Research At a Glance
- Research Category
- Neurological & Cognitive Research
- Peptide Length
- 7 amino acids (ACTH(4-10) analogue)
- Purity
- ≥ 98% (HPLC)
- Published Studies
- ~230 indexed
- Storage
- Lyophilized: 2–8 °C, protected from light. Reconstituted: 2–8 °C, use within 30 days.
Published-study figures are approximate PubMed result counts and indicate the volume of available literature only. Purity reflects third-party analytical testing on the corresponding lot; see the Quality Assurance Center for lot-matched certificates.
What Is Semax?
Semax (Met-Glu-His-Phe-Pro-Gly-Pro) is a synthetic heptapeptide developed as an analog of ACTH (4-10), a fragment of adrenocorticotropic hormone. A C-terminal Pro-Gly-Pro extension protects the peptide against proteolytic degradation while eliminating the steroidogenic (cortisol-stimulating) activity of full-length ACTH, giving researchers a tool for studying ACTH-fragment receptor interactions independent of HPA-axis effects.
Why Researchers Study It
- BDNF pathway research — the most consistently reported finding in the literature is Semax's upregulation of brain-derived neurotrophic factor (BDNF) mRNA and protein, particularly in hippocampal tissue, relevant to synaptic plasticity and neuronal survival research
- Dopaminergic and serotonergic signaling — research has examined Semax's effects on dopamine synthesis and receptor sensitivity in striatal and frontal cortical regions, relevant to attention and executive function pathway research
- Neuroprotection and ischemia models — research in cerebral ischemia models has examined reduced neuronal death associated with Semax administration, with proposed BDNF-mediated survival signaling
- Blood-brain barrier and stability research — Semax's Pro-Gly-Pro stabilization is itself studied as a model for peptide modification strategies addressing enzymatic degradation and CNS penetration
What the Published Literature Shows
Animal model research has consistently reported increased BDNF protein levels, altered BDNF gene expression, and activation of TrkB-related signaling following Semax administration, findings researchers have interpreted as evidence of an effect on neuroplasticity rather than transient stimulation alone. Electroencephalography research has documented functional changes associated with Semax administration in preclinical models. Separate mechanistic research has identified a BDNF-independent neuroprotective pathway, with one 2025 study reporting that Semax reduced reactive oxygen species production associated with amyloid-beta/copper interactions.
Researchers reviewing this literature note that while the animal-model and mechanistic evidence base for Semax is substantial, human clinical evidence remains comparatively limited in scope, and conclusions about translational relevance should be drawn cautiously.
Source
Review literature available via PubMed — Semax BDNF neuroprotection research .
Compound Specifications
| Classification | Synthetic ACTH (4-10) analog heptapeptide |
|---|---|
| Format | Lyophilized powder |
| Purity | ≥99% (HPLC-verified per lot) |
| Storage | −20°C; refrigerate 2–8°C after laboratory handling |
Certificate of Analysis
Every lot is independently tested and lot-matched. View Certificates of Analysis