemistry student Corey Compton, and the Massachusetts Institute of Technology have used a novel compound to exploit an Achilles’ heel in the bacterium that causes tuberculosis.

In a series of laboratory experiments, the researchers have shown that it is possible to kill Mycobacterium tuberculosis by inhibiting ClpP, a cellular enzyme that is not targeted by any antibacterial drug on the market. The work is preliminary, but the researchers are hopeful it could point the way to new drugs to treat tuberculosis and other infections that are becoming resistant to traditional antibiotics.

“ClpP has emerged over the last decade or so as a potential drug target in bacteria because they require it to either live or to cause disease,” said Jason Sello, associate professor of chemistry at Brown, who led the research. “Our findings indicate that chemical inhibition of the essential ClpP enzyme in Mycobacterium tuberculosis is a viable strategy in anti-tuberculosis drug development.”

A paper describing the research has been accepted by the journal ACS Chemical Biology and published online.

Read more of Kevin Stacey's article about the TB bacterium.