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Semax vs selank: shared tail, different origins

Semax and selank are synthetic heptapeptides that end in the same Pro-Gly-Pro tripeptide but take their first four residues from different natural peptides.[1],[2],[3]

Semax joins the ACTH(4-7) fragment to Pro-Gly-Pro, while selank extends the tetrapeptide tuftsin with the same three residues.[1],[3],[4],[5]

Their recorded laboratory targets differ, and this page lays out the structural relationship and those records without setting reported effects against each other.

Identity side by side

AttributeSemaxSelank
Sequence[6],[5]Met-Glu-His-Phe-Pro-Gly-ProThr-Lys-Pro-Arg-Pro-Gly-Pro
First four residues taken from[1],[3],[4]ACTH(4-7)Tuftsin (Thr-Lys-Pro-Arg)
Shared C-terminal tripeptide[1],[2]Pro-Gly-ProPro-Gly-Pro
FDA UNII[1],[2]I5FAL2585HTS9JR8EP1G
CAS Registry Number[1],[2]80714-61-0129954-34-3
Molecular formula[6],[5]C37H51N9O10SC33H57N11O9
Main breakdown products reported[7]HFPGP and PGP (with nerve cells)TKPRP, TKP, RP and GP (blood plasma)
Targets recorded (library)[6],[5]BDNF/trkB system (rat hippocampus)Enkephalin-degrading enzymes; [3H]GABA binding sites on brain cell membranes

How are the two built?

The substance registry files semax under the descriptive name ACTH (4-7), Pro-Gly-Pro, and a 2017 transcriptome paper describes it the same way, as the ACTH(4-7) fragment joined to that tripeptide.[1],[3]

Earlier literature, including the 2006 rat hippocampus study, calls semax an analogue of ACTH(4-10), and both descriptions refer to the same seven-residue molecule.[8],[6]

Selank's first four residues, Thr-Lys-Pro-Arg, match the registry sequence of tuftsin, a peptide first named in 1970.[2],[4],[9]

Where do their recorded pathways meet and part?

One 2001 study tested both peptides against the enkephalin-degrading enzymes of human serum and found that each inhibited them, with the effect scaling with the amount added.[10]

In that work, five-residue fragments of each heptapeptide still inhibited the enzymes, whereas the three-, four- and six-residue fragments tested showed no such effect.[10]

Tritium-labelling work reported HFPGP and PGP as the main products of semax breakdown in the presence of nerve cells, and TKPRP, TKP, RP and GP as the main products of selank in blood plasma.[7]

Past that shared enzyme work the records diverge: semax's centres on BDNF and trkB measurements in rat hippocampus, and selank's adds [3H]GABA binding on isolated brain cell membranes.[8],[11]

What is left out of this comparison?

The 2001 serum study printed a separate inhibition value for each peptide, but one assay does not establish a general difference, so those values stay on the selank compound page.[10]

A 2020 functional connectivity study that included both peptides reports outcome measures, which fall outside the identity and pathway scope of this page.[12]

Limitations

Enzyme inhibition, receptor-binding and gene-expression findings here come from serum, membrane preparations, cultured cells or rats, and none establishes an effect in a person.[6],[5]

Two of the pathway sources were published in Russian, and only their English abstracts were read for this page.[10],[7]

Compound profiles

References

  1. U.S. FDA Global Substance Registration System (GSRS), Semax, UNII I5FAL2585H. UNII I5FAL2585H · CAS 80714-61-0
  2. U.S. FDA Global Substance Registration System (GSRS), Selank, UNII TS9JR8EP1G. UNII TS9JR8EP1G · CAS 129954-34-3
  3. Medvedeva EV, Dmitrieva VG, Limborska SA, Myasoedov NF, Dergunova LV. Semax, an analog of ACTH(4-7), regulates expression of immune response genes during ischemic brain injury in rats. Mol Genet Genomics. 2017;292(3):635-653. PMID 28255762 · DOI 10.1007/s00438-017-1297-1
  4. U.S. FDA Global Substance Registration System (GSRS), Tuftsin, UNII QF5336J16C. UNII QF5336J16C · CAS 9063-57-4
  5. Selank research profile, PepGenex Science (identity and records, with their sources).
  6. Semax research profile, PepGenex Science (identity and records, with their sources).
  7. Zolotarev IuA, Dadaian AK, Dolotov OV, et al. [Evenly tritium-labeled peptides and their in vivo and in vitro biodegradation]. Bioorg Khim. 2006;32(2):183-191. (In Russian.) PMID 16637290
  8. Dolotov OV, Karpenko EA, Inozemtseva LS, et al. Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Res. 2006;1117(1):54-60. PMID 16996037 · DOI 10.1016/j.brainres.2006.07.108
  9. Najjar VA, Nishioka K. "Tuftsin": a natural phagocytosis stimulating peptide. Nature. 1970;228(5272):672-673. PMID 4097539 · DOI 10.1038/228672a0
  10. Kost NV, Sokolov OIu, Gabaeva MV, et al. [Semax and selank inhibit the enkephalin-degrading enzymes from human serum]. Bioorg Khim. 2001;27(3):180-183. (In Russian.) PMID 11443939 · DOI 10.1023/a:1011373002885
  11. Vyunova TV, Andreeva L, Shevchenko K, Myasoedov N. Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. Protein Pept Lett. 2018;25(10):914-923. PMID 30255741 · DOI 10.2174/0929866525666180925144642
  12. Panikratova YR, Lebedeva IS, Sokolov OY, et al.. Functional Connectomic Approach to Studying Selank and Semax Effects.. Doklady Biological Sciences 2020. PMID 32342318 · DOI 10.1134/S001249662001007X