KPV.
KPV is the three-amino acid C-terminal fragment of alpha-Melanocyte Stimulating Hormone (α-MSH), retaining its anti-inflammatory activity in a minimal tripeptide sequence studied primarily for intestinal inflammation and wound healing.
Want the full narrative? Read the KPV Research Guide for the published-study discussion and mechanism deep-dive.
- Key Signals
- Gut Health · Anti-inflammatory · Wound Healing
- Origin
- Synthetic (α-MSH C-terminal fragment)
- Investigator
- Catania et al. (Univ. Groningen), 1990s
- Class
- Anti-inflammatory tripeptide (α-MSH fragment)
- Status (UAE)
- Research compound (off-label)
α-MSH's Repair Signal, Stripped to Three Residues
KPV is identified as the anti-inflammatory C-terminal tripeptide of α-MSH, retaining receptor binding activity in a minimal three-residue sequence.
Preclinical IBD models demonstrate KPV's ability to reduce colonic inflammation through direct epithelial MC1R and intracellular NLRP3 signalling.
Oral and nanoparticle-encapsulated KPV formulations achieve gut epithelial penetration, enabling direct delivery to inflamed intestinal tissue.
Three residues, one anti-inflammatory signal.
Lys-Pro-Val
C₁₆H₃₀N₄O₄ · MW 342.4 Da
KPV retains the anti-inflammatory activity of α-MSH in three residues, binding MC1R and NLRP3 in gut epithelium to suppress inflammatory signalling without the parent hormone's melanotropic effects.
Solid preclinical signal, no human trial data.
Consistent anti-inflammatory effects in animal IBD models; no Phase 1 human study completed in any indication.
- Colitis reduction (DSS models)
- NLRP3 inflammasome inhibition
- NF-κB suppression confirmed
- Wound healing accelerated
- Partial oral absorption shown
- MC1R binding confirmed (human cells)
- IL-1β and TNF-α reduction (in vitro)
- Epithelial barrier protection shown
- No human clinical trial data
- Systemic autoimmune modulation
- Dermatitis and skin inflammation
- Neuroprotective signalling (early)
- Oral nanoparticle drug delivery
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Derived from an Approved Hormone, Not Approved Itself
In the UAE, research-grade peptides occupy a defined regulatory category distinct from licensed medicines. Compounds sold under this classification — including those offered by Dubai Peptides — are intended exclusively for qualified research applications, not for human administration.
KPV has no regulatory approval in any jurisdiction. While α-MSH, its parent hormone, is endogenous and well characterised, the isolated tripeptide has not been subject to IND filing, clinical trial registration, or marketing authorisation in the US, EU, or UAE. Research interest centres on oral and nanoparticle formulations for IBD, but no Phase 1 study in human subjects has been completed or registered.
Catania and colleagues demonstrate that the C-terminal tripeptide KPV of α-MSH independently activates anti-inflammatory signalling in the early 1990s.
Preclinical studies in DSS-induced colitis models establish KPV as a direct-delivery anti-inflammatory candidate for intestinal disease.
Nanoparticle and oral encapsulation research demonstrates partial gut epithelial penetration, opening a non-injectable delivery route for IBD research.