KPV: Evidence, Stability, Dosing and the FDA Record

What is inflamed, what keeps it inflamed, and what would have to calm down

The tissue at the centre of this compound's whole record is a lining: the single layer of cells covering the inside of your gut, the surface of your eye, your airway, your gums, the underside of your skin. Every controlled win KPV has is in one of those.

What breaks down. A lining cell is held to its neighbour by tight junctions. Inflammation loosens them. Once loose, gut contents leak into the wall, immune cells arrive, and the cells release IL-1β, IL-6 and TNF-α — the three signals that show up in every KPV paper. Those signals loosen the junctions further. It is a loop that keeps itself running.

What makes it break down faster. More of the same signals. The master switch that turns them on is a protein pair called NF-κB, which sits idle in the body of the cell until inflammation frees it, at which point it walks into the nucleus and switches on the genes for all three cytokines. Every cycle of that loop damages more lining.

What builds it back. Lining cells divide fast — the gut resurfaces itself roughly every five days. The layer will rebuild itself if the inflammation stops. That is unusual and it is the reason this class of compound gets attention: you do not need to add anything, you need to remove the thing preventing repair.

What makes it build back faster, and how strong each link is. KPV walks into the nucleus itself and physically blocks NF-κB's ride into the nucleus — shown in a human airway cell line with the binding site identified, strong for a dish. That drops IL-1β, IL-6 and TNF-α — shown in mouse gut, rat gum, rabbit eye, human skin cells, consistent across four tissues, strong. Lower cytokines let the lining reseal — shown in mice and rats by wound closure and colon length, moderate. The same happens in a person — never tested by anyone, in any published study, by any route.

That last line is a row in the table, not the story. What follows is everything above it.

The tanning half was cut off and the calming half stayed

Alpha-MSH is thirteen residues — SYSMEHFRWGKPV. The last three are K, P and V. KPV as a free base is C16H30N4O4, molecular weight 342.43 g/mol, CAS 67727-97-3. The acetate salt adds an acetic acid molecule for 402.5 g/mol and carries the same CAS number in most references. Neither form has a UNII code, a United States Pharmacopeia monograph, a European Pharmacopoeia monograph or a Japanese Pharmacopoeia monograph.

Alpha-MSH itself was studied as an anti-inflammatory for decades and never became one, because it drives melanin production and nobody wanted to tan a colitis patient to treat their colon. Cutting the molecule down to its last three residues removed that problem: KPV keeps almost all of the anti-inflammatory capacity of the full hormone and produces no pigment change at all.

That is the design idea, stated by the people who proposed it, and it is the one claim about KPV that the literature and the regulator both accept without argument.

The obvious receptor was checked three times and it is not the one

Alpha-MSH works by docking onto melanocortin receptors, MC1 through MC5. The obvious guess was that its three-residue tail docks onto the same ones, more selectively. Three separate lines of evidence say it does not.

KPV cannot push radiolabelled alpha-MSH off rat brain tissue, off mouse melanoma cells, or off mouse immune cells carrying MC1R. Unlike alpha-MSH, it raises no cyclic AMP in those cells — meaning the docking signal never fires. Drug-blocking and gene-knockout approaches both failed to pin KPV's anti-inflammatory and wound-healing effects on MC2, MC3 or MC4.

Statement

Official disclosure

FDA Evaluation of KPV-Related Bulk Drug Substances (KPV free base and KPV acetate) for Inclusion on the 503A Bulk Drug Substances List — PCAC briefing document, 12 May 2026

“There is a lack of evidence to evaluate the effectiveness of KPV (free base) and KPV acetate products for the nominated uses of wound healing and inflammatory conditions. The nomination did not include, and FDA did not find any information on the use of KPV (free base) or KPV acetate administered in humans.”

Aug 4, 2026 · fda.gov

2026-08-04 08:30w_4lw9q2jv · #fb0b00b413a6

Human skin cells read the same. Neither alpha-MSH nor KPV produced any rise in cyclic AMP in HaCaT cells or in ordinary human skin cells. What did move was calcium inside the cell, across concentrations from 10⁻¹⁵ to 10⁻⁷ M.

The structural argument is blunter. KPV does not contain the sequence a molecule needs in order to bind any known melanocortin receptor at all — and it keeps the activity anyway. What it uses instead is not known.

So two things are settled. The anti-inflammatory effect is real in cells and animals. It is not a melanocortin receptor effect. What is open is what it is instead — and note the shape of that: this is a negative answer to a specific question, not an unexplored area. People were looking, and they found out it was not that.

It stops the inflammation switch from reaching the nucleus

The best-worked-out candidate is physical interference. KPV gets in the way of the ride NF-κB takes into the nucleus.

In an immortalised human airway lining cell line, KPV cut NF-κB reporter activity, matrix metalloproteinase-9 activity, and release of IL-8 and eotaxin, and it did more of all of that at higher doses. The effect tracked with KPV's own movement into the nucleus, with stabilisation of IκBα, and with tagged p65RelA failing to get into the nucleus. Competition experiments put KPV at the importin-α3 binding site on p65RelA — importin-α3 is the shuttle protein that carries NF-κB in — probably jamming armadillo domains 7 and 8. A comparison peptide, γ-MSH, needed MC3R in the same experiment. KPV did not.

Downstream, the pattern is the same everywhere it has been looked at: IL-1β, IL-6 and TNF-α fall. In immune cells stimulated with bacterial wall fragments, in colon tissue from mice with colitis, in rat gum tissue and in human skin cells stressed with air pollution particles, those three are what move.

Calming inflammation in a dish is not the same as calming inflammation in a person, and the gap between those two is where every unanswered question about KPV lives.

A door in the gut wall that opens wider the sicker the gut gets

PepT1 is a transporter built to pull two- and three-amino-acid fragments out of the gut and into the cell. It sits in the small intestine normally, is barely present in a healthy colon, and appears in large amounts in the colon lining during inflammatory bowel disease. KPV is a tripeptide. It fits through.

Radiolabelled KPV is carried by human PepT1 with a half-saturation point of roughly 160 µM in Caco2-BBE gut lining cells and roughly 700 µM in Jurkat immune cells, and unlabelled KPV competes with glycyl-sarcosine, the standard test substrate for that transporter. Once inside, concentrations in the billionths of a molar were enough to shut down NF-κB and MAP kinase signalling.

The transporter is not incidental to the story — it is the story. In mice given azoxymethane plus dextran sodium sulfate to trigger colitis and then colon cancer, KPV prevented the cancer in normal animals and did nothing whatsoever in animals bred without PepT1. Take the door away and the drug stops working.

This is why swallowing and rectal use get discussed at all for a peptide you would otherwise assume needs a needle. It also makes a specific, testable prediction: the sicker the colon, the more doors, and therefore the more gets in. That prediction has been confirmed in mice. It has never been checked in a person.

Every controlled result comes from a dish, a mouse, a rat or a rabbit

The three tables below are the complete usable evidence base, split by what kind of system produced each result. Doses are exactly as the papers report them.

In a dish

In animals

In people

Asking the ClinicalTrials.gov programming interface for KPV peptide on 4 August 2026 returned {"totalCount": 0}.

FDA searched independently and found the same. The nomination that put KPV in front of the agency cited nine references: eight were animal studies of various alpha-MSH derivatives, and the ninth was a skin-permeation experiment on cadaver skin.

Statement

Official disclosure

FDA Evaluation of KPV-Related Bulk Drug Substances (KPV free base and KPV acetate) for Inclusion on the 503A Bulk Drug Substances List — PCAC briefing document, 12 May 2026

“There is a lack of evidence to evaluate the effectiveness of KPV (free base) and KPV acetate products for the nominated uses of wound healing and inflammatory conditions. The nomination did not include, and FDA did not find any information on the use of KPV (free base) or KPV acetate administered in humans.”

Aug 4, 2026 · fda.gov

2026-08-04 08:30w_4lw9q2jv · #fb0b00b413a6

Plain KPV falls apart, which is why most of the research is about packaging

Read the animal table again and one thing is impossible to miss: hydrogels, nanoparticles, liposomes, film dressings, prodrugs, gels that set at body heat. That is not fashion. That is a whole field routing around a defect.

Put KPV under acid, alkali or hydrogen peroxide and the main thing you get back is lysine-proline-diketopiperazine. The lysine and proline ends curl round and bond to each other, the ring closes, and the peptide is gone.

KPV solution given rectally was described flatly as "very unstable", which is why the rat colitis work needed a thiolated polymer gel just to hold it together for two hours at body temperature.

The 2026 prodrug paper is the cleanest measurement of what that costs. Plain KPV swallowed at 1 mg/kg did nothing in mouse colitis. The same peptide, chemically caged so it survives the stomach and uncages only where reactive oxygen marks inflamed tissue, worked at half that dose and reached 3.8 times the concentration in the colon.

Trying to toughen the molecule by chemistry rather than packaging has cost the activity outright. Sticking a sugar-alkyl group on the lysine produced versions that shrugged off protein-cutting enzymes and killed nothing under any condition tested — including the acetylated parent.

Two things follow, and both are practical.

Nothing in the animal record shows that plain, unpackaged KPV swallowed reaches inflamed tissue in a useful amount. One paper specifically shows it does not.

And the storage numbers in the regulatory file are the ones to work from: dry powder is reported good for up to three years at −20 °C, two years at 4 °C, and three months at 15 °C, while once it is in water it is reported at six months at −80 °C, one month at −2 °C and one week at 10 °C.

Statement

Official disclosure

FDA Evaluation of KPV-Related Bulk Drug Substances (KPV free base and KPV acetate) for Inclusion on the 503A Bulk Drug Substances List — PCAC briefing document, 12 May 2026

“There is a lack of evidence to evaluate the effectiveness of KPV (free base) and KPV acetate products for the nominated uses of wound healing and inflammatory conditions. The nomination did not include, and FDA did not find any information on the use of KPV (free base) or KPV acetate administered in humans.”

Aug 4, 2026 · fda.gov

2026-08-04 08:30w_4lw9q2jv · #fb0b00b413a6

The two salts differ in how much will dissolve by a factor of seven

This is the detail most likely to leave you holding a cloudy vial and wondering whether you ruined it.

KPV free base dissolves in water only up to 0.70 mg/mL. KPV acetate is reported to dissolve at 5 mg/mL.

Statement

Official disclosure

FDA Evaluation of KPV-Related Bulk Drug Substances (KPV free base and KPV acetate) for Inclusion on the 503A Bulk Drug Substances List — PCAC briefing document, 12 May 2026

“There is a lack of evidence to evaluate the effectiveness of KPV (free base) and KPV acetate products for the nominated uses of wound healing and inflammatory conditions. The nomination did not include, and FDA did not find any information on the use of KPV (free base) or KPV acetate administered in humans.”

Aug 4, 2026 · fda.gov

2026-08-04 08:30w_4lw9q2jv · #fb0b00b413a6

Now do the arithmetic everyone does. A 10 mg vial with 2 mL of water in it is aiming for 5 mg/mL.

If the powder is the acetate salt, 5 mg/mL sits exactly on the reported ceiling — it will go in, with nothing to spare.

If the powder is the free base, 5 mg/mL is about seven times more than will dissolve. It physically cannot all go into solution. What you get is a suspension that looks nearly right, and the amount of actual peptide in each syringe depends on how recently you swirled it.

The part that makes this a real problem rather than a solvable one: the two forms share the same CAS number and are labelled inconsistently, so the container often does not tell you which one you have. FDA said exactly that, and called the naming conventions non-compliant with INN, IUPAC and USAN standards for that reason. If you want a fill that works either way, 0.70 mg/mL is the number that clears both — a 10 mg vial in 14 mL, which nobody does, or a smaller vial in more water.

One mark on the syringe is fifty micrograms

A U-100 insulin syringe holds 1 mL across 100 marks. One mark is 0.01 mL. Everything else falls out of the concentration.

Start there:

• 10 mg powder ÷ 2 mL bacteriostatic water = 5 mg/mL = 5,000 mcg/mL
• 1 mark = 0.01 mL × 5,000 mcg/mL = 50 mcg per mark

Putting the same 10 mg into 4 mL instead of 2 mL halves every number in the column and doubles the volume you inject for a given dose. That is usually the point: small doses are easier to measure when each mark is worth less. It also drops you to 2.5 mg/mL, which is under the acetate ceiling with room to spare and still five times over the free base's, so it does not solve the salt problem.

The dose people actually take rests on a unit conversion, not a trial. Scaled from rodent studies by body surface area, a human-equivalent starting dose has been published at around 0.2 mg — four marks on a 5 mg/mL fill.

That number carries the weight of an arithmetic conversion and nothing else. Nobody has measured how the body absorbs and clears KPV free base or KPV acetate, in any species. There is no measured half-life, no figure for how much reaches the blood, and no dose-response curve anywhere that would let a human dose be worked out rather than scaled from a mouse.

Statement

Official disclosure

FDA Evaluation of KPV-Related Bulk Drug Substances (KPV free base and KPV acetate) for Inclusion on the 503A Bulk Drug Substances List — PCAC briefing document, 12 May 2026

“There is a lack of evidence to evaluate the effectiveness of KPV (free base) and KPV acetate products for the nominated uses of wound healing and inflammatory conditions. The nomination did not include, and FDA did not find any information on the use of KPV (free base) or KPV acetate administered in humans.”

Aug 4, 2026 · fda.gov

2026-08-04 08:30w_4lw9q2jv · #fb0b00b413a6

What people taking it report, counted: 28 helped, 4 worse, 3 both, of 35

Sixty first-hand posts about KPV are catalogued as sources on this page — fifty from Reddit, ten from X, all pulled on 29 June 2026. Twenty-five of them are guides, product write-ups, questions, or regulatory commentary with no outcome in them. That leaves 35 posts where a named person says what they took and what happened.

Sorted by what they actually reported:

Read that honestly in both directions. This is a curated set, pulled from threads people started because they had something to say, and the direction of that bias is upward — nobody posts "took a peptide, nothing occurred, no further questions." The zero in the bottom row is the tell. For DSIP, catalogued the same way on the same day, five of thirty-five reports said nothing happened. Here, none did. Either KPV does something noticeable to nearly everyone who takes it, or the silent non-responders are not in the sample. Both of those can be true at once.

What the set is genuinely good for is a dose survey and a side-effect list, and on those two it is consistent. On a 10 mg vial in 2 mL — 50 mcg per mark — the reported range runs from four marks to ten. 200 to 500 mcg a day under the skin is what people take.

The 28 who said something got better

Twelve days under the skin at 200 mcg, one 5 mg vial, for gut symptoms — labelled anecdotal:

Forty days at 500 mcg a day, for mast cell symptoms:

Same condition, a different person, putting a number on it:

r/MCAS again, on fatigue and food tolerance:

Roughly 300 mcg a night by injection, from r/MCAS — and, from the same thread, the swallowed form causing flares where the injected form did not:

Skin is the second cluster. Eczema, four to five weeks in, with symptoms returning within two days of stopping:

Hidradenitis, in a stack:

Then the reports where the benefit is real but short. Two people independently describe roughly forty-eight hours of relief per injection and then a return to baseline:

And the outliers, which are worth keeping visible precisely because a single report proves nothing: a person whose supraventricular tachycardia episodes stopped for two months and came back two days after stopping the peptide:

The rest of the 28 — histamine tolerance, general inflammation, skin, nail fungus, dandruff, food reactions, rheumatoid arthritis alongside prescribed drugs, sacroiliac pain in a stack, hair thickening in a blend, and several "keeps it in the stack year-round" posts:

The 4 where a bad effect was the whole report

At the same doses. This matters — the negatives are not from people megadosing.

200 mcg, and the complaint is not physical at all:

250 mcg a night, day four:

An acute reaction within an hour of a small injected volume:

Dizziness, broken sleep, headaches, brain fog and fatigue, from a long-covid gut thread:

The 3 who got both

Eight days of clear improvement, then red bumps out of nowhere:

Gut repair, but only after months of climbing the dose slowly, with paradoxical reactions early:

And the one that splits by route rather than by person — swallowed did nothing measurable, injected moved a blood marker a long way:

Two patterns worth naming out loud

The first is a frame, not a finding. Fatigue, apathy and flu-like malaise appear over and over at 200–500 mcg, and the standard community explanation is a die-off or healing flare. That explanation cannot be wrong, because there is no result it excludes — every bad reaction becomes evidence the compound is working. Treat it as what it is: an unfalsifiable story wrapped around an adverse effect.

The second is a real, testable claim, and it appears in enough reports to take seriously: people who started very low and climbed slowly report the paradoxical reactions going away. That is a dose-response observation, and it is the only actionable thing the whole self-report record produces.

Duration is the other thing the reports agree on and the animal literature never measured. The effect is described as lasting days, not weeks — which fits a three-amino-acid peptide with no measured half-life and a known tendency to curl up into a diketopiperazine and stop existing.

None of this substitutes for a trial. It does establish three facts you would otherwise learn by accident: the dose is 200–500 mcg under the skin, bad reactions at that dose are common enough to fill threads, and the swallowed and injected forms are not experienced as the same thing.

Swallowed, injected, rubbed on, sprayed up the nose — what changes

All four are sold. The evidence behind each is not remotely equal.

Swallowed has the strongest mechanical case, because PepT1 is a real door, KPV is a real fit for it, and the door opens wider in inflamed bowel. Against that: the single experiment that pitted plain swallowed KPV against a packaged version found the plain version inert.

Rectal puts the peptide against the target tissue directly, and was shown to need a stabilising gel to survive long enough to do anything.

Rubbed on has an explicit measurement against it. Across human cadaver skin, KPV left on the surface crossed at a rate below the 0.01 µg/mL detection limit. It took microneedles punching through the outer layer to reach 4.4 µg/cm²/h, and a small electric current on top of that to multiply it further. Nothing crosses intact skin on its own in any amount you can measure.

FDA reached the same conclusion and pointed out that it cuts both ways: poor skin crossing limits how much reaches the bloodstream and therefore limits systemic toxicity, and it equally limits KPV's usefulness as a cream, because it may never reach the living skin layers under the dead outer one.

Statement

Official disclosure

FDA Evaluation of KPV-Related Bulk Drug Substances (KPV free base and KPV acetate) for Inclusion on the 503A Bulk Drug Substances List — PCAC briefing document, 12 May 2026

“There is a lack of evidence to evaluate the effectiveness of KPV (free base) and KPV acetate products for the nominated uses of wound healing and inflammatory conditions. The nomination did not include, and FDA did not find any information on the use of KPV (free base) or KPV acetate administered in humans.”

Aug 4, 2026 · fda.gov

2026-08-04 08:30w_4lw9q2jv · #fb0b00b413a6

Sprayed up the nose has no published measurement of any kind.

It kills bacteria and yeast in a dish and has never been measured in a body

Alpha-MSH peptides including KPV stopped Staphylococcus aureus forming colonies and cut Candida albicans survival and germ-tube formation, down to concentrations in the trillionths of a molar. Unusually for an anti-inflammatory, they made white blood cells kill both organisms better rather than worse — most things that calm inflammation blunt that.

The version taken furthest toward antifungal development is the double, [Ac-CKPV]₂, built by joining two KPV units through a cysteine-cysteine bridge. It works against Candida strains that azole drugs no longer touch.

The MRSA result in the rat mouth-ulcer model is the closest thing to a confirmation in a living animal, and it needed a sticky gel holding the peptide against the wound for seven hours to get there.

Where the evidence stops, and the swap that gets made

Two things in this file are solid enough to act on, and neither is a musculoskeletal finding.

The first is inflammation in a lining. Every controlled win KPV has is in one — bowel, cornea, airway, skin, gum. If your problem is a gut that is inflamed, that is the strongest part of this record and it is genuinely the strongest part.

The second is the pairing with BPC-157, which is what most gut protocols actually run.

Now the swap, because it is made constantly and it is worth being able to spot.

No study in any table above used a tendon, a ligament, a disc or a joint. There is no rat Achilles study. No ligament cut study. No cartilage study. The wound-healing results are all in linings — a scraped cornea, a diabetic skin wound, a mouth ulcer — and resealing a one-cell-thick lining is a different job from rebuilding collagen in a tendon. Lining cells divide every few days and re-cover a surface. Tendon rebuilds by laying down and remodelling collagen fibres over months, using different cells and a different signal set.

So the sentence "KPV helps tissue heal" is true and useless, and it is the sentence that does the work. Someone reads it and hears "KPV will help my rotator cuff." That is a cornea result laundered into a shoulder claim, and the laundering happens in the word tissue.

The honest version is four clauses long. KPV reduces inflammatory signalling in the linings of animals. It has never been given to a person in a published study. It has no measured human dose. And it is currently proposed for exclusion from legal compounding in the United States.

FDA proposed in July 2026 that KPV stay off the compounding list

The regulatory position has two layers and they get conflated constantly.

The older layer: KPV sits on FDA's table of bulk drug substances that were nominated for compounding and then withdrawn by whoever nominated them, filed under substances that may present significant safety risks. The agency's entry says it "has not identified any human exposure data on drug products containing KPV administered via any route of administration" and "lacks important information regarding any safety issues raised by KPV, including whether it would cause harm if administered to humans."

Statement

Official disclosure

Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks — FDA

“KPV — FDA has not identified any human exposure data on drug products containing KPV administered via any route of administration. FDA lacks important information regarding any safety issues raised by KPV, including whether it would cause harm if administered to humans.”

Aug 4, 2026 · fda.gov

2026-08-04 08:31w_fquamfa9 · #bbafed64a833

The newer layer matters more. The nomination was withdrawn, and FDA chose to take KPV to its advisory committee anyway. On 23 July 2026 the Pharmacy Compounding Advisory Committee heard KPV free base and KPV acetate alongside BPC-157, TB-500 and MOTS-c, with the uses under evaluation recorded as wound healing and inflammatory conditions.

Statement

Official disclosure

Pharmacy Compounding Advisory Committee; Notice of Meeting — Bulk Drug Substances Nominated for Inclusion on the Section 503A Bulk Drug Substances List, 91 FR (16 April 2026)

“KPV (free base), KPV acetate — Uses evaluated: Wound healing and inflammatory conditions.”

Aug 4, 2026 · federalregister.gov

2026-08-04 08:32w_x3r14ud2 · #5b44dcbde045

FDA's position going in was not ambiguous: "FDA is proposing that KPV (free base) NOT be included on the 503A Bulks List" and "FDA is proposing that KPV acetate NOT be included on the 503A Bulks List."

Statement

Official disclosure

FDA Briefing Document Introduction, Pharmacy Compounding Advisory Committee, July 23-24 2026 — Points to Consider

“3. FDA is proposing that KPV (free base) NOT be included on the 503A Bulks List. 4. FDA is proposing that KPV acetate NOT be included on the 503A Bulks List.”

Aug 4, 2026 · fda.gov

2026-08-04 08:31w_b5ztk84s · #5e38ccfea1e1

The reasoning, dated 12 May 2026, weighed four criteria and found against on all four.

Neither form is well characterised: the naming is inconsistent, and no certificate of analysis, impurity profile, clumping test or microbiology data was supplied or found in the literature.

How much it has historically been compounded is unknown: outsourcing facilities reported compounding no KPV products at all between January 2017 and June 2025, while telehealth and compounding websites sell injectable, swallowed, topical and nasal-spray KPV for inflammatory conditions, wound healing, skin health, gut health, killing microbes, and protection against nerve damage and stroke.

There is no evidence it works, because there is no human data.

And there is no safety evidence in either direction.

Statement

Official disclosure

FDA Evaluation of KPV-Related Bulk Drug Substances (KPV free base and KPV acetate) for Inclusion on the 503A Bulk Drug Substances List — PCAC briefing document, 12 May 2026

“There is a lack of evidence to evaluate the effectiveness of KPV (free base) and KPV acetate products for the nominated uses of wound healing and inflammatory conditions. The nomination did not include, and FDA did not find any information on the use of KPV (free base) or KPV acetate administered in humans.”

Aug 4, 2026 · fda.gov

2026-08-04 08:30w_4lw9q2jv · #fb0b00b413a6

What that means in practice: getting onto the 503A Bulks List is what makes a substance lawfully compoundable when it has no monograph and is not part of an approved drug. FDA has proposed it not get on.

Unknown is not the same as safe

FDA's Office of Surveillance and Epidemiology searched the FDA Adverse Event Reporting System and the medical literature for harms linked to KPV, through 3 December 2025. The reporting system returned nothing. The literature search found no cases. A separate search of the Human Foods Program adverse event system covering 1 January 2004 to 3 December 2025 also came back empty.

Statement

Official disclosure

FDA Evaluation of KPV-Related Bulk Drug Substances (KPV free base and KPV acetate) for Inclusion on the 503A Bulk Drug Substances List — PCAC briefing document, 12 May 2026

“There is a lack of evidence to evaluate the effectiveness of KPV (free base) and KPV acetate products for the nominated uses of wound healing and inflammatory conditions. The nomination did not include, and FDA did not find any information on the use of KPV (free base) or KPV acetate administered in humans.”

Aug 4, 2026 · fda.gov

2026-08-04 08:30w_4lw9q2jv · #fb0b00b413a6

An empty harm database for a substance nobody has published on giving to humans measures the literature, not the compound. Reporting to that system is voluntary, and compounders working under section 503A generally do not report to FDA at all. Meanwhile four of the thirty-five first-hand posts above describe a bad reaction, and none of those four is in any database.

No acute toxicity study exists. No repeat-dose toxicity study. No genotoxicity study. No developmental or reproductive toxicity study, of either form. FDA's stated worry is clumping and whether the immune system reacts to it, and neither can be assessed without the impurity and aggregate data the nomination never supplied.

The narrower operative fact: what circulates is research-grade powder from suppliers whose certificates of analysis FDA could not locate, and the agency's specific objection is that nobody can tell from the label whether a given vial holds the free base or the acetate — which, per the section above, decides whether your 10 mg in 2 mL is a solution or a suspension.

Where every number above came from

Primary literature, by PubMed identifier. PMID 18061177 (PepT1 uptake, Gastroenterology 2008); PMID 18092346 (DSS and transfer colitis, Inflammatory Bowel Diseases 2008); PMID 27458604 (PepT1 knockout and colitis-driven cancer, 2016); PMID 22837805 (p65RelA blocked from the nucleus, 2012); PMID 21222263 and PMID 18612139 (the melanocortin-receptor-independence argument); PMID 15102092 (skin cell cyclic AMP and calcium); PMID 10670585 and PMID 15946192 (killing microbes, and the CKPV double); PMID 16965771 (rabbit cornea); PMID 2550304 and PMID 6333677 (the original mouse and rabbit work, 1989 and 1984); PMID 25298219 (the stability assay and the diketopiperazine breakdown product); PMID 28343991 (human cadaver skin); PMID 19909746, PMID 28143741, PMID 34547895, PMID 34846053, PMID 36240893, PMID 39252648 and PMC12802832 (the packaging literature); PMID 29953505 (sugar-alkyl versions, activity lost); PMID 40073467 and PMID 42064835 (recent skin and liver cell work).

Trial registries. ClinicalTrials.gov programming interface v2, query "KPV peptide", 4 August 2026: {"totalCount": 0}. No registered study of KPV in people exists.

Regulatory record. FDA's evaluation of KPV-related bulk drug substances dated 12 May 2026; the briefing document proposing exclusion from the 503A Bulks List; the Federal Register notice of 16 April 2026 announcing the meeting and the uses evaluated; and the standing FDA page listing KPV among bulk substances nominated but withdrawn.

Statement

Official disclosure

July 23-24, 2026: Meeting of the Pharmacy Compounding Advisory Committee — FDA

“On July 23, 2026, the Committee will discuss the following bulk drug substances being considered for inclusion on the 503A Bulks List: BPC-157-related bulk drug substances, KPV-related bulk drug substances (KPV (free base)/ KPV acetate), TB-500-related bulk drug substances, and MOTs-C-related bulk drug substances. Uses evaluated for KPV: Wound healing and inflammatory conditions.”

Aug 4, 2026 · fda.gov

2026-08-04 08:31w_zjkqhidi · #9ec597559e73

Chemistry. PubChem CID 125672 for the free base; CAS 67727-97-3 for both forms; molecular weight 342.43 g/mol free base and 402.5 g/mol acetate; water solubility 0.70 mg/mL free base and 5 mg/mL acetate.

Both sides on the record. In favour, the researchers who characterised the molecule: Brzoska and colleagues concluded that keeping the anti-inflammatory effect while losing the pigment effect makes KPV "an alternative for antiinflammatory therapy", and that its physical properties and low expected production cost suit inflammatory skin and bowel disease. Böhm and Luger, cited in FDA's own nonclinical review, went further and called for clinical studies to find out whether KPV could heal skin wounds and ulcers — a call that, as of August 2026, nobody has answered. Against, the regulator, in its own words: "There is a lack of clinical and nonclinical safety information on the use of KPV (free base) and KPV acetate. FDA is particularly concerned about the lack of any human data on drug products containing these substances…"

Statement

Official disclosure

FDA Evaluation of KPV-Related Bulk Drug Substances (KPV free base and KPV acetate) for Inclusion on the 503A Bulk Drug Substances List — PCAC briefing document, 12 May 2026

“There is a lack of evidence to evaluate the effectiveness of KPV (free base) and KPV acetate products for the nominated uses of wound healing and inflammatory conditions. The nomination did not include, and FDA did not find any information on the use of KPV (free base) or KPV acetate administered in humans.”

Aug 4, 2026 · fda.gov

2026-08-04 08:30w_4lw9q2jv · #fb0b00b413a6

The three hardest numbers in the file, because everything else is softer than they are: nothing measurable crosses intact human skin, at a detection limit of 0.01 µg/mL; the PepT1 half-saturation point in gut lining is 160 µM; and the main breakdown product under stress is lysine-proline-diketopiperazine.

KPV is not an approved drug in any country. Nothing here is a dosing or treatment recommendation.

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