Longeveron Inc. (NASDAQ:LGVN), a clinical stage biotechnology company developing cellular therapy for life-threatening, rare pediatric and chronic aging-related conditions, today announced that additional analysis of data from the Phase 2a clinical trial evaluating its stem cell therapy laromestrocel in mild Alzheimer’s disease (AD) is being presented in a Poster Presentation at the 2026 Alzheimer’s Association International Conference® (AAIC®), being held July 12-15, 2026 in London, United Kingdom and online.

Results presented in "Laromestrocel Stabilizes Brain Inflammation In Key Alzheimer’s Disease Gray And White Matter Regions As Assessed Using Free Water MRI" provide support for a clinically relevant and durable anti-inflammatory mechanism of action of laromestrocel in gray and white matter and indicate potential blood biomarker correlates. Importantly, the reduction on free water detected by MRI correlates with both improved clinical outcomes and the anti-atrophic responses in the brain.

A key contributor to AD brain atrophy and clinical pathology is progressive neuroinflammation, and no therapeutic to date has been successful in mitigating the destructive inflammation of AD. Brain inflammation can be indexed using free water MRI. Longeveron previously found that free water rose substantially during AD pathogenesis in the brains of individuals in the placebo group, particularly in the hippocampus, temporal lobe, and other key AD regions, but subjects treated with laromestrocel showed no increase. Together with previously published data, these results showed that laromestrocel, a human bone marrow-derived, mesenchymal stem cell therapy with anti-inflammatory and pro-vascular effects, substantially reduced brain atrophy and lowered free water in a proof of concept, randomized Phase 2a trial (CLEAR-MIND).

In this new post-hoc exploratory analysis of CLEAR-MIND results, the anti-inflammatory effect was observed to be most prominent in the hippocampus, temporal lobe, and other AD-associated areas and correlated (Spearman) with both increased brain volume and improved cognitive and quality of life scores.

Laromestrocel infusion groups were: 1) placebo, 2) 25 million cells, single dose (25Mx1), 3) 25M cells over 4 monthly doses (25Mx4) or 4) 100M cells over 4 monthly doses (100Mx4), vs placebo. Data were statistically modeled using Mixed Model Repeated Measures (MMRM). In the placebo population (N=10), free water rose over 39 weeks in key white matter regions: the fornix, sagittal stratum, uncinate fasciculus. However, free water was numerically reduced compared with placebo in all groups receiving laromestrocel (fornix at week 26: 25Mx4, N=11, p=0.058; sagittal stratum at week 39: pooled 25Mx4 and 100Mx4 treatment groups, N=21, p=0.063; uncinate fasciculus (left) at week 39: 100Mx4, N=10, p=0.064). This reduction trend in free water correlated (Spearman) with Longeveron’s recent findings showing significantly reduced free water compared with placebo at 39 weeks in key gray matter regions: hippocampus, the temporal, parietal, and occipital lobes, and medulla, and with improvements in clinical scores.

Blood plasma samples from the trial were assessed using NuLISA. Plasma NuLISA indicated a reduction compared with placebo (N=11) at 39 weeks in neurogranin, a marker of neuronal degradation (25Mx4, N=12, p=0.023), and an increase in IL-13, an anti-inflammatory cytokine that regulates brain microglia activation (25Mx1, N=12, p=0.043).