A patient at home
Pioneering immunotherapy

Target neurodegenerative disease at its source.

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
Approach

Vaccine therapies to eradicate neurodegenerative disease.

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.

01
Platform

One universal MultiTEP backbone, adaptable to any disease-driving target protein.

02
Pipeline

Four clinical-stage vaccines spanning amyloid-beta, tau and alpha-synuclein pathologies.

03
Prevention

Built for primary and secondary prevention in at-risk, cognitively unimpaired individuals — acting before symptoms emerge.

Competitive advantage

One universal construct, any target.

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.

3× B-CELL EPITOPE 12 TH EPITOPES · MULTITEP ADJUVANT PADREP23P32P21P30P2P7P17P28HBsAgHBVncMT + Three copies of the targetmaximize antibody titers A library of non-self Th epitopesdrives a robust T-helper signal Formulated with the protein —not conjugated to it
· AV-1959R Aβ + tau · Duvax tau · AV-1980R α-syn · PV-1950R
Our approach

Immunotherapy that clears disease-driving proteins.

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.

Step 01

Targeted antibody response

Each vaccine prompts the immune system to generate antibodies that specifically recognize and bind pathological Aβ, tau and α-synuclein.

Step 02

Preventing progression

By forming antigen-antibody complexes, the immunotherapies help prevent harmful oligomers, plaques and tangles from ever forming.

Step 03

Clearing pathological agents

Once bound, harmful molecules are neutralized and marked for clearance — before they can deposit in the brain and damage neurons.

Where the vaccines act

Prevention, years before symptoms.

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.

Preclinical AD
AV-1959R
At-risk to amyloid-positive, cognition intact (A−/T−/N− → A+/T−/N−).
Primary + secondary prevention
Preclinical AD
Duvax
Amyloid-positive with early tau, still cognitively unimpaired (A+/Tlow+/N−).
Secondary prevention
MCI
Anti-Aβ mAbs
Mild cognitive impairment — subtle decline already present (A+/T+/N+).
mAb treatment
Dementia
Anti-Aβ mAbs
Alzheimer's dementia — neuronal injury, clinical decline (A+/T+/N+).
mAb treatment
Phase 1 · randomized, placebo-controlled, double-blind

AV-1959R is safe and highly immunogenic.

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.

100%
of vaccinated participants induced anti-Aβ antibodies
65,000+
geometric mean titer (GMT)
1
annual booster projected to sustain protective titers

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.

The active immunotherapy advantage

One vaccine. A durable, self-made response.

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.

Prevention-first

Acts before injury

Built for the preclinical window — enabling primary and secondary prevention before irreversible neuronal injury.

Durable

A single annual booster

Two-shot priming followed by one annual booster is modeled to sustain protective antibody levels.

Convenient

A simple injection

A 100 μg intramuscular injection given in a standard outpatient setting — no infusion required.

Specific

Targets pathology

Antibodies bind pathological aggregates while largely sparing the healthy forms of the protein.

Pipeline

Four vaccines across the neurodegeneration spectrum.

One universal platform, organized by the disease each program targets — from Alzheimer's disease to tauopathies and synucleinopathies. Developed primarily with non-dilutive funding.

Alzheimer's diseaseAmyloid-β & tau
Aβ · AV-1959R
Amyloid-β recombinant vaccine
Phase 2 IND cleared
Aβ + tau · Duvax
Dual-target vaccine
Phase 1 ongoing
TauopathiesPSP · CBD · FTD · CTE
tau · AV-1980R
Tau recombinant vaccine
Phase 1 ongoing
SynucleinopathiesDLB · Parkinson's · MSA
α-syn · PV-1950R
α-synuclein vaccine
IND-ready
Expanding the platform

Beyond Alzheimer's: tau and α-synuclein.

Because only the B-cell epitope changes, the MultiTEP platform extends naturally to other proteinopathies — addressing a broad spectrum of neurodegenerative disease.

AV-1980RPhase 1
Tau vaccine · tauopathies
  • Progressive supranuclear palsy — movement, balance and eye control
  • Corticobasal degeneration — stiffness, limb control, cognition
  • Frontotemporal dementia — behavior and personality
  • Chronic traumatic encephalopathy — repetitive head impacts in contact-sport athletes & military personnel
PV-1950RIND-ready
α-synuclein vaccine · synucleinopathies
  • Dementia with Lewy bodies — lead indication
  • Parkinson's disease — the most common synucleinopathy
  • Multiple system atrophy — rapid, severe; glial aggregates
Up to 90% of people with REM sleep behavior disorder may progress to a synucleinopathy over 10–14 years.
Leadership

Scientists who have spent careers on this problem.

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.

Michael Agadjanyan
Michael Agadjanyan
Head of Immunology, IMM
30+ years in immunology & vaccines; developer of the MultiTEP platform.
Roman Kniazev
Roman Kniazev
Acting CEO / COO
Former biotech VC and biotech co-founder.
Anahit Ghochikyan
Anahit Ghochikyan
Immunotherapy scientist
Neurodegeneration-focused vaccine design.
James Callaway
James Callaway
Ex-CEO, Cebix & ArmaGen
Elan (AN-1792) veteran; early-stage clinical strategy and execution.
Robert Alexander
Robert Alexander
CSO, Alzheimer's Prevention Initiative (Banner)
Former VP Neuroscience, Takeda.
David H. Cribbs
David H. Cribbs
Professor in Residence, UCI MIND
Antibody-mediated Aβ clearance research.
Guriq Basi
Guriq Basi
Former CSO, Elan (AN-1792)
Protein and antibody engineering.
Lon S. Schneider
Lon S. Schneider
Director, USC CADC
Della Martin Professor; leader in AD clinical trials.
On the record

Built on peer-reviewed evidence.

Press releases
Partnering & collaboration

Let's prevent neurodegeneration, together.

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