Selank — Tuftsin-Derived Heptapeptide (RUO)

Selank is a synthetic heptapeptide structurally derived from the endogenous tetrapeptide tuftsin. It serves as a specialized mechanistic probe for investigating peptide stability and neuroimmune-associated signaling markers. While structurally related to tuftsin, research indicates Selank possesses a distinct pharmacological profile and does not strictly replicate the biological activity of its parent molecule.

Peptide Name:
Selank
Peptide Class:
Synthetic Heptapeptide
Sequence Length:
7 Amino Acids
Primary Research Focus:
Neuroimmune-Associated Signaling
Form:
Lyophilized Powder
Regulatory Status:
Research Grade Material (RUO)
Amino Acid Sequence:
Thr–Lys–Pro–Arg–Pro–Gly–Pro
Chemical Formula:
C₃₃H₅₇N₁₁O₉
Molecular Weight
~751.9 g/mol
Molecular Design Note:
Selank incorporates the C-terminal Pro–Gly–Pro (PGP) tripeptide sequence. This modification is critical to enhanced structural stability and resistance to rapid enzymatic degradation in biological matrices.
Store powder at +4°C (short term) or -20°C (long term). Keep desiccated.
For laboratory research use only. Reconstitute using sterile bacteriostatic water consistent with established laboratory research protocols. Preparation should be performed under aseptic conditions. Reconstituted material is not intended for long-term storage.
Molecular Weight

Selank is utilized as a reference compound to investigate modulation of monoamine neurotransmitter metabolism within the central nervous system.

  • Monoamine Metabolism: Studies measuring turnover rates of norepinephrine, dopamine, and serotonin in discrete brain regions (e.g., hypothalamus, frontal cortex).
  • Enzymatic Regulation: Investigation of peptide influence on tyrosine hydroxylase activity, the rate-limiting enzyme in catecholamine synthesis.

Transcriptomic analyses in rodent models suggest Selank may influence expression of gene clusters associated with neuronal plasticity and membrane dynamics.

  • BDNF Expression: Measurement of Brain-Derived Neurotrophic Factor (BDNF) mRNA upregulation in hippocampal tissue following peptide exposure.
  • GABAergic System: Evaluation of modulation in GABA receptor subunit gene expression, distinguishing Selank’s signaling profile from classical benzodiazepines.

Given its derivation from tuftsin (an immunomodulatory peptide), Selank is employed to study crosstalk between nervous and immune systems.

  • Cytokine Modulation: Assays measuring changes in pro-inflammatory cytokine profiles (e.g., IL-6) in stress-exposed models.
  • Immune Signaling: Investigation into whether Selank retains partial phagocytosis-associated signaling properties of native tuftsin in microglial cells.

The C-terminal PGP motif makes Selank a valuable model for evaluating peptide stability and enzymatic resistance.

  • Enkephalinase Inhibition: Studies suggesting Selank may inhibit enzymes responsible for endogenous enkephalin degradation.
  • Serum Stability: Comparative degradation assays versus native tuftsin to quantify stabilization effects of the PGP modification.
  • Mechanism Complexity: Precise receptor targets remain incompletely defined; observed effects may be pleiotropic or allosteric.
  • Model Dependency: Behavioral outcomes vary depending on stress paradigms employed (e.g., elevated plus maze vs. open field).
  • Translation Gaps: While gene expression changes are measurable, direct correlation to behavioral phenotypes remains under investigation.
  • Volkova, A. A., et al. (2016) “Selank, a tuftsin analog, and its fragments affect the expression of genes involved in GABAergic neurotransmission.” Frontiers in Pharmacology.
  • Sokolov, O. Y., et al. (2002) “Effects of Selank on behavioral reactions and monoamine content in rat brain structures.” Vestnik Rossiiskoi Akademii Meditsinskikh Nauk.
  • Uchakina, O. N., et al. (2008) “Immunomodulatory effects of Selank in patients with anxiety-asthenic disorders.” Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova.
  • Kost, N. V., et al. (2001) “Beta-casomorphins-7 and the tuftsin analogue Selank inhibit enkephalin degradation.” Bioorganicheskaia Khimiia.
  • Semenova, T. P., et al. (2009) “Comparison of Selank and tuftsin effects on serotonin metabolism.” Neuroscience and Behavioral Physiology.
  • Inozemtseva, L. S., et al. (2008) “The role of the dopamine system in the mechanism of action of Selank.” Doklady Biological Sciences.
The compound listed below is referenced in research contexts related to the mechanisms discussed in this article.
Selank is a chemical reference standard intended strictly for in-vitro and laboratory research applications (e.g., receptor binding assays, gene expression analysis). It is not a drug, dietary supplement, or anxiolytic for human consumption. It is not intended for therapeutic use or injection. All handling must be performed by qualified professionals in a laboratory setting.

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