KPV (Lys-Pro-Val) Dosage Guide

Evidence-based protocols for the minimal anti-inflammatory fragment of alpha-MSH — oral, subcutaneous, and topical dosing for gut inflammation, IBD, skin conditions, NF-κB inhibition, and stacking strategies.

Compiled by PeptideWiki Editorial Team·Last reviewed February 24, 2026

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Research Peptides

KPV

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What Is KPV?

KPV (Lys-Pro-Val) is a naturally occurring tripeptide derived from the C-terminal sequence of alpha-melanocyte stimulating hormone (α-MSH). It is the minimal anti-inflammatory fragment of α-MSH — the smallest piece of the hormone that retains potent anti-inflammatory activity. Its amino acid sequence is simply Lysine-Proline-Valine, making it one of the smallest bioactive peptides used in research.

What makes KPV unique is its mechanism of action. Unlike melanocyte-stimulating peptides such as MT-II (which activate melanocortin receptors to cause tanning, appetite changes, and sexual effects), KPV works through a completely different pathway. KPV enters cells and directly inhibits NF-κB nuclear translocation — the master switch that controls production of pro-inflammatory cytokines including TNF-α, IL-6, and IL-1β. This means KPV is purely anti-inflammatory with no tanning, sexual, or appetite effects whatsoever.

Another distinguishing feature is KPV's potential for oral bioavailability. Most peptides are destroyed by stomach acid and digestive enzymes, making oral administration impractical. However, KPV's extremely small size (only 3 amino acids) may allow some absorption through the gastrointestinal tract — making oral dosing the most popular community route, particularly for gut-targeted inflammation. This is highly unusual in the peptide world.

Use our Peptide Dosage to calculate your exact subcutaneous dose based on vial size and concentration.

Dosing information in this guide is derived from preclinical studies and community protocols — not from approved pharmaceutical labeling.

Key Characteristics:

Minimal anti-inflammatory fragment of α-MSH — the smallest piece of alpha-MSH that retains full anti-inflammatory potency; amino acid sequence Lys-Pro-Val
NF-κB pathway inhibition — enters cells and directly blocks NF-κB nuclear translocation, reducing TNF-α, IL-6, IL-1β, and other pro-inflammatory cytokines
NOT a melanocortin receptor agonist — does NOT cause tanning, sexual effects, or appetite changes — works through melanocortin-independent pathways entirely
Multiple administration routes — oral (most popular for gut inflammation), subcutaneous injection (systemic), topical (skin), and intranasal
Potential oral bioavailability — tripeptide size may allow some GI absorption — highly unusual for peptides; oral is the most common community route
Very mild side effect profile — no hormone manipulation, no receptor desensitization, no feedback loops; rare GI discomfort (oral) or injection site reactions (SubQ)

For a complete overview of its mechanism and research, see our full KPV profile. New to peptides? Start with the Beginner's Guide to Peptides.

How KPV Dosage Is Determined

KPV dosing is primarily informed by preclinical research (animal models of inflammatory bowel disease and skin inflammation) and community experience. Unlike some peptides with extensive human clinical pharmacology data, KPV's dosing protocols are largely extrapolated from animal studies and refined by community use. The dose ranges below represent the most commonly reported effective ranges.

Preclinical IBD Research

Multiple animal studies have demonstrated KPV's efficacy in models of inflammatory bowel disease. Dalmasso et al. showed that KPV significantly reduced colonic inflammation in murine colitis models when administered orally — demonstrating that the tripeptide can survive GI transit in sufficient quantities to exert local anti-inflammatory effects. These studies used doses in the range of micrograms per kilogram, which community practitioners have extrapolated to the 200–500 mcg oral range for humans.

NF-κB Mechanism Studies

Kannengiesser et al. and other groups characterized KPV's mechanism of action at the cellular level. KPV enters cells (including colonocytes and keratinocytes) and directly interacts with NF-κB subunits, preventing their translocation to the nucleus. Without nuclear NF-κB, transcription of pro-inflammatory genes (TNF-α, IL-6, IL-1β, COX-2) is markedly reduced. This mechanism is dose-dependent and occurs at micromolar concentrations, supporting the microgram-range dosing used in practice.

Skin Inflammation Research

Preclinical studies on skin inflammation models demonstrated that topical application of KPV reduces contact dermatitis, accelerates wound healing, and decreases local cytokine production. These findings support topical administration as a viable route for localized skin conditions, with KPV applied directly to affected areas.

Community-Derived Protocols

Given limited human clinical data, much of the practical dosing knowledge for KPV comes from community experience. The oral range of 200–500 mcg (1–2x daily) and subcutaneous range of 100–500 mcg daily represent the most commonly reported effective doses across peptide research communities. These ranges align well with extrapolations from preclinical dose-response data.

Strength of evidence: Moderate preclinical, limited clinical. KPV has good preclinical data in animal IBD and skin inflammation models, with well-characterized NF-κB mechanism of action at the cellular level. However, published human clinical trials are lacking. Dosing protocols are based on preclinical pharmacology and community experience. This is a research peptide — not an approved therapeutic.

Standard KPV Dosage Ranges

KPV is unique among peptides in offering multiple practical administration routes. The optimal route depends on the target condition: oral for gut inflammation, subcutaneous for systemic effects, and topical for skin conditions. Dosing varies by route due to differences in bioavailability.

Oral Dosing

Level	Dose per Administration	Frequency	Daily Total	Notes
Starting	200 mcg	1x daily	200 mcg	Assess tolerance; take on empty stomach
Standard	200–500 mcg	1–2x daily	200–1,000 mcg	Most common oral protocol for gut inflammation and IBD support
Higher Range	500 mcg	2x daily	1,000 mcg	Upper end of community-reported oral dosing; for persistent inflammation

Subcutaneous Injection

Level	Dose per Injection	Frequency	Daily Total	Notes
Starting	100 mcg	1x daily	100 mcg	Assess tolerance; injection site rotation
Standard	200–300 mcg	1x daily	200–300 mcg	Most common SubQ protocol for systemic anti-inflammatory support
Higher Range	500 mcg	1x daily	500 mcg	Upper community-reported dose; for active inflammatory conditions

Topical Application

Preparation: KPV can be reconstituted and applied directly to affected skin areas, or compounded into a topical cream or gel
Frequency: 1–2x daily to affected areas
Best for: Localized skin inflammation — dermatitis, eczema flares, psoriasis plaques, wound healing
Note: Topical dosing is less standardized than oral or SubQ; concentration depends on preparation method

Route selection matters: Use oral KPV for gut-targeted inflammation (IBD, colitis, GI issues) where the peptide contacts the intestinal lining directly. Use subcutaneous injection for reliable systemic anti-inflammatory delivery. Use topical for localized skin conditions. Many users combine routes — for example, oral for gut inflammation plus topical for concurrent skin issues.

Administration Routes Compared

KPV is unusual among peptides in offering multiple viable routes of administration. Each route has distinct advantages depending on the target condition. Understanding these differences is critical for selecting the right protocol.

Parameter	Oral	Subcutaneous	Topical	Intranasal
Typical Dose	200–500 mcg	100–500 mcg	Applied to area	100–200 mcg
Bioavailability	Lower (partial GI absorption)	Highest	Local delivery	Moderate (mucosal)
Best For	Gut inflammation, IBD	Systemic inflammation	Skin conditions	Sinus / upper airway
Systemic Reach	Moderate	Full systemic	Minimal	Moderate
Ease of Use	Easiest (capsule/liquid)	Requires injection	Easy (apply to skin)	Easy (spray)
Community Popularity	Most popular	Second most common	Niche use	Less common
Key Advantage	Direct gut lining contact	Reliable absorption	Direct skin delivery	Mucosal absorption

Why oral works for KPV (but not most peptides): Most peptides are large molecules that are rapidly destroyed by stomach acid and digestive proteases. KPV is only 3 amino acids — one of the smallest bioactive peptides in use. This tiny size may provide partial resistance to enzymatic degradation, allowing enough intact KPV to reach the intestinal lining. For gut inflammation specifically, even partial survival through the GI tract is advantageous because the target tissue (intestinal mucosa) is in direct contact with the oral dose. This is why oral KPV is most effective for gut conditions and less reliable for systemic targets.

Calculate Your KPV Dose

For subcutaneous injection, KPV is supplied as a lyophilized (freeze-dried) powder, typically in 5 mg vials. You reconstitute it with bacteriostatic water, then draw your dose using an insulin syringe. The concentration depends on how much water you add to the vial. For oral capsules, dosing is pre-measured — no reconstitution math is needed.

Worked Example (Subcutaneous):

Vial size: 5 mg (5,000 mcg) of KPV
Bacteriostatic water added: 2 mL
Concentration: 5,000 mcg ÷ 2 mL = 2,500 mcg per mL
Target dose: 250 mcg
Volume to draw: 250 ÷ 2,500 = 0.1 mL = 10 units on an insulin syringe

Quick Reference — 5 mg Vial (Subcutaneous)

Bac Water Added	Concentration	200 mcg Dose	500 mcg Dose
1 mL	5,000 mcg/mL	4 units (0.04 mL)	10 units (0.1 mL)
2 mL	2,500 mcg/mL	8 units (0.08 mL)	20 units (0.2 mL)
2.5 mL	2,000 mcg/mL	10 units (0.1 mL)	25 units (0.25 mL)
5 mL	1,000 mcg/mL	20 units (0.2 mL)	50 units (0.5 mL)

Skip the Math — Use Our

Enter your vial size, water volume, and desired dose — get instant calculations with zero manual math.

KPV Dosage by Goal

KPV's NF-κB inhibition mechanism makes it applicable across multiple inflammatory conditions. The optimal protocol varies depending on whether you are targeting gut inflammation, skin conditions, systemic inflammation, or wound healing.

Gut Inflammation & IBD Support (Crohn's, Ulcerative Colitis)

The most common use case for KPV. Oral administration delivers the peptide directly to the intestinal lining where it can inhibit NF-κB locally in colonocytes and immune cells within the gut mucosa. This is the protocol with the strongest preclinical support (animal IBD models).

Route: Oral (capsules or liquid)
Dose: 200–500 mcg per administration
Frequency: 1–2x daily on an empty stomach
Duration: 4–8 weeks; reassess at 4 weeks
Stack: + BPC-157 250–500 mcg oral or SubQ for synergistic gut mucosal repair (the most popular KPV stack)

Skin Inflammation (Dermatitis, Eczema, Psoriasis)

Topical KPV delivers the peptide directly to inflamed skin tissue. NF-κB inhibition in keratinocytes and local immune cells reduces cytokine production at the site of inflammation. Can be combined with oral or SubQ dosing for conditions involving both skin and systemic inflammation.

Route: Topical (applied to affected areas)
Frequency: 1–2x daily
Duration: Continue as long as needed; reassess every 4 weeks
Optional addition: Oral KPV 200–500 mcg daily for systemic anti-inflammatory support alongside topical treatment

Systemic Inflammation & Immune Modulation

For systemic inflammatory conditions not limited to the gut or skin, subcutaneous injection provides the most reliable and complete absorption. This route ensures full systemic delivery of KPV for NF-κB inhibition throughout the body.

Route: Subcutaneous injection
Dose: 200–500 mcg per injection
Frequency: 1x daily
Duration: 4–8 weeks
Stack: + Thymosin Alpha-1 for comprehensive immune modulation (NF-κB inhibition + adaptive immune support)

Wound Healing & Post-Procedure Recovery

KPV's anti-inflammatory properties support wound healing by reducing excessive inflammation at the injury site. NF-κB inhibition dampens the pro-inflammatory phase, allowing the tissue to transition more efficiently to the proliferative and remodeling phases of wound repair.

Route: Topical (to wound site) and/or SubQ (systemic support)
Dose: Topical to affected area + optional SubQ 200–300 mcg daily
Duration: Until healing is satisfactory; typically 2–6 weeks
Stack: + BPC-157 250 mcg + TB-500 750 mcg for comprehensive wound healing (anti-inflammatory + angiogenesis + tissue remodeling)

Match the route to the target. Oral KPV is optimal when the gut itself is the target (the peptide contacts the intestinal lining directly). Subcutaneous injection is optimal for systemic delivery. Topical is optimal for localized skin conditions. Do not assume one route is universally superior — the best choice depends entirely on the target tissue.

Cycling & Duration

Unlike GHRPs (which require strict cycling due to receptor desensitization), KPV does not act on receptors that downregulate with continuous use. Its mechanism — direct NF-κB translocation inhibition — does not involve receptor binding at the cell surface in the same way. This means KPV has a lower tolerance/desensitization risk than many peptides. However, structured cycling is still recommended as a general best practice.

Protocol	On-Period	Off-Period	Notes
Standard (Gut)	4–8 weeks	2–4 weeks off	Most common for gut inflammation; reassess symptoms at 4 weeks
Extended (Chronic IBD)	8–12 weeks	4 weeks off	For persistent conditions; monitor and reassess regularly
Maintenance	Ongoing at lower dose	N/A	Some users maintain at 200 mcg/day after initial cycle; limited long-term data
Skin (Topical)	As needed	As needed	Topical use is typically used during active flares and discontinued when resolved
Acute (Wound Healing)	2–6 weeks	Stop when healed	Duration matches healing timeline; no need for extended cycling

Lower desensitization risk than GHRPs: KPV does not stimulate cell-surface receptors that downregulate with repeated use (like GHS-R1a in the case of Hexarelin). Its intracellular NF-κB mechanism does not appear to develop the same tolerance pattern. However, cycling is still recommended to reassess the inflammatory condition, ensure the peptide remains effective, and follow general best practices for research peptide use.

When to Extend or Shorten a Cycle

Extend beyond 8 weeks if chronic gut inflammation is improving but not fully resolved. Monitor closely and consult a healthcare provider for IBD management.
Shorten to 4 weeks or less if the acute inflammatory episode resolves quickly (e.g., a short IBD flare that calms within weeks).
Consider maintenance dosing (lower dose, ongoing) for chronic conditions where symptoms recur upon discontinuation — but recognize that long-term human safety data is limited.
Topical use does not require strict cycling — apply during active skin inflammation and discontinue when the condition resolves.

KPV Stacking Protocols

KPV stacks well with peptides that target complementary mechanisms. Because KPV's anti-inflammatory action (NF-κB inhibition) is mechanistically distinct from tissue repair peptides, antimicrobial peptides, and immune modulators, combining them creates synergistic protocols for complex inflammatory conditions.

KPV + BPC-157 — The Gut Healing Stack (Most Popular)

The most widely used KPV stack and arguably the most popular peptide combination for gut inflammation and IBD. KPV reduces inflammation via NF-κB inhibition (dampening the fire), while BPC-157 promotes mucosal repair through angiogenesis, growth factor upregulation (VEGF, EGF), and nitric oxide modulation (rebuilding the tissue). These mechanisms are fully complementary.

Compound	Dose	Route	Purpose
KPV	200–500 mcg, 1–2x daily	Oral (empty stomach)	NF-κB inhibition; reduces gut inflammatory cytokines
BPC-157	250–500 mcg, 1–2x daily	Oral or SubQ	Gut mucosal repair; angiogenesis; growth factor upregulation

Protocol note: For gut-targeted protocols, oral BPC-157 is often preferred alongside oral KPV so both peptides contact the intestinal lining directly. For more severe conditions or when systemic repair support is also desired, subcutaneous BPC-157 can be used instead of or in addition to oral dosing.

KPV + LL-37 (Anti-Inflammatory + Antimicrobial)

Combines KPV's NF-κB-mediated anti-inflammatory effects with LL-37's broad-spectrum antimicrobial and immunomodulatory activity. This stack addresses both the inflammatory response and potential microbial contributions to chronic inflammation — particularly relevant for conditions where infection or dysbiosis contributes to inflammation.

Compound	Dose	Route	Purpose
KPV	200–500 mcg, 1x daily	Oral or SubQ	NF-κB inhibition; cytokine reduction
LL-37	50–100 mcg, 1x daily	SubQ	Antimicrobial defense; immunomodulation; biofilm disruption

KPV + Thymosin Alpha-1 (Anti-Inflammatory + Immune Modulation)

Pairs KPV's direct NF-κB anti-inflammatory mechanism with Thymosin Alpha-1's adaptive immune system modulation. Thymosin Alpha-1 enhances T-cell function and immune surveillance while KPV dampens excessive inflammatory signaling. This stack is designed for conditions involving both dysregulated inflammation and suboptimal immune function.

Compound	Dose	Route	Purpose
KPV	200–500 mcg, 1x daily	Oral or SubQ	NF-κB inhibition; inflammatory cytokine reduction
Thymosin Alpha-1	1.6 mg, 2–3x per week	SubQ	T-cell modulation; adaptive immune support; immune surveillance

KPV + BPC-157 + TB-500 (Comprehensive Healing Stack)

A three-peptide approach for significant tissue damage or chronic inflammatory conditions that require both anti-inflammatory action and comprehensive tissue repair. KPV handles NF-κB inhibition, BPC-157 drives angiogenesis and growth factor production, and TB-500 promotes tissue remodeling, reduces fibrosis, and supports stem cell migration to injury sites.

Compound	Dose	Route	Purpose
KPV	200–500 mcg, 1–2x daily	Oral or SubQ	NF-κB inhibition; anti-inflammatory foundation
BPC-157	250–500 mcg, 1–2x daily	Oral or SubQ	Angiogenesis; growth factor upregulation; mucosal repair
TB-500	750 mcg, 1x daily (or 2 mg 2x/week)	SubQ	Tissue remodeling; anti-fibrotic; stem cell migration

Do NOT confuse KPV with melanocortin agonists. KPV does not interact with the same receptors as MT-II, PT-141, or other melanocortin-active peptides. There is no synergy or conflict with melanocortin pathways because KPV simply does not engage them. Stacking KPV with melanocortin peptides is neither beneficial nor harmful from a receptor perspective — they operate on entirely separate pathways.

Explore more combinations with our Peptide Stack Builder or browse the Top 10 Peptide Stacks guide.

Safety, Side Effects & Contraindications

Safety Profile: KPV has one of the mildest side effect profiles of any research peptide. It does not manipulate hormones, does not activate cell-surface receptors that desensitize, and does not affect endocrine feedback loops. The NF-κB inhibition mechanism is well-characterized and targeted. Reported side effects are rare and generally mild. However, long-term human safety data is limited, and KPV remains a research peptide — not an approved drug.

Reported Side Effects

Rare and generally mild:

Mild GI discomfort (oral route) — occasional nausea or stomach upset, usually transient and resolves within the first few days
Injection site reactions (SubQ route) — minor redness, soreness, or swelling at the injection site; standard for any subcutaneous peptide
Rare headache — reported by a small minority of users, typically mild and self-resolving
Mild skin irritation (topical route) — possible with topical application in individuals with very sensitive skin

NOT associated with KPV:

No tanning, skin darkening, or pigmentation changes (KPV does not activate melanocortin receptors)
No sexual side effects (no effect on libido, arousal, or reproductive function)
No appetite changes (no orexigenic or anorexigenic effects)
No cortisol or prolactin elevation
No known receptor desensitization or tolerance development
No water retention or bloating

Compared to other anti-inflammatory approaches: KPV's side effect profile is considerably milder than conventional anti-inflammatory drugs (NSAIDs, corticosteroids, biologics). NSAIDs carry GI ulceration risk, corticosteroids cause systemic metabolic effects, and biologics suppress immune function broadly. KPV's targeted NF-κB mechanism avoids these issues. However, it is not FDA-approved and does not replace prescribed treatments for serious conditions.

Contraindications

Pregnancy and breastfeeding — no safety data exists for KPV during pregnancy or nursing. Avoid entirely.
Active infections requiring NF-κB signaling — NF-κB plays a role in the immune response to infections. Theoretically, inhibiting NF-κB during an active severe infection could impair the immune defense. Use caution and consult a healthcare provider if dealing with acute infections.
Immunosuppressed individuals — those on immunosuppressive medications or with compromised immune function should consult a healthcare provider before using any peptide that modulates inflammatory pathways.
Known hypersensitivity — discontinue use if allergic reactions occur (rash, hives, difficulty breathing).

When to Stop or Reduce Dose

Persistent GI discomfort that does not resolve within the first week of oral use
Any signs of allergic reaction (rash, hives, swelling, difficulty breathing)
Worsening of the underlying condition despite 4+ weeks of consistent use
Development of new infections while on KPV — consult a healthcare provider about whether to continue
Any symptom that feels unusual or concerning — err on the side of caution

Regulatory Status: KPV is not FDA-approved for human use. It is classified as a research peptide. In some jurisdictions it is available as a dietary supplement or wellness product due to its tripeptide nature. Regulations vary significantly by country and state — verify your local laws before purchasing.

Common KPV Dosing Mistakes

Avoid these common errors to get the most out of your KPV protocol:

Expecting melanocortin effects (tanning, libido, appetite changes): KPV is derived from alpha-MSH but does NOT activate melanocortin receptors. It works through direct NF-κB inhibition — a completely different mechanism. Do not confuse it with MT-II or other melanocortin agonists. KPV is purely anti-inflammatory with no tanning, sexual, or appetite effects.

Using injectable doses for oral administration (or vice versa): Oral and subcutaneous bioavailability are different. Oral doses are typically higher (200–500 mcg) to compensate for reduced GI absorption, while subcutaneous doses can be lower (100–500 mcg) due to direct systemic delivery. Do not assume the same dose applies to both routes.

Stopping too early before effects develop: KPV’s anti-inflammatory effects build over time as NF-κB inhibition reduces chronic cytokine production. Gut inflammation improvements typically take 1–2 weeks, and full benefits for IBD may require 4–8 weeks. Do not abandon the protocol after a few days if symptoms have not yet resolved.

Using KPV alone for severe IBD without medical supervision: While KPV shows promise for gut inflammation in preclinical models, severe IBD (Crohn’s disease, ulcerative colitis) requires proper medical management. KPV should complement — not replace — evidence-based treatments prescribed by a gastroenterologist. Never discontinue prescribed medications in favor of a research peptide.

Not storing reconstituted KPV properly: Like all reconstituted peptides, KPV solution should be stored refrigerated (2–8°C) and used within 3–4 weeks. Do not leave reconstituted vials at room temperature or expose them to direct light. Use bacteriostatic water for reconstitution to prevent bacterial growth.

Taking oral KPV with a large meal: While KPV does not require the strict fasting protocols of GH-releasing peptides, taking it with a large meal increases exposure to digestive enzymes and dilutes concentration in the GI tract. Take oral KPV on an empty stomach or at least 30 minutes before eating for optimal gut contact.

Assuming oral bioavailability equals injectable bioavailability: Even though KPV’s tripeptide size allows some oral absorption, subcutaneous injection still provides more reliable and complete systemic delivery. If targeting systemic inflammation (not gut-specific), subcutaneous injection is the preferred route. Use oral for gut-targeted protocols.

Confusing KPV with full-length alpha-MSH: KPV (Lys-Pro-Val) is only the minimal anti-inflammatory fragment of alpha-MSH. Full-length alpha-MSH activates melanocortin receptors and has broad hormonal effects. KPV retains ONLY the anti-inflammatory activity (NF-κB inhibition) without the melanocortin receptor activation. They are not interchangeable.

Frequently Asked Questions

Key Takeaways

KPV (Lys-Pro-Val) is the minimal anti-inflammatory fragment of α-MSH — it works through direct NF-κB pathway inhibition, NOT melanocortin receptor activation
No tanning, sexual, or appetite effects — KPV is purely anti-inflammatory; do not confuse it with MT-II or other melanocortin agonists
Oral dosing is viable and most popular: 200–500 mcg, 1–2x daily on an empty stomach — the tripeptide size allows some GI absorption (unusual for peptides)
SubQ for systemic effects: 100–500 mcg daily provides the most reliable systemic anti-inflammatory delivery
Topical for skin conditions: apply directly to affected areas 1–2x daily for localized dermatitis, eczema, or psoriasis
Match the route to the target: oral for gut, SubQ for systemic, topical for skin
Gold standard stack: KPV + BPC-157 for gut inflammation and IBD (NF-κB inhibition + mucosal repair)
Cycling: 4–8 weeks recommended — lower desensitization risk than GHRPs, but cycling is still best practice for reassessment
Very mild side effect profile — rare GI discomfort (oral), rare injection site reactions (SubQ), no hormonal effects, no known tolerance
Not FDA-approved — classified as a research peptide. Good preclinical data (animal IBD models) but limited human clinical data. Consult a healthcare provider.

This article is for educational and informational purposes only. See our Disclaimer.

References

Dalmasso G, et al. “PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation.” Gastroenterology. 2008;134(1):166-178. PubMed
Kannengiesser K, et al. “Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease.” Inflamm Bowel Dis. 2008;14(3):324-331. PubMed
Brzoska T, et al. “Alpha-melanocyte-stimulating hormone and related tripeptides: biochemistry, antiinflammatory and protective effects in vitro and in vivo, and future perspectives for the treatment of immune-mediated inflammatory diseases.” Endocr Rev. 2008;29(5):581-602. PubMed
Luger TA, et al. “New insights into the functions of alpha-MSH and related peptides in the immune system.” Ann N Y Acad Sci. 2003;994:133-140. PubMed
Getting SJ, et al. “Molecular determinants of the anti-inflammatory actions of the melanocortin peptides.” Pharmacol Ther. 2006;111(1):1-15. PubMed
Ichiyama T, et al. “Alpha-melanocyte-stimulating hormone inhibits NF-kappaB activation and IkappaBalpha degradation in human glioma cells and in experimental brain inflammation.” Exp Neurol. 1999;157(2):359-365. PubMed
Mandrika I, et al. “Effects of melanocortin peptides on lipopolysaccharide/ interferon-gamma-induced NF-kappaB DNA binding and nitric oxide production.” Peptides. 2001;22(9):1553-1559. PubMed
Capsoni F, et al. “Effect of alpha-MSH on human monocyte and neutrophil activation.” J Leukoc Biol. 2007;81(3):845-855.
Dalmasso G, et al. “Saccharomyces boulardii inhibits inflammatory bowel disease by trapping T cells in mesenteric lymph nodes.” Gastroenterology. 2006;131(6):1812-1825. PubMed

Next Steps

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