← Back to library
Cell + animal research · no established human drug dataResearch / investigational · not FDA approved

KPV

Lys-Pro-Val · C-terminal α-MSH tripeptide

Melanocortin-derived tripeptide studied for anti-inflammatory effects in cell and animal models, with no established human drug-exposure data.

Vial / injectable research formatsTopical / oral research formatsInflammation & Gut

Reference dose

200–500 mcg daily

Source-specific educational reference, not an individualized recommendation.

Reference schedule

Daily · 4–8 weeks

New to peptide research?

This page gets detailed quickly.

Profiles include evidence, formats, units, source-specific reference amounts and, where relevant, device details. If any of those terms are unfamiliar, do not guess your way through them. Start with a Personalised Guide and we will put the foundations in the right order for you.

Start here

At a glance

Structure

Lys-Pro-Val

The C-terminal tripeptide corresponding to α-MSH residues 11–13.

Evidence base

Cell + animal

Most direct efficacy evidence is preclinical.

Human exposure data

Not identified by FDA

FDA reports no identified KPV drug-product exposure data by any route.

Regulatory status

Not FDA approved

Reviewed in the 2026 503A compounding process.

What it is

KPV is the three-amino-acid sequence lysine-proline-valine, corresponding to the C-terminal residues 11–13 of α-melanocyte-stimulating hormone.

It was developed as an anti-inflammatory research fragment intended to retain some of α-MSH's anti-inflammatory activity without its pigmentary effects.

Research focus

InflammationGut / colitis modelsBarrier biologySkin inflammationWound research

How it works

KPV is the Lys-Pro-Val C-terminal tripeptide of α-MSH. Preclinical work reports anti-inflammatory effects involving NF-κB, cytokine signalling and intestinal peptide transport, although FDA notes that its precise molecular targets remain unknown.

Important context

KPV has a coherent preclinical anti-inflammatory literature, especially in gut and inflammatory models, but there is a major human-evidence gap. FDA states that it has not identified human exposure data for drug products containing KPV by any route.

What it is studied for

Gut research examines intestinal epithelial inflammation, peptide transport, cytokine signalling and experimental colitis.

Skin and wound research is interested in whether KPV can reduce inflammatory signalling without melanocortin-associated pigmentation.

Broader inflammatory research explores NF-κB, MAPK and cytokine pathways across immune and non-immune cell systems.

More contextWhy KPV should remain a preclinical profileSee the deeper context, evidence details and practical distinctions behind this profile.

Cell studies and mouse colitis models show reproducible anti-inflammatory signals, including reduced inflammatory signalling and improved disease measures in experimental colitis.

Those findings make KPV scientifically interesting, but they do not establish a human oral, topical or injectable dose, clinical efficacy or long-term safety.

  • KPV corresponds to amino acids 11–13 of α-MSH and is commonly described as Lys-Pro-Val.
  • Published mouse studies report anti-inflammatory effects in DSS, TNBS and transfer-colitis models.
  • Cell work has linked KPV uptake in intestinal cells to the PepT1 transporter and inhibition of NF-κB/MAPK-related inflammatory signalling.
  • FDA's 2026 review states that it did not identify human clinical studies for the nominated wound-healing or inflammatory uses and proposed that KPV free base and acetate not be included on the 503A Bulks List.

Why people are interested

What makes KPV worth researching.

Animal research

Intestinal inflammation

Mouse colitis models report reduced inflammatory activity and improved disease measures after KPV treatment.

Cell + animal research

PepT1 transport

Cell studies indicate that KPV can be transported by PepT1 in intestinal epithelial and immune cells and can suppress inflammatory signalling.

Mechanistic / preclinical

NF-κB / cytokine signalling

Preclinical work reports inhibition of NF-κB and related inflammatory pathways, but FDA notes that KPV's precise molecular targets remain unknown.

No established human drug data

Human evidence gap

FDA found no human clinical evidence for the nominated wound-healing or inflammatory uses and no identified human exposure data for KPV drug products.

Evidence

Where the evidence is strongest, and what kind of evidence it is.

Animal · multiple experimental models

Colitis models

KPV reduced inflammatory measures in DSS, TNBS and transfer-colitis mouse models in published preclinical studies.

Cell research

Cellular mechanism

KPV has been reported to reduce NF-κB and MAPK-related signalling and pro-inflammatory cytokine output in intestinal epithelial and immune-cell systems.

Not established

Human therapeutic evidence

FDA's 2026 review did not identify clinical studies supporting KPV for wound healing or inflammatory conditions and reported no identified human drug-product exposure data.

Regulatory evaluation · 2026

FDA compounding review

FDA proposed that KPV free base and KPV acetate not be included on the 503A Bulks List.

Human research

FDA's 2026 evaluation states that it did not identify human exposure data for drug products containing KPV administered by any route.

FDA also reported that its literature review did not identify clinical studies supporting KPV for the nominated wound-healing or inflammatory-condition uses.

Accordingly, commonly marketed oral, topical and injectable KPV protocols should not be described as clinically validated human treatments.

Preclinical research

Published mouse studies report anti-inflammatory effects in multiple experimental colitis models, including improvements in histology and inflammatory markers.

Cell studies indicate PepT1-mediated uptake and suppression of NF-κB, MAPK and pro-inflammatory cytokine signalling.

Review literature describes KPV as retaining anti-inflammatory properties of α-MSH while lacking its pigmentary action, but the translational clinical evidence remains absent.

Reference dosing

Reference amount, schedule and conversion.

A reference amount is only useful when you know the formulation, concentration and delivery device it belongs to. Do not transfer a vial amount into a pen, a pen click count into another pen, or a syringe-unit number into a different concentration.

01

Identify the format

Vial, reusable cartridge pen, prefilled multi-dose pen or single-dose autoinjector.

02

Confirm concentration

Know the total peptide amount and liquid volume or the manufacturer/vendor concentration.

03

Understand the units

Keep mg/mcg, mL and syringe units or device clicks separate.

04

Then use the reference

Only convert a known reference amount with the calculator that matches the actual device.

Source-specific reference

200–500 mcg daily

Daily · 4–8 weeks

The 200–500 mcg range is a Pep Report research reference. It is educational context rather than a clinically validated individualized dose.

Calculator connection

Choose the calculator that matches the actual formulation. The calculator converts numbers you already know; it does not choose the target amount.

The vial calculator can convert a known vial amount and liquid volume into concentration. It does not establish that injectable administration is appropriate or that the research dose range is clinically supported.

Storage

Start with the format. Then verify the exact product.

Learn the storage framework

Rule of thumb, not a product instruction

Storage belongs to the exact formulation. Generic advice can orient you, but the label, pharmacy directions or formulation-specific stability data should determine the final temperature and usable-life limits.

Pens

Treat a pen as a finished drug-device product: protect it from unnecessary heat and light, do not freeze unless the exact label explicitly permits it, and use that device's own unopened and in-use storage window.

Vials

Treat dry and reconstituted vials as different stability states. Refrigeration after mixing is common for some formulations but is not a universal peptide rule.

Product-specific notes

There is no FDA-approved KPV product label establishing standardized therapeutic storage conditions.

Research-product storage should follow formulation-specific supplier documentation rather than assuming all peptide formats are equivalent.

Practical reference

Formats

Vial / injectable research formats

Topical / oral research formats

Reconstitution & units

The vial calculator applies only to vial concentration arithmetic. Oral and topical products require route- and formulation-specific information.

There is no clinically validated human KPV reconstitution or injection protocol.

mcg or mg describe peptide amount; mL and U-100 units describe liquid volume.

The calculator does not validate the research dose reference or establish that an injectable route is clinically appropriate.

Safety, status & open questionsOpen the practical cautionsKPV is an investigational research peptide, not an approved treatment for inflammatory bowel disease, eczema, psoriasis, wound healing or other inflammatory conditions. Its evidence is predominantly cellular and animal.

Open questions

The precise molecular target or targets responsible for KPV's anti-inflammatory activity remain incompletely established.

Human pharmacokinetics, route-specific bioavailability, dose-response and long-term safety are not established.

Preclinical gut findings do not establish efficacy for human inflammatory bowel disease.

Commercial products may vary in chemical form, identity, concentration and purity.

Regulatory notes

KPV is not an FDA-approved drug.

FDA reports that it has not identified human exposure data for drug products containing KPV by any route.

In July 2026 FDA proposed that KPV free base and KPV acetate not be included on the 503A Bulks List.

Practical notes

Human safety data are insufficient to define a reliable adverse-effect profile for oral, topical or injectable KPV.

FDA states that it lacks important information needed to determine whether KPV drug products would cause harm in humans.

Injectable research products add risks around sterility, identity, purity and concentration.

Route-specific absorption and systemic exposure are uncertain, so evidence from one experimental route should not be transferred automatically to another.

Common mistakes

Calling KPV a proven human anti-inflammatory or IBD treatment because it works in mouse colitis models.

Treating a proposed mechanism such as NF-κB inhibition as proof of clinical benefit.

Presenting the 200–500 mcg research range as a validated human dose.

Using injectable-vial arithmetic for oral or topical formulations without route-specific evidence.

Common questions

Does KPV have human clinical trials?

FDA's 2026 review states that it did not identify human exposure data for KPV drug products or clinical studies supporting the nominated wound-healing and inflammatory uses.

Why is KPV discussed for gut inflammation?

Published cell and mouse studies show anti-inflammatory effects in intestinal systems and experimental colitis models, including PepT1-related uptake and reduced inflammatory signalling.

Is KPV an approved treatment for IBD, eczema or psoriasis?

No. KPV is not an FDA-approved drug for those or any other therapeutic indication.

Why does the profile still have a vial calculator?

Only for arithmetic when a research vial's exact strength and liquid volume are already known. It does not provide or validate a human treatment dose.

Related peptides & blends

References