Investigational melanocortin tripeptide (Melanocortin research — anti-inflammatory C-terminal α-MSH(11–13) fragment, MELANOCORTIN-RECEPTOR-INDEPENDENT, NOT a tanning peptide) Limited Human Data

KPV

Also Known As: Lys-Pro-Val, Lys-Pro-Val tripeptide, α-MSH(11-13), MSH 11-13, H-Lys-Pro-Val-OH (free acid)

KPV is the linear tripeptide Lys-Pro-Val — the three C-terminal residues (positions 11–13) of α-melanocyte-stimulating hormone (α-MSH). The chemical entity described on this page is the free-acid form H-Lys-Pro-Val-OH (CAS 67727-97-3, PubChem CID 125672, molecular formula C₁₆H₃₀N₄O₄, molecular weight ≈ 342.43 g·mol⁻¹). #1 EDITORIAL READER-CONFLATION GUARDRAIL: KPV belongs to the melanocortin family and shares an α-MSH lineage with afamelanotide, bremelanotide (PT-141), and Melanotan II — but is pharmacologically OPPOSITE on the axes that matter to most readers. KPV does NOT cause skin pigmentation (unlike afamelanotide and Melanotan II, which are MC1R agonists for tanning). KPV does NOT have a sexual-function indication (unlike PT-141 / bremelanotide, an MC4R agonist for hypoactive sexual desire disorder). KPV does NOT meaningfully bind MC1R / MC3R / MC4R / MC5R as a full agonist. KPV is a 3-amino-acid C-terminal fragment, not a 13-residue full-length analogue (afamelanotide) or cyclic 7-residue analogue (Melanotan II). Studies report that the anti-inflammatory action of KPV is largely MELANOCORTIN-RECEPTOR-INDEPENDENT (Brzoska 2008 Endocr Rev review) and is mediated through NF-κB and MAP-kinase suppression together with SLC15A1 / PepT1-mediated intracellular uptake into inflamed colonic epithelium (Dalmasso 2008 Gastroenterology, PMID 18061177). REGISTRY GAP — IMPORTANT: a systematic ClinicalTrials.gov v2 API audit on 2 May 2026 for "KPV", "Lys-Pro-Val", and "tripeptide KPV" returned ZERO active registered human trials. The common misattribution of PCK3145 as a "KPV-amide formulation" is INCORRECT — PCK3145 is a 15-residue synthetic peptide derived from Prostate Secretory Protein 94 (PSP94), developed by Procyon Biopharma for metastatic castration-resistant prostate cancer (NCT00695851 at Memorial Sloan Kettering Cancer Center, 2005–2009 — a prostate cancer trial, NOT IBD, NOT KPV). PCK3145 is structurally and pharmacologically UNRELATED to KPV and must NEVER be cited as a KPV development programme. WADA Class S0 (catch-all for non-approved substances); KPV does NOT fall under S2 (peptide hormones, growth factors) because it is not a hormone analogue with anabolic or EPO-mimetic activity. Vendor-market caveat: KPV is widely sold by research-peptide vendors and discussed on bodybuilding, autoimmune-recovery, IBD-self-treatment, gut-health and biohacker forums as a "gut-healing peptide" — none of those framings reflects approved-medicine status. Limited human data — preclinical reports only. Research use only.

Identity & Chemistry

PubChem 2D rendering of KPV (CID 125672), a linear tripeptide of L-lysine, L-proline, and L-valine — the C-terminal three residues (positions 11–13) of α-melanocyte-stimulating hormone. Free-acid form (H-Lys-Pro-Val-OH).
Image credit: Structure data from PubChem CID 125672, U.S. National Library of Medicine (no canonical Wikimedia file as of 2026-05-02 — Wikimedia Commons returned zero hits for "KPV tripeptide", "Lys-Pro-Val", and "lysylprolylvaline"; PubChem 2D fallback used per Image Acquisition Policy). · Public Domain (U.S. Government work — National Library of Medicine)
Amino Acid Sequence
H-Lys-Pro-Val-OH (free-acid linear tripeptide; one-letter K-P-V). Corresponds to residues 11–13 (Lys¹¹-Pro¹²-Val¹³) of α-melanocyte-stimulating hormone (α-MSH). The free-acid form (CAS 67727-97-3, PubChem CID 125672) is the canonical chemical entity described here. Two closely related but chemically DISTINCT forms — the C-terminal amide H-Lys-Pro-Val-NH₂ and the N-acetyl/C-amide Ac-Lys-Pro-Val-NH₂ — are used in much of the original Hiltz / Catania / Lipton mouse work and in many vendor preparations and have different masses and stability profiles; the dossier preserves the form actually tested in each cited study where stated.
Molecular Formula
C₁₆H₃₀N₄O₄
Molecular Weight
342.43 g·mol⁻¹ (free acid; ≈ 342.43–342.44 Da across PubChem / Wikipedia / supplier SDS sheets, rounding variance only). The C-terminal amide H-Lys-Pro-Val-NH₂ is ≈ 341.45 g·mol⁻¹ (one fewer oxygen, one extra nitrogen relative to the free acid; amidation protects the C-terminus from carboxypeptidase cleavage). The N-acetyl/C-amide Ac-Lys-Pro-Val-NH₂ is ≈ 383 g·mol⁻¹. These are SEPARATE chemical entities, not interchangeable, and vendor catalogues frequently fail to disambiguate which form is shipped — the page MUST surface this caveat.
CAS Number
67727-97-3 (free acid)
PubChem CID
125672
IUPAC Name
(2S)-2-[[(2S)-1-[(2S)-2,6-diaminohexanoyl]pyrrolidine-2-carbonyl]amino]-3-methylbutanoic acid. PubChem CID 125672 indexes this entity under the synonym "MSH (11-13)". No DrugBank monograph identified at audit date 2026-05-02. ChEMBL and UNII identifiers not located at audit date.
Solubility
Soluble in water and aqueous buffers; hygroscopic. Reconstitution typically performed in sterile bacteriostatic or distilled water for laboratory use. Quantitative aqueous solubility data are not publicly disclosed at PubChem CID 125672; for research use only.
Storage
Lyophilised powder: store at −20 °C protected from light. Reconstituted peptide: store at 2–8 °C and use within days; long-term aliquot storage at −20 to −80 °C. As a small linear tripeptide it is more stable to heat and freeze-thaw than larger peptides, but the free-acid C-terminus is susceptible to carboxypeptidase action; amidated forms (H-Lys-Pro-Val-NH₂ or Ac-Lys-Pro-Val-NH₂) are more enzymatically stable. Vendor / supplier certificate of analysis governs; for research use only.

Mechanism of Action

Studies report two parallel mechanisms for KPV: (1) anti-inflammatory NF-κB and MAP-kinase suppression with SLC15A1 / PepT1-mediated intracellular uptake into inflamed colonic epithelium, and (2) antimicrobial activity against Staphylococcus aureus and Candida albicans in vitro. Both mechanisms are described as LARGELY MELANOCORTIN-RECEPTOR-INDEPENDENT (Brzoska 2008 review). KPV is NOT a full MC1R / MC3R / MC4R / MC5R agonist and does NOT drive cutaneous melanogenesis — a critical disambiguation against afamelanotide and Melanotan II. Observed in research settings.

The mechanistic narrative built around KPV is that it captures the anti-inflammatory pharmacophore region of α-MSH without the receptor-activating full-length sequence, so it reproduces the anti-inflammatory effects of α-MSH without the pigmentation-driving MC1R-agonist effects. In Dalmasso 2008 KPV was characterised as a PepT1 substrate (Kₘ ≈ 160 μmol/L); PepT1 is normally expressed in the small intestine and is upregulated in inflamed colonic epithelium during ulcerative colitis and Crohn's disease — providing an inflammation-localised intracellular delivery mechanism that allows low oral doses to reach the cytoplasm of inflamed enterocytes. In the DSS-colitis murine model and the TNBS-colitis murine model, oral KPV administration reduced disease severity, body-weight loss and histological inflammation. In the CD45RBhi T-cell transfer colitis model, KPV improved weight regain and histological scores; the effect was partially preserved in MC1R-deficient mice — supporting receptor-independent activity (Kannengiesser 2008). Antimicrobial activity (Cutuli 2000) was reported at higher micromolar to picomolar concentrations depending on assay; the literature is sparse and predominantly in vitro, and no clinical antimicrobial application is established. IMPORTANT EDITORIAL SCOPING: KPV does NOT drive cutaneous melanogenesis, does NOT cause skin pigmentation, and does NOT mediate sexual-arousal function — those effects are mediated respectively by afamelanotide (MC1R agonism, FDA / EMA approved for erythropoietic protoporphyria), Melanotan II (cyclic MC1R / MC4R agonist), and PT-141 / bremelanotide (MC4R agonist, FDA approved for hypoactive sexual desire disorder in pre-menopausal women) — three pharmacologically OPPOSITE profiles in the same melanocortin family category. Mechanism statements here are intentionally hedged — studies report, observed in research settings — and never framed as established human pharmacology. Research use only.

Molecular Targets

  • NF-κB / MAP-kinase axis — Dalmasso 2008 (Gastroenterology, PMID 18061177): nanomolar KPV concentrations inhibit NF-κB and MAP-kinase signalling in cultured intestinal epithelial cells and immune cells
  • SLC15A1 / PepT1 (proton-coupled di/tripeptide transporter) — Dalmasso 2008 reports KPV as a PepT1 substrate (Kₘ ≈ 160 μmol/L); PepT1 is UPREGULATED in inflamed colonic epithelium during IBD, providing inflammation-localised intracellular delivery
  • Pro-inflammatory cytokines — IL-6, TNF-α, IL-1β; reduced expression in DSS-colitis and TNBS-colitis murine models (Dalmasso 2008; Kannengiesser 2008, Inflamm Bowel Dis, PMID 18092346)
  • Antimicrobial activity — Staphylococcus aureus (colony-formation inhibition) and Candida albicans (viability and germ-tube formation reduction) in vitro (Cutuli 2000, J Leukoc Biol, PMID 10670585); proposed mechanism: elevation of microbial cAMP
  • Human keratinocyte calcium signalling — Elliott 2004 (J Invest Dermatol, PMID 15102092) reports calcium-mediated responses in human keratinocytes WITHOUT the canonical MC1R-cAMP pathway
  • NOT a full MC1R / MC3R / MC4R / MC5R agonist — Brzoska 2008 review places KPV in a class of α-MSH C-terminal fragments whose anti-inflammatory effects are largely MELANOCORTIN-RECEPTOR-INDEPENDENT; pharmacologically OPPOSITE to afamelanotide (MC1R agonist), PT-141 (MC4R agonist) and Melanotan II (cyclic full-length analogue) despite a shared α-MSH lineage

Signaling Pathways

  • NF-κB suppression → reduced pro-inflammatory cytokine expression (IL-6, TNF-α, IL-1β) → histological improvement in DSS- and TNBS-colitis murine models (Dalmasso 2008; Kannengiesser 2008)
  • PepT1-mediated apical uptake → inflammation-localised intracellular delivery → NF-κB suppression in the cytoplasm of inflamed enterocytes — low oral doses reach functionally relevant intracellular concentrations because PepT1 is upregulated during IBD inflammation (Dalmasso 2008)
  • Antimicrobial: KPV / α-MSH elevate microbial cAMP → adenylyl cyclase inhibitor ddAdo partly reverses the antimicrobial activity (Cutuli 2000)
  • NOT classical MC1R-cAMP signalling in keratinocytes — Elliott 2004 specifically reported NO elevation of cAMP in keratinocytes under their conditions, in contrast to full-length α-MSH; calcium-mediated responses were observed instead

Research Applications

The published evidence base is predominantly preclinical (mouse in vivo + in-vitro cell culture and antimicrobial assays). The Hiltz / Catania / Lipton lineage of 1989–1991 established the α-MSH(11–13) pharmacophore concept; the Dalmasso 2008 / Kannengiesser 2008 IBD papers provided the murine colitis efficacy data and the PepT1 mechanism description. The Brzoska 2008 Endocr Rev review provides the receptor-independent synthesis. ClinicalTrials.gov v2 API audit on 2 May 2026: ZERO active registered human trials for KPV-as-tripeptide (see REGISTRY GAP above). Observed in research settings.

DSS-induced colitis (mouse) — in vivo, IBD efficacy

in vivo

Studies report that oral KPV administration reduced body-weight loss, histological inflammation and pro-inflammatory cytokine expression (IL-6, TNF-α, IL-1β) versus vehicle controls. Mechanistically linked to SLC15A1 / PepT1-mediated apical uptake into inflamed colonic epithelium.

— Dalmasso et al. 2008, Gastroenterology 134(1):166-178 (PMID 18061177)

TNBS-induced colitis (mouse) — in vivo, IBD efficacy

in vivo

Studies report that oral KPV administration reduced disease activity index (DAI) and histological inflammation versus vehicle controls. Consistent with the PepT1-mediated delivery model.

— Dalmasso et al. 2008, Gastroenterology 134(1):166-178 (PMID 18061177)

CD45RBhi T-cell transfer colitis (mouse) — in vivo, receptor-independence test

in vivo

Studies report that KPV improved weight regain and histological scores; the effect was partially preserved in MC1R-deficient mice and supports receptor-independent anti-inflammatory activity.

— Kannengiesser et al. 2008, Inflamm Bowel Dis 14(3):324-331 (PMID 18092346)

PepT1-mediated cellular uptake — in vitro, Caco-2 / HT29 cell cultures

in vitro

Studies report that KPV is a substrate of the proton-coupled di/tripeptide transporter SLC15A1 / PepT1 (Kₘ ≈ 160 μmol/L) and inhibits NF-κB and MAP-kinase signalling at nanomolar concentrations in intestinal epithelial cells and immune cells.

— Dalmasso et al. 2008, Gastroenterology 134(1):166-178 (PMID 18061177)

Antimicrobial activity — in vitro, Staphylococcus aureus and Candida albicans

in vitro

Studies report that α-MSH and the C-terminal tripeptide KPV inhibited S. aureus colony formation and reduced C. albicans viability and germ-tube formation. Proposed mechanism: elevation of microbial cAMP; the adenylyl cyclase inhibitor ddAdo partly reversed the killing activity. NOTE: concentrations are higher than the nanomolar anti-inflammatory range; no clinical antimicrobial application is established.

— Cutuli et al. 2000, J Leukoc Biol 67(2):233-239 (PMID 10670585)

Human keratinocyte signalling — in vitro, calcium-mediated responses

in vitro

Studies report that KPV elicits calcium-mediated responses in human keratinocytes without elevation of cAMP — DISTINCT from the canonical MC1R-cAMP pathway activated by full-length α-MSH. Supports the receptor-independent mechanism narrative.

— Elliott et al. 2004, J Invest Dermatol 122(4):1010-1019 (PMID 15102092)

Anti-inflammatory pharmacophore characterisation — in vivo, early mouse models

in vivo

Studies report that the α-MSH(11–13) sequence and stereochemical analogues (D-Lys, D-Pro, D-Val substitutions) retain anti-inflammatory / antipyretic activity in mouse models — establishing that the anti-inflammatory pharmacophore region of α-MSH is localised within the C-terminal three residues. The Hiltz / Catania / Lipton papers form the foundational citations of the KPV research lineage.

— Hiltz et al. 1991, Peptides 12(4):767-771 (PMID 1788140)

Receptor-independent model synthesis — review

preclinical

Review synthesises the hypothesis that α-MSH C-terminal tripeptides (KPV and similar analogues) exert anti-inflammatory effects LARGELY WITHOUT classical melanocortin-receptor agonism — a key disambiguation against MC1R pigmentation agonists (afamelanotide, Melanotan II) and MC4R sexual-function agonists (PT-141 / bremelanotide).

— Brzoska et al. 2008, Endocrine Reviews 29(5):581-602 (PMID 18612139, review)

Clinical Status

Regulatory Status
KPV is NOT approved — by the FDA, EMA, MHRA, PMDA, Health Canada, TGA, NMPA or ANVISA — and does not appear in any Western or international pharmacopoeia as an active substance. A systematic ClinicalTrials.gov v2 API query on 2 May 2026 for "KPV", "Lys-Pro-Val" and "tripeptide KPV" returned ZERO active registered human trials of KPV-as-tripeptide. Highest published phase: preclinical (mouse in vivo + in-vitro cell culture and antimicrobial assays); isolated topical or oral exploratory studies in humans without large registered RCTs. CRITICAL EDITORIAL CORRECTION — PCK3145 IS NOT KPV: earlier Triscience editorial drafts and external secondary sources may refer to PCK3145 as a "KPV-amide formulation" advanced by Procyon Biopharma in IBD research circa 2003–2008. THIS IS INCORRECT. PCK3145 is a 15-residue synthetic peptide derived from Prostate Secretory Protein 94 (PSP94), developed by Procyon Biopharma for METASTATIC HORMONE-REFRACTORY PROSTATE CANCER. The corresponding registered trial NCT00695851 ("Dose-Seeking Trial of PCK3145 in Asymptomatic, Castrate Metastatic Prostate Cancer Patients", Memorial Sloan Kettering Cancer Center, 2005–2009) is a PROSTATE CANCER trial, not an IBD trial, and PCK3145 has no structural or pharmacological relationship to KPV. NCT00695851 must NEVER be cited as a KPV development programme — it is a PCK3145 prostate cancer trial and is explicitly EXCLUDED from this KPV page. Anti-doping: KPV is not explicitly named on the WADA Prohibited List 2026, but as an unapproved peptide it falls under WADA Class S0 (Non-Approved Substances) by default for athletes-in-competition use. KPV does NOT fall under S2 (peptide hormones, growth factors, related substances and mimetics) because it is not a hormone analogue with anabolic or EPO-mimetic activity. No published WADA monograph or AAF (Adverse Analytical Finding) is associated with KPV at the time of audit.
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Highest Trial Phase
Highest published phase: preclinical (mouse in vivo + in-vitro cell culture). No registered human Phase 1/2/3 trial as of audit date 2026-05-02. ClinicalTrials.gov v2 API audit result: ZERO hits for "KPV", ZERO hits for "Lys-Pro-Val", ZERO hits for "tripeptide KPV".
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Sponsor
Academic research lineage: Hiltz / Catania / Lipton (Saint Louis University, early pharmacophore characterisation 1989–1991); Dalmasso / Merlin (Emory University, PepT1 mechanism and IBD efficacy 2008); Kannengiesser / Maaser / Brzoska / Luger (Universities of Münster and Heidelberg, IBD efficacy and melanocortin-receptor-independent model 2008). NO commercial development programme for KPV-as-tripeptide identifiable at audit date. Editorial correction: PCK3145 (Procyon Biopharma, NCT00695851 metastatic prostate cancer MSKCC 2005–2009) is NOT a KPV formulation and NOT a KPV development — it is a 15-residue PSP94-derived peptide for a different indication and is explicitly EXCLUDED from this page.
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Safety Profile

Observed in research settings

Limited human data — preclinical reports only. No large-scale RCTs of KPV-as-tripeptide have been completed or registered as of audit date 2026-05-02. No FDA-issued safety label exists. Statements about human safety are therefore OBSERVATIONAL AND UNCERTAIN. Observed in research settings; for research use only.

Adverse Events Reported in Studies

  • Murine studies: oral and intraperitoneal KPV administration (Dalmasso 2008; Kannengiesser 2008; Hiltz 1991) reported no overt acute toxicity at doses tested for anti-inflammatory effect — these studies were not designed as formal toxicology and did not characterise long-term, reproductive or carcinogenicity endpoints
  • Hypersensitivity and immunogenicity characterisation: as a short tripeptide KPV is generally regarded as low-immunogenicity, but post-translational modifications (acetylation, amidation) and impurities in research-grade preparations could in principle drive hypersensitivity — no published case series quantifies this
  • Mechanistic theoretical drug interaction: KPV's PepT1 dependency raises a theoretical interaction with other PepT1 substrates (β-lactam antibiotics, ACE inhibitors, valacyclovir) and with luminal pH — this is mechanistic speculation and not a clinical observation
  • Human studies: ZERO — no systematically captured adverse events from human studies exist because zero registered human KPV-as-tripeptide trials exist at audit date 2026-05-02

Serious Adverse Events

  • Human data gap: ZERO independent long-term pharmacovigilance dataset for KPV — multi-month or multi-year human safety data have not been published. Safety statements should be tagged exclusively as "limited human data — preclinical reports only"
  • Pregnancy / lactation: unknown; no data
  • Vendor-market caveat: KPV is widely sold by research-peptide vendors and prominent on bodybuilding, autoimmune-recovery, IBD-self-treatment, gut-health and biohacker forums (Reddit /r/Peptides, vendor blogs, podcast hosts) framed as an oral or sublingual "gut-healing peptide" — none of those framings reflects approved-medicine status. Triscience keeps KPV copy strictly research-only, not for human consumption
  • Anti-doping: WADA Class S0 (Non-Approved Substances) — default classification for non-approved peptides; NOT S2 (peptide hormones, growth factors, related substances and mimetics) because KPV is not a hormone analogue with anabolic or EPO-mimetic activity
  • Adverse-event registry signals: none located at audit date

References

  1. Hiltz ME, Catania A, Lipton JM Anti-inflammatory activity of alpha-MSH(11-13) analogs: influences of alteration in stereochemistry Peptides 1991;12(4):767-771. 1991 .

    DOI: 10.1016/0196-9781(91)90131-8 PMID: 1788140 View Source

  2. Cutuli M, Cristiani S, Lipton JM, Catania A Antimicrobial effects of alpha-MSH peptides Journal of Leukocyte Biology 2000;67(2):233-239. 2000 .

    DOI: 10.1002/jlb.67.2.233 PMID: 10670585 View Source

  3. Elliott RJ, Szabo M, Wagner MJ, Kemp EH, MacNeil S, Haycock JW alpha-Melanocyte-stimulating hormone, MSH 11-13 KPV and adrenocorticotropic hormone signalling in human keratinocyte cells Journal of Investigative Dermatology 2004;122(4):1010-1019. 2004 .

    DOI: 10.1111/j.0022-202X.2004.22404.x PMID: 15102092 View Source

  4. Dalmasso G, Charrier-Hisamuddin L, Nguyen HTT, Yan Y, Sitaraman S, Merlin D PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation Gastroenterology 2008;134(1):166-178. 2008 .

    DOI: 10.1053/j.gastro.2007.10.026 PMID: 18061177 View Source

  5. Kannengiesser K, Maaser C, Heidemann J, Luegering A, Ross M, Brzoska T, Bohm M, Luger TA, Domschke W, Kucharzik T Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease Inflammatory Bowel Diseases 2008;14(3):324-331. 2008 .

    DOI: 10.1002/ibd.20334 PMID: 18092346 View Source

  6. Brzoska T, Luger TA, Maaser C, Abels C, Böhm M α-Melanocyte-stimulating hormone and related tripeptides: biochemistry, antiinflammatory and protective effects in vitro and in vivo, and future perspectives for the treatment of immune-mediated inflammatory diseases (review) Endocrine Reviews 2008;29(5):581-602. 2008 .

    DOI: 10.1210/er.2007-0027 PMID: 18612139 View Source

Frequently Asked Questions

How is KPV different from afamelanotide, Melanotan II and PT-141?
KPV is the C-terminal tripeptide (3 amino acids: Lys-Pro-Val) of α-MSH. Afamelanotide is a full-length, 13-residue α-MSH analogue and an MC1R agonist, FDA / EMA approved to drive skin pigmentation in erythropoietic protoporphyria. Melanotan II is a cyclic 7-residue α-MSH analogue used recreationally (and not approved) for tanning. PT-141 / bremelanotide is a closely related cyclic peptide used clinically as an MC4R agonist for hypoactive sexual desire disorder. KPV does NOT drive pigmentation, does NOT have a sexual-function indication, and does NOT function as a classical melanocortin-receptor agonist; its primary reported activities are NF-κB inhibition and PepT1-mediated intestinal anti-inflammatory action — pharmacologically OPPOSITE to the three compounds above despite a shared α-MSH lineage.
Is KPV FDA-approved?
No. KPV has NO FDA approval and NO EMA marketing authorisation for any indication. It is an investigational research peptide. As of 2 May 2026 there are ZERO registered trials of KPV-as-tripeptide on ClinicalTrials.gov.
What is PCK3145, and is it the same as KPV?
PCK3145 is a DIFFERENT peptide — a 15-residue fragment of Prostate Secretory Protein 94 (PSP94), developed by Procyon Biopharma for METASTATIC PROSTATE CANCER (Phase I/II, e.g. NCT00695851 at Memorial Sloan Kettering Cancer Center, 2005–2009). PCK3145 is structurally and pharmacologically UNRELATED to KPV. Some secondary sources confuse the two; the dossier explicitly disambiguates them. NCT00695851 must never be cited as a KPV development programme — it is a prostate cancer trial of a structurally distinct peptide.
Has KPV been tested in inflammatory bowel disease?
KPV has been studied PRECLINICALLY in murine DSS-colitis, TNBS-colitis, and T-cell transfer colitis models (Dalmasso 2008; Kannengiesser 2008), with reductions in disease activity, body-weight loss and pro-inflammatory cytokine expression. There is NO published Phase 2 or Phase 3 randomised controlled trial in IBD, and no currently registered KPV-tripeptide IBD trial on ClinicalTrials.gov as of 2 May 2026.
What is the PepT1 transporter and why does it matter for KPV?
PepT1 (gene SLC15A1) is a proton-coupled di- and tripeptide transporter expressed on the apical surface of small-intestinal enterocytes. In inflammatory bowel disease, PepT1 expression is UPREGULATED IN INFLAMED COLONIC EPITHELIUM. Dalmasso et al. (2008) reported that KPV is a substrate of PepT1 (Kₘ ≈ 160 μmol/L), so oral KPV is preferentially delivered into the cytoplasm of inflamed colonic cells where it can suppress NF-κB. This inflammation-targeted delivery is a key mechanistic argument for KPV's preclinical IBD activity.
Is KPV banned by WADA?
KPV is not explicitly named on the WADA Prohibited List 2026. As an unapproved peptide, however, it falls under Class S0 (Non-Approved Substances) by default for athletes in competition. KPV is NOT classified under S2 (peptide hormones, growth factors, related substances and mimetics) because it is not a hormone analogue with anabolic or EPO-mimetic activity.

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