N-Acetyl Semax – 25MG
$58.00
Discount per Quantity
Quantity | Discount | Price |
---|---|---|
5 - 8 | 5% | $55.10 |
9 + | 10% | $52.20 |
N-Acetyl Semax
N-Acetyl Semax Peptide N-Acetyl Semax is a synthetic polypeptide analog of the ACTH naturally produced in the body. This peptide is a modified version of a fragment of the adrenocorticotropic hormone ACTH 4-7, which consists of 4 amino acids: methionine, glutamic acid, histidine, and phenylalanine, the so-called Met-Glu-His-Phe. An additional C-terminus extension of proline-glycine-proline or Pro-Gly-Pro is attached to the latter amino acid. N-Acetyl PGP Semax may have an increased permeability of the blood-brain barrier 2 due to the fact that the added Pro-Gly-Pro to the C-terminus increases the lipophilicity of the peptide. This potentially allows for its active diffusion through tight junctions or uptake via lipid raft-mediated endocytosis, bypassing the BBB. Furthermore, the PGP addition may alter the peptide’s interaction with an unspecified receptor or transport through BB barrier, promoting receptor-mediated transcytosis. In addition, acetylation of the peptide can inactivate acetylases, increasing the half-life of the peptide in the blood by maintaining the half-life Semax experiment. Overall Researchers have suggested that N-Acetyl Semax may be a nootropic and possess neuroprotective properties due to the following: It may interact with dopamine, serotonin, enkephalin, or BDNF levels, as noted previously. Furthermore, it may modulate gene expression or enhance immuno-response. It is largely accepted that since experimental studies have proven that this peptide inhibits serum enkephalin-degrading enzymes, it can, therefore, be hypothesized that this is where the interaction between Semax and enkephalins occurs as a matter of probability. The researchers assume that this neuropeptide’s inhibition of the serum enkephalin substrate enzyme activity will prevent enkephalins’ enzymatic degradation and increase their concentration in the brain. Enkephalins are endogenous opioid peptides that mediate nociception and stress. Furthermore, activation of the opioid system directly or indirectly influences DA and 5-HT release in brain neurons. Semax may increase the levels of its metabolite 5-HIAA in the striatum as optimal, suggesting possible amplification of serotonergic activity. The effect might be explained by the direct involvement of Semax in serotonin metabolism.
On the other hand, the peptide does not affect the concentration of DA and its metabolites. However, it can increase the responsiveness of the dopaminergic system and the agonist’s action.
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