N-Acetyl Semax 30mg

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N-Actetyl Semax

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N-Acetyl Semax

N-Acetyl Semax 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).

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.[3][5][6][9]

Sometimes referred to simply as Semax, N-Acetyl Semax 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.[1]


 

Semax Peptide

SEMAX

Molecular formula: C39H54N10O10S
Molar Mass: 854.97


 


 

N-Acetyl Semax Research Effects

N-Acetyl Semax’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.[4]

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.[12] 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.[12] 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).[12]

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.[5] 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.[5] 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.[5]


 

Clinical Studies with N-Acetyl Semax

A recent 2017 study published in Molecular Genetics and Genomics demonstrated N-Acetyl Semax’s powerful protective effect in rat subjects with ischemic brain injury (brain stroke).[9] Researchers noted that the peptide markedly affected the rats’ immune response.[9] The Semax peptide was observed to enhance the antigen presentation signaling pathway, intensify ischemia’s effect on the interferon signaling pathways, and affect the processes for synthesizing immunoglobulins.[9] Additionally, the peptide was seen to significantly increase expression of the gene encoding the immunoglobulin heavy chain.[9] Study researchers postulated that Semax’s neuroprotective mechanism was achieved through “neuroimmune crosstalk” and newly identified properties of Pro-Gly-Pro (PGP), a component of the Semax peptide.[9]

Moreover, further research has indicated that decreased vascular injury and enhanced mRNA neurotrophin synthesis occurs after Semax administration in rats that have suffered cerebral ischemia due to stroke.[10] In a 2013 study, Semax was observed to have anti-inflammatory properties which manifested in reduced levels of vascular endothelial growth factor (VEGFA) in rat study subjects after ischemic brain injury.[10]

In 2007, researchers published a paper in Medical Hypothesis suggesting N-Acetyl Semax as a potential future treatment for Attention-Deficit Hyperactivity Disorder (ADHD) and Rett Syndrome.[2] Researchers noted that evidence gleaned from previous animal studies suggested that Semax was able to augment the effects of psychostimulants on central dopamine release while additionally stimulating central brain-derived neurotrophic factor (BDNF) synthesis.[2] Importantly, it was also noted in previous study that Semax could improve selective attention and modulate brain development.[2] As a result, they suggested that the increased central BDNF activity as a result of Semax administration could prove highly therapeutic in regards to Rett syndrome, while noting that BDNF and increased dopamine release could also highly benefit cases of ADHD.


 

N-Acetyl Semax Cognitive Effects

Remarkably, N-Acetyl Semax has exhibited cognitive effects in animal studies that seem to go far beyond protection and recovery from acute brain injury. In fact, studies have shown it to have a measureable effect on animal behavior.

A 2007 study analyzed the effects of the Semax peptide on the exploratory activity, anxiety level, and depression-like behavior in white rats.[4] While it was shown that chronic Semax administration did not significantly influence exploratory activity of the rats in a “non-stressogenic environment,” it did however stimulate anxiolytic (anti-anxiety) and antidepressant effects.[4] Researchers in the study concluded that the results gained from N-Acetyl Semax administration may be traced to the activation of the brain serotoninergic system as well as to increased BDNF expression in the hippocampus.[4]

In addition, the Semax peptide has been shown to reduce memory and learning deficits in rat study subjects treated with amphetamines in utero.[11] In this study, published in BMC Pharmacology, it was observed that Semax induced delayed memory deficits and significant learning impairments in juvenile offspring of rats.[11] Therefore, researchers concluded that the peptide may lead to a significant recovery of the memory functions of brain-damaged rat subjects, opening new approaches for neuroprotection and cognitive rehabilitation of prenatal brain damage.[11]

Further, a 2001 study examined the effects of N-Acetyl Semax administration on subjects with glaucomatous optic neuropathy, an eye disorder.[6] Intriguingly, it was shown by electrophysiological and computer methods of examination that the Semax peptide outperformed traditional neuroprotective treatments for glaucoma. Researchers concluded that the success of Semax was due to its powerful neuroprotective and neurotrophic effects, further demonstrating the potent healing effect the peptide seems to exhibit on the neurological system.[6]


 

Further Protective Effects

The neuroprotective properties of Semax peptides have been demonstrated in animal studies to protect against damaging effects of heavy metal poisoning as well. A recent 2016 study published in Doklady Biological Sciences observed the effects of Semax on heavy metal poisoning in rats compared with ascorbic acid.[8] Researchers established that heavy metal salts inhibited the avoidance response in rat subjects, and that Semax counteracted this effect as strongly as ascorbic acid.[8] As a result, researchers confirmed the peptide’s antioxidant properties.[8]

Moreover, the N-Acetyl Semax peptide has been shown to moderate the effects of copper cytotoxicity in animal studies as well.[7] Researchers in a 2015 study published in the Journal of Inorganic Biochemistry noted that Semax exhibits marked neuroprotective activities on cognitive brain functions.[7] Dys-homeostasis of metal ions is involved in several neurodegenerative disorders, so it was hypothesized that N-Acetyl Semax would be effective in mitigating these disorders.[7] Ultimately, they found that a reduced copper induced cytotoxicity was indeed observed following Semax administration.[7]

Certainly, clinical study has shown that N-Acetyl Semax’s possible therapeutic value may well extend beyond mental and cognitive disorders. In a 2002 study published in the Bulletin of Experimental Biology and Medicine, researchers studied the effects of the Semax peptide on healing peptic ulcers.[3] Remarkably, it was observed that ulcer healing occurred in 89.5% patients receiving intranasal Semax compared to just over 30% in the control group.[3] Researchers did note that further study of Semax in different combinations with common antiulcer drugs was needed, but these findings proved quite promising for future therapeutic applications.[3]


 

References:

1. Biophysical Journal. Volume 95. November 2008 4879–4889. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2576403/pdf/4879.pdf
2. Med Hypotheses. 2007;68(5):1144-6. Epub 2006 Sep 25. https://www.ncbi.nlm.nih.gov/pubmed/16996699
3. Ivanikov, I.O., Brekhova, M.E., Samonina, G.E. et al. Bulletin of Experimental Biology and Medicine (2002) 134: 73. doi:10.1023/A:1020621124776. https://link.springer.com/article/10.1023%2FA%3A1020621124776
4. Ross Fiziol Zh Im I M Sechenova. 2007 Jun;93(6):661-9. https://www.ncbi.nlm.nih.gov/pubmed/17850024
5. Brain Res. 2006 Oct 30;1117(1):54-60. Epub 2006 Sep 22. https://www.ncbi.nlm.nih.gov/pubmed/16996037
6. Vestn Oftalmol. 2001 Jul-Aug;117(4):5-8. https://www.ncbi.nlm.nih.gov/pubmed/11569188
7. J Inorg Biochem. 2015 Jan;142:39-46. doi: 10.1016/j.jinorgbio.2014.09.008. Epub 2014 Sep 28. https://www.ncbi.nlm.nih.gov/pubmed/25310602
8. Dokl Biol Sci. 2016 May;468(1):112-4. doi: 10.1134/S0012496616030066. Epub 2016 Jul 14. https://www.ncbi.nlm.nih.gov/pubmed/27411820
9. Mol Genet Genomics. 2017 Jun;292(3):635-653. doi: 10.1007/s00438-017-1297-1. Epub 2017 Mar 2. https://www.ncbi.nlm.nih.gov/pubmed/28255762
10. Mol Biol (Mosk). 2013 May-Jun;47(3):461-6. https://www.ncbi.nlm.nih.gov/pubmed/23888777
11. BMC Pharmacol. 2009; 9(Suppl 2): A26. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2778896/
12. BMC Genomics. 2014; 15: 228. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3987924/