Etifoxine (and therefore GRX-917) was recently shown to reduce neuroinflammation via inhibition of the NLRP3 inflammasome pathway (https://www.biorxiv.org/content/10.1101/2023.09.19.558428v1). Etifoxine inhibits the NLRP3 inflammasome pathway broadly, as shown by marked reductions of NLRP3, IL-1beta, and TNF. In addition, significant improvement in clinical scores were observed in the mouse EAE model of acute inflammation, confirming prior studies with etifoxine. NLRP3 inflammasome pathway inhibition thus appears to underlie etifoxine’s efficacy in animal models of neuroinflammation and neurodegeneration, including multiple sclerosis, Alzheimer’s Disease, Parkinson’s Disease, stroke, head trauma, pain, and neuropathy.
GABA Therapeutics’ lead clinical asset, GRX-917 (deuterated-etifoxine), exhibits equivalent pharmacology, MOA, safety, and efficacy. This new mechanistic insight not only supports assessment of GRX-917 for neuroinflammatory disorders, but also points to GRX-917’s potential for the treatment of peripheral NLRP3 inflammatory pathway disorders, such as inflammatory bowel disease, osteoarthritis, rheumatoid arthritis, lupus, asthma, gout, NASH, chronic kidney disease, and others. anxiety NLRP3 neuroinflammation neurodegeneration IBD multiplesclerosis neuropathy
For questions contact:
Richard G. Farrell
Chief Financial Officer
Follow us on LinkedIn
We post current progress and developments on our GABA Therapeutics’ LinkedIn page. Click here to follow us LinkedIn.