Salt Lake City – Clene Inc. today unveiled preclinical findings that, according to the company, demonstrate CNM-Au8® improves cellular health in a novel dopaminergic neuron model of Parkinson’s disease. The firm said the model—derived from skin cells of both familial and sporadic Parkinson’s disease patients—retains age-related features, enabling more disease-relevant observations (according to the company).
In the study, Clene said that CNM-Au8 enhanced mitochondrial health by increasing membrane potential and mitochondrial volume while reducing reactive oxygen species, particularly in familial Parkinson’s disease neurons, with milder effects in sporadic cases. The company claims the treatment also lowered inflammatory proteins linked to senescence (CD40 and CXCL10) in sporadic neurons.
Clene noted that CNM-Au8 restored cellular metabolism by increasing the NAD+/NADH ratio in a dose-dependent manner and normalized about 36% of metabolites in familial and 17% in sporadic neurons—especially those involved in the TCA cycle and nucleotide metabolism. According to the company, it also reversed dysregulated gene expression toward control levels in both neuron types, without showing toxicity at tested doses—consistent with its clinical safety record from over 1,000 patient-years of use in ALS and MS (according to the company).
Clene said the data were presented at the Michael J. Fox Foundation’s H2 Therapeutics Stewardship Meeting in New York City. The company claims these findings strengthen support for further clinical development of CNM-Au8 for Parkinson’s disease.
