Semax
clinical trialsAlso known as: ACTH (4-7) Pro-Gly-Pro, N-Acetyl Semax
Semax (ACTH(4-7) Pro-Gly-Pro, N-Acetyl Semax) is a synthetic heptapeptide derived from the adrenocorticotropic hormone fragment ACTH(4-10). Its primary mechanism involves upregulation of brain-derived neurotrophic factor (BDNF) and modulation of the melanocortin system, particularly through MC1 and MC4 receptor interactions. This leads to enhanced neuroplasticity, increased neuronal survival, and improved synaptic transmission. Additionally, Semax inhibits enkephalin degradation and reduces oxidative stress, contributing to its neuroprotective and nootropic effects. Key research findings from clinical trials indicate that Semax significantly improves cognitive function, attention, and memory in patients with ischemic stroke and chronic cerebrovascular insufficiency. It has also demonstrated efficacy in accelerating recovery of motor and speech functions post-stroke. Preclinical studies show that Semax increases BDNF mRNA expression in the hippocampus and cortex, and enhances long-term potentiation. The peptide exhibits a favorable safety profile with minimal side effects, primarily mild transient hypertension or nausea. Clinically, Semax is approved in Russia for the treatment of acute ischemic stroke, cognitive impairment, and optic nerve atrophy. It is administered intranasally, allowing rapid blood-brain barrier penetration. Ongoing research explores its potential in neurodegenerative diseases, traumatic brain injury, and attention-deficit/hyperactivity disorder. Despite promising results, larger multicenter trials are needed to establish standardized protocols for broader clinical application. For research purposes only — not medical advice.
Key data
C37H51N9O10SResearch & studies
Semax improved functional recovery and inhibited LMP-related pyroptosis in SCI mice and neuroinflammation models.; Semax targeted the μ-opioid receptor (Oprm1) to regulate USP18 and deubiquitination of FTO.; USP18 knockdown confirmed its role in Semax-mediated SCI recovery.; Semax reduced oxidative stress in SCI models.
3774 DEGs were identified under ischemia conditions, while 1539 and 2066 DEGs were found under Semax and ACTH(6-9)PGP, respectively, at 24 hours post-tMCAO.; Both peptides significantly reduced expression distortions for 1171 genes associated with immune and neurosignaling pathways.; Only 32 DEGs differed between ACTH(6-9)PGP and Semax administration at 24 hours post-tMCAO, indicating similar effects.; The pattern of peptide action on the transcriptome depended on the time elapsed after tMCAO, as shown by comparison with 4.5-hour data.
Psychotropic drugs with immunomodulatory/antiviral properties affect adult neurogenesis and neuronal survival while altering key proinflammatory cytokines.; Pharmacological changes in one system (nervous or immune) lead to functional reorganization in the other.; Amantadine, originally antiviral, was approved as an anti-parkinsonian drug after wide medical use.; Interferon alpha causes depression in 30-45% of patients, limiting its clinical use.
Frequently asked questions
What is Semax?
Semax (ACTH(4-7) Pro-Gly-Pro, N-Acetyl Semax) is a synthetic heptapeptide derived from the adrenocorticotropic hormone fragment ACTH(4-10). Its primary mechanism involves upregulation of brain-derived neurotrophic factor (BDNF) and modulation of the melanocortin system, particularly through MC1 and MC4 receptor interac
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 206 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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