Clene Inc. (NASDAQ: CLNN) presented combined results from its REPAIR-MS trial at the 41st Congress of the European Committee for Treatment and Research in Multiple Sclerosis in Barcelona, demonstrating significant improvements in brain energy metabolism for multiple sclerosis patients treated with CNM-Au8. The investigational therapy showed enhanced brain NAD+/NADH ratios, a critical marker of energetic capacity, across both relapsing and non-active progressive MS patient groups.
The treatment produced significant changes in brain NAD+ and NADH fractions, with researchers identifying correlations between baseline brain energy metabolism and key clinical measures including disability progression, cognitive function, and motor performance. CNM-Au8 demonstrated a favorable safety profile and was well tolerated by patients throughout the trial period, reinforcing its potential as a disease-modifying therapy for multiple sclerosis. For detailed trial information, visit the official results page.
This development represents a significant advancement in the understanding and treatment of multiple sclerosis, a chronic neurodegenerative disease affecting approximately 2.8 million people worldwide. The focus on addressing bioenergetic failure in MS represents a novel therapeutic approach that could potentially slow disease progression by improving mitochondrial function and neuronal protection. The correlation between improved energy metabolism and clinical outcomes suggests that targeting cellular energy production may be fundamental to managing MS progression.
For investors and stakeholders following Clene's progress, additional company information and updates are available through the corporate newsroom. The positive REPAIR-MS results position CNM-Au8 as a promising candidate in the neurodegenerative disease treatment landscape, potentially offering new hope for patients with limited therapeutic options. The company's focus on mitochondrial health and neuronal protection represents an emerging area of research that could have broader implications for treating other neurodegenerative conditions beyond multiple sclerosis.
