Semax

Semax is a synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) derived from the N-terminal fragment (ACTH 4-7) of adrenocorticotropic hormone (ACTH), with a Pro-Gly-Pro extension for enhanced metabolic stability. Unlike full-length ACTH, Semax lacks corticotropic activity (it does not stimulate adrenal cortisol production) but retains and enhances the neurotrophic and cognitive effects of the ACTH 4-7 fragment. Semax's primary mechanism centres on its upregulation of brain-derived neurotrophic factor (BDNF) — a key neurotrophin that supports neuronal survival, differentiation, and synaptic plasticity. By increasing BDNF expression in the hippocampus and cerebral cortex, Semax enhances the neuroplasticity underlying learning and memory formation. Additionally, Semax modulates dopaminergic and serotonergic neurotransmitter systems, influencing cognitive performance, attention, and mood regulation. The peptide also exhibits neuroprotective effects through modulation of oxidative stress pathways and anti-apoptotic signalling in neurons. Semax's unique combination of BDNF upregulation, monoamine neurotransmitter modulation, and neuroprotective activity — all without corticotropic effects — makes it a valuable research tool for studying cognitive enhancement signalling, neuroprotection, and the neurotrophic basis of learning and memory.