KPV is a synthetic tripeptide (lysine–proline–valine) corresponding to residues 11–13, the C-terminal fragment, of the endogenous hormone α-melanocyte-stimulating hormone (α-MSH).1 It is supplied strictly as a research-use-only chemical for laboratory study and is not an approved drug for human or veterinary use. Because the pigment-driving portion of α-MSH is absent, researchers have reported that KPV retains anti-inflammatory activity without the melanocortin-receptor signalling associated with the parent hormone.2 The published evidence base is limited to animal models and cell-culture systems; no controlled human clinical trials establish efficacy or safety, so claims should be read with that caveat. Where dosing appears below, it reflects only the concentrations used in primary studies and should not be read as a usage recommendation.
Sequence & identity
Chemical identity verified against PubChem CID 125672 (InChIKey YSPZCHGIWAQVKQ-AVGNSLFASA-N).5
Mechanisms studied
KPV lacks the core melanocortin-receptor binding motif of α-MSH, and researchers have reported that it acts largely independently of cell-surface melanocortin receptors. In intestinal epithelial and immune cells, Dalmasso and colleagues observed that KPV is carried into the cytoplasm by the di/tripeptide transporter PepT1 (hPepT1), and that this transport was required for its anti-inflammatory effect.1 Once intracellular, researchers reported suppression of the NF-κB pathway: in human bronchial epithelial cells, Land observed that KPV translocates to the nucleus and competitively blocks the interaction between the p65/RelA subunit of NF-κB and importin-α3, reducing NF-κB nuclear translocation and downstream IL-8 secretion in a dose-dependent manner.3 Across these models, researchers described attenuation of pro-inflammatory cytokine signalling rather than activation of a classical receptor.2
Dosing in the research literature
The figures below summarise regimens as reported in published research — they are not recommendations or directions for use.
| Source / model | Regimen reported | Notes |
|---|---|---|
| Dalmasso et al., 2008 (Gastroenterology) — in vitro1 | 10 nM KPV applied to cytokine-stimulated Caco2-BBE epithelial and Jurkat T cells | Concentration used in cell culture to study PepT1-mediated uptake and NF-κB-related signalling; not a human regimen. |
| Dalmasso et al., 2008 (Gastroenterology) — murine1 | 100 µM KPV in drinking water (ad libitum) in C57BL/6 mice | Oral exposure in DSS- and TNBS-induced colitis models; reported ~50% reduction in DSS-induced colonic myeloperoxidase. Animal model only. |
| Land, 2012 (Int J Physiol Pathophysiol Pharmacol)3 | ≈0–10 µg/mL KPV on human bronchial epithelial cells (16HBE14o-) | Dose-ranging in vitro; dose-dependent suppression of TNFα-evoked NF-κB activity and IL-8 at concentrations ≥1 µg/mL. Not a dosing guideline. |
| Human use | Not established | No controlled human clinical trials define a human dose, route, or safety profile. RUO only. |
Effects observed in research
In animal and cell-based studies, researchers reported anti-inflammatory effects rather than confirmed clinical outcomes. In two murine models of inflammatory bowel disease (DSS- and TNBS-induced colitis), Dalmasso and colleagues observed that oral KPV reduced body-weight loss, lowered colonic myeloperoxidase activity by roughly half, and decreased pro-inflammatory cytokine mRNA.1 Kannengiesser and colleagues similarly reported reduced colonic inflammatory infiltrate and improved recovery in murine IBD models.4 In epithelial cell systems, researchers observed reduced IL-8/IL-1β-driven signalling and lower NF-κB activity.13 These are preclinical observations in laboratory models; they have not been shown to translate into therapeutic benefit in humans, and KPV is not approved to treat, cure, or prevent any condition.
Strength of evidence
Evidence grade C. The published record for KPV consists of animal models (chiefly murine DSS/TNBS colitis)14 and in-vitro work in epithelial and immune cell lines.13 Mechanistic data (PepT1 uptake; NF-κB/importin-α3 inhibition) are reasonably consistent across these models. However, there are no controlled human clinical trials establishing efficacy, dosing, or long-term safety, and most human-facing claims circulate through vendor and commentary sources rather than peer-reviewed clinical data. KPV should be regarded as an early-stage research compound, not a validated therapeutic.
Reconstitution & storage
Reconstitute with bacteriostatic water for laboratory handling. Store lyophilised material frozen and reconstituted material refrigerated. Use Peptigo’s reconstitution calculator and storage cheat sheet for working figures.
References
- Dalmasso G, Charrier-Hisamuddin L, Nguyen HTT, Yan Y, Sitaraman S, Merlin D. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008;134(1):166–178. PMID: 18061177.
- Brzoska T, Luger TA, Maaser C, Abels C, Böhm M. α-Melanocyte-stimulating hormone and related tripeptides: biochemistry, antiinflammatory and protective effects in vitro and in vivo, and future perspectives for the treatment of immune-mediated inflammatory diseases. Endocr Rev. 2008;29(5):581–602. PMID: 18612139.
- Land SC. Inhibition of cellular and systemic inflammation cues in human bronchial epithelial cells by melanocortin-related peptides: mechanism of KPV action and a role for MC3R agonists. Int J Physiol Pathophysiol Pharmacol. 2012;4(2):59–73. PMID: 22837805; PMCID: PMC3403564.
- Kannengiesser K, Maaser C, Heidemann J, Luegering A, Ross M, Brzoska T, Böhm M, Luger TA, Domschke W, Kucharzik T. Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease. Inflamm Bowel Dis. 2008;14(3):324–331. PMID: 18092346.
- National Center for Biotechnology Information. PubChem Compound Summary for CID 125672, Lys-Pro-Val (KPV). InChIKey YSPZCHGIWAQVKQ-AVGNSLFASA-N; CAS 67727-97-3. Accessed 2026.