For laboratory research use only - not for human consumption

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
7

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)
1.4×

Approximate 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, 2006
394

Genes 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), 2020

Why 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.

Semax research catalogue presentation

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.

Pathway 01

Peptide identity

The Form Labs catalogue record names Semax as MEHFPGP. It is an ACTH-fragment analog with a Pro-Gly-Pro tail.

Pathway 02

Rat hippocampal tissue

Dolotov et al. (2006) reported higher BDNF and TrkB signalling in rat hippocampal tissue. These are animal measurements.

Pathway 03

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.
One long horizontal bar labelled Hormone, joined by a thin line to a shorter solid bar of two parts labelled Fragment and Stability tail. The diagram is not to scale.
Semax is built from the ACTH(4-7) fragment of the hormone ACTH with a Pro-Gly-Pro tail added for stability (Form Labs catalogue record). It is an ACTH(4-10) analog, not ACTH itself (Dolotov et al., Brain Research, 2006). The diagram is an abstract sketch, not to scale.

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.

01

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, 2018
02

BDNF & 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, 2006
03

Dopamine & serotonin systems

Eremin et al. (2005) reported dopamine and serotonin measures in rodent brain research.

Eremin et al., Neurochemical Research, 2005
04

Gene 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, 2020
05

Peptidase / enzyme stability

Studied for how fast peptidase enzymes in blood and tissue break down the Semax sequence.

Potaman et al., Biochem Biophys Res Commun, 1991

The 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.

Where 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).

1980s

The Institute of Molecular Genetics develops Semax as an ACTH(4-10) analog. It has an added stability tail.

1991

Early biochemical work shows how peptidase enzymes break Semax down (Potaman et al.).

2005

Eremin et al. (2005) reported dopamine and serotonin measures in rodents.

2006

A rat study reports that Semax raised BDNF and TrkB signalling in the hippocampus (Dolotov et al.).

2014

A genome-wide screening study finds 68-96 genes with changed activity in rat brain tissue after Semax (Medvedeva et al.).

2018

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.).

2020

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.

References

Every figure, sourced.

Educational references to third-party literature. Form Labs is unaffiliated with the study authors.

01

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).

DOI
02

Gusev 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.

DOI
03

Filippenkov 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.

DOI
04

Eremin KO et al. Neurochemical Research, 2005, 30:1493-1500 - a laboratory study of Semax and dopaminergic/serotoninergic (monoamine) signalling systems in rodents.

DOI
05

Medvedeva 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.

DOI
06

Potaman VN et al. Biochemical and Biophysical Research Communications, 1991, 176 - a laboratory study of enzymatic (peptidase) degradation of Semax.

DOI
07

Deigin 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.

DOI

Citations 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
Form Laboratories - Semax

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11 mg - 2-8 C

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