Antipodean Pharmaceuticals Completes Phase 2 Trial Enrollment For MitoQ In Parkinson’s Disease

Antipodean Pharmaceuticals, a privately held pharmaceutical company developing treatments for disorders associated with mitochondrial dysfunction, today announced that it completed enrollment in a Phase 2 study to evaluate its lead compound, MitoQ (mitoquinone), in Parkinson’s disease, a neurodegenerative disorder that affects up to four million people worldwide.

“We believe that MitoQ’s novel mechanism of action may yield additional therapeutic options for Parkinson’s disease patients, who have limited treatments available for symptom relief, and none to halt disease progression,” said Ken Taylor, CEO, Antipodean Pharmaceuticals. “MitoQ blocks the effects of oxidation, a chemical reaction that generates oxygen free radicals, which can attack and destroy cells. We achieved enrollment in this Phase 2 trial ahead of schedule, demonstrating the rapid advancement of our clinical programs.”

The randomized, double-blind multi-center clinical trial is evaluating 128 patients in New Zealand and Australia who have met the diagnosis criteria for Parkinson’s, but have not begun any treatment. Patients were randomized into one of three treatment arms to compare treatment with MitoQ at 40 mg and 80 mg to placebo, orally administered once daily. The primary endpoint is disease progression according to the Unified Parkinson’s disease Rating Scale (UPDRS). An independent data safety monitoring board is reviewing safety data periodically.

“Several neurodegenerative disorders, including Parkinson’s, are associated with mitochondrial dysfunction from oxidative damage,” said Dr. Barry Snow, Head of Department of Neurology, Auckland Hospital, and lead investigator of the trial. “MitoQ may be able to stem the progression of these difficult-to-treat conditions.”

About MitoQ

MitoQ is based on a novel technology, targeted lipophilic cations, that transport and concentrate antioxidants into the mitochondria — organelles inside cells that provide energy for life processes — where they accumulate up to a thousand fold. In 2004, a genomic study of hereditary early-onset Parkinson’s disease demonstrated a direct molecular link between mitochondrial dysfunction and the pathogenesis of Parkinson’s disease. Mitochondrial dysfunction also has been shown to represent an early critical event in the pathogenesis of the sporadic form of Parkinson’s disease. Clinical studies by the Parkinson’s Study Group show that very high doses of an antioxidant called Coenzyme Q (which MitoQ effectively targets into mitochondria) appear to slow the progression of Parkinson’s disease symptoms.

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