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Product Name: Selank

CAS No: 129954-34-3

CAT No: P100123

Molar Mass:751.90

Chemical Formula:C38H49N9O5


Storage:Store at -20°C

Sequence: TKPRPGP

Target Indicators: Selank is a synthetic analog of the endogenous tuftsin molecule


Application: Selank is a synthetic peptide analog derived from the naturally occurring peptide tuftsin. It has anxiolytic and nootropic properties, meaning it can reduce anxiety and improve cognitive function. In pharmaceutical chemistry, Selank is studied for its potential therapeutic applications in treating anxiety disorders, depression, and cognitive decline. It acts by modulating the levels of neurotransmitters such as serotonin, dopamine, and norepinephrine in the brain, which are involved in mood regulation and cognitive function. Additionally, Selank has been shown to enhance memory and learning abilities, making it a promising candidate for improving cognitive performance and treating neurodegenerative diseases such as Alzheimer’s and Parkinson’s. Its mechanism of action and favorable safety profile make Selank a valuable tool in psychiatry and neurology for managing anxiety and cognitive impairment

Current Research:Selank, a synthetic regulatory peptide, holds promise as a safe drug with specific clinical properties and direct physiological effects due to its pronounced anxiolytic, neuropsychotropic, antidepressant, antistress, and nootropic activities, along with its immunomodulatory effects. While its mechanisms of action are not fully understood, Selank’s design, inspired by the endogenous tuftsin molecule, incorporates additional amino acids to enhance its metabolic stability and duration of action. Notably, Selank’s anxiolytic effects resemble those of benzodiazepines, but without the accompanying unwanted side effects such as amnesia, withdrawal, and dependence.


Previous studies have suggested that Selank modulates the activity of the GABAergic system, particularly through allosteric modulation of GABAA receptors, similar to benzodiazepines. Further investigations aimed at elucidating Selank’s mechanism of action have focused on changes in mRNA levels of genes related to neurotransmission in response to Selank administration. These studies have revealed that Selank influences the expression of genes involved in neurotransmission, suggesting a direct effect on nerve cells. Additionally, Selank’s effects on gene expression profiles partially overlap with those induced by GABA administration, further supporting its involvement in modulating the GABAergic system.


Interestingly, Selank’s effects extend beyond the GABAergic system to include modulation of dopamine and serotonin receptors, indicating its multifaceted actions on various neurotransmitter systems. For instance, Selank activates genes associated with synaptic plasticity and memory formation, suggesting a potential role in enhancing cognitive function. Moreover, Selank has been shown to influence the expression of genes involved in regulating the balance between sleep and wakefulness, providing insights into its therapeutic effects on sleep patterns in individuals with generalized anxiety disorders.


Overall, Selank exhibits complex effects on nerve cells, acting through multiple neurotransmitter systems to exert its therapeutic benefits. While its mechanism of action involves allosteric modulation of GABAA receptors, Selank’s effects on gene expression profiles suggest broader interactions with other neurotransmitter systems. Further research is needed to fully elucidate Selank’s mechanisms of action and its therapeutic potential in various clinical applications.

Reference:Medvedev, V. E., Tereshchenko, O. N., Kost, N. V., Ter-Israelyan, A. Y., Gushanskaya, E. V., Chobanu, I. K., … & Myasoedov, N. F. (2015). Optimization of the treatment of anxiety disorders with selank. Zhurnal Nevrologii i Psikhiatrii Imeni SS Korsakova, 115(6), 33-40.

Volkova, A., Shadrina, M., Kolomin, T., Andreeva, L., Limborska, S., Myasoedov, N., & Slominsky, P. (2016). Selank administration affects the expression of some genes involved in GABAergic neurotransmission. Frontiers in Pharmacology, 7, 31.

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