Posted On: 04/12/2014 6:25:28 PM
Post# of 2022
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Consequently, the responsibility for research is falling increasingly to academic researchers. Michael Gilmore organized Harvard’s Program on Antibiotic Resistance in 2009: a multimillion-dollar project grant from the National Institutes of Health (NIH) currently funds the collaborative effort of HWPAR’s seven independent laboratories to study antibiotic-resistant S. aureus. The goal of the academic program is less to develop new drugs—a task better suited to companies, given their superior financial resources and specialized pharmacological knowledge—than to develop innovative approaches to finding them. “We explore new drug targets that are higher risk than those a company would work on,” explains professor of microbiology and immunobiology Suzanne Walker, one of Gilmore’s collaborators. “It’s hard to beat a company at developing a compound, and there’s no reason to do that. But I think it’s up to academics to lay the groundwork.”
In 2009, Walker’s lab discovered the compound targocil, which prevents bacterial growth by interfering with a cellular pathway that creates a critical component of the S. aureus cell wall. Targocil is potentially useful for treating drug-resistant strains like MRSA: the compound restores the lethal effect of antibiotics like penicillin and methicillin by disabling bacterial modes of resistance. Other such molecules have been clinically useful; to combat the naturally penicillin-resistant species E. coli, for instance, some treatments like augmentin combine a penicillin-like antibiotic with a second compound that inhibits the enzyme that confers resistance, and targocil combination treatments have likewise succeeded in overcoming MRSA in mice. Moreover, targocil has proven to be a useful tool for understanding S. aureus biology. “The more we understand about the physiology of MRSA, the more likely we are to find new ways to intervene,” says Walker.
http://harvardmagazine.com/2014/05/superbug
In 2009, Walker’s lab discovered the compound targocil, which prevents bacterial growth by interfering with a cellular pathway that creates a critical component of the S. aureus cell wall. Targocil is potentially useful for treating drug-resistant strains like MRSA: the compound restores the lethal effect of antibiotics like penicillin and methicillin by disabling bacterial modes of resistance. Other such molecules have been clinically useful; to combat the naturally penicillin-resistant species E. coli, for instance, some treatments like augmentin combine a penicillin-like antibiotic with a second compound that inhibits the enzyme that confers resistance, and targocil combination treatments have likewise succeeded in overcoming MRSA in mice. Moreover, targocil has proven to be a useful tool for understanding S. aureus biology. “The more we understand about the physiology of MRSA, the more likely we are to find new ways to intervene,” says Walker.
http://harvardmagazine.com/2014/05/superbug
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