Alpha-MSH Tripeptide · Ingredient Guide
KPV: The Honest Guide to an Ingredient You Cannot Buy on Its Own
KPV is three amino acids from the tail of a hormone your body already makes. It has interesting preclinical data, no human trials, and no standalone product. This guide explains all three.
- FDA Status
- Not FDA approved; 503A compounded
- Availability
- Ingredient only, never dispensed alone
- Evidence
- Preclinical; no human trials
- Access
- 28 U.S. States
Our promise: This page exists because a lot of people search for KPV and almost nobody explains it honestly. KPV has real preclinical data, mostly in mouse colitis models, and zero human trials. We say that plainly, and we tell you up front that you cannot buy it on its own here.
On this page
Section 01
What KPV Actually Is
KPV is a tripeptide. Three amino acids: lysine, proline, valine. The name is simply their one-letter codes, K-P-V. It is not a synthetic invention so much as a fragment of something your body already produces: it is the C-terminal tail of alpha-melanocyte-stimulating hormone, written in the literature as alpha-MSH(11-13).
Alpha-MSH is a thirteen-amino-acid hormone with two well-described roles: it drives pigmentation through the melanocortin receptors, and it dampens inflammatory signalling. The interesting observation behind KPV is that those two functions appear to separate. In laboratory models the three-amino-acid tail retains a good deal of the anti-inflammatory activity while no longer binding the melanocortin receptors responsible for pigment. That is the whole rationale for using the fragment instead of the hormone.
KPV is not an FDA-approved drug, and it is small enough to be worth saying plainly: at three amino acids it sits at the very bottom of the size range people mean by “peptide”, and its small size is part of why it is being investigated for oral and colon-targeted delivery.
3
Amino acids (Lys-Pro-Val)
α-MSH(11-13)
Parent hormone fragment
0
Published human trials
Section 02
Why You Cannot Buy KPV on Its Own
RxPepsDirect does not dispense KPV as a standalone product. There is no KPV-only vial and no KPV-only capsule. It reaches patients only as one ingredient inside a combination, and there are three of them.
| Product | KPV content | Form | What else is in it |
|---|---|---|---|
| BPC-157/TB-500/KPV | 15mg (3mg/mL) | 5mL injectable vial | BPC-157 15mg, TB-500 15mg. No copper. |
| KLOW | 15mg (3mg/mL) | 5mL injectable vial | BPC-157 15mg, TB-500 15mg, GHK-Cu 50mg. |
| BPC-157/KPV Capsules | 500mcg per capsule | Oral capsule | BPC-157 500mcg. |
Product
KPV content
Form
What else is in it
Product
KPV content
Form
What else is in it
Product
KPV content
Form
What else is in it
The practical difference between the two injectables is copper. KLOW adds GHK-Cu, a copper-carrying tripeptide, and the three-peptide vial deliberately leaves it out. If copper is a concern, whether because of a copper-handling condition or simple preference, the no-copper vial is the one to discuss with your prescriber. Between the injectable and the capsule the difference is route rather than formula philosophy.
Section 03
How It Is Proposed To Work
The mechanism most often cited for KPV is suppression of NF-kB signalling. NF-kB is a transcription factor that sits near the top of the inflammatory cascade: when it is activated it switches on a large set of genes that produce inflammatory cytokines. A compound that dampens NF-kB activity would, in principle, reduce inflammatory output broadly rather than blocking one specific mediator.
In cell and animal work KPV appears to act inside the cell rather than at a surface receptor, and at least one of the colitis studies found effects that persisted in animals lacking the MC1R melanocortin receptor, which is part of why the fragment is thought to work through a different route than the parent hormone’s pigment pathway.
Section 04
What the Evidence Actually Shows
The KPV literature is small, genuinely interesting, and entirely preclinical. It clusters around gut inflammation.
| Study | Model | Finding | Evidence level |
|---|---|---|---|
| Kannengiesser 2008 | Two murine colitis models | Reduced intestinal inflammation, with effect partly independent of the MC1R receptor | Animal |
| Laroui 2010 | Mouse colitis, colon-targeted nanoparticles | Delivered locally to the colon, KPV reduced colitis at far lower quantities than systemic dosing | Animal |
| Brzoska 2008 review | Review of alpha-MSH and related tripeptides | Summarises the anti-inflammatory case for the fragment across in vitro and in vivo work | Review, preclinical |
| Human trials | None published | No controlled human trial of KPV for any indication, by any route | None |
Study
Model
Finding
Evidence level
Study
Model
Finding
Evidence level
Study
Model
Finding
Evidence level
Study
Model
Finding
Evidence level
Two things follow from that table. First, the strongest KPV data is in the gut, which is why it turns up in gut-focused protocols and in an oral capsule alongside BPC-157. Second, and more important, the gap between a mouse colitis model and a person taking a compounded capsule is very large. Dose, route, delivery and species all differ, and the Laroui result in particular depended on targeting the compound directly to the colon.
Section 05
Why KPV Has No Dose of Its Own
“KPV dosage” is one of the most common searches about this molecule, and the honest answer is that the question does not have a standalone answer here. Your KPV dose is a consequence of which combination you were prescribed and how much of it you draw.
| Product | Listed protocol | KPV delivered | Note |
|---|---|---|---|
| BPC-157/TB-500/KPV | 20 units, Mon-Fri | 0.6mg | 0.2mL at 3mg/mL, alongside 0.6mg each of BPC-157 and TB-500 |
| KLOW | 20 units, Mon-Fri | 0.6mg | Same volume also delivers 2mg of GHK-Cu |
| BPC-157/KPV Capsules | 1 capsule daily | 500mcg | Taken by mouth, typically on an empty stomach |
Product
Listed protocol
KPV delivered
Note
Product
Listed protocol
KPV delivered
Note
Product
Listed protocol
KPV delivered
Note
Your prescription label and your prescriber’s directions control your dose. No clinically validated KPV dose exists to check it against.
Section 06
Safety and Screening
There is no human safety dataset for KPV. That is not the same as saying it is dangerous; it means the honest position is uncertainty rather than reassurance. Reported tolerability comes from clinic observation and patient report, not from controlled study.
Because KPV is only dispensed inside a combination, the screening that matters is the screening for the product you are actually prescribed, and those products carry more established concerns than KPV does on its own. Discuss with your prescriber: autoimmune conditions, cancer history or active malignancy, pregnancy or breastfeeding, current medications and supplements, and, for KLOW specifically, copper-handling disorders such as Wilson’s disease and copper sensitivity.
Section 07
Regulatory Status
KPV is not an FDA-approved drug and has no approved labelling. That makes its use here unapproved rather than off-label, which is a distinction worth keeping straight: off-label describes an approved drug used outside its approved labelling, and there is no label here to be outside of.
In July 2026 the Pharmacy Compounding Advisory Committee voted to recommend adding KPV, alongside BPC-157 and TB-500, to the 503A Bulks List. That vote is a recommendation. It is advisory and nonbinding, and it does not by itself create FDA approval or final placement on the list. Anyone presenting it as an approval is overstating it.
Compounded, Not FDA Approved
Prescribed patient-specifically under Section 503A
Preclinical Evidence Base
No published human trial for any indication
Section 08
Community Q&A
What does KPV stand for?
Nothing, in the acronym sense. K, P and V are the one-letter codes for its three amino acids: lysine, proline and valine. The name is the sequence.
Is KPV the same as alpha-MSH?
No. Alpha-MSH is a thirteen-amino-acid hormone. KPV is its three-amino-acid C-terminal fragment. They are related the way a sentence is related to its last three words, and the practical difference is that KPV appears to keep part of the anti-inflammatory activity in laboratory models without acting on the melanocortin receptors that drive pigmentation.
Which product should I choose if I want KPV?
That is a prescriber decision, and the honest framing is that no study compares them. The practical differences are copper and route: BPC-157/TB-500/KPV has no copper, KLOW adds GHK-Cu, and BPC-157/KPV capsules are oral rather than injected.
Does KPV help with gut problems?
The preclinical evidence is strongest in the gut, specifically in mouse models of colitis, which is why it appears in gut-focused protocols. That is a reason it is being studied, not evidence that it treats a gut condition in people. No human trial has tested it, and it is not an approved treatment for inflammatory bowel disease or any other condition.
Why does the oral capsule use a much smaller amount?
The capsule contains 500mcg of KPV against 0.6mg, or 600mcg, in a 20-unit injectable dose, so the amounts are closer than they look. Route matters more than the number: an oral capsule and a subcutaneous injection are not interchangeable, and there is no human data establishing what proportion of an oral KPV dose is absorbed.
Section 09
The RxPepsDirect Model
Provider Review First
A licensed provider reviews your intake, decides whether a KPV-containing combination is appropriate, and chooses which one. RxPepsDirect bills a flat $39 medical visit fee for that review.
Honest About the Evidence
This guide states that KPV has no human trials, no human dose, and no human safety dataset. We would rather you understand that before you order than after.
Filled by a 503A Pharmacy
Optimal Balance Pharmacy compounds and ships the combination product against your prescription. RxPepsDirect does not sell, dispense or ship peptides.
Ingredient, Not a Product
We list KPV so you can understand what is in your vial. We do not sell it separately, and we do not claim the blend is better than the isolate, because nobody has tested that.
References
- 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. PMID: 18288644
- Laroui H, Dalmasso G, Nguyen HT, et al. Drug-loaded nanoparticles targeted to the colon with polysaccharide hydrogel reduce colitis in a mouse model. Gastroenterology. 2010. PMID: 20347818
- Brzoska T, Luger TA, Maaser C, et al. Alpha-melanocyte-stimulating hormone and related tripeptides: biochemistry, antiinflammatory and protective effects in vitro and in vivo, and future perspectives. Endocr Rev. 2008. PMID: 18292088
Related protocol guides
Other protocols in the same clinical territory. Each guide is co-bylined by a licensed RxPepsDirect prescriber.
Three-peptide recovery stack, no copper
BPC-157/TB-500/KPV protocol guide: the no-copper three-peptide vial, who it is actually for, and what the evidence supports
The middle rung of the recovery ladder: BPC-157 and TB-500 for repair, KPV for inflammation, and GHK-Cu deliberately left out. Explains the four situations that call for a no-copper vial, and states plainly that no study compares it against the four-peptide version.
Four-peptide recovery stack
KLOW (KPV stack) protocol guide: the anti-inflammatory tripeptide lead, the four-peptide blend, and the limits of the evidence
Leads with KPV, the alpha-MSH tripeptide with the clearest preclinical anti-inflammatory data, then explains the BPC-157 / TB-500 / GHK-Cu stack and states plainly that the four-peptide blend has no combined human trial. Honest about what is mechanism and what is proof.
Recovery peptide protocol
BPC-157 protocol guide: clinical data, physician dosing, and the limits of the evidence
Mechanism, dosing, non-response rates, the angiogenesis question, WADA status, and the 503A pathway. Honest about what the human evidence is and is not.
Zonulin receptor antagonist (gut permeability)
Larazotide protocol guide: the zonulin receptor antagonist, the celiac Phase 2 trials, and the leaky-gut evidence gap
An oral octapeptide that blocks the zonulin receptor to keep intestinal tight junctions closed. More human trial data than most compounded peptides: Phase 2 showed benefit during gluten challenge; Phase 2b primary endpoint narrowly missed but secondary endpoints were significant. Evidence is celiac-specific.
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