Research Guide · Selank

What is Selank?

A synthetic tuftsin-derived heptapeptide developed in Russia for anxiolytic, immunomodulatory and neuroprotective research without sedation or dependence liability.

Updated September 2026 Research Use Only 11 min read

What is Selank

A heptapeptide tuftsin analogue developed at the Russian Academy of Sciences for anxiolytic and immunomodulatory research.

Structure & Chemistry

Selank is a synthetic heptapeptide Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP). Built from natural tuftsin (T-K-P-R, derived from immunoglobulin G) extended C-terminally with -Pro-Gly-Pro for enzymatic stability. CAS 129954-34-3; MW 751.85 Da.

Origins & Development

Developed at the Institute of Molecular Genetics, Russian Academy of Sciences (Ashmarin lab). Registered by the Russian Ministry of Health in 2009 for generalised anxiety disorder and neurasthenia.

Mechanism Class

Anxiolytic via enkephalinase inhibition with downstream GABAergic enhancement. Distinct from benzodiazepines: no sedation, no dependence, no muscle relaxation, no cognitive impairment in research subjects.

Mechanism of Action

Anxiolytic, neuropeptide modulatory, and immunomodulatory pathways.

Enkephalinase Inhibition

Selank inhibits enzymes that degrade endogenous enkephalins (met- and leu-enkephalin). Elevated enkephalin tone enhances opioid receptor signalling, indirectly modulating GABAergic inhibition and limbic anxiety circuits without direct GABA-A receptor agonism (Vyunova et al.).

Indirect GABAergic Modulation

Through enkephalinergic enhancement, Selank augments GABA-A receptor function in anxiety-related circuits. Unlike benzodiazepines, this is indirect and does not cause sedation, tolerance, or dependence — distinguishing Selank in research models of chronic anxiolytic use (Kozlovskaya et al.).

Monoaminergic Effects

Selank modulates serotonin and dopamine systems, contributing to mood stability and stress resilience research outcomes. Effects are indirect through neurotrophic and neuropeptide cascades rather than direct receptor binding.

Tuftsin-Derived Immunomodulation

Selank retains immunomodulatory activity from its tuftsin parent. Modulates pro-inflammatory cytokine balance (IL-6, TNF-α reduction; IL-2 modulation), enabling research into immune-CNS interactions and stress-induced immune dysregulation (Zozulya et al.).

Selank vs Related Anxiolytics

Comparison with benzodiazepines, Semax, buspirone, and tuftsin parent.

Compound

Mechanism

Distinguishing Feature

Selank

Heptapeptide; enkephalinase inhibitor

Anxiolytic without sedation, dependence, cognitive impairment

Semax

ACTH(4-10) heptapeptide; BDNF/NGF inducer

Cognitive enhancement focus; companion to Selank from same Russian lab

Benzodiazepines

Direct GABA-A allosteric agonists

Strong anxiolytic but sedation, dependence, tolerance, cognitive impairment

Buspirone

5-HT1A partial agonist

Non-sedating anxiolytic; slow onset (weeks); different receptor target

Tuftsin (T-K-P-R)

Endogenous immunomodulatory tetrapeptide

Selank’s parent; lacks Selank’s enzymatic stability and CNS activity

Research Context: Selank’s parallel design philosophy with Semax (same lab, same C-terminal stabiliser) makes them complementary research tools — Semax for cognitive enhancement and neuroprotection, Selank for anxiolysis. Together they offer a non-sedating, non-dependence research alternative to benzodiazepines.

Key Research Applications

Primary research domains.

Anxiety Models (GAD)

Russian clinical and preclinical literature establish Selank for generalised anxiety disorder. Animal anxiety models (open field, elevated plus maze) demonstrate anxiolytic activity equivalent to medazepam at standard research doses, without sedation.

Stress Resilience & Cognitive Performance Under Stress

Research models of acute and chronic stress investigate Selank’s ability to preserve cognitive performance whilst reducing anxiety. Distinct from benzodiazepines which impair cognition during anxiolysis.

Neuroinflammation & Immune-CNS Interaction

Tuftsin-derived immunomodulation makes Selank valuable for studying CNS-immune crosstalk in anxiety and stress models. Cytokine modulation (IL-6, TNF-α) intersects with hypothalamic-pituitary-adrenal axis dysregulation.

Neuroprotection & Memory Consolidation

Emerging research explores Selank in memory consolidation under stress and neuroprotection in ischaemia models, leveraging both anxiolytic and indirect neurotrophic effects.

Opioid Withdrawal Research

Through enkephalinase inhibition and endogenous enkephalin elevation, Selank is investigated in opioid withdrawal and dependence models, providing a non-opioid means of supporting endogenous opioid signalling.

Quick Reference Specifications

Key biochemical parameters.

P · 01

Designation

Selank (tuftsin analogue heptapeptide)

P · 02

Sequence

Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP)

P · 03

CAS Number

129954-34-3

P · 04

Molecular Weight

751.85 Da

P · 05

Molecular Formula

C33H57N11O9

P · 06

Origin

Institute of Molecular Genetics, Russian Academy of Sciences (Ashmarin lab)

P · 07

Russian Approval

Registered 2009 for generalised anxiety disorder and neurasthenia

P · 08

Mechanism

Enkephalinase inhibition; indirect GABAergic modulation; immunomodulation

P · 09

Route

Intranasal spray (signature); subcutaneous in animal studies

P · 10

Storage

Lyophilised: 2–8°C; reconstituted: 2–8°C, stable 2–4 weeks

Reconstitution & Storage

Handling guidance.

Reconstitution

Reconstitute lyophilised Selank with sterile bacteriostatic water. For nasal preparation, dissolve to typical research concentration of 0.1–1 mg/mL. Use sterile syringes; gentle dissolution; avoid shaking.

Nasal Solution Preparation

Transfer to sterile metered nasal spray bottle for animal-model intranasal delivery. Typical research dose ranges (rodent models) are 100–300 µg per dose.

Storage Timeline

Lyophilised vials stable for years at 2–8°C. Reconstituted solutions maintain bioactivity 2–4 weeks at 2–8°C. Protect from light. Avoid freeze-thaw cycles.

Handling Best Practices

Maintain refrigeration; document reconstitution date; aliquot for extended programmes; use fresh sterile dispensers per research subject; discard solutions older than 4 weeks.

Key Published Research

Peer-reviewed studies behind Selank’s research profile.

2001

Enkephalinase inhibition

Selank inhibited enzymes that break down enkephalins — the basis for the enkephalinase mechanism described above.¹

2008

Clinical anxiety study

A Russian clinical study reported anxiolytic effects in patients with generalised anxiety disorder and neurasthenia.²

2016

GABAergic gene expression

Selank altered the expression of genes involved in GABAergic neurotransmission in rat brain tissue, supporting the indirect GABAergic mechanism.³

2017

Chronic stress model

In rats under unpredictable chronic mild stress, Selank enhanced the anxiety-reducing effect of diazepam.⁴

Regulatory & Research Status

Where Selank stands in 2026.

RUSSIA

Registered medicine

Selank nasal drops are registered in Russia for generalised anxiety disorder and neurasthenia.

UK / EU / US

Not approved

Selank is not an approved medicine in the UK, EU or US, and it was not among the peptides reviewed by the US FDA in 2026. Its sister peptide Semax was recommended for the 503A bulks list by an FDA advisory committee in July 2026.

Evidence Quality & Limitations

The clinical evidence for Selank consists mainly of small Russian-language studies by the developing institutes, and independent replication is limited. Claims that it causes no sedation, tolerance or dependence come from this literature and have not been tested in large controlled trials. Mechanistic findings — enkephalinase inhibition, GABAergic gene changes and cytokine effects — are largely from rodent and in-vitro work.

References

Zozulya AA, et al. The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity. Bull Exp Biol Med. 2001;131:315–7. PubMed
Zozulia AA, et al. 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;108:38–48. PubMed
Volkova A, et al. Selank administration affects the expression of some genes involved in GABAergic neurotransmission. Front Pharmacol. 2016;7:31. PubMed
Kasian A, et al. Peptide Selank enhances the effect of diazepam in reducing anxiety in unpredictable chronic mild stress conditions in rats. Behav Neurol. 2017;2017:5091027. PubMed

⚠ Research Use Only. The compounds discussed in this guide are intended strictly for in-vitro laboratory research. Not for human consumption, therapeutic use, or veterinary application. Researchers must comply with all applicable local regulations.