KPV
Published research and evidence base
KPV is the C-terminal tripeptide of alpha-melanocyte-stimulating hormone, alpha-MSH(11-13). Its evidence base is entirely preclinical and is concentrated in gut inflammation, where oral or rectal delivery via the PepT1 di/tripeptide transporter reduces colitis severity in rodent models, and in topical or barrier-protective applications in keratinocytes. A substantial share of the recent literature is formulation science (nanoparticles, hydrogels, microneedles) rather than new pharmacology. There are no human trials of KPV for any indication.
- Studies cited
- 15
- Published 2023+
- 6
- Newest paper
- 2026
- Last reviewed
- Aug 2026
Recurring themes in the literature
- NF-kappaB suppression and cytokine reduction
- PepT1-mediated intestinal uptake
- colitis and gut barrier repair
- keratinocyte protection and skin inflammation
- antimicrobial activity of alpha-MSH fragments
- targeted oral and topical delivery systems
Compound identifiers
- CAS
- 67727-97-3
- PubChem
- 125672
Recommended by an FDA advisory committee.
On 23–24 July 2026 the FDA’s Pharmacy Compounding Advisory Committee considered KPV for the 503A Bulks List and recommended its addition on a reported vote of 8–6 with one abstention. Heard as KPV free base and KPV acetate, and recommended on a divided vote.
This is not an approval. The committee advises; it does not decide. The recommendation is not binding, the FDA has not completed the rulemaking that would formally change anything, and inclusion on the 503A Bulks List is not equivalent to FDA approval of a drug. The list also governs pharmacy compounding for patients, which is a separate activity from research-use-only supply.
What the July 2026 advisory vote actually did sets out the process, the other compounds heard, and the four things the vote is routinely misreported as meaning.
What KPV is, chemically.
- Molecular formula
- C16H30N4O4
- Molecular weight
- 342.43 g/mol
- CAS number
- 67727-97-3
- PubChem CID
- 125672
These figures come from the PubChem record for this compound and describe the free base. Lyophilised peptide is normally supplied as an acetate or trifluoroacetate salt and carries residual water, so the mass of powder in a vial is not the same quantity as the molecular weight above would suggest. Chromatographic purity on a certificate of analysis does not resolve that difference either — how to read a certificate of analysis explains why.
15 published studies.
Ordered by strength of study design, then by recency. Every entry links to its source record so the finding can be checked against the paper rather than taken on our word.
- 01Animal in vivo2024
KPV and RAPA Self-Assembled into Carrier-Free Nanodrugs for Vascular Calcification Therapy
Zhang L, et al. · Adv Healthc Mater · carrier-free self-assembled KPV plus rapamycin nanodrug tested in vascular calcification models
KPV and rapamycin self-assembled into a carrier-free nanodrug that reduced vascular calcification, avoiding the low drug-loading and safety limitations of conventional nanomedicine carriers.
- 02Animal in vivo2024
Growth Factors-Loaded Temperature-Sensitive Hydrogel as Biomimetic Mucus Attenuated Murine Ulcerative Colitis via Repairing the Mucosal Barriers
Li D, et al. · ACS Appl Mater Interfaces · murine ulcerative colitis treated with a thermosensitive poloxamer hydrogel carrying hyaluronic acid, epigallocatechin-3-gallate, KPV tripeptide and epidermal growth factor
The KPV-containing biomimetic mucus hydrogel attenuated murine ulcerative colitis by repairing the mucosal barrier.
- 03Animal in vivo2021
Self-Cross-Linked Hydrogel of Cysteamine-Grafted gamma-Polyglutamic Acid Stabilized Tripeptide KPV for Alleviating TNBS-Induced Ulcerative Colitis in Rats
Sun J, et al. · ACS Biomater Sci Eng · TNBS-induced ulcerative colitis in rats; rectally administered KPV stabilised in a self-cross-linked thiolated gamma-polyglutamic acid hydrogel
Free KPV solution was unstable on rectal administration, which compromised efficacy; the hydrogel-stabilised formulation alleviated TNBS-induced colitis in rats.
- 04Animal in vivo2021
In situ mucoadhesive hydrogel capturing tripeptide KPV: the anti-inflammatory, antibacterial and repairing effect on chemotherapy-induced oral mucositis
Shao W, et al. · Biomater Sci · chemotherapy-induced oral mucositis model treated with a temperature-sensitive PLGA-PEG-PLGA hydrogel with epigallocatechin-3-gallate as adhesion enhancer, loaded with KPV
The KPV-loaded mucoadhesive hydrogel produced anti-inflammatory, antibacterial and reparative effects on chemotherapy-induced oral mucositis.
- 05Animal in vivo2017
Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis
Xiao B, et al. · Mol Ther · murine ulcerative colitis; KPV loaded into hyaluronic acid-functionalised polymeric nanoparticles (~272 nm) given orally
Hyaluronic acid-functionalised nanoparticles mediated targeted delivery of KPV to inflamed colonic tissue and alleviated ulcerative colitis in mice more effectively than free peptide.
- 06Animal in vivo2016
Critical role of PepT1 in promoting colitis-associated cancer and therapeutic benefits of the anti-inflammatory PepT1-mediated tripeptide KPV in a murine model
Viennois E, et al. · Cell Mol Gastroenterol Hepatol · AOM/DSS-induced colitis-associated cancer in mice overexpressing human PepT1 in intestinal epithelial cells and in PepT1-knockout mice
PepT1 expression promoted colitis-associated cancer development, and PepT1-transported KPV reduced inflammation and tumour burden in the murine model.
- 07Animal in vivo2013
Single administration of tripeptide alpha-MSH(11-13) attenuates brain damage by reduced inflammation and apoptosis after experimental traumatic brain injury in mice
Schaible EV, et al. · PLoS One · experimental traumatic brain injury in mice; single administration of alpha-MSH(11-13), with POMC, MC1R and MC4R mRNA profiling
A single dose of the tripeptide attenuated brain damage after experimental traumatic brain injury, with reduced inflammation and apoptosis relative to controls.
- 08Animal in vivo2008
Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease
Kannengiesser K, et al. · Inflamm Bowel Dis · two murine models of intestinal inflammation, including dextran sodium sulfate colitis
KPV reduced intestinal inflammation in both murine models, supporting the melanocortin-derived tripeptide as an anti-inflammatory agent independent of the full alpha-MSH sequence.
- 09Animal in vivo2008
PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation
Dalmasso G, et al. · Gastroenterology · human Caco2 intestinal epithelial cells and immune cells in vitro, plus two mouse colitis models
KPV entered intestinal epithelial and immune cells via the PepT1 di/tripeptide transporter, and this transporter-mediated uptake accounted for its anti-inflammatory effect in mouse colitis. This established the mechanism underlying oral KPV dosing.
- 10Animal in vivo2003
Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) alpha-melanocyte-stimulating hormone peptides
Getting SJ, et al. · J Pharmacol Exp Ther · murine crystal-induced peritonitis, comparing KPV with alpha-MSH, the core melanocortin peptide, an MC3/MC4 agonist and a selective MC1R agonist
Systemic KPV significantly reduced leukocyte accumulation in crystal-induced peritonitis, as did alpha-MSH and the MC3/MC4 agonist, whereas the selective MC1R agonist did not. This separated KPV's anti-inflammatory action from MC1R signalling.
- 11In vitro2026
KPV attenuates adipogenesis and lipid metabolism through modulation of ROS-mediated AKT/mTORC1/PPARgamma signaling
An SH, et al. · Tissue Cell · MDI-induced adipocyte differentiation in 3T3-L1 preadipocytes
KPV dose-dependently suppressed adipocyte differentiation, with 100 ug/mL reducing Oil Red O staining intensity, through modulation of ROS-mediated AKT/mTORC1/PPARgamma signalling.
- 12In vitro2026
Lysine-proline-valine peptide attenuates hepatic lipid accumulation through ROS-dependent regulation of the PPARgamma pathway in HepG2 cells
Lee JY, et al. · Cytotechnology · oleic acid-induced lipid accumulation in HepG2 hepatic epithelial cells
KPV reduced oleic acid-induced lipid deposition and oxidative damage in HepG2 cells, with effects mapped to ROS-dependent regulation of the PPARgamma pathway and fatty acid synthase expression.
- 13In vitro2025
Lysine-Proline-Valine peptide mitigates fine dust-induced keratinocyte apoptosis and inflammation by regulating oxidative stress and modulating the MAPK/NF-kappaB pathway
Sung J, et al. · Tissue Cell · human HaCaT keratinocytes exposed to fine particulate matter (PM10)
PM10 suppressed HaCaT proliferation and induced a pro-inflammatory response; KPV mitigated the resulting apoptosis and inflammation by reducing oxidative stress and modulating MAPK/NF-kappaB signalling.
- 14Review2025
Exploring the Role of Tripeptides in Wound Healing and Skin Regeneration: A Comprehensive Review
Adnan SB, et al. · Int J Med Sci · review of tripeptides in wound healing and skin regeneration
The review summarised how short peptides regulate cell migration, proliferation and differentiation during tissue repair, and noted that optimising outcomes in chronic wounds remains an unmet challenge.
- 15Review2008
Alpha-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
Brzoska T, et al. · Endocr Rev · review of alpha-MSH and related tripeptides across melanocortin receptor biology and immune-mediated inflammatory disease
The review consolidated evidence that alpha-MSH and its C-terminal tripeptides exert protective and anti-inflammatory effects via central and peripheral melanocortin receptors and via direct effects on immune cells. It remains the standard mechanistic reference for KPV.
What this evidence does not establish.
No human clinical trial of KPV has been published for colitis, wound healing, skin inflammation or any other indication, so effective human dose, route and safety profile are unknown. Free KPV is unstable in aqueous and rectal administration, which is why most recent work uses engineered delivery vehicles rather than the plain peptide sold to consumers; results from those formulations do not transfer to unformulated KPV.
Common questions about the research.
- What is KPV?
KPV is a three-amino-acid peptide — lysine, proline, valine — corresponding to residues 11–13 of alpha-melanocyte-stimulating hormone. It is the minimal C-terminal fragment of that hormone shown to retain anti-inflammatory activity in published models.
- Why does the literature include oral protocols?
KPV is a substrate for PepT1, the di/tripeptide transporter expressed in intestinal epithelial and immune cells, so it can enter target cells after oral delivery. Colitis studies exploit that route directly.
- How does KPV relate to alpha-MSH?
KPV is the C-terminal tripeptide of alpha-MSH. Research interest centres on the fact that it retains anti-inflammatory activity in models while lacking the pigmentary signalling of the full-length hormone, and that part of its effect appears to be independent of classical melanocortin-receptor signalling.
Available from our catalog
For research purposes only. Not for human consumption, diagnosis, treatment, or prevention of any condition. Nothing on this page is medical advice, and no study summarised here should be read as a recommendation.