Selank: what the research literature shows

What it is

From tuftsin to Selank

Review Tuftsin is the tetrapeptide Thr-Lys-Pro-Arg. It lies in the Fc region of the heavy chain of immunoglobulin G and is released from it by enzymes.² A 1989 review describes it as acting mainly on phagocytic cells, macrophages above all, where it raises phagocytosis, motility and bactericidal activity through specific receptors.²

Animal study Selank adds Pro-Gly-Pro to that sequence. A 1995 paper compared tuftsin with the heptapeptide, then coded TP-7, in rats whose serotonin system had been depleted soon after birth.⁵ Both peptides changed behaviour in stress tests and brought brain serotonin toward normal, and the authors described the effects of TP-7 as the more pronounced.⁵

Much of the later work cited here comes from Moscow institutes, among them the Institute of Molecular Genetics of the Russian Academy of Sciences and the Mental Health Research Center.⁷¹⁶

Sequence and chemistry

Values are from the two PubChem records.¹¹⁷

Three of the seven residues are proline. Two, lysine and arginine, are basic, so the peptide carries a net positive charge at neutral pH. It has no cysteine, methionine or tryptophan.¹

The tail and what enzymes do to it

Review A 2005 paper from Moscow describes short peptides that contain Pro-Gly-Pro as about as stable as major pharmacological preparations, and presents Selank and Semax as hybrids in which pieces of natural regulatory peptides help to stabilize the whole molecule in the body.³ Its abstract states this as a concept and reports no measurements.³ The wider idea is set out in our guide to half-life extension strategies.

Cell study The peptide is still cut. A study that labelled every residue with tritium followed the breakdown of Selank in blood plasma and, after administration in vivo, in brain tissue, and found its major products to be Thr-Lys-Pro-Arg-Pro, Thr-Lys-Pro, Arg-Pro and Gly-Pro.¹⁸ Tuftsin itself, Thr-Lys-Pro-Arg, is not among the major products that the abstract names.¹⁸

How it is studied

Three kinds of experiment recur, and they sit on different rungs of the evidence ladder.

• Cell study Bench and cell work: enzyme assays that follow the breakdown of enkephalin in blood plasma;⁶ binding of labelled GABA to brain-cell membranes;⁸ electrical recording from neurons in rat hippocampal slices;⁹ and gene-expression panels in a neuroblastoma cell line.¹⁹
• Animal study Rodent work: two mouse strains that differ in their emotional and stress reactions, scored in an open field;²⁰ and PCR panels or microarrays of rat frontal cortex, rat hippocampus and mouse spleen.⁷²¹²²
• Human study Clinical work: patients with anxiety-related disorders rated on psychometric scales against a benzodiazepine comparator;¹⁰ and healthy volunteers scanned with resting-state functional MRI.¹⁶

What the literature reports

Enkephalin-degrading enzymes

Enkephalins are opioid peptides made by the body, and enzymes in blood plasma break them down.²⁰²³

Cell study In a plasma assay, Selank inhibited the enzymatic hydrolysis of enkephalin in a concentration-dependent way, with half-maximal inhibition at 15 micromolar, and it was more potent than the peptidase inhibitors bacitracin and puromycin.⁶ The title offers this as a possible mechanism of its anxiolytic activity.⁶

Animal study In BALB/c mice, Selank was followed by less anxiety-like behaviour in the open field and a longer half-life of plasma leu-enkephalin; in C57Bl/6 mice it changed neither.²⁰ In a second mouse study, Selank reduced a behaviour induced by apomorphine, a drug that overstimulates the dopamine system, and the opioid blocker naloxone blocked that effect.²³ Selank did not displace labelled ligands from dopamine D2 or opioid receptors on rat brain membranes, so the authors proposed an indirect action through the enzymes.²³

GABA signalling

Animal study In the frontal cortex of rats, a panel of 84 neurotransmission genes was read one and three hours after Selank or GABA itself.⁷ Forty-five genes had changed at one hour and 22 at three hours, and the changes after Selank correlated positively with those after GABA at one hour.⁷

Cell study A later study in IMR-32 neuroblastoma cells gave a different picture. Selank alone changed the mRNA level of none of the genes studied; applied together with GABA, it almost completely suppressed the changes that GABA caused.¹⁹

Cell study In a radioligand assay, Selank changed the binding of labelled GABA to brain-cell membranes in the manner of a positive allosteric modulator, and it blocked the modulating activity of diazepam and olanzapine.⁸ In rat hippocampal slices, it raised the amplitude and frequency of spontaneous inhibitory currents in pyramidal neurons, sometimes after a brief fall, with no clear dependence on concentration across the range tested.⁹ The authors of the gene-expression and binding papers describe allosteric modulation of the GABA system as one possible mechanism.⁷⁸

Gene expression in brain and spleen

Animal study In the rat hippocampus, a microarray study found 36 genes whose mRNA changed more than two-fold after a single administration and 20 after a course; most encode proteins associated with the plasma membrane.²¹

Animal study A study of mouse spleen tested Selank and two fragments of it against a panel of 84 inflammation-related genes; 34 genes changed, and the gene Bcl6 changed after each of the three peptides.²²

Human evidence

The human studies we found are few, small and Russian. PubMed holds 68 records with Selank in the title or abstract; 29 are written in Russian and three are indexed as clinical trials.²⁴ Two of those are indexed as randomized controlled trials, though neither abstract describes randomization or blinding.¹⁰¹² For the Russian papers below we read the abstracts, not the full text.

• Human study Generalized anxiety disorder and neurasthenia, 2008. Thirty patients received Selank and 32 the benzodiazepine medazepam.¹⁰ The authors described the anxiolytic effects as similar, with added antiasthenic and psychostimulant effects for Selank, and reported that the half-life of leu-enkephalin in serum, short at baseline, rose during Selank treatment, mostly in generalized anxiety disorder.¹⁰
• Human study Phobic-anxiety and somatoform disorders, 2014. Sixty patients were studied in a comparison with phenazepam, another benzodiazepine.¹¹ The abstract describes the anxiolytic effect of Selank as pronounced and as lasting a week beyond treatment, and gives no group sizes or scores.¹¹
• Human study Add-on study, 2015. Thirty patients received phenazepam alone and 40 received phenazepam with Selank.¹² The authors reported an earlier response and a lower level of the benzodiazepine’s side effects, such as impaired attention and sedation, in the combined group.¹²
• Human study Healthy volunteers, 2020. Fifty-two participants received Selank, Semax or placebo and were scanned three times.¹⁶ Groups differed in functional connectivity between the right amygdala and the right temporal cortex; the abstract reports no measure of anxiety or cognition.¹⁶

A search of ClinicalTrials.gov on 8 October 2026 for Selank as an intervention returned two studies, both of non-invasive brain stimulation and neither of the peptide.²⁵

Regulatory status

• Russia. We could not search the Russian State Register of Medicines, so we state no registration details. Selank’s chemical name is absent from the government’s list of vital and essential medicines approved in December 2025.²⁶ A Russian clinical paper calls it a peptide preparation and a US review calls it a Russian drug; neither is a regulator’s statement.⁴¹²
• Canada. A search of Health Canada’s Drug Product Database on 8 October 2026 for Selank as an active ingredient returned no products.¹³ A Health Canada advisory of 9 April 2026 on unauthorized injectable peptide drugs does not name Selank among its examples; it states that a “For Research Use Only” label does not make such products legal or exempt them from regulatory requirements.²⁷
• United States. A search of the FDA’s approved-drug data on the same day returned no matches.¹⁴ An FDA page on compounding, current as of 22 April 2026, lists “Selank acetate (TP-7)” among bulk substances that were once in category 2 of its interim policies, the category for substances that may present significant safety risks, and were later withdrawn by their nominators.¹⁵ The entry says that compounded drugs containing it may pose a risk of immunogenicity because of possible aggregation and peptide-related impurities, and that the agency lacks important safety information.¹⁵
• European Union. The European Commission’s Union Register, which lists centrally authorized medicines, had no entry for Selank among its active or its no-longer-active products on 8 October 2026.²⁸ The register does not cover medicines authorized by single member states, which we did not check.

Material sold on this site is for laboratory research use only.

In the laboratory

Selank is supplied here as a lyophilized powder in sealed vials. A pre-mixed liquid format is also listed.

Mass is the first identity check. PubChem gives 751.9 g/mol for Selank and 500.6 g/mol for tuftsin, so a mass spectrum, where a batch document gives one, separates the heptapeptide from its parent and from shorter breakdown products.¹¹⁷ Our guide to analytical methods for peptides explains how a spectrum is read, and batch documents are posted on the Lab Results page when they exist.

With no cysteine, methionine or tryptophan, the sequence lacks the residues usually watched for oxidation.¹ The other routes of change are explained in peptide stability and degradation.

Cell study Enzymes cut Selank into four main fragments, and in the mouse spleen study two fragments of Selank changed gene expression when given on their own, so an assay run in plasma or serum may be reporting on fragments as well as on the parent peptide.¹⁸²²

For temperature, light and moisture, sealed and once opened, follow the peptide storage guide.