LUYE PHARMA (02186) has announced that the Phase II clinical trial in China for its self-developed Class 1 innovative drug LY03015 for treating Tardive Dyskinesia (TD) has been completed, yielding positive results and meeting its primary endpoint.

LY03015 is the world's first dual-target innovative drug targeting both vesicular monoamine transporter 2 (VMAT2) and Sigma-1 receptor to enter clinical trials, with intended indications for TD and chorea associated with Huntington's disease (HD).

TD is a hyperkinetic movement disorder that can occur following long-term use of antipsychotic drugs, characterized by involuntary, rhythmic, repetitive, and stereotyped movements, including abnormal muscle movements in the face or trunk.

Symptoms often persist even after discontinuing the causative medication, significantly impacting patients' mental health and quality of life.

Global data indicates that among patients receiving antipsychotic treatment, the average prevalence of TD is approximately 25.3%.

According to the Cortellis database, the current market size for drugs treating this condition is about $5 billion annually and is showing a rapid growth trend.

Public information suggests that existing treatments may carry serious safety concerns, either due to off-target effects of metabolites or because they are inactivated via metabolism by CYP2D6, which exhibits significant genetic polymorphism.

Results from registration double-blind clinical trials for existing treatments show that after treatment with single-target VMAT2 inhibitors, approximately 60% of patients still fail to achieve a clinically meaningful level of efficacy, defined as an improvement of ≥50% on the Abnormal Involuntary Movement Scale (AIMS 1-7), indicating insufficient effectiveness and a significant unmet treatment need.

Utilizing its self-developed AI drug design platform, the group has designed the novel small-molecule drug LY03015, which not only addresses the aforementioned safety risks but also highly targets both VMAT2 and Sigma-1R, exerting a dual effect of "symptom control" and "pathological improvement".

On one hand, it inhibits VMAT2 transport function to reduce the release of dopamine (DA) from presynaptic neurons, thereby decreasing DA stimulation of hypersensitive D2 receptors and alleviating disease symptoms.

On the other hand, by activating Sigma-1R, it can promote the release of brain-derived neurotrophic factor (BDNF) and synaptic remodeling, repairing damaged cortical-striatal synaptic connections, which holds promise for achieving sustained symptom remission and reducing the disease recurrence rate.