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Neuropsychiatric

Selank

Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) is a synthetic heptapeptide analog of the immunopeptide tuftsin, developed in Russia and marketed there as an intranasal anxiolytic/nootropic. Small Russian trials report anxiolytic and mild "nootropic"/anti-asthenic effects in generalized anxiety disorder and neurasthenia, roughly comparable to benzodiazepines (medazepam, phenazepam) but with less sedation. The entire human evidence base is small, mostly non-blinded, non-English, and from one research group, and it has not been independently replicated or approved outside Russia. There is essentially no systematic human safety data by organ system (cardiac, hepatic, renal, endocrine, hematologic monitoring was not performed in the published trials). In the US/EU it is unapproved and is sold illicitly as a "dietary supplement" of unknown identity, purity, and dose; a US clinical-pharmacology review explicitly flags it as poorly studied and GABAergic/CNS-active. Because it is CNS-active and often self-administered as an unregulated research chemical, it should be treated as an investigational agent, not a proven safe anxiolytic.

Clinical readoutPeptide · neuropeptide
Hepatic strainNone
CardiovascularNone
HPTA suppressionNone
Half-life
Very short in blo…
Route
Clinically administered…
Evidence
C
Active
Pharmacodynamic effect…
1·t½2·t½3·t½4·t½5·t½
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ Very short in blood — the peptide is rapidly hydrolyzed by plasma peptidases; tritium-labeling studies in plasma show degradation on the order of minutes, generating fragments TKPRP, TKP, RP, and GP (glyprolines). No validated human half-life is published.
Pharmacology

Mechanism of action

Selank is a synthetic analog of the endogenous tetrapeptide tuftsin, extended with a Pro-Gly-Pro (glyproline) tail that slows enzymatic degradation. Proposed, largely preclinical mechanisms: (1) positive allosteric modulation of GABA-A receptor GABA binding — radioligand studies in rat brain membranes show Selank alters [3H]GABA binding and can interact with/block benzodiazepine (diazepam) and olanzapine modulatory sites, though not identically; (2) modulation of the enkephalin/opioid system — it inhibits enkephalin-degrading enzymes and raises leu-enkephalin activity in human serum, and its anxiolytic effect is partly naloxone-sensitive in mice; (3) effects on brain monoamines (dopamine synthesis/turnover, tyrosine hydroxylase) underlying an antidepressant/psychostimulant component in rodents; (4) modulation of BDNF and expression of GABAergic, cytokine, and chemokine genes (immunomodulatory/antiviral activity inherited from tuftsin). No single receptor target fully explains its action, and the definitive human mechanism is not established.
Kinetics

Pharmacokinetics

Half-life

Very short in blood — the peptide is rapidly hydrolyzed by plasma peptidases; tritium-labeling studies in plasma show degradation on the order of minutes, generating fragments TKPRP, TKP, RP, and GP (glyprolines). No validated human half-life is published.

Active duration

Pharmacodynamic effect markedly outlasts plasma presence: Russian trials describe an anxiolytic effect persisting up to ~1 week after the last dose, attributed to downstream/neurotrophic changes rather than sustained plasma levels. This is not established by rigorous PK/PD studies.

Route

Clinically administered intranasally (aqueous drops, typically a 0.15% solution) to exploit nose-to-brain delivery; intraperitoneal/intravenous routes used only in animal research. Reported clinical dosing (as reported in Russian trials, always paired with the caveat that safety monitoring was minimal): roughly 900 µg–2700 µg/day intranasally over 10–14 days.

Metabolism & clearance

Metabolized by extracellular/plasma peptidases (aminopeptidases, other exopeptidases) into shorter peptides and amino acids; no cytochrome-P450 hepatic metabolism is implicated. Metabolite handling and renal clearance in humans are not characterized. Washout of the parent peptide from blood is fast (minutes), but centrally mediated effects may persist longer.

For monitoring and washout planning, not drug-test evasion.

Reported effects

Physiological & performance effects

  • Anxiolytic effect in generalized anxiety disorder and neurasthenia, reported comparable to benzodiazepines (medazepam, phenazepam) in small Russian trials
  • Mild 'nootropic'/attention and anti-asthenic (anti-fatigue) effect, and reduced sedation/psychomotor impairment relative to benzodiazepines
  • Reported reduction of benzodiazepine side effects and easing of withdrawal when used as add-on to phenazepam (single small RCT)
  • Antidepressant/psychostimulant-like component seen only in rodent models (forced swim, WAG/Rij), not established in humans
  • Preclinical: attenuation of alcohol- and morphine-withdrawal anxiety signs, modulation of BDNF, and immunomodulatory/antiviral gene-expression effects (rodent/cell only)
Safety

Adverse effects by system

Cardiovascular

No adequate human data. Published trials did not systematically monitor blood pressure, heart rate, or ECG; no cardiovascular signal has been reported, but absence of reporting is not evidence of safety.

Hepatic

No adequate human data. Liver enzymes were not systematically measured in the published trials; hepatic effects are unknown. No CYP-mediated metabolism is implicated mechanistically.

Endocrine / HPTA

No adequate human data. Selank is a neuropeptide with no known androgenic, estrogenic, or gonadotropic activity and is not an anabolic-androgenic agent; effects on the hypothalamic-pituitary-gonadal axis have not been studied in humans.

Reproductive

No adequate human data. No studies of fertility, pregnancy, or lactation outcomes; must be considered unstudied and therefore avoided in pregnancy/breastfeeding.

Neuropsychiatric

CNS-active (GABAergic/opioid-modulating). Trials emphasize low sedation versus benzodiazepines, but rigorous neuropsychiatric adverse-effect surveillance was not done. A US clinical-pharmacology review groups it with GABAergic sedative-hypnotics and raises theoretical concern about CNS depression and misuse potential when combined with other depressants; human dependence/withdrawal data specific to Selank are lacking.

Renal

No adequate human data. Renal function was not systematically monitored in published trials; renal handling of the peptide and its fragments is uncharacterized.

Hematologic

No adequate human data. As a tuftsin analog it has immunomodulatory (cytokine/chemokine gene-expression) activity in preclinical models, but human hematologic or immune safety endpoints were not measured.

Dermatologic

No adequate human data. Intranasal administration could plausibly cause local nasal mucosal irritation, but this was not systematically reported. No systemic dermatologic effects described.

Recovery

HPTA suppression & recovery

Suppression: None expected / not studied

Selank is a non-steroidal neuropeptide with no known sex-hormone or gonadotropic activity and no evidence of HPTA/HPG-axis suppression; it is not an anabolic-androgenic agent, and HPTA/HPG effects have not been formally studied in humans. No SERM or post-cycle intervention is indicated or supported for Selank, and none should be inferred. Anyone with existing endocrine concerns, or who is using it alongside hormonal agents, should consult an endocrinologist rather than self-managing; this monograph defers all endocrine decision-making to a qualified clinician.

Bloodwork & vitals

Monitoring

Recommended labs & checks
No Selank-specific validated monitoring exists; because human organ-system safety is uncharacterized, a conservative baseline and periodic panel is reasonable if used: CBC, comprehensive metabolic panel (including liver enzymes and renal function)Clinician-directed mental-health assessment of anxiety/mood rather than self-tracking

Cadence: Baseline before any use and clinician-guided follow-up; do not rely on self-monitoring. Given short courses reported in trials (10–14 days), any use beyond a brief period warrants medical review.

Warning signs — seek care
  • Excessive sedation, drowsiness, confusion, or slowed breathing — especially if combined with alcohol/benzodiazepines/opioids (seek urgent care)
  • Worsening anxiety, depression, or new suicidal thoughts
  • Allergic reaction: rash, facial/throat swelling, difficulty breathing (emergency)
  • Persistent nasal irritation, bleeding, or congestion with intranasal use
  • Any unexplained systemic symptoms — stop and consult a clinician, since safety is not established
Do not use if

Contraindications

  • Pregnancy and breastfeeding — no reproductive/developmental safety data
  • Concurrent use with benzodiazepines, alcohol, or other CNS depressants without medical supervision — Selank is GABAergic/CNS-active and combined depressant effects are not characterized in humans
  • Use as a substitute for evaluation/treatment of a diagnosed anxiety or mood disorder by a clinician
  • Product obtained as an unregulated 'research chemical'/supplement of unverified identity, purity, or dose (the typical real-world source outside Russia)
  • Known hypersensitivity to the peptide or excipients; active nasal/sinus pathology for intranasal use
  • Children/adolescents — no adequate data outside the specific Russian study populations
Combinations

Interaction profile

  • ContraindicatedWith DNP: Additive cardiovascular strain

Check a specific combination in the interaction checker.

Harm reduction

Reducing harm & when to stop

  • Treat Selank as an investigational, unapproved agent: there is no rigorous human organ-system safety data and no independent replication of the Russian efficacy trials. Do not use it as a substitute for clinician-directed evaluation of anxiety or depression.
  • Do not combine with alcohol, benzodiazepines, opioids, or other CNS depressants without medical supervision — it is GABAergic/CNS-active and combined effects are uncharacterized.
  • Avoid entirely in pregnancy, breastfeeding, and in adolescents due to absence of safety data.
  • Products sold outside Russia are unregulated and of unverified identity, purity, and dose; contamination and mislabeling are real risks with 'research chemical'/supplement sources.
  • Get baseline bloodwork (CBC, liver, renal) and involve a clinician before and during any use; keep any course short and reassess.
  • Stop and seek medical care for excessive sedation or slowed breathing, allergic reaction (swelling, difficulty breathing), worsening mood or suicidal thoughts, or persistent nasal irritation/bleeding.
  • Anyone with existing cardiac, hepatic, renal, psychiatric, or endocrine conditions should consult the relevant specialist before considering use; defer endocrine questions to an endocrinologist.
Evidence

Citations (15)

Every clinical claim above is tied to a primary source. Overall evidence grade C — graded to the best available evidence for its core claims.

  1. 01

    Selank has an anxiolytic effect in generalized anxiety disorder and neurasthenia comparable to the benzodiazepine medazepam, with additional anti-asthenic/psychostimulant effects, in a comparative human trial (n=62); it also raised leu-enkephalin activity in serum.

    RCT[Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia].PMID 18454096 ↗

  2. 02

    In 60 patients with anxiety/somatoform disorders, Selank produced anxiolytic and mild nootropic effects comparable to phenazepam, with the anxiolytic effect lasting about a week after the last dose.

    RCT[A comparison of the anxiolytic effect and tolerability of selank and phenazepam in the treatment of anxiety disorders].PMID 25176261 ↗

  3. 03

    Adding Selank to phenazepam in patients with anxiety disorders reduced benzodiazepine side effects (memory/attention impairment, sedation, sexual disturbance) and eased withdrawal, improving quality of life (randomized comparative trial, n=70).

    RCT[Optimization of the treatment of anxiety disorders with selank].DOI 10.17116/jnevro20151156133-40 ↗

  4. 04

    Selank acts as a positive allosteric modulator of GABA binding at brain GABA-A receptors and interacts with benzodiazepine/olanzapine modulatory sites (rat brain membrane radioligand study).

    PreclinicalDOI 10.2174/0929866525666180925144642 ↗

  5. 05

    Selank increases amplitude and rate of spontaneous inhibitory postsynaptic currents in rat hippocampal CA1 neurons, consistent with enhanced GABAergic inhibition.

    PreclinicalEffect of Selank on Spontaneous Synaptic Activity of Rat Hippocampal CA1 Neurons.DOI 10.1007/s10517-017-3676-3 ↗

  6. 06

    Selank does not directly change mRNA levels of GABAergic-system genes in IMR-32 neuroblastoma cells but appears to modulate GABA's interaction with its receptors, supporting an indirect/allosteric mechanism.

    PreclinicalDOI 10.3389/fphar.2017.00089 ↗

  7. 07

    The anxiolytic effect of Selank is partly mediated by the enkephalin/opioid system and is naloxone-sensitive in mice.

    Preclinical[The role of opioid system in peculiarities of anti-anxiety effect of peptide anxiolytic selank].PMID 22550852 ↗

  8. 08

    Selank is a tuftsin analog with an antidepressant/psychostimulant component in rodent depression models, linked to activation of brain monoaminergic systems and dopamine turnover.

    PreclinicalPMID 18661785 ↗

  9. 09

    Selank is rapidly degraded in blood plasma by peptidases into fragments (TKPRP, TKP, RP, GP), and intranasal administration delivers it to brain tissue (tritium-labeling pharmacokinetic study).

    Preclinical[Evenly tritium-labeled peptides and their in vivo and in vitro biodegradation].PMID 16637290 ↗

  10. 10

    Route of administration (intranasal vs intraperitoneal) changes Selank's receptor-binding profile (GABA vs NMDA) due to differing pharmacokinetics/biotransformation, in mice.

    PreclinicalPMID 29787664 ↗

  11. 11

    Selank has immunomodulatory/antiviral activity, altering expression of cytokine, chemokine, and receptor genes; the Gly-Pro fragment is a key pharmacophore (mouse spleen).

    PreclinicalPMID 21786679 ↗

  12. 12

    Selank modulates BDNF content in hippocampus and prefrontal cortex and mitigates ethanol-withdrawal-associated memory impairment in rats.

    PreclinicalSelank, Peptide Analogue of Tuftsin, Protects Against Ethanol-Induced Memory Impairment by Regulating of BDNF Content in the Hippocampus and Prefrontal Cortex in Rats.DOI 10.1007/s10517-019-04588-9 ↗

  13. 13

    Selank attenuates aversive signs of naloxone-precipitated morphine withdrawal in rats, comparable to (slightly less than) diazepam.

    PreclinicalSelank, a Peptide Analog of Tuftsin, Attenuates Aversive Signs of Morphine Withdrawal in Rats.DOI 10.1007/s10517-022-05624-x ↗

  14. 14

    Selank reduces ethanol-withdrawal anxiety and allodynia in alcohol-preferring rats without affecting ethanol consumption.

    PreclinicalEfficacy of peptide anxiolytic selank during modeling of withdrawal syndrome in rats with stable alcoholic motivation.DOI 10.1007/s10517-014-2490-4 ↗

  15. 15

    Selank is a poorly studied Russian GABAergic drug sold to US consumers as an unregulated dietary supplement; it is grouped with GABA-modulating sedative-hypnotics and flagged for insufficient safety/abuse-potential evaluation.

    ReviewDOI 10.1002/jcph.1922 ↗

Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice