Semax
DESCRIPTION
Semax is a synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) analog of adrenocorticotropic hormone (ACTH) fragment 4-10 with an added C-terminal Pro-Gly-Pro tripeptide that enhances enzymatic resistance and bioavailability.
Purity: 99.15%
Semax demonstrated clinically meaningful neuroprotection and recovery enhancement in acute ischemic stroke, supporting its approved indication in Russia.
Semax provides sustained neurotrophic support through BDNF/TrkB signaling without neuroendocrine disruption, confirming its selective neuroprotective mechanism.
Developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, Semax is approved in Russia and Ukraine for clinical use as a neuroprotective and nootropic agent.
It has over 25 years of clinical safety data and works primarily through BDNF (brain-derived neurotrophic factor) and NGF (nerve growth factor) upregulation.
Clinical dosing in Russia: 200-600 μg per dose, administered intranasally 2-3 times daily. Common research protocols: 0.1% solution (1mg/mL), 1-3 drops per nostril per dose.
Typical cycle duration: 10-20 days with equivalent rest periods. Intranasal route provides rapid CNS delivery bypassing the blood-brain barrier.
- Unit size: 30mg/vial
- Unit quantity: 1 vial
- Molecular formula: C37H51N9O10S
- Molecular weight: 813.9 g/mol
Cognitive Enhancement & Nootropic Effects
Semax has demonstrated significant cognitive enhancement in both clinical populations (stroke patients, cognitive impairment) and healthy subjects. It improves attention, working memory, information processing speed, and learning acquisition through neurotrophic factor modulation.
Mechanism of Action
Upregulates BDNF expression 2-8 fold, enhancing long-term potentiation (LTP) and synaptic plasticity in hippocampal and cortical neurons. Increases NGF levels supporting cholinergic neuron function. Activates TrkB signaling cascades that promote dendritic growth and synaptic connectivity.
Neuroprotection & Stroke Recovery
Semax is clinically approved in Russia for treatment of ischemic stroke. It provides neuroprotection against oxidative stress, excitotoxicity, and ischemic damage. Clinical studies show improved neurological recovery outcomes when administered early after stroke.
Mechanism of Action
Reduces oxidative stress through upregulation of antioxidant enzymes (SOD, catalase). Inhibits excitotoxic NMDA receptor-mediated calcium influx. Promotes neurotrophic factor expression (BDNF, NGF) to support neuronal survival and axonal regeneration in damaged brain regions.
Anxiolytic Effects
Semax demonstrates anxiolytic properties without the sedation, cognitive impairment, or dependence associated with benzodiazepines. It reduces anxiety while simultaneously enhancing cognitive function — a unique combination among anxiolytic agents.
Mechanism of Action
Modulates the melanocortin system (MC3R/MC4R) to regulate stress response pathways. Influences serotonergic and dopaminergic neurotransmission. Normalizes HPA axis activity without suppressing basal cortisol, maintaining physiological stress response capability.
Immune Modulation
Through its melanocortin receptor activity, Semax demonstrates immunomodulatory properties. It can regulate inflammatory responses and influence immune cell function, providing secondary immunological benefits beyond its primary neurological effects.
Mechanism of Action
Activates melanocortin receptors on immune cells, modulating cytokine production and inflammatory signaling. Influences expression of genes involved in innate immunity and inflammatory regulation through ACTH-derived signaling pathways.
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