Semax is a synthetic heptapeptide analogue of the ACTH(4-7) sequence (Met-Glu-His-Phe-Pro-Gly-Pro), developed at the Institute of Molecular Genetics of the Russian Academy of Sciences. The compound retains the neuroprotective and cognitive-modulating properties of the parent ACTH fragment while eliminating its steroidogenic and hormonal activity. It has been studied extensively in models of neuroplasticity, cerebral ischemia, BDNF regulation, and anxiety-related behavior.
Semax exerts its primary effects through two complementary pathways. First, it activates melanocortin receptors (primarily MC4R) in the CNS, modulating dopaminergic neurotransmission and attention-related signaling cascades. Second, it upregulates BDNF and its high-affinity receptor TrkB in hippocampal and cortical neurons, promoting synaptic plasticity, LTP (long-term potentiation), and neuronal survival under stress conditions. In ischemia models, Semax reduces infarct volume through both BDNF-dependent mechanisms and suppression of NF-κB-mediated neuroinflammation. The Pro-Gly-Pro C-terminal extension, absent in native ACTH(4-7), is essential for CNS activity and resistance to enzymatic degradation.
Semax crosses the blood-brain barrier efficiently despite its peptide nature, attributed to the Pro-Gly-Pro tail. For in vitro neuronal models, concentrations of 10 nM to 1 μM are typical depending on the endpoint. Semax has no ACTH-like steroidogenic activity, making it suitable for neuromodulatory studies without confounding glucocorticoid effects. Methionine oxidation can occur with improper storage; lyophilized Semax should be stored at −20°C and reconstituted immediately before use.
For in vitro laboratory research only. Not for human consumption. Not FDA approved.
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