Selank Peptide

Selank is a short synthetic heptapeptide composed of seven amino acids. It was developed as an analogue of the naturally occurring peptide Tuftsin,(5) which is a tetrapeptide fragment derived from immunoglobulin G (IgG). Tuftsin has been studied for its involvement in immune system regulation and is thought to influence the activity of phagocytic cells.

Early research suggested that Tuftsin may play a role in processes such as phagocytosis, cellular motility, and broader immunological functions.(2) Building on these findings, scientists have developed synthetic analogues like Selank using established chemical synthesis methods, with the aim of exploring and potentially enhancing the biological properties associated with Tuftsin.(4)

Overview

Selank is structured as a peptide chain consisting of two key fragments: Tuftsin at the N-terminus and a tripeptide sequence—Pro-Gly-Pro (PGP)—at the C-terminus. This structural design is considered significant, as the inclusion of the PGP motif may enhance the peptide’s ability to cross biological barriers, including the blood–brain barrier (BBB).(6)

The BBB is a highly selective, semi-permeable membrane that regulates the movement of substances from the bloodstream into the central nervous system. The addition of the PGP sequence may influence the peptide’s physicochemical properties, such as its hydrophilicity or lipophilicity, potentially improving its compatibility with the lipid-rich environment of the BBB. It has also been proposed that the PGP motif may interact with specific transport mechanisms or receptors on the BBB, possibly facilitating receptor-mediated transport or endocytosis.

Additionally, the presence of the PGP sequence may alter the tertiary structure of Selank, which could affect how the peptide interacts with cellular components of the BBB. These structural and functional characteristics are hypothesised to assist Selank in navigating or bypassing the restrictive tight junctions that typically limit the passage of larger molecules into brain tissue, although these mechanisms remain under investigation.(6)

Chemical Makeup
  • Molecular Formula: C33H57N11O9
  • Molecular Weight: 751.88 g/mol
  • Other Known Titles: TP-7, Selanc
Research and Clinical Studies
Selank Peptide and BDNF Levels

There is a possibility that Selank may influence the expression of brain-derived neurotrophic factor (BDNF), a protein considered essential for neuronal survival, growth, and synaptic function.(1) Research suggests that Selank may increase levels of BDNF mRNA in the hippocampus, a key brain region involved in memory formation and emotional regulation.

This potential effect is particularly notable under conditions of stress, where glucocorticoids are known to suppress BDNF expression. By possibly counteracting this suppression, Selank may be relevant in studies examining neuroplasticity and the brain’s ability to adapt and reorganise. Given BDNF’s role in synaptic signalling and neuronal resilience, these findings highlight Selank’s potential involvement in mechanisms related to cognitive function and emotional processing, although further research is required to fully understand these effects.

Selank Peptide and Serotonin Signaling

Selank has been suggested to potentially influence serotonin signalling pathways, which are widely regarded as central to the regulation of mood and anxiety. Research using murine models, particularly those with inhibited serotonin synthesis, has indicated that Selank may alter serotonin dynamics when the serotonergic system is compromised.

Researchers have proposed that Selank may enhance serotonin metabolism within the brainstem, suggesting a possible modulatory effect on the serotonin system. More specifically, the peptide is thought to increase the metabolic processing of serotonin in brain regions associated with emotional regulation and stress response.

This proposed enhancement of serotonin metabolism may represent a pathway through which Selank could help counterbalance reduced serotonergic activity. These findings point toward a potential role in modulating mood-related neurochemistry, although the exact mechanisms and broader implications remain under investigation.

Selank Peptide and GABA Signaling

Studies have suggested that Selank may interact with the gamma-aminobutyric acid (GABA) system, a major inhibitory neurotransmitter network involved in reducing neuronal excitability, promoting relaxation, and modulating anxiety-related responses.

In one study,(7) researchers examined the expression of 84 genes associated with neurotransmission in murine models following exposure to either Selank or GABA. Gene expression was analysed at one and three hours using PCR techniques. The findings indicated a positive correlation between the gene expression profiles observed with Selank and those seen with GABA, suggesting that Selank may influence neurotransmission in a manner related to the GABAergic system.

However, the data also suggested that Selank’s effects may extend beyond simple direct activation of GABA receptors. Differences in gene expression patterns between Selank and GABA exposure led researchers to hypothesise that Selank may act as a modulator of the GABAergic system, potentially through allosteric mechanisms rather than direct receptor binding alone. This implies a more complex interaction, where Selank may alter how GABA receptors respond rather than simply mimicking GABA itself.

Additionally, Selank has been proposed to induce longer-lasting changes in neurotransmitter systems, which may contribute to sustained effects observed in experimental settings. These findings suggest that Selank’s influence on neural regulation may involve both immediate and longer-term modulation of neurotransmitter activity, although the precise mechanisms remain under ongoing investigation.

Selank Peptide and Genome Expression

Studies have explored the potential effects of Selank on gene expression and its possible involvement in inflammatory processes. In one such investigation,(8) male murine models were divided into three groups: a control group, a group receiving a single exposure to Selank, and a group subjected to repeated exposure. Following the experiment, RNA was extracted from both the spleen and hippocampus and analysed using PCR techniques.

The findings suggested that Selank may influence gene expression, with more pronounced effects observed in the spleen and hippocampus. Notably, changes were reported in the expression of the CX3CR1 gene, which is associated with inflammatory signalling pathways. These observations led researchers to propose that Selank may play a role in modulating inflammation through gene expression mechanisms, particularly via alterations in CX3CR1 activity, although further research is required to clarify these effects.

Selank Peptide and Enkephalin Signaling

In a clinical study,(9) 62 research models diagnosed with Generalized Anxiety Disorder (GAD) were evaluated to assess the potential effects of Selank. The subjects were divided into two groups, with approximately 48% receiving Selank and 52% receiving a standard benzodiazepine compound. Following the intervention, psychometric assessments suggested that the effects of Selank were comparable to those observed with the benzodiazepine.

Researchers also noted changes in enkephalin levels, specifically tau leu-enkephalin. Prior to the study, levels appeared reduced in the Selank group, and exposure to the peptide was associated with a reversal of this trend. It has been hypothesised that Selank may inhibit enzymes responsible for the breakdown of enkephalins. Since enkephalins are endogenous ligands of opioid receptors involved in regulating pain, mood, and stress responses, reduced degradation may lead to increased enkephalin availability.

This proposed mechanism suggests that Selank may enhance the physiological actions of enkephalins, potentially contributing to its observed effects in anxiety-related models. However, these mechanisms remain under investigation and require further validation.

Selank Peptide and Memory

This study(11) examined the effects of Selank on learning and memory using murine models trained over four days in a conditioned avoidance response (CAR) task—a behavioural model used to assess learning efficiency. Selank was administered 15 minutes prior to each training session. Over the course of the study, researchers observed that the models exposed to Selank appeared to show improved learning performance, demonstrated by a reduction in errors and an increase in correct responses.

These effects are hypothesised to involve multiple interconnected mechanisms. Selank may influence neuropeptide systems in the brain, which are considered important for cognitive processes such as learning and memory. It may also affect neural circuits involved in memory consolidation, potentially enhancing synaptic stability and efficiency.

Additionally, Selank’s proposed modulation of anxiety-related pathways may indirectly support cognitive performance, as reduced anxiety can improve focus and learning outcomes. The peptide has also been suggested to promote neural plasticity—the brain’s ability to adapt and reorganise—particularly in circuits that are underperforming. Collectively, these findings suggest that Selank may influence both the cognitive and emotional components of learning, highlighting its potential relevance in neurocognitive research, although further studies are required to confirm these mechanisms.

Selank Peptide and Immunomodulation

This clinical study(12) investigated the potential effects of Selank in research models diagnosed with Generalized Anxiety Disorder (GAD) accompanied by neurasthenia. The subjects were divided into control and experimental groups, with the experimental group receiving Selank exposure over a 14-day period. Following the study, peripheral blood samples were collected and analysed.

The results suggested a peak elevation in interleukin-6 (IL-6) levels, along with alterations in the balance between Th1 and Th2 cytokines—key components involved in immune system regulation. These findings indicate that Selank may influence immune signalling pathways, potentially modulating the immune response, although the precise implications of these changes remain to be fully understood.

Selank Peptide and Withdrawal

In this study,(13) murine models were provided with 10% ethanol as their sole fluid source over a 24-week period, after which ethanol was withdrawn to induce alcohol withdrawal symptoms. Following this, the models were exposed to Selank to assess its potential effects on withdrawal-related behaviours.

After 48 hours, researchers reported an apparent reduction in withdrawal symptoms, as indicated by improved outcomes in behavioural assessments such as social interaction tests and maze-based evaluations. These findings suggest that Selank may influence behavioural responses associated with withdrawal in experimental settings, although the underlying mechanisms and broader implications require further investigation.

Selank Peptide and Cardiovascular Activity

In this study,(14) Selank was administered to feline models to evaluate its potential effects on cardiovascular and respiratory function. Following exposure, researchers reported an approximate 32% decrease in arterial blood pressure within the first 3 minutes. Additionally, there appeared to be a 24% increase in cerebral blood flow within the first 10 minutes, which gradually returned toward baseline levels thereafter.

Notably, Selank did not appear to produce any significant changes in respiratory function or heart rate in this model. These findings suggest a potential influence on vascular dynamics, particularly cerebral circulation, although further research is needed to better understand the mechanisms and broader implications of these effects.

Selank Peptide and Weight, Cholesterol

In this study,(15) murine models were first subjected to a high-fat diet for six weeks until their body weight reached approximately 280–300g. The models were then divided into groups: a control group receiving sodium chloride, an experimental group exposed to Selank, and an additional baseline control group that received no intervention.

Following analysis, researchers reported that the Selank-exposed group appeared to show reductions in lipid-related markers, with decreases in cholesterol and fat levels ranging between approximately 25% and 58%. More specifically, reductions were noted in low-density lipoprotein (LDL), very-low-density lipoprotein (VLDL), and triglycerides. These findings suggest that Selank may influence lipid metabolism, potentially exhibiting hypocholesterolemic and hypolipidemic effects.

The study also observed improvements in haemostasis-related parameters, including increased fibrinolytic activity and reduced platelet aggregation, which may indicate a shift toward conditions less favourable for clot formation. Additionally, Selank exposure was associated with potential modulation of glucose homeostasis, suggesting a role in maintaining stable blood glucose levels.

In terms of overall metabolism and body composition, the Selank group appeared to demonstrate improved fat metabolism rates, eventually aligning with those of the baseline control group. While the control group gained an average of 40g during the study period, the Selank group maintained their weight and later exhibited gradual weight reduction following peptide exposure. These findings indicate a potential influence of Selank on metabolic regulation, although further research is required to confirm these effects and underlying mechanisms.

Selank peptide is available for research and laboratory purposes only. Please speak to our friendly research team to find out more and for sourcing options.

References:

  1. Inozemtseva, L. S., Karpenko, E. A., Dolotov, O. V., Levitskaya, N. G., Kamensky, A. A., Andreeva, L. A., & Grivennikov, I. A. (2008). Intranasal administration of the peptide Selank regulates BDNF expression in the rat hippocampus in vivo. Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections, 421, 241–243.  https://doi.org/10.1134/s0012496608040066

  2. Najjar VA. Tuftsin, a natural activator of phagocyte cells: an overview. Ann N Y Acad Sci. 1983;419:1-11. doi: 10.1111/j.1749-6632.1983.tb37086.x.  https://pubmed.ncbi.nlm.nih.gov/6370072/

  3. Semenova, T. P., kozlovskiĭ, I. I., Zakharova, N. M., & Kozlovskaia, M. M. (2009). Eksperimental'naia i klinicheskaia farmakologiia, 72(4), 6–8.

  4. Fridkin M, Stabinsky Y, Zakuth V, Spirer Z. Tuftsin and some analogs: synthesis and interaction with human polymorphonuclear leukocytes. Biochim Biophys Acta. 1977 Jan 24;496(1):203-11.  https://pubmed.ncbi.nlm.nih.gov/576412/

  5. Kozlovskaya MM, Kozlovskii II, Val'dman EA, Seredenin SB. Selank and short peptides of the tuftsin family in the regulation of adaptive behavior in stress. Neurosci Behav Physiol. 2003 Nov;33(9):853-60.  https://pubmed.ncbi.nlm.nih.gov/14969422/

  6. Elena Filatova et al., GABA, Selank, and Olanzapine Affect the Expression of Genes Involved in GABAergic Neurotransmission in IMR-32 Cells.  https://doi.org/10.3389/fphar.2017.00089

  7. Volkova, A., Shadrina, M., Kolomin, T., Andreeva, L., Limborska, S., Myasoedov, N., & Slominsky, P. (2016). Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Frontiers in pharmacology, 7, 31.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4757669/

  8. T.A Kolomin et al., Transcriptomic Response of Rat Hippocampus and Spleen Cells to Single and Chronic Administration of the Peptide Selank. June 2, 2009.  DOI: 10.1134/S1607672910010023

  9. Zozulia AA, Neznamov GG, Siuniakov TS, Kost NV, Gabaeva MV, Sokolov OIu, Serebriakova EV, Siranchieva OA, Andriushenko AV, Telesheva ES, Siuniakov SA, Smulevich AB, Miasoedov NF, Seredenin SB. Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia. Zh Nevrol Psikhiatr Im S S Korsakova. 2008;108(4):38-48. Russian.  https://pubmed.ncbi.nlm.nih.gov/18454096/

  10. Medvedev VE, Tereshchenko ON, Israelian AIu, Chobanu IK, Kost NV, Sokolov OIu, Miasoedov NF. 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. 2014;114(7):17-22. Russian.  https://pubmed.ncbi.nlm.nih.gov/25176261/

  11. Kozlovskii II, Danchev ND. The optimizing action of the synthetic peptide Selank on a conditioned active avoidance reflex in rats. Neurosci Behav Physiol. 2003 Sep;33(7):639-43.  https://pubmed.ncbi.nlm.nih.gov/14552529/

  12. Uchakina ON, Uchakin PN, Miasoedov NF, Andreeva LA, Shcherbenko VE, Mezentseva MV, Gabaeva MV, Sokolov OIu, Zozulia AA, Ershov FI. Immunomodulatory effects of selank in patients with anxiety-asthenic disorders. Zh Nevrol Psikhiatr Im S S Korsakova. 2008;108(5):71-5. Russian.  https://pubmed.ncbi.nlm.nih.gov/18577961/

  13. Kolik LG, Nadorova AV, Kozlovskaya MM. Efficacy of peptide anxiolytic selank during modeling of withdrawal syndrome in rats with stable alcoholic motivation. Bull Exp Biol Med. 2014 May;157(1):52-5.  https://pubmed.ncbi.nlm.nih.gov/24913576/

  14. Gan'shina TS, Kozlovskiĭ II. [Effects of the new peptide anxiolytic drug selank on the cardiovascular system functioning and respiration in cats]. Eksp Klin Farmakol. 2005 Jul-Aug;68(4):33-5. Russian.  https://pubmed.ncbi.nlm.nih.gov/16193654/

  15. N.F. Mjasoedov et al, The Influence of Selank on the Parameters of the Hemostasis System, Lipid Profile, and Blood Sugar Level in the Course of Experimental Metabolic Syndrome. April 14, 2014.

Dr. Marinov

Dr. Marinov (MD, Ph.D.) is a researcher and chief assistant professor in Preventative Medicine & Public Health. Prior to his professorship, Dr. Marinov practiced preventative, evidence-based medicine with an emphasis on Nutrition and Dietetics. He is widely published in international peer-reviewed scientific journals and specializes in peptide therapy research.

Selank Peptide