Peptide Name
KPV
Updated February 2026
KPV Dosing Protocol
Definitive KPV (Lys-Pro-Val) protocol reference covering oral and injectable dosing, PepT1-mediated anti-inflammatory mechanism, reconstitution precision, and evidence boundaries.
Half-life
Short; exact human PK not established
Dose range
200-500 mcg daily (oral or SubQ)
Status
Not FDA-approved
Clinical depth
Preclinical evidence only
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Discount code: PEPPAL
Quick Reference Card
Aliases
Lysine-Proline-Valine; Lys-Pro-Val; alpha-MSH (11-13); C-terminal tripeptide of alpha-MSH
Category / Class
Anti-Inflammatory / Melanocortin-Derived Peptide
Half-Life
Short; exact human plasma half-life is not established, but functional anti-inflammatory effects persist beyond circulation window
Dosing Frequency
Once daily SubQ or oral; some oral protocols are twice daily
Dose Range
200-500 mcg daily; some protocols use up to 1,000 mcg/day
Common Vial Sizes
5mg, 10mg
Route of Administration
Subcutaneous, oral, topical, and nasal (less common)
Regulatory Status
Not FDA-approved. No completed human trials. Evidence base is preclinical and mechanistic.
Key Stat
Oral KPV significantly reduced inflammation severity in DSS and TNBS colitis models in the 2008 Gastroenterology PepT1 study.
What Is KPV?
KPV is a tripeptide (lysine-proline-valine) derived from the C-terminal segment of alpha-MSH and is one of the most studied melanocortin-derived fragments for inflammation control.
Its small size supports PepT1-mediated epithelial uptake, which is central to oral gut-focused protocol interest and distinguishes it from many peptides that require injection-only administration.
KPV retains anti-inflammatory activity while lacking the receptor-binding sequence responsible for classic melanocortin pigmentation effects, which is why it is generally positioned as non-tanning.
KPV is not FDA-approved for any indication and has no completed human efficacy trials. This page is educational research reference only.
How KPV Works: PepT1-Mediated NF-kB Inhibition and Barrier-Support Signaling
KPV is studied for intracellular inflammatory-pathway modulation after PepT1-mediated uptake, especially in inflamed epithelial tissues.
NF-kB Pathway Dampening
KPV is reported to reduce NF-kB signaling duration and downstream inflammatory gene expression, helping lower cytokine burden without the broad suppression profile seen in steroid-like approaches.
PepT1-Mediated Cellular Uptake
A key finding from colitis research is PepT1-mediated transport. PepT1 upregulation in inflamed intestinal tissue may create preferential uptake where inflammatory burden is highest.
Barrier and Mucosal Support
KPV-associated effects include epithelial barrier support and improved mucosal-healing dynamics in preclinical models, relevant to leaky-gut and IBD-style research contexts.
Antimicrobial Dimension
KPV literature also describes antimicrobial activity against selected pathogens, making it notable as a dual anti-inflammatory and antimicrobial candidate in mixed inflammation-infection scenarios.
This combination of small-peptide transportability and pathway-level inflammation control drives KPV's role in gut and skin inflammation protocol models.
KPV Dosing Protocol and Administration Schedule
Initiation (injectable)
Weeks 1-2
200 mcg/day SubQ
Low-start tolerance and response check.
Titration (injectable)
Weeks 3-4
300-400 mcg/day SubQ
Increase by about 100 mcg/week as tolerated.
Maintenance (injectable)
Weeks 5-12
400-500 mcg/day SubQ
Common anti-inflammatory maintenance window.
Oral standard
Weeks 1-8+
200-500 mcg once or twice daily
Preferred route for gut-focused workflows; take on empty stomach.
Oral intensive
Weeks 1-8+
500 mcg twice daily
Used in higher-burden inflammatory contexts.
Topical skin use
4-8+ weeks
Compounded topical, 1-2x daily
Applied to localized inflammatory skin targets.
Cycle standard
4-8 weeks on
Active dose
Typical 2-4 week off period.
Cycle extended
8-16 weeks on
Active dose
Longer protocols with periodic off windows.
Evidence Level Notice and Dosing Notes
Evidence level: No completed human dose-finding trials define optimal KPV dosing. Protocols are preclinical extrapolation and practitioner/community derived.
Route selection: Oral route is typically favored for gut-focused applications; SubQ route is favored for systemic delivery goals.
Empty-stomach guidance: Oral KPV is commonly taken on an empty stomach to reduce transporter competition from dietary peptides.
Pigmentation context: KPV does not have the receptor-binding sequence associated with tanning peptides and is generally modeled as non-pigmenting.
Missed dose: Resume next scheduled dose without doubling.
KPV Reconstitution Guide
Vial Size: 5 mg
BAC Water: 1 mL
Concentration: 5,000 mcg/mL
200 mcg: 0.04 mL (4 units)
300 mcg: 0.06 mL (6 units)
500 mcg: 0.10 mL (10 units)
Vial Size: 5 mg
BAC Water: 2 mL
Concentration: 2,500 mcg/mL
200 mcg: 0.08 mL (8 units)
300 mcg: 0.12 mL (12 units)
500 mcg: 0.20 mL (20 units)
Vial Size: 10 mg
BAC Water: 2 mL
Concentration: 5,000 mcg/mL
200 mcg: 0.04 mL (4 units)
300 mcg: 0.06 mL (6 units)
500 mcg: 0.10 mL (10 units)
Vial Size: 10 mg
BAC Water: 3 mL
Concentration: 3,333 mcg/mL
200 mcg: 0.06 mL (6 units)
300 mcg: 0.09 mL (9 units)
500 mcg: 0.15 mL (15 units)
Vial Size: 10 mg
BAC Water: 5 mL
Concentration: 2,000 mcg/mL
200 mcg: 0.10 mL (10 units)
300 mcg: 0.15 mL (15 units)
500 mcg: 0.25 mL (25 units)
Step-by-Step Reconstitution Instructions
- Wipe vial stopper with alcohol and allow to dry.
- Draw planned BAC water volume with a sterile syringe.
- Inject water against vial wall instead of directly onto powder.
- Allow gentle flow; avoid forced pressure.
- Roll vial gently for 30-60 seconds; do not shake.
- Inspect for clear, colorless solution before use.
- Label concentration/date and refrigerate at 2-8C. Use within 30 days.
KPV Side Effects and Safety
KPV has a favorable preclinical tolerability profile, but there are no completed human clinical safety programs.
Evidence boundary: No completed human efficacy/safety trials currently define long-term dosing safety outcomes.
Common reports: Community-reported effects are usually mild: transient injection-site irritation, occasional mild headache, and occasional GI upset at higher oral doses.
Pigmentation effects: KPV is generally considered non-tanning and non-pigmenting in standard protocol use.
Immune profile: KPV is studied for pathway-targeted inflammation control rather than broad immunosuppression.
General cautions: Avoid use in pregnancy/breastfeeding and seek clinician oversight in complex inflammatory/infectious conditions.
KPV Research Evidence
Dalmasso et al. 2008
Preclinical + in vitro • Model-dependent
DSS/TNBS colitis models and epithelial cell systems
Oral KPV reduced colitis severity with PepT1-mediated uptake as a central mechanism finding.
Xiao et al. 2017
Preclinical • Model period
DSS colitis mouse model
Nanoparticle-delivered KPV improved targeting to inflamed colonic tissues and reduced inflammatory markers.
Kannengiesser et al. 2008
Preclinical + in vitro • Cell-assay based
Bronchial epithelial cell models
Dose-dependent suppression of TNF-driven inflammatory signaling and matrix-remodeling markers.
Catania et al. 2000
In vitro • Laboratory assay
S. aureus and C. albicans cultures
Reported direct antimicrobial activity, adding a dual anti-inflammatory/antimicrobial dimension.
Getting et al. 2006
Review • N/A
Multiple inflammation models
Summarized melanocortin-derived anti-inflammatory pharmacology and receptor-pathway distinctions relevant to KPV.
KPV evidence is currently preclinical and mechanistic, led by gut-inflammation model data and PepT1 transport findings. The translational gap is the absence of completed human RCTs establishing definitive dosing, efficacy magnitude, and long-term safety.
Storage and Handling
Lyophilized (powder)
-20C (freezer)
Long-term (years)
Lyophilized (powder)
2-8C (refrigerator)
Months
Lyophilized (powder)
15-25C (room)
Weeks (shipping tolerance)
Reconstituted
2-8C (refrigerator)
Up to 30 days
Reconstituted
Do not freeze
N/A
Protect from light/moisture, avoid freeze-thaw cycling, and use bacteriostatic water for multi-dose workflows.
KPV vs BPC-157 vs alpha-MSH
Origin
KPV: C-terminal tripeptide fragment of alpha-MSH
BPC-157: Synthetic 15-AA gastric-protein fragment
alpha-MSH (full-length): Endogenous 13-AA melanocortin hormone
Primary Mechanism
KPV: NF-kB-focused anti-inflammatory signaling via PepT1 uptake
BPC-157: VEGF/NO modulation with cytoprotective repair signaling
alpha-MSH (full-length): Broad melanocortin receptor agonism
Primary Use Model
KPV: Inflammation control and gut barrier support
BPC-157: Structural tissue repair
alpha-MSH (full-length): Pigmentation and melanocortin-system signaling
Oral Viability
KPV: Yes (PepT1-mediated)
BPC-157: Yes
alpha-MSH (full-length): Limited practical oral utility
Pigmentation Effects
KPV: No
BPC-157: No
alpha-MSH (full-length): Yes
Clinical Evidence
KPV: Preclinical only
BPC-157: Limited human + broad preclinical
alpha-MSH (full-length): Extensive hormonal research
KPV and BPC-157 are often paired in gut-focused protocols because KPV emphasizes inflammation control while BPC-157 emphasizes structural repair.
KPV should not be confused with melanotan compounds; pigmentation effects are not the target profile.
Dose units and route selection should be matched to protocol goals (gut-local, systemic, or skin-local models).
See the BPC-157 Protocol, TB-500 Protocol and GHK-Cu Protocol for compound-specific guides.
KPV Stacking Protocols
Stack 1
KPV + BPC-157 (Gut Healing Stack)
KPV handles inflammatory signaling load while BPC-157 supports structural mucosal repair. Often run orally for gut-targeted workflows.
See the compound-specific See BPC-157 protocol for additional context.
View protocolStack 2
KPV + TB-500 (Systemic Inflammation + Repair)
Pairs inflammation control with deep tissue and migration support where multi-system recovery is needed.
See the compound-specific See TB-500 protocol for additional context.
View protocolStack 3
KPV + GHK-Cu (Anti-Inflammatory Skin Stack)
Combines inflammatory pathway control with collagen/remodeling support for skin-focused inflammatory contexts.
See the compound-specific See GHK-Cu protocol for additional context.
View protocolFrequently Asked Questions - KPV
Q1: What is the starting dose of KPV?
A common starting point is 200 mcg once daily (oral or SubQ), then titration toward 400-500 mcg/day based on response and tolerance.
Q2: What is KPV's half-life?
Exact human PK half-life is not firmly established. As a tripeptide, rapid degradation is expected, while intracellular pathway effects can persist longer.
Q3: What results can be expected from KPV?
Reported timelines often include early symptom shifts in 2-4 weeks, with broader anti-inflammatory trend changes over 6-12 weeks depending on context.
Q4: How do you reconstitute KPV?
Common setup is 10 mg with 2 mL (5,000 mcg/mL), where a 500 mcg dose equals 0.10 mL or 10 units on a U-100 syringe.
Q5: Is KPV FDA-approved?
No. KPV is not FDA-approved for any indication and currently has no completed human clinical efficacy trials.
Q6: What are the most common side effects of KPV?
Community reports are usually mild and infrequent, such as temporary injection-site irritation, mild GI discomfort at higher oral doses, or occasional headache.
Q7: How does KPV compare to BPC-157?
KPV is primarily anti-inflammatory (NF-kB-focused), while BPC-157 is primarily repair-focused. They are commonly combined for inflammation-plus-repair goals.
Q8: What vial sizes is KPV available in?
Most common lyophilized vial sizes are 5 mg and 10 mg.
Q9: How much bacteriostatic water should be added to KPV?
10 mg with 2 mL or 3 mL are common choices. Lower concentration can improve draw precision for microgram-level dosing.
Q10: Can KPV be taken orally?
Yes. Oral KPV is a common protocol route, especially for gut-focused use, and is generally taken on an empty stomach.
Q11: How should reconstituted KPV be stored?
Store refrigerated at 2-8C, protect from light, and use within around 30 days. Do not freeze the reconstituted solution.
Q12: Does KPV cause skin tanning or pigmentation changes?
No. KPV is generally modeled as non-pigmenting and should not be confused with melanotan peptides.
Sources & Research
- Dalmasso G, Charrier-Hisamuddin L, et al. "PepT1-Mediated Tripeptide KPV Uptake Reduces Intestinal Inflammation." Gastroenterology, 2008 PubMed.
- Xiao B, Laroui H, et al. "Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis." Molecular Therapy, 2017 Link.
- Kannengiesser K, et al. "Kannengiesser et al. 2008 preclinical epithelial-cell KPV findings." Journal of Leukocyte Biology, 2008.
- Catania A, et al. "The peptide NDP-MSH induces phenotype changes in the heart that resemble those induced by melanocortin receptor agonists." Journal of Leukocyte Biology, 2000.
- Brzoska T, Luger TA, Maaser C, et al. "alpha-MSH related peptides: a new class of anti-inflammatory and immunomodulating drugs." Annals of the Rheumatic Diseases, 2008 Link.
- Star RA, Rajora N, et al. "Evidence for autocrine modulation of macrophage nitric oxide synthase by alpha-melanocyte-stimulating hormone." PNAS, 1995.
- Getting SJ. "Targeting melanocortin receptors as potential novel therapeutics." Pharmacology and Therapeutics, 2006.
- Rajora N, Boccoli G, et al. "alpha-MSH modulates experimental inflammatory bowel disease." Peptides, 1997.
- Lee DJ, Kwon JY, et al. "The therapeutic potential of melanocortin peptides in inflammatory bowel disease." Nature Reviews Gastroenterology and Hepatology, 2018.
- Wang W, et al. "Melanocortin Regulation of Inflammation." Frontiers in Endocrinology, 2019 Link.
- Recent Advances in KPV Peptide Delivery (review article). Link.
- Wikipedia: Alpha-melanocyte-stimulating hormone. Link.
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The information on this page is for educational and research reference purposes only. KPV is not FDA-approved for any indication. No completed human clinical trials exist. No compounds discussed on this site are intended for human consumption. This is not medical advice.
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