The precise pharmacological action of the synthetic peptide Semax, which is a heptapeptide fragment of the endogenous Adrenocorticotropic Hormone (ACTH), to specifically and measurably elevate the concentration of Brain-Derived Neurotrophic Factor (BDNF) within the central nervous system. BDNF is a critical neurotrophin that promotes the survival of existing neurons and actively encourages the growth, differentiation, and branching of new neurons and synapses. This powerful mechanism is central to Semax’s profound potential for robust cognitive enhancement and comprehensive neuroprotection.
Origin
Semax was originally developed in Russia as a pharmaceutical agent, based on the structure of the endogenous neuropeptide ACTH, specifically for its adaptogenic and neuroprotective properties. The subsequent observation of its profound neurotrophic effects led to the identification of the “BDNF increase” as a key, quantifiable part of its primary mechanism of action. This highlights the therapeutic utility and scientific promise of peptide mimetics in advanced neurological health interventions.
Mechanism
Semax is believed to exert its effect by binding to specific, high-affinity receptors on both neuronal and glial support cells, initiating a complex intracellular signaling cascade that potently upregulates the transcription of the BDNF gene. This increased expression of BDNF leads directly to enhanced synaptic plasticity, a process known as long-term potentiation, which is the essential cellular basis of learning and memory formation. The peptide’s action also fundamentally contributes to increased neuronal resilience against ischemic damage and chronic oxidative stress.
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