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The development of histone deacetylase inhibitors to treat a variety of diseases has been somewhat hampered by HDAC-related toxicity concerns. A team from the Stanley Center for Psychiatric Research at Ó³»­´«Ã½, led by the Center’s director of medicinal chemistry Ed Holson and Ó³»­´«Ã½ postdoctoral associate David Olson, has discovered a new HDAC-independent mechanism by which some hydroxamate-based HDAC inhibitors protect neurons from oxidative stress, such as during stroke. The molecules bind iron within the cell and form catalase mimetic complexes with antioxidant activity, a mechanism that also holds therapeutic potential for other diseases involving oxidative stress. was published online in the journal Chemistry & Biology.