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NOT FOR HUMAN CONSUMPTION
Semax is a synthetic peptide developed in Russia in the 1980s by the Institute of Molecular Genetics at the Russian Academy of Sciences. Originally intended for stroke treatment, Semax is recognized for its nootropic, neuroprotective, neurogenic, and cognitive-enhancing properties. It is utilized clinically in Russia and parts of Eastern Europe, notably prescribed for cognitive disorders, brain injuries, and neurological deficits.
Chemical Composition: Synthetic analogue of adrenocorticotropic hormone (ACTH); specifically, the peptide ACTH(4-10): Met-Glu-His-Phe-Pro-Gly-Pro.
Molecular Weight: Approximately 813.9 g/mol.
Classification: Synthetic peptide; neuropeptide, nootropic, neuroprotective agent.
Formulations: Commonly administered intranasally or via subcutaneous injection.
Semax operates via multiple neurochemical pathways, explaining its diverse effects:
Significantly increases levels of Brain-Derived Neurotrophic Factor (BDNF) and other neurotrophic factors.
Promotes neurogenesis, neuronal differentiation, survival, and improved neural plasticity.
Enhances dopamine and serotonin signaling pathways, potentially improving mood, motivation, cognition, and emotional regulation.
As a melanocortin receptor agonist (specifically MC4 receptors), Semax modulates stress responses, attention, memory, anxiety levels, and immune responses.
Reduces oxidative stress, inflammation, and neuronal damage following injury.
Promotes recovery after traumatic brain injury, stroke, ischemia, or neurodegeneration.
Improves blood flow in cerebral tissues, delivering oxygen and nutrients more effectively, thus potentially improving cognitive function and brain health.
Semax is clinically approved and prescribed in Russia for numerous neurological conditions and cognitive disorders:
Improves attention, memory, mental clarity, and learning capacity.
Potential applications for cognitive decline, ADHD, memory impairment, or cognitive fatigue.
Promotes recovery of neurological functions after stroke, transient ischemic attacks, or brain ischemia.
Clinically employed to reduce neurological deficits post-stroke.
Potential therapeutic use in Parkinson’s, Alzheimer’s, dementia, or age-related cognitive decline due to neuroprotective and neurotrophic effects.
Reduces anxiety and stress symptoms via modulation of stress-related neurochemical pathways.
Potential use in anxiety disorders, mild depression, PTSD, or stress-induced cognitive dysfunction.
Supports neuronal regeneration, reduces inflammation, and improves outcomes following traumatic brain injury.
Semax is primarily administered intranasally or subcutaneously due to limited bioavailability orally.
Typical Dosage Ranges (Clinical and Experimental Use):
Intranasal Administration:
Standard Dose: 50–150 mcg per spray, usually 1–3 sprays per nostril, 1–3 times daily.
Daily Total: Usually ranges from 300 mcg to 900 mcg/day; higher doses occasionally used temporarily under medical supervision.
Subcutaneous Injection (less common outside clinical environments):
Typical Dosage: 200–1000 mcg/day, usually split into 1–3 injections.
Cycle Duration:
Typically used in cycles lasting several weeks, followed by breaks to monitor effects and avoid potential tolerance.
Semax demonstrates a notably favorable safety profile, with minimal side effects commonly reported:
Mild nasal irritation or discomfort from intranasal use.
Mild headache or transient dizziness (rarely reported).
Rare or unreported at therapeutic dosages.
Currently no strong evidence suggesting tolerance, addiction, or withdrawal risk at therapeutic doses.
Limited, but clinical experience in Russia suggests generally safe long-term usage with medical supervision.
Hypersensitivity or allergic reactions to peptide-based drugs.
Severe psychiatric conditions without medical supervision.
Few well-documented drug interactions.
Due to neurochemical modulation, caution is advised if combining Semax with psychotropic medications (SSRIs, MAOIs, stimulants) due to theoretical (though rarely reported) risks.
Russia & Eastern Europe: Semax is officially approved and prescribed by medical practitioners, available as prescription medication.
United States, Canada, EU, Australia: Not approved or regulated as a pharmaceutical. It is usually marketed through specialty supplement retailers or research chemical suppliers, typically labeled “for research purposes only.”
WADA (Sports Regulatory Agencies): Semax is currently not listed as a prohibited substance by WADA, but always consult updated prohibited substance lists.
Semax has been studied primarily in Russian research, though growing interest internationally has increased visibility:
Significant increases in BDNF, neuronal growth, cognitive function, and reductions in oxidative stress demonstrated in animal and clinical studies.
Proven efficacy in stroke recovery and cognitive disorders in Russian clinical studies.
Limited availability of large-scale, randomized, placebo-controlled clinical trials in Western countries.
More comprehensive international research is needed to confirm the extent of therapeutic efficacy, optimal dosing, and long-term safety profile.
Potential Benefits | Possible Risks/Limitations |
---|---|
Cognitive enhancement (memory, attention, focus) | Limited robust international clinical data |
Neuroprotection, neurogenesis, anti-aging potential | Limited long-term safety evidence internationally |
Improved mood, reduced anxiety, emotional stability | Rare mild nasal irritation or transient headache |
Stroke, ischemia, TBI recovery | Regulatory status uncertain outside Eastern Europe |
Low incidence of side effects | Few documented drug interactions, but caution advised |
Ashmarin, I. P., et al. (1997). "Semax, an analog of ACTH(4–10) with cognitive-enhancing and neuroprotective properties." Neuroscience and Behavioral Physiology, 27(6), 607–612.
Levitskaya, N. G., et al. (2004). "Neuroprotective and nootropic effects of Semax in ischemic stroke." Bulletin of Experimental Biology and Medicine, 138(1), 1–4.
Kaplan, A. Y., et al. (1996). "Semax attenuates cognitive impairment after acute ischemic stroke." Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 96(9), 22–25.