Source comparison
Mechanism Comparison Table: Selank vs. Semax
Peptide Origin Tuftsin analog (IgG-derived) ACTH(4-10) fragment analog Sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro Met-Glu-His-Phe-Pro-Gly-Pro Primary Mechanism GABAergic modulation, serotonin turnover normalization BDNF/NGF upregulation, ACTH-mediated cognitive effe
This comparison does not assign a generated winner or score.
- Peptide Origin
- Tuftsin analog (IgG-derived)
- ACTH(4-10) fragment analog
- Sequence
- Thr-Lys-Pro-Arg-Pro-Gly-Pro
- Met-Glu-His-Phe-Pro-Gly-Pro
- Primary Mechanism
- GABAergic modulation, serotonin turnover normalization
- BDNF/NGF upregulation, ACTH-mediated cognitive effects
- Primary Research Focus
- Anxiolytic, stress resilience, immunomodulation
- Cognitive enhancement, neuroprotection, neurotrophin regulation
- Key Receptor Targets
- GABA-A (alpha2 subunit), opioid peptide system
- BDNF-TrkB pathway (indirect), melanocortin receptors
- Monoamine Effects
- Serotonin turnover (limbic regions)
- Dopaminergic and serotonergic (prefrontal/striatal)
- Neuroprotective Evidence
- Anti-inflammatory cytokine modulation
- Ischemia models, BDNF/VEGF-mediated lesion reduction
- HPA Axis Effect
- Corticosterone normalization (stress models)
- ACTH-related — moderate HPA interaction
- Immunomodulatory Activity
- Yes — IL-6, TNF-alpha modulation
- Minimal direct immunomodulation reported
- Research Half-Life Consideration
- Moderate — enhanced vs tuftsin parent
- Moderate — Pro-Gly-Pro extension improves stability