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BDNF and TrkB Upregulation The most extensively documented mechanism of Semax in pre-clinical research is its rapid upregulation of brain-derived neurotrophic factor (BDNF) and its primary signalling receptor, tropomyosin receptor kinase B (TrkB)

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Early studies suggest potential benefits in conditions involving impaired intestinal motility or altered gut hormone signaling, including metabolic disorders and certain gastrointestinal diseases