Selank, which was developed in Russia, is a short peptide with nootropic and anxiolytic properties. It is a synthetic analogue of naturally occurring Tuftsin, an immunomodulatory peptide that modulates IL-6, T helper cells, monoamine neurotransmitters, and brain-derived neurotropic factor (BDNF). In fact, Selank and Tuftsin are essentially the same except that Selank has an additional four amino acids in its chain that help to improve metabolic stability and half-life. Selank has been tested in clinical trials as a potential treatment for generalized anxiety disorder.

Sequence: Thr-lys-pro-arg-pro-gly-pro Molecular Formula: C₃₃H₅₇N₁₁O₉ Molecular Weight: 751.887 g / mol PubChem CID: 11765600 CAS Number: 129954-34-3 Synonyms: Selanc Source: PubChem

Effets d'anxiété de selank basés sur les gènes liés au neurotransmetteur GABA

According to Dr. Anastasiya Volkova of L'Institut de génétique moléculaire en Russie, “numerous clinical studies have shown that Selank has strong antianxiety and neuroprotective effects in the treatment of anxiety. The clinical effects of Selank are similar to those of the classical antianxiety medications such as benzodiazepine, which are allosteric modulators of GABAA receptors and increase the inhibitory action of GABA.” Selank’s effects include reducing anxiety, improving mood, lower stress levels, and positively influencing memory and learning. Like benzodiazepines, low doses of Selank have a sedating effect. Unlike benzodiazepines, Selank does not appear to be habit-forming and does not lead to symptoms of withdrawal or amnesia. Research in rats shows that of the 84 genes known to be connected to GABA signaling in some way, seven are heavily modulated by Selank and 45 show some change in expression when the peptide is administered. Overall, 52 genes related to GABA signaling are affected by Selank to some degree. These results indicate that Selank can directly influence the expression of genes in nerve cells and that it likely produces effects by changing the affinity of the GABA receptor for GABA^[1]. Cette altération de l'affinité des récepteurs explique probablement pourquoi Sellank est synergique avec les benzodiazépines et d'autres agonistes des récepteurs du GABA. Changes in gene expression as a function of time in rats treated with Selank. Source: Pubment La recherche chez le rat montre que Selank et les benzodiazépines, lorsqu'ils sont utilisés seuls, ont des effets similaires sur l'anxiété, en particulier le trouble d'anxiété généralisée. Selank peut détenir un léger avantage sur les benzodiazépines lorsqu'ils tentent de réduire les niveaux élevés d'anxiété, mais une combinaison des deux traitements semble être la meilleure pour traiter le stress léger chronique imprévisible^[2]. The effects that Selank has on GABA receptors may be modulated, to some degree, by the peptide’s effect on enkephalin degradation. Testing indicates that people with anxiety and phobic disorders demonstrate increased enkephalinase activity in the blood during generalized anxiety and, as a result, the enkephalins they produce have shorter half-lives^[3]. En empêchant la dégradation des enképhalines par l'inhibition de l'ekephalinase, Selank peut réinitialiser cette voie enzymatique et aider à protéger les peptides anxiolytiques naturels du corps. La recherche sur des souris sujette à l'anxiété soutient l'hypothèse qu'au moins une partie de l'impact que Selank a est le résultat de la prévention de la dégradation de l'enképhaline^[4].

Sellank et le système immunitaire dans l'anxiété

La recherche chez les patients souffrant de dépression indique que Selank peut supprimer le gène responsable de la production de la cytokine inflammatoire IL-6. Fait intéressant, cet effet n'est observé que chez les patients souffrant de dépression et ne semble pas avoir lieu chez des individus en bonne santé^[5]. This suggests that Selank may be useful in treating people with anxiety-asthenic disorders, severe disorders in which anxiety is associated with fatigue, headache, heart palpitations, high blood pressure, nerve pain, and depression. When comparing Selank to standard anxiolytic treatments, like benzodiazepines, the two treatments show similar benefits in reducing anxiety, but only Selank has any effect on asthenic symptoms like fatigue and pain^[6]. Part of the effect is likely due to Selank’s ability to modulated IL-6 expression while part is likely due to the peptide’s ability to alter the rate of breakdown of the body’s natural pain killers, enkephalins. Testing of Selank in rats has revealed that the peptide regulates the expression of some 34 genes involved in the inflammatory process. These genes affect chemokines, cytokines, and receptors for both. In particular, Selank has been found to alter expression of BcI6, a gene that is heavily involved in the development of the immune system^[7]. This study, more than any other, revealed that Selank has very complex biological effects, but may help to deepen our understanding of how the immune system develops. Selank and even fragments of Selank have been shown to temporarily alter gene expression for C3, CAsp1, Il2rf, and Xcr1 in the mouse spleen. By affecting these genes, Selank is able to alter the balance of the immune system and thereby modulate inflammation^[8].

Selank Research avec mémoire et apprentissage

There has long been an association between anxiety and learning/memory. The correlation is a negative one, with increased anxiety leading to decreased ability to recall memories or store new information. Traditional anxiety treatments can reduce this effect, as can Selank, but Selank appears to do more than simply reduce the impact of anxiety on cognitive function. There is good reason to believe that Selank actually boosts cognition directly. Research in rats trains with food rewards and injected with either saline or Selank has shown that Selank boosts memory trace stability and thus enhances the memory storage process^[9]. It is important to note that this benefit was seen regardless of the anxiety levels of the rats, indicating that the peptide has effects beyond its ability to simply reduce stress-related impairment of memory. It appears that Selank may alter memory by affecting the expression of a number of genes in the hippocampus. Research in rats shows changes in mRNA levels of 36 different genes after intranasal administration of Selank. Most of the genes encode proteins associated with the plasma membrane and may therefore modulate ion-dependent processes in learning and memory^[10]. Though much research needs to be done to understand the mechanism by which Selank works to improve memory and learning, this research offers a tantalizing early clue to suggest that it alters the way neurons function in such a way that both forming and accessing memories is easier. Research even suggests that Selank can help to rescue memory and learning following damage to the brain. Rats treated with a neurotoxin and then Selank showed restored cognitive processes in at least one study. This effect appears to be related to an artificial inhibition of the catecholamine system in the brain by Selank^[11]. Il y a un certain espoir que Selank aidera à faire la lumière sur la façon dont la fonction cognitive peut être restaurée ou du moins améliorée après une lésion cérébrale traumatique, en particulier les types de blessures qui se produisent pendant le processus de naissance.

Recherche et douleur de Selank

Selank peut agir pour réduire la dégradation des enképhalines naturelles en inhibant les enzymes, trouvées dans le sang humain, qui les décompose^[12]. Enkephalins are natural peptides that bind to opioid receptors and help to blunt the severity of pain. They also function in the human stress response and are found in high levels in the brain and adrenal glands. By reducing levels of enkephalins in the brain, Selank may help to blunt the normal stress response and the effects that it has on memory, learning, and concentration. Selank exhibits minimal side effects, low oral and excellent subcutaneous bioavailability in mice. Per kg dosage in mice does not scale to humans. Selank for sale at Peptide Sciences is limited to educational and scientific research only, not for human consumption. Only buy Selank if you are a licensed researcher.

The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.

Dr. Petr Slominsky‘s 169 research works with 803 citations. 12 of those papers pertain to the examination of Selank’s diverse, multifaceted effects e.g. anxiety reduction, changes in the transcription profile of the hippocampus, and changes in expression of the genes for chemokines, cytokines, and their receptors. Dr. Slominsky is particularly interested in the epigenetic effects of Selank and other disease-state pathologies. Dr. Petr Slominsky is being referenced as one of the leading scientists involved in the research and development of Selank. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Peptide Sciences and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide. Dr. Petr Slominsky is listed in [7] under the referenced citations.

1. A. Volkova et al., «L'administration de Selank affecte l'expression de certains gènes impliqués dans la neurotransmission GABAergique», Front. Pharmacol., Vol. 7, février 2016. [PubMed]
2. A. Kasian et al., “Peptide Selank Enhances the Effect of Diazepam in Reducing Anxiety in Unpredictable Chronic Mild Stress Conditions in Rats,” Behavioural Neurology, 2017. [Online]. Available: https://www.hindawi.com/journals/bn/2017/5091027/.
3. A. A. Zozulya et al., «L'effet inhibiteur de Selank sur les enzymes dégradés enképhalines comme mécanisme possible de son activité anxiolytique», Bull. Exp. Biol. Med., Vol. 131, no. 4, pp. 315–317, avril 2001. [PubMed]
4. O. Y. Sokolov, V. K. Meshavkin, N. V. Kost et A. A. Zozulya, «Effets de Selank sur les réactions comportementales et les activités des enzymes plasmatiques dégradant les enkephalines chez les souris avec différents phénotypes de réactions émotionnelles et de stress», Bull. Exp. Biol. Med. [PubMed]
5. O. N. Uchakina et al., «[Effets immunomodulatoires de Selank chez les patients atteints de troubles anxieux-asthéniques]», Zh. Nevrol. Psikhiatr. Je suis. S. S. Korsakova, vol. 108, no. 5, pp. 71–75, 2008. [PubMed]
6. A. Nevrol. Psikhiatr. Je suis. S. S. Korsakova, vol. 108, no. 4, pp. 38–48, 2008. [PubMed]
7. T. Kolomin, M. Shadrina, L. Andreva, P. Slominsky, S. Limborska et N. Myasoedov, «Expression de l'inflammation-rammation-Rammation-Rammation-Rammation-Rammation-Rammation Speen sous le selank analogique de Tuftssine», Regul. Pept., Vol. 170, no. 1–3, pp. 10-1 18–23, octobre 2011. [PubMed]
8. T. I. Agapova et al., «[Effet de Semax sur la dynamique temporaire du facteur neurotrophique dérivé du cerveau et de l'expression des gènes du facteur de croissance nerveuse dans l'hippocampe du rat et le cortex frontal]», Mol. Genet. Mikrobiol. Virusol., Non. 3, pp. 28–32, 2008. [PubMed]
9. T. P. Semenova, I. I. Kozlovskiĭ, N. M. Zakharova et M. M. Kozlovskaia, «[Optimisation expérimentale des processus d'apprentissage et de mémoire par Selank]», Ekp. Klin. Farmakol., Vol. 73, no. 8, pp. 2–5, août 2010. [PubMed]
10. S. I. Aimny est Niash. NLV. Nous sommes notre cœur. Il est. Y .. Woving Up, Vuid. 63, sachez. 3, pp. 365–374, juin. 201
11. T. P. Semenova, M. M. Kozlovskaya, N. M. Zakharova, I. I. Kozlovskii et A. V. Zuikov, «Effet de Selank sur les processus cognitifs après des dommages infligés au système cérébral des catécholamines au début de l'ontogénie», Bull. Exp. Biol. Med., Vol. 144, no. [PubMed]
12. N. V. Kost et al., «[Semax et Selank inhibent les enzymes dégradant de l'eckephaline du sérum humain]]», Bioorg. Khim., Vol. 27, no. 3, pp. 180–183, juin 2001. [Springer]

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