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Two Proposals from HWI Funded

 

Two research scientists from the Hauptman-Woodward Institute (HWI) have been notified that their recent grant applications will be funded.

malkowskiDr. Michael Malkowski’s proposal entitled “Structure and Dynamics of Cyclooxygenase Catalysis and Inhibition” has been funded by the National Institutes of Health for four years at a total of $1.5M.

The cyclooxygenase enzymes (COX-1 and COX-2) are associated with several disease pathologies.  COX-1 and COX-2 are the targets of aspirin, ibuprofen, and other nonsteroidal anti-inflammatory drugs (NSAIDs) as well as COX-2 selective inhibitors (coxibs) such as Celebrex.

NSAIDs and coxibs are used to decrease acute and chronic inflammation, protect against adverse cardiovascular events, and reduce the risk of developing certain cancers.  They are among the most heavily utilized drugs in the world, but their use is not without risk. Over 15,000 deaths per year can be ascribed to harmful effects resulting from their consumption.  The goal of Dr. Malkowski's project is to understand the molecular basis of how these drugs interact with the cyclooxygenase enzymes and then use this knowledge to provide a foundation for the development of new drugs and the repurposing of existing ones to provide maximum efficacy while minimizing risks.

gewirthAnother HWI scientist, Dr. Daniel Gewirth, has been informed by the New York State Department of Health that his proposal "Targeting the Androgen Receptor in Prostate Cancer" has been funded for $75K to be spent in the 15-month period beginning November 1, 2015.

The growth of prostate cancer cells is dependent on a protein known as the androgen receptor (AR).  Current drugs that inhibit the AR and cause remission target a specific region of the AR molecule known as the ligand-binding domain.  However, over time prostate cancer cells often become resistant to these drugs.  The Gewirth lab will study alternative regions of the AR molecule with the ultimate goal of developing a new class of drugs that will inhibit AR activity when current drugs fail.

 
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