RESEARCH MONOGRAPH · KDC-MN-009

KPV

May 9, 2026 Kodiac biolabs Research Revised May 30, 2026 2 min read

Our opinion on this compound

74/100

The forgotten tripeptide. Anti-inflammatory mechanism is real and people sleep on this constantly

KPV is alpha-MSH(11-13), the C-terminal tripeptide (Lys-Pro-Val) of the larger melanocortin. The full alpha-MSH peptide is well characterized as an anti-inflammatory mediator (the melanocortin system is one of the body's endogenous anti-inflammatory arms, alongside cortisol), and KPV preserves most of that anti-inflammatory activity while losing the pigmentation effects associated with melanocortin receptor binding at MC1R.

That last point is the interesting one. KPV doesn't seem to act primarily through the classical melanocortin receptors. The leading mechanism story involves intracellular signaling effects (inhibition of NF-kB nuclear translocation, suppression of NLRP3 inflammasome activation) that are receptor-independent or work through novel binding partners. The Lipton group and the Maaser/Kannengiesser collaborations have published on this in colitis and ocular inflammation models for over two decades now.

The IBD literature is where KPV looks most interesting. Multiple animal models (DSS colitis, TNBS colitis) show meaningful reduction in mucosal inflammation, and there's a small human pilot in ulcerative colitis from the Buchman group that showed signal. Topical and oral routes both seem to produce effects, which is unusual for a tripeptide (most short peptides get destroyed in the gut) and suggests either active transport via PEPT1 or local action on enterocytes before degradation.

Sourcing is trivial. Three residues, dead simple to synthesize, very cheap per mg. Purity is easy to achieve and verify. Stability is good. This is a peptide that should be in every researcher's freezer who works on inflammation models.

Whats holding it back? Honestly, the lack of marketing volume. KPV doesn't have a strong brand, doesn't have a major pharma backing, and falls between the cracks of the peptide-research community and the gastroenterology community. The published evidence is consistent enough that we think it deserves more attention than it gets.

One caveat. Some of the human signal comes from one company's proprietary oral formulation, so the route-of-administration story isn't as clean as you'd hope.

Underrated. Take a look at the colitis literature, you'll see what we mean.

Evidence: 60
Mechanism: 70
Reliability: 70
Safety: 85
Sourcing: 85
Value: 85
Signal: 70
Staying power: 70

Plain-language summary Intrigue 66 / 100

KPV is a tiny three-amino-acid peptide derived from the C-terminal end of alpha-MSH (the melanocyte-stimulating hormone). It has anti-inflammatory effects, particularly in the gut, and is being studied for inflammatory bowel disease. Stocked in the Kodiac catalog as a research-only powder for laboratory work; not a medicine, not for human consumption.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Tripeptide C-terminal fragment of alpha-melanocyte stimulating hormone

A 3-amino-acid tripeptide derived from the C-terminus of alpha-MSH, characterized for anti-inflammatory effects in colitis, dermatitis, and hepatic injury models.

Abstract

KPV (sequence Lys-Pro-Val-OH; CAS 67727-97-3; molecular formula C16H30N4O4; molecular weight 342.43) is a synthetic tripeptide corresponding to residues 11-13 of alpha-melanocyte stimulating hormone (alpha-MSH), the C-terminal fragment that retains anti-inflammatory activity in many of the published preclinical models of acute and chronic inflammation. The tripeptide was originally characterized by Catania and Lipton in the early 1990s as part of a structure-activity relationship study of the alpha-MSH inflammatory pharmacology, with the goal of identifying a small fragment that retained the parent hormone's anti-inflammatory effects without the pigmentation, body temperature, and feeding-behavior effects mediated by the N-terminal portion of the hormone. KPV reproduced the anti-inflammatory effects of alpha-MSH in rodent models of acute lung injury, dextran sulfate sodium-induced colitis, contact dermatitis, and hepatic ischemia-reperfusion injury. The mechanism involves attenuation of NF-kappa-B activation, reduced pro-inflammatory cytokine production by activated immune cells, and modulation of the melanocortin system through receptors that are not yet fully characterized for the tripeptide fragment. There is no FDA-approved IND for KPV in any indication; preliminary clinical work has explored topical KPV preparations for ulcerative colitis and inflammatory dermatologic conditions. The compound is widely used in research-grade work on inflammation and tissue injury. The principal limitations on the strength of the evidence are the relatively small published literature compared to BPC-157 or TB-500 and the limited human pharmacokinetic data.

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The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, reported research dose ranges, sourcing and quality verification, reconstitution and handling, stack interaction considerations, and a curated reference list. Available as a research-use-only PDF download.

KDC-MN-009

The full reference document is provided strictly for research use only. It reports research dose ranges from the published literature, not instructions for use in humans or animals.

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FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

Kodiac sells research compounds for investigative use only.

KPV

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