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.
- 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 Russian Academy of Sciences as an extended, plasma-stable analogue of tuftsin.
- Granted clinical approval in the Russian Federation as an anxiolytic; used in human research for generalised anxiety, adjustment disorder, and stress-related symptomatology.
- Studied internationally as a tool peptide for probing the relationship between enkephalin tone, anxiety, and attention.
- An N-acetylated analogue (N-Acetyl Selank Amidate) was later developed for extended duration of action.
Section 3
Mechanism of Action
- 1Inhibition of enkephalinase enzymes, prolonging the half-life of endogenous enkephalins and producing anxiolytic effects without direct opioid receptor agonism.
- 2Modulation of GABAergic tone indirectly via the enkephalin system; no direct GABA-A binding has been demonstrated.
- 3Upregulation of BDNF expression in the hippocampus, similar to Semax but generally lower magnitude.
- 4Influence on monoamine turnover — increased serotonergic and dopaminergic metabolite levels in regions associated with mood and motivation.
- 5Immunomodulatory effects via the tuftsin pharmacophore — measurable changes in cytokine balance, particularly interleukin profiles, in stressed animals.
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 animal models (open-field, elevated plus-maze paradigms).
- 2Improved attention and cognitive performance under stress in early human studies.
- 3Anti-asthenic effect — reduction of mental fatigue and improvement in subjective wellbeing in published trials.
- 4No sedative, amnestic, or motor-impairing effects at studied doses, in contrast to benzodiazepines.
- 5Immunomodulation — observed normalisation of cytokine profiles in subjects with stress-related immune dysregulation.
- 6Synergistic profile with cognitive peptides such as Semax in stack research.
Section 5
Theoretical Dosing & Protocols
| Route | Dosage | Frequency | Duration |
|---|---|---|---|
| Intranasal (research) | Typically 75–300 μg per session in published protocols | 2–3 times daily in study protocols | Studies generally run 10–21 days |
Note: Cyclical use is more common than continuous administration in published research.
Section 6
Administration Routes
- Intranasal — the established research route, with the same nose-to-brain rationale as Semax.
- Parenteral routes used in animal research; oral administration is not viable due to proteolytic degradation.
Section 7
Safety Profile
Commonly reported
- · Mild nasal irritation
- · Occasional transient headache or lightheadedness
- · Subtle changes in arousal level (typically reduced anxiety, not sedation)
Rare / theoretical
- · Hypersensitivity reactions
- · Long-term Western safety data is limited
- · Possible interaction with opioid-modulating medications (theoretical, via enkephalin pathway)
Contraindications
- · Not authorised for human use outside Russia
- · Pregnancy and lactation — insufficient data
- · Concomitant opioid antagonist therapy — theoretical interference with mechanism
Section 8
UK & EU Regulatory Context
United Kingdom
Not licensed as a medicine in the United Kingdom. Available strictly as a research chemical for laboratory use.
European Union
Not approved by the European Medicines Agency. Clinically approved in the Russian Federation.
Section 9
Clinical Studies Summary
Selank in generalised anxiety disorder — controlled trial
Russian clinical trial reporting significant reduction in anxiety scores comparable to a benzodiazepine comparator, without sedation or cognitive impairment.
Selank effects on cytokine profile in stressed subjects
Normalisation of pro-/anti-inflammatory cytokine balance following a course of intranasal Selank.
Enkephalinase inhibition by Selank — mechanistic study
Demonstration of dose-dependent inhibition of plasma and brain enkephalin-degrading activity, providing a molecular basis for the observed anxiolytic effect.
Section 10
Frequently Asked Questions
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: research peptides are sold strictly for in vitro and preclinical laboratory purposes. Importation or supply for human consumption is not permitted under UK medicines legislation.