Selank

Selank is a synthetic seven-amino-acid peptide developed from tuftsin, a small fragment of an immune-system protein. Researchers have studied it in anxiety-related clinical reports, animal behavior and experiments on brain signaling. Small Russian treatment studies reported favorable symptom changes using benzodiazepine treatments as references. Laboratory work offers several possible explanations involving GABA and the breakdown of enkephalins, with responses affected by the biological system and other compounds present. Zozulia and colleagues (2008), Vyunova and colleagues (2018).

Overview

Molecular profile

Form: Selank parent free-base peptide; acetate/diacetate salts described separately Source
Sequence: TKPRPGP — Thr-Lys-Pro-Arg-Pro-Gly-Pro Source
Length: 7 amino-acid residues Source
Molecular formula: C33H57N11O9 (estimated neutral parent composition) Source
Molecular mass: Approximately 752 Da (estimated average, parent peptide) Source
Related research name: TP-7 Source

Forms and derivatives

Selank acetate / Selank diacetate

Acetate salt forms of the parent heptapeptide. FDA separates Selank and Selank diacetate in its substance hierarchy; the rat expression study explicitly identifies a diacetate preparation.

NA-Selank / N-acetyl Selank

The name ordinarily denotes the Selank sequence with an N-terminal acetyl group. This covalent terminal modification differs from an acetate salt.

NA-Selank Amidate / N-acetyl Selank amidate

The stated name denotes an N-acetylated Selank sequence with C-terminal amidation. A material needs an explicit terminal structure before matching it to evidence.

The Selank sequence is Thr-Lys-Pro-Arg-Pro-Gly-Pro, abbreviated TKPRPGP. The first four residues form tuftsin; the remaining Pro-Gly-Pro extension creates the heptapeptide. TP-7 is another name used for Selank. FDA's substance registry distinguishes the parent peptide from Selank diacetate, a salt form containing acetate counterions. An acetate salt and a peptide with a covalently attached acetyl group have different chemical identities. FDA substance record.

This structural context helps explain why Selank papers can be relevant to several biological questions. Changing tuftsin's sequence creates a new research material whose activities require their own experiments. Sarkisova and colleagues identified the seven-residue sequence in their rat and mouse behavioral study; the responses differed with the animal strain and exposure conditions. Sarkisova and colleagues (2008).

NA-Selank and NA-Selank Amidate

NA-Selank usually denotes N-acetyl Selank: the seven-residue parent sequence with an acetyl group attached at its amino terminus. NA-Selank Amidate additionally denotes an amide at the carboxyl terminus. Those changes alter the chemical groups available at the ends of the chain. Comparative human measurements of stability, brain exposure, clinical effect and safety remain unavailable in the primary literature reviewed here. An explicit terminal structure is needed to match each derivative to evidence; the cited Selank trials concern the preparations their investigators identified as Selank.

Uses and research areas

The clinical literature centers on anxiety-related disorders. A 2008 report examined generalized anxiety disorder and neurasthenia, a diagnostic term used in that study for a pattern including fatigue and reduced stamina. A later report examined Selank alongside phenazepam in anxiety-phobic, hypochondriacal and somatoform disorders. These populations explain the original treatment questions more precisely than a broad label such as stress relief. Zozulia and colleagues (2008), Medvedev and colleagues (2015).

Animal studies approach related questions through observable behavior: time spent in exposed maze arms, immobility during a forced-swim test, and sucrose consumption. Each task samples a particular response to its laboratory setting. Differences across these tasks are useful when investigating how a peptide affects stress-related behavior, especially when an effect appears in one strain or condition and fades in another. Sarkisova and colleagues (2008), Kasian and colleagues (2017).

Mechanism of action

GABA is a chemical messenger that helps restrain activity in the nervous system. Its effects depend on receptors, transporters and the surrounding cell network. Vyunova and colleagues used isolated brain-cell membranes and radiolabeled GABA to examine whether Selank altered ligand binding. They reported concentration-dependent modulation and complex interactions with diazepam and olanzapine. The combined effects differed from the effects of each substance alone, suggesting that the surroundings of the binding interaction influence its response. The authors proposed allosteric modulation, in which an interaction changes how a receptor responds to its usual messenger. Vyunova and colleagues (2018).

Enkephalins provide another proposed route. These small signaling peptides are broken down by enzymes in blood and tissues. Zozulya and colleagues found that Selank slowed enkephalin hydrolysis in a plasma assay. Their work connects Selank with the persistence of another signaling molecule, which also clarifies an easily confused measurement: a change in enkephalin half-life describes the assay's substrate. Zozulya and colleagues (2001).

Gene-expression experiments measure the amount of messenger RNA, which carries copies of the genetic instructions cells use to make proteins. Changes in these messages help researchers identify how a cell responds, alongside measurements of the proteins and cell behavior. The rat and cell experiments below examine those responses in their particular biological settings.

Pharmacokinetics

Zolotarev and colleagues used tritium labeling and chromatographic separation to examine Selank biodegradation in blood plasma and its distribution in brain tissue after intranasal administration. They identified TKPRP, TKP, RP and GP among the breakdown products. A label can remain in a fragment after the parent peptide is cleaved, so separating the molecular species is essential when measuring how much intact Selank persists. The accessible study provides preclinical distribution and breakdown information; a human concentration-time profile remains unavailable in the reviewed sources. Zolotarev and colleagues (2006).

The clinical enkephalin work concerns how rapidly enkephalin breaks down in the assay. It therefore cannot supply Selank's plasma half-life. A duration of symptom change also measures a pharmacological outcome rather than peptide clearance. These distinctions leave the principal exposure questions open: how much intact peptide reaches particular tissues, how the route changes that exposure, and how terminally modified derivatives compare.

Research findings

Anxiety scores in two small treatment reports

Zozulia and colleagues studied 62 patients: 30 received Selank and 32 medazepam. Assessments included Hamilton, Zung and Clinical Global Impression scales, alongside an enkephalin-related blood measurement. The authors described similar anxiety improvement and additional effects on fatigue and activity with Selank. PubMed indexes the paper as a randomized controlled trial. The accessible English abstract omits the allocation procedure, blinding, numerical symptom differences and confidence intervals, so the reported similarity cannot establish a formal equivalence or noninferiority result. Zozulia and colleagues (2008).

Medvedev and colleagues compared phenazepam alone in 30 patients with phenazepam plus Selank in 40 patients. The authors reported a faster initial response and fewer selected cognitive, sedative and other treatment-associated symptoms in the combined group. This paper also carries an indexed randomized-trial label. Its accessible abstract does not reveal enough allocation detail or a complete event table to quantify how reliably the groups differed. Because both groups received phenazepam, the finding applies to that add-on comparison. Medvedev and colleagues (2015).

Expression findings depend on the experimental system

Volkova and colleagues measured RNA messages from 84 neurotransmission-related genes in rat frontal cortex, part of the brain, at one and three hours after intranasal Selank or GABA. The early pattern of increases and decreases was similar after the two compounds. The methods identify Selank diacetate and describe tissue pooled within each group and time point. Measuring the same pooled tissue repeatedly improves measurement precision but does not add independent animals to the experiment. Volkova and colleagues (2016).

Filatova and colleagues tested a related gene panel in IMR-32 neuroblastoma cells. Selank alone produced no detected changes in the measured messenger-RNA levels. Combining it with GABA largely suppressed the expression changes produced by GABA alone, while combining it with olanzapine altered more genes than olanzapine alone. The contrast across these experiments suggests that cell type, tissue organization and co-exposure influence the response. Filatova and colleagues (2017).

Behavioral context and brain-network measurements

Kasian and colleagues compared Selank, diazepam, their combination and saline in rats with and without unpredictable chronic mild stress. In a raised maze with open and enclosed arms, stressed rats given the combination spent more time in the open arms and less in the enclosed arms than saline-treated controls. Their anxiety indicators did not clearly differ from their own prestress values. Without the chronic-stress condition, even the saline course worsened some measures; the changes after Selank were less pronounced. This mixed response belongs beside the positive finding because the initial state affected the outcome. Kasian and colleagues (2017).

Panikratova and colleagues studied resting-state brain connectivity in 52 healthy participants receiving Selank, Semax or placebo. Regional connectivity differences involved the right amygdala and temporal cortex. Such scans can locate an acute network response and help guide further hypotheses. Demonstrating a useful change in symptoms, memory or daily function would require outcomes assessing those abilities directly. Panikratova and colleagues (2020).

Safety and tolerability

Selank has no FDA-approved therapeutic indication identified in this review. FDA's current compounding-risk page specifically lists Selank acetate (TP-7), noting possible immune reactions associated with peptide aggregation or impurities and important gaps in human safety information. Small symptom studies provide too little follow-up and too few participants to estimate uncommon or delayed harms. FDA compounding-risk record.

The phenazepam add-on report offers a preliminary tolerability observation in a particular co-treatment setting. It does not establish a general absence of sedation, dependence, interactions or withdrawal effects. Direct assessment of each outcome would need an appropriate comparator, a defined preparation and adequate follow-up.

What the research means

Selank's literature has a coherent scientific theme: a short tuftsin-derived peptide may influence the way cells and neural networks respond to inhibitory signaling and stress. The enzyme, membrane-binding, gene-expression and behavioral experiments investigate different parts of that theme. Their value grows when their methods explain both the favorable and null findings.

Larger, clearly reported anxiety trials would show whether the small clinical findings reproduce with a characterized Selank preparation. A convincing result would connect a symptom difference with functional improvement, adverse-event monitoring and transparent allocation methods. Derivative comparisons would then need their own structural and exposure evidence.

FAQs

Is Selank the same peptide as tuftsin?

Selank contains tuftsin's four-residue sequence followed by Pro-Gly-Pro, producing seven residues. The extension creates a separate peptide with its own experimental responses. Sarkisova and colleagues (2008).

Does the medazepam comparison establish equivalent effectiveness?

The authors reported similar anxiety effects, but the accessible report provides no formal noninferiority margin or adequate numerical uncertainty for an equivalence conclusion. Its indexed randomized-trial label is retained; detailed allocation and blinding methods remain unavailable. Zozulia and colleagues (2008).

What does the null IMR-32 result contribute?

IMR-32 is a laboratory cell line derived from a neuroblastoma, a tumor of nerve-related cells. Investigators measured messenger RNA, the cellular messages used to make proteins. They did not detect a change in the measured messages after Selank alone. Adding Selank to GABA or olanzapine changed the response compared with those compounds alone. The result shows that the cell type and the other substances present matter when testing a proposed mechanism. Filatova and colleagues (2017).

Are NA-Selank and NA-Selank Amidate established improvements?

Their names describe terminal chemical modifications. The cited primary literature supplies no direct comparative human measurements establishing greater benefit, longer exposure or improved safety for either form.

Can an enkephalin half-life supply Selank's half-life?

The measured half-life belongs to enkephalin, whose breakdown the assay examines. Quantifying intact Selank clearance requires a separate peptide-specific exposure study. Zozulya and colleagues (2001).

Selank and Semax share a Pro-Gly-Pro extension but begin with different peptide sequences. Their related chemical design does not assign them the same clinical effects. Oxytocin offers another example of the distance between an acute brain measurement and a reproducible behavioral treatment result. Epitalon's profile examines how a precise peptide identity determines which aging studies apply.

References

The selected sources include original clinical reports, laboratory studies and FDA identity and safety records. Full citations and source-specific annotations follow.

U.S. Food and Drug Administration. Global Substance Registration System: Selank, UNII TS9JR8EP1G. Public substance record, accessed 13 October 2026.
Records the seven-residue parent sequence, estimated neutral composition and mass, and Selank-diacetate relationship.
Sarkisova KIu, Kozlovskiĭ II, Kozlovskaia MM. [Effects of heptapeptide selank on genetically-based and situation-provoked symptoms of depression in behavior in WAG/Rij and Wistar rats, and in BALB/c mice]. Zhurnal Vysshei Nervnoi Deiatelnosti imeni I. P. Pavlova. 2008;58(2):226–237. PMID: 18661785.
Identifies TKPRPGP and reports strain- and exposure-dependent behavioral responses, including several null conditions.
Zozulia AA, Neznamov GG, Siuniakov TS, Kost NV, Gabaeva MV, Sokolov OIu, Serebriakova EV, Siranchieva OA, Andriushenko AV, Telesheva ES, Siuniakov SA, Smulevich AB, Miasoedov NF, Seredenin SB. [Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia]. Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova. 2008;108(4):38–48. PMID: 18454096.
Compares 30 Selank and 32 medazepam recipients using symptom scales and a serum enkephalin-related measurement.
Medvedev VE, Tereshchenko ON, Kost NV, Ter-Israelyan AY, Gushanskaya EV, Chobanu IK, Sokolov OY, Myasoedov NF. [Optimization of the treatment of anxiety disorders with selank]. Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova. 2015;115(6):33–40. DOI: 10.17116/jnevro20151156133-40.
Compares phenazepam alone in 30 patients with the Selank combination in 40, reporting earlier symptom response and fewer selected undesirable symptoms.
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. Frontiers in pharmacology. 2016;7:31. DOI: 10.3389/fphar.2016.00031.
Examines a rat frontal-cortex expression panel and records the diacetate preparation and pooled tissue design.
Filatova E, Kasian A, Kolomin T, Rybalkina E, Alieva A, Andreeva L, Limborska S, Myasoedov N, Pavlova G, Slominsky P, Shadrina M. GABA, Selank, and Olanzapine Affect the Expression of Genes Involved in GABAergic Neurotransmission in IMR-32 Cells. Frontiers in pharmacology. 2017;8:89. DOI: 10.3389/fphar.2017.00089.
In IMR-32 neuroblastoma cells, investigators detected no change in the measured RNA messages with Selank alone. Adding Selank to GABA or olanzapine changed the responses seen with those substances alone.
Kasian A, Kolomin T, Andreeva L, Bondarenko E, Myasoedov N, Slominsky P, Shadrina M. Peptide Selank Enhances the Effect of Diazepam in Reducing Anxiety in Unpredictable Chronic Mild Stress Conditions in Rats. Behavioural neurology. 2017;2017:5091027. DOI: 10.1155/2017/5091027.
Reports stronger normalization with the combination in stressed rats and deterioration of some measures in nonstressed conditions.
Zozulya AA, Kost NV, Yu Sokolov O, Gabaeva MV, Grivennikov IA, Andreeva LN, Zolotarev YA, Ivanov SV, Andryushchenko AV, Myasoedov NF, Smulevich AB. The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity. Bulletin of experimental biology and medicine. 2001;131(4):315–317. DOI: 10.1023/a:1017979514274.
Investigates enzymatic enkephalin hydrolysis in plasma, clarifying which molecule's persistence the assay measures.
Vyunova TV, Andreeva L, Shevchenko K, Myasoedov N. Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. Protein and Peptide Letters. 2018;25(10):914–923. DOI: 10.2174/0929866525666180925144642.
Uses radiolabeled GABA binding to examine concentration-dependent modulation and interactions with other compounds in membrane preparations.
Panikratova YR, Lebedeva IS, Sokolov OY, Rumshiskaya AD, Kupriyanov DA, Kost NV, Myasoedov NF. Functional Connectomic Approach to Studying Selank and Semax Effects. Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections. 2020;490(1):9–11. DOI: 10.1134/S001249662001007X.
Reports acute resting-state connectivity differences in 52 healthy participants; symptom and cognitive-task efficacy were not measured in the accessible abstract.
Zolotarev IuA, Dadaian AK, Dolotov OV, Kozik VS, Kost NV, Sokolov OIu, Dorokhova EM, Meshavkin VK, Inozemtseva LS, Gabaeva MV, Andreeva LA, Alfeeva LIu, Pavlov TS, Badmaeva KE, Badmaeva SE, Bakaeva ZV, Kopylova GN, Samonina GE, Vas'kovskiĭ BV, Grivennikov IA, Zozulia AA, Miasoedov NF. [Evenly tritium-labeled peptides and their in vivo and in vitro biodegradation]. Bioorganicheskaia Khimiia. 2006;32(2):183–191. Russian article; English translation in Russian Journal of Bioorganic Chemistry 32:166–173, DOI: 10.1134/S1068162006020099.
Identifies Selank and Semax breakdown products through chromatographic separation of labeled peptides; the abstract supplies no human exposure curve.
U.S. Food and Drug Administration. Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks. Current agency webpage, accessed 13 October 2026.
Identifies substance-specific gaps in safety, aggregation, impurities and characterization for compounded peptide products.

Glossary

GABA: A chemical messenger that helps restrain activity in the nervous system.
Enkephalin: A small endogenous signaling peptide examined in the cited breakdown assays.
Allosteric modulation: A change in receptor behavior produced through an interaction affecting how another molecule acts.
Messenger RNA: A temporary cellular copy of genetic instructions used to make proteins.
Active comparator: Another treatment used as the reference condition in a study.
Acetate salt: A peptide form associated with acetate counterions; this differs chemically from covalent N-terminal acetylation.