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Semax is a synthetic peptide derived from a fragment of adrenocorticotropic hormone (ACTH 4-10). Developed at the Institute of Molecular Genetics, it has been extensively researched for neuroprotective and nootropic applications. Studies indicate effects on BDNF expression, cognitive function, and neuronal survival.
Semax is a synthetic heptapeptide corresponding to the 4-10 fragment of adrenocorticotropic hormone (ACTH), with an added Pro-Gly-Pro C-terminal tripeptide that confers enhanced metabolic stability. Developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, Semax has been one of the most extensively studied neuropeptides in preclinical and clinical research settings.
The peptide's primary mechanism of action involves the modulation of brain-derived neurotrophic factor (BDNF) and its receptor TrkB, which play critical roles in neuronal survival, differentiation, and synaptic plasticity. Research has demonstrated that Semax administration leads to significant upregulation of BDNF mRNA expression in multiple brain regions, including the hippocampus and cortex, areas essential for learning and memory processes.
Beyond its neurotrophic effects, Semax has been investigated for its influence on the expression of neurotrophins NGF and NT-3, as well as its modulation of serotonergic and dopaminergic neurotransmission. Studies suggest that these combined mechanisms contribute to measurable improvements in cognitive performance, attention, and memory consolidation in various experimental paradigms.
Neuroprotective research has explored Semax's potential to mitigate oxidative stress-induced neuronal damage, support mitochondrial function, and promote neuronal survival under ischemic conditions. These investigations have provided valuable insights into the peptide's broad spectrum of neurobiological activity and its utility as a research tool for studying neurodegenerative processes.