Semax (Research Overview)
Semax is a synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) derived from the ACTH(4-10) fragment with a C-terminal Pro-Gly-Pro extension. The literature describes it as a neuropeptide analog that lacks the corticotropic activity of full-length ACTH.
Mechanism of Action
Semax retains the Met-Glu-His-Phe core of ACTH(4-10) and adds a Pro-Gly-Pro tail that is described in the literature as improving resistance to peptidase degradation. Published work has examined its effects on neurotrophin signaling, including expression of BDNF and NGF and their receptors in rodent hippocampus and cortex.
Additional mechanism studies have looked at interactions with melanocortin receptor pathways and modulation of monoaminergic (serotonergic and dopaminergic) systems in animal models. Mechanistic conclusions remain preliminary and vary by model and by research group.
Research Areas
Preclinical research has used Semax in rodent models of focal and global cerebral ischemia, where investigators have measured neuronal survival markers, gene-expression profiles, and inflammatory-signaling changes.
A second area is cognitive-function paradigms in animals, including learning and memory tasks, where Semax has been used as a tool compound to examine neurotrophin-dependent signaling. Gene-expression profiling studies have also characterized transcriptional responses in brain tissue following exposure in vivo.
Findings from animal or in-vitro systems do not establish safety or efficacy for any indication and should not be interpreted as medical claims.
Specification summary
Semax
Stated purity ≥99%. For laboratory research use only.
Related materials
References
- Agapova TY, Agniullin YV, Shadrina MI, Shram SI, Slominsky PA, Lymborska SA, et al. Neurotrophin gene expression in rat brain under the action of Semax, an analogue of ACTH 4-10. Neurosci Lett. 2007;417(2):201-5. PMID 17353092 · DOI
- Shadrina M, Kolomin T, Agapova T, Agniullin Y, Shram S, Slominsky P, et al. Comparison of the temporary dynamics of NGF and BDNF gene expression in rat hippocampus, frontal cortex, and retina under Semax action. J Mol Neurosci. 2010;41(1):30-5. PMID 19662538 · DOI
- Dmitrieva VG, Povarova OV, Skvortsova VI, Limborska SA, Myasoedov NF, Dergunova LV. Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia. Cell Mol Neurobiol. 2010;30(1):71-9. PMID 19633950 · DOI
- Medvedeva EV, Dmitrieva VG, Povarova OV, Limborska SA, Skvortsova VI, Myasoedov NF, 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. 2014;15:228. PMID 24661604 · DOI
Cited literature is provided for scientific context only and does not describe or endorse any use of these products.
For laboratory research use only. Not for human or veterinary use. Not intended to diagnose, treat, cure, or prevent any disease.