# Semax: A Field Log of the Neurotrophin and Cognition Research > Semax is a synthetic ACTH(4-10) analog that rapidly and region-specifically raises brain BDNF and NGF in rodent studies. A plain-English digest of the published literature, every claim cited. A field log of the published record — what the studies measured, what the research-use community reports, and the cautions the literature actually records. Every quantitative claim is cited. ## Start here Semax is a small lab-made peptide — a short chain of seven amino acids. It was built in Russia in the 1980s from a piece of a natural hormone (ACTH), keeping the part that talks to the brain and dropping the part that triggers stress hormones. People take an interest in it as a *nootropic* — a substance studied for sharper thinking, focus, and memory — and as a *neuroprotective* agent, meaning something that may shield brain cells from harm. What have the studies actually shown? In rats, Semax quickly raises two growth signals the brain uses to keep neurons healthy and learning — BDNF and NGF. In rat stroke models it shrank the damaged area. Most of this work is in animals, and almost all of it comes from one country, so the human picture is thin. People who use it report a quick, calm clarity, but a fair number feel little or nothing. The honest upsides and downsides — including what to watch for — are on [the effects page](/effects). ## What the Semax record actually shows Semax (Met-Glu-His-Phe-Pro-Gly-Pro, one-letter MEHFPGP) is a synthetic *heptapeptide* — a peptide seven amino acids long. It was engineered from the natural ACTH(4-7) fragment of adrenocorticotropic hormone, with a Pro-Gly-Pro tail grafted on to slow how fast the body breaks it down. Crucially, it lacks ACTH's cortisol-releasing (steroidogenic) activity — it is the brain-signaling part without the stress-hormone part. The single most reproduced finding is neurotrophic. Intranasal Semax at 50 and 250 microg/kg produced a rapid, region-specific increase in BDNF protein in rat basal forebrain — but not cerebellum — three hours after dosing, and bound a specific, reversible, calcium-dependent site with a dissociation constant of 2.4 nM [1]. A single 50 microg/kg intranasal dose shifted neurotrophin gene expression across regions: NGF and BDNF mRNA rose in hippocampus while NGF mRNA fell in frontal cortex [2]. The pattern is consistent: Semax does not flood the brain with one signal everywhere — it nudges specific regions in specific directions. A second, separate action is enzyme inhibition. In human serum in vitro, Semax inhibited enkephalin-degrading enzymes with an IC50 of about 10 microM, more potently than reference inhibitors [3] — a mechanism thought to prolong the brain's own opioid-peptide signaling. ## Neuroprotection: the strongest preclinical signal Where the literature is most developed is brain injury. Intranasal Semax given for 6 days in a rat model of focal photoinduced prefrontal-cortex ischemia (reduced blood flow) decreased the volume of cortical *infarction* — dead tissue — and improved retention of a learned avoidance task, an antiamnesic effect [4]. How it protects appears to be less about a single receptor and more about reshaping which genes the injured brain switches on. Genome-wide analysis after permanent middle-cerebral-artery occlusion showed Semax predominantly modulated immune-system genes — immunoglobulins and chemokines made up more than half of the affected genes — and altered vascular-system genes [5]. The protective effect reads as an immune and blood-vessel shift, not a tidy lock-and-key drug action. This is why Semax became a registered stroke drug in Russia, and why that record is worth reading carefully rather than dismissing or overselling. See the full [Semax research](/research). ## A short residence time, a longer effect Semax does not linger. After a 50 microg/kg intranasal dose of radiolabeled Semax in rats, only about 0.093% of the administered radioactivity per gram appeared in brain at 2 minutes — about 80% of it still intact Semax, the rest already broken into metabolites — and the peptide is degraded fast by enzymes [6]. The intact heptapeptide therefore has a very short residence time. That raises an obvious question the field has answered with an inference: if the molecule is gone in minutes, why do behavioral effects last hours? The common explanation is the Pro-Gly-Pro (PGP) metabolite — the tail that was grafted on for stability is itself biologically active. It is a reasonable account, but it is an inference, not a fully resolved pharmacokinetic picture, and that distinction is worth keeping in view. ## What this site is This is a field log: Semax watched as a phenomenon and its record tabulated, not sold. The pages here summarize the peer-reviewed literature, label what is animal data versus human data, and keep the community's reports clearly separate from the studies. You will find [what is semax peptide used for](/what-is-semax), a side-by-side on [Semax vs Selank](/vs-selank), the dosing research context, an honest [Semax effects](/effects) page, and the full [Semax references](/references). No product is sold here. The aim is simply an accurate reading of what is on the record. --- A field log of the published Semax research — observed and tabulated, never prescribed.