Semax

clinical trials

Also 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

Category
Cognitive & Neuroprotective
Molecular weight
813.9 g/mol
Molecular formula
C37H51N9O10S
CAS number
80714-61-0
Administration
intranasal
Research status
clinical trials
References
206
Tags
nootropic, bdnf, neuroprotective

Research & studies

Modulation of neuropathological pathways by bioactive peptides and proteins/polypeptides: Targeting oxidative stress in neurodegenerative diseases
Neuropeptides · 2025 · PubMed
Semax peptide targets the μ opioid receptor gene Oprm1 to promote deubiquitination and functional recovery after spinal cord injury in female mice
British journal of pharmacology · 2025 · PubMed

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.

The Potential of the Peptide Drug Semax and Its Derivative for Correcting Pathological Impairments in the Animal Model of Alzheimer's Disease
Acta naturae · 2025 · PubMed
Genes That Associated with Action of ACTH-like Peptides with Neuroprotective Potential in Rat Brain Regions with Different Degrees of Ischemic Damage
International journal of molecular sciences · 2025 · PubMed
ACTH-like Peptides Compensate Rat Brain Gene Expression Profile Disrupted by Ischemia a Day After Experimental Stroke
Biomedicines · 2024 · PubMed

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.

Insight into Glyproline Peptides' Activity through the Modulation of the Inflammatory and Neurosignaling Genetic Response Following Cerebral Ischemia-Reperfusion
Genes · 2022 · PubMed
Semax, a Synthetic Regulatory Peptide, Affects Copper-Induced Abeta Aggregation and Amyloid Formation in Artificial Membrane Models
ACS chemical neuroscience · 2022 · PubMed
Pharmacological Aspects of Neuro-Immune Interactions
Current pharmaceutical design · 2018 · PubMed

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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