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Cognitive & nootropic

Selank

SelancTP-7TP-7 diacetateThr-Lys-Pro-Arg-Pro-Gly-Pro

Selank is a synthetic tuftsin-derived heptapeptide studied for anxiolytic and nootropic activity and registered as a prescription anxiolytic in Russia, though it is not FDA-approved.

Sequence fingerprint

TKPRPGP

  • Nonpolar4
  • Polar1
  • Basic (+)2
  • 7 residues

Thr-Lys-Pro-Arg-Pro-Gly-Pro

Overview

Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP). It is an analogue of the endogenous immunomodulatory peptide tuftsin, modified with a C-terminal Pro-Gly-Pro extension intended to improve metabolic stability relative to the parent tetrapeptide.

In preclinical and in vitro research, Selank has been reported to interact with the GABAergic system and to influence serotonergic and dopaminergic signalling, to alter the expression of brain-derived neurotrophic factor (BDNF) in the hippocampus, and to modulate cytokine balance (including interleukin-6) consistent with its tuftsin-derived origin. It has also been described as inhibiting enzymes that degrade enkephalins. Its reported anxiolytic-like activity is generally attributed to GABAergic modulation rather than to direct benzodiazepine-receptor binding.

Selank was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences and is registered in Russia as a prescription anxiolytic nasal spray (marketed as Selank/Selanc), with availability also reported in Ukraine. It is not approved by the US FDA or the UK MHRA, and most of the published efficacy and safety data come from Russian research groups, with limited independent international validation and limited long-term human safety, pharmacokinetic and drug-interaction data.

Outside Russia and Ukraine, Selank is handled as a research chemical. Material sold for laboratory use is not manufactured, tested, or labelled to pharmaceutical standards and is not intended for human or veterinary use.

Mechanism, evidence & status

Selank is a synthetic heptapeptide analogue of the endogenous immunomodulatory peptide tuftsin, extended at the C-terminus with a Pro-Gly-Pro tripeptide to improve metabolic stability. Preclinical reports describe modulation of GABAergic, serotonergic and dopaminergic signalling, inhibition of enkephalin-degrading enzymes, and altered expression of BDNF and cytokines such as IL-6. Its reported anxiolytic-like activity is attributed primarily to effects on the GABAergic system rather than to direct benzodiazepine-receptor binding.

Human evidence
Preclinical plus small Russian clinical studies; limited independent validation
Regulatory status
Registered and marketed as a prescription anxiolytic nasal spray (Selank/Selanc) in Russia, with availability also reported in Ukraine. NOT approved by the US FDA or the UK MHRA; outside Russia/Ukraine it is unlicensed and handled only as a research chemical.
Research applications
  • Investigated in animal and in vitro models as an anxiolytic-like and antiasthenic agent acting on GABAergic and monoaminergic pathways.
  • Studied as a nootropic / neuroprotective candidate, including effects on BDNF expression in the hippocampus.
  • Examined for immunomodulatory activity (cytokine and IL-6 expression) reflecting its tuftsin-derived origin.
  • Used as a tool compound to probe enkephalin metabolism and peptide-based modulation of neurotransmitter systems.
Safety considerations
  • Most published safety and efficacy data derive from Russian research institutions; independent international trials and long-term human safety data are limited (Wikipedia; review literature).
  • Reported pharmacology suggests anxiolytic activity without the tolerance, dependence or marked sedation associated with benzodiazepines, but this profile has not been confirmed by large independent trials (PMC review).
  • Not approved by the FDA or MHRA; material sold for research is not manufactured, tested, or labelled to pharmaceutical standards and is not intended for human or veterinary use.
  • Comprehensive human pharmacokinetic, drug-interaction and chronic-toxicity data are not well characterized in the international literature.
References