N-Acetyl Semax Amidate | The A-Z Guide

Russian researchers created the nootropic peptide Semax in the 1980s, and N-Acetyl Semax Amidate is an improved form. N-Acetyl Semax Amidate and Semax have a seven-amino-acid sequence and are structurally similar.

This sequence combines a portion of adrenocorticotropic hormone (ACTH, more precisely ACTH 4-7, or Met-Glu-His-Phe) with an extension at the C-terminus that reads Pro-Gly-Pro.

Studies suggest that N-acetyl Semax Amidate may have several potential downstream impacts, including resistance to hydrolysis and degradation caused by leucine aminopeptidase. This is believed to result from the amidation and acetic acid integrated at the C-terminus.

According to reports, N-Acetyl Semax Amidate may have a half-life of 30 minutes longer than Semax before breaking it down into blood plasma. It also suggests more stability in brain tissue, meaning the nootropic action may remain longer in the organism.

Research on the mechanisms and possible properties of N-Acetyl Semax Amidate is severely deficient, whereas data on the compound’s pharmacokinetics are heavily concentrated. Nevertheless, the peptide is expected to have research potential similar to Semax, which is licensed in Russia for the investigations of cognitive disorders and stroke.

The existing scientific facts may, therefore, inform N-Acetyl Semax Amidate’s prospective pharmacodynamics on Semax’s mechanisms:

Research indicates that Semax may raise neurotrophic factors that help neurons survive and adapt, such as Brain-Derived Neurotrophic Factor (BDNF) and Nerve Growth Factor (NGF). Studies have suggested that Semax may raise BDNF levels by 40%.

Investigations purport that the peptide may potentially cause a one-hundred percent increase in the brain’s tropomyosin receptor kinase B (TrkB) receptor expression. These receptors mediate many of BDNF’s neuroprotective potential actions.

The findings imply that Semax may possibly influence mood, stress, cognitive functions, and reward-driven behavior by enhancing the signaling of serotonin, dopamine, and enkephalin. In addition to its nootropic potential, Semax is believed to exert possible anti-ulcer action via controlling microcirculation, vascular permeability, and gastrointestinal blood flow.

Future studies should determine if N-Acetyl Semax Amidate may reproduce these impacts. The peptide is only accessible as a research chemical in laboratories.

N-Acetyl Semax Amidst Potential

There is a lack of information on the properties of N-Acetyl Semax Amidate. However, the altered peptide should have better pharmacokinetics and the same impacts as Semax. The potential of N-Acetyl Semax Amidate may be better understood by outlining the most recent research on the perceived action of Semax.

N-Acetyl Semax Amidate and the Brain

Data suggests that N-Acetyl Semax Amidate may help protect neurons after a stroke, nerve injury, or neurotoxin exposure. A study of animal research models of stroke indicated that routine exposure following ischemic activity suggested increased BDNF levels and enhanced motor function. Decreased inflammation, as speculated in another experiment involving stroke research models, may aid in recovery.

N-Acetyl Semax Amidate and Nerves

One experimental study suggested that the research models of glaucoma that were exposed to Semax peptide appeared to have had less pressure-driven nerve damage.

N-Acetyl Semax Amidate and Neurotoxicity

Research models exposed to Semax while induced with alcohol delirium appeared to have exhibited signs of being able to withstand the neurotoxic effects of alcohol, as suggested by an exploratory animal-based study.

N-Acetyl Semax Amidate and Cognition

Before performing tests using N-Acetyl Semax Amidate, researchers wanted to review substantial nootropic research on Semax. The peptide’s impact on brain activity and mental exhaustion has been extensively studied:

Brain activity:

Researchers aimed to see how a 1% Semax solution or a placebo may have affected the Default Mode Network (DMN) in brain activity. The findings implied that Semax may have significantly increased volume in the rostral subcomponent of the DMN, especially in the medial frontal cortex, according to functional magnetic resonance imaging (fMRI) scans, which may indicate better information processing and episodic memory.

Fatigue:

Researchers evaluated the actions of Semax in relation to cognitive function. Following Semax exposure, the findings suggested a recall accuracy of 71%, which was significantly higher than the 41% reported in the control model.

N-Acetyl Semax Amidate and Ulcers

The extra-neurological impacts of N-Acetyl Semax Amidate are believed to be comparable to those of Semax. One study postulated that exposure to 1% Semax appeared to have accelerated the healing of peptic ulcers.

According to a 2002 study by Russian researchers Ivanikov et al., the healing rate for peptic ulcers following Semax exposure appeared to be 90%, about three times more than the control 30% healing rate. Investigations purport that because it seems to regulate blood flow and maintain blood vessels, Semax may hasten the recovery of peptic ulcers.

Although promising, the study above falls short of the rigorous standards required to be considered a non-inferiority study. The findings imply that the sequential approach may have aided over 94% of instances of peptic ulcers caused by helicobacter pylori.

For scientific studies, N-Acetyl Semax may be purchased online. Please note that none of the substances mentioned in this article have been approved for human or animal consumption.

References

[i] Kolomin, T., Shadrina, M., Slominsky, P., Limborska, S., &Myasoedov, N. (2013). A new generation of drugs: synthetic peptides based on natural regulatory peptides. Neuroscience and Medicine, 4(04), 223-252.

[ii] Khavinson, V., Ilina, A., Kraskovskaya, N., Linkova, N., Kolchina, N., Mironova, E., Erofeev, A., &Petukhov, M. (2021). Neuroprotective Effects of Tripeptides-Epigenetic Regulators in Mouse Models of Alzheimer’s Disease. Pharmaceuticals (Basel, Switzerland), 14(6), 515. https://doi.org/10.3390/ph14060515

[iii] Shevchenko, K. V., Nagaev, I.u, Alfeeva, L. I.u, Andreeva, L. A., Kamenskiĭ, A. A., Levitskaia, N. G., Shevchenko, V. P., Grivennikov, I. A., & Miasoedov, N. F. (2006). Bioorganicheskaia khimiia, 32(1), 64–70. https://doi.org/10.1134/s1068162006010055

[iv] Tsai S. J. (2007). Semax, an analog of adrenocorticotropin (4-10), is a potential agent for the treatment of attention-deficit hyperactivity disorder and Rett syndrome. Medical hypotheses, 68(5), 1144–1146. https://doi.org/10.1016/j.mehy.2006.07.017

[v] Shevchenko, K. V., Nagaev, I. Y., Andreeva, L. A., Shevchenko, V. P., & Myasoedov, N. F. (2019). Prospects for Intranasal Delivery of Neuropeptides to the Brain. Pharmaceutical Chemistry Journal, 53, 89-100.

[vi] Markov, D. D., Dolotov, O. V., & Grivennikov, I. A. (2023). Melanocortin System: A Promising Target for the Development of New Antidepressant Drugs. International journal of molecular sciences, 24(7), 6664. https://doi.org/10.3390/ijms24076664

[vii] Shevchenko, K. V., Nagaev, I. Y., Andreeva, L. A., Shevchenko, V. P., & Myasoedov, N. F. (2013). Stability of Semax acetyl to proteolysis in various biological media. Doklady biological sciences: proceedings of the Academy of Sciences of the USSR, Biological Sciences sections, 449, 110–112. https://doi.org/10.1134/S0012496613020166

[viii] Shadrina, M., Kolomin, T., Agapova, T., Agniullin, Y., Shram, S., Slominsky, P., Lymborska, S., & Myasoedov, N. (2010). Comparison of the temporary dynamics of NGF and BDNF gene expression in rat hippocampus, frontal cortex, and retina under Semax action. Journal of molecular neuroscience: MN, 41(1), 30–35. https://doi.org/10.1007/s12031-009-9270-z