Clene Inc. Presents Preclinical Data Showing CNM-Au8 Improves Cellular Health in Parkinson’s Disease Model
TL;DR
Clene's CNM-Au8 offers a first-in-class therapeutic advantage by improving mitochondrial function and reducing inflammation in Parkinson's disease neurons.
CNM-Au8 works by correcting metabolic imbalances, normalizing gene expression, and improving mitochondrial health with no observed toxicity in preclinical models.
This neuroprotective therapy could significantly improve quality of life for Parkinson's patients by addressing both familial and sporadic forms of the disease.
Gold nanocrystals from Clene restored cellular metabolism in Parkinson's neurons through a novel mechanism targeting mitochondrial function.
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Clene Inc. (NASDAQ: CLNN) has released new preclinical data indicating that its investigational therapy CNM-Au8® improves mitochondrial function, reduces inflammation, and restores cellular metabolism in a dopaminergic neuron model of Parkinson’s disease. The findings, presented at the Michael J. Fox Foundation H2 Therapeutics Stewardship Meeting in New York City, showed that CNM-Au8 corrected metabolic imbalances, normalized dysregulated gene expression, and exhibited 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 funding from the Michael J. Fox Foundation, underscores CNM-Au8’s potential as a neuroprotective therapy for both familial and sporadic forms of Parkinson’s disease. This development is significant for the neurodegenerative disease research community, as it addresses critical cellular dysfunctions associated with Parkinson’s, potentially offering a new approach to slowing or halting disease progression.
CNM-Au8 is an investigational first-in-class therapy designed to improve central nervous system cell survival and function by targeting mitochondrial health and the NAD pathway while reducing oxidative stress. For more information about Clene Inc., visit https://www.clene.com. The full press release can be accessed at https://ibn.fm/B9Coc.
The implications of these findings extend beyond Parkinson’s disease, as mitochondrial dysfunction and oxidative stress are common features in other neurodegenerative conditions such as amyotrophic lateral sclerosis and multiple sclerosis. This research could pave the way for broader applications of CNM-Au8, potentially benefiting patients across multiple neurological disorders and advancing the field of neuroprotective therapeutics.
Curated from InvestorBrandNetwork (IBN)
