Selank Research: What the Studies Show

Selank (TP-7) is a synthetic heptapeptide derived from the immunomodulator tuftsin, developed at the Institute of Molecular Genetics of the Russian Academy of Sciences. It is studied for anxiolytic, nootropic and immunomodulatory activity. Selank is registered for clinical use in Russia; it is not approved by the U.S. FDA. The published literature therefore comes mainly from Russian and Eastern European research institutions.

Mechanism of action

Selank is a tuftsin analogue — the parent peptide is an immune-signalling fragment — extended with a Pro-Gly-Pro tail that resists enzymatic breakdown and gives it central nervous system activity.

Molecular work points to positive allosteric modulation of GABAergic signalling rather than direct receptor agonism, which is the leading explanation for anxiolytic effects without sedation or dependence.

A second mechanism is inhibition of enkephalin-degrading enzymes, extending the half-life of the body's own opioid-like stress-buffering peptides.

Its tuftsin origin also gives it measurable effects on pro-inflammatory cytokine output under stress conditions.

The studies

The generalised anxiety comparison below is human clinical research conducted in Russia; the remaining entries are animal and biochemical studies.

Human clinical efficacy

Comparative clinical trial (human)2008Completed

Selank versus medazepam in generalized anxiety disorder and neurasthenia

Whether a peptide anxiolytic can match a benzodiazepine without the sedative and cognitive cost.

Comparative human trial in 62 patients with generalized anxiety disorder and neurasthenia · Selank compared against the benzodiazepine medazepam · anxiolytic, sedative and cognitive endpoints

62
Patients
Comparable
Anxiolytic effect vs medazepam
Not observed
Sedation / cognitive impairment
Present
Anti-asthenic & psychostimulant activity
  • Selank's anxiolytic effect was statistically comparable to the benzodiazepine medazepam in this cohort.
  • Unlike the benzodiazepine comparator, it produced no sedative or cognitive-impairing effects.
  • It additionally showed anti-asthenic (anti-fatigue) and mild psychostimulant activity — the opposite of the benzodiazepine side-effect direction.
  • Sample size is modest at 62 patients and the work has not been replicated in large Western trials.

GABAergic mechanism

Preclinical molecular (rat)2016Completed

Selank and the expression of genes involved in GABAergic neurotransmission

Which neurotransmitter gene programmes Selank switches on, and how fast.

Expression analysis of 84 neurotransmitter-related genes in rat frontal cortex · sampling at 1 and 3 hours post-administration

84
Genes profiled
1-3 hours
Time to expression change
Substantially altered
GABAergic signalling genes
  • Selank drastically altered expression of genes governing GABAergic signalling — the brain's primary inhibitory, calming pathway — within one to three hours.
  • The pattern is consistent with Selank acting as a positive allosteric modulator of GABA receptors rather than a direct agonist.
  • That distinction is the proposed reason it does not produce the dependence associated with benzodiazepines.
Preclinical (rat)2017Completed

Selank enhances the effect of diazepam under unpredictable chronic mild stress

Whether combining Selank with a benzodiazepine outperforms either alone under chronic stress.

Unpredictable chronic mild stress (UCMS) model in rats · Selank alone, diazepam alone and combination arms · anxiety-related behavioural endpoints

Selank + diazepam
Most effective arm
Suppressed
Stress-induced behaviour
Reduced
Implied benzodiazepine dose
  • The Selank plus diazepam combination gave the strongest suppression of stress-induced behaviour.
  • The authors concluded co-administration could allow a lower benzodiazepine dose, reducing side-effect burden and addiction liability.
  • This is a rodent chronic-stress model, not a clinical dosing recommendation.

Endogenous opioid pathway

Biochemical study2001Completed

Inhibition of enkephalin-degrading enzymes as a mechanism of anxiolytic activity

Why anxious subjects burn through their own calming peptides — and whether Selank slows that down.

Biochemical assay of enkephalin degradation in blood · dose-response testing of Selank against enkephalin-degrading enzymes

Accelerated at baseline
Enkephalin degradation in severe anxiety
Dose-dependent
Enzyme inhibition by Selank
Extended
Enkephalin half-life
  • Patients with severe generalized anxiety showed rapid degradation of enkephalins — the body's own mood- and pain-regulating opioid peptides.
  • Selank dose-dependently inhibited the enzymes responsible, extending enkephalin half-life.
  • This gives a second, non-GABA route by which Selank may support stress resilience.

Cognition & learning

Preclinical (animal learning models)2018Completed

Optimizing action of Selank on the Schaffer collateral-CA1 pathway and associative learning

Whether Selank improves memory consolidation, and in which subjects the effect is largest.

Monosynaptic Schaffer collateral-CA1 pyramidal cell pathway recordings · associative learning tasks scoring correct choices and errors

Increased
Correct choices
Reduced
Errors
Poor-learner subgroup
Largest effect
  • Selank progressively optimised associative learning and memory consolidation across training sessions.
  • The effect was strongest in subjects with initially poor learning ability — correct choices rose and errors fell.
  • Upregulation of BDNF in the hippocampus is the proposed underlying mechanism, linking it to the same neurotrophic axis as Semax.

Immunomodulation

Preclinical (animal)2020Completed

Influence of Selank on cytokine levels under conditions of social stress

Whether a tuftsin-derived peptide can damp the inflammatory response to behavioural stress.

Social stress model · measurement of pro-inflammatory cytokines interleukin-1β, interleukin-6 and TNF-α

Suppressed
Interleukin-1β
Suppressed
Interleukin-6
Suppressed
TNF-α
  • Selank significantly suppressed the pro-inflammatory cytokines IL-1β, IL-6 and TNF-α raised by behavioural stress.
  • Consistent with its origin as a derivative of the immune peptide tuftsin.
  • Suggests Selank stabilises central nervous system and immune responses together rather than acting on mood alone.

Receptor pharmacology

Biochemical (receptor binding assay)2016Completed

Radioligand-receptor binding and GABA-A modulation

How Selank calms the central nervous system without the heavy sedation of conventional tranquillisers.

Radioligand-receptor binding assay on isolated brain cell membranes · testing whether Selank behaves as a positive allosteric modulator of GABA-A receptors

Altered
GABA receptor binding efficiency
Not observed
Benzodiazepine sub-site binding
Positive allosteric modulation
Proposed action
  • Selank changed the binding efficiency of GABA receptors, the brain's principal inhibitory system, letting endogenous GABA act more effectively.
  • It did not bind the benzodiazepine sub-site — the leading explanation for anxiolytic activity without marked muscle relaxation or cognitive dulling.
  • Receptor-level data of this kind is mechanistic; it does not by itself establish clinical benefit.

Neuroprotection

Preclinical (ex vivo)2019Completed

BDNF regulation and protection against ethanol-induced memory impairment

Whether Selank stabilises brain-derived neurotrophic factor during an ethanol-induced memory challenge.

Rat model of ethanol-induced memory impairment · BDNF content measured in the hippocampus and prefrontal cortex · memory-disturbance endpoints

Stabilised
Hippocampal BDNF
Regulated
Prefrontal cortex BDNF
Reduced
Ethanol-induced memory impairment
  • Selank regulated BDNF — the principal growth factor for neuronal survival and plasticity — in the two regions most associated with memory and attention.
  • Memory impairment provoked by the ethanol challenge was attenuated relative to controls.
  • Animal data only; no equivalent human neuroprotection trial has been published.

Human clinical efficacy

Clinical trial (human)2014-2015Completed

Selank versus phenazepam, and optimisation of anxiety treatment

How Selank compares with a benzodiazepine on both effect and tolerability in anxiety disorders.

Clinical comparison of Selank against phenazepam in patients with anxiety disorders, plus a follow-up treatment-optimisation study · anxiolytic efficacy, tolerability and side-effect endpoints

Comparable
Anxiolytic effect
Favoured Selank
Tolerability
Fewer
Sedative side effects
  • Selank's anxiolytic effect was comparable to phenazepam in this patient population.
  • Tolerability favoured Selank — fewer reports of drowsiness and attention or memory complaints than the benzodiazepine arm.
  • The follow-up optimisation paper is why Selank is discussed in the Russian literature as a way to reduce reliance on benzodiazepines rather than as a stand-alone replacement.

Storage & handling

Selank is supplied as a lyophilised powder. Keep sealed vials refrigerated or frozen, protected from light and moisture.

Reconstitute with bacteriostatic water directed slowly down the inner wall of the vial and swirl gently until clear. Do not shake.

Store reconstituted solution at 2-8 °C and use within the stability window set by your lab's standard operating procedures.

All information on this page is provided for laboratory and educational reference only. Peptides Lab SA (PTY) Ltd supplies compounds strictly for in-vitro research use. Nothing here is medical advice, a dosing recommendation, or a claim of human safety or efficacy.

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