A reference work, not a recommendation to use: this profile describes mechanism and evidence and does not replace medical advice. The claims come from marketing and forums and are tested here, not endorsed.

Mechanism of action

Evidence map: Selank

Each line stands for a published finding; line style and color show where it comes from. The filter hides weaker evidence levels. Sources: see references.

Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) [1] is a derivative of the endogenous peptide tuftsin, extended by Pro-Gly-Pro [2]. In Russia it is registered as an anxiolytic [3]. The mechanism described first is inhibition of enkephalin-degrading enzymes: in human plasma, selank inhibited enkephalin degradation with an IC50 of 15 µM, that is, only at micromolar concentrations [1].

The approach most discussed today is the GABA system. In radioligand studies on brain membranes, selank behaved like a positive allosteric modulator of GABA binding; together with benzodiazepines, the result was not an additive but a distinct pattern, and selank blocked the modulating effect of diazepam [4]. After administration to rats, selank altered the expression of numerous neurotransmission genes in the frontal cortex, after one hour with a pattern similar to GABA [5]. In human neuroblastoma cells, by contrast, selank alone did not change gene expression, but it almost completely suppressed the changes triggered by GABA [6]. In mice, depending on the route of administration, selank raised either the GABA binding sites in the frontal cortex (by 38%) or the NMDA binding sites (by 23%); it acted as an anxiolytic only in the more anxious mouse strain [7].

Further findings come from animal experiments: in mice, selank raised noradrenaline in the hypothalamus and altered dopamine and serotonin breakdown products in opposite directions depending on the strain [8]. In rats after long-term alcohol consumption, it improved object recognition and prevented an alcohol-induced rise in BDNF [2]. In the spleen of mice, it lowered the mRNA of complement factor C3 threefold within 30 minutes; the cleavage fragment Gly-Pro acted similarly [9]. Almost all studies come from a few Moscow research groups.

Assigned to the site of action NMDA receptor (GluN1/GluN2B) in the postsynaptic membrane of a dendritic spine; not drawn in its figure: only changed numbers of binding sites (mice).

Assigned to the site of action GABA-A receptor (benzodiazepine, GABA and membrane sites), GABA-B with GIRK, glycine receptor; not drawn in its figure: binding site unresolved.

Targets

TargetTypeActionKey dataEvidence
GABA-A receptor (binding site unresolved)ReceptorPositive modulator Laboratory[4]
Enkephalin-degrading enzymes (plasma)EnzymeInhibitorIC50 15 µM (human plasma) Laboratory[1]
GABA binding sites, frontal cortexReceptorExpression ↑+38% (mouse, intraperitoneal administration) Animal study[7]
NMDA receptor binding sitesReceptorExpression ↑+23% (mouse, intranasal administration) Animal study[7]

Effect profile

Which signaling systems the compound affects according to current data. ↑ enhanced, ↓ dampened, ≈ modulated, ○ no effect; dots = evidence level.

  • Dopaminemodulated · Dopamine breakdown products raised or lowered depending on mouse strain[8]
  • Noradrenaline↑ · Noradrenaline raised in the hypothalamus (two mouse strains)[8]
  • Serotoninmodulated · Serotonin and 5-HIAA lowered in the hippocampus in only one mouse strain[8]
  • Acetylcholineno data
  • Glutamate · AMPAno data
  • Glutamate · NMDAmodulated · more NMDA binding sites after intranasal administration (mouse)[7]
  • GABAmodulated · positive allosteric modulation of GABA binding (laboratory); GABA-like gene patterns and more binding sites (rodent)[4][5][7]
  • Histamineno data
  • Orexinno data
  • Adenosineno data
  • Opioidsmodulated · inhibits enkephalin degradation in plasma (micromolar); longer enkephalin half-life in treated patients[1][11]
  • Melatoninno data
  • Neurotrophinsmodulated · prevented the alcohol-induced BDNF rise (rat)[2]
  • Blood flowno data
  • Nitric oxideno data
  • Energy metabolismno data
  • Insulin · glucoseno data
  • Inflammation · oxidativemodulated · inflammation-related genes altered in the spleen, C3 lowered (mouse)[9]
  • Stress axisno data
  • Testosterone axisno data
  • Endocannabinoidsno data
  • Autophagy · senescenceno data
  • Immune systemno data
  • Lipid metabolismno data
  • Coagulation · fibrinolysisno data
  • Methylationno data

Human studies

  • Generalized anxiety disorder and neurasthenia, comparison with medazepam

    comparative study; indexed in PubMed as an RCT, randomization and blinding not described in the abstract · Patients: generalized anxiety disorder, neurasthenia · n = 62 · not verified

    Measured: Hamilton, Zung and CGI scales; enkephalin half-life in serum

    Result: Anxiolytic effect similar to medazepam; additionally described as anti-asthenic. Enkephalin half-life rose under selank.[11]

    Human, non-randomised

  • Selank in addition to phenazepam in anxiety disorders

    comparative study; indexed in PubMed as an RCT, randomization not described in the abstract · Patients: anxiety, hypochondriacal and somatoform disorders · n = 70 · not verified

    Measured: HDRS, CGI, Spielberger; UKU side effect scale; Stroop and word fluency test; SF-36

    Result: With selank, the effect set in earlier, and side effects of phenazepam such as impairment of attention and memory were smaller.[12]

    Human, non-randomised

  • Resting-state fMRI in healthy people

    placebo-controlled · healthy · n = 52 · Single dose, measurement after 5 and 20 minutes

    Measured: functional connectivity of the amygdala and dorsolateral prefrontal cortex

    Result: Altered connectivity between right amygdala and right temporal lobe; no cognitive tests.[13]

    Human, randomised

Risks and warnings

  • Lack of safety data

    A US review describes selank as a barely studied Russian drug with a GABA-related mechanism, whose abuse potential should be examined before free sale [10].

    No data

  • Unclear identity and purity

    Selank was detected in confiscated, uncontrolled products and is sold online as a powder or nasal spray [14].

    No data

  • Influence on nerve cell differentiation (cell culture)

    At a high concentration (100 µM), selank reduced the proportion of GABA-containing neurons from mouse embryonic stem cells by 61%; the research team nevertheless judged the peptides overall to be nontoxic. Relevance for humans unclear [15].

    Laboratory

Interactions

  • Benzodiazepines (diazepam, phenazepam): In the laboratory, selank altered the effect of benzodiazepines on GABA binding [4]; in patients, it was given together with phenazepam, with earlier onset of effect and fewer side effects [12].
  • Olanzapine: In neuroblastoma cells, selank enhanced the effect of olanzapine on gene expression [6].

Fact check: common claims

  • partly supported

    “Selank is anxiolytic like a benzodiazepine, but without its drawbacks”

    In small Russian comparative studies, similar anxiolytic effect to medazepam [11]; randomization not described. Dependence and withdrawal effects were not studied systematically [10].

  • not supported

    “Selank improves memory and concentration in healthy people”

    Memory findings only in rats [2]; the only study in healthy people contained no cognitive tests [13].

  • not supported

    “Selank raises BDNF”

    In the rat study examined, selank prevented an alcohol-induced BDNF rise instead of raising BDNF [2]. Human data are lacking.

  • not supported

    “Selank strengthens the immune system”

    Only altered expression of immune genes in the mouse spleen [9]; clinical endpoints such as infections were not studied in the studies examined.

Pharmacokinetics

Absorption
In studies, intranasal administration or (in animal experiments) intraperitoneal administration; the activity profile in mice differed depending on the route of administration [7].
Half-life
Not verified.
Metabolism
Peptide cleavage; the fragment Gly-Pro showed effects on immune genes in mice similar to selank [9].
Entry into the brain
Not verified.

Legal status

Germany
No marketing authorization known; not checked in medicines registers.
EU
No marketing authorization known; not verified.
USA
No FDA approval known; according to a review, sold as a dietary supplement in the US [10].
Other countries
Russia: listed as an anxiolytic among the 14 peptide drugs registered there [3].

Related compounds

Semaxsame classN-Acetyl-Semaxsame class (German only)

Open questions

  • At which site of the GABA-A receptor does selank bind, and does it reach effective concentrations in the brain after intranasal administration?
  • Can the anxiolytic effects be confirmed in randomized, blinded studies by independent groups?
  • Does selank have dependence or withdrawal potential, as is known for other GABA-modulating substances?

References

  1. Zozulya AA, Kost NV, Yu Sokolov O, Gabaeva MV, Grivennikov IA, Andreeva LN, et al. The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity. Bull Exp Biol Med. 2001;131(4):315–7. doi:10.1023/a:1017979514274 · PubMed
  2. 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):641–4. doi:10.1007/s10517-019-04588-9 · PubMed
  3. Deigin VI, Poluektova EA, Beniashvili AG, Kozin SA, Poluektov YM. Development of peptide biopharmaceuticals in Russia. Pharmaceutics. 2022;14(4):716. doi:10.3390/pharmaceutics14040716 · PubMed
  4. Vyunova TV, Andreeva L, Shevchenko K, Myasoedov N. Peptide-based anxiolytics: the molecular aspects of heptapeptide Selank biological activity. Protein Pept Lett. 2018;25(10):914–23. doi:10.2174/0929866525666180925144642 · PubMed
  5. Volkova A, Shadrina M, Kolomin T, Andreeva L, Limborska S, Myasoedov N, et al. Selank administration affects the expression of some genes involved in GABAergic neurotransmission. Front Pharmacol. 2016;7:31. doi:10.3389/fphar.2016.00031 · PubMed
  6. Filatova E, Kasian A, Kolomin T, Rybalkina E, Alieva A, Andreeva L, et al. GABA, Selank, and olanzapine affect the expression of genes involved in GABAergic neurotransmission in IMR-32 cells. Front Pharmacol. 2017;8:89. doi:10.3389/fphar.2017.00089 · PubMed
  7. Vasil’eva EV, Kondrakhin EA, Salimov RM, Kovalev GI. [Comparison of pharmacological effects of heptapeptide Selank after intranasal and intraperitoneal administration to BALB/c and C57BL/6 mice]. Eksp Klin Farmakol. 2016;79(9):3–11. PubMed
  8. Narkevich VB, Kudrin VS, Klodt PM, Pokrovskiĭ AA, Kozlovskaia MM, Maĭskiĭ AI, et al. [Effects of heptapeptide selank on the content of monoamines and their metabolites in the brain of BALB/C and C57Bl/6 mice: a comparative study]. Eksp Klin Farmakol. 2008;71(5):8–12. PubMed
  9. Kolomin T, Morozova M, Volkova A, Shadrina M, Andreeva L, Slominsky P, et al. The temporary dynamics of inflammation-related genes expression under tuftsin analog Selank action. Mol Immunol. 2014;58(1):50–5. doi:10.1016/j.molimm.2013.11.002 · PubMed
  10. Doyno CR, White CM. Sedative-hypnotic agents that impact gamma-aminobutyric acid receptors: focus on flunitrazepam, gamma-hydroxybutyric acid, phenibut, and selank. J Clin Pharmacol. 2021;61 Suppl 2:S114–28. doi:10.1002/jcph.1922 · PubMed
  11. Zozulia AA, Neznamov GG, Siuniakov TS, Kost NV, Gabaeva MV, Sokolov OIu, 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. PubMed
  12. Medvedev VE, Tereshchenko ON, Kost NV, Ter-Israelyan AY, Gushanskaya EV, Chobanu IK, et al. [Optimization of the treatment of anxiety disorders with selank]. Zh Nevrol Psikhiatr Im S S Korsakova. 2015;115(6):33–40. doi:10.17116/jnevro20151156133-40 · PubMed
  13. Panikratova YR, Lebedeva IS, Sokolov OY, Rumshiskaya AD, Kupriyanov DA, Kost NV, et al. Functional connectomic approach to studying Selank and Semax effects. Dokl Biol Sci. 2020;490(1):9–11. doi:10.1134/S001249662001007X · PubMed
  14. 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):371–81. doi:10.1002/dta.2717 · PubMed
  15. Kobylyanskii AG, Zolotarev YA, Andreeva LA, Grivennikov IA, Myasoedov NF. Studying the toxic effects of some biologically active peptides on the model of mouse embryonic stem cells. Bull Exp Biol Med. 2017;163(6):731–6. doi:10.1007/s10517-017-3891-y · PubMed
How this profile was checked

Last reviewed: 2026-10-23. All sources with a DOI or PMID were resolved automatically via Crossref or doi.org and PubMed.

Translated from the German profile (version of 2026-10-23); translation checked on 2026-10-26.

Checked

  • All DOIs resolved via Crossref, PMIDs match the DOIs; three Russian papers without a DOI, via PMID only.
  • Key figures checked against abstracts: sequence and IC50 15 µM [1]; object recognition and BDNF [2]; positive allosteric modulation, diazepam blocked [4]; 84 genes, correlation with GABA after 1 h [5]; no effect alone in IMR-32, dampening of the GABA effect, olanzapine [6]; +38% GABA, +23% NMDA binding sites, BALB/c only [7]; noradrenaline, dopamine and serotonin metabolites [8]; C3 threefold after 30 min, Gly-Pro [9]; 62 patients (30 vs. 32), enkephalin half-life [11]; 30 vs. 40 patients, side effects, Stroop [12]; 52 healthy people, placebo, fMRI [13]; “poorly studied Russian drugs … sold … as dietary supplements” [10]; selank in confiscated products [14]; −61% GABA-positive neurons at 100 µM [15].
  • In the full text [3]: 14 peptide drugs registered in Russia, selank as an anxiolytic in Table 1.
  • ClinicalTrials.gov (October 23, 2026): no entry with selank as an intervention; the free-text search returned only irrelevant hits.

Not verified

  • Duration of treatment and exact methodology of [11] and [12] (Russian-language, abstract only); whether randomization actually took place.
  • A Russian brief communication (Inozemtseva 2008, PMID 18841804) describes, according to its title, a regulation of BDNF in the rat hippocampus after intranasal administration; no abstract, therefore not used.
  • Half-life and brain penetration in humans; no verified source found.
  • Authorization status in Germany and the EU not checked in registers.

No dosages, no sources of supply. This information does not replace medical advice.

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