What Is Selank?
Selank is a synthetic heptapeptide analogue of the immunomodulatory peptide Tuftsin, most researched for anxiolytic effects, GABAergic modulation, cognitive enhancement, and memory improvement in animal models.
Selank is a synthetic heptapeptide with the amino acid sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP), developed and patented at the Institute of Molecular Genetics of the Russian Academy of Sciences (RAS) under the research direction of Professor Sergei Seredenin. It was created as a stabilised synthetic analogue of tuftsin — a naturally occurring immunomodulatory tetrapeptide (Thr-Lys-Pro-Arg) derived from the Fc fragment of immunoglobulin G. Tuftsin itself was first characterised by Victor Najjar at Tufts University in the 1970s, and Selank represents an engineered extension of tuftsin's C-terminal with a Pro-Gly-Pro sequence added to enhance metabolic stability and CNS bioavailability.
Unlike tuftsin, which acts primarily as an immunostimulant through activation of phagocytic neutrophils and macrophages, Selank appears to exert its predominant research-relevant effects on the central nervous system — specifically on anxiety circuitry, GABAergic signalling, and neurotrophic factor expression. This CNS-directed profile, combined with its notably low keyword difficulty (KD 3–5) in research search terms, reflects an emerging but relatively underexplored research compound with growing scientific interest.
Selank has been registered as a pharmaceutical drug in Russia under the trade name Selank (Cеланк) by the State Research Institute of Highly Pure Biopreparations. However, it has not received regulatory approval from the FDA, EMA, or TGA and remains outside approved therapeutic use in Western markets. All Selank provided by Rainbow Peptide is strictly For Research Use Only and is not intended for, nor suitable for, human administration. Research applications include studying GABAergic modulation, neuropeptide-cytokine interactions, and cognitive pathway biology in in vitro and controlled animal model settings.
Mechanism of Action
Selank produces anxiolytic effects primarily through GABAergic potentiation, BDNF upregulation in hippocampal tissue, and modulation of serotonin/dopamine metabolism — without the sedation or dependence risk associated with benzodiazepines in animal models.
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GABA-A Receptor Modulation Research indicates Selank modulates GABA-A receptor activity through a mechanism distinct from classical benzodiazepine binding. Studies suggest Selank may act at a novel allosteric site on the GABA-A receptor complex, potentiating inhibitory GABAergic neurotransmission without the full receptor occupancy and tolerance risk associated with benzodiazepines. This pharmacological profile has made it an interesting subject for studying non-sedating anxiolysis.
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IL-6 Expression Modulation Selank has demonstrated significant effects on cytokine expression patterns in rodent stress models. Of particular research interest is its ability to modulate interleukin-6 (IL-6) expression — a cytokine with established roles in neuroimmune communication, HPA axis regulation, and anxiety-related behaviour. Downregulation of IL-6 in the hippocampus has been associated with anxiolytic behavioural outcomes in chronic stress paradigms.
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BDNF Upregulation and Synaptic Plasticity Multiple studies have reported Selank-induced upregulation of brain-derived neurotrophic factor (BDNF) in hippocampal and prefrontal cortex tissue. BDNF is a master regulator of synaptic plasticity, long-term potentiation (LTP), and neuronal survival. Enhanced BDNF signalling correlates with improved learning and memory performance in rodent models, providing a potential mechanistic basis for the nootropic dimension of Selank research.
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Enkephalin Degradation Inhibition Selank appears to inhibit enkephalinase enzymes responsible for degrading endogenous enkephalins — opioid peptides with roles in pain modulation, stress response, and mood regulation. By slowing enkephalin breakdown, Selank may prolong the effects of endogenous opioid peptide signalling, contributing to its anxiolytic profile through non-GABAergic mechanisms.
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Serotonergic System Interaction Research has identified Selank interactions with serotonergic pathways, including effects on serotonin transporter (SERT) expression and 5-HT1A receptor sensitivity. Serotonergic modulation is proposed as a contributing mechanism to Selank's anxiolytic properties, complementing the primary GABAergic and neurotrophic mechanisms and offering researchers a multi-pathway model for studying anxiety biology.
Reconstitution Reference
The following reference is provided for licensed research professionals only. All reconstitution must comply with your institution's biosafety protocols.
| Vial Size | BAC Water Volume | Resulting Concentration | Storage (reconstituted) | Peptide Calculator |
| 5 mg | 2.0 mL | 2,500 mcg/mL | 2–8°C, use within 28 days | Calculate Dose → |
Selank is highly water-soluble and typically dissolves quickly upon addition of bacteriostatic water. Lyophilised powder should be stored at -20°C, protected from light. Do not freeze reconstituted solutions.
Competitive Pricing Comparison
Market price data from independent competitor analysis. All products are For Research Use Only.
| Supplier | Price Range (per vial) | Avg Market Price | COA Available |
| Competitor Low | $52 | — | Varies |
| Competitor High | $141 | — | Varies |
| Market Average | — | $85 | — |
| Rainbow Peptide | View Price → | ✓ Yes — HPLC + MS |
Published Research References
Studies cited for scientific reference. All data from preclinical models or limited Russian clinical literature unless stated. Not medical advice.
- Semenova TP, et al. "Behavioral effects of Selank in rats under conditions of emotional stress." Ross Fiziol Zh Im I M Sechenova. 2010;96(5):480–490. PubMed 20614214 ↗
- Volkova AV, et al. "Effects of Selank on gene expression in mouse frontal cortex." Mol Biol. 2016;50(5):779–787. PubMed 27700421 ↗
- Uchakina ON, et al. "Immunomodulatory effects of Selank on cytokine balance in patients with anxiety-asthenic disorders." Zh Nevrol Psikhiatr. 2008;108(5):71–75. PubMed 18562897 ↗