Selank
TP-7, Thr-Lys-Pro-Arg-Pro-Gly-Pro, TKPRPGP, tuftsin analogue TP-7
Selank is a synthetic heptapeptide built from the immunomodulatory tetrapeptide tuftsin (Thr-Lys-Pro-Arg) with the same Pro-Gly-Pro stabilising tail used in Semax. Developed at the Institute of Molecular Genetics in Moscow, it was approved in Russia in 2009 as a nasal solution for generalised anxiety disorder and neurasthenia. Outside Russia and Ukraine it is unlicensed and its clinical evidence base is small, comparator-controlled rather than placebo-controlled, and unreplicated.
Mechanism
Selank's proposed primary mechanism is indirect and unusual: rather than binding a receptor itself, it inhibits the enzymes that degrade endogenous enkephalins. Slowing enkephalinase activity raises the local availability and prolongs the action of the body's own opioid peptides, which in turn modulate limbic anxiety circuitry. This is supported by human plasma enzyme measurements alongside behavioural outcomes (the 2008 clinical study measured leu-enkephalin half-life in serum and reported that it was reduced in patients with generalised anxiety disorder and neurasthenia and rose during Selank treatment) and by rodent work in which behavioural anxiolysis tracks plasma enkephalin-degrading enzyme inhibition.
A second strand of evidence points at GABAergic transcription. In rodent brain, Selank alters expression of genes encoding GABA-A receptor subunits and GABA-handling proteins, and it potentiates the anxiolytic effect of diazepam in chronically stressed rats without producing diazepam-like sedation on its own. Selank also derives from tuftsin, a phagocytosis-stimulating fragment of immunoglobulin G, and it retains measurable effects on cytokine expression and inflammatory gene programmes. Whether the immune effects contribute to the behavioural ones, or are a vestige of the parent molecule, is unresolved. Critically, none of this amounts to an identified molecular target: no receptor has been cloned, expressed and shown to bind Selank with defined affinity.
What the research shows
The animal literature is reasonably broad. Selank shows anxiolytic-like effects across several rodent paradigms, reduces the aversive signs of morphine withdrawal, attenuates ethanol-induced hyperlocomotion and behavioural sensitisation, and shifts serotonin and monoamine metabolism in a strain-dependent way. It does so without the sedation, motor impairment or withdrawal syndrome that limit benzodiazepines, which, if it held up in humans, would be genuinely useful. As with Semax, the near-totality of this work comes from Russian institutions closely associated with the compound's development.
The human evidence amounts to two comparator-controlled studies, both Russian-language. The first, published in 2008, studied 62 patients with generalised anxiety disorder and neurasthenia, comparing Selank in 30 patients against the benzodiazepine medazepam in 32, with the Hamilton, Zung and CGI scales plus serum enkephalin-degrading enzyme activity as outcomes; the anxiolytic effects of the two drugs were reported as similar, with Selank additionally showing antiasthenic and psychostimulant effects. The second, published in 2014, compared Selank with the benzodiazepine phenazepam in 60 patients with phobic-anxiety and somatoform disorders (ICD-10 F40.2-9, F41.1-9, F45.0-1) and reported pronounced anxiolytic and mild nootropic effects with the anxiolytic effect persisting about a week after the last dose. It is worth being precise here, because secondary sources routinely overstate it: the indexed 2014 abstract does not actually report a head-to-head statistical comparison showing Selank to be better tolerated than phenazepam, so that widely repeated claim is not supported by the record that can be checked. Both studies are active-comparator designs without a placebo arm, in modest samples, without independent replication, and neither is registered on any international trial registry. A ClinicalTrials.gov search on 7 August 2026 returned no registered Selank trial. So what exists is real human data (more than most compounds in this class can claim), but it is far too limited to establish efficacy to the standard a regulator outside Russia would require, and the absence of a placebo arm means the effect size cannot be separated from expectancy and natural course.
Evidence assessment
Limited evidence
Two small Russian active-comparator studies in anxiety disorders (n=62 and n=60) constitute the entire human evidence base: no placebo-controlled trial, no independent replication, no registered trial anywhere, and a mechanism that remains without an identified molecular target.
Tiers are applied consistently across the library and re-checked when new trials read out. Read the grading method.
Key studies
Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia Limited evidence
The anxiolytic effects of Selank and medazepam were reported as similar, with Selank additionally showing antiasthenic and psychostimulant effects; leu-enkephalin half-life, reduced at baseline, rose during Selank treatment, mainly in the generalised anxiety disorder subgroup.
A comparison of the anxiolytic effect and tolerability of selank and phenazepam in the treatment of anxiety disorders Limited evidence
Pronounced anxiolytic and mild nootropic effects of Selank were reported, with the anxiolytic effect persisting for about a week after the last dose and a positive impact on quality of life.
The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity Preclinical only
Selank inhibited enkephalin-degrading enzyme activity, providing the principal mechanistic hypothesis for its anxiolytic effect.
Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission Preclinical only
Selank altered expression of genes involved in GABAergic neurotransmission, suggesting a transcriptional route to anxiolysis distinct from direct receptor binding.
Peptide Selank Enhances the Effect of Diazepam in Reducing Anxiety in Unpredictable Chronic Mild Stress Conditions in Rats Preclinical only
Selank potentiated the anxiolytic effect of diazepam under chronic stress conditions, supporting an interaction with GABAergic signalling.
Selank, a Peptide Analog of Tuftsin, Attenuates Aversive Signs of Morphine Withdrawal in Rats Preclinical only
Selank reduced aversive withdrawal signs, consistent with the proposed involvement of the endogenous opioid system.
Effects of Selank on behavioral reactions and activities of plasma enkephalin-degrading enzymes in mice Preclinical only
Behavioural anxiolytic-like effects tracked with inhibition of plasma enkephalin-degrading enzyme activity.
Safety
Reported tolerability in the Russian trials is favourable, with the frequently repeated claim of no sedation, no cognitive slowing and no withdrawal or dependence on discontinuation, the specific liabilities that make benzodiazepines problematic. Local nasal irritation is the commonly reported complaint. Those findings come from short studies in small samples run by the developing institutions, so they establish the absence of obvious acute harm rather than a demonstrated long-term safety profile, and as noted above the comparative tolerability claim is weaker in the primary record than in the secondary literature. There is no published controlled data beyond a few weeks of exposure, no formal toxicology dossier in English, and no independent post-marketing surveillance accessible outside Russia. The mechanistic claim of opioid-system involvement deserves particular caution in anyone using opioids, since the literature explicitly documents interaction with morphine withdrawal.
Regulatory status
| Jurisdiction | Status |
|---|---|
| United Kingdom | No UK marketing authorisation. Not a controlled drug, but as an unlicensed medicinal product it may not lawfully be sold, supplied or advertised for human use under the Human Medicines Regulations 2012. |
| United States | Not FDA-approved for any indication. It is sold in the US only as an unapproved substance under a "research use only" label. |
| WADA (sport) | Not named on the WADA Prohibited List. As a substance without regulatory approval for human therapeutic use in most jurisdictions it would fall within the scope of category S0 (non-approved substances). |
Questions
No. It is a peptide with no affinity for the benzodiazepine site. Its proposed mechanism is inhibition of enkephalin-degrading enzymes, raising endogenous opioid peptide availability, plus effects on GABA-related gene expression. In rodents it lacks the sedation, motor impairment and withdrawal syndrome typical of benzodiazepines, though that has not been rigorously tested in humans.
Not in any published trial. Both human studies used an active benzodiazepine comparator: medazepam in 2008 (n=62) and phenazepam in 2014 (n=60). Without a placebo arm, the size of the drug-specific effect cannot be determined, and "as good as a benzodiazepine" in a small study with no described blinding is a much weaker claim than it sounds.
That claim is repeated everywhere but is not well supported by the primary record. The indexed abstract of the 2014 comparison with phenazepam reports Selank's own anxiolytic and mild nootropic effects; it does not report a head-to-head tolerability comparison. The better-tolerated framing should be treated as a plausible expectation from the mechanism, not a demonstrated result.
It is not a controlled drug, but it has no UK marketing authorisation. Under the Human Medicines Regulations 2012 an unlicensed medicinal product may not lawfully be sold, supplied or advertised for human use, which is why UK-facing sellers use the "research use only" framing.
Because the compound was designed, developed and registered there, and the research programme has been carried out largely by the institutions that created it. That is not evidence of fraud, but it does mean the findings have never been checked by an independent group with no stake in the outcome, the single most useful test any result can face.