Semax is a heptapeptide, which is a peptide built from seven amino acids (sequence MEHFPGP). This is 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.
Adults with ischemic stroke studied alongside standard care in a published Russian clinical study. This is a study record. It is not a claim that Semax treats stroke. It is not a Form Labs product claim.
Gusev et al., Zhurnal Nevrologii i Psikhiatrii, 2018Approximate rise in BDNF measured in rat hippocampus after Semax, alongside more TrkB signalling. This is a lab measure in rats, not a Form Labs product claim.
Dolotov et al., Brain Research, 2006Genes with changed activity in injured rat brain tissue after Semax, in a genome-wide RNA-sequencing study. This is far short of the "4,000 genes" figure sometimes seen in marketing. It is a lab finding, not a Form Labs product claim.
Filippenkov et al., Genes (Basel), 2020Why it matters
Why is Semax studied?
Semax is a synthetic heptapeptide. This means it has seven amino acids, in the order MEHFPGP (Form Labs catalogue record). Researchers in Russia developed it as an ACTH(4-10) analog. This is a fragment analog of the hormone ACTH. Published research studies it for protecting nerve cells and for thinking. Most work is in cells and animal brains. There is also one clinical study in Russian stroke patients (Gusev et al., 2018).
Mostly animal research, plus one Russian clinical study.
Semax was developed in Russia in the 1980s at the Institute of Molecular Genetics. It is built from a fragment of the hormone ACTH (adrenocorticotropic hormone) with an added stability tail. It is registered as a medicine there. Most of what is published studies nerve protection and thinking. This includes how the peptide behaves in cells and animal brains. In one notable study, it was given alongside standard care for ischemic stroke in Russian patients.
The evidence looks different from a Western drug development programme. No Phase 1-3 trial series has been reviewed by the TGA, the FDA or EU regulators. Instead there is a long-running Russian research literature. It has rodent studies on BDNF and on dopamine and serotonin systems. It has genome-wide screening studies. It has one published clinical study in stroke patients. This guide uses all of it as research context. It is not a product claim or a promise about what happens in a person.

Study observations
What laboratory observations have Semax studies reported?
Dolotov et al. (2006) reported higher BDNF and TrkB signalling in rat hippocampal tissue after Semax. Filippenkov et al. (2020) reported changed gene activity in injured rat brain tissue. These are lab animal findings. The separate Russian clinical record measured stroke-recovery scores and plasma BDNF. It does not give 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 names Semax as MEHFPGP. It is an ACTH-fragment analog with a Pro-Gly-Pro tail.
Rat hippocampal tissue
Dolotov et al. (2006) reported higher BDNF and TrkB signalling in rat hippocampal tissue. These are animal measurements.
Rat brain gene activity
Filippenkov et al. (2020) reported changed gene activity in injured rat brain tissue. This is a lab 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. (1991) reported fast breakdown of Semax 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. The TGA (Australia) and the FDA (US) have not approved it. It has 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. The first is nerve protection and ischemic stroke, in a Russian clinical study. The second is BDNF and TrkB signalling in rat brain tissue. The third is dopamine and serotonin systems in rodents. The fourth is gene activity found by genome-wide screening. The fifth is how fast peptidase enzymes break Semax down. Apart from the one clinical study, the work is lab research in animals and cells.
Study areas from the published literature.
Neuroprotection & ischemic stroke
Studied in a Russian clinical study alongside standard stroke care. It tracked plasma BDNF and recovery of function.
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. (2005) reported dopamine and serotonin measures 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 fast peptidase enzymes in blood and tissue break down the Semax sequence.
Potaman et al., Biochem Biophys Res Commun, 1991The studies
What did the Semax studies find?
The six Semax studies in this guide are one Russian clinical study and five lab studies. Dolotov et al. (2006) reported that Semax raised BDNF in rat hippocampus by roughly 1.4-fold. Gusev et al. (2018) measured plasma BDNF and recovery in stroke patients. The patients were given Semax alongside standard care. Filippenkov et al. (2020) found 394 genes with changed 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. (2006) measured BDNF and TrkB signalling in rat hippocampal tissue after Semax.
- Studied in
- Adult rats.
- Design
- A lab experiment on rat hippocampal tissue after Semax (Dolotov et al., 2006).
- Measured
- BDNF levels and TrkB receptor signalling in the hippocampus.
Dolotov et al. (2006) reported roughly 1.4-fold higher hippocampal BDNF and more TrkB signalling in rats. These are lab animal measurements.
DOI 10.1016/j.brainres.2006.07.108A published Russian clinical study. It measured plasma BDNF and a recovery score in stroke patients. The patients were given Semax alongside standard care.
- Studied in
- 110 adults with ischemic stroke.
- Design
- A clinical study that measured plasma BDNF and the Barthel Index (a score of recovery of function) alongside standard stroke treatment.
- Measured
- Plasma BDNF levels and Barthel Index scores.
This is a published clinical study in the Russian literature. It measured plasma BDNF and recovery scores in stroke patients given Semax alongside standard care (Gusev et al., 2018). It is the human anchor for Semax. But it is not a Western regulatory trial. This guide draws no conclusion about how well Semax works for any one person.
DOI 10.17116/jnevro20181183261-68A genome-wide RNA-sequencing study. It measured how Semax changed gene activity after an induced stroke-like injury in rats.
- Studied in
- Rat brain tissue after induced cerebral ischemia-reperfusion, which is a model of stroke-like injury.
- Design
- Genome-wide RNA-sequencing.
- Measured
- How many genes had changed activity after Semax, and which ones.
394 genes showed changed activity in the injured brain tissue after Semax, compared with untreated injury (Filippenkov et al., 2020). This is a lab finding in rats. It is not a claim about people. It is far short of the "thousands of genes" figure sometimes seen in marketing.
DOI 10.3390/genes11060681An earlier genome-wide gene-activity screening study in rat brain tissue.
- Studied in
- Rat brain tissue.
- Design
- Genome-wide gene-expression screening.
- Measured
- Genes with changed activity after Semax.
This study found a smaller set of genes with changed activity. The set was on the order of 68 to 96 genes (Medvedeva et al., 2014). Again this is a lab measure in rats. It is not a claim about people.
DOI 10.1186/1471-2164-15-228A rodent lab study. It measured activity of the dopamine and serotonin (monoamine) systems after Semax.
- Studied in
- Rodent brain tissue.
- Design
- Lab measure of monoamine system activity in rodent brain tissue (Eremin et al., 2005).
- Measured
- Signalling markers linked to dopamine and serotonin.
The study reported changes in the activity of the dopamine and serotonin systems in the animals studied (Eremin et al., 2005). This is a lab finding. It is not a claim about mood or thinking in people.
DOI 10.1007/s11064-005-8826-8A biochemical study. It measured how peptidase enzymes in blood and tissue break down the Semax sequence.
- Studied in
- Lab enzyme/biochemical assays.
- Design
- An in-vitro degradation assay.
- Measured
- How fast peptidase enzymes broke down the Semax sequence.
Potaman et al. (1991) reported fast breakdown of Semax 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 in this guide are rodent lab work and one Russian clinical study (Gusev et al., 2018). They are not a Western Phase 1-3 programme. The research gives no direction for use in or on people or animals. It describes the molecule in general, not what a specific batch does.
- Large Western clinical trials: no Phase 1-3 programme has been 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?
This guide does not state Semax's approval status. Its sources include no regulator record of an approval decision. The research record starts with 1991 enzyme work (Potaman et al., 1991). It moves through the 2006 rat BDNF study (Dolotov et al., 2006). It ends with a 2018 Russian clinical study in 110 stroke patients (Gusev et al., 2018).
The Institute of Molecular Genetics develops Semax as an ACTH(4-10) analog. It has an added stability tail.
Early biochemical work shows how peptidase enzymes break Semax down (Potaman et al.).
Eremin et al. (2005) reported dopamine and serotonin measures in rodents.
A rat study reports that Semax raised BDNF and TrkB signalling in the hippocampus (Dolotov et al.).
A genome-wide screening study finds 68-96 genes with changed activity in rat brain tissue after Semax (Medvedeva et al.).
A published Russian clinical study measures plasma BDNF and recovery of function in 110 ischemic stroke patients. The patients were given Semax alongside standard care (Gusev et al.).
An RNA-sequencing study finds 394 genes with changed activity in rat brain tissue. The rats had a stroke-like injury and Semax (Filippenkov et al.).
Approval status: Registered as a medicine in Russia. The TGA (Australia) and the FDA (US) have not approved it. It has 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 is mostly rat and rodent lab work. There is also one published human clinical study in Russian ischemic stroke patients (Gusev et al., 2018). This is a much smaller and different body of evidence than a Western drug development programme. You may see a claim that Semax changes thousands of genes. The studies cited here do not support it. The genome-wide studies found about 68-96 genes (Medvedeva et al., 2014) and 394 genes (Filippenkov et al., 2020).
Mostly animal research, plus one human study
Most of the Semax evidence is rat and rodent lab work. It covers 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 is a much smaller and different body of evidence than a Western drug development programme.
No TGA or FDA approval, no EU marketing authorisation
Semax is registered as a medicine in Russia. The TGA (Australia) and the FDA (US) have not approved it. It has no marketing authorisation in the EU. Do not read anything here as Western regulatory approval.
The "4,000 genes" figure is wrong
A common marketing claim says Semax changes thousands of genes. The actual genome-wide studies found dozens to a few hundred. One 2014 study found about 68-96 genes. A 2020 study found 394. See the FAQ below for the full picture.
Where Form Labs fits
This guide is a plain-English summary of published research. Form Labs did not run that research. It is 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 lab research.
Lab handling
How is Semax handled as reference material?
Semax is lab reference material. It is not for human consumption or veterinary use. Storage and lot checks follow the product label. They also follow any verified matching certificate of analysis (COA). The catalogue record notes storage at 2-8 C and protection from light.
Research-use boundary
Semax is supplied strictly for lab research. It is not for human, veterinary, medical or any other use.
COA and label
Each lab report covers only the sample, amount and lot it names. Match the lot number on your vial to the reports in the certificate library.
Storage
Supplied freeze-dried. Keep it at 2-8°C (fridge-cold) and out of light. Follow the vial label, any verified matching lab report for the batch. 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. The Form Labs catalogue record calls Semax an ACTH-fragment analog.
- 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. It is a protein that researchers measure as a marker of nerve-cell growth and survival.
- TrkB
- The receptor (cell signal receiver) that BDNF switches on. Researchers measure TrkB signalling alongside BDNF levels.
- Peptidase
- An enzyme that breaks peptides down. Potaman et al. (1991) reported fast 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 scoring scale for recovery of function. The Russian stroke study used it to track how well patients could manage daily activities.
- Research use only (RUO)
- A lab-only boundary. It means not for human consumption, or for 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). Researchers in Russia developed it as an ACTH(4-10) analog. It is studied mostly in animal and cell research. The common questions cover its sequence and how it relates to BDNF. They also cover whether it is a nootropic, how it differs from Selank, and the thousands-of-genes claim. Form Labs supplies reference material for research use only.
Semax is a synthetic heptapeptide (a peptide of seven amino acids) with the sequence MEHFPGP. Researchers at the Institute of Molecular Genetics in Russia developed it as an ACTH(4-10) analog. That is a fragment analog of the hormone ACTH with a Pro-Gly-Pro tail for stability. Published research studies it for nerve protection and thinking. Most of that is animal and cell work, plus some human clinical research in Russia. Form Labs supplies Semax strictly as reference material for research use only, not for human or veterinary use.
Semax's sequence is MEHFPGP (Met-Glu-His-Phe-Pro-Gly-Pro). It is 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. 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. Its molecular formula is C37H51N9O10S. Its molecular weight is about 813.9 g/mol.
Dolotov et al. (2006) reported roughly 1.4-fold higher BDNF in rat hippocampal tissue and more TrkB signalling after Semax. BDNF and TrkB were lab measures in that animal model. The experiment did not show a clinical outcome in people.
Popular writing often calls Semax a nootropic. That label describes how it is discussed. It is not something Form Labs claims. Published research studies it for nerve protection and thinking. It is mostly in animal and cell models, plus some Russian clinical work. Form Labs supplies Semax strictly as reference material for research use only. Nothing on this page claims that it improves memory, focus or mood in people.
Semax and Selank are two different synthetic peptides. Semax has the sequence MEHFPGP. It is an analog of a fragment of the hormone ACTH. It is studied mostly in nerve protection and thinking research. Selank has the sequence TKPRPGP. It is an analog of the peptide tuftsin. It is studied more in anxiety and immune marker research. Form Labs supplies both only as reference material for research use only.
A widely repeated marketing claim says Semax changes the activity of several thousand genes. The actual studies do not show that. Genome-wide studies in rat brain tissue found dozens to a few hundred genes changing after Semax. One 2014 study found about 68-96 genes. A 2020 study found 394. None found thousands. The "thousands" figure seems to mix up the total number of genes screened with the far smaller number actually affected. Either way, these are lab measures in animals. They are not a claim about people.
Semax is registered as a medicine in Russia, where it was developed. The Therapeutic Goods Administration (TGA) in Australia and the FDA in the United States have not approved it. It has no marketing authorisation in the European Union. Form Labs supplies it for research use only, not as a medicine and not for human or veterinary use.
Form Labs supplies Semax strictly as lab research material. This guide is a plain-English summary of published research that Form Labs did not run. It is not medical advice, not a product claim, and not guidance for any human or veterinary use.
Semax is supplied freeze-dried. The published handling notes call for storing it at 2-8°C (fridge-cold), protected from light. Follow 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.
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