Clene Inc. (NASDAQ: CLNN) has presented new preclinical data showing that its lead investigational therapy CNM-Au8 improves mitochondrial health, reduces inflammation, and normalizes gene expression in Parkinson's disease models. The findings, presented at the Michael J. Fox Foundation's H2 Therapeutics Stewardship Meeting in New York City, demonstrate the drug candidate's potential to address key cellular deficits driving Parkinson's disease progression.
The preclinical results revealed that CNM-Au8 improved mitochondrial function, restored cellular energy metabolism, reduced harmful inflammation, and normalized disrupted gene expression in dopaminergic neurons. These findings align with previous Phase 2 trial results that showed positive energetic and metabolic effects in Parkinson's patients, suggesting a consistent mechanism of action across study types.
Notably, the treatment demonstrated no toxicity in neuronal models, consistent with safety data accumulated from over 1,000 patient-years in clinical trials for amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS). This safety profile is particularly important for a potential chronic treatment for neurodegenerative diseases that require long-term medication.
The implications of these findings are significant for the approximately 10 million people worldwide living with Parkinson's disease. Current treatments primarily address symptoms rather than modifying the underlying disease progression. CNM-Au8's ability to improve cellular health and energy metabolism represents a potential disease-modifying approach that could slow or halt disease advancement.
Clene plans to design a Phase 2 clinical study specifically for Parkinson's disease while continuing to advance its ALS and MS programs. The company's focus on improving mitochondrial health and protecting neuronal function addresses a fundamental aspect of neurodegenerative diseases that has been challenging to target effectively with existing therapies.
The research findings were initially announced in September 2025 and detailed further at the scientific meeting. For investors seeking additional information, the latest updates relating to CLNN are available through the company's newsroom at https://ibn.fm/CLNN. The convergence of positive preclinical data with previous clinical results suggests CNM-Au8 may represent a promising new therapeutic approach for neurodegenerative disorders where treatment options remain limited.
