Repligen Corporation (Nasdaq: RGEN) announced today that it has entered into an exclusive license agreement with the University of California, Irvine (UCI) for a patent application covering the use of histone deacetylase 3 (HDAC3) inhibitors for the treatment of disorders involving preservation or extinction of memory including Alzheimer's disease, memory impairment and post traumatic stress disorder. The patent application is based on work conducted at UCI by Dr. Marcelo A. Wood, which demonstrated that one of Repligen's HDAC3 inhibitors improved both the acquisition and persistence of long-term memory in an animal model. These data were published in the January 12th issue of The Journal of Neuroscience in a manuscript entitled "HDAC3 Is a Critical Negative Regulator of Long-Term Memory Formation" (McQuown, S., et al., J. Neurosci. (2011) 31:764 –774). Under the terms of the license agreement, UCI will receive an upfront payment, development milestones and royalties upon successful commercialization of an HDAC3 inhibitor for certain memory disorders. Upon issue, the patent will remain in force until 2031 prior to any regulatory extensions.
"These new data indicate that HDAC3 inhibitors should be further evaluated for use in a variety of disorders in which the acquisition or extinction of a long-term memory is a factor," stated Walter C. Herlihy, President and Chief Executive Officer of Repligen Corporation. "We intend to continue to investigate the potential of our selective HDAC3 inhibitors in a variety of disease models."
The manuscript published in The Journal of Neuroscience examined the role of HDAC3 inhibitors in long-term memory using a combined genetic and pharmacologic approach. In the study, a genetic approach was used to delete HDAC3 in the hippocampus of normal mice. These mice showed improved acquisition of long-term memory which persisted longer than in control mice. Similar results were seen when normal mice were treated with a proprietary Repligen compound which inhibits HDAC3. The authors conclude that the "results suggest that HDAC3 deletion leads to long-term memory formation that is persistent and lasts beyond the point at which normal long-term memory fails."
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