KPV (4mg)

KPV Peptide

KPV, the C-terminal peptide stretch of alpha-melanocyte-stimulating hormone (alpha-MSH), has been explored for its potential photoprotective characteristics, possible action against ischemia, and other consequences in feeding behavior, inflammation, and energy homeostasis.^[1]

Specifications

Other Known Titles: MSH(11-13), ACTH(11-13), alpha-MSH(11-13)

Molecular Formula: C₁₆H₃₀N₄O₄

Molecular Weight: 342.43 g/mol

Sequence: Lys-Pro-Val

KPV Peptide Research

KPV Peptide and Intestinal Inflammation
The primary subject of KPV research has been focused on its potential for reducing intestinal inflammation. In mouse models of inflammatory bowel disease (IBD), it appeared to reduce inflammatory infiltrates, MPO activity, and overall histological evidence of inflammation. KPV appeared to help mice to recover faster and gain weight. Delivery of KPV using nanoparticles functionalized with hyaluronic acid appeared to help direct inflammation to targeted intestinal locations.^[2] Thus the suppression of TNF-alpha may reduce inflammation and cause mucosal healing in mice. The researchers note that: “These results collectively demonstrate that our HA-KPV-NP/hydrogel system has the capacity to release HA-KPV-NPs in the colonic lumen and that these NPs subsequently penetrate into colitis tissues and enable KPV to be internalized into target cells, thereby alleviating ulcerative colitis.” Studies have suggested that the peptide also may reduce NF-kappaB and mitogen-activated protein kinase (MAPK) activity.^[3] TNF-alpha, NF-kappaB, and MAPK inhibition together ameliorate the inflammatory changes in the intestine. Mice exposed to KPV appeared to exhibit less colonic infiltration and average colon lengths than the control group.

KPV Peptide and General Inflammation
Studies in rabbits dating back to 1984 posited that KPV may have anti-inflammatory and fever reducing (antipyretic) characteristics.^[4] However, the peptide exhibited lower potency in these trials than the total length alpha-MSH molecule, suggesting that KPV lacked crucial sequences of alpha-MSH necessary for complete antipyretic activity. Researchers explored various analogs of alpha-MSH to reduce inflammation in a broad spectrum of diseases such as fever, irritant, allergic contact dermatitis, vasculitis, fibrosis, arthritis, and inflammation of the eyes, brain, lungs, and gastrointestinal tract.^[5] The scientists reported that “This study indicates that KPV is transported into cells by PepT1 and might be a new [research] agent for IBD.”  The apparent anti-inflammatory impact of KPV may differ from alpha-MSH only marginally. The parent molecule is suggested to be better at suppressing late inflammatory responses, indicating that it might be influencing immune modulation, which is separate from immediate inflammatory responses only marginally. Wound healing is a complex process that involves three general phases in the wound healing process: inflammatory, proliferative, and remodeling. Most of these cells involved in wound healing express a Melanocortin 1 receptor (MC1R) that binds alpha-melanocyte-stimulating hormone and analogs like KPV and KdPT. KVP peptide researchers found that the peptide appeared to reduce the inflammatory properties without inducing the pigmentation associated with natural scar formation in the study setting. KPV may have both anti-inflammatory and anti-microbial activities. It appears to inhibit the growth of both Candida albicans and Staphylococcus aureus and may prevent infection in the setting of severe wounds like burns.

KPV Peptide and Scar Formation
KPV may decrease chronic inflammation, which appears to lead to hypertrophic scarring (e.g., keloid).^[6] Hypertrophic scarring is considered to be caused by widespread macrophage infiltration, TNF immunoreactivity, and neutrophil abundance. Use of alpha-MSH in this setting may induce comparatively more minor scars and a less of an harsh inflammatory response. In comparison to related hormones, Alpha-MSH appears to exhibit greater potential impact than KPV but researchers posit that the molecule may have one serious disadvantage to KPV, inducing an increase in melanin production and pigmentation along the skin surface. The possible anti-inflammatory effects of KPV are mediated through a different pathway compared to those of alpha-MSH. Whereas alpha-MSH binds to specific melanocortin receptors, KPV does not appear to.

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References