Semax Spray

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Synthetic ACTH-derived neuropeptide-signalling — increases BDNF, sharpens focus, and supports neuroprotection.

Semax is a synthetic heptapeptide analog of ACTH(4-10) that enhances BDNF and NGF expression, modulates dopaminergic, serotonergic, and cholinergic systems, and demonstrates neuroprotective effects through inhibition of nitric oxide synthesis, improved cerebral blood flow, and anti-inflammatory gene modulation in stroke research.

Semax is a synthetic heptapeptide analog of ACTH(4-10) that enhances BDNF and NGF expression, modulates dopaminergic, serotonergic, and cholinergic systems, and demonstrates neuroprotective effects through inhibition of nitric oxide synthesis, improved cerebral blood flow, and anti-inflammatory gene modulation in stroke research. It has a molecular formula C37H51N9O10S, mass 813.93 Da. Its published amino-acid sequence is Met-Glu-His-Phe-Pro-Gly-Pro. Common synonyms in the literature include ACTH 4-7 PGP, Heptapeptide Semax, and ACTH(4-10) analog.

Investigation of Semax to date is a mix of preclinical and early clinical, with the majority of citations concentrated in animal models and in-vitro assays rather than randomized controlled human trials. Published work referencing Semax spans Stroke and ischemia research: Extensive preclinical and Russian clinical studies have examined Semax in stroke contexts. Animal studies show reduced infarct size, decreased oxidative stress, and improved cerebral blood flow. Human stroke patients in Russia reportedly show accelerated recovery with elevated plasma BDNF levels, BDNF and neurotrophic factor studies: Research demonstrates Semax rapidly elevates BDNF expression and its receptor TrkB in hippocampus, frontal cortex, and basal forebrain within 3-8 hours post-dose. Nerve growth factor (NGF) is also upregulated, supporting neuronal survival and synaptic plasticity, and Alzheimer's disease models: In APP/PS1 transgenic mice, Semax improved cognition in novel object recognition and Barnes maze tests, reduced amyloid plaques and inclusions in cortex and hippocampus, and showed neuroprotective effects. Proposed mechanisms in the literature include BDNF/NGF pathway: rapidly upregulates BDNF and NGF expression supporting neuronal survival and neurogenesis and Neurotransmitter enhancement: modulates dopaminergic (motivation), serotonergic (mood), and cholinergic (memory) activity. None of this material describes therapeutic outcomes in humans, and No vendor listed here provides dosing guidance for Semax outside laboratory research.

For the full mechanistic profile, published references, and constraint notes on Semax, see the Semax research page. All references cited on that page are peer-reviewed primary literature.