N-Acetyl Semax - 20MG

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N-Acetyl Semax - 20MG
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Product Overview

Semax: Neuroprotective Peptide Profile

N-Acetyl Semax is a heptapeptide analog of ACTH(4-10) with N-terminal acetylation, characterized by neuroprotective, neurotrophic, and anti-inflammatory actions across ischemic stroke, spinal cord injury (SCI), cognition, and stress-related models.

Neuroprotection & Functional Recovery

  • In cerebral ischemia/reperfusion, Semax upregulates active CREB and suppresses MMP-9, c-Fos, and JNK—counteracting ischemia-driven transcriptomic disruption and supporting neuronal survival.[1,2]
  • In SCI, Semax targets Oprm1 (μ-opioid receptor), modulates USP18-mediated deubiquitination, and reduces lysosomal membrane permeabilization and pyroptosis, improving recovery and oxidative stress indices.[3]

Immune/Vascular Gene Programs & Neurotrophins

  • Enhances expression of immune/vascular genes (immunoglobulins, chemokines, endothelial migration/vasculogenesis) after focal ischemia.[4]
  • Rapid, region-specific induction of neurotrophins (NGF, BDNF) and increases in BDNF protein and TrkB phosphorylation—linked to learning, memory, and synaptic plasticity.[5–9]

N-Acetylation & Metal-Ion Interactions

  • N-acetylation (Ac-Semax) shifts Cu(II) coordination to a [CuLH] species with a distorted CuNO chromophore and more positive redox potential; unlike non-acetylated Semax, Ac-Semax does not protect against Cu(II)-induced toxicity in neuroblastoma cells, underscoring the role of a free N-terminus.[10,11]
  • Both Semax and Ac-Semax form Zn(II) complexes of comparable strength; acetylation does not affect Zn(II) influx or localization.[10]

Stress, Mood & Monoaminergic Systems

  • Antidepressant-like and antistress effects in chronic unpredictable stress, reversing anhedonia, adrenal hypertrophy, and hippocampal BDNF depletion.[12]
  • Activates dopaminergic and serotonergic systems; augments psychostimulant-evoked dopamine release; proposed utility in ADHD and Rett syndrome.[14,15]

Angiogenesis & Cellular Repair

  • Promotes proliferation of neuroglia, endothelial cells, and SVZ progenitors; activates capillary networks in normal and ischemic brain, improving perfusion and limiting damage.[13]

Key Takeaways

  • Multi-modal neuroprotection: anti-inflammatory, anti-apoptotic/anti-pyroptotic, pro-plasticity.
  • Gene-level reprogramming: boosts immune/vascular pathways and neurotrophin signaling.
  • Chemistry matters: N-terminal acetylation modulates Cu/Zn binding and may tune bioactivity in metal-dyshomeostasis states.

References

  1. Sudarkina OY, et al. Int J Mol Sci. 2021;22(12):6179.[1]
  2. Filippenkov IB, et al. Genes. 2020;11(6):E681.[2]
  3. Liu R, et al. Br J Pharmacol. 2025.[3]
  4. Medvedeva EV, et al. BMC Genomics. 2014;15:228.[4]
  5. Agapova TY, et al. Neurosci Lett. 2007;417(2):201–205.[5]
  6. Shadrina M, et al. J Mol Neurosci. 2010;41(1):30–35.[6]
  7. Dolotov OV, et al. Brain Res. 2006;1117(1):54–60.[7]
  8. Dmitrieva VG, et al. Cell Mol Neurobiol. 2010;30(1):71–79.[8]
  9. Dolotov OV, et al. J Neurochem. 2006;97(S1):82–86.[9]
  10. Magrì A, et al. J Inorg Biochem. 2016;164:59–69.[10]
  11. Tabbì G, et al. J Inorg Biochem. 2015;142:39–46.[11]
  12. Inozemtseva LS, et al. Eur J Pharmacol. 2024;984:177068.[12]
  13. Stavchansky VV, et al. J Mol Neurosci. 2011;45(2):177–185.[13]
  14. Tsai SJ. Med Hypotheses. 2007;68(5):1144–1146.[14]
  15. Eremin KO, et al. Neurochem Res. 2005;30(12):1493–1500.[15]

All information provided is for research purposes only.

ALL ARTICLES AND PRODUCT INFORMATION PROVIDED ON THIS WEBSITE ARE FOR INFORMATIONAL AND EDUCATIONAL PURPOSES ONLY. The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body. These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law.