Research Overview
Semax and Selank get compared constantly because they look like siblings on paper. Both are synthetic heptapeptides developed at the same Russian research institutes, both take a short natural fragment and extend it with the same C-terminal Pro-Gly-Pro tripeptide to slow peptidase cleavage, and both turn up in the same behavioural and gene-expression literature.
Their parent molecules are unrelated: Semax is built on the adrenocorticotropic hormone fragment ACTH(4-7), Selank on tuftsin, a four-residue fragment of the immunoglobulin G heavy chain. Semax reports cluster around neurotrophin signaling, brain ischemia transcriptomes and stress behaviour; Selank reports cluster around enkephalin-degrading enzymes, the GABAergic system and immune gene expression.
Both are also registered medicines in Russia, a regulatory fact worth stating plainly. Semax is described as included in the Russian list of vital and essential drugs for medical application (Radchenko et al., Acta Naturae 2025, PMID 41479572), and a 2026 review states both are approved as drugs there, Semax indicated for stroke and neurological disease and Selank for mild anxiety (Renke et al., Int J Mol Sci 2026, PMID 42123471). Research material in this catalog is not that medicine.
Structure and Class
Semax is Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP), ACTH(4-7) with Pro-Gly-Pro appended: C37H51N9O10S, approximately 813.9 g/mol, CAS 80714-61-0, PubChem CID 9811102. The catalog page prints 813.94 g/mol and gives the class as an ACTH(4-10) analog heptapeptide. Its single sulfur atom is the N-terminal methionine, which makes Semax the oxidation-sensitive one of the pair.
Selank is Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP), the tuftsin sequence Thr-Lys-Pro-Arg with the same extension. Reported identity data: C33H57N11O9, approximately 751.9 g/mol, CAS 129954-34-3, PubChem CID 11765600, printed as 751.87 g/mol with the class given as a tuftsin analog heptapeptide. Selank has no sulfur, and its lysine and arginine make it the more basic peptide. Both are commonly supplied as acetate or diacetate salts, so net peptide content, salt form and purity are certificate values for the specific lot rather than free-base figures.
Side by Side
| Attribute | Semax | Selank |
|---|---|---|
| Compound class | Synthetic heptapeptide, melanocortin fragment analog | Synthetic heptapeptide, tuftsin analog |
| Sequence | Met-Glu-His-Phe-Pro-Gly-Pro | Thr-Lys-Pro-Arg-Pro-Gly-Pro |
| Parent fragment | ACTH(4-7), plus Pro-Gly-Pro | Tuftsin (Thr-Lys-Pro-Arg), plus Pro-Gly-Pro |
| Identity data | C37H51N9O10S, approximately 813.9 g/mol, CAS 80714-61-0 | C33H57N11O9, approximately 751.9 g/mol, CAS 129954-34-3 |
| Mechanism as reported | Raises BDNF protein and trkB phosphorylation; specific saturable binding in basal forebrain membranes; shifts gene expression after ischemia | Inhibits enkephalin-degrading enzyme activity; shifts GABA receptor subunit, transporter and dopamine receptor gene expression |
| Study models cited | Rat hippocampus and basal forebrain, rat artery occlusion, rat chronic stress, transgenic mice, human imaging | Human plasma in vitro, rat frontal cortex, rat morphine withdrawal, human imaging |
| Regulatory status cited | Registered medicine in Russia, listed as vital and essential; not approved in the United States | Registered medicine in Russia for mild anxiety; not approved in the United States |
| Supplied form | Lyophilized powder, single vial, also in a blend with Selank | Lyophilized powder, single vial, also in a blend with Semax |
Research Context: Semax
The neurotrophin link is the most cited mechanism. In rat hippocampus, a single application was reported to raise BDNF protein roughly 1.4 fold alongside a 1.6 fold increase in trkB tyrosine phosphorylation, with exon III BDNF mRNA up about three fold, and treated animals showed more conditioned avoidance reactions (Dolotov et al., Brain Res 2006, PMID 16996037). Model: rat.
A companion study looked for a binding site. Tritium-labelled Semax bound rat basal forebrain membranes in a time-dependent, specific, reversible and calcium-requiring manner with a dissociation constant near 2.4 nM, and intranasal application raised BDNF in basal forebrain but not cerebellum (Dolotov et al., J Neurochem 2006, PMID 16635254). Models: rat tissue membranes and rat.
The ischemia literature is transcriptomic. In rats after permanent middle cerebral artery occlusion, Semax predominantly altered immune-response genes, more than half the differentially expressed set at 24 hours (Medvedeva et al., BMC Genomics 2014, PMID 24661604). Model: rat.
Two recent studies extend the behavioural side. In male rats under chronic unpredictable stress, Semax was reported to attenuate anhedonia in the sucrose preference test and to suppress adrenal hypertrophy and the fall in hippocampal BDNF (Inozemtseva et al., Eur J Pharmacol 2024, PMID 39442746). In APPswe/PS1dE9 transgenic mice, Semax and a derivative were reported to improve open field, novel object recognition and Barnes maze performance and to reduce amyloid inclusion counts in cortex and hippocampus (Radchenko et al., Acta Naturae 2025, PMID 41479572).
Research Context: Selank
Selank's oldest mechanistic claim is enzymatic. In human plasma in vitro, it dose-dependently inhibited enzymatic hydrolysis of enkephalin with a reported half-maximal inhibitory concentration near 15 micromolar, more potently than bacitracin or puromycin in the same assay; the same report described reduced total enkephalinase activity in patients with generalized anxiety (Zozulya et al., Bull Exp Biol Med 2001, PMID 11550013). Models: human plasma in vitro and a clinical cohort.
The GABAergic hypothesis has been tested at the transcript level. In rat frontal cortex, Selank or GABA shifted mRNA levels of 45 of 77 analyzable neurotransmission genes at one hour with a strong positive correlation between treatments, and at three hours Selank produced large increases in the GABA-A epsilon and theta subunit genes and in hypocretin where GABA did not. The authors read that partial overlap as consistent with allosteric modulation rather than action at the GABA binding site (Volkova et al., Front Pharmacol 2016, PMID 26924987). Model: rat.
Behavioural work uses classical rodent paradigms. In outbred rats under naloxone-precipitated morphine withdrawal, Selank was reported to reduce the total withdrawal index by about 40 percent and to attenuate convulsive reactions, ptosis and posture disorders, performing slightly below diazepam (Konstantinopolsky et al., Bull Exp Biol Med 2022, PMID 36322304). Model: rat.
One study puts both peptides in the same human protocol. Resting-state functional MRI in 52 healthy participants, scanned before and at two timepoints after Semax, Selank or placebo, reported differences in connectivity between the right amygdala and a right-hemisphere temporal region (Panikratova et al., Dokl Biol Sci 2020, PMID 32342318). Model: human imaging, not an efficacy trial.
Choosing Between Them for a Research Question
The split is cleaner than the shared Pro-Gly-Pro tail suggests. A study on neurotrophin signaling, ischemic cortex transcriptomes, amyloid models or stress-induced anhedonia has direct precedent with Semax. A study on enkephalin-degrading enzymes, GABA-A subunit and transporter expression, or withdrawal behaviour has direct precedent with Selank.
Route matters as much as compound: much of the cited rodent work for both used intranasal delivery, so replication designs need to match the route as well as the molecule. Where a design calls for both in one preparation, the catalog stocks a fixed blend, which suits an overlap question and cannot attribute an effect to one peptide. The registered-medicine status in Russia is background only and transfers no approval or safety conclusion to research material.
Handling and Storage
Both ship lyophilized and are most stable that way. Keep the sealed vial cold and dark, warm it to room temperature before opening so moisture does not condense onto the cake, add diluent slowly down the wall, and let the powder dissolve without shaking. The Disguised Alpha pages for both state minus 20 C for the powder as shipped and 2 to 8 C after reconstitution, protected from light, avoiding freeze-thaw cycles.
Semax deserves more care in solution because of its N-terminal methionine, whose thioether side chain is oxidation-prone; protect it from air, light and oxidizing agents. Both peptides degrade in biological media by sequential cleavage, so aliquot into single-use volumes, keep solutions cold and dark, and use the certificate molecular weight for molarity.
Questions Researchers Ask
Are Semax and Selank the same class of compound?
They share a format and a stabilizing tail, not a class. Both are synthetic heptapeptides ending in Pro-Gly-Pro, but Semax derives from an adrenocorticotropic hormone fragment and Selank from the immunoglobulin-derived tuftsin sequence.
Are these approved drugs?
In Russia, yes: Semax is described as included in the Russian list of vital and essential drugs (Radchenko et al., Acta Naturae 2025, PMID 41479572), and a 2026 review states both are approved there (Renke et al., Int J Mol Sci 2026, PMID 42123471). Neither is approved in the United States, and research-grade material is not a medicine.
Which one has human data?
Both appear in a single human imaging protocol against placebo in 52 participants, reporting connectivity differences rather than clinical outcomes (Panikratova et al., Dokl Biol Sci 2020, PMID 32342318). The Selank enzyme report also included a clinical cohort (Zozulya et al., Bull Exp Biol Med 2001, PMID 11550013).
What should be confirmed on the certificate?
Printed lot identity, HPLC purity against specification, identity confirmation, measured net peptide content, and the salt form. Use the certificate molecular weight for concentration work.
Semax and Selank are supplied strictly for laboratory and in-vitro research use. They are not for human consumption, veterinary use, or any diagnostic or therapeutic application. Nothing on this page is medical, dosing, or therapeutic advice.