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BRAD-R13 (also known as R13) is a small-molecule flavonoid prodrug and a potent, selective agonist of the tropomyosin receptor kinase B (TrkB), which is the main signaling receptor for brain-derived neurotrophic factor (BDNF). It was developed to improve upon earlier TrkB agonists by enhancing oral bioavailability and pharmacokinetics. BRAD-R13 is hydrolyzed in vivo to release tropoflavin (7,8-dihydroxyflavone), which mimics BDNF activity in the brain. Preclinical studies have shown that chronic administration of R13 activates TrkB signaling pathways, reduces amyloid-beta deposition, attenuates synaptic loss, and rescues memory deficits in Alzheimer's disease mouse models. The drug also represses asparagine endopeptidase (AEP) activation—a process implicated in neurodegenerative disease pathogenesis—by activating TrkB. BRAD-R13 has demonstrated safety and efficacy in animal models and is currently being evaluated for its safety, tolerability, pharmacokinetics, and potential therapeutic effects primarily for Alzheimer's disease[1][2][5][10].
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