Semax: ACTH-Derived Neuropeptide Research Guide

Semax (Met-Glu-His-Phe-Pro-Gly-Pro) is a synthetic heptapeptide derived from ACTH(4-10). It combines the ACTH(4-7) fragment with a stabilizing Pro-Gly-Pro C-terminal tripeptide, extending its half-life while eliminating hormonal effects. Molecular Weight: 813.92 Da Administration: Intranasal or subcutaneous (poor oral bioavailability) Half-life: 20-24 hours Research demonstrates Semax may affect: - Memory and learning through neurotrophin modulation (BDNF/TrkB) - Serotonergic and dopaminergic pathway activation - Attention and short-term memory processes - BDNF levels in hippocampus within hours of administration Studies in ischemia models show: - 394 differentially expressed genes at 24 hours post-treatment - Reduced inflammatory cytokine expression (IL-17, TNF) - Decreased neutrophil activation - Restored dopaminergic, cholinergic, and glutamatergic synapse genes - Modulated stress kinase and tissue damage markers Anti-aggregation studies reveal: - Inhibition of copper-induced amyloid-beta aggregation - Cu²⁺ ion sequestration preventing toxic complex formation - Protection of neuronal cells from amyloid-induced cytotoxicity Proposed mechanisms include: 1. Melanocortin receptor modulation 2. Potential enkephalinase inhibition 3. Neurotrophin (BDNF/TrkB) regulation 4. Immune cell modulation 5. Metal ion chelation reducing oxidative stress 6. Broad transcriptome changes affecting multiple signaling pathways Gene expression research shows effects on: - Immune response pathways - Vascular system regulation - Neurotransmitter signaling - Calcium signaling pathways Studies demonstrate modulation of: - pJNK (stress kinase) - MMP-9 (tissue damage marker) - c-Fos (apoptosis marker) - pCREB (neuroprotection marker) - Store lyophilized powder at -20°C - Protect from light - Reconstitute immediately before use Note: This compound is for research purposes only and is not approved for therapeutic use outside specific jurisdictions.