NA Selank Amidate (60mg – 300mg)

N-Acetyl Selank Amidate

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Peptide Partners Manufacturer Id: VI32

Batch Id: SEK202601

Research Studies

(for educational purposes only)

Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission

Authors: Anastasiya Volkova, Maria Shadrina, Timur Kolomin, Lyudmila Andreeva, Svetlana Limborska, Nikolay Myasoedov, Petr Slominsky

Published: Frontiers in Pharmacology, 2016 Feb 18;7:31

URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC4757669/

Scientific Summary

The study analyzed the expression of 84 genes involved in neurotransmission (including major subunits of the GABA receptor, transporters, ion channels, dopamine, and serotonin receptors) in the frontal cortex of rats 1 and 3 hours after administration of Selank or GABA (300 μg/kg) using real-time PCR method. Frontal cortex tissues were extracted from rats, and total RNA was isolated using the RNeasy Mini Kit. First-strand cDNAs were synthesized using the RT2 First Strand Kit, and real-time quantitative RT-PCR was performed using a Custom RT2 Profiler PCR Array. The study found significant changes in the expression of 45 genes 1 hour after administration of the compounds, and 22 genes changed their expression 3 hours after Selank or GABA administration. A positive correlation was found between the changes in gene expression within 1 hour after administration of Selank or GABA. The results showed that Selank caused alterations in the expression of genes involved in neurotransmission, including GABA receptor subunits (Gabrb3, Gabre, Gabrq), dopamine receptors (Drd1a, Drd2, Drd3, Drd5), serotonin receptors (Htr3a), ion channels (Cacna1a, Cacna1b, P2rx7), and GABA transporters (Slc32a1, Slc6a1, Slc6a11, Slc6a13). The data indicate that Selank’s molecular mechanism is associated with allosteric modulation of the GABAergic system.

Plain English Interpretation

This research examined how Selank affects the activity of genes in the brain that control neurotransmitters, which are chemical messengers that help brain cells communicate. Scientists gave rats either Selank or GABA (a natural calming brain chemical) and then looked at which genes became more or less active in the frontal cortex, a brain region involved in thinking and decision-making. They used a technique called real-time PCR to measure gene activity at two time points: 1 hour and 3 hours after giving the compounds. The researchers found that Selank changed the activity of many genes related to the GABA system, which is the brain’s main calming mechanism. Specifically, Selank affected genes that make GABA receptors (the “docking stations” where GABA attaches to brain cells), dopamine receptors (involved in reward and motivation), serotonin receptors (involved in mood), and proteins that transport GABA around the brain. The pattern of gene changes caused by Selank was similar to those caused by GABA itself, suggesting that Selank works by fine-tuning the GABA system rather than activating it directly. This helps explain why Selank has calming and anti-anxiety effects without causing the sedation or dependence problems associated with traditional anti-anxiety drugs like benzodiazepines.

GABA, Selank, and Olanzapine Affect the Expression of Genes Involved in GABAergic Neurotransmission in IMR-32 Cells

Authors: Elena Filatova, Anastasiya Kasian, Timur Kolomin, Ekaterina Rybalkina, Anelya Alieva, Lyudmila Andreeva, Svetlana Limborska, Nikolay Myasoedov, Galina Pavlova, Petr Slominsky, Maria Shadrina

Published: Frontiers in Pharmacology, 28 February 2017, Volume 8, Article 89

URL: https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2017.00089/full

Scientific Summary

The study examined changes in expression of 84 genes involved in neurotransmission in the human neuroblastoma cell line IMR-32 using quantitative PCR (qPCR) method. IMR-32 cells were seeded into 6-well plates at 1-2 million cells per well and incubated for 24 hours to allow adherence. After 24 hours, cells were treated with Selank (1 nmol per well), GABA (1 nmol per well), olanzapine (1 nmol per well), or combinations (Selank+GABA; Selank+olanzapine) for 1 hour. RNA was extracted using Trizol reagent and QIAamp RNA mini kit, and first-strand cDNAs were synthesized using the RT2 First Strand Kit. qPCR was performed using Custom Human RT2 Profiler PCR Array on the StepOnePlus Real-Time qPCR System. The study found no changes in mRNA levels of the genes studied under the effect of Selank alone in IMR-32 cells. However, the combined effect of GABA and Selank led to nearly complete suppression of changes in expression of genes in which mRNA levels changed under the effect of GABA alone. When Selank was used in conjunction with olanzapine, expression alterations of 35 genes were observed (compared with 25 genes for olanzapine alone), including decreased mRNA levels of ADORA2A, CSF2, CX3CL1, DRD3, FOS, GABBR1, JUNB, MMP10, NPFFR1, and SLC32A1. The data indicate that Selank has no direct effect on mRNA levels of GABAergic system genes in neuroblastoma IMR-32 cells, but may affect the interaction of GABA with GABAA receptors and may enhance the effect of olanzapine on gene expression.

Plain English Interpretation

This study investigated how Selank affects gene activity in human brain-like cells (neuroblastoma cells) grown in laboratory dishes. The researchers treated these cells with Selank alone, GABA alone, olanzapine (an antipsychotic medication) alone, or combinations of these compounds, then measured which genes turned on or off after one hour. Surprisingly, when Selank was added to the cells by itself, it didn’t change the activity of any of the genes they were monitoring. This was different from what happens in living animals, suggesting that Selank needs the complex environment of a living brain to show its effects. However, when Selank was combined with GABA, something interesting happened: Selank almost completely blocked the gene changes that GABA normally causes. This suggests that Selank might work by modifying how GABA interacts with its receptors on brain cells, rather than by directly activating those receptors itself. When Selank was combined with olanzapine, it amplified the drug’s effects, causing changes in even more genes than olanzapine alone. These findings help explain why Selank doesn’t cause sedation or addiction like traditional anti-anxiety drugs—it acts as a modulator that fine-tunes the GABA system rather than directly activating it. The results also suggest that Selank might enhance the effects of certain psychiatric medications, which could have implications for combination therapies.

Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity

Authors: Tatiana V. Vyunova, Lioudmila Andreeva, Konstantin Shevchenko, Nikolay Myasoedov

Published: Protein and Peptide Letters, Volume 25, Number 10, 2018, pp. 914-923(10)

URL: https://www.ingentaconnect.com/content/ben/ppl/2018/00000025/00000010/art00006

Scientific Summary

The study used the radioligand-receptor method of analysis to investigate Selank’s molecular mechanisms. Brain cell plasmatic membranes were isolated and protein concentration was detected in membrane samples. HPLC was used to obtain and ensure reagents and Selank purity. The radioligand binding assay used tritiated GABA ([3H]GABA) to measure binding to GABA receptors in the presence of Selank. The study showed that Selank affects [3H]GABA binding as a positive allosteric modulator. The joint action of Selank and some benzodiazepines (Diazepam and Olanzapine) also regulates activity of [3H]GABA binding in a specific manner, which is not cumulative and differs from either substance individually. Selank was able to block the modulatory activity of Diazepam and Olanzapine, suggesting that the location of their binding sites and the peptide binding sites are apparently not the same, but potentially may partially overlap. The study demonstrated concentration-dependent effects of Selank on GABA receptor binding. The results showed that one of Selank’s anti-anxiety molecular mechanisms can be associated with subtype selective concentration-dependent allosteric modulation of GABA receptors.

Plain English Interpretation

This research used a sophisticated technique to understand exactly how Selank interacts with GABA receptors in the brain. The scientists isolated membranes from brain cells and used radioactive GABA molecules as tracers to see how Selank affects GABA’s ability to bind to its receptors. They discovered that Selank acts as what’s called a “positive allosteric modulator,” which means it doesn’t directly activate GABA receptors itself, but instead changes the shape of the receptor in a way that makes GABA work better. Think of it like adjusting the tuning on a radio—Selank fine-tunes the receptor to make it more responsive to GABA’s signal. Interestingly, when the researchers combined Selank with benzodiazepine drugs like Diazepam (Valium) or Olanzapine, Selank actually blocked some of the drugs’ effects rather than adding to them. This suggests that Selank and these drugs bind to different but overlapping spots on the GABA receptor. The effect of Selank depended on how much was present—higher concentrations had stronger effects. This concentration-dependent action is important because it means Selank’s effects are self-limiting and less likely to cause overdose problems. The findings help explain why Selank provides anxiety relief without the drowsiness, memory problems, and addiction risks associated with benzodiazepines—it works through a gentler, more nuanced mechanism that enhances the brain’s natural calming system rather than overwhelming it.