Semax

$126.00 USD

Semax is a synthetic heptapeptide analog of ACTH(4–10) widely explored in neuroprotective and cognitive research. In controlled studies, Semax has demonstrated potential to promote memory retention, enhance attention, and support recovery following brain ischemia. Its mechanisms include modulation of BDNF/trkB signaling, regulation of neurotransmitters such as serotonin and dopamine, and immunomodulatory activity.

Laboratory models have shown Semax may help maintain vascular integrity and gene expression tied to cognitive and immune resilience. It is frequently evaluated in stroke, neurodegeneration, and neurocognitive research contexts.

Semax, chemically defined as Met‑Glu‑His‑Phe‑Pro‑Gly‑Pro, is a neuropeptide developed for experimental use in neurology and brain research. It is derived from ACTH(4–10) and has been extensively investigated in Eastern Europe for its neuroprotective and nootropic properties.

Cognitive & Neurotrophic Effects

Preclinical research has demonstrated that Semax significantly enhances BDNF expression and trkB receptor activation in the hippocampus, increasing exon III BDNF mRNA by threefold and trkB phosphorylation by 1.6-fold in rodent models within hours of administration. These changes correlate with measurable improvements in memory consolidation and cognitive resilience in passive avoidance tasks Enhanced Wellness+13Peptide Sciences+13Wikipedia+13.

Neuroprotection & Vascular Support

Genomic studies in ischemic rat brain models revealed that Semax modulates gene expression tied to immune response, vascular formation, and cellular repair. Significant upregulation of immunoglobulin and chemokine genes was observed, along with altered vascular gene expression associated with endothelial migration and tissue regeneration PMC.

Neurotransmitter Modulation & Mood Regulation
Semax has been shown to increase levels of serotonin and dopamine in the central nervous system and blunt the effects of psychostimulants like amphetamine through regulatory pathways. These actions suggest implications for mood stabilization and stress responsiveness PARTICLE, s. r. o.+14Synapse+14Peptide Sciences+14.

Clinical & Human-Model Findings
In pilot human studies, intranasal Semax improved EEG patterns, attention, and short-term memory in shift workers—even under fatigue. Functional neuroimaging studies also showed enhanced activity in the default mode network after Semax administration in healthy volunteers Alzheimer's Drug Discovery Foundation+1Wikipedia+1.

Mechanistic Insights & Tissue Protection
Semax may also offer protection against protein aggregation and copper-induced cytotoxicity. In cell models, Semax interfered with amyloid β fibrillogenesis and reduced oxidative stress markers. Additionally, it normalized circadian rhythms and prevented adverse cardiac remodeling post-ischemia in animal studies Wikipedia+11PMC+11Peptide Sciences+11.

Together, these findings position Semax as a versatile compound for research into CNS repair, cognitive resilience, neurovascular integrity, and neuroimmune interaction. Its multiple mechanisms—ranging from neurotrophic support to genomic modulation—make it a robust agent for exploratory laboratory studies.

Research & References:

V. Khavinson et al., “Epithalon peptide induces telomerase activity and telomere elongation in human somatic cells,” Bull Exp Biol Med. 2003. (PubMed)
O.V. Korkushko et al., “Epithalamin increases pineal melatonin secretion in aged rats and elderly humans,” Bull Exp Biol Med. and related follow‑up studies. (ResearchGate)
Aging‑cell/oocyte model study: Epithalon reduced oxidative stress and improved oocyte integrity, including increased SOD activity and reduced ROS in aging models (Aging-US)