KPV

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(2S)-2-[[(2S)-1-[(2S)-2,6-diaminohexanoyl]pyrrolidine-2-carbonyl] amino]-3-methylbutanoic acid

CC(C)[C@@H](C(=O)O)NC(=O)[C@@H]1CCCN1C(=O)[C@H](CCCCN)N

C-terminal residues 11-13 of α-melanocyte-stimulating hormone (α-MSH), a 13-residue peptide hormone.

Hiltz ME, Lipton JM. Antiinflammatory activity of a COOH-terminal fragment of the neuropeptide alpha-MSH. FASEB J. 1989;3(11):2282-4.

α-MSH engages melanocortin receptors (MC1R, MC3R, MC4R, MC5R) through the central His-Phe-Arg-Trp (HFRW) tetrapeptide pharmacophore at residues 6-9. The C-terminal Lys-Pro-Val tripeptide does not contain that motif.

Multiple primary studies report KPV anti-inflammatory activity that proceeds without melanocortin-receptor signaling. Kannengiesser et al. (2008) examined the MC1R contribution specifically and described KPV activity as at least partially independent of MC1R.

KPV carries no reported pigmentary action, in contrast to the parent hormone.

KPV is taken up by intestinal epithelial and immune cells via the PepT1 peptide transporter. Transport is required for activity; competitive blockade abolishes the effect. Dalmasso et al. (2008) established this route. Viennois et al. (2016) examined PepT1 in colitis-associated models.

Once internalized, KPV inhibits NF-κB activation and nuclear translocation, reported at nanomolar concentrations.

Reported modulation alongside NF-κB.

Reported reductions in TNF-α and other pro-inflammatory cytokines in intestinal and epithelial cell models. Xiao et al. (2017) reported TNF-α downregulation in colonic tissue.

Bonfiglio et al. (2006) reported accelerated corneal epithelial re-epithelialization with KPV exposure, an effect attenuated by pre-treatment with the nitric oxide synthase inhibitor L-NAME, indicating NO involvement in that model.

The central proline imposes a conformational constraint that the structure-activity literature treats as material to activity.

Intestinal inflammation — the largest body of work PepT1-mediated uptake reducing intestinal inflammation (Dalmasso 2008); murine IBD models with reported reductions in inflammatory infiltrate and myeloperoxidase activity (Kannengiesser 2008); hyaluronic-acid-functionalized nanoparticle oral delivery in ulcerative colitis (Xiao 2017); hydrogel-based delivery systems (Sun 2021, Zhao 2022).

α-MSH and related tripeptides, anti-inflammatory and protective effects (Brzoska 2008); keratinocyte signaling (Elliott 2004); murine incisional wound healing and scar area (de Souza 2015).

Corneal epithelial wound healing and the role of nitric oxide (Bonfiglio 2006).

Inhibition of inflammation cues in bronchial epithelial cells (Land 2012).

Dissection of the anti-inflammatory effect of core and C-terminal α-MSH peptides (Getting 2003); structural modification by reductive glycoalkylation of the lysine residue (Songok 2018).

Effect of α-MSH 11-13 on fever in the rabbit (Richards & Lipton 1984).

Stability-indicating HPLC assay for KPV in aqueous solutions and skin homogenates (Pawar 2015); transdermal iontophoretic delivery across microporated skin (Pawar 2017).

Oral, topical, transdermal, and intraperitoneal.

KPV is not approved as a drug by the FDA, EMA, or any other regulatory agency. No approved formulation exists in any jurisdiction. It is supplied as a research chemical for in-vitro and preclinical laboratory use only.