Cenna Biosciences is moving its synthetic peptide 8M2D — also referred to as Nubytide in prior company disclosures and as P8 in earlier academic literature — into its first human study, with the NCT07568041 clinical trial registered in April 2026 and a start date of September 2026. The La Jolla, California-based company is testing the subcutaneously administered compound in healthy volunteers and people with early Alzheimer's disease, targeting amyloid beta production through a non-enzymatic mechanism that the company describes as potential first-in-class. The asset originates from UCSD Alzheimer's research conducted by Nazneen Dewji, PhD, who serves as both founder of Cenna Biosciences and principal investigator on the trial.
The Phase Ia/b study enrolls approximately 54 participants across three sequential parts. Parts I and II are randomized, double-blind, and placebo-controlled, evaluating single ascending doses (up to five dose levels, 30 healthy adults aged 18–55) and multiple ascending doses (up to three dose levels, 18 healthy adults) of 8M2D delivered by subcutaneous injection. Part III is an open-label cohort of approximately six participants with early Alzheimer's disease, aged 55–80, diagnosed with mild cognitive impairment of probable Alzheimer's disease, and carry a qualifying amyloid burden. Primary endpoints across the Phase 1a/b trial assess safety and tolerability alongside pharmacokinetic parameters.
In the Alzheimer's disease cohort, the trial also measures changes in plasma and CSF biomarkers including Aβ42, Aβ40, P-tau217, and NP-tau217 from baseline after 14 days of dosing. Primary completion is expected by September 2027, with full study completion in December 2027.
The mechanistic rationale for 8M2D rests on a body of preclinical work arising from UCSD Alzheimer's research published by Dewji and colleagues. The compound belongs to a class of synthetic peptides derived from a fragment of Presenilin-1, a catalytic subunit of the γ-secretase complex. Rather than inhibiting γ-secretase or β-secretase directly — the approach taken by earlier small-molecule secretase inhibitors, several of which failed in late-stage trials due to toxicity or lack of efficacy — 8M2D appears to bind the ectodomain of the amyloid precursor protein (APP) itself, blocking the APP–Presenilin interaction that initiates amyloidogenic cleavage.