Is Selank approved in the UK?

No. It has a Russian registration history but holds no MHRA, EMA or FDA authorisation, and is supplied for laboratory research only.

No. Reported work describes it slowing the breakdown of the body's own enkephalins by inhibiting enkephalin-degrading enzymes, rather than binding opioid receptors itself.

Selank (Tuftsin Analogue)

What Is Selank? A Complete Research Overview

JMWritten & reviewed by Jack Muncaster · Founder, UK PeptidesLast reviewed 2026-08-234 cited sources

Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro, developed at the Institute of Molecular Genetics of the Russian Academy of Sciences. It combines tuftsin, an immunomodulatory tetrapeptide from immunoglobulin G, with a Pro-Gly-Pro extension that confers resistance to enzymatic degradation.

Key facts

Sequence: Thr-Lys-Pro-Arg-Pro-Gly-Pro
Single-letter: TKPRPGP
Length: 7 residues (heptapeptide)
Molecular weight: 751.9 Da
Molecular formula: C33H57N11O9
CAS number: 129954-34-3
PubChem CID: 11765600
Development code: TP-7
Western approval: None — not MHRA, EMA or FDA approved

What it is built from

Selank has two parts. The first four residues, Thr-Lys-Pro-Arg, are tuftsin — a naturally occurring tetrapeptide released from the heavy chain of immunoglobulin G, long studied for immunomodulatory activity. The remaining three, Pro-Gly-Pro, are a stabilising extension. The design intent is to retain tuftsin's activity while giving it a useful duration in circulation.

Why the extension was necessary

Tuftsin on its own is degraded rapidly. Proline-containing motifs resist most peptidases, because proline's side chain bonds back to its own backbone nitrogen and locks the rotation that proteolytic enzymes need at their active site. Appending Pro-Gly-Pro therefore converts a fragile tetrapeptide into something that survives long enough to be studied — the same approach, from the same institute, that produced Semax from an ACTH fragment.

Research material referenced

Selank 10mg — third-party HPLC tested

View — £24.99

The mechanism that distinguishes it

The most specific reported activity is not receptor binding at all. Selank has been reported to inhibit enkephalin-degrading enzymes, extending the half-life of the body's own enkephalins rather than acting as an opioid ligand itself. Work from 2001 and 2002 in the Bulletin of Experimental Biology and Medicine measured this directly on plasma enkephalinase activity.

Other reported activity

Published work also describes effects on GABAergic signalling, on serotonergic and dopaminergic transmission, and on brain-derived neurotrophic factor expression. A 2008 study reported that intranasally administered Selank regulates BDNF expression in the rat hippocampus. As with Semax, the great majority of this is rodent work.

The evidence base, described honestly

PubMed indexes roughly 135 Selank records — a smaller literature than its parent peptide tuftsin, which has around 690. The mechanistic work appears in international journals; the clinical work is concentrated in Russian-language publications, principally the Korsakov Journal of Neurology and Psychiatry. That is a description of where the evidence sits, not a dismissal of it.

Regulatory position

Selank has a registration history in the Russian Federation. It holds no marketing authorisation from the MHRA, EMA or FDA, cannot be prescribed or dispensed in the UK, and is supplied here for laboratory research only. A registration granted by one national regulator confers nothing in any other jurisdiction.

Extended research context

The Selank (Tuftsin Analogue) deep dive

Deep dive: preserving a signal rather than supplying one

Selank's most specifically characterised activity is not receptor binding. Work published in the Bulletin of Experimental Biology and Medicine in 2001 and 2002 reported that it inhibits enkephalin-degrading enzymes, measured directly on plasma enkephalinase activity, thereby extending the half-life of endogenous enkephalins rather than acting at opioid receptors itself. That distinction is routinely muddled and it matters: an agonist activates the receptor wherever the drug reaches, at whatever concentration is given, while a degradation inhibitor only lets the ligand the body is already releasing persist longer. The effect is bounded by endogenous release and occurs only where that release happens. The same logic underlies DPP-4 inhibitors in the incretin field, which prolong native GLP-1 rather than supplying an analogue - and instructively, that class produces much smaller effects than the receptor agonists do.

Deep dive: what the sequence does and does not contain

TKPRPGP is unusual among research peptides for what is absent from it. There is no cysteine, so no disulfide bonds form or scramble and no reducing agent is needed. There is no methionine, so the thioether oxidation that adds 16 Da and dominates handling guidance for MOTS-c and Semax does not apply. There is no asparagine or glutamine either, ruling out deamidation. What remains is straightforward hydrolysis, and three prolines in seven residues resist even enzymatic cleavage well, because proline locks the backbone rotation peptidases require. One practical cost of that composition: no aromatic residues means almost no absorbance at 280 nm, so the standard spectrophotometric quantification method does not work on it.

Deep dive: reading a two-literature evidence base

PubMed indexes roughly 135 Selank records against about 690 for its parent peptide tuftsin - an inversion worth noticing, since most designed analogues eventually outgrow the parent they replaced. Most of the tuftsin literature is immunological and predates Selank entirely, so it is not evidence about Selank. Within Selank's own record the split is the same one Semax shows: mechanistic work in internationally indexed journals, assessable directly; clinical work concentrated in Russian-language publications, indexed by translated title and often without accessible English full text. That is evidence which is hard to verify independently, which is not the same as evidence that is absent, and not the same as evidence that is established.

Research applications

▸Enkephalin and enkephalinase pathway research
▸GABAergic receptor expression studies in rodent models
▸BDNF expression research, including intranasal administration routes
▸Comparative work on proline-stabilised peptide design
▸Tuftsin and immunopeptide structure-activity research

Handling checklist

✓Store lyophilised material cold, dry and protected from light
✓No reducing agent needed — the sequence contains no cysteine
✓No methionine oxidation to expect; a +16 Da satellite warrants explanation
✓Do not rely on 280 nm absorbance — there are no aromatic residues
✓Introduce diluent gently against the vial wall; swirl rather than shake
✓Aliquot to avoid repeated freeze-thaw cycles

Common research-handling mistakes

Learnt from thousands of researcher orders across our UK labs.

✗ Describing Selank as an opioid or opioid agonist

Fix: Reported work describes inhibition of enkephalin-degrading enzymes, not receptor binding. It preserves endogenous enkephalins rather than supplying an agonist.

✗ Treating the benzodiazepine contrast as a safety claim

Fix: The mechanistic difference is real — expression-level rather than direct allosteric modulation — but it supports no comparative claim about safety or dependence.

✗ Citing tuftsin literature as evidence about Selank

Fix: Tuftsin has roughly five times more papers, most of them immunological and predating Selank. They are different compounds.

✗ Reading a BDNF expression change as a demonstrated outcome

Fix: The work measured expression in rat hippocampus. Expression is upstream of function and upstream again of any clinical claim.

✗ Treating Russian registration as equivalent to MHRA approval

Fix: Authorisations are jurisdictional and do not transfer. Selank has never been assessed by the MHRA, EMA or FDA.

Continue researching

Peer-reviewed guides, comparators and matched reference materials.

Frequently asked questions

Is Selank approved in the UK?: No. It has a Russian registration history but holds no MHRA, EMA or FDA authorisation, and is supplied for laboratory research only.
What is Selank made from?: Tuftsin, a tetrapeptide from immunoglobulin G, with a Pro-Gly-Pro extension appended for stability.
Is Selank an opioid?: No. Reported work describes it slowing the breakdown of the body's own enkephalins by inhibiting enkephalin-degrading enzymes, rather than binding opioid receptors itself.

Primary sources & clinical trials

Peer-reviewed research and registered trials from PubMed, ClinicalTrials.gov, PubChem, FDA and NIH. All links open in a new tab and point to the primary source, so every claim can be verified at origin.

Written and reviewed by

Jack Muncaster · Founder, UK Peptides

Jack founded UK Peptides in Manchester after repeatedly receiving research compounds with missing or recycled paperwork. He is responsible for supplier selection, batch release decisions and the content published in this research library. Every article here is sourced to primary literature and every product page to a signed third-party certificate.

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