# Selank vs semax - Canonical: https://residue.info/vs/selank-vs-semax/ - Compounds: Selank (https://residue.info/c/selank/), Semax (https://residue.info/c/semax/) - Updated: 2026-10-19 · Reviewed by: Residue Editorial Team 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 medazepam [1]. Semax (ACTH(4-7) plus Pro-Gly-Pro) was studied in ischemic stroke, with reports of better recovery and higher BDNF [2]. Neither has large randomized trials or FDA approval [3]. ## Side by side | | Selank | Semax | |---|---|---| | Sequence | Thr-Lys-Pro-Arg-Pro-Gly-Pro [4] | Met-Glu-His-Phe-Pro-Gly-Pro [5] | | Studied for | Anxiety, neurasthenia [1] | Ischemic stroke [2][6] | | Largest clinical study | 62 patients vs medazepam [1] | 110 stroke patients, 5 months [2] | | Proposed mechanism | GABA allosteric modulation; enkephalinase inhibition [7][4] | BDNF; immune and vascular gene expression after ischemia [2][8] | | Registered trials | None; the 2 search hits are unrelated device studies [9] | None on ClinicalTrials.gov at fetch [10] | | FDA | Withdrawn nomination [3] | Withdrawn nomination [3] | | Evidence grade | C | C | ## How are their designs related?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-Pro [4]. Semax joins the ACTH(4-7) fragment to Pro-Gly-Pro, giving Met-Glu-His-Phe-Pro-Gly-Pro [5][11]. ## 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 effects [1]. Laboratory work found it inhibited enzymatic breakdown of plasma enkephalin (IC50 15 µM) [4], acted as a positive allosteric modulator of GABA binding [7], and in rat frontal cortex changed expression of 45 of 84 neurotransmission genes within an hour [12]. ## 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 rehabilitation [2]. A 1997 study added semax to therapy in 30 acute stroke patients and compared them with 80 conventionally treated controls, reporting faster neurological recovery [6]. In rats after focal brain ischemia, semax mainly altered immune-response genes plus 24 vascular genes at 3 hours [8]. ## 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 fetch [9][10]. That is why both sit at Grade C on our [evidence scale](https://residue.info/methodology/). ## Are they FDA-approved? FDA lists selank acetate and semax among withdrawn compounding nominations and says it lacks important safety information for humans [3]. Neither is FDA-approved. ## Frequently asked questions **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-Arg [4], while semax builds on the ACTH(4-7) fragment [5]. Selank was studied for anxiety [1], semax for stroke [2]. **Are selank and semax FDA-approved?** No. FDA lists both among withdrawn compounding nominations and states it lacks safety information about them [3]. **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 controls [6], and the selank study compared two active treatments without placebo [1]. **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 nominations [3]. ## Sources [1] [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. https://pubmed.ncbi.nlm.nih.gov/18454096/ [2] [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. https://pubmed.ncbi.nlm.nih.gov/29798983/ [3] Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks. U.S. FDA, content current as of 04/22/2026. https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks [4] The 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. https://pubmed.ncbi.nlm.nih.gov/11550013/ [5] Semax, 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. https://pubmed.ncbi.nlm.nih.gov/28255762/ [6] [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. https://pubmed.ncbi.nlm.nih.gov/11517472/ [7] Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. Vyunova TV et al. Protein Pept Lett. 2018. https://pubmed.ncbi.nlm.nih.gov/30255741/ [8] The 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. https://pubmed.ncbi.nlm.nih.gov/24661604/ [9] ClinicalTrials.gov registry search: selank. 2 registered studies at fetch. https://clinicaltrials.gov/search?intr=selank [10] ClinicalTrials.gov registry search: semax. 0 registered studies at fetch. https://clinicaltrials.gov/search?intr=semax [11] PubChem compound record: ACTH (4-7), Pro-Gly-Pro-. C37H51N9O10S · MW 813.9 g/mol. https://pubchem.ncbi.nlm.nih.gov/compound/9811102 [12] Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Volkova A et al. Front Pharmacol. 2016. https://pubmed.ncbi.nlm.nih.gov/26924987/ --- From Residue. Research and education only; not medical advice. Quote with attribution and a link to the canonical page.