Semax

Effects documented in the literature

Semax is a heptapeptide derived from the ACTH(4-10) fragment with no corticotropic activity. Studies (PMID 16996699, 16635254) demonstrated a rapid increase in the expression of BDNF (Brain-Derived Neurotrophic Factor) and NGF (Nerve Growth Factor) in the hippocampus and frontal cortex of murine models, as well as modulation of TrkA/TrkB receptors. At the hormonal level, unlike ACTH(1-24) fragments, Semax does not stimulate the HPA axis and does not elevate cortisol. The studies describe modulation of the dopaminergic, serotonergic, and cholinergic systems, an increase in endogenous enkephalin, and a reduction in neuronal oxidative stress. Functionally, the studies observe improved memory and attention performance in models of cerebral ischemia and stroke, as well as a neuroprotective effect via inhibition of BAX-mediated neuronal apoptosis. These data come from the scientific literature and are provided strictly for informational purposes in a research context. This product is not intended for veterinary, diagnostic or therapeutic use and is not recommended for any use outside a scientific, professional and research setting. [1][2][3]