Kpv Research
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KPV: Alpha-MSH Derived Tripeptide and Melanocortin Research
KPV (Lys-Pro-Val) is a synthetic tripeptide derived from the C-terminal of alpha-melanocyte-stimulating hormone (alpha-MSH). It is studied in laboratory settings for its role in melanocortin receptor pharmacology and anti-inflammatory signalling pathway research. Despite its small size, KPV has been the subject of substantial research interest due to its activity in inflammatory cell models.
Chemical and Molecular Data
| Property | Value |
|---|---|
| Molecular formula | C16H31N3O4 |
| Molecular weight | 329.43 g/mol |
| CAS number | 1101-61-7 |
| Sequence | Lys-Pro-Val |
| Amino acid count | 3 |
| Parent peptide | Alpha-MSH (C-terminal fragment, positions 11-13) |
| Purity | greater than or equal to 98% as verified by HPLC |
| Form | Lyophilised powder |
| Storage | -20 degrees C, protected from light and moisture |
| Reconstitution | Sterile water recommended |
KPV: Alpha-MSH C-terminal Tripeptide and Melanocortin Pathway
Alpha-MSH and Melanocortin Biology
Alpha-melanocyte-stimulating hormone (alpha-MSH) is a 13 amino acid neuropeptide derived from pro-opiomelanocortin (POMC) processing. In addition to its well-known role in pigmentation through MC1R, alpha-MSH exerts potent anti-inflammatory effects through melanocortin receptors (MC1R, MC3R, MC5R) expressed on immune cells. The C-terminal KPV tripeptide (residues 11-13 of alpha-MSH) retains significant anti-inflammatory activity in laboratory models despite lacking the full receptor binding pharmacophore of the parent peptide.
Melanocortin Receptor Pharmacology Research
Laboratory research has examined KPV's interactions with melanocortin receptors, particularly MC1R, MC3R, and MC5R expressed on macrophages, monocytes, and other immune cells. Research has investigated whether KPV's anti-inflammatory effects are receptor-mediated or operate through receptor-independent mechanisms.
The melanocortin system and its anti-inflammatory signalling through cAMP/PKA pathways and NFkB suppression has been studied as a context for understanding KPV's mechanism of action in inflammatory models.
Anti-inflammatory Signalling Research
The primary research focus on KPV involves its effects on inflammatory signalling pathways in cell culture models. Laboratory studies have examined:
NFkB pathway modulation. Research has investigated KPV's effects on NFkB nuclear translocation, IkB phosphorylation, and expression of NFkB-dependent inflammatory genes in macrophage and epithelial cell models.
Cytokine regulation. Studies have examined KPV's effects on pro-inflammatory cytokine production (IL-1beta, TNF-alpha, IL-6, IL-8) and anti-inflammatory mediators in stimulated immune cell models.
Intestinal epithelial research. KPV has been studied in intestinal epithelial cell models relevant to mucosal immunology research, with investigations of barrier function and inflammatory signalling in Caco-2 and similar cell systems.
Research Applications
KPV is used in melanocortin receptor pharmacology studies, NFkB pathway anti-inflammatory research, cytokine regulation studies in macrophage models, intestinal epithelial barrier research, and as a minimal active fragment reference compound in alpha-MSH pharmacology studies.
Alpha-MSH Derived Peptides: Research Comparison
| Peptide | Sequence | Length | Receptor activity | Research focus |
|---|---|---|---|---|
| Alpha-MSH | Ac-SYSMEHFRWGKPV-NH2 | 13aa | MC1R, MC3R, MC5R | Broad melanocortin |
| KPV | Lys-Pro-Val | 3aa | Partial MC1/3/5 | Anti-inflammatory signalling |
| [Nle4-D-Phe7]-alpha-MSH | Modified alpha-MSH | 13aa | Full MC1-5 | Pan-melanocortin research |
| MT-II | Ac-Nle-cyc[Asp-His-D-Phe-Arg-Trp-Lys]-OH | 7aa cyclic | Full MC1-5 | SAR studies |
Melanocortin System Overview
The melanocortin system comprises five G-protein coupled receptors (MC1R-MC5R), two endogenous agonists (alpha-MSH, ACTH, and related POMC-derived peptides), and two endogenous antagonists (AgRP and agouti protein). Key features relevant to KPV research:
- MC1R is expressed on melanocytes, macrophages, and dendritic cells. MC1R activation reduces pro-inflammatory cytokine production and increases anti-inflammatory mediators.
- MC3R is expressed in the hypothalamus, immune cells, and gut. Research has examined MC3R's role in energy homeostasis and immune regulation.
- MC5R is expressed on immune cells, exocrine glands, and other tissues. MC5R activation has been studied in the context of immune cell activation and exocrine secretion.
KPV's ability to interact with these receptors despite being only 3 amino acids has made it a useful minimal pharmacophore for studying melanocortin biology in inflammatory research models.
Frequently Asked Questions
Does KPV interact with melanocortin receptors directly or through a different mechanism?
The mechanistic basis of KPV's effects in laboratory models is not fully resolved. Some research suggests KPV can interact with MC1R, MC3R, and MC5R, though with lower affinity than full-length alpha-MSH. Other research has proposed receptor-independent mechanisms involving direct inhibition of NFkB pathway components. In practical terms, most laboratory research uses KPV as a functional tool and characterises downstream pathway changes (NFkB nuclear translocation, cytokine production, calcium signalling) rather than relying on a single defined mechanism.
Why does KPV retain activity despite losing most of the alpha-MSH sequence?
The C-terminal tripeptide Lys-Pro-Val represents the very end of the alpha-MSH sequence. Structure-activity relationship research with alpha-MSH analogues has demonstrated that the C-terminal region contributes to receptor binding, while the central His-Phe-Arg-Trp core is the primary receptor activation pharmacophore. KPV's activity in inflammatory models at concentrations higher than those required for alpha-MSH suggests it acts as a weak partial agonist or modulator rather than a potent receptor agonist, making it useful for studying the concentration-dependent aspects of melanocortin signalling.
Published Research References
For laboratory and analytical research purposes only. Not for human or veterinary use. No dosage or administration guidance is provided or implied.
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