Selank Benefits: What the Research Actually Shows
Dr. Sieglinde Klaus
Scientific Editorial Team · Bergdorf Bioscience
Table of Contents
- 01What is Selank and what does the research say about its benefits?
- 02What do the human studies of Selank show?
- 03What distinguishes monotherapy from combination treatment?
- 04Which GABA-related findings have been measured?
- 05Which BDNF and gene expression findings exist?
- 06What do the animal models mean for the research question?
- 07Which endpoints are most informative?
- 08What is known about tolerability and unresolved points?
- 09How do Selank and Semax differ?
- 10How does Selank fit as a research material?
- 11What questions about Selank come up most often?
- Are there human studies of Selank?
- How long does the effect last?
- Does Selank cause dependence?
- Which side effects are documented?
- Is Selank the same as Semax?
- 12Which primary papers inform this article?
Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro. It builds on the immune peptide tuftsin and carries Pro-Gly-Pro at its C-terminus. In controlled human studies with 60 to 70 participants, anxiety symptoms declined to a similar degree as with a benzodiazepine comparator, quality of life improved, and in combination several side effects of the benzodiazepine were less pronounced. A placebo-controlled imaging study with 52 healthy participants showed altered functional connectivity between the right amygdala and the right temporal cortex. Those findings come first here.
What matters is which measurement stands behind the word effect. Research measures Selank on three levels: binding and gene expression, behavior and tissue in animal models, and clinical scales in humans. This article sorts the studies by those levels, names participant count, comparison group and endpoint, and shows where the data hold. Substance identity is documented in the Selank peptide lexicon; the findings are the subject here.
What is Selank and what does the research say about its benefits?
Selank is a synthetic analog of tuftsin, studied in research for anxiolytic, antiasthenic and cognitive endpoints. What gets measured are anxiety scales, attention and memory, stress and immune parameters, monoamines, receptor binding and gene expression. The substance consists of seven amino acids and appears in the literature under the development designation TP-7.
The sequence combines two building blocks. The core Thr-Lys-Pro-Arg comes from tuftsin, an immune peptide from the heavy chain of immunoglobulin G. The C-terminal extension Pro-Gly-Pro is described in the literature as a stabilizer and carrier element (Siebert et al., 2017). The result is a peptide of immune origin that is studied mainly for behavior and anxiety.
Effect here means a measurable difference from a control. A binding assay shows an interaction with a receptor system, a gene expression experiment shifted mRNA values, a behavioral test a group difference under defined stress conditions, a clinical scale the rating of symptoms. These levels are not interchangeable. The strength of the Selank literature is that all four have been addressed. Its weakness is that the clinical papers are small and mostly available only as abstracts.
In a distribution experiment with tritium-labeled glyprolines, intranasal administration in rats was the most favorable route for accumulation in the central nervous system; all routes showed a high affinity for stomach tissue (Ashmarin et al., 2008). The degradation products described were TKPRP, TKP, RP and GP (Zolotarev et al., 2006). Anyone looking for Selank as a research material will find the lyophilized 10 mg product on the Selank product page. The pack size describes the quantity in the package, not a use.
What do the human studies of Selank show?
The controlled human studies show a clear anxiolytic effect: in three comparison studies with 60 to 70 participants, scale scores under Selank were similar to those under medazepam or phenazepam, and under the combination with phenazepam the scale effect appeared earlier. Add to that an imaging study with 52 healthy volunteers and smaller papers on anxiety, asthenia and immune parameters.
The first controlled paper compared Selank with medazepam in 2008. 62 patients with generalized anxiety disorder or neurasthenia were assigned to the two treatments, 30 received Selank and 32 medazepam. Hamilton, Zung and CGI scales were recorded, together with the half-life of Leu-enkephalin in serum. The authors report a similar anxiolytic effect for both substances, plus antiasthenic and psychostimulant effects under Selank; the Leu-enkephalin half-life rose, mainly in generalized anxiety disorder (Zozulia et al., 2008). The study thus connects clinic and molecule: a peptide that inhibits the breakdown of enkephalins changes a measurable serum value.
The second paper compared Selank with phenazepam in 60 patients with phobic-anxious and somatoform disorders in 2014. It reports a pronounced anxiolytic effect, a mild nootropic effect and better quality of life. The anxiolytic effect persisted one week after the last administration (Medvedev et al., 2014). That describes the duration in the protocol used at the time, not a general duration of effect.
The third clinical paper tested the combination in 2015. 70 patients with anxiety disorders received either phenazepam alone (30 people) or phenazepam plus Selank (40 people). HDRS, CGI, the Spielberger scale, the UKU side effect scale, the Stroop test, a verbal fluency test and SF-36 were recorded. Under the combination the scale effect appeared earlier, several unwanted phenazepam effects were less pronounced, and quality of life was better (Medvedev et al., 2015). This is the clinically strongest finding in the literature: it shows an added benefit over an established treatment and a tolerability advantage.
The imaging study examined 52 healthy participants with resting-state fMRI before and 5 and 20 minutes after administration of Selank, Semax or placebo. The groups differed in functional connectivity between the right amygdala and a region in the right temporal cortex. Selank and Semax showed shared and specific effects (Panikratova et al., 2020). The endpoint is imaging, not clinical; the study demonstrates a measurable central response, not symptom improvement.
Further human papers with reported content add to the picture:
- Zozulya et al. (2001): In generalized anxiety, the half-life of plasma enkephalin was shortened and enkephalinase activity reduced, but not in panic disorder and agoraphobia. Selank inhibited hydrolysis in a dose-dependent manner with an IC50 of 15 micromoles (DOI).
- Uchakina et al. (2008): In patients with anxiety-asthenia, Selank shifted the Th1/Th2 cytokine balance over 14 days. In peripheral blood cell cultures, a concentration of 10 to the power of minus 7 moles per liter suppressed IL-6 gene expression completely in depressed patients, but not in healthy subjects (PubMed).
- Verbenko (2018): In an open controlled study with 30 patients with adjustment disorder, PHQ values were lower under a two-week Selank treatment than in the waiting-list group. For somatic symptoms 1.2 versus 3.6 were reported, for nutritional problems 0.1 versus 3.4, and for alcohol misuse 0.3 versus 1.5, each p<0.05 (DOI).
- Pogodina and Nikiforova (2024): 64 patients with post-COVID asthenia received neuroprotectives with or without Selank nasal drops over 30 days. A good effect on asthenia and mental performance is reported, along with a decline in anxiety and depression symptoms (DOI).
- Dontsova et al. (2020): In 124 patients with moderate atopic dermatitis, Selank strengthened the anti-inflammatory effect of baseline therapy, most strongly with UV phototherapy (p<0.001) (DOI).
Four further human papers are documented but evidenced only by their titles: an application in climacteric syndrome (Starikov and Fedorov, 2019), a potentiation of SSRIs (Verbenko and Shakina, 2019), a Phase II conference abstract (Neznamov et al., 200580332-3)) and a conference abstract on response in generalized anxiety disorder (Syunyakov et al., 201275281-1)). They document research in these fields, not content.
The methodological limit is the same in every clinical paper: the Russian-language full texts were not accessible, and all statements rest on abstracts. Randomization, blinding, dropouts, effect sizes and adverse events are not described there. Participant numbers between 30 and 124 limit precision, and the large anxiety studies used active comparators instead of placebo.
What distinguishes monotherapy from combination treatment?
The monotherapy studies show Selank's standalone anxiolytic effect; the combination study shows the added benefit: under phenazepam plus Selank the scale effect appeared earlier, and several side effects of the benzodiazepine were less pronounced. That answers two questions: whether Selank reduces anxiety on its own and whether it improves an existing treatment.
For monotherapy, the papers from 2008 and 2014 speak. Both compared Selank with a benzodiazepine and reported comparable anxiolytic effects. A comparison against placebo is missing. That does not mean the effects are placebo; it means the substance's share of the observed effect cannot be isolated from these designs.
For the combination, the 2015 paper speaks. It shows an earlier scale effect and a more favorable side effect profile. Because both groups received phenazepam, the difference between the groups is attributable to the addition of Selank. Within this study that is a clean comparison; it does not demonstrate Selank monotherapy.
The animal literature supports the combination logic. In the rat chronic stress model, Selank plus diazepam showed the strongest anxiolytic behavioral effect of the conditions tested (Kasian et al., 2017). In BALB/c mice with elevated baseline anxiety, Selank increased the time spent in the open arms compared with a tranquilizer alone and blocked the locomotor suppression caused by therapeutic diazepam and olanzapine doses, but not by haloperidol (Kost et al., 2025). Both papers describe an interaction, not the addition of two identical effects.
Which GABA-related findings have been measured?
Selank changes GABA binding in membrane preparations and the mRNA of GABA-related genes in the rat frontal cortex; in the human neuroblastoma cell line IMR-32 it does not change the evaluated mRNA values on its own but shifts the effect of GABA and olanzapine. That gives three measurement levels for the same hypothesis: binding, tissue and cell culture. The results point in the same direction but differ in size and evidentiary weight.
The binding level was addressed by a radioligand study with labeled GABA on brain cell membrane preparations. Selank influenced GABA binding and was interpreted as a positive allosteric modulator; the effect together with benzodiazepines was not cumulative (Vyunova et al., 2018). That is a proposed molecular mechanism, not clinical proof of receptor engagement.
The tissue level was addressed by a rat study with a single intranasal dose of 300 micrograms per kilogram. mRNA in the frontal cortex was examined after one and three hours. The paper found altered expression patterns of genes of GABAergic neurotransmission (Volkova et al., 2016). Because tissue pools were measured, the values are not a sum of independent single measurements.
The cell level was addressed by a study on IMR-32 cells. Selank alone at 1 nanomole per well and one hour of incubation did not change the evaluated mRNA values; of 84 genes examined, 69 were evaluable. Together with GABA it suppressed the GABA-induced expression changes almost completely; together with olanzapine, more genes changed than under olanzapine alone (Filatova et al., 2017). In this cell model Selank alone is not a strong transcriptional trigger but a modulator.
Two further preparations support this reading. In hippocampal slices from rats, Selank at 1 to 8 micromoles increased the inhibitory synaptic activity of CA1 neurons, without a clear dose dependence (Povarov et al., 2017). In murine embryonic stem cells, a concentration of 100 micromoles lowered the share of GABA-producing neurons by 61 percent, without a toxicity signal (Kobylyanskii et al., 2017).
Taken together, this yields a consistent but indirect picture. Selank acts on GABAergic systems, depending on what is measured. Whether a clinical anxiety effect follows is decided not by the binding assay but by the controlled human study.
Which BDNF and gene expression findings exist?
The gene expression data show a consistent pattern: in stress, addiction and ischemia models Selank shifts mRNA programs, and BDNF changes as part of those programs. The strongest finding comes from a long-term ethanol model. Rats received ten percent ethanol for 30 weeks; Selank was injected over seven days at 0.3 milligrams per kilogram daily. The treatment prevented ethanol-induced memory and attention deficits (p<0.01) and prevented the ethanol-induced BDNF increase in the hippocampus and prefrontal cortex (p<0.05). In nine-month-old rats without ethanol, Selank increased cognition (p<0.05) (Kolik et al., 2019).
A second strand concerns the breadth of the transcriptome response. After intranasal administration of 200 micrograms per kilogram, 36 genes in the rat hippocampus changed more than twofold, and 20 after a treatment course; the genes belonged mainly to membrane proteins (Kolomin et al., 2013). The title of a 2024 paper names changes in hippocampal gene expression in the first hours after acute restraint stress (Filippenkov et al., 2024); no abstract was available. In the ischemia model, 118 genes were differentially expressed 4.5 hours after the insult, 99 of them downregulated (Molecular Biology, 2026).
For BDNF in the hippocampus after intranasal Selank administration, a 2008 paper is often cited. It is documented by DOI and title, but no abstract was available (Inozemtseva et al., 2008). A substantive statement on direction, size or conditions cannot be derived from it.
The classification is therefore clear: gene expression and BDNF are plasticity markers. They show that Selank leaves traces in neuronal tissue. They do not show that this becomes a clinical effect. Human BDNF was not measured in the papers evaluated.
What do the animal models mean for the research question?
The animal models show measurable effects in anxiety, addiction, ischemia and stress models and at the same time show that strain, dose, route of administration and stress context determine the outcome. They therefore deliver hypotheses about mechanisms and limits, not evidence of human efficacy.
- Anxiety and long-term use: 24 Wistar rats received TP-7 daily at 0.3 milligrams per kilogram intraperitoneally. Anxiety scores fell from the second day and remained altered over four weeks; body mass was unchanged (Czabak-Garbacz et al., 2006).
- Chronic stress: Rats underwent 14 days of unpredictable chronic mild stress and received Selank intranasally, diazepam orally, or both. In the elevated plus maze the combination showed the strongest anxiolytic effect. Without stress, anxiety indicators worsened under repeated administration, less so under Selank (Kasian et al., 2017).
- Strain dependence: In BALB/c mice Selank acted anxiolytically, in C57BL/6 mice it did not; sedative effects did not occur even at high doses (Seredenin et al., 1998). In BALB/c it also prolonged the plasma half-life of Leu-enkephalin, in C57BL/6 it did not (Sokolov et al., 2002).
- Cognition after hypoxia: Rats after prenatal hypoxia showed, under 300 micrograms per kilogram, two to three times higher sensory attention and a learning performance improved by a factor of 1.5 (each p<0.01) (Semenova et al., 2008).
- Opioid withdrawal: In naloxone-precipitated morphine withdrawal, Selank at 0.3 milligrams per kilogram lowered the total withdrawal index by 39.6 percent (p<0.0001) and raised the tactile threshold by a factor of 9; diazepam reached 49.3 percent and a factor of 13 (Konstantinopolsky et al., 2022).
- Stroke model: In rats with intracerebral hemorrhage, neurological function improved on day 10 only in the peptide groups; the groups comprised five animals (Skvortsova et al., 2009).
- Stress, liver and gut: Under restraint stress Selank changed antioxidants and transaminases, without a monotonic dose dependence (Fomenko et al., 2017), and normalized the disturbed colon microbiota; 750 micrograms per kilogram reached values of unstressed animals (Mukhina et al., 2019).
- Route of administration: In BALB/c mice intraperitoneal administration increased GABA binding sites in the frontal cortex by 38 percent, intranasal administration increased MK-801 binding sites by 23 percent (Vasilyeva et al., 2020).
Three consequences follow from this. The effect depends on the model: an effect in the elevated plus maze is not an effect on a clinical scale. The dose-response relationship is not linear; several papers report a maximum at intermediate doses. And mouse strains respond differently. The animal models are a good map of possibilities and no substitute for controlled human studies.
Which endpoints are most informative?
The most informative are prespecified clinical scales with an active or placebo control; imaging and behavioral endpoints are intermediate steps, binding and gene expression are mechanisms. Anyone comparing studies of Selank should therefore ask first what was measured, and only then what came out.
- Hamilton, Zung and CGI scales: Observer-rated anxiety, depressiveness and global impression. Clinically relevant, dependent on rater training and blinding.
- HDRS: Observer-rated depression. In the combination study, the earlier effect under Selank was the main finding.
- Spielberger scale: State and trait anxiety as self-report. It complements observer ratings, it does not replace them.
- UKU scale: Systematic recording of adverse events. It makes the combination study valuable for the tolerability profile.
- SF-36: Health-related quality of life, close to patients' experience and reported only once in the Selank literature.
- PHQ: Self-report on somatic and psychological complaints. The 2018 paper reports individual items.
- Resting-state fMRI: Functional connectivity between brain regions. The endpoint shows a central response, not a symptom change.
- Elevated plus maze and open field: Behavioral measures for anxiety and locomotion in rodents. Sensitive to stress protocol, prior experience and strain.
- Withdrawal index and tactile threshold: Measures of physical withdrawal symptoms. They describe a state, not the effect of continuous administration.
A good endpoint is defined in advance, recorded blinded and reported for all participants, including those without improvement. That includes an effect size with a measure of variance. Precisely these details are missing from the abstracts of the clinical Selank papers. The scales are clinically relevant, the reporting is not.
What is known about tolerability and unresolved points?
The available summaries name good tolerability and, under phenazepam plus Selank, less pronounced benzodiazepine side effects; an independent long-term safety profile for Selank is missing.
In the 2015 paper, adverse effects were recorded with the UKU scale. Under phenazepam plus Selank, attention and memory disturbances, asthenia, sedation, prolonged sleep duration, sexual dysfunction, emotional indifference and orthostasis were less pronounced than under phenazepam alone (Medvedev et al., 2015). That concerns the accompanying effects of the benzodiazepine, not a separate profile of Selank. The 2014 paper names tolerability in its title and reports a mild nootropic effect without giving rates (Medvedev et al., 2014).
An independent review classifies Selank as a little-studied Russian drug sold in the US as a dietary supplement and calls for an assessment of misuse potential (Doyno and White, 2021). That is an assessment, not data collection. None of the studies examined had dependence, withdrawal or tolerance as an endpoint; the withdrawal data from the animal model concern morphine (Konstantinopolsky et al., 2022).
Four points remain open. First, pharmacokinetics: no half-life, bioavailability or clearance value is available for Selank. The IC50 of 15 micromoles describes the inhibition of enkephalinases in human plasma in vitro, not a concentration after administration. Second, independence: the papers come from a few Moscow institutes; replication by an independent group is missing. Third, the registry situation: name queries at ClinicalTrials.gov on October 25, 2026 returned no record with a Selank intervention. An empty name search is not proof of absence. Fourth, language: the Russian-language full texts were not accessible.
What the data do not support is a statement on long-term safety, dependence or transferability to other populations. What they do support is a consistent signal for an anxiolytic effect with a plausible mechanism and a measurable central response.
How do Selank and Semax differ?
Selank is a tuftsin analog, Semax an analog of an ACTH fragment; both are heptapeptides with a C-terminal Pro-Gly-Pro sequence but differ in origin, effect profile and evidence base. The full comparison is set out under Selank and Semax compared.
- Origin: Selank builds on the immune peptide tuftsin, Semax on a fragment of adrenocorticotropic hormone.
- Structure: Both carry the C-terminal Pro-Gly-Pro extension but differ in the rest of their structure.
- Research profile: Selank is studied mainly in anxiety, asthenia and stress, Semax at cognitive endpoints.
- Shared data: In the imaging study with 52 healthy participants, both peptides showed shared and specific effects on connectivity between the right amygdala and the right temporal cortex (Panikratova et al., 2020).
The Semax guide describes the other perspective.
How does Selank fit as a research material?
As a research material, Selank is a lyophilized 10 mg product for laboratory work; the preparations used in studies are not automatically identical with the material offered. Batch, purity, formulation and route of administration differ between a clinical trial preparation and a lyophilized research peptide.
The studies used injectable solutions, nasal drops, and intraperitoneal and intranasal administration. The 10 mg figure on the Selank product page describes the package size, not a dose and not a usage recommendation.
For laboratory work, reconstitution remains an arithmetic task. Anyone who dissolves the vial in a defined volume obtains a concentration from mass and volume. The Selank calculator performs this conversion; it carries no dosing instruction. The Selank product information describes the material offered, the Selank peptide lexicon the substance identity, and the guide overview further guides.
What questions about Selank come up most often?
Are there human studies of Selank?
Yes. Nine human papers with reported content are documented, including three controlled comparison studies in anxiety disorders and neurasthenia, a placebo-controlled imaging study with 52 healthy participants, and papers on adjustment disorder, post-COVID asthenia, atopic dermatitis and immune parameters. Four further papers are documented only by title. Most clinical statements rest on abstracts.
How long does the effect last?
In the 2014 comparison study, the anxiolytic effect persisted one week after the last administration. That describes the duration in the protocol used at the time, not a general duration of effect. No half-life value for Selank is available in the evaluated studies.
Does Selank cause dependence?
There are no robust data on this. No study examined dependence, withdrawal or tolerance as an endpoint. An independent review calls for an assessment of misuse potential; that is an open question, not a finding. The withdrawal data from the animal model concern morphine.
Which side effects are documented?
No available summary gives systematic rates. In the combination study with phenazepam, several unwanted effects of the benzodiazepine were less pronounced; that concerns phenazepam. A long-term profile for Selank is not documented.
Is Selank the same as Semax?
No. Selank is a tuftsin analog, Semax an analog of an ACTH fragment. Both carry a C-terminal Pro-Gly-Pro extension and were examined in the same imaging study. The comparison is set out under Selank and Semax compared.
Which primary papers inform this article?
- Zozulia et al. (2008). Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia. Zh Nevrol Psikhiatr Im S S Korsakova 108(4):38-48. PubMed
- Uchakina et al. (2008). Immunomodulatory effects of selank in patients with anxiety-asthenic disorders. Zh Nevrol Psikhiatr Im S S Korsakova 108(5):71-75. PubMed
- Medvedev et al. (2014). A comparison of the anxiolytic effect and tolerability of selank and phenazepam in the treatment of anxiety disorders. Zh Nevrol Psikhiatr Im S S Korsakova 114(7):17-22. PubMed
- Medvedev et al. (2015). Optimization of the treatment of anxiety disorders with selank. Zh Nevrol Psikhiatr Im S S Korsakova 115(6):33-40. DOI
- Panikratova et al. (2020). Functional connectomic approach to studying selank and semax effects. Doklady Biological Sciences 490(1):9-11. DOI
- Zozulya et al. (2001). The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity. Bulletin of Experimental Biology and Medicine 131(4):315-317. DOI
- Verbenko (2018). The effectiveness of selank in the treatment of adjustment disorder. Psychosomatic Medicine and General Practice. DOI
- Pogodina and Nikiforova (2024). Post-COVID syndrome, possibilities for therapy of asthenic disorders with Selank. Vrach. DOI
- Dontsova et al. (2020). Effect of combined phototherapy and regulatory polypeptide selank on cytokine blood profile of patients with atopic dermatitis. Medical Alphabet. DOI
- Starikov and Fedorov (2019). The use of Selank in the treatment of autonomic and psychoemotional disorders in women with climacteric syndrome. Vrach. DOI
- Verbenko and Shakina (2019). New possibilities for potentiating the effects of antidepressants of the group of selective serotonin reuptake inhibitors by the regulatory peptide Selank. Vrach. DOI
- Neznamov et al. (2005). Novel anxiolytic Selank: results of the Phase II clinical trials. European Neuropsychopharmacology. DOI80332-3)
- Syunyakov et al. (2012). Rapid and slow response during treatment of generalized anxiety disorder with peptide anxiolytic selank. European Psychiatry. DOI75281-1)
- Vyunova et al. (2018). Peptide-based anxiolytics: the molecular aspects of heptapeptide Selank biological activity. Protein and Peptide Letters 25(10):914-923. DOI
- Volkova et al. (2016). Selank administration affects the expression of some genes involved in GABAergic neurotransmission. Frontiers in Pharmacology 7:31. DOI
- Filatova et al. (2017). GABA, Selank, and Olanzapine affect the expression of genes involved in GABAergic neurotransmission in IMR-32 cells. Frontiers in Pharmacology 8:89. DOI
- Povarov et al. (2017). Effect of selank on spontaneous inhibitory postsynaptic currents in hippocampal slices. Bulletin of Experimental Biology and Medicine. DOI
- Kobylyanskii et al. (2017). Effect of peptides on the differentiation of murine embryonic stem cells. Bulletin of Experimental Biology and Medicine. DOI
- Kolik et al. (2019). Selank, peptide analogue of tuftsin, protects against ethanol-induced memory impairment by regulating BDNF content in the hippocampus and prefrontal cortex in rats. Bulletin of Experimental Biology and Medicine 167(5):641-644. DOI
- Kolomin et al. (2013). Changes in the hippocampal transcriptome after intranasal selank administration. Bulletin of Experimental Biology and Medicine. DOI
- Filippenkov et al. (2024). Selank peptide causes changes in gene expression in the hippocampus of rats in the early hours after acute restraint stress. Nanobiotechnology Reports. DOI
- Molecular Biology (2026). Transcriptomic effects of peptide drug Selank during early experimental cerebral ischemia in rats. DOI
- Inozemtseva et al. (2008). Intranasal administration of the peptide Selank regulates BDNF expression in the rat hippocampus in vivo. Doklady Biological Sciences 421:241-243. DOI
- Czabak-Garbacz et al. (2006). Influence of long-term treatment with tuftsin analogue TP-7 on the anxiety-phobic states and body weight. Pharmacological Reports 58(4):562-567. PubMed
- Kasian et al. (2017). Peptide Selank enhances the effect of diazepam in reducing anxiety in unpredictable chronic mild stress conditions in rats. Behavioural Neurology 2017:5091027. DOI
- Seredenin et al. (1998). Anxiolytic action of Selank in mice with different emotionality. Bulletin of Experimental Biology and Medicine. PubMed
- Sokolov et al. (2002). Selank and enkephalin half-life in BALB/c and C57BL/6 mice. Bulletin of Experimental Biology and Medicine. DOI
- Semenova et al. (2008). Use of Selank to correct measures of integrative brain activity and biogenic amine levels in adult rats resulting from antenatal hypoxia. Neuroscience and Behavioral Physiology 38(2):203-207. DOI
- Konstantinopolsky et al. (2022). Selank, a peptide analog of tuftsin, attenuates aversive signs of morphine withdrawal in rats. Bulletin of Experimental Biology and Medicine 173(6):730-733. DOI
- Skvortsova et al. (2009). Experimental hemorrhagic stroke: the study of neuropeptides (MIF, selank) in the intraperitoneal injection. Zh Nevrol Psikhiatr Im S S Korsakova 109(12 Suppl 2):62-66. PubMed
- Fomenko et al. (2017). Effect of Selank on functional state of rat hepatocytes under conditions of restraint stress. Bulletin of Experimental Biology and Medicine 163(4):415-418. DOI
- Mukhina et al. (2019). State of colon microbiota in rats during chronic restraint stress and Selank treatment. Bulletin of Experimental Biology and Medicine 167(2):226-228. DOI
- Vasilyeva et al. (2020). Route-dependent effects of Selank on receptor binding in the mouse brain. Neurochemical Journal. DOI
- Kost et al. (2025). Combined action of benzodiazepine tranquilizers and peptide anxiolytic Selank in BALB/c mice. Neurochemical Journal. DOI
- Ashmarin et al. (2008). Tissue distribution of glyprolines after different routes of administration. Russian Journal of Bioorganic Chemistry. DOI
- Zolotarev et al. (2006). Degradation and brain distribution of intranasal Selank in rats. Bulletin of Experimental Biology and Medicine. PubMed
- Siebert et al. (2017). Tuftsin: properties and analogs. Current Medicinal Chemistry 24(34):3711-3727. DOI
- Doyno and White (2021). Sedative-hypnotic agents that impact gamma-aminobutyric acid receptors: focus on flunitrazepam, gamma-hydroxybutyric acid, phenibut, and selank. Journal of Clinical Pharmacology 61 Suppl 2:S114-S128. DOI
For research use only. Not for human consumption. Scientific Editorial Team: Dr. Sieglinde Klaus
References
- Siebert A., et al. Tuftsin – Properties and Analogs. Current Medicinal Chemistry. 2017.DOI
- Ashmarin I., et al. A comparative analysis of the distribution of glyprolines after their administration by different ways. Russian Journal of Bioorganic Chemistry. 2008.DOI
- Zolotarev IuA, et al. Evenly tritium-labeled peptides and their in vivo and in vitro biodegradation]. Bioorganicheskaia khimiia. 2006.PMID
- https://pubmed.ncbi.nlm.nih.gov/18454096/
- https://pubmed.ncbi.nlm.nih.gov/25176261/
- Medvedev V., et al. Optimization of the treatment of anxiety disorders with selank. Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova. 2015.
