An evidence page. It grades what the literature shows, and no more. Nothing here is a recommendation; the lab concentrations mentioned describe how a study was run, not how to use anything.

01 Identity

Common name	KPV
Sequence	Lys-Pro-Val (K-P-V)
Class	Synthetic tripeptide; C-terminal fragment (residues 11–13) of α-melanocyte-stimulating hormone (α-MSH)
Molecular formula	C₁₆H₃₀N₄O₄
Molecular weight	342.43 g/mol
CAS number	67727-97-3 · PubChem CID 125672
Synonyms	α-MSH (11–13); MSH (11–13); ACTH (11–13)

KPV is the last three residues of α-MSH (SYSMEHFRWGKPV). Much of α-MSH's anti-inflammatory activity has been attributed to this motif, which is why the isolated tripeptide became a research subject in its own right. It lacks the central sequence α-MSH uses to bind melanocortin receptors, and so does not produce the parent hormone's pigmentary effect. Identifiers anchored to PubChem CID 125672; salt forms may carry a different CAS.

02 Regulatory status

KPV holds no marketing authorisation anywhere. It is not approved by the FDA, EMA, or MHRA for any indication, and is not an approved medicine in any market as of the review date.

In the United States it has been drawn into the FDA's review of bulk drug substances eligible for pharmacy compounding under section 503A; its compounding status is under ongoing regulatory review. It is otherwise sold widely as a "research chemical, not for human use." There is no controlled-substance scheduling. The FDA compounding position changes over time and should be confirmed against the FDA's own 503A and advisory-committee documentation, not secondary summaries.

03 Mechanism of action

KPV is studied as a receptor-independent anti-inflammatory peptide. The proposed mechanism, characterised mainly in vitro, has several reported components:

Cellular uptake via PepT1. In intestinal cells, KPV is reported to enter via the di/tripeptide transporter PepT1, which is upregulated in the inflamed colon. The inference often drawn — that inflamed tissue imports more KPV — follows from PepT1 biology, not a measured clinical effect.

NF-κB inhibition. At nanomolar concentrations in cell culture, KPV is reported to inhibit NF-κB activation with reduced pro-inflammatory cytokine output. In-vitro mechanism.

MAP-kinase modulation and reduced cytokine secretion from epithelial and immune cells, and reported antimicrobial activity in vitro. In-vitro; clinical relevance untested.

The mechanism is reasonably characterised at the cellular level. None of it has been confirmed to produce a clinical outcome in humans.

04 Pharmacokinetics / pharmacodynamics

A notable preclinical property is oral activity: unlike many peptides, KPV reduced inflammation when given orally in animal colitis models, attributed to PepT1-mediated epithelial uptake rather than survival intact in circulation.

No human pharmacokinetic data exist — no measured absorption, half-life, or exposure–response in humans. KPV is expected to degrade to its constituent amino acids; this is a plausibility argument, not a measured human profile, and not evidence of safe systemic exposure.

05 Evidence by endpoint

Graded one use-case at a time, the picture barely moves. There is cell and animal work to point to. For efficacy or safety in people there is nothing — no human trials, for any indication.

5.1 — Intestinal inflammation / inflammatory bowel disease

The most developed evidence base. In the principal study (Dalmasso et al., Gastroenterology 2008), KPV inhibited NF-κB and MAP-kinase signalling and reduced cytokine secretion in human intestinal cell lines and human T cells in vitro, and reduced DSS- and TNBS-induced colitis in mice when given by mouth. Concordant murine IBD results (Kannengiesser et al., 2008), a PepT1-dependent reduction in colitis-associated cancer in mice, and nanoparticle-delivered oral KPV in mouse ulcerative colitis (Xiao et al., 2017) followed.

Preclinical only — no human trials

5.2 — Skin inflammation / dermatitis

α-MSH and its C-terminal fragment have anti-inflammatory activity in skin models. A 2017 study examined transdermal delivery of KPV across ex-vivo microporated human skin. That is a permeation study, not a clinical efficacy trial. Vendor claims that KPV "treats" eczema or psoriasis frequently cite this permeation paper; it does not support an efficacy claim.

Preclinical only

5.3 — Antimicrobial activity

α-MSH-derived peptides including KPV have been reported to inhibit organisms such as S. aureus and C. albicans in vitro.

Preclinical only (in vitro)

5.4 — Wound healing & systemic anti-inflammation

Promoted widely for wound healing and general "systemic inflammation," these uses rest on mechanistic plausibility and extrapolation from the colitis and cell-culture work rather than direct outcome studies.

Mechanistic / preclinical

5.5 — Any human efficacy or safety endpoint

A search of the trial registry and approval databases shows no registered human clinical trials of KPV and no FDA-approved labelled use. All proposed human benefits are extrapolated from cell-culture and animal studies.

No human data

06 Safety and adverse events

There is no human safety data for KPV. No human pharmacokinetic, tolerability, or adverse-event data exist, because no human trials have been conducted.

Claims of a "favourable" safety profile — common in commercial material — rest largely on the absence of reported harm plus the rationale that a short peptide degrades to common amino acids. Absence of evidence of harm is not evidence of safety, and degradation-to-amino-acids is a plausibility argument, not a finding.

No long-term safety data of any kind exist in humans. Effects of repeated or prolonged human exposure are unknown. In the animal models studied, KPV was generally reported as tolerated at the exposures used, but those were not human-relevant safety studies.

07 Evidence summary

Endpoint	Grade
Intestinal inflammation / IBD	Preclinical only
Skin inflammation / dermatitis	Preclinical only
Antimicrobial	Preclinical (in vitro)
Wound healing / systemic	Mechanistic / preclinical
Any human efficacy or safety endpoint	No human data
Long-term human safety	No data

08 References

Dalmasso G, Charrier-Hisamuddin L, Nguyen HTT, Yan Y, Sitaraman S, Merlin D. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008;134(1):166–178.DOI 10.1053/j.gastro.2007.10.026 · PMC2431115
Kannengiesser K, et al. Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease. Inflammatory Bowel Diseases. 2008.Confirm full citation before publication
Brzoska T, Luger TA, Maaser C, Abels C, Böhm M. α-MSH and related tripeptides: biochemistry, anti-inflammatory and protective effects in vitro and in vivo. Endocrine Reviews. 2008;29(5):581–602. Review
Xiao B, Xu Z, Viennois E, et al. Orally targeted delivery of tripeptide KPV via hyaluronic acid-functionalized nanoparticles efficiently alleviates ulcerative colitis. Molecular Therapy. 2017;25(7):1628–1640.
Hiltz ME, Lipton JM. Antiinflammatory activity of a COOH-terminal fragment of the neuropeptide α-MSH. FASEB J. 1989.Foundational; confirm exact citation before publication
Transdermal iontophoretic delivery of lysine-proline-valine (KPV) peptide across microporated human skin. Journal of Pharmaceutical Sciences. 2017;106(7):1814–1820.Ex-vivo permeation study, not a clinical trial
PubChem CID 125672 (Lysyl-prolyl-valine, KPV). Identity reference
ClinicalTrials.gov and Drugs@FDA — searched for KPV / Lys-Pro-Val: no registered human trials and no approved labelled use identified as of the review date.Negative finding; re-check at each review