CervoMed Inc. (NASDAQ:CRVO), a clinical-stage biotechnology company developing treatments for age-related brain disorders (CervoMed or the Company), today announced that it has completed enrollment in the Phase 2a study of neflamapimod for the treatment of nfvPPA, a type of FTD. Interim biomarker data from the study will be presented at the 19th CTAD Conference in Boston, Massachusetts, taking place November 16–19, 2026.

"The rapid enrollment of this trial reflects the belief of the FTD academic medical community in the potential of neflamapimod to address this disease and the critical need for treatments for nfvPPA," said Dr. John A. Alam, Chief Executive Officer of CervoMed. "Recently published preclinical data help elucidate the mechanisms behind FTD that are driven by tau pathology and demonstrate the potential of neflamapimod to reverse the neuronal deficits associated with forms of tau-related FTD, such as nfvPPA, via the inhibition of p38α. We look forward to sharing the first biomarker data with neflamapimod in patients with nfvPPA early in the fourth quarter of 2026 and the first clinical data in the first quarter of 2027."

The Phase 2a study was designed to evaluate the safety, pharmacokinetics, and clinical effects of neflamapimod in participants with nfvPPA. The trial enrolled 25 participants, taking oral neflamapimod (40 milligram TID [n = 19] or 80 milligram BID [n = 6]) for 24 weeks, followed by a 12-week, randomized, double-blind placebo-controlled extension. The study is being conducted at leading academic centers in the U.S.

Recent Nature Neuroscience publication supports inhibition of p38α as potential therapeutic approach in FTD

A recent preclinical study published in Nature Neuroscience1 demonstrated that axonal transport dysfunction occurs in the early stages of genetic forms of FTD where the primary mutation is in the microtubule-associated protein tau, leading to the abnormal build-up of misfolded tau proteins in the brain that is the pathologic driver in approximately half of patients with FTD. Axonal transport is critical for nerve development, function, and survival.

After establishing that p38α inhibition reduced axonal transport deficits in transgenic mice harboring tau mutations associated with human disease (FTD-Tau), the authors used neflamapimod, a known pharmacological inhibitor of p38α, to test whether it could reproduce the effect. Imaging the mice before and after treatment, they found that sustained inhibition improved axonal transport and reversed the underlying deficits, strengthening the link between p38α and the mechanism of tau pathology.