Palmetto Peptides Guide to the Research Peptide KPV

Palmetto Peptides Research Team

April 19, 2026

kpvtripeptideanti-inflammatoryresearch-peptide

Research Notice: This article covers research on KPV research peptide and GHK-KPV research peptide — available from Palmetto Peptides for laboratory use only.

title: "Palmetto Peptides Guide to the Research Peptide KPV"

meta_title: "KPV Peptide: Complete Research Guide | Palmetto Peptides"

meta_description: "The definitive research guide to KPV (Lys-Pro-Val): mechanism of action, NF-κB pathway, murine colitis models, oral delivery systems, purity standards, and lab protocols. For research use only."

last_updated: "2025-01-15"

author: "Palmetto Peptides Research Team"

schema: "Article, FAQPage"

Research Disclaimer: KPV is sold exclusively for in vitro and laboratory research purposes. It is not approved for human or veterinary use, is not a dietary supplement, and is not intended to diagnose, treat, cure, or prevent any condition. All information presented here is for scientific and educational purposes only. Researchers should comply with all applicable institutional, local, and federal regulations governing research peptide use.

Last Updated: January 15, 2025

KPV (Lys-Pro-Val) is a synthetic tripeptide derived from the C-terminal sequence of alpha-melanocyte-stimulating hormone (alpha-MSH) that has been studied in preclinical research for its effects on NF-κB-mediated inflammatory signaling, intestinal epithelial models, and oral bioavailability via the PepT1 transporter. It is available for laboratory and in vitro research purposes.

This guide covers everything a researcher needs to know about KPV — from its molecular structure and mechanism to delivery systems, lab protocols, and sourcing standards. Whether you are designing a new in vitro assay, reviewing the colitis model literature, or evaluating KPV as a research tool alongside other peptides, this reference compiles the core science in one place.

Order KPV Research Peptide from Palmetto Peptides

[What Is KPV?](#what-is-kpv)
[KPV Chemical Structure and Properties](#kpv-chemical-structure-and-properties)
[How KPV Works: NF-κB Pathway Modulation](#how-kpv-works-nfkb-pathway-modulation)
[PepT1 Transporter and Oral Uptake Research](#pept1-transporter-and-oral-uptake-research)
[KPV in Murine Colitis Models](#kpv-in-murine-colitis-models)
[KPV Wound Healing and Tissue Repair Research](#kpv-wound-healing-and-tissue-repair-research)
[KPV Antimicrobial Properties: In Vitro Evidence](#kpv-antimicrobial-properties-in-vitro-evidence)
[KPV Oral Delivery Systems and Nanoparticle Research](#kpv-oral-delivery-systems-and-nanoparticle-research)
[KPV vs. Alpha-MSH: Research Comparison](#kpv-vs-alpha-msh-research-comparison)
[KPV vs. Other Research Peptides](#kpv-vs-other-research-peptides)
[Purity Standards and What to Look for in a Supplier](#purity-standards-and-what-to-look-for-in-a-supplier)
[Storage, Reconstitution, and Lab Handling](#storage-reconstitution-and-lab-handling)
[Animal Model Protocols](#animal-model-protocols)
[Frequently Asked Questions](#frequently-asked-questions)
[Citations](#citations)

What Is KPV?

KPV is the three-amino-acid sequence Lysine-Proline-Valine, corresponding to residues 11, 12, and 13 of alpha-melanocyte-stimulating hormone (alpha-MSH). The peptide came under research interest after investigators discovered that the C-terminal tripeptide fragment of alpha-MSH retained meaningful anti-inflammatory activity in cell culture models, independent of the melanocortin receptor (MCR) signaling pathway that drives alpha-MSH's broader biological effects.

In plain terms: alpha-MSH is a 13-amino-acid hormone produced naturally in the body. Its last three amino acids — KPV — appear to carry a distinct functional profile that can be studied on its own. That separation matters for researchers because KPV does not significantly engage the MCR family of receptors responsible for pigmentation and a range of other systemic effects, which makes it a cleaner tool for isolating certain inflammatory signaling questions.

The scientific interest in KPV has been concentrated in a few areas:

Intestinal inflammation research, particularly in DSS (dextran sodium sulfate) and TNBS (trinitrobenzenesulfonic acid) colitis models in mice
NF-κB pathway studies in intestinal epithelial cell lines and macrophages
Oral delivery research leveraging the PepT1 transporter expressed in intestinal epithelium
Wound healing and epithelial restitution assays
Antimicrobial in vitro assays

KPV is available as a lyophilized white powder for research use. It is not a drug, supplement, or therapeutic agent.

View KPV Research Peptide at Palmetto Peptides

KPV Chemical Structure and Properties

Understanding what you are working with chemically is the first step for any rigorous research application. Here is a reference summary of KPV's core chemical identity:

Property	Value
Full name	Lysyl-Prolyl-Valine
CAS number	69079-94-3
Molecular formula	C16H31N5O4
Molecular weight	357.45 g/mol
Sequence	H-Lys-Pro-Val-OH
Stereochemistry	L-Lys, L-Pro, L-Val
Appearance	White lyophilized powder
Solubility	Aqueous (water, 0.1% acetic acid); limited in DMSO
Storage (lyophilized)	-20°C to -80°C, desiccated, away from light

Amino acid residue roles explained simply:

Lysine (Lys) is a positively charged amino acid that contributes to the peptide's water solubility and is believed to play a role in its antimicrobial membrane interactions. Proline (Pro) is a rigid, cyclic amino acid that constrains the peptide's shape and contributes to its metabolic stability — this structural rigidity is part of why KPV resists rapid enzymatic degradation compared to more flexible peptides. Valine (Val) is a hydrophobic amino acid that likely contributes to how KPV interacts with lipid-containing structures like bacterial membranes and cell surfaces.

KPV is synthesized using solid-phase peptide synthesis (SPPS), either Fmoc (9-fluorenylmethyloxycarbonyl) or Boc (tert-butyloxycarbonyl) chemistry. Research-grade material is purified by reverse-phase high-performance liquid chromatography (RP-HPLC) and confirmed by LC-MS or MALDI-TOF mass spectrometry. For cell culture and in vivo models, 98%+ purity is the standard required to generate reliable, reproducible data.

For a full deep dive into KPV synthesis and characterization methods, see: KPV Tripeptide Chemical Structure and Synthesis

How KPV Works: NF-κB Pathway Modulation

The primary mechanism under investigation for KPV is its apparent ability to modulate the NF-κB signaling pathway inside cells, independent of surface receptor binding. This is the molecular explanation that researchers point to when describing KPV's anti-inflammatory activity in cell culture models.

What is NF-κB? (Layman's explanation)

NF-κB stands for Nuclear Factor kappa-light-chain-enhancer of activated B cells. That name is a mouthful, but the concept is straightforward: NF-κB is a protein complex that acts like an alarm system inside cells. When a cell detects a threat — a bacterial signal, a pro-inflammatory cytokine, physical damage — NF-κB gets activated. Once active, it moves from the cytoplasm (the general interior of the cell) into the nucleus (where genetic instructions are stored) and turns on genes that produce inflammatory proteins like TNF-alpha, IL-6, IL-1beta, and interferon-gamma. These are the proteins that drive inflammation.

Normally, NF-κB is kept inactive by a protective protein called IκB. An enzyme complex called IKK (IκB kinase) can tag IκB for destruction. Once IκB is broken down, NF-κB is free to move into the nucleus and start the inflammatory cascade.

Where KPV appears to act in this pathway:

In vitro studies using intestinal epithelial cell lines (IEC-6, HT-29, Caco-2) and macrophage models (RAW264.7) suggest that KPV interferes with this cascade at the IKK step. When cells pre-treated with KPV are challenged with a pro-inflammatory stimulus, researchers have observed:

Reduced IKK activity
Preserved IκB levels (less degradation)
Lower levels of NF-κB's p65 subunit found in the nucleus
Downstream reduction in TNF-alpha, IL-6, IL-1beta, and IFN-gamma expression

The key observation that distinguishes KPV from alpha-MSH mechanistically is that KPV appears to act intracellularly rather than through surface receptor binding. Alpha-MSH modulates NF-κB partly through MC1R and MC3R receptor engagement, which triggers intracellular cAMP signaling. KPV does not show meaningful MC receptor binding affinity. Researchers have added MC receptor antagonists to cell culture models alongside KPV and found no reduction in KPV's effects, supporting the theory that KPV works through a receptor-independent intracellular route.

NF-κB pathway summary — simplified:

It is important to note that all of this evidence comes from cell culture experiments. NF-κB pathway biology is extremely well-characterized, but KPV's precise binding partners, intracellular localization, and dose-response kinetics in different cell types remain active areas of investigation.

For the full mechanistic deep dive, see: KPV and NF-κB Pathway Modulation: In Vitro Evidence

PepT1 Transporter and Oral Uptake Research

One of the reasons KPV has attracted attention beyond standard injectable peptide research is its relationship with the PepT1 transporter — a mechanism that could make oral delivery viable in ways that most peptides are not.

What is PepT1? (Layman's explanation)

PepT1 (also called SLC15A1) is a protein channel found primarily in the cells lining the small intestine. Its job is to pull small peptides — specifically di- and tripeptides — from the gut into the bloodstream. The body evolved this transporter because digesting proteins produces huge numbers of two- and three-amino-acid fragments, and absorbing them efficiently is nutritionally important.

KPV, as a tripeptide, fits the structural profile that PepT1 recognizes. This is unusual in peptide research — most larger peptides are broken down or poorly absorbed orally, which is why injectable delivery is standard. KPV's small size and proline-constrained rigidity appear to make it a PepT1 substrate.

What the research shows:

Caco-2 cell monolayers (a standard lab model for intestinal epithelial absorption) have been used to characterize KPV uptake. Studies have found that KPV transport across these monolayers is:

pH-dependent: Uptake increases under mildly acidic conditions consistent with the intestinal lumen environment
Saturable: At higher concentrations, transport rate levels off, consistent with a carrier-mediated (not simple diffusion) mechanism
Competitively inhibitable: Adding known PepT1 substrates reduces KPV uptake, suggesting they compete for the same transporter

A particularly interesting finding for colitis research is that PepT1 expression is normally very low in the colon. However, in inflamed colonic tissue, PepT1 expression appears to increase significantly — which has led researchers to theorize that colonic KPV uptake may be preferentially enhanced in the inflammatory context where researchers want activity.

This PepT1 biology has also driven much of the interest in nanoparticle encapsulation research, with hyaluronic acid (HA) functionalization used to add CD44-receptor targeting on top of PepT1-mediated transport, improving delivery specificity in inflamed tissue models.

For the full transporter research review, see: KPV and PepT1 Transporter Uptake: In Vitro Evidence

KPV in Murine Colitis Models

The most substantial body of preclinical research on KPV involves murine colitis models. Researchers have evaluated KPV across both DSS (dextran sodium sulfate) and TNBS (trinitrobenzenesulfonic acid) colitis induction protocols in mice, using multiple delivery routes.

Colitis model overview:

Model	Induction method	Primary research use
DSS colitis	Oral DSS administration; disrupts mucosal barrier	Acute and chronic colitis; epithelial damage
TNBS colitis	Intracolonic TNBS/ethanol instillation	T-cell mediated immune response; Crohn's-like

Summary of KPV findings in murine models:

Across the published literature, KPV administration in colitis models has been associated with measurable changes in several standard readout parameters:

Disease Activity Index (DAI): A composite score tracking weight loss, stool consistency, and fecal blood. Lower DAI scores have been observed in KPV-treated animals compared to untreated colitis controls.
Colon histology: Histological sections from KPV-treated animals have shown reduced crypt loss, better epithelial continuity, and lower immune cell infiltration scores versus controls in multiple studies.
Myeloperoxidase (MPO) activity: MPO is an enzyme released by neutrophils and is used as a proxy for intestinal inflammation severity. KPV-treated animals have shown reduced colonic MPO activity in DSS models.
Cytokine profiles: Tissue cytokine measurements from colonic samples have shown reduced TNF-alpha, IL-6, and IL-1beta in KPV treatment arms, consistent with the NF-κB mechanism.

Delivery method matters:

One of the practical lessons from the murine model research is that how KPV is delivered significantly affects outcomes. Oral free KPV shows limited effect in some models, while nanoparticle-encapsulated KPV designed for colonic targeting has shown stronger activity — likely due to the protection from gastric degradation and the enhanced delivery to inflamed colonic epithelium that nanoparticle carriers provide.

Intracolonic (IC) instillation delivers KPV directly to the affected tissue and bypasses oral stability concerns, making it a cleaner tool for mechanistic studies even if it is less translationally relevant than oral delivery.

For full model details, dosing protocols, and study comparison tables, see: KPV in Murine Colitis Models: Research Summary

KPV Wound Healing and Tissue Repair Research

Beyond the colitis model literature, KPV has been evaluated in wound healing and epithelial repair assay contexts. This research largely connects back to the same NF-κB suppression mechanism — in wound environments, excessive inflammatory signaling can impair the organized cellular migration and tissue deposition needed for efficient healing.

Intestinal epithelial restitution research:

The primary wound healing context for KPV is intestinal epithelial restitution — the process by which intestinal epithelial cells migrate to cover areas where the epithelial barrier has been disrupted. Scratch assay models (where a defined scratch is made in a cell monolayer and closure rate is measured over time) have been used to evaluate whether KPV treatment affects migration rate and barrier recovery.

Skin and keratinocyte models:

KPV has also been evaluated in keratinocyte (skin epithelial cell) wound models. UV-irradiation models and scratch assays using primary keratinocytes and keratinocyte cell lines have shown effects on migration and inflammatory marker expression consistent with the broader NF-κB evidence base.

Fibroblast and collagen considerations:

Some wound healing research adjacent to KPV involves the comparison with GHK-Cu, a peptide with established collagen synthesis-promoting activity. KPV's mechanism is distinct — it does not appear to directly promote collagen synthesis the way GHK-Cu does. Instead, the research interest is in whether suppressing the inflammatory microenvironment creates conditions more conducive to normal repair processes. These are complementary rather than overlapping research questions.

For the full review of wound healing assay methods and findings, see: KPV in Wound Healing and Tissue Repair Research Models

KPV Antimicrobial Properties: In Vitro Evidence

A separate but growing line of KPV research addresses its antimicrobial activity. This is structurally logical given KPV's sequence: the positively charged lysine residue and the proline-constrained backbone are features shared by many known antimicrobial peptides (AMPs), which disrupt bacterial membranes through charge-mediated interactions.

What in vitro antimicrobial assays measure:

Assay type	What it measures
Minimum Inhibitory Concentration (MIC)	Lowest concentration that visibly inhibits growth
Minimum Bactericidal Concentration (MBC)	Lowest concentration that kills 99.9% of organisms
Time-kill assay	How rapidly killing occurs at a given concentration
Membrane integrity assay	Whether membrane disruption is the kill mechanism

Organisms tested in published research:

KPV has been evaluated against a range of organisms in cell-free in vitro assays including gram-positive bacteria (Staphylococcus aureus), gram-negative bacteria (Escherichia coli), and fungal organisms (Candida albicans). The cyclic CKPV analog has also been investigated, with structural constraints that may enhance membrane interaction compared to the linear KPV sequence.

Important context: in vitro antimicrobial activity against isolated organisms does not predict efficacy in complex biological environments. Serum proteins, competing microbiota, and biofilm formation all affect how antimicrobial peptides perform outside controlled lab conditions.

For MIC/MBC data tables and full assay methodology, see: KPV Antimicrobial Properties: In Vitro Evidence Review

KPV Oral Delivery Systems and Nanoparticle Research

The structural compatibility with PepT1-mediated transport has made KPV a model peptide for oral delivery system development. A substantial portion of the KPV literature is not about the peptide's biological activity per se, but about testing nanoparticle and hydrogel encapsulation strategies that improve its delivery to colonic tissue.

Why encapsulation matters:

Free peptides face three challenges in oral delivery: (1) acid and enzyme degradation in the stomach and small intestine, (2) rapid clearance before reaching target tissue, and (3) limited targeting to inflamed versus healthy tissue. Encapsulation addresses all three.

Delivery system comparison:

Delivery system	Key feature	Research context
HA-functionalized PLGA nanoparticles	CD44 targeting + PepT1 uptake	Colitis model oral delivery; most published data
Chitosan hydrogels	Mucoadhesive; pH-responsive	Colonic retention; direct instillation models
Plant-derived nanoparticles (GDNPs)	Ginger-derived exosome-like	Oral delivery with natural colonic uptake
ROS-responsive hydrogels	Release triggered by oxidative stress	Targeted release in inflamed tissue specifically
Self-assembling peptide nanostructures	Intrinsic biocompatibility	Emerging platform; reduced polymer concerns

Hyaluronic acid (HA) coating is particularly well-studied because inflamed intestinal epithelium overexpresses CD44, the HA receptor. This means HA-coated nanoparticles bind preferentially to inflamed tissue rather than distributing nonspecifically — a meaningful targeting advantage for colitis research models.

For the full delivery system comparison and 2025 technology review, see:

KPV vs. Alpha-MSH: Research Comparison

KPV and alpha-MSH are closely related but functionally distinct in ways that matter for experimental design.

Feature	Alpha-MSH	KPV
Size	13 amino acids	3 amino acids
Receptor binding	MC1R, MC3R, MC4R, MC5R	Minimal/none detected
Primary mechanism	MCR-cAMP-PKA signaling	Intracellular NF-κB modulation
Oral stability	Poor (enzymatic degradation)	Better (PepT1 substrate, proline stability)
PepT1 uptake	Not demonstrated	Demonstrated in Caco-2 models
Pigmentation effects	Yes (MC1R-mediated)	Not observed
Colitis model literature	Yes	Yes (growing)
Research use case	Broader melanocortin biology	Intestinal inflammation focus

The practical implication: if a researcher wants to study melanocortin receptor biology, alpha-MSH is the appropriate tool. If the research question is specifically about NF-κB-mediated intestinal inflammatory signaling with an orally deliverable peptide, KPV's cleaner receptor profile and PepT1 compatibility make it a distinct and often preferable research tool.

For the full structural and pharmacological comparison, see: KPV vs. Alpha-MSH: Research Comparison

KPV vs. Other Research Peptides

Researchers designing experiments often need to decide between several peptides with overlapping or related research profiles. Here is how KPV compares to commonly co-evaluated peptides in the Palmetto Peptides catalog:

Feature	KPV	BPC-157	TB-500	GHK-Cu	Selank
Primary mechanism	NF-κB modulation	Angiogenesis/GI mucosal repair	Actin sequestration (Tβ4)	Copper-mediated collagen synthesis	Immunomodulation/neuropeptide
Size	Tripeptide	15 aa	Tetrapeptide (Tβ4 fragment)	Tripeptide (copper complex)	Heptapeptide
Primary research area	Intestinal inflammation	GI/systemic tissue repair	Tissue repair, actin dynamics	Wound healing/skin models	Anxiety/immune/cognitive models
Oral delivery research	Yes (PepT1)	Orally active in murine models	Limited	Limited	Limited
Colitis model data	Yes	Yes	Limited	No	No
Receptor mechanism	Receptor-independent	Growth factor-mediated	Actin-G-actin equilibrium	Copper-dependent signaling	GABA/serotonin/immune

Research pairing considerations:

KPV and BPC-157 represent complementary tools in GI research — KPV focuses on the NF-κB-mediated inflammatory component while BPC-157 has a broader mucosal repair and angiogenesis profile. Researchers studying both pathways independently may include both in a study design to dissect which contributes more to observed outcomes.

KPV and GHK-Cu both address inflammatory environments but through mechanistically distinct pathways. GHK-Cu promotes collagen remodeling; KPV addresses upstream inflammatory signaling. In wound healing models, these functions can be studied in parallel.

Explore related research peptides:

For the full comparative analysis, see: KPV vs. Other Research Peptides: Comparison Guide

Purity Standards and What to Look for in a Supplier

For any experiment using KPV, the quality of the peptide directly determines the reliability of the results. This section outlines what research-grade KPV should look like and what to verify before placing an order.

Minimum standards for research-grade KPV:

Requirement	Standard
HPLC purity	98%+ for cell culture and in vivo use
Identity confirmation	LC-MS or MALDI-TOF matching theoretical MW (357.45 Da)
Counterion	Acetate preferred for biological assays (TFA can affect cell viability)
Endotoxin testing	LAL test; critical for in vivo models (endotoxin confounds inflammation readouts)
Lot number	Required for methods section reproducibility
Certificate of Analysis	Available per lot with analytical data

What to avoid:

Suppliers who list purity without providing the underlying HPLC chromatogram
Material sold at prices significantly below market (5mg of 98%+ purity KPV should cost $30-80 from a legitimate supplier)
Vague documentation, no lot traceability, or CoAs with suspicious round-number purity values
TFA salt form for biological assays without documented TFA removal

At Palmetto Peptides, every lot of KPV ships with a full Certificate of Analysis including HPLC trace and MS confirmation. We do not sell sub-98% material for research use.

View KPV Documentation Standards at Palmetto Peptides

For the full purity guide and supplier evaluation checklist, see: KPV Purity Standards and Third-Party Testing Guide

Storage, Reconstitution, and Lab Handling

Proper handling is the difference between reliable assay results and data that cannot be reproduced. Here are the key guidelines for KPV in a research laboratory setting.

Storage summary:

Form	Recommended temperature	Estimated stability
Lyophilized, sealed	-20°C	2+ years
Lyophilized, sealed	-80°C	5+ years
Reconstituted in sterile water	-20°C	3-6 months (3 freeze-thaw max)
Reconstituted in 0.1% AcOH	-20°C	6-12 months
In aqueous solution at 4°C	Refrigerator	1-2 weeks

Reconstitution quick guide:

Bring the vial to room temperature before opening to prevent moisture condensation on the peptide
Use sterile water or 0.1% acetic acid for aqueous stock solutions (PBS is acceptable for short-term use; avoid PBS for long-term storage due to salt crystallization during freeze-thaw)
Add solvent slowly down the side of the vial; do not inject directly onto the lyophilized cake
Gently swirl or pipette to mix; do not vortex vigorously
Target a stock concentration of 1 mg/mL unless the assay protocol specifies otherwise
Aliquot into single-use volumes to minimize freeze-thaw cycles
Label with: peptide name, lot number, concentration, solvent, date reconstituted
Store at -20°C; use within 3-6 months

Concentration reference (MW 357.45 g/mol):

Stock concentration	Molar equivalent
1 mg/mL	~2.80 mM
0.5 mg/mL	~1.40 mM
0.1 mg/mL	~280 µM
0.01 mg/mL	~28 µM

For the complete reconstitution protocol and freeze-thaw guidance, see: KPV Storage, Reconstitution, and Lab Handling Guidelines

Animal Model Protocols

Researchers using KPV in murine colitis models should have clear protocols for reconstitution, dose calculation, and delivery. This section provides a working reference.

Administration route selection:

Route	Research use case	Notes
Oral gavage (PO)	Oral bioavailability and delivery system studies	Most translationally relevant for oral delivery research
Intracolonic instillation (IC)	Direct colonic tissue delivery; mechanistic clarity	Bypasses oral stability variables
Intraperitoneal injection (IP)	Systemic exposure; faster absorption	Less common for KPV; used in some alpha-MSH studies
Subcutaneous (SC)	Sustained release or depot models	Less published data for KPV specifically

Dose calculation example:

To prepare a 1 mg/kg dose for a 25g mouse using a 1 mg/mL KPV stock:

For oral gavage in mice, a typical volume is 100-200 µL. If the calculated volume is too small for accurate delivery, dilute the stock further and recalculate.

Common doses in the murine literature: Most published KPV studies in colitis models have used doses ranging from 0.5 to 10 mg/kg. Intracolonic instillation volumes are typically limited to 100-150 µL in mice to avoid reflux.

All animal research using KPV or any research peptide requires IACUC approval and must comply with institutional and federal animal welfare regulations.

For full protocol tables and step-by-step administration guides, see: KPV Animal Model Reconstitution and Administration Protocols

Frequently Asked Questions

Citations

Dalmasso G, et al. "The PepT1 oligopeptide transporter induces inflammatory signaling in the intestinal epithelium." *Cellular and Molecular Life Sciences.* 2011;68(11):1923-1934.

Kannengiesser K, et al. "Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of experimental colitis." *Inflammatory Bowel Diseases.* 2008;14(3):324-331.

Hartmann RM, et al. "KPV (alpha-melanocyte-stimulating hormone tripeptide) downregulates TNF-alpha-induced NF-κB signaling in intestinal epithelial cells." *Peptides.* 2020;127:170298.

Laroui H, et al. "Targeting intestinal inflammation with CD98 siRNA/PEI-loaded nanoparticles." *Biomaterials.* 2014;35(5):1790-1800.

Vong LB, et al. "Orally administered redox nanoparticles for the treatment of DSS-induced colitis in mice." *Biomaterials.* 2012;33(9):2647-2655.

Brzoska T, et al. "Alpha-melanocyte-stimulating hormone and related tripeptides: biochemistry, anti-inflammatory, and protective effects in vitro and in vivo, and future perspectives for the treatment of immune-mediated inflammatory diseases." *Endocrine Reviews.* 2008;29(5):581-602.

Gonscherowski V, et al. "Melanocortin receptor agonism mediates anti-inflammatory effects of the melanocortin tripeptide Lys-Pro-Val." *Journal of Dermatological Science.* 2005;40(3):211-217.

Smalley SG, et al. "Oligopeptide transport by PepT1 in Caco-2 cell monolayers: evidence for a pH-dependent proton-coupled mechanism." *Journal of Pharmacy and Pharmacology.* 1995;47(7):562-567.

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This article was written and reviewed by the Palmetto Peptides Research Team. All content is intended for scientific and educational purposes only. KPV is sold for laboratory research use only and is not approved for human or veterinary administration.

Author: Palmetto Peptides Research Team