Evidence review
What human evidence exists for KPV?
The answer
None. Four name variants return 97 indexed papers and no record at all under the clinical-trial or randomized-trial publication types, while the parent hormone searched the same way in the same session returns 86 clinical trials and 48 randomized ones.
KPV is the tripeptide lysine-proline-valine: three amino acids, and the tail end of alpha-melanocyte-stimulating hormone. The parent hormone has broad anti-inflammatory signaling roles, and the fragment keeps a measurable share of that activity in laboratory models without the pigmentation effects the whole hormone produces [1].
That is a genuinely interesting piece of pharmacology and it is why the compound has a literature at all. It is also the precise point at which a marketing claim usually detaches from the record, because a fragment retaining activity in a cell assay is a finding about a cell assay. The monograph records the regulatory position with the date it was verified; this page counts what has been done in people.
Zero. Searched in August 2026 across four name variants, the tripeptide returns 97 indexed records. Under the clinical-trial publication type it returns 0. Under the stricter randomized-controlled-trial publication type it also returns 0 [4].
A publication-type filter that has stopped matching returns zero for every substance in the database, and a dead filter is indistinguishable from a true absence by looking at the output. The same session therefore put a control term with a large and undisputed trial literature through the identical filter: it returned 8,904 records under the clinical-trial type and 6,113 under the randomized type. The invalid tag that once produced a false zero on this site was run against that same control term and returned 0, and a deliberately invalid record identifier errored in the same run [4]. The instrument was answering, and the answer for this compound was nothing.
The reference below carries the query rather than a description of it, so the count can be repeated rather than trusted. That is the standard the method page sets out, and it is the standard any claim about this compound's evidence should be held to elsewhere.
Thirty-two of the 97 records carry the Humans subject heading, and a reader who stops at that number will conclude the opposite of the truth. All 32 were read [4].
They are melanocortin receptor pharmacology — binding affinities, agonist selectivity across receptor subtypes, three-dimensional models of the receptor. They are assays run in human cell lines. They are delivery-vehicle papers: hyaluronic-acid-functionalized nanoparticles carrying the tripeptide to the colon, hydrogel microspheres, carrier-free nanodrugs. One is an iontophoresis study measuring transport across microporated human skin outside the body [4].
The heading marks human tissue, human receptors, and human-derived cells. It does not mark a person who was given the compound and followed, and the difference between those two things is the entire question a reader arrives with. This is the same class of error as counting a search hit without opening it, and the correction is the same: read the records.
It is real work and it is worth describing accurately rather than dismissing. The central paper showed that the intestinal peptide transporter PepT1, which is induced in the colon during inflammatory bowel disease, carries KPV into epithelial and immune cells, where it reduced inflammatory signaling in human cell lines and improved two mouse models of colitis [2]. A separate murine study reached a similar conclusion in the same year [3].
So the compound has a plausible transport mechanism, an identified target, and effects in animals with an induced disease. That is the beginning of a drug development program, and for a great many molecules it is where the story ends, because the step from a mouse to a person is the step most compounds do not survive.
The contrast with the parent hormone makes the gap legible. Searched the same way in the same session, alpha-melanocyte-stimulating hormone returns 6,405 records, 86 clinical trials, and 48 randomized trials [4]. The molecular family has been carried into human research repeatedly. This fragment has not, and its literature cannot borrow the family's.
KPV was removed from Category 2 of the interim 503A bulks list in April 2026 without being added to Category 1, and in July 2026 the Pharmacy Compounding Advisory Committee voted to recommend adding it to the section 503A list. The margin is reported as 8–6 with one abstention — the same margin BPC-157 and TB-500 received — by McDermott Will & Schulte and by LumaLex Law, whose separate accounts of the meeting agree substance by substance [5, 6]; the FDA has published no minutes, transcript or vote summary for it, so that figure is secondary and this review says so where it prints one. The vote is advisory, no FDA final rule has issued, and no licensed United States pharmacy may lawfully compound it.
That sequence is worth reading beside the count above. A committee recommended a compounding listing for a substance with no published human trial of any kind, which is a fact about what the committee was asked to decide rather than a criticism of how it decided. The vote ledger carries the arithmetic of the whole meeting, and the pending page explains what an advisory recommendation changes, which is nothing yet.
Meanwhile the compound is sold as an oral capsule, a topical, and an injectable, and material offered under the name is research-use-only chemical supply produced outside pharmacy licensure. The research-use-only entry sets out what that labeling posture does and does not mean, and the repair peptides class collects the molecules that share this position.
Monographs
Reference tables
Every source below is inherited from a monograph in this index, where it was verified at writing time; this review introduces none of its own. The pointer beside each entry names the monograph and the reference number it came from.