XenoPort, Inc. (Nasdaq:XNPT) announced today that it has been awarded a grant from The Michael J. Fox Foundation (MJFF) for Parkinson’s Research to support preclinical studies to explore XP23829 for its ability to protect against neurodegeneration in experimental preclinical models of Parkinson’s disease. The grant of $347,075 was awarded under the Foundation's Therapeutics Development Initiative Program aimed at supporting preclinical development of Parkinson's disease therapies that have the potential for fundamentally altering disease course and improving treatment of symptoms.
“Evaluating drugs that could potentially slow the progression of Parkinson’s disease is a high-priority research area for The Michael J. Fox Foundation,” said Kuldip Dave, PhD, associate director of research programs at MJFF. “We are encouraged by research that suggests that fumaric acid esters could slow the progression of the neurodegenerative process. We are hopeful that XenoPort’s efforts to this end could help to speed progress toward a breakthrough treatment for patients with Parkinson’s disease.”
XenoPort is evaluating XP23829, a fumaric acid ester compound and a prodrug of monomethyl fumarate (MMF). Fumaric acid ester compounds have shown immuno-modulatory and neuroprotective effects in cell-based systems and preclinical models of disease. Dimethyl fumarate (DMF), also a fumaric acid ester compound and a prodrug of MMF, has been shown to be effective in clinical trials in patients with relapsing-remitting multiple sclerosis (RRMS) and psoriasis. A potential shortcoming of DMF-based therapy is that patients can suffer from gastrointestinal adverse events.
The biological mechanisms underlying the beneficial effects of fumaric acid ester prodrugs may be due to Nrf2 activation by MMF. Nrf2 activation is thought to combat oxidative neurodegeneration by increasing the genetic expression of a number of antioxidant enzymes and downregulating, or reducing, production of proinflammatory molecules. In human genetic studies, patients with genetic sequences associated with high Nrf2 transcriptional activity also showed decreased risk of developing Parkinson’s disease or an increased age of onset of the disease. In preclinical models of Parkinson’s disease, MPTP-induced neurotoxicity of dopaminergic neurons was reduced by activation of Nrf2 either through addition of Nrf2-inducing compounds or by over expression of Nrf2.
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