Clene's CNM-Au8 Shows Neuroprotective Potential in Parkinson's Disease Preclinical Study
September 4th, 2025 3:39 PM
By: Newsworthy Staff
Clene Inc.'s CNM-Au8 demonstrated improved mitochondrial function, reduced inflammation, and restored cellular metabolism in Parkinson's disease models, suggesting potential as a neuroprotective therapy for both familial and sporadic forms of the disease.

Clene Inc. (NASDAQ: CLNN) has presented new preclinical data showing that its investigational drug CNM-Au8® improved mitochondrial function, reduced inflammation, and restored cellular metabolism in a novel dopaminergic neuron model of Parkinson's disease. The findings, presented at the Michael J. Fox Foundation H2 Therapeutics Stewardship Meeting, revealed that CNM-Au8 corrected metabolic imbalances and normalized dysregulated gene expression while exhibiting a favorable safety profile with no observed toxicity in Parkinson's disease neurons.
The study, conducted in collaboration with the Salk Institute and supported by Michael J. Fox Foundation funding, underscores CNM-Au8's potential as a neuroprotective therapy for both familial and sporadic Parkinson's disease. This research is particularly significant given the urgent need for disease-modifying treatments that can address the underlying cellular dysfunction in Parkinson's rather than merely managing symptoms. The demonstration of improved mitochondrial health and reduced inflammation suggests CNM-Au8 may target fundamental pathological mechanisms common to various forms of the neurodegenerative disorder.
For more information about the company's research, visit https://www.clene.com. The full press release detailing these preclinical findings can be accessed at https://ibn.fm/B9Coc. These results build upon previous research showing CNM-Au8's potential in other neurodegenerative conditions, positioning it as a promising candidate for addressing the cellular basis of Parkinson's disease progression rather than just symptomatic relief.
Source Statement
This news article relied primarily on a press release disributed by InvestorBrandNetwork (IBN). You can read the source press release here,
