Selank

Selank, possessing the amino acid sequence H-Thr-Lys-Pro-Arg-Pro-Gly-Pro-OH, is a potent and long-lasting anti-anxiety drug.

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Selank, possessing the amino acid sequence H-Thr-Lys-Pro-Arg-Pro-Gly-Pro-OH, is a potent and long-lasting anti-anxiety drug.

Derived from the retention and subsequent modification of a tuftsin core fragment, this process significantly enhances its ability to cross the sanguine cerebrum obice; unique central nervous system activity is a direct result of said modification.

Since the beginning of this century numerous clinical trials have been performed on Selank; complex pharmacological properties spanning multiple modalities and multiple potential targets have been documented.

A stable mechanism of action is what makes Selank particularly valuable; rebound effects do not occur upon discontinuation.

Neurological diseases benefit from a triple regulatory path: neurotransmitters, neuroplasticity and immune system regulation.

Sequentia

Thr-Lys Pro Arg-Pro-Gly-Pro

CAS Number

129954-34-3

Formulae hypotheticae

C33H57N11O9

M. Pondus

751.887

Research Of Selank

1.Mechanisms of Action and Therapeutic Effects

Its core function is the regulation of the balance within key neurotransmitter systems in the brain.

Modulating the transmission of γ-aminobutyric acid (GABA) nominatim, along with various regulatory effects on serotonin and dopaminergic systems, leads to excellent anti-anxiety and antidepressant effects.

Enhanced hippocampal neuronal plasticity has also been shown; cognitiva amplificationem (learning, memory consolidation, attention being prime examples) is at least partially attributable to this line of regulation.

The retention of the original tuftsin core allows for significant efficacy in regulating the cellular immune status, cytokines (interferon being one of the better studied) – an immunomodulatory effect the body can use to cope with various stress.

Clinical studies support the improvement of mood and enhanced psychological resilience that Selank facilitates.

2.Anti-anxiety and antidepressant effects

Unlike traditional anti-anxiety and antidepressant drugs, selank does not act directly on GABA receptors.

Instead, it works by regulating various key neurotransmitters within the brain.

Experiments have shown that selank enhances the transmission efficiency of this inhibitoriae neurotransmitter, GABA; inhibiting excessive neuronal activity and subsequently anxiety being the primary outcome of this process.

Further regulation of neurotransmitters – dopamine being a prime example – allows selank to significantly increase the nervous system’s stress resilience.

Mood swings and associated positive/negative feelings of pleasure are at least partially controlled; stable, long term anti-anxiety and antidepressant effects are the result.

Notable side effects (drowsiness, cognitive impairment, addiction being the most well documented) are avoided, making selank a uniquely positioned treatment for certain neurological diseases.

3.Enhancing Cognitive Function and Promoting Neuroplasticity

Selank has demonstrated efficacy in enhancing cognitive function.

Brain Derived Neurotrophic Factor (BDNF) is the focus of much of this research; upregulation of its activity is central to neuronal survival, differentiation and all forms of synaptic plasticity.

Hippocampal cells specifically show increased BDNF related activity when treated with selank.

Neural reorganization through new connections has been observed – memory consolidation, learning ability and attention/concentration all improve.

Clearer thinking, faster information processing and positive results in cognitive tests have all been recorded in patients.

4.Neuroimmune System Regulation

Tuftsin is a natural immune peptide.

Selank retains a core fragment of tuftsin, thus possessing a powerful, though subtle, immunomodulatory effect.

Neuromodulation and this neuro-immune interaction are complementary.

Chronic stress studies show Selank to be particularly well suited to psychological and physiological adaptation.

Improved or at least balanced immune responses contribute to the end result of these mechanisms.

Psychological and physical well-being are interdependent.

5.Potential for treating obsessive-compulsive disorder and agitation

Some reports indicate that selank influences the connection between the amygdala et prefrontal cortex; promoting fear extinction being one of the more directly observable effects.

Obsessive-compulsive disorder and various forms of agitation fall under this category as primary targets for treatment.

Animal experiments have shown a significant reduction of agitation-induced fur-puffing behavior, a validated measure of pure agitation.

Scientists have begun to speculate the mechanisms behind this – regulation of at least some aspect of the serotonin system being a leading theory, stress adaptation being enhanced in multiple studies.

Related research is still ongoing, but exploring these potential lines of treatment is important; treating the aforementioned diseases (psychiatric or otherwise) remains a significant and achievable goal.

COA

HPLC

MS

(1) volumus, C. R.; White, C. M. Agentia sedativa-hypnotica Impact Gamma-Aminobutyric Acidum Receptores: Focus in Flunitrazepam, Gamma-Hydroxybutyric Acidum, Phenibut, et Selank. J Clin Pharmacol 2021, 61 Suppl 2, S114-S128. DOI': 10.1002/jcph.1922 From NLM Medline.

(2) Rem pauperem, A.; Kolomin, T^.; Andreeva, L.; Bondarenko, Ej.; Myasoedov, N.; Slominsky, P .; Shadrina, M. Peptide Selank auget effectum Diazepam in reducendo maeror in vagus Chronica mitis accentus Conditiones in carborundum. Behav Neurol 2017, 2017, 5091027. DOI': 10.1155/2017/5091027 Ex NLM Medline.

(3) Pin, L. G.; Nadorova, A. V.; Antipova, T. A.; Kruglov, S. V.; Kudrin, V. S .; Durnev, A. D. Selank, Peptide Analogia Tuftsin, Protects Against Ethanol-Induced Memory Impairment by Regulating of BDNF Content in the Hippocampus and Prefrontal Cortex in Rats. Bulla Exp Biol Med 2019, 167 (5), 641-644. DOI': 10.1007/s10517-019-04588-9 From NLM Medline.

(4) Pin, L. G.; Nadorova, A. V.; Seredenin, S. B. Selank Inhibits Ethanol-inducti Hyperlocomotionis et Manifestationis Behavioural Sensitization in DBA/2 Mures. Bulla Exp Biol Med 2016, 162 (1), 56-59. DOI': 10.1007/s10517-016-3544-6 Ex NLM Medline.

(5) Pretium, N. V.; Sokolov, Domine.; Gabaeva, M. V.; Grivennikov, I. A.; Andreeva, L. A.; Miasoedov, N. F.; Zozulia, A. A. [Semax et selank enzymes ab humano Serum inhibent enkephalin]]. Bioorg Khim 2001, 27 (3), 180-183. DOI': 10.1023/a:1011373002885 Ex NLM Medline.

(6) nescio, G. G.; Teleshova, E. S .; Bochkarev, V. K.; Koschelev, V. V.; Syunyakov, T. S. P.3.036 Novus anxiolyticus Selank: Proventus thePhase II de iudiciis clinicis. Neuropsychopharmacologiae Europaeae 2005, 15, S159-S160. DOI': 10.1016/s0924-977x(05)80332-3.

(7) Slominsky, P. A.; Shadrina, M. Et ego.; Kolomin, T. A.; Stavrovskaya, A. V.; Filatova, E. V.; Andreeva, L. A.; Illariishkin, S. N.; Myasoedov, N. F. Peptides semax et selank mores mures inclusi cum 6-OHDA adducti PD sicut parkinsonismi. Quamdiu Biol Sci 2017, 474 (1), 106-109. DOI': 10.1134/S0012496617030048 From NLM Medline.

(8) Sollertinskaja, T. N.; Shorokhov, M. V.; Myasoedov, N. F. Effectus cerebroprotectivos Semax et Selank in primatibus in diversis generibus neurosis. Acta Internationalis Psychophysiologiae 2008, 69 (3). DOI': 10.1016/j.ijpsycho.2008.05.356.

(9) Sollertinskaya, T. N.; Shorokhov, M. V.; Kozlovskaya, M. M.; Kozlovskii, I. Et ego.; Sudakov, K. V. Compensatory and antiamnestic effects of heptapeptide Selank in monkeys. Journal of Evolutionary Biochemistry and Physiology 2008, 44 (3), 332-340. DOI': 10.1134/s0022093008030101.

Sequentia:

Thr-Lys Pro Arg-Pro-Gly-Pro

CAS:

129954-34-3

M.W:

751.887 g / mol

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