KPV

KPV is a peptide three amino acids long: lysine, proline, valine. It is the tail end of alpha-melanocyte-stimulating hormone (alpha-MSH), a hormone the body makes, and it drew attention in the late 1980s because that fragment carried anti-inflammatory activity in animals while the rest of the hormone carried the pigmentation activity. Researchers have worked on it since, mostly in rodent models of gut inflammation and mostly as a way of getting an anti-inflammatory signal into the lining of the colon.

What people research it for follows from that work. Gut inflammation is the dominant interest and it is the one the published literature actually addresses: colitis models, inflammatory bowel disease models, and the transporter that carries KPV into the cells lining the intestine. Skin is the second interest, driven by a 2015 nomination asking the FDA to let pharmacies compound KPV as a topical cream for wound healing and inflammatory skin conditions. A third group of claims circulates in community and vendor sources covering mast cell problems, histamine intolerance and post-viral illness, and those are covered on this page too, graded like everything else.

Each claim area is graded separately below, with the species and the model named on every result and the human record stated plainly. The reference list runs to 32 numbered sources: 23 primary research papers, four formal reviews and five agency documents, every identifier checked against PubMed, the DOI handle system or the issuing agency. The regulatory section is current to 2 August 2026, which matters this year: the FDA's Pharmacy Compounding Advisory Committee took KPV up on 23 July 2026, and what that meeting did and did not do is widely misreported.

Key takeaways

• KPV is not an approved drug anywhere, it is not on the FDA 503A Bulks List, and the advisory committee vote of 23 July 2026 changed neither of those things.
• Zero human studies of KPV exist on any route, confirmed three ways: a ClinicalTrials.gov search, a PubMed clinical-trial filter, and the FDA's own search across PubMed, Embase, DailyMed, Drugs@FDA and FAERS.
• Every result behind KPV comes from rodents, rabbits or cell culture: seven rodent colitis studies, a rabbit corneal wound model, a diabetic mouse wound model, and a body of work in human cell lines. [Animal] [1] [2] [6] [7] [8] [9] [11] [12] [13] [14] [15] [19] [20]
• KPV does not appear to act through melanocortin receptors: it fails to displace radiolabelled alpha-MSH, it produces no rise in cyclic AMP, and its anti-inflammatory effect in mice holds up under a melanocortin antagonist and in animals with a nonfunctional MC1 receptor. [Animal] [2] [3] [4] [5] [22]
• The FDA's own reviewers proposed not adding KPV free base or KPV acetate to the 503A Bulks List, in a document FDA published. That the committee then recommended inclusion over that proposal is reported by press and law-firm coverage only: FDA has published no minutes, transcript or vote record, and two separate voting questions were put.
• Passive movement of KPV across intact human skin fell below the limit of detection in a laboratory permeation study, which cuts directly against the topical cream the 2015 nomination asked for. [In-vitro] [17] [25]
• There is no toxicology package: neither the nominator nor the FDA identified an acute, repeat-dose, genotoxicity, reproductive or carcinogenicity study of either KPV form.
• Almost none of the animal work gave KPV in the form that is sold. The studies delivered it in drinking water, in eye drops, or inside an engineered hydrogel, nanoparticle or prodrug conjugate. [Animal] [7] [9] [11] [12] [13] [14] [15]
• Claims about mast cell activation, histamine intolerance, post-viral illness, Lyme disease and mould exposure circulate in community and vendor sources, and the FDA compiled that same list from promotional websites as evidence of drug marketing. [Anecdote] [25]

Who researches KPV?

Three groups arrive at this compound from different directions, and the published work speaks to them unevenly.

The largest group is reading about gut inflammation, usually after a diagnosis of ulcerative colitis or Crohn's disease, or after being told about intestinal permeability. That is where the literature sits: seven of the rodent studies on this page are colitis models. It is also where the distance between the literature and a person is greatest, because every one of those studies is a chemical injury created deliberately in a mouse or a rat over days, not a chronic illness lived with over years.

The second group is reading about skin, and often arrives from a cosmetic or wound-care angle. The 2015 compounding nomination that put KPV in front of the FDA was for a topical cream at 0.1 percent, and the strongest single piece of laboratory work on that route is a permeation study that measured essentially nothing crossing intact human skin.

The third group is reading about mast cells, histamine, post-viral symptoms, or chronic inflammatory conditions with no settled treatment. Nothing in the published record addresses any of those, and the matrix below grades those claims as what they are.

What is KPV?

Plain-English version: a chain of three amino acids, lysine then proline then valine, cut from the end of a hormone the body already makes.

Alpha-melanocyte-stimulating hormone is thirteen amino acids long and does two separate jobs. It drives pigmentation through a family of receptors called the melanocortin receptors, and a large literature reports that it damps down inflammation [21]. In 1989 two researchers gave mice graded amounts of just the last three residues, positions 11 to 13, and reported that the fragment lowered ear swelling in a graded way against both saline and a large corticosteroid comparison [1]. That fragment is KPV, and the reason anyone cares about it is that it appeared to carry the anti-inflammatory half of the hormone without the pigmentation half.

The second half of that description has held up better than the first. Four separate lines of work place KPV outside the melanocortin receptor family, and a 2010 review states that it lacks the entire sequence motif required to bind any of those receptors [22]. The four studies, and the one 2021 paper that reports the opposite, are set out in the mechanism section below.

So the common description of KPV as the business end of alpha-MSH is wrong in the way that matters. It is a fragment that produces anti-inflammatory readouts in laboratory systems by a route nobody has identified. The FDA said the same thing in its own review: the molecular targets underlying the pharmacological effects of KPV-related bulk drug substances remain unknown [25].

Lys-Pro-Val · C16H30N4O4, 342.4 g/mol

How strong is the evidence, claim by claim?

Every claim area this compound is discussed for gets a row, including the ones with the weakest support. The tier records what the row rests on, and the last column states what that work can and cannot show. Each tier links to its definition on the methodology page.

Rolled up, that puts KPV at evidence grade D Animals and anecdote . No completed human study of this compound for any use. The claim set is animal, in-vitro, and anecdote. A grade describes the quality of the research, not whether something works and not whether anyone should use it. The derivation is published.

How KPV is thought to work

Mechanism work on KPV splits into two questions that get conflated constantly. What KPV does to a cell has a reasonable amount of consistent evidence behind it. What KPV binds to in order to do it has none. The subsections below run in order of how well supported each one is.

What we do not know

The molecular target is the large gap. Four studies rule out the melanocortin receptors, one proposes importin-alpha-3, and nothing has confirmed it. The FDA reached the same conclusion in its 2026 review and wrote it in those words [25].

How much KPV reaches anything, in a person, is unknown on every route. No pharmacokinetic or pharmacodynamic measurement of KPV in a human being has been published, and the FDA's search across PubMed, Embase, ClinicalTrials.gov, DailyMed, Drugs@FDA and FAERS found none [25].

Whether free KPV survives long enough to act is also open. A stability study found it degrades under acid, alkaline and oxidative stress, with lysine-proline diketopiperazine identified as the major degradation product [16]. Nearly every recent KPV paper exists because free KPV does not survive delivery, which is why the literature is dominated by hydrogels, nanoparticles and prodrug conjugates.

And the pigmentation question is less settled than the standard framing suggests. The usual claim is that KPV keeps the anti-inflammatory half of alpha-MSH and drops the pigmentation half [21] [23]. A 2021 paper building KPV-modified liposomes for a vitiligo mouse model states the opposite in passing, describing a specific affinity for the MC1 receptor and reporting that the binding of KPV and its receptor contributed to activating the cyclic AMP and tyrosinase pathway and raising melanin content [29]. That paper is about a delivery vehicle carrying two other agents, so it is weak evidence for a receptor claim, but it is a published statement running against the consensus and it is not this site's job to hide it. Those two positions cannot both be right, and this site is not going to pretend one of them has been resolved.

Has KPV been tested in humans?

Two independent checks were run for this page on 2 August 2026, and two more were run by the FDA and published in its own review. All four returned the same answer.

The table records what each check covered, because in this category the difference between no trial, no completed trial and no published trial usually matters. For KPV all three are the same number.

Why we are not calling this proof

Nothing in that table is a failed trial. There is no discontinued program, no missed endpoint, no withdrawn registration. KPV has no clinical record at all, which is a different situation from a compound that was tested and did not deliver, and the difference matters when reading anything written about it.

The animal work is real work and some of it is careful work. What it cannot do is stand in for a human result. Every colitis study on this page created the injury on purpose, in a young healthy rodent, over days, and measured the outcome at a fixed point. Human inflammatory bowel disease is none of those things. The corneal study is a rabbit eye. The wound study delivered a growth factor alongside KPV and never separated the two.

The FTC sets the substantiation bar for a health claim at randomized controlled human trials, and says animal work, laboratory work and observational data are generally not enough on their own. For KPV there is none of the first and a reasonable amount of the rest. That is the whole picture, and it is why this page grades every claim area rather than answering the question most readers arrive with.

Benefits: what the research shows

Each heading below is a claim people make about KPV, not a finding. Under each one is what was measured, in what, and by whom.

Two formal reviews cover this ground and are worth naming, because they are frequently cited as though they contained data of their own. A 2008 review in Endocrine Reviews surveys the alpha-MSH and tripeptide literature [21], and a 2023 review covers the melanocortin system in inflammatory bowel disease [24]. Both summarise animal and cell work. Neither adds a human result, and neither is cited on this page as evidence of an effect.

The honest bottom line on benefits

None of the ten claim areas above is supported by a human result. That is not a hedge, it is the count: zero, on every route, confirmed four separate ways.

There is a second thing to say about the count, and it cuts the other way from the way counts usually get used. The studies behind these claims are not independent of each other. Author lists were checked against PubMed for this page, and two clusters run through most of the file. One investigator, Merlin D, is an author on references 7, 9, 10 and 11: four papers that between them carry the gut-inflammation row, the PepT1 transporter row and the tumour-model row. References 10 and 11 share five authors with each other, and references 7 and 9 share four. A second cluster covers references 12, 13 and 19: 12 and 13 share four authors, and 13 shares five with 19. Reference 19 is the only source for the wound-healing claim, and it comes from the same group as two of the seven colitis studies.

Put together, five of the seven colitis studies sit inside one of those two clusters. Only references 8 and 14 sit outside both. Overlapping authorship is not proof of a single laboratory and it is not an accusation about anyone's work: small fields are small, and a group that builds an assay tends to keep using it. But this site treats concentration of authorship as a quality signal when it reads other compounds, and a reader weighing seven studies should know that they are closer to three or four independent lines of evidence than to seven.

What anyone does with that is a judgement rather than a fact, and it belongs to the reader. This site reports what has been documented. It does not prescribe what should be done.

How long KPV stays in the body

There is no published half-life for KPV in a person, and there is no published half-life for KPV in an animal either. Nobody has reported a clearance figure or a bioavailability figure for it in any species. The FDA searched for human pharmacokinetic and pharmacodynamic data as part of its 2026 review and reported finding none [25].

Any half-life figure circulating online therefore came from somewhere other than a measurement of KPV. Some of them look borrowed from alpha-MSH, a different and much larger molecule with a different clearance route. Others have no traceable origin at all.

What has been measured is stability, which is a different property and a genuinely useful one. A 2015 assay identified lysine-proline diketopiperazine as the major degradation product under acid, alkaline and oxidative stress [16], a 2021 paper states that KPV solution is very unstable when given rectally [12], and a 2026 prodrug paper reports a conjugated form reaching 3.8 times the colonic accumulation of free KPV [14]. Three routes to the same conclusion about the free peptide.

No pharmacokinetic parameter has been reported for KPV in any species: no half-life, no clearance, no bioavailability. What exists instead is a relative colonic-accumulation comparison in colitis mice and laboratory stability work. [Animal] [12] [14] [16]

What is documented about dosing

No study has established an amount of KPV for a person, so there is no dosing section on this site in the sense other properties use the phrase. What can be reported is what published studies gave to their animals or their cells, in the model they used, and what kind of figures circulate elsewhere.

Commonly cited protocols (extrapolated, not validated)

Nothing here is a dosing recommendation. Statements about dosing reflect community and research reports only.

One thing in that table is worth pulling out: the marketed presentation, a lyophilised powder in a vial, has never been studied in any animal, let alone a person.

The second is that a concentration in a culture dish and a concentration in a rodent's drinking water are not doses and do not convert into one. Body-weight scaling between species is unreliable even between two mammals given the same route, and none of these studies used the route the compound is sold for.

Main routes people compare, and what each source class actually reported, are set out on the documented protocols page.

Reported effects and what has been measured

What the toxicology record contains

The FDA's 2026 review lists, item by item, what the nominator submitted and what the agency's own search returned for both KPV free base and KPV acetate: no acute toxicity study, no repeat-dose toxicity study, no genotoxicity study, no developmental and reproductive toxicity study, and no carcinogenicity study [25].

That is a complete absence rather than a set of reassuring results, and the two are not the same thing. A compound with a clean fourteen-day rodent toxicology study has a measurement behind it. KPV has none.

What has been reported to regulators

The FDA's Office of Surveillance and Epidemiology searched FAERS and the medical literature through 3 December 2025 and retrieved no adverse event reports and no literature cases for KPV [25].

The agency's own document states the limitation on that result, and the limitation is the important half. There is no documented clinical exposure to KPV, and the compounding channel it circulates through does not report adverse events to the FDA. A null return from a surveillance system nobody is reporting into measures the reporting, not the compound.

So the honest reading is that nothing is known in either direction. This site makes no claim about tolerability, because no data exists that could establish one.

Immunogenicity and aggregation, unassessed

The FDA's review notes that peptides as short as two amino acids have been shown to aggregate, that aggregation is itself a risk factor for immunogenicity, and that neither was assessed for KPV. Its conclusion, verbatim: based on available information there is insufficient data to conclude that KPV (free base) or KPV acetate do not present these risks [25].

That is a statement about what has not been ruled out rather than a statement that a problem exists. Both halves of it belong on this page.

The transporter finding, and why it sits in this section

The tumour-model result in the benefits section above has a second half that belongs here. In the same experiments, mice engineered to overexpress human PepT1 carried a larger tumour burden, knockout mice carried less, and human colorectal cancer biopsies showed increased PepT1 expression [10]. So the transporter that carries KPV into the gut lining is the same transporter that paper associates with tumour promotion, and nobody has followed up on what the combination means. [Animal] [10]

Chemical stability and the degradation product

A 2015 stability-indicating HPLC assay put KPV through acid, alkaline and oxidative stress in aqueous solution and in skin homogenate, and identified lysine-proline diketopiperazine as the major degradation product [16]. It is the only published account of what KPV turns into when it breaks down.

Nobody has characterised what that degradation product does, in any system. [In-vitro] [12] [16]

What has not been characterised

The FDA's reviewers concluded that both forms are not well characterized from the physical and chemical characterization perspective, on two grounds that do apply to both: naming conventions that do not follow INN, IUPAC or USAN standards, and the absence from both the public literature and the nomination package of substance-specific quality attributes including impurities, aggregates and microbiological tests [25].

On solubility the agency reached opposite conclusions for the two forms, and the difference is worth keeping straight. For the free base it recorded 0.7 mg per millilitre, called that limited, and said it could not evaluate the proposed 0.1 percent cream or gel because the nominator supplied no formulation information. For KPV acetate it recorded 5 mg per millilitre and concluded that solubility and particle size would not be issues of concern for those same dosage forms [25]. Worth noting where the free-base figure comes from: FDA's footnote sources it to a peptide vendor's certificate of analysis, which is the kind of document the sourcing section above is about.

Those are identity and quality findings rather than harm findings, and they are the reason the agency's own reviewers proposed against listing. A substance whose impurity profile has never been described cannot have its risks described either.

Talk to a licensed clinician about anything concerning your health.

Sourcing and quality

What a credible product should show

A certificate of analysis is the document that matters, and most of the work is in reading it rather than in having one. Three things make a certificate checkable: a lot number that matches the vial in front of you, a test date, and the name of the laboratory that ran the test rather than the name of the company selling the material.

What the common tests establish is narrower than it looks. High performance liquid chromatography separates what is in a sample and reports relative peak area, which is a statement about chromatographic purity. It does not establish the identity of the main peak. Mass spectrometry addresses identity by measuring molecular weight, which for KPV should land at 342.4. Neither test says how much peptide is in the vial: that is net peptide content, and it is reported separately, if at all.

For a compound like KPV the analytical questions worth asking are specific. Was the material tested for the diketopiperazine degradation product the stability literature identifies [16]? Is there an endotoxin result? Is there a sterility result? Those three are absent from most certificates circulating in this market, and their absence is a fact about the document rather than about any particular seller.

Red flags

A certificate with no lot number cannot be tied to the vial in your hand, whatever else it says. A certificate reproduced from a supplier without an independent test is a supplier's claim rather than a verification. A certificate dated well before the material was made covers a different batch.

A purity figure with no method named is not a purity figure. Ninety-nine percent by which measurement, against which reference standard, and with how much peptide in the vial are four separate questions, and one percentage answers none of them.

Widely circulated statistics about what fraction of products in this market are underdosed, or what fraction of certificates are fabricated, trace back to affiliate content sites rather than to a published testing program. This site does not publish them, because nobody has traced them to primary data. If a figure like that ever appears with a real methodology behind it, it will be cited here by number.

This site names no company adversely and names none favourably either. There is no best-vendor list here, no rating and no top pick, and there will not be one.

Will it show on a drug test?

For a tested athlete the answer is that KPV is prohibited, and the route to that answer is worth understanding because it is not the obvious one. KPV does not appear anywhere on the WADA 2026 Prohibited List. Neither does the word melanocyte, nor any melanocortin fragment [28].

It is reached instead by the S0 category, Non-Approved Substances, whose definition covers any pharmacological substance not addressed by another section of the list and with no current approval by any governmental regulatory health authority for human therapeutic use. That covers KPV exactly. S0 substances are prohibited at all times, in competition and out of it [28].

One precision point gets inverted constantly. The 2026 list states under the S0 heading that all prohibited substances in that class are Specified Substances. Specified status changes how a sanction is calculated, not whether the substance is banned. BPC-157 is named on the face of S0; KPV is not named on the list at all and is caught only by the general definition.

The US Department of Defense has no KPV-specific position. The Operation Supplement Safety ingredient and substance index and the DoD prohibited dietary supplement ingredients page, both checked on 2 August 2026, return no KPV entry, and OPSS carries no KPV article, unlike BPC-157, which appears on that index [30]. The general rule still reaches it: OPSS states that service members are prohibited from taking unapproved drugs as ingredients in dietary supplements, and KPV is an unapproved drug. Anyone writing that the Department of Defense has banned KPV by name is describing something that is not in the record.

Whether any other testing program looks for it is a question for that program. Anti-doping testing and workplace testing are different systems with different panels, and only the anti-doping side has published a position that reaches KPV at all.

Storage

The only published stability work on KPV is the 2015 forced-degradation study, which measured what happens under acid, alkaline and oxidative stress in aqueous solution and in skin homogenate and identified the major breakdown product [16]. It is a laboratory stress test rather than a shelf-life study, and nobody has published a shelf life for KPV in any presentation.

Read alongside the 2021 stability observation in the pharmacokinetics section, the picture is that KPV in solution is a moving target, and that the published literature has treated that as a formulation problem rather than a handling one.

This site publishes no handling or preparation procedure. That is a standing rule and the reasoning is on the editorial policy page.

Regulatory status, as of 8 August 2026

The 23 July 2026 meeting is the reason KPV is being written about this year, and most of what has been written about it goes wrong in the same two ways. The first is calling the outcome an approval. It was not one, and an advisory committee cannot issue one. The second is reporting a single vote.

The meeting itself was announced in the Federal Register on 16 April 2026, in a notice that also established a public docket and requested comments on the substances under review, under Docket No. FDA-2025-N-6895 [27]. That docket is where any comment on KPV had to go, and it is where the next step in the process will appear if the FDA takes one.

The FDA's published questions document for the meeting put two separate voting questions on KPV, one on KPV free base and one on KPV acetate, under the heading asking whether the agency should include certain bulk drug substances on the 503A Bulks List [26]. That document establishes what was asked. It does not record what was answered, and nothing FDA has published does. What is on the record from FDA is the other side of it: the agency's own reviewers wrote in their briefing document that on balance the physicochemical characterization, the information on historical use, and the lack of any effectiveness and safety information in humans for both forms weighed against adding them, and proposed not adding either [25]. That the committee then recommended inclusion over that proposal comes from press and law-firm coverage of the meeting, not from an FDA document.

A tally of 8 in favour, 6 against and 1 abstention has circulated in press and law-firm write-ups. As of 2 August 2026 the FDA has posted no minutes, no transcript and no vote record for that meeting: the 2026 meeting materials page carries the briefing documents, the questions, the agenda, the roster, webcast information and the FDA's own slides, and nothing else. So that tally has no primary source. And because two questions were put while every report gives one number, there is no way to say which question the number belongs to, or whether both went the same way. This page will carry the tally when the minutes exist and not before. Two things the meeting documents do establish, and the 503A record on this site reads them in full: FDA proposed that every one of the fourteen substances be kept off the list, and every nomination had already been withdrawn by the party that filed it, with FDA electing to proceed anyway.

What a listing would mean, if the FDA accepted the recommendation and finished the process, is that a licensed pharmacy could compound KPV for an identified patient against a valid prescription under section 503A. It would not be an approval, it would not create an over-the-counter product, and it would not make a direct unlicensed sale lawful. The process runs through a notice of proposed rulemaking, a comment period and a final rule [27], and that requirement cannot be bypassed. This page publishes no estimate of how long it takes, because no agency document states one.

Two facts about the nomination rarely appear in coverage. It was submitted by a compounding pharmacy in 2015 and later withdrawn, and the FDA evaluated KPV on its own initiative anyway [25]. And it asked only for a 0.1 percent topical cream or gel, for wound healing and inflammatory skin conditions, which is a much narrower question than most coverage implies [25]. There is also a mismatch worth recording: the nomination form answered yes to whether the substance had previously been compounded, while the FDA's check of the outsourcing facility product report database found no reported KPV compounding across eight and a half years [25].

Nothing about KPV's compounding status changed on 23 July 2026. It remains off the 503A Bulks List, for the reasons in the first row of the table above [25].

KPV compared with other anti-inflammatory peptides

Two of these five carry a grade and three do not, and that is deliberate: a grade is derived from tiered claim rows, and the source review behind them has been run only on KPV and GHK-Cu. BPC-157's registrations were pulled from the ClinicalTrials.gov API for this page; the TB-500 and larazotide rows repeat this project's earlier survey and say so, because a count carried across from internal notes is not a count checked against a registry.

The GHK-Cu row is worth reading against this one, because the two compounds sit at opposite ends of what the grade scale can express. KPV is D because nobody has tested it. GHK-Cu is B because it was tested twice and did not separate from its control either time. The higher letter belongs to the compound that failed, which is why the sentence beside every badge carries the direction in words.

The comparison people actually search for is KPV against BPC-157, and it is set out in full on its own page.

What KPV typically costs

KPV is sold both as lyophilised powder in vials and as capsule products, in a range of vial sizes. What any of it costs is not published here, and the price comparison page sets out why, along with the four things that actually move a listing.

The one thing worth carrying away is that nothing in a price says anything about identity, content or testing. Those are certificate questions, and they are covered in the sourcing section above.

See the price comparison.

Frequently asked questions

References

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2. Getting SJ, Schioth 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. PMID 12750433 DOI 10.1124/jpet.103.051623
3. 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. PMID 11239505 DOI 10.1016/s0006-2952(00)00583-9
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6. 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. PMID 22837805
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10. Viennois E, Ingersoll SA, Ayyadurai S, Zhao Y, Wang L, Zhang M, Han MK, Garg P, Xiao B, Merlin D. 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. PMID 27458604 DOI 10.1016/j.jcmgh.2016.01.006
11. Xiao B, Xu Z, Viennois E, Zhang Y, Zhang Z, Zhang M, Han MK, Kang Y, Merlin D. Orally targeted delivery of tripeptide KPV via hyaluronic acid-functionalized nanoparticles efficiently alleviates ulcerative colitis. Mol Ther. 2017. PMID 28143741 DOI 10.1016/j.ymthe.2016.11.020
12. Sun J, Xue P, Liu J, Huang L, Lin G, Ran K, Yang J, Lu C, Zhao YZ, Xu HL. Self-cross-linked hydrogel of cysteamine-grafted gamma-polyglutamic acid stabilized tripeptide KPV for alleviating TNBS-induced ulcerative colitis in rats. ACS Biomater Sci Eng. 2021. PMID 34547895 DOI 10.1021/acsbiomaterials.1c00792
13. Zhao Y, Xue P, Lin G, Tong M, Yang J, Zhang Y, Ran K, Zhuge D, Yao Q, Xu H. A KPV-binding double-network hydrogel restores gut mucosal barrier in an inflamed colon. Acta Biomater. 2022. PMID 35245681 DOI 10.1016/j.actbio.2022.02.039
14. Cheng J, Wu P, Li C, Han Y, Sun M, Dou Y, Chen S, Zhang J. Inflammation-triggered self-immolative conjugates enable oral peptide delivery by overcoming gastrointestinal barriers. Sci Adv. 2026. PMID 41533788 DOI 10.1126/sciadv.aea2989
15. 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. PMID 16965771 DOI 10.1016/j.exer.2006.07.014
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