PMID: 15088389
Eremin et al./PubMed/2004
Why It Matters
This paper caught my attention because Semax is marketed as a nootropic, but most human data is published in Russian journals that are hard to access. This rodent study shows it does something to brain chemistry—specifically dopamine and serotonin pathways—but we're looking at metabolites in mouse and rat brains, not actual cognitive outcomes in humans. Worth knowing if you're considering Semax, but this is basic neuropharmacology, not proof it'll make you sharper.
Key Findings
- Semax altered levels of DOPAC (3,4-dihydroxyphenylacetic acid), a dopamine metabolite, in rodent brains
- The peptide also affected 5-HIAA (hydroxyindoleacetic acid) levels, indicating changes in serotonin metabolism
- Studies used both C57BL/6 mice and Sprague-Dawley rats, suggesting effects replicate across rodent strains
- Semax is a synthetic fragment derived from ACTH (adrenocorticotropic hormone), giving it structural similarity to endogenous stress hormones
- No human data provided—all findings are from animal models with uncertain translation to human neuropharmacology
Read the Paper↗PMID: 15088389