Description


Chemical Properties


Storage

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  1. Overview
  
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  2. Biochemical Characteristics
  
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  3. Research Applications
  

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  4. Summary of Preclinical Research
  
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  5. Form & Analysis Testing
  
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  6. Referenced Citations
  
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  7. RUO Disclaimer
  

Overview

Semax (ACTH(4–7)-PGP; also referred to as Pro-Gly-Pro-ACTH in registration records) is a synthetic heptapeptide derived from a defined segment of adrenocorticotropic hormone (ACTH). In the scientific literature, Semax has been used as a research tool in neurobiology and molecular signaling studies, including investigations of activity-dependent genetic programs, neurotrophin-linked transcriptional responses, monoaminergic pathway markers, and systems-level network activity measured using experimental imaging and omics-based approaches.

Preclinical publications describe Semax-associated changes in transcriptional signatures within relevant CNS tissues and report modulation of neurotrophin-related gene expression (including BDNF and NGF) in controlled animal- and cell-based experimental designs.

Biochemical Characteristics

Semax structure without the N-acetyl side chain

Source: PubChem

Sequence: Met-Glu-His-Phe-Pro-Gly-Pro Molecular Formula: C37H51N9O10S Molecular Weight: 813.92 g/mol CAS Number: 80714-61-0 Synonyms: Pro-Gly-Pro-ACTH

Research Applications

Semax is a synthetic analog of an ACTH fragment corresponding to amino acids 4–10 of ACTH with a Pro-Gly-Pro motif at the C-terminus. In laboratory research, Semax is used in preclinical models to investigate pathway-level regulation of:

• Neurotrophin-linked transcription: experimental measurements involving BDNF and NGF gene expression dynamics in relevant CNS regions [5].
• Systems-level brain network activity: research imaging endpoints evaluating resting-state network behavior and connectivity patterns [1].
• Neurovascular and immune genetic programs: whole-genome transcriptional profiling in animal models with emphasis on vascular and immune system gene sets in brain tissue [3].
• Learning/memory model endpoints: mechanistic comparisons using ACTH-related peptides in genetic rodent models with cognition-focused behavioral readouts [6].
• Monoaminergic signaling markers: studies measuring serotonergic pathway endpoints and neurotrophin-dependent behavioral paradigms in rodents.
• Oxidative stress biomarker panels: morphofunctional and lipid peroxidation endpoints associated with the liver under stress model conditions [8] [9].

Summary of Preclinical Research

Pathway / Mechanistic Context

In the cited preclinical literature, Semax is evaluated as a modulator of gene expression programs and systems-level neuronal network activity. Reported parameters include transcriptomic changes in CNS tissue, neurotrophin-associated transcriptional dynamics, and network-level activity patterns measured using experimental neuroimaging techniques. In addition, publications describe Semax-associated changes in peripheral oxidative stress biomarker panels and liver tissue parameters under stress model conditions.

1. Resting-State Network Readouts

Experimental imaging studies report changes in resting-state network behavior following Semax exposure, including measured effects within the default mode network as defined by the analytical framework of the study [1]. The reference literature on the default mode network and social cognition network relationships is commonly used to interpret these types of resting-state measurements in neuroscience research [2].

Image showing the overlap in activation between the resting-state neural network and the regions of the brain responsible for social cognition.

Source: PubMed

2. Genome-Wide Gene Expression Profiling in a Rodent Ischemia Model

In a rat model of focal cerebral ischemia, genome-wide gene expression analysis revealed Semax-associated expression changes in gene sets related to the immune and vascular systems in brain tissue, providing molecular context for mechanistic research into neurovascular and inflammatory pathway regulation in this model [3].

3. Neurotrophin-Related Gene Expression Dynamics

Rodent studies report that Semax exposure is associated with time-dependent changes in gene expression in the hippocampus and frontal cortex, including reported effects on BDNF and NGF gene expression measurements within the study design [5].

4. ACTH-Related Peptides in a Genetic Epilepsy Model

Preclinical studies in a Kcna1-deficient mouse model indicate that ACTH exposure is associated with preservation of learning and memory within the experimental paradigm, providing comparative context for research involving ACTH-derived peptide fragments such as Semax [6].

5. Serotonin- and Neurotrophin-Linked Behavioral Paradigms

Rodent studies evaluating altered hippocampal BDNF levels report behavioral and serotonergic consequences in experimental models, supporting broader mechanistic frameworks connecting neurotrophin abundance, serotonergic pathway markers, and behavioral outcomes in preclinical research [7].

6. Peripheral Oxidative Stress and Hepatic Biomarkers

Other cited studies describe Semax-associated effects on liver morphofunctional parameters and lipid peroxidation markers in rat stress models, including biochemical measurements relevant to oxidative stress research workflows [8] [9].

Form & Analysis Testing

Semax is a synthetic peptide supplied for controlled laboratory workflows. Laboratories may reference the sequence, CAS number, and registry identifiers for internal documentation and study design. Analytical characterization of peptides typically includes chromatographic purity analysis and mass spectrometry confirmation in accordance with internal qualification standards.

Article Author

The above bibliography was researched, edited, and organized by Dr. Logan, M.D. Dr. Logan earned his medical degree from the Case Western Reserve University School of Medicine and holds a bachelor’s degree in Molecular Biology.

Scientific Journal Author

Dr. Igor Ivanovich Bobyntsev conducts research at Kursk State Medical University in the Department of Pathophysiology. His primary objective is to develop new and more effective methods for teaching morphological disciplines, including histology, cytology, embryology, human anatomy, pathological anatomy, and the study of the morphological manifestations of the stress-limiting effects of neuropeptides and their synthetic analogs. His key research interests include 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 under conditions of chronic emotional and painful stress.

Dr. Igor Ivanovich Bobyntsev is referenced as one of the leading scientists involved in the research and development of Semax. This physician/scientist is in no way endorsing or promoting the purchase, sale, or use of this product for any purpose. There is no affiliation or relationship, implied or otherwise, between Peptide Sciences and this physician. The purpose of referencing the physician is to recognize and credit the extensive research and development efforts carried out by the scientists studying this peptide. Dr. Igor Ivanovich Bobyntsev is listed under references [8] and [9].

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 treatment 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 temporal 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 ACTH4-7-PGP (Semax) on Morphofunctional State of Hepatocytes in Chronic Emotional and Painful Stress. Bulletin of Experimental Biology and Medicine. 163. [ResearchGate]
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. [ResearchGate]

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The products offered on this website are supplied for in vitro research only. In vitro studies (Latin: “in glass”) are performed outside the body. These products are not medicines or drugs and have not been approved by the FDA to prevent, treat, or cure any medical condition, illness, or disease. Bodily administration of any kind to humans or animals is strictly prohibited by law.

For laboratory research use only. Not for human, medical, diagnostic, or veterinary use.