tuneTypical Dose
Short-course protocols with intranasal or oral delivery. No robust standardized regimen in public sources
Peptide
Thr-Lys-Pro-Arg-Pro-Gly-Pro
tuneTypical Dose
Short-course protocols with intranasal or oral delivery. No robust standardized regimen in public sources
watchEffect Window
Rapid-to-short latency in comparative trials. Persistence about one week post-course in one study
check_circleCompliance
WADA NOT PROHIBITED
Overview
Selank is a synthetic peptide based on tuftsin studied for anxiolytic effects. It is used for calm focus and stress resilience claims, with evidence largely limited to regional clinical research.
Limited studies suggest reduced anxiety symptoms without strong sedation, with proposed modulation of GABA and serotonin systems. Some reports describe improved stress tolerance and attention. Minority research explores immune marker effects, but data are limited. Large, well-controlled trials are lacking, so benefits remain uncertain and depend on product quality and study context.
Selank is a heptapeptide with proposed enkephalinergic and GABA-related modulation, but clinical efficacy remains protocol-limited and dose data are weakly reported.
Outcomes
Safety
Evidence
Zozulia AA et al. 2008. "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. [PubMed: 18454096](https://pubmed.ncbi.nlm.nih.gov/18454096/)
Population: Adults with generalized anxiety disorder and neurasthenia
Dose protocol: Selank (n=30) compared with medazepam (n=32). Psychometric scales and enkephalin biomarkers measured. Route not fully detailed in abstract.
Key findings: Comparable anxiolytic effect to medazepam. Selank also showed antiasthenic/psychostimulant signal.
Notes: Good first-pass human signal but publication language and reporting granularity limit confidence.
Comparable anxiolytic effect to medazepam; selank also showed antiasthenic/psychostimulant signal.
Medvedev VE et al. 2014. "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. [PubMed: 25176261](https://pubmed.ncbi.nlm.nih.gov/25176261/)
Population: Adults with phobic-anxiety and somatoform disorders
Dose protocol: 60-patient comparator study against phenazepam. Detailed regimen not fully in abstract.
Key findings: Selank showed pronounced anxiolytic and mild nootropic effects. Reported effect persisted about one week post-treatment.
Notes: Stronger inference on symptom persistence than on dosing/AE details.
Selank showed pronounced anxiolytic and mild nootropic effects; reported effect persisted about one week post-treatment.
Uchakina ON et al. 2008. "Immunomodulatory effects of selank in patients with anxiety-asthenic disorders." Zh Nevrol Psikhiatr Im S S Korsakova. 2008;108(5): 71-75. [PubMed: 18577961](https://pubmed.ncbi.nlm.nih.gov/18577961/)
Population: Adults with GAD/neurasthenia
Dose protocol: Selank for 14 days, in vitro + in vivo cytokine observations.
Key findings: Reported Th1/Th2 balance changes after Selank exposure.
Notes: Biological signal only. Clinical endpoint coupling is exploratory.
Reported Th1/Th2 balance changes after Selank exposure.
Zozulya AA et al. 2001. "The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity." Bull Exp Biol Med. [PMID: 11550013](https://pubmed.ncbi.nlm.nih.gov/11550013/)
Population: Human-derived plasma/neuropeptide context and anxiety cohort framing
Dose protocol: Enkephalinase inhibition characterized with IC50. No clinical dose schedule tested in this mechanism arm.
Key findings: Dose-dependent enkephalinase inhibition and reduced enkephalin hydrolysis signature.
Notes: Helpful mechanistic evidence, not direct clinical efficacy proof.
Dose-dependent enkephalinase inhibition and reduced enkephalin hydrolysis signature.
Kost NV et al. 2001. "Semax and selank inhibit the enkephalin-degrading enzymes from human serum." Bioorg Khim. 2001;27(3): 180-183. [PMID: 11443939](https://pubmed.ncbi.nlm.nih.gov/11443939/)
Population: Human serum biology context
Dose protocol: IC50 values: Selank IC50 20 μM.
Key findings: Supports mechanistic plausibility through enkephalinase inhibition potency.
Notes: Mechanistic signal only.
Supports mechanistic plausibility through enkephalinase inhibition potency.
Sokolov OY et al. 2002. "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): 133–135. [PMID: 12432865](https://pubmed.ncbi.nlm.nih.gov/12432865/)
Population: Mice BALB/c and C57Bl/6
Dose protocol: 100 µg/kg Selank, phenotype-specific response to anxiety behaviors.
Key findings: Supports dose-related anxiolytic effects and enkephalinase-related mechanism in select phenotypes.
Notes: Translation to human dosing remains uncertain.
Supports dose-related anxiolytic effects and enkephalinase-related mechanism in select phenotypes.
Vyunova TV et al. 2018. "Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity." Protein Pept Lett. 2018;25(10): 914–923. [PMID: 30255741](https://pubmed.ncbi.nlm.nih.gov/30255741/)
Population: Aggregate human + animal literature synthesis
Dose protocol: Not dose-finding (mechanistic synthesis).
Key findings: Concludes Selank effects are linked to GABAergic modulation and prolonged anxiolytic/nootropic context.
Notes: Review-level certainty is lower than direct trial-level certainty.
Concludes Selank effects are linked to GABAergic modulation and prolonged anxiolytic/nootropic context.
Povarov IS et al. 2017. "GABA, Selank, and Olanzapine affect expression of genes involved in GABAergic neurotransmission." Front Pharmacol. [PMID: 28293190](https://pubmed.ncbi.nlm.nih.gov/28293190/)
Population: IMR-32 neuroblastoma model cells
Dose protocol: Preclinical expression profiling under selank/GABA/olanzapine conditions.
Key findings: No major mRNA changes with Selank alone. Interaction effects on gene signatures when combined with GABA.
Notes: Mechanistic context only.
No major mRNA changes with Selank alone; interaction effects on gene signatures when combined with GABA.
Fomenko EV et al. 2019. "Effect of Selank on Morphological Parameters of Rat Liver in Chronic Foot-Shock Stress." Bull Exp Biol Med. [PMID: 31243679](https://pubmed.ncbi.nlm.nih.gov/31243679/)
Population: Wistar rats
Dose protocol: 100, 300, 1000 µg/kg i.p., 15 min pre-stress.
Key findings: Reduced stress-linked hepatic morphological damage markers, with strongest effect around 300 µg/kg in this model.
Notes: Stress/organ protection signal is secondary to anxiety core claims.
Reduced stress-linked hepatic morphological damage markers, with strongest effect around 300 µg/kg in this model.
Sarkisova KI et al. 2008. Selank in behavioral models of inherited and induced depression-like symptoms. [PMID: 18661785](https://pubmed.ncbi.nlm.nih.gov/18661785/)
Population: Rats and mice
Dose protocol: Preclinical only. Mixed acute dosing in depression-like paradigms.
Key findings: Reported anxiolytic/psychostimulant features and monoaminergic hypotheses.
Notes: Useful exploratory signal. Does not establish clinical antidepressant effect.
Reported anxiolytic/psychostimulant features and monoaminergic hypotheses.
Konstantinopolsky MA et al. 2022. Selank attenuates aversive signs in morphine withdrawal (animal model). [PMID: 36322304](https://pubmed.ncbi.nlm.nih.gov/36322304/)
Population: Outbred rats
Dose protocol: 0.3 mg/kg i.p. anxiolytic dose.
Key findings: Reduced withdrawal severity versus control and lower efficacy than diazepam 2 mg/kg in one metric.
Notes: Not core anxiety-indication evidence for typical human use.
Reduced withdrawal severity versus control and lower efficacy than diazepam 2 mg/kg in one metric.
USADA Prohibited List page (includes link to WADA 2026 Prohibited List and substance consultation process). [USADA prohibited list](https: //www.usada.org/substances/prohibited-list/)
Population: Competitive athletes and support staff
Dose protocol: Not applicable
Key findings: Selank is not a named compound in these summary pages. Practical compliance depends on direct list consultation.
Notes: Use athlete-side checks at medication-time, not just static assumptions.
Selank is not a named compound in these summary pages; practical compliance depends on direct list consultation.
Panikratova YR, Lebedeva IS, Sokolov OY, et al. Functional connectomic approach to studying Selank and Semax effects. Dokl Biol Sci. 2020;490(1):9-11. doi:10.1134/S001249662001007X. PMID:32342318.
Population: Healthy adult volunteers.
Dose protocol: Single-dose intranasal Selank, Semax, or placebo with fMRI at baseline, 5 min, and 20 min (n=52).
Key findings: Selank produced measurable changes in right amygdala-temporal functional connectivity versus control conditions.
Notes: Objective neuroimaging evidence of CNS activity in healthy humans. Amygdala changes consistent with anxiolytic mechanism.
This controlled neuroimaging study assessed Selank and Semax effects on brain functional connectivity in 52 healthy adults using resting-state fMRI. Participants received Selank, Semax, or placebo and were scanned at baseline, 5 minutes, and 20 minutes post-administration. Selank produced differences in right amygdala-temporal region connectivity compared to control conditions. The study provides objective neuroimaging evidence of Selank's central nervous system activity in healthy humans, complementing the earlier clinical anxiety trials. The amygdala connectivity changes are consistent with Selank's proposed anxiolytic mechanism, as the amygdala is a key structure in anxiety processing. The sample size of 52 is reasonable for an fMRI study design.
Medvedev VE, Tereshchenko ON, Kost NV, et al. Optimization of the treatment of anxiety disorders with Selank. Zh Nevrol Psikhiatr Im S S Korsakova. 2015;115(6):33-40. doi:10.17116/jnevro20151156133-40. PMID:26356395.
Population: Adults with anxiety-spectrum disorders.
Dose protocol: Selank plus phenazepam (n=40) vs phenazepam monotherapy (n=30) in anxiety disorders.
Key findings: Combination achieved faster anxiolytic response and reduced benzodiazepine side effects including sedation and memory impairment.
Notes: Extends Selank evidence by showing adjunctive benefit that reduces benzodiazepine side-effect burden. Same Russian research group.
This RCT randomized 70 patients with anxiety disorders to either phenazepam monotherapy (n=30) or combined Selank plus phenazepam (n=40). The combination group achieved therapeutic anxiolytic response earlier and experienced fewer benzodiazepine side effects, including less sedation, fewer memory problems, and fewer sexual disturbances. The study extends the Selank evidence base by showing potential as an adjunct that reduces benzodiazepine side-effect burden while maintaining or accelerating anxiolytic response. Published in a Russian neurology journal, the study shares the same methodological limitations as other Selank trials (limited reporting detail, single research group). However, the practical clinical framing of reduced side effects is relevant and distinct from the earlier pure efficacy comparisons.