CervoMed Announces New Data at the AD/PD™ 2026 Scientific Conference that Reinforce Neflamapimod’s Positive Effects in Dementia with Lewy Bodies (DLB) in Patients without Alzheimer’s Disease Co-Pathology

New analyses show DLB patients with lower plasma pTau181 levels — indicating an earlier stage of disease and absence of Alzheimer’s disease (AD) co-pathology — experienced greater clinical benefit with neflamapimod in Phase 2b clinical trial

PK/PD analyses of Phase 2b clinical data provide further insight into the drug plasma concentration levels of neflamapimod associated with a clinical effect

Findings further support neflamapimod’s potential to target the underlying cause of disease in DLB and the Company’s patient enrichment strategy and dosing regimen for planned Phase 3 trial

BOSTON, March 19, 2026 (GLOBE NEWSWIRE) -- This week, in an oral session at the AD/PD™ 2026 Conference in Copenhagen, Denmark, investigators will present new analyses from the Phase 2b RewinD-LB clinical trial of neflamapimod, being developed by CervoMed Inc. (NASDAQ: CRVO) (CervoMed or the Company) for the treatment of dementia with Lewy bodies (DLB). The new data analyses reinforce that neflamapimod, which targets the neuroinflammation and synaptic dysfunction associated with DLB, has the potential to slow disease progression by acting on the underlying disease biology.

“In these analyses, the treatment response progressively increases across DLB patient subgroups that are less likely to have Alzheimer’s disease (AD) co-pathology, as identified by the pTau181 blood test,” said Dr. John-Paul Taylor, MBBS, MRCPsych, PhD, Professor of Translational Dementia Research at Newcastle University and the chief investigator of the RewinD-LB trial for the United Kingdom. “These data further validate the use of plasma pTau181 to exclude patients with AD co-pathology, potentially enabling us to focus on those most likely to experience a treatment benefit with neflamapimod. In addition, because neflamapimod targets the biology driving ‘pure’ DLB, the robust association between neflamapimod response and absence of AD co-pathology strengthens our confidence that neflamapimod can slow disease progression in these patients.”

“The clinical and biomarker activity that we are seeing with neflamapimod provides a strong indication that we are successfully targeting the underlying cause of disease in the basal forebrain and supports our belief that the inhibition of p38α by neflamapimod can reverse the synaptic dysfunction that drives disease progression in ’pure‘ DLB patients,” said Dr. John Alam, Chief Executive Officer of CervoMed. “As we look forward to initiating our planned Phase 3 clinical trial, these findings reinforce our conviction that, based on their plasma pTau181 levels at the initiation of the study and our dose selection of 50mg TID, we are further increasing the opportunity for patients to respond to neflamapimod treatment.”

New analyses of data from RewinD-LB Trial stratified by plasma pTau181 subset demonstrate greater treatment effect with reduced likelihood of AD co-pathologyThe RewinD-LB Phase 2b trial was comprised of an initial, randomized phase comparing neflamapimod to placebo, followed by a neflamapimod-only extension phase. In the initial phase, the participants did not achieve expected plasma drug concentration levels with the neflamapimod capsules used (DP Batch A) and did not demonstrate a statistically significant improvement on the trial’s primary endpoint.

In the extension phase, administration of a new batch of capsules (DP Batch B) was associated with expected plasma drug concentration levels and DP Batch B compared to DP Batch A treatment within the extension phase demonstrated a statistically significant and clinically meaningful slowing of clinical progression. Importantly, though, treatment in extension phase capsule batch identity (DP Batch A vs. DP Batch B) remained blinded to participants and site personnel.

The analyses presented at AD/PD reveal a consistently improving treatment effect in multiple clinical end points at progressively lower plasma pTau181 levels, which are associated with a higher percentage of DLB patients without AD co-pathology.

Table 1. Within-participant comparison of change in Clinical Dementia Rating Sum of Boxes (CDR-SB) over 16 weeks in those who received placebo and then DP Batch B stratified by level of enrichment for absence of AD co-pathology