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Research use only
· 7 min read
Tuftsin is four residues long and degrades in serum within minutes. Selank is tuftsin with three residues bolted onto its C-terminus, and that modest addition is the entire design rationale: buy stability by extending the parent fragment into a heptapeptide. The result is Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP), developer code TP-7, and a compound that the Soviet-era pharmacology literature spent considerable effort characterising at the receptor and enzyme level. Supplied strictly as a research reagent; everything below describes what published studies investigated, not any human use.
| Compound | Selank |
|---|---|
| Synonyms / development code | TP-7; TKPRPGP |
| Class / mechanism | Synthetic tuftsin-analogue regulatory heptapeptide (glyproline class) |
| Amino-acid sequence | Thr-Lys-Pro-Arg-Pro-Gly-Pro |
| Molecular formula | C33H57N11O9 |
| Molecular weight | ~751.9 g/mol (average) |
| CAS number | 129954-34-3 |
| PubChem CID | 11765600 |
| Supply status | Research use only - not for human or veterinary use |
PubChem CID 11765600 is the record to verify against. It carries the formula C33H57N11O9, an average molecular weight of approximately 751.9 g/mol, CAS 129954-34-3, the three-letter sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro, and TP-7 as a synonym - all cross-consistent on forward and reverse lookup. That four-way check (name to CID, CAS to CID, sequence to CID, code to CID) closes with no collision, which is the level of adversarial verification a well-run lab should expect from any reagent supplier.
One identity trap worth flagging: N-Acetyl Selank is a distinct compound. It sits at PubChem CID 133082488 with the formula C35H59N11O10 - two additional carbons, one additional oxygen, and a meaningfully different molecular entity. The two names look similar enough that catalogue errors are plausible; the CID check is the reliable discriminator.
| Property | Selank | Tuftsin (parent fragment) | Semax (related glyproline peptide) |
|---|---|---|---|
| Sequence (three-letter) | Thr-Lys-Pro-Arg-Pro-Gly-Pro | Thr-Lys-Pro-Arg | Met-Glu-His-Phe-Pro-Gly-Pro |
| Sequence (single-letter) | TKPRPGP | TKPR | MEHFPGP |
| Peptide length | Heptapeptide (7 residues) | Tetrapeptide (4 residues) | Heptapeptide (7 residues) |
| C-terminal motif | Pro-Gly-Pro | None (unextended) | Pro-Gly-Pro |
| Structural relationship | Tuftsin extended at C-terminus | Endogenous immunomodulatory fragment | Independent ACTH(4-7)-derived analogue |
| Class grouping | Tuftsin-analogue regulatory peptide | Regulatory tetrapeptide | Regulatory heptapeptide |
Selank is grouped here by molecular and structural pharmacology as a tuftsin-analogue regulatory peptide, not by any therapeutic indication. The logic of that grouping is straightforward: the N-terminal Thr-Lys-Pro-Arg block is native tuftsin, and the C-terminal Pro-Gly-Pro extension is the design element that sets Selank apart from it. That terminal Pro-Gly-Pro motif - shared with Semax (Met-Glu-His-Phe-Pro-Gly-Pro) - is reported in the literature to confer resistance to prolyl endopeptidase cleavage, relative to the unextended parent tetrapeptide. This is a structure-stability relationship at the molecular level, a documented design rationale, and not an in-vivo outcome. The on-page comparison table sets out the full sequence and motif relationships between Selank, tuftsin and Semax. Researchers working across the glyproline class may also consult the companion profile for Semax.
Each entry below is stated as the study design and the named endpoint only. No result, effect size, or outcome is reproduced.
Enkephalin-degrading enzyme inhibition (human serum). Kost et al. (Bioorg Khim, 2001; PMID 11443939) ran an in-vitro assay using human serum, testing Selank and Semax as inhibitors of enkephalin-degrading enzymes. The investigation measured dose-dependent inhibition of enzymatic enkephalin hydrolysis and evaluated peptide fragments of varying length. The named in-vitro IC50 values reported were approximately 20 microM for Selank and 10 microM for Semax; pentapeptide fragments retained inhibitory activity while tri-, tetra- and hexapeptide fragments did not. This is a biochemical enzyme-inhibition endpoint, measured entirely in vitro.
GABAergic receptor binding (brain-cell membranes). Vyunova et al. (Protein Pept Lett, 2018; PMID 30255741) characterised how Selank interacts with the GABAergic system in isolated brain-cell plasma membranes, using [3H]GABA binding as the measured endpoint, with HPLC for reagent purity control. An in-vitro molecular-mechanism investigation.
The studies below span cell culture, rodent, non-standard animal (arctic ground squirrel, for reasons explained below), and one healthy-participant imaging study. Each is described by design and named endpoint. No result is reproduced; the neutralising note on each study is load-bearing and intentional. Listed here as research context, not as findings a reader should expect to replicate or rely on.
Gene expression, cultured cells. Filatova et al. (Front Pharmacol, 2017; PMID 28293190) treated cultured human IMR-32 neuroblastoma cells with the peptide, GABA, olanzapine and combinations, then used quantitative PCR to measure mRNA levels of 84 genes involved in GABAergic neurotransmission. Endpoint: change in mRNA expression; study design only, no effect of the compound is asserted.
Inflammation-related gene expression, mouse spleen. Kolomin et al. (Regul Pept, 2011; PMID 21609736) administered a single intraperitoneal injection to mice and measured real-time PCR expression of 84 inflammation-related genes in spleen at 6 h and 24 h. Endpoint: expression level of inflammation-related genes; study design only, no effect is asserted.
Fragment characterisation and antiviral assay, in vitro. Andreeva et al. (Dokl Biol Sci, 2010; PMID 20506839) characterised structural fragments by chromatography and mass spectrometry and evaluated them in cell-culture systems, using Vero cells with encephalomyocarditis virus as the model agent. Endpoint: antiviral activity of fragments in vitro; study design only, no effect is asserted.
Behavioural models, rat (alcohol withdrawal). Kolik et al. (Bull Exp Biol Med, 2014; PMID 24913576) used outbred rats and a single intraperitoneal injection, with behaviour assessed in the elevated plus maze and social interaction tests plus a mechanical-sensitivity measure in a 48-h alcohol-withdrawal model. Study design only, no effect is asserted.
Elevated plus maze under chronic mild stress, rat. Kasian et al. (Behav Neurol, 2017; PMID 28280289) placed Wistar rats under unpredictable chronic mild stress and administered the peptide and diazepam individually and in combination, measuring elevated plus maze performance. Study design only, no effect is asserted.
Object recognition and tissue BDNF content, rat. Kolik et al. (Bull Exp Biol Med, 2019; PMID 31625062) studied outbred rats receiving chronic ethanol, measuring object-recognition testing and ex vivo BDNF content in hippocampus and frontal cortex. Study design only, no effect is asserted.
Liver morphology under chronic stress, rat. Fomenko et al. (Bull Exp Biol Med, 2019; PMID 31243679) administered 100, 300 and 1000 mcg/kg to Wistar rats under chronic foot-shock stress and analysed liver tissue morphologically and morphometrically. Endpoints: hepatocyte morphology and nucleus-to-cytoplasm ratio; study design only, no effect is asserted.
Serum cytokines in social-stress model, rat. Yasenyavskaya et al. (Curr Rev Clin Exp Pharmacol, 2021; PMID 32621722) used a sensory-contact social-stress model, administering 100 mcg/kg/day for 20 days and measuring serum cytokines (IL-1-beta, IL-6, IL-4, TGF-beta1, TNF-alpha) by ELISA. Endpoint: serum cytokine concentrations; study design only, no effect is asserted.
Morphine-withdrawal model, rat. Konstantinopolsky et al. (Bull Exp Biol Med, 2022; PMID 36322304) used a naloxone-precipitated morphine-withdrawal model, comparing a single 0.3 mg/kg injection of the peptide against diazepam 2 mg/kg. Endpoints: total index of withdrawal signs and tactile sensitivity threshold; study design only, no effect is asserted.
Seasonal behavioural study, arctic ground squirrel. Semenova et al. (Bull Exp Biol Med, 2005; PMID 16848230) assessed arctic ground squirrels across seasons in open-field and hole-board tests. Endpoints: orientation and exploratory activity, locomotor activity. The choice of model species reflects a particular interest in seasonal variation in regulatory-peptide responsiveness; study design only, no effect is asserted.
Resting-state functional connectivity, healthy participants. Panikratova et al. (Dokl Biol Sci, 2020; PMID 32342318) imaged 52 healthy participants before and at 5 and 20 min after administration of the peptide, Semax or placebo using resting-state functional MRI, with amygdala and dorsolateral prefrontal cortex as regions of interest. Endpoint: whole-brain resting-state functional connectivity between predefined regions. This is a brain-connectivity-mapping study reported at the mechanism level; study design only, no effect is asserted.
Selank is typically supplied as a white-to-off-white lyophilised powder. As a short water-soluble heptapeptide with no disulphide bond, it follows standard short-peptide handling conventions: store the dry powder sealed, protected from moisture and light, with long-term storage at -20 C. Allow vials to equilibrate to room temperature before opening to prevent condensation on the hygroscopic powder.
The Pro-Gly-Pro C-terminal extension was introduced specifically to increase metabolic and enzymatic stability relative to native tuftsin - a design feature that is relevant to bench expectations when working with Selank as a research reagent. Being a hydrophilic, non-cysteine heptapeptide, Selank is conventionally dissolved in an appropriate aqueous laboratory solvent for analysis, then aliquoted to limit freeze-thaw cycling. This is a description of conventional bench practice, not a preparation method for any use in humans or animals. See the reconstitution guide for the standard laboratory workflow. Purity and identity should be verifiable rather than assumed: current certificates of analysis are available for every batch.
Three tiers, sorted by how much weight each can bear. Well established: the chemistry. Selank is a defined heptapeptide, Thr-Lys-Pro-Arg-Pro-Gly-Pro, with a confirmed PubChem record (CID 11765600), CAS number and formula that survive forward and reverse lookup, and its N-terminal block is native tuftsin - none of that is in dispute. The middle ground: the mechanism work. Enzyme-inhibition assays in human serum and [3H]GABA binding in isolated brain-cell membranes are real measurements, but they sit in test tubes and cell preparations, alongside rodent gene-panel and behavioural models. A cell in a dish is not a person. Weakest of all: human evidence, which here amounts to a single resting-state imaging study of brain connectivity - a mechanism readout, not a tested outcome. It is not a licensed medicine, and it has not been shown to produce defined outcomes in humans. Curiosity is warranted; certainty is not.
Kovalabs supplies Selank strictly as a research chemical for laboratory research use only. It is not a medicine, supplement, or veterinary product, is not for human or veterinary use, and nothing on this page constitutes a medicinal, therapeutic, efficacy, dosing, or human-outcome claim. The descriptions above are restricted to molecular, structural and biochemical endpoints, stated only as what each study investigated. Purchasers are responsible for handling, storing and using the material in compliance with all applicable laws and institutional requirements. Full terms are set out on the research disclaimer page.
Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP). It is classified here by its molecular pharmacology as a tuftsin-analogue regulatory peptide (glyproline class), being the endogenous tetrapeptide tuftsin extended at the C-terminus with a Pro-Gly-Pro motif. It is supplied for research use only.
Selank corresponds to PubChem CID 11765600, CAS 129954-34-3, molecular formula C33H57N11O9 and an average molecular weight of approximately 751.9 g/mol. These were cross-checked by forward and reverse lookup in PubChem. Note that N-Acetyl Selank is a different compound (CID 133082488, C35H59N11O10) and should not be confused with Selank base.
Selank shares its N-terminal Thr-Lys-Pro-Arg tetrapeptide with the endogenous peptide tuftsin and adds a C-terminal Pro-Gly-Pro motif. That same Pro-Gly-Pro motif appears in the related heptapeptide Semax (Met-Glu-His-Phe-Pro-Gly-Pro) and is described as a stabilising element relative to the unextended fragment. The on-page table compares all three sequences in both three-letter and single-letter notation.
Published study designs name endpoints such as in-vitro inhibition of enkephalin-degrading enzymes (PMID 11443939), [3H]GABA receptor binding (PMID 30255741), mRNA expression of GABAergic and inflammation-related gene panels (PMID 28293190, PMID 21609736), serum cytokine concentrations and tissue BDNF content in animal models, and resting-state functional connectivity in a healthy-participant imaging study (PMID 32342318). These are named endpoints only; no result or outcome is asserted.
By convention for short synthetic peptides, the lyophilised powder is stored sealed, away from moisture and light, with long-term storage at -20 C, and vials are equilibrated to room temperature before opening. As a hydrophilic non-cysteine heptapeptide, Selank is conventionally dissolved in an appropriate aqueous laboratory solvent, then aliquoted and stored cold to avoid repeated freeze-thaw cycles. See the reconstitution guide for the standard workflow. This is not a preparation method for any use in humans or animals.
No. Kovalabs supplies Selank as a research chemical for laboratory research use only. It is not for human or veterinary use, diagnosis, or treatment, and nothing on this page constitutes a medicinal, therapeutic, efficacy, or dosing claim. See the research disclaimer for full terms.