Oct 23, 2026
Study testing Mission Therapeutics' therapy recruiting in several locations
Written by Andrea Lobo | Oct. 19, 2026
- The first patient was dosed in a Phase 1b clinical trial testing MTX325, an oral treatment for Parkinson’s.
- The trial is still recruiting participants at several locations.
- MTX325 aims to be a disease-modifying therapy by improving mitochondrial quality control through the blocking of the USP30 enzyme.
The first patient has been dosed in Mission Therapeutics’ Phase 1b clinical trial of MTX325, an oral treatment for Parkinson’s disease.
With several locations open in the U.K., France, Germany, and Australia, the Phase 1b clinical trial (NCT07630545) is still recruiting up to 36 adults aged 40-75 with mild to moderate idiopathic (of unknown cause) Parkinson’s.
The first patient was dosed at the Royal Liverpool University Hospital in the U.K. Initial data are expected in 2027.
The start of this part of the trial follows the successful completion of an earlier part conducted in healthy volunteers, which showed that the treatment was generally safe and could reach functional brain tissue.
“Dosing the first Parkinson’s disease patient is a significant milestone in the development of MTX325, a potential disease-modifying treatment for this serious neurodegenerative disease,” Sarah Fritchley, PhD, Mission’s chief development officer, said in a company press release.
Oct 22, 2026
Research funding, chemical bans among suggestions from experts
Written by Marisa Horak, MS | Oct. 16, 2026
- Experts outlined an eight-step strategy focused on primary prevention to eliminate Parkinson’s disease and address rising incidence rates.
- Key risk factors include genetic variations and environmental exposures to toxic chemicals like paraquat and trichloroethylene.
- Primary prevention efforts require policy changes to ban harmful chemicals and $600 million in annual NIH research funding.
In late 2025, the Parkinson’s Foundation and the Fixel Institute at the University of Florida brought together dozens of experts to ask a bold question: What will it take to bring about a world where no one has Parkinson’s disease?
Now, that group — the Parkinson’s Disease Prevention Think Tank — has put out a paper outlining the key steps that will need to be taken. The paper, “Primary prevention of Parkinson’s disease: proceedings, the 8C’s and a position statement from the Parkinson’s disease prevention think tank,” was published in npj Parkinson’s disease.
The group identified what it called “eight Cs,” priority actions needed to eliminate the disease: Count incidence and prevalence, conduct studies, create policy change — this includes urging the U.S. Environmental Protection Agency to ban toxic chemicals linked to Parkinsons’ — counsel on risk, communicate clearly, form coalitions across disease organizations, apply cross-disciplinary approaches involving health economists and toxicologists, and financial commitment in the form of $600 million in research funding from the National Institutes of Health.
“Our goal is to draw attention to primary prevention by advancing research and shaping policy,” Sneha Mantri, MD, chief medical officer of the Parkinson’s Foundation and the paper’s lead author, said in a foundation press release. “ Our report outlines the actions needed on the individual and system level to make this vision a reality.”
Oct 21, 2026
4-week program on food-med interaction boosts physical, mental quality of life
Written by Michela Luciano, PhD | Oct. 15, 2026
- Dietary proteins compete with Parkinson's medication for intestinal absorption and brain transport.
- A four-week nutrition education program focusing on food-drug interactions significantly improved patients' physical and mental quality of life.
- Patients learned to optimize treatment efficacy by timing protein-rich meals away from levodopa doses and shifting protein intake.
A four-week nutrition education program focused on how food interacts with Parkinson’s disease medications was tied to improved physical and mental quality of life for patients, a small study in Turkey found.
The program helped participants adjust their eating habits, providing guidance on timing protein-rich meals around doses of levodopa, the main treatment for Parkinson’s disease. After the intervention, participants reported improved physical and mental well-being, along with changes in their nutrient intake.
The findings suggest that helping people with Parkinson’s understand food/medication interactions could improve their quality of life and dietary habits. However, the researchers cautioned that the study involved only 30 participants and lacked a comparison group, making it difficult to determine whether the improvements were attributable to the education program.
“To further validate and expand upon these promising findings, the long‐term efficacy of such targeted nutritional interventions should be demonstrated in future large‐scale, randomized controlled trials,” the researchers wrote.
The study, “Effects of food–drug interaction-oriented nutritional education on quality of life in Parkinson’s disease: A pilot quasi-experimental study,” was published in Nutrition in Clinical Practice.
Oct 20, 2026
150 mg dose also improved on time without troublesome dyskinesia
Written by Andrea Lobo | Oct. 13, 2026
- Solengepras (CVN424) is an investigational oral treatment being studied for motor and non-motor Parkinson’s symptoms.
- The Phase 3 ARISE trial found 150 mg significantly reduced average daily off time and improved daily motor function.
- Cerevance plans to discuss the results with the FDA and next steps for a potential New Drug Application.
The 150 mg dose of solengepras (CVN424), Cerevance’s investigational oral treatment for Parkinson’s disease, significantly reduced average daily off time — periods when symptoms reappear despite medication — compared with placebo, according to topline results from a Phase 3 trial.
The Phase 3 ARISE trial (NCT06553027) evaluated the safety and efficacy of solengepras in addition to standard treatments in people with Parkinson’s disease who experience motor fluctuations. The trial enrolled 341 participants at sites worldwide, completing enrollment earlier this year.
“ARISE met its primary endpoint and showed a consistent pattern of benefit across OFF time, ON time, daily motor function, daytime alertness and quality of life, together with favorable tolerability,” Craig Thompson, Cerevance’s CEO, said in a company press release. “We look forward to discussing these results with the FDA to determine next steps.”
How solengepras may help control Parkinson’s motor symptoms
Parkinson’s disease is caused by the loss of nerve cells that produce dopamine, a chemical messenger that helps control movement. Levodopa, which the brain converts into dopamine, is a standard treatment for easing Parkinson’s motor symptoms. However, long-term use of levodopa can lead to off periods and dyskinesia, or sudden, involuntary movements.
Solengepras is designed to block GPR6, a receptor found on specific nerve cells in the striatum, a brain region involved in controlling voluntary movement. By blocking GPR6, solengepras is designed to help restore balance between brain pathways involved in movement without directly altering dopamine levels or signaling.
The ARISE trial evaluated once-daily solengepras at 75 or 150 mg versus placebo in people with Parkinson’s who averaged at least three hours of off time per day despite treatment with levodopa and other Parkinson’s medications.
According to the company, the 150 mg dose met the trial’s primary goal, significantly reducing average daily off time by 0.61 hours, or about 37 minutes, versus placebo at Week 12. A difference between the treatment and placebo groups was seen as early as Week 2, the first assessment after treatment began, and at each subsequent visit through Week 12.
The 150 mg dose also increased on time without troublesome dyskinesia by 36 minutes versus placebo.
The 150 mg dose also significantly improved motor experiences of daily living, with a 1.91-point improvement versus placebo, as measured by Part 2 of the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale. Participants receiving the 150 mg dose also had less daytime sleepiness on a secondary measure and better quality of life on an exploratory measure.
Oct 19, 2026
Arvinas' ARV-102 linked to improved eye movement control in Phase 1 study
Written by Andrea Lobo | Oct. 14, 2026
- ARV-102 successfully crossed the blood-brain barrier, reduced LRRK2 levels, and improved eye movement in a Phase 1 trial.
- The results build on earlier data showing promise for the experimental treatment.
- The drug's developer said the study supports further clinical evaluation of ARV-102.
Phase 1 trial results showed an experimental oral therapy was associated with improved eye movement control, lower levels of neuroinflammatory biomarkers, and higher markers of nerve cell health in people with Parkinson’s disease.
The results from the ARV-102-103 trial (EUCT 2024-516888-84-00) build on findings presented earlier this year showing that Arvinas‘ ARV-102 reached the brain and reduced levels of its target protein, LRRK2, in the cerebrospinal fluid (CSF, the fluid that surrounds the brain and spinal cord). ARV-102 was also found to be generally safe and well tolerated.
The findings were shared at the Movement Disorders Society International Congress of Parkinson’s Disease and Movement Disorders, held last week in Seoul, South Korea. The data were presented as late-breaking oral and poster presentations titled “Phase 1 Study of ARV-102, a PROTAC LRRK2 Degrader, in Parkinson’s Disease: Oculomotor and Biomarker Data.”
“Although this study was not designed to assess clinical efficacy, we are encouraged by the exploratory dose-related changes in [abnormal eye movements] and their associations with LRRK2 degradation and changes in pathway biomarkers,” Ilaria Conti, MD, PhD, Arvinas’ vice president of clinical research, said in a company press release. “These findings support further clinical evaluation of ARV-102.”
Mutations in the LRRK2 gene, which encodes a protein of the same name, are one of the most common genetic causes of Parkinson’s. LRRK2 is often overactive in Parkinson’s, which can disrupt waste recycling within cells and exacerbate inflammation, causing damage to nerve cells.
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