PolyCore Advances PCT-3012 to Treat Parkinson’s Without Dyskinesia
PolyCore Therapeutics has secured a seed investment to advance its lead compound PCT-3012, designed to treat motor symptoms in Parkinson’s disease without triggering levodopa-induced dyskinesia, or uncontrollable body movements.
The investment, by Xontogeny and Ben Franklin Technology Partners, will enable studies supporting a potential investigational new drug (IND) application — a mandatory step to conduct clinical trials in humans.
“We are excited to support the PolyCore team in advancing their novel compound through pre-clinical trials, as we believe this new therapeutic could substantially improve the lives of patients living with Parkinson’s disease by improving motor symptoms without the development of tolerance or dyskinesia,” Chris Garabedian, chairman and CEO of Xontogeny, said in a press release.
The biopharmaceutical company, based in Philadelphia, noted that it’s currently testing PCT-3012 in preclinical studies.
“We are thrilled to welcome a collaboration with the team at Xontogeny as we work to advance our lead compound through IND-enabling studies,” said Kelly Beck, CEO of PolyCore Therapeutics. “In addition, we are appreciative of the continued support from Ben Franklin Technology Partners in this round.”
Parkinson’s disease is characterized by the loss of nerve cells (neurons) that produce the neurotransmitter dopamine. A chemical messenger, dopamine is essential for muscle control.
Levodopa, or L-dopa, is a precursor to dopamine and has long been one of the gold standards for Parkinson’s treatment.
“Nearly 60,000 new cases of Parkinson’s disease are diagnosed in the United States each year, and the current gold standard for motor symptom management results in dyskinesias for nearly 50% of patients who are treated for more than four years,” said Garabedian.
“Concern around developing these involuntary, erratic motions of the face and body cause some patients to delay treatment,” he said.
A new small molecule, PCT-3012 is designed to selectively bind to a dopamine receptor called D3 (D3R), which is similar to levodopa but via a different mechanism of action. Traditionally, L-dopa binding to D3R triggers the recruitment of two other proteins, called G-protein and beta-arrestin. The latter is believed to cause the desensitization of the D3R, which means the receptor becomes less sensitive to L-dopa binding. This leads to dyskinesia.
PCT-3012 was designed to bypass the recruitment of beta-arrestin, reducing dyskinesia while maintaining the therapeutic benefits of L-dopa.
“As the global population continues to age, it is important that we continue to identify treatments that not only address the symptoms of PD [Parkinson’s disease] but also do not create new side effects, like dyskinesias, which can be incredibly disruptive to a patient’s quality of life,” said Beck.
“The resources provided through this seed investment will allow us to rapidly advance our technology and accelerate our ability to bring our technology into the clinic,” she added.
The amount of the seed investment was not made public.