- Clene Inc., a late clinical-stage biopharmaceutical company focused on developing solutions that improve mitochondrial health and protect neuronal function to treat neurodegenerative diseases, recently announced the publication of a peer-reviewed article
- The article describes results from two Phase 2a clinical trials, REPAIR-PD and REPAIR-MS, which evaluated the effects of CNM-Au8, the company’s lead drug candidate, on brain energy metabolite levels in participants with Parkinson’s Disease and Multiple Sclerosis, respectively
- Researchers measured key brain metabolites, such as NADH and NAD+, which are involved in neuronal energy production, utilization, and maintenance, for changes from baseline with daily, oral treatment of CNM-Au8 over 12 weeks
- Results from the studies showed that treatment with CNM-Au8 increased the brain NAD+/NADH ratio by a statistically significant (p < 0.05) 10.4%
Energy metabolism involves the conversion of the potential energy contained in food-borne fuels, including some amino acids, glucose, lactate, fatty acids, and ethanol, among others, into chemical energy. Usually, this chemical energy exists in the form of adenosine triphosphate (“ATP”), the universal energy-containing molecule that powers most cellular functions, including brain function.
ATP is produced through oxidative phosphorylation (“OXPHOS”) or glycolysis. The former, however, requires mitochondria and yields considerably more ATP than the latter (https://ibn.fm/9pQ6P). Unfortunately, oxidative phosphorylation can sometimes become impaired, affecting skeletal muscle, cardiac, and nervous tissues normally characterized by high energy metabolism. Causes of the impairments to oxidative phosphorylation vary from…
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