Semax is a synthetic heptapeptide consisting of a fragment of adrenocorticotropic hormone (ACTH 4-7), the sequence Met-Glu-His-Phe, extended with the tripeptide Pro-Gly-Pro to improve metabolic stability. It was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences.
The N-Acetyl (NA) form provides enhanced resistance to aminopeptidase degradation, increasing the peptide’s effective half-life in biological systems.
Preclinical and clinical research has investigated Semax in models of neuroprotection, cognitive function, and neurovascular regulation. A 2025 study reported improved cognitive function in a mouse model of Alzheimer’s disease together with reduced amyloid load in the brain.
Mechanistic studies have identified multiple pathways under investigation including BDNF upregulation, suppression of MMP-9 and JNK inflammatory signalling, activation of CREB-mediated neuronal recovery pathways, and inhibition of amyloid-beta fibrillogenesis.
A 2025 publication in the British Journal of Pharmacology identified a mechanism involving the mu-opioid receptor gene Oprm1 in spinal cord injury recovery models, complementing the existing body of Russian-origin studies.
Semax’s BDNF-stimulating activity has been reported with neurotrophin mRNA levels elevated for 24-72 hours post-administration, and VEGF plus angiogenesis-related gene upregulation has been documented following focal brain ischaemia models.
For In-Vitro Research Use Only. Not for human consumption, veterinary use, or clinical application. No dosing guidance is provided or implied.




