KPV is a tripeptide made of lysine, proline, and valine that corresponds to the C-terminal fragment of α-melanocyte-stimulating hormone (α-MSH), specifically residues 11–13. It has been investigated since the 1990s as the minimal anti-inflammatory fragment of α-MSH. It is not FDA-approved.

KPV is taken up by cells through the PepT1 di/tripeptide transporter, which is expressed on intestinal epithelial cells and immune cells. Unlike full-length α-MSH, KPV does not bind the melanocortin receptors MC1R, MC3R, or MC5R and does not compete with α-MSH at those receptors — its activity is not melanocortin-receptor-mediated. Intracellularly, nanomolar concentrations of KPV inhibit activation of the NF-κB and MAP kinase inflammatory signaling pathways and reduce pro-inflammatory cytokine secretion.

What is the half-life of KPV?

A specific, peer-reviewed human elimination half-life for KPV is not established. Published reviews of anti-inflammatory peptides identify human pharmacokinetics — including plasma half-life and clearance — as a critical barrier to clinical translation for KPV. Available evidence is preclinical, and no registered human clinical trials have been reported to date.

How do I reconstitute a 10 mg KPV vial?

For 10 mg of lyophilized KPV reconstituted with 2 mL of bacteriostatic water, the concentration is 5 mg/mL. On a 100-unit insulin syringe, 1 unit equals 0.01 mL = 50 mcg of KPV. A 250 mcg amount equals 5 units; 500 mcg equals 10 units; 1 mg equals 20 units. Using 1 mL of bacteriostatic water gives 10 mg/mL (100 mcg per unit); using 5 mL gives 2 mg/mL (20 mcg per unit). The reconstitution volume is a concentration choice; it does not change the total mass in the vial.

No. KPV is a research peptide and is not approved by the FDA for any clinical indication. In the FDA's April 15, 2026 503A categories update, KPV was slated for removal from Category 2 after seven calendar days because the nomination was withdrawn, with FDA intending to consult the Pharmacy Compounding Advisory Committee (PCAC) on KPV-related bulk drug substances (KPV free base / acetate) on July 23, 2026. Removal from Category 2 does not itself authorize compounding; PCAC must review inclusion on the 503A bulks list.

Is KPV given orally or by injection?

Both routes have been studied preclinically. Because KPV is small enough to be taken up by the PepT1 transporter in the intestinal epithelium, oral administration has been explored in animal models — including orally targeted nanoparticle formulations that deliver KPV to inflamed colonic tissue in DSS- and TNBS-induced colitis models. Injectable routes are also used in research-vendor preparations. No route is FDA-approved for clinical use.

Anti-inflammatory tripeptide · research peptide

KPV (Lys-Pro-Val)

Studied for: anti-inflammatory signaling, ulcerative colitis and IBD models (preclinical)

KPV is the Lys-Pro-Val tripeptide that corresponds to the C-terminal fragment of α-melanocyte-stimulating hormone (α-MSH 11–13). It has been studied for roughly three decades in preclinical models of inflammation, particularly intestinal inflammation. It is not FDA-approved, and no registered human clinical trials have been reported to date.

Class: Tripeptide (3 amino acids)
Sequence: Lys-Pro-Val
Origin: C-terminal fragment of α-MSH (residues 11–13)^[1]
Primary cellular uptake: PepT1 di/tripeptide transporter^[2]
Primary signaling: NF-κB · MAP kinase inhibition^[2][3]
Melanocortin receptor activity: None (does not bind MC1/3/5R)^[3]
Human PK: Not well established^[4]
FDA status: Not approved · April 15 2026 503A action^[5]

Educational reference only. KPV has no approved human clinical use and no registered human clinical trials have been reported. This page summarizes published preclinical research and documents reconstitution math for lyophilized research vials. It does not recommend a dose, an indication, or a source.

Last reviewed April 22, 2026 by the Enhanced Health Editorial Team. See the editorial policy.

What KPV is

KPV is a short peptide consisting of just three amino acids — lysine (K), proline (P), and valine (V) — in that order. It corresponds to the C-terminal three residues of α-melanocyte-stimulating hormone (α-MSH), a 13-residue peptide hormone derived from proopiomelanocortin (POMC). In the scientific literature KPV is often written as "α-MSH(11-13)" to indicate its position within the parent hormone.^[1][4]

Interest in KPV began in the 1990s, when researchers identified this C-terminal tripeptide as the minimal fragment of α-MSH that retains most of the anti-inflammatory activity of the full-length hormone. The finding was striking because KPV is far too small to engage the melanocortin G-protein-coupled receptors that α-MSH normally activates.^[3][4]

Mechanism

KPV's anti-inflammatory activity is mediated not by receptor binding but by intracellular uptake and interference with inflammatory signaling:

PepT1 transport. KPV is a substrate for PepT1 (SLC15A1), the proton-coupled di/tripeptide transporter expressed on intestinal epithelial cells and, notably, on activated immune cells. PepT1 transports KPV across the cell membrane without requiring a surface receptor.^[2]
NF-κB inhibition. Inside the cell, KPV inhibits the canonical NF-κB pathway by blocking nuclear translocation of the active p65/p50 heterodimer. NF-κB is a master regulator of pro-inflammatory gene expression, and blocking its nuclear entry damps down cytokine production.^[3]
MAP kinase inhibition. Nanomolar concentrations of KPV have been reported to inhibit the MAP kinase inflammatory signaling pathway in parallel, with resulting reductions in pro-inflammatory cytokine secretion.^[2]
No melanocortin receptor engagement. Biochemical work has confirmed that KPV does not bind or activate MC1R, MC3R, or MC5R, and does not compete with α-MSH at those receptors. This is why KPV's mechanism is described as non-melanocortin-receptor-mediated.^[3]

Preclinical evidence

The most developed body of preclinical evidence for KPV is in inflammatory bowel disease (IBD) models:

DSS- and TNBS-induced colitis. Oral administration of KPV reduces disease severity in chemically induced murine colitis models, with decreased pro-inflammatory cytokine expression.^[2]
Orally targeted nanoparticle delivery. KPV encapsulated in hyaluronic-acid-functionalized nanoparticles has been shown to deliver the peptide preferentially to inflamed colonic tissue and reduce disease activity in ulcerative colitis models.^[6]
Cytokine and immune cell effects. In cell-culture work, KPV reduces secretion of pro-inflammatory cytokines from activated immune cells in a concentration-dependent manner.^[2][3]

No human Phase 2 or Phase 3 clinical trial data is available for KPV. Reviews of anti-inflammatory peptides for IBD identify human pharmacokinetic characterization as a critical barrier to clinical translation.^[4]

Pharmacokinetics

Plasma half-life. A specific peer-reviewed human elimination half-life for KPV is not established.
Oral bioavailability. Because KPV is a PepT1 substrate, oral administration achieves cellular uptake via intestinal epithelium and on activated immune cells — a notable feature relative to larger peptides, which typically require injection.^[2]
Routes studied. Oral, intraperitoneal, and subcutaneous routes have been used in preclinical work. Research-vendor preparations are typically sold as lyophilized powder for reconstitution.

Storage and stability

Lyophilized powder. Store sealed per the supplier's certificate of analysis — typically refrigerated at 2–8 °C or frozen at −20 °C.
After reconstitution. Store refrigerated at 2–8 °C. Bacteriostatic water (0.9% benzyl alcohol) is commonly used when multi-draw use is planned; sterile water is used for single-draw preparations.
Handling. Swirl to mix — do not shake vigorously. Avoid freeze–thaw cycles. Discard any solution that is cloudy, discolored, or contains particulates.

Reconstitution math

Math only — no dose recommendation. The concentration after reconstitution determines how many insulin-syringe units equal a given mcg or mg amount.

Example 1 · 10 mg vial + 2 mL bac water concentration = 10 mg / 2 mL = 5 mg/mL = 5000 mcg/mL
1 unit = 0.01 mL = 50 mcg
→ 250 mcg = 5 units
→ 500 mcg = 10 units
→ 1 mg = 20 units
→ 5 mg = 100 units (full syringe)

Example 2 · 10 mg vial + 1 mL bac water concentration = 10 mg / 1 mL = 10 mg/mL = 10,000 mcg/mL
1 unit = 0.01 mL = 100 mcg = 0.1 mg
→ 500 mcg = 5 units
→ 1 mg = 10 units
→ 5 mg = 50 units
→ 10 mg = 100 units (full syringe)

Example 3 · 5 mg vial + 2 mL bac water concentration = 5 mg / 2 mL = 2.5 mg/mL = 2500 mcg/mL
1 unit = 0.01 mL = 25 mcg
→ 250 mcg = 10 units
→ 500 mcg = 20 units
→ 1 mg = 40 units
→ 2.5 mg = 100 units (full syringe)

Frequently asked questions

What is KPV?

A tripeptide of lysine, proline, and valine — the C-terminal fragment of α-MSH (residues 11–13). Identified in the 1990s as the minimal anti-inflammatory fragment of α-MSH. Not FDA-approved.^[1][4]

How does it work?

Enters cells via the PepT1 di/tripeptide transporter (not via melanocortin receptors). Inhibits NF-κB and MAP kinase inflammatory signaling intracellularly, reducing pro-inflammatory cytokine secretion.^[2][3]

What is the half-life?

Not established in peer-reviewed human pharmacokinetic work. Reviews identify human PK as a critical barrier to clinical translation.^[4]

How do I reconstitute a 10 mg vial?

Typical: 10 mg + 2 mL bacteriostatic water = 5 mg/mL → 1 unit = 50 mcg; 1 mg = 20 units. Using 1 mL gives 10 mg/mL (100 mcg per unit).

Is it FDA-approved?

No. In the FDA's April 15, 2026 503A categories update, KPV was listed for removal from Category 2 after seven calendar days because the nomination was withdrawn; FDA will consult PCAC on KPV-related bulk drug substances on July 23, 2026. Removal from Category 2 does not itself permit compounding.^[5]

Oral or injectable?

Both routes have preclinical data. KPV's PepT1 substrate status makes oral uptake feasible — a distinguishing feature relative to larger peptides that typically require injection. Oral nanoparticle delivery has been studied in ulcerative colitis models.^[2][6]

Primary references

Brzoska T, Luger TA, Maaser C, Abels C, Böhm M. α-MSH and related peptides: a new class of anti-inflammatory and immunomodulating drugs. Endocr Rev (2008 review in PMC). PMC2095288
Kannengiesser K, Maaser C, Heidemann J, Luegering A, Ross M, Brzoska T, Bohm M, Luger TA, Domschke W, Kucharzik T. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Inflamm Bowel Dis / Gastroenterology 2008 (PubMed 18061177, PMC2431115). PubMed 18061177
Mandrika I, Muceniece R, Wikberg JE. Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) α-melanocyte-stimulating hormone peptides. Biochem Pharmacol 2003 (PubMed 12750433). PubMed 12750433
Ghazvini S, et al. Anti-inflammatory peptides as promising therapeutics against inflammatory bowel diseases: a systematic review. JGH Open 2025. Wiley Online Library
U.S. Food and Drug Administration. 503A Categories Update for April 2026 — notice that KPV was slated for removal from Category 2 after seven calendar days because the nomination was withdrawn, with PCAC consultation on KPV-related bulk drug substances scheduled for July 23, 2026. fda.gov/media/94155
Xiao B, Xu Z, Viennois E, Zhang Y, Zhang Z, Zhang M, Han MK, Kang Y, Merlin D. Orally targeted delivery of tripeptide KPV via hyaluronic acid-functionalized nanoparticles efficiently alleviates ulcerative colitis. Mol Ther 2017 (PubMed 28143741, PMC5498804). PubMed 28143741

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