KPV 10 mg
Peptide Library · Profile
KPV 10 mg
KPV has one claim that stands up better than almost anything else in this library, and one problem that undoes most of the case for injecting it. The claim is that it works without touching melanocortin receptors — true, and well evidenced. The problem is that its best evidence is a gut mechanism, and an injection goes around the gut.
The short version
Plain English first. Everything below this section is the same material with the sources, the numbers and the caveats attached.
What it is
A three-amino-acid fragment of a hormone, sold for inflammation and gut problems.
What has actually been measured
One claim that genuinely stands up: it works without touching melanocortin receptors. That is true and reasonably well evidenced in animals, and it matters because it means none of the melanotan-style side effects apply.
What has not been measured
Any human study, by any route. FDA went looking in 2026 and found none.
What most people get wrong
The route. Its best evidence is a gut mechanism — delivered in mouse drinking water, through a transporter in the intestinal wall. An injection goes around the gut entirely, which is most of the case against injecting it.
What KPV is
KPV is three amino acids — lysine, proline, valine — and it is the tail end of alpha-MSH, the hormone that colours your skin and, less famously, damps down inflammation. It is one of the smallest things anyone sells. It is also sold under one name in at least three different chemical forms, and almost nobody says which.
| Form | Notation | Formula | Weight |
|---|---|---|---|
| Free acid | H-Lys-Pro-Val-OH | C16H30N4O4 | 342.4 Da |
| Acetate salt | H-Lys-Pro-Val-OH · acetate | — | 402.5 Da |
| Acetylated and amidated | Ac-Lys-Pro-Val-NH2 | C18H33N5O4 | 383.5 Da |
CAS 67727-97-3 for the free acid; 57899-96-4 for the acetylated amide.
The one sold as "the C-terminal tripeptide of alpha-MSH" usually isn't
In alpha-MSH itself, that final valine is amidated. So the natural fragment is Lys-Pro-Val-NH2. The substance FDA evaluated in 2026 is the free acid, H-Lys-Pro-Val-OH — its own document notes Figure 1 shows "the carboxylic acid terminus, not an amide group." That is a des-amido analogue of the natural fragment, not the fragment.
Meanwhile a large part of the market sells the acetylated amide. Two molecules twelve per cent apart in mass, one product name, and no way to tell them apart without a mass spectrometer. A 5 mg dose of one is not a 5 mg dose of the other in molar terms.
The published chemistry for this compound is unusually bad
We checked what suppliers print. A sample of what we found:
- One vendor monograph gives two different CAS numbers on the same page. One of them, 65189-71-1, is Kemptide — a seven-residue protein kinase substrate, an entirely unrelated molecule. The other resolves to nothing.
- Another gives the acetylated amide a formula one carbon short and one nitrogen over, with a CAS that resolves to nothing.
- A third pairs the amide name with the free acid CAS number.
- PubChem's high-ranking near-match for these searches is Lys-Val-Pro — same formula, wrong order of residues.
None of that means the powder in any given vial is wrong. It means the paperwork culture around this particular compound is careless, and paperwork is the only thing standing between you and a white powder that all looks identical.
How it is said to work
This is the section where KPV does better than most compounds in this library, and we want to say so plainly before we get to the problems.
"It works without binding melanocortin receptors" is true
That claim sounds like the sort of thing a vendor invents. It is not. Three independent lines of evidence support it, and one of them is pure structural logic you can check yourself.
Every melanocortin peptide shares a four-residue motif — His-Phe-Arg-Trp — described in the review literature as "the minimum sequence required for receptor binding and activation." In alpha-MSH those are residues 6 to 9. KPV is residues 11 to 13. It contains not one residue of the pharmacophore. It structurally cannot be a melanocortin agonist, and the experiments agree:
| Test | Result |
|---|---|
| Displacing radiolabelled alpha-MSH from rat brain tissue | KPV was unable to |
| cAMP response — the canonical melanocortin readout | KPV failed to evoke one |
| Anti-inflammatory effect with an MC3/MC4 receptor antagonist on board | Retained |
So whatever KPV does, it does not do it through the receptors its parent hormone uses. That is a real and well-supported distinction, and it is the honest reason someone might be interested in this molecule rather than alpha-MSH itself — no pigmentation effects, no melanocortin pharmacology.
What it does instead: NF-κB, in cells and in mice
The core finding is Dalmasso and colleagues, 2008, in Gastroenterology. Nanomolar concentrations of KPV inhibited activation of NF-κB and MAP kinase inflammatory signalling and reduced pro-inflammatory cytokine secretion — measured properly, by reporter assay, Western blot, PCR and ELISA. FDA's own summary describes the mechanism as "KPV-induced inhibition of nuclear factor-κB activation leading to a reduction in the expression of proinflammatory cytokines."
And here is the part that decides this page
How does KPV get into those cells? Through PepT1 — a di- and tripeptide transporter that sits on the lining of your intestine. It is a gut absorption transporter. It is there to pull small peptides out of what you have eaten.
In the study the whole anti-inflammatory case rests on, KPV was dissolved in the drinking water of mice. The mechanism is: peptide in the gut lumen, taken up by intestinal cells through a gut transporter, NF-κB suppressed in those cells. An injection skips every step of that.
The antimicrobial claim did not replicate
You will read that KPV kills Staphylococcus aureus and Candida albicans at picomolar concentrations. That comes from Cutuli and colleagues in 2000, and it is a real paper.
In 2018 a group used the acetylated amide form of KPV as their reference compound in antibacterial assays and reported no inhibition of bacterial growth. Different assay format, and possibly a different form of the molecule — both fair caveats. But a failure to reproduce a picomolar antibacterial effect is exactly the sort of thing that belongs on a page about a compound, and we could not find a single vendor page that mentions it.
One claim we looked for and could not source at all: mast cell stabilisation. We found no primary study measuring KPV against mast cell degranulation or histamine release. If you see that claim, ask where it comes from.
Pharmacokinetics
None exists. No half-life, no Cmax, no bioavailability, no clearance — in humans or in animals, by any route.
FDA, in its 2026 evaluation, verbatim: "FDA did not identify clinical studies in humans assessing pharmacokinetics or pharmacodynamics of KPV (free base) or KPV acetate via any route of administration."
The "one to two hour plasma half-life" that circulates on peptide reference sites carries no citation, on any page in the chain we could follow. Treat it as unsourced.
Two things that have actually been measured, and neither is a half-life
It is not protease-resistant. A 2018 study followed the acetylated amide by NMR under enzymatic digestion and found it "degraded to its three constituent amino acids within 24 hours." That is a test tube with an enzyme in it, not plasma — but it tells you the molecule has no special stability.
It does not cross intact skin on its own. A 2017 study on human cadaver skin found that "KPV permeation via passive diffusion was below the limit of detection." It took microneedles or iontophoresis to move any across. That is worth knowing because it undercuts the topical creams as much as anything undercuts the injectables.
What the evidence shows
There is no human evidence for KPV. Not weak human evidence — none, by any route, anywhere.
FDA, verbatim: "The nomination did not include, and FDA did not find information on products containing KPV (free base) or KPV acetate administered in humans."
And on the evidence the nominator actually supplied: "The nomination cited nine literature references in support of the nomination; none were studies of KPV administered in humans." Eight were animal studies of alpha-MSH derivatives. The ninth was skin permeation through cadaver skin.
The inflammatory bowel disease story, stated exactly
KPV's reputation rests on Dalmasso 2008. Here is precisely what that study was:
| Species | Mice |
| Model | DSS- and TNBS-induced colitis |
| Route | Oral — added to the drinking water |
| Concentration | 100 µM in water |
| Uptake mechanism | PepT1, an intestinal peptide transporter |
| Cell work alongside | Caco2-BBE, HT29-Cl.19A and Jurkat cell lines |
The authors' own sentence is "oral administration of KPV reduces the incidence of DSS- and TNBS-induced colitis." Oral. In mice. Through a gut transporter.
What has been injected
One study. Getting and colleagues, 2003: mice, subcutaneous, a monosodium urate crystal peritonitis model, 3 to 88 nanomoles per mouse, with maximal effect around 9 nmol producing a 42% reduction in neutrophil migration. A single acute inflammation model in one species. That is the entire injectable evidence base for this compound — and it is also the study that demonstrated the melanocortin independence, so it is doing double duty.
There is no registered clinical trial of KPV. Not injected, not oral, not topical, not by enema. Not completed, not recruiting, not planned.
What FDA was actually asked to approve
Worth knowing what the July 2026 nomination was for: a topical cream or gel at 0.1%, for wound healing, psoriasis and eczema. Nobody has formally asked any regulator to consider injectable KPV at all. FDA noted separately that "several websites promote KPV as single-API injectable, oral, topical, and nasal spray drug products" — which is a regulator observing the gap between what is being sold and what anyone has put forward for assessment.
Reconstitution
A 10 mg vial, against doses commonly quoted in the hundreds of micrograms:
| Bacteriostatic water | Concentration | 1 unit (U-100) = | 500 mcg draw |
|---|---|---|---|
| 2 mL | 5 mg/mL | 50 mcg | 10 units · 0.10 mL |
| 3 mL | 3.33 mg/mL | 33.3 mcg | 15 units · 0.15 mL |
| 5 mL | 2 mg/mL | 20 mcg | 25 units · 0.25 mL |
A solubility check worth doing yourself
FDA's own record gives the water solubility of KPV free base as 0.70 mg/mL, and of the acetate as 5 mg/mL — a sevenfold difference between two things sold under the same name.
A 10 mg vial reconstituted into 2 mL is 5 mg/mL. If your vial is genuinely free base and it dissolves clear at that concentration, then either it is not free base or that solubility figure is wrong. If a vial does not go fully clear, add more water rather than shaking it harder — and treat cloudiness as information about what you were sold, not as a handling failure.
On supply: at 500 mcg a day a 10 mg vial is 20 days, comfortably inside the 28 days bacteriostatic water's preservative is validated for. At 200 mcg a day it is 50 days, which is not — reconstitute part of the vial at a time. The supply planner will work it out.
Reported protocols
The circulating figure is 200 to 500 mcg a day, subcutaneous. One of the most-copied sources for that number says outright where it comes from, and it is worth quoting.
"The recommended dosage according to anecdotal evidence and expert opinions is 200-400mcg/daily." The same page concedes that "human trial data indicating an appropriate KPV dosage are limited, as most studies involving this tripeptide have been carried out on rodents."
No citation accompanies it. That is the entire provenance of the injectable convention for this compound — not a bad extrapolation, not an aggressive one. Just a number somebody wrote down, which other people then copied.
What the arithmetic gives, for comparison
Converting the one injected animal study by body surface area, FDA's standard method, for a 70 kg adult:
| Mouse dose (subcutaneous) | Human equivalent |
|---|---|
| 3 nmol — the lowest tested | ~280 mcg |
| 9 nmol — maximal effect | ~840 mcg |
| 88 nmol — the highest tested | ~8.2 mg |
So the marketed 200 to 500 mcg sits near the bottom of that range, around the least effective dose tested, and well under the human equivalent of the optimum. That is a coincidence rather than a derivation — nobody did this sum before setting the convention, and we are showing it so you can see how far apart the two things are, not as a recommendation. A single acute peritonitis model in mice is not a basis for chronic daily dosing in a person at any number.
For scale in the other direction: the oral colitis study's 100 µM in drinking water works out to something like 40 mg a day for a 70 kg human — roughly a hundred times the injectable convention, by a completely different route, through a transporter that an injection never meets. The two numbers are not versions of each other.
Storage
Lyophilised, sealed, cold, dark and dry. Our storage guide covers the general conventions.
Here there is a real, sourced difference between the two forms, and it is another reason to know which one you have. FDA's record gives the lyophilised free base as "stable up to 3 years when stored at -20 °C in a tightly closed container," and the acetate as stored "in a sealed container at 2 °C to 8 °C." Different forms, different storage, same label.
Do not freeze a reconstituted solution. FDA also flagged, for peptide injectables generally and this one specifically, that "significant amounts of aggregates can form in formulated products, especially during storage or when exposed to stress conditions" — and that nobody has measured whether that happens here.
Reported effects
There is no human safety dataset for KPV. Not for injection, not for anything.
The toxicology package is empty in all five domains
FDA searched for and did not find acute toxicity studies, repeat-dose toxicity studies, genotoxicity studies, developmental and reproductive toxicity studies, or carcinogenicity studies — for either form, in any species. There is no long-term data of any kind, by any route.
An empty adverse-event database, and why it means nothing here
FDA, verbatim: "The FAERS search did not retrieve any reports and the literature search did not identify any cases of adverse events."
Read that with the rest of the picture. FDA also found that compounding pharmacies reported preparing no KPV products at all between January 2017 and June 2025, and that "the earliest and extent of KPV use in compounding is unknown." There is no approved product, no prescriber, no pharmacy in the chain. Nothing about the grey market reports into that database. Zero reports here measures the absence of a reporting pathway, not the presence of safety.
The certificate problem, which is our kind of problem
One finding from FDA's review is worth singling out for anyone who buys peptides on published certificates. Reviewing the certificates submitted with the nomination, FDA wrote that "most of CoA for KPV (free base) only contains purity testing result. However, there is no information on the impurity limits/testing results."
Those are two different things and they get conflated constantly. A purity figure says what proportion of the peptide present is the right peptide. An impurity profile says what else is in the vial. A certificate carrying only the first has answered the easier question. It is worth knowing which one you are looking at — on our certificates and on anyone else's.
What FDA said it could not rule out
Verbatim: "The nominators did not provide, and FDA did not identify clinical studies or human exposure data assessing immunogenicity or aggregation of KPV-related BDSs. Based on available information there is insufficient data to conclude that KPV (free base) or KPV acetate do not present these risks."
Regulatory status
Approval. None, anywhere. FDA searched and found no monograph in the United States Pharmacopeia or National Formulary, none in the European Pharmacopoeia, none in the Japanese Pharmacopoeia, and no authorised European product. Neither form is a component of any approved drug.
United States — reviewed in July 2026
FDA published a briefing document on KPV ahead of its Pharmacy Compounding Advisory Committee, which heard it on 23 July 2026 alongside BPC-157, TB-500 and MOTS-c under docket FDA-2025-N-6895. Its conclusion, verbatim:
"On balance, the physicochemical characterization, information on historical use, lack of any effectiveness and safety information in humans for both KPV (free base) and KPV acetate weigh against their being added to the 503A Bulks List... Accordingly, we propose not adding KPV (free base) or KPV acetate to the 503A Bulks List."
The committee voted 8 to 6 with one abstention to recommend adding it anyway, against FDA's own scientists. The next step, if FDA takes it, is notice-and-comment rulemaking that reporting suggests "could occur in 2027 or extend into a multi-year process." Nothing has changed in law, and a committee recommendation is advice rather than a decision.
On the separate bulk drug substances page, FDA's standing text on KPV reads: "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."
Canada
Health Canada's public advisory of 9 April 2026 names KPV among fourteen peptides given as "examples of unauthorized injectable peptide drugs seized by Health Canada." The advisory states that peptides function as prescription drugs in Canada, and that research-use-only labelling "does not make these products legal or exempt from regulatory requirements."
Sport
KPV is not named on the 2026 WADA Prohibited List — we read the list and searched it for "KPV", "Lys-Pro-Val", "melanocortin" and alpha-MSH. That is not permission. Section S0 prohibits at all times "any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use." KPV has no approval anywhere, so it sits inside S0 by definition. An athlete should treat it as prohibited.
Sentient Biogenix supplies KPV for laboratory research use only. It is not for human or veterinary use.
Questions we actually get
Isn't KPV the anti-inflammatory one that works on the gut?
The gut evidence is real and it is the best evidence this compound has. It is also the reason to be careful about injecting it. In the study everyone cites, KPV was put in mouse drinking water and absorbed through PepT1, a transporter on the lining of the intestine. That is a gut-lumen mechanism. An injection never encounters it.
Does it act on melanocortin receptors like alpha-MSH?
No, and unusually, that claim is well proven rather than merely asserted. Melanocortin receptor binding needs a four-residue motif, His-Phe-Arg-Trp, which sits at positions 6 to 9 of alpha-MSH. KPV is positions 11 to 13 and contains none of it. It does not displace alpha-MSH from brain tissue, it produces no cAMP response, and its anti-inflammatory effect survives a melanocortin receptor blocker. It is a genuinely receptor-independent molecule.
Have there been human trials?
None. Not one registered trial exists, by any route. When FDA reviewed the compound in 2026 it found no human exposure data at all — and noted that the nine references submitted in support of the nomination included not a single study of KPV given to a person.
Which form am I buying — acid or amide?
Ask, and ask for it in writing. The free acid is 342.4 Da; the acetylated amide is 383.5 Da. They are different molecules with different water solubility and different storage requirements, and they are routinely sold under the same three-letter name. If a supplier cannot tell you, that is itself an answer.
Does it kill bacteria?
A 2000 paper reported activity against Staph aureus and Candida at very low concentrations. A 2018 group using the amide form found no inhibition of bacterial growth at all. Different assays, possibly different molecules — but the failure to replicate is real and nobody selling the compound mentions it.
Where does 200 to 500 mcg a day come from?
The most-copied source for it says, in its own words, "anecdotal evidence and expert opinions." There is no citation behind it. The only injected animal study puts the human equivalent of its most effective dose nearer 840 mcg — which is not a recommendation, just a demonstration that the marketed number was not derived from the science people cite for it.
References
- US Food and Drug Administration. FDA Briefing Document, Pharmacy Compounding Advisory Committee — KPV-related bulk drug substances, July 2026. fda.gov — the free-acid structure, both forms' solubility and storage, the absence of human exposure data and pharmacokinetics, the five empty toxicology domains, the FAERS and compounding-history searches, the certificate-of-analysis finding, and the conclusion against listing.
- US Food and Drug Administration. Presentation slides, Pharmacy Compounding Advisory Committee, 23 July 2026. fda.gov
- US Food and Drug Administration. Certain bulk drug substances for use in compounding that may present significant safety risks. fda.gov
- Dalmasso G, Charrier-Hisamuddin L, Nguyen HTT, et al. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology 2008;134(1):166–178. PMID 18061177. pubmed.ncbi.nlm.nih.gov — the colitis work: mice, oral, KPV in drinking water at 100 µM, uptake via PepT1, and the NF-κB and MAP kinase findings in cell lines.
- Getting SJ, Schiöth HB, Perretti M. Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) alpha-melanocyte-stimulating hormone peptides. Journal of Pharmacology and Experimental Therapeutics 2003;306(2):631–637. PMID 12750433. pubmed.ncbi.nlm.nih.gov — the only injected efficacy study: mice, subcutaneous, 3 to 88 nmol, and the demonstration that the effect survives melanocortin receptor blockade and produces no cAMP response.
- Cutuli M, Cristiani S, Lipton JM, Catania A. Antimicrobial effects of alpha-MSH peptides. Journal of Leukocyte Biology 2000;67(2):233–239. academic.oup.com — the original antimicrobial claim.
- Songok J, et al. PLOS ONE 2018;13(6):e0199686. journals.plos.org — the acetylated amide as reference compound, "no inhibition of bacterial growth," and the 24-hour enzymatic degradation to free amino acids.
- Pawar KR, et al. Enhanced transdermal delivery of KPV. Journal of Pharmaceutical Sciences 2017;106(7):1814–1820. jpharmsci.org — human cadaver skin; passive KPV permeation below the limit of detection.
- Melanocortin regulation of inflammation. Frontiers in Endocrinology 2019;10:683. frontiersin.org — the His-Phe-Arg-Trp pharmacophore requirement, which KPV does not contain.
- Health Canada. Think twice before injecting peptides bought online: unauthorized products can seriously harm you. Public advisory, 9 April 2026. recalls-rappels.canada.ca
- World Anti-Doping Agency. The 2026 Prohibited List, in force 1 January 2026, section S0. Read via the Austrian Federal Law Gazette's official reproduction (BGBl. III Nr. 219/2025) because WADA blocks automated access to its own copy.
Some sources we could not open directly and have reported through secondary records, marked here rather than hidden: the nanomole figures from the 2003 injected mouse study were read from an institutional repository rather than the publisher's PDF; the ocular wound-healing work of Bonfiglio 2006 is real and indexed but we could not verify its dosing, so no numbers from it appear above; and our oral human-equivalent estimate assumes a mouse's daily water intake, which the paper does not state. We have also been unable to confirm a distinct CAS number for the acetate salt as against the free base.