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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 collaboration with the W.W. Zakusov Institute of Pharmacology. The peptide is an analog of the ACTH(4-10) fragment (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 while lacking its hormonal action on the adrenal cortex. The ACTH(4-7) fragment (Met-Glu-His-Phe) is 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 conditions, and as an immunomodulator. The peptide is mainly available as a nasal solution (0.1% and 1%).
The mechanism of action of Semax is multifaceted and includes effects on neurotrophic systems, neurotransmitter systems, and gene expression:
BDNF/TrkB system modulation – Semax significantly increases levels of brain-derived neurotrophic factor (BDNF) and its receptor TrkB in the hippocampus. A single application of Semax (50 µg/kg) in rats caused 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 brain’s monoaminergic systems. The peptide increases 5-HIAA levels (a serotonin metabolite) in the striatum 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 more than 1500 genes in the brain under ischemic conditions. The peptide modulates genes related to:
Immunomodulatory action – Semax affects the activity of microglia and immune system 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 action – Semax forms stable complexes with Cu²⁺ ions, which may inhibit copper-dependent aggregation of β-amyloid protein (Aβ). In vitro studies have shown that Semax delays amyloid fibril formation and protects neuroblastoma cells from the neurotoxicity of Aβ oligomers.
Semax is the subject of extensive preclinical research and limited clinical studies, mainly in Russia and the countries of the former USSR.
Research in stroke and ischemia
Semax is registered in Russia for use in the acute phase of ischemic stroke. Studies in animal models (pMCAO – permanent middle cerebral artery occlusion; tMCAO – transient) have shown the peptide’s neuroprotective effects. RNA-Seq analysis identified 394 differentially expressed genes (DEGs) in the brains of rats treated with Semax 24 hours after tMCAO compared with saline. Semax suppressed the expression of genes associated with inflammatory processes and activated genes related to neurotransmission, reversing the expression pattern induced by ischemia alone.
Nootropic and cognitive studies
In animal studies, Semax improved learning and memory, 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 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 those of other neuroprotective drugs.
Studies in Alzheimer’s disease
Due to Semax’s ability to chelate copper and inhibit Aβ aggregation, the peptide is being investigated as a potential candidate for the prevention and treatment of Alzheimer’s disease. In vitro studies have shown that Semax:
Studies in Parkinson’s disease
In a rat model of Parkinson’s disease (MPTP injection), four daily intranasal doses of Semax improved some behavioral aspects, although the results were mixed.
Studies in other neurological conditions
Semax is being studied and clinically used in Russia for:
Studies on VEGF gene expression
Analysis of the effects of Semax and its C-terminal fragment PGP 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 angiogenesis pathways under conditions of cerebral ischemia.
Semax fits into the tradition of research on melanocortin peptides and ACTH fragments as neurotropic factors. In the 1950s, it was discovered that ACTH could exert cognitive effects independently of its hormonal action. Further research on ACTH fragments led to the identification of ACTH(4-10) as the minimal neurotropic sequence.
Modification of the C-terminus with the PGP tripeptide was crucial for creating a drug with practical utility – native ACTH fragments have a half-life measured in minutes, whereas Semax acts for 20-24 hours.
Compared with other nootropic peptides:
These two peptides are sometimes used together because of complementary mechanisms – Semax for cognitive function and neuroprotection, Selank for mood regulation and anxiety reduction.
In published studies, Semax showed a favorable safety profile with minimal adverse effects:
Reported adverse events (rare):
No typical side effects:
However, most data come from Russian studies, and the English-language scientific literature is limited. The long-term safety profile in Western populations has not been fully studied.
