We clear the pathological Alzheimer's- and Parkinson's-causing proteins before they deposit in the brain and damage neurons — using the patient's own immune system.
Nuravax is committed to preventing and curing central nervous system disorders through the patient's own immune system. We design highly specific vaccine therapies using our proprietary MultiTEP platform to target the root causes of neurological disease — beginning with Alzheimer's and Parkinson's.
One universal MultiTEP backbone, adaptable to any disease-driving target protein.
Four clinical-stage vaccines spanning amyloid-beta, tau and alpha-synuclein pathologies.
Built for primary and secondary prevention in at-risk, cognitively unimpaired individuals — acting before symptoms emerge.
Three copies of a target B-cell epitope are fused to a string of 12 promiscuous, non-self helper T-cell (Th) epitopes to form a single recombinant protein. That protein is then formulated with an adjuvant — not conjugated to it — driving a robust, durable antibody response across diverse genetic backgrounds. Only the B-cell epitope changes.
Our vaccines direct the body's own immune system against the pathological proteins — amyloid-β, tau and α-synuclein — associated with neurodegenerative disorders, helping to halt or reverse disease progression before it takes hold.
Each vaccine prompts the immune system to generate antibodies that specifically recognize and bind pathological Aβ, tau and α-synuclein.
By forming antigen-antibody complexes, the immunotherapies help prevent harmful oligomers, plaques and tangles from ever forming.
Once bound, harmful molecules are neutralized and marked for clearance — before they can deposit in the brain and damage neurons.
Amyloid accumulates first — decades before symptoms — followed by tau, then neuronal injury. Our vaccines act in the preclinical AD window, well before the MCI and dementia stages where anti-Aβ monoclonal antibodies are used. AV-1959R enables both primary and secondary prevention; Duvax targets secondary prevention.
In a randomized, placebo-controlled, double-blind Phase 1 study, our lead amyloid-β vaccine was safe and well-tolerated across both dose cohorts, and induced a strong, specific anti-Aβ antibody response.
Antibodies are specific to the pathological aggregates — fibrils, protofibrils and oligomers — while largely sparing healthy monomers. The response is so durable that, based on Phase 1 data and mathematical modeling, we expect a single annual boost to be enough to sustain protective antibody levels.
Rather than delivering antibodies by infusion, our vaccines prompt the body to generate its own — a durable, convenient and prevention-first approach to neurodegenerative disease.
Built for the preclinical window — enabling primary and secondary prevention before irreversible neuronal injury.
Two-shot priming followed by one annual booster is modeled to sustain protective antibody levels.
A 100 μg intramuscular injection given in a standard outpatient setting — no infusion required.
Antibodies bind pathological aggregates while largely sparing the healthy forms of the protein.
One universal platform, organized by the disease each program targets — from Alzheimer's disease to tauopathies and synucleinopathies. Developed primarily with non-dilutive funding.
Because only the B-cell epitope changes, the MultiTEP platform extends naturally to other proteinopathies — addressing a broad spectrum of neurodegenerative disease.
MultiTEP was developed over two decades with the Institute for Molecular Medicine, leading universities and the NIH. Our team has carried neurodegeneration programs from discovery into the clinic.