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Research · October 10, 2026 · By Prime Peptide Solutions

Selank: Mechanism of Action and Research Applications

A research overview of Selank, the tuftsin-derived heptapeptide: identity data, GABA-binding, gene-expression and monoamine findings by study model, key studies and handling.

Selank: Mechanism of Action and Research Applications

What Is Selank?

Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro (one-letter code TKPRPGP). Its first four residues are tuftsin, an immunoglobulin-derived tetrapeptide, and the last three are a Pro-Gly-Pro extension. In laboratory research Selank is studied for its effects on gene expression in rodent brain and spleen, on GABA receptor binding in brain membranes, on monoamine levels in rodents, and on peptide-degrading enzymes. The literature refers to it simply as Selank or by its sequence; it is sometimes described as a tuftsin analog.

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Selank shares its Pro-Gly-Pro ending with Semax, which is built on a fragment of ACTH instead of tuftsin. This page covers Selank on its own. For the pair, see the Selank vs Semax comparison and the combined Selank and Semax overview; for a different neuropeptide pairing, see DSIP vs Selank.

This article is a scientific overview for laboratory researchers. The research-grade Selank supplied by Prime Peptide Solutions is sold strictly for in-vitro laboratory research. It is not approved for human use and is not for human or animal consumption.

Structure and Background

Tuftsin, the parent sequence

Tuftsin was described in 1970 as a natural peptide that stimulates phagocytosis (Najjar and Nishioka, 1970). It is the tetrapeptide Thr-Lys-Pro-Arg, located in the Fc domain of the immunoglobulin G heavy chain and released from it by enzymatic processing (Fridkin and Najjar, 1989). A 1983 overview describes two cleavage steps: a splenic enzyme that cuts after the arginine and an enzyme on the outer side of the cell membrane that cuts before the threonine (Najjar, 1983).

Selank adds Pro-Gly-Pro to that tetrapeptide. A 2005 review places Pro-Gly-Pro among the glyprolines, describes them as unusually stable for regulatory peptides, and presents Selank and Semax as hybrid peptides in which the PGP part helps stabilize the whole molecule (Ashmarin et al., 2005). The extension also changes what the peptide does in some models: in one rat study, Selank and tuftsin had different effects on brain serotonin metabolism (see below).

Molecule at a Glance

  • Sequence: H-Thr-Lys-Pro-Arg-Pro-Gly-Pro-OH (7 residues)
  • Termini: free N-terminal amine and free C-terminal carboxylic acid
  • Molecular formula: C33H57N11O9
  • Molecular weight: 751.9 g/mol (monoisotopic mass 751.43 Da)
  • CAS number: 129954-34-3
  • PubChem CID: 11765600
  • Composition notes: three prolines (positions 3, 5 and 7); no cysteine or methionine, so no sulfur; no aromatic residues
  • Charge: lysine, arginine and the free N-terminus against one C-terminal carboxyl give a net charge of roughly +2 near pH 7
  • Not the same as: N-acetyl Selank amidate, a separate compound with both ends modified

Why molecular weights differ between sources

The formula and molecular weight above are for the free peptide, as PubChem lists it. Synthetic peptides are often isolated as acetate or trifluoroacetate salts, so the mass of a weighed powder is not all peptide. Molecular weight, HPLC purity and net peptide content are separate numbers, and a batch lab report states which were measured.

Proposed Mechanism of Action

No receptor that binds Selank directly has been identified. Published work points to several indirect routes: modulation of GABA binding to GABA receptors, broad shifts in gene expression in brain and spleen, strain-dependent changes in monoamine levels, and inhibition of enzymes that break down enkephalins and other regulatory peptides. The findings below are grouped by study model, and they come from cell-free systems, cell lines and rodents.

Research Findings by Study Model

Cell-free systems and cell lines

  • GABA receptor binding. In radioligand assays with rat brain plasma membranes, Selank changed [3H]GABA binding in the manner of a positive allosteric modulator. Combined with benzodiazepines, its effect was not additive, and it blocked the modulatory activity of diazepam and olanzapine; the authors conclude the binding sites are not the same but may partly overlap (Vyunova et al., 2018).
  • GABAergic gene expression in a neuroblastoma line. In IMR-32 human neuroblastoma cells, Selank alone did not change mRNA levels of 84 genes linked to GABAergic signaling and neurotransmission. Added together with GABA, it almost completely suppressed the expression changes that GABA caused on its own, and with olanzapine it widened the set of genes that changed (Filatova et al., 2017).
  • Peptidase inhibition. In human serum in vitro, Selank inhibited enkephalin-degrading enzymes with an IC50 of about 20 micromolar, against about 10 micromolar for Semax; pentapeptide fragments of both peptides were also active, while tri-, tetra- and hexapeptide fragments were not (Kost et al., 2001).
  • Breakdown in plasma. Using evenly tritium-labelled peptide, the main products of Selank degradation in blood plasma were the pentapeptide TKPRP, the tripeptide TKP and the dipeptides RP and GP (Zolotarev et al., 2006).

Rodent studies

  • Neurotransmission genes in rat frontal cortex. Real-time PCR of 84 genes involved in neurotransmission, including GABA receptor subunits, transporters, ion channels and dopamine and serotonin receptors, showed significant changes in 45 genes one hour after Selank or GABA and in 22 genes three hours after either compound. The changes after Selank correlated positively with those after GABA, which the authors interpret as support for allosteric modulation of the GABAergic system (Volkova et al., 2016).
  • Hippocampal transcriptome. A cDNA microarray study in rats found more than two-fold changes in the mRNA levels of 36 genes after a single administration and 20 genes after repeated administration, most encoding plasma-membrane-associated proteins, which led the authors to propose effects on ion homeostasis in hippocampal cells (Kolomin et al., 2013). The same group reported transcriptomic responses in both rat hippocampus and spleen cells (Kolomin et al., 2010).
  • BDNF. Selank regulated expression of brain-derived neurotrophic factor (BDNF) in the rat hippocampus in vivo (Inozemtseva et al., 2008).
  • Inflammation-related genes in mouse spleen. Of 84 genes for chemokines, cytokines and their receptors, 34 changed significantly 6 and 24 hours after Selank. Bcl6, a regulator of immune-cell development, changed after Selank and after each of two Selank fragments (Kolomin et al., 2011). A time-course study found a three-fold drop in complement C3 mRNA 30 minutes after Selank, a wave-like pattern for Casp1, early changes in Il2rg and a fall in Xcr1 at 90 minutes, with closely matching profiles for the dipeptide Gly-Pro (Kolomin et al., 2014).
  • Monoamines in two mouse strains. In BALB/c and C57Bl/6 mice, Selank raised hypothalamic norepinephrine in both strains, but its effects on dopamine metabolites ran in opposite directions: up in frontal cortex and hippocampus of C57Bl/6 mice, down in BALB/c mice. Hippocampal serotonin and 5-HIAA fell in BALB/c mice only (Narkevich et al., 2008).
  • Selank vs tuftsin. In rats given the serotonin-synthesis inhibitor PCPA beforehand, Selank increased serotonin metabolism in the brain stem 30 minutes later, while tuftsin did not and instead lowered it in the neocortex (Semenova et al., 2009).

Human data

This laboratory overview is limited to cell-free, cell line and rodent studies. Clinical literature is outside its scope and is not summarized here.

Key Studies

  • Vyunova et al., 2018 (Protein Pept Lett): radioligand study of Selank and [3H]GABA binding in rat brain membranes. PubMed 30255741
  • Volkova et al., 2016 (Front Pharmacol): expression of 84 neurotransmission genes in rat frontal cortex. PubMed 26924987
  • Filatova et al., 2017 (Front Pharmacol): GABAergic gene expression in IMR-32 cells with Selank, GABA and olanzapine. PubMed 28293190
  • Kolomin et al., 2011 (Regul Pept): inflammation-related gene expression in mouse spleen. PubMed 21609736
  • Kolomin et al., 2014 (Mol Immunol): time course of C3, Casp1, Il2rg and Xcr1 expression; Selank vs Gly-Pro. PubMed 24291245
  • Narkevich et al., 2008 (Eksp Klin Farmakol): monoamines and metabolites in two mouse strains. PubMed 19093364
  • Kost et al., 2001 (Bioorg Khim): enkephalin-degrading enzyme inhibition in human serum. PubMed 11443939
  • Zolotarev et al., 2006 (Bioorg Khim): biodegradation products of tritium-labelled Selank. PubMed 16637290

Stability and Laboratory Handling

Storing the lyophilized peptide

Selank in our catalog is supplied as a lyophilized powder in a sealed vial; the product page gives storage at 2-8 °C, or -20 °C for long-term storage. Keep vials cold, dry and away from light. With no methionine or cysteine, Selank lacks the residues most prone to oxidation, but like most lyophilized peptides it takes up moisture, so a cold vial should reach room temperature, ideally in a desiccator, before it is opened, and be resealed tightly afterward. See our guides to storing research peptides and lyophilization.

Detection and degradation products

Because Selank has no tryptophan, tyrosine or phenylalanine, it absorbs very little at 280 nm, and HPLC methods detect it through peptide-bond absorbance in the low-UV range (around 214-220 nm). In plasma it is cut into TKPRP, TKP, RP and GP, so labs that run it in biological media can use those fragment masses to read chromatograms and mass spectra.

Verifying identity and purity

A batch lab report documents identity and purity: HPLC gives a purity figure, and mass spectrometry checks that the observed mass matches the expected one, about 751.43 Da (monoisotopic) for Selank. See how to read a peptide COA and how HPLC and mass spec verify purity.

Frequently Asked Research Questions

What is Selank?

A synthetic seven-residue peptide, Thr-Lys-Pro-Arg-Pro-Gly-Pro: the tuftsin tetrapeptide extended with Pro-Gly-Pro. It is studied in cell, membrane and rodent models for effects on GABA receptor binding, gene expression and monoamine levels.

Is Selank the same as tuftsin?

No. Tuftsin is the four-residue peptide Thr-Lys-Pro-Arg from immunoglobulin G. Selank adds Pro-Gly-Pro, and in a rat study the two peptides had different effects on brain serotonin metabolism.

What receptor does Selank act on?

No direct receptor has been identified. In rat brain membranes it behaves like a positive allosteric modulator of GABA binding, while in IMR-32 cells it did not change GABAergic gene expression on its own.

Why do Selank studies also test Gly-Pro?

Gly-Pro is one of the fragments Selank breaks down into. In mouse spleen, Gly-Pro produced expression profiles that closely matched those of Selank for several immune genes, which suggests the dipeptide may contribute to the parent peptide's effects.

How does Selank differ from Semax?

Both end in Pro-Gly-Pro, but Selank starts from tuftsin and Semax from the ACTH(4-7) core. Semax contains a methionine and Selank does not. See the Selank vs Semax comparison.

What is the research-grade Selank sold here intended for?

The research-grade Selank sold by Prime Peptide Solutions is supplied strictly for in-vitro laboratory research. It is not for human or animal consumption.

Conclusion

Selank is the tuftsin tetrapeptide extended with Pro-Gly-Pro: seven residues, three prolines, no sulfur and no aromatic side chains. No direct receptor is known. Membrane binding studies point to allosteric modulation of GABA binding, rodent studies show broad and time-dependent changes in brain and spleen gene expression and strain-dependent monoamine shifts, and in vitro work shows inhibition of serum enkephalin-degrading enzymes and a defined set of breakdown fragments. For laboratories, the practical points are cold, dry storage, low-UV detection and identity checks against a monoisotopic mass of about 751.43 Da.

Disclaimer: This article is provided for educational and research purposes only. It summarizes publicly available scientific literature and does not constitute medical advice. Selank and all peptide compounds sold by Prime Peptide Solutions are intended strictly for laboratory research, are not approved for human use, and are not for human or animal consumption. Researchers are responsible for compliance with all applicable regulations in their jurisdiction.

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Selank · 10mg
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References & Further Reading

Research-Grade Selank

In our catalog, research-grade Selank is listed as Selank, supplied as a lyophilized powder in one size, a 10mg vial. Published lab reports (COAs) are listed on our COAs page.

Sold strictly for in-vitro laboratory research. Not for human or animal consumption.

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