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Despite descending from a hormone fragment, Semax has no meaningful hormonal (ACTH-like) activity of its own — the melanocortin backbone was retained but the corticotropic function was engineered out. Instead, it's characterized as neurotrophic: it upregulates BDNF and TrkB signaling and influences dopaminergic pathways, effects studied for cognitive support, focus, and neuroprotection after ischemic injury.