Selank.
Selank is a synthetic heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, with the laboratory designation TP-7.
Selank is a synthetic heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, with the laboratory designation TP-7. Selank is research / preclinical, and PepCue grades its published evidence D tier (41/100). This is a research reference, not medical or dosing advice.
What it is
Selank is a synthetic heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, with the laboratory designation TP-7. It is a stabilized analog of tuftsin, an endogenous immunomodulatory tetrapeptide (Thr-Lys-Pro-Arg) derived from the Fc region of immunoglobulin G; the added Pro-Gly-Pro tail confers resistance to enzymatic degradation. It is studied primarily as an anxiolytic and nootropic agent and is most associated with Russian neuropharmacology research.
How it works
Selank's parent peptide tuftsin acts on immune cells, and Selank retains immunomodulatory activity while shifting toward neuromodulation. Proposed central mechanisms include modulation of monoamine systems (serotonin, dopamine, noradrenaline) and interaction with the GABAergic and enkephalin/opioid systems; Selank has been reported to inhibit enkephalin-degrading enzymes, prolonging the action of endogenous enkephalins. It has also been reported to influence expression of brain-derived neurotrophic factor (BDNF) and to alter cytokine balance (e.g., IL-6 and interferon-related signaling). These mechanisms are largely characterized in rodent and in vitro models rather than established in humans.
Mechanism pathways
Peptides that tune monoamine, GABA, opioid, ion-channel, and social-behaviour circuits.
Neuromodulation differs from neurotransmission. A neurotransmitter carries a discrete signal across a synapse; a neuromodulator adjusts how strongly and for how long many synapses respond, acting over a broader area and a longer timescale. Most of the compounds grouped here are neuromodulators, which is why their reported effects are described as shifts in tone rather than as switching a function on or off, and why their effects are often bidirectional depending on the starting state. Several routes are represented. One compound is a selective blocker of TREK-1, a two-pore-domain potassium channel. These channels set the resting membrane potential and therefore how easily a neuron fires. TREK-1 is expressed in mood-relevant regions and has been implicated in resistance to conventional antidepressants, and blocking it is proposed to increase serotonergic neurotransmission and support hippocampal neurogenesis. This is a well-defined molecular target, which distinguishes it from most of the group. Another is derived from an immune-active parent peptide and retains immunomodulatory activity while shifting toward central effects. Its proposed actions include modulation of serotonin, dopamine, and noradrenaline systems, interaction with GABAergic signalling, and inhibition of enkephalin-degrading enzymes, which prolongs the action of the body's own opioid peptides rather than adding an exogenous one. A third acts on the oxytocin receptor, a G-protein-coupled receptor. Peripherally this drives uterine contraction and the milk ejection reflex, which is the basis of its approved obstetric use. Centrally, oxytocin signalling in the amygdala, nucleus accumbens, and hypothalamus is associated with social salience, threat processing, and reward related to social interaction. Effects here are strongly context-dependent and are not reliably prosocial. A fourth has no confirmed receptor at all despite decades of study. Reported interactions are diffuse and concentration-dependent, spanning NMDA receptor modulation, stress-axis regulation, and several neuropeptide systems, and it has been framed as a homeostatic regulator with dose- and timing-dependent effects rather than as a sedative acting at a defined site. Honest assessment: one member is an approved medicine for a narrow peripheral indication, and its central effects remain an active research question rather than an established therapy. The others are unapproved research compounds whose mechanisms rest largely on rodent and in vitro work, with limited independent human evidence. Compounds affecting mood and arousal circuits also interact unpredictably with psychiatric medication.
The evidence
The great majority of Selank evidence is preclinical (rodent and in vitro), covering anxiolytic-like behavior, stress models, immune/cytokine modulation, and tissue effects under chronic stress (e.g., Bull Exp Biol Med studies on rat intestine and liver under restraint/foot-shock stress, and a cytokine study under 'social' stress). Human clinical data are limited and come almost entirely from Russian-language trials and registry approval rather than large, independently replicated, placebo-controlled studies indexed in Western literature; reported uses include generalized anxiety disorder and asthenic/neurasthenic conditions. A frequently cited molecular review (Protein and Peptide Letters, 2018, PMID 30255741) summarizes the proposed biology. Overall, robust, independently replicated human efficacy data are thin, and mechanistic plausibility should not be read as proven clinical benefit.
The evidence, in brief
A synthetic heptapeptide derived from the immune peptide tuftsin, developed in Russia as an anxiolytic with reported nootropic effects. Human evidence is limited and largely confined to Russian-language studies (e.g. comparison with a benzodiazepine in anxiety); not approved in the US or EU.
- Efficacy and mechanisms of the peptide anxiolytic selank in generalized anxiety disorder and neurastheniaZh Nevrol Psikhiatr (Korsakov J), 2008 (PMID 18454096)
Evidence maturity
An evidence-only reading: approval status, human vs preclinical data, mechanism and safety. Popularity never raises it. Research file #055
Some human signal atop preclinical work; gaps remain.
Some early human evidence exists but isn't definitive.
Claim receipts
Popular claims about Selank, checked against the state of the evidence. The verdict describes evidence maturity, never an invented study result.
The favorable sedation, dependence and withdrawal profile is reported mostly by the developing groups in small studies, not established in independent head-to-head comparisons.
It is registered in Russia for anxiety and asthenic conditions, but human data come almost entirely from Russian-language trials without large, independently replicated, placebo-controlled confirmation in indexed Western literature.
Nootropic effects are characterized mainly in rodent and in vitro models, and subjective feelings of being calmer or sharper are among the most placebo-responsive outcomes in medicine.
Cytokine and immune effects come from rodent stress models and cell work; none of this has been established as a clinical benefit in people.
Rigorous long-term, large-sample safety data from independent groups are lacking, and most of the existing record comes from the originating institutions and small studies.
Safety profile
Published reports, mostly from the developing Russian groups, describe Selank as generally well tolerated with a notably low sedation, dependence, and withdrawal profile compared with benzodiazepines, but rigorous long-term and large-sample safety data from independent groups are lacking. Because much of the safety record comes from the originating institutions and small studies, the true adverse-event and long-term safety profile in humans is not well established. As a peptide typically administered intranasally in research, purity, contamination, and product-quality concerns apply to non-pharmaceutical material. It has not undergone the comprehensive safety review required for major regulatory approval outside its country of origin.
Compound notes
- Selank is a synthetic analog of the immunomodulatory peptide tuftsin.
- It is studied (mainly in Russia) for anxiety and mood, framed as an anxiolytic without sedation/dependence.
- Not FDA-approved; research-only in most countries.
- Robust independent human trials are limited.
Regulatory status
Selank is reported to have been registered/approved in Russia (around 2009) for anxiety and asthenic conditions, marketed as an intranasal preparation. It is not approved by the US FDA and is not an approved drug in the EU; outside Russia it is effectively investigational and is widely sold as a research-use-only / not-for-human-consumption chemical. It is not a controlled substance and is not a standard WADA-prohibited agent, but its unapproved status means quality and legality vary by jurisdiction.
Sold research-use-only; human evidence is limited or preclinical.
By the numbers
- 01Heptapeptide TP-7 (Thr-Lys-Pro-Arg-Pro-Gly-Pro); a metabolically stabilized analog of the endogenous immunopeptide tuftsin
- 02Developed at the Institute of Molecular Genetics, Russian Academy of Sciences
- 03Studied as an anxiolytic/nootropic; proposed to act via monoamine, GABAergic, enkephalin, BDNF, and cytokine pathways
- 04Most evidence is preclinical (rodent/in vitro); independently replicated human trial data are limited
- 05Reported to be approved/registered in Russia (~2009); not FDA- or EMA-approved
- 06Commonly marketed outside Russia as a research-use-only chemical, not for human consumption
Selank: research formats
Choose the format you are researching to see route-specific notes.
Standard format. Selank is a registered nasal spray in Russia (0.15% solution).
Selank is commercially registered in Russia as a 0.15% nasal spray (1.5 mg/mL). The intranasal route offers efficient absorption via the olfactory mucosa. Research contexts outside Russia use reconstituted lyophilized powder in preserved water, typically at 1.5–5 mg/mL.
0.15% = 1.5 mg/mL. One standard nasal drop (0.03–0.05 mL) delivers approximately 45–75 mcg of Selank at the registered 0.15% concentration.
Selank is more anxiolytic than cognitive-enhancing; the intranasal route produces effects within 15–30 minutes in most research reports.
Sources
Every factual claim above resolves to a real, published source.
- Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological ActivityProtein and Peptide Letters, 2018, PMID 30255741
- Sedative-Hypnotic Agents That Impact Gamma-Aminobutyric Acid Receptors: Focus on Flunitrazepam, Gamma-Hydroxybutyric Acid, Phenibut, and SelankJournal of Clinical Pharmacology, 2021, PMID 34396551
- The Influence of Selank on the Level of Cytokines Under the Conditions of 'Social' StressCurrent Reviews in Clinical and Experimental Pharmacology, 2021, PMID 32621722
- Selank: PubMed search of indexed primary and review literaturePubMed (NCBI) topic search, all years
Cite this page
PepCue. “Selank: the evidence.” PepCue, reviewed June 1, 2026. https://www.pepcue.app/p/selank.
Log your doses, run the vial math, and keep a provider-ready record in PepCue.