in animals, Semax rapidly elevates the levels and expression of brain-derived neurotrophic factor (BDNF) and its signalling receptor TrkB in the hippocampus and rapidly activates serotonergic and dopaminergic brain systems. In accordance, it has been found to produce antidepressant-like and anxiolytic-like effects, attenuate the behavioural effects of exposure to chronic stress and potentiate the locomotor activity produced by D-amphetamine. As such, it has been suggested that Semax may be effective in the treatment of depression, as well as in attention deficit hyperactivity disorder (ADHD)
Though the exact mechanism of action of Semax is unclear, there is evidence that it may act through melanocortin receptors. Specifically, there is a report of Semax competitively antagonizing the action of the melanocortin receptor full agonist α-melanocyte-stimulating hormone (α-MSH) at the MC4 and MC5 receptors in both in vitro and in vivo experimental conditions, indicating that it may act as an antagonist or partial agonist of these receptors. Semax did not antagonize α-MSH at the MC3 receptor, though this receptor could still be a target of the drug. As for the MC1 and MC2 receptors, they were not assayed. In addition to actions at receptors, Semax, as well as a related peptide drug, Selank, have been found to inhibit enzymes involved in the degradation of enkephalins and other endogenous regulatory peptides , though the clinical significance of this property is uncertain.
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