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Free U.S. shipping on orders over $150Selank is a 7-amino acid peptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP). It was developed at the Russian Institute of Molecular Genetics in the 1990s for its potential anxiolytic, neuroprotective, and nootropic properties. The peptide is an analog of the tuftsin molecule, which is naturally produced in the human body. It works primarily by allosterically modulating GABA receptors, similarly to benzodiazepines but without the same impairing side effects.
Selank can function as a neuropsychotropic, antidepressant, and antistress, nootropic and immunomodulatory drug due to its anxiolytic activity [1].
Selank has similar effects to tranquilizers like benzodiazepines at low doses without the unwanted side effects such as dependence, withdrawal, and amnesia. Moreover, animal studies suggest that Selank relieves aggression and fear reaction [1].
In addition, Selank modulates the expression of genes that influence different types of immune responses, suggesting that it may also work through immunomodulation [2]. A rat study suggests that Selank may help maintain immune homeostasis during stress [3].
The pharmacological investigation of Selank has primarily focused on its anxiolytic and antidepressant properties. In patients with anxiety and depressive disorders, Selank effectively reduced anxiety, mood swings, and somatic symptoms [4].
In the experimental model of chronic mild stress, the combination of Selank with benzodiazepines was the most effective in reducing anxiety levels, and Selank independently was the most efficient in reducing anxiety levels after individual stressful events [5].
Adults living in Ukraine with adjustment disorder who were admitted to hospital for routine check ups were either given Selank or placebo. Selank reduced complaints in patients with adjustment disorders. Even two weeks after treatment, patients receiving Selank reported reduced somatic symptoms, nutritional problems, and alcohol misuse [6].
A 2016 rat study [1] examined the effect of intranasal Selank and GABA on the expression of genes related to neurotransmission in the frontal cortex. The study concluded that Selank exerts a significant and time-dependent effect on the expression of genes related to neurotransmission, supporting its pivotal role in modulating anxiolytic and antidepressant pathways.
Moreover, Selank works as a GABA receptor modulator. If administered together, Selank and benzodiazepines can regulate the activity of GABA receptors in a peculiar manner, which is not cumulative and is different from either substance individually. Thus, Selank's anti-anxiety mechanism of action is also concentration-dependent allosteric modulation of GABA receptors [7].
A rat study suggests that intranasal selank may improve memory and learning by increasing BDNF in the hippocampus [1, 8].
Another study examined rats with strong alcohol preference fed with 10% ethanol as the only fluid source for 30 weeks to induce attention and memory disturbances mimicking chronic alcohol intoxication. Subsequently, both alcohol-fed and age-matched control rats received Selank intraperitoneally at 0.3 mg/kg. Both alcohol-fed and control rats experienced a cognitive stimulating effect with increased exploration time and reduced discrimination index in novel object recognition tests. In control animals, BDNF was unchanged. However, in alcohol-fed animals, alcohol cessation after 30 weeks elevated BDNF in the hippocampus and cortex, while administration of selank restored BDNF levels to values comparable to those of the control group. In conclusion, Selank helps modulate BDNF and other reparative processes in rats cognitively impaired from chronic alcohol [9].
A Russian article investigated the effects of Selank on behavior and serotonin/noradrenalin concentrations in the brains of adult rats exposed to hypoxia during 14-16 days of gestation. Intraperitoneal Selank resulted in [10]:
These results suggest that Selank has a normalizing impact on neurobehavioral functions impaired by prenatal hypoxia, indicating its potential role in enhancing stress resilience and supporting recovery of serotonergic and noradrenergic system activity. Moreover, Selank was shown to have positive emotional effects and antistress actions [11].
Inflammation is a complex process mediated by the interaction of various immune cells and cytokines including IL-1β, IL-6, and TGF-β1. A recent study [12] has evaluated the effect of Selank on the level of the cytokines in rats that have been exposed to inflammatory stress. There was a significant decrease in the concentration of IL-1β and IL-6 and restoration of the level of IL-4, as well as suppression of the production of TGF-β1 and TNF-α in the serum of rats treated with Selank.
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). Selank is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
Selank is a heptapeptide, a synthetic regulatory peptide, with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro. It is described as a peptide anxiolytic synthesized on the basis of the endogenous peptide tuftsin, and as an analog of the immunomodulatory peptide taftsin. In outbred rats receiving 10% ethanol as their only fluid source for 30 weeks, Selank was studied for effects on memory impairment and brain-derived neurotrophic factor content in brain structures. In rats with 6-hydroxidopamine-induced parkinsonism-like conditions, its effects on behavior were examined.
In clinical studies in people, Selank was reported to have an anxiolytic (anxiety-reducing) effect comparable to that of classical benzodiazepine drugs. Clinical studies have also reported similarities between the spectrum of physiological effects of Selank and those of benzodiazepines such as diazepam and phenazepam. Selank is described as a heptapeptide with anxiolytic and nootropic properties, and in one mouse study it was given at 300 μg/kg/day for 5 days by intraperitoneal and intranasal routes. In that mouse study, the effects were assessed by elevated-plus-maze behavior in BALB/c and C57BL/6 mice and by measuring the binding of markers to NMDA and GABA receptors in the brain.
In an animal study, one possible molecular mechanism of Selank is associated with allosteric modulation of the GABAergic system, and the authors describe its effects on nerve cells as complex. In in vitro experiments, Selank affected [3H]GABA binding as a positive allosteric modulator. In in vitro work, one proposed anti-anxiety mechanism of Selank is subtype-selective, concentration-dependent allosteric modulation of GABA receptors.
In BALB/c mice given Selank intraperitoneally, the number of GABA receptor binding sites in the frontal cortex increased by 38%, with no change in NMDA receptor binding in the hippocampus. In a separate study in BALB/c mice given Selank intranasally, the density of MK-801 binding sites increased by 23%, with no effect on GABA receptors. The two studies used different routes of administration and reported different outcomes.
In rat studies, Selank given alone was the most effective at reducing elevated anxiety induced by a course of test substances. In the same rat studies, combining diazepam with Selank was the most effective at reducing anxiety under unpredictable chronic mild stress. In rats, the maximum stress-limiting effect of Selank was reached after administration of 300 μg/kg.
In ex vivo experiments in rats, Selank prevented the ethanol-induced increase in BDNF content in the hippocampus and frontal cortex. A separate animal study suggests that Selank's effects on memory involve a neurotrophin mechanism related to BDNF production. A review lists Selank among neuroactive peptides said to enhance brain-derived neurotrophic factor and HGF/c-Met pathways, though this statement is a general one and is not tied to a specific rodent measurement.
In a study in male DBA/2 mice, Selank at 0.3 mg/kg given intraperitoneally prevented the development of ethanol-induced hyperlocomotion caused by 2.0 g/kg ethanol given intraperitoneally. The effect was similar to that of the nonselective opiate receptor blocker naloxone at 1.0 mg/kg intraperitoneally, whereas the sigma-1 receptor agonist Afobazole at 1.0 mg/kg did not inhibit the ethanol-induced behavioral stimulation. The authors suggest that Selank can modulate the motivational effects of ethanol.
In rats subjected to chronic restraint stress, Selank restored the intestinal microbiota, presumably via central (neurotropic) and peripheral (immunotropic) mechanisms. In rats under stress, colon signs included wall atrophy, inflammatory reaction, and changes in the number and functional activity of mast cells, alongside increased corticosterone levels.
In a resting-state fMRI study of 52 healthy participants, Selank and Semax were each compared against placebo on functional connectivity of predefined regions of interest. In this human clinical study, both Selank and Semax showed between-group and between-condition differences in connectivity between the right amygdala and a region spanning the fusiform, inferior and middle temporal, and parahippocampal gyri in the right hemisphere. A post hoc analysis in these human participants identified both general and specific effects of Selank and Semax on connectivity between the right amygdala and the right temporal cortex.
In animal studies, the two routes of selank administration produced differing pharmacological spectra. The researchers suggested these differences are determined by selank's pharmacokinetics and biotransformation, as well as by how its anxiolytic and nootropic effects develop over time. In mice, the anxiolytic and nootropic effect of selank given by either route was observed only in BALB/c mice, which initially showed reduced exploratory activity and higher anxiety than C57BL/6 mice.
A new combined LC-MS/MS method was developed and used to analyze 10 putative cognitive enhancing polypeptides, including Selank, that were being sold online. The method was designed to work for both hydrophilic and more hydrophobic peptides. In the in vitro work, HPLC was used to obtain and ensure the purity of reagents and Selank.
In rats, expression of 22 genes in the frontal cortex changed three hours after Selank or GABA was given. In this rat study, expression of 84 neurotransmission-related genes in the frontal cortex was measured by real-time PCR at 1 and 3 hours after Selank or GABA at 300 μg/kg. The provided facts do not say which of these genes changed or whether their expression went up or down.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.