Long-term functional rescue of trauma-induced vision loss by a novel, small molecule TrkB modulator.
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ABSTRACT: Brain-derived neurotrophic factor (BDNF) signaling through the tropomyosin-related kinase B (TrkB) receptor promotes neuronal growth and survival following an injury. However, its short half-life and pleiotropic effects limit the clinical use of BDNF as a therapy in neurodegenerative disorders. Identification of novel and selective TrkB activators may ameliorate the damage caused to retinal neurons during eye-related injuries and may reduce adverse visual outcomes associated with visual trauma. We previously described a small molecule, N-[2-(5-hydroxy-1H-indol-3-yl) ethyl]-2-oxopiperidine-3-carboxamide (HIOC), that activates TrkB and reduces the decline in visual function in a mouse model of ocular trauma. Using the lead optimization approach, we subsequently synthesized a fluoropyridine a
SUBMITTER: Modgil S
PROVIDER: S-EPMC12478906 | biostudies-literature | 2025
REPOSITORIES: biostudies-literature
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