N-Acetyl Semax is a synthetic peptide derived from the ACTH(4-7) fragment and chemically modified through N-terminal acetylation. In laboratory research, this modification is used to investigate peptide stability, intracellular signaling, and transcriptional responses in neural and peripheral tissues. N-Acetyl Semax is studied exclusively in controlled experimental systems, including cellular assays and in vivo animal models, as a tool for probing peptide-mediated regulatory mechanisms.

Image of Semax core peptide without the N-acetyl modification
Source: PubChem

Sequence: Ac-Met-Glu-His-Phe-Pro-Gly-Pro-NH₂
Molecular Formula: C₃₉H₅₃N₉O₁₁S
Molecular Weight: 855.97 g/mol
CAS Number: 2920938-90-3

The N-terminal acetyl group and C-terminal amidation are commonly examined in peptide chemistry for their effects on enzymatic stability and receptor interaction kinetics in experimental systems.

N-Acetyl Semax is used in preclinical research settings to examine peptide-driven modulation of molecular and transcriptional networks. Common laboratory applications include:

• Gene expression analysis in neural tissue following peptide exposure
• Investigation of signaling pathways associated with neurotrophic factor regulation
• Assessment of vascular- and immune-related transcriptional responses in animal models
• Exploration of peptide effects on mitochondrial and oxidative-stress–related pathways

Mechanistic studies report that N-Acetyl Semax exposure is associated with altered transcription of genes involved in neurotrophic signaling, vascular regulation, and immune-related pathways in rodent models. Genome-wide analyses have identified modulation of transcripts linked to endothelial signaling, mitochondrial function, and stress-responsive regulatory networks.

At the molecular level, these observations are used to map peptide-mediated interactions with intracellular signaling cascades rather than to infer organism-level outcomes.

Preclinical investigations of N-Acetyl Semax primarily involve in vivo rodent models and in vitro molecular assays. Published studies describe time-dependent changes in gene expression within the hippocampus, frontal cortex, and vascular-associated tissues. These data sets are used to characterize transcriptional dynamics and pathway-level responses following peptide exposure.

Additional studies evaluate N-Acetyl Semax as a research tool for examining relationships between neurotrophic factor signaling and cellular adaptation under experimentally induced stress conditions.

N-Acetyl Semax is supplied as a synthetic research peptide. Analytical characterization typically includes high-performance liquid chromatography (HPLC) and mass spectrometry (MS) to verify identity, molecular mass, and purity in accordance with standard laboratory practices.

The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.

Dr. Igor Ivanovich Bobyntsev researches at the Kursk State Medical University within the Department of Pathophysiology. His main goal is to find new, more effective methods for teaching morphological disciplines… such as histology, cytology, embryology, human anatomy, pathological anatomy, the study of the morphological manifestation of stress-limiting effects of neuropeptides and their synthetic analogues. His key interests pertain to Antioxidants, Free Radicals, Antioxidant Activity, Free Radical Scavengers, Reactive Oxygen Species, Lipid Peroxidation, SOD, Oxidative Stress Biomarkers, Inflammatory Biomarkers, and Oxidative Stress. He specifically studied the influence of Semax on the morphofunctional state of hepatocytes, and lipid peroxidation in the liver, when under chronic emotional and painful stress.

Dr. Igor Ivanovich Bobyntsev is being referenced as one of the leading scientists involved in the research and development of Semax. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Peptide Sciences and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide. Dr. Igor Ivanovich Bobyntsev is listed in [8] and [9] under the referenced citations.

1. I. S. Lebedeva et al., “Effects of Semax on the Default Mode Network of the Brain,” Bull. Exp. Biol. Med., vol. 165, no. 5, pp. 653–656, Sep. 2018. [PubMed]
2. R. B. Mars, F.-X. Neubert, M. P. Noonan, J. Sallet, I. Toni, and M. F. S. Rushworth, “On the relationship between the ‘default mode network’ and the ‘social brain,’” Front. Hum. Neurosci., vol. 6, 2012. [PMC]
3. E. V. Medvedeva et al., “The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis,” BMC Genomics, vol. 15, p. 228, Mar. 2014. [PubMed]
4. E. I. Gusev, M. Y. Martynov, E. V. Kostenko, L. V. Petrova, and S. N. Bobyreva, “[The efficacy of semax in the tretament of patients at different stages of ischemic stroke],” Zh. Nevrol. Psikhiatr. Im. S. S. Korsakova, vol. 118, no. 3. Vyp. 2, pp. 61–68, 2018. [PubMed]
5. T. I. Agapova et al., “[Effect of semax on the temporary dynamics of brain-derived neurotrophic factor and nerve growth factor gene expression in the rat hippocampus and frontal cortex],” Mol. Genet. Mikrobiol. Virusol., no. 3, pp. 28–32, 2008. [PubMed]
6. M. H. Scantlebury, K.-C. Chun, S.-C. Ma, J. M. Rho, and D. Y. Kim, “Adrenocorticotropic Hormone Protects Learning and Memory Function in Epileptic Kcna1-null mice,” Neurosci. Lett., vol. 645, pp. 14–18, Apr. 2017. [PubMed]
7. T. Deltheil et al., “Behavioral and serotonergic consequences of decreasing or increasing hippocampus brain-derived neurotrophic factor protein levels in mice,” Neuropharmacology, vol. 55, no. 6, pp. 1006–1014, Nov. 2008. [PubMed]
8. Ivanov, Alexander & Bobyntsev, Igor & Shepeleva, Olga & Kryukov, Alexey & Andreeva, L & Myasoedov, N. (2017). Influence of ACTG4-7-PGP (Semax) on Morphofunctional State of Hepatocytes in Chronic Emotional and Painful Stress. Bulletin of experimental biology and medicine. 163. [Research Gate]
9. Bobyntsev, Igor & Kryukov, Alexey & Shepeleva, Olga & Ivanov, Alexander. (2015). The effect of ACTH-4-7-PGP peptide on lipid peroxidation in liver and activity of serum transaminases in rats under acute and chronic immobilization stress conditions. 78. 18-21. [Research Gate]

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