Compound Profiles
Semax and Selank: Two Neuropeptides in Published Research
Healthy Aminos Research Team · · 7 min read
Semax: ACTH(4-10) Analog
[Semax](/peptides/cognitive/semax) is a synthetic heptapeptide analog of ACTH(4-10) with the sequence Met-Glu-His-Phe-Pro-Gly-Pro. MW: 813.97 Da (CAS: 80714-61-0). Developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, semax retains neurotropic properties without adrenocorticotropic (steroidogenic) activity.
### BDNF Upregulation
[Dolotov et al. (2006)](https://pubmed.ncbi.nlm.nih.gov/16996037/) examined semax's effects on brain-derived neurotrophic factor (BDNF) expression in rat hippocampal and cortical tissues. The study reported increased BDNF mRNA levels in treated animals compared to controls, with the effect observed in both hippocampal and basal forebrain regions.
Selank: Tuftsin Analog
[Selank](/peptides/cognitive/selank) is a synthetic analog of the naturally occurring immunomodulatory peptide tuftsin (Thr-Lys-Pro-Arg) with an added Gly-Pro sequence for metabolic stability. MW: 751.87 Da (CAS: 129954-34-3).
### Human Clinical Data
[Zozulia et al. (2008)](https://pubmed.ncbi.nlm.nih.gov/18454096/) published data from a human clinical trial comparing selank to a benzodiazepine reference compound in patients with anxiety disorders. The study reported observations on anxiety rating scales with both compounds, noting that selank did not produce sedation or dependence markers observed with the reference compound.
### GABA-A Modulation
[Kasian et al. (2019)](https://pubmed.ncbi.nlm.nih.gov/30255741/) examined selank's interactions with GABA-A receptors in vitro. The study used electrophysiological recordings and reported positive allosteric modulation of GABA-A receptor currents in cell preparations.
Comparative Notes
Both peptides were developed in the same laboratory and share the Pro-Gly C-terminal motif that enhances metabolic stability. They target distinct pathways: semax primarily through neurotrophic factor modulation, selank primarily through GABAergic and enkephalinergic systems.
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