Selank

Research · Selank

Overview

Selank is a synthetic seven-residue analog of tuftsin, an immunomodulatory tetramer derived from the Fc region of immunoglobulin G. Its sequence, Thr-Lys-Pro-Arg-Pro-Gly-Pro, extends the native Thr-Lys-Pro-Arg motif with a C-terminal Pro-Gly-Pro glyproline segment that increases metabolic stability. Developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, it is studied as a reference compound in anxiolytic, stress-response, and immunomodulation research. It shares the glyproline stabilizing strategy with Semax, and the two compounds are frequently compared in Russian neuropharmacology literature. Studies have examined its behavioral, gene-expression, and immunological profiles in rodent models and cultured neuronal cells.

Mechanism of action

A single high-affinity receptor has not been identified, and the proposed mechanisms are multiple. The compound has been reported to inhibit enkephalin-degrading enzymes in human plasma, prolonging the half-life of endogenous enkephalins. Gene-expression studies report modulation of transcripts involved in GABAergic neurotransmission, and allosteric interaction with GABA-A receptors has been proposed. Further reported effects include altered expression of inflammation-related genes and cytokines, consistent with the immunomodulatory activity of the parent tuftsin sequence, as well as effects on monoamine metabolism in rodent brain. Its metabolic fragments, including shorter glyproline-containing sequences, have been proposed to contribute independently to the observed activity profile, complicating attribution to the intact seven-residue molecule.

Key research findings

1. 01

   In vitro assays demonstrate inhibition of enkephalin-degrading enzyme activity in human serum, proposed as a contributor to its behavioral profile.

2. 02

   Rodent and cell-culture studies characterize changes in expression of genes involved in GABAergic neurotransmission following exposure.

3. 03

   Preclinical stress models characterize behavioral endpoints in anxiety-related paradigms and associated changes in cytokine levels.

4. 04

   Primary research is published in Russian-language journals and remains uncharacterized in Western clinical databases.

Published references

• The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity

  Zozulya AA et al. — Bull Exp Biol Med, 2001 · PMID: 11550013

• Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission

  Volkova A et al. — Front Pharmacol, 2016 · PMID: 26924987

The information above is derived from published preclinical and clinical research. It is provided for educational purposes only and does not constitute medical advice, diagnosis, or treatment recommendations.