Semax
Semax
Research Use Only
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Semax Overview
Semax is a synthetic heptapeptide derived from adrenocorticotropic hormone (ACTH 4-10) with the addition of a C-terminal Pro-Gly-Pro sequence. It is studied in laboratory and preclinical models for its influence on neuronal signaling, CNS pathway dynamics, and molecular stress responses. Research has investigated its ability to modulate neurotrophic factor expression, neurotransmitter systems, and oxidative stress pathways.
History
Semax was developed in Russia in the 1980s–1990s at the Institute of Molecular Genetics of the Russian Academy of Sciences as part of research on synthetic peptides with potential neuromodulatory effects. It was designed to retain the neuroactive core of ACTH while eliminating hormonal activity, thereby providing a stable, non-hormonal peptide for CNS research. Over time, studies expanded into its roles in neuronal signaling characterization, synaptic plasticity, and regulation of gene expression in experimental brain models.
Structure
Molecular Formula: C₃₇H₅₁N₉O₁₀S
Molecular Weight: 813.9 g/mol
CAS: 80714-61-0
Sequence: Met-Glu-His-Phe-Pro-Gly-Pro
Research Findings
Semax has been studied in neurological, CNS, and systemic models, with research highlighting its role in neuronal signaling, synaptic pathway dynamics, and stress response. Studies also report activity in neurotransmitter modulation, oxidative stress pathways, and signaling dynamics in preclinical settings.
Key Areas of Research:
- Neurological: Neuronal signaling, pathways, cascades
- CNS: Synaptic plasticity, signaling, function
- Systemic: Stress pathways, remodeling, resilience
Together, these findings suggest broad experimental potential for Semax across neurological, CNS, and systemic pathways. By influencing neurotransmitter systems and supporting signaling and pathway responses, Semax provides a versatile platform for research into CNS dynamics, stress biology, and systemic resilience in laboratory settings.
References
Ashmarin, I.P., et al. (1997). A nootropic adrenocorticotropin analog 4-10-Semax (15 years of design and study). Zhurnal Vysshei Nervnoi Deyatelnosti, 47(2), 420–430.
Dolotov, O.V., et al. (2006). Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Research, 1117(1), 54–60.
Dergunova, L.V., et al. (2014). 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, 15, 228.