Semax and Selank: two peptides, one structural trick
Both bolt Pro-Gly-Pro onto a short bioactive fragment to survive peptidases. What each one is derived from, and what the literature actually measures.
Semax and Selank come from the same Russian research programme and share an engineering decision worth understanding, because it explains why both exist in the form they do.
The shared trick: Pro-Gly-Pro
Short peptides are cleared fast. Both compounds take a short bioactive sequence and append the tripeptide Pro-Gly-Pro, which blocks rapid enzymatic degradation and markedly extends stability relative to the parent fragment. Same solution, two different starting molecules.
| Semax | Selank | |
|---|---|---|
| Derived from | ACTH(4-7) | Tuftsin (Thr-Lys-Pro-Arg) |
| Sequence | Met-Glu-His-Phe-Pro-Gly-Pro | Thr-Lys-Pro-Arg-Pro-Gly-Pro |
| Molecular weight | 813.94 g/mol | 751.88 g/mol |
| Main research axis | Neurotrophic (BDNF) | GABAergic / neuroimmune |
Semax: neurotrophic without the endocrine activity
ACTH(4-7) is a fragment of adrenocorticotropic hormone, but Semax does not carry the corticotropic activity of the parent — it does not drive steroidogenesis. What the literature reports instead is elevated BDNF and TrkB receptor expression in hippocampal tissue, together with shifts in monoamine turnover. That separation, neurotrophic signalling without the endocrine axis, is what makes it a clean probe in cognition and cerebral-ischemia models.
Selank: anxiolytic and immune literature at once
Selank is built on tuftsin, which is itself an immunomodulatory peptide. Published work describes modulation of GABA-A receptor expression and inhibition of enkephalin-degrading enzymes, which stabilises endogenous enkephalin levels. Because the backbone is tuftsin, it also has documented effects on interleukin expression — which is why the same compound shows up in anxiolytic studies and in neuroimmune studies, a pairing that confuses people reading only one half of the literature.
Selected literature
- Dolotov OV et al. Semax, an ACTH(4-7) analog, regulates BDNF expression in the rat hippocampus. J Neurosci Res. 2006;84(8):1670-1677.
- Zozulya AA et al. Efficacy and possible mechanisms of action of Selank. Bull Exp Biol Med. 2001;131(4):315-317.
- Kolomin T et al. Transcriptomic response of rat hippocampus to Selank. J Mol Neurosci. 2014;53(3):440-446.
See Semax 10 mg and Selank 10 mg. COAs for both are temporarily unavailable. For laboratory research use only.
For laboratory research use only. Reference information, not medical advice or human-use guidance.
