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Trapidil-Derived Drug Candidate Boosts Levodopa Benefits and Cuts Dyskinesia in Animals

Computational transcriptomics guided the design of a trapidil-derived, PKA-targeting molecule, with toxicology under way ahead of planned human trials next year.

Overview

  • The preclinical study published July 15 reported that SB-0110 significantly reduced levodopa-induced dyskinesia and improved motor response in both rodent and macaque models of Parkinson’s disease.
  • SB-0110 is a derivative of trapidil that acts on PKA signaling, a brain enzyme system linked to movement control and dopamine responses.
  • Researchers used transcriptomics-driven, computation-based repurposing to match levodopa-induced gene programs to existing drug signatures and select compounds that preserve levodopa benefits while opposing dyskinesia-related programs.
  • Sinopia Biosciences is finishing regulatory toxicology studies required for an investigational new drug filing and plans first-in-human testing next year, but human safety and effectiveness remain unproven.
  • The program is funded by NIH SBIR grants with support from the Michael J. Fox Foundation, and if clinical development succeeds Sinopia projects patient access could take roughly six to seven years while offering a potential alternative to amantadine, which has limiting psychiatric and vascular side effects.