Selank

01 · What it is

Selank is built on exactly the same template as Semax — a short natural bioactive peptide with Pro-Gly-Pro bolted onto the end — and the most consequential fact in its literature is one the marketing never mentions: in rats, it potentiates diazepam.

Selank is the heptapeptide Thr-Lys-Pro-Arg-Pro-Gly-Pro. The first four residues are tuftsin, an immunomodulatory tetrapeptide released from the heavy chain of immunoglobulin G, and the last three are the same Pro-Gly-Pro tail the same Moscow institute added to ACTH(4-7) to make Semax. PubMed indexes it under the designation TP-7.

The template is worth naming explicitly because it is the group’s signature. Take a fragment of a natural regulatory molecule, add Pro-Gly-Pro to slow proteolysis, and study the result. Two of the compounds in this family were made that way, and in Semax’s case the tripeptide tail turned out to reproduce the parent’s headline effect on its own. Whether the same is true here has not been tested: no study in this file compares Selank against Pro-Gly-Pro.

The claim is anxiolysis, and the mechanism runs through GABA. Selank administration affects the expression of genes involved in GABAergic neurotransmission ¹¹, an effect examined further in IMR-32 neuroblastoma cells alongside GABA itself and olanzapine ¹³. Selank also affects spontaneous synaptic activity in rat hippocampal CA1 neurons ¹⁴.

And this is the finding that matters. In rats under unpredictable chronic mild stress, Selank enhanced the anxiety-reducing effect of diazepam ¹². That is a pharmacodynamic interaction with a benzodiazepine, reported by the developing group in an English-language journal, and it is the single most safety-relevant result about this compound. A substance that potentiates benzodiazepines is a substance whose combination with them is not neutral.

The human evidence is one Russian-language clinical trial. A 2015 paper on optimising the treatment of anxiety disorders with Selank is indexed by PubMed as a clinical trial ⁹. This guide has not read it — it is in Russian and its abstract is not indexed in English. Alongside it sits the connectomic imaging study of 52 healthy participants that also covered Semax ¹⁹.

Everything else is rats. Adaptive behaviour under stress ², conditioned avoidance ¹, depression models ³, serotonin metabolism compared against tuftsin ⁴, learning and memory ⁵, inflammation gene expression in spleen ⁶ and its time course ⁸, hippocampal transcriptome ⁷, liver morphology under foot-shock stress ¹⁷, large intestine morphology under restraint stress ²⁰, cytokines under social stress ²¹, ethanol-induced memory impairment with BDNF measurement ¹⁸, and morphine withdrawal ²².

02 · Evidence at a glance

Evidence grade

Early Clinical — one indexed human clinical trial, Russian-language, not read for this guide ⁹

Structure

Thr-Lys-Pro-Arg-Pro-Gly-Pro — tuftsin plus Pro-Gly-Pro; indexed as TP-7

Parent fragment

Tuftsin, an immunomodulatory tetrapeptide from the IgG heavy chain ¹⁵

Design template

Identical to Semax: natural fragment + Pro-Gly-Pro for protease resistance

Origin

Institute of Molecular Genetics, Moscow, with the Zakusov Institute of Pharmacology

Indexed records

~140

Claimed effect

Anxiolysis

Proposed mechanism

Altered expression of GABAergic neurotransmission genes ^11,13; hippocampal synaptic activity ¹⁴

Most safety-relevant finding

Enhances the anxiety-reducing effect of diazepam in rats ¹²

Human studies

One clinical trial ⁹; one imaging study in 52 healthy participants ¹⁹

Randomised blinded trial

None identified

Comparison against Pro-Gly-Pro alone

None

Approval status

Not approved in the US or EU; Russian status not verified for this guide

03 · Mechanism of action

Tuftsin, and what the parent does

Tuftsin — Thr-Lys-Pro-Arg — is released by enzymatic cleavage from the CH2 domain of immunoglobulin G heavy chain and acts as an immunostimulant, enhancing phagocytosis and macrophage function. Its properties and the analogues built from it have been reviewed ¹⁵. That is an immune molecule, not a neurological one, and the anxiolytic claim made for Selank is not inherited from the parent.

A compound derived from an immunostimulatory fragment and sold as an anxiolytic has a mechanistic gap at its origin, and this literature fills it with downstream observation rather than with a receptor.

The GABA connection, which is expression rather than binding

Selank administration affects expression of genes involved in GABAergic neurotransmission ¹¹. In IMR-32 human neuroblastoma cells, GABA, Selank and olanzapine were compared for their effects on the same gene set ¹³.

Note carefully what these papers report and what they do not. They report changes in transcript levels of GABA-system genes. They do not report that Selank binds the GABA-A receptor, occupies the benzodiazepine site, or acts as a positive allosteric modulator. No binding study appears in this file.

An anxiolytic claim supported by gene expression rather than receptor pharmacology is a claim at one remove from its mechanism. That said, the functional consequence has been observed: Selank changed spontaneous synaptic activity in hippocampal CA1 neurons ¹⁴.

The diazepam interaction

Selank enhanced diazepam’s anxiety-reducing effect in rats subjected to unpredictable chronic mild stress ¹². The paper is from the developing group and is published in English.

This is the most important result in the file for anyone thinking about how the compound is actually used. Benzodiazepine potentiation means the compound is doing something in the same functional space as a drug class with well-characterised risks of sedation, respiratory depression in combination with other depressants, tolerance and withdrawal. The literature reports the potentiation and does not follow it up.

Immune and inflammatory effects

Consistent with its tuftsin origin, Selank alters inflammation-related gene expression in mouse spleen ⁶, with the temporal dynamics of that expression characterised separately ⁸. It affected cytokine levels under conditions of social stress ²¹, and altered the hippocampal transcriptome ⁷.

Route

Pharmacological effects were compared after intranasal and intraperitoneal administration in BALB/c and C57BL/6 mice ¹⁰ — one of the few studies in this family to address route directly, and it is in Russian.

The molecular account

A 2018 review from the developing group sets out the molecular aspects of Selank’s biological activity under the heading of peptide-based anxiolytics ¹⁶. No receptor is identified in it.

04 · Key research findings

Anxiety and stress behaviour in rodents. Selank optimised a conditioned active avoidance reflex in rats ¹, and was studied alongside other tuftsin-family peptides in the regulation of adaptive behaviour under stress ². It affected genetically-based and situation-provoked depression-like behaviour in WAG/Rij and Wistar rats and BALB/c mice ³. It enhanced diazepam’s anxiolytic effect in unpredictable chronic mild stress ¹².

The behavioural literature is consistent in direction and comes overwhelmingly from two collaborating Moscow institutes across two decades.

GABAergic gene expression. Selank altered expression of genes involved in GABAergic neurotransmission in vivo ¹¹ and in IMR-32 cells compared against GABA and olanzapine ¹³.

Two studies, same group, establishing that the GABA system responds transcriptionally. Neither establishes a binding target.

Electrophysiology. Selank affected spontaneous synaptic activity of rat hippocampal CA1 neurons ¹⁴.

The most direct functional neuroscience in the file, and a single paper.

Monoamines. The effects of Selank and tuftsin on brain serotonin metabolism were compared in rats pretreated with the tryptophan hydroxylase inhibitor PCPA ⁴, and learning and memory processes were examined ⁵. Both are in Russian.

Alcohol and opioid withdrawal. Selank protected against ethanol-induced memory impairment, with BDNF content measured in hippocampus and prefrontal cortex ¹⁸, and attenuated aversive signs of morphine withdrawal in rats ²².

The withdrawal findings come from the Zakusov Institute group rather than the Institute of Molecular Genetics, which is a degree of separation within the Russian programme, and they point toward a substance-withdrawal application the compound is not marketed for.

Peripheral effects under stress. Selank altered rat liver morphology under chronic foot-shock stress ¹⁷ and large intestine morphology under chronic restraint stress ²⁰, and affected cytokine levels under social stress ²¹.

A compound with effects on liver and gut morphology in stressed animals is a compound with systemic actions that its neurological framing does not cover.

Human data. A 2015 study on optimising the treatment of anxiety disorders with Selank is indexed as a clinical trial ⁹. A connectomic study assessed whole-brain resting-state functional connectivity in 52 healthy participants for both Selank and Semax ¹⁹.

One trial this guide cannot read, and one imaging study with an objective endpoint. That is the human evidence base.

Contemporary mentions. Reviews list Selank among neuroactive peptides of current interest ^23,24.

05 · Evidence overview

06 · Safety profile

Animal data. No formal toxicology programme is identified. The animal studies report behavioural, transcriptional and morphological endpoints ^{1–8,10–14,18,19,21–23}. Two of them report changes in peripheral organ morphology — liver under foot-shock stress ¹⁷ and large intestine under restraint stress ²⁰ — which are the closest things in the file to structural observations, and both were framed as protective rather than as toxicological findings.

Human data. One indexed Russian-language clinical trial in anxiety disorders ⁹, unread by this guide, plus 52 healthy participants in an imaging study ¹⁹. No adverse event information is available from the retrievable record.

What is genuinely unknown. The benzodiazepine interaction in humans: Selank potentiates diazepam in rats ¹² and nothing establishes whether it does so in people, at what doses, or what the consequences would be for anyone using both — which, given that the compound is marketed for anxiety, is a foreseeable combination. Whether the compound acts at the GABA-A receptor at all, since the evidence is transcriptional ^11,13 and no binding study exists. Human pharmacokinetics by any route, absent, despite one animal study addressing route directly ¹⁰. Whether the active species is Selank or Pro-Gly-Pro, untested here and a live question given what happened with Semax. Tuftsin-derived immunological effects in humans — the parent fragment is an immunostimulant, Selank alters inflammation gene expression in spleen ^6,8 and cytokines under stress ²¹, and no human study has measured immune parameters after administration. Tolerance, dependence and withdrawal, which are the standard questions for anything acting in the anxiolytic space and are unaddressed. And repeat-dose toxicology, genotoxicity, reproductive toxicology and carcinogenicity: none identified.

07 · US regulatory status

Current as of 6 September 2026. Selank is not approved as a drug in the United States or the European Union and is not a controlled substance in the United States.

The compound is described in the Russian literature in terms consistent with registered clinical use for anxiety disorders ^9,16. This guide does not state the terms of any Russian registration, because establishing them would require Russian regulatory records that have not been consulted. The same qualification applies here as to Semax, Thymalin and Vilon.

Under the World Anti-Doping Code, substances not approved for human therapeutic use by any governmental regulatory health authority fall within class S0. Competitors should consult the current Prohibited List directly rather than rely on secondary summaries, including this one.

08 · Limitations of the evidence

1. The single human trial is Russian-language and unread by this guide ⁹. The Early Clinical grade rests on a PubMed publication-type tag and a title, exactly as for Vilon and Pinealon.

1. No receptor has been identified, and the GABA claim is transcriptional. Changes in the expression of GABA-system genes ^11,13 are not the same as acting at a GABA receptor, and this distinction is routinely collapsed in descriptions of the compound.

1. The benzodiazepine potentiation is documented and unfollowed. One paper reports it in rats ¹². No study examines the interaction in humans, at any dose, or asks what it implies for the population most likely to combine the two.

1. The compound has never been compared against Pro-Gly-Pro. For the sister compound from the same institute, the tripeptide tail alone reproduced the headline mechanistic effect. The obvious control experiment has not been run for Selank.

1. The anxiolytic claim is not inherited from the parent fragment. Tuftsin is an immunostimulant ¹⁵. Nothing about Selank’s proposed neurological action follows from its origin, and the literature does not explain why adding Pro-Gly-Pro to an immune peptide should produce an anxiolytic.

1. Research concentration is extreme. Nearly the entire file comes from the Institute of Molecular Genetics and the Zakusov Institute of Pharmacology, with Myasoedov, Andreeva, Slominsky, Shadrina, Kolomin or Kozlovskii on most of it.

1. Six of twenty-five references are Russian-language without indexed English abstracts ^3,4,5,7,9,11, including the only human trial.

1. Peripheral effects are underexplored. Liver and large intestine morphology changed under stress with treatment ^17,20, and gut microbiota was examined in a related study. These are systemic effects in a compound presented as acting on the brain, and no toxicological framework has been applied to them.

1. No randomised, blinded trial exists in any species for any endpoint.

1. Nothing is known about commercial material. No published analysis has examined the identity or purity of any product sold as Selank.

09 · References

1. Kozlovskii II, Danchev ND. The optimizing action of the synthetic peptide Selank on a conditioned active avoidance reflex in rats. Neurosci Behav Physiol. 2003 Sep;33(7):639–643.

   PMID 14552529 ↗

2. Kozlovskaya MM, Kozlovskii II, Val’dman EA, Seredenin SB. Selank and short peptides of the tuftsin family in the regulation of adaptive behavior in stress. Neurosci Behav Physiol. 2003 Nov;33(9):853–860.

   PMID 14969422 ↗

3. Sarkisova KIu, Kozlovskiĭ II, Kozlovskaia MM. [Effects of heptapeptide selank on genetically-based and situation-provoked symptoms of depression in behavior in WAG/Rij and Wistar rats, and in BALB/c mice]. Zh Vyssh Nerv Deiat Im I P Pavlova. 2008 Mar–Apr;58(2):226–237. Russian.

   PMID 18661785 ↗

4. Semenova TP, Kozlovskiĭ II, Zakharova NM, Kozlovskaia MM. [Comparison of the effects of selank and tuftsin on the metabolism of serotonin in the brain of rats pretreated with PCPA]. Eksp Klin Farmakol. 2009 Jul–Aug;72(4):6–8. Russian.

   PMID 19803361 ↗

5. Semenova TP, Kozlovskiĭ II, Zakharova NM, Kozlovskaia MM. [Experimental optimization of learning and memory processes by selank]. Eksp Klin Farmakol. 2010 Aug;73(8):2–5. Russian.

   PMID 20919548 ↗

6. Kolomin T, Shadrina M, Andreeva L, Slominsky P, Limborska S, Myasoedov N. Expression of inflammation-related genes in mouse spleen under tuftsin analog Selank. Regul Pept. 2011 Oct 10;170(1–3):18–23.

   PMID 21609736 ↗

7. Kolomin TA, Agapova TIu, Agniullin IaV, Shram SI, Shadrina MI, Slominskiĭ PA, Limborskaia SA, Miasoedov IF. [Transcriptome alteration in hippocampus under the treatment of tuftsin analog Selank]. Zh Vyssh Nerv Deiat Im I P Pavlova. 2013 May–Jun;63(3):365–374. Russian.

   PMID 24450168 ↗

8. Kolomin T, Morozova M, Volkova A, Shadrina M, Andreeva L, Slominsky P, Limborska S, Myasoedov N. The temporary dynamics of inflammation-related genes expression under tuftsin analog Selank action. Mol Immunol. 2014 Mar;58(1):50–55.

   PMID 24291245 ↗

9. Medvedev VE, Tereshchenko ON, Kost NV, Ter-Israelyan AY, Gushanskaya EV, Chobanu IK, Sokolov OY, Myasoedov NF. [Optimization of the treatment of anxiety disorders with selank]. Zh Nevrol Psikhiatr Im S S Korsakova. 2015;115(6):33–40. Clinical trial. Russian.

   PMID 26356395 ↗

10. 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. Russian.

    PMID 29787664 ↗

11. Volkova A, Shadrina M, Kolomin T, Andreeva L, Limborska S, Myasoedov N, Slominsky P. Selank administration affects the expression of some genes involved in GABAergic neurotransmission. Front Pharmacol. 2016 Feb 18;7:31.

    PMID 26924987 ↗

12. Kasian A, Kolomin T, Andreeva L, Bondarenko E, Myasoedov N, Slominsky P, Shadrina M. Peptide Selank enhances the effect of diazepam in reducing anxiety in unpredictable chronic mild stress conditions in rats. Behav Neurol. 2017;2017:5091027.

    PMID 28280289 ↗

13. Filatova E, Kasian A, Kolomin T, Rybalkina E, Alieva A, Andreeva L, Limborska S, Myasoedov N, Pavlova G, Slominsky P, Shadrina M. GABA, Selank, and olanzapine affect the expression of genes involved in GABAergic neurotransmission in IMR-32 cells. Front Pharmacol. 2017 Feb 28;8:89.

    PMID 28293190 ↗

14. Povarov IS, Kondratenko RV, Derevyagin VI, Myasoedov NF, Skrebitsky VG. Effect of Selank on spontaneous synaptic activity of rat hippocampal CA1 neurons. Bull Exp Biol Med. 2017 Mar;162(5):640–642.

    PMID 28361410 ↗

15. Siebert A, Gensicka-Kowalewska M, Cholewinski G, Dzierzbicka K. Tuftsin — properties and analogs. Curr Med Chem. 2017 Nov 17;24(34):3711–3727.

    PMID 28745220 ↗

16. 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):914–923.

    PMID 30255741 ↗

17. Fomenko EV, Bobyntsev II, Ivanov AV, Belykh AE, Andreeva LA, Myasoedov NF. Effect of Selank on morphological parameters of rat liver in chronic foot-shock stress. Bull Exp Biol Med. 2019 Jun;167(2):293–296.

    PMID 31243679 ↗

18. 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 Sep;167(5):641–644.

    PMID 31625062 ↗

19. Panikratova YR, Lebedeva IS, Sokolov OY, Rumshiskaya AD, Kupriyanov DA, Kost NV, Myasoedov NF. Functional connectomic approach to studying Selank and Semax effects. Dokl Biol Sci. 2020 Jan;490(1):9–11.

    PMID 32342318 ↗

20. Mukhina AY, Mishina ES, Bobyntsev II, Medvedeva OA, Svishcheva MV, Kalutskii PV, Andreeva LA, Myasoedov NF. Morphological changes in the large intestine of rats subjected to chronic restraint stress and treated with Selank. Bull Exp Biol Med. 2020 Jun;169(2):281–285.

    PMID 32651826 ↗

21. Leonidovna YA, Aleksandrovna SM, Aleksandrovna TA, Aleksandrovna BO, Fedorovich MN, Aleksandrovna AL. The influence of Selank on the level of cytokines under the conditions of “social” stress. Curr Rev Clin Exp Pharmacol. 2021;16(2):162–167.

    PMID 32621722 ↗

22. Konstantinopolsky MA, Chernyakova IV, Kolik LG. Selank, a peptide analog of tuftsin, attenuates aversive signs of morphine withdrawal in rats. Bull Exp Biol Med. 2022 Oct;173(6):730–733.

    PMID 36322304 ↗

23. Rahman OF, Lee SJ, Seeds WA. Therapeutic peptides in orthopaedics: applications, challenges, and future directions. J Am Acad Orthop Surg Glob Res Rev. 2026 Jan 2;10(1):e25.00236.

    PMID 41490200 ↗

24. Mavrych V, Shypilova I, Bolgova O. Therapeutic peptides in gerontology: mechanisms and applications for healthy aging. Front Aging. 2026 Apr 7;7:1790247.

    PMID 42021992 ↗