Semax is a synthetic heptapeptide derived from the ACTH(4-10) fragment, with a Pro-Gly-Pro motif added to extend bioactivity to 20–24 hours in animal models. Developed at the Russian Academy of Sciences, it is registered as a medical drug in Russia and Ukraine for stroke, dyscirculatory encephalopathy, and optic nerve atrophy. It represents one of the most clinically advanced synthetic neuropeptides in the world.
This item is not currently in stock. Message us on Telegram to check availability or place a request.
Join TelegramSemax's neuroprotective mechanisms have been characterised through multiple complementary approaches. At the cellular level, Semax promotes neuronal survival under hypoxia and glutamate-mediated excitotoxicity — the primary injury mechanisms in ischaemic stroke. It contributes to mitochondrial stability under calcium dysregulation stress and inhibits nitric oxide synthesis, reducing NO-mediated neuronal damage post-ischaemia.
At the transcriptomic level, genome-wide studies of rat brain cortex under focal ischaemia showed Semax predominantly enhanced the expression of immune system genes — over 50% of Semax-modulated genes were immune-response related — alongside 24–36 vascular system genes associated with endothelial migration and vasculogenesis, suggesting an immunomodulatory and pro-vascular mechanism underlying its neuroprotection.
In cognitive research, Semax modulates monoamine neurotransmission — increasing serotonin levels and potentiating dopaminergic compounds in animal models. A single intranasal dose (50 µg/kg) increased BDNF in rat basal forebrain within 3 hours, and in human stroke patients, multi-course treatment elevated plasma BDNF significantly, with high-BDNF patients showing improved rehabilitation timing.
Semax has been used in clinical practice in Russia since the 1990s as an adjunct in stroke management. Human studies in the Russian clinical registry document differences in neurological function scores when added to standard care protocols, and reduced infarction size measurements in photothrombosis models. These are not regulatory-approved findings outside Russia/Ukraine. Multi-course dosing (6,000 µg/day × 10 days) produced significant plasma BDNF elevation compared to controls.
EEG studies in healthy adults demonstrated that Semax (250–1000 µg/kg) produced electroencephalographic changes similar to other established neuroprotective drugs, providing objective physiological evidence of CNS activity in healthy volunteers.
Semax and Selank are often compared as they were developed concurrently at the Russian Academy of Sciences. Semax is ACTH-derived and is primarily linked to dopaminergic activity and BDNF-related neuroplasticity — making it relevant to research paradigms studying attention, learning, and memory consolidation pathway markers.
Selank, by contrast, is tuftsin-derived and acts mainly through GABAergic and cytokine-modulating pathways — positioning it within studies examining stress signalling, emotional regulatory pathway markers, and anxiolytic mechanisms in preclinical contexts. Their distinct mechanisms make them complementary rather than interchangeable in research contexts.