Research Peptide · For laboratory research use only
Also known as ACTH 4-7 Pro8-Gly9-Pro10
Semax is a synthetic heptapeptide, Met-Glu-His-Phe-Pro-Gly-Pro, that joins the adrenocorticotropic hormone fragment ACTH(4-7) to a C-terminal Pro-Gly-Pro tripeptide; it is described in the literature as an analogue of ACTH(4-10)1,3. It is a different compound from N-acetyl Semax, which carries an acetylated N-terminus and has its own profile.
Published work, largely from groups in Moscow, comprises rodent studies of neurotrophin expression, rat models of focal cerebral ischaemia with transcriptome-wide analyses, neurochemical studies of monoamine systems, and in vitro work on copper binding1,2,3,4,5,6.
As described in the research literature
As described in the research literature, mechanistic interest in Semax has centred on brain-derived neurotrophic factor (BDNF). Membranes from rat basal forebrain contained specific, reversible, calcium-dependent binding sites for tritium-labelled Semax, and increased BDNF protein was reported in the basal forebrain but not the cerebellum1. In rat hippocampus, increases in BDNF protein, trkB tyrosine phosphorylation, and exon III BDNF and trkB mRNA were reported2.
In the rat permanent middle cerebral artery occlusion (pMCAO) model, Semax altered transcription of neurotrophins and their receptors selectively in the ischaemic cortex, compared with intact and sham-operated animals3. Genome-wide analysis in the same model found that most of the genes whose expression Semax altered were linked to the immune response, with a further group linked to the vascular system4. Neurochemical work in rodents reported increased striatal 5-hydroxyindoleacetic acid and an enhanced response to D-amphetamine, without changes in dopamine from Semax alone5.
What published studies have examined
Radioligand binding to rat basal forebrain membranes and BDNF protein levels in the basal forebrain were examined in one study1. A second measured BDNF and trkB protein, trkB phosphorylation and mRNA in rat hippocampus, alongside conditioned avoidance behaviour2.
Transcription of Bdnf, Ngf, Nt-3 and the Trk receptors was measured in rat cortex at three time points after pMCAO, comparing Semax with its C-terminal fragment Pro-Gly-Pro3. A genome-wide transcriptional analysis at 3 and 24 hours after pMCAO examined immune-related and vascular genes4.
Tissue and extracellular levels of dopamine, serotonin and their metabolites were measured in rodent striatum, including by microdialysis, and the interaction with D-amphetamine-induced dopamine release and locomotion was examined5.
Sources [5]
Equilibrium studies characterised the copper(II) complexes formed by Semax across a range of pH values, and MTT assays in SH-SY5Y neuroblastoma and RBE4 endothelial cells examined copper-induced cytotoxicity in its presence6.
Sources [6]
Semax, an analogue of adrenocorticotropin (4-10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain.
Dolotov OV, Karpenko EA, Seredenina TS, et al. Journal of Neurochemistry, 2006.
Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus.
Dolotov OV, Karpenko EA, Inozemtseva LS, et al. Brain Research, 2006.
Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia.
Dmitrieva VG, Povarova OV, Skvortsova VI, et al. Cellular and Molecular Neurobiology, 2010.
The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis.
Medvedeva EV, Dmitrieva VG, Povarova OV, et al. BMC Genomics, 2014.
Semax, an ACTH(4-10) analogue with nootropic properties, activates dopaminergic and serotoninergic brain systems in rodents.
Eremin KO, Kudrin VS, Saransaari P, et al. Neurochemical Research, 2005.
Semax, an ACTH4-10 peptide analog with high affinity for copper(II) ion and protective ability against metal induced cell toxicity.
Tabbì G, Magrì A, Giuffrida A, et al. Journal of Inorganic Biochemistry, 2015.
This page is provided for research and educational reference only. It does not constitute medical advice, dosing guidance, or a recommendation for use. All compounds are strictly for laboratory and in-vitro research purposes.