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Product description
Semax (Met-Glu-His-Phe-Pro-Gly-Pro) is a synthetic heptapeptide developed at the Institute of Molecular Genetics of the Russian Academy of Sciences in cooperation with the Institute of Pharmacology. W.W. Zakusowa. The peptide is an analogue of a fragment of ACTH(4-10) (adrenocorticotropic hormone), modified by the addition of the C-terminal tripeptide Pro-Gly-Pro (PGP) to increase metabolic stability.
Semax retains the neurotrophic properties of native ACTH, but is devoid of its hormonal effect on the adrenal cortex. The ACTH(4-7) (Met-Glu-His-Phe) fragment constitutes the minimal sequence responsible for cognitive effects, while the C-terminal tripeptide PGP provides resistance to peptidases and extends the duration of action from minutes to 20-24 hours in animal models.
In Russia, Semax is a registered drug used in the treatment of stroke, vascular encephalopathy, cognitive disorders, optic nerve disorders and as an immunomodulator. The peptide is mainly available in the form of an intranasal solution (0.1% and 1%).
The mechanism of action of Semax is multidirectional and includes effects on neurotrophic and neurotransmitter systems and gene expression:
BDNF/TrkB system modulation – Semax significantly increases the levels of brain-derived neurotrophic factor (BDNF) and its receptor TrkB in the hippocampus. A single application of Semax (50 µg/kg) in rats resulted in a maximum 1.4-fold increase in BDNF protein, a 1.6-fold increase in TrkB phosphorylation (receptor activation), a 3-fold increase in BDNF exon III mRNA, and a 2-fold increase in TrkB mRNA. BDNF is crucial for synaptic plasticity, learning and memory.
Activation of dopaminergic and serotonergic systems – Semax activates the monoaminergic systems of the brain. The peptide increases striatal 5-HIAA (a serotonin metabolite) levels by 25% in tissue and up to 180% in extracellular fluid within 1-4 hours after administration. Semax itself does not change dopamine levels, but it dramatically enhances the effects of D-amphetamine on extracellular dopamine levels and locomotor activity.
Regulation of gene expression – Transcriptomic studies have shown that Semax affects the expression of over 1,500 genes in the brain under ischemic conditions. The peptide modulates genes related to:
Immunomodulatory effect – Semax affects the activity of microglia and immune cells in the CNS. Under ischemic conditions, the peptide enhances the expression of chemokine and immunoglobulin genes, modulating the neuroimmune response to injury.
Copper chelation and anti-amyloid effect – Semax forms stable complexes with Cu²⁺ ions, which may inhibit the copper-dependent aggregation of β-amyloid (Aβ) protein. In vitro studies have shown that Semax delays the formation of amyloid fibers and protects neuroblastoma cells against the neurotoxicity of Aβ oligomers.
Semax is the subject of extensive preclinical research and limited clinical trials, mainly in Russia and the former USSR countries.
Tests in stroke and ischemia
Semax is registered in Russia for use in the acute phase of ischemic stroke. Studies on animal models (pMCAO - permanent occlusion of the middle cerebral artery; tMCAO - transient) have demonstrated the neuroprotective effect of the peptide. RNA-Seq analysis identified 394 differentially expressed genes (DEGs) in the brains of Semax-treated rats 24 hours after tMCAO compared to saline. Semax inhibited the expression of genes related to inflammatory processes and activated genes related to neurotransmission - reversing the expression pattern induced by ischemia itself.
Nootropic and cognitive research
In animal studies, Semax improved learning and memory, as measured by the conditioned avoidance test. Rats treated with Semax showed a marked increase in the number of conditioned avoidance responses. This effect correlated with the activation of the BDNF/TrkB system in the hippocampus. In healthy humans (pilot study, n=24), intranasal 1% Semax solution (total dose 1.2 mg) improved attention and short-term memory and induced EEG changes similar to other neuroprotective drugs.
Alzheimer's disease research
Due to Semax's ability to chelate copper and inhibit Aβ aggregation, the peptide is being investigated as a potential candidate in the prevention and treatment of Alzheimer's disease. In vitro studies have shown that Semax:
Research in Parkinson's disease
In a rat model of Parkinson's disease (MPTP injection), four daily administrations of intranasal Semax improved some behavioral aspects, although results were mixed.
Tests in other neurological conditions
Semax is being studied and clinically used in Russia in:
Studies on VEGF gene expression
The analysis of the influence of Semax and its C-terminal PGP fragment on the expression of VEGF family genes (Vegf-a, Vegf-b, Vegf-c, Vegf-d, Plgf) and their receptors (Vegfr-1, Vegfr-2, Vegfr-3) showed modulation of the pathways angiogenesis in conditions of cerebral ischemia.
Semax is part of the tradition of research on melanocortin peptides and ACTH fragments as neurotrophic factors. In the 1950s, it was discovered that ACTH could exert cognitive effects independent of hormonal action. Further research on ACTH fragments led to the identification of ACTH(4-10) as a minimal neurotropic sequence.
Modification of the C-terminus of the PGP tripeptide was crucial to creating a drug with practical utility - native ACTH fragments have a half-life of minutes, while Semax works for 20-24 hours.
Compared to other nootropic peptides:
These two peptides are sometimes used together for complementary mechanisms - Semax for cognitive function and neuroprotection, Selank for mood regulation and anxiety reduction.
In published studies, Semax demonstrated a favorable safety profile with minimal side effects:
Reported adverse events (rare):
No common side effects:
However, most of the data comes from Russian studies, and there is limited English-language scientific literature. The long-term safety profile in Western populations has not been fully investigated.
