KPV Peptide: Structure, Research Findings and Lot Data

What is KPV peptide?

KPV is a tripeptide. Its three amino acids are lysine, proline and valine, in that order. The name is simply their one-letter codes: K, P and V.

The KPV tripeptide matches the last three residues of alpha-melanocyte-stimulating hormone (alpha-MSH), a 13-residue peptide cut from the precursor protein POMC (UniProt P01189). Researchers have studied this short fragment on its own since at least 1989 (Hiltz and Lipton, 1989).

Peptide KPV is not an FDA-approved drug. The published work on it comes from cell cultures, mouse models and human skin samples studied in vitro. Astramide supplies it as a research chemical, for research use only.

KPV is also one of the four components of the KLOW peptide blend, where it sits beside GHK-Cu, BPC-157 and TB-500. It is the component that separates KLOW from the three-peptide GLOW blend, as our GLOW vs KLOW comparison explains.

What is the molecular structure of KPV?

KPV is small: 16 carbon atoms and about 342 g/mol.

The two masses matter on a certificate. The acetate adds one acetic acid, about 60 g/mol, so it is about 17.5% heavier than the free acid. A mass match means something only against a stated reference form. The KPV Pro lot record states the free acid.

Where does KPV sit in alpha-MSH?

Alpha-MSH is residues 138 to 150 of the POMC precursor, with the sequence SYSMEHFRWGKPV (UniProt P01189). Count from the left: S is 1, and the final K, P and V are 11, 12 and 13. Those last three are KPV.

One structural detail differs. In alpha-MSH, the final valine carries a C-terminal amide. KPV as listed in PubChem and on the pH Solutions certificate is the free acid, ending in -OH (PubChem CID 125672).

A 2008 review placed KPV in a family of alpha-MSH-derived tripeptides, alongside the related tripeptide KdPT (Brzoska et al., 2008). The 1989 study described the C-terminal tripeptide as the message sequence of the parent hormone for one of its effects (Hiltz and Lipton, 1989).

what was measured

What does KPV do in research models?

"What does KPV peptide do" is best answered as what studies measured. KPV has been studied in inflammatory signalling research. The results below come from cells, mouse models and skin samples, not from people.

1989: ear swelling in mice

In a picryl chloride ear swelling model in mice, alpha-MSH 11 to 13 inhibited swelling. The response varied with the amount given to the mice (Hiltz and Lipton, 1989).

2000: microbes in culture

Alpha-MSH and KPV had antimicrobial influences against Staphylococcus aureus and Candida albicans in vitro. Effects were seen over a broad concentration range, including picomolar levels, and were linked to increased cAMP (Cutuli et al., 2000).

2008: NF-κB in intestinal and immune cell lines

In Caco2-BBE, HT29-Cl.19A and Jurkat cells, KPV at nanomolar concentrations inhibited NF-κB and MAPK activation and lowered pro-inflammatory cytokine secretion (Dalmasso et al., 2008). The same paper also used chemically induced (DSS and TNBS) mouse models.

2025: keratinocytes exposed to fine particles

HaCaT human keratinocytes were exposed to PM10 particulate matter. KPV at 50 µg/mL was associated with higher cell viability and lower IL-1β secretion, ROS, ERK and p38 signalling, NF-κB and caspase-1. The authors also used a 3D skin model (Sung et al., 2025).

2026: macrophages exposed to oxidized LDL

Mouse RAW264.7 macrophages were exposed to oxidized LDL. The study measured lipid accumulation and foam cell formation, which were lower with KPV in this cell line, along with ROS, p38 and NF-κB signalling, NLRP3 inflammasome assembly and IL-1β maturation. The authors reported no cytotoxicity in RAW264.7 cells at the concentrations tested (Bai et al., 2026). This was a mouse cell line, in vitro only.

Which research models have examined KPV?

Each cited study, by year, system and what was measured. "Skin in vitro" means human skin tissue studied in the lab.

Two papers looked at how KPV moves. A 2010 study examined KPV loaded into nanoparticles in cell and mouse models (Laroui et al., 2010). A 2017 study measured KPV permeation through dermatomed human skin in vitro, as a physicochemical measurement (Pawar et al., 2017).

How does KPV enter cells? PepT1 and the melanocortin question

The KPV peptide mechanism question has two parts: how the tripeptide gets into cells, and which receptor, if any, it uses.

The PepT1 transporter

PepT1 is a membrane transporter for small peptides (Dalmasso et al., 2008). In the 2008 cell work, KPV competed with a radiolabelled PepT1 substrate for uptake. The authors concluded that KPV enters cells through PepT1 (Dalmasso et al., 2008).

Does KPV need melanocortin receptors?

Alpha-MSH acts on melanocortin receptors (Brzoska et al., 2008), so a natural question is whether its fragment does too. One 2008 study tested this directly. It used mice with a nonfunctional melanocortin 1 receptor (MC1Re/e). The effects of KPV were at least partially independent of MC1R signalling (Kannengiesser et al., 2008).

An earlier study in microbes linked the activity of alpha-MSH and KPV to increased cAMP (Cutuli et al., 2000). A 2023 review covered the wider melanocortin system in mouse intestinal models (Gravina et al., 2023). For background on the parent hormone and its tripeptides, see the 2008 review (Brzoska et al., 2008).

In short: PepT1 for uptake, and MC1R not required for every effect measured.

What is not known about KPV?

Four gaps stand out in the sources on this page.

• No clinical trial is among the cited studies. Every study above used cells, mice, microbes or skin tissue in vitro.
• Concentrations vary by orders of magnitude. One study reported effects at picomolar levels (Cutuli et al., 2000), another at nanomolar levels (Dalmasso et al., 2008). The 2025 study used 50 µg/mL (Sung et al., 2025).
• The receptor picture is incomplete. MC1R was not required for all effects (Kannengiesser et al., 2008), and the cited work names no single receptor in its place.
• The newest work is in cell lines. The 2026 study used a mouse macrophage line, in vitro only (Bai et al., 2026).

two labs, two menus

How do the two published KPV certificates compare?

Two published KPV lots, two labs, two test menus. Line by line, including what each does not report:

Krause reports an endotoxin result that pH Solutions does not. pH Solutions reports nine further tests that Krause does not. "Not performed" means the Krause report lists the test and states it was not run. "Not reported" means the test does not appear on that certificate.

On identity, Krause reports a mass spectral match, while pH Solutions prints the free acid formula and mass it matched. Both purity figures come from HPLC, but at different detection settings, so the two numbers are not a direct ranking. Our guide to how HPLC and mass spectrometry differ explains what each method confirms.

What is the regulatory status of KPV?

This is general information, not legal advice.

KPV is not an FDA-approved drug. Astramide supplies KPV and KPV Pro as research chemicals, for research use only.

On October 30, 2026, HHS published an interim 503A enforcement discretion policy for listed peptides (FR Doc 2026-22192, 91 FR 68526). It lists six peptides, and KPV is one of them. Its appendix gives KPV as H-Lys-Pro-Val-OH acetate, C16H30N4O4·CH3COOH, 402.5 g/mol (HHS, 2026). Condition 7 limits the policy to a single listed active ingredient.

The listing does not make KPV an approved drug. The notice itself states: "Compounded drugs are not FDA-approved." The comment period closes November 13, 2026, under docket HHS-OASH-2026-0496.

For the full picture, read our HHS peptide policy explainer and our overview of whether peptides are legal.

published, lot by lot

Batch Verification Standards

The two published KPV lots, as printed:

Both lots carry the same 10 mg label, and each record links to the full certificate. Both products are supplied for research use only. Both KPV lot records are in the Astramide COA library, and our testing process page explains how lot records are produced. For a field-by-field method, see how to read a peptide COA. Terms such as LAL and water activity are defined in the peptide glossary.

This content is prepared by the Astramide Science Team and reviewed by the Chief Science Officer, overseeing analytical quality assurance and third-party laboratory partnerships with a focus on HPLC-based purity verification and research-grade peptide compound validation. All research peptides sold by Astramide are intended strictly for laboratory research use only.

Update log

• November 9, 2026: Rewritten. Corrected the molecular formula to C16H30N4O4, replaced the testing description with the two published lot records, added the 2025 and 2026 cell studies and the HHS policy status, linked every citation.
• July 19, 2026: Published.

Sources

• Hiltz ME, Lipton JM. FASEB J. 1989;3(11):2282-4. PMID 2550304. PubMed
• Cutuli M, Cristiani S, Lipton JM, Catania A. J Leukoc Biol. 2000;67(2):233-9. PMID 10670585. PubMed
• Dalmasso G, et al. Gastroenterology. 2008;134(1):166-78. PMID 18061177. PMC2431115
• Kannengiesser K, et al. Inflamm Bowel Dis. 2008;14(3):324-31. PMID 18092346. PubMed
• Brzoska T, Luger TA, Maaser C, Abels C, Bohm M. Endocr Rev. 2008;29(5):581-602. PMID 18612139. PubMed
• Laroui H, et al. Gastroenterology. 2010;138(3):843-53. PMID 19909746. PubMed
• Pawar K, Kolli CS, Rangari VK, Babu RJ. J Pharm Sci. 2017;106(7):1814-20. PMID 28343991. PubMed
• Gravina AG, et al. Cells. 2023;12(14):1889. PMID 37508552. PMC10378568
• Sung J, et al. Tissue Cell. 2025;95:102837. PMID 40073467. PubMed
• Bai JS, et al. Tissue Cell. 2026;104:104036. PMID 42854645. PubMed
• US HHS. 503A Peptide Enforcement Discretion Policy, Appendix B. 2026. HHS PDF
• US HHS. Federal Register. FR Doc 2026-22192, 91 FR 68526. October 30, 2026. Docket HHS-OASH-2026-0496. Public inspection PDF
• Databases: PubChem CID 125672; UniProt entry P01189.