Selank (Tuftsin Analogue)
A Co-Receptor That Binds Almost Nothing in Common
Neuropilin-1 is a transmembrane protein that acts mainly as a co-receptor, partnering with other receptors to modify their signalling. It binds structurally unrelated ligands including semaphorins, vascular endothelial growth factor and tuftsin.
Key facts
- Type
- Single-pass transmembrane co-receptor
- Ligands include
- Semaphorins, VEGF, tuftsin
- Roles
- Axon guidance, vascular biology, immunity
- Short cytoplasmic tail
- Limited independent signalling
- Tuftsin route
- TGF-beta pathway (Nissen 2013)
- Cell types
- Includes microglia and macrophages
What a co-receptor does
A conventional receptor binds a ligand and initiates signalling itself. A co-receptor binds the ligand too, but hands the signalling to a partner receptor — increasing affinity, changing selectivity, or enabling a response that the partner alone would not produce. Neuropilin-1 has a very short intracellular tail, which is the structural reason it depends on partners.
Why one protein binds such different molecules
Its extracellular region is built from several distinct domains, and different ligands engage different domains. That modular construction is what allows a single protein to serve axon guidance, blood vessel development and immune signalling without those ligands resembling each other in any way.
Research material referenced
Selank 10mg — third-party HPLC tested
The axon guidance role
Neuropilin-1 partners with plexins to receive semaphorin signals, which steer growing axons during nervous system development — frequently by repelling them from inappropriate territory. This is the context in which the protein was originally characterised, and it explains the name.
The vascular role
It also acts as a co-receptor for vascular endothelial growth factor, enhancing signalling through VEGF receptors. Nervous system wiring and blood vessel patterning share guidance machinery more generally, and neuropilin-1 is among the clearest examples of one protein serving both.
The immune role, and why it matters here
Neuropilin-1 is expressed on immune cells including macrophages and microglia. That is the context in which tuftsin signalling through it makes sense — a peptide released from an antibody, acting on an immune cell co-receptor, onto the TGF-beta pathway that helps set immune tone.
Why this is worth knowing when reading peptide claims
A protein that binds unrelated ligands and partners with several receptors will show up in many literatures. That breadth means an effect attributed to neuropilin-1 engagement needs care about which partnership and which cell type is involved, because the same receptor does entirely different work depending on both.
Extended research context
The Selank (Tuftsin Analogue) deep dive
Deep dive: preserving a signal rather than supplying one
Selank's most specifically characterised activity is not receptor binding. Work published in the Bulletin of Experimental Biology and Medicine in 2001 and 2002 reported that it inhibits enkephalin-degrading enzymes, measured directly on plasma enkephalinase activity, thereby extending the half-life of endogenous enkephalins rather than acting at opioid receptors itself. That distinction is routinely muddled and it matters: an agonist activates the receptor wherever the drug reaches, at whatever concentration is given, while a degradation inhibitor only lets the ligand the body is already releasing persist longer. The effect is bounded by endogenous release and occurs only where that release happens. The same logic underlies DPP-4 inhibitors in the incretin field, which prolong native GLP-1 rather than supplying an analogue - and instructively, that class produces much smaller effects than the receptor agonists do.
Deep dive: what the sequence does and does not contain
TKPRPGP is unusual among research peptides for what is absent from it. There is no cysteine, so no disulfide bonds form or scramble and no reducing agent is needed. There is no methionine, so the thioether oxidation that adds 16 Da and dominates handling guidance for MOTS-c and Semax does not apply. There is no asparagine or glutamine either, ruling out deamidation. What remains is straightforward hydrolysis, and three prolines in seven residues resist even enzymatic cleavage well, because proline locks the backbone rotation peptidases require. One practical cost of that composition: no aromatic residues means almost no absorbance at 280 nm, so the standard spectrophotometric quantification method does not work on it.
Deep dive: reading a two-literature evidence base
PubMed indexes roughly 135 Selank records against about 690 for its parent peptide tuftsin - an inversion worth noticing, since most designed analogues eventually outgrow the parent they replaced. Most of the tuftsin literature is immunological and predates Selank entirely, so it is not evidence about Selank. Within Selank's own record the split is the same one Semax shows: mechanistic work in internationally indexed journals, assessable directly; clinical work concentrated in Russian-language publications, indexed by translated title and often without accessible English full text. That is evidence which is hard to verify independently, which is not the same as evidence that is absent, and not the same as evidence that is established.
Research applications
- ▸Enkephalin and enkephalinase pathway research
- ▸GABAergic receptor expression studies in rodent models
- ▸BDNF expression research, including intranasal administration routes
- ▸Comparative work on proline-stabilised peptide design
- ▸Tuftsin and immunopeptide structure-activity research
Handling checklist
- ✓Store lyophilised material cold, dry and protected from light
- ✓No reducing agent needed — the sequence contains no cysteine
- ✓No methionine oxidation to expect; a +16 Da satellite warrants explanation
- ✓Do not rely on 280 nm absorbance — there are no aromatic residues
- ✓Introduce diluent gently against the vial wall; swirl rather than shake
- ✓Aliquot to avoid repeated freeze-thaw cycles
Common research-handling mistakes
Learnt from thousands of researcher orders across our UK labs.
✗ Describing Selank as an opioid or opioid agonist
Fix: Reported work describes inhibition of enkephalin-degrading enzymes, not receptor binding. It preserves endogenous enkephalins rather than supplying an agonist.
✗ Treating the benzodiazepine contrast as a safety claim
Fix: The mechanistic difference is real — expression-level rather than direct allosteric modulation — but it supports no comparative claim about safety or dependence.
✗ Citing tuftsin literature as evidence about Selank
Fix: Tuftsin has roughly five times more papers, most of them immunological and predating Selank. They are different compounds.
✗ Reading a BDNF expression change as a demonstrated outcome
Fix: The work measured expression in rat hippocampus. Expression is upstream of function and upstream again of any clinical claim.
✗ Treating Russian registration as equivalent to MHRA approval
Fix: Authorisations are jurisdictional and do not transfer. Selank has never been assessed by the MHRA, EMA or FDA.
Continue researching
Peer-reviewed guides, comparators and matched reference materials.
Related questions researchers ask
- What is Selank?
- What is tuftsin?
- How does Selank affect enkephalins?
- Does Selank work like a benzodiazepine?
- Is Selank approved in the UK?
- How does Selank differ from Semax?
Frequently asked questions
- What does a co-receptor do?
- It binds a ligand but hands signalling to a partner receptor, modifying affinity, selectivity or the response. Neuropilin-1's short intracellular tail is why it depends on partners.
- How can it bind unrelated ligands?
- Its extracellular region has several distinct domains, and different ligands engage different ones.
- Why is it relevant to tuftsin?
- It is expressed on macrophages and microglia, which is where a peptide released from an antibody acting on immune tone would need a receptor.
Primary sources & clinical trials
Peer-reviewed research and registered trials from PubMed, ClinicalTrials.gov, PubChem, FDA and NIH. All links open in a new tab and point to the primary source, so every claim can be verified at origin.
- PubMedNissen JC et al., Tuftsin signals through its receptor neuropilin-1 via the TGF-beta pathway — J Neurochem 2013 (PMID 24033337)pubmed.ncbi.nlm.nih.gov
- PubMedTweedle MF, Peptide-targeted diagnostics and radiotherapeutics — Acc Chem Res 2009 (PMID 19552403)pubmed.ncbi.nlm.nih.gov
- PubMedZozulya AA et al., Inhibitory effect of Selank on enkephalin-degrading enzymes — Bull Exp Biol Med 2001 (PMID 11550013)pubmed.ncbi.nlm.nih.gov
- PubMedSokolov OY et al., Selank and plasma enkephalin-degrading enzyme activity — Bull Exp Biol Med 2002 (PMID 12432865)pubmed.ncbi.nlm.nih.gov
- PubMedInozemtseva LS et al., Intranasal Selank regulates BDNF expression — Dokl Biol Sci 2008 (PMID 18841804)pubmed.ncbi.nlm.nih.gov
- PubMedZozulia AA et al., Efficacy and mechanisms of the peptide anxiolytic selank — 2008 (PMID 18454096)pubmed.ncbi.nlm.nih.gov
- PubMedKolik LG et al., Selank, peptide analogue of tuftsin — Bull Exp Biol Med 2019 (PMID 31625062)pubmed.ncbi.nlm.nih.gov
- PubMedFridkin M, Tuftsin: its chemistry, biology, and clinical potential — Crit Rev Biochem Mol Biol 1989 (PMID 2667894)pubmed.ncbi.nlm.nih.gov
- PubChemPubChem · Selank (CID 11765600)pubchem.ncbi.nlm.nih.gov
- RefMHRA — Medicines and Healthcare products Regulatory Agencygov.uk
- GuidelineGoogle — Creating helpful, reliable, people-first contentdevelopers.google.com
Written and reviewed by
Jack Muncaster · Founder, UK Peptides
Jack founded UK Peptides in Manchester after repeatedly receiving research compounds with missing or recycled paperwork. He is responsible for supplier selection, batch release decisions and the content published in this research library. Every article here is sourced to primary literature and every product page to a signed third-party certificate.
More Selank (Tuftsin Analogue) articles
- The Question the Fragment Literature Does Not AnswerSelank is tuftsin plus Pro-Gly-Pro. Tuftsin has a receptor; Selank has no identified one. Whether the extension preserves engagement is unresolved.
- Tuftsin and the Antigenicity QuestionNaim 1989 reported tuftsin's lack of antigenicity. A sequence excised from the body's own IgG has no reason to look foreign to the immune system.
- Why Proline Keeps Appearing in These SequencesSelank has three prolines in seven residues, Semax two in seven, BPC-157 four in fifteen. A 2019 review treats proline-containing peptides as a class.
- An Induced-Deficit Model With a Biochemical ReadoutKolik 2019 examined Selank against ethanol-induced memory impairment in rats, linking the effect to BDNF content in hippocampus and prefrontal cortex.
- What an Aversive-Signs Model MeasuresKonstantinopolsky 2022 reported Selank attenuating aversive signs of morphine withdrawal in rats. What that endpoint is, and what it is not.
Popular across the research hub
One flagship guide from every other research category — keep exploring.
- Retatrutide ResearchWhat Does "Reta" Mean?
- GHK-Cu (Copper Peptide)GHK vs GHK-Cu: Peptide and Complex Compared
- TB-500 (Thymosin β4 fragment)TB-500 CAS Number and Chemical Identity
- BPC-157 (Pentadecapeptide)The Zagreb Research Programme
- CJC-1295 & IpamorelinCJC-1295 CAS Number and Chemical Identity
- Peptide ReferenceAspartimide Formation and Why It Hides
- Bacteriostatic WaterWhy Bacteriostatic Water Is the Default Peptide Diluent
- Research & Regulatory NewsWhat the Cardiovascular and Kidney Data Actually Is
- GLP-1 & Incretin ScienceSix Trials Out of Forty-Two
- MOTS-c (Mitochondrial Peptide)The Residue That Oxidises So Others Do Not
- Semax (ACTH Fragment Peptide)Semax, MT-2 and KPV Are Pieces of the Same Sequence
- DSIP (Delta Sleep-Inducing Peptide)How DSIP Was Discovered
- KLOW (Blend)KLOW and GLOW Compared
- GLOW (Blend)A Blend Fixes the Ratio and Keeps the Complexity
- MT-2 (Melanotan II)MT-2 Structure: Four Stability Features in Seven Residues
- IGF-1 LR3IGF-1 LR3 Structure: Three Disulfides and Why They Matter
- GlutathioneThe Gamma-Glutamyl Bond
- NAD+NAD+ Molecular Structure
- KPVHow KPV Is Reported to Act