Selank – 5mg
Selank is a synthetic analog of the immune peptide tuftsin — an anxiolytic neuropeptide studied for calm and cognition without the drawbacks of classical sedatives.
In preclinical research, Selank produced an anxiolytic effect comparable to benzodiazepines (diazepam) in stress models — but without the sedation or dependence associated with them[1].
It is thought to act by modulating GABA and serotonin signaling and BDNF expression, and is investigated for anxiety, focus and memory research.
Supplied as a lyophilized powder for reconstitution. Figures above summarize published preclinical (animal) research on this molecule and are provided as scientific reference for laboratory research only.
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Anxiolytic Heptapeptide
Calm Without Sedation: The Tuftsin Analog That Matches Benzodiazepines
Selank is a synthetic heptapeptide analog of tuftsin (sequence: Thr-Lys-Pro-Arg-Pro-Gly-Pro) engineered for enhanced metabolic stability. In clinical trials for generalized anxiety disorder, Selank matched the anxiolytic efficacy of medazepam (a benzodiazepine) while adding anti-asthenic and psychostimulant benefits — without sedation, cognitive impairment, or dependence potential. This unique "calm yet clear" profile makes it central to anxiety and cognition research.
- Heptapeptide: Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP)
- Tuftsin analog with glyproline motif for stability
- Anxiolytic efficacy comparable to benzodiazepines
- No sedation, amnesia, or dependence potential
- Anti-asthenic (energy-boosting) properties
Multi-Axis Mechanism
How Selank Achieves Anxiolysis Without Trade-Offs
Selank operates through a rare multi-system mechanism. It modulates 52 GABA-related genes, increases hippocampal BDNF, and inhibits enkephalin-degrading enzymes (IC₅₀ ~20 µM) — prolonging the body's natural anti-stress peptides. Unlike benzodiazepines that directly enhance GABA receptor activity, Selank changes receptor affinity through gene expression, explaining its synergy with classical anxiolytics and lack of tolerance development.
- Modulates 52 genes related to GABA signaling
- Increases BDNF in hippocampus (intranasal-confirmed)
- Inhibits enkephalinases (preserves endogenous anti-stress peptides)
- Regulates IL-6 and 34 inflammation-related genes
- Alters GABA receptor affinity (not direct agonism)
Research Applications
From Memory Enhancement to Pain Modulation
Selank research extends far beyond anxiety. Studies demonstrate enhanced memory trace stability independent of anxiety reduction — suggesting direct nootropic properties. It modulates 36 hippocampal genes encoding plasma membrane proteins involved in learning. Pain research shows enkephalinase inhibition helps protect natural analgesic peptides. Additional applications include immune modulation, cognitive rescue after brain injury, and even antiviral activity against influenza A.
- Memory and learning: Enhanced trace stability, 36 hippocampal genes
- Pain modulation: Enkephalinase inhibition preserves natural analgesia
- Cognitive rescue: Restores function after neurotoxin damage
- Immune modulation: IL-6 suppression, 34 cytokine-related genes
- Antiviral research: Activity against influenza A/H3N2
The Science Behind Calm Clarity: Why Selank Redefines Anxiolytic Research
Selank represents a breakthrough in anxiolytic peptide research. As a synthetic analog of the immunomodulatory peptide tuftsin, it retains the parent compound's immune benefits while adding profound anxiolytic and nootropic properties. The additional glyproline (PGP) motif dramatically improves metabolic stability, allowing consistent research protocols impossible with native tuftsin.
The clinical evidence is compelling. In head-to-head trials against medazepam (a benzodiazepine), Selank matched anxiolytic efficacy while adding anti-asthenic and psychostimulant benefits — the opposite of benzodiazepine sedation. Unlike classical anxiolytics, Selank shows no amnesia, cognitive impairment, tolerance, or withdrawal symptoms. This "calm without sedation" profile has made it a reference compound for anxiety research.
Mechanistically, Selank operates on multiple axes simultaneously. It modulates 52 genes related to GABA signaling — not through direct receptor agonism, but by changing receptor affinity through gene expression. It increases hippocampal BDNF (supporting neuroplasticity), inhibits enkephalin-degrading enzymes (preserving natural stress-relief peptides), and regulates inflammatory cytokines including IL-6. This multi-system approach explains both its efficacy and favorable side-effect profile.
Research applications extend well beyond anxiety. Memory studies show enhanced trace stability independent of anxiety reduction, suggesting direct nootropic effects. Pain research demonstrates prolonged enkephalin half-life through enkephalinase inhibition. Immune studies reveal regulation of 34 inflammation-related genes. For teams investigating anxiety disorders, cognitive enhancement, neuroimmune interactions, or pain modulation, Selank provides a uniquely clean, multi-target research tool with extensive clinical validation.
For research use only. Not for human consumption.
Scientific Literature
- Vyunova TV, et al. Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. Protein Pept Lett. 2018;25(10):914-923.
- Zozulya AA, et al. The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity. Bull Exp Biol Med. 2001;131(4):315-317.
- Volkova A, et al. Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Front Pharmacol. 2016;7:31.
- Kasian A, et al. Peptide Selank Enhances the Effect of Diazepam in Reducing Anxiety in Unpredictable Chronic Mild Stress Conditions in Rats. Behav Neurol. 2017;2017:5091027.
- Zozulia AA, et al. [Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia]. Zh Nevrol Psikhiatr Im S S Korsakova. 2008;108(4):38-48. Russian.
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