KPV
Lysine-Proline-Valine (α-MSH 11-13)
Tripeptide consisting of the C-terminal three amino acids (Lys-Pro-Val) of α-melanocyte stimulating hormone. Carries most of α-MSH's anti-inflammatory activity in a stable, non-pigmenting form. Used primarily for gut inflammation (IBD-adjacent), systemic auto-immune flares, and skin / mast-cell conditions.
At a glance
- Routes
- Oral · SubQ · Topical
- Vial sizes
- 5 mg · 10 mg · 20 mg
- Evidence base
- 3 studies 1 review · 2 preclinical
Mechanism
Anti-inflammatory action runs through the PepT1 di/tripeptide transporter on intestinal epithelial cells and activated immune cells, not melanocortin receptors. Once intracellular, KPV inhibits NF-κB nuclear translocation (p65/p50 heterodimer) and dampens MAPK signaling (ERK1/2, JNK, p38), reducing transcription of IL-6, IL-8, IL-12, IL-1β, TNF-α, IFN-γ. Oral KPV at 100 μM cut MPO activity ~50% (DSS) and ~30% (TNBS) with marked histological improvement in murine colitis. KPV carries most of α-MSH's immune-modulating activity without pigmenting or metabolic effects. Hyaluronic-acid nanoparticle delivery achieved 3.8x greater colonic accumulation vs free KPV with efficacy at 20x lower dose. In α-MSH-receptor-expressing tissues (skin, brain) KPV may engage MC1R/MC5R, but PepT1 dominates in gut and immune cells.
Dosing
No standardized human dosing has been established. Every catalogued study for KPV is preclinical or a literature review. Amounts used in animal models do not translate directly to humans.
Published evidence
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Review 2008
α-MSH and Related Tripeptides: Biochemistry, Anti-Inflammatory and Protective Effects
Comprehensive review establishing KPV as carrying most of α-MSH's immune-modulating activity without pigmenting / metabolic effects.
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Animal in vivo 2017
Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis
HA-functionalized nanoparticle delivery of oral KPV achieved 3.8x greater colonic accumulation vs free KPV with efficacy at 20x lower dose.
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Animal in vivo 2008
PepT1-Mediated Tripeptide KPV Uptake Reduces Intestinal Inflammation
Defined PepT1-mediated uptake. In murine colitis, oral KPV at 100μM cut MPO activity ~50% (DSS) and ~30% (TNBS), with marked histological improvement and suppression of IL-8/IL-6/IL-12/IL-1β/TNF-α/IFN-γ.
Reported side effects
- Injection site irritation
- Occasional Mild · SC route only. Mild redness or transient burn, usually carrier-related.
- GI cramping / loose stool
- Rare Mild · Oral route. Anecdotal, usually dose-related.
- Long-term safety unknown
- Unknown Mild · No human chronic-use safety database. α-MSH parent has cardiovascular and endocrine effects at supraphysiologic doses; KPV lacks the cyclic core driving MC4R binding, but residual MCR engagement not excluded.
Interactions
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BPC-157 Synergy
KPV + BPC-157 oral is the most-cited community gut-healing stack. Complementary mechanisms: KPV suppresses cytokine-driven inflammation via NF-κB; BPC-157 drives angiogenesis and epithelial repair.
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LL-37 Synergy
KPV (anti-inflammatory) and LL-37 (anti-microbial + biofilm-disrupting) target complementary arms of mucosal dysfunction.
Reconstitution and storage
5 mg vial + 2 mL BAC water = 2,500 mcg/mL = 250 mcg per 0.1 mL (10 units on insulin syringe). 10 mg + 2 mL = 5,000 mcg/mL = 250 mcg per 0.05 mL. Drip water down vial wall. Do not shake.
Lyophilized: freezer (-20°C) for long-term, fridge (2-8°C) acceptable short-term. Reconstituted: refrigerate 2-8°C, use within 28-30 days. Protect from light.