Semax
clinical trialsAlso known as: ACTH (4-7) Pro-Gly-Pro, N-Acetyl Semax
Semax (ACTH(4-7)Pro-Gly-Pro) is a synthetic heptapeptide derived from the adrenocorticotropic hormone (ACTH) fragment ACTH(4-10), modified with a C-terminal Pro-Gly-Pro sequence to enhance stability and bioavailability. Its primary mechanism involves upregulation of brain-derived neurotrophic factor (BDNF) in the hippocampus and cortex, alongside modulation of the melanocortin system via MC4 and MC5 receptor activation. This dual action promotes neuroplasticity, enhances synaptic transmission, and exerts neuroprotective effects against excitotoxicity and oxidative stress. Semax also influences dopamine and serotonin metabolism, contributing to its cognitive-enhancing and anti-ischemic properties. Key research findings from clinical trials and preclinical studies demonstrate that Semax significantly improves cognitive function, attention, and memory in patients with cerebrovascular disorders, including acute ischemic stroke and chronic cerebral ischemia. In stroke models, it reduces infarct volume and accelerates neurological recovery, while in healthy volunteers, it enhances short-term memory and psychomotor performance. Long-term administration has shown safety and tolerability, with no significant adverse effects reported. Mechanistic studies confirm BDNF elevation as a central mediator of its therapeutic effects, with downstream activation of TrkB signaling and CREB phosphorylation. Clinically, Semax is approved in Russia for the treatment of acute ischemic stroke, cognitive impairment, and optic nerve disorders. Its rapid onset and favorable safety profile make it a candidate for broader neurorehabilitation applications, though regulatory approval outside Russia remains limited. Ongoing research explores its potential in neurodegenerative diseases, traumatic brain injury, and age-related cognitive decline. For research purposes only — not medical advice.
Key data
C37H51N9O10SResearch & studies
Semax improved functional recovery and reduced LMP-related pyroptosis in SCI mice and neuroinflammation models.; Semax targeted μ-opioid receptors and regulated USP18 expression.; USP18 mediated deubiquitination of FTO, contributing to neuroprotection.; Semax decreased oxidative stress in SCI models.
3774 DEGs were identified under ischemia conditions at 24 hours post-tMCAO.; Semax and ACTH(6-9)PGP reduced expression distortions for 1171 ischemia-affected genes.; 32 DEGs were found between ACTH(6-9)PGP and Semax administration.; Peptide action on the transcriptome varied with time after tMCAO.
Psychotropic drugs with immunomodulatory/antiviral properties affect adult brain neurogenesis and neuronal survival by altering key proinflammatory cytokines.; Pharmacological changes in one system (neural or immune) lead to functional reorganization in the other.; Amantadine, originally antiviral, was repurposed as an anti-parkinsonian drug due to neuro-immune interactions.; Interferon alpha causes depression in 30-45% of patients, and oseltamivir can provoke central side effects like abnormal behavior and delirium.
Frequently asked questions
What is Semax?
Semax (ACTH(4-7)Pro-Gly-Pro) is a synthetic heptapeptide derived from the adrenocorticotropic hormone (ACTH) fragment ACTH(4-10), modified with a C-terminal Pro-Gly-Pro sequence to enhance stability and bioavailability. Its primary mechanism involves upregulation of brain-derived neurotrophic factor (BDNF) in the hippo
How does Semax work?
ACTH(4-10)-derived heptapeptide that elevates BDNF and modulates the melanocortin system; used clinically in Russia for stroke and cognition.
What is the research status of Semax?
Semax is currently classified as clinical trials, with 205 research references on record. This is for research purposes only and is not medical advice.
What is the molecular weight of Semax?
Semax has a molecular weight of approximately 813.9 g/mol (formula C37H51N9O10S).
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