SEMAX (Met-Glu-His-Phe-Pro-Gly-Pro) is a synthetic heptapeptide analog of the endogenous ACTH(4-7) tetrapeptide sequence, with a C-terminal Pro-Gly-Pro extension that confers resistance to proteolytic degradation and enhances CNS bioavailability. It was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences in Moscow by Nikolai F. Myasoedov and colleagues beginning in the 1980s.

Preclinical research has focused on SEMAX’s ability to upregulate brain-derived neurotrophic factor (BDNF) and its receptor TrkB in hippocampal and frontal cortical tissue under conditions of AF64A-induced neurodegeneration and acute hypoxia. Dolotov, Karpenko, and colleagues at the Institute of Molecular Genetics documented SEMAX-induced changes in hippocampal BDNF and NGF transcription in rodent stress models. Separate lines of research examined the compound’s effects on dopaminergic and serotonergic signaling, enkephalin-degrading enzyme inhibition, and cortical EEG activity. All findings referenced here derive from preclinical models and have not been validated in controlled human clinical trials.

SEMAX research appears in European Journal of Pharmacology, Bulletin of Experimental Biology and Medicine, and Peptides. It is not approved by the U.S. Food and Drug Administration for any diagnostic, therapeutic, or preventive application. It is classified as a research compound only.