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PCL Semax 10mg

$349.99

SKU: TIR 60mg Categories: ,

What is Semax?

Semax is a synthetic heptapeptide (Met–Glu–His–Phe–Pro–Gly–Pro) derived from the adrenocorticotropic hormone fragment ACTH(4–10), with the addition of a C-terminal Pro–Gly–Pro sequence that enhances its metabolic stability and extends its biological activity while eliminating hormonal properties (Eremin et al. 2003; Ivanova et al. 2005). Experimental studies have shown that Semax modulates monoaminergic systems in animal models, particularly the serotoninergic pathway. Intraperitoneal administration increased tissue and extracellular concentrations of 5-hydroxyindoleacetic acid (5-HIAA) in the hypothalamus and striatum of mice and rats, indicating enhanced serotonin turnover, while dopaminergic metabolites remained largely unchanged (Eremin et al. 2003). These findings suggest that Semax acts through selective modulation of serotonin metabolism, potentially involving interaction with melanocortin-4 receptors (Eremin et al. 2003).

Transcriptomic analyses in rat models of focal cerebral ischemia revealed that Semax influences the expression of genes related to immune and vascular regulation (Medvedeva et al. 2014). Specifically, it upregulated genes encoding immunoglobulins and chemokines, altered the transcription of endothelial and smooth muscle cell migration genes, and affected calcium-dependent signaling processes (Medvedeva et al. 2014). These molecular responses indicate a coordinated modulation of immune activity and vascular development under ischemic conditions.

In behavioral stress paradigms, Semax demonstrated dose-dependent effects on stress-induced analgesia and exploratory behavior in rats subjected to forced swimming (Ivanova et al. 2005). Lower doses (0.05 mg/kg) attenuated stress-induced analgesia, whereas higher doses (0.5 mg/kg) enhanced analgesic and anxiety-like responses. The authors attributed these effects to modulation of serotonergic pathways rather than opioid or melanocortin receptor mechanisms (Ivanova et al. 2005). Collectively, these findings describe Semax as a stable ACTH-derived peptide that exerts diverse regulatory influences on monoaminergic, immunogenic, and vascular systems in experimental models.

References

Eremin, K. O., Kudrin, V. S., Grivennikov, I. A., Miasoedov, N. F., & Rayevsky, K. S. (2003). Effects of Semax on dopaminergic and serotoninergic systems of the brain. Doklady Biological Sciences, 394, 1–3.

Ivanova, D. M., Vilenskii, D. A., Levitskaya, N. G., Andreeva, L. A., Alfeeva, L. Y., Kamenskii, A. A., & Myasoedov, N. F. (2005). Effect of Semax on changes in pain sensitivity and behavior of animals induced by forced swimming. Doklady Biological Sciences, 407, 123–127.

Medvedeva, E. V., Dmitrieva, V. G., Povarova, O. V., Limborska, S. A., Skvortsova, V. I., Myasoedov, N. F., & Dergunova, L. V. (2014). The peptide Semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis. BMC Genomics, 15, 228. https://doi.org/10.1186/1471-2164-15-228

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