All information below describes the compound's chemical identity, laboratory handling, and the published research literature. It describes molecular targets and results in laboratory and animal models only — not effects in humans — and is not evidence of any human benefit.
What Are Selank and Semax?
Selank and Semax are synthetic neuropeptides developed at the Institute of Molecular Genetics of the Russian Academy of Sciences. Both were designed as stable synthetic analogues of naturally occurring peptide sequences, with modifications intended to give greater resistance to enzymatic degradation and central nervous system penetration relative to the native fragments they are derived from. Neither occurs freely in nature; both are subjects of preclinical neuroscience investigation.
Selank (also designated TP-7) is a heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro, derived from the endogenous immunomodulatory tetrapeptide tuftsin. Semax is a heptapeptide with the sequence Met-Glu-His-Phe-Pro-Gly-Pro, an analogue of the ACTH(4-7) fragment of adrenocorticotropic hormone extended with a Pro-Gly-Pro C-terminal addition. Both are supplied as reference compounds for in vitro and animal research use only. The sections below summarize their chemical identity, laboratory handling, the molecular targets and model systems examined in the published literature, and the primary references — without describing outcomes, efficacy, or effects in humans.
Research Targets & Pathways
Published preclinical literature has examined Selank and Semax in relation to several molecular systems. These are pathway associations reported in laboratory and animal models; refer to the cited studies for methods and findings.
- GABA-A receptor / GABAergic neurotransmission — examined in relation to Selank in behavioral and receptor-binding assays.
- Serotonergic signaling — examined in relation to Selank, including tryptophan hydroxylase activity in rodent brain tissue.
- Enkephalin-degrading enzyme activity / endogenous opioid peptides — examined in relation to Selank in studies of enkephalin turnover.
- Tuftsin receptor / immunoregulatory signaling — examined in relation to Selank in lymphocyte and cytokine assay systems.
- BDNF / TrkB neurotrophin signaling — examined in relation to both Selank and Semax in hippocampal and cortical tissue.
- NGF neurotrophin expression — examined in relation to Semax across rat brain regions.
- Melanocortin receptor (MC4R) / ACTH(4-7) activity — examined in relation to Semax in receptor-binding assays.
- Mu opioid receptor (Oprm1) — examined in relation to Semax in a spinal cord injury model.
- Cytokine signaling (IL-6, TNF-α, IL-10) — examined in relation to both compounds in stress-model and immune assay systems.
Model Systems Studied
Selank and Semax have been used as test compounds across a range of published preclinical model systems, primarily in rodents and in vitro cell assays. Refer to the cited literature for study designs, endpoints, and findings.
- Anxiety-related behavior — elevated plus-maze, open-field, and conditioned active avoidance assays (primarily Selank).
- Learning and memory — Morris water maze and passive avoidance paradigms (both compounds).
- Cerebral ischemia — middle cerebral artery occlusion and ischemia-reperfusion rodent models (primarily Semax).
- Spinal cord injury — rodent spinal cord injury models (Semax).
- Stress models — chronic unpredictable and social stress paradigms (both compounds).
- Neurodegeneration models — rodent Alzheimer's disease models (Semax).
- Electrophysiology — hippocampal-slice long-term potentiation and inhibitory-tone measurements (Selank).
- In vitro — neuronal and glial cell lines, lymphocyte cultures, and receptor-binding assays (both compounds).
- Imaging — fMRI functional connectome mapping in rodents (both compounds).
Note: the published Selank and Semax literature originates predominantly from Russian and Eastern European research institutions; independent replication outside those groups remains limited.
Molecular & Technical Profile
Selank · C33H57N11O9 | MW 751.86 g/mol | CAS 129954-34-3 | Sequence: Thr-Lys-Pro-Arg-Pro-Gly-Pro
Semax · C37H51N9O10S | MW 813.94 g/mol | CAS 80714-61-0 | Sequence: Met-Glu-His-Phe-Pro-Gly-Pro
Selank — Storage, Reconstitution & Working Concentrations
Semax — Storage, Reconstitution & Working Concentrations
Storage, reconstitution, and working-concentration values are general laboratory guidance for in vitro and animal research; always confirm against the lot-specific Certificate of Analysis.
Current Research Status
As of the time of this writing, neither Selank nor Semax has been approved by the U.S. Food and Drug Administration (FDA) for any human therapeutic use. Both compounds have been registered for clinical use in Russia, but the evidence base reviewed here is primarily preclinical, derived from rodent and in vitro models, and the published literature originates predominantly from Russian and Eastern European research institutions. Translation to human clinical contexts under FDA standards has not been established through large-scale controlled clinical trials. Ongoing research continues to characterize the mechanistic profiles of both compounds and identify which experimental findings may have translational relevance.
Research FAQ
Are Selank and Semax approved for human use?
No. Neither Selank nor Semax has been approved by the FDA for any human therapeutic use. Both have been registered for clinical use in Russia, but the evidence base reviewed here is preclinical (rodent and in vitro models), and the compounds are supplied for laboratory research use only — not for human consumption.
What are Selank's and Semax's molecular formulas and sequences?
Selank is a synthetic heptapeptide, sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro — molecular formula C33H57N11O9, MW 751.86 g/mol, CAS 129954-34-3. Semax is a synthetic heptapeptide, sequence Met-Glu-His-Phe-Pro-Gly-Pro — molecular formula C37H51N9O10S, MW 813.94 g/mol, CAS 80714-61-0.
How are Selank and Semax stored and reconstituted?
Store lyophilized at −20°C, protected from light and moisture. Reconstitute each in sterile or bacteriostatic water (or saline/PBS); store the reconstituted solution at 2–8°C for up to ~28 days and avoid repeated freeze–thaw.
What targets and model systems have Selank and Semax been studied in?
Preclinical work has examined Selank in relation to GABA-A receptor and serotonergic signaling, enkephalin-degrading enzyme activity, and BDNF/TrkB signaling, and Semax in relation to BDNF and NGF neurotrophin signaling, melanocortin/ACTH-fragment activity, and cytokine signaling. Model systems include rodent elevated plus-maze and water-maze assays, cerebral ischemia and spinal cord injury models, chronic stress models, and in vitro neuronal, glial, and lymphocyte cultures. Note the predominantly single-region literature caveat noted above.
Selected References
- Kozlovskaya et al. — Review of molecular aspects of Selank heptapeptide biological activity across preclinical assay systems — Protein Pept Lett, 2018.
- Semenova et al. — Characterization of Selank as a tuftsin analogue with enhanced CNS stability and anxiolytic profile in rodent models — Bull Exp Biol Med, 2001.
- Zozulya et al. — Review of tuftsin-derived peptide pharmacology including receptor binding and metabolic stability assays — Peptides, 2009.
- Voin et al. — Pharmacological review measuring GABA-A receptor modulation profiles of Selank, phenibut, and flunitrazepam in behavioral and receptor-binding assays — J Clin Pharmacol, 2021.
- Semenova et al. — Elevated plus-maze and open-field assay measurements of anxiolytic activity in Selank-treated rats versus diazepam controls — Bull Exp Biol Med, 2005.
- Inozemtseva et al. — ELISA-measured BDNF protein levels in hippocampus and prefrontal cortex of rats after Selank administration under ethanol-induced memory impairment model — Bull Exp Biol Med, 2019.
- Dolotov et al. — Measured BDNF and NGF protein levels in multiple rat brain regions following Semax administration — Bull Exp Biol Med, 2007.
- Shadrina et al. — Measured transcription of neurotrophin and neurotrophin receptor genes following Semax and Pro-Gly-Pro administration after cerebral ischemia in rat models — Cell Mol Neurobiol, 2010.
- Glazova et al. — Measured BDNF and TrkB receptor expression in rat brain following repeated Semax administration — Bull Exp Biol Med, 2004.
- Ashmarin et al. — Measured learning and memory performance in rodent behavioral models following ACTH(4-10) analogue (Semax) administration; compared to reference nootropic compounds — Zh Vyssh Nerv Deiat Im I P Pavlova, 1995.
- Kolomin et al. — Analyzed brain protein expression profile to assess protective effect of Semax in a rat cerebral ischemia-reperfusion model — Int J Mol Sci, 2021.
- Gusev et al. — Evaluation of therapeutic effect of Semax in optic nerve disease; early clinical characterization of compound — Vestn Oftalmol, 2000.