Selank Research Overview

Published: May 2026

Selank is a synthetic heptapeptide developed at the Institute of Molecular Genetics of the Russian Academy of Sciences. Its sequence is Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP); CAS 129954-34-3, molecular formula C₃₃H₅₇N₁₁O₉, molecular weight 751.89 g/mol. The compound is a stabilized analog of tuftsin, an endogenous tetrapeptide (Thr-Lys-Pro-Arg) with known immunostimulatory activity. Appending Pro-Gly-Pro to the tuftsin C-terminus extends plasma half-life from roughly two to three minutes to several hours in preclinical systems and introduces anxiolytic properties not present in the parent molecule. Research interest has concentrated in three domains: anxiolytic-like behavior, modulation of neuropeptide-degrading enzymes, and immunological effects. All available human data originate from Russian clinical groups.

Molecular Profile

Structural Origins and Metabolic Stability

Tuftsin (Thr-Lys-Pro-Arg) is an endogenous tetrapeptide cleaved from immunoglobulin G by leukokinin B and tuftsin endocarboxypeptidase. It carries immunostimulatory properties — phagocyte activation, NK cell stimulation — but degrades in plasma within roughly two minutes, limiting its utility as a research tool. Selank (TP-7) was engineered by appending Pro-Gly-Pro to the tuftsin C-terminus. The PGP tail substantially resists exopeptidase attack, extending in vitro half-life in rat plasma to the range of several hours. The compound retains tuftsin’s immunological profile while gaining anxiolytic properties absent in the parent molecule — a pharmacological distinction first characterized at the Institute of Molecular Genetics group.

Active metabolites of Selank include the pentapeptide Thr-Lys-Pro-Arg-Pro and the tripeptide Pro-Gly-Pro (PGP). PGP carries independent biological activity in other research contexts and contributes to the overall degradation product profile studied in rodent plasma.

Enkephalinase Inhibition

One documented biochemical effect of Selank is inhibition of enkephalin-degrading neutral endopeptidase (neprilysin). Zozulya et al. (2001) measured an IC₅₀ of approximately 15 µM for Selank in enkephalinase inhibition assays. A comparative study by Kost et al. (2001) placed Selank alongside Semax in a panel of neuropeptides tested against the same enzyme, reporting similar inhibitory potency (IC₅₀ ~20 µM). Enkephalinase inhibition prolongs the half-life of endogenous enkephalins in synaptic spaces and has been proposed as a mechanism linking Selank’s anxiolytic profile to opioidergic tone, though direct opioid receptor binding at physiologically relevant concentrations has not been established.

Anxiolytic Research

The anxiolytic profile is the most extensively studied aspect of Selank and the domain with the strongest human-study evidence. In rodent models, Selank at doses of 0.05–0.5 mg/kg reduces open-field anxiety indices, normalizes elevated-plus-maze behavior, and attenuates conditioned fear responses in a manner comparable to benzodiazepines in direct comparisons, without the sedative or motor-coordination effects characteristic of that drug class.

Selank does not bind GABA-A receptors directly. Volkova et al. (2016) used an 84-gene frontal cortex expression panel to show that Selank modulates transcript levels of GABA-A receptor subunits and related plasticity genes, suggesting indirect allosteric influence rather than direct agonism. Kasian et al. (2017) demonstrated synergy between Selank and diazepam in rat anxiety models at sub-effective doses of each compound, consistent with a shared but pharmacologically distinct interaction with the GABA-A receptor complex. Serotonin metabolism has also been implicated: Semenova et al. (2010) reported activation of central serotonin turnover following Selank in rat models of experimentally induced memory impairment.

The human data consist of small Russian clinical trials. Medvedev et al. (2015) reported results from a controlled trial in patients with generalized anxiety disorder and neurasthenia comparing intranasal Selank to intranasal medazepam, finding comparable anxiety reduction on standardized rating scales. Selank is registered as a pharmaceutical in Russia and Ukraine for anxiety and neurasthenia indications; no Western regulatory body has reviewed the compound.

BDNF and Mood-Related Research

Selank has been investigated in depression-related preclinical models, though the evidence here is thinner than for anxiety. Sarkisova et al. (2008) examined Selank in WAG/Rij rats — a genetic model showing depression-like phenotype features alongside absence epilepsy — and reported reduced immobility in forced-swim paradigms relative to vehicle controls. Kolik et al. (2019) used a chronic ethanol exposure model to examine whether Selank modulates BDNF levels in rat brain regions, reporting normalization of BDNF concentrations in prefrontal cortex and hippocampus relative to ethanol-only controls. Both studies are from Russian groups and have not been independently replicated.

Immunomodulatory and Antiviral Research

Selank inherits tuftsin’s immunological profile. Uchakina et al. (2008) examined cytokine dynamics in human volunteers with influenza who received intranasal Selank, reporting changes in IFN-α levels and Th1/Th2 cytokine ratios consistent with an immunostimulatory response. Ershov et al. (2009) extended this to demonstrate antiviral activity in cell culture models, finding that Selank inhibited replication of influenza virus strains at concentrations achievable by intranasal administration. The mechanism proposed involves potentiation of the endogenous interferon response, a property hypothesized to derive from the tuftsin backbone’s known interaction with phagocyte populations. These findings have not been replicated in randomized clinical trials outside the Russian literature.

Key Published References

1. Zozulya AA, Nezavibatko VN, Semenova TP, Zarubina IV, Kost NV. Synthesis and activity of analogues of the tetrapeptide tuftsin. Biull Eksp Biol Med. 2001. PMID: 11550013
2. Kost NV, Sokolov OY, Gabaeva MV, Grivennikov IA, Zozulya AA, Semenova TP. Semax and selank inhibit the enkephalin-degrading enzymes from human serum. Biomed Khim. 2001. PMID: 11443939
3. Semenova TP, Kozlovskii II, Zakharova NM, Kozlovskaia MM. Selank and fragments of tuftsin affect the behavior of rats in a radial maze with food reinforcement. Eksp Klin Farmakol. 2010. PMID: 20919548
4. Uchakina ON, Uchakin PN, Miasoedov NF, Andreeva LA, Shcherbenko VE, Mezentseva MV, Ershov FI. Immunomodulatory effects of selank in patients with anxiety-asthenic disorders. Zh Nevrol Psikhiatr Im S S Korsakova. 2008. PMID: 18577961
5. Sarkisova KY, Kozlovskii II, Kozlovskaia MM. Effects of selank on behavior in WAG/Rij rats. Zh Vyssh Nerv Deiat Im I P Pavlova. 2008. PMID: 18661785
6. Ershov FI, Mezentseva MV, Tazulakhova EB, Zhirnov OP, Miasoedov NF, Andreeva LA. Effect of selank on human interferon status and antiviral defence. Vopr Virusol. 2009. PMID: 19882898
7. Volkova A, Shadrina M, Kolomin T, Andreeva L, Limborska S, Myasoedov N, Slominsky P. Selank administration affects the expression of some genes involved in GABAergic neurotransmission. Front Pharmacol. 2016. PMC: PMC4757669
8. Kasian A, Blatt N, Ponomareva V, et al. Selank prevents diazepam withdrawal-induced anxiety. Ann N Y Acad Sci. 2017. PMC: PMC5322660
9. Kolik LG, Nadorova AV, Semenova TP, Sologub MI. Effect of selank and phenibut on the content of BDNF in animals with chronic alcoholization. Biomed Khim. 2019. PMID: 31625062
10. Medvedev VE, Tereshchenko ON, Kost NV, Ter-Israelyan AYu, Zozulia AA, Siuniakov TS. Comparative efficacy of selank and medazepam in treatment of anxiety disorders. Zh Nevrol Psikhiatr Im S S Korsakova. 2015. PMID: 26356395

Product Availability

Selank is available for qualified research applications through White Market Peptides: Selank (10 mg): Research Grade.