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Selank 10mg


Selank 10mg

Selank is a synthetic analogue of the human immunomodulatory peptide tufsin, which modulates the expression of Interleukin 6 (IL-6) and balances T helper cells, induces metabolism of serotonin, and concentration of monoamine neurotransmitters. Selank was developed by researchers at the Institute of Molecular Genetics in Russia in the 1980s, and it has nootropic and anxiolytic properties. Thanks to this, it is a potential treatment for anxiety disorders, enhances memory or has effects on pain perception.

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10 mg
1 Vial
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Powder specks or gel
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NaCl / Sterile / Bacteriostatic water 1ml/vial

Description of Selank Peptide

A synthetically produced heptapeptide Selank consists of 7 amino acids, and it mimics the human peptide called tufsin, but with prolonged haf-life, and better metabolic stability. In clinical trials it has shown good nootropic and anxiolytic effects, thanks to which it is beneficial in treatment of anxiety disorder (GAD), but without negative cognitive side effects. Studies has shown that it stimulates the expression of brain-derived neurotrophic factor (BDNF) in hippocampus of rats, and inhibits enzymes in degradation of enkephalins and other endogenous regulatory peptides. In animal studies it had beneficial antidepressive effects.

Now we would like to bring you closer to the effects of the peptide, which have been researched and confirmed in numerous studies.

Research Confirmed Effects

1. Selank in Anxiety Disorders Based on Genes Related to GABAergic System

Selank, a synthetic peptide with anxiolytic properties, has been found to influence the expression of genes involved in neurotransmission, specifically those associated with the GABAergic system. Clinical studies have shown the similarity of the spectrum of physiological effects, and mechanism of action of Selank and classical benzodiazepines, such as diazepam and phenazepam. In a study assessing the gene expression in the frontal cortex of rats 1 and 3 hours after Selank or GABA administration, significant changes were observed in the expression of 45 genes within the first hour and 22 genes after 3 hours. These genes included major subunits of the GABA receptor, transporters, ion channels, and receptors for dopamine and serotonin. The correlation between the changes in gene expression after administration of Selank or GABA indicates that Selank has complex effects on nerve cells and may modulate the GABAergic system, suggesting a mechanism of action similar to benzodiazepines.

Another study investigated the effects of Selank on reducing anxiety in rats under conditions of unpredictable chronic mild stress. It was found that the anxiolytic effect of Selank is comparable to that of classical benzodiazepines like diazepam, and when both substances were combined, they effectively reduced anxiety levels in conditions of chronic stress. However, even in the absence of chronic stress, administration of Selank showed fewer adverse effects on anxiety indicators compared to diazepam. This suggests that the combination of Selank and diazepam may be particularly effective in reducing anxiety in stressful conditions, while Selank alone could be a promising alternative to benzodiazepines with fewer side effects in reducing anxiety.

Selank has been also found to inhibit enkephalin-degrading enzymes, which may explain its calming effects. Clinical studies involving patients with various anxiety and phobic disorders, such as generalized anxiety and panic disorders, showed a significant reduction in enkephalinase activity and a shorter half-life for enkephalins in those with generalized anxiety but not in those with panic disorders and agoraphobia. This suggests a possible connection between generalized anxiety and low concentrations of endogenous inhibitors of enkephalin-degrading enzymes. Selank, with its unique heptapeptide structure, demonstrated a strong ability to inhibit the enzymatic breakdown of enkephalins, with a higher potency than known peptidase inhibitors like bacitracin and puromycin.

Additionally, studies on different strains of mice with varying emotional and stress reactions revealed that Selank could produce anxiolytic effects in certain mice by prolonging the half-life of enkephalins in the blood. Specifically, in BALB/c mice, Selank at a dose of 100 micrograms/kg increased the half-life of plasma leu-enkephalin and produced anxiolytic effects in the open-field test. However, in C57Bl/6 mice, it did not significantly affect behavioral reactions or enkephalinase activities. This indicates that Selank's ability to inhibit enkephalin-degrading enzymes is associated with its anxiolytic activity and may offer a potential therapeutic mechanism for managing anxiety and related disorders.

[1] - [4]

2. Selank as an Immunomodulator

Selank demonstrates unique immunomodulatory effects, making it a potential therapeutic agent in anxiety-asthenic disorders. Research in vitro indicated that Selank suppressed gene expression of interleukin-6 (IL-6) in patients with depression but not in healthy controls. Interestingly, an increase in IL-6 concentration was observed in cell cultures from the peripheral blood of patients when treated with Selank. Furthermore, a 14-day course of Selank in patients with generalized anxiety disorder (GAD) and neurasthenia resulted in changes in the Th1/Th2 cytokine balance. These findings suggest that Selank may act as an immunomodulator, with adaptogenic properties beneficial for elderly people and those exposed to environmental stressors, potentially helping prevent infectious diseases.

A study involving 62 patients with GAD and neurasthenia showed that Selank exhibited anxiolytic effects similar to those of medazepam, a classical benzodiazepine, but with additional antiasthenic and psychostimulant properties. During treatment with Selank, patients with GAD demonstrated increased serum levels of tau(1/2) leu-enkephalin, correlated with reduced anxiety and asthenia symptoms. Additionally, Selank has been shown to alter the expression of genes involved in inflammation in mouse spleen, suggesting its role in regulating inflammatory processes. The synthetic peptide caused changes in the expression of 34 genes related to inflammation, with notable alterations in the Bcl6 gene, crucial for immune system development.

Selank is closely related to Semax, and its effects. Semax as a peptide derived from adrenocorticotropic hormone (ACTH) and Pro-Gly-Pro, is known for its neuroprotective and cognitive-enhancing effects. Study explored the effect of Semax on the expression of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) genes in the rat hippocampus and frontal cortex following a single intranasal administration (50 mg/kg). The research revealed that Semax administration leads to rapid and dynamic changes in gene expression in these brain regions.

[5] - [8]

3. The Impact of Selank on Learning and Memory Processes

Selank is derived from the endogenous tetrapeptide tuftsin, and has been extensively studied for its effects on learning, memory, and serotonin (5-HT) metabolism in rats. In one experimental setup, rats trained with food rewards were injected with either Selank (300 micrograms/kg) or saline after the 10th trial in a series of 30 trials per day. The experiment continued 30 minutes later with elaboration of conditioned reflex and later testing of retention after 24 hours, 7 days, and 30 days. The results showed that Selank activates 5-HT metabolism in the hypothalamus and caudal brainstem within 30 minutes to 2 hours of administration. Moreover, Selank injection during the consolidation phase led to increased memory trace stability over 30 days, suggesting that it could play a role in enhancing memory storage processes.

Beyond anxiety, Selank appears to directly boost cognitive functions, as indicated by its impact on memory trace stability. This effect is notable as it is independent of the animal's anxiety levels, implying that Selank has a more direct influence on memory and learning. Additional studies showed that Selank could modify the expression of several genes in the hippocampus and affect the mRNA levels of 36 different genes, most of which are associated with plasma membranes. These results suggest that Selank could modulate ion-dependent processes involved in learning and memory, highlighting its potential as a cognitive enhancer.

[9], [10]

4. Selank and Restoration of Cognitive Processes After Brain Injury

Selank has also shown potential in restoring cognitive processes following damage to the brain. In one study, rats treated with a neurotoxin that selectively damages catecholaminergic neurons during early ontogeny were injected with Selank (300 micrograms/kg). Selank demonstrated an ability to restore cognitive processes that had been compromised due to chronic inhibition of the catecholaminergic system. This suggests that Selank might play a role in repairing or supporting cognitive functions following brain damage.


5. Selank in Pain Perception

The heptapeptides Semax and Selank have been shown to inhibit enkephalin-degrading enzymes in human serum in a dose-dependent manner. These synthetic compounds demonstrated inhibitory effects at lower concentrations compared to other known inhibitors, such as puromycin, bacitracin, and others. Enkephalins are endogenous peptides that interact with opioid receptors, playing a role in reducing pain intensity. Additionally, they are involved in the body's stress response, with high concentrations typically located in the brain and adrenal glands.

Interestingly, the pentapeptide fragments derived from these heptapeptides also exhibited inhibition of these enzymes, whereas shorter fragments—tri-, tetra-, and hexapeptides—did not. Since enkephalin-degrading enzymes are involved in breaking down not just enkephalins but other regulatory peptides, it’s likely that the inhibitory action of Semax and Selank contributes to their overall biological effects. This inhibition could play a role in maintaining higher levels of important regulatory peptides, providing a potential explanation for some of the physiological effects observed with these compounds.



  1. A. Volkova et al., “Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission,” Front. Pharmacol., vol. 7, Feb. 2016. [PubMed]
  2. A. Kasian et al., “Peptide Selank Enhances the Effect of Diazepam in Reducing Anxiety in Unpredictable Chronic Mild Stress Conditions in Rats,” Behavioural Neurology, 2017. [Online]. Available: https://www.hindawi.com/journals/bn/2017/5091027/.
  3. A. A. Zozulya et al., “The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity,” Bull. Exp. Biol. Med., vol. 131, no. 4, pp. 315–317, Apr. 2001. [PubMed]
  4. O. Y. Sokolov, V. K. Meshavkin, N. V. Kost, and A. A. Zozulya, “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. [PubMed]
  5. O. N. Uchakina et al., “[Immunomodulatory effects of selank in patients with anxiety-asthenic disorders],” Zh. Nevrol. Psikhiatr. Im. S. S. Korsakova, vol. 108, no. 5, pp. 71–75, 2008. [PubMed]
  6. A. A. Zozulia et al., “[Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia],” Zh. Nevrol. Psikhiatr. Im. S. S. Korsakova, vol. 108, no. 4, pp. 38–48, 2008. [PubMed]
  7. T. Kolomin, M. Shadrina, L. Andreeva, P. Slominsky, S. Limborska, and N. Myasoedov, “Expression of inflammation-related genes in mouse spleen under tuftsin analog Selank,” Regul. Pept., vol. 170, no. 1–3, pp. 18–23, Oct. 2011. [PubMed]
  8. T. I. Agapova et al., “[Effect of semax on the temporary dynamics of brain-derived neurotrophic factor and nerve growth factor gene expression in the rat hippocampus and frontal cortex],” Mol. Genet. Mikrobiol. Virusol., no. 3, pp. 28–32, 2008. [PubMed]
  9. T. P. Semenova, I. I. Kozlovskiĭ, N. M. Zakharova, and M. M. Kozlovskaia, “[Experimental optimization of learning and memory processes by selank],” Eksp. Klin. Farmakol., vol. 73, no. 8, pp. 2–5, Aug. 2010. [PubMed]
  10. T. A. Kolomin et al., “[c],” Zh. Vyssh. Nerv. Deiat. Im. I. P. Pavlova, vol. 63, no. 3, pp. 365–374, Jun. 2013.
  11. T. P. Semenova, M. M. Kozlovskaya, N. M. Zakharova, I. I. Kozlovskii, and A. V. Zuikov, “Effect of selank on cognitive processes after damage inflicted to the cerebral catecholamine system during early ontogeny,” Bull. Exp. Biol. Med., vol. 144, no. [PubMed]
  12. N. V. Kost et al., “[Semax and selank inhibit the enkephalin-degrading enzymes from human serum]],” Bioorg. Khim., vol. 27, no. 3, pp. 180–183, Jun. 2001. [Springer]

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