Selank, N-Acetyl Selank and Adalank: A Tuftsin Analog, Its Mechanism and the State of the Evidence

Selank is a short peptide designed in Moscow on the basis of tuftsin, an antibody fragment. Russia registers it as nasal drops available without prescription, while the European Union and the United States do not recognize it as a medicine. Most research on Selank was done in Russia, and every clinical study involved its developers. Online descriptions also mix data on Selank with promises about derivatives that no peer-reviewed paper has described.

This article separates those layers: the origin of the molecule, results from laboratory models, human studies, the derivatives N-Acetyl Selank and Adalank, and the differences from Semax. You will find no doses or protocols here, for reasons given in the closing questions.

In our catalog, the compounds discussed in this article are chemical reagents intended solely for laboratory research (Research Use Only). They are not medicinal products, dietary supplements or foods, and they are not intended for use in humans or animals. What this status means is explained in our material on the legal status of research reagents.

An essential distinction: in Russia, Selank is a registered medicine in the form of nasal drops available without prescription. Research material containing the same peptide is not a substitute for a medicinal product and does not replace medical consultation. The three clinical studies discussed below enrolled diagnosed patients in Russia, and their findings do not apply to research material.

What is Selank

Selank is a heptapeptide, a chain of seven amino acids: Thr-Lys-Pro-Arg-Pro-Gly-Pro (one-letter code TKPRPGP). The first four form tuftsin, a tetrapeptide in the Fc region of the immunoglobulin G heavy chain, from which enzymes release it (Fridkin and Najjar, 1989, PMID 2667894). Tuftsin was isolated in 1970 at Tufts University. This tetrapeptide stimulates some white blood cells, including macrophages and neutrophils (Wardowska et al., 2007, PMID 17718389).

Selank’s developers extended tuftsin by three amino acids, Pro-Gly-Pro. In their words, the aim was to improve its metabolic stability and prolong its action (Volkova et al., 2016, PMID 26924987). Some enzymes cut peptides from the ends of the chain, and such a tail works like the plastic tip of a shoelace that stops it from fraying. The molecule came from the Institute of Molecular Genetics of the Russian Academy of Sciences and the Zakusov Institute of Pharmacology (PMID 26924987). It has appeared in the literature since 1995, at first under the code TP-7 (Seredenin et al., 1995, PMID 8704608).

In rats, intact Selank was detectable in plasma for 7–10 minutes, and tuftsin itself turned out to be the main active metabolite (Boĭko et al., 1998, PMID 9854633). Some of the reported effects may therefore come from breakdown products rather than from the whole molecule.

Mechanism: what laboratory models showed

Data on the mechanism come from rodent studies, cell cultures and blood samples tested in vitro. None of the leads described below has been confirmed directly in humans.

Enkephalins: slower breakdown instead of an opioid receptor

Enkephalins are short opioid peptides made by the body and broken down by enzymes called enkephalinases. In vitro, Selank inhibited enkephalin breakdown in plasma more strongly than the classic peptidase inhibitors bacitracin and puromycin. The concentration inhibiting half of the activity (IC50) was 15 µM (Zozulya et al., 2001, PMID 11550013). In the same group’s measurement in human serum, it was 20 µM (Kost et al., 2001, PMID 11443939).

At the same time, Selank did not displace opioid or dopamine D2 receptor ligands from rat brain membranes. In mice, however, naloxone, which blocks opioid receptors, abolished its effect on apomorphine-induced behavior. The authors concluded that Selank acts indirectly, by slowing the breakdown of the body’s own enkephalins (Meshavkin et al., 2006, PMID 17415472). Think of it as cleaning up later: no extra signaling molecules arrive, but those already present stay in place longer.

GABA and gene expression

GABA-A receptors work as the main brakes of the nervous system and are the target of benzodiazepines. In a radioligand study on brain cell membranes, Selank changed the binding of labeled GABA in the way a positive allosteric modulator does. It also blocked the modulating action of diazepam (Vyunova et al., 2018, PMID 30255741). In the rat frontal cortex, one hour after Selank or GABA, the expression of 45 of 84 genes studied changed. The abstract does not separate the results for the two substances, however (PMID 26924987).

In human IMR-32 neuroblastoma cells, Selank alone did not change the mRNA level of any gene studied. Given together with GABA, it almost completely cancelled the changes caused by GABA (Filatova et al., 2017, PMID 28293190). Its effect on the GABA system therefore looks different from one model to another.

An effect that depends on baseline anxiety

Selank reduced signs of anxiety in BALB/c mice, which are genetically more anxious, and did not change the behavior of low-anxiety C57BL/6 mice (Seredenin et al., 1998, PMID 9583175). This dependence has not been tested in humans.

BDNF: what was actually measured

Descriptions of Selank often repeat that it “raises BDNF”, the neurotrophic factor that supports the survival and plasticity of neurons. PubMed holds two experimental papers on this question (search on 24 October 2026). The first, from 2008, speaks in its title of “regulating” BDNF expression in the rat hippocampus. Without an abstract, though, the direction of change cannot be determined (Inozemtseva et al., 2008, PMID 18841804).

The second concerned rats given an ethanol solution to drink for 30 weeks. In that study, Selank blocked the alcohol-induced rise in BDNF in the hippocampus and frontal cortex (Kolik et al., 2019, PMID 31625062). This is a return toward normal in one addiction model, and no general “raising” of BDNF can be inferred from it.

Human studies: who was studied and against what

PubMed lists three clinical studies of Selank and one imaging study in healthy volunteers. All were conducted in Russia, and each names among its authors N.F. Myasoedov of the Institute of Molecular Genetics, the team that developed Selank.

None of the three clinical studies had a placebo group. PubMed tags the 2008 study as randomized, yet its abstract does not describe blinding (Zozulia et al., 2008, PMID 18454096). The 2014 abstract gives neither group sizes nor the result of the comparison with phenazepam (Medvedev et al., 2014, PMID 25176261). In 2015 Selank was added to a benzodiazepine, so its own effect cannot be isolated (Medvedev et al., 2015, PMID 26356395). The fMRI study measured the activity of brain networks, not mood or behavior (Panikratova et al., 2020, PMID 32342318).

ClinicalTrials.gov contains no study with Selank as an intervention, and PubMed has no systematic review or meta-analysis (searches on 24 October 2026). A review in the Journal of Clinical Pharmacology described phenibut and Selank as “poorly studied Russian drugs with GABAergic mechanisms”. According to its authors, both “are inexplicably sold to US consumers as dietary supplements” (Doyno and White, 2021, PMID 34396551).

N-Acetyl Selank and Adalank: the literature versus online claims

N-Acetyl Selank carries an acetyl group on the first amino acid of Selank (Ac-TKPRPGP). N-Acetyl Selank Amidate also has the end of the chain converted to an amide (Ac-TKPRPGP-NH₂), and in our catalog it goes by the name Adalank. Despite the similar name, Adalank is not related to Adamax, which is described as a Semax derivative.

In PubMed, Europe PMC and ClinicalTrials.gov we found no paper or study on N-acetylated Selank, its amide or Adalank (search by name and sequence, 24 October 2026). PubChem has an “N-acetyl selank” record with a free chain end and no linked literature. One of its synonyms even gives a sequence with a proline missing (PubChem, CID 133082488). An entry in a substance database is an identifier, not evidence of activity.

A common misunderstanding concerns the word “acetate”. The Russian medicine contains Selank diacetate (Vidal, 2026), a salt: the same molecule with two acetate ions. Rat studies also used Selank in this form (PMID 26924987). N-acetylation, by contrast, is a permanent change in structure that creates a new molecule.

Online descriptions credit the derivatives with better brain penetration and longer action, although no published data support this. Changing the ends of the chain can also alter activity, not only stability. For Semax, the only paper with an abstract on the acetylated form showed a loss of protective properties in cell culture. That is why we do not extrapolate from Selank to its derivatives.

In the lab, the name on the label does not settle which variant is in the vial. “N-Acetyl Selank” is used for both the free-end form and the amide, and their masses differ by about 1 Da (793.9 vs 792.9 g/mol). A mass spectrum in the batch certificate will show such a difference, and we explain how to read one in our article on the certificate of analysis.

Semax and Selank: how they differ

Both peptides were created with the involvement of the Moscow Institute of Molecular Genetics and belong to the glyprolines, peptides containing the Pro-Gly-Pro sequence. Glyproline researchers described this family as having stability comparable to that of typical drugs (Ashmarin et al., 2005, PMID 15837162).

• Selank
  • origin: tuftsin (an antibody fragment) + Pro-Gly-Pro
  • sequence: TKPRPGP
  • registration in Russia: 0.15% nasal drops, no prescription needed, “other anxiolytics”
  • main research areas: anxiety and stress in animals, enkephalinases, GABA
  • enkephalinase inhibition in human serum (IC50): 20 µM
• Semax
  • origin: fragment of the hormone ACTH(4-7) + Pro-Gly-Pro
  • sequence: MEHFPGP
  • registration in Russia: 0.1% and 1% nasal drops, prescription-only, nootropics
  • main research areas: ischemic stroke, neuroprotection, BDNF
  • enkephalinase inhibition in human serum (IC50): 10 µM

Three papers compared them directly. Semax inhibited enkephalinases more strongly (PMID 11443939), and on fMRI both peptides produced shared and distinct changes in amygdala connectivity (PMID 32342318). In rats with damaged dopamine neurons, neither changed motor activity, while Selank reduced anxiety-like behavior (Slominsky et al., 2017, PMID 28702721). Semax, along with the derivatives N-Acetyl Semax and Adamax, is the subject of a separate article, Semax peptide: mechanism and evidence.

Regulatory status

In Russia, Selank® is registered as 0.15% nasal drops dispensed without prescription, first on 30 April 2009. The current registration certificate, valid without a time limit, dates from 15 July 2025 (GRLS, as of 23 October 2026). The product information classes it as “other anxiolytics” (ATC N05BX) and names Selank diacetate as the active substance (Vidal, 2026). Registration in one country does not establish efficacy by EU or US standards.

No medicine containing Selank is approved in the EU or the US. EMA’s Article 57 data contain none (EMA, data as of 9 October 2026), and Drugs@FDA lists none either (checked 27 October 2026). FDA placed “Selank acetate (TP-7)” among bulk substances for compounding whose nominations were withdrawn. It warned of immunogenicity risk from aggregation and peptide-related impurities and said it lacks important information on safety in humans (FDA, 2026).

Selank was not among the seven peptides that FDA’s Pharmacy Compounding Advisory Committee reviewed on 23–24 July 2026 (FDA, 2026). It is also absent from the federal list of bulk substances usable in pharmacy compounding (21 CFR 216.23). N-Acetyl Selank and Adalank have no registration that we could find in Russia, the EU or the United States.

Anti-doping note

The name Selank does not appear on the WADA 2026 Prohibited List. Class S0 covers substances without approval for human therapeutic use from any governmental regulatory health authority, and Selank holds a current registration in Russia. By the wording of the List, class S0 does not apply to it. A 2025 review, several of whose authors sit on the scientific team of Poland’s anti-doping agency (POLADA), nevertheless listed Selank among substances of unclear status. It did not name a similar prohibited substance (Pokrywka et al., 2025, PMID 41048238). The absence of a name from the List therefore does not mean that a substance is allowed.

N-Acetyl Selank and Adalank have no registration as a medicine in any country we know of, and they fit the “designer drugs” example in the text of class S0. They are therefore prohibited at all times. From 1 January 2027, the new List also names peptides as an example in class S0 (USADA, 2026). USADA, the national anti-doping organization of the United States, applies the same List as a Code signatory (USADA, 2026). The final interpretation rests with WADA and national agencies, and our article on how the WADA Prohibited List approaches research compounds describes the classification rules in detail.

Frequently asked questions

Is Selank an anti-anxiety drug?
In Russia it is registered as a non-prescription medicine in the “other anxiolytics” group. The clinical evidence consists of three small Russian studies without placebo, involving the developers, in which Selank was compared with benzodiazepines or added to them. In the EU and the US it has no status as a medicine, and in our catalog it is a laboratory research reagent.

Does Selank raise BDNF?
The abstracts in PubMed do not confirm this. In the only paper with an abstract, Selank prevented an alcohol-induced rise in BDNF in rats (PMID 31625062).

What is Adalank, and is it more potent than Selank?
Adalank is the name of N-Acetyl Selank Amidate in our catalog. There are no data on its potency: neither it nor N-Acetyl Selank has a peer-reviewed paper or a registered clinical trial. Claims of better brain penetration come from product listings.

Is the Selank in the Russian medicine acetylated?
No. The medicine contains Selank diacetate, a salt of the same molecule, not its N-acetylated derivative.

Why are there no doses in this article?
Selank in our catalog is material for laboratory research, not a product for administration to humans. The registered dosing we know of concerns the Russian drops and applies only within the terms of their product information. For N-Acetyl Selank and Adalank, we know of no clinical data from which any numbers could be derived.

Is Selank banned in sport?
The 2026 List does not name it, and the Russian registration rules out class S0. Authors linked to the POLADA scientific team nevertheless listed it among substances of unclear status, so the decision rests with WADA and national agencies. Derivatives without registration fall under class S0, and from 1 January 2027 that class also lists peptides as an example.

Summary

Selank is tuftsin extended by Pro-Gly-Pro, developed in Moscow and registered in Russia as non-prescription nasal drops. Laboratory models describe slower enkephalin breakdown, an influence on GABA binding and an effect in mice that depends on baseline anxiety. Human data consist of three small Russian trials without placebo, involving the developers, and one imaging study. The peer-reviewed literature is silent on N-Acetyl Selank and Adalank, so data on Selank cannot be carried over to them. The anti-doping status of Selank itself remains unclear. In the US it is not an approved drug, and it was not among the peptides FDA advisers reviewed for compounding in July 2026.

Product documentation

Reagent pages with batch documentation cover Selank spray, Selank 10mg and the derivatives N-Acetyl Selank Spray 10mg, N-Acetyl Selank in a vial, Adalank 10mg and Adalank 10mg Spray. Compounds studied for cognitive function are collected in peptides for brain function, and those studied for stress and mood in peptides for well-being. Intranasal forms are grouped in peptides in spray. For wider background, see our guide to nootropic substances. All materials listed here are for laboratory research only.

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