KPV
KPV (Lys-Pro-Val)
The gut anti-inflammatory
A tripeptide derived from the C-terminal end of alpha-melanocyte-stimulating hormone (alpha-MSH). KPV retains the potent anti-inflammatory properties of the parent hormone without melanogenic (skin-darkening) effects. It targets gut inflammation through MC1R signaling and NF-kB suppression, making it a focused tool for IBD, colitis, and intestinal permeability.
Key Benefits
Reduction of intestinal inflammation and mucosal damage
Preservation of gut barrier integrity (tight junctions)
Suppression of pro-inflammatory cytokines in the gut
Potential relief from IBD and colitis symptoms
Mechanism of Action
How KPV works
KPV reduces gut inflammation through targeted molecular pathways:
- MC1R activation — binds melanocortin-1 receptor on intestinal epithelial cells and macrophages, triggering an anti-inflammatory signaling cascade that dampens mucosal immune overactivation
- NF-kB inhibition — directly suppresses nuclear translocation of NF-kB, the master transcription factor driving inflammatory cytokine production (TNF-alpha, IL-1beta, IL-6) in the gut
- Epithelial barrier support — preserves tight junction protein expression (claudin-1, occludin, ZO-1) under inflammatory stress, reducing intestinal permeability ("leaky gut")
- Macrophage polarization — shifts intestinal macrophages from pro-inflammatory M1 to anti-inflammatory M2 phenotype, promoting tissue resolution rather than chronic inflammation
Your Genetics & KPV
Genetic variants that affect your response
These SNPs determine how effectively KPV works for you specifically. A genetic peptide report identifies your variants before you start.
The Arg160Trp variant reduces MC1R function. Since KPV acts through MC1R, carriers of loss-of-function variants may have a diminished anti-inflammatory response and could require higher doses or alternative stacking strategies.
NOD2 variants are the strongest genetic risk factor for Crohn's disease. Carriers have dysregulated mucosal immunity — KPV's NF-kB suppression targets exactly this pathway, potentially offering proportionally greater benefit.
Non-secretors (AA genotype) lack fucosylated glycans on the gut mucosa, altering microbiome composition and increasing susceptibility to gut inflammation. KPV's barrier-protective effects may be especially valuable for non-secretors.
The -1082A>G variant affects IL-10 production. Low IL-10 producers (AA genotype) have reduced natural anti-inflammatory capacity — KPV's M2 macrophage polarization may partially compensate for this deficit.
Which variants do you carry?
Upload your DNA data or order a kit to find out.
Evidence & Research
15+
Published studies
Animal studies and in vitro data with promising but limited clinical validation
Common Stacks
KPV is commonly combined with:
Frequently Asked Questions
What is KPV used for?
KPV is used primarily for gut inflammation — conditions like IBD, ulcerative colitis, and intestinal permeability (leaky gut). As a fragment of alpha-MSH, it delivers potent anti-inflammatory effects specifically in the gut via MC1R receptor activation and NF-kB suppression, without the skin-darkening effects of full-length melanocortin peptides.
Does genetics affect KPV response?
Yes. MC1R variants directly affect the receptor KPV binds to — loss-of-function variants may reduce response. NOD2 variants (linked to Crohn's disease) indicate dysregulated gut immunity that KPV specifically targets. FUT2 secretor status affects gut mucosal defense and microbiome composition, influencing baseline gut vulnerability.
Can KPV be taken orally?
KPV is one of the few peptides being explored for oral delivery. As a tripeptide, it is small enough to potentially survive partial digestion, and its target (intestinal epithelium) is directly accessible via oral route. Some practitioners use oral KPV specifically for gut conditions, though bioavailability data is still limited.
Personalize your protocol
Does KPV match your DNA?
Upload your existing genetic data or order a kit. Your report scores KPV against your unique genetic profile — CYP metabolism, receptor variants, pathway markers — in minutes.