What Is Selank? The Tuftsin-Derived Heptapeptide

Selank is a synthetic heptapeptide, Thr-Lys-Pro-Arg-Pro-Gly-Pro. It extends tuftsin, a tetrapeptide fragment of immunoglobulin G, with a Pro-Gly-Pro tail. Like Semax, it came out of the Institute of Molecular Genetics in Moscow, and the two share that C-terminal PGP motif. Its research literature centres on GABA signalling and on enzymes that degrade enkephalins.

For laboratory research use only. The compounds discussed are not approved for human or veterinary use and are not drugs, foods or cosmetics. This article summarises published research and is not medical advice.

Key points

Sequence TKPRPGP; C₃₃H₅₇N₁₁O₉, 751.9 g/mol.
Built on tuftsin (Thr-Lys-Pro-Arg) plus Pro-Gly-Pro.
Basic peptide: lysine and arginine give it a net positive charge.
Described as a positive allosteric modulator of GABA binding in rat brain membranes.
Degraded in plasma to TKPRP, TKP, RP and GP.

Quick facts

Property	Value
Sequence	Thr-Lys-Pro-Arg-Pro-Gly-Pro
Formula / weight	C₃₃H₅₇N₁₁O₉, 751.9 g/mol (PubChem CID 11765600)
Parent peptide	Tuftsin (Thr-Lys-Pro-Arg), from immunoglobulin G
C-terminal extension	Pro-Gly-Pro
Charge at neutral pH	Net positive (Lys, Arg)
Status	Not approved in the US or EU

Our Selank research peptide is supplied in 5 mg and 10 mg vials with lot-level HPLC and MS data.

GABA-related research

Two strands of work connect Selank to GABAergic signalling:

Approach	Finding	Study
Radioligand binding, rat brain membranes	Selank affected [³H]GABA binding as a positive allosteric modulator; its combined action with benzodiazepines was not simply additive	Vyunova et al., 2018
Real-time PCR, 84 neurotransmission genes, rat frontal cortex	45 genes changed 1 h after Selank or GABA; 22 genes at 3 h; changes correlated between the two substances	Volkova et al., 2016

The second study is notable because it compared Selank directly with GABA itself and found correlated expression changes, which the authors interpreted as evidence of a shared basis of action. Other rodent work has examined Selank in models of morphine withdrawal (Konstantinopolsky et al., 2022) and ethanol-induced memory impairment, where BDNF content in the hippocampus and prefrontal cortex was measured (Kolik et al., 2019).

Enkephalinase inhibition

Selank also acts on enzymes rather than receptors. Using tritium-labelled Leu-enkephalin to measure peptidase activity in human plasma, Zolotarev and colleagues found that aminopeptidases accounted for about 80% of total enkephalin-degrading activity, dipeptidylaminopeptidases about 2% and dipeptidylcarboxypeptidases about 10%. Against this background, Selank was more specific for carboxypeptidases and dicarboxypeptidases, whereas the reference inhibitor bestatin acted mainly on aminopeptidases (Zolotarev et al., 2004). Slowing enkephalin breakdown is a different kind of mechanism from direct receptor binding, and it may explain some findings in opioid-related models.

How Selank is broken down

Tritium-labelling work in blood plasma identified the major degradation products as the pentapeptide TKPRP, the tripeptide TKP, and the dipeptides RP and GP (Zolotarev et al., 2006). Degradation therefore proceeds from both ends. The same paper examined Semax in parallel, which is why the two peptides are often discussed together; see Semax vs Selank.

Fragment	Origin
TKPRP	Loss of the C-terminal Gly-Pro
TKP	Further N-terminal-side fragment
RP, GP	Dipeptide products

The shared Pro-Gly-Pro motif

Selank and Semax were developed by the same institute and share the C-terminal Pro-Gly-Pro extension, added to short regulatory peptides as a stabilising modification. The front halves differ completely: tuftsin in Selank, an ACTH fragment in Semax. PGP is not inert, since it activated neurotrophin transcription on its own in a rat ischemia model, so experiments comparing the two peptides often include PGP as a separate control.

Half-life

We did not find a peer-reviewed human pharmacokinetic study reporting a half-life for Selank. The plasma degradation data above are consistent with rapid processing, which is typical for small unmodified peptides. N-acetylated versions are sold on the basis of improved stability; see N-acetyl Selank amidate.

Handling in the lab

Store lyophilized powder at −20 °C, sealed and dark.
Highly water-soluble thanks to its basic residues; reconstitute with bacteriostatic or sterile water (method).
No methionine or cysteine, so Selank is less oxidation-sensitive than Semax.
Keep solutions at 2–8 °C and avoid repeated freeze–thaw (storage guide).
Calculate concentrations with the peptide reconstitution calculator.

Open questions

What is Selank’s human pharmacokinetic profile, including half-life and brain exposure?
Does it interact with a specific binding site, or are its effects secondary to peptidase inhibition and gene-expression changes?
Have the GABA findings been replicated outside the originating research network?

Related research

Frequently asked questions

What is Selank?

Selank is a synthetic heptapeptide, Thr-Lys-Pro-Arg-Pro-Gly-Pro. It combines tuftsin, a tetrapeptide derived from immunoglobulin G, with a C-terminal Pro-Gly-Pro tripeptide. It was developed at the Institute of Molecular Genetics in Moscow.

What does Selank do in research models?

Radioligand studies describe it as a positive allosteric modulator of GABA binding in rat brain membranes. Gene-expression work found changes in many neurotransmission-related genes after administration, and it inhibits enkephalin-degrading enzymes in human plasma.

How is Selank broken down?

In blood plasma, tritium-labelling studies identified the pentapeptide TKPRP, the tripeptide TKP and the dipeptides RP and GP as the major degradation products.

What is the half-life of Selank?

We did not find a peer-reviewed human half-life value. The degradation data indicate rapid enzymatic processing in plasma, as expected for a short unmodified peptide.

What is Selank's molecular weight?

About 751.9 g/mol (C33H57N11O9).

References

Vyunova TV, et al. Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. Protein Pept Lett. 2018. PMID: 30255741 https://pubmed.ncbi.nlm.nih.gov/30255741/
Volkova A, et al. Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Front Pharmacol. 2016. PMID: 26924987 https://pubmed.ncbi.nlm.nih.gov/26924987/
Zolotarev IuA, et al. [Leu-enkephalin homogeneously labeled with tritium in studying the Selank inhibiting effect on the enkephalin-degrading enzymes of human plasma]. Bioorg Khim. 2004. PMID: 15344652 https://pubmed.ncbi.nlm.nih.gov/15344652/
Zolotarev IuA, et al. [Evenly tritium-labeled peptides and their in vivo and in vitro biodegradation]. Bioorg Khim. 2006. PMID: 16637290 https://pubmed.ncbi.nlm.nih.gov/16637290/
Konstantinopolsky MA, et al. Selank, a Peptide Analog of Tuftsin, Attenuates Aversive Signs of Morphine Withdrawal in Rats. Bull Exp Biol Med. 2022. PMID: 36322304 https://pubmed.ncbi.nlm.nih.gov/36322304/
Kolik LG, et al. Selank, Peptide Analogue of Tuftsin, Protects Against Ethanol-Induced Memory Impairment by Regulating of BDNF Content in the Hippocampus and Prefrontal Cortex in Rats. Bull Exp Biol Med. 2019. PMID: 31625062 https://pubmed.ncbi.nlm.nih.gov/31625062/
PubChem Compound Summary for CID 11765600, Selank. National Center for Biotechnology Information. https://pubchem.ncbi.nlm.nih.gov/compound/11765600