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Research monograph · α-msh-derived tripeptide (α-msh 11–13)
KPVResearch monograph
Inflammation Pathway Studies
This monograph collects what the published literature reports about KPV — its mechanisms, the areas it is studied in, its molecular record and the sources behind them. That short tail carries much of the parent hormone's anti-inflammatory signaling while leaving behind its effect on pigmentation, which is the property that made the fragment worth isolating.
For laboratory research use only — not for human or animal use
Mechanisms
How KPV works
Inflammatory Pathway Suppression
NF-κB Inhibition
Reported to inhibit NF-κB and MAP-kinase signalling at nanomolar concentrations — the transcriptional step upstream of pro-inflammatory cytokine production, rather than the cytokines themselves.
Inhibits NF-kB and MAP-kinase at nanomolar levels
Reduces TNF-a, IL-6 and IL-1b
Suppresses inflammatory output rather than raising anti-inflammatory signal
Cellular Transport & Action
PepT1-Mediated Uptake
Uptake is described via PepT1, an intestinal peptide transporter. That route matters because it lets the tripeptide reach the cell interior, where the signalling it acts on takes place.
Enters cells via the PepT1 transporter
PepT1 sits on immune and intestinal epithelial cells
Allows modulation from inside the cell
Melanocortin Fragment
α-MSH-Derived Activity
As the C-terminal tripeptide of alpha-MSH it retains the parent hormone's anti-inflammatory signalling while leaving the pigmentation activity behind. Isolating that fragment is the reason it exists as a separate compound.
C-terminal tripeptide of alpha-MSH
Carries much of the parent's anti-inflammatory activity
Antimicrobial effects reported against S. aureus and C. albicans
Studied applications
What KPV is researched for
GASTROENTEROLOGY
Intestinal Inflammation & Colitis
Colitis models are the most-studied application, which follows from uptake via an intestinal peptide transporter.
Dalmasso et al. 2008
IMMUNOLOGY
α-MSH Anti-Inflammatory Signaling
Inflammatory transcription is the measured endpoint, inherited from the parent hormone minus its pigmentation activity.
Brzoska et al.
DERMATOLOGY
Epithelial Wound Healing
Epithelial closure is measured in gut and skin models, where the anti-inflammatory and repair endpoints overlap.
Bonfiglio et al. 2006
MICROBIOLOGY
Antimicrobial Activity
Direct antimicrobial effects have been reported, distinct from the anti-inflammatory signalling and less well characterized.
Cutuli et al. 2000
What the published work measures
The endpoints reported across the literature for this compound. The figures belong to the individual papers, not to us.
NF-κB Activation
Pro-inflammatory Cytokines (TNF-α, IL-6)
Colitis Severity (DSS / TNBS models)
Corneal Re-epithelialization (rabbit study, 60 h)
Reference values
KPV molecular data
Scroll for full molecular data →
Sequence
L-Lysyl-L-Prolyl-L-Valine (α-MSH 11–13)
Molecular weight
342.43 g/mol
Molecular formula
C₁₆H₃₀N₄O₄
Physical form
Lyophilized powder
Documented purity
Quantified by HPLC, reported per lot
Storage
-20°C for long-term stability
Solubility
Water-soluble
Available sizes
10mg
FAQ
Common questions about KPV
What is KPV?
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KPV is a tripeptide of lysine, proline and valine, corresponding to the C-terminal tripeptide of alpha-MSH. That short tail carries much of the parent hormone's anti-inflammatory signaling while leaving behind its effect on pigmentation, which is the property that made the fragment worth isolating.
What is KPV researched for?
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Published research on KPV concentrates on Intestinal Inflammation & Colitis, α-MSH Anti-Inflammatory Signaling, Epithelial Wound Healing and Antimicrobial Activity. Each of those areas is summarised further up this page with the citation it comes from, and the full reference list — 4 indexed publications — sits at the bottom. Study designs and concentrations vary considerably between publications, so the primary sources are worth reading directly.
How does KPV work?
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The literature describes KPV acting across Inflammatory Pathway Suppression, Cellular Transport & Action and Melanocortin Fragment, reported respectively as NF-κB Inhibition, PepT1-Mediated Uptake and α-MSH-Derived Activity. Those pathways are drawn from preclinical models rather than clinical work, and they describe what has been observed rather than a settled mechanism — the individual pathway cards above cite what each one is based on.
What are the molecular specifications for KPV?
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KPV has a molecular formula of C16H30N4O4, an average mass of 342.43 g/mol and the sequence L-Lysyl-L-Prolyl-L-Valine (α-MSH 11–13). It ships as lyophilized powder. Those are nominal reference values for the parent compound. The identity of the specific material you receive is confirmed by mass spectrometry and reported on that lot's certificate.
How should KPV be stored and reconstituted?
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Store the sealed vial at -20°C, protected from light and moisture, and let it reach room temperature before opening so condensation does not form on cold powder. KPV is water-soluble; reconstitute by directing the diluent down the vial wall rather than onto the powder, then swirl to dissolve rather than shaking. Keep reconstituted solution refrigerated and avoid repeated freeze-thaw cycles — solutions are far less stable than lyophilized powder.
Is KPV approved for human use?
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No. KPV is supplied strictly for in-vitro laboratory research and development. It is not a drug, food, supplement or cosmetic, it has not been evaluated by the FDA, and it is not intended for human or animal consumption, ingestion, injection or any in-vivo use. Ordering confirms you are a qualified researcher or institution purchasing on that basis.
Cited sources
Peer-reviewed literature
Independent published research indexed from PubMed — not Routine Peptides claims.
Every production run is analyzed by an independent laboratory, and the certificate for your lot travels with the order — not a catalog-wide document, and not a summary written by us.