KPV
KPV in the Published Literature
PubMed indexes roughly 34 records on KPV's anti-inflammatory work. The literature is predominantly murine and cell culture, with the alpha-MSH parent literature providing broader context. There is no established human clinical programme.
Key facts
- Indexed records
- ~34 on anti-inflammatory work
- Dominant evidence
- Murine models, cell culture
- Key model paper
- Kannengiesser 2008 (PMID 18092346)
- Delivery work
- Xiao 2017 (PMID 28143741)
- Parent context
- Luger 2003, Brzoska 2010
- Clinical trials
- None established
A small literature with a clear shape
Around 34 indexed records is modest — smaller than Selank's 135, far smaller than DSIP's 519. What it lacks in volume it makes up in consistency: the work runs from mechanism through disease models to delivery, which is a coherent trajectory rather than scattered observations.
The parent literature is larger and relevant
Alpha-MSH has a substantially bigger literature, and Luger's 2003 review in the Annals of the New York Academy of Sciences and Brzoska's 2010 chapter both cover the anti-inflammatory arm. Much of it concerns the whole hormone rather than the tripeptide, so the same read-across caution applies here as for TB-500 and thymosin beta-4.
Research material referenced
KPV 10mg — third-party HPLC tested
Searching it
KPV alone returns a mix, since the abbreviation is short and collides with unrelated terms — the same problem that puts an organic acid at the top of a PubChem search. Combining it with peptide or with anti-inflammatory narrows it usefully. Lys-Pro-Val finds chemical records; alpha-MSH finds the parent literature.
What is absent
Human clinical trials. Independent replication across many groups. And a defined molecular target — NF-κB interference is described as an effect rather than mapped to a binding interaction. These gaps are ordinary for a compound at this stage rather than remarkable.
How it compares within this library
Less studied than BPC-157, which has a Phase 2 recruiting, or GHK-Cu with its decades of work. Better motivated than DSIP, whose central claim has never resolved. KPV sits in the middle: a clear rationale, a small consistent literature, and no human data.
Extended research context
The KPV deep dive
Deep dive: two functions in one hormone, and the case for splitting them
Alpha-MSH is a thirteen-residue peptide cleaved from proopiomelanocortin, and it does two things that have almost nothing to do with each other. Its core sequence engages melanocortin receptors on melanocytes and drives melanin synthesis - the activity it is named for. Separately, it carries anti-inflammatory activity that Brzoska and colleagues localised to its C-terminal end, a paper titled 'terminal signal' precisely because the finding was that the signal sits at the terminus rather than in the receptor-binding core. That is an unusually clean functional separation, and it produced two research compounds pulling in opposite directions from one parent. KPV takes the C-terminal three residues and discards the pigmentation activity. Melanotan II does the reverse - a cyclic analogue built around the receptor-binding portion to maximise exactly what KPV was designed to leave behind. Same hormone, opposite halves.
Deep dive: what happens when you shrink a molecule fivefold
Going from alpha-MSH at 1,664.9 Da to KPV at 342.43 Da is not a trim, it is a change of category. A 1,665 Da peptide is firmly a cell-surface ligand - far too large to cross a membrane passively, so whatever it does must begin at a receptor. A 342 Da tripeptide is small enough that intracellular access becomes plausible, which is why KPV's reported mechanism is described in terms of NF-kappaB signalling rather than melanocortin receptor engagement. The consequence is rarely stated: if the fragment acts inside the cell and the parent acts at its surface, then the anti-inflammatory activity of the two is not necessarily the same phenomenon, and read-across between them should run cautiously in both directions. Fragment logic assumes the fragment is the parent minus something. Here it may be the parent minus something plus a different route of access.
Deep dive: the delivery paper is the most informative thing in the literature
Xiao and colleagues published in Molecular Therapy in 2017 on delivering KPV orally using hyaluronic acid-functionalised nanoparticles targeted to inflamed intestinal tissue. Read as a result it is a delivery success. Read as a statement about the compound it is more interesting: nobody builds a targeted nanoparticle carrier for a molecule that already reaches its target. The existence of that work says the free tripeptide's arrival at inflamed tissue was the limiting problem - which follows directly from being 342 Da, highly soluble and rapidly cleared. It is the same signal that CJC-1295's DAC modification carries for growth hormone secretagogues, or that lipidation carries across the whole incretin class: when the engineering effort goes into getting a compound to stay and arrive rather than into making it more active, the pharmacokinetics were the bottleneck.
Research applications
- ▸Melanocortin fragment structure-activity research
- ▸NF-kappaB pathway and cytokine production studies in culture
- ▸Murine models of induced intestinal inflammation
- ▸Targeted peptide delivery and carrier system development
- ▸Comparative work on parent hormones and isolated fragments
- ▸Analytical method development for very short peptides
Handling checklist
- ✓Verify identity against Lys-Pro-Val, CID 125672, at 342.43 Da
- ✓Do not search PubChem for 'KPV' - it returns an unrelated organic acid
- ✓Store lyophilised, cold, dry and dark
- ✓Use low-binding consumables; a small cationic peptide adsorbs to surfaces
- ✓Reconstitute gently down the vial wall and swirl, never shake
- ✓Aliquot into single-use volumes to avoid freeze-thaw cycling
- ✓Expect no disulfide or oxidation satellites - no cysteine, no methionine
Common research-handling mistakes
Learnt from thousands of researcher orders across our UK labs.
✗ Searching PubChem for 'KPV' to verify a certificate
Fix: That returns CID 13294447, 2-oxo-5-phenylpentanoic acid at 192.21 Da, an unrelated compound. Search Lys-Pro-Val for CID 125672.
✗ Treating KPV and alpha-MSH findings as interchangeable
Fix: They differ fivefold in mass and the fragment may act intracellularly where the parent cannot. Read across cautiously in both directions.
✗ Assuming a colitis model result speaks to inflammatory bowel disease
Fix: Induced colitis in a mouse is acute and chemical; human IBD is chronic, heterogeneous and immunologically complex.
✗ Expecting to quantify KPV by absorbance at 280 nm
Fix: There is no aromatic residue in the sequence, so there is no usable absorbance there.
✗ Attributing unexplained low recovery to degradation
Fix: KPV is chemically robust - no cysteine, methionine or asparagine. Adsorption to glass and plastic is the more likely cause.
Continue researching
Peer-reviewed guides, comparators and matched reference materials.
Related questions researchers ask
- Why does searching PubChem for KPV return the wrong compound?
- Is KPV's anti-inflammatory mechanism the same as alpha-MSH's?
- What does the targeted delivery literature imply about KPV's pharmacokinetics?
- How does a three-residue peptide have activity without secondary structure?
- Why is KPV harder to characterise analytically than longer peptides?
- What is the relationship between KPV and Melanotan II?
Frequently asked questions
- How large is the KPV literature?
- Roughly 34 indexed records on the anti-inflammatory work — modest, but consistent in direction.
- Are there clinical trials?
- None established. The evidence is murine models and cell culture.
- How should I search for it?
- KPV alone collides with unrelated terms. Combine it with peptide or anti-inflammatory, and search Lys-Pro-Val for chemical records.
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.
- PubMedKannengiesser K et al. — Inflamm Bowel Dis 2008 (PMID 18092346)pubmed.ncbi.nlm.nih.gov
- PubMedXiao B et al. — Mol Ther 2017 (PMID 28143741)pubmed.ncbi.nlm.nih.gov
- PubMedLuger TA et al. — Ann N Y Acad Sci 2003 (PMID 12851308)pubmed.ncbi.nlm.nih.gov
- PubMedPubMed — KPV peptide literaturepubmed.ncbi.nlm.nih.gov
- PubMedBrzoska T et al., Terminal signal: anti-inflammatory effects of alpha-MSH — Adv Exp Med Biol 2010 (PMID 21222263)pubmed.ncbi.nlm.nih.gov
- PubChemPubChem · Lys-Pro-Val (CID 125672)pubchem.ncbi.nlm.nih.gov
- PubChemPubChem · alpha-MSH (CID 16133793)pubchem.ncbi.nlm.nih.gov
- 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 KPV articles
- KPV Regulatory StatusNo marketing authorisation anywhere. Why an anti-inflammatory literature makes the claims boundary particularly easy to cross.
- What Is KPV? A Complete Research OverviewKPV is Lys-Pro-Val, the C-terminal tripeptide of alpha-MSH, at 342.43 Da. It carries reported anti-inflammatory activity without the pigmentation effects.
- Alpha-MSH: Pigmentation and Inflammation in One HormoneA 13-residue hormone doing two unrelated jobs. Why separating its anti-inflammatory C-terminus from its pigmentation activity was worth attempting.
- How KPV Is Reported to ActReported effects centre on NF-kB signalling and pro-inflammatory cytokine production. Why the mechanism is described intracellularly rather than at a receptor.
- KPV Structure and Physical PropertiesThree residues, 342.43 Da, one proline and one lysine. What a tripeptide can and cannot do structurally, and why analysis is difficult.
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