N-Acetyl Semax Amidate - 20MG

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N-Acetyl Semax Amidate - 20MG
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Product Overview

Semax Amidate

N-Acetyl Semax Amidate (Ac-Semax) is a heptapeptide analog of ACTH(4-10) (Met-Glu-His-Phe-Pro-Gly-Pro) with N-terminal acetylation. Semax derivatives exhibit neuroprotective, neurotrophic, and anti-inflammatory properties with clinical use in ischemic stroke and emerging data in spinal cord injury (SCI) and cognitive disorders.

Neuroprotective & Recovery Effects

  • In cerebral ischemia/SCl models, Semax downregulates injury pathways (e.g., MMP-9, c-Fos, JNK) and upregulates recovery proteins (active CREB), reducing oxidative stress and cell death.[1]
  • After SCI, Semax promotes functional recovery via μ-opioid receptor targeting (Oprm1), USP18-mediated deubiquitination, and reduced lysosomal permeabilization/pyroptosis.[2]

Gene Expression & Immune Modulation

  • Genome-wide analyses in focal ischemia show Semax increases expression of immune/vascular genes (immunoglobulins, chemokines; endothelial migration/angiogenesis).[3]
  • Rapid induction of neurotrophins (NGF, BDNF) with region-specific effects (hippocampus, cortex, retina); modulation of BDNF/TrkB signaling supports plasticity and repair.[4–6]

N-Terminal Acetylation & Metal-Ion Binding

  • N-acetylation alters Cu(II) coordination: Ac-Semax forms a [CuLH] species with distorted CuNO chromophore and more positive redox potential; lacks protection against Cu(II)-induced toxicity seen with non-acetylated Semax—highlighting the role of a free N-terminus.[7,8]
  • Both Semax and Ac-Semax form Zn(II) complexes of comparable strength; acetylation does not affect Zn(II) influx/subcellular localization in neuroblastoma cells.[7]

Cognitive & Nootropic Effects

  • Enhances learning, memory, and attention; increases BDNF synthesis; modulates dopaminergic/serotonergic systems; augments psychostimulant-evoked dopamine release.[6,9–11]
  • Hypothesized utility in ADHD and Rett syndrome based on neurotransmitter/BDNF effects.[10]

Vascular & Cellular Repair

  • Increases proliferation of neuroglia, endothelial cells, and SVZ progenitors; activates capillary networks in normal and ischemic brain tissue, improving perfusion and limiting ischemic damage.[12]

Key Takeaways

  • Multi-modal neuroprotection: anti-inflammatory, anti-apoptotic, pro-plasticity.
  • Transcriptomic reprogramming: boosts immune/vascular and neurotrophin pathways.
  • Chemistry matters: N-acetylation modifies Cu(II) interactions and may tune bioactivity in metal-dyshomeostasis contexts.

References

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

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.