Mitochon Pharmaceuticals announced that it was awarded a grant from The Michael J. Fox Foundation for Parkinson’s Research (MJFF) to help develop its mitochondrial targeted compounds for treating Parkinson’s disease. The funding will go to pivotal animal studies to assess the benefits of Mitochon’s compounds in ameliorating the deficits associated with dopaminergic neuron loss, the hallmark of Parkinson’s disease. If successful, Mitochon’s compounds, MP101 ad MP201 could be in patients as early as 2019.

 “We are delighted to receive funding from The Michael J. Fox Foundation, the preeminent institution in the field of Parkinson’s research. By harnessing the power of the mitochondria, our compounds are able to protect cells from the destructive effects of age-related degeneration. Importantly, this funding will pave the way for human clinical development, with the hope of helping the millions of people with Parkinson’s disease,” said Robert Alonso, co-founder and CEO of Mitochon.

“Abnormalities in the mitochondrial processes can have severe consequences for the function and survival of dopamine neurons in people with PD,” said Shalini Padmanabhan, Ph.D., Associate Director of Research Programs at MJFF. “The Foundation supports Mitochon’s work toward discovery and development of mitochondrial-targeted therapies to speed breakthroughs for patients.”

MP101 and MP201 are mitochondrial targeted, once-a-day, oral therapies that have been shown to shield cells from damage caused by a host of degenerative processes (genetic and non-genetic, auto-immune and injury). In preclinical studies, these compounds have exhibited striking protective and functional benefits in disease models. These include: brain volume sparing in Huntington’s disease; axonal protection from demyelination in Multiple Sclerosis and dopaminergic neuron loss in Parkinson’s disease. To understand the critical step of translation, Mitochon will initiate Phase I studies in normal healthy volunteers in 2018 and is expected to be in Phase II studies in 2019.