- PRI-101 inhibited aggregation of α-synuclein and actively disassembled fibrils across in vitro and in vivo models relevant to Parkinson’s disease
Dusseldorf, Germany, March 19, 2026 - Priavoid GmbH (“Priavoid”) today announced preclinical proof-of-concept data for PRI-101, its orally available all-d-peptide candidate being developed for the treatment of Parkinson’s disease (PD) and related synucleinopathies. The data will be presented in a poster session by Dr. Marc Sevenich at the International Conference on Alzheimer’s and Parkinson’s Diseases and Related Neurological Disorders (AD/PDTM 2026) in Copenhagen, Denmark.
PRI-101 was developed using Priavoid’s proprietary detangler platform and is designed to target and disassemble α-synuclein (α-syn) aggregates, which play a key role in the disease pathology and in the induction of toxicity that leads to neurodegeneration in PD, multiple system atrophy (MSA), and other synucleinopathies. PRI-101 is binding to the α-syn subunit within toxic and self-replicating neurodegenerative aggregates and promoting their conversion back towards native, non-toxic forms, with the aim of counteracting disease-driving aggregation processes.
“Parkinson’s disease affects more than 6 million people worldwide and remains an area of profound unmet medical need, with patients still lacking therapies that meaningfully alter the course of disease,” said Dr. Antje Willuweit, Director Preclinical Development at Priavoid GmbH. “Taken together, these preclinical data suggest that PRI-101 has the potential to be a first-in-class therapeutic candidate with disease-modifying potential for Parkinson’s disease and other related synucleinopathies. We look forward to advancing this candidate towards the clinic to address a substantial need for new disease-modifying therapeutic options.”
Preclinical data presented at the conference demonstrated that PRI-101 can directly target and reduce pathological α-syn aggregates across multiple Parkinson’s disease models. In vitro studies showed that PRI-101 disassembled α-syn preformed fibrils (PFFs) and deactivated their seeding activity in a concentration- and time-dependent manner. It also demonstrated ex vivo target engagement, reducing α-syn aggregate levels in postmortem brain samples from patients with PD, MSA, and dementia with Lewy bodies. Pharmacokinetic studies following single and multiple doses confirmed that PRI-101 efficiently crosses the blood brain barrier and achieves meaningful penetration into the brain. In a human brain organoid model system for synucleinopathies and two distinct PD mouse models, PRI-101 reduced α-syn aggregates and levels of phosphorylated α-syn, a marker of α-syn aggregation. In vivo, PRI-101 was associated with prolonged median survival versus placebo. Short- and long-term treatment also led to a dose-dependent reduction of α-syn aggregates in the brain (including in the substantia nigra), accompanied by significant improvements in behavioral performance.
This work is funded by a grant from The Michael J. Fox Foundation for Parkinson’s Research.
About Priavoid
Priavoid’s novel class of orally available all-d-peptide therapeutics detangle neurotoxic oligomer species to inhibit and reverse disease-specific protein aggregation in neurodegenerative disorders. We aim to establish clinical proof-of-concept through our lead program, PRI-002, which will complete a Phase 2 trial in Alzheimer’s disease in 2026. Priavoid has built a focused pipeline of detangler compounds that are non-immunogenic and reach their oligomer targets in the brain and inside the affected cells. Our goal is to develop disease-modifying therapies that address the underlying biology of neurodegeneration and drive meaningful clinical benefit for patients.
Contacts:
Priavoid GmbH
Email: media@priavoid.com
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Trophic Communications
Anja Heuer and Marie Weickert, PhD
Phone: +49 151 106 199 05
Email: priavoid@trophic.eu
