Semax

Semax is a synthetic heptapeptide, Met-Glu-His-Phe-Pro-Gly-Pro, that joins the ACTH(4-7) sequence of adrenocorticotropic hormone to a C-terminal Pro-Gly-Pro tripeptide. Rodent studies of the Semax peptide have examined brain-derived neurotrophic factor (BDNF) and trkB expression in the hippocampus and basal forebrain, serotonin and dopamine turnover in the striatum, and gene expression in the cortex after experimental cerebral ischemia. Research Market supplies Semax as a lyophilized research reagent, with purity and identity data for each lot reported on its certificate of analysis. It is sold strictly for laboratory research use.

Chemical structure and identification

• Molecular formula: C₃₇H₅₁N₉O₁₀S
• Molecular weight: 813.9 g/mol
• CAS number: 80714-61-0
• PubChem CID: 9811102
• Amino acid sequence: Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP)
• Synonyms: ACTH (4-7), Pro-Gly-Pro-; Pro-Gly-Pro-ACTH (4-7)
• Form: Lyophilized powder
• Analytical methods: RP-HPLC for purity and mass spectrometry for identity, reported on the batch certificate of analysis

Research applications

• Hippocampal BDNF and trkB: A single application of Semax in rats was followed by a 1.4-fold rise in hippocampal BDNF protein and a 1.6-fold rise in trkB tyrosine phosphorylation, with higher exon III BDNF and trkB mRNA levels [1]
• Binding sites in basal forebrain: Tritium-labeled Semax bound rat basal forebrain membranes specifically and reversibly (calcium-dependent, K_D about 2.4 nM), and intranasal application raised BDNF levels in the basal forebrain but not the cerebellum after 3 hours [2]
• Monoamine systems: In rodents, Semax increased striatal 5-HIAA without changing dopamine levels on its own, and enhanced D-amphetamine-evoked striatal dopamine release and locomotor activity [3]
• Ischemia transcriptome: Genome-wide analysis of rat cortex after permanent middle cerebral artery occlusion found that Semax mainly altered immune-related genes, notably immunoglobulin and chemokine genes, along with genes tied to vascular processes [4]
• VEGF family genes: In the same rat focal ischemia model, Semax and its C-terminal tripeptide Pro-Gly-Pro changed Vegf-b and Vegf-d mRNA levels in the frontoparietal cortex between 3 and 72 hours, opposite to the changes caused by ischemia [5]

Reference citations

1. 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 Res, 1117(1):54–60. PMID 16996037 · DOI
2. Dolotov O.V. et al. (2006). Semax, an analogue of adrenocorticotropin (4-10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain. J Neurochem, 97(Suppl 1):82–86. PMID 16635254 · DOI
3. Eremin K.O. et al. (2005). Semax, an ACTH(4-10) analogue with nootropic properties, activates dopaminergic and serotoninergic brain systems in rodents. Neurochem Res, 30(12):1493–1500. PMID 16362768 · DOI
4. Medvedeva E.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. PMID 24661604 · DOI
5. Medvedeva E.V. et al. (2013). Effect of semax and its C-terminal fragment Pro-Gly-Pro on the expression of VEGF family genes and their receptors in experimental focal ischemia of the rat brain. J Mol Neurosci, 49(2):328–333. PMID 22772900 · DOI

Compound data from PubChem CID 9811102. Literature summaries describe published preclinical research and are not claims about this product’s effects in humans or animals.