Improving Parkinson’s disease treatment
August 11, 2026
Improving Parkinson’s disease treatment
At a Glance
- Researchers identified a drug candidate that enhanced effectiveness and reduced side effects of the standard Parkinson’s disease treatment in animal models.
- If the drug candidate proves effective in people, it could be an effective way to improve treatment for Parkinson’s disease.
The brain needs a precise balance of chemicals to work correctly. Even small shifts in that balance can cause problems. This makes it challenging to develop treatments for brain disorders without causing side effects.
The standard treatment for Parkinson’s disease involves such a trade-off. Parkinson’s disease occurs when brain cells that produce the chemical dopamine die. This leads to movement problems such as shaking, stiffness, and difficulty with balance.
A medication called levodopa helps patients by increasing dopamine levels in the brain. However, it can also cause rapid, involuntary twisting or writhing movements. This side effect is called dyskinesia. Levodopa also becomes less effective the longer patients take it.
An NIH-funded research team led by Dr. Aarash Bordbar at Sinopia Biosciences looked into how levodopa reduces Parkinson’s symptoms and causes dyskinesia. They used that knowledge to find a drug candidate that could boost levodopa’s benefits and reduce its side effects. The results were published in Science Translational Medicine on July 15, 2026.
Prior research in a mouse model of Parkinson’s disease showed levodopa changes gene activity in brain cells that respond to dopamine. The team linked some of those changes to levodopa’s beneficial effects and others to dyskinesia.
The researchers then looked for a drug candidate with the same effects on genes linked to levodopa’s benefits, but the opposite effects on genes linked to dyskinesia. Their search of a database of existing candidates turned up a chemical compound called SB-0107.
They tested combinations of SB-0107 and levodopa in rodent models of Parkinson’s disease. The team looked at how the treatment affected movement and gene activity in a brain region containing cells that respond to dopamine. SB-0107 had similar effects as levodopa on genes linked to levodopa’s benefits. It also boosted levodopa’s beneficial effects on movement symptoms. Additionally, SB-0107 countered levodopa’s effects on genes linked to dyskinesia and avoided inducing or exacerbating dyskinesia in rats.
The researchers then tested the combination treatment in a nonhuman primate model of Parkinson’s. SB-0107 again boosted the beneficial effects of levodopa. It also reduced dyskinesia. When the scientists altered SB-0107 to make it last longer in the body, the new versions, including one called SB-0110, reduced dyskinesia even more.
Parkinson’s disease can also make it harder to learn, remember, and use information. SB-0107 improved performance on some tasks that measure those cognitive abilities in the nonhuman primate model of Parkinson’s.
Based on the study’s results, Sinopia Biosciences is advancing SB-0110 as a potential treatment that could help levodopa stay effective and reduce its side effects. The team is aiming to begin clinical trials in people next year.
"Patients face two major problems with [levodopa]: the reappearance of Parkinson’s symptoms and dyskinesia,” Bordbar says. “There is no drug that can be added to levodopa to address both simultaneously in a robust manner, and that’s what our drug candidate is doing.”
—by Brandon Levy
Related Links
- Personalized deep brain stimulation for Parkinson's disease
- A potential blood test for Parkinson's disease
- Night breathing patterns identify people with Parkinson's disease
- Progress in Parkinson’s
- Parkinson’s disease
References
A small molecule reduces both parkinsonism and l-dopa-induced dyskinesia in animal models of Parkinson's disease. Bordbar A, Bloem B, Lloyd C, Johnston TH, Schneider JS, Bezard E, Pioli E, Li Q, Tawfeeq C, Vu Pham N, Huber G, Wu J, Hill MP, Brotchie JM, McCammon JA, Herberg FW, Taylor S, Weiner DM, Merchant K, Famili I. Sci Transl Med. 2026 Jul 15;18(858):eaec7409. doi: 10.1126/scitranslmed.aec7409. Epub 2026 Jul 15. PMID: 42455901.
Funding
NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and National Institute of General Medical Sciences (NIGMS); Michael J. Fox Foundation for Parkinson’s Research.
