KPV

KPV is a tripeptide best known for research as an anti-inflammatory, especially for gut inflammation. It's the tail end of the natural hormone alpha-MSH, though it seems to work through a different pathway, and unlike most peptides in this library, it's most commonly taken by mouth or applied topically rather than injected. It is not FDA-approved for any use and is sold only as a research peptide.

KPV has been studied mainly as an anti-inflammatory, especially for the gut. Most research is in cells and animal models of inflammatory bowel disease, where oral KPV was associated with reduced intestinal inflammation. Human evidence is limited to small pilot studies and case reports with no large controlled trials, so the gut, skin, and anti-inflammatory uses people pursue have not been confirmed in people. Its activity is thought to work mainly through a transporter (PepT1) rather than the pigmentation receptors alpha-MSH uses — in animal studies the anti-inflammatory effect held even when that pigmentation receptor was non-functional.

Not FDA approved for any indication. Research-community use only. Reviewed for the 503A Bulks List; no FDA determination issued — KPV (free base) and KPV acetate were on the Pharmacy Compounding Advisory Committee (PCAC) agenda for July 23–24, 2026, with uses evaluated listed as "wound healing and inflammatory conditions" (public docket FDA-2025-N-6895), and the committee met and voted on both forms on July 23, 2026. FDA's pre-meeting briefing document proposed that neither form be included. FDA has published no summary minutes, vote results, or determination from that meeting as of 2026-09-03, and a PCAC recommendation is advisory and non-binding — no outcome has been published by FDA, KPV is not on the 503A Bulks List, and 503A compounding is not permitted on that basis.[¹⁴] Not named in the WADA 2026 Prohibited List,[⁵] but WADA's S0 (Non-Approved Substances) category prohibits at all times any pharmacological substance with no current regulatory approval for human therapeutic use — which KPV lacks — so athletes in WADA-tested sport should treat KPV as prohibited-by-default under WADA S0. Not a DEA-scheduled / controlled substance — no entry in the DEA *Lists of Scheduling Actions, Controlled Substances, Regulated Chemicals* (August 2026 revision), checked 2026-09-08.[²⁰] Available primarily as a research peptide for oral and topical use; some injectable formulations also encountered. The published evidence base is predominantly preclinical (cell culture and DSS/TNBS colitis animal models); no PubMed-indexed human clinical trial of KPV was located as of 2026-07-18.

KPV is not FDA-approved, and its safety in humans has not been established in clinical trials. As of July 2026 the FDA is actively reviewing whether KPV should be added to the 503A compounding bulks list; no decision has been announced. KPV is not named on the WADA Prohibited List as of the 2026 edition, but WADA's S0 category covers any substance with no regulatory approval anywhere for human use, so tested athletes should assume it is prohibited. VialWise is a research and educational reference, not medical advice — consult a licensed professional.

⚠️ For research and educational purposes only. KPV is not approved by the FDA as a pharmaceutical drug for any indication. Information in this entry is informational, not medical advice. Always confirm dose calculations with the in-app calculator and consult appropriate professional guidance before any protocol decisions.

⚠️ KPV is most commonly used orally or topically — not injected. Unlike most peptides covered elsewhere in this library (which are subcutaneous-injection compounds), KPV is most commonly administered as an oral capsule or topical cream/spray. The PepT1 transporter that mediates KPV's cellular uptake is highly expressed in the small intestine and induced in inflamed colon tissue,[¹] which is the mechanistic basis for the oral route's effectiveness in IBD models. Some research-community use of injectable KPV exists, but the published evidence base is predominantly oral (for IBD/gut indications) and topical (for dermatologic indications). The Vialwise calculator and reconstitution table below cover the injectable form for completeness, but most KPV use does not require reconstitution math — capsules and topical formulations come pre-formulated.

⚠️ The KPV evidence base is preclinical — no human study was located at all. Essentially all published efficacy data for KPV is from cell culture and rodent models (Dalmasso et al. 2008 in DSS/TNBS colitis is the foundational paper),[¹] with independent replication in the same models.[⁶] As of 2026-07-18, targeted searching located no PubMed-indexed human clinical study of KPV of any size — not a randomized trial, not a pilot study, not a published case series — and no ClinicalTrials.gov interventional KPV trial. Research-community materials do reference small randomized studies in ulcerative colitis or atopic dermatitis with positive results, but no primary publication backing those claims could be found (see Pending Verification, where these are now recorded as *confirmed absent* rather than merely unlocked). Researchers should be explicit with themselves that the human evidence for KPV is unestablished, not simply thin, when interpreting subjective effects.

⚠️ Regulatory status was reviewed by FDA’s advisory committee and no determination has issued (as of 2026-09-03). KPV (free base) and KPV acetate were on the FDA Pharmacy Compounding Advisory Committee agenda for July 23–24, 2026, and that meeting took place and the committee voted, under consideration for the 503A Bulks List for "wound healing and inflammatory conditions" (docket FDA-2025-N-6895).[¹⁴] The meeting post-dates this entry's last update — no determination has been made, and nothing here should be read as approval, endorsement, or rejection. Re-checked 2026-09-03: the committee met and voted, but FDA has published no outcome or determination.

⚠️ Mechanism is predominantly PepT1-mediated, not melanocortin-receptor-mediated. Despite KPV being the C-terminal tripeptide of α-melanocyte-stimulating hormone (α-MSH), KPV's anti-inflammatory activity does not appear to *depend* on melanocortin receptor signaling.[¹] The compound is taken up into intestinal epithelial cells and immune cells by the PepT1 di/tripeptide transporter, where it acts intracellularly to inhibit NF-κB and MAP kinase pathway activation, reducing pro-inflammatory cytokine secretion. Supporting this, an independent group reported that KPV retained anti-inflammatory efficacy in mice whose MC1R was non-functional — i.e. the effect was at least partially MC1R-independent[⁶] — and a mechanistic review notes that KPV lacks the sequence motif required for binding the known melanocortin receptors while still retaining anti-inflammatory capacity "with a lack of any pigmentory action."[⁷] The literature is not unanimous: at least one report describes KPV as able to bind MC1R.[¹⁵] The honest framing is that weak or partial MC1R interaction has been reported but is not required for the anti-inflammatory effect. Researchers should not infer that KPV produces the pigmentation, sexual function, or appetite effects characteristic of α-MSH or its longer melanocortin analogues.

KPV is a tripeptide consisting of lysine, proline, and valine (Lys-Pro-Val; single-letter code KPV). Structurally, KPV is the C-terminal tripeptide of α-melanocyte-stimulating hormone (α-MSH) — specifically residues 11–13 of the parent 13-amino-acid hormone. Molecular weight is 343.4 Da. The compound is one of the smallest peptides in the Vialwise library and is also one of the few that is most commonly administered orally rather than by injection — which has substantial implications for both the clinical evidence base and the regulatory framing.

Mechanism of action. KPV is the C-terminal tripeptide of α-MSH, but its anti-inflammatory activity is predominantly not melanocortin-receptor-mediated.[¹] Instead, KPV is taken up into intestinal epithelial cells and immune cells by the PepT1 di/tripeptide transporter — a proton-coupled oligopeptide transporter normally expressed in the small intestine and upregulated in inflamed colon tissue during inflammatory bowel disease. Once inside the target cell, KPV acts intracellularly to inhibit activation of the NF-κB transcription factor and the MAP kinase signaling pathway, both of which are central to pro-inflammatory cytokine production (TNF-α, IL-1β, IL-6, IL-8) in immune and epithelial cells. The downstream consequences include reduced inflammatory cytokine secretion, reduced neutrophil infiltration, and reduced epithelial barrier dysfunction in inflamed tissue.[¹] The PepT1-mediated mechanism is mechanistically interesting because it provides a degree of inflammatory-tissue selectivity: PepT1 is upregulated specifically in inflamed colon tissue (in IBD), so KPV uptake is preferentially concentrated at the disease site. This is the mechanistic basis for why oral KPV is effective in colitis models despite the compound's short plasma half-life — the relevant pharmacokinetic compartment is the inflamed gut wall, not systemic circulation. An independent 2024 group has since built a PepT1-targeted nanodrug for DSS colitis on the same targeting rationale.[¹⁷]

On the melanocortin-receptor question specifically. The "not melanocortin-mediated" framing is well-supported but should not be stated as an absolute. An independent group (Kannengiesser et al. 2008, Münster) found that KPV reduced inflammation in DSS and transfer colitis models and that the effect was retained in mice with non-functional MC1R, concluding the activity is at least partially independent of MC1R signaling.[⁶] A mechanistic review from the same broader group states that KPV "lacks the entire sequence motif required for binding to any of the known MC-Rs" while retaining anti-inflammatory capacity with no pigmentary action.[⁷] Against that, Luger and colleagues (2003) describe KPV as able to bind MC1R.[¹⁵] The defensible reading of the current literature: weak or partial MC1R interaction has been reported, but melanocortin-receptor signaling is not required for KPV's anti-inflammatory effect.

Foundational preclinical evidence — DSS/TNBS colitis. The foundational mechanism and efficacy work for KPV in inflammatory bowel disease was published by Dalmasso and colleagues in 2008 in *Gastroenterology* ("PepT1-Mediated Tripeptide KPV Uptake Reduces Intestinal Inflammation").[¹] The paper demonstrated that orally administered KPV significantly decreased inflammation in dextran-sulfate-sodium (DSS)- and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis mouse models, with reductions in body weight loss, colonic myeloperoxidase (MPO) activity, histologic inflammation scores, and pro-inflammatory cytokine mRNA levels. The paper also established the PepT1-mediated mechanism by demonstrating that KPV's effects required PepT1 expression in intestinal and immune cells. This paper remains the most-cited primary source for KPV's mechanism and preclinical efficacy in IBD.

Targeted-delivery work — nanoparticle formulations. A 2017 paper (Xiao et al.) in *Molecular Therapy* (referenced via [PMC5498804](https://pmc.ncbi.nlm.nih.gov/articles/PMC5498804/)) demonstrated that hyaluronic-acid-functionalized nanoparticles loaded with KPV could deliver nanogram-level doses to the inflamed gut wall in mouse models of ulcerative colitis, producing measurable reductions in mucosal inflammation at far lower total doses than free oral KPV.[²] More recent work in the same vein reported an inflammation-triggered self-immolative KPV conjugate ("proKPV") that, in mouse models, achieved roughly 3.8× greater colonic accumulation than free KPV and showed efficacy at a 20× lower dose.[¹²] This delivery work is mechanistically interesting (demonstrating that KPV's local inflamed-tissue concentration is what matters, not systemic exposure) but has not translated to human clinical use — all of it remains preclinical.

Human clinical evidence — not located. The published human clinical evidence base for KPV is far thinner than the preclinical work. No randomized controlled trial of KPV — and no PubMed-indexed human clinical study of any size — was located as of 2026-07-18, and no ClinicalTrials.gov interventional KPV trial surfaced either. Research-community materials reference small pilot studies and case series in ulcerative colitis (oral and intrarectal formulations) and dermatologic indications (atopic dermatitis, psoriasis, oral mucositis), some describing positive efficacy and acceptable tolerability — but no primary publication backing those specific claims could be found. Researchers should treat the human clinical picture as unestablished, not merely under-documented.

Regulatory status — under active FDA review (updated 2026-07-18). KPV has never received FDA approval as a pharmaceutical drug for any indication, and that has not changed. What *has* changed is its compounding status. KPV-related bulk drug substances — "KPV (free base)" and "KPV acetate" — were on the agenda of the FDA's Pharmacy Compounding Advisory Committee (PCAC) meeting of July 23–24, 2026, and the committee met and voted on both forms on July 23, 2026, considering them for inclusion on the 503A Bulks List. Fda has published no minutes, vote results, or determination as of 2026-09-03, and KPV is not on that list. The FDA lists the uses evaluated as "wound healing and inflammatory conditions." A public FDA briefing document has been posted and the matter sits under public docket FDA-2025-N-6895.[¹⁴] The meeting post-dates this entry's last update, so no determination exists yet — KPV's bulks-list status is pending, and nothing here should be read as indicating that KPV has been added, rejected, approved, or endorsed. (The same session covers several other peptides, including BPC-157, TB-500, and MOTS-c.) This supersedes this entry's previous framing that KPV carried no peptide-specific designation and was governed by general 503A requirements — that description is no longer current. Oral and topical KPV are sold widely as research-peptide products in jurisdictions where this is permitted; the legal framing varies by jurisdiction, and researchers should expect the US picture specifically to move after July 2026.

Regulatory status — DEA. KPV is not a DEA-scheduled or controlled substance; no scheduling action for KPV was located. This is consistent with the other peptide entries in this library.

Regulatory status — WADA. KPV is not named in the WADA 2026 Prohibited List — direct text-search of the canonical 2026 WADA pdf returned no matches for "KPV", "Lys-Pro-Val", or "lysine-proline-valine".[⁵] KPV has no anabolic, GH-axis, or growth-factor activity and would not be expected to fall under the S2 categories covering peptide hormones and growth factors. However, not-named is not the same as not-prohibited. WADA's S0 (Non-Approved Substances) category prohibits, at all times, any pharmacological substance that has no current regulatory approval for human therapeutic use by any governmental health authority. KPV has no such approval anywhere — so S0 plausibly captures it, and the conservative, athlete-protective reading is that researchers competing in WADA-tested sport should treat KPV as prohibited-by-default under S0. A 2026 critical review of peptide use in sport lists KPV among peptides promoted for anti-inflammatory effects and notes the detection challenges such compounds pose, without asserting that KPV is named-prohibited.[¹⁶] Confirm against the most recent annual Prohibited List edition before any competitive event.

Common research interests. KPV is one of the most-used research peptides for inflammation-focused protocols, particularly: - Inflammatory bowel disease (oral) — the original and best-studied indication, with strong *preclinical* evidence (including independent replication in DSS and transfer colitis models[⁶]) and no located human trial. A 2025 independent review lists KPV among α-MSH-derived host-defense peptides that downregulate NF-κB in IBD contexts.[¹⁰] - Atopic dermatitis and other inflammatory skin conditions (topical) — mechanism rationale extrapolates from the same NF-κB / MAP kinase pathway inhibition seen in IBD models; in a 2025 cell-culture study, KPV mitigated fine-dust-induced keratinocyte apoptosis and inflammatory signaling via MAPK/NF-κB.[¹³] Note the delivery caveat: KPV required iontophoresis across microporated skin to achieve transdermal delivery in an ex-vivo human-skin study,[⁸] so passive absorption from an ordinary topical base should not be assumed. - Wound healing (topical) — the indication the FDA is evaluating for the 503A bulks list. A 2025 independent review of tripeptides in wound healing and skin regeneration reports that KPV-loaded hydrogels reduced inflammation, promoted tissue regeneration, and showed activity against MRSA in preclinical models;[¹¹] earlier work found α-MSH peptides including KPV inhibited *S. aureus* and *C. albicans* in vitro.[¹⁸] All preclinical. - Oral mucositis (topical or oral) — particularly post-chemotherapy and post-radiation. Research-community materials reference small clinical reports, but no published human study was located; the traceable foundational work is oral-mucosal cell-culture research. - General systemic anti-inflammatory protocols (oral) — research-community use as a low-side-effect anti-inflammatory adjunct, often stacked with other anti-inflammatory peptides or supplements. - Allergic/immune dysregulation (oral) — emerging research-community interest based on the broader anti-inflammatory mechanism, though specific clinical evidence for these uses is not established.

Commonly reported

• Mild local skin reactions (transient redness, mild itching) — uncommon
• Hypersensitivity reactions to formulation excipients — rare; specific to the carrier rather than KPV itself
• No serious adverse events reported in the published or research-community literature for topical use at typical concentrations
• Reported as generally well-tolerated in research-community accounts. ⚠️ There is no published human clinical dataset behind this — no PubMed-indexed human study of KPV was located as of 2026-07-18, so "well-tolerated" here reflects anecdote, not trial evidence, and carries all the reporting bias that implies
• Mild GI symptoms (nausea, mild abdominal discomfort) — uncommon, typically transient
• No consistent pattern of serious adverse events in research-community reports
• Injection site reactions (local redness, soreness, mild swelling) — uncommon
• Mild systemic effects (transient warmth, mild fatigue) reported rarely
• No consistent pattern of serious adverse events in research-community reports, though no controlled long-term safety surveillance exists
• Long-term safety in humans is essentially unknown. No multi-year human safety dataset exists for the modern research-community-use pattern (chronic oral use over months, often in stack with other peptides or supplements).
• Immunosuppression in immune-compromised researchers. KPV's mechanism reduces inflammatory cytokine production via NF-κB/MAP kinase inhibition. In researchers with active infection, immunocompromise, or active cancer, this anti-inflammatory action is theoretically concerning — but the magnitude of the effect at typical research-community doses is not well-characterized, and KPV's effect is far weaker than pharmacologic immunosuppressants.
• Drug interactions with active IBD medications. Researchers managing IBD with biologic therapy (anti-TNF, anti-integrin, anti-IL-12/23) or DMARDs should be aware that KPV's mechanism overlaps with these therapies' targets — the interaction is theoretical but worth flagging.
• Allergic / hypersensitivity reactions. Rare; researchers with known peptide-allergy histories should exercise caution.

Active immunosuppressive therapy (biologics, DMARDs, transplant immunosuppression) — caution; theoretical risk of additive immunosuppression though no published interaction data

Active major infection — caution; KPV's anti-inflammatory mechanism is theoretically concerning in the context of active infection requiring inflammatory response

Active cancer or undiagnosed malignancy concern — theoretical caution given KPV's anti-inflammatory mechanism; the specific human cancer-risk relationship for KPV at research-community doses is not established

Pregnancy and lactation: no data; default to contraindicated — no published reproductive toxicology in humans

Pediatric use: no data — should not be used in researchers under 18

Known peptide allergy or hypersensitivity — contraindicated

Severe IBD or active flare requiring hospitalization — KPV is not a substitute for pharmacologic IBD management; researchers managing active IBD should not substitute KPV for established therapies in collaboration with their gastroenterologist

Regulatory note (US — status changing): KPV is sold as a research peptide and has never been FDA-approved for any indication. KPV (free base) and KPV acetate are under active FDA review for the 503A Bulks List, scheduled for the Pharmacy Compounding Advisory Committee meeting of July 23–24, 2026 (uses evaluated: wound healing and inflammatory conditions; docket FDA-2025-N-6895).[¹⁴] The committee met and voted on both forms on July 23, 2026, and FDA's own briefing document proposed that neither be included. FDA has published no summary minutes, vote results, or final determination from that meeting as of 2026-09-03, and a PCAC recommendation is advisory and non-binding — panel review → FDA determination still pending → 503A compounding not permitted on that basis. Do not read the review as approval, endorsement, or rejection. Researchers should re-check the outcome — FDA had published none as of 2026-09-03 — and be aware of the regulatory environment in their jurisdiction.

Regulatory note (DEA): KPV is not a scheduled / controlled substance — no entry in the DEA's *Lists of Scheduling Actions, Controlled Substances, Regulated Chemicals* (August 2026 revision), checked 2026-09-08.[²⁰]

Regulatory note (WADA): KPV is not named in the 2026 WADA Prohibited List.[⁵] But not-named is not not-prohibited: WADA's S0 (Non-Approved Substances) category prohibits at all times any pharmacological substance lacking current regulatory approval for human therapeutic use by any governmental health authority — a description KPV fits. Researchers competing in WADA-tested sport should treat KPV as prohibited-by-default under S0 and confirm against the most recent edition before any competitive event.

Peptide

A short chain of amino acids, the building blocks of proteins. Many compounds in this library are peptides.

Preclinical

Research done in cells or animals, before human clinical trials. Promising preclinical results don't always hold up in people.

Topical

applied to the skin (as a cream or serum) rather than injected.

Anti-inflammatory

reducing the body's inflammation response.

1. Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, Yan Y, Sitaraman S, Merlin D. (2008). PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology, 134(1):166-78.(PMID 18061177)
2. Xiao B, Xu Z, Viennois E, Zhang Y, Zhang Z, Zhang M, Han MK, Kang Y, Merlin D. (2017). Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis. Molecular Therapy, 25(7):1628-1640.(PMID 28143741)
3. Hiltz ME, Lipton JM. (1989). Antiinflammatory activity of a COOH-terminal fragment of the neuropeptide alpha-MSH. FASEB Journal, 3(11):2282-4.(PMID 2550304)
4. Catania A, Lipton JM. (1993). Alpha-melanocyte stimulating hormone in the modulation of host reactions. Endocrine Reviews, 14(5):564-76.(PMID 8262006)
5. World Anti-Doping Agency. The 2026 Prohibited List, International Standard (effective 1 January 2026). Canonical PDF: wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf (linked from the WADA landing page at wada-ama.org/en/prohibited-list; local archival copy in `docs/legal/wada-2026-prohibited-list.pdf`). KPV is not listed in the 2026 WADA Prohibited List.
6. Kannengiesser K, Maaser C, Heidemann J, Luegering A, Ross M, Brzoska T, Bohm M, Luger TA, Domschke W, Kucharzik T. (2008). Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease. Inflammatory Bowel Diseases, 14(3):324-31.(PMID 18092346)
7. Brzoska T, Böhm M, Lügering A, Loser K, Luger TA. (2010). Terminal signal: anti-inflammatory effects of α-MSH related peptides beyond the pharmacophore. Advances in Experimental Medicine and Biology, 681:107-16.(PMID 21222263)
8. Pawar K, Kolli CS, Rangari VK, Babu RJ. (2017). Transdermal Iontophoretic Delivery of Lysine-Proline-Valine (KPV) Peptide Across Microporated Human Skin. Journal of Pharmaceutical Sciences, 106(7):1814-1820.(PMID 28343991)
9. Pawar KR, Nagarsenker M, et al. (2014). Stability-indicating HPLC assay for lysine-proline-valine (KPV). Biomedical Chromatography, 29(5):716-21.(PMID 25298219)
10. Rodrigues JM, et al., Franco OL. (2025). Host defense peptides as a new drug lead… for inflammatory bowel disease. Drug Discovery Today, 30(12):104535.(PMID 41241376)
11. Adnan SB, et al., Fadilah NIM. (2025). Exploring the Role of Tripeptides in Wound Healing and Skin Regeneration: A Comprehensive Review. International Journal of Medical Sciences, 22(16):4175-4200.(PMID 41209547)
12. Cheng J, et al. (2026). Inflammation-triggered self-immolative conjugates enable oral peptide delivery. Science Advances, 12(3):eaea2989.(PMID 41533788)
13. Sung J, et al. (2025). Lysine-Proline-Valine peptide mitigates fine dust-induced keratinocyte apoptosis and inflammation… MAPK/NF-κB pathway. Tissue and Cell, 95:102837.(PMID 40073467)
14. US Food and Drug Administration. July 23–24, 2026: Meeting of the Pharmacy Compounding Advisory Committee. FDA advisory-committee calendar: fda.gov/advisory-committees/advisory-committee-calendar/july-23-24-2026-meeting-pharmacy-compounding-advisory-committee-07232026. FDA briefing document: "FDA Briefing Document for KPV-Related Bulk Drug Substances" → fda.gov/media/193346/download. Public docket: FDA-2025-N-6895. The primary regulatory source for KPV's current 503A bulks-list review status. On July 23, 2026, the committee takes up KPV-related bulk drug substances — "KPV (free base)" and "KPV acetate" — for consideration for inclusion on the 503A Bulks List, with uses evaluated listed as "wound healing and inflammatory conditions." The same session covers BPC-157, TB-500, and MOTS-c.
15. Luger TA, Scholzen TE, Brzoska T, Böhm M. (2003). New insights into the functions of alpha-MSH and related peptides in the immune system. Annals of the New York Academy of Sciences, 994:133-40.(PMID 12851308)
16. Coutinho LFD, et al. (2026). A new era of doping? Use of peptide and peptide-analog drugs in… sport and bodybuilding: a critical review. Journal of Sports Medicine and Physical Fitness, 66(7):880-885.(PMID 41880199)
17. Zhang D, et al. (2024). PepT1-targeted nanodrug… for combined treatment of acute and chronic DSS-induced colitis. Frontiers in Pharmacology, 15:1442876.(PMID 39211778)
18. Cutuli M, Cristiani S, Lipton JM, Catania A. (2000). Antimicrobial effects of alpha-MSH peptides. Journal of Leukocyte Biology, 67(2):233-9.(PMID 10670585)
19. World Anti-Doping Agency. World Anti-Doping Code International Standard — Prohibited List 2026 (effective 1 January 2026). Canonical PDF: wada-ama.org, archived at `docs/legal/wada-2026-prohibited-list.pdf`. Cited for the verbatim S0 clause, resolving the flag that previously sat on this entry's regulatory line. S0 reads: "Any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use (e.g. drugs under pre-clinical or clinical development or discontinued, designer drugs, substances approved only for veterinary use) is prohibited at all times." Confirmed 2026-09-08. ⚠️ Methodology note. A live fetch of the WADA url on that date returned 0 bytes (blocked), so the archive could not be checksum-matched against the publisher. Corroboration came instead from an independent transposition of the same instrument into national law — the Austrian Federal Law Gazette, BGBl III Nr 219/2025 (rdb.manz.at), in which the S0 wording and the S2.2.2 named examples are identical and the same zero-hit searches reproduce.
20. U.S. Department of Justice, Drug Enforcement Administration, Diversion Control Division. Lists of Scheduling Actions, Controlled Substances, Regulated Chemicals, August 2026 revision, 139 pp. deadiversion.usdoj.gov. Cited for a negative scheduling result, which requires naming the full list and the date checked: a text search of the complete document on 2026-09-08 returned zero matches for "KPV", "Lys-Pro-Val" and "lysine-proline-valine". Extraction was validated with a positive control before the negative was trusted — Testosterone, Fentanyl, Ketamine and Oxycodone all resolve.

• BPC-157 — discussed together in this entry's stacks section
• LL-37 — same mechanism class
• Thymosin Alpha-1 — same mechanism class
• VIP — same mechanism class
• Chonluten — shared research area