Selank

1. Studied for

   Anxiety-related endpoints in human clinical studies (Russian literature)

   3 small studies conducted in Russia make up the entire human record. In the first, 62 people enrolled on anxiety-related diagnoses were split between selank (30 people) and the benzodiazepine medazepam (32 people); the researchers reported that the two eased anxiety about equally on standard rating scales, and that selank additionally appeared to reduce fatigue and to have a mild stimulating quality. They also measured a marker of how long a natural calming molecule survives in blood, found it was shortened in these people at the start, and reported it rising while selank was being given, mostly in the group enrolled for generalized anxiety. The second compared selank against the benzodiazepine phenazepam in 60 people enrolled on anxiety-related diagnoses and reported a pronounced anxiety-reducing effect plus a mild memory-and-attention effect, with the anxiety effect described as persisting for a week after the last administration. The third compared phenazepam alone (30 people) against phenazepam plus selank (40 people) and reported the benefit arriving sooner on a clinician-rated symptom scale, along with fewer of the unwanted effects that come with the benzodiazepine. These limitations are part of the finding and must travel with it: all 3 are small, published in Russian, come from overlapping investigator groups at the same Russian institutions, report no blinding in the retrievable abstracts, and none has been repeated in a Western registration trial. This is a research record about investigational endpoints, not evidence of a benefit to any person. human clinical studies (62, 60 and 70 participants), all conducted in Russia Preclinical moderate A well-described result with several independent outcome measures, but from a single laboratory or a single study design. Open for the full finding and the paper it came from.

   In the literature

   Anxiety-related endpoints in human clinical studies (Russian literature)

   3 small studies conducted in Russia make up the entire human record. In the first, 62 people enrolled on anxiety-related diagnoses were split between selank (30 people) and the benzodiazepine medazepam (32 people); the researchers reported that the two eased anxiety about equally on standard rating scales, and that selank additionally appeared to reduce fatigue and to have a mild stimulating quality. They also measured a marker of how long a natural calming molecule survives in blood, found it was shortened in these people at the start, and reported it rising while selank was being given, mostly in the group enrolled for generalized anxiety. The second compared selank against the benzodiazepine phenazepam in 60 people enrolled on anxiety-related diagnoses and reported a pronounced anxiety-reducing effect plus a mild memory-and-attention effect, with the anxiety effect described as persisting for a week after the last administration. The third compared phenazepam alone (30 people) against phenazepam plus selank (40 people) and reported the benefit arriving sooner on a clinician-rated symptom scale, along with fewer of the unwanted effects that come with the benzodiazepine. These limitations are part of the finding and must travel with it: all 3 are small, published in Russian, come from overlapping investigator groups at the same Russian institutions, report no blinding in the retrievable abstracts, and none has been repeated in a Western registration trial. This is a research record about investigational endpoints, not evidence of a benefit to any person.^{References 1, 2, 3}

   Modelhuman clinical studies (62, 60 and 70 participants), all conducted in Russia

   Confidence: moderate

   A well-described result with several independent outcome measures, but from a single laboratory or a single study design.

   Source

   Zozulia AA et al., Zh Nevrol Psikhiatr Im S S Korsakova, 2008;108(4):38-48, PMID: 18454096; Medvedev VE et al., Zh Nevrol Psikhiatr Im S S Korsakova, 2014;114(7):17-22, PMID: 25176261; Medvedev VE et al., Zh Nevrol Psikhiatr Im S S Korsakova, 2015;115(6):33-40, doi:10.17116/jnevro20151156133-40, PMID: 26356395

   PubMed 18454096 PubMed 25176261 PubMed 26356395

   How this citation was checked

   Re-resolved on 2026-07-28 via PubMed E-utilities efetch (XML, nested markup included so no abstract text is silently truncated). PMID 18454096 returns first author Zozulia AA, Zh Nevrol Psikhiatr Im S S Korsakova 2008;108(4):38-48; the abstract independently confirms 62 participants, selank 30 versus medazepam 32, the Hamilton, Zung and CGI scales, verbatim 'The anxiolytic effects of both drugs were similar but selank had also antiasthenic and psychostimulant effects', and the shortened tau(1/2) leu-enkephalin at baseline with an increase while selank was being given, mostly in the generalized-anxiety group. PMID 25176261 returns first author Medvedev VE, same journal 2014;114(7):17-22; the abstract confirms 60 participants, the ICD-10 code ranges F40.2-9, F41.1-9 and F45.0-1, the phenazepam comparison, verbatim 'Pronounced anxiolytic and mild nootropic effects of selank were demonstrated' and 'The anxiolytic effect lasted for a week after last receiving the peptide'. PMID 26356395 returns first author Medvedev VE, same journal 2015;115(6):33-40, DOI 10.17116/jnevro20151156133-40; the abstract confirms 30 on phenazepam alone versus 40 on the combination, the HDRS, CGI, Spielberger, UKU and SF-36 instrument set, the earlier onset on HDRS, and the reduced phenazepam side effects. No blinding statement appears in any of the 3 abstracts, which is why none is claimed. The specific diagnostic labels carried in those abstracts are deliberately not printed in the finding above, per this store's standing rule that its own prose names no disease; the ICD-10 ranges are recorded here instead so a checker can still resolve who was enrolled.

2. Studied for

   Inhibition of enkephalin-degrading enzymes (proposed mechanism)

   The body makes its own calming molecules, called enkephalins, and enzymes in the blood chop them up. In test tubes using human blood serum, Selank slowed those enzymes down, and did so more strongly than 2 standard laboratory enzyme blockers, puromycin and bacitracin (the concentration needed to halve enzyme activity was about 20 micromolar for Selank and about 10 micromolar for the related peptide Semax; a second report measured about 15 micromolar for Selank acting on enkephalin breakdown in plasma). That second report also observed, in people assessed against DSM-IV criteria, a shortened enkephalin lifetime and reduced total enkephalin-degrading activity in 1 anxiety-related group but not in the other 2; that is an observation about the people themselves, not an effect of Selank on them. In mice, Selank lengthened the plasma lifetime of one enkephalin and produced calmer behavior in the open-field test, but only in BALB/c animals: in C57Bl/6 animals it changed neither behavior nor enzyme activity at all. That strain-dependence is part of the finding and limits how far the proposed mechanism generalizes. A further mouse study gave the opioid blocker naloxone beforehand and reported that this dampened sensitivity to Selank in BALB/c mice while increasing the response in C57Bl/6 mice, which the authors read as evidence that the enkephalin-opioid system governs how strongly an individual animal responds to the peptide. IN VITRO in vitro (human blood serum and plasma) and in mice (BALB/c and C57Bl/6 strains) Preclinical moderate A well-described result with several independent outcome measures, but from a single laboratory or a single study design. Open for the full finding and the paper it came from.

   In the literature

   Inhibition of enkephalin-degrading enzymes (proposed mechanism)

   The body makes its own calming molecules, called enkephalins, and enzymes in the blood chop them up. In test tubes using human blood serum, Selank slowed those enzymes down, and did so more strongly than 2 standard laboratory enzyme blockers, puromycin and bacitracin (the concentration needed to halve enzyme activity was about 20 micromolar for Selank and about 10 micromolar for the related peptide Semax; a second report measured about 15 micromolar for Selank acting on enkephalin breakdown in plasma). That second report also observed, in people assessed against DSM-IV criteria, a shortened enkephalin lifetime and reduced total enkephalin-degrading activity in 1 anxiety-related group but not in the other 2; that is an observation about the people themselves, not an effect of Selank on them. In mice, Selank lengthened the plasma lifetime of one enkephalin and produced calmer behavior in the open-field test, but only in BALB/c animals: in C57Bl/6 animals it changed neither behavior nor enzyme activity at all. That strain-dependence is part of the finding and limits how far the proposed mechanism generalizes. A further mouse study gave the opioid blocker naloxone beforehand and reported that this dampened sensitivity to Selank in BALB/c mice while increasing the response in C57Bl/6 mice, which the authors read as evidence that the enkephalin-opioid system governs how strongly an individual animal responds to the peptide.^{References 4, 5, 6, 7}

   Modelin vitro (human blood serum and plasma) and in mice (BALB/c and C57Bl/6 strains)

   Confidence: moderate

   A well-described result with several independent outcome measures, but from a single laboratory or a single study design.

   Source

   Kost NV et al., Bioorg Khim, 2001;27(3):180-183, doi:10.1023/a:1011373002885, PMID: 11443939; Zozulya AA et al., Bull Exp Biol Med, 2001;131(4):315-317, doi:10.1023/a:1017979514274, PMID: 11550013; Sokolov OY et al., Effects of Selank on behavioral reactions and activities of plasma enkephalin-degrading enzymes in mice with different phenotypes of emotional and stress reactions, Bull Exp Biol Med, 2002;133(2):133-135, doi:10.1023/a:1015582302311, PMID: 12432865; Kozlovskii II et al., Eksp Klin Farmakol, 2012;75(2):10-13, PMID: 22550852

   PubMed 11443939 PubMed 11550013 PubMed 12432865 PubMed 22550852

   How this citation was checked

   Re-resolved on 2026-07-28 via PubMed efetch. 11443939: first author Kost NV, Bioorg Khim 2001;27(3):180-3, DOI 10.1023/a:1011373002885; the abstract states the Semax IC50 of 10 microM and the Selank IC50 of 20 microM against human serum enkephalin-degrading enzymes and that both are more pronounced than puromycin and bacitracin. 11550013: first author Zozulya AA, Bull Exp Biol Med 2001;131(4):315-7, DOI 10.1023/a:1017979514274; the abstract states the IC50 of 15 microM for inhibition of plasma enkephalin hydrolysis, greater potency than bacitracin and puromycin, and the DSM-IV observation of a shortened enkephalin half-life and reduced total enkephalinase activity in 1 of the 3 enrolled anxiety-related groups. 12432865: first author Sokolov OY, Bull Exp Biol Med 2002;133(2):133-5, DOI 10.1023/a:1015582302311; the full title carries the 'different phenotypes' qualifier and the abstract states verbatim that Selank acted in BALB/c mice 'but had no effect on behavioral reactions and enkephalinase activities in C57Bl/6 mice'. 22550852: first author Kozlovskii II, Eksp Klin Farmakol 2012;75(2):10-13; the abstract confirms verbatim that naloxone given beforehand 'attenuated the sensitivity to selank in BALB/C mice whereas the response to anxiolytic effects of peptide was increased in C57BL/6 mice'. The authors' own efficacy conclusion in 11550013 is deliberately not carried over: it is their recommendation, not their measured result. Every numeric quantity for administration present in these abstracts is omitted; the IC50 values retained are test-tube enzyme-potency constants.

3. Studied for

   GABAergic system: gene expression, receptor binding, and synaptic electrophysiology

   GABA is the brain's main braking signal, and 3 preclinical lines have probed whether Selank works through it. They do not fully agree. (1) Gene readouts in rat frontal cortex: researchers measured 84 neurotransmission genes 1 and 3 hours after a single intranasal administration, discarded 7 for having too little readable mRNA, and analyzed the remaining 77. Pooled across the Selank arm and the GABA arm together, 45 of those 77 genes changed at 1 hour and 22 at 3 hours; taken alone, the Selank arm accounted for 29 of 77 at 1 hour and 17 of 77 at 3 hours. Among GABA-A receptor subunits specifically, and in the Selank arm specifically, Gabrb3 rose about 1.6-fold at 1 hour, while Gabre and Gabrq each fell roughly 20-fold at 1 hour and then rose 16.1-fold and 13.3-fold at 3 hours. The authors proposed that Selank nudges the GABA system indirectly, from a side site rather than the main one. (2) Receptor binding in isolated brain-cell membrane preparations: radioligand assays described Selank as a positive side-site modulator of GABA binding, and reported that Selank BLOCKS the modulating activity of both diazepam and olanzapine, with the authors concluding that the peptide and benzodiazepine binding sites are apparently not the same though they may partially overlap. (3) Electrophysiology in rat brain slices: applying Selank to hippocampal slices increased the size and rate of the spontaneous inhibitory signals arriving at CA1 neurons, in some neurons preceded by a brief dip, with no clear dependence on concentration across the range tested. IMPORTANT COUNTERWEIGHT: in a human neuroblastoma cell line (IMR-32), Selank on its own changed none of the GABA-system genes studied; it only altered what GABA or olanzapine did when the two were incubated together. THE LINES CONFLICT: one rat behavior study reports Selank enhancing diazepam's calming effect, while the binding study reports Selank blocking diazepam's modulating activity. Both sit in the record and have not been reconciled. The mechanism is an active hypothesis, not a settled one. in rats (frontal cortex gene expression and hippocampal brain slices), in isolated brain-cell membrane preparations, and in cultured human neuroblastoma cells Preclinical moderate A well-described result with several independent outcome measures, but from a single laboratory or a single study design. Open for the full finding and the paper it came from.

   In the literature

   GABAergic system: gene expression, receptor binding, and synaptic electrophysiology

   GABA is the brain's main braking signal, and 3 preclinical lines have probed whether Selank works through it. They do not fully agree. (1) Gene readouts in rat frontal cortex: researchers measured 84 neurotransmission genes 1 and 3 hours after a single intranasal administration, discarded 7 for having too little readable mRNA, and analyzed the remaining 77. Pooled across the Selank arm and the GABA arm together, 45 of those 77 genes changed at 1 hour and 22 at 3 hours; taken alone, the Selank arm accounted for 29 of 77 at 1 hour and 17 of 77 at 3 hours. Among GABA-A receptor subunits specifically, and in the Selank arm specifically, Gabrb3 rose about 1.6-fold at 1 hour, while Gabre and Gabrq each fell roughly 20-fold at 1 hour and then rose 16.1-fold and 13.3-fold at 3 hours. The authors proposed that Selank nudges the GABA system indirectly, from a side site rather than the main one. (2) Receptor binding in isolated brain-cell membrane preparations: radioligand assays described Selank as a positive side-site modulator of GABA binding, and reported that Selank BLOCKS the modulating activity of both diazepam and olanzapine, with the authors concluding that the peptide and benzodiazepine binding sites are apparently not the same though they may partially overlap. (3) Electrophysiology in rat brain slices: applying Selank to hippocampal slices increased the size and rate of the spontaneous inhibitory signals arriving at CA1 neurons, in some neurons preceded by a brief dip, with no clear dependence on concentration across the range tested. IMPORTANT COUNTERWEIGHT: in a human neuroblastoma cell line (IMR-32), Selank on its own changed none of the GABA-system genes studied; it only altered what GABA or olanzapine did when the two were incubated together. THE LINES CONFLICT: one rat behavior study reports Selank enhancing diazepam's calming effect, while the binding study reports Selank blocking diazepam's modulating activity. Both sit in the record and have not been reconciled. The mechanism is an active hypothesis, not a settled one.^{References 8, 9, 10, 11}

   Modelin rats (frontal cortex gene expression and hippocampal brain slices), in isolated brain-cell membrane preparations, and in cultured human neuroblastoma cells

   Confidence: moderate

   A well-described result with several independent outcome measures, but from a single laboratory or a single study design.

   Source

   Volkova A et al., Front Pharmacol, 2016;7:31, doi:10.3389/fphar.2016.00031, PMID: 26924987; Vyunova TV et al., Protein Pept Lett, 2018;25(10):914-923, doi:10.2174/0929866525666180925144642, PMID: 30255741; Povarov IS et al., Bull Exp Biol Med, 2017;162(5):640-642, doi:10.1007/s10517-017-3676-3, PMID: 28361410; Filatova E et al., Front Pharmacol, 2017;8:89, doi:10.3389/fphar.2017.00089, PMID: 28293190

   PubMed 26924987 PubMed 30255741 PubMed 28361410 PubMed 28293190

   How this citation was checked

   Re-resolved on 2026-07-28 three ways. 26924987: Crossref /works/10.3389/fphar.2016.00031 returns title 'Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission', Frontiers in Pharmacology, 2016-02-18, volume 7, authors Volkova/Shadrina/Kolomin/Andreeva/Limborska/Myasoedov/Slominsky; PubMed efetch returns the same with article 31. The gene counts come from the open-access full text at Europe PMC (PMC4757669), which states verbatim 'among the 84 studied genes, seven genes (Csf2, Drd4, Htr3b, Il2, Mmp7, Mmp10, and Npffr2) had a high threshold reaction cycle (Ct > 35) ... Therefore, these genes were excluded', then 'Of the remaining 77 genes, summarily 45 genes showed changes in mRNA level 1 h after Selank OR GABA administration', 'Expression changed in only 22 of the 77 genes' at 3 h, and the Selank-only breakdown 'Selank affected the expression of fewer genes 1 h after the administration (38%, 29 of 77 genes) ... (22%, 17 of 77 genes)' at 3 h. The pooled 45 and 22 are deliberately not attributed to Selank alone. Table 1 of the same full text gives the Selank-arm fold changes Gabrb3 1.58 at 1 h, Gabre 0.05 and Gabrq 0.05 at 1 h, Gabre 16.10 and Gabrq 13.30 at 3 h. 30255741: PubMed efetch returns first author Vyunova TV, Protein Pept Lett 2018;25(10):914-923; the abstract confirms the radioligand method, brain-cell plasma membrane isolation, positive allosteric modulation of [3H]GABA binding, and verbatim 'Selank is able to block the modulatory activity of Diazepam and Olanzapine, the location of their and peptide binding sites apparently not the same, but potentially may partially overlaps'. The abstract states no species for the membrane preparations, so no species is asserted. 28361410: PubMed efetch returns first author Povarov IS, Bull Exp Biol Med 2017;162(5):640-642, DOI 10.1007/s10517-017-3676-3; the abstract confirms increased amplitude and discharge rate of spontaneous inhibitory postsynaptic currents in rat CA1 pyramidal neurons, the transient decrease in some neurons, and no significant concentration-dependence. The numeric bath concentration range is omitted, so that every numeric concentration on this page is an enzyme-potency constant. 28293190: PubMed efetch returns first author Filatova E, Front Pharmacol 2017;8:89; the abstract states verbatim 'We found no changes in the mRNA levels of the genes studied under the effect of Selank', 'The combined effect of GABA and Selank led to nearly complete suppression of changes in expression of genes in which mRNA levels changed under the effect of GABA', and 'When Selank was used in conjunction with olanzapine, the expression alterations of more genes were observed compared with olanzapine alone'. Audit-trail note: a plain-text PubMed fetch truncates this abstract at a superscript character; the XML efetch used here preserves nested markup and returns the complete text, cross-checked against the Europe PMC core record.

4. Studied for

   BDNF and the hippocampal transcriptome

   BDNF is a protein that helps brain cells grow and survive, and it is the single most over-claimed Selank endpoint in consumer marketing. 3 rodent studies exist and they do not tell one story. (1) A rat study reported that intranasal Selank regulates BDNF expression in the hippocampus. LIMIT OF VERIFICATION: neither PubMed nor Europe PMC carries an abstract for this record, so the direction, timing and size of the reported BDNF change could not be independently confirmed and are not asserted here. (2) In outbred rats given 10 percent ethanol as their only fluid for 30 weeks, chronic alcohol RAISED BDNF, and Selank PREVENTED that rise in the hippocampus and frontal cortex. Selank also prevented the memory and attention problems that developed during alcohol withdrawal in an object-recognition test, and produced a cognition-stimulating effect in 9-month-old rats that had never been given ethanol. Read the direction carefully: here Selank normalized an elevated BDNF level rather than raising it. (3) Using gene-chip arrays on rat hippocampus, a single intranasal administration changed the levels of 36 genes by more than 2-fold, and a repeated course changed 20; most of those genes encode proteins sitting in the cell membrane, which the authors linked to control of ion balance. Taken together, these do NOT establish that Selank raises BDNF, and there is no human BDNF data at all. in rats Preclinical moderate A well-described result with several independent outcome measures, but from a single laboratory or a single study design. Open for the full finding and the paper it came from.

   In the literature

   BDNF and the hippocampal transcriptome

   BDNF is a protein that helps brain cells grow and survive, and it is the single most over-claimed Selank endpoint in consumer marketing. 3 rodent studies exist and they do not tell one story. (1) A rat study reported that intranasal Selank regulates BDNF expression in the hippocampus. LIMIT OF VERIFICATION: neither PubMed nor Europe PMC carries an abstract for this record, so the direction, timing and size of the reported BDNF change could not be independently confirmed and are not asserted here. (2) In outbred rats given 10 percent ethanol as their only fluid for 30 weeks, chronic alcohol RAISED BDNF, and Selank PREVENTED that rise in the hippocampus and frontal cortex. Selank also prevented the memory and attention problems that developed during alcohol withdrawal in an object-recognition test, and produced a cognition-stimulating effect in 9-month-old rats that had never been given ethanol. Read the direction carefully: here Selank normalized an elevated BDNF level rather than raising it. (3) Using gene-chip arrays on rat hippocampus, a single intranasal administration changed the levels of 36 genes by more than 2-fold, and a repeated course changed 20; most of those genes encode proteins sitting in the cell membrane, which the authors linked to control of ion balance. Taken together, these do NOT establish that Selank raises BDNF, and there is no human BDNF data at all.^{References 12, 13, 14}

   Modelin rats

   Confidence: moderate

   A well-described result with several independent outcome measures, but from a single laboratory or a single study design.

   Source

   Inozemtseva LS, Karpenko EA, Dolotov OV, Levitskaya NG, Kamensky AA, Andreeva LA, Grivennikov IA. Intranasal administration of the peptide Selank regulates BDNF expression in the rat hippocampus in vivo. Dokl Biol Sci. 2008;421:241-243. doi:10.1134/S0012496608040066. PMID: 18841804; Kolik LG et al., Bull Exp Biol Med, 2019;167(5):641-644, doi:10.1007/s10517-019-04588-9, PMID: 31625062; Kolomin TA et al., Zh Vyssh Nerv Deiat Im I P Pavlova, 2013;63(3):365-374, doi:10.7868/s0044467713030052, PMID: 24450168

   PubMed 18841804 PubMed 31625062 PubMed 24450168

   How this citation was checked

   Re-resolved on 2026-07-28. 18841804 checked two ways: Crossref /works/10.1134/s0012496608040066 returns title 'Intranasal administration of the peptide Selank regulates BDNF expression in the rat hippocampus in vivo', Doklady Biological Sciences, 2008, volume 421, pages 241-243, author list Inozemtseva L.S., Karpenko E.A., Dolotov O.V., Levitskaya N.G., Kamensky A.A., Andreeva L.A., Grivennikov I.A.; PubMed efetch returns the identical record and, critically, NO abstract text, which is why only the title-level claim is made. An earlier draft of the source research attributed this paper to Semenova TP; that was wrong and is not repeated. Also dropped as unconfirmable: the authors' reading of local neurotrophic stimulation versus transport, and the 3-hour mRNA and 24-hour protein time course. 31625062: PubMed efetch returns first author Kolik LG, Bull Exp Biol Med 2019;167(5):641-644, DOI 10.1007/s10517-019-04588-9; the abstract states 30 weeks of 10 percent ethanol as the only fluid source, the object recognition test, the cognitive-stimulating effect in 9-month rats not exposed to ethanol, prevention of ethanol-induced memory and attention disturbances during withdrawal, and verbatim 'Selank prevented ethanol-induced increase in BDNF content in the hippocampus and frontal cortex (p<0.05)'. 24450168: PubMed efetch returns first author Kolomin TA, Zh Vyssh Nerv Deiat Im I P Pavlova 2013;63(3):365-74, DOI 10.7868/s0044467713030052; the abstract states verbatim 'mRNA levels of 36 genes changed more than 2-fold after a single intranasal Selank administration, and 20 genes--after course administration' and that most encode plasma-membrane-associated proteins. Every numeric quantity for administration in the Kolik and Kolomin abstracts is omitted.

5. Studied for

   Learning, memory and attention in animal models

   In rats that started out poor at learning a task, repeated Selank administration significantly improved how quickly they learned an active-avoidance task, with more correct solutions and fewer errors, and an effect already visible after the first administration; in normal rats the peak effect landed on day 3, and the study ran the reference nootropic piracetam as a comparator. In adult Wistar rats that had been given a toxin during their first 3 days of life to damage catecholamine-producing nerve cells, Selank restored the learning, memory and attention that this permanent damage had disrupted. In monkeys with experimentally induced neurosis, intranasal Selank was reported to produce long-lasting changes in disturbed behavior (the authors describe elimination of fear and aggression and increased exploratory activity) and lasting compensation of disrupted memory. These are exploratory animal studies of learning and memory endpoints. NO controlled human cognition trial was located in this search, and the single human imaging study in this dossier carried no cognitive outcome measure. in rats and in monkeys Preclinical moderate A well-described result with several independent outcome measures, but from a single laboratory or a single study design. Open for the full finding and the paper it came from.

   In the literature

   Learning, memory and attention in animal models

   In rats that started out poor at learning a task, repeated Selank administration significantly improved how quickly they learned an active-avoidance task, with more correct solutions and fewer errors, and an effect already visible after the first administration; in normal rats the peak effect landed on day 3, and the study ran the reference nootropic piracetam as a comparator. In adult Wistar rats that had been given a toxin during their first 3 days of life to damage catecholamine-producing nerve cells, Selank restored the learning, memory and attention that this permanent damage had disrupted. In monkeys with experimentally induced neurosis, intranasal Selank was reported to produce long-lasting changes in disturbed behavior (the authors describe elimination of fear and aggression and increased exploratory activity) and lasting compensation of disrupted memory. These are exploratory animal studies of learning and memory endpoints. NO controlled human cognition trial was located in this search, and the single human imaging study in this dossier carried no cognitive outcome measure.^{References 15, 16, 17}

   Modelin rats and in monkeys

   Confidence: moderate

   A well-described result with several independent outcome measures, but from a single laboratory or a single study design.

   Source

   Kozlovskii II, Danchev ND. Neurosci Behav Physiol. 2003;33(7):639-643. doi:10.1023/a:1024444321191. PMID: 14552529; Semenova TP et al., Bull Exp Biol Med, 2007;144(5):689-691, doi:10.1007/s10517-007-0406-2, PMID: 18683497; [Compensatory and antiamnestic effects of heptapeptide Selank in monkeys]. Zh Evol Biokhim Fiziol. 2008;44(3):284-290. PMID: 18727417 (the PubMed and Europe PMC records for this article list no authors)

   PubMed 14552529 PubMed 18683497 PubMed 18727417

   How this citation was checked

   Re-resolved on 2026-07-28 via PubMed efetch. 14552529: first author Kozlovskii II with Danchev ND, Neurosci Behav Physiol 2003;33(7):639-43, DOI 10.1023/a:1024444321191; the abstract confirms the conditioned active avoidance paradigm, rats with initially low learning ability, the piracetam comparator, effects apparent after the first administration on training day 1, the increase in correct solutions and decrease in errors at p<0.05, and the day-3 maximum in normal rats. 18683497: first author Semenova TP, Bull Exp Biol Med 2007;144(5):689-91, DOI 10.1007/s10517-007-0406-2; the abstract confirms adult Wistar rats, 6-hydroxydopamine given during the first 3 days of life, and verbatim 'Selank ... restored cognitive processes disordered by chronic artificial inhibition of the cerebral catecholaminergic system'. 18727417: Zh Evol Biokhim Fiziol 2008;44(3):284-90; PubMed efetch returns an empty author list, so no author is asserted; the abstract confirms intranasal administration in monkeys with neurosis and states verbatim 'elimination of fear and aggression and an increase of orientational-explorative activity' plus 'a long compensation of disturbed psychic functions (processes of memory)'. The authors' forward-looking 'promising agent for correction' conclusion is not carried over. Every numeric quantity for administration in 14552529 and 18683497 is omitted. 'Experimentally induced neurosis' is retained as the published name of an animal model, which is not a statement that this compound addresses any condition in a person.

6. Studied for

   Co-administration with a benzodiazepine under chronic stress

   48 male Wistar rats were split evenly: 24 left alone and 24 put through 14 days of unpredictable mild stress. Anxiety was measured on an elevated plus maze before and after a 14-day course of test substances. Under chronic stress, the animals that received diazepam and Selank together ended up with anxiety readings that did not differ from what they had shown before the stress began, and the authors identified that combination as the most effective condition under chronic stress. AN IMPORTANT NUANCE THE HEADLINE HIDES: in the animals that were never stressed, the course of test substances actually moved anxiety readings in the direction of getting worse, though less so for Selank than for the others, and in that unstressed condition Selank alone was the most effective at reducing the substance-driven rise. This is also the study whose binding-level counterpart above reports Selank blocking diazepam's modulating activity, so the interaction between the two is not characterized in a single direction. Rodent only, and nothing here is a combination suggestion. in rats (48 male Wistar rats) Preclinical moderate A well-described result with several independent outcome measures, but from a single laboratory or a single study design. Open for the full finding and the paper it came from.

   In the literature

   Co-administration with a benzodiazepine under chronic stress

   48 male Wistar rats were split evenly: 24 left alone and 24 put through 14 days of unpredictable mild stress. Anxiety was measured on an elevated plus maze before and after a 14-day course of test substances. Under chronic stress, the animals that received diazepam and Selank together ended up with anxiety readings that did not differ from what they had shown before the stress began, and the authors identified that combination as the most effective condition under chronic stress. AN IMPORTANT NUANCE THE HEADLINE HIDES: in the animals that were never stressed, the course of test substances actually moved anxiety readings in the direction of getting worse, though less so for Selank than for the others, and in that unstressed condition Selank alone was the most effective at reducing the substance-driven rise. This is also the study whose binding-level counterpart above reports Selank blocking diazepam's modulating activity, so the interaction between the two is not characterized in a single direction. Rodent only, and nothing here is a combination suggestion.^{References 18}

   Modelin rats (48 male Wistar rats)

   Confidence: moderate

   A well-described result with several independent outcome measures, but from a single laboratory or a single study design.

   Source

   Kasian A et al., Behav Neurol, 2017;2017:5091027, doi:10.1155/2017/5091027, PMID: 28280289

   PubMed 28280289

   How this citation was checked

   Re-resolved on 2026-07-28 two ways. Crossref /works/10.1155/2017/5091027 returns title 'Peptide Selank Enhances the Effect of Diazepam in Reducing Anxiety in Unpredictable Chronic Mild Stress Conditions in Rats', Behavioural Neurology, 2017, volume 2017, authors Kasian Anastasiya, Kolomin Timur, Andreeva Lyudmila, Bondarenko Elena, Myasoedov Nikolay, Slominsky Petr, Shadrina Maria; PubMed efetch for 28280289 returns the same record with article number 5091027. The abstract confirms verbatim 'even in the absence of chronic stress, the administration of a course of test substances changed anxiety indicators toward their deterioration, but the changes after the administration of a course of Selank were less pronounced', 'In conditions of chronic stress, anxiety indicator values after the simultaneous use of diazepam and Selank did not differ from the respective values observed before chronic stress exposure', and that individual Selank was most effective against the substance-driven elevation while the combination was most effective under chronic stress. The open-access full text was retrieved from Europe PMC (PMC5322660) and confirms 'The animals (n = 48) were divided into 2 groups: a rest group (n1 = 24) ... and a stress group (n2 = 24)', male Wistar rats, the 14-day randomized stressor schedule, the 14-day once-daily administration, and the elevated plus maze testing before and after. Diazepam is present in this finding as an experimental arm and is deliberately absent from the co-marketed section, where it would render as a pairing suggestion for a prescription medicine this store does not sell.

7. Studied for

   Withdrawal-related and ethanol-related behavior in rodents

   In outbred rats that had drunk 10 percent ethanol as their only fluid for 24 weeks, the researchers then worked with the alcohol-preferring animals (those above a defined average daily intake) and gave them a free choice between ethanol and water. In that selected subgroup, a single administration of Selank eliminated the anxiety brought on by 48 hours of alcohol withdrawal on 2 separate behavioral tests, and prevented touch-triggered pain sensitivity from developing, without changing how much ethanol the animals drank. Note the scope: this is a selected alcohol-preferring subgroup under free-choice conditions, not the whole cohort. In a separate model where morphine withdrawal was triggered in dependent rats, a single administration of Selank reduced the overall withdrawal score by 39.6 percent, significantly reduced convulsive reactions, drooping eyelids and posture problems, and raised the touch-sensitivity threshold 9-fold; the authors explicitly described Selank as slightly inferior to diazepam, which reduced the score by 49.3 percent and raised the threshold 13-fold. Not equivalent to a benzodiazepine, on the authors' own reading. In DBA/2 mice, Selank prevented alcohol-induced hyperactivity from developing and blocked the display of motor sensitization, though not its formation. in rats (outbred) and in DBA/2 mice Preclinical moderate A well-described result with several independent outcome measures, but from a single laboratory or a single study design. Open for the full finding and the paper it came from.

   In the literature

   Withdrawal-related and ethanol-related behavior in rodents

   In outbred rats that had drunk 10 percent ethanol as their only fluid for 24 weeks, the researchers then worked with the alcohol-preferring animals (those above a defined average daily intake) and gave them a free choice between ethanol and water. In that selected subgroup, a single administration of Selank eliminated the anxiety brought on by 48 hours of alcohol withdrawal on 2 separate behavioral tests, and prevented touch-triggered pain sensitivity from developing, without changing how much ethanol the animals drank. Note the scope: this is a selected alcohol-preferring subgroup under free-choice conditions, not the whole cohort. In a separate model where morphine withdrawal was triggered in dependent rats, a single administration of Selank reduced the overall withdrawal score by 39.6 percent, significantly reduced convulsive reactions, drooping eyelids and posture problems, and raised the touch-sensitivity threshold 9-fold; the authors explicitly described Selank as slightly inferior to diazepam, which reduced the score by 49.3 percent and raised the threshold 13-fold. Not equivalent to a benzodiazepine, on the authors' own reading. In DBA/2 mice, Selank prevented alcohol-induced hyperactivity from developing and blocked the display of motor sensitization, though not its formation.^{References 19, 20, 21}

   Modelin rats (outbred) and in DBA/2 mice

   Confidence: moderate

   A well-described result with several independent outcome measures, but from a single laboratory or a single study design.

   Source

   Kolik LG et al., Bull Exp Biol Med, 2014;157(1):52-55, doi:10.1007/s10517-014-2490-4, PMID: 24913576; Konstantinopolsky MA et al., Bull Exp Biol Med, 2022;173(6):730-733, doi:10.1007/s10517-022-05624-x, PMID: 36322304; Kolik LG et al., Bull Exp Biol Med, 2016;162(1):56-59, doi:10.1007/s10517-016-3544-6, PMID: 27878720

   PubMed 24913576 PubMed 36322304 PubMed 27878720

   How this citation was checked

   Re-resolved on 2026-07-28. 24913576: PubMed efetch returns first author Kolik LG, Bull Exp Biol Med 2014;157(1):52-5, DOI 10.1007/s10517-014-2490-4; the abstract scopes the result to alcohol-preferring animals allowed free choice between 10 percent ethanol and water, after 24 weeks of 10 percent ethanol as the only fluid source, and states verbatim that Selank 'eliminated anxiety induced by ethanol withdrawal in tests elevated plus maze and social interaction tests and prevented the formation of mechanical allodynia without affecting ethanol consumption'. The alcohol-preferring free-choice qualifier is carried in the finding above rather than left out, and the numeric intake threshold is stated only as 'a defined average daily intake'. 36322304: Crossref /works/10.1007/s10517-022-05624-x returns title 'Selank, a Peptide Analog of Tuftsin, Attenuates Aversive Signs of Morphine Withdrawal in Rats', Bulletin of Experimental Biology and Medicine, 2022-10, volume 173, issue 6, pages 730-733, authors Konstantinopolsky M.A., Chernyakova I.V., Kolik L.G.; PubMed efetch returns the same and the abstract states verbatim the 39.6 percent reduction, p<0.0001 for convulsive reactions, ptosis and posture disorders, the 9-fold threshold increase, and 'Selank was slightly inferior to diazepam' with the 49.3 percent and 13-fold diazepam figures. An earlier draft of the source research had described this as comparable to diazepam; the authors' own hedge and their own figures are used instead. 27878720: PubMed efetch returns first author Kolik LG, Bull Exp Biol Med 2016;162(1):56-59, DOI 10.1007/s10517-016-3544-6; the abstract confirms male DBA/2 mice, prevention of ethanol-induced hyperlocomotion, and verbatim 'blocked manifestation of motor sensitization without affecting its formation'. Every numeric quantity for administration in all 3 abstracts is omitted.

8. Studied for

   Immune and cytokine signaling

   Selank descends from tuftsin, an immune-signaling fragment, which keeps immune endpoints in the research picture. The reported changes are time-dependent and go in both directions rather than being a one-way immune boost. In mouse spleen after a single administration, the C3 gene's message level fell about 3-fold within 30 minutes, the Casp1 message rose and fell in a wave, Il2rg changed at early timepoints, and Xcr1 fell at 90 minutes; a 2-amino-acid fragment of Selank produced largely the same profiles, which the authors read as the fragment contributing to the whole peptide's effect. In outbred white rats put through a 20-day social-confrontation stress model, the authors concluded that Selank brought serum IL-1-beta, IL-6, TNF-alpha and TGF-beta1 back down to close to control values. A precision point worth stating rather than smoothing over: the restoration of IL-4 reported in that same paper is attributed by its authors to Semax, not to Selank, and the paper also states that the stress-driven change in IL-4 was not statistically significant, so no IL-4 claim is made here for Selank. In a small human study, Selank added to cells in a dish completely suppressed IL-6 gene expression in blood cells from one enrolled clinical group but not in blood cells from healthy controls, while raising IL-6 concentration in those same cell cultures; separately, over 14 days of administration, shifts in Th1/Th2 cytokine balance were observed in the serum of a second enrolled group. Nothing here supports a directional consumer immunity claim. in mice (spleen), in outbred white rats, and one small human study with both cell-culture and in-body arms Preclinical moderate A well-described result with several independent outcome measures, but from a single laboratory or a single study design. Open for the full finding and the paper it came from.

   In the literature

   Immune and cytokine signaling

   Selank descends from tuftsin, an immune-signaling fragment, which keeps immune endpoints in the research picture. The reported changes are time-dependent and go in both directions rather than being a one-way immune boost. In mouse spleen after a single administration, the C3 gene's message level fell about 3-fold within 30 minutes, the Casp1 message rose and fell in a wave, Il2rg changed at early timepoints, and Xcr1 fell at 90 minutes; a 2-amino-acid fragment of Selank produced largely the same profiles, which the authors read as the fragment contributing to the whole peptide's effect. In outbred white rats put through a 20-day social-confrontation stress model, the authors concluded that Selank brought serum IL-1-beta, IL-6, TNF-alpha and TGF-beta1 back down to close to control values. A precision point worth stating rather than smoothing over: the restoration of IL-4 reported in that same paper is attributed by its authors to Semax, not to Selank, and the paper also states that the stress-driven change in IL-4 was not statistically significant, so no IL-4 claim is made here for Selank. In a small human study, Selank added to cells in a dish completely suppressed IL-6 gene expression in blood cells from one enrolled clinical group but not in blood cells from healthy controls, while raising IL-6 concentration in those same cell cultures; separately, over 14 days of administration, shifts in Th1/Th2 cytokine balance were observed in the serum of a second enrolled group. Nothing here supports a directional consumer immunity claim.^{References 22, 23, 24}

   Modelin mice (spleen), in outbred white rats, and one small human study with both cell-culture and in-body arms

   Confidence: moderate

   A well-described result with several independent outcome measures, but from a single laboratory or a single study design.

   Source

   Kolomin T et al., Mol Immunol, 2014;58(1):50-55, doi:10.1016/j.molimm.2013.11.002, PMID: 24291245; Yasenyavskaya AL (indexed in PubMed as Leonidovna YA) et al., Curr Rev Clin Exp Pharmacol, 2021;16(2):162-167, doi:10.2174/1574884715666200704152810, PMID: 32621722; Uchakina ON et al., Zh Nevrol Psikhiatr Im S S Korsakova, 2008;108(5):71-75, PMID: 18577961

   PubMed 24291245 PubMed 32621722 PubMed 18577961

   How this citation was checked

   Re-resolved on 2026-07-28. 24291245: PubMed efetch returns first author Kolomin T, Mol Immunol 2014;58(1):50-5, DOI 10.1016/j.molimm.2013.11.002; the abstract confirms mouse spleen, a single intraperitoneal administration, a significant 3-fold decrease in the C3 mRNA level 30 min afterward, the wave-like Casp1 alteration, the early Il2rg change, the Xcr1 reduction at 90 min, and the Gly-Pro coincidence. 32621722: Crossref /works/10.2174/1574884715666200704152810 returns title 'The Influence of Selank on the Level of Cytokines Under the Conditions of Social Stress', Current Reviews in Clinical and Experimental Pharmacology, 2021, volume 16, issue 2, pages 162-167, with the first author parsed as Yasenyavskaya A. Leonidovna, which is why PubMed indexes the surname as 'Leonidovna YA'; PubMed efetch returns the same bibliographic record, and both index forms are printed in the citation so it is checkable either way. The Selank-naming sentence is verbatim 'This peptide is able to reduce the concentration of IL-1beta, IL-6 and TNF-alpha, as well as TGF-beta1, practically reaching control values, when studying the effect of Selank on the level of cytokines under conditions of social stress'. The IL-4 restoration appears only in the preceding sentence, which begins 'Evaluation of the effect of Semax on the level of the cytokines', and the abstract separately states verbatim 'there was a tendency to decrease the concentration of IL-4 and increase the level of TNF-alpha but these indicators were not statistically significant'. An earlier draft of the source research carried 'and restored IL-4' for Selank; it was unsupported at this model and for this compound and is deleted. 18577961: PubMed efetch returns first author Uchakina ON, Zh Nevrol Psikhiatr Im S S Korsakova 2008;108(5):71-5; the abstract confirms complete suppression of peripheral blood IL-6 gene expression in the enrolled clinical group but not in the healthy controls, the significant IL-6 concentration increase in that group's cell culture, and the 14-day in-body Th1/Th2 balance change in a separate enrolled group. The two enrolled groups differ between the two arms and their specific diagnostic labels are deliberately not printed, per this store's standing rule that its own prose names no disease. The authors' own immunomodulator and infection-prevention recommendations are not carried over.

9. Studied for

   Monoamine and serotonin neurochemistry in rodents

   In Wistar rats whose serotonin production had been chemically blocked beforehand, Selank increased serotonin turnover in the brain stem 30 minutes after a single administration, whereas its parent peptide tuftsin did nothing in the brain stem and lowered turnover in the neocortex. In a strain-comparison study in BALB/c and C57Bl/6 mice, Selank raised norepinephrine in the hypothalamus of both strains, but produced OPPOSITE effects on dopamine breakdown products: those rose in the frontal cortex and hippocampus of C57Bl/6 mice and fell in BALB/c mice. Selank also lowered serotonin and its breakdown product in the hippocampus of BALB/c mice while leaving both untouched in C57Bl/6 mice. The strain-dependence and the outright reversal of direction are the notable results. These are mechanistic animal neurochemistry studies and establish nothing about human neurotransmitter levels, which is why no statement anywhere on this page says the compound balances or optimizes anyone's neurotransmitters. in rats (Wistar) and in mice (BALB/c and C57Bl/6) Preclinical moderate A well-described result with several independent outcome measures, but from a single laboratory or a single study design. Open for the full finding and the paper it came from.

   In the literature

   Monoamine and serotonin neurochemistry in rodents

   In Wistar rats whose serotonin production had been chemically blocked beforehand, Selank increased serotonin turnover in the brain stem 30 minutes after a single administration, whereas its parent peptide tuftsin did nothing in the brain stem and lowered turnover in the neocortex. In a strain-comparison study in BALB/c and C57Bl/6 mice, Selank raised norepinephrine in the hypothalamus of both strains, but produced OPPOSITE effects on dopamine breakdown products: those rose in the frontal cortex and hippocampus of C57Bl/6 mice and fell in BALB/c mice. Selank also lowered serotonin and its breakdown product in the hippocampus of BALB/c mice while leaving both untouched in C57Bl/6 mice. The strain-dependence and the outright reversal of direction are the notable results. These are mechanistic animal neurochemistry studies and establish nothing about human neurotransmitter levels, which is why no statement anywhere on this page says the compound balances or optimizes anyone's neurotransmitters.^{References 25, 26}

   Modelin rats (Wistar) and in mice (BALB/c and C57Bl/6)

   Confidence: moderate

   A well-described result with several independent outcome measures, but from a single laboratory or a single study design.

   Source

   Semenova TP et al., Eksp Klin Farmakol, 2009;72(4):6-8, PMID: 19803361; Narkevich VB et al., Eksp Klin Farmakol, 2008;71(5):8-12, PMID: 19093364

   PubMed 19803361 PubMed 19093364

   How this citation was checked

   Re-resolved on 2026-07-28 via PubMed efetch. 19803361: first author Semenova TP, Eksp Klin Farmakol 2009;72(4):6-8; the title specifies rats given PCPA beforehand and the abstract confirms Wistar rats, a group of 87 mature animals, that selank enhances 5-HT metabolism in the brain stem 30 min after a single administration to animals given PCPA beforehand, and verbatim that 'tuftsin induced no changes in the 5-HT metabolism in the brain stem and decreased it in the neocortex'. The authors' own 'can be used for the correction of disturbances' conclusion is not carried over, and the PCPA quantity is omitted. 19093364: first author Narkevich VB, same journal 2008;71(5):8-12; the abstract confirms BALB/C and C57Bl/6 mice in the open-field test, states verbatim that selank 'led to an increase in the NE level in the hypothalamus of both mice strains', gives the opposite directions for DOPAC and homovanillic acid between the two strains in frontal cortex and hippocampus, and states verbatim 'Selank induced a decrease in 5-HT and 5-HIAA levels in the hippocampus of BALB/C mice, but did not affect these parameters in C57Bl/6 animals'.

10. Studied for

    Despair-like behavior in rodent strain models

    Selank was tested against despair-like behavior that is built into the genetics of inbred WAG/Rij rats and against despair-like behavior provoked by circumstance in BALB/c mice, with ordinary outbred Wistar rats as controls. Given repeatedly at higher amounts, Selank counteracted the WAG/Rij pattern: those rats normally give up sooner in a forced-swim test and drink less sugar water, and both signs were reduced. In BALB/c mice, a single administration at lower amounts shortened the time spent immobile in the forced-swim test, but repeated administration and higher amounts did not. Selank did not meaningfully change the behavior of the control Wistar rats and did not change general movement or anxiety in the WAG/Rij rats. The strain-dependence and the fact that more was not better are themselves the notable results, and they limit how far this generalizes. This same report is also the source of the uncorroborated Russian third-phase claim flagged in the description above. in rats (WAG/Rij and Wistar) and in BALB/c mice Preclinical moderate A well-described result with several independent outcome measures, but from a single laboratory or a single study design. Open for the full finding and the paper it came from.

    In the literature

    Despair-like behavior in rodent strain models

    Selank was tested against despair-like behavior that is built into the genetics of inbred WAG/Rij rats and against despair-like behavior provoked by circumstance in BALB/c mice, with ordinary outbred Wistar rats as controls. Given repeatedly at higher amounts, Selank counteracted the WAG/Rij pattern: those rats normally give up sooner in a forced-swim test and drink less sugar water, and both signs were reduced. In BALB/c mice, a single administration at lower amounts shortened the time spent immobile in the forced-swim test, but repeated administration and higher amounts did not. Selank did not meaningfully change the behavior of the control Wistar rats and did not change general movement or anxiety in the WAG/Rij rats. The strain-dependence and the fact that more was not better are themselves the notable results, and they limit how far this generalizes. This same report is also the source of the uncorroborated Russian third-phase claim flagged in the description above.^{References 27}

    Modelin rats (WAG/Rij and Wistar) and in BALB/c mice

    Confidence: moderate

    A well-described result with several independent outcome measures, but from a single laboratory or a single study design.

    Source

    Sarkisova KIu, Kozlovskii II, Kozlovskaia MM. Zh Vyssh Nerv Deiat Im I P Pavlova. 2008;58(2):226-237. PMID: 18661785

    PubMed 18661785

    How this citation was checked

    Re-resolved on 2026-07-28 via PubMed efetch: PMID 18661785 returns first author Sarkisova KIu with Kozlovskii II and Kozlovskaia MM, Zh Vyssh Nerv Deiat Im I P Pavlova 2008;58(2):226-37, article in Russian. The abstract confirms the WAG/Rij, control Wistar and BALB/c arms, the repeated higher-amount effect against increased immobility in forced swimming and decreased sucrose intake or preference in WAG/Rij rats, the single lower-amount reduction of immobility in BALB/c mice with explicitly no significant effect after repeated administration or at higher amounts, and verbatim 'Selank did not affect the level of general locomotor activity and anxiety in WAG/Rij rats, and did not exert substantial effect on the behavior of control Wistar rats'. All specific numeric quantities are omitted and rendered only as relative higher and lower amounts. This abstract also carries the Russian claim of completed third-phase clinical testing that is flagged and contextualized in what_it_is. The area name departs from the source research file, which titled it with a disease name; the endpoints measured are named instead.

11. Studied for

    Anxiety-like behavior in rats with dopamine-neuron lesions

    In rats given a toxin that destroys dopamine-producing neurons, neither Semax nor Selank changed how much the animals moved in a maze or how they responded defensively. Selank did lower the anxiety level of these rats with damaged dopamine neurons, an effect the authors noted had already been seen in healthy rodents, leading them to conclude that damage to the substantia nigra does not change how the animal responds to this peptide. The 2 peptides were tested as separate arms, not given together. in rats with 6-hydroxydopamine lesions Preclinical moderate A well-described result with several independent outcome measures, but from a single laboratory or a single study design. Open for the full finding and the paper it came from.

    In the literature

    Anxiety-like behavior in rats with dopamine-neuron lesions

    In rats given a toxin that destroys dopamine-producing neurons, neither Semax nor Selank changed how much the animals moved in a maze or how they responded defensively. Selank did lower the anxiety level of these rats with damaged dopamine neurons, an effect the authors noted had already been seen in healthy rodents, leading them to conclude that damage to the substantia nigra does not change how the animal responds to this peptide. The 2 peptides were tested as separate arms, not given together.^{References 28}

    Modelin rats with 6-hydroxydopamine lesions

    Confidence: moderate

    A well-described result with several independent outcome measures, but from a single laboratory or a single study design.

    Source

    Slominsky PA et al., Dokl Biol Sci, 2017;474(1):106-109, doi:10.1134/S0012496617030048, PMID: 28702721

    PubMed 28702721

    How this citation was checked

    Re-resolved on 2026-07-28 via PubMed efetch: PMID 28702721 returns first author Slominsky PA, Dokl Biol Sci 2017;474(1):106-109, DOI 10.1134/S0012496617030048, with co-authors Shadrina MI, Kolomin TA, Stavrovskaya AV, Filatova EV, Andreeva LA, Illarioshkin SN and Myasoedov NF. The abstract confirms the 6-hydroxydopamine lesion model, verbatim 'both peptides did not affect motor activity of rats in elevated cross shaped maze and passive defensive behavior of the animals', 'Selank decreased level of anxiety of rats with toxic damage of DA neurons', the note that such effects were previously seen in healthy rodents, and the conclusion 'toxic damage of substantia nigra does not affect the response of the rat organism on this peptide'. The abstract describes Semax and Selank as separate arms with no co-administration anywhere. The area name departs from the source research file, which framed the model by a disease analogy; the lesion itself is named instead, which is also the more precise description.

12. Studied for

    Analytical identification, quality control and regulatory context

    Belgium's official medicines control laboratory analyzed 2 suspicious seized pharmaceutical preparations, from 2017 and 2018, and identified their contents as the research peptides Selank and Semax. The authors state that, to their knowledge, these peptides 'have not completed any clinical trials', and that an online search found them freely available as lyophilized powder or in nasal sprays. The paper's real contribution is a validated LC-MS/MS testing method, built to comply with the European official medicines control laboratory network's recommendation on interpreting screening results for unknown peptides and validated to the ISO 17025 standard, able to identify 10 putative cognitive-enhancing polypeptides sold online. This is the most useful citation in this dossier for the question 'can an independent laboratory confirm what is in a vial', and it is also the clearest independent statement of Selank's non-approved status outside Russia. analytical chemistry only (LC-MS/MS on seized preparations and reference peptides; no biological model at all) Preclinical moderate A well-described result with several independent outcome measures, but from a single laboratory or a single study design. Open for the full finding and the paper it came from.

    In the literature

    Analytical identification, quality control and regulatory context

    Belgium's official medicines control laboratory analyzed 2 suspicious seized pharmaceutical preparations, from 2017 and 2018, and identified their contents as the research peptides Selank and Semax. The authors state that, to their knowledge, these peptides 'have not completed any clinical trials', and that an online search found them freely available as lyophilized powder or in nasal sprays. The paper's real contribution is a validated LC-MS/MS testing method, built to comply with the European official medicines control laboratory network's recommendation on interpreting screening results for unknown peptides and validated to the ISO 17025 standard, able to identify 10 putative cognitive-enhancing polypeptides sold online. This is the most useful citation in this dossier for the question 'can an independent laboratory confirm what is in a vial', and it is also the clearest independent statement of Selank's non-approved status outside Russia.^{References 29}

    Modelanalytical chemistry only (LC-MS/MS on seized preparations and reference peptides; no biological model at all)

    Confidence: moderate

    A well-described result with several independent outcome measures, but from a single laboratory or a single study design.

    Source

    Vanhee C, Francotte A, Janvier S, Deconinck E. Drug Test Anal. 2020;12(3):371-381. doi:10.1002/dta.2717. PMID: 31667971

    PubMed 31667971

    How this citation was checked

    Re-resolved on 2026-07-28 two ways. Crossref /works/10.1002/dta.2717 returns the exact title, Drug Testing and Analysis, 2020-01-29, volume 12, issue 3, pages 371-381, authors Vanhee Celine, Francotte Antoine, Janvier Steven, Deconinck Eric; PubMed efetch for 31667971 returns the same record with the Sciensano, Brussels affiliations. The abstract confirms the 2 suspicious preparations from the end of 2017 and 2018, their identification as Selank and Semax, verbatim 'which, to our knowledge, have not completed any clinical trials', the online availability as lyophilized powder or in nasal sprays, the total of 10 putative cognitive enhancing polypeptides analyzed, and the OMCL recommendation-paper and ISO 17025 validation framing. This is the only citation in this dossier from a laboratory with no connection to the Russian research program that produced the rest of it.

13. Studied for

    Antiviral endpoints against one influenza A strain

    Against one influenza strain, A/Aichi 2/68 (H3N2), antiviral effects of Selank were reported both in cell culture and in infected laboratory animals. Adding Selank to the cell culture 24 hours before the virus was introduced was the most effective schedule and completely stopped the virus from reproducing in that arm; in the animals, survival was likewise highest when the peptide was given before infection rather than after. In the animals, Selank switched on the gene for interferon-alpha, a natural antiviral signal, without changing IL-4, IL-10 or TNF-alpha, and the authors proposed that the antiviral action may come from rebalancing Th1/Th2/Treg cytokines both directly and indirectly by way of the central nervous system. This is preclinical only. No human infection study was located, and no protective claim for a person is made anywhere on this page. in cultured cells and in infected laboratory animals Preclinical preliminary A single study, an early mechanistic observation, or a result whose interpretation is the authors' own inference. Open for the full finding and the paper it came from.

    In the literature

    Antiviral endpoints against one influenza A strain

    Against one influenza strain, A/Aichi 2/68 (H3N2), antiviral effects of Selank were reported both in cell culture and in infected laboratory animals. Adding Selank to the cell culture 24 hours before the virus was introduced was the most effective schedule and completely stopped the virus from reproducing in that arm; in the animals, survival was likewise highest when the peptide was given before infection rather than after. In the animals, Selank switched on the gene for interferon-alpha, a natural antiviral signal, without changing IL-4, IL-10 or TNF-alpha, and the authors proposed that the antiviral action may come from rebalancing Th1/Th2/Treg cytokines both directly and indirectly by way of the central nervous system. This is preclinical only. No human infection study was located, and no protective claim for a person is made anywhere on this page.^{References 30}

    Modelin cultured cells and in infected laboratory animals

    Confidence: preliminary

    A single study, an early mechanistic observation, or a result whose interpretation is the authors' own inference.

    Source

    Ershov FI et al., Vopr Virusol, 2009;54(5):19-24. PMID: 19882898

    PubMed 19882898

    How this citation was checked

    Re-resolved on 2026-07-28 via PubMed efetch: PMID 19882898 returns first author Ershov FI, Vopr Virusol 2009;54(5):19-24, article in Russian, with co-authors Uchakin PN, Uchakina ON, Mezentseva MV, Alekseeva LA and Miasoedov NF. The abstract confirms strain A/Aichi 2/68 (H3N2), effects in both systems, verbatim 'Selank added to the cell culture 24 hours before inoculation (a preventive use scheme) showed the highest efficiency, by completely suppressing viral reproduction', the highest animal survival under the prevention scheme, verbatim 'induced the gene expression of interferon-alpha (IFN-alpha), without affecting that of interleukin (IL)-4, IL-10, or tumor necrosis factor-alpha', and the Th1/Th2/Treg cytokine equilibrium mechanism hypothesis. The abstract names no species for the in vivo arm, so none is asserted. The authors' closing 'it has no negative effects' remark is deliberately not carried over. An earlier draft of the source research claimed the authors linked the effect to interferon-alpha induction rather than direct antiviral action; that contrast is contradicted by the complete suppression of viral reproduction in the pre-inoculation cell-culture arm and is not repeated. The area name departs from the source research file so the row label names the virus and the experimental system rather than an infection.

14. Studied for

    Resting-state brain connectivity (human imaging)

    52 healthy volunteers were scanned by resting-state MRI 3 times: before, then 5 and 20 minutes after receiving Semax, Selank or a placebo. The researchers looked at the amygdala (a fear and anxiety hub) and the dorsolateral prefrontal cortex (an executive-control region) on both sides of the brain. They found differences between groups and between timepoints in how strongly the right amygdala was coupled to a right-hemisphere region spanning the fusiform, inferior and middle temporal, and parahippocampal gyri. This is an exploratory observation about brain network measures with no cognitive or clinical outcome measured at all, and it is a single study. It is also the only placebo-controlled human study in this dossier, which is worth knowing in both directions. HUMAN in a human trial (52 healthy volunteers, placebo-controlled, resting-state fMRI) Preclinical preliminary A single study, an early mechanistic observation, or a result whose interpretation is the authors' own inference. Open for the full finding and the paper it came from.

    In the literature

    Resting-state brain connectivity (human imaging)

    52 healthy volunteers were scanned by resting-state MRI 3 times: before, then 5 and 20 minutes after receiving Semax, Selank or a placebo. The researchers looked at the amygdala (a fear and anxiety hub) and the dorsolateral prefrontal cortex (an executive-control region) on both sides of the brain. They found differences between groups and between timepoints in how strongly the right amygdala was coupled to a right-hemisphere region spanning the fusiform, inferior and middle temporal, and parahippocampal gyri. This is an exploratory observation about brain network measures with no cognitive or clinical outcome measured at all, and it is a single study. It is also the only placebo-controlled human study in this dossier, which is worth knowing in both directions.^{References 31}

    Modelin a human trial (52 healthy volunteers, placebo-controlled, resting-state fMRI)

    Confidence: preliminary

    A single study, an early mechanistic observation, or a result whose interpretation is the authors' own inference.

    Source

    Panikratova YR et al., Dokl Biol Sci, 2020;490(1):9-11, doi:10.1134/S001249662001007X, PMID: 32342318

    PubMed 32342318

    How this citation was checked

    Re-resolved on 2026-07-28 two ways. Crossref /works/10.1134/S001249662001007X returns title 'Functional Connectomic Approach to Studying Selank and Semax Effects', Doklady Biological Sciences, 2020-01, volume 490, issue 1, pages 9-11, authors Panikratova Ya.R., Lebedeva I.S., Sokolov O.Yu., Rumshiskaya A.D., Kupriyanov D.A., Kost N.V., Myasoedov N.F.; PubMed efetch for 32342318 returns the same record. The abstract confirms 52 healthy participants, the amygdala and dorsolateral prefrontal cortex regions of interest in both hemispheres, the 3 scan timepoints, the Semax, Selank and placebo arms, and verbatim 'Between-group alongwith between-condition differences were revealed in FC between the right amygdala and a region in fusiform, inferior and middle temporal as well as parahippocampal gyri in the right hemisphere'. No cognitive or clinical outcome measure appears anywhere in the abstract, which is why none is claimed.

15. Studied for

    Cell-level toxicity screening

    In a screen of several peptides applied to mouse embryonic stem cells and the cells they turn into, Selank had only an insignificant effect on the formation of mature neurons, and the authors concluded that the peptides studied do not produce a toxic effect during the embryonic and fetal period of life. One measured change is worth stating plainly rather than burying inside that conclusion: when the researchers looked specifically at stem cells turning into GABA-producing neurons, Selank reduced the proportion of those cells by 61 percent compared with control cells that received nothing (the comparators thyroliberin and nerve growth factor reduced them by 58 and 87 percent). This is a cell-culture observation, not a safety conclusion for any living organism, and it is a single study. It is carried here because it is the only toxicity work in the record and because the number inside it runs against the sentence wrapped around it. in cultured mouse embryonic stem cells and their derivatives Preclinical preliminary A single study, an early mechanistic observation, or a result whose interpretation is the authors' own inference. Open for the full finding and the paper it came from.

    In the literature

    Cell-level toxicity screening

    In a screen of several peptides applied to mouse embryonic stem cells and the cells they turn into, Selank had only an insignificant effect on the formation of mature neurons, and the authors concluded that the peptides studied do not produce a toxic effect during the embryonic and fetal period of life. One measured change is worth stating plainly rather than burying inside that conclusion: when the researchers looked specifically at stem cells turning into GABA-producing neurons, Selank reduced the proportion of those cells by 61 percent compared with control cells that received nothing (the comparators thyroliberin and nerve growth factor reduced them by 58 and 87 percent). This is a cell-culture observation, not a safety conclusion for any living organism, and it is a single study. It is carried here because it is the only toxicity work in the record and because the number inside it runs against the sentence wrapped around it.^{References 32}

    Modelin cultured mouse embryonic stem cells and their derivatives

    Confidence: preliminary

    A single study, an early mechanistic observation, or a result whose interpretation is the authors' own inference.

    Source

    Kobylyanskii AG et al., Bull Exp Biol Med, 2017;163(6):731-736, doi:10.1007/s10517-017-3891-y, PMID: 29063333

    PubMed 29063333

    How this citation was checked

    Re-resolved on 2026-07-28 via PubMed efetch requested as XML with nested markup preserved, because a plain-text PubMed fetch truncates this abstract mid-sentence at a superscript character and drops exactly the numbers cited here; the same content was cross-checked against the Europe PMC core record. PMID 29063333 returns first author Kobylyanskii AG, Bull Exp Biol Med 2017;163(6):731-736, DOI 10.1007/s10517-017-3891-y. The complete abstract confirms mouse embryonic stem cells and derivatives, the peptide panel including Selank, verbatim 'HLDF-6, Selank, and thyroliberin produced an insignificant effect on the differentiation of these cells into mature neurons', verbatim 'Analysis of differentiation of embryonic stem cells into GABA+ neurons showed that Selank, thyroliberin ... and NGF ... decrease the ratio of these cells by 61, 58, and 87%, respectively, in comparison with the control', and the closing non-toxicity conclusion. The comparator concentrations are omitted.

16. Studied for

    Blood clotting behavior (test tube)

    A clot-formation test run on 3 related glyproline peptides, including Selank, plus His-Phe-Arg-Trp-Pro-Gly-Pro and Pro-Gly-Pro, showed anticoagulant effects across the concentrations tested, with every measured clotting parameter shifting toward slower, weaker clot formation compared with control. Of the 3 peptides, Selank showed the strongest anticoagulant potency. This is a single test-tube observation and no clinical significance is claimed, but it is included because a blood-thinning signal is exactly the kind of finding a research dossier should not omit. IN VITRO in vitro only (thromboelastography) Preclinical preliminary A single study, an early mechanistic observation, or a result whose interpretation is the authors' own inference. Open for the full finding and the paper it came from.

    In the literature

    Blood clotting behavior (test tube)

    A clot-formation test run on 3 related glyproline peptides, including Selank, plus His-Phe-Arg-Trp-Pro-Gly-Pro and Pro-Gly-Pro, showed anticoagulant effects across the concentrations tested, with every measured clotting parameter shifting toward slower, weaker clot formation compared with control. Of the 3 peptides, Selank showed the strongest anticoagulant potency. This is a single test-tube observation and no clinical significance is claimed, but it is included because a blood-thinning signal is exactly the kind of finding a research dossier should not omit.^{References 33}

    Modelin vitro only (thromboelastography)

    Confidence: preliminary

    A single study, an early mechanistic observation, or a result whose interpretation is the authors' own inference.

    Source

    Rogozinskaya EY, Lyapina MG. Bull Exp Biol Med. 2017;164(2):170-172. doi:10.1007/s10517-017-3950-4. PMID: 29181670

    PubMed 29181670

    How this citation was checked

    Re-resolved on 2026-07-28 two ways. Crossref /works/10.1007/s10517-017-3950-4 returns the full title 'Anticoagulant Effects of Arginine-Containing Peptides of the Glyproline Family (His-Phe-Arg-Trp-Pro-Gly-Pro and Thr-Lys-Pro-Arg-Pro-Gly-Pro) Revealed by Thromboelastography', Bulletin of Experimental Biology and Medicine, volume 164, issue 2, pages 170-172, authors Rogozinskaya E. Ya. and Lyapina M. G.; PubMed efetch for 29181670 returns the same record. The abstract confirms thromboelastography on the 3 named glyproline oligopeptides, that 'The parameters R, K, MA, S, TMA, and J changed to hypocoagulation direction in comparison to the control', and verbatim 'Selank demonstrated the maximal anticoagulation potency'. The title itself independently confirms that Thr-Lys-Pro-Arg-Pro-Gly-Pro is the sequence being called Selank, which is a second attestation of the identity recorded in molecular_facts.

17. Studied for

    Gut, liver and stomach endpoints under stress

    This is a scattered set of small single-group rodent reports rather than a developed line of evidence, and it is presented that way. Across 3 different laboratory models of stomach ulcer formation, Selank and the breakdown products the body makes from it reduced the area of the ulcers. In Wistar rats held under chronic restraint stress, where stress reduced the beneficial resident gut bacteria and let opportunistic organisms increase, Selank restored the gut bacterial balance. A companion study in the same model found that stress produced thinning of the colon wall, an inflammatory reaction and changes in mast cells alongside raised corticosterone, and that Selank lowered corticosterone and reduced those tissue changes. A separate liver study needs its 2 conditions kept apart, because merging them misleads. Under ACUTE restraint stress, Selank lowered catalase activity, superoxide dismutase activity and malondialdehyde in the liver and raised total antioxidant activity there, and at the highest amount tested it also lowered aminotransferase levels in blood serum. Under CHRONIC restraint stress, the picture was narrower: lower superoxide dismutase activity and lower malondialdehyde in liver tissue plus lower AST in serum, with the other measured parameters unchanged. Note that corticosterone is the rodent stress hormone; this says nothing about cortisol in humans. in rats (Wistar) and in animal gastric ulcer models Preclinical preliminary A single study, an early mechanistic observation, or a result whose interpretation is the authors' own inference. Open for the full finding and the paper it came from.

    In the literature

    Gut, liver and stomach endpoints under stress

    This is a scattered set of small single-group rodent reports rather than a developed line of evidence, and it is presented that way. Across 3 different laboratory models of stomach ulcer formation, Selank and the breakdown products the body makes from it reduced the area of the ulcers. In Wistar rats held under chronic restraint stress, where stress reduced the beneficial resident gut bacteria and let opportunistic organisms increase, Selank restored the gut bacterial balance. A companion study in the same model found that stress produced thinning of the colon wall, an inflammatory reaction and changes in mast cells alongside raised corticosterone, and that Selank lowered corticosterone and reduced those tissue changes. A separate liver study needs its 2 conditions kept apart, because merging them misleads. Under ACUTE restraint stress, Selank lowered catalase activity, superoxide dismutase activity and malondialdehyde in the liver and raised total antioxidant activity there, and at the highest amount tested it also lowered aminotransferase levels in blood serum. Under CHRONIC restraint stress, the picture was narrower: lower superoxide dismutase activity and lower malondialdehyde in liver tissue plus lower AST in serum, with the other measured parameters unchanged. Note that corticosterone is the rodent stress hormone; this says nothing about cortisol in humans.^{References 34, 35, 36, 37}

    Modelin rats (Wistar) and in animal gastric ulcer models

    Confidence: preliminary

    A single study, an early mechanistic observation, or a result whose interpretation is the authors' own inference.

    Source

    Pavlov TS et al., Bull Exp Biol Med, 2007;143(1):51-53, doi:10.1007/s10517-007-0014-1, PMID: 18019011; Mukhina AY et al., Bull Exp Biol Med, 2019;167(2):226-228, doi:10.1007/s10517-019-04496-y, PMID: 31236882; Mukhina AY et al., Bull Exp Biol Med, 2020;169(2):281-285, doi:10.1007/s10517-020-04868-9, PMID: 32651826; Fomenko EV et al., Bull Exp Biol Med, 2017;163(4):415-418, doi:10.1007/s10517-017-3817-8, PMID: 28853100

    PubMed 18019011 PubMed 31236882 PubMed 32651826 PubMed 28853100

    How this citation was checked

    Re-resolved on 2026-07-28 via PubMed efetch for all 4. 18019011: first author Pavlov TS, Bull Exp Biol Med 2007;143(1):51-3, DOI 10.1007/s10517-007-0014-1; the entire abstract reads that antiulcer properties of Selank and its in vivo formed metabolites were studied on 3 experimental models of ulceration and that 'The test peptides decreased the area of experimental gastric ulcers'. No species is named in the record, so none is asserted. 31236882: first author Mukhina AY, Bull Exp Biol Med 2019;167(2):226-228, DOI 10.1007/s10517-019-04496-y; the abstract confirms Wistar male rats under chronic restraint stress, the decrease in obligate microflora with an increase in opportunistic microorganisms, and verbatim 'Selank restored intestinal microbiota'. 32651826: first author Mukhina AY, Bull Exp Biol Med 2020;169(2):281-285, DOI 10.1007/s10517-020-04868-9; the abstract confirms Wistar male rats and verbatim 'signs of atrophy, inflammatory reaction, and changes in the number and functional activity of mast cells were observed against the background of increased corticosterone level', and that Selank decreased corticosterone and reduced the pathomorphological manifestations. 28853100: first author Fomenko EV, Bull Exp Biol Med 2017;163(4):415-418, DOI 10.1007/s10517-017-3817-8; the abstract splits its results by condition and an earlier draft of the source research merged them. Verbatim for the acute arm: 'Under conditions of acute restraint stress, Selank ... decreased catalase and superoxide dismutase activities and malondialdehyde concentration and increased total antioxidant activity in the liver homogenate', with the highest-amount arm reducing aminotransferases in blood serum. Verbatim for the chronic arm: 'Under conditions of chronic stress, Selank ... reduced superoxide dismutase activity and malondialdehyde concentration in the liver tissue and AST activity in the serum. The other parameters remained unchanged.' The split is kept and every numeric quantity is omitted.

12 moderate / 5 preliminaryRated by how many independent labs and how many kinds of experiment found the same thing.