Overview
Semax is a heptapeptide analog of ACTH(4-10) developed at the Institute of Molecular Genetics in Moscow and approved in Russia for stroke, cognitive decline, and optic nerve disease. It dramatically upregulates BDNF (brain-derived neurotrophic factor) and its receptor TrkB, enhancing synaptic plasticity and neuronal survival. It also modulates dopaminergic, serotonergic, and cholinergic systems for acute cognitive enhancement.
Mechanism of action
Semax binds melanocortin receptors (MC4R) and activates BDNF/TrkB signaling, stimulating synaptic potentiation and neurogenesis in the hippocampus. It increases enkephalins and modulates the dopamine/serotonin balance in prefrontal cortex. It also exhibits anti-inflammatory neuroprotective effects by reducing pro-inflammatory cytokine expression following ischemic injury.
Selected literature
- [01]
Semax and BDNF upregulation in rat brain
Shadrina M.I. et al. · Journal of Molecular Neuroscience · 2010
Semax administration produced a 1.6-fold increase in BDNF mRNA expression in the rat hippocampus within 24 hours.
- [02]
Neuroprotective effects of Semax in ischemic stroke
Miasoedov N.F. et al. · Zhurnal Nevrologii i Psikhiatrii · 1999
Semax reduced infarct volume and improved neurological outcomes in a randomized controlled trial of acute ischemic stroke patients.
- [03]
ACTH(4-10) analogs and cognitive performance
De Wied D. · Progress in Brain Research · 1990
ACTH fragment analogs improved attention, memory consolidation, and cognitive flexibility in both animal models and human trials.
The information on this page is summarized from the published research literature and is provided for reference and educational purposes only. It is not medical advice and should not be used to guide treatment decisions. Our peptides are sold for in-vitro research and laboratory use only.