蜜桃视频-Meridian pharmacy researcher Kirk Hevener awarded NIH grant to study deadly bacteria
September 20, 2016
The National Institutes of Health has awarded 蜜桃视频 assistant professor Kirk Hevener a $415,000 grant that may one day lead to the discovery of a new drug to battle the deadly intestinal bacteria Clostridium difficile.
Difficile鈥攁s it鈥檚 commonly known鈥攊s a stubborn, antibiotic-resistant bacteria that can wreak havoc in the lower bowel, causing severe diarrhea, dehydration and even death, said Hevener, an assistant professor of biomedical and pharmaceutical sciences at the 蜜桃视频-Meridian Health Science Center.
The New England Journal of Medicine reports that C. difficile afflicted 500,000 Americans and caused 29,000 deaths in 2011鈥攚ith the majority of cases occurring in hospitals, nursing homes or community health care settings.
鈥淚t鈥檚 highly contagious and easily spread. The bacteria forms spores that are resistant to antiseptics typically used to clean a hospital room,鈥 said Hevener, whose research involves the design of small molecule compounds that can inhibit a key enzyme in C. difficile to stop or slow the growth of the disease-causing bacteria.
The NIH鈥檚 National Institute of Allergy and Infectious Disease awarded the exploratory grant June 25. For the next two years, Hevener and his research team will target FabK, an enzyme found in the fatty acid synthetic pathway of C. difficile. This enzyme isn鈥檛 found in most non-disease causing bacteria in the healthy gut or in humans.
鈥淭his will allow us to more narrowly target C. difficile and avoid off-target effects against nonpathogenic organisms,鈥 Hevener said. In other words, narrowly targeting a bad bug will avoid the destruction of the good bugs which can protect the body from disease.
Hevener鈥檚 research team consists of ISU-Meridian graduate students, a microbiologist from Texas A&M University and a chemist from University of Hawaii. In addition to determining if FabK is a targetable enzyme, the researchers want to prove that compounds they are developing to inhibit FabK will work in vivo or in living organisms, such as mice. That鈥檚 a vital step to securing additional funds for further research and clinical trials.
鈥淭his could lead to the discovery of a new drug that could likely be tested in humans one day,鈥 Hevener said.
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