KPV

What it actually is

KPV is three amino acids: lysine, proline, valine. It is the tail end of alpha-melanocyte-stimulating hormone, residues 11 to 13, and it is about as small as a peptide gets while still being called one. That size is the reason it shows up in four different delivery formats, from capsules to nasal sprays to compounded creams, because a tripeptide is small enough that people assume it will go anywhere.

The mechanism everyone repeats, and what FDA actually says

Search KPV and you will be told it is a melanocortin agonist that calms inflammation by acting on MC1R. FDA's 2026 briefing document says that is probably not what is happening. In its words, several lines of evidence suggest melanocortin receptors are unlikely to be the molecular targets underlying the anti-inflammatory and wound-healing properties of KPV. KPV could not displace radiolabelled alpha-MSH from rat brain tissue, from murine melanoma cells, or from MC1R-expressing macrophages, and it did not raise cAMP in those macrophages. If it were an MC receptor agonist, all three of those experiments should have gone the other way.

What FDA does treat as plausible is more prosaic and, if anything, more interesting. KPV appears to inhibit activation of NF-κB, the transcription factor that switches on most of the pro-inflammatory cytokine programme, and to blunt the downstream effects of interleukin-1β. And it gets into cells through PepT1, a peptide transporter found on intestinal epithelial cells and on T cells, which is upregulated in inflamed intestinal tissue. That is a coherent story for a gut compound: the transporter that carries it in is most abundant exactly where you want it.

What the evidence actually supports

Nothing, in humans. That is not a rhetorical flourish. FDA searched, and reported that it identified no clinical studies, no pharmacokinetic data and no pharmacodynamic data for KPV by any route of administration. There is no half-life to publish. There is no bioavailability figure. There is no dose-finding study.

The preclinical work is real. Rodent colitis models and wound-healing models show consistent anti-inflammatory effects, and the PepT1 transport work is well characterised. But between a mouse colon and a dosing schedule for a person sits every question KPV has never been asked.

In July 2026 FDA's Pharmacy Compounding Advisory Committee voted 8–6 with one abstention to recommend KPV for the 503A bulks list, for wound healing and inflammatory conditions, over the explicit recommendation of FDA's own scientific reviewers. That vote is advisory. It is not a rule: FDA would still have to write one, and it has not proposed one. KPV is not lawfully compoundable today.

The topical problem

The most common consumer form of KPV is a compounded cream for eczema, psoriasis or general skin inflammation. In vitro testing on human cadaver skin found that KPV does not permeate skin well, and that penetration improved only when the skin barrier was actively breached with iontophoresis or microneedle abrasion. FDA's own comment is that this could limit the usefulness of KPV as a topical therapeutic. Nobody selling the cream mentions it.

Running it

Every figure on this page is community practice with a vendor-tier label attached, and the ranges vary because nothing anchors them. Two things we deliberately do not publish, both circulating widely: the "most people respond well to 300 mcg daily" line, and a disease-specific protocol giving numbers against named diagnoses like Crohn's disease and ulcerative colitis. Publishing a dose against a diagnosis for a compound with zero human data is the single most dangerous thing a page like this could do.

Storage carries an unresolved conflict and we ship the conservative side. Our sourcing places KPV among the compounds that need sterile water rather than bacteriostatic water, which means a 24-hour window, not 28 days. Both community dosing guides say bacteriostatic water. There is no stability study to settle it. Separately, the free base dissolves at about 0.70 mg/mL against 5 mg/mL for the acetate, so if you reconstitute free base as though it were acetate you will end up with a suspension, not a solution.

What the marketing claims

FDA's briefing document catalogues the claims it found in the market for KPV: a wide array of inflammatory conditions, wound healing, skin health, immune strengthening, protection against nerve damage and stroke, gut health, antimicrobial action, reduced tumour growth, psoriasis, inflammatory bowel disease, colitis, Crohn's disease, mast cell activation syndrome, histamine intolerance, recovery from COVID-19, Lyme disease, mould toxicity and pain syndromes.

That is a federal regulator, in a public document, listing the exact claim stack you will meet on the first page of search results. It is worth reading twice, because a compound that treats everything is a compound that has been tested for nothing.