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KPV

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Research use only. For laboratory and research use only (RUO). Not for human or veterinary use, not for consumption, and not a medicine. Information is a research summary, not medical advice, and contains no dosing guidance.

Snapshot

Field Value
Full name / aliases Lys-Pro-Val; L-lysyl-L-prolyl-L-valine; alpha-MSH (11-13); the C-terminal tripeptide of alpha-melanocyte-stimulating hormone
Class / mechanism Anti-inflammatory tripeptide; NF-kB / IKK inhibitor, taken up by the PepT1 di/tripeptide transporter; melanocortin-receptor-independent
Sequence Lys-Pro-Val (KPV)
Molecular formula C16H30N4O4 (free base)
MW (free base) ~342.43 g/mol
CAS / PubChem CID CID 125672, CAS 67727-97-3
Category Cosmetic / skin, anti-inflammatory; also studied for gut
Salt forms seen Free base and acetate (the common lyophilised salt); confirm salt on CoA
AxYn SKU + strengths Live: the added ingredient that turns Glow into KLOW (KLOW = Glow blend + KPV)

Chemistry and make-up

KPV is just three residues, lysine then proline then valine, and it is the last three amino acids (positions 11 to 13) of the 13-residue hormone alpha-MSH [A]. That heritage matters: KPV keeps much of the anti-inflammatory activity of the parent hormone but drops the message-sequence that drives pigmentation, so it does not darken skin and does not act through the classic melanocortin receptors [A]. There is no cysteine, so no disulfide bridges, and no metal binding; the central proline gives a rigid turn that is part of why the tripeptide is comparatively stable. Because it is so small it is a substrate for the PepT1 di/tripeptide transporter, which actively carries it into intestinal epithelial and immune cells, the basis for its oral and gut-targeted interest [A]. As a small acetate-salt peptide, the QC priorities are identity and purity confirmed by mass spec and HPLC, plus a stated salt form, since counterion changes the effective peptide content.

What it is studied for (evidence)

  • Mechanism: KPV enters cells (partly via PepT1) and inhibits the NF-kB inflammatory pathway, reported to act at the level of IkB kinase (IKK) and NF-kB nuclear translocation, reducing production of pro-inflammatory cytokines such as TNF-alpha, IL-1beta and IL-6, and dampening NLRP3 inflammasome signalling [A]. Crucially the effect is PepT1-mediated, not melanocortin-receptor-mediated (Dalmasso et al., *Gastroenterology* 200801852-5/fulltext)).
  • Established (in preclinical models):
  • Reduces intestinal inflammation: oral KPV lowered the incidence and severity of DSS- and TNBS-induced colitis in mice, cutting colonic myeloperoxidase and pro-inflammatory cytokine expression [A] (Dalmasso 2008). Later work tied PepT1-mediated KPV uptake to benefit in colitis-associated cancer models (CMGH 201600015-1/fulltext)).
  • Anti-inflammatory activity in skin models: topical KPV has reduced contact-dermatitis-type inflammation and local cytokine output, and is described as supporting wound closure and modulating collagen to limit hypertrophic scarring [A/D].
  • Direct antimicrobial action: alpha-MSH and KPV have shown killing of *Staphylococcus aureus* and *Candida albicans* at physiological concentrations, relevant to skin and wound context [A].
  • Emerging / thin / preclinical only: Broader claims for systemic anti-inflammatory, gut-barrier, allergy and dermatological use rest almost entirely on cell and rodent data plus older dermatological patents (for example US6894028B2, “Use of KPV tripeptide for dermatological disorders”). Human data is very limited.
  • Marketing claims vs data: Vendors present KPV as a proven fix for IBD, leaky gut, eczema, mast-cell and autoimmune conditions, often with dosing. The mechanism is genuine and the preclinical anti-inflammatory signal is consistent, but there is no completed, published randomised human efficacy trial. Treat all human-outcome and dosing claims as extrapolation from animal work.
  • Human clinical status: Not an approved drug, no USP monograph, no approved labeling. On 23 July 2026 the FDA PCAC voted 8 to 6 (1 abstention) to recommend KPV (free base and acetate) for the 503A compounding bulks list, over the objection of FDA scientific staff, who cited insufficient safety and efficacy evidence. That is an advisory recommendation only, not a rule, and still requires FDA rulemaking (realistically into 2027) [B].

Handling, format and stability

Supplied lyophilised, usually as the acetate salt; reconstitution is a research-handling note only, no dosing here. Store the lyophilised powder cold and protected from light; reconstituted peptide is less stable and cold-chain dependent. KPV is regarded as relatively robust for a peptide because of its small size and central proline, but standard peptide care applies: avoid repeated freeze-thaw and prolonged warmth. For a tripeptide, identity by mass spec is especially important because short peptides are easy to mis-synthesise or substitute.

Regulatory and trade status

  • UK/EU: No medicines approval; sell strictly research use only and avoid anti-inflammatory or treatment claims, which could pull it into “medicinal by presentation” territory. It is used in some cosmetic contexts as an anti-inflammatory skin peptide; confirm any INCI/CosIng listing before cosmetic labelling [B — verify].
  • US: Not FDA approved. On 23 July 2026 the PCAC recommended KPV for the 503A bulks list by an 8-6 vote (1 abstention) against FDA staff advice; this is advisory only and final status depends on FDA rulemaking, not settled [B] (FDA PCAC July 2026).
  • WADA: Not specifically named; as a non-approved substance a sport-context user should treat it cautiously under the S0 logic and check the current list [B — verify].
  • Customs / trade: Low profile. Identity and purity are the practical risks, not legal status.

Sources

  • [A] Dalmasso et al., “PepT1-Mediated Tripeptide KPV Uptake Reduces Intestinal Inflammation,” *Gastroenterology* 2008 — https://www.gastrojournal.org/article/S0016-5085(07)01852-5/fulltext
  • [A] “Critical Role of PepT1 in Promoting Colitis-Associated Cancer and Therapeutic Benefits of the Anti-inflammatory PepT1-Mediated Tripeptide KPV,” *CMGH* 2016 — https://www.cmghjournal.org/article/S2352-345X(16)00015-1/fulltext
  • [A] “Terminal Signal: Anti-Inflammatory Effects of alpha-MSH Related Peptides Beyond the Pharmacophore,” Springer — https://link.springer.com/chapter/10.1007/978-1-4419-6354-3_8
  • [A] alpha-MSH / KPV antimicrobial activity vs *S. aureus* and *C. albicans*, *J Leukoc Biol* — https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6915932/
  • [B] FDA Pharmacy Compounding Advisory Committee, 23-24 July 2026 (KPV 8-6 recommendation) — https://www.fda.gov/advisory-committees/advisory-committee-calendar/july-23-24-2026-meeting-pharmacy-compounding-advisory-committee-07232026
  • [B] PubChem CID 125672 (Lys-Pro-Val), CAS 67727-97-3
  • [C] Patent US6894028B2, “Use of KPV tripeptide for dermatological disorders” — https://patents.google.com/patent/US6894028B2/en
  • [D] Vendor / community pages (BSCG, Peptidepedia, klow-peptide) — commercial, publish dosing and human claims we do not use.

Plain summary

KPV is a three-amino-acid piece (Lys-Pro-Val) of the hormone alpha-MSH that keeps the anti-inflammatory action but not the skin-darkening effect, working by getting inside cells and calming the NF-kB inflammation pathway. The evidence is genuine but almost entirely preclinical (cells and mice, strongest in gut inflammation and skin), with no completed human efficacy trial, so all “treats IBD/eczema” and dosing claims are extrapolation. For AxYn it is the added ingredient that turns the Glow blend into KLOW, so its identity and purity (mass spec, salt form) are what make the KLOW upgrade real.

For laboratory and research use only (RUO). Not for human or veterinary use, not for consumption, and not a medicine. Information is a research summary, not medical advice, and contains no dosing guidance.

For laboratory research use only. Not for human or veterinary use, not for consumption, and not a medicine. This is a research summary, not medical advice, and contains no dosing guidance.