Compound research
KPV: Research Overview & Current Status
KPV is a Alpha-MSH-derived tripeptide / anti-inflammatory peptide fragment. Current research status: preclinical research. KPV has no FDA or EMA approval and, per current research, no completed human clinical trials have been identified. Roughly two dozen studies published between 2001 and 2025 have examined KPV exclusively in cell culture, animal models (IBD, dermatitis, bronchial inflammation), and delivery-system experiments.
Overview
KPV (Lysine-Proline-Valine) is the minimal C-terminal tripeptide fragment (positions 11-13) of alpha-melanocyte-stimulating hormone (alpha-MSH), first shown by Hiltz and Lipton in 1989 to retain anti-inflammatory activity independent of alpha-MSH's pigmentation effects and without activating melanocortin receptors.
Alpha-MSH-derived tripeptide / anti-inflammatory peptide fragment
Research timeline
1989
Hiltz and Lipton first identified the KPV tripeptide fragment as retaining autonomous anti-inflammatory activity independent of alpha-MSH's melanocortin receptor-mediated pigmentation effects.
Source →1980s-1990s
Broader research by Catania, Lipton, and colleagues at Weill Cornell established that alpha-MSH and its fragments reduce fever, suppress inflammation, and modulate immune cell activity beyond pigmentation.
Source →2000s
Preclinical studies began characterizing KPV's efficacy in animal models of inflammatory bowel disease, contact dermatitis, and bronchial inflammation.
Source →2000s-2010s
Mechanistic studies identified inhibition of IkB kinase, preservation of IkBalpha, and prevention of NF-kB nuclear translocation as key anti-inflammatory pathways, along with inflammasome modulation (reduced IL-1beta, IL-18).
Source →2010s-2020s
Oral bioavailability of KPV demonstrated in colitis animal models via PepT1 transporter-mediated cellular uptake, notable because most peptides are degraded in the digestive tract.
Source →2001-2025
Cumulative body of roughly two dozen published studies on KPV's anti-inflammatory mechanisms across gut, skin, and lung models, entirely preclinical.
Source →
Active & recent research
KPV in inflammatory bowel disease models
Oral bioavailability and anti-inflammatory efficacy via PepT1-mediated uptake and NF-kB pathway inhibition
KPV mechanism of NF-kB inhibition
IkB kinase inhibition and preservation of IkBalpha to block NF-kB nuclear translocation and downstream cytokine production (TNF-alpha, IL-6, IL-1beta)
KPV in dermatitis and bronchial inflammation models
Reduction of inflammatory cytokine production and immune cell activation in non-gut tissue models
Key findings
- Foundational 1989 research by Hiltz and Lipton established that KPV retains the anti-inflammatory activity of full-length alpha-MSH despite lacking the receptor-binding motif needed to activate known melanocortin receptors, suggesting a distinct, not-fully-characterized signaling mechanism.
- Preclinical mechanistic studies report that KPV inhibits NF-kB signaling via IkB kinase inhibition and modulates the inflammasome pathway (reducing IL-1beta and IL-18), providing a plausible molecular basis for its reported anti-inflammatory effects across multiple animal models.
- A notable and unusual property reported in animal colitis models is oral bioavailability — KPV reportedly retains efficacy when taken by mouth, which is atypical for peptides that are usually degraded in digestion.
- As of current research, no human clinical trials of KPV have been completed; every reported finding derives from cell culture or animal models, and reviewers explicitly caution about possible publication bias favoring positive preclinical results.
Safety & regulatory notes
KPV has no FDA or EMA approval and, per current research, has not been evaluated in any completed human clinical trial. There is no established human safety, dosing, or pharmacokinetic profile. All available efficacy and safety signals come from preclinical cell-culture and animal-model research.
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Where it's sold for research
We haven't built a dedicated vendor-availability page for KPV yet. See our full research-peptide vendor rankings →
KPV FAQ
Has KPV been tested in humans?+
No completed human clinical trials of KPV have been identified in current research; all available evidence comes from cell culture and animal models (inflammatory bowel disease, dermatitis, bronchial inflammation).
How does KPV reduce inflammation mechanistically?+
Preclinical studies report that KPV inhibits NF-kB signaling by blocking IkB kinase activity and modulates the inflammasome pathway, reducing production of inflammatory cytokines like TNF-alpha, IL-6, and IL-1beta, though researchers note the exact signaling mechanism remains incompletely characterized.
Is KPV related to alpha-MSH and does it share its pigmentation effects?+
KPV is the minimal C-terminal tripeptide fragment of alpha-MSH, but it lacks the receptor-binding motif needed to activate melanocortin receptors, so research indicates it does not produce alpha-MSH's pigmentation effects while apparently retaining much of its anti-inflammatory activity.
Is KPV FDA-approved?+
No. KPV is an investigational research compound with no FDA or EMA approval and no completed human trials to date.
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