Semax

Semax is a synthetic heptapeptide derived from the ACTH (adrenocorticotropic hormone) fragment 4-10, with a Pro-Gly-Pro tripeptide extension at the C-terminus. It was developed at the Institute of Molecular Genetics in Russia.

Unlike full-length ACTH, Semax lacks hormonal activity and does not stimulate cortisol release. The modifications enhance metabolic stability while retaining and amplifying the cognitive-enhancing properties associated with the ACTH(4-10) fragment, known as the "active core" for neurotropic effects.

Semax exerts its effects through several neurobiological mechanisms:

Neurotrophic Factor Regulation Semax significantly increases expression of BDNF, NGF, and their receptors (TrkA, TrkB). These neurotrophins are essential for neuronal survival, differentiation, and synaptic plasticity.

Dopaminergic System Modulation The peptide affects dopamine and serotonin neurotransmission, particularly in frontal cortex regions involved in attention, working memory, and executive function.

Neuroprotection Semax provides protection against various neurological insults including hypoxia, ischemia, and neurotoxicity through antioxidant effects and mitochondrial stabilization.

Gene Expression Effects Studies show Semax modulates expression of hundreds of genes involved in neurotransmission, immune function, vascular regulation, and cellular stress responses.