Selank is a synthetic peptide derived froSelank is a synthetic heptapeptide analogue of the naturally occurring human peptide tuftsin. Developed in Russia, it has been utilized for its potential neuroprotective and cognitive-enhancing properties. Selank's structure is designed to be more stable and longer-lasting than its parent peptide, tuftsin.
Selank's effects are believed to arise from its interaction with various neurotransmitter systems:
Additionally, Selank has been found to elevate brain-derived neurotrophic factor (BDNF) levels in the hippocampus, supporting neuroplasticity and cognitive function.
Dr. Anastasiya Volkova of the Institute of Molecular Genetics in Russia reports that numerous clinical studies demonstrate Selank’s strong anti-anxiety and neuroprotective effects, comparable to classical anxiolytics like benzodiazepines, which modulate GABA_A receptors and enhance GABA’s inhibitory action. Selank reduces anxiety, improves mood, lowers stress, and positively influences memory and learning. Unlike benzodiazepines, it is not habit-forming and does not cause withdrawal symptoms or amnesia.
Animal studies reveal that Selank modulates the expression of 52 genes related to GABA signaling, including 7 genes heavily influenced and 45 showing some expression changes. This suggests Selank directly affects gene expression in neurons, likely altering the affinity of GABA receptors for GABA, which may explain its synergistic effect with benzodiazepines and other GABA agonists.
Selank and benzodiazepines show similar efficacy in reducing anxiety, particularly generalized anxiety disorder, but combined therapy may better treat unpredictable chronic mild stress.
Selank may modulate anxiety partly through inhibition of enkephalin degradation. Anxiety and phobic disorders correlate with increased blood enkephalinase activity, reducing the half-life of natural enkephalins. By preventing their breakdown, Selank helps preserve endogenous anxiolytic peptides. Animal studies support this mechanism.
In depression patients, Selank suppresses IL-6 gene expression, an inflammatory cytokine, but this effect is absent in healthy individuals. This suggests Selank may be especially useful in anxiety-asthenic disorders, which involve anxiety with fatigue, pain, and other somatic symptoms. Unlike benzodiazepines, Selank can alleviate these asthenic symptoms, likely due to IL-6 modulation and protection of enkephalins.
Selank regulates 34 inflammation-related genes in rats, including chemokines, cytokines, and receptors. It notably alters expression of the Bel6 gene, critical in immune development. These findings reveal complex immunomodulatory effects of Selank.
Anxiety negatively impacts memory and learning, but Selank not only reduces anxiety-related cognitive impairment but may directly enhance cognition. Rat studies show Selank stabilizes memory traces and improves memory storage independent of anxiety level.
Gene expression changes in the hippocampus after Selank administration include modulation of 36 genes, many encoding plasma membrane proteins involved in ion-dependent learning and memory processes. Selank may ease the formation and recall of memories.
It has also shown potential to restore cognitive function after brain injury in rats, possibly via inhibition of the catecholamine system, with implications for traumatic brain injury therapy.
Selank inhibits enzymes degrading natural enkephalins—opioid peptides that modulate pain and stress responses. By preserving enkephalins, Selank may blunt stress effects on cognition, learning, and concentration.
Selank exhibits minimal side effects, with low oral and excellent subcutaneous bioavailability in mice. Dosages in mice do not scale directly to humans. Selank is sold strictly for educational and scientific research and is not intended for human consumption. Purchase only if licensed.
Selank is primarily utilized in scientific studies focusing on:
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