Now reading Entry 042 / 102 Last revised Jan 22, 2026 18 sources 2 comparisons Methodology →
A specimen of the Immune drawer Drawer F · Immune

KPV

Research Only

A naturally occurring tripeptide derived from the C-terminus of alpha-melanocyte-stimulating hormone (alpha-MSH). Preclinical studies demonstrate potent anti-inflammatory effects via NF-kB inhibition, but no human clinical trials have been conducted. Research has focused on inflammatory bowel disease and skin inflammation models.

Lys-Pro-Val · Lysine-Proline-Valine · alpha-MSH(11-13) · C-terminal alpha-MSH tripeptide

Research evidence
Low

Mostly preclinical · 1 human study

Preclinical
94%
Clinical
6%

Based on 18 cited sources

Evidence Score48/100
Early / limited
Research Depth19/100
Mechanism67/100
Plausibility76/100
Global Coverage48/100
Community Experience42/100
EffectivenessNot Established

Demonstrated effect magnitude — not a recommendation or safety claim.

Research Depth 19: highest human tier is animal-only (1A=6) — no human clinical study; the dossier's single "human" source is human cell lines (Caco2/HT29/Jurkat in 18061177), not a trial — so best-study RoB is high (1B=3), total human N<50 (1C=1), evidence indirect via animal models (1D=2); substantial multi-model preclinical program (DSS/TNBS colitis, peritonitis, contact hypersensitivity) earns 1E=7. Mechanism 67: PepT1 transporter functionally and genetically implicated (oral efficacy PepT1-dependent, MC1R-independence shown in MC1Re/e knockout mice, SHU9119 fails to block; 18061177/18092346/12750433) but the effector target lacks measured binding affinity (2A~25); NF-kB/IkBa pathway to gene transcription well mapped (2B=20); nanomolar dose-response across cell+in-vivo models (2C=13); confirmed in mouse models (2D=9). Plausibility 76: mechanism->surrogate (cytokine/MPO/histology) established in animals, surrogate->human benefit only inferred (3A=24); fully coherent with melanocortin/NF-kB anti-inflammatory biology (3B=24); class analogy via parent alpha-MSH and melanocortin peptides (3C=17); tightly scoped anti-inflammatory claim applied across tissues (3D=11). Global Coverage 48: independent replication across Emory(US), Munster(DE), London(UK), Houston(US), Dallas(US) groups (4A=22); 3+ countries (4B=13); ~18 studies with diverse contexts (4C=13); no regulatory recognition, research-only (4D=0). Community Experience 42: niche but persistent enthusiast use (5A=9), multi-year track record (5B=15), limited/consistent reports (5C=8), no notable adverse signal over modest exposure (5D=10). Effectiveness not-established: zero quantified human efficacy estimate and no meaningful documented community effect signal (dossier reports no positive/negative anecdotes).

Scored June 2026 How we rate →
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Evidence Level
low
Not approved for human use by any regulatory agency
Limited human clinical trial data
Consult a healthcare provider before use
Not FDA Approved WADA Prohibited
Identity
SCALE · 1:1 N-TERMINUS C-TERMINUS 3 AA · 342.43 Da
Also Known As
Lys-Pro-Val • Lysine-Proline-Valine • alpha-MSH(11-13) • C-terminal alpha-MSH tripeptide
Class
Tripeptide
Length
3 amino acids
Mol. weight
342.43 Da
Sequence
KPV
Molecular Structure
K
P
V
Hydrophobic
Polar
Positive
Negative

The proposed mechanisms of KPV are based on animal models and cell culture studies. No human mechanistic data exists.

How It Works (Simplified)

KPV acts as an “inflammation brake” that works at the cellular level through several pathways:

NF-kB Inhibition

Blocks the master inflammation switch by preventing IkBa degradation. Keeps NF-kB trapped in cytoplasm, unable to turn on inflammatory genes.

PepT1 Transport

Uses intestinal peptide transporter PepT1 for cellular uptake - unusual for peptides and suggests potential oral bioavailability.

Cytokine Reduction

Reduces production of inflammatory messengers (TNF-alpha, IL-1, IL-6, IL-8) while potentially increasing anti-inflammatory IL-10.

No Tanning Effect

Unlike parent alpha-MSH, KPV doesn’t bind melanocortin receptors. Provides anti-inflammatory benefits without skin pigmentation changes.

Key Research: Dalmasso G et al. demonstrated PepT1-mediated uptake is essential for KPV’s anti-inflammatory effects in colitis models. PMID:18061177

Important Limitations

  • Nearly all mechanistic studies from limited research groups
  • Translation to human physiology is unconfirmed
  • Optimal administration route for systemic effects unknown
  • Bioavailability and pharmacokinetics in humans not characterized
i. NF-κB Pathway Inhibition · Primary Anti-Inflammatory
Inflammatory stimulus (LPS, TNF-α, IL-1)IKK activationIκBα phosphorylationKPV stabilizes IκBαNF-κB sequestered in cytoplasmInflammatory gene transcription prevented
ii. PepT1-Mediated Uptake · Oral Bioavailability
Oral KPVIntestinal epitheliumPepT1 transporterIntracellular accumulationNF-κB/MAPK inhibition
Mechanism NF-kB pathway inhibition via IkBa stabilization
Supported 6 direct studies
Benefit appears to reduce inflammation in various tissue types
Evidence Level
Low
8 Animal
5 In Vitro
Mechanism PepT1 transporter-mediated cellular uptake in intestinal epithelium
Supported 4 direct studies
Benefit may provide oral bioavailability for intestinal anti-inflammatory effects
Evidence Level
Low
5 Animal
3 In Vitro
Mechanism MAPK pathway modulation (p38, JNK, ERK inhibition)
Emerging 3 direct studies
Benefit may suppress inflammatory cytokine production
Evidence Level
Very Low
4 Animal
3 In Vitro
Mechanism Melanocortin receptor-independent anti-inflammatory signaling
Supported 4 direct studies
Benefit appears to reduce inflammation without melanotropic (tanning) effects
Evidence Level
Low
5 Animal
4 In Vitro
Mechanism Confidence
Established
Supported
Emerging
Evidence Level
High
Moderate
Low
Very Low
NCT ID Title Peptide Phase Status Completion
No registered trials
KPV Phase N/A No clinical trials registered on ClinicalTrials.gov -
No registered trials No clinical trials registered on ClinicalTrials.gov

KPV Phase N/A Est. -
Phase 01 1
Week 1-2

Based on preclinical data: NF-kB inhibition begins within hours of administration. Reduction in pro-inflammatory cytokine production (TNF-alpha, IL-1, IL-6) observed in cell studies. Animal colitis studies showed reduced inflammation markers within the first week.

PMID:9743348
Phase 02 2
Week 2-4

Animal studies demonstrate sustained anti-inflammatory effects with continued administration. Improved intestinal barrier function and reduced immune cell infiltration observed in colitis models.

PMID:18061177
Phase 03 3
Week 4-8

Preclinical models show ongoing suppression of inflammatory pathways. Oral bioavailability via PepT1 transporter enables sustained intestinal effects in animal studies.

PMID:18092346
Phase 04 4
Week 8+

Long-term effects in humans are completely unknown. No clinical trials have established duration of treatment, optimal dosing, or sustained efficacy. All timeline data is extrapolated from short-term animal studies.

Research-based observations

This timeline reflects observations from published clinical and preclinical studies. Individual responses may vary significantly. This is not a guarantee of effects or a dosing schedule. Consult qualified healthcare providers for personalized guidance.

Good Signs (6 indicators)
White to off-white lyophilized powder
Dissolves completely in bacteriostatic water
Clear, colorless solution after reconstitution
Certificate of analysis showing >95% purity
HPLC verification of identity and purity
Proper vacuum seal intact before reconstitution
Warning Signs (5 indicators)
Slightly off-white or cream-colored powder
Takes longer than expected to dissolve
No third-party testing verification
COA from manufacturer only
Purity listed below 95% but above 90%
Bad Signs (6 indicators)
Yellow, brown, or discolored powder
Visible particles or cloudiness after reconstitution
Gel-like consistency or clumping
No COA provided or COA appears fraudulent
Unusual odor
Vial seal compromised or previously opened
Positive quality indicator
Requires evaluation
Potential quality issue

For Research Evaluation Only

These quality indicators are general guidelines based on typical peptide characteristics. Professional laboratory testing (HPLC, mass spectrometry) provides definitive quality verification. This checklist is for initial visual evaluation only.

Synergistic
Compatible
Caution
Avoid

Both have anti-inflammatory properties through different mechanisms. KPV targets NF-kB pathway while BPC-157 acts via VEGF/angiogenesis. No known contraindications.

LL-37

Compatible
Compatible

LL-37's antimicrobial properties may complement KPV's anti-inflammatory effects in wound healing contexts. Different immune modulation mechanisms.

Both modulate immune function through different pathways. KPV inhibits NF-kB while Ta1 enhances T-cell and dendritic cell responses. May have complementary effects.

KPV's anti-inflammatory effects may complement GHK-Cu's wound healing and collagen synthesis properties. Different target pathways.

Both derive from melanocortin family. Unlike full alpha-MSH or Melanotan-II, KPV lacks melanocortin receptor binding. However, theoretical pathway overlap warrants caution.

Research Note: Interaction data is based on published literature, mechanistic understanding, and theoretical considerations. Most peptide combinations lack direct clinical study. This information is for educational purposes only and does not constitute medical advice. Always consult qualified healthcare providers.

This dossier synthesizes available evidence from peer-reviewed literature, regulatory documents, and clinical trial registries. Evidence strength ratings follow a modified GRADE approach.

For complete methodology details, see our Methodology page.

Important Disclaimer

This dossier is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before making health decisions.

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