RecoveryLys-Pro-ValKPV tripeptide

KPV

C-terminal tripeptide of α-MSH · anti-inflammatory

KPV is a tripeptide — lysine-proline-valine — that corresponds to the C-terminal three residues of α-melanocyte-stimulating hormone (α-MSH), the fragment to which much of α-MSH's anti-inflammatory activity has been attributed. In laboratory and rodent studies it dampens inflammation from inside the cell: it is carried into intestinal and immune cells by the peptide transporter PepT1 and there inhibits NF-κB and MAP-kinase signaling, lowering pro-inflammatory cytokine output. Its best-developed evidence is in models of inflammatory bowel disease, where oral KPV reduced colitis severity in mice. Notably, that protection persists even in mice lacking functional melanocortin receptors, so the gut effect does not depend on the classic α-MSH receptor. KPV has not been studied in human clinical trials, has no published pharmacokinetics or half-life, and is not an FDA-approved drug.

The short version

KPV is one of the smallest peptides in this catalog — just three amino acids (lysine, proline, valine) strung together. It is the tail end of a larger natural hormone called α-MSH, and it carries that hormone's anti-inflammatory punch in a much simpler package.

The way it works is unusual: instead of acting on a receptor on the cell surface, it gets carried inside the cell (by a transporter called PepT1) and quiets the inflammation machinery from within — turning down the master switch, NF-κB, that drives inflammatory signaling.

Most of what is known comes from studies of gut inflammation in mice, where giving KPV by mouth calmed colitis. Importantly, this still worked in mice engineered to lack the usual α-MSH receptor, which tells researchers the gut effect runs through a different route.

An honest caveat: KPV has never been tested in a human clinical trial, and there is no published data on how long it lasts in the body. Anything you read claiming a specific human dose or half-life is not backed by the scientific literature.

Molecular identity

Specs

Molecular weight: 342.43 g/mol (average)
Molecular formula: C16H30N4O4
Monoisotopic mass: 342.2267 Da
Sequence (3 AA): Lys-Pro-Val (KPV)
CAS number: 67727-97-3

Structure / class: Free-acid tripeptide; C-terminal fragment of α-MSH (residues 11-13)PubChem CID 125672; research literature
Molecular target: Intracellular NF-κB and MAPK signaling (anti-inflammatory); cell entry via the PepT1 di/tripeptide transporter — melanocortin-receptor-independent in gut modelsPMID 18061177; PMID 18092346
Half-life: Not established — no published human pharmacokinetics; expected rapid peptidase degradationNot established (PubMed, May 2026)
Regulatory status: Not FDA-approved; research compound. No human clinical trials. Nominated for FDA 503A compounding bulks-list review (PCAC scheduled 2026-07-23)No approval record; FDA 503A nomination docket

Plain English

Mechanism

KPV is the C-terminal tripeptide of α-melanocyte-stimulating hormone (the tail-end three building blocks, residues 11-13, of that hormone); a long line of research attributes much of α-MSH's anti-inflammatory activity to this small fragment. Its best-characterized mechanism is intracellular (acting inside the cell rather than on its surface): in human intestinal epithelial cells (the cells lining the gut) and T cells (a type of immune cell), nanomolar KPV — an extremely low concentration — inhibits activation of the NF-κB and MAP-kinase signaling pathways (two of the cell's master inflammation switches) and reduces the secretion of pro-inflammatory cytokines (the chemical alarm signals immune cells release to drive inflammation).

To act inside the cell, KPV first has to get there. It is transported into intestinal and immune cells by PepT1, the di/tripeptide transporter (a doorway protein that pulls small two- and three-amino-acid peptides into the cell) — normally a small-intestinal protein that becomes induced (switched on in greater amounts) in the colon during inflammation. The dependence on this transporter is not incidental: in mice engineered to lack PepT1, KPV lost its effect, establishing PepT1-mediated uptake as essential to its action in that model.

A key point about the receptor question: although KPV comes from α-MSH, its anti-inflammatory effect in the gut does NOT require functional melanocortin receptors (the cell-surface docking sites the parent hormone normally acts through). In colitis (gut-inflammation) experiments, KPV still rescued mice that lacked a working MC1 receptor — consistent with the PepT1-uptake / intracellular-NF-κB model rather than classic surface-receptor signaling. A parallel cell-surface route has been proposed in some skin and cell-line studies, so receptor involvement appears to be context-dependent; but in the tissue where KPV is best studied, the effect is melanocortin-receptor-independent.

A note on identity: KPV (Lys-Pro-Val) is distinct from KdPT (Lys-D-Pro-Thr), a different molecule derived from interleukin-1β that signals through the IL-1 receptor — the two are sometimes conflated but are not the same compound. The values on this page are for the free-acid tripeptide KPV (PubChem CID 125672).

Sources:PMID 18061177 PMID 27458604 PMID 18092346 PMID 17934097

Why people reach for it

Potential benefits

KPV is the small, anti-inflammatory tripeptide people reach for when calming an overactive immune or gut response is the goal. Here's what draws them to it.

Calm an overactive inflammatory response — Its headline appeal. KPV is carried inside gut and immune cells and turns down NF-κB and MAP-kinase — the master switches that drive inflammatory cytokine output — so it's reached for when the goal is dialing inflammation down rather than masking it.
A go-to for gut-lining flares — KPV's best-developed research is in gut inflammation — oral KPV reduced colitis severity across rodent models — which is why it's a favorite when digestive inflammation and a settled gut lining are the target.
A favorite for MCAS and histamine-driven days — Because it suppresses cytokine release from immune cells, people reach for it on mast-cell and histamine-flare contexts, often on-demand around a known trigger.
The anti-inflammatory half of a recovery stack — It works through inflammation control rather than tissue-building, so it slots cleanly alongside repair peptides — most commonly BPC-157, which rebuilds the structure while KPV calms the environment around it.
A small, α-MSH-derived molecule with a light footprint — KPV carries much of α-MSH's anti-inflammatory activity in just three amino acids, and the rodent evidence reported tolerability and benefit — though its safety picture is entirely preclinical, with no human trials.

Sources:PMID 18061177 PMID 18092346 PMID 27458604 PMID 17934097

What people reach for KPV for, drawn from what the research reports (entirely preclinical — rodent and cell models) and how it's used — not proven human outcomes or medical claims.

Implied timing

Best time to dose

Implied best time

Anytime (consistent)

KPV has no clock-driven timing — most people pick a consistent daily time and stick to it, with a slight evening lean for gut and overnight-repair goals.

KPV works through a steady anti-inflammatory mechanism (intracellular NF-κB / MAP-kinase suppression), not a circadian one — so there's no hour of the day that biologically suits it best. Consistency matters far more than the exact time.
For gut-lining and recovery goals, an evening dose is a reasonable lean — it lines the calm-inflammation signal up with the body's overnight repair window, the same logic used for the common BPC-157 pairing.
For a split acute-flare dose, the two doses are spaced ~10–12 hours apart (e.g. 8 AM and 8 PM) — that spacing, not a specific time of day, is what's being optimized.
On-demand users time it around a known trigger or exposure rather than a daily clock, which is its own kind of timing — situational, not scheduled.

No study establishes an ideal time of day for KPV — this is reasoned from its anti-inflammatory mechanism and how it's used. As a rule of thumb most peptide dosing lands in the midday-to-evening window; for KPV the time is flexible, with a mild evening lean for gut and overnight-repair goals.

How to run it

Dosing & protocol

KPV is dosed here as a subcutaneous injection — the form sold as a research peptide and the route the on-page calculator is built for. It has no published human-trial dose, so the ranges and schedule below are community-and-practitioner convention, extrapolated from its anti-inflammatory mechanism. Read it as a map of how people actually run injectable KPV — not a validated prescription.

Community convention, not trial-proven: KPV has zero human trials and no published human dose, and it is not an FDA-approved drug. Its strongest published evidence is in animal models of gut inflammation; subcutaneous use for whole-body anti-inflammatory goals is reasoned from mechanism, not shown in a trial. Every number here is a usage pattern, not evidence.

Tiered dose ranges

Most protocols scale the subcutaneous dose to how active the inflammation is.

Low / maintenance:: 200 mcg once daily — mild inflammatory maintenance, general recovery, or first testing tolerance to the compound.
Standard:: 300–500 mcg once daily — the baseline range most often used for ongoing inflammatory goals.
Acute flare:: 400–500 mcg twice daily (≈ 800–1,000 mcg/day) — reserved for intense flares or severe MCAS episodes, typically held to 7–10 days before dropping back to a standard daily dose.

Subcutaneous administration

KPV is injected into subcutaneous fat; site and timing are the actionable choices.

Injection site:: The abdomen (staying a couple of inches clear of the navel), the love-handle area, or the outer thigh. Rotate sites between doses so one spot isn't used repeatedly — that prevents local irritation and fatty lumps (lipohypertrophy).
Measuring the dose:: Drawn on a U-100 insulin syringe from the reconstituted vial; the reconstitution card below converts each dose to syringe units (e.g. 300 mcg = 15 IU at the standard mix), and the calculator does it for any vial size.
Time of day:: There's no circadian constraint, so a consistent daily time matters more than the exact hour — see Best time to dose above; many lean evening for gut and overnight-repair goals. For a split acute-flare dose, space the two ~10–12 hours apart (e.g. 8 AM and 8 PM).
Food window:: Subcutaneous KPV doesn't compete with food for absorption, so it can be injected independent of meals.

Cycle & washout

Peptides that modulate immune and inflammatory pathways are generally pulsed rather than run indefinitely — thought to prevent receptor desensitization.

Standard cycle:: 4–8 weeks of continuous daily use, then reassess.
Washout:: Follow with a 2–4-week break. Re-check inflammatory markers (hs-CRP, or a specific cytokine panel) during the break to see whether the body's baseline inflammatory setpoint has lowered.
On-demand alternative:: For intermittent MCAS or environmental allergies, KPV is sometimes used strictly on-demand for 3–5 days around a known exposure or symptom flare, rather than on a fixed cycle.

Reconstitution at a glance

The on-page calculator does this live; the quick reference for a 10 mg vial:

Mixing:: 10 mg vial + 5 mL bacteriostatic water = 2,000 mcg per mL. On a 100-unit (1 mL) insulin syringe: 200 mcg = 10 IU · 300 mcg = 15 IU · 400 mcg = 20 IU · 500 mcg = 25 IU.
Why 5 mL:: The higher dilution spreads small microgram doses across more syringe units, so you're not measuring microscopic increments — which reduces dosing errors.

Sources:PMID 18061177 PMID 27458604 PMID 18092346 PMID 28143741

Substrate the signal needs

Nutritional cofactor precision

KPV calms inflammation by getting inside gut and immune cells and turning down NF-κB, the master inflammatory switch. The useful cofactors push that same lever with food and supplements, or give the gut lining what it needs to rebuild.

Reasoned from KPV's NF-κB / gut-barrier mechanism plus general anti-inflammatory nutrition — not a KPV cofactor study. Supplement doses are common community ranges, not KPV-specific findings.

Quercetin (mast-cell stabilizer & zinc ionophore)

The single best-matched partner if you're using KPV for MCAS or a leaky-gut goal.

Mechanism:: Quercetin stabilizes mast-cell membranes (curbing histamine release) while KPV works downstream to suppress cytokine output — two angles on the same flare. It also acts as a zinc ionophore, shuttling zinc into the cell where it reinforces NF-κB inhibition.
Protocol integration:: 500 mg isoquercetin (a more bioavailable form), or quercetin phytosome, twice daily — taken ~20 minutes before meals.

Zinc & copper (balanced ratio)

Mechanism:: Zinc is a natural brake on NF-κB — a deficiency lets inflammatory signaling run hotter. Pairing it with a little copper keeps the metalloenzyme balance intact over a long course.
Protocol integration:: 30–50 mg zinc picolinate or bisglycinate daily, paired with 2 mg copper bisglycinate to prevent copper depletion.

Gut-barrier substrate (L-glutamine · zinc-carnosine · vitamin D)

Mechanism:: KPV's best evidence is in the gut, so feeding the lining it acts on matters: L-glutamine is the primary fuel of gut-lining cells, zinc-carnosine is a gut-directed zinc form used to support the barrier, and vitamin D regulates intestinal immune tone.
Protocol integration:: L-glutamine 5 g once or twice daily; zinc-carnosine 75 mg/day; vitamin D dosed to a blood level in the sufficient range. Prebiotic fiber and fermented foods push the microbiome toward butyrate, an anti-inflammatory short-chain fat.

Anti-inflammatory diet (omega-3 + polyphenols)

Mechanism:: Omega-3 fats (EPA/DHA) and plant polyphenols (curcumin, berries, leafy greens) independently dampen the same NF-κB-driven signaling KPV targets, so diet and peptide pull in the same direction rather than at cross purposes.
Protocol integration:: ~2–3 g combined EPA/DHA daily and a polyphenol-rich, colorful-plant diet. For the whole-body, tissue-repair side, the usual connective-tissue substrate also applies — adequate protein, vitamin C for collagen, and zinc for remodeling.

Combinations + timing

Stacking notes + timing windows

KPV is highly focused — it halts the cytokine cascade and lowers NF-κB. The best pairings come at the same problem from a different angle: rebuilding tissue, or regulating the immune system more deeply. Pairing KPV with another anti-inflammatory would just push the same lever twice — redundant, not synergistic.

User combinations reasoned from complementary mechanisms — not regimens studied head-to-head, and KPV itself has no human trial, so any stack is doubly unproven. Doses are community convention; "reached for" describes where users go, not a proven indication.

KPV + BPC-157

The most common KPV pairing — KPV calms the fire, BPC-157 rebuilds the structure.

Why it works:: BPC-157 is studied for healing the gut lining and bringing new blood supply (angiogenesis) to repairing tissue; KPV suppresses the local NF-κB inflammation so that tissue heals in a calmer environment, with less scarring. Complementary levers — repair and calm — not the same one twice.
The protocol:: KPV 300–500 mcg + BPC-157 250–500 mcg, co-injected subcutaneously once daily — drawn together or as two nearby sites, rotated across the week. Time it around the affected area for a recovery/injury focus.
Outcome:: The combination users reach for on inflammatory-flare, gut-inflammation, and ligament/tendon-recovery goals.

KPV + BPC-157 + TB-500

The soft-tissue recovery trio — adds a cell-migration signal to the calm-and-rebuild pair.

Why it works:: TB-500 promotes the migration of repair cells into injured tissue, BPC-157 rebuilds the structure, and KPV calms the inflammation around the repair — three distinct jobs on one injury, each a different lever.
The protocol:: KPV 300–500 mcg daily alongside the standard BPC-157 + TB-500 recovery pairing; TB-500 is typically run on its own loading-then-maintenance schedule (a higher weekly load for the first weeks, then a lower maintenance dose).
Outcome:: Reached for on broader soft-tissue and connective-tissue recovery, where inflammation and structural damage overlap.

KPV + Thymosin Alpha-1

An immune-modulator pairing for inflammation with an underlying immune driver.

Why it works:: KPV dampens the over-reactive innate / mast-cell response while Thymosin Alpha-1 tunes the adaptive immune system — two different arms of immunity, so the body doesn't damage itself in the crossfire. Different levers, not a doubled one.
The protocol:: KPV 300 mcg subcutaneously daily, with Thymosin Alpha-1 on its own typical schedule (commonly ~1.5 mg twice weekly).
Outcome:: Reached for on MCAS and chronic-inflammatory contexts where the immune system is both over-reactive and under-effective. Note the honesty axis on the Thymosin Alpha-1 page — its most rigorous trial was null.

Reconstitution math

Reconstitution calculator

Calculated for a 1 mL U-100 insulin syringe (100 units/mL).

Peptide per vial

BAC water added

Desired dose

Units per dose

Draw to this mark on a U-100 syringe

Volume per dose: 0.1 mL
Doses per vial: 20
Concentration: 5 mg/mL

One vial lasts

Daily: 20 days
Every other day: 40 days
5×/week: 28 days

Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.

From the studies

Side effects from research

Because KPV has not been studied in human clinical trials, there is no human safety or toxicology dataset, and no adverse-event profile can be stated. The rodent colitis studies that form its evidence base reported tolerability and benefit, but they are efficacy experiments in animals, not formal safety studies — they cannot be read as establishing human safety.

KPV is not an FDA-approved drug. It has been nominated for evaluation for the FDA's 503A compounding bulks list, with an advisory-committee review pending; absent approval, it remains a research-grade substance without an established human safety record. Anyone considering it should weigh that the entire safety picture is preclinical.

Sources:PMID 18092346

As reported in literature

Research dosing ranges

This is the cited preclinical evidence the practical framing above leans on — shown separately so research data is never mistaken for a human dose. There is no established human dose for KPV: no human clinical trial has been located in PubMed or on ClinicalTrials.gov (as of May 2026), so there is no clinical dosing schedule to report, and any specific human protocol circulated by vendors is extrapolation rather than evidence. What follows is the in-vitro (cell-dish) and rodent models in which KPV has actually been studied — not a dosing recommendation. Several rodent studies dosed KPV in drinking water without stating a precise mg figure in the published abstract; those cells are marked accordingly.

Dose	Route	Model	Outcome	Sources:
Nanomolar	In vitro (cell culture)	Human intestinal epithelial cells & T cells	Inhibited NF-κB and MAP-kinase activation; reduced pro-inflammatory cytokine secretion	PMID 18061177
Oral (drinking water)	Oral	Mouse — DSS & TNBS colitis	Reduced colitis severity and pro-inflammatory cytokine expression	PMID 18061177
Not specified	Oral	Mouse — DSS & T-cell-transfer colitis (incl. MC1R-deficient)	Earlier recovery, reduced colonic myeloperoxidase; protective even without functional MC1R	PMID 18092346
Nanoparticle-delivered	Oral	Mouse — DSS ulcerative colitis	Hyaluronic-acid-functionalized KPV nanoparticles reduced mucosal damage and downregulated TNF-α	PMID 28143741

Quick answers

Frequently asked

What is KPV?

KPV is a tripeptide made of lysine, proline, and valine. It is the C-terminal three-residue fragment of α-MSH (α-melanocyte-stimulating hormone), and it carries much of that hormone's anti-inflammatory activity in a far smaller molecule.

How does KPV reduce inflammation?

Its best-characterized mechanism is intracellular. It is carried into intestinal and immune cells by the transporter PepT1, and once inside it inhibits the NF-κB and MAP-kinase signaling pathways, lowering pro-inflammatory cytokine output. In gut models this works even without functional melanocortin receptors, so it does not depend on the classic α-MSH surface receptor.

Is there a recommended human dose of KPV?

No. KPV has not been tested in any human clinical trial (PubMed and ClinicalTrials.gov, May 2026), so there is no established human dose. The evidence base is rodent and in-vitro only. Specific human dosing protocols circulated by vendors are extrapolations, not findings.

What is KPV's half-life?

There is no published half-life or pharmacokinetic data for KPV. As a small tripeptide it is expected to be broken down quickly by peptidases, but no measured value exists in the scientific literature — any specific number you see quoted is unsourced.

Is KPV the same as KdPT?

No. KPV (Lys-Pro-Val) comes from α-MSH and acts largely through PepT1 uptake and intracellular NF-κB inhibition. KdPT (Lys-D-Pro-Thr) is a different molecule derived from interleukin-1β that signals through the IL-1 receptor. They are frequently confused but are chemically and mechanistically distinct.

Is KPV an approved medicine?

No. KPV is not an FDA-approved drug. It has been nominated for evaluation for the FDA's 503A compounding bulks list, with advisory-committee review pending. This page presents the research literature only and makes no therapeutic claims.

Primary sources

References

PubChem CID 125672PubChem CID 125672 (KPV / Lys-Pro-Val, α-MSH 11-13)
PMID 18061177Dalmasso et al., Gastroenterology 2008 (PepT1 uptake, NF-κB/MAPK inhibition, DSS/TNBS colitis)
PMID 18092346Kannengiesser et al., Inflamm Bowel Dis 2008 (colitis; protective in MC1R-deficient mice)
PMID 27458604Viennois et al., Cell Mol Gastroenterol Hepatol 2016 (PepT1 genetic proof; no effect in PepT1-KO)
PMID 28143741Xiao et al., Mol Ther 2017 (oral hyaluronic-acid-functionalized KPV nanoparticles, DSS colitis)
PMID 17934097Luger & Brzoska, review 2007 (α-MSH anti-inflammatory activity attributed to C-terminal KPV)
PMID 29953505Glycoalkylated KPV analogs 2018 (modified KPV shows improved proteolytic stability vs native)

Research use only · Not medical advice · Updated 2026-06-01