Semax (10 mg) 195€ + Shipping ^{En solde}

Semax is a synthetic neurotrophic heptapeptide built from the ACTH(4–7) core plus a C-terminal Pro-Gly-Pro (PGP) extension that improves proteolytic stability. It lacks the corticotropic (adrenal) activity of ACTH and is studied primarily for BDNF/TrkB-mediated neurotrophic signaling and ischemic-injury transcriptomics. This product is supplied as a research-grade aqueous nasal-spray solution for in vitro, ex vivo and analytical research only.

Investigational directions enabled by the published mechanism — not therapeutic claims.

• ◆Neurotrophic signaling: BDNF exon III transcription and TrkB phosphorylation in rat hippocampus
• ◆Ischemic-injury research: post-ischemic transcriptome (394 DEGs, tMCAO 24 h)
• ◆Monoaminergic modulation: dopaminergic/serotonergic activation in rodent striatum
• ◆Neuroimmune transcriptomics: immune-response and vasculogenesis gene programs post-ischemia

In published models, Semax upregulates BDNF exon III transcription and increases TrkB tyrosine phosphorylation in rat hippocampus, with rapid BDNF/NGF mRNA induction in basal-forebrain glial cultures. In ischemia models the transcriptome shifts — inflammatory genes down, neurotransmission genes up — and dopaminergic/serotonergic systems are activated in the rodent striatum.

Key literature: Dolotov et al., 2006, J Neurochem · Shadrina et al., 2001 · Filippenkov et al., 2020 · Medvedeva et al., 2014 / 2017.

Evidence note: neurotrophin induction is the best-characterized axis; the primary receptor remains unidentified. Early screening reported MC4R antagonism (Adan 1994), but whether melanocortin receptors mediate the neurotrophic effects is unresolved.