Semax

Mechanism

Semax (Met-Glu-His-Phe-Pro-Gly-Pro) is a synthetic analog of the ACTH(4-10) fragment, specifically the ACTH(4-7) sequence with a Pro-Gly-Pro stabilizing extension. Unlike ACTH, semax does not stimulate adrenal cortisol production. Its primary mechanisms include upregulation of BDNF and its receptor TrkB, modulation of serotonergic systems, enhancement of neuronal survival through the MAPK/ERK signaling cascade, and modulation of cerebral blood flow. Semax has demonstrated neuroprotective effects in stroke models by reducing infarct volume, promoting neuroplasticity, and modulating the expression of neurotrophins and their receptors in the central nervous system.

What the literature has looked at

• Studies have investigated its neuroprotective signaling in cerebral ischemia research models
• Studies have examined BDNF upregulation and cognitive signaling pathways
• Research has explored neuroprotective mechanisms in cerebral ischemia models
• Studies have assessed effects on attention, memory, and learning signaling in research subjects

Research context, not a claim about what this compound does. Research Use Only — not for human or animal consumption. 21+.

Cited work

• Dolotov OV, et al. Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Res. 2006;1117(1):54-60.

  Semax increased BDNF mRNA expression and TrkB receptor levels in the rat hippocampus, establishing a neurotrophic mechanism for its cognitive-modulating effects.

• Gusev EI, et al. Semax in prevention of disease progress and development of exacerbations in patients with cerebrovascular insufficiency. Zh Nevrol Psikhiatr Im S S Korsakova. 2005;105(2):35-40.

  Research examined semax-mediated neuroprotective signaling pathways in a cerebrovascular insufficiency model, observing modulation of neurological signaling parameters and cognitive function markers.

Properties

type

Peptide (heptapeptide, ACTH analog)