What Is KPV? Sequence, Analytical Identity and Research Models

What does KPV mean?

The one-letter amino-acid code is direct:

• K = lysine
• P = proline
• V = valine

The sequence is therefore Lys-Pro-Val, written as H-Lys-Pro-Val-OH for the unmodified free-acid reference structure.

PubChem’s standardized free-acid record identifies that structure as CID 125672, with molecular formula C16H30N4O4, average molecular weight 342.43 g/mol, and CAS Registry Number 67727-97-3. Those identifiers describe the all-L free-acid reference record. PubChem maintains a separate component record for L-lysyl-L-prolyl-L-valine acetate, CID 90474670.

That difference is not cosmetic. Free acid, acetate, another counterion, a hydrate, or a formulated mixture can have different reported composition and mass accounting. The name KPV or a free-acid database record should not be used to invent a salt form for a lot whose specification does not state one.

How is KPV related to alpha-MSH?

A primary antimicrobial study printed the 13-residue alpha-MSH sequence as SYSMEHFRWGKPV and tested both the complete peptide and its carboxyl-terminal KPV tripeptide. KPV is therefore alpha-MSH residues 11-13 in that nomenclature.

The relationship is structural, not proof of interchangeable behavior. Alpha-MSH and KPV differ in length and in the experimental responses reported across model systems. A source that studied complete alpha-MSH should not be presented as a KPV study unless KPV was a defined experimental condition.

How should BulkGLP’s current KPV record be used?

Start with the KPV research material page and follow its current batch-record link. Match the physical vial, product name, lot, and original laboratory report before interpreting identity.

An LC-MS identity result, an HPLC-UV purity result, measured content, appearance, and endotoxin are distinct lot-specific findings. A sequence, molecular formula, counterion, salt form, sterility result, or microbial result should be stated only when the applicable record supports it.

Current lot data changes with inventory. The product page and batch ledger show the active lot, accession, purity, and measured content recorded for that sample. Primary literature and standardized chemical records describe the KPV reference entity, but they do not determine the form of a specific lot.

Where has KPV appeared in primary research?

The evidence below is grouped by model and endpoint. It is not a list of established human outcomes.

Intestinal epithelial and T-cell models

Dalmasso and colleagues studied KPV in Caco2-BBE and HT29-Cl.19A human intestinal epithelial cell lines and in Jurkat human T cells. Their experiments included radiolabeled uptake and competition assays, PepT1 expression conditions, NF-kappaB reporter activity, I-kappaB and MAP-kinase measurements, cytokine messenger RNA, and secreted-cytokine assays.

The paper reported PepT1-associated KPV uptake and changes in the measured inflammatory-signaling endpoints under its defined cell-culture conditions. Those results are specific to the cell lines, stimulation conditions, concentrations, transport assays, and endpoints used by the investigators.

DSS- and TNBS-induced mouse models

The same paper studied KPV in two induced mouse colitis models. The DSS experiment reported five mice per group for the displayed body-weight, myeloperoxidase, colon, and histology comparisons. The TNBS experiment reported ten mice per group for the displayed body-weight, myeloperoxidase, and cytokine-mRNA comparisons.

These were induced animal models, not human clinical trials. The exposure route, model induction, group size, time window, tissues, and endpoints limit what can be inferred beyond the experiment.

Human keratinocyte signaling experiments

Elliott and colleagues compared alpha-MSH, KPV, related peptides, and ACTH-derived materials in HaCaT cells and normal human keratinocytes. They measured cyclic AMP and intracellular calcium and also used Chinese hamster ovary cells transfected with the melanocortin-1 receptor.

The study reported no cyclic-AMP elevation in the keratinocyte conditions described in its abstract and reported context-dependent calcium responses. It did not test a finished BulkGLP vial, a KLOW blend, or a clinical intervention.

Microbial and neutrophil assays

Cutuli and colleagues tested alpha-MSH and KPV against Staphylococcus aureus and Candida albicans under in-vitro assay conditions. Their endpoints included colony formation, yeast viability, germ-tube formation, cyclic AMP in yeast, and pathogen killing by human neutrophils.

Those are organism and ex-vivo cellular assays. They do not establish that a KPV product treats an infection or produces the same observation in another model.

Mouse peritonitis and macrophage experiments

Getting and colleagues compared KPV with other melanocortin-related peptides in mouse peritonitis models and in cultured macrophage experiments. The study reported model-dependent differences among leukocyte accumulation, cytokine release, and cyclic-AMP findings and concluded that KPV was unlikely to act through the melanocortin receptors tested in that design.

This does not establish one universal KPV mechanism. Taken with the PepT1 and keratinocyte papers, it shows why the model, receptor context, transport system, assay, and endpoint must remain attached to each statement.

What the research does not establish

• A human clinical outcome
• A dosing or administration protocol
• That every cell type transports KPV through PepT1
• One universal receptor or signaling mechanism across models
• That an isolated-KPV result applies to KLOW or another multi-component formulation
• That a current lot will reproduce a published biological result
• That identity, HPLC-UV purity, measured content, endotoxin, and microbial status are interchangeable findings

The scientific papers explain what defined reference materials did in particular experiments. The lot report answers narrower analytical questions about the submitted sample.

How to interpret KPV identity, purity, and content

• Sequence identity defines the order Lys-Pro-Val for the reference compound.
• Chemical form distinguishes the free acid from an acetate or another documented form.
• LC-MS identity addresses the laboratory’s mass-spectral identity result under its method.
• HPLC-UV purity reports a chromatographic result; it does not by itself state the amount of KPV in the vial.
• Net content reports the measured amount for the submitted sample.
• Endotoxin is a separate assay with its own sensitivity and result.

Read how to read a peptide COA for the limits of each field, and use current and historical batch records to keep the vial, lot, and report connected.

KPV as a standalone material versus KPV inside KLOW

Standalone KPV is a single tripeptide. KLOW is a multi-component blend that includes KPV alongside other listed analytes. Its composition, component quantities, and lot record describe the finished formulation rather than KPV alone.

An observation made with KLOW cannot be assigned to KPV alone unless the experimental design isolates KPV’s contribution and controls the other components. Conversely, the cellular or animal findings summarized above do not establish the behavior of the finished KLOW formulation.

For blend-specific context, read What Is KLOW Peptide? and the KLOW vs GLOW comparison. Those references cover formulation composition and comparison; the identity and literature above concern standalone KPV.

Frequently asked questions

What is the KPV amino-acid sequence?

KPV is Lys-Pro-Val. The free-acid reference structure is written H-Lys-Pro-Val-OH.

Is KPV the same as alpha-MSH?

No. KPV is the carboxyl-terminal tripeptide, residues 11-13, of the 13-residue alpha-MSH sequence. It is not the complete alpha-MSH peptide.

Does the name KPV establish free acid or acetate?

No. The applicable specification and lot record must establish the chemical form. A counterion cannot be assigned from the name alone.

What models are summarized here?

The cited primary studies include human intestinal epithelial cell lines, Jurkat T cells, normal and immortalized human keratinocytes, microbial assays, human-neutrophil assays, cultured macrophages, and induced mouse inflammation models. They are not presented as human clinical evidence.

Is a KLOW result evidence for KPV alone?

No. KLOW contains multiple listed components. Attribution requires controls that isolate KPV while accounting for the remaining analytes, quantities, chemical forms, and lot variation.

Continue through the research library

• Structural and Binding Peptides
• TB-500 and thymosin beta-4 identity guide

Primary and authoritative sources

1. Dalmasso G, et al. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008;134(1):166-178. DOI 10.1053/j.gastro.2007.10.026; PMID 18061177; PMCID PMC2431115.
2. Elliott RJ, et al. Alpha-melanocyte-stimulating hormone, MSH 11-13 KPV and adrenocorticotropic hormone signalling in human keratinocyte cells. Journal of Investigative Dermatology. 2004;122(4):1010-1019. DOI 10.1111/j.0022-202X.2004.22404.x; PMID 15102092.
3. Cutuli M, Cristiani S, Lipton JM, Catania A. Antimicrobial effects of alpha-MSH peptides. Journal of Leukocyte Biology. 2000;67(2):233-239. DOI 10.1002/jlb.67.2.233; PMID 10670585.
4. Getting SJ, Schioth HB, Perretti M. Dissection of the anti-inflammatory effect of the core and C-terminal KPV alpha-melanocyte-stimulating hormone peptides. Journal of Pharmacology and Experimental Therapeutics. 2003;306(2):631-637. DOI 10.1124/jpet.103.051623; PMID 12750433.
5. PubChem. MSH (11-13), CID 125672. Standardized record for the all-L free-acid KPV structure and identifiers.
6. PubChem. L-lysyl-L-prolyl-L-valine acetate, CID 90474670. Separate component record used only to show why chemical form must be stated.