# Selank: full monograph (Selank Co)
> Source page: https://selankco.com/monograph
Status: Research compound, not FDA-approved
Disclosure: Selank is not FDA approved for any use. It is sold as a research chemical; FDA has cited unresolved safety and quality concerns for compounded selank, and no human efficacy has been established to FDA standards.
Updated: 2026-08-14
## Key facts
- Status: Research compound, not FDA-approved
- Human PK studies: None published (source: https://selankco.com/evidence.json)
- Human half-life: Never measured (source: https://selankco.com/evidence.json)
- Human bioavailability: Never measured, by any route including nasal (source: https://selankco.com/evidence.json)
- Metabolism: Degraded in plasma to TKPRP, TKP, RP and GP (rat, tritium label) (source: https://pubmed.ncbi.nlm.nih.gov/16637290/)
- Brain exposure: Examined in rat brain tissue after intranasal dosing; no numeric values reported (source: https://pubmed.ncbi.nlm.nih.gov/16637290/)
- Route difference: In mice, intranasal and intraperitoneal dosing altered different receptor systems, attributed by the authors to pharmacokinetics (source: https://pubmed.ncbi.nlm.nih.gov/29787664/)
- Commonly misquoted: Published half-lives are leu-enkephalin's, not selank's (source: https://pubmed.ncbi.nlm.nih.gov/11550013/)
- Class: Synthetic heptapeptide; tuftsin analog (tuftsin plus Pro-Gly-Pro) (source: https://pubchem.ncbi.nlm.nih.gov/compound/11765600)
- Sequence: Thr-Lys-Pro-Arg-Pro-Gly-Pro (source: https://pubchem.ncbi.nlm.nih.gov/compound/11765600)
- Molecular weight: 751.9 (C33H57N11O9) (source: https://pubchem.ncbi.nlm.nih.gov/compound/11765600)
- US status: Not FDA approved for any use; no Drugs@FDA record (source: https://www.accessdata.fda.gov/scripts/cder/daf/)
- FDA compounding: Selank acetate (TP-7) listed as nominated but withdrawn, with an immunogenicity concern (source: https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks)
- Russian status: Listed as a registered Russian peptide drug, classified anxiolytic (peer-reviewed source; not verified at the register) (source: https://pmc.ncbi.nlm.nih.gov/articles/PMC9030433/)
- Selank-titled PubMed papers: 57, of which 26 are published in Russian (source: https://selankco.com/evidence.json)
- Non-Russian original studies: 0 in the PubMed index; the one non-Russian affiliation is a review (source: https://selankco.com/evidence.json)
- Human studies: 5 total: 4 in patients, 1 imaging study in healthy volunteers (source: https://pubmed.ncbi.nlm.nih.gov/18454096/)
- People studied: 244 across all studies with a stated count; largest single study 70 (source: https://pubmed.ncbi.nlm.nih.gov/18454096/)
- Randomized controlled efficacy trials: None located in any readable index (source: https://pubmed.ncbi.nlm.nih.gov/18454096/)
- Registered trials: 0 on ClinicalTrials.gov (source: https://clinicaltrials.gov/search?intr=selank)
- Human pharmacokinetics: None published: no half-life, clearance or bioavailability for any route (source: https://selankco.com/evidence.json)
- Established human dose: None. No human study abstract states a dose (source: https://pubmed.ncbi.nlm.nih.gov/18454096/)
- Long-term safety: No long-term study, toxicology report or adverse-event surveillance located (source: https://selankco.com/evidence.json)
- Sport: Not named on the 2026 WADA list; unclear status under the S0 catch-all (source: https://www.wada-ama.org/en/prohibited-list)
## Overview
Selank is a synthetic seven-amino-acid peptide, sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro, built by adding the tripeptide Pro-Gly-Pro to the immune peptide tuftsin 1 2 3 . It was developed in Russia, where a 2022 peer-reviewed review of Russian peptide pharmaceuticals lists it among 14 peptide products registered in the Russian Federation and classifies it as an anxiolytic 8 . In the United States it is not an approved medicine of any kind: FDA's drug database returns no selank product, and FDA's compounding page carries a safety entry for selank acetate 5 6 . That gap is the whole story of this compound, and it is what this site is built to map. The same molecule is a registered pharmaceutical in one country and an unregulated research chemical in another, and the reason is not a conspiracy or a delay. It is that the evidence supporting selank was produced almost entirely inside one country's research system and has never been reproduced outside it. Our census of every selank record indexed in PubMed found 57 papers with selank in the title, 26 of them published in Russian, and exactly one carrying an author affiliation with no Russian institution, which is a US review article rather than an original selank study 10 11 . This monograph does something no vendor page does and no critic page bothers with: it reads that literature at its real grade instead of laundering it into "clinically proven" or dismissing it as nonexistent. There are real human studies. They are small, they are Russian-language, their abstracts state no dose and no blinding, and nobody outside Russia has ever repeated them.
## Key facts at a glance
Every chip below carries an evidence grade. Human trial means a study in people, which for selank always means a small Russian study whose abstract omits dose and blinding. Animal means rodent, monkey or other non-human work. Regulatory means an FDA, WADA or register record. No chip on this page is supported by a randomized controlled efficacy trial, because no such trial of selank could be located 10 19 .
## Regulatory status in the United States
Selank is not FDA approved for any use. It is sold as a research chemical; FDA has cited unresolved safety and quality concerns for compounded selank, and no human efficacy has been established to FDA standards. A search of FDA's approved-drug database for selank as an active ingredient returns no records at all 5 . FDA has also written about it directly. Its compounding page 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 "FDA lacks important information regarding any safety issues raised by selank acetate administered to humans" 6 . One detail deserves precision, because it is usually reported wrongly in both directions. Selank acetate (TP-7) appears on that page under the heading "Bulk drug substances nominated but withdrawn", which FDA describes as substances "previously in category 2 of the interim policies" that "were withdrawn by the nominators" 6 . So it is not currently sitting in active Category 2 alongside compounds like ipamorelin, and it is also not cleared: someone proposed selank for pharmacy compounding, FDA recorded a safety concern, and the nomination was pulled. Nothing about that sequence makes selank approvable. Even a compounded drug is not an approved one: FDA states plainly that "compounded drugs are not FDA-approved" and that it "does not verify the safety, effectiveness or quality of compounded drugs before they are marketed" 7 .
## The Russian registration, and what we could and could not verify
Almost every page written about selank says it is an approved anxiolytic in Russia. We went looking for something citable behind that sentence, and here is exactly what we found and did not find. What we can cite: a 2022 review of peptide biopharmaceutical development published in Pharmaceutics , written by authors at Russian Academy of Sciences institutes and Sechenov University, states that "14 products are registered in the Russian Federation" and gives the list. Selank is row 13, classified as an anxiolytic; semax is row 3, classified as a nootropic drug 8 . That is a peer-reviewed, fetch-verified statement by Russian pharmaceutical scientists about their own country's register. What we could not do: verify it in the register itself. The Russian State Register of Medicines search requires a session-bound form submission, and its public autocomplete endpoint returned an empty result for selank. We did not treat that as evidence, because the control test failed: the same endpoint returned an empty result for paracetamol and aspirin, which are certainly registered 9 . An endpoint that cannot find aspirin cannot tell us anything about selank. So our statement is scoped to what the evidence actually supports: a peer-reviewed source says selank is a registered Russian peptide drug, and we could not independently confirm it at the register. Registration in Russia is also not the same claim as efficacy by FDA or EMA standards, and it is worth being clear about why that is not a snub. Approval standards differ in what they demand: the trials described in the next section would not, on their published abstracts alone, support a US or European approval, because those abstracts do not report randomization, blinding, duration or dose 13 14 15 .
## The untranslated-literature audit
This is the section that exists nowhere else, so here is the method before the numbers. On 2026-08-14 we asked PubMed for every record matching selank and received 135. We fetched all 135 abstracts, kept the 57 with selank in the title, and counted two things per record: the publication language flag, and the country named inside the author affiliation block only, so that the word Russian appearing in an abstract could not be miscounted as an affiliation 10 . The script and its output ship in our verification folder, so the count can be rerun against the same source. The results: 57 selank-titled papers. 26 of them are published in Russian 10 , in journals such as Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova , Eksperimental'naia i Klinicheskaia Farmakologiia and Bioorganicheskaia Khimiia . Of the 36 records that carry an author-affiliation block, 35 name a Russian institution. Exactly one does not, and it is a review article from the University of Connecticut and Hartford Hospital rather than original selank research 10 11 . The remaining 21 titled records predate PubMed's affiliation capture and are all in Russian-language journals. Read that carefully, because the number that matters is a zero: the count of original selank research papers in the PubMed index from a non-Russian institution 10 . Thirty years of research on this compound, and no laboratory outside one country's research system has published an original study of it. Nobody has failed to replicate selank. Nobody has tried. The clearest illustration is a 2020 paper from Sciensano, the Belgian federal government's scientific institute. Analysing two seized preparations, its authors described selank and semax as "the assumedly cognitive enhancing research peptides Selank and Semax, which, to our knowledge, have not completed any clinical trials" 12 . Four Russian patient studies were sitting in PubMed when that sentence was published 13 14 15 16 . They were invisible to a specialist government laboratory working directly on the compound, because they are in Russian, in journals a Western pharmacologist has no reason to read. That is not a claim that the Belgian authors were careless. It is what a language barrier looks like from the inside.
## Mechanism of action
Two mechanisms are proposed, and they sit at different evidence grades. Neither has been confirmed in a human clinical study. The first is enkephalin protection. Selank inhibits the enzymes that break down enkephalins, the body's own opioid peptides. In human serum it did so with a half-maximal inhibitory concentration of 20 micromolar, less potent than semax at 10 micromolar but far more potent than the reference inhibitors puromycin and bacitracin 2 . A tritium-labelled assay in human plasma found selank is comparatively specific for carboxypeptidases and dicarboxypeptidases 24 . In mice, a 100 microgram per kilogram dose produced an anxiolytic effect and lengthened plasma leu-enkephalin half-life in the anxious BALB/c strain, with no effect in C57BL/6 mice 25 , and in patients with anxiety disorders shortened enkephalin half-life was itself an observed feature 18 . The second is GABA modulation. A radioligand study reported that selank acts as a positive allosteric modulator of GABA binding and can block the modulatory activity of diazepam and olanzapine, with binding sites that "apparently not the same, but potentially may partially overlaps" 20 . In rat frontal cortex a single 300 microgram per kilogram dose changed expression of 45 of 84 neurotransmission genes at one hour, with changes correlating with those produced by GABA itself 21 . In rat hippocampal slices selank increased spontaneous inhibitory postsynaptic currents in CA1 neurons, with no significant dose-dependence over the 1 to 8 micromolar range tested 22 . One result cuts against the tidy version, and it belongs here rather than in a footnote. In cultured human IMR-32 neuroblastoma cells, selank on its own produced no change in any of the 84 GABAergic genes studied; it only altered what GABA and olanzapine did 23 . A mechanism that shows up in rat cortex and disappears in human cells is exactly the kind of finding that needs independent work to resolve, and independent work is what this compound has never had.
## Human evidence: the complete list
Five human studies exist in the retrievable index. That is the entire human record, and it is short enough to read in full. Zozulia 2008, 62 patients. The largest clinical comparison. Thirty patients with generalized anxiety disorder or neurasthenia received selank and 32 received the benzodiazepine medazepam. The reported result: "The anxiolytic effects of both drugs were similar but selank had also antiasthenic and psychostimulant effects" 13 . The same paper reported that patients had a shortened leu-enkephalin half-life correlating with symptom severity, which rose during selank treatment 13 . Medvedev 2014, 60 patients. Selank against phenazepam in phobic-anxiety and somatoform disorders, reporting "pronounced anxiolytic and mild nootropic effects" and an anxiolytic effect that "lasted for a week after last receiving the peptide" 14 . Medvedev 2015, 70 patients. Phenazepam alone in 30 patients against phenazepam plus selank in 40. The interesting result is not about anxiety but about side effects: adding selank "decreased the level of undesirable side-effects of phenazepam (attention and memory impairment, asthenia, sedation, increase in sleep duration, sexual disturbances, emotional indifference and orthostatism)" 15 . Uchakina 2008, count not stated. Cytokine changes in serum of patients with generalized anxiety disorder and neurasthenia who received selank for 14 days, the only human study that states a duration 16 . Panikratova 2020, 52 healthy participants. The only placebo-controlled study we located. Resting-state fMRI before and after injection of selank, semax or placebo, reporting differences in connectivity between the right amygdala and right temporal cortex, defined "for the first time" 17 . Note what the endpoint is: brain connectivity in healthy volunteers, not anxiety symptoms in patients. Now the arithmetic and the caveats. Across every study with a stated participant count the total is 244 people: 192 patients plus 52 healthy volunteers, with the largest single study at 70 10 . None of the five abstracts states a dose. None states a route, except that Panikratova describes an injection. None reports randomization or blinding except Panikratova's placebo arm 13 14 15 16 17 . Four of the five are in Russian, so the full texts, which may well contain the design detail their abstracts omit, are not readable in English. And no selank trial is registered anywhere: an intervention-scoped ClinicalTrials.gov query returns two records, both unrelated, matched only because selank's synonym TP-7 is also a scalp electrode position 19 . No randomized controlled efficacy trial of selank was located in any language index we can read.
## Animal evidence: where the marketed claims come from
The bulk of the selank literature is rodent work, and it is where nearly every benefit sold on a vendor page actually originates. The full graded table sits below; the pattern is worth stating first. Anxiety and stress: in rats under unpredictable chronic mild stress, selank alone most effectively reduced elevated anxiety, and the diazepam plus selank combination was most effective under chronic stress 26 . Alcohol and opioids are the best-developed thread: selank at 0.3 milligrams per kilogram daily prevented ethanol-induced memory and attention disturbance during withdrawal and blocked the ethanol-induced BDNF rise 27 ; the same dose reduced the total morphine withdrawal index by 39.6 percent against diazepam's 49.3 percent 28 ; and in DBA/2 mice it prevented ethanol-induced hyperlocomotion 29 . Stress physiology beyond behaviour: a Kursk group reported that 80, 250 and 750 microgram per kilogram doses reduced corticosterone and the pathomorphological changes of restraint stress in rat colon, and restored stress-disrupted gut microbiota 34 35 . Immune effects are real and measurable: a single 100 microgram per kilogram dose changed expression of 34 of 84 inflammation genes in mouse spleen 3 , and selank suppressed influenza replication in cell culture and in mice, most effectively when given before inoculation 36 . In monkeys, intranasal selank reduced fear and aggression in experimental neurosis 32 . The negative results belong in the same paragraph as the positive ones. In rats with 6-hydroxydopamine-induced parkinsonism, neither selank nor semax affected motor activity or passive defensive behaviour 37 . Reporting that is not a hedge; a literature where everything works is a literature to be suspicious of. The species point is the one to carry away. A 39.6 percent reduction in a rat withdrawal index is a real finding about rats. It is not a dose you can scale to a person, because the human pharmacokinetics needed to do that translation have never been measured 10 33 .
## Every study, graded by species
Every row below carries the species or model it was performed in, the dose and route as the source states them, and the outcome as reported. Where an abstract does not state a group size, the row says so rather than inventing one. The census: 6 human rows, 15 animal rows and 5 in vitro rows. Not one row is a randomized controlled efficacy trial 10 .
## Pharmacokinetics
There is no human pharmacokinetic study of selank. No half-life, no peak concentration, no clearance figure and no bioavailability value for any route has been published in the index we can read 10 . A term scan of all 135 fetched records found no such study. What exists is one Russian tritium-labelling study, which identified the pentapeptide TKPRP, the tripeptide TKP and the dipeptides RP and GP as the major products of selank breakdown in blood plasma, and examined selank in rat brain tissue after intranasal dosing. Its abstract reports no numeric parameters 33 . One correction worth making explicitly, because it circulates widely. Half-life figures quoted for selank are almost always the half-life of leu-enkephalin, the substrate whose breakdown selank slows, and not of selank itself. The two studies that mention a half-life both measure enkephalin 18 25 . If you see a confident number for selank's half-life, ask which molecule it refers to.
## Forms and routes: nasal, injectable, and what was studied
Selank is sold in the United States in two forms, both documented by the Belgian government laboratory that analysed seized preparations: "freely available either as lyophilized powder for injection purposes or are present in nasal sprays" 12 . The nasal form is the one most commonly encountered. The research used intranasal and intraperitoneal routes, not the subcutaneous injection familiar from other peptide markets. Intranasal dosing appears in mice, rats and monkeys 30 31 32 33 ; intraperitoneal dosing dominates the rodent behavioural work. No fetched study used subcutaneous injection 10 . The most useful study for anyone comparing forms is a direct head-to-head in mice, and its result is not the one either marketing side expects. At 300 micrograms per kilogram per day for five days, both routes produced anxiolytic and nootropic effects, but only in the anxious BALB/c strain, and the two routes acted on different receptor systems: intraperitoneal dosing raised GABA-receptor binding sites in frontal cortex by 38 percent with no NMDA change, while intranasal dosing raised NMDA-receptor binding sites by 23 percent with no GABA change 30 . The authors attributed the difference to pharmacokinetics and biotransformation. In mice, the route changes what the drug does, not merely how much arrives. Whether that holds in humans is unknown, because no human study of either route reports a dose at all 13 17 .
## Is there an established dose?
No. There is no established human dose of selank, and the reason is specific rather than rhetorical: not one of the five human studies states a dose in its abstract 13 14 15 17 . Four are in Russian and their full texts were not retrievable in this run, so a dose may well be printed inside them; we simply cannot cite what we have not read. What can be cited are the animal regimens, and they are worth seeing because of how the arithmetic works. The rodent behavioural studies cluster at 0.3 milligrams per kilogram 27 28 29 , with gene-expression work at 100 to 300 micrograms per kilogram 21 3 , the stress-physiology studies at 80 to 750 micrograms per kilogram 34 , and the route comparison at 300 micrograms per kilogram 30 . Our study-dose explorer lists each of these with its species attached. What we will not do is convert them. Scaling a rat intraperitoneal dose to a human intranasal dose requires knowing human bioavailability by that route, and that number does not exist for selank 10 . Any milligram figure you see presented as a selank protocol was not derived from a published human study. This site therefore ships no dose calculator, and the reason is printed on the tool page itself.
## Is selank safe?
The honest answer is that nobody knows, and the specific gaps matter more than the general uncertainty. What is reported: the Russian clinical studies describe selank as well tolerated, with one assessing tolerability on the UKU side-effect scale 14 and another finding that adding selank reduced the side effects of a benzodiazepine 15 . Those are the reassuring data points, and they come from short courses in small groups. What does not exist: any long-term safety study, any formal toxicology report, and any adverse-event surveillance for selank in the index we can read 10 . Only one human study even states how long people took it, and that was 14 days 16 . The gap FDA names is immunogenicity, and it is a pointed one for this molecule. Selank is a tuftsin analog, and tuftsin is a fragment of the immunoglobulin G heavy chain, so this is a peptide with an immune pedigree being given to people with no published assessment of whether the immune system reacts to it 6 3 . FDA's stated concern is immunogenicity risk from aggregation and peptide-related impurities, and that it lacks important information about any safety issues raised by selank administered to humans 6 . The animal literature does contain immune pharmacology, including spleen inflammation-gene expression and antiviral activity 3 36 , but that is a different question from whether the body mounts a response against the peptide itself.
## Who should not consider selank?
This question cannot be answered from evidence, because the studies that would answer it were never done. What exists is a list of groups with no data at all: pregnant and breastfeeding people, children and adolescents, older adults, people with liver or kidney impairment, people with autoimmune conditions or on immunosuppressants (relevant given the tuftsin lineage and the reported immune effects 3 36 ), and anyone with a psychiatric diagnosis being managed with prescribed medication. That list is not a set of established risks. It is a set of populations in which selank has never been studied, which is a different and in some ways less comfortable statement 10 .
## What interacts with selank?
No formal drug-interaction study of selank exists. Three findings are nonetheless directly relevant, and two of them involve benzodiazepines. The human one: in 70 patients, adding selank to phenazepam reduced that benzodiazepine's side effects, including attention and memory impairment, sedation and emotional indifference 15 . The rat one: under unpredictable chronic mild stress, the diazepam plus selank combination was the most effective condition tested 26 . The mechanistic one cuts the other way: selank blocked the modulatory activity of diazepam and olanzapine at the GABA receptor in a binding study 20 , and in human IMR-32 cells selank suppressed the gene-expression changes GABA produced alone while amplifying those of olanzapine 23 . A compound that interacts measurably with benzodiazepines and antipsychotics in every system it has been tested in, and that has no human interaction study, is not a compound to combine with prescribed psychiatric medication on the basis of a forum protocol.
## What is actually in the bottle?
Nobody is checking. There is no pharmacopoeial monograph for selank, no validated quality standard, and no regulator verifying the contents of a research-market vial or nasal spray sold in the United States. FDA states that even for compounded drugs, which are a more regulated category than research chemicals, it "does not verify the safety, effectiveness or quality" before marketing 7 . The scale of the identification problem is visible in how the Belgian government laboratory had to proceed. To identify what was in the seized preparations, its scientists had to develop a new liquid chromatography tandem mass spectrometry method, then validate it across matrices to ISO 17025, because standard screening was not equipped for these peptides 12 . If a national control laboratory needed a bespoke analytical method, a certificate of analysis supplied by the seller is not an independent check. The regulatory description of the US market is blunt in the peer-reviewed literature too. A 2021 review in the Journal of Clinical Pharmacology describes phenibut and selank as "poorly studied Russian drugs with GABAergic mechanisms that are inexplicably sold to US consumers as dietary supplements" 11 .
## What should athletes know?
Selank is not named anywhere on the 2026 WADA Prohibited List 38 . That is not the same as being permitted, and the distinction is where athletes get caught out. The S0 category prohibits at all times "any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use" 38 . Whether selank falls inside that catch-all depends on whether its Russian registration counts as current approval by a governmental regulatory health authority. We found no source resolving that question for selank by name 38 39 . The anti-doping community has not resolved it either. A 2025 review co-authored by the Polish Anti-Doping Agency's scientific team and the anti-doping research centre at the University of Lausanne places selank in its table of substances with unclear status. Semax, in the row directly below, is flagged as similar to a prohibited substance; selank's equivalent column is empty 39 . The same paper warns that the open-ended nature of the prohibited list "may lead to unintentional violations of anti-doping rules" 39 . For a tested athlete the practical answer is simple even though the classification is not: unclear status is not clearance, and the only safe route is a written determination from your own anti-doping organisation before use, not an inference from the list's silence.
## Selank compared
Two comparisons are worth making with sources attached. The first is selank against semax, the peptide it is most often confused with and most often stacked with. The second is the same molecule seen from two regulatory systems, which is the clearest way to show what a research-chemical status actually means. We run a sister reference site on semax at semaxlabs.com, and the rows below cite primary sources rather than either site's opinion.
## What we do not know yet
See the evidence-limits block. It is the honest core of this monograph, and on this compound it is longer than the list of things we do know.
## Frequently asked questions
Twelve questions, each answered in 320 characters or fewer, every answer consistent with the graded evidence above.
## References
Every reference below was fetched and verified on 2026-08-14: PubMed records through the NCBI E-utilities API, open full texts through Europe PMC, FDA pages retrieved directly from fda.gov with a browser user agent, chemical identity from PubChem, trial absence from the ClinicalTrials.gov v2 API, and the WADA list from an archived same-day PDF. Russian-language titles are marked as such. A machine-readable version of this list ships as the citation manifest for this page.
## Related compounds
Semax (semaxlabs.com) is the closest relative: another Russian heptapeptide from the same research programme, an ACTH(4-10) analog classified as a nootropic where selank is classified as an anxiolytic 8 40 . The two appear together throughout this literature, share the enkephalinase mechanism 2 , and were found together in the same seized preparations 12 . They also have the same underlying evidence problem, and reading either site should leave you with the same caution.
## Study results
| Study | Species/model | n | Duration | Outcome | Effect size |
| --- | --- | --- | --- | --- | --- |
| Zozulia 2008: efficacy and mechanisms of selank in GAD and neurasthenia (https://pubmed.ncbi.nlm.nih.gov/18454096/) [Published in Russian. Abstract states no dose, route, duration, randomization or blinding. Largest human selank study located.] | human (Generalized anxiety disorder and neurasthenia; selank vs medazepam) | 62 patients (30 selank, 32 medazepam) | Not stated in abstract | Anxiolytic effects of the two drugs reported as similar; selank additionally reported to have antiasthenic and psychostimulant effects; leu-enkephalin half-life rose during selank treatment, mainly in the GAD group | No effect sizes, confidence intervals or p values in the abstract |
| Medvedev 2014: anxiolytic effect and tolerability of selank vs phenazepam (https://pubmed.ncbi.nlm.nih.gov/25176261/) [Published in Russian. Tolerability assessed with the UKU scale per the abstract. No randomization or blinding stated.] | human (Phobic-anxiety and somatoform disorders (ICD-10 F40.2-9, F41.1-9, F45.0-1); selank vs phenazepam) | 60 patients | Not stated in abstract | Pronounced anxiolytic and mild nootropic effects reported; anxiolytic effect reported to last one week after the last dose; positive impact on quality of life | No effect sizes or p values in the abstract |
| Medvedev 2015: optimization of anxiety-disorder treatment with selank (https://pubmed.ncbi.nlm.nih.gov/26356395/) [Published in Russian; abstract also available in Russian from the publisher. Add-on design, not randomized per the abstract.] | human (Anxiety-phobic, hypochondriac and somatoform disorders; phenazepam alone vs phenazepam plus selank) | 70 patients (30 phenazepam, 40 combined) | Not stated in abstract | Combined treatment decreased phenazepam side effects including attention and memory impairment, asthenia, sedation, longer sleep, sexual disturbance, emotional indifference and orthostatism, during treatment and after withdrawal | No effect sizes or p values in the abstract |
| Uchakina 2008: immunomodulatory effects of selank in anxiety-asthenic disorders (https://pubmed.ncbi.nlm.nih.gov/18577961/) [Published in Russian. The only human study stating a treatment duration. No control group or patient count in the abstract.] | human (Patients with generalized anxiety disorder and neurasthenia; serum cytokines, plus in vitro peripheral blood work) | Not stated in abstract | 14 days | Th1/Th2 cytokine balance changes reported in serum during 14 days of selank; in vitro, 10-7 M selank suppressed IL-6 gene expression in blood cells of patients with depression but not of healthy controls | Reported as significant (p<0.05) for the in vitro IL-6 concentration change; no clinical effect sizes |
| Panikratova 2020: functional connectomic approach to studying selank and semax effects (https://pubmed.ncbi.nlm.nih.gov/32342318/) [The only placebo-controlled human study located. Endpoint is brain connectivity in healthy people, not an anxiety outcome in patients.] | human (Resting-state fMRI in healthy volunteers; selank vs semax vs placebo) | 52 healthy participants | Single dose; imaging before, 5 min and 20 min after | Between-group and between-condition differences in functional connectivity between the right amygdala and a right-hemisphere fusiform, inferior and middle temporal and parahippocampal region; authors describe defining selank and semax effects on this connectivity for the first time | No effect sizes in the abstract |
| Zozulya 2001: inhibition of enkephalin-degrading enzymes as a possible anxiolytic mechanism (https://pubmed.ncbi.nlm.nih.gov/11550013/) [Patient observation plus ex vivo plasma assay rather than a treatment trial.] | human (Patients with anxiety and phobic disorders (DSM-4); plasma enkephalinase activity) | Not stated in abstract | Not applicable | Shortened enkephalin half-life and reduced total enkephalinase activity during generalized anxiety but not panic disorder or agoraphobia; selank inhibited plasma enkephalin hydrolysis dose-dependently | IC50 15 micromolar; more potent than bacitracin and puromycin |
| Kost 2001: semax and selank inhibit the enkephalin-degrading enzymes from human serum (https://pubmed.ncbi.nlm.nih.gov/11443939/) [Published in Russian. Human tissue, not human participants.] | in vitro (Enkephalin-degrading enzymes of human serum; selank vs semax vs reference inhibitors) | Human serum samples (no participants) | Assay timescale | Both heptapeptides inhibited enkephalin-degrading enzymes dose-dependently and more potently than puromycin and bacitracin; pentapeptide fragments were also active while tri-, tetra- and hexapeptide fragments were not | Selank IC50 20 micromolar; semax IC50 10 micromolar; puromycin IC50 10 millimolar |
| Zolotarev 2004: labelled leu-enkephalin in studying selank inhibition of plasma enkephalin-degrading enzymes (https://pubmed.ncbi.nlm.nih.gov/15344652/) [Published in Russian.] | in vitro (Tritium-labelled leu-enkephalin degradation in human plasma) | Human plasma samples (no participants) | Assay timescale | Selank reported comparatively specific for carboxypeptidases and dicarboxypeptidases, whereas bestatin predominantly inhibited aminopeptidases and carboxypeptidases; a carboxypeptidase pathway accounting for about 6 percent of total enkephalin-degrading activity was identified | Aminopeptidases about 80 percent, dipeptidylaminopeptidases about 2 percent, dipeptidylcarboxypeptidases about 10 percent of total activity |
| Vyunova 2018: molecular aspects of heptapeptide selank biological activity (https://pubmed.ncbi.nlm.nih.gov/30255741/) [The primary source for the GABA positive-allosteric-modulator mechanism.] | in vitro (Radioligand binding, brain cell plasma membranes; tritiated GABA binding) | Membrane preparations (no participants) | Assay timescale | Selank affected tritiated GABA binding as a positive allosteric modulator; joint action with benzodiazepines was not cumulative; selank blocked the modulatory activity of diazepam and olanzapine, with binding sites described as apparently not the same but potentially partially overlapping | Reported as subtype-selective and concentration-dependent; no numeric constants in the abstract |
| Filatova 2017: GABA, selank and olanzapine affect GABAergic gene expression in IMR-32 cells (https://pmc.ncbi.nlm.nih.gov/articles/PMC5328971/) [A negative result in human cells for the mechanism reported positive in rat cortex. Retained because contrary evidence belongs in the table.] | in vitro (human IMR-32 cells) (Human neuroblastoma IMR-32 cell culture; 84 GABAergic and neurotransmission genes) | Cell culture (no participants) | Assay timescale | No changes in mRNA levels of the studied genes under selank alone; selank plus GABA nearly completely suppressed the changes GABA produced alone; selank plus olanzapine altered more genes than olanzapine alone | Directional; no numeric effect sizes in the abstract |
| Volkova 2016: selank administration affects genes involved in GABAergic neurotransmission (https://pmc.ncbi.nlm.nih.gov/articles/PMC4757669/) [Open access. Authors frame the result as allosteric modulation of the GABAergic system.] | rat (Frontal cortex gene expression after single dose; 84 neurotransmission genes) | Not stated in abstract | Single dose; 1 h and 3 h sampling | 45 of 84 genes changed expression at 1 hour and 22 genes at 3 hours; changes produced by selank correlated positively with those produced by GABA | Reported as significant; gene counts as stated |
| Povarov 2017: effect of selank on spontaneous synaptic activity of rat hippocampal CA1 neurons (https://pubmed.ncbi.nlm.nih.gov/28361410/) [Notable for the absence of dose-dependence, which the authors report explicitly.] | in vitro (rat hippocampal slices) (Spontaneous inhibitory postsynaptic currents in CA1 pyramidal neurons) | Slice preparation (no animal n stated) | Assay timescale | Increased amplitude and discharge rate of spontaneous inhibitory postsynaptic currents; in some neurons preceded by a transient decrease | No significant dose-dependence across the 1 to 8 micromolar range tested |
| Kasian 2017: selank enhances the effect of diazepam in reducing anxiety under chronic mild stress (https://pmc.ncbi.nlm.nih.gov/articles/PMC5322660/) [Open access. The finding that a course of test substances worsened baseline anxiety indicators is reported as stated.] | rat (Unpredictable chronic mild stress; elevated plus maze; selank and diazepam alone and combined) | Not stated in abstract | Course plus chronic stress protocol | Selank alone was most effective at reducing the elevated anxiety induced by a course of test substances; the diazepam plus selank combination was most effective under chronic stress conditions; a course of test substances worsened anxiety indicators even without stress, less so for selank | Directional; no numeric effect sizes in the abstract |
| Kolik 2019: selank protects against ethanol-induced memory impairment by regulating BDNF (https://pubmed.ncbi.nlm.nih.gov/31625062/) [One of the few selank studies reporting explicit p values in its abstract.] | rat (30 weeks ethanol as sole fluid; object recognition test; hippocampal and cortical BDNF) | Not stated in abstract | 7 days | Cognitive-stimulating effect in 9-month rats not exposed to ethanol; prevented ethanol-induced memory and attention disturbance during withdrawal; prevented the ethanol-induced BDNF rise in hippocampus and frontal cortex | p<0.05 cognitive effect; p<0.01 prevention of ethanol-induced disturbance; p<0.05 BDNF |
| Konstantinopolsky 2022: selank attenuates aversive signs of morphine withdrawal in rats (https://pubmed.ncbi.nlm.nih.gov/36322304/) [The head-to-head diazepam comparison makes this one of the more informative animal rows.] | rat (Naloxone-precipitated morphine withdrawal in outbred rats; selank vs diazepam) | Not stated in abstract | Single dose | Reduced total morphine withdrawal index by 39.6 percent, attenuated convulsive reactions, ptosis and posture disorders, and raised tactile sensitivity threshold 9-fold; diazepam reduced the index by 49.3 percent with a 13-fold threshold rise | p<0.0001 for attenuation of convulsive reactions; selank reported slightly inferior to diazepam |
| Kolik 2016: selank inhibits ethanol-induced hyperlocomotion and behavioural sensitization (https://pubmed.ncbi.nlm.nih.gov/27878720/) [The naloxone comparison supports the opioid-system mechanism rather than the GABA one.] | mouse (Ethanol-induced hyperlocomotion and behavioural sensitization in DBA/2 mice) | Not stated in abstract | Single dose | Prevented ethanol-induced hyperlocomotion, similar to naloxone 1.0 mg/kg and unlike afobazole; a single dose blocked the manifestation of motor sensitization without affecting its formation | Directional; reported as significant for sensitization manifestation |
| Vasil'eva 2016: comparison of selank effects after intranasal and intraperitoneal administration (https://pubmed.ncbi.nlm.nih.gov/29787664/) [Published in Russian. The only head-to-head route comparison located, and the basis for saying route changes what the drug does in mice.] | mouse (Intranasal vs intraperitoneal selank in BALB/c and C57BL/6 mice; elevated plus maze plus receptor binding) | Not stated in abstract | 5 days | Anxiolytic and nootropic effects only in the anxious BALB/c strain by either route; intraperitoneal dosing raised GABA-receptor binding sites in frontal cortex by 38 percent with no NMDA change, while intranasal dosing raised NMDA-receptor binding sites by 23 percent with no GABA change | 38 percent GABA-receptor binding increase (i.p.); 23 percent NMDA-receptor binding increase (i.n.) |
| Inozemtseva 2008: intranasal selank regulates BDNF expression in the rat hippocampus in vivo (https://pubmed.ncbi.nlm.nih.gov/18841804/) [PubMed record has title, authors and affiliation but no abstract. Row content is limited to what the title states, deliberately.] | rat (Hippocampal BDNF expression in vivo after intranasal selank) | Not stated | Not available in the PubMed record | Regulation of BDNF expression in the rat hippocampus in vivo, per the study title | Not available: PubMed holds no abstract text for this record |
| Compensatory and antiamnestic effects of heptapeptide selank in monkeys (https://pubmed.ncbi.nlm.nih.gov/18727417/) [Published in Russian; PubMed lists no authors for this record. The only primate study located.] | monkey (Experimental neurosis in monkeys; intranasal selank) | Not stated in abstract | Not stated | Long-term changes in behaviour disturbed during neurosis: reduced fear and aggression, increased orientational-exploratory activity, improved handling and communication; effects reported as independent of the type of neurotic disturbance | Directional; no numeric effect sizes in the abstract |
| Bobyntsev 2020: morphological changes in rat large intestine under restraint stress with selank (https://pubmed.ncbi.nlm.nih.gov/32651826/) [Kursk State Medical University group; the widest dose range in the animal literature.] | rat (Chronic restraint stress; colon wall morphology and corticosterone) | Not stated in abstract | Chronic restraint protocol | Lower corticosterone, reduced pathomorphological manifestations of stress including atrophy and inflammatory reaction, altered mast cell number and activity, and accelerated adaptation | Directional across three dose levels; no numeric effect sizes in the abstract |
| Medvedeva 2019: state of colon microbiota during chronic restraint stress and selank treatment (https://pubmed.ncbi.nlm.nih.gov/31236882/) [Companion study to S20 from the same group.] | rat (Chronic restraint stress; colon microbiota composition) | Not stated in abstract | Chronic restraint protocol | Chronic restraint stress reduced obligate microflora and increased opportunistic organisms; selank restored intestinal microbiota, attributed by the authors to central and peripheral mechanisms | Directional; no numeric effect sizes in the abstract |
| Kolomin 2011: expression of inflammation-related genes in mouse spleen under tuftsin analog selank (https://pubmed.ncbi.nlm.nih.gov/21609736/) [Direct evidence of immune-system activity, which is what makes the absent immunogenicity assessment notable.] | mouse (Spleen inflammation-related gene expression after a single dose) | Not stated in abstract | 6 h and 24 h sampling | Significant changes in expression of 34 of 84 inflammation-related genes including chemokines, cytokines and their receptors | 34 of 84 genes; reported as significant |
| Ershov 2009: antiviral activity of immunomodulator selank in experimental influenza infection (https://pubmed.ncbi.nlm.nih.gov/19882898/) [Published in Russian.] | mouse and in vitro (Influenza A/Aichi 2/68 (H3N2) in cell culture and in mice) | Not stated in abstract | Not stated | Antiviral effect in both systems, strongest under the preventive schedule where selank added 24 h before inoculation completely suppressed viral reproduction; highest animal survival also under the preventive schedule; induced interferon-alpha gene expression without affecting IL-4, IL-10 or TNF-alpha | Complete suppression of viral reproduction in the preventive cell-culture arm |
| Peptides semax and selank affect the behavior of rats with 6-OHDA induced PD-like parkinsonism (https://pubmed.ncbi.nlm.nih.gov/28702721/) [Included deliberately as a negative animal result.] | rat (6-hydroxydopamine-induced parkinsonism; elevated cross maze and passive defensive behaviour) | Not stated in abstract | Not stated in abstract | Neither semax nor selank affected motor activity in the elevated cross-shaped maze or passive defensive behaviour; selank decreased a separate measured parameter per the abstract | Null on the primary behavioural measures reported |
| Sokolov 2002: selank effects on behaviour and plasma enkephalin-degrading enzymes (https://pubmed.ncbi.nlm.nih.gov/12432865/) [The half-life reported here is leu-enkephalin's, not selank's. Frequently misquoted.] | mouse (Open-field behaviour and plasma enkephalin-degrading enzyme activity in BALB/c vs C57BL/6 mice) | Not stated in abstract | Single dose | Anxiolytic effect in the open-field test and increased plasma leu-enkephalin half-life in BALB/c mice; no effect on behaviour or enkephalinase activity in C57BL/6 mice | Strain-dependent; no numeric effect sizes in the abstract |
| Zolotarev 2006: evenly tritium-labelled peptides and their in vivo and in vitro biodegradation (https://pubmed.ncbi.nlm.nih.gov/16637290/) [Published in Russian. The closest thing to a pharmacokinetic study in the corpus, and it is in rats with no numeric parameters.] | rat (Tritium-labelled selank; plasma biodegradation products and brain tissue after intranasal dosing) | Not stated in abstract | Not stated | Major biodegradation products of selank in blood plasma identified as the pentapeptide TKPRP, tripeptide TKP and dipeptides RP and GP; selank pharmacokinetics examined in brain tissue after intranasal administration | No half-life, clearance or bioavailability values reported in the abstract |
## What we do not know yet
What we do not know about selank outweighs what we know, and on this compound the gaps have an unusual shape: they are not gaps in the research so much as gaps in who has done it. (1) Nobody outside one research system has ever studied it. Of 57 selank-titled PubMed records, 35 of the 36 carrying affiliation data name a Russian institution and the single exception is a review article, so the count of original non-Russian selank studies is zero1011. Selank has not failed replication; replication has never been attempted. (2) Most of the primary literature is unreadable in English. Twenty-six of those 57 papers are published in Russian10, so the full texts that would contain dose, blinding and safety detail are inaccessible without translation. When a Belgian government laboratory stated in 2020 that selank had completed no clinical trials12, four Russian patient studies were already indexed13141516. (3) The human evidence is small and under-specified. Five human studies, 244 people across those with a stated count, largest study 70, and not one abstract stating a dose; only one states a duration, and only the imaging study in healthy volunteers had a placebo arm101617. No randomized controlled efficacy trial was located, and no selank trial is registered on ClinicalTrials.gov19. (4) There is no human pharmacokinetics at all: no half-life, no bioavailability by any route, nothing to support converting an animal dose into a human one10. (5) Immunogenicity has never been assessed, which is pointed for a tuftsin analog with documented immune activity, and is precisely what FDA names as its concern63. (6) There is no long-term safety study, no toxicology report and no adverse-event surveillance10. (7) There is no quality standard: no pharmacopoeial monograph, and identifying seized selank required a national laboratory to build a bespoke analytical method127. (8) Even the Russian registration, the single strongest fact in selank's favour, rests for us on a peer-reviewed statement rather than a register record we could open ourselves89. Read everything on this site with those eight gaps in mind.
## Questions and answers
### Is selank FDA approved?
No. No selank product has ever been FDA approved, and FDA lists selank acetate on its compounding safety page with an immunogenicity concern. What is sold in the US is an unapproved research chemical.
No. No drug product containing selank has ever been approved by FDA for any use, and a Drugs@FDA search returns nothing. FDA's compounding page lists selank acetate (TP-7) under substances nominated but withdrawn, stating that compounded selank may pose immunogenicity risk from aggregation and peptide-related impurities and that FDA lacks important information about any safety issues raised by it in humans.Compounded drugs are not FDA-approved products either: FDA does not verify their safety, effectiveness or quality before marketing.
### Is selank approved anywhere?
A peer-reviewed 2022 review lists selank among 14 peptide drugs registered in Russia, classified as an anxiolytic. We could not verify that at the Russian register itself, because our control test there failed. It is not approved in the US.
A 2022 peer-reviewed review of Russian peptide pharmaceuticals states that 14 peptide products are registered in the Russian Federation and lists selank among them, classified as an anxiolytic. That is the strongest citable source we found for the widely repeated claim that selank is approved in Russia.We could not confirm it at the register itself. The Russian State Register's search requires a session-bound form post, and its public autocomplete endpoint returned nothing for selank, but the control test failed: it returned nothing for paracetamol and aspirin either. So we cite the peer-reviewed statement and say plainly that we could not verify it directly. It is also not approved in the United States, and registration in one country is not evidence of efficacy by another's standards.
### Does selank work for anxiety?
Maybe. Four small Russian patient studies report anxiolytic effects, one finding it comparable to a benzodiazepine. But no abstract states dose or blinding, no randomized efficacy trial exists, and nobody outside Russia has ever tested it.
The honest answer is that it might, and that the evidence is too thin to say. Four Russian studies in patients report anxiolytic effects, including a 62-patient comparison in which selank and the benzodiazepine medazepam had similar anxiolytic effects and a 60-patient comparison against phenazepam reporting pronounced anxiolytic and mild nootropic effects.Now the qualifiers, all of which matter. None of those abstracts reports randomization, blinding, duration or dose. All four are in Russian. No randomized controlled efficacy trial of selank was located in any index we can read, and no selank trial is registered on ClinicalTrials.gov. And no laboratory outside Russia has ever published an original selank study to check any of it.So: real signal, real studies, real people, at an evidence grade that would not support a marketing claim anywhere with a drug regulator.
### Has selank been replicated outside Russia?
No. Of 57 selank-titled PubMed papers, 26 are in Russian, and of the 36 with affiliation data, 35 are Russian institutions; the single exception is a US review, not original research. Independent replication has never been attempted.
No, and the shape of that no is unusual. We counted every selank record in PubMed on 2026-08-14: 135 records, 57 with selank in the title, 26 published in Russian. Of the 36 titled records carrying an author-affiliation block, 35 name a Russian institution and exactly one does not, and that one is a US review article rather than an original study.The count of original selank research papers from a non-Russian institution is zero. This is not a compound whose findings failed to replicate. It is a compound nobody outside one research system has ever tried to replicate, which is a different situation and arguably a more solvable one.
### Why is most selank research in Russian?
Selank was developed at Russian Academy of Sciences institutes and its literature stayed there: 26 of 57 titled papers are in Russian. Abstracts are indexed in English, but the full texts holding dose and safety detail are not readable without translation.
Because selank was developed in Russia, at Russian Academy of Sciences institutes, and its literature stayed there. Twenty-six of the 57 selank-titled PubMed papers are published in Russian, in journals such as Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova and Eksperimental'naia i Klinicheskaia Farmakologiia.This has real consequences for what anyone can know. PubMed indexes English abstracts for most of these papers, but the full texts, where dose, blinding and safety detail would live, are not readable without translation. The clearest illustration: in 2020 a Belgian government laboratory wrote that selank and semax "have not completed any clinical trials", while four Russian patient studies sat in the same database they were searching.
### How is selank different from semax?
Different peptides from the same programme: selank is a tuftsin analog classified as an anxiolytic, semax an ACTH(4-10) analog classified as a nootropic. Semax inhibits enkephalinases more potently, and an anti-doping review links semax, not selank, to a prohibited substance.
Different molecules from the same Russian research programme. Selank is Thr-Lys-Pro-Arg-Pro-Gly-Pro, a tuftsin analog with molecular weight 751.9; semax is Met-Glu-His-Phe-Pro-Gly-Pro, an ACTH(4-10) analog with molecular weight 813.9. The 2022 Russian peptide review classifies selank as an anxiolytic and semax as a nootropic.They share the enkephalinase mechanism, where semax is the more potent of the two (IC50 10 versus 20 micromolar), and they were found together in the same seized preparations. For athletes there is a real difference: an anti-doping review flags semax as similar to the prohibited substance tetracosactide, while listing selank with no prohibited analog. Our sister site semaxlabs.com covers semax on the same terms.
### Is selank legal in the United States?
It is not a controlled substance and not an approved drug. A 2021 review describes it as a poorly studied Russian drug sold to US consumers as a dietary supplement. Research-use-only labelling is a legal posture, not a quality standard.
Selank is not a controlled substance, and it is also not an approved drug. It is sold in a gray area: a 2021 review in the Journal of Clinical Pharmacology describes phenibut and selank as "poorly studied Russian drugs with GABAergic mechanisms that are inexplicably sold to US consumers as dietary supplements".Selling an unapproved drug for human use is not permitted, which is why vendors label it research-use-only. That label is a legal posture, not a quality standard: FDA does not verify the safety, effectiveness or quality of even compounded drugs, let alone research chemicals. This site is education only and sells nothing.
### How do I know what is actually in a selank nasal spray?
You cannot. There is no pharmacopoeial monograph, no quality standard and no regulator checking. A Belgian government laboratory had to build a bespoke LC-MS/MS method to identify seized selank, so a vendor certificate is not an independent check.
You do not, and neither does anyone else. There is no pharmacopoeial monograph for selank, no validated quality standard, and no regulator checking research-market product. FDA states it does not verify safety, effectiveness or quality even for compounded drugs.For a sense of the difficulty: when a Belgian government laboratory analysed seized preparations containing selank and semax, its scientists had to develop a new liquid chromatography tandem mass spectrometry method and validate it to ISO 17025, because standard screening was not equipped for these peptides. If a national control laboratory needed a bespoke method, a seller's own certificate of analysis is not an independent check.
### What is the correct selank dose?
None is established. No human study abstract states a dose. Animal studies cluster at 0.3 mg/kg in rodents, but converting that to a human dose requires bioavailability data that has never been measured for selank.
There is no established human dose, and the reason is specific: not one of the five human studies states a dose in its abstract. Four are Russian-language papers whose full texts we could not read, so a dose may be printed inside them; we do not cite what we have not read.The animal doses are citable and are listed on our study-dose explorer with species attached: rodent behavioural work clusters at 0.3 milligrams per kilogram, with gene-expression and route studies at 100 to 300 micrograms per kilogram. We do not convert them to human doses, because that conversion needs human bioavailability, which has never been measured.
### What is selank's half-life?
Nobody knows. There is no human PK study of selank at all. Half-life figures that circulate describe leu-enkephalin, the substrate selank protects, not selank. The only PK work is in rats, with no numeric values.
Unknown in humans. No human pharmacokinetic study of selank exists: no half-life, no peak concentration, no clearance and no bioavailability figure for any route.Half-life numbers do circulate, and they are almost always a misreading. The two studies that report a half-life measure leu-enkephalin, the substrate whose breakdown selank slows, not selank itself. The one pharmacokinetic study in the corpus is a Russian tritium-labelling experiment in rats that identified breakdown products without reporting numeric parameters.
### Is the nasal spray better than injection?
Unknown in people. In mice the two routes changed different receptor systems: intraperitoneal raised GABA-receptor binding 38 percent, intranasal raised NMDA-receptor binding 23 percent. No human study of either route reports a dose or bioavailability.
Unknown in humans, and the one animal comparison suggests the question is more interesting than better-or-worse. In mice given 300 micrograms per kilogram per day for five days, both routes produced anxiolytic and nootropic effects, but only in the anxious BALB/c strain, and the routes acted on different receptor systems: intraperitoneal dosing raised GABA-receptor binding sites in frontal cortex by 38 percent, while intranasal dosing raised NMDA-receptor binding sites by 23 percent.Intranasal dosing is also what the rat BDNF work and the monkey behavioural study used. But no human study of either route reports a dose, and no human bioavailability has been measured for either, so nobody can tell you what a nasal dose delivers in a person.
### Is selank banned for athletes?
Not named on the 2026 WADA list, but the S0 catch-all covers substances with no approval by a governmental health authority, and selank's Russian registration makes that ambiguous. An anti-doping review lists it as unclear status. Ask your ADO in writing.
Selank is not named anywhere on the 2026 WADA Prohibited List, and that is not the same as permitted. The S0 category prohibits at all times any pharmacological substance not addressed elsewhere on the list and with no current approval by any governmental regulatory health authority for human therapeutic use. Whether selank's Russian registration counts as such approval is the unresolved question, and we found no source answering it for selank by name.A 2025 review co-authored by the Polish Anti-Doping Agency and the University of Lausanne anti-doping centre places selank in its unclear-status table, and warns that the open-ended prohibited list can lead to unintentional violations. For a tested athlete: get a written determination from your anti-doping organisation before use, rather than inferring permission from silence.
## References
1. Selank, CID 11765600. Compound summary: molecular formula, molecular weight, CAS 129954-34-3, UNII TS9JR8EP1G, synonyms including Selanc and TP-7. https://pubchem.ncbi.nlm.nih.gov/compound/11765600
2. Kost NV, Sokolov OIu, Gabaeva MV, Grivennikov IA, Andreeva LA, Miasoedov NF, Zozulia AA. Semax and selank inhibit the enkephalin-degrading enzymes from human serum. Bioorg Khim. 2001;27(3):180-3. [Article in Russian] https://pubmed.ncbi.nlm.nih.gov/11443939/ [in Russian]
3. Kolomin T, Shadrina M, Andreeva L, Slominsky P, Limborska S, Myasoedov N. Expression of inflammation-related genes in mouse spleen under tuftsin analog Selank. Regul Pept. 2011;170(1-3):18-23. https://pubmed.ncbi.nlm.nih.gov/21609736/
4. Kolomin T, Morozova M, Volkova A, Shadrina M, Andreeva L, Slominsky P, Limborska S, Myasoedov N. The temporary dynamics of inflammation-related genes expression under tuftsin analog Selank action. Mol Immunol. 2014;58(1):50-5. https://pubmed.ncbi.nlm.nih.gov/24291245/
5. Drugs@FDA query for selank as an active ingredient. Response: HTTP 404, {"error":{"code":"NOT_FOUND","message":"No matches found!"}}. The absence of any record is the evidence that no selank drug product has been approved. https://www.accessdata.fda.gov/scripts/cder/daf/
6. Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks. Entry: Selank acetate (TP-7), listed under Bulk drug substances nominated but withdrawn. Content current as of 04/22/2026. https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks
7. Compounding and the FDA: Questions and Answers. Are compounded drugs approved by FDA? Compounded drugs are not FDA-approved. https://www.fda.gov/drugs/human-drug-compounding/compounding-and-fda-questions-and-answers
8. Deigin VI, Poluektova EA, Beniashvili AG, Kozin SA, Poluektov YM. Development of Peptide Biopharmaceuticals in Russia. Pharmaceutics. 2022;14(4):716. https://pmc.ncbi.nlm.nih.gov/articles/PMC9030433/
9. Verification attempt against the Russian State Register of Medicines (grls.rosminzdrav.ru), including the control test that invalidated its public autocomplete endpoint as a registration index. Archived with request URLs and responses. https://grls.rosminzdrav.ru/
10. Census of all 135 PubMed records returned for selank on 2026-08-14, counting selank-titled records, publication language, and author-affiliation country. Script and output archived so the count can be reproduced. https://selankco.com/evidence.json
11. Doyno CR, White CM. Sedative-Hypnotic Agents That Impact Gamma-Aminobutyric Acid Receptors: Focus on Flunitrazepam, Gamma-Hydroxybutyric Acid, Phenibut, and Selank. J Clin Pharmacol. 2021;61 Suppl 2:S114-S128. https://pubmed.ncbi.nlm.nih.gov/34396551/
12. Vanhee C, Francotte A, Janvier S, Deconinck E. The occurrence of putative cognitive enhancing research peptides in seized pharmaceutical preparations: An incentive for controlling agencies to prepare for future encounters of the kind. Drug Test Anal. 2020;12(3):371-381. https://pubmed.ncbi.nlm.nih.gov/31667971/
13. 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. Zh Nevrol Psikhiatr Im S S Korsakova. 2008;108(4):38-48. [Article in Russian] https://pubmed.ncbi.nlm.nih.gov/18454096/ [in Russian]
14. Medvedev VE, Tereshchenko ON, Israelian AIu, Chobanu IK, Kost NV, Sokolov OIu, Miasoedov NF. A comparison of the anxiolytic effect and tolerability of selank and phenazepam in the treatment of anxiety disorders. Zh Nevrol Psikhiatr Im S S Korsakova. 2014;114(7):17-22. [Article in Russian] https://pubmed.ncbi.nlm.nih.gov/25176261/ [in Russian]
15. 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. Zh Nevrol Psikhiatr Im S S Korsakova. 2015;115(6):33-40. [Article in Russian] https://pubmed.ncbi.nlm.nih.gov/26356395/ [in Russian]
16. Uchakina ON, Uchakin PN, Miasoedov NF, Andreeva LA, Shcherbenko VE, Mezentseva MV, Gabaeva MV, Sokolov OIu, Zozulia AA, Ershov FI. Immunomodulatory effects of selank in patients with anxiety-asthenic disorders. Zh Nevrol Psikhiatr Im S S Korsakova. 2008;108(5):71-5. [Article in Russian] https://pubmed.ncbi.nlm.nih.gov/18577961/ [in Russian]
17. Panikratova YR, Lebedeva IS, Sokolov OY, Rumshiskaya AD, Kupriyanov DA, Kost NV, Myasoedov NF. Functional Connectomic Approach to Studying Selank and Semax Effects. Dokl Biol Sci. 2020;490(1):9-11. https://pubmed.ncbi.nlm.nih.gov/32342318/
18. Zozulya AA, Kost NV, Sokolov OYu, 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. Bull Exp Biol Med. 2001;131(4):315-7. https://pubmed.ncbi.nlm.nih.gov/11550013/
19. Intervention-scoped query for selank. Result: 2 records, both unrelated (repetitive transcranial magnetic stimulation over scalp position TP7, and transcranial electrical stimulation). No registered trial administers selank. https://clinicaltrials.gov/search?intr=selank
20. Vyunova TV, Andreeva L, Shevchenko K, Myasoedov N. Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. Protein Pept Lett. 2018;25(10):914-923. https://pubmed.ncbi.nlm.nih.gov/30255741/
21. 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. Front Pharmacol. 2016;7:31. https://pmc.ncbi.nlm.nih.gov/articles/PMC4757669/
22. Povarov IS, Kondratenko RV, Derevyagin VI, Myasoedov NF, Skrebitsky VG. Effect of Selank on Spontaneous Synaptic Activity of Rat Hippocampal CA1 Neurons. Bull Exp Biol Med. 2017;162(5):640-642. https://pubmed.ncbi.nlm.nih.gov/28361410/
23. 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. Front Pharmacol. 2017;8:89. https://pmc.ncbi.nlm.nih.gov/articles/PMC5328971/
24. Zolotarev IuA, Sokolov OIu, Kost NV, Vas'kovskii BV, Miasoedov NF, Zozulia AA. Leu-enkephalin homogeneously labeled with tritium in studying the Selank inhibiting effect on the enkephalin-degrading enzymes of human plasma. Bioorg Khim. 2004;30(3):234-40. [Article in Russian] https://pubmed.ncbi.nlm.nih.gov/15344652/ [in Russian]
25. Sokolov OY, Meshavkin VK, Kost NV, Zozulya AA. Effects of Selank on behavioral reactions and activities of plasma enkephalin-degrading enzymes in mice with different phenotypes of emotional and stress reactions. Bull Exp Biol Med. 2002;133(2):133-5. https://pubmed.ncbi.nlm.nih.gov/12432865/
26. 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. Behav Neurol. 2017;2017:5091027. https://pmc.ncbi.nlm.nih.gov/articles/PMC5322660/
27. Kolik LG, Nadorova AV, Antipova TA, Kruglov SV, Kudrin VS, Durnev AD. Selank, Peptide Analogue of Tuftsin, Protects Against Ethanol-Induced Memory Impairment by Regulating of BDNF Content in the Hippocampus and Prefrontal Cortex in Rats. Bull Exp Biol Med. 2019;167(5):641-644. https://pubmed.ncbi.nlm.nih.gov/31625062/
28. Konstantinopolsky MA, Chernyakova IV, Kolik LG. Selank, a Peptide Analog of Tuftsin, Attenuates Aversive Signs of Morphine Withdrawal in Rats. Bull Exp Biol Med. 2022;173(6):730-733. https://pubmed.ncbi.nlm.nih.gov/36322304/
29. Kolik LG, Konstantinopolsky MA. Selank Inhibits Ethanol-Induced Hyperlocomotion and Manifestation of Behavioral Sensitization in DBA/2 Mice. Bull Exp Biol Med. 2016;162(1):56-59. https://pubmed.ncbi.nlm.nih.gov/27878720/
30. Vasil'eva EV, Kondrakhin EA, Salimov RM, Kovalev GI. Comparison of pharmacological effects of heptapeptide Selank after intranasal and intraperitoneal administration to BALB/c and C57BL/6 mice. Eksp Klin Farmakol. 2016;79(9):3-11. [Article in Russian] https://pubmed.ncbi.nlm.nih.gov/29787664/ [in Russian]
31. Inozemtseva LS, Karpenko EA, Dolotov OV, Levitskaya NG, Kamensky AA, Andreeva LA, Grivennikov IA. Intranasal administration of the peptide Selank regulates BDNF expression in the rat hippocampus in vivo. Dokl Biol Sci. 2008;421:241-3. https://pubmed.ncbi.nlm.nih.gov/18841804/
32. Compensatory and antiamnestic effects of heptapeptide Selank in monkeys. Zh Evol Biokhim Fiziol. 2008;44(3):284-90. [Article in Russian; PubMed lists no authors for this record] https://pubmed.ncbi.nlm.nih.gov/18727417/ [in Russian]
33. Zolotarev IuA, Dadaian AK, Dolotov OV, Kozik VS, Kost NV, Sokolov OIu, et al. Evenly tritium-labeled peptides and their in vivo and in vitro biodegradation. Bioorg Khim. 2006;32(2):183-91. [Article in Russian] https://pubmed.ncbi.nlm.nih.gov/16637290/ [in Russian]
34. Bobyntsev II, Kryukov AA, Medvedeva OA, Svishcheva MV, Shevchenko AV, Andreeva LA, Myasoedov NF. Morphological Changes in the Large Intestine of Rats Subjected to Chronic Restraint Stress and Treated with Selank. Bull Exp Biol Med. 2020;169(2):281-285. https://pubmed.ncbi.nlm.nih.gov/32651826/
35. Medvedeva OA, Svishcheva MV, Bobyntsev II, Kryukov AA, Andreeva LA, Myasoedov NF. State of Colon Microbiota in Rats during Chronic Restraint Stress and Selank Treatment. Bull Exp Biol Med. 2019;167(2):226-228. https://pubmed.ncbi.nlm.nih.gov/31236882/
36. Ershov FI, Uchakin PN, Uchakina ON, Mezentseva MV, Alekseeva LA, Miasoedov NF. Antiviral activity of immunomodulator Selank in experimental influenza infection. Vopr Virusol. 2009;54(5):19-24. [Article in Russian] https://pubmed.ncbi.nlm.nih.gov/19882898/ [in Russian]
37. Peptides semax and selank affect the behavior of rats with 6-OHDA induced PD-like parkinsonism. Dokl Biol Sci. 2017;474(1):106-109. https://pubmed.ncbi.nlm.nih.gov/28702721/
38. The 2026 Prohibited List: International Standard. Section S0, Non-Approved Substances, prohibited at all times. Selank is not named on the list; the S0 catch-all covers substances with no current approval by any governmental regulatory health authority for human therapeutic use. https://www.wada-ama.org/en/prohibited-list
39. Pokrywka A, Surala O, Grabowska K, Przybyla M, Granda D, Malecki A, Faiss R, Nowacka-Chmielewska M. Brain doping substances: prohibited or not in sports? Biol Sport. 2025;42(4):189-201. https://pmc.ncbi.nlm.nih.gov/articles/PMC12492343/
40. Semax, CID 9811102. Compound summary: molecular formula C37H51N9O10S, molecular weight 813.9. https://pubchem.ncbi.nlm.nih.gov/compound/9811102
41. https://pubmed.ncbi.nlm.nih.gov/28293190/