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MapLight's M1/M4 agonist aces Phase II schizophrenia trial

MapLight's M1/M4 agonist aces Phase II schizophrenia trial

MapLight Therapeutics (Nasdaq: MPLT) reported positive topline results from its Phase II ZEPHYR trial of ML-007C-MA in adults with acute exacerbation of schizophrenia, with the 210/3 mg twice-daily dose meeting the primary endpoint and demonstrating a statistically significant reduction in PANSS total score versus placebo at Week 5 — results the company says were designed and sized to support registration.

The trial enrolled 307 inpatient adults randomized 1:1:1 to placebo, ML-007C-MA 210/3 mg BID, or 330/6 mg once daily across 25 US sites. In the modified intent-to-treat population, the BID arm produced a least-squares mean difference of −4.5 points on the PANSS total score versus placebo (effect size 0.37, p=0.015). Among completers, the effect size reached 0.50 (LS mean difference −6.0, p=0.002). The BID dose also achieved separation on CGI-S (effect size 0.48, p=0.002) and PANSS positive Marder factor (effect size 0.39, p=0.012). The once-daily 330/6 mg dose showed numerical improvement but did not reach statistical significance on the primary endpoint, though it separated on CGI-S (p=0.036) and PANSS positive Marder factor (p=0.045).

A prespecified secondary endpoint assessed cognitive performance via the Cogstate battery in participants with baseline cognitive impairment. The BID arm produced an effect size of 0.51 (0.44 points versus placebo, p=0.041), and MapLight reported that this cognitive benefit did not correlate with PANSS score change — indicating an effect independent of antipsychotic symptom improvement. No approved therapy currently carries an indication for cognitive impairment associated with schizophrenia.

ML-007C-MA is an oral, extended-release fixed-dose combination of betovumeline, an investigational M1/M4 muscarinic agonist, co-formulated with fesoterodine, a peripherally acting anticholinergic. The design activates M1 and M4 muscarinic receptors in the central nervous system to drive antipsychotic and cognitive effects, while the co-formulated anticholinergic mitigates peripheral cholinergic side effects by synchronizing the pharmacokinetics of both components. The mechanism is non-dopaminergic, placing ML-007C-MA in the same mechanistic class as Bristol Myers Squibb's Cobenfy (xanomeline-trospium chloride), which received FDA approval in September 2024 as the first non-D2 antipsychotic. Every other approved agent in schizophrenia — including cariprazine, lumateperone, and paliperidone — works primarily through dopamine D2 receptor blockade.

Tolerability in the ZEPHYR trial was generally favorable. Treatment-emergent adverse events in the BID arm were reported in 74.7% of participants versus 48.1% on placebo, mostly mild and cholinergic in nature. There were no serious adverse events or drug-related severe TEAEs in either active arm. GI-related discontinuations occurred in only two participants (2.0%) in the BID arm, and no participant failed to reach target dose due to tolerability. All-cause discontinuation across both active arms was 19.9%. Small increases in heart rate were observed, consistent with the known fesoterodine profile.

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MapLight plans to request an End-of-Phase 2 meeting with the FDA to discuss the design of a confirmatory Phase III trial that, together with ZEPHYR, would support an initial NDA submission. Site identification for the confirmatory trial is already underway. The company also intends to evaluate a once-daily regimen alongside the BID dose in a separate confirmatory study.

The ZEPHYR data carry direct implications for MapLight's broader pipeline. The ongoing VISTA trial is evaluating the same 210/3 mg BID dose for hallucinations and delusions associated with Alzheimer's disease psychosis — an indication with no approved therapy — with topline results expected in the second half of 2027. The cognitive signal observed in ZEPHYR, if replicated in VISTA, would strengthen the mechanistic rationale for the Alzheimer's disease psychosis program, where cognitive function is a central clinical concern.


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