Also known as: TP-7 · Selanc · Selank heptapeptide
Selank is a synthetic heptapeptide developed at the Russian Institute of Molecular Genetics, derived from the endogenous immunomodulatory peptide tuftsin (Thr-Lys-Pro-Arg) with a Pro-Gly-Pro extension that dramatically extends its half-life and CNS activity. It is approved in Russia as an anxiolytic and nootropic and is one of the most extensively studied Russian peptides, with a unique profile combining anxiety reduction, cognitive enhancement, and immune modulation without sedation.
Selank (TKPRPGP) was developed by the V.V. Zakusov Institute of Pharmacology of the Russian Academy of Sciences as a synthetic analogue of tuftsin — a naturally occurring tetrapeptide fragment of IgG that modulates immune function. The C-terminal Pro-Gly-Pro extension increases metabolic stability from minutes to several hours, enabling practical clinical use.
Unlike classical anxiolytics (benzodiazepines), Selank does not cause sedation, muscle relaxation, or physical dependence. It acts via GABAergic modulation, serotonin system interaction, and BDNF upregulation — producing anxiolysis while simultaneously enhancing working memory, attention, and mental clarity.
Selank is approved by the Russian Ministry of Health as an anxiolytic and is administered intranasally (nasal drops) in clinical practice. It has been evaluated in multiple controlled trials for generalised anxiety disorder, neurasthenia, and cognitive impairment associated with anxiety.
Selank enhances GABAergic neurotransmission through positive allosteric modulation of GABA-A receptors, explaining its anxiolytic effects. Unlike benzodiazepines, it does not bind the benzodiazepine site directly, producing anxiolysis without the sedation, tolerance, or dependence associated with classical GABA modulators.
Selank significantly increases BDNF (brain-derived neurotrophic factor) expression in the hippocampus and frontal cortex. This neurotrophin elevation underlies its cognitive-enhancing and neuroprotective properties, promoting synaptic plasticity, neurogenesis, and long-term memory consolidation.
Selank modulates serotonergic transmission (5-HT1A, 5-HT2A receptors) and has secondary effects on dopaminergic pathways. This dual modulation is likely responsible for its mood-stabilising and procognitive effects that go beyond pure anxiolysis.
Selank is non-sedating and does not impair cognitive performance — making daytime dosing practical. No dependence or withdrawal has been documented in clinical use. Typical research courses run 10–14 days. Longer-term use has been studied without significant adverse findings but long-term data are limited outside Russian literature.
Unlike benzodiazepines, Selank does not require tapering. No rebound anxiety on cessation has been reported in clinical studies. BDNF-mediated effects on memory and neuroplasticity may persist after the acute anxiolytic effect wears off.
Russian clinical trials (1990s–2010s) consistently showed Selank superior to placebo for GAD with a favourable safety profile. Head-to-head comparisons with medazepam showed equivalent anxiolytic efficacy without cognitive impairment side effects. Western peer-reviewed replication is limited but growing.
Cognitive studies show improvement in attention, short-term memory, and information processing speed in both anxious and non-anxious populations — suggesting a direct nootropic effect independent of anxiety reduction.
Ask anything about Selank — mechanisms, dosing protocols, interactions, or research comparisons.
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