August 11, 2026 - National Institutes of Health
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.
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