Selank

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Anxiolytic and neuropeptide research compound — benzodiazepine-equivalent calm without sedation or dependency.

Selank is a synthetic heptapeptide analog of tuftsin with additional glyproline residues, developed in Russia and investigated for anxiolytic, neuropeptide-signalling, neuroprotective, and immunomodulatory effects through GABAergic and neurotransmitter system modulation.

Selank is a synthetic heptapeptide analog of tuftsin with additional glyproline residues, developed in Russia and investigated for anxiolytic, neuropeptide-signalling, neuroprotective, and immunomodulatory effects through GABAergic and neurotransmitter system modulation. It has a molecular formula C33H57N11O9, mass 751.88 Da. Its published amino-acid sequence is Thr-Lys-Pro-Arg-Pro-Gly-Pro. Common synonyms in the literature include Selanc, TP-7, and Selanc peptide.

Investigation of Selank to date is a mix of preclinical and early clinical, with the majority of citations concentrated in animal models and in-vitro assays rather than randomized controlled human trials. Published work referencing Selank spans GABA mechanism studies: Selank acts as a positive allosteric modulator of GABA_A receptors, enhancing [3H]GABA binding in concentration-dependent, subtype-selective manner without cumulative effects when combined with benzodiazepines like diazepam. It blocks modulatory activity of diazepam and olanzapine, suggesting distinct binding sites. Gene expression shows positive correlation to GABA effects at 1 hour (r=0.86, p≤0.05), Human clinical studies (Russia): Clinical trials in patients with generalized anxiety disorder have demonstrated anxiolytic efficacy comparable to low-dose benzodiazepines (diazepam, medazepam, phenazepam). Studies report reduced anxiety without hypnosedative effects or withdrawal symptoms, and Ethanol withdrawal models: Selank (0.3 mg/kg IP) reduces anxiety in elevated plus maze and social interaction tests during ethanol withdrawal. In combination with chronic mild stress, standalone Selank (300 μg/kg intranasal) is most effective for elevated anxiety. Proposed mechanisms in the literature include GABA-A receptor allosteric modulation: increases GABA binding affinity, mimicking benzodiazepine-like actions without side effects and Enkephalin system: inhibits enkephalin-degrading enzymes, increasing leu-enkephalin half-life. None of this material describes therapeutic outcomes in humans, and No vendor listed here provides dosing guidance for Selank outside laboratory research.

For the full mechanistic profile, published references, and constraint notes on Selank, see the Selank research page. All references cited on that page are peer-reviewed primary literature.