Selank vs Semax
Selank and Semax are heptapeptides developed in Russia that share a Pro-Gly-Pro tail but derive from different parent molecules: Selank is an analog of tuftsin, and Semax is an analog of an ACTH fragment 1,2,8. Both have been studied mainly in rodents and in Russian-language clinical reports, and the FDA lists both among bulk substances for compounding about which it has limited or no safety information 9.
Side by side
| Field | Selank | Semax |
|---|---|---|
| Class | Synthetic heptapeptide, analog of tuftsin 7,8 | Synthetic heptapeptide, analog of an ACTH fragment 2,3 |
| Origin and structure | Thr-Lys-Pro-Arg-Pro-Gly-Pro: the tuftsin sequence with Pro-Gly-Pro attached; the FDA lists it as selank acetate (TP-7) 1,8,9 | Met-Glu-His-Phe-Pro-Gly-Pro: an ACTH(4-7) fragment with Pro-Gly-Pro attached, also described as an ACTH(4-10) analog 1,2,3 |
| Proposed mechanism | Inhibited enkephalin-degrading enzymes in human serum in vitro 1; changed expression of genes tied to GABAergic neurotransmission in rat frontal cortex (animal data) 6 | Inhibited enkephalin-degrading enzymes in human serum in vitro 1; increased BDNF and trkB signaling in rat hippocampus (animal data) 2; altered immune-response gene expression in rat ischemia (animal data) 3 |
| Half-life | Not identified in the sources reviewed | Not identified in the sources reviewed |
| Highest human trial phase | Comparative clinical study versus medazepam in 62 patients, published in Russian 5 | Clinical study in 110 post-stroke patients, published in Russian 4 |
| FDA status | Listed by the FDA (as selank acetate, TP-7) among bulk substances for compounding that may present significant safety risks; FDA lacks important information on safety in humans 9 | Listed by the FDA (as semax, heptapeptide) on the same page; FDA has no, or limited, safety information for the proposed routes 9 |
| Published human outcomes | In 62 patients with generalized anxiety disorder or neurasthenia, anxiolytic effects on psychometric scales were similar to medazepam, and the authors also described antiasthenic and psychostimulant effects 5 | In 110 post-stroke patients, groups receiving Semax had higher plasma BDNF and a faster rise in Barthel index scores than groups that did not 4 |
| Safety signals | No safety findings were given in the abstract of the clinical study; the FDA notes it lacks information on safety in humans 5,9 | No safety findings were given in the abstract of the clinical study; the FDA notes limited safety information 4,9 |
| WADA status | Not individually named in the 2026 Prohibited List text reviewed; class S0 covers substances with no current governmental approval for human therapeutic use, and this was not assessed here 10 | Not individually named in the 2026 Prohibited List text reviewed; class S0 covers substances with no current governmental approval for human therapeutic use, and this was not assessed here 10 |
| Evidence level | Mostly rodent and in vitro data, with one small Russian-language comparative clinical study 1,5,6,7 | Mostly rodent and in vitro data, with one Russian-language clinical study 1,2,3,4 |
Selank: what the data says
In the human literature identified, a Russian-language study of 62 patients with generalized anxiety disorder and neurasthenia compared Selank (30 patients) with medazepam (32 patients) and reported similar anxiolytic effects on the Hamilton, Zung and CGI scales, along with antiasthenic and psychostimulant effects for Selank 5. The abstract does not describe blinding or randomization 5.
In rats (animal-only evidence), Selank prevented ethanol-induced memory and attention disturbances and prevented the ethanol-induced rise in BDNF content in the hippocampus and frontal cortex 7. In rat frontal cortex, it changed the expression of 45 of 84 neurotransmission-related genes one hour after administration, and the changes correlated with those produced by GABA, leading the authors to propose allosteric modulation of the GABAergic system 6. A separate rat study of the analog TP-7 reported reduced anxiety-phobic behavior over four weeks 8.
Semax: what the data says
In rats (animal-only evidence), a single application of Semax increased BDNF protein and trkB phosphorylation in the hippocampus, and treated animals made more conditioned avoidance responses 2. In rats with focal cerebral ischemia, transcriptome analysis found that immune-response genes were the most markedly affected by Semax 3.
In a Russian-language study of 110 patients after ischemic stroke, those who received Semax had higher plasma BDNF throughout the study and a faster improvement in Barthel index scores than those who did not 4. The abstract describes subgroups by rehabilitation timing and Semax use but does not state that allocation was randomized or blinded 4. In human serum in vitro, both Semax and Selank inhibited enkephalin-degrading enzymes, which the authors suggested could contribute to their biological activity 1.
Key research differences
- Parent molecule: Selank is a tuftsin analog and Semax is an analog of an ACTH fragment, each with a Pro-Gly-Pro tail 1,3,8.
- Shared in vitro activity: both inhibited enkephalin-degrading enzymes in human serum, with a lower IC50 reported for Semax (10 micromolar) than for Selank (20 micromolar) 1.
- Studied mechanisms in rodents differ: Semax with hippocampal BDNF/trkB signaling and immune-response gene expression 2,3, Selank with GABAergic gene expression and BDNF content after ethanol exposure (animal data) 6,7.
- Clinical focus differs: the human report on Selank concerns anxiety disorders and neurasthenia 5, whereas the human report on Semax concerns recovery after ischemic stroke 4.
- Both human reports were published in Russian, and their abstracts do not describe blinding or randomization 4,5.
- The FDA lists both and states that it lacks important safety information on Selank and has no or limited safety information on Semax for the proposed routes 9.
Where the evidence is limited
Evidence for both compounds is limited 4,5. Most of the data identified come from Russian research groups, the two human reports identified are Russian-language studies whose abstracts do not describe blinding or randomization, and no independent replication was identified 4,5. The rodent studies use different models and are not directly comparable 2,6. No check of regulatory status outside the United States was made in this review.
Frequently asked questions
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References
- Semax and selank inhibit the enkephalin-degrading enzymes from human serum (in Russian) Bioorganicheskaia Khimiia. 2001
- Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus Brain Research. 2006
- Semax, an analog of ACTH(4-7), regulates expression of immune response genes during ischemic brain injury in rats Molecular Genetics and Genomics. 2017
- The efficacy of semax in the treatment of patients at different stages of ischemic stroke (in Russian) Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova. 2018
- Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia (in Russian) Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova. 2008
- Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission Frontiers in Pharmacology. 2016
- Selank, Peptide Analogue of Tuftsin, Protects Against Ethanol-Induced Memory Impairment by Regulating of BDNF Content in the Hippocampus and Prefrontal Cortex in Rats Bulletin of Experimental Biology and Medicine. 2019
- Influence of long-term treatment with tuftsin analogue TP-7 on the anxiety-phobic states and body weight Pharmacological Reports. 2006
- Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks (Category 2; content current as of 04/22/2026) FDA (Human Drug Compounding). 2026
- International Standard: Prohibited List 2026 WADA. 2026
For research use only. Not for human or veterinary use. Not a drug, food, or dietary supplement. This page compares published research and is not medical advice or a recommendation.

