3AA Animal Models
KPV
Alpha-MSH's anti-inflammatory core — a tripeptide that enters inflamed gut cells via PepT1 and shuts down NF-kB at the nuclear level.
In Plain English: KPV is a three-amino-acid fragment (Lys-Pro-Val) from the tail end of alpha-MSH. It enters inflamed intestinal cells via the PepT1 transporter, shuts down NF-kB and MAPK inflammatory switches, and dials back cytokine storms (TNF-a, IL-6, IL-12) without broadly suppressing the immune system. Preclinical evidence in colitis, wound healing, and skin inflammation is strong; zero human RCTs exist.
Research Maturity
Animal Models (~47 indexed publications on PubMed for KPV peptide / Lys-Pro-Val (verified 2026-05-04)+ Studies)
Quick Facts
Focus
Gut Health
Immune Regulating
Inflammation
Skin & Hair
Route
Oral
SubQ
Topical
Origin
C-terminal fragment (positions 11-13) of alpha-MSH, produced from POMC cleavage. First identified as the minimal active anti-inflammatory sequence in the early 1990s. Major gut-targeting mechanism (PepT1 uptake) established at Emory University 2003-2016.
Mechanism
Enters cells via hPepT1 transporter (upregulated in inflamed gut, creating self-targeting). Inside cell: (1) inhibits IKK complex blocking NF-kB nuclear entry; (2) suppresses MAPK/ERK cascades; (3) blocks importin-a3 interaction with p65RelA. Result: reduced TNF-a, IL-6, IL-8, IL-12, IFN-g transcription. In keratinocytes, triggers intracellular calcium signalling (receptor-independent pathway).
Outcome
Murine colitis models (DSS, TNBS, T-cell transfer): reduced MPO ~50%, preserved colon length, lowered TNF-a mRNA. HA-PLGA nanoparticle delivery significantly outperformed free KPV in UC mouse models. Prevented colitis-associated carcinogenesis in PepT1+ mice (2016).
Safety Flags & Warnings
No Human Clinical Trials
No Human Pharmacokinetics
Cancer History Contraindication
Always consult a licensed physician. Research purposes only.
€6.4 / mg
