Clinical Research, Pharma & Healthcare Financing

Nuravax, IMM to Present Alzheimer’s Vaccine Data at CTAD 2025

Two oral presentations to highlight the safety, immunogenicity, and future development of AV-1959R for primary and secondary prevention of Alzheimer’s disease

Nuravax Inc., a clinical-stage biopharmaceutical company developing active immunotherapies for neurodegenerative diseases, announced today that two oral presentations—the Phase 1 clinical results and the Phase 2 secondary prevention study design for its licensed lead Drug Product, the amyloid-beta (Aβ) vaccine, AV-1959R—have been accepted at the 18th Clinical Trials on Alzheimer’s Disease (CTAD-25) conference, scheduled for December 3–5 in San Diego, California.

Presentation Details:

Session: Oral Communications – Phase 1
Date/Time: Thursday, December 4, 2025 | 2:30 PM – 4:00 PM (PST)
Title: The MultiTEP-based vaccine, AV-1959R, safely elicits high concentrations of antibodies specific to Aβ42 protofibrils/fibrils/plaques in vaccinated healthy volunteers.
Authors: Michael G. Agadjanyan, Lon Schneider, Alex Grinberg, Anahit Ghochikyan

Session: Oral Communications – Phase 2 Design
Date/Time: Thursday, December 4, 2025 | 2:30 PM – 4:00 PM (PST)
Title: Considerations for Phase 2 Trials of an Aβ Vaccine, AV-1959R, for Secondary Therapeutic Prevention of Alzheimer’s Disease
Authors: Lon Schneider, Michael G. Agadjanyan, Anahit Ghochikyan

Roman Kniazev, CEO of Nuravax, Inc., said, “The MultiTEP platform behind AV-1959R was specifically engineered to overcome immunological tolerance and safely induce strong anti-Aβ antibody responses across diverse populations at risk,” and he continued, “The Phase 1 outcomes may validate decades of translational vaccine research and offer a path forward for active immunization and prevention or mitigation of risk.”

The AV-1959R is an adjuvanted, Aβ epitope-specific vaccine built on the proprietary MultiTEP platform, designed to induce high levels of antibodies while avoiding autoreactive T cell responses. It is intended for both secondary prevention in individuals with biomarker-positive disease and primary preventive therapy for individuals at elevated risk of Alzheimer’s pathology  due to known factors, including a family history of the disease, the presence of the APOE4 genotype, mutations in APP, PSEN1, PSEN2, TREM2, and CASP8 genes as well as comorbid conditions (e.g., hypertension, hyperlipidemia, type 2 diabetes mellitus, obesity, etc)

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