Semax vs Selank: differences, evidence and regulatory status

Last reviewed 26 August 2026

Two 10 mg vials of white lyophilised powder, each holding a synthetic heptapeptide. Both peptides were designed at the same Moscow institute. Both end in the same three residues. Both are registered medicines in one country, and no marketing authorisation for either was identified anywhere else. Almost everything a comparison of the pair can honestly establish sits in that last sentence.

What follows compares two molecules and two regulatory records: what each sequence is, what it was derived from, why one of them travels under four different names in the indexed literature, and where each is registered. No amount, frequency or route appears below; the working vocabulary is reconstitution, solution and concentration.

The two molecules, side by side

Both mass figures are for the free peptide; a counterion contributes mass these numbers exclude, which is one legitimate reason a certificate figure and a figure calculated from a sequence disagree. The notation conventions used above are set out in peptide nomenclature.

One design, two different parents

Set the sequences under one another and the relationship is immediate. Each is a naturally occurring tetrapeptide carrying the same three appended residues:

• Semax = Met–Glu–His–Phe (ACTH 4–7) + Pro–Gly–Pro
• Selank = Thr–Lys–Pro–Arg (tuftsin) + Pro–Gly–Pro

Pro–Gly–Pro is not decorative. Stavchansky and colleagues (2022) state the rationale in one line: The Pro-Gly-Pro (PGP) tripeptide is an active factor of resistance to the biodegradation of peptide drugs. What the two do not share is the parent: one tetrapeptide is a fragment of a pituitary hormone, the other a fragment of an antibody. The same stabilising strategy was applied to two unrelated pieces of biology, and a shared C-terminal motif is the whole of the structural resemblance.

Why one heptapeptide carries four designations

Searching for Semax is harder than it should be, because the indexed record uses at least four names for one molecule: Semax; ACTH(4–7)–PGP, the form PubChem files it under and the form Liu and colleagues (2025) use when they describe a synthetic heptapeptide, comprising the ACTH (4-7) fragment and a C-terminal Pro-Gly-Pro tripeptide; synthetic ACTH(4–10) analogue, the designation in the title of Glazova and colleagues (2021); and ACTH4-10Pro⁸-Gly⁹-Pro¹⁰, used throughout by Indharty (2013), a paper in which the trade name itself appears once, in a parenthesis in the methods.

The second and third look contradictory and are not. Corticotropin runs Ser–Tyr–Ser–Met–Glu–His–Phe–Arg–Trp–Gly…, so ACTH(4–10) is Met–Glu–His–Phe–Arg–Trp–Gly — itself a heptapeptide. Semax is also seven residues, so it is not ACTH(4–10) with a tripeptide added; that arithmetic gives ten. It is ACTH(4–10) with positions 8, 9 and 10 replaced by Pro, Gly and Pro, which is what the fourth designation spells out and what the second describes from the other end. The practical consequence is mundane: a search on any one of the four returns an incomplete set.

What the substitution removes

The replaced residues are not arbitrary. Fridmanis and colleagues (2017), reviewing melanocortin receptor specificity, record that All MCs share an identical –H–F–R–W– pharmacophore sequence, and separately that The –K–K–R–R–P– motif within adrenocorticotropic hormone (ACTH) is considered the second pharmacophore and is required for successful activation of adrenocorticotropic hormone receptor.

Read against MEHFPGP as sequence arithmetic: His and Phe are present, and Arg and Trp — the other half of that four-residue motif — are exactly what the substitution removed. The K–K–R–R–P motif sits at corticotropin positions 15 to 19, so no seven-residue construct beginning at position 4 could contain it in any case. Consistent with this, Indharty (2013) describes the compound as a synthetic short fragment of ACTH devoid of hormonal effects.

Tuftsin, and what Selank adds to it

Tuftsin has the longer pedigree. Navolotskaya (2014) describes its 1970 discovery as the endogenous tetrapeptide tuftsin (Thr-Lys-Pro-Arg, fragment 289-292 of the C(H2)-domain of the heavy (H) chain of IgG) and dates a whole search programme into peptides of immunoglobulin origin from it. Volkova and colleagues (2016) put the derivation plainly — Selank is a synthetic analog of the endogenous tuftsin molecule … which was elongated at the C terminus — and describe their material as the diacetate salt. Filatova and colleagues (2017) record that it was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, the same institute Deigin and colleagues (2022) name for Semax.

The regulatory records, which is where the two actually differ

Deigin and colleagues (2022), reviewing peptide biopharmaceutical development in Russia, write that 14 products are registered in the Russian Federation and list both compounds in the accompanying table of peptide drugs developed there, classifying Semax as a Nootropic drug and Selank as an Anxiolytic. That is a statement about a national register, and its scope is exactly that: a medicine registered in one jurisdiction is registered in that jurisdiction and confers nothing elsewhere.

No marketing authorisation was identified for either compound in the United Kingdom, the European Union or the United States. That is a search result rather than a proven negative, and is stated as one. The UK position for material of this kind turns on the attachment of a claim rather than on the identity of a molecule, and is set out in the MHRA position.

The records then diverge again, recently enough to be easy to miss. At its meeting of 23–24 July 2026, the United States Food and Drug Administration’s Pharmacy Compounding Advisory Committee voted 8–5, with one abstention, in favour of recommending Semax for inclusion on the section 503A Bulks List. Selank was not among the substances considered. Three qualifications matter more than the headline: the committee’s votes are recommendations and are not binding on the FDA; a 503A listing governs eligibility for use as a bulk substance in US pharmacy compounding and is not a marketing authorisation; and it has no effect in the United Kingdom.

The one European laboratory record

Vanhee and colleagues (2020) reported encountering two suspicious pharmaceutical preparations, in late 2017 and in 2018, containing Selank and Semax. They developed a liquid chromatography–tandem mass spectrometry method for peptides of this class and applied it to ten polypeptides then marketed online, following the General European Official Medicines Control Laboratory network’s recommendations for interpreting mass spectrometry results for unknown peptides. Their stated purpose, in the paper’s own subtitle, was An incentive for controlling agencies to prepare for future encounters of the kind. It is the only European control-laboratory record identified for either compound, and it names both.

The shape of the published literature

Volume is measurable, so it is reported as a measurement. All figures were obtained on 9 August 2026 from PubMed title/abstract searches and the ClinicalTrials.gov intervention field.

A count measures volume and nothing else — not quality, not direction, not replication — and the Semax figure is a floor rather than a total, for the four-designations reason above. What follows reports individual studies, grouped by the class of model each used.

In vitro

• Filatova and colleagues (2017) measured 84 genes involved in GABAergic neurotransmission in cultured IMR-32 human neuroblastoma cells exposed to GABA, olanzapine, Selank and combinations. They reported that Selank has no direct effect on the mRNA levels of the GABAergic system genes in neuroblastoma IMR-32 cells, and that with GABA it led to nearly complete suppression of changes in expression of genes in which mRNA levels changed under the effect of GABA.
• Sciacca and colleagues (2022) examined Semax in cell-free and cell-based systems using thioflavin T fluorescence, differential scanning calorimetry, dye leakage from lipid vesicles and an MTT viability assay. They reported that the peptide interfered with fibrillogenesis of amyloid-β:Cu²⁺ complexes, and reported anti-aggregating properties especially in the presence of Cu²⁺.

Rodent models

• Medvedeva and colleagues (2014) compared brain gene expression in Wistar rats subjected to permanent middle cerebral artery occlusion, with and without the peptide, at 3 and 24 hours. They reported that the transcripts whose expression changed were predominantly immune-system genes — over half of the altered genes at 24 hours — alongside a further set associated with vascular development.
• Stavchansky and colleagues (2022) compared PGP, PGP–Leu and Semax in Wistar rats subjected to transient middle cerebral artery occlusion, measuring gene expression by real-time RT-PCR at 24 hours.
• Volkova and colleagues (2016) measured 84 neurotransmission-related genes in rat frontal cortex at two time points after administration of Selank or of GABA. They reported significant changes in 45 genes at the earlier point and 22 at the later, and a positive correlation between the changes produced by the two agents.
• Kolik and colleagues (2019) examined outbred rats maintained on ethanol as their sole fluid source, using an object recognition task and measuring BDNF in hippocampus and prefrontal cortex. They reported what they described as a cognitive-stimulating effect in nine-month-old animals not exposed to ethanol, and reported that Selank blocked the ethanol-associated rise in BDNF content in both regions.

Human studies

• Serdiuk and colleagues (2007) studied 27 patients with motor neurone disease; PubMed types the record as a randomised controlled trial. They reported that semax does not influence either the course of CPD or the dynamics of clinical estimates — chronic partial denervation, assessed by needle electromyography alongside the Norris ALS, ALSFRS and ALSAQ-40 scales — while reporting a change in the total quality-of-life score.
• Zozulia and colleagues (2008) studied 62 patients with generalised anxiety disorder and neurasthenia, comparing selank in 30 against medazepam in 32 using psychometric instruments and serum enkephalin activity. They reported comparable anxiety measures between the two agents, and reported additional effects they characterised as antiasthenic and psychostimulant.
• Medvedev and colleagues (2015) studied 70 patients with anxiety-phobic, hypochondriac and somatoform disorders, comparing phenazepam alone in 30 against selank with phenazepam in 40, and reported that the combined arm decreased the level of undesirable side-effects.
• Gusev and colleagues (2018) studied 110 patients at early and late rehabilitation intervals after ischaemic stroke, measuring plasma BDNF alongside the Medical Research Council motor scale and the Barthel index. They reported that Administration of semax, regardless of the timing of rehabilitation, increased BDNF plasma levels.
• Indharty (2013) studied 40 consecutive patients with moderate head injury in a prospective comparative design, measuring serum Bcl-2. The compound is designated ACTH4-10Pro⁸-Gly⁹-Pro¹⁰ throughout; the name Semax appears once, in a parenthesis in the methods, and the one-letter sequence MEHFPGP once, which is what fixes the identification.

What this literature does not contain

• No systematic review and no meta-analysis of either compound is indexed in PubMed.
• No study of either is registered on ClinicalTrials.gov. Russian trials are commonly registered nationally instead, so this is a statement about one register rather than about the existence of trials.
• The human reports cluster tightly. Four of the five above were published in Russian, and all four appeared in the same journal, Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova.
• Authorship concentrates. N. F. Myasoedov is an author on eight of the works cited here, spanning both compounds and both the human and the animal literature, and Deigin and colleagues (2022) record Semax as synthesised by scientists at the Institute of Molecular Genetics of the RAS under the guidance of two academicians, I. P. Ashmarin and N. F. Myasoedov.
• No independent replication outside that group was identified for any of the human findings above.

None of that is a finding against either compound. An absence of data is an absence of data, and it constrains what can be said in either direction. How evidence of this shape is graded, and why a grade is a property of the literature rather than of the material, is set out in the grading method.

Anti-doping status, which this page does not settle

Category S0 of the WADA Prohibited List covers, in the wording reproduced by national anti-doping authorities, all pharmacological substances which are not addressed by any of the sections of the Prohibited List and have no current approval by any governmental regulatory health authority for human therapeutic use.

The operative question is therefore narrow, and genuinely unresolved on the face of the rule: both compounds hold registration with the health authority of the Russian Federation, and whether that answers the phrase any governmental regulatory health authority is a determination for an anti-doping organisation, not something a reference page should assert. A ruling under a particular code comes from the relevant organisation or from Global DRO; it cannot be inferred from a structural resemblance in either direction.

Four things a side-by-side comparison cannot establish

1. Which is the better compound. The two literatures use different models, endpoints and comparators, and no study has compared them against one another.
2. That Russian registration travels. A national register records one authority’s decision under one legal framework. Neither compound has an equivalent record elsewhere.
3. That the July 2026 committee vote changed anything. It was non-binding, concerned US compounding eligibility rather than approval, and Selank was not before the committee at all.
4. That a shared tail implies shared behaviour. Pro–Gly–Pro was appended to both for stability; the tetrapeptides it was appended to are unrelated in origin.

Handling, storage and the arithmetic

The two are handled identically, because handling follows from physical form rather than from sequence. Both are supplied as 10 mg of lyophilised powder in a sealed vial, without diluent, stored sealed at −20 °C and protected from light; short periods at 2–8 °C in transit do not affect lyophilised material, and once in solution the material is held at 2–8 °C and not frozen. The wider picture is in the storage and stability reference.

Reconstitution arithmetic is likewise indifferent to which of the two is in the vial: concentration is the mass of solid divided by the volume of diluent, so 10 mg into 2 ml gives 5 mg/ml and the same 10 mg into 1 ml gives 10 mg/ml. A preserved or unpreserved diluent changes the composition of the liquid, not that relation — the difference is set out in the diluent comparison. The reconstitution calculator resolves vial strength against diluent volume, and its presets fill in strength only: the volume is ours to calculate, a target amount is not, and the calculator does not produce one.

The two presentations in this catalogue

• Semax 10mg (XA10) — 10 mg lyophilised powder, sealed vial. Technical reference: the Semax library entry.
• Selank 10mg (SK10) — 10 mg lyophilised powder, sealed vial. Technical reference: the Selank library entry.

Both sit in the Cognitive & Nootropic catalogue category, and both carry the same purity statement: Third-party tested at greater than 99% purity. That is a statement about composition, not a statement that either compound does anything.

References

1. National Center for Biotechnology Information. PubChem Compound Summary for CID 9811102, ACTH (4-7), Pro-Gly-Pro- (Semax). Chemical database record.
2. National Center for Biotechnology Information. PubChem Compound Summary for CID 11765600, Selank. Chemical database record.
3. UniProt Consortium. UniProtKB entry P01189, Pro-opiomelanocortin, Homo sapiens; corticotropin chain, residues 138–176. Sequence database record.
4. Fridmanis D, Roga A, Klovins J. ACTH receptor (MC2R) specificity: what do we know about underlying molecular mechanisms? Front Endocrinol (Lausanne). 2017;8:13. PMID 28220105. DOI 10.3389/fendo.2017.00013. Review.
5. Navolotskaya EV. The second life of antibodies. Biochemistry (Mosc). 2014;79(1):1–7. PMID 24512657. DOI 10.1134/S0006297914010015. Review.
6. Deigin VI, Poluektova EA, Beniashvili AG, Kozin SA, Poluektov YM. Development of peptide biopharmaceuticals in Russia. Pharmaceutics. 2022;14(4):716. PMID 35456550. DOI 10.3390/pharmaceutics14040716. Review; includes a table of peptide products registered in the Russian Federation.
7. Liu R, Chen Y, Huang H, et al. Semax peptide targets the mu opioid receptor gene Oprm1 to promote deubiquitination and functional recovery after spinal cord injury in female mice. Br J Pharmacol. 2025;182(22):5489–5516. PMID 40692165. DOI 10.1111/bph.70122. Rodent (female C57BL/6 mice); cited here for its definitional opening sentence only.
8. Glazova NY, Manchenko DM, Volodina MA, et al. Semax, synthetic ACTH(4-10) analogue, attenuates behavioural and neurochemical alterations following early-life fluvoxamine exposure in white rats. Neuropeptides. 2021;86:102114. PMID 33418449. DOI 10.1016/j.npep.2020.102114. Rodent; cited here for its title designation only.
9. Indharty RS. The increase of serum Bcl-2 concentration in moderate head injury outcome: the role of ACTH4-10Pro(8)-Gly(9)-Pro(10). Asian J Neurosurg. 2013;8(2):83–89. PMID 24049550. DOI 10.4103/1793-5482.116381. Human trial; the paper designates the compound ACTH4-10Pro(8)-Gly(9)-Pro(10) throughout and names Semax once.
10. Stavchansky VV, Filippenkov IB, Remizova JA, et al. Insight into glyproline peptides’ activity through the modulation of the inflammatory and neurosignaling genetic response following cerebral ischemia-reperfusion. Genes (Basel). 2022;13(12):2380. PMID 36553646. DOI 10.3390/genes13122380. Rodent (Wistar rat, transient MCAO).
11. Medvedeva EV, Dmitrieva VG, Povarova OV, 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. PMID 24661604. DOI 10.1186/1471-2164-15-228. Rodent (Wistar rat, permanent MCAO).
12. Sciacca MFM, Naletova I, Giuffrida ML, Attanasio F. Semax, a synthetic regulatory peptide, affects copper-induced Aβ aggregation and amyloid formation in artificial membrane models. ACS Chem Neurosci. 2022;13(4):486–496. PMID 35080861. DOI 10.1021/acschemneuro.1c00707. In vitro and cell-free.
13. Volkova A, Shadrina M, Kolomin T, et al. Selank administration affects the expression of some genes involved in GABAergic neurotransmission. Front Pharmacol. 2016;7:31. PMID 26924987. DOI 10.3389/fphar.2016.00031. Rodent.
14. Filatova E, Kasian A, Kolomin T, et al. GABA, Selank, and olanzapine affect the expression of genes involved in GABAergic neurotransmission in IMR-32 cells. Front Pharmacol. 2017;8:89. PMID 28293190. DOI 10.3389/fphar.2017.00089. In vitro (human IMR-32 neuroblastoma cell line).
15. Kolik LG, Nadorova AV, Antipova TA, Kruglov SV, Kudrin VS, Durnev AD. Selank, peptide analogue of tuftsin, protects against ethanol-induced memory impairment by regulating of BDNF content in the hippocampus and prefrontal cortex in rats. Bull Exp Biol Med. 2019;167(5):641–644. PMID 31625062. DOI 10.1007/s10517-019-04588-9. Rodent.
16. Serdiuk AV, Levitskiï GN, Miasoedov NF, Skvortsova VI. [The study of chronic partial denervation and quality of life in patients with motor neuron disease treated with semax.] Zh Nevrol Psikhiatr Im S S Korsakova. 2007;107(4):29–39. PMID 18379501. Russian. Human trial (randomised controlled trial, comparative study; n = 27).
17. Zozulia AA, Neznamov GG, Siuniakov TS, 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. PMID 18454096. Russian. Human trial (n = 62).
18. Medvedev VE, Tereshchenko ON, Kost NV, et al. [Optimization of the treatment of anxiety disorders with selank.] Zh Nevrol Psikhiatr Im S S Korsakova. 2015;115(6):33–40. PMID 26356395. DOI 10.17116/jnevro20151156133-40. Russian. Human trial (n = 70).
19. Gusev EI, Martynov MY, Kostenko EV, Petrova LV, Bobyreva SN. [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 Pt 2):61–68. PMID 29798983. DOI 10.17116/jnevro20181183261-68. Russian. Human trial (n = 110).
20. Vanhee C, Francotte A, Janvier S, Deconinck E. 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. PMID 31667971. DOI 10.1002/dta.2717. Analytical and regulatory laboratory study.
21. United States Food and Drug Administration, Pharmacy Compounding Advisory Committee. Meeting of 23–24 July 2026; vote on inclusion of Semax on the section 503A Bulks List. Regulatory proceeding. Vote tally and non-binding status as reported by the Regulatory Affairs Professionals Society and the National Community Pharmacists Association; FDA’s own briefing document did not resolve to automated retrieval and has not been read directly.
22. World Anti-Doping Agency. Prohibited List, category S0, Non-approved substances. Regulatory document; wording taken from a national anti-doping authority’s reproduction, the WADA PDF having yielded no text to automated retrieval.
23. PubMed and ClinicalTrials.gov record counts in the table above were obtained on 9 August 2026 using title/abstract and intervention-field queries respectively. Database queries.