KPV

Lys-Pro-Val, α-MSH(11–13), alpha-MSH C-terminal tripeptide

Recovery, repair & tissue

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Summary

Class: Tripeptide (3 amino acids) — the last three residues of the natural hormone alpha-melanocyte-stimulating hormone (α-MSH). Occurs naturally as part of α-MSH; supplied as a synthetic fragment
Mechanism: Dampens inflammatory signalling (NF-κB) inside immune and gut-lining cells, partly by being carried into cells through the PepT1 transporter, without the pigmentation effects of full α-MSH
Routes studied: Oral and intrarectal (mouse colitis models), intraperitoneal and intravenous (rodents), topical and in-vitro. Community: oral capsules, subcutaneous injection, topical, nasal
Dose range reported: Animal: roughly 10–100 µg per mouse per day orally or by injection in colitis models; in vitro micromolar. Community: 200–500 µg/day subcutaneous or 500 µg oral, sometimes topical creams. No human dose exists
Half-life: Not characterised in humans; as a small unprotected tripeptide it is expected to be degraded within minutes in plasma. Oral activity in mice is attributed to local gut uptake
Storage: Lyophilised: refrigerate, protect from light. Reconstituted: refrigerate; community practice is use within ~4 weeks
Regulatory status: Not approved for any indication anywhere. See region table

Doses are as reported in studies or by the community — never recommendations.

1What it is

KPV is the three-amino-acid tail of α-MSH, a hormone your body makes from the larger precursor POMC. Full α-MSH has two well-known jobs: it tells skin cells to make pigment, and it calms inflammation. In the late 1980s researchers found that the pigment effect and much of the anti-inflammatory effect could be separated — the short C-terminal piece, KPV, kept the anti-inflammatory action without darkening skin (Hiltz & Lipton 1989).

Most work since has come from gut-inflammation research, where KPV's small size turned out to matter: it is taken up by PepT1, a transporter that gut-lining cells and some immune cells use to absorb dipeptides and tripeptides from food. That gives it a route into exactly the cells involved in inflammatory bowel disease, and most of the published studies are in mouse colitis models.

There are no published human trials of KPV.

2How it's thought to work

NF-κB inhibition. inside cells, KPV reduces activation of NF-κB, the master switch for many inflammatory genes, lowering production of cytokines such as TNF-α, IL-6 and IL-8 (Dalmasso 2008; Brzoska 2008 review).

PepT1 transport. KPV is carried into colonic epithelial cells and immune cells by the PepT1 transporter; blocking PepT1 blocks the anti-inflammatory effect in those cells (Dalmasso 2008).

Receptor-independent action. unlike full α-MSH, KPV does not meaningfully activate melanocortin receptors, which is why it has no tanning effect. Some anti-inflammatory activity may still involve MC1R on certain immune cells; this is debated.

Antimicrobial activity. α-MSH and KPV reduce growth of Staphylococcus aureus and Candida albicans , possibly by raising cAMP in the microbe (Cutuli 2000).

Proposed: carried into gut-lining cells by the PepT1 transporter; inside, it damps the NF-κB inflammatory signal before it reaches the nucleus.Schematic — not to scale

3What the research shows

Colitis (inflammatory bowel disease models)

Oral or rectal KPV reduced weight loss, tissue damage and inflammatory cytokines in mouse models of colitis induced by DSS or TNBS (Dalmasso 2008, Gastroenterology; Kannengiesser 2008, Inflamm Bowel Dis). Later work packaged KPV in nanoparticles for oral delivery and reported similar protection at lower doses in mice (Xiao 2017, Mol Ther). All rodent. [2][3][4]

Graded C/D

General anti-inflammatory activity

The original fragment studies showed KPV reduced fever and inflammation in rodent models comparably to full α-MSH (Hiltz & Lipton 1989, FASEB J). Reviews summarise effects in models of skin inflammation, arthritis and endotoxaemia (Brzoska 2008, Endocr Rev). [1][5]

Antimicrobial effect

In-vitro reductions in S. aureus and C. albicans viability (Cutuli 2000, J Leukoc Biol). No animal infection model or human data. [6]

Graded D/—

Wound healing, skin conditions, mast-cell stabilisation

Mechanistic cell work and community anecdote. No controlled studies.

Any human indication

None published. Full α-MSH analogues have reached humans (afamelanotide is an approved medicine), but KPV itself has not been trialled. Community use for gut inflammation, skin conditions, mast-cell symptoms and "immune calming" rests on the mouse colitis data and anecdote.

4Reported side effects and interactions

Literature-reported

No human safety data. Rodent studies report no obvious toxicity at the doses used, but these were short-term.

Community-reported

generally described as well tolerated; occasional injection-site irritation, mild nausea when taken orally, headache. A minority report fatigue.

Theoretical. broad suppression of NF-κB could blunt useful immune responses if sustained; α-MSH fragments interact with mast cells and could in principle affect allergic responses in either direction. Because KPV is a food-like tripeptide, immunogenicity is expected to be low.

Interactions. none established. Additive anti-inflammatory effect with other NF-κB-targeting compounds is plausible but unstudied.

Markers researchers commonly monitor

No compound-specific markers are established. Where KPV is used in a gut-inflammation context, protocols commonly track:

Marker	Why it's watched
Faecal calprotectin	a stool marker of gut inflammation; the most direct readout for the main research use.
CRP (preferably high-sensitivity)	general systemic inflammation.
CBC with differential	baseline immune status; theoretical concern about immune suppression with sustained NF-κB inhibition.
Symptom diaries (stool frequency, skin scores)	because no biochemical marker of KPV effect exists in humans.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Common vial sizes 5 mg and 10 mg. with ; swirl rather than shake. Oral capsules and topical preparations are also used in the community; the oral route has animal support for gut-local effects, not for systemic absorption.

Open in calculator, pre-loaded →

6Commonly studied alongside

BPC-157 (community "gut-repair" pairing; no combined study), larazotide (research context), thymosin alpha-1, LL-37.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved. Placed in Category 2 of the FDA's 2023 compounding bulk-substances list, restricting compounding pharmacies from using it
European Union	Not authorised as a medicine or permitted supplement ingredient
United Kingdom	Not licensed
Australia	Not an approved product †
South Africa	Not registered
Sport	Not specifically named by WADA; as a non-approved substance it falls under S0 †

8Open questions

Does oral KPV act only locally in the gut, or does any reach the bloodstream intact?
Is there any human efficacy at all? Zero trials.
How much of the anti-inflammatory effect depends on PepT1 expression, which is itself altered in inflamed tissue?

9References

1Hiltz ME, Lipton JM (1989). Antiinflammatory activity of a COOH-terminal fragment of the neuropeptide alpha-MSH. FASEB J. PubMed
2Dalmasso G et al. (2008). PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. PubMed · DOI
3Kannengiesser K et al. (2008). Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease. Inflamm Bowel Dis. PubMed · DOI
4Xiao B et al. (2017). Orally targeted delivery of tripeptide KPV via hyaluronic acid-functionalized nanoparticles efficiently alleviates ulcerative colitis. Mol Ther. PubMed · DOI
5Brzoska T et al. (2008). 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. Endocr Rev. PubMed · DOI
6Cutuli M et al. (2000). Antimicrobial effects of alpha-MSH peptides. J Leukoc Biol. PubMed · DOI
7FDA (2023). Bulk drug substances for compounding — KPV category 2 listing. PubMed

References are being resolved to PubMed/DOI identifiers; links search PubMed for the citation until then.

† Being confirmed by our reviewers against current sources.

10Community

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Self-reported side effects Phase 2

Not enough data yet. 0 of the 50 members needed have logged this compound for 4+ weeks. We don't show anything below 50, so no one can be identified.

11Page history

25 Oct 2026Profile published — awaiting medical review

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