Sleep & Cognition

Selank

Also known as TP-7, Selank acetate, Thr-Lys-Pro-Arg-Pro-Gly-Pro, TKPRPGP

A seven-amino-acid Russian anxiolytic built from a fragment of an antibody, registered as a prescription intranasal medicine in the Russian Federation and tested there in a handful of small anxiety trials, with no approval and no independently replicated trial anywhere else.

How it works

A synthetic analog of Tuftsin that modulates the GABAergic system to stabilize mood and anxiety.

Performance edge

Used for mental focus and stress reduction; provides a "calm focus" without cognitive impairment.

Plain-English guide

Selank, without the jargon

What it is

Selank is a chain of seven amino acids made at the Institute of Molecular Genetics of the Russian Academy of Sciences. It is built from tuftsin, a natural four-amino-acid immune signal that the body cuts out of the heavy chain of immunoglobulin G, one of the antibodies in your blood; the chemists bolted a short tail of three more amino acids onto the end to slow the body down from chewing it up (Filatova 2017). In Russia it is a registered prescription medicine for mild anxiety, given intranasally, and that intranasal form is what was given to patients in the published human studies (Renke 2026). It is not approved by any regulator outside Russia. In the United States it is sold as a research chemical and as a supplement ingredient, and the US Food and Drug Administration lists selank acetate among bulk substances that may present significant safety risks in pharmacy compounding.

What people use it for

Generalised anxiety disorder and neurasthenia, the indications the Russian clinical trials were built around (Zozulia 2008)
Phobic, anxious and somatoform disorders, where it was compared head to head with the benzodiazepine phenazepam (Medvedev 2014)
Reducing the side effects of a benzodiazepine, by adding Selank on top of phenazepam rather than replacing it (Medvedev 2015)
Off-label use in nootropic and biohacking circles for so-called calm focus, mental fatigue and stress, which is not what the trials measured
Claimed immune and antiviral effects, which rest mostly on cell and animal work rather than on outcome trials

How it works, simply

A benzodiazepine turns up the volume on the brain's main braking signal, GABA, wherever that signal is being used. Selank behaves more like a hand resting on the volume knob: in binding experiments it does not switch GABA receptors on by itself, it changes how strongly they respond when GABA is already there (Vyunova 2018). That is the working explanation for why the Russian trials described an anxiety effect without the heavy sedation and clumsiness that benzodiazepines cause. Whether that translation from a test tube to a person holds up outside those trials has not been shown.

What to expect, and when

First 20 minIn 52 healthy volunteers scanned with resting-state functional MRI, Selank changed connectivity between the right amygdala and the right temporal cortex within 20 minutes of dosing, compared with placebo (Panikratova 2020). A brain-scan change is not the same as feeling different.
Days 1-7In the trial that added Selank to phenazepam, the combined group reached a measurable improvement on the Hamilton depression rating scale earlier than the group on phenazepam alone (Medvedev 2015). No study located reports how fast a single dose works on its own.
Week 2The two-week mark is where the Russian anxiety trials took their main readings; a 2026 review summarises intranasal Selank in mild generalised anxiety disorder as producing a significant reduction in anxiety scores after two weeks without sedation (Renke 2026).
Week 3+In the comparison against phenazepam, the anxiolytic effect was reported to last for a week after the last dose of the peptide (Medvedev 2014), which is unusual and has not been independently replicated.
Month 2+No controlled human data past roughly one to two months was located. A 2026 narrative review states it can be used for weeks to months with no reported complications, but that is a summary of a thin literature rather than a long-term safety study.

Side effects and interactions

Mild daytime drowsiness and dry mouth are the uncommon adverse effects named in a 2026 narrative review of the peptide literature (Renke 2026)
No sedation, memory impairment or motor slowing was attributed to Selank in the trials; in the phenazepam add-on trial those problems came from the benzodiazepine and were reported to be lower when Selank was added (Medvedev 2015)
The 2008 trial reported antiasthenic and psychostimulant effects alongside the anxiolytic effect (Zozulia 2008), so a stimulating rather than calming response is possible and may affect sleep
The US Food and Drug Administration states that compounded drugs containing selank acetate may pose risk for immunogenicity for certain routes of administration, meaning an immune reaction raised against the peptide, because of the potential for aggregation and peptide-related impurities
Total published human exposure is in the low hundreds of patients across a few small Russian trials, so uncommon adverse effects would not have been detected; absence of reports is not evidence of absence
Nothing in the human literature located characterises injection-site reactions, because the human studies used the intranasal formulation rather than the subcutaneous injection that off-label users give themselves

Who should avoid it

You are pregnant, trying to conceive, or breastfeeding; no human reproductive or developmental safety data for Selank was located
You are taking a benzodiazepine, an SSRI, an SNRI or any other psychiatric medication without telling the prescriber; the only combination that has been studied at all is Selank plus phenazepam (Medvedev 2015), and nothing else has interaction data
You have an anxiety disorder that has never been assessed by a clinician; the trial patients had diagnosed generalised anxiety disorder, neurasthenia or somatoform disorders, and self-treating an undiagnosed condition can delay care that works
You have an autoimmune condition or are on immune-modifying treatment; Selank is built from tuftsin, a fragment of immunoglobulin G that acts as an immune signal, and what an antibody-derived peptide does in that setting is unstudied
You are a competitive athlete under the World Anti-Doping Agency code, since a substance with no approval outside one country falls foul of the non-approved substances category
You are under 18, or you are not working with a physician who knows you are taking it

Common mistakes

Assuming the injected route reproduces the trial. Every human efficacy result located came from the intranasal formulation registered in Russia, not from subcutaneous injection. In mice, the same 300 micrograms per kilogram dose given intranasally and intraperitoneally produced different receptor changes in the brain, with the intranasal route raising NMDA receptor binding and the injected route raising GABA receptor binding (Vasil'eva 2016). Route is not a detail here.
Expecting a benzodiazepine. The trials measured change on anxiety rating scales over two weeks in diagnosed patients, not an acute calming hit, and one trial reported psychostimulant effects alongside the anxiolytic ones.
Stacking it with alcohol, sedatives or several other unapproved peptides at once. No interaction data exists outside the single phenazepam study, and combining compounds makes any adverse effect impossible to attribute.
Reconstituting or storing it carelessly. Use bacteriostatic water, run it slowly down the vial wall, swirl rather than shake, keep the lyophilised powder cold and dark, refrigerate after reconstitution, and discard on the timeline your pharmacist gives rather than stretching one vial for months.
Trusting the label on grey-market material. Selank and Semax have both turned up in seized pharmaceutical preparations analysed by forensic chemists (Vanhee 2020), and the US Food and Drug Administration flags peptide-related impurities and aggregation as a specific concern for compounded selank acetate.

Deep research

What the literature actually shows

Mechanism

Selank is the heptapeptide Thr-Lys-Pro-Arg-Pro-Gly-Pro. The first four residues, Thr-Lys-Pro-Arg, are tuftsin, a short immunomodulatory peptide released from the heavy chain of human immunoglobulin G; the appended tripeptide Pro-Gly-Pro at the carboxyl end was added to give metabolic stability and duration of action, since bare tuftsin is degraded quickly (Filatova 2017). The molecule was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, the same laboratory that produced Semax.

The best-characterised mechanism is allosteric modulation of the GABA-A receptor, the receptor benzodiazepines act on. Radioligand binding work reported that Selank behaves as a positive allosteric modulator of tritiated GABA binding, with subtype-selective and concentration-dependent effects, and that when Selank and a benzodiazepine are present together the result is not simply the sum of the two and differs from either alone (Vyunova 2018). That last point is the mechanistic counterpart of the clinical claim that adding Selank to phenazepam changes how the benzodiazepine behaves rather than just adding to it.

The gene-expression story is more equivocal than it is usually reported. In human IMR-32 neuroblastoma cells, Selank on its own had no direct effect on the messenger RNA levels of GABAergic system genes; its effect appeared only in combination, where it nearly abolished the changes GABA alone produced and enhanced the changes produced by olanzapine (Filatova 2017). In other words, the cell data supports a modulator that only matters when something else is acting, not a drug with an effect of its own at the transcriptional level.

Two further threads run through the animal and patient literature without being settled. One is brain-derived neurotrophic factor: intranasal Selank changed BDNF expression in the rat hippocampus (Doklady Biological Sciences, 2008), and a 2026 review repeats that Selank raises BDNF in regions such as the prefrontal cortex (Renke 2026), but no human study located measured it. The other is the endogenous opioid system: the 2008 anxiety trial reported that patients with anxiety disorders had lower enkephalin-degrading activity in serum, correlated with symptom severity, and that Selank treatment raised the parameter, most strongly in the generalised anxiety disorder group (Zozulia 2008). Neither thread has been tested as a mechanism in a controlled human experiment.

Strength of evidence

Limited human dataFour human studies of Selank itself were located, including one PubMed-indexed randomized controlled trial, so this is genuinely human data rather than animal extrapolation; it stays at limited-human for two reasons. First, the trials are small (52 to 70 participants), all Russian, published in one journal family, mostly compared against an active benzodiazepine rather than placebo, and none has been independently replicated or registered on ClinicalTrials.gov. Second, the route does not match this cheatsheet: the human efficacy evidence is for the intranasal formulation registered in Russia (Renke 2026), while the dosing figures here describe a reconstituted vial given by subcutaneous injection, and a mouse study found that the same dose given intranasally and intraperitoneally changed different receptor systems in the brain (Vasil'eva 2016). The one human study that names a route, the 2020 imaging study, describes an injection but measures brain connectivity rather than any clinical outcome.

Key studies

Randomised controlled trial2008Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakovan = 62
Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia
Sixty-two patients with generalised anxiety disorder or neurasthenia were treated with either selank (30 patients) or the benzodiazepine medazepam (32 patients), with Hamilton, Zung and Clinical Global Impression scales plus serum enkephalin measurements. The anxiolytic effects of the two drugs were similar, but selank also showed antiasthenic and psychostimulant effects. Enkephalin activity was lower in more severely affected patients and rose with selank treatment, most clearly in the generalised anxiety disorder group. There was no placebo arm and the abstract does not state the dose or route.
Human trial2014Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakovan = 60
A comparison of the anxiolytic effect and tolerability of selank and phenazepam in the treatment of anxiety disorders
Sixty patients with phobic-anxiety and somatoform disorders, coded ICD-10 F40.2-9, F41.1-9 and F45.0-1, received selank or the benzodiazepine phenazepam. The authors reported pronounced anxiolytic and mild nootropic effects of selank, with the anxiolytic effect lasting for a week after the last dose of the peptide, and a positive effect on quality of life. The report is an active-comparator study without a placebo arm, and the abstract states neither dose nor route.
Randomised controlled trial2015Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakovan = 70
Optimization of the treatment of anxiety disorders with selank
Indexed by PubMed as a randomized controlled trial. Seventy patients with anxiety-spectrum disorders received either phenazepam alone (30 patients) or phenazepam combined with selank (40 patients), assessed with the Hamilton depression rating scale, Clinical Global Impression, Spielberger scales, the UKU side-effect rating scale, cognitive testing and SF-36. The combination reached a positive effect earlier on the Hamilton scale and lowered the rate of benzodiazepine side effects, including attention and memory impairment, sedation, lengthened sleep, sexual dysfunction and emotional blunting, both during treatment and after the tranquilliser was stopped, with better quality-of-life scores. This is an add-on design, so it does not establish what selank does by itself.
Human trial2020Doklady Biological Sciencesn = 52
Functional Connectomic Approach to Studying Selank and Semax Effects
Fifty-two healthy participants underwent resting-state functional MRI before and at 5 and 20 minutes after administration of Semax, Selank or placebo. Both general and specific effects of Selank and Semax on functional connectivity between the right amygdala and the right temporal cortex, including the fusiform and parahippocampal gyri, were reported for the first time. The abstract describes the administration as an injection and does not state the dose or how participants were allocated. This is a brain-imaging endpoint in healthy volunteers, not a clinical outcome.
In vitro2018Protein and Peptide Letters
Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity
Radioligand-receptor binding analysis reporting that Selank affects tritiated GABA binding as a positive allosteric modulator, with subtype-selective, concentration-dependent allosteric modulation of GABA receptors proposed as one molecular mechanism of its anti-anxiety effect. Selank combined with benzodiazepines regulated GABA binding in a specific manner that was not cumulative and differed from either substance alone.
In vitro2017Frontiers in Pharmacology
GABA, Selank, and Olanzapine Affect the Expression of Genes Involved in GABAergic Neurotransmission in IMR-32 Cells
Quantitative PCR of 84 neurotransmission genes in human IMR-32 neuroblastoma cells. Selank had no direct effect on the messenger RNA levels of GABAergic system genes on its own. Combined with GABA it nearly completely suppressed the expression changes that GABA produced alone, and combined with olanzapine it enhanced that drug's effect on the genes studied. The paper also sets out Selank's structure as the tuftsin fragment Thr-Lys-Pro-Arg plus a Pro-Gly-Pro tail added for metabolic stability, developed at the Institute of Molecular Genetics of the Russian Academy of Sciences.
Animal study2016Eksperimental'naia i Klinicheskaia Farmakologiia
Comparison of pharmacological effects of heptapeptide Selank after intranasal and intraperitoneal administration to BALB/c and C57BL/6 mice
Selank at 300 micrograms per kilogram per day for five days was given to two mouse strains either intraperitoneally or intranasally. In the anxiety-prone BALB/c strain the intraperitoneal route increased GABA receptor binding in the frontal cortex by 38 percent without affecting hippocampal NMDA receptors, while the intranasal route increased NMDA receptor binding by 23 percent without affecting GABA receptors. Anxiolytic and nootropic effects appeared only in BALB/c mice and not in the less anxious C57BL/6 strain. The authors attributed the difference to route-specific pharmacokinetics and biotransformation.
Review2026International Journal of Molecular Sciences
Therapeutic Peptides in Aesthetic, Metabolic and Endocrine Conditions: Effects, Safety, Clinical Applications, and Future Perspectives
Narrative review describing Selank as a heptapeptide derived from a tuftsin fragment with anxiolytic and nootropic properties and no significant sedative effect. It states that in humans, intranasal Selank has been tested in patients with mild generalised anxiety disorder, producing a significant reduction in anxiety scores after two weeks without sedative effects, that Selank is officially indicated in Russia for mild anxiety, that uncommon adverse effects include mild daytime drowsiness or dry mouth, and that it can be used for weeks to months with no reported complications. As a narrative review it summarises the same small Russian trial literature rather than adding new data.

Safety data

The reported tolerability record is unremarkable and very thin. Across the Russian anxiety trials Selank was described as anxiolytic without the sedation, cognitive dulling and motor effects of the benzodiazepine comparators, and in the add-on trial the rate of those benzodiazepine side effects fell when Selank was added to phenazepam (Medvedev 2015). A 2026 narrative review names mild daytime drowsiness and dry mouth as uncommon adverse effects and reports no complications over weeks to months of use (Renke 2026). The total published human exposure is in the low hundreds of patients, concentrated in a small number of short trials in one country, so this record can only exclude common, short-term, obvious harms. One trial also reported psychostimulant effects (Zozulia 2008), which is worth knowing if you are taking it for anxiety and expecting calm.

Two structural gaps matter more than the reported events. First, every human efficacy result located is for the intranasal formulation, whereas off-label use outside Russia is subcutaneous self-injection from a reconstituted vial; the mouse comparison of the two routes found different receptor changes from the same dose (Vasil'eva 2016), so the tolerability record for nasal drops does not automatically transfer. Second, interaction data essentially does not exist: the only combination studied is Selank with phenazepam, and nothing was located on Selank with SSRIs, SNRIs, alcohol, or the other peptides it is commonly stacked with. A compound whose proposed mechanism is allosteric modulation of the same receptor benzodiazepines act on (Vyunova 2018) is exactly the kind of compound where interaction data would matter.

Product quality is a separate risk from the molecule. The US Food and Drug Administration states that compounded drugs containing selank acetate may pose risk for immunogenicity for certain routes of administration due to the potential for aggregation and peptide-related impurities, and that it lacks important information regarding any safety issues raised by selank acetate administered to humans. Selank has also turned up alongside Semax in seized pharmaceutical preparations examined by forensic laboratories (Vanhee 2020). Material bought outside a regulated supply chain carries the additional and unquantified risk of not being what the label says.

Regulatory status

FDA: As of 2026-09-19, Selank is not approved by the US Food and Drug Administration for any indication; selank acetate appears on the agency's bulk drug substances safety-risk page as a nomination that was later withdrawn, with the agency noting risk for immunogenicity for certain routes of administration due to potential aggregation and peptide-related impurities, and stating that it lacks important information regarding any safety issues raised by selank acetate administered to humans.
WADA: As of 2026-09-19, Selank is not named individually on the World Anti-Doping Agency Prohibited List, but section S0 prohibits at all times any pharmacological substance with no current approval by a governmental regulatory health authority for human therapeutic use, which is how a substance registered only in the Russian Federation is generally read, and at least one 2026 review instead places Selank under section S2; either way an athlete under the Code should treat it as prohibited and get a written ruling from their anti-doping organisation before using it.
Source: https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks

Open questions

Does Selank work when injected? Every human efficacy result located is for the intranasal formulation, and the only route comparison located, in mice, found that intranasal and intraperitoneal dosing changed different receptor systems in the brain (Vasil'eva 2016).
Would the Russian results survive a placebo-controlled trial run elsewhere? The anxiety trials compared Selank against an active benzodiazepine rather than placebo, were conducted in one country, and no Selank trial was located on ClinicalTrials.gov.
How can the anxiolytic effect persist for a week after the last dose, as reported in the phenazepam comparison (Medvedev 2014), when the peptide itself is cleared far faster than that?
Is the GABA-A mechanism the real one? Selank modulates GABA binding allosterically in binding assays (Vyunova 2018) yet had no effect of its own on GABAergic gene expression in human neuroblastoma cells (Filatova 2017), and the enkephalin and BDNF threads have never been tested as mechanisms in a controlled human study.
What are the long-term effects? Nothing controlled was located past roughly two months, and no study has looked for tolerance, withdrawal or dependence, which is the specific worry a reviewer raised about poorly studied GABA-active compounds sold as supplements.