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Is a synthetic analog of adrenocorticotropic hormone, ACTH 4-10, and is a heptapeptide with the structure Met-Glu-His-Phe-Pro-Gly-Pro. The Semax peptide consists of the ACTH fragment and the tripeptide Pro-Gly-Pro (PGP).Buy N-Acetyl Selank online
Created in Russia, N-Acetyl Semax has been observed in animal studies to have very potent nootropic, neuroprotective, neurogenic, and neurorestorative effects. As a result, it has been researched extensively in mammalian studies involving brain injuries like stroke and transient ischemic attack, disorders of the memory and cognitive faculties, as well as optic nerve disease, peptic ulcers, and immune system enhancement.
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Sometimes referred to simply as Semax, N-Acetyl Selank undergoes an important transformation via N-terminal acetylation. This is performed in order to increase the peptide’s stability and biological activity. Research on peptide N-terminal acetylation has suggested that the process may offer distinct advantages, including increasing the efficiency of the peptide’s specific mechanism of action.
N-Acetyl Semax Research Effects
N-Acetyl Selank’s action mechanisms are not entirely clear, but research has suggested that much of its neuroprotective and restorative effects may be traced to the activation of the brain serotoninergic system in addition to increased BDNF expression in the hippocampus.
In addition, the Semax peptide is known to affect several biological processes involved in the function of various systems. The peptide markedly affects the immune response, altering the expression of genes that modulate the amount and mobility of immune cells and enhancing the expression of genes that encode chemokines and immunoglobulins. In studies conducted on rats, Semax is also observed to influence the expression of genes that promote the formation and functioning of the vascular system.
As a result, it is believed that the key mechanisms of the peptide’s neuroprotective effects are likely to be its immunomodulating effect and its impact on the vascular system during ischemia (inadequate blood flow).
Moreover, a 2006 study published in Brain Research concluded that the Semax peptide affects cognitive brain functions by modulating the expression and the activation of the hippocampal BDNF/trkB system.Researchers in the study analyzed the effects of Semax administration on the brains of rat subjects, observing that a 1.4-fold increase of BDNF protein levels along with a 1.6-fold increase of trkB tyrosine phosporylation levels occurred.
Additionally, a 3-fold increase of exon III BDNF and a 2-fold increase of trkB mRNA levels occurred in the rat hippocampus as well. This supports the view that activation of the hippocampal BDNF/trkB system is key to the action mechanisms of Semax.