KPV

Areas of active research — not promised effects

Each tag links to other compounds with research into that goal. Research use only: these are areas of study, not human-use claims.

Related by research scope · open each to compare

KPV is not an FDA-approved drug and has no cleared indication. It is not currently on the 503A Bulk Drug Substances list that would permit compounding pharmacies to prepare it for patient use. As of April 23 2026, KPV was removed from FDA Category 2 (the list of substances under active regulatory review for prohibition from compounding), clearing it for PCAC advisory committee evaluation. That evaluation is scheduled for July 23 2026 (docket FDA-2025-N-6895). Until FDA acts on any PCAC recommendation and formally adds KPV to the 503A Bulks List, it remains outside the legal compounding pathway and is available only as a research-use-only material.

Transparent blend · bci-1.0 · never paid-placement

Primary name

KPV

Origin

KPV corresponds to residues 11–13 (Lys-Pro-Val) of the 13-amino-acid neuropeptide α-MSH. It is derived by conceptual or synthetic truncation of α-MSH, retaining the anti-inflammatory C-terminal domain while discarding the melanocortin-receptor-binding core responsible for pigmentation and appetite effects.

Registry IDs

PubChem CID

13294447

CAS

88768-11-0

InChIKey

MJXXAPORLGKVLB-UHFFFAOYSA-N

DrugBank

DB08050

Molecular formula

C16H30N4O4

Molar mass

192.21 g/mol

Monoisotopic

192.078644241 Da

InChIKey

MJXXAPORLGKVLB-UHFFFAOYSA-N

Appearance

White to off-white lyophilized powder (vendor-typical for synthetic tripeptide)

Solubility

Freely soluble in water; soluble in aqueous buffers at physiological pH; limited…

Sequence not available in current seed.

Stability: Short linear tripeptide; susceptible to proteolytic degradation in biological fluids. Stability in solution is limited. Nanoparticle encapsulation has been expl

Vial sizes

5 mg · 10 mg

Purity grades

≥98% (HPLC)

Salt forms

Free base (primary)

• GHS hazard class on file
• PPE & spill response
• Disposal guidance
• Not-for-human-consumption posture

How much research exists, and of what maturity — never a verdict on whether it works.

Mechanism of action

• KPV inhibits the NF-κB signaling pathway, blocking nuclear translocation of the p65 subunit and reducing downstream transcription of pro-inflammatory cytokines including TNF-α, IL-1β, and IL-6
• Unlike the full α-MSH molecule, KPV's anti-inflammatory activity appears to be partially independent of classical melanocortin receptor engagement, suggesting intracellular or alternative receptor mechanisms that remain under investigation
• In intestinal epithelia, KPV is actively transported into cells via the proton-coupled oligopeptide transporter PepT1 (SLC15A1), which is upregulated in inflamed colonic mucosa, potentially creating preferential delivery to inflamed sites
• Additional activity in keratinocytes and macrophages involves suppression of MAP-kinase signaling cascades alongside NF-κB, consistent with broad attenuation of innate immune activation

Pharmacokinetics (ADME)

Half-life

Approximately 1–2 hours (estimated from preclinical data; no formal human PK studies identified)

PK–PD note: As a short linear tripeptide, KPV is susceptible to rapid proteolytic degradation in plasma and gastrointestinal fluids. Oral delivery exploiting PepT1-mediated uptake has been demonstrated in murine …

Reading the evidence

• Evidence quality and gaps vary by application — see the cited grades above.
• Indexed-article counts span all evidence tiers, not only completed human trials.
• No first-party human-dosing, efficacy, or benefit claims are made here.

Key reviews & evidence-gap sources

• α-MSH related peptides: a new class of anti-inflammatory and anti-infectious agents (review) — Narrative review of α-MSH-derived peptides including KPV; not a KPV-specific systematic review.
• Ichiyama T et al. The neuroimmunomodulatory peptide alpha-MSH. Ann N Y Acad Sci 2000 — Review covering α-MSH and C-terminal fragments (KPV) anti-inflammatory activity.
• Land SC. Inhibition of cellular and systemic inflammation cues in human bronchial epithelial cells by melanocortin-related peptides. Int J Physiol Pathophysiol Pharmacol 2012 — Mechanistic study in human bronchial epithelial cells characterizing KPV NF-κB inhibition via p65RelA/importin-α3; primary mechanistic anchor.
• Dalmasso G et al. PepT1-Mediated Tripeptide KPV Uptake Reduces Intestinal Inflammation. Gastroenterology 2008 — Primary mechanistic + animal (DSS/TNBS colitis mice) study; PepT1-mediated uptake, NF-κB/MAPK inhibition.

No registered human trials found for this compound.

Status

No registered trials found

Summary (literature)

No formal human safety data are available for KPV as an isolated compound. As a tripeptide derived from an endogenous neuropeptide, it is expected to have a favorable safety profile relative to full-length α-MSH, which carries melanotropic and central nervous system effects. Prec…

WADA status

Not specifically listed on the WADA 2026 Prohibited List. KPV is not a melanocortin receptor agonist in the classical sense and is not named under prohibited pe…

Dominant research route: Oral

Oral KPV added to drinking water in DSS- and TNBS-induced colitis models in mice; PepT1-mediated uptake characterized in human intestinal epithelial (Caco2-BBE, HT29-Cl.19A) and Jurkat T cells in vitro

Bioavailability: KPV is actively transported into intestinal epithelial and immune cells via the H+-coupled di/tripeptide transporter PepT1; oral administration reduced colitis severity in mice. No human oral PK data located.

Foundational KPV-specific study (Dalmasso et al., 2008, Gastroenterology) used the oral route in murine colitis models; PepT1 is upregulated in inflamed colon, providing a mechanistic rationale for gut-targeted oral delivery. This is the most-studied route for KPV itself.

Mice treated subcutaneously with KPV (9 nmol) 30 min before intraperitoneal IL-1β challenge; anti-inflammatory effect assessed via PMN migration and KC release

Bioavailability: SC KPV produced an anti-inflammatory response in a murine IL-1β-induced inflammation model; no formal SC pharmacokinetic/bioavailability parameters reported in the primary study.

Getting et al. (2003, J Pharmacol Exp Ther) dissected the anti-inflammatory effect of KPV vs. core MSH peptides using the SC route in mice. Community aggregator sources (Layer B) describe SC as the most commonly discussed administration route, with a reported plasma half-life of ~2 hours, but no primary human PK study supports this value.

Single intraperitoneal injection of α-MSH(11-13)/KPV (1 mg/kg) 30 min after controlled cortical impact (TBI) in mice

Bioavailability: IP administration reduced secondary lesion volume and neuronal apoptosis after experimental TBI in mice; no bioavailability fraction reported.

Schaible et al. (2013, PLOS ONE) used IP KPV (α-MSH 11-13) for neuroprotection study; IP served as the systemic delivery route in this murine TBI model. IP was also the route of the IL-1β inflammatory challenge (not KPV) in Getting et al.

Transdermal delivery of KPV across dermatomed human skin ex vivo using iontophoresis, microneedles, and combined iontophoresis+microneedles

Bioavailability: Iontophoresis and microneedle-enhanced strategies were investigated to enhance KPV flux across human skin ex vivo; no in vivo topical bioavailability data located.

A transdermal iontophoretic delivery study (ScienceDirect, 2017) examined KPV penetration across microporated human skin, supporting feasibility of topical/transdermal delivery for dermatologic indications. Note: topical anti-inflammatory efficacy claims in secondary sources derive largely from α-MSH (parent hormone) studies rather than KPV-specific human trials.

Aggregate community-reported route; no primary human PK trial identified

Bioavailability: Community aggregator sources describe SC as the dominant non-oral route, with a reported plasma half-life of approximately 2 hours; this value is unsourced to any primary human pharmacokinetic study and should be treated as unverified.

De-identified aggregate community sources consistently identify SC injection as the most commonly discussed administration route for systemic applications outside the GI tract. No human RCT or controlled PK trial supports specific bioavailability or half-life figures.

Animal & human figures are kept visibly separate so studied animal doses are never misread as human guidance.

Sorted A–Z by vendor — never by price

Weekly median $/mg from the live vendor crawl.

Researched storefront prices, bucketed

p25 $5.50 · median $9.50 · p75 $10.00 · 10 researched vendors

Legit, COA-backed band: $5.50–$11.00/mg.

Value rule: don't just buy the cheapest — a price under $3/mg is a red flag. Pair price with COA and independent-test grade.

Estimated cost of research (10 mg)

Vial (best researched price)

$35

Bacteriostatic water (generic estimate)

$6

Syringes / supplies (generic estimate)

$12

What each test proves — general guidance, plus this compound's researched purity data

Purity on the current market (researched)

99.22% HPLC purity reported for a single KPV 10mg batch (Janoshik Analytical, Panda Peptides batch, published Feb–May 2026). Insufficient independent data to establish a range.

Independent labs cited for this compound

No KPV-specific FDA recalls, market withdrawals, or safety alerts found in FDA enforcement databases as of search date.

Buyer red-flag checklist

• No FDA-approved KPV drug product exists for any indication
• FDA flagged 'absence of human exposure data for KPV' when placing it on Category 2 in 2023
• KPV was on the FDA Category 2 restricted compounding list (significant safety risk) from 2023 until the 2026 reclassification announcement
• Gray-market KPV sold as 'research use only' / 'not for human consumption' to circumvent FDA drug oversight
• Chinese-sourced raw peptide powders marketed 'not for human use' are unaffected by compounding-list changes
• No KPV-specific import alert, recall, or warning letter found — but no pharmaceutical-grade manufacturing standard applies to gray-market supply

GMP vs research-grade: the chemistry (SPPS + HPLC + MS) is identical — the difference is the quality system.

Underdosing / mislabeling: No KPV-specific underdosing prevalence data identified from Janoshik, MZ Biolabs, or Finnrick aggregates. KPV is not currently tracked on Finnrick's product testing leaderboard. General risk of label mismatch noted in secondary sources but without compound-specific quantification.

• An RUO label is not an import exemption — CBP judges actual intended use.
• Lyophilized powder is ambient-stable in transit; temperature control needed for > 7-day transit.
• US-warehouse vendors dodge import scrutiny — they cost more but ship more reliably.

Every item dated & sourced

KPV is not a named substance on the WADA 2026 Prohibited List. As a peptide without approval by any governmental regulatory health authority for human therapeutic use, it would fall under the S0 (Non-Approved Substances) catch-all, which is prohibited at all times and classified as a Specified Substance.

No granted patents identified in current seed. Composition-of-matter coverage is limited given the peptide's synthetic origin.

• IACUC / IRB research context
• RUO buyer responsibilities & documentation
• Veterinary / alternative-use where lawful
• Jurisdiction-aware "who may lawfully obtain"

What people discuss

Reported concerns — discussion, not established effects

Reading caveats

• vendor-affiliated content present (Amino Innovations, RealPeptides are sellers)
• self-reported anecdotal logs, no controlled human trials
• subreddit promotion / ambassador-linked posts
• survivorship bias toward positive gut/skin outcomes

Manually researched from reddit, youtube, x— theme weights are research estimates, not live counts; aggregated & de-identified. No individual posts, quotes, or usernames are ever shown.

Relative research / market volume — populated once the activity stream is wired

Inline tooltips for lyophilized, RUO, EU/mg, SPPS, 503A and more.

Toggle plain-language ↔ scientific in the header.

• How to read a COA
• Free base vs acetate
• Understanding evidence grades

C-terminal tripeptide of α-MSH (Lys-Pro-Val) that suppresses NF-κB-driven inflammation and is absorbed by intestinal PepT1 transporters in preclinical models. Approximately 111 articles are indexed (literature last scanned 2026-05-29). US regulatory status: Research Use Only; not approved; PCAC review pending July 2026. Research use only.

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