Neurolixis today announced the publication of the results from its successful Phase 2A proof-of-concept clinical trial of NLX-112 (befiradol) in Parkinson’s disease. The findings, published in the prestigious journal 𝘔𝘰𝘷𝘦𝘮𝘦𝘯𝘵 𝘋𝘪𝘴𝘰𝘳𝘥𝘦𝘳𝘴, highlight NLX-112’s potential as a first-in-class, non-dopaminergic therapy with dual efficacy in addressing both levodopa-induced dyskinesia (LID) and motor impairment in Parkinson’s patients. The randomized, double-blind, placebo-controlled trial, supported by The Michael J. Fox Foundation and Parkinson’s UK, evaluated NLX-112 in patients with troubling LID. The study successfully met its primary endpoint of safety and tolerability, as well as its secondary endpoint of significantly reducing LID. Notably, NLX-112 also demonstrated anti-parkinsonian effects, significantly improving motor function in study participants.
See the full publication (Open Access): 𝗡𝗟𝗫-𝟭𝟭𝟮 𝗿𝗮𝗻𝗱𝗼𝗺𝗶𝘇𝗲𝗱 𝗣𝗵𝟮𝗔 𝘁𝗿𝗶𝗮𝗹: 𝘀𝗮𝗳𝗲𝘁𝘆, 𝘁𝗼𝗹𝗲𝗿𝗮𝗯𝗶𝗹𝗶𝘁𝘆, 𝗮𝗻𝘁𝗶-𝗱𝘆𝘀𝗸𝗶𝗻𝗲𝘁𝗶𝗰 𝗮𝗻𝗱 𝗮𝗻𝘁𝗶-𝗽𝗮𝗿𝗸𝗶𝗻𝘀𝗼𝗻𝗶𝗮𝗻 𝗲𝗳𝗳𝗶𝗰𝗮𝗰𝘆. 𝘔𝘰𝘷𝘦𝘮𝘦𝘯𝘵 𝘋𝘪𝘴𝘰𝘳𝘥𝘦𝘳𝘴, 2025 (https://doi.org/10.1002/mds.30175)
𝗔 𝗡𝗼𝘃𝗲𝗹 𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺 𝗼𝗳 𝗔𝗰𝘁𝗶𝗼𝗻: Unlike current Parkinson’s treatments that target the dopamine system, NLX-112 acts on the serotonin (5-HT) system, as a highly selective full activator of 5-HT1A receptors. This unique mechanism differentiates NLX-112 from previous serotonergic drugs and is believed to underlie its dual efficacy in reducing dyskinesia and improving motor function. The promising results from this Phase 2A trial support further development of NLX-112 as a transformative therapy for movement disorders. Neurolixis is actively planning next steps in the clinical development program to advance NLX-112 toward potential regulatory approval.
𝗔𝗯𝗼𝘂𝘁 𝗣𝗮𝗿𝗸𝗶𝗻𝘀𝗼𝗻’𝘀 𝗗𝗶𝘀𝗲𝗮𝘀𝗲 𝗮𝗻𝗱 𝗥𝗲𝗹𝗮𝘁𝗲𝗱 𝗠𝗼𝘃𝗲𝗺𝗲𝗻𝘁 𝗗𝗶𝘀𝗼𝗿𝗱𝗲𝗿𝘀: Parkinson’s disease is the second most common neurodegenerative disorder, affecting over 10 million people worldwide. Levodopa, the mainstay treatment for Parkinson’s, often leads to debilitating dyskinesias (involuntary movements) after prolonged use. Up to 80% of patients develop LID within ten years of levodopa therapy. Current treatments for LID, such as amantadine, are limited by side effects and variable efficacy, underscoring the need for new therapeutic options.
As well as Parkinson’s disease, other disorders also involve dysfunction in the basal ganglia, a brain region critical for coordinating movement. Such disorders include spinocerebellar ataxia, Huntington’s disease, essential tremor and dystonia, and lead symptoms such as tremors, rigidity, and impaired motor control.
