Our Pipeline
Priavoid is advancing a streamlined pipeline of orally available all-d-peptide treatments derived from our differentiated platform. Each program applies the same core principle: detangling toxic protein oligomers at the root cause of disease to provide new disease-modifying treatment options for patients in need.
Our clinical lead program, PRI-002 for Alzheimer’s disease, is the most advanced asset in our pipeline. In parallel, we are progressing key programs in synucleinopathies, including multiple system atrophy (MSA) and Parkinson’s disease (PRI-101), tauopathies (PRI-200), and additional discovery programs targeting protein aggregation across further neurodegenerative disorders.
Our Focus Indications
Neurodegenerative disorders 1, 2, 3
Neurodegenerative disorders are a group of chronic, progressive diseases characterized by the gradual loss of functional neurons in the central nervous system. As neurons have limited capacity for regeneration, their degeneration leads to irreversible and worsening impairments in cognition, movement, behavior, and/or autonomic function. This group includes conditions such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and related disorders.
From a biological perspective, decades of research have shown that neurodegenerative diseases share common pathogenic mechanisms, despite affecting different brain regions and producing distinct clinical syndromes. Central among these mechanisms is the abnormal accumulation of misfolded proteins, which disrupt cellular function and progressively spread through neural networks.
Current research has shifted scientific focus toward biomarkers and disease trajectories, aiming to better understand how molecular and cellular changes translate into clinical decline. This framework underpins current efforts to improve diagnosis, monitor progression, and develop disease-modifying therapies grounded in biological evidence.
About Alzheimer’s disease 1, 2
Alzheimer’s disease is associated with abnormal aggregation of amyloid-β (Aβ) and tau proteins. Increasing evidence suggests that soluble Aβ oligomers are among the most neurotoxic species, disrupting synaptic function and neuronal communication. They spread through the brain and contribute to progressive cognitive decline. With dementia affecting approximately 57 million people worldwide, Alzheimer’s disease accounts for an estimated 60-70% of cases, making it the leading cause of dementia globally. The growing prevalence and limited disease-modifying options underscore the need for treatments that address underlying disease biology.
About Parkinson’s disease
Parkinson’s disease is linked to the misfolding and aggregation of α-synuclein, which can be particularly neurotoxic, disrupting synaptic function, mitochondrial health, and cellular homeostasis, and may contribute to progressive neuronal dysfunction and degeneration. Parkinson’s disease is the fastest-growing neurological disorder worldwide. According to the WHO, neurodegenerative diseases, including Parkinson’s disease, will become the second leading cause of death worldwide by 2040, highlighting a significant and increasing unmet medical need for disease-modifying treatment options.
About Tauopathies
Tau is a microtubule-associated protein that becomes abnormally modified and aggregated in Alzheimer’s disease and other tauopathies like Pick’s disease and frontotemporal dementia (FTD). These pathological tau aggregates disrupt intracellular transport and neuronal function, correlate with disease progression and clinical severity, and may propagate between neurons, contributing to disease spread. Tauopathies display varied clinical phenotypes including dementia, movement disorders, and motor neuron disease.