Selank
Also known as: TP-7 · Thr-Lys-Pro-Arg-Pro-Gly-Pro
A synthetic heptapeptide analogue of tuftsin developed for anxiolytic and immunomodulatory research, with measurable effects on attention and mood.
Selank is a tuftsin-derived heptapeptide anxiolytic studied intranasally; enkephalinase inhibition rather than GABA-A binding, without sedation or dependence.
Evidence tier: A — ≥1 RCT + meta-analysis or approved clinical use
- Category
- Anxiolytic / Mood
- Half-life
- Intranasal: minutes; pharmacodynamic effects 24h+
- Formula
- C₃₃H₅₇N₁₁O₉
- Weight
- 751.87 g/mol
- Sequence
- Thr-Lys-Pro-Arg-Pro-Gly-Pro
Section 1
Overview
Selank is a synthetic seven-amino-acid peptide built around the tetrapeptide tuftsin (Thr-Lys-Pro-Arg), an endogenous immunomodulator. Tuftsin itself has a vanishingly short half-life; Selank extends the molecule with a proline-glycine-proline tail that confers stability and produces a peptide with measurable anxiolytic and pro-cognitive activity in research models.
Selank was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences as part of the same research programme that produced Semax. The two are commonly studied as complementary tools: Selank is broadly positioned as anxiolytic, while Semax leans cognitive/attentional.
In animal anxiety paradigms, Selank produces effects comparable to classical benzodiazepines without the sedation, motor impairment, dependence liability, or amnestic side effects associated with that drug class — a profile attributed to its action on enkephalin metabolism rather than direct GABA-A binding.
Section 2
Discovery & History
- Synthesised in the 1990s at the Institute of Molecular Genetics of the Russian Academy of Sciences under the direction of the same group that produced Semax, extending the endogenous immunomodulator tuftsin into a plasma-stable heptapeptide.
- Granted clinical approval in the Russian Federation as an anxiolytic and anti-asthenic agent; entered routine use in Russian psychiatric and psychoneurological practice for generalised anxiety, adjustment disorder, and stress-related asthenic syndromes.
- Studied internationally as a tool peptide for probing the relationship between the enkephalin system, anxiety phenotypes, and attention — a mechanistic angle distinct from every other clinically deployed anxiolytic drug class.
- The 2005–2015 Russian trial programme produced comparative work against benzodiazepines (medazepam, phenazepam) in generalised anxiety populations, reporting comparable anxiolytic magnitude without the sedation-and-dependence liability.
- An N-acetylated, C-terminally amidated analogue (N-Acetyl Selank Amidate, NA-Selank) was developed to further extend the pharmacodynamic half-life; the parent compound remains the reference for the clinical evidence base.
Section 3
Mechanism of Action
- 1Inhibition of enkephalin-degrading enzymes (neprilysin / neutral endopeptidase and the aminopeptidases that cleave Met- and Leu-enkephalin), prolonging endogenous enkephalin half-life and producing anxiolytic tone via the delta-opioid system without direct receptor agonism.
- 2Indirect modulation of GABAergic tone via the enkephalin system rather than direct GABA-A binding; this is the mechanistic root of Selank's non-sedating, non-dependence-forming profile relative to benzodiazepines.
- 3Upregulation of hippocampal and cortical BDNF expression in rodent models — smaller in magnitude than Semax but measurable and reproducible, plausibly contributing to the peptide's pro-cognitive effect under stress.
- 4Modulation of monoamine turnover — increased serotonergic and dopaminergic metabolite levels have been reported in the prefrontal cortex and hippocampus, aligning with the observed mood and motivational effects.
- 5Immunomodulatory effects via the tuftsin pharmacophore — normalisation of pro- and anti-inflammatory cytokine balance (IL-6, TNF-α, IL-4, IL-10 shifts) in stressed animals and in published Russian clinical work on stress-related immune dysregulation.
- 6Attenuation of the acute HPA-axis stress response — reduction in stress-induced cortisol / corticosterone rise, consistent with the observed anxiolytic effect but distinct from cortisol-suppressive corticosteroids.
Section 4
Researched Benefits
Findings reported in the published preclinical and clinical literature. Effects in research contexts do not constitute claims of therapeutic benefit in humans.
- 1Reduction of anxiety-like behaviour in the standard rodent anxiety paradigms (elevated plus-maze, open-field test, novelty-suppressed feeding), with effect sizes comparable to diazepam without the associated motor and cognitive costs.
- 2Improved attention and cognitive performance under psychological or physiological stress in published Russian clinical trials on operator-population subjects.
- 3Anti-asthenic effect — measurable reduction in mental fatigue and improvement in subjective wellbeing scores in clinical trials for post-viral and post-traumatic asthenic syndromes.
- 4Absence of sedation, amnestic effect, motor impairment, or dependence liability at studied doses, in contrast to the benzodiazepine class — the mechanistically-predicted clinical differentiator.
- 5Immunomodulatory normalisation — measurable stabilisation of cytokine profiles and lymphocyte subsets in subjects with stress-related immune dysregulation, distinguishing Selank from purely CNS-active anxiolytics.
- 6Synergistic profile with cognitive peptides such as Semax and Noopept in published Russian stack research — the most studied multi-peptide protocol combines Selank (anxiolytic) with Semax (cognitive) for stress-under-cognitive-load research designs.
- 7Reported normalisation of sleep quality without direct sedative or sleep-onset-inducing effect — an indirect benefit of reduced sympathetic tone and stress-axis attenuation.
Section 5
Theoretical Dosing & Protocols
| Route | Dosage | Frequency | Duration | Source |
|---|---|---|---|---|
| Intranasal (research) | No sourced dose | Not stated | Not stated | None cited |
Note: No dose figure is shown because none could be confirmed from the abstract of a human Selank trial (PubMed abstracts checked: 18454096, 25176261, 26356395, 18577961).
Section 6
Administration Routes
- Intranasal — the established research route, exploiting the nose-to-brain olfactory and trigeminal pathways in the same rationale that dominates the whole Russian cognitive-peptide programme.
- Parenteral (intramuscular / subcutaneous) routes used in animal research and in some Russian clinical protocols where a sustained plasma exposure is desired.
- Oral administration is not viable — the peptide is efficiently degraded by gastrointestinal proteases and undergoes near-complete first-pass metabolism.
- Sublingual administration is anecdotally reported outside published literature but has not been characterised in the peer-reviewed pharmacokinetic record.
Section 7
Safety Profile
Commonly reported
- · Mild transient nasal irritation, congestion, or dryness — the most common tolerability finding in intranasal protocols, generally self-limiting within the first 2–3 doses.
- · Occasional transient headache or lightheadedness, reported at higher frequency in initial-dose exposure than in maintenance dosing.
- · Subtle changes in arousal level — the characteristic effect is reduced anxiety without accompanying sedation, distinguishing it clinically from the benzodiazepine class.
- · Rare reports of altered dream quality or vivid dreaming during the first week of a course, without accompanying sleep-quality disturbance.
Rare / theoretical
- · Hypersensitivity reactions — theoretical based on peptide chemistry, not documented at significant frequency in published Russian clinical work.
- · Long-term Western safety data is limited to the Russian clinical experience; chronic-use safety beyond ~12 weeks of continuous administration is not well-characterised.
- · Possible pharmacodynamic interaction with opioid-antagonist medications (naltrexone, naloxone) — theoretical mechanism-based interference at the enkephalin arm.
- · Theoretical interaction with monoamine-oxidase inhibitors given Selank's modulation of monoamine turnover — no documented clinical events but a prudent research-context consideration.
Contraindications
- · No entry for Selank was found in the electronic medicines compendium (emc) on 17 October 2026. Regulation 46(1) of the Human Medicines Regulations 2012 prohibits selling or supplying an unauthorised medicinal product.
- · Pregnancy and lactation — insufficient controlled data; excluded from published Russian trial protocols in these populations.
- · Concomitant opioid antagonist therapy — theoretical interference with the enkephalin-arm mechanism of action.
- · Active severe nasal pathology (structural, surgical, or infectious) — practical route contraindication for the intranasal formulation.
Section 8
UK & EU Regulatory Context
United Kingdom
No entry for Selank was found in the electronic medicines compendium (emc) on 17 October 2026. The emc is not a complete record of UK authorisations, so check the MHRA Products database.
European Union
Not approved by the European Medicines Agency. Registered in the Russian Federation (Vidal.ru lists Selank nasal drops under registration number ЛП-№(010951)-(РГ-RU)).
Section 9
Clinical Studies Summary
Selank in generalised anxiety disorder — controlled trial
Multicentre Russian controlled trial in generalised anxiety disorder (n>60) reporting significant reduction in Hamilton Anxiety Rating Scale scores over a 14-day treatment course, with anxiolytic magnitude comparable to a benzodiazepine (medazepam) comparator arm and without the sedation, motor impairment, or short-term dependence signal seen in the benzodiazepine group. Notable for using standardised Western anxiety-rating instruments alongside the Russian clinical assessment scales.
Read studySelank effects on cytokine profile in stressed subjects
Clinical immunology study in a stress-exposed adult population reporting normalisation of pro- and anti-inflammatory cytokine balance (measurable IL-6 decrease, IL-4/IL-10 increase) following an intranasal Selank course. Interpreted as evidence for a peripherally-active tuftsin-pharmacophore immunomodulatory effect operating alongside the CNS anxiolytic effect.
Enkephalinase inhibition by Selank — mechanistic study
Preclinical biochemistry study demonstrating dose-dependent inhibition of plasma and brain enkephalin-degrading enzymatic activity following Selank administration in rodents, providing the molecular basis for the observed anxiolytic behavioural effect and firmly locating the mechanism upstream of GABA-A rather than at the receptor itself.
Selank in post-traumatic asthenic syndrome — open-label trial
Russian open-label clinical experience in post-traumatic and post-viral asthenic syndromes reporting significant improvement in the standardised asthenia inventories over a treatment course, with the anti-asthenic effect emerging by day 4–5 and consolidating over the second week.
Selank effect on operator performance under stress
Russian applied-psychology trial in a shift-worker / operator population reporting improved sustained-attention performance under high-stress workload conditions in the Selank arm relative to placebo, with cognitive-performance differentials most pronounced in the second half of the shift.
Section 10
Frequently Asked Questions
Section 10a
Practical Research Guidance
Cycle guidance
Reconstitution & storage
UK sourcing notes
Section 11
Sourcing for Laboratory Research
Sourcing Selank for laboratory research
Researchers in the United Kingdom and elsewhere typically obtain Selank from specialist research-chemical suppliers. Purity, third-party testing, and supplier transparency are the principal differentiators worth evaluating before placing an order. The two suppliers below are commonly referenced in UK research contexts.
Reminder: this page is educational. Regulation 46(1) of the Human Medicines Regulations 2012 prohibits selling or supplying an unauthorised medicinal product, and some compounds on this site, such as semaglutide, are authorised prescription-only medicines in the UK.