Charles River Laboratories International, Inc. has announced a significant expansion of its work with small molecule LRRK2 inhibitors, funded by The Michael J. Fox Foundation for Parkinson’s Research (MJFF), a leading organization working to support the diagnosis and treatment of Parkinson’s disease (PD).
“Since 2011, we have worked together with The Michael J. Fox Foundation and its partners to accelerate the discovery of therapies and potential cures for Parkinson’s disease,” said Emily Hickey, DVM, PhD, Corporate Senior Vice President, Global Discovery Services, Charles River. “We are delighted to have the opportunity to continue to contribute to this cutting-edge research.”
The work will build on previous research that advanced efforts to identify novel small molecule LRRK2 inhibitors. The inhibition of the kinase LRRK2, which in humans has been genetically linked to development of PD, is one of the most promising novel therapeutic strategies. The goal is to determine optimal dosing strategies to achieve efficacy with LRRK2 inhibitors while avoiding the lung alterations that have been reported in previous research.
“Continued research into LRRK2 is extremely important to developing a successful therapy to slow or stop the progression of Parkinson’s disease,” said Marco Baptista, PhD, MJFF senior associate director of research programs. “We’re grateful to Charles River for their important work in researching the optimal use strategies of LRRK2.”
The pre-competitive Parkinson’s Disease Research Tools Consortium has also provided Charles River funding because of its in vitro biology expertise. The consortium will focus on developing a screening assay in human primary cells to observe and modulate protein aggregation and associated neurotoxicity.
In addition to these new projects, Charles River will continue to work with a MJFF-sponsored consortium—which includes Charles River, the University of Pennsylvania, Washington University, and the University of Pittsburgh—on the development of an α-synuclein imaging agent.