Semax is described as a heptapeptide - a peptide built from seven amino acids (sequence MEHFPGP). An identity fact, not a Form Labs product claim.
Semax sequence identity (MEHFPGP)Plain-English research guideMEHFPGP
Semax research guide
Everything worth knowing, without the jargon.
Semax is a synthetic heptapeptide (seven amino acids, sequence MEHFPGP) developed in Russia as an ACTH(4-10) analog - a fragment analog of the hormone ACTH - and studied in published research for its role in neuroprotection and cognition.
Form Labs materials are research reference materials, not the approved medicines; no Form Labs product is approved for human or veterinary use.
REV 2026-10 · 1 Oct 20266 peer-reviewed studiesResearch-use-only context
What the papers reportThird-party literature - not product claims
Adults with ischemic stroke studied alongside standard care in a published Russian clinical study. A study record, not a claim that Semax treats stroke - not a Form Labs product claim.
Gusev et al., Zhurnal Nevrologii i Psikhiatrii, 2018Approximate rise in BDNF measured in rat hippocampus after Semax, alongside increased TrkB signalling. A laboratory measurement in rats, not a Form Labs product claim.
Dolotov et al., Brain Research, 2006Genes with altered activity in injured rat brain tissue after Semax, in a genome-wide RNA-sequencing study - far short of the "4,000 genes" figure sometimes seen in marketing. A laboratory finding, not a Form Labs product claim.
Filippenkov et al., Genes (Basel), 2020Why it matters
Why is Semax studied?
Semax is studied because it is a synthetic heptapeptide, seven amino acids with the sequence MEHFPGP (Form Labs catalogue record), developed in Russia as an ACTH(4-10) analog, a fragment analog of the hormone ACTH. Semax is studied in published research for neuroprotection and cognition-related questions, mostly in cells and animal brains, plus one clinical study in Russian ischemic-stroke patients (Gusev et al., Zhurnal Nevrologii i Psikhiatrii, 2018).
Mostly animal research, plus one Russian clinical study.
Semax was developed in Russia in the 1980s at the Institute of Molecular Genetics, built from a fragment of the hormone ACTH (adrenocorticotropic hormone) with an added stability tail. It's registered as a medicine there, and most of what's published about it studies cognition- and neuroprotection-related questions: how the peptide behaves in cells and animal brains, and, in one notable study, alongside standard care for ischemic stroke in Russian patients.
The evidence base looks different from a Western drug-development programme. There's no Phase 1-3 trial series reviewed by the TGA, the FDA, or EU regulators - instead there's a long-running Russian research literature: rodent studies on BDNF and dopamine/serotonin systems, genome-wide screening studies, and one published clinical study in stroke patients. This guide treats all of it as research context, not as a product claim or a promise about what happens in a person.
Study observations
What laboratory observations have Semax studies reported?
Dolotov et al. (Brain Research, 2006) reported higher BDNF and TrkB signalling in rat hippocampal tissue after Semax. Filippenkov et al. (Genes, 2020) reported altered gene activity in injured rat brain tissue. These are laboratory animal findings. The separate Russian clinical record measured stroke-recovery scores and plasma BDNF, without establishing a result for Form Labs material.
Semax laboratory measurements Findings stay tied to the cited study and its model.
Peptide identity
The Form Labs catalogue record identifies Semax as MEHFPGP, an ACTH-fragment analog with a Pro-Gly-Pro tail.
Rat hippocampal tissue
Dolotov et al. (Brain Research, 2006) reported higher BDNF and TrkB signalling in rat hippocampal tissue; these are animal measurements.
Rat brain gene activity
Filippenkov et al. (Genes, 2020) reported altered gene activity in injured rat brain tissue; this is a laboratory observation.
Pharmacology at a glance
- Research code
- MEHFPGP
- Class
- ACTH(4-10) analog - a fragment analog of the hormone ACTH, built with a Pro-Gly-Pro tail added for stability.
- Molecule
- A synthetic heptapeptide (seven amino acids). CAS 80714-61-0, molecular formula C37H51N9O10S, molecular weight about 813.9 g/mol.
- Reported half-life
- Potaman et al. (Biochemical and Biophysical Research Communications, 1991) reported rapid Semax breakdown by peptidase enzymes in biochemical experiments; this guide records no specific half-life figure.
- Originator
- Institute of Molecular Genetics, Russian Academy of Sciences (Russia)
- Approval status
- Registered as a medicine in Russia; not approved by the TGA (Australia) or the FDA (US), and no marketing authorisation in the EU.
What it has been studied for
What has Semax been studied for?
Semax has been studied in five areas: neuroprotection and ischemic stroke in a Russian clinical study, BDNF and TrkB signalling in rat brain tissue, dopamine and serotonin systems in rodents, gene expression by genome-wide screening, and how quickly peptidase enzymes break Semax down. Apart from the one clinical study, the work is laboratory research in animals and cells.
Study areas from the published literature.
Neuroprotection & ischemic stroke
Studied in a Russian clinical study alongside standard stroke care, tracking plasma BDNF and functional recovery.
Gusev et al., Zhurnal Nevrologii i Psikhiatrii, 2018BDNF & TrkB signalling
Studied for whether it raises BDNF (a nerve-growth marker) and TrkB receptor signalling in rat brain tissue.
Dolotov et al., Brain Research, 2006Dopamine & serotonin systems
Eremin et al. (Neurochemical Research, 2005) reported dopaminergic and serotoninergic measurements in rodent brain research.
Eremin et al., Neurochemical Research, 2005Gene expression / transcriptome
Studied with genome-wide screening to see which genes change activity after Semax in rat brain-injury models.
Medvedeva et al., BMC Genomics, 2014; Filippenkov et al., Genes, 2020Peptidase / enzyme stability
Studied for how quickly peptidase enzymes in blood and tissue break the Semax sequence down.
Potaman et al., Biochem Biophys Res Commun, 1991The studies
What did the Semax studies find?
The six Semax studies cited in this guide are one Russian clinical study and five laboratory records. Dolotov et al. (Brain Research, 2006) reported that Semax raised BDNF in rat hippocampus by roughly 1.4-fold. Gusev et al. (Zhurnal Nevrologii i Psikhiatrii, 2018) measured plasma BDNF and functional recovery in stroke patients given Semax alongside standard care. Filippenkov et al. (Genes, 2020) found 394 genes with altered activity in injured rat brain tissue.
Open any study for a plain summary, what it measured, the finding, and a link to the paper.
Dolotov et al. (Brain Research, 2006) measured BDNF and TrkB signalling in rat hippocampal tissue after Semax.
- Studied in
- Adult rats.
- Design
- A laboratory experiment examining rat hippocampal tissue after Semax (Dolotov et al., Brain Research, 2006).
- Measured
- BDNF levels and TrkB receptor signalling in the hippocampus.
Dolotov et al. (Brain Research, 2006) reported roughly 1.4-fold higher hippocampal BDNF and increased TrkB signalling in rats; these are laboratory animal measurements.
DOI 10.1016/j.brainres.2006.07.108A published Russian clinical study measuring plasma BDNF and a functional-recovery score in stroke patients given Semax alongside standard care.
- Studied in
- 110 adults with ischemic stroke.
- Design
- A clinical study measuring plasma BDNF and the Barthel Index (a functional-recovery score) alongside standard stroke treatment.
- Measured
- Plasma BDNF levels and Barthel Index scores.
This is a published clinical study in the Russian literature that measured plasma BDNF and functional-recovery scores in stroke patients given Semax alongside standard care (Gusev EI et al. - Zhurnal Nevrologii i Psikhiatrii - 2018). It's the human-research anchor for Semax, but it is not a Western regulatory trial, and this guide draws no efficacy conclusion from it for any individual (Gusev EI et al. - Zhurnal Nevrologii i Psikhiatrii - 2018).
DOI 10.17116/jnevro20181183261-68A genome-wide RNA-sequencing study measuring how Semax changed gene activity after an induced stroke-like injury in rats.
- Studied in
- Rat brain tissue after induced cerebral ischemia-reperfusion (a stroke-like injury model).
- Design
- Genome-wide RNA-sequencing.
- Measured
- Number and identity of genes with altered activity after Semax.
394 genes showed altered activity in the injured brain tissue after Semax, compared with untreated injury - a laboratory finding in rats, not a claim about people, and far short of the "thousands of genes" figure sometimes seen in marketing (Filippenkov IB et al. - Genes (Basel) - 2020).
DOI 10.3390/genes11060681An earlier genome-wide gene-expression screening study in rat brain tissue.
- Studied in
- Rat brain tissue.
- Design
- Genome-wide gene-expression screening.
- Measured
- Genes with altered activity after Semax.
This study found a smaller set - on the order of 68 to 96 genes - with altered activity, again a laboratory measurement in rats, not a claim about people (Medvedeva EV et al. - BMC Genomics - 2014).
DOI 10.1186/1471-2164-15-228A rodent laboratory study measuring dopaminergic and serotoninergic (monoamine) system activity after Semax.
- Studied in
- Rodent brain tissue.
- Design
- Laboratory measurement of monoamine system activity in rodent brain tissue (Eremin et al., Neurochemical Research, 2005).
- Measured
- Dopamine- and serotonin-related signalling markers.
The study reported changes in dopaminergic and serotoninergic system activity in the animals studied - a laboratory finding, not a claim about mood or cognition in people (Eremin KO et al. - Neurochemical Research - 2005).
DOI 10.1007/s11064-005-8826-8A biochemical study measuring how blood and tissue peptidase enzymes degrade the Semax sequence.
- Studied in
- Laboratory enzyme/biochemical assays.
- Design
- An in-vitro degradation assay.
- Measured
- How quickly peptidase enzymes broke down the Semax sequence.
Potaman et al. (Biochemical and Biophysical Research Communications, 1991) reported rapid Semax breakdown by peptidase enzymes in biochemical experiments.
DOI 10.1016/S0006-291X(05)80247-5Where evidence stops
What has Semax research not established?
The Semax studies cited in this guide are rodent laboratory work and one Russian clinical study (Gusev et al., Zhurnal Nevrologii i Psikhiatrii, 2018), not a Western Phase 1-3 programme. The research cited in this guide gives no direction for use in or on people or animals, and describes the molecule in general, not what a specific batch does.
- Large Western clinical trials: there is no Phase 1-3 programme reviewed by the TGA, FDA, or EU regulators.
- Any use in or on people or animals: none of the research on this page is a use direction.
- What a specific batch does: the studies are about the molecule in general, not this vial.
Development and status
Is Semax approved, and where does the research stand?
Semax's approval status is not stated here, because this guide's sources include no regulator record of an approval decision for it. The research record runs from 1991 enzyme work (Potaman et al., Biochem Biophys Res Commun, 1991) through the 2006 rat BDNF study (Dolotov et al., Brain Research, 2006) to a 2018 Russian clinical study in 110 stroke patients (Gusev et al., Zhurnal Nevrologii i Psikhiatrii, 2018).
Semax is developed at the Institute of Molecular Genetics, Russian Academy of Sciences, as an ACTH(4-10) analog with an added stability tail.
Early biochemical work describes how peptidase enzymes break Semax down (Potaman et al.).
Eremin et al. (Neurochemical Research, 2005) reported dopaminergic and serotoninergic measurements in rodents.
A rat study reports Semax raising BDNF and TrkB signalling in the hippocampus (Dolotov et al.).
A genome-wide screening study finds 68-96 genes with altered activity in rat brain tissue after Semax (Medvedeva et al.).
A published Russian clinical study measures plasma BDNF and functional recovery in 110 ischemic-stroke patients given Semax alongside standard care (Gusev et al.).
An RNA-sequencing study finds 394 differentially expressed genes in rat brain tissue after stroke-like injury and Semax (Filippenkov et al.).
Approval status: Registered as a medicine in Russia; not approved by the TGA (Australia) or the FDA (US), and no marketing authorisation in the EU.Whatever the molecule’s status elsewhere, what Form Labs supplies is research-use-only reference material - for laboratory work, not for people or animals.
Evidence and limitations
What does the Semax research mean, and what does it not?
The Semax evidence base is mostly rat and rodent laboratory work, plus one published human clinical study in Russian ischemic-stroke patients (Gusev et al., Zhurnal Nevrologii i Psikhiatrii, 2018), a much smaller and different evidence base than a Western drug-development programme. A commonly repeated claim that Semax changes thousands of genes is not supported by the studies cited here: the genome-wide studies found about 68-96 genes (Medvedeva et al., BMC Genomics, 2014) and 394 genes (Filippenkov et al., Genes, 2020).
Mostly animal research, plus one human study
Most of the Semax evidence base is rat and rodent laboratory work - BDNF/TrkB signalling, dopamine and serotonin systems, and genome-wide gene screening. There is one published human clinical study, in Russian ischemic-stroke patients. That's a much smaller and different evidence base than a Western drug-development programme.
No TGA or FDA approval, no EU marketing authorisation
Semax is registered as a medicine in Russia, but it is not approved by the TGA (Australia) or the FDA (US), and it has no marketing authorisation in the EU. Nothing here should be read as Western regulatory approval.
The "4,000 genes" figure is wrong
A commonly repeated marketing claim says Semax changes thousands of genes. The actual genome-wide studies found dozens to a few hundred - about 68-96 genes in one 2014 study and 394 in a 2020 study. See the FAQ below for the full picture.
Where Form Labs fits
This guide is a plain-English summary of published research that Form Labs did not run. It's not medical advice, not a product claim, and not use guidance. Form Labs supplies Semax strictly as reference material, with a catalog lot record, for laboratory research. Matching current certification is unverified.
Lab handling
How is Semax handled as reference material?
Semax is laboratory reference material, not for human consumption or veterinary use. Storage and lot checks follow the product label and any verified matching certificate of analysis (COA). This guide's catalogue record notes storage at 2-8 C and protection from light. Historical sample reports do not verify current lot identity, purity or release status.
Research-use boundary
Semax is supplied strictly for laboratory research. It's not for human, veterinary, medical, or any other use.
COA and label
Historical sample reports do not establish current identity, purity or release status.
Storage
Supplied freeze-dried. Keep it at 2-8°C (fridge-cold) and out of light, following the vial label, any verified matching lab report for the batch, and the receiving lab's own written procedures.
Glossary
Plain-English definitions.
- Heptapeptide
- A peptide made from seven amino acids; Semax's sequence is MEHFPGP.
- ACTH
- Adrenocorticotropic hormone; Semax is an ACTH-fragment analog according to the Form Labs catalogue record.
- ACTH(4-10) analog
- A lab-made peptide built from amino acids 4 through 10 of ACTH, with an added Pro-Gly-Pro tail for stability.
- BDNF
- Brain-derived neurotrophic factor - a protein researchers measure as a marker of nerve-cell growth and survival.
- TrkB
- The receptor (cell signal receiver) that BDNF activates; researchers measure TrkB signalling alongside BDNF levels.
- Peptidase
- An enzyme that breaks peptides down; Potaman et al. (1991) reported rapid Semax breakdown in biochemical experiments.
- Monoamine
- A group of signalling chemicals in the brain that includes dopamine and serotonin.
- Transcriptome / RNA-sequencing
- A genome-wide method for measuring which genes are active in a tissue sample, and by how much.
- Barthel Index
- A functional-recovery scoring scale used in the Russian stroke study to track patients' daily-activity ability.
- Research use only (RUO)
- A lab-only boundary: not for human consumption, veterinary, medical, or cosmetic use.
FAQ
What are the most common questions about Semax?
Semax is a synthetic heptapeptide with the sequence MEHFPGP (Form Labs catalogue record), developed in Russia as an ACTH(4-10) analog and studied mostly in animal and cell research. The most common questions about Semax cover its sequence, how it relates to BDNF, whether it is a nootropic, how it differs from Selank and the thousands-of-genes claim. Form Labs supplies research-use-only reference material.
Semax is a synthetic heptapeptide (a seven-amino-acid peptide) with the sequence MEHFPGP, developed in Russia at the Institute of Molecular Genetics as an ACTH(4-10) analog - a fragment analog of the hormone ACTH with a stability-enhancing Pro-Gly-Pro tail. It's studied in published research for its role in neuroprotection and cognition, mostly in animal and cell studies, plus some human clinical research in Russia. Form Labs supplies Semax strictly as research-use-only reference material, not for human or veterinary use.
Semax's sequence is MEHFPGP (Met-Glu-His-Phe-Pro-Gly-Pro), a synthetic heptapeptide built as an ACTH(4-10) analog. The first four amino acids match the ACTH(4-7) fragment of the hormone ACTH, and the Pro-Gly-Pro tail was added to make the peptide more stable against enzyme breakdown. Its chemical registry number is CAS 80714-61-0, with molecular formula C37H51N9O10S and a molecular weight of about 813.9 g/mol.
Dolotov et al. (Brain Research, 2006) reported roughly 1.4-fold higher BDNF in rat hippocampal tissue and increased TrkB signalling after Semax. BDNF and TrkB were laboratory measurements in that animal model; the experiment did not establish a clinical outcome in people.
Semax is often described in popular writing as a nootropic, but that label refers to how it is discussed, not to anything Form Labs is claiming. In the published research it is studied for its role in neuroprotection and cognition-related experiments, mostly in animal and cell models plus some Russian clinical work. Form Labs supplies Semax strictly as research-use-only reference material, and nothing on this page is a claim that it improves memory, focus, or mood in people.
Semax and Selank are two different synthetic peptides. Semax is the sequence MEHFPGP, an analog of a fragment of the hormone ACTH, and is studied mostly in neuroprotection and cognition research; Selank is the sequence TKPRPGP, an analog of the peptide tuftsin, and is studied more in anxiety- and immune-marker research. Form Labs supplies both only as research-use-only reference material.
A widely repeated marketing claim says Semax changes the activity of several thousand genes, but the actual studies don't show that. Genome-wide studies in rat brain tissue found on the order of dozens to a few hundred genes changing after Semax - about 68-96 genes in one 2014 study and 394 in a 2020 study - not thousands. The "thousands" figure appears to confuse the total number of genes screened with the far smaller number actually affected, and either way these are laboratory measurements in animals, not a claim about people.
Semax is registered as a medicine in Russia, where it was developed, but it is not approved by the Therapeutic Goods Administration (TGA) in Australia or the FDA in the United States, and it has no marketing authorisation in the European Union. Form Labs supplies it only as research-use-only reference material, not as a medicine and not for human or veterinary use.
Form Labs supplies Semax strictly as laboratory research material. This guide is a plain-English summary of published research that Form Labs did not run - not medical advice, not a product claim, and not guidance for any human or veterinary use.
Semax is supplied freeze-dried, and the published handling notes call for storing it at 2-8°C (fridge-cold), protected from light, following the vial label and any verified matching lab report (COA) for the batch.
References
Every figure, sourced.
Educational references to third-party literature. Form Labs is unaffiliated with the study authors.
Dolotov OV et al. Brain Research, 2006, 1117:54-60 - reported Semax regulating BDNF and TrkB signalling in rat hippocampus (~1.4-fold BDNF rise).
DOIGusev EI et al. Zhurnal Nevrologii i Psikhiatrii, 2018 - a published Russian clinical study of Semax in 110 patients with ischemic stroke, measuring plasma BDNF and the Barthel Index alongside standard care.
DOIFilippenkov IB et al. Genes (Basel), 2020, 11(6):681 - an RNA-sequencing study reporting 394 differentially expressed genes in rat brain tissue after cerebral ischaemia-reperfusion and Semax.
DOIEremin KO et al. Neurochemical Research, 2005, 30:1493-1500 - a laboratory study of Semax and dopaminergic/serotoninergic (monoamine) signalling systems in rodents.
DOIMedvedeva EV et al. BMC Genomics, 2014, 15:228 - a genome-wide screening study reporting 96/68 genes with altered activity in rat brain tissue after Semax.
DOIPotaman VN et al. Biochemical and Biophysical Research Communications, 1991, 176 - a laboratory study of enzymatic (peptidase) degradation of Semax.
DOIDeigin Y et al. Pharmaceutics, 2022, 14(4):716 - a peer-reviewed review of Russian peptide biopharmaceuticals that discusses Semax; general background context, not a Semax-dedicated study.
DOICitations are provided for education only. No therapeutic, weight-loss, or efficacy claims are made.
How we produce these guides
These guides are written and maintained in-house by the Form Laboratories research team. They summarise published literature and link to the cited papers. Form Laboratories did not run those studies. They are not authored by a named clinician and are not medical advice.
Findings remain tied to the study population, model and limits. Cell and animal observations remain separate from clinical results. Everything we supply is research-use-only reference material, not for people or animals.
The product
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