Selank
Synthetic tuftsin analogue heptapeptide · Research-grade reference material
Identity
- Molecular formula
- C33H57N11O9
- Molecular weight
- 751.87 g/mol
- CAS number
- 129954-34-3
Research Background
Selank is a synthetic analog of tuftsin, a naturally occurring tetrapeptide (Thr-Lys-Pro-Arg) released when immunoglobulin G is cleaved. A Pro-Gly-Pro tripeptide extension was added, the same modification used in Semax, to substantially slow enzymatic degradation and extend biological half-life from minutes to hours.
Developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, working alongside the Zakusov Institute of Pharmacology. Selank is studied primarily as an anxiolytic, distinct from Semax’s cognitive/neurotrophic focus despite sharing the same research origin and Pro-Gly-Pro modification strategy.
Lab-tested research material
Mechanism
Rather than binding a receptor directly, Selank modulates expression of genes involved in GABAergic neurotransmission, including GABA-A receptor subunits, GABA transporters, and GABA-synthesizing enzymes (Volkova et al.), a transcriptional effect rather than a direct allosteric one. Separately, Selank has been shown to increase BDNF expression in the rat hippocampus (Inozemtseva et al.), and in a rat model of opioid withdrawal, attenuated aversive withdrawal signs following naloxone-precipitated morphine withdrawal (Konstantinopolsky et al.).
Selank has been studied predominantly by Russian and Eastern European research groups since the 1990s, in anxiety, cognition and immune-signaling models. Its tuftsin origin gives it a dual research profile spanning both CNS and peripheral immune activity — unusual among neuroactive peptides. Findings below derive from animal and cell-culture systems. They are not established effects in humans.
GABAergic modulation. Described in the literature as acting on GABA binding / receptor affinity rather than as a direct receptor agonist.
BDNF regulation. Kolik et al. (2019) reported Selank (0.3 mg/kg IP, 7 days) prevented memory and attention impairment during alcohol withdrawal in rats and prevented ethanol-induced BDNF elevation in hippocampus and prefrontal cortex.
Gene-expression effects. Kolomin et al. (2010) reported a single intranasal dose produced measurable gene-expression changes in both rat hippocampus and spleen — consistent with dual CNS/immune activity.
Behavioral models. Seregin et al. reported anxiolytic activity in elevated plus-maze models without motor impairment or sedation.
Monoaminergic & enkephalin systems. Reported modulation of serotonergic signaling and enkephalin metabolism.
Proposed pathways investigated in preclinical (animal / in-vitro) models. Schematic only; not a claim of established human effect.
State of the Evidence
Like Semax, Selank’s research base is large but concentrated almost entirely in Russian-language literature and Russian institutions. Independent, large-scale trials from outside that system remain limited, and neither compound is approved by a Western regulator.
1. Animal — “Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission,” Frontiers in Pharmacology, 2016. PMID 26924987
2. Animal — “Selank Increases the Expression of Brain-Derived Neurotrophic Factor in Rat Hippocampus,” Doklady Biological Sciences, 2008.
3. Animal — “Selank, a Peptide Analog of Tuftsin, Attenuates Aversive Signs of Morphine Withdrawal in Rats,” Bulletin of Experimental Biology and Medicine, 2022. DOI 10.1007/s10517-022-05624-x
What the Literature Supports — and What It Doesn’t
Selank follows the same evidentiary pattern as Semax: a substantial preclinical record and a national regulatory approval, alongside an absence of independent Western replication. Both facts belong in an honest reference.
Evidence at a glance
Russian clinical reports describe anxiolytic activity in generalized anxiety disorder without sedation; numeric effect sizes are frequently absent from English-language abstracts, limiting independent appraisal.
No Western randomized controlled trials have replicated the reported clinical findings.
Preclinical findings are specific and quantified (dose, duration, statistical significance), which is a genuine strength of the animal literature.
Comparisons to benzodiazepines appear in the Russian literature; these should not be read as establishing equivalence under Western regulatory standards.
Appropriate characterization: a metabolically stabilized tuftsin analogue with a coherent preclinical GABAergic/BDNF profile and a national regulatory approval, lacking the independent controlled human evidence required for FDA authorization.
Regulatory & status notes
Selected references
- 1. Kolik LG, et al. Selank, Peptide Analogue of Tuftsin, Protects Against Ethanol-Induced Memory Impairment by Regulating BDNF Content in the Hippocampus and Prefrontal Cortex in Rats. Bull Exp Biol Med. 2019.
- 2. Kolomin T, et al. Changes in gene expression in rat hippocampus and spleen following a single intranasal dose of Selank. Dokl Biochem Biophys. 2010.
- 3. Seregin et al. Anxiolytic activity of Selank in elevated plus-maze models. PMID 19916388.
- 4. Teleshova ES, et al. Results of clinical and pharmacological studies of the peptide anxiolytic Selank. Psikhiatriya. 2010;(4):26–35. [Russian]
Safety Information
Research-use compound with limited human data. Evidence strength varies — see the Evidence section above.
No established clinical contraindications. This is an investigational compound with limited human data and has not been evaluated by the FDA for safety in this context. Consult a qualified clinician. For research and educational purposes only, not for human or veterinary use.
Related Compounds
For research and educational purposes only. Not for human or veterinary use.