ProMIS Neurosciences Inc (PMN) News & EventsPMNProMIS Neurosciences Inc

ProMIS Neurosciences Reports Positive Interim Results for PMN310 Trial

ProMIS Neurosciences announced positive blinded six-month interim safety and biomarker results from PRECISE-AD, the Phase 1b trial of its lead drug candidate, PMN310, in patients with mild cognitive impairment due to Alzheimer's disease or mild Alzheimer's disease, or AD. In the blinded interim analysis evaluating 136 AD patients, PMN310 was observed to have a favorable safety profile across all genotypes, with no cases of amyloid-related imaging abnormalities-edema reported as of the data cutoff date, and early, directionally consistent movement in disease-relevant biomarkers potentially reflective of the randomization pattern. The trial remains blinded and ongoing with topline 12-month results expected in 1Q27. A majority of patients showed reductions in disease-relevant biomarkers against expected increases in natural-history trajectories: 68.5% of patients had a decline from baseline in plasma pTau217 and 62.5% had a decline in CSF MTBR-tau243, consistent with a potential beneficial drug effect and potentially reflective of the trial's 3:1 active-to-placebo randomization. These observed biomarker trends are not a determination of efficacy, and trends in biomarkers may not ultimately be reflective of clinical effects. Unblinded 12-month topline data is expected Q1 2027, including efficacy data.

ProMIS PMN310 Shows Dose-Dependent AbetaO Reduction at 3 and 29 Days at AAIC 2026

ProMIS Neurosciences announced the first human evidence of dose-dependent amyloid-beta oligomer reduction by its Alzheimer's drug candidate, PMN310, presented at AAIC 2026. The findings, drawn from analysis of samples collected during the company's Phase 1a trial in healthy volunteers, showed that individuals receiving PMN310 exhibited a dose-dependent reduction in detectable AssO in cerebrospinal fluid at both three and 29 days after dosing. While healthy individuals carry lower oligomer burdens than Alzheimer's patients, amyloid-beta oligomers are detectable in CSF even in cognitively normal adults, making this a meaningful measure of target engagement. This represents one of the first quantitative demonstrations of treatment-related oligomer reduction in humans. Amyloid-beta oligomers in CSF were measured using surface-based fluorescence intensity distribution analysis developed by attyloid, an assay which enables direct quantification of oligomer particles with unprecedented sensitivity. While the assay is currently exploratory, it provides pharmacodynamic evidence of target engagement by PMN310. Placebo-treated healthy volunteers in the Phase 1a trial exhibited low levels of AbetaO in CSF. PMN310 administration resulted in a dose-dependent reduction in detectable AbetaO particles in CSF. PMN310 demonstrated binding to AbetaO with no interaction with monomers by surface plasmon resonance, and no detectable reactivity with plaques or vascular deposits of Abeta in AD brain tissue sections, representing the potential for a differentiated clinical profile. PMN310 was generally well-tolerated, with CSF concentrations linearly dose-dependent, reaching 100-600 times the estimated molar concentration of AbetaO, and a CSF half-life of approximately 27 days. In a transgenic AD mouse model, PMN310 preserved memory and learning performance in the Morris Water Maze task.