Multiple disease hallmarks underlie central nervous system disorders, including neuronal loss, synaptic and neuronal dysfunction, pathological protein aggregation, inflammation and mitochondrial dysfunction. These processes drive progressive loss of neurons, leading to impairment in memory, cognition, behavior and motor function.

Target

Our R&D programs focus on the tropomyosin receptor kinase B (TrkB) receptor pathway. Impaired TrkB signaling is implicated in a range of neurological and psychiatric conditions. Activation of the TrkB receptor engages downstream signaling pathways enhancing neuronal survival, promoting neuronal and synaptic plasticity, and reducing neuroinflammation and pathological protein aggregates including α-synuclein, amyloid-β and tau. In addition, TrkB activation leads to an improvement in mitochondrial function and an increase in BDNF production, the brain's growth receptor.

Compound

Our lead asset OT-003 selectively binds to the TrkB receptor, leading to activation of the downstream signaling pathways and promoting these effects in both cellular and in vivo experiments. This pharmacology leads to significant improvements in memory, cognition and motor function as shown in a range of in vivo studies.