Bial has stopped development in a subpopulation of Parkinson’s disease patients after its phase 2b trial missed its primary and key secondary efficacy endpoints.
Portugal-based Bial designed the study to compare BIA 28-6156 to placebo in 273 Parkinson’s patients with a pathogenic variant in the GBA1 gene. People in the treatment arms received one of two doses of BIA 28-6156, a molecule that activates the GCase enzyme to restore lipid metabolism and lysosomal function. Studies have linked compromised GCase activity to the decline of Parkinson’s patients.
While the mechanism of action suggested BIA 28-6156 could be a disease-modifying therapy, the phase 2b failed to generate evidence that the molecule improves outcomes. The primary endpoint looked at the time to clinically meaningful progression on motor aspects of experiences of daily living.
The study missed its primary endpoint. And with BIA 28-6156 also performing no better than placebo on key secondary endpoints, Bial has ended development of the drug candidate in the trial population. Bial is running one other BIA 28-6156 study, which is evaluating the molecule in people with varying degrees of renal impairment.
Bial has yet to share data from the failed phase 2b trial, saying only that the study missed its key efficacy endpoints but found BIA 28-6156 to be generally well tolerated. No unexpected safety concerns were seen, Bial said. The drugmaker plans to share data from the trial through peer-reviewed publications and scientific meetings.
Pulling back from BIA 28-6156 blows a hole in Bial’s R&D pipeline. Beyond BIA 28-6156, the company is only running non-interventional studies of opicapone and a sublingual apomorphine formulation. Both trials are enrolling Parkinson’s patients. Bial acquired the European rights to a sublingual apomorphine drug, Kynmobi, in 2021. The company won European approval for opicapone, sold as Ongentys, in 2016.
