Literature on Semax (Met-Glu-His-Phe-Pro-Gly-Pro), its derivation from the natural ACTH(4–10) sequence, structural modifications described in published synthesis methodology, and preclinical investigations of melanocortin-receptor binding and BDNF expression reported across the research record.
Semax is a synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) derived from the natural ACTH(4–10) fragment of adrenocorticotropic hormone, modified at the C-terminus to extend plasma stability. Reported mechanisms in published animal and cell-culture work include competitive antagonism at melanocortin MC4 and MC5 receptors and modulation of enkephalin-degrading enzyme activity.
A recurring theme in the Semax literature is its observed effect on BDNF (brain-derived neurotrophic factor) and trkB expression in rodent hippocampus and basal forebrain. Transcriptome-level studies after experimentally induced cerebral ischaemia describe gene-expression patterns related to inflammation, apoptosis, and neurotransmission. The references below are entry points into that body of work.
Disclaimer · Citations are provided as reference material from the published research literature. Strata sells research compounds for laboratory use only and does not interpret, recommend, or extrapolate findings to human application.