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Semax — 10mg

$45.00Price
Quantity

Research-grade Semax, a synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) derived from the ACTH(4-10) fragment. Studied for neuroprotective, nootropic, and neurotrophic properties including BDNF modulation and cerebrovascular research. 10mg lyophilized powder, 99%+ purity verified by Janoshik Analytical via HPLC and mass spectrometry.


  • For laboratory research use only.

  • Not for human or veterinary use.

  • Not intended for diagnosis, treatment, cure, or prevention of any disease.

  • Use only in controlled laboratory settings by qualified personnel following appropriate safety procedures.

  • Semax is a synthetic heptapeptide analog of adrenocorticotropic hormone fragment ACTH(4-10), developed at the Institute of Molecular Genetics of the Russian Academy of Sciences. The C-terminal Pro-Gly-Pro tripeptide extension enhances metabolic stability and bioavailability compared to the native ACTH fragment. Semax has been the subject of extensive research in Russia, where it appears on the List of Vital & Essential Drugs, and has been studied in clinical settings for cerebrovascular and cognitive research. It is frequently studied alongside Selank, another Russian-developed neuropeptide.


    BENEFITS


    • Neurotrophic signaling — studied for BDNF (brain-derived neurotrophic factor) expression modulation

    • Neuroprotection — investigated in cerebral ischemia and stroke models

    • Cognitive research — explored for effects on learning, memory, and attention pathways

    • Blood-brain barrier penetration — compact heptapeptide structure enables CNS access

    • Well-characterized — decades of published research including clinical studies


    WHAT RESEARCHERS LOOK AT


    • BDNF and TrkB expression in hippocampal and cortical tissue models

    • Neuroprotective effects in focal ischemia (pMCAO) models

    • Monoaminergic neurotransmitter metabolism (serotonin, dopamine, norepinephrine)

    • Gene expression profiling of immune and vascular systems post-ischemia

    • Copper(II) chelation and amyloid-beta aggregation modulation

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