No.Β 12Tuftsin analoguePhase II

Selank β€” Research Dossier

Compiled by the Nexyra Research TeamPublished 30 June 2026Last reviewed 30 June 2026

Evidence grading

Preclinical
Phase I
Phase II
Phase III
Approved

Sequence

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

Tuftsin + Pro-Gly-Pro enzymatic stabiliser

GAD comparator (n)

62

Selank vs medazepam; Zozulia et al. 2008

Large Western RCTs

0

Clinical data concentrated in Russian literature

Parent peptide

Tuftsin

Naturally occurring immunomodulatory tetrapeptide

Selank has the closest human-trial evidence of any anxiolytic research peptide in its class β€” a comparator-controlled study versus medazepam finding comparable effect without sedation β€” but like its sibling Semax carries almost no independent Western replication.

Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) is a synthetic heptapeptide derivative of tuftsin (Thr-Lys-Pro-Arg), a naturally occurring immunomodulatory tetrapeptide found in immunoglobulin G. It was developed by the Institute of Molecular Genetics of the Russian Academy of Sciences with the V.V. Zakusov Institute of Pharmacology. The Pro-Gly-Pro C-terminal extension, shared with Semax, confers enzymatic stability and prolongs biological activity.

Its studied profile is primarily anxiolytic and nootropic, with secondary immunomodulatory activity inherited from its tuftsin lineage. Like Semax it carries a genuine Russian clinical record β€” here concentrated on anxiety and neurasthenia rather than cognition β€” with effectively absent Western replication.


β€œSelank produced anxiolytic effects comparable to medazepam across 62 patients with generalised anxiety disorder and neurasthenia, without the sedation associated with benzodiazepine treatment.”

β€” Zozulia AA et al., Zh Nevrol Psikhiatr Im S S Korsakova 2008

Mechanism

Selank's actions span several systems rather than a single receptor, distinguishing it from classical anxiolytics:

  • GABAergic modulation: affects expression of genes involved in GABAergic neurotransmission and is described as influencing GABA binding β€” the basis for anxiolytic effect without benzodiazepine-type sedation or dependence.
  • BDNF regulation: intranasal Selank upregulates BDNF in the rat hippocampus and preserves BDNF balance in stress and ethanol-withdrawal models.
  • Enkephalin stabilisation: inhibits enkephalin-degrading enzymes, preserving endogenous opioid tone β€” associated with anxiolytic activity without dependence.
  • Immunomodulation: consistent with its tuftsin origin, modulates cytokine expression (including IL-6) and Th1/Th2 balance in patient-derived cells.

Clinical evidence base

Generalised anxiety disorder (strongest signal)

A controlled clinical study (Zozulia, Seredenin et al., 2008; PMID 18454096) compared Selank (30 patients) with the benzodiazepine medazepam (32 patients) across 62 patients with GAD and neurasthenia, using Hamilton, Zung and CGI rating scales. Selank produced anxiolytic effects comparable to medazepam, with additional benefit in neurasthenia and without sedation. Effect sizes versus the active comparator were not reported in the English-language abstract.

Immunological

Uchakina et al. (2008) reported Selank suppressed IL-6 gene expression in cells from depressed patients and altered serum Th1/Th2 cytokine dynamics over 14 days in GAD/neurasthenia subjects, supporting its immunomodulatory mechanism.

Preclinical

BDNF regulation in the rat hippocampus (Inozemtseva et al., 2008), hippocampal transcriptome changes, and anxiolytic activity in ethanol-withdrawal models (Kolik et al., 2014) form a coherent rodent evidence base consistent with the proposed mechanism.

The replication gap

As with Semax, the substantive clinical literature is Russian-language, conducted at institutions where Selank was developed, and has not been replicated in large Western randomised trials. The comparator-controlled GAD study is real and informative but small, and effect-size reporting in accessible sources is limited.

Regulatory status

Selank is a registered pharmaceutical in Russia for anxiety and asthenic disorders. It is not approved by the FDA, MHRA, or EMA. Material supplied for laboratory work is research-use only.


Nexyra Lab Catalogue

This dossier covers published clinical research on Selank. Nexyra Lab supplies research-grade Selank for in vitro laboratory use.

View Selank in the Nexyra catalogue (research use only) β†’

References

  1. 1

    Zozulia AA, Neznamov GG, Siuniakov TS, Seredenin SB, et al. Efficacy and possible mechanisms of action of a new peptide anxiolytic Selank in the therapy of generalised anxiety disorders and neurasthenia. Zh Nevrol Psikhiatr Im S S Korsakova. 2008. PMID: 18454096 https://pubmed.ncbi.nlm.nih.gov/18454096/

  2. 2

    Volkov NV, Slominsky PA, et al. Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Front Pharmacol. 2016.

  3. 3

    Inozemtseva LS, Karpenko EA, Dolotov OV, et al. Intranasal administration of the peptide Selank regulates BDNF expression in the rat hippocampus in vivo. Dokl Biol Sci. 2008.

  4. 4

    Kolik LG, Nadorova AV, Kozlovskaya MM. Efficacy of peptide anxiolytic Selank during modeling of withdrawal syndrome in rats with different anxiety levels. Bull Exp Biol Med. 2014.


Research & Laboratory Use Only

This dossier is compiled for research planning and educational purposes only. It summarises published scientific literature and does not constitute medical advice, dosing guidance, or a therapeutic claim. All Nexyra Lab products are for research purposes only and are not for human or veterinary use. Nothing in this document should be interpreted as recommending, endorsing, or facilitating the self-administration of any compound.

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