KPV[Lys-Pro-Val; the C-terminal tripeptide of alpha-MSH]
Compound snapshot
Class
Research peptide
FDA approved
No
Clinical development
Phase 2
Last reviewed
September 2026
Research areas
Immune signalling / Inflammation / Longevity research
Regulatory status
Research use only — not approved
Internet attention
Moderate
Registry query
KPV
A three-amino-acid fragment (lysine-proline-valine) of alpha-melanocyte-stimulating hormone, the natural melanocortin hormone. It is studied in laboratory models of gut and skin inflammation, and it is the 'K' in the KLOW blend.
Reality check — what we actually know
Supported by human evidence
- No adequately powered randomised human trials establish the outcomes this compound is marketed for.
Animal research only
- Reduced colitis severity in two separate mouse models of inflammatory bowel disease
- Lowered inflammatory cytokine release in cultured human intestinal and T cells
- Studied for skin irritation and wound inflammation in animal and cell work
Mechanistically plausible
- KPV is carried into intestinal and immune cells by the di/tripeptide transporter PepT1, which is normally found in the small intestine and is switched on in the colon during inflammatory bowel disease. Inside the cell it dampens NF-kB and MAP-kinase inflammatory signalling and lowers pro-inflammatory cytokine output — without the pigment and appetite effects of full-length alpha-MSH, which it is too short to trigger.
Common internet claims
- Online discussion frequently presents KPV as a proven treatment rather than a research compound.
Not established
- Human efficacy for the outcomes commonly claimed
- Optimal route, quantity and duration in humans
- Long-term human safety
Evidence distribution
Each band is a live PubMed search for KPV, filtered to that kind of study. Top is the strongest evidence; the base is reasoning, not proof. A band with no records means that kind of study has not been published for this compound yet.
Mechanism and reported findings
KPV is carried into intestinal and immune cells by the di/tripeptide transporter PepT1, which is normally found in the small intestine and is switched on in the colon during inflammatory bowel disease. Inside the cell it dampens NF-kB and MAP-kinase inflammatory signalling and lowers pro-inflammatory cytokine output — without the pigment and appetite effects of full-length alpha-MSH, which it is too short to trigger.
- Reduced colitis severity in two separate mouse models of inflammatory bowel disease
- Lowered inflammatory cytokine release in cultured human intestinal and T cells
- Studied for skin irritation and wound inflammation in animal and cell work
- Explored as an oral or topical anti-inflammatory rather than a growth or repair signal
Strength of the evidence: Preclinical only. The core work is cell and rodent research from the mid-2000s onward (Dalmasso 2008 in Gastroenterology; Kannengiesser 2008 in Inflammatory Bowel Diseases). There are no published human trials of KPV in any indication, and how much of an oral or injected dose reaches inflamed tissue in people has never been established.
Safety and known cautions
No human safety data, no approved product, no established dose. Anything sold online is unapproved and unregulated, so purity, content and labelling vary by vendor. Inflammatory bowel disease, autoimmune conditions and persistent skin inflammation need proper medical care — not a research chemical.
Evidence at a glance
No single score, on purpose. The line beside each bar shows how much reported outcomes vary between studies.
Development stage
- Discovery
- Preclinical
- Phase 1
- Phase 2Current
- Phase 3
- Regulatory review
- Approved