Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro): what it is, where it comes from, and what the published studies actually tested

What Selank is#

Selank is a synthetic peptide of seven amino acids: threonine, lysine, proline, arginine, proline, glycine and proline, written Thr-Lys-Pro-Arg-Pro-Gly-Pro or TKPRPGP in single-letter code.^[1][2] Its developers describe it as a synthetic analogue of tuftsin, a natural four-residue peptide, Thr-Lys-Pro-Arg, that corresponds to a short fragment of the heavy chain of human immunoglobulin G. The first four residues of Selank are tuftsin itself. The last three, Pro-Gly-Pro, were added to the C-terminal end to make the molecule more stable against breakdown.^[1][3]

Selank was designed and produced at the Institute of Molecular Genetics of the Russian Academy of Sciences, in cooperation with the V.V. Zakusov Research Institute of Pharmacology, and most of the published work on it comes from those groups and their collaborators.^[1][3] That concentration matters when reading the literature, and it is a theme this page returns to below.

Selank sequence, form and identifiers#

The sequence above is the one recorded for Selank in the FDA Global Substance Registration System and used in the primary papers. In the 2016 rat gene-expression study, for example, the material was described as the diacetate salt of Thr-Lys-Pro-Arg-Pro-Gly-Pro.^[1] FDA's compounding list refers to the substance as selank acetate.^[4] The salt form changes how much of a weighed powder is peptide and how much is counter-ion, so the form should be stated on any lot's Certificate of Analysis rather than assumed. The Selank product page lists the sequence alongside the lot records for our vials.

Why Selank was studied#

Tuftsin was originally of interest as an immune-related peptide. Selank's developers set out to build a more stable tuftsin derivative and then examined it in two directions at once: behavior in rodent stress models and immune signaling. The papers by this group frame Selank as a molecule that touches both the nervous system and the immune system, and much of the later work tries to identify which molecular pathways are involved.^[3][5] Three lines of laboratory work stand out: rodent behavior studies, gene-expression studies centered on the GABA neurotransmitter system and on inflammation-related genes, and enzyme studies on the breakdown of enkephalins, small opioid peptides made in the body.

Animal and cell studies, and what each measured#

Kozlovskaya et al., Neuroscience and Behavioral Physiology, 2003#

This paper compared Selank with ten other peptides from the tuftsin family in rats and in inbred C57BL/6 and BALB/c mice. Animals were first grouped by their type of emotional reactivity, then tested in a conflict situation used to produce behavioral signs of emotional stress. The authors reported that the peptides altered those behavioral measures and attributed some effects to the molecules' structures or to their breakdown fragments. The abstract does not list the individual tests.^[6] All of this work was in rodents.

Semenova et al., Experimental and Clinical Pharmacology, 2010#

In Wistar rats trained on a food-rewarded learning task, the authors gave a single administration of Selank or saline during training and then tested retention at 24 hours, 7 days and 30 days. They also measured serotonin metabolism in the hypothalamus and brain stem, and reported activation of serotonin metabolism in those regions from 30 minutes to two hours after administration, together with greater stability of the learned task over 30 days. They proposed a link between the two.^[7] The paper is in Russian; this summary is drawn from the English abstract.

Volkova et al., Frontiers in Pharmacology, 2016#

This is one of the few Selank gene-expression papers with an English full text. Thirty male Wistar rats were split into control, Selank and GABA groups of ten. The authors used real-time PCR to measure the expression of 84 genes involved in neurotransmission in the frontal cortex 1 hour and 3 hours after a single administration. They reported significant expression changes in 45 genes at 1 hour and 22 genes at 3 hours, and a positive correlation between the changes produced by Selank and by GABA at 1 hour. From this pattern they proposed that one possible mechanism is allosteric modulation of the GABAergic system, which they presented as a hypothesis rather than a demonstrated mechanism.^[1]

Filatova et al., Frontiers in Pharmacology, 2017#

The same group then moved to cultured human neuroblastoma cells (the IMR-32 line) to test the GABA idea in a simpler system. They measured mRNA levels of 84 genes related to the GABAergic system after exposure to Selank, GABA, the antipsychotic olanzapine, and Selank combined with each. Selank on its own did not change the measured mRNA levels. Combined with GABA, it largely cancelled the changes GABA produced alone; combined with olanzapine, significant changes were seen in more genes (35 of the 69 analyzed) than with olanzapine alone. The authors concluded that Selank had no direct effect on these genes in this cell line and that their data partly supported an effect on how GABA interacts with GABA-A receptors.^[2] That negative single-agent result is worth noting, because it is often left out when the 2016 rat paper is summarized.

Kolomin et al., Molecular Immunology, 2014#

Following the tuftsin thread, this study looked at immune-related genes. Male mice were given a single administration of Selank or of its two-residue fragment Gly-Pro, and the authors measured spleen mRNA for four inflammation-related genes (C3, Casp1, Il2rg and Xcr1) at several time points. They reported changes in each, including a roughly threefold fall in C3 mRNA at 30 minutes, and found that the profiles after Selank and after Gly-Pro were largely similar, suggesting the fragment contributes to the activity they measured.^[5] This was mouse spleen tissue, not human tissue.

Kost et al., Bioorganic Chemistry (Russian), 2001#

This in-vitro enzyme study is the origin of the enkephalinase theme in Selank discussions. The authors incubated Selank and the related peptide Semax with enkephalin-degrading enzymes from human serum and reported inhibition, with an IC50 of about 20 micromolar for Selank and 10 micromolar for Semax. Five-residue fragments of both peptides also inhibited the enzymes, while three-, four- and six-residue fragments did not. The authors suggested this inhibition might contribute to the peptides' biological activity.^[8] The experiment used serum enzymes in a test tube; it did not measure anything in a living person. A 2019 review by the developers' group summarizes the experimental and clinical literature and proposes that Selank's activity runs through the enkephalin system, which remains the group's working model rather than an independently confirmed one.^[3]

Human research on Selank#

Published human data are thin. The clearest example is a study by Zozulia and colleagues, 2008, published in Russian in a Russian neurology and psychiatry journal. It enrolled 62 patients diagnosed with generalized anxiety disorder or neurasthenia; 30 received Selank and 32 received medazepam, a benzodiazepine marketed in Russia. The investigators rated participants on the Hamilton, Zung and Clinical Global Impression scales and measured the half-life of leu-enkephalin in blood serum. The authors reported comparable changes on the rating scales in both groups, lower values of this serum measure in the patients, correlations between it and symptom ratings and illness duration, and an increase in the measure in the Selank group.^[9]

That is one small comparison from investigators connected to the developers. PubMed indexes it as a randomized controlled trial, but the English abstract does not describe how participants were allocated, whether anyone was blinded, or any follow-up. It has not been independently replicated in the peer-reviewed literature we reviewed, and it is not evidence that Selank is safe or useful for anyone. FDA's own assessment, discussed below, states that the agency lacks important information about safety issues when selank acetate is given to humans.^[4]

Regulatory status: FDA and WADA#

Selank is not an FDA-approved drug. On its list of bulk drug substances for compounding that may present significant safety risks, FDA lists selank acetate (TP-7) in the table of substances that were previously in category 2 and whose nominations were withdrawn by the nominators; it is not in the page's main category 2 table. The entry states that compounded drugs containing selank acetate may pose a risk of immunogenicity for certain routes of administration because of the potential for aggregation and peptide-related impurities, and that FDA lacks important information on safety issues in humans.^[4]

Selank does not appear by name on the World Anti-Doping Agency's 2026 Prohibited List. The list's S0 section prohibits at all times any pharmacological substance not addressed elsewhere on the list that has no current approval by a government health authority for human therapeutic use.^[10] Whether S0 applies to a particular substance is a determination for anti-doping authorities, not for a supplier.

Selank vs Semax#

Selank is often searched alongside Semax, another seven-residue peptide from the same Russian research program. The two share the Pro-Gly-Pro tail but have different starting fragments: Selank begins with tuftsin, while Semax has the sequence Met-Glu-His-Phe-Pro-Gly-Pro.^[8] They were tested side by side in the 2001 serum-enzyme study described above.^[8] Our Selank vs Semax comparison sets out the differences in origin and in the published research for each.

What has not been studied#

• No large, independently run clinical trials of Selank appear in the peer-reviewed literature reviewed for this page.
• No regulatory approval by the FDA, and no FDA review of human safety data; FDA states it lacks important human safety information.
• The proposed GABAergic mechanism rests on rat gene-expression data and was not reproduced as a direct effect in the IMR-32 cell study.
• The enkephalinase findings come from human serum enzymes in a test tube, not from measurements in living animals or people, apart from the serum measure in one small clinical comparison.
• Most studies come from a small number of connected Russian groups, and many are available only in Russian, which limits independent scrutiny.
• Long-term behavior of the molecule in any species is not described in the sources reviewed here.

Reading a Selank listing with this in mind#

Listings that call Selank an "anti-anxiety peptide" are restating the conclusions of rodent studies and one small Russian clinical comparison as if they were settled. A listing that gives the sequence, the salt form, the amount of peptide per vial, the lot number and where that lot's analytical report can be read is describing a reagent. For a seven-residue peptide that FDA has flagged for aggregation and impurity risk, identity and purity data are the part that matters to a laboratory. Our guide to reading a Certificate of Analysis explains what the report should show, HPLC and mass spectrometry explained covers the two methods behind it, and the COA library lists every Renuvia lot and its current testing status.