TRANSMISSION 01 / HEPTAPEPTIDE SELANK
Selank: a tuftsin-derived heptapeptide studied as an anxiolytic and nootropic across twenty preclinical models and one published human trial.
Compound summary, mechanism pathways, dosage research, and full citation index — drawn from the peer-reviewed record.
What Is Selank?
Selank is a synthetic heptapeptide with the amino acid sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro and a molecular weight of 751.9 Da. It was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences as a structural analogue of tuftsin — a naturally occurring immunomodulatory tetrapeptide (Thr-Lys-Pro-Arg) derived from the Fc fragment of IgG heavy chain. The Pro-Gly-Pro C-terminal extension was added to improve metabolic stability relative to the parent tetrapeptide. Selank carries the designation TP-7 in the Russian pharmacological literature and was registered in Russia as a prescription nasal spray anxiolytic in 2009.
In preclinical models, Selank modulates GABA-A receptor sensitivity through indirect allosteric interaction, inhibits enzymatic degradation of enkephalins, and upregulates hippocampal BDNF expression. These converging pathways produce anxiolytic effects without the direct receptor binding associated with conventional benzodiazepines. Published preclinical toxicology and the single available Russian clinical trial report a favorable safety profile at study doses. Outside Russia, Selank is classified as a research compound — it is not approved by the FDA or EMA for any indication.
This site indexes the peer-reviewed research literature on Selank. Every quantitative claim is cited. All dosing figures represent study administration protocols in specific species — not recommendations for humans. See Selank mechanism of action for pathway detail, Selank dosage research for the preclinical and clinical dose data, and frequently asked questions about Selank for the full question inventory.
Key Findings from the Research Record
Thirty years of publications from Russian academic and state institutions have produced a consistent finding: Selank reduces anxiety behavior without the tolerance and withdrawal phenomena associated with benzodiazepines. The mechanism literature identifies at least seven converging pathways — GABA-A allosteric modulation, enkephalinase inhibition, BDNF upregulation, serotonin turnover enhancement, HPA axis normalization, dopamine modulation, and cytokine regulation via the tuftsin lineage [1][3][4][12][14].
The single published human trial (N=62, GAD and neurasthenia patients) found Selank at 2,700 micrograms per day intranasal over 14 days produced anxiolytic activity equivalent to medazepam on Hamilton, Zung, and Clinical Global Impression scales, while additionally demonstrating antiasthenic and psychostimulant effects not observed with the benzodiazepine [5]. An fMRI study in 52 healthy adults confirmed measurable changes in resting-state functional connectivity between the right amygdala and right temporal cortex within 20 minutes of intranasal administration — direct human neuroimaging evidence of CNS activity [20].
The evidence base has limitations. Most research originates from Russian institutions; independent Western replication is limited. Human data consists of a single 62-patient trial. Long-term human safety data is absent. Preclinical toxicology is favorable but narrow in scope.
For the full comparative analysis, see Selank vs Semax comparison. For dependence and tolerance data, see Selank withdrawal research.
Compound Profile
Sequence: Thr-Lys-Pro-Arg-Pro-Gly-Pro Synonyms: TP-7; tuftsin analogue; heptapeptide Selank Molecular weight: 751.9 Da Category: Neuropeptide — anxiolytic and nootropic class Plasma half-life: approximately 3–5 minutes (rapid enzymatic cleavage; behavioral effects persist well beyond plasma clearance via active metabolite formation) dosage literature — see [Selank half-life and duration] Routes studied: intranasal (primary clinical route), intraperitoneal (preclinical), subcutaneous (preclinical) Regulatory status: registered Russia 2009 (prescription nasal spray); not FDA-approved; not EMA-approved; research compound outside Russia
Structural variants: N-Acetyl Selank Amidate (N-terminal acetylation + C-terminal amidation) is a modification proposed to increase enzymatic resistance and extend half-life. Independent peer-reviewed pharmacokinetic comparison studies are limited. See N-Acetyl Selank and Selank Amidate Variants for current data.