Key Takeaways
- •KPV is Lys-Pro-Val, residues 11 to 13 of alpha-melanocyte-stimulating hormone (alpha-MSH): CAS 67727-97-3, C16H30N4O4, 342.43 g/mol. The acetate salt is 402.5 g/mol.
- •It does not act like its parent hormone at the melanocortin receptors. KPV failed to displace alpha-MSH binding and failed to raise cAMP in receptor-bearing cells, and the FDA's 2026 review says melanocortin receptors are "unlikely to be the molecular targets" of its effects.
- •Every published effect comes from cell lines and animal models, chiefly mouse colitis. No clinical trial has tested it, and the FDA found no human exposure data by any route.
- •In the United States it is not an approved drug. FDA staff originally recommended against adding it to the 503A compounding list, the advisory committee voted the other way in July 2026, and a draft HHS enforcement policy published on 30 October 2026 covers compounding by licensed pharmacies only.
- •In Canada it has no Drug Identification Number and no Notice of Compliance, so it cannot be sold as a medicine and is a research material.
- •For a tripeptide, identity is the real test. A three-residue peptide reaches a high HPLC purity easily, so mass spectrometry (MS) identity is what confirms the vial holds Lys-Pro-Val.
KPV is three amino acids long, it is cut from the tail of a hormone thirteen residues long, and it is described more loosely than almost any compound on the market. Other pages in both Canada and the United States incorrectly call it a melanocortin agonist, credit it with outcomes no human study has measured, and describe its US legal position as anything from "banned" to "now legal". This guide sets out what the molecule really is, what the published cell and animal research measured, what the FDA's own July 2026 review concluded, where KPV stands in Canada and in the United States today, and how to verify that a vial holds it.
It is written for laboratory and in-vitro research procurement. It reports what published studies recorded in cell lines and animal models because that is the whole of the evidence base. It contains no dosing, administration or human-use guidance, and none should be inferred.
What KPV Is
Alpha-MSH is a thirteen-residue peptide, Ser-Tyr-Ser-Met-Glu-His-Phe-Arg-Trp-Gly-Lys-Pro-Val, made from the precursor protein pro-opiomelanocortin. KPV is its last three residues, lysine, proline and valine, taken on their own. The literature also calls it alpha-MSH(11-13).
A dipeptide is a compound built from two amino acids, and a tripeptide, as the name suggests, is built from three. That size is not a detail. It decides how KPV gets into cells, how it is measured, and why its analytical profile looks nothing like a 30-residue peptide's.
| Property | Value |
|---|---|
| Sequence | Lys-Pro-Val (KPV) |
| Position in alpha-MSH | Residues 11 to 13, C-terminal |
| CAS number | 67727-97-3 |
| Molecular formula (free base) | C16H30N4O4 |
| Average mass (free base) | 342.43 g/mol |
| Monoisotopic mass | 342.2267 Da |
| Acetate salt | C16H30N4O4 · CH3COOH, 402.5 g/mol |
| Form | Lyophilized powder |
Free-base figures are from PubChem CID 125672; acetate figures are from the FDA's 2026 briefing document.
Free base and acetate are not interchangeable on paper
Synthetic peptides are usually isolated as a salt, and the counterion adds mass. KPV acetate is 402.5 g/mol against 342.43 for the free base, so the peptide is about 85% of the acetate's mass. The FDA treated the two as different active ingredients and evaluated them separately. For a researcher the practical point is net peptide content: a vial labelled by the mass of material inside it holds less peptide than that figure if the material is a salt, and a certificate that reports net peptide content is the one that tells you how much.
How KPV Works in the Published Research
It does not behave like alpha-MSH at the melanocortin receptors
Alpha-MSH acts by binding and activating the melanocortin receptors MC1R, MC3R, MC4R and MC5R. Because KPV is cut from alpha-MSH, many pages assume it acts at the same receptors. The experiments that tested that assumption found otherwise:
- Binding. In B16 mouse melanoma cells, which carry alpha-MSH receptors, KPV did not inhibit binding of a radiolabelled alpha-MSH analogue (Lyson et al. 1994). In RAW 264.7 macrophages carrying MC1R binding sites, KPV did not compete for binding "even in concentrations up to 1 mM" (Mandrika et al. 2001).
- Signalling. Alpha-MSH stimulated cAMP strongly in those macrophages, and KPV "was ineffective" (Mandrika et al. 2001). In mouse macrophages, a melanocortin agonist raised cAMP and KPV "failed to increase cAMP" (Getting et al. 2003).
- Blockade. KPV's effect on white-cell migration in mouse peritonitis was not blocked by an MC3/MC4 receptor antagonist, and it persisted in mice carrying a non-functional MC1R (Getting et al. 2003). Getting and colleagues concluded that KPV "is unlikely to mediate its effects through melanocortin receptors."
The FDA reviewed this same evidence in 2026 and wrote that "several lines of evidence suggest that MC receptors are unlikely to be the molecular targets underlying the anti-inflammatory and wound-healing properties of KPV." That is why a description of KPV as a melanocortin agonist is wrong, and why Volta files it under peptides on composition grounds rather than beside the melanocortin compounds.
The precise wording matters in one case. Kannengiesser and colleagues reported that KPV's effect in mouse colitis "seem[s] to be at least partially independent of MC1R signaling." That is a narrower statement than "never touches a melanocortin receptor."
It enters cells through PepT1, a transporter for small peptides
PepT1 is a membrane transporter that carries di- and tripeptides into cells. It is a transporter, not a receptor, meaning it moves small peptides across the membrane rather than being switched on by them.
Dalmasso and colleagues (Gastroenterology 2008) showed that KPV enters human intestinal epithelial cells (Caco2-BBE, HT29-Cl.19A) and human T cells (Jurkat) through PepT1. That route is a property of KPV's size, not of its parent hormone, since a 13-residue peptide is far too large for it. PepT1 is expressed at low levels in the healthy colon and rises during inflammation (Viennois et al. 2016), which researchers have proposed as a reason KPV reaches inflamed tissue more readily than healthy tissue. In the same 2016 study, KPV had no effect on tumour development in mice lacking PepT1, which is direct evidence that the transporter matters to what it does in that model.
Once inside, it damps NF-kappaB signalling
The intracellular findings converge on one pathway. NF-kappaB is a transcription factor that switches on many inflammatory genes.
- At nanomolar concentrations, KPV reduced NF-kappaB and MAP kinase activation and the secretion of inflammatory cytokines in intestinal and immune cell lines (Dalmasso et al. 2008).
- In macrophages it inhibited NF-kappaB nuclear translocation, by a route that did not depend on cAMP (Mandrika et al. 2001).
- In human bronchial epithelial cells, KPV was imported into the nucleus, stabilised the NF-kappaB inhibitor IkappaB-alpha, and blocked nuclear entry of the p65 subunit, apparently by interfering with the importin binding site on p65 (Land 2012).
So the current model, in cell culture, is uptake through PepT1 followed by interference with NF-kappaB at the nucleus. It is a model built from cell-line work, and the FDA describes these as mechanisms "researchers have proposed."
What the Animal and Cell Research Measured
Everything below is preclinical. Each line reports what one study recorded in its own model.
| Area | Model | What was reported | Study |
|---|---|---|---|
| Colitis | Mice, DSS and TNBS colitis, oral KPV | Reduced histological inflammation and lower pro-inflammatory cytokine expression | Dalmasso et al. 2008 |
| Colitis | Mice, DSS and T-cell transfer colitis | Earlier recovery, reduced inflammatory infiltrates and myeloperoxidase activity; in MC1R-deficient mice, all treated animals survived DSS colitis | Kannengiesser et al. 2008 |
| Colitis-associated tumours | Mice, AOM/DSS model | Fewer tumours in normal mice; no effect in mice lacking PepT1 | Viennois et al. 2016 |
| Oral delivery | Mice, ulcerative colitis | KPV in hyaluronic-acid nanoparticles reduced mucosal damage and TNF-alpha more than an untargeted form | Xiao et al. 2017 |
| Peritonitis | Mice | Reduced white-cell accumulation, not blocked by melanocortin antagonists | Getting et al. 2003 |
| Corneal wound | Rabbits, topical | Faster re-epithelialisation of an abraded cornea, reversed by a nitric oxide synthase inhibitor | Bonfiglio et al. 2006 |
| Antimicrobial | In vitro | Alpha-MSH and KPV reduced S. aureus colony formation and C. albicans viability | Cutuli et al. 2000 |
| Airway | Human bronchial epithelial cell line | Dose-dependent inhibition of NF-kappaB, IL-8 and eotaxin | Land 2012 |
| Skin permeation | Human cadaver skin, in vitro | Poor passive permeation; iontophoresis and microneedles increased it | Pawar et al. 2017 |
Three things about this body of work matter when reading anything written about KPV:
- Most of it is gut research in mice. The colitis models are where KPV has been studied most, and they are where the PepT1 finding gives a mechanistic reason for the result. The skin, eye and antimicrobial findings each rest on one or two studies.
- Much of the newer literature is about delivery, not new pharmacology. Nanoparticles, hydrogels, iontophoresis and prodrugs make up a large share of what has been published since 2017. These are formulation questions: how to get a small, water-soluble peptide to a target tissue intact.
- The percentages that circulate online come from animals. A figure such as a reduction in colonic myeloperoxidase is a measurement in a mouse colon. It is not a predicted human effect.
Is There Any Human Evidence?
No. The FDA's 2026 briefing document states that the agency "did not identify clinical studies in humans assessing pharmacokinetics or pharmacodynamics" of KPV by any route. Its search of the FDA Adverse Event Reporting System and the medical literature through 3 December 2025 retrieved no reports. It also found no acute toxicity, repeat-dose toxicity, genotoxicity or developmental and reproductive toxicity studies.
That last point is easy to misread. "No adverse events reported" is not the same as "shown to be safe": it means nobody has studied the question, so there is nothing to report. The FDA's own conclusion was that potential safety risks in humans "are unknown." A ClinicalTrials.gov search for KPV and lysine-proline-valine, checked 10 November 2026, returned no registered trial testing KPV as an investigational drug.
KPV in the United States
The US position changed four times between 2023 and October 2026, which is why pages written at different moments contradict each other. In order:
| Date | What happened | Source |
|---|---|---|
| 29 September 2023 | FDA placed KPV in Category 2 of nominated bulk substances, those raising potential significant safety risks in compounding | FDA, Certain Bulk Drug Substances list |
| 22 April 2026 | KPV removed from Category 2 because the nominator withdrew its nomination; FDA chose to evaluate KPV on its own initiative | FDA, 503A categories update |
| 23 July 2026 | FDA staff recommended against adding KPV free base or KPV acetate to the 503A Bulks List; the Pharmacy Compounding Advisory Committee voted to recommend adding it | FDA briefing document; trade press reported the vote as 8 to 6 with one abstention |
| 30 October 2026 | HHS published a draft enforcement discretion policy covering 503A compounding with six peptides, KPV among them | Federal Register, FR Doc. 2026-22192 |
What the FDA review concluded
FDA staff found that "a balancing of the criteria weighs against" placing either form of KPV on the list. Their reasons were that both forms are "not well-characterized" (no recognised naming standard, no public data on impurity identity, aggregates or microbiological quality), that no human data exist by any route, and that approved therapies already exist for the nominated uses of wound healing and inflammatory conditions. The committee's vote is advisory. It does not approve anything and does not bind the FDA.
What the October 2026 HHS policy does and does not do
The notice states that HHS "does not intend to take enforcement action against a State-licensed pharmacy, Federal facility, or licensed physician compounding a drug product" using a peptide on its Appendix A while FDA rulemaking on the 503A list proceeds. Read narrowly, which is how it is written:
- It is a draft and it is not binding. The notice says the policy "does not establish any rights for any person and is not binding on HHS or the public," and that HHS may revisit it if a safety or quality signal arises.
- It is not an FDA approval and does not add KPV to the 503A Bulks List.
- It covers prescription compounding by state-licensed pharmacies and physicians, and state pharmacy boards keep their own authority. Law-firm summaries of the appendix read it as limited to KPV acetate in topical and oral forms, and as not extending to material sold as research use only.
- Comments were open for two weeks after publication, on docket HHS-OASH-2026-0496.
None of this changes what a research-use-only vial is. Material sold for laboratory research is not a compounded drug, is not covered by the policy, and is not for human use.
KPV in Canada
| Question | Answer |
|---|---|
| Drug Identification Number | None |
| Notice of Compliance | None |
| Authorized as a medicine in Canada | No |
| Lawfully sold as a medicine | No |
KPV has no marketing authorization in Canada. An active-ingredient search of Health Canada's Drug Product Database for "KPV", "lysine-proline-valine" and "lysylprolylvaline" returned no result, checked 10 November 2026. With no DIN and no Notice of Compliance, no pharmacy stocks it and no product containing it may be sold as a drug. What is available is research-grade material, and what that means in Canadian law is set out separately.
Canada has no equivalent of the US 503A compounding lists, so the US advisory vote and the HHS policy have no effect here. Health Canada does act on peptides sold outside that framework: recall RA-82047, dated 5 May 2026, covered BPC-157 and GHK-Cu powder supplied to pharmacies as unauthorized active pharmaceutical ingredients.
Side by side
| Canada | United States | |
|---|---|---|
| Approved drug | No DIN, no Notice of Compliance | Not FDA-approved for any use |
| Compounding | No 503A equivalent | Draft HHS enforcement policy, 30 October 2026, licensed pharmacies only |
| Regulator's safety view | No published assessment | FDA 2026: human safety risks "unknown" |
| Research-use supply | Permitted for laboratory use | Permitted for laboratory use, outside the HHS policy |
| Human clinical trials | None registered | None registered |
How KPV Compares With BPC-157
KPV is often listed beside BPC-157 because both turn up in gut research. Chemically they have little in common.
| KPV | BPC-157 | |
|---|---|---|
| Length | 3 residues | 15 residues |
| Mass | 342.43 g/mol | 1419.5 g/mol |
| Origin | C-terminal fragment of alpha-MSH | Sequence from a gastric protein |
| Proposed uptake | PepT1 transporter | Not established |
| Main research focus | Intestinal inflammation, NF-kappaB | Gut and connective tissue models |
| Human clinical trials | None registered | None completed |
| US status, Nov 2026 | Not approved; in draft HHS compounding policy | Not approved; in draft HHS compounding policy |
| Canadian status | No DIN | No DIN; named in recall RA-82047, May 2026 |
The mass difference has an analytical consequence: BPC-157 is about four times larger, and a longer sequence has many more ways to go wrong during synthesis, so its impurity profile is richer and its HPLC purity figure carries more information. KPV is the opposite case, covered next. Both are stocked as single vials, BPC-157 10 mg and KPV 10 mg.
How to Verify a KPV Lot
A high HPLC purity figure is weak evidence for a three-residue peptide. Chromatographic purity is the share of the main peak, and the impurities it catches are mostly truncated or deletion sequences from synthesis. A 39-residue peptide has many ways to go wrong and a chromatogram that shows them. Three residues have very few, so a high figure is easy to reach and distinguishes little.
Mass spectrometry is the test that identifies it. KPV's monoisotopic mass is 342.2267 Da. A mass spectrometric identity check against a reference standard distinguishes Lys-Pro-Val from a different tripeptide of similar size, or from the same residues in the wrong order. For a compound this small, look for the identity method and the mass or transition reported, not just the purity percentage. More on the methods is in what actually proves a peptide sequence.
Know the degradation product to look for. Under acid, alkaline and oxidative stress, KPV acetate forms lysyl-proline diketopiperazine (Lys-Pro-DKP) as a major degradation product, per work the FDA cites. A cyclic dipeptide of that kind is a specific impurity a stability-indicating method should separate from the parent peak.
Check net peptide content as well as purity. Purity is a ratio of peaks and says nothing about how much peptide is in the vial. For a salt form in particular, net peptide content is the figure that tells you how much KPV you actually have.
Check the three things that make a certificate checkable:
- The laboratory is named, with its report number.
- The lot number on the document matches the vial in your hand.
- The laboratory publishes a verification page where the report number can be looked up independently.
A certificate that names no laboratory, or whose lot number matches nothing on the container, describes some other material. Volta publishes its certificates as page images in its published certificate archive with the issuing laboratory's own verification link. Those reports carry both HPLC and MS results. If you want a second opinion from outside the supplier, the peptide testing labs directory lists independent laboratories in both countries.
Storage and Handling
The figures below are the stability data the FDA's briefing document reported from the literature, for laboratory storage of the material.
| Form | Condition | Reported stability |
|---|---|---|
| Lyophilized free base | -20 °C, tightly closed | Up to 3 years |
| Lyophilized free base | 4 °C | Up to 2 years |
| Acetate (supplier CoA) | 2 °C to 8 °C, sealed | Long-term storage condition |
| Aqueous solution | -80 °C | Up to 6 months |
KPV free base is only modestly soluble in water, reported at 0.7 mg/mL, while the acetate dissolves at about 5 mg/mL. That difference is one more reason the salt form matters when a protocol depends on a stock concentration.
KPV Alone and Inside Multi-Component Vials
KPV is stocked on its own as a 10 mg vial, and it is one of four compounds in an 80 mg vial alongside GHK-Cu, BPC-157 and TB-500. The compound hub is KPV.
A composition certificate for a multi-component vial measures each compound separately, as covered in the analytical tradeoffs of a blend. It reports a purity and a net peptide content per component and states no single purity for the vial, because the vial is not one substance. When a figure is given for such a vial, the honest form is an average across the measured components with each component's own figure printed beside it, so the arithmetic can be repeated.
This matters when comparing a blend with a single-compound vial. The blend's 80 mg is divided across four compounds, so the quantity of any one of them is not the headline figure, and the per-component masses are on the certificate rather than the label.
Frequently Asked Questions
What is KPV peptide?
KPV is the tripeptide lysine-proline-valine, residues 11 to 13 at the C-terminal end of alpha-melanocyte-stimulating hormone. Its CAS number is 67727-97-3, its formula is C16H30N4O4 and its average mass is 342.43 g/mol as the free base.
What has KPV been studied for?
Mainly intestinal inflammation in mouse colitis models, where it reduced histological inflammation and inflammatory markers. Smaller bodies of work cover corneal wound healing in rabbits, antimicrobial activity in vitro, and airway epithelial cells in culture. All of it is preclinical.
How does KPV work?
In cell studies, KPV enters cells through PepT1, a transporter for di- and tripeptides, and then reduces NF-kappaB signalling, apparently by blocking nuclear entry of the p65 subunit. These are mechanisms proposed from cell-line work and have not been studied in humans.
Is KPV a melanocortin agonist?
No. KPV did not displace alpha-MSH from its receptors and did not raise cAMP in receptor-bearing cells, and its anti-inflammatory effect persisted when melanocortin receptors were blocked or non-functional. The FDA's 2026 review concluded the melanocortin receptors are unlikely to be its targets.
Is KPV FDA-approved?
No. KPV is not approved for any use. FDA staff recommended against adding it to the 503A compounding list in July 2026, the advisory committee recommended adding it, and on 30 October 2026 HHS published a draft enforcement discretion policy covering compounding by licensed pharmacies. None of those steps is an approval.
Is KPV legal in Canada?
KPV has no Drug Identification Number and no Notice of Compliance from Health Canada, so it cannot lawfully be sold as a medicine in Canada and no pharmacy stocks it. It is supplied as a research material for laboratory use only.
Is KPV legal in the United States?
It is not an approved drug and cannot be marketed as one. The October 2026 HHS draft policy describes when HHS will not take enforcement action against licensed pharmacies compounding it on prescription. Research-grade material is sold for laboratory use and falls outside that policy.
Is there an established dose of KPV?
No. The FDA found no human pharmacokinetic, clinical or toxicity studies, so no human dose has been established, and this guide gives none. Concentrations in the published literature are specific to cell cultures and animal models and do not translate to people.
Is KPV safe?
That has not been established. The FDA found no human data and no animal toxicity studies, and described the potential safety risks in humans as unknown. The absence of adverse-event reports reflects the absence of study, not evidence of safety.
Is KPV on the WADA Prohibited List?
KPV is not named on the list. WADA's section S0 prohibits at all times any pharmacological substance not approved by a government health authority for human therapeutic use, and KPV has no such approval in Canada or the United States.
What is the difference between KPV and BPC-157?
KPV is a three-residue fragment of alpha-MSH at 342 g/mol; BPC-157 is a fifteen-residue peptide at about 1,420 g/mol. KPV's uptake through PepT1 has been demonstrated in cell studies; no equivalent route has been established for BPC-157. Neither is approved in either country.
Why does purity matter less for KPV than for a longer peptide?
Chromatographic purity mainly detects synthesis impurities such as truncated sequences, and a three-residue peptide has very few ways to produce them. A high purity figure is therefore easy to reach and distinguishes little. Mass spectrometric identity against a reference standard is what confirms which molecule is present.
How is a multi-component vial's certificate different?
Each compound in the vial is measured on its own, so the certificate carries a purity and a net peptide content per component rather than one figure for the vial.
Sources
- Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, Yan Y, Sitaraman S, Merlin D. "PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation." Gastroenterology. 2008;134(1):166-178. doi:10.1053/j.gastro.2007.10.026. PMID 18061177. PMC2431115.
- Kannengiesser K, Maaser C, Heidemann J, et al. "Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease." Inflamm Bowel Dis. 2008;14(3):324-331. doi:10.1002/ibd.20334. PMID 18092346.
- Getting SJ, Schiöth HB, Perretti M. "Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) alpha-melanocyte-stimulating hormone peptides." J Pharmacol Exp Ther. 2003;306(2):631-637. doi:10.1124/jpet.103.051623. PMID 12750433.
- Mandrika I, Muceniece R, Wikberg JE. "Effects of melanocortin peptides on lipopolysaccharide/interferon-gamma-induced NF-kappaB DNA binding and nitric oxide production in macrophage-like RAW 264.7 cells: evidence for dual mechanisms of action." Biochem Pharmacol. 2001;61(5):613-621. PMID 11239505.
- Lyson K, Ceriani G, Takashima A, Catania A, Lipton JM. "Binding of anti-inflammatory alpha-melanocyte-stimulating-hormone peptides and proinflammatory cytokines to receptors on melanoma cells." Neuroimmunomodulation. 1994;1(2):121-126. PMID 7489322.
- Land SC. "Inhibition of cellular and systemic inflammation cues in human bronchial epithelial cells by melanocortin-related peptides: mechanism of KPV action and a role for MC3R agonists." Int J Physiol Pathophysiol Pharmacol. 2012;4(2):59-73. PMID 22837805. PMC3403564.
- Viennois E, Ingersoll SA, Ayyadurai S, et al. "Critical role of PepT1 in promoting colitis-associated cancer and therapeutic benefits of the anti-inflammatory PepT1-mediated tripeptide KPV in a murine model." Cell Mol Gastroenterol Hepatol. 2016;2(3):340-357. PMID 27458604. PMC4957955.
- Xiao B, Xu Z, Viennois E, et al. "Orally targeted delivery of tripeptide KPV via hyaluronic acid-functionalized nanoparticles efficiently alleviates ulcerative colitis." Mol Ther. 2017;25(7):1628-1640. PMID 28143741. PMC5498804.
- Bonfiglio V, Camillieri G, Avitabile T, Leggio GM, Drago F. "Effects of the COOH-terminal tripeptide alpha-MSH(11-13) on corneal epithelial wound healing: role of nitric oxide." Exp Eye Res. 2006;83(6):1366-1372. PMID 16965771.
- Cutuli M, Cristiani S, Lipton JM, Catania A. "Antimicrobial effects of alpha-MSH peptides." J Leukoc Biol. 2000;67(2):233-239. PMID 10670585.
- Pawar K, et al. "Transdermal iontophoretic delivery of lysine-proline-valine (KPV) peptide across microporated human skin." J Pharm Sci. 2017;106(7):1814-1820. PMID 28343991.
- Brzoska T, Luger TA, Maaser C, Abels C, Böhm M. "Alpha-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." Endocr Rev. 2008;29(5):581-602. PMID 18612139.
- US Food and Drug Administration. FDA Evaluation of KPV (Free Base) and KPV Acetate for Inclusion on the 503A Bulk Drug Substances List. Briefing document, Pharmacy Compounding Advisory Committee, 23-24 July 2026.
- US Food and Drug Administration. Pharmacy Compounding Advisory Committee; Notice of Meeting. Federal Register 91(73), 16 April 2026, FR Doc. 2026-07361, Docket FDA-2025-N-6895.
- US Department of Health and Human Services. Enforcement Discretion Policy Regarding 503A Compounding Using Certain Peptide Bulk Drug Substances; Notice of Availability. Federal Register, 30 October 2026, FR Doc. 2026-22192, Docket HHS-OASH-2026-0496.
- PubChem Compound Summary, CID 125672 (Lys-Pro-Val). National Library of Medicine.
- Health Canada Drug Product Database, active-ingredient search for KPV, lysine-proline-valine and lysylprolylvaline: no result returned, checked 10 November 2026.
- ClinicalTrials.gov search for KPV and lysine-proline-valine, checked 10 November 2026.
