PE 22-28 vs Semax
A side-by-side research comparison of PE 22-28 and Semax across mechanism, dosing, half-life, benefits, side effects and research status.
Comparison table
| Attribute | PE 22-28 | Semax |
|---|---|---|
| Full name | PE 22-28 (Spadin-Derived TREK-1 Peptide) | Semax (ACTH 4-10 analog) |
| Category | Cognitive & Nootropic | Cognitive & Nootropic |
| Status | Research peptide (preclinical) | Research compound |
| Mechanism | Selectively blocks the TREK-1 background potassium channel. TREK-1 inhibition enhances serotonergic signaling and rapidly increases synaptogenesis and neurogenesis, producing antidepressant-like effects faster than SSRIs in animal models. | Activates MC3/4R, increases BDNF and NGF, modulates dopamine/serotonin, enhances neuronal survival via TrkB, and promotes CREB-mediated neuroplasticity. |
| Molecular weight | ~ (7-residue peptide) | 813.9 Da |
| Half-life | Short (peptide; improved vs spadin) | 3-5 min (systemic) / extended (intranasal) |
| Bioavailability | Intranasal or injection (research) | Moderate (intranasal) |
| Typical dose | Not established for humans | 200-600 mcg per dose |
| Frequency | Research only | 2-3x daily |
| Route | Intranasal or injection (research) | Intranasal drops/spray |
PE 22-28 reported benefits
- Rapid antidepressant effects (preclinical)
- Promotes neurogenesis and synaptogenesis
- TREK-1 channel blockade
- Neuroplasticity research interest
Semax reported benefits
- Enhanced attention/focus
- Memory improvement
- Neuroprotection (stroke)
- BDNF/NGF upregulation
- Improved learning
- Optic nerve support
Related comparisons
Research and educational reference only. Not medical advice.