Semax (MEHFPGP) is built on the ACTH(4-7) fragment; Selank (TKPRPGP) is built on the immune peptide tuftsin. Both end in the same Pro-Gly-Pro tail.
Semax research centres on experimental stroke, BDNF signalling and learning; Selank research centres on anxiety models, GABA-A receptor binding and GABAergic gene expression.
Direct comparisons are rare: an in vitro enzyme study and one small fMRI study in 52 healthy volunteers.
Both are listed as medicines in Russia; neither is FDA-approved, authorised through the EU centralised procedure or named in Australia's Poisons Standard.
The human evidence for both is small, Russian-language and not placebo-controlled, so neither can be called better than the other.
Semax vs Selank comes down to parent molecule and research focus. Both are synthetic seven-amino-acid peptides developed in Russia, and both end in the same Pro-Gly-Pro tail, but Semax is built on a fragment of the hormone ACTH1 while Selank is built on the immune peptide tuftsin2. In Russia, Selank is approved for anxiety and Semax has been used for neurological conditions including ischaemic stroke3; neither is an FDA-approved drug4, neither is authorised through the EU's centralised procedure5, and neither is named in Australia's Poisons Standard6.
Because the two are so often mentioned in the same breath, it is easy to assume they are variations on one compound. They are not. This comparison sets out how they differ in structure, in the models they have been studied in, in the mechanisms proposed for them and in the quality of the evidence behind each.
Semax vs Selank at a glance
Chemical identifiers are as listed by PubChem.7,8 The other rows summarise the studies discussed below.
Semax
Selank
Sequence
Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP)
Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP)
Parent molecule
ACTH(4-7), a fragment of adrenocorticotropic hormone
Tuftsin (Thr-Lys-Pro-Arg), a fragment of the immunoglobulin G heavy chain
Molecular formula
C37H51N9O10S
C33H57N11O9
Molar mass
813.9 g/mol
751.9 g/mol
CAS number
80714-61-0
129954-34-3
PubChem CID
9811102
11765600
Main research models
Experimental stroke in rats; learning tasks; neurotrophin signalling
Rodent anxiety and stress models; GABAergic gene expression
Leading proposed mechanism
Raised BDNF and trkB activation
Allosteric modulation of GABA-A binding; inhibition of enkephalin breakdown
Human evidence
Small Russian-language stroke studies
Small Russian-language anxiety trials against benzodiazepines
The same stabilising tail. Both peptides were built by attaching the tripeptide Pro-Gly-Pro, a "glyproline", to a short natural peptide. In Semax the tail increases resistance to peptidases1; in Selank it was added to improve metabolic stability and prolong action.2 The tail is the design feature intended to help both short peptides survive enzymatic breakdown for longer.
The same scientific home. Selank was designed at the Institute of Molecular Genetics of the Russian Academy of Sciences with the Zakusov Research Institute of Pharmacology2, and much of the Semax literature comes from the same institute and its collaborators.10 That shared origin is why the two are paired, and it is also a shared weakness: independent replication outside this network is limited for both.
Medicine status in Russia only. Semax is on Russia's list of vital and essential medicines1 and Selank is described as approved there for anxiety.3 Outside Russia, both are research compounds.
Where Semax and Selank differ
Parent molecule
Semax takes positions 4 to 7 of ACTH (Met-Glu-His-Phe). ACTH is a pituitary hormone, but Semax is reported to have no hormonal activity.1 Selank takes tuftsin, a four-residue fragment of the heavy chain of human immunoglobulin G with immunomodulatory properties.2,3 The two parent peptides share no sequence, so any overlap in reported effects cannot be put down to a common active motif other than the tail.
Semax research concentrates on the brain's response to injury and on learning. A representative 2006 rat study reported that a single application of Semax raised hippocampal BDNF protein about 1.4-fold and increased activation of its receptor, trkB, alongside more conditioned avoidance responses.10 Much of the rest of the Semax literature measures gene expression after experimental stroke.
Selank research concentrates on anxiety-like behaviour. A 2018 radioligand study reported that Selank altered GABA binding in brain membrane preparations in a way consistent with positive allosteric modulation of GABA-A receptors, the site where benzodiazepines act.11 A 2016 rat study reported expression changes in 45 of 84 neurotransmission-related genes in the frontal cortex one hour after Selank, changes that correlated with those produced by GABA itself.2
How each has been tested
The models differ as much as the molecules. Semax stroke studies typically use middle cerebral artery occlusion in rats, in which one of the brain's main arteries is blocked permanently or for a set time, then measure infarct size, behaviour or gene expression at fixed intervals. Selank studies lean on behavioural paradigms such as the elevated plus maze, which scores how much time a rodent spends in the open arms of a raised platform, often after weeks of unpredictable mild stress. Results from one family of models say little about the other, which is one reason the two literatures rarely meet.
In other words, Semax is studied mainly as a neurotrophic and neuroprotective candidate and Selank mainly as an anxiolytic candidate. Both descriptions come from preclinical work.
Studies that tested Semax and Selank side by side
Head-to-head data are scarce. Two studies stand out.
Enkephalin-degrading enzymes, 2001. Working with human serum in vitro, a Moscow group reported that both peptides inhibited the enzymes that break down enkephalins, with IC50 values of 10 µM for Semax and 20 µM for Selank, more potent than the reference inhibitor puromycin. Five-residue fragments of each were also active; shorter fragments were not.12 This is the clearest mechanistic overlap between the two, though it was shown only in a test tube and at micromolar concentrations.
Brain connectivity imaging, 2020. In 52 healthy participants, resting-state functional MRI was recorded before and 5 and 20 minutes after administration of Semax, Selank or placebo. The authors reported between-group differences in connectivity between the right amygdala and regions of the right temporal cortex, with some effects shared by both peptides and some specific to each.13 It is a short communication with a small sample, and connectivity changes are not the same as functional effects.
What is missing is the obvious experiment: both peptides tested in the same animal model, at matched molar amounts, alongside a Pro-Gly-Pro-only control, with blinded scoring. None of the studies reviewed here used that design, so claims that one peptide outperforms the other in any model rest on comparisons across different papers, laboratories and methods.
Human evidence compared
For both peptides the clinical literature is small and published mostly in Russian.
Semax has been studied in people after ischaemic stroke. In a 2018 study, 110 patients in early or late rehabilitation were subdivided by whether they received Semax; the authors reported higher plasma BDNF and better Barthel index recovery in the Semax subgroups. The abstract does not describe randomisation, blinding or a placebo.14
Selank has been studied in anxiety-related disorders, with benzodiazepines as comparators. In a 2008 study, 62 patients with generalised anxiety disorder or neurasthenia received Selank or medazepam, and the authors reported similar anxiolytic effects in both groups.15 Clinical studies have been described as showing a spectrum of effects similar to benzodiazepines such as diazepam and phenazepam.2
Neither peptide has a trial registered on ClinicalTrials.gov (searched September 2026), and neither has been tested in the kind of large, independent, placebo-controlled trial that would support firm conclusions. That is why the popular question "which is better?" has no evidence-based answer.
Common misconceptions about Semax and Selank
"They are the same peptide in different forms." They share only the Pro-Gly-Pro tail. The active parent sequences, ACTH(4-7) and tuftsin, are unrelated.1,2
"Semax is a hormone because it comes from ACTH." Semax contains an ACTH fragment, but it is reported to have no hormonal activity.1
"Selank is a kind of benzodiazepine." Selank is a peptide, not a benzodiazepine. One laboratory study proposes that it modulates GABA-A receptor binding allosterically, and that its binding site differs from, though may partly overlap with, that of diazepam.11
"Approval in Russia means approval elsewhere." It does not. Neither peptide is FDA-approved or authorised through the EU centralised procedure.4,5
"Research-grade material is the Russian medicine." A lyophilised research compound is not the registered Russian product and has not been evaluated by any regulator as a medicine.
Regulatory status side by side
Russia: Semax is on the list of vital and essential medicines1; Selank is described as approved for anxiety.3
United States: neither is FDA-approved.4 The FDA's page on bulk substances that may present significant safety risks lists both "semax (heptapeptide)" and "selank acetate (TP-7)" as substances previously in category 2 whose nominations were withdrawn, and says the agency lacks sufficient or important safety information for each.9
European Union: no centrally authorised medicine contains either.5
Australia: neither is named in the June 2026 Poisons Standard.6
Choosing between them as research tools
For laboratory researchers the choice follows the question being asked. Work on ischaemia models, neurotrophin signalling or learning tasks has more Semax precedent to build on. Work on anxiety-like behaviour, GABAergic transmission, enkephalin metabolism or immune gene expression has more Selank precedent. Because both carry the same Pro-Gly-Pro tail, comparative designs benefit from controls that separate the effect of the tail from the effect of the parent sequence.
One practical point for comparative work: equal masses are not equal amounts. Using the PubChem molar masses, 1 mg of Semax free peptide is about 1.229 µmol, while 1 mg of Selank is about 1.330 µmol, roughly 8% more molecules. Salt forms such as acetates, and residual water, shift the real figures further, so equimolar designs should be calculated from each lot's stated net peptide content rather than from the label mass.7,8
Chemical stability also differs. Semax contains methionine, an amino acid whose sulphur-containing side chain is prone to oxidation; Selank's sequence has no methionine, cysteine or tryptophan. That can matter for storage and for solution stability over long experiments; see how to store peptides.
They are built on different natural peptides. Semax adds a Pro-Gly-Pro tail to ACTH(4-7), a fragment of the hormone ACTH, while Selank adds the same tail to tuftsin, a fragment of immunoglobulin G. Semax research focuses on experimental stroke and BDNF signalling; Selank research focuses on rodent anxiety models and GABA-A receptor binding.
Is Semax or Selank better?
There is no evidence-based answer. The two have never been compared in a large controlled trial, and their human studies are small, Russian-language and not placebo-controlled. They have mostly been studied in different models, so the useful question for researchers is which compound has more precedent for the model and endpoint being investigated.
Have Semax and Selank been compared directly?
Rarely. A 2001 in vitro study found that both inhibited enkephalin-degrading enzymes in human serum, with IC50 values of 10 µM for Semax and 20 µM for Selank. A 2020 imaging study in 52 healthy volunteers reported shared and distinct changes in amygdala connectivity after each peptide compared with placebo.
Are Semax and Selank approved anywhere?
In Russia, Semax is on the list of vital and essential medicines and Selank is described as approved for anxiety. Neither is FDA-approved, neither is authorised through the EU centralised procedure, and neither is named in Australia's June 2026 Poisons Standard. Research-grade material is supplied for laboratory research only.
Why do Semax and Selank both end in Pro-Gly-Pro?
Pro-Gly-Pro is a glyproline tripeptide that the developers attached to both parent peptides to improve metabolic stability. According to papers from the developing institute, the tail increases resistance to peptidases, the enzymes that cut peptides apart, and lengthens duration of action. It is the main structural feature the two peptides share.
References
Radchenko AI, et al. The Potential of the Peptide Drug Semax and Its Derivative for Correcting Pathological Impairments in the Animal Model of Alzheimer's Disease. Acta Naturae. 2025;17(4):110-120. PubMed 41479572
Volkova A, et al. Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Front Pharmacol. 2016;7:31. PubMed 26924987
Rahman OF, et al. Therapeutic Peptides in Orthopaedics: Applications, Challenges, and Future Directions. J Am Acad Orthop Surg Glob Res Rev. 2026;10(1). PubMed 41490200
U.S. Food and Drug Administration. Drugs@FDA: FDA-Approved Drugs database. Searched for "semax" and "selank" via the openFDA drugsfda endpoint, 21 September 2026: no matching products. Source
European Medicines Agency. Medicines data (human and veterinary medicines JSON report), retrieved 21 September 2026: 2,746 records, none containing semax or selank. Source
Therapeutic Goods (Poisons Standard—June 2026) Instrument 2026 (SUSMP No. 48), F2026L00633, commenced 1 June 2026. Federal Register of Legislation. Source
National Center for Biotechnology Information. PubChem Compound Summary for CID 9811102, Semax. Accessed 21 September 2026. Source
National Center for Biotechnology Information. PubChem Compound Summary for CID 11765600, Selank. Accessed 21 September 2026. Source
U.S. Food and Drug Administration. Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks. Content current as of 22 April 2026. Source
Dolotov OV, 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
Vyunova TV, et al. Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. Protein Pept Lett. 2018;25(10):914-923. PubMed 30255741
Kost NV, et al. [Semax and selank inhibit the enkephalin-degrading enzymes from human serum]. Bioorg Khim. 2001;27(3):180-183. Article in Russian. PubMed 11443939
Panikratova YR, et al. Functional Connectomic Approach to Studying Selank and Semax Effects. Dokl Biol Sci. 2020;490(1):9-11. PubMed 32342318
Gusev EI, et al. [The efficacy of semax in the treatment of patients at different stages of ischemic stroke]. Zh Nevrol Psikhiatr Im S S Korsakova. 2018;118(3 Vyp 2):61-68. Article in Russian. PubMed 29798983
Zozulia AA, et al. [Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia]. Zh Nevrol Psikhiatr Im S S Korsakova. 2008;108(4):38-48. Article in Russian. PubMed 18454096
Research use only. This article summarises published scientific literature
for educational purposes. It is not medical advice and does not describe or endorse human
or veterinary use. Compounds supplied by Titan Peptides are for laboratory research only
and are not approved therapeutic goods in Australia.
Semax is a seven-amino-acid ACTH fragment analogue listed as an essential medicine in Russia but not approved in the US or EU. Here is what the rodent and small clinical studies report, and how much weight they can bear.
Selank is a seven-amino-acid analogue of the immune peptide tuftsin, approved in Russia as an anti-anxiety medicine but not in the US or EU. This is what the published studies report, and how far they go.
A plain-English primer on research peptides: what a peptide is, how peptides are built one amino acid at a time on a resin bead, why they arrive as a freeze-dried powder, and what "research use only" does and does not mean.