By Erica Slaughter Huntington disease (HD), a genetically dominant trinucleotide repeat disorder resulting from cytosine-adenine-guanine (CAG) repeats within the huntingtin (HTT) gene, has a near-full pene- trance and onset of symptomatology and neuronal loss typically by the third decade of life. A neuropathological hallmark of HD is cortical atrophy, as indicated in…(Read More)

In the sanctity of pure drug discovery, objective reasoning can become clouded when pursuing ideas that appear unorthodox, but are spot on physiologically. To put this into historical perspective, it was an unorthodox idea in the 1950’s to suggest that warfarin, a rat poison, could be repositioned into a breakthrough drug in humans…(Read More)

Blue Bell, Pennsylvania (BUSINESS WIRE) — Mitochon Pharmaceuticals today announced that it was awarded Orphan Drug Designation by FDA for its mitochondrial targeted compound, MP-101 for treating Huntington’s Disease. This important allowance, along with the Company’s open IND will help secure the path forward for the continued clinical development of MP101 in Huntington…(Read More)

Blue Bell, Pennsylvania (BUSINESS WIRE) — Mitochon Pharmaceuticals today announced that it was notified by the US Patent and Trade Mark Office of allowance on its first patent, US 15/002,531 “INDUCED EXPRESSION OF BRAIN DERIVED NEUROTROPHIC FACTOR (BDNF) FOR TREATMENT OF NEUROMUSCULAR, NEURODEGENERATIVE, AUTOIMMUNE, DEVELOPMENTAL AND/OR METABOLIC DISEASE”. This patent allowance will help…(Read More)

Blue Bell, Pennsylvania (BUSINESS WIRE)–Mitochon Pharmaceuticals today 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…(Read More)

Huntington’s disease (HD) is a neurodegenerative disorder caused by a CAG repeat expansion in the first exon of the gene huntingtin. There is no treatment to prevent or delay the disease course of HDcurrently. Oxidative stress and mitochondrial dysfunction have emerged as key determinants of the disease progression in HD. Therefore, counteracting mutant huntingtin…(Read More)

Recent findings have elucidated roles for mitochondrial uncoupling proteins (UCPs) in neuronal plasticity and resistance tometabolic and oxidative stress. UCPs are induced by bioenergetic challenges such as caloric restriction and exercise and may protect neurons against dysfunction and degeneration. The pharmacological uncoupler 2,4-dinitrophenol (DNP), which was once prescribed to >100,000 people as…(Read More)