Selank vs semax
Residue Editorial Team · updated
In brief
Selank and semax are synthetic heptapeptides studied mainly in Russia. Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) was studied for anxiety: in 62 patients its effect was similar to the benzodiazepine medazepam1PubMed[Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia]. Zozulia AA et al. Zh Nevrol Psikhiatr Im S S Korsakova. 2008.. Semax (ACTH(4-7) plus Pro-Gly-Pro) was studied in ischemic stroke, with reports of better recovery and higher BDNF2PubMed[The efficacy of semax in the tretament of patients at different stages of ischemic stroke]. Gusev EI et al. Zh Nevrol Psikhiatr Im S S Korsakova. 2018.. Neither has large randomized trials or FDA approval3FDACertain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks. U.S. FDA, content current as of 04/22/2026..
How do Selank and Semax compare at a glance?
| Dimension | Selank | Semax |
|---|---|---|
| Sequence | Thr-Lys-Pro-Arg-Pro-Gly-Pro4PubMedThe inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity. Zozulya AA et al. Bull Exp Biol Med. 2001. | Met-Glu-His-Phe-Pro-Gly-Pro5PubMedSemax, an analog of ACTH((4-7)), regulates expression of immune response genes during ischemic brain injury in rats. Medvedeva EV et al. Mol Genet Genomics. 2017. |
| Studied for | Anxiety, neurasthenia1 | Ischemic stroke2,6PubMed[Effectiveness of semax in acute period of hemispheric ischemic stroke (a clinical and electrophysiological study)]. Gusev EI et al. Zh Nevrol Psikhiatr Im S S Korsakova. 1997. |
| Largest clinical study | 62 patients vs medazepam1 | 110 stroke patients, 5 months2 |
| Proposed mechanism | GABA allosteric modulation; enkephalinase inhibition7PubMedPeptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. Vyunova TV et al. Protein Pept Lett. 2018.,4 | BDNF; immune and vascular gene expression after ischemia2,8PubMedThe peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis. Medvedeva EV et al. BMC Genomics. 2014. |
| Registered trials | None; the 2 search hits are unrelated device studies9TrialClinicalTrials.gov registry search: selank. 2 registered studies at fetch. | None on ClinicalTrials.gov at fetch10TrialClinicalTrials.gov registry search: semax. 0 registered studies at fetch. |
| FDA | Withdrawn nomination3 | Withdrawn nomination3 |
| Evidence grade | C | C |
How are their designs related?
Both peptides end in the tripeptide Pro-Gly-Pro. Selank is Thr-Lys-Pro-Arg-Pro-Gly-Pro4. Semax joins the ACTH(4-7) fragment to Pro-Gly-Pro, giving Met-Glu-His-Phe-Pro-Gly-Pro5,11PubChemPubChem compound record: ACTH (4-7), Pro-Gly-Pro-. C37H51N9O10S · MW 813.9 g/mol..
What is the evidence for Selank?
In 62 patients with generalized anxiety disorder or neurasthenia, selank (30 patients) and medazepam (32) had similar anxiolytic effects, and selank also showed anti-asthenic and psychostimulant effects1. Laboratory work found it inhibited enzymatic breakdown of plasma enkephalin (IC50 15 µM)4, acted as a positive allosteric modulator of GABA binding7, and in rat frontal cortex changed expression of 45 of 84 neurotransmission genes within an hour12PubMedSelank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Volkova A et al. Front Pharmacol. 2016..
What is the evidence for Semax?
In 110 ischemic-stroke patients followed for five months, semax raised plasma BDNF and was associated with better Barthel index outcomes, particularly alongside early rehabilitation2. A 1997 study added semax to therapy in 30 acute stroke patients and compared them with 80 conventionally treated controls, reporting faster neurological recovery6. In rats after focal brain ischemia, semax mainly altered immune-response genes plus 24 vascular genes at 3 hours8.
How should this evidence be read?
Neither record includes a large, placebo-controlled, multicenter trial, and ClinicalTrials.gov held no registered trial testing either peptide at our fetch9,10. That is why both sit at Grade C on our evidence scale.
Are they FDA-approved?
FDA lists selank acetate and semax among withdrawn compounding nominations and says it lacks important safety information for humans3. Neither is FDA-approved.
Why do they get these evidence grades?
- C Selank
- Small clinical studies in Russian journals, including a 62-patient comparison with medazepam; no large randomized placebo-controlled trial indexed in PubMed. Grade C: Limited / early human data.
- C Semax
- Small clinical studies in stroke published in Russian journals, without large randomized controlled trials; mechanism work is in rats. Grade C: Limited / early human data.
Questions readers ask
What is the difference between selank and semax?
They share a Pro-Gly-Pro tail but differ otherwise: selank's other residues are Thr-Lys-Pro-Arg4, while semax builds on the ACTH(4-7) fragment5. Selank was studied for anxiety1, semax for stroke2.
Are selank and semax FDA-approved?
No. FDA lists both among withdrawn compounding nominations and states it lacks safety information about them3.
How strong is the clinical evidence?
Limited. The studies are small and published in Russian journals; the 1997 semax stroke study compared 30 treated patients with 80 conventionally treated controls6, and the selank study compared two active treatments without placebo1.
Can you take selank and semax together?
No published trial among the sources we cite tested them together. Both remain unapproved in the US, and FDA lists them among withdrawn compounding nominations3.
References
Every source below was retrieved from its official API or page and cached on the data-edition date. Numbers match the margin notes.
- 1 PubMed Zozulia AA, Neznamov GG, Siuniakov TS, et al. [Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia]. Zh Nevrol Psikhiatr Im S S Korsakova 2008. PMID 18454096.
- 2 PubMed Gusev EI, Martynov MY, Kostenko EV, et al. [The efficacy of semax in the tretament of patients at different stages of ischemic stroke]. Zh Nevrol Psikhiatr Im S S Korsakova 2018. PMID 29798983; doi:10.17116/jnevro20181183261-68.
- 3 FDA Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks. U.S. FDA, content current as of 04/22/2026.
- 4 PubMed Zozulya AA, Kost NV, Yu Sokolov O, et al. The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity. Bull Exp Biol Med 2001. PMID 11550013; doi:10.1023/a:1017979514274.
- 5 PubMed Medvedeva EV, Dmitrieva VG, Limborska SA, et al. Semax, an analog of ACTH((4-7)), regulates expression of immune response genes during ischemic brain injury in rats. Mol Genet Genomics 2017. PMID 28255762; doi:10.1007/s00438-017-1297-1.
- 6 PubMed Gusev EI, Skvortsova VI, Miasoedov NF, et al. [Effectiveness of semax in acute period of hemispheric ischemic stroke (a clinical and electrophysiological study)]. Zh Nevrol Psikhiatr Im S S Korsakova 1997. PMID 11517472.
- 7 PubMed Vyunova TV, Andreeva L, Shevchenko K, et al. Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. Protein Pept Lett 2018. PMID 30255741; doi:10.2174/0929866525666180925144642.
- 8 PubMed Medvedeva EV, Dmitrieva VG, Povarova OV, et al. The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis. BMC Genomics 2014. PMID 24661604; doi:10.1186/1471-2164-15-228.
- 9 ClinicalTrials.gov ClinicalTrials.gov registry search: selank. 2 registered studies at fetch.
- 10 ClinicalTrials.gov ClinicalTrials.gov registry search: semax. 0 registered studies at fetch.
- 11 PubChem PubChem compound record: ACTH (4-7), Pro-Gly-Pro-. C37H51N9O10S · MW 813.9 g/mol.
- 12 PubMed Volkova A, Shadrina M, Kolomin T, et al. Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Front Pharmacol 2016. PMID 26924987; doi:10.3389/fphar.2016.00031.