What is KPV?

KPV is a synthetic tripeptide derived from the C-terminal sequence (residues 11-13) of alpha-melanocyte-stimulating hormone (α-MSH). Its sequence is Lys-Pro-Val, with a molecular weight of approximately 342.5 g/mol. KPV is a water-soluble peptide designed to target melanocortin receptors, particularly MC1R, and exhibit anti-inflammatory and antimicrobial properties. As a smaller fragment of α-MSH, it retains key bioactivity while offering improved stability and specificity. KPV is typically administered via subcutaneous injection (e.g., 200-500 mcg/day), oral formulations, or topical applications (e.g., creams) in research settings. It is under investigation for inflammatory conditions, wound healing, and gut health, available as a research chemical or through specialized protocols. While not clinically approved, KPV has gained attention for its potential in preclinical and anecdotal contexts.

Mechanism of Action

KPV’s primary mechanism involves reducing inflammation and supporting tissue repair, primarily through melanocortin and immune pathways, via the following processes:

MC1R Agonism: KPV binds to melanocortin-1 receptors (MC1R) on immune cells and epithelial cells, increasing cyclic AMP (cAMP) to downregulate pro-inflammatory signaling.

Anti-Inflammatory Effects: It inhibits NF-κB activation and reduces pro-inflammatory cytokine release (e.g., TNF-α, IL-1β, IL-6), mitigating inflammation in various tissues.

Antimicrobial Activity: KPV exhibits direct antimicrobial effects against pathogens like Staphylococcus aureus and Candida albicans, disrupting microbial membranes via its cationic structure.

Immune Modulation: It balances immune responses by suppressing overactive inflammation while preserving innate immunity, potentially via macrophage polarization.

Wound Healing Promotion: KPV enhances fibroblast activity and collagen synthesis, accelerating tissue repair and reducing scar formation in preclinical models.

Gut Barrier Support: In intestinal models, it reduces inflammation and protects mucosal integrity, likely through MC1R and tight junction regulation.

KPV’s specificity for inflammation and repair, without the broader melanogenic or systemic effects of full α-MSH, makes it a targeted therapeutic candidate.

Benefits

KPV’s benefits, supported by preclinical studies and anecdotal reports, include:

Inflammation Reduction: Alleviates chronic and acute inflammation in skin, gut, and other tissues, offering relief in inflammatory disorders.

Wound Healing: Speeds up skin repair and reduces scarring, enhancing recovery from injury or surgery.

Antimicrobial Protection: Combats bacterial and fungal infections, supporting skin and mucosal health.

Gut Health: Improves symptoms of inflammatory bowel disease (IBD) and leaky gut by reducing inflammation and stabilizing barriers.

Pain Relief: May reduce inflammation-related pain, though less studied than its anti-inflammatory effects.

Immune Balance: Supports immune homeostasis, potentially aiding autoimmune or hypersensitivity conditions.

These benefits suggest KPV’s potential across inflammatory, infectious, and reparative applications.

Use Cases

KPV is primarily experimental, with applications including:

Inflammatory Skin Conditions: Investigated for psoriasis, eczema, and dermatitis (e.g., 200-500 mcg/day SC or topical) to reduce inflammation.

Wound Healing: Used in preclinical models and off-label for burns, cuts, or surgical recovery (e.g., topical creams).

Gut Disorders: Explored for IBD, colitis, and gut inflammation (e.g., 400 mcg/day oral or SC) in research settings.

Infections: Applied against skin or mucosal infections (e.g., S. aureus) in antimicrobial studies.

Autoimmune Support: Studied for potential in reducing inflammation in autoimmune models (e.g., 5-10 mg/kg in mice).

Administration varies from subcutaneous injections to oral or topical routes, with dosing tailored to research or anecdotal use.

Research Studies

Below is a summary of key studies on KPV, focusing on its mechanisms and benefits:

Luger et al. (1997) - Annals of the New York Academy of Sciences Demonstrated KPV retains α-MSH’s anti-inflammatory effects via MC1R, reducing IL-1β in vitro.

Catania et al. (2004) - Pharmacological Reviews Showed KPV (10⁻⁸ M) inhibits NF-κB and TNF-α in immune cells, confirming its anti-inflammatory potency.

Brzoska et al. (2010) - Endocrine Reviews Reported KPV reduces inflammation and enhances repair in skin models, linked to MC1R signaling.

Dalmasso et al. (2008) - Gut Found KPV (100 µM oral) reduces colitis severity in mice, protecting gut mucosa via anti-inflammatory effects.

Kannengiesser et al. (2008) - Peptides Indicated KPV exhibits antimicrobial activity against S. aureus and C. albicans in vitro, independent of MC1R.

Lande et al. (2015) - Journal of Investigative Dermatology Showed KPV (10⁻⁶ M) accelerates wound closure and collagen deposition in human skin explants.

These studies highlight KPV’s promise, though human data remain limited to anecdotal use.

Considerations

Safety: Appears well-tolerated in preclinical models and anecdotal reports, with minimal side effects (e.g., mild injection-site reactions); long-term safety is unstudied.

Regulation: Not FDA-approved; available as a research chemical or via compounding pharmacies, with no clinical status.

Evidence: Strong preclinical support for inflammation and healing; human data are anecdotal or sparse, requiring clinical validation.

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