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Peptides · Cognitive
Semax
99.90% purity · Lot KVPNWJ · tested Apr 22, 2026CAS80714-61-0FormulaC37H51N9O10SMW813.93
ACTH (4-10) analogue studied in BDNF-expression research.
- Independently tested
- Lot-matched COA
- Lyophilized for stability
- Ships from the USA
Research use only. Not for human or veterinary use. Sold to qualified researchers aged 21+.
$70.002 for $70 — $35 per vial
1
Lot-matched documentation. Every order ships with the certificate for its lot. If a vial arrives damaged or doesn't match its paperwork, tell us within 72 hours and we'll replace it.
Latest lab results
Third-party testedSemax 10 mg
- Purity (HPLC-UV)
- 99.90%
- Identity (LC-MS)
- Confirmed — Semax
- Lot
- KVPNWJ
- Tested
- Apr 22, 2026
- Lab
- Freedom Diagnostics Testing
Your order ships with the certificate for its own lot.
About Semax
ACTH (4-10) analogue studied in BDNF-expression research.
Supplied as
10 mg per vial, as a lyophilized powder in a sealed glass vial with a crimped cap. The lot number on the label matches the certificate of analysis in the COA library.
Storage and handling
Store lyophilized powder frozen (−20 °C) or refrigerated, sealed and away from light. Once reconstituted, keep refrigerated (2–8 °C).
Handle in a laboratory setting using appropriate protective equipment. Consult the certificate of analysis and safety data for lot-specific information.
Important research notice. This product is intended solely for in-vitro and laboratory research. It is not a drug, food, supplement or cosmetic, has not been evaluated by the FDA, and must not be used in humans or animals. Peptides Only does not provide usage or dosing information.
Research summary
Semax is a synthetic seven-amino-acid peptide (Met-Glu-His-Phe-Pro-Gly-Pro) that joins the ACTH(4-7) fragment of adrenocorticotropic hormone to a stabilizing Pro-Gly-Pro tail. It is studied mainly for its effects on brain-derived neurotrophic factor (BDNF) and on gene expression in rodent models of cerebral ischemia, in a literature that comes largely from Russian research groups. Peptides Only supplies Semax as a lyophilized compound for laboratory research only.
- Also known as
- ACTH(4-7)-Pro-Gly-Pro · ACTH(4-7)PGP · MEHFPGP · ACTH(4-10) analog
- Sequence
- Met-Glu-His-Phe-Pro-Gly-Pro
What is Semax?
Semax is a synthetic analog of ACTH(4-10), a fragment of adrenocorticotropic hormone. Its sequence, Met-Glu-His-Phe-Pro-Gly-Pro, keeps the ACTH(4-7) segment and ends in the tripeptide Pro-Gly-Pro, which is why Russian papers often call it ACTH(4-7)PGP1,2.
The Pro-Gly-Pro ending is deliberate. Pro-Gly-Pro belongs to the glyprolines, a peptide family that Moscow physiologists described as far more resistant to breakdown than most regulatory peptides, and Semax and its sister peptide Selank were designed as hybrids that pair an active fragment with this glyproline tail3. Semax is still metabolized: in experiments with tritium-labeled peptide and nerve cells, its main breakdown products were the pentapeptide His-Phe-Pro-Gly-Pro and the tripeptide Pro-Gly-Pro4.
BDNF and TrkB: the most-cited Semax research
The best-known Semax findings concern brain-derived neurotrophic factor (BDNF), a growth factor involved in synaptic plasticity, and its receptor TrkB. In glial cells cultured from the basal forebrain of newborn rats, Semax raised BDNF mRNA about eightfold and NGF mRNA about fivefold, with the largest change at 30 minutes5.
In adult rats given Semax intranasally, BDNF protein rose within three hours in the basal forebrain but not in the cerebellum, and membranes from the basal forebrain showed specific, calcium-dependent binding sites for labeled Semax6. A follow-up study in the rat hippocampus reported increases in BDNF protein, TrkB phosphorylation, and BDNF and TrkB mRNA, together with more conditioned avoidance responses in a learning task1.
These are short-term expression measurements, mostly in healthy rodents. They show that Semax changes neurotrophin signaling in specific brain regions, but the binding site described in rat forebrain has not been tied to a named receptor in these studies6.
Semax in cerebral ischemia models
A second body of work uses rat models of stroke-like injury, chiefly occlusion of the middle cerebral artery. After permanent occlusion, Semax increased transcription of Bdnf, Ngf, Nt-3 and Trk receptor genes in the ischemic cortex at time points from 3 to 72 hours; the Pro-Gly-Pro fragment alone also changed these genes, but in a largely non-specific way2. A genome-wide analysis of the same model found that more than half of the genes Semax altered at 24 hours were immune-related, with further changes in genes linked to blood-vessel formation7.
With transient occlusion followed by reperfusion, RNA sequencing identified 394 genes expressed differently in Semax-treated rats than in saline controls at 24 hours. Semax suppressed inflammation-related genes and activated neurotransmission-related genes, roughly the reverse of the pattern produced by ischemia-reperfusion alone8. These studies measure gene expression at fixed time points; they are not long-term recovery studies.
Enzymes and human imaging studies
In human serum tested in vitro, Semax and Selank both inhibited enkephalin-degrading enzymes more strongly than reference peptidase inhibitors such as puromycin and bacitracin. Because these enzymes also break down other regulatory peptides, the authors proposed this as one route by which the two heptapeptides could act9.
Human data are limited. A resting-state fMRI study in 24 healthy volunteers compared intranasal Semax with placebo and reported a larger rostral subcomponent of the brain's default mode network in the Semax group10. In a Russian study of 110 patients in rehabilitation after ischemic stroke, plasma BDNF levels were higher in the subgroups that received Semax; the abstract does not describe randomization or blinding11.
Limitations of the evidence
Most Semax research comes from a small network of Moscow institutions, especially the Institute of Molecular Genetics of the Russian Academy of Sciences, and much of it appears in Russian-language or Russian-edited journals1,7. Western regulators have not evaluated it: Belgian control-laboratory scientists who identified Semax and Selank in seized preparations described them as research peptides sold online that, to their knowledge, had not completed clinical trials12.
- Most mechanistic data come from rats, often measured hours after a single exposure.
- Human studies are small, and the published abstracts give limited design detail.
- A specific receptor for Semax has not been characterized; the BDNF findings describe associations rather than a defined pathway.
- Semax is not approved by the FDA or the European Medicines Agency.
Sourcing Semax for research
Every Peptides Only lot of Semax is independently tested and ships from the USA with a lot-matched certificate of analysis showing HPLC purity and mass-spec identity, published in our certificate library. Semax is also available with Selank and Pinealon in the Semax / Selank / Pinealon Set.
Semax FAQ
Is Semax approved by the FDA?
No. Semax is not an FDA-approved drug and has not been authorized by the European Medicines Agency. Russian authors describe it as a medicine used in Russia for patients with disorders of cerebral circulation8. Peptides Only sells it strictly as a research compound for laboratory use.
What is the difference between Semax and Selank?
Both are Russian-developed heptapeptides that end in Pro-Gly-Pro, but they start from different parent sequences: Semax from the ACTH(4-7) fragment, Selank from the tuftsin sequence Thr-Lys-Pro-Arg9,3. Semax research centers on BDNF and ischemia models; Selank research centers on GABAergic signaling and stress behavior in rodents. See Semax vs Selank for a side-by-side comparison.
Is Semax the same as ACTH(4-10)?
No. ACTH(4-10) is a natural fragment of adrenocorticotropic hormone (Met-Glu-His-Phe-Arg-Trp-Gly). Semax keeps the first four of those residues and replaces the last three with Pro-Gly-Pro, so the literature describes it as an ACTH(4-10) analog rather than the fragment itself1,2.
Why does most Semax research come from Russia?
Semax was developed by Russian researchers, and nearly all mechanistic studies come from Moscow institutes such as the Institute of Molecular Genetics5,2. That concentration is a reason for caution: independent replication outside Russia is sparse.
How is lyophilized Semax stored?
Like most lyophilized peptides, sealed vials are generally kept cold, dry and protected from light. Our guide to peptide storage and stability covers the general principles.
Further reading
References
- Dolotov OV, Karpenko EA, et al. Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Res. 2006;1117(1):54-60. PubMed 16996037
- Dmitrieva VG, Povarova OV, et al. Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia. Cell Mol Neurobiol. 2010;30(1):71-9. PubMed 19633950
- Ashmarin IP, Samonina GE, et al. Natural and hybrid (chimeric) stable regulatory glyproline peptides. Pathophysiology. 2005;11(4):179-185. PubMed 15837162
- Zolotarev IuA, Dadaian AK, et al. Evenly tritium-labeled peptides and their in vivo and in vitro biodegradation. Bioorg Khim. 2006;32(2):183-91. PubMed 16637290
- Shadrina MI, Dolotov OV, et al. Rapid induction of neurotrophin mRNAs in rat glial cell cultures by Semax, an adrenocorticotropic hormone analog. Neurosci Lett. 2001;308(2):115-8. PubMed 11457573
- Dolotov OV, Karpenko EA, et al. Semax, an analogue of adrenocorticotropin (4-10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain. J Neurochem. 2006;97 Suppl 1:82-6. PubMed 16635254
- Medvedeva EV, Dmitrieva VG, et al. The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis. BMC Genomics. 2014;15:228. PubMed 24661604
- Filippenkov IB, Stavchansky VV, et al. Novel Insights into the Protective Properties of ACTH(4-7)PGP (Semax) Peptide at the Transcriptome Level Following Cerebral Ischaemia-Reperfusion in Rats. Genes (Basel). 2020;11(6):681. PubMed 32580520
- Kost NV, Sokolov OIu, et al. Semax and selank inhibit the enkephalin-degrading enzymes from human serum. Bioorg Khim. 2001;27(3):180-3. PubMed 11443939
- Lebedeva IS, Panikratova YR, et al. Effects of Semax on the Default Mode Network of the Brain. Bull Exp Biol Med. 2018;165(5):653-656. PubMed 30225715
- Gusev EI, Martynov MY, et al. The efficacy of semax in the tretament of patients at different stages of ischemic stroke. Zh Nevrol Psikhiatr Im S S Korsakova. 2018;118(3. Vyp. 2):61-68. PubMed 29798983
- Vanhee C, Francotte A, et al. The occurrence of putative cognitive enhancing research peptides in seized pharmaceutical preparations: An incentive for controlling agencies to prepare for future encounters of the kind. Drug Test Anal. 2020;12(3):371-381. PubMed 31667971
Research summary reviewed 2026-10-26 against the cited literature.
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