N-Acetyl Semax is a heptapeptide and synthetic analog of adrenocorticotropic hormone, ACTH 4-10, which was developed in Russia. This peptide has potent nootropic, neuroprotective, neurogenic, and neurorestorative effects, as observed in animal studies. N-Acetyl Semax has been extensively researched in mammalian studies involving brain injuries such as stroke, transient ischemic attack, memory and cognitive disorders, optic nerve disease, peptic ulcers, and immune system enhancement. It undergoes an important transformation via N-terminal acetylation to increase stability and biological activity, which has been shown to increase the efficiency of the peptide’s specific mechanism of action.
A 2017 study published in Molecular Genetics and Genomics demonstrated the neuroprotective properties of N-Acetyl Semax in rat subjects with ischemic brain trauma. The 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. Furthermore, the peptide significantly increased expression of the gene encoding the immunoglobulin heavy chain. Researchers postulated that Semax’s neuroprotective mechanism was achieved through “neuroimmune crosstalk” and newly identified properties of Pro-Gly-Pro (PGP).
In addition, further research has indicated that Semax administration can lead to decreased vascular injury and enhanced mRNA neurotrophin synthesis in rats that have suffered cerebral ischemia due to stroke. Semax was also observed to have anti-inflammatory properties, manifesting in reduced levels of vascular endothelial growth factor (VEGFA) in rat study subjects after ischemic brain injury.
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. They noted that 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. The increased central BDNF activity as a result of Semax administration could prove highly therapeutic in regards to Rett syndrome, while BDNF and increased dopamine release could also highly benefit cases of ADHD.
N-Acetyl Semax has demonstrated significant cognitive effects in animal studies that go beyond protection and recovery from acute brain injury. For instance, a study conducted on white rats in 2007 showed that chronic Semax administration had anxiolytic and antidepressant effects, which may be attributed to the activation of the brain serotoninergic system and increased BDNF expression in the hippocampus.
Semax has also been shown to reduce memory and learning deficits in rat subjects treated with amphetamines in utero, leading researchers to conclude that the peptide may aid in neuroprotection and cognitive rehabilitation of prenatal brain damage.
In addition, Semax has demonstrated its potential in treating glaucomatous optic neuropathy by outperforming traditional neuroprotective treatments. Semax has also exhibited neuroprotective properties in animal studies by counteracting the effects of heavy metal poisoning and copper cytotoxicity, and reducing cytotoxicity induced by reduced copper.
Moreover, a clinical study in 2002 found that Semax administration led to healing of peptic ulcers in a significantly higher percentage of patients compared to the control group, providing promising prospects for future therapeutic applications.
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