KPV - 10mg

Structured public compound identifiers and computed chemical properties. Product-specific stability, purity, lot results, and shelf life are not inferred from this record.

Why linked: Official PubChem identity record returned for the resolved component KPV.

Airborne particulate matter (PM) poses a major environmental risk that impairs skin health by triggering oxidative stress, inflammation, and cell death. In this study, we investigated the protective effects of Lysine-Proline-Valine (KPV)-an endogenous peptide derived from α-melanocyte-stimulating hormone-against oxidative damage and inflammation induced by fine PM (PM 10 ) in human HaCaT keratinocytes. Our results show that PM 10 markedly suppresses HaCaT cell proliferation via cytotoxic effects and induces a pro-inflammatory response by increasing IL-1β secretion. Notably, treatment with 50 μg/mL of KPV restored cell viability and reduced IL-1β secretion disrupted by PM 10 exposure. To counteract PM 10 -induced cell death, KPV inhibited reactive oxygen species (ROS) production, which is responsible for activating extracellular signal-regulated kinase and p

Why linked: The title contains the resolved identity “Lysine-Proline-Valine”.

A simple, sensitive and stability-indicating high-performance liquid chromatographic (HPLC) assay method was developed and validated for a bioactive peptide, lysine-proline-valine (KPV) in aqueous solutions and skin homogenates. Chromatographic separation was achieved on a reversed phase Phenomenex C18 column (4.6 &#xd7; 250 mm, packed with 5 &#xb5;m silica particles) with a gradient mobile phase consisting of 0.1% trifluoroacetic acid (TFA) in water (A) and 0.1% TFA in acetonitrile (B). The proposed HPLC method was validated with respect to accuracy, precision, linearity, repeatability, limit of detection (LOD) and limit of quantitation (LOQ). The calibration curve was linear with a correlation coefficient (r) of 0.9999. Relative standard deviation values of accuracy and precision experiments were <2. The LOD and LOQ of KPV were 0.01 and 0.25 &#xb5;g/mL, respectively. Under stress condi

Why linked: The title contains the resolved identity “KPV”.

Lysine-proline-valine (KPV) is a C-terminal peptide fragment of &#x3b1;-melanocyte stimulating hormone with potent anti-inflammatory properties. Present study investigates various transdermal enhancement strategies such as iontophoresis (ITP), microneedles (MN), and their combination (ITP&#xa0;+ MN) on KPV delivery across dermatomed human skin. KPV attains a positive charge at pH less than 7.0, thus anodal ITP was used. The influence of current strength, KPV concentration, and duration of current application on the KPV delivery was investigated. At defined ITP parameters, the influence of MN on KPV delivery (ITP&#xa0;+ MN) across skin was also determined. KPV permeation was less than detectable levels (limit of detection, 0.01 &#x3bc;g/mL) by simple passive diffusion. However, KPV permeation was increased to 4.4 &#x3bc;g/cm 2 /h by MN treatment. Furthermore, ITP and ITP&#xa0;+ MN increas

Why linked: The title contains the resolved identity “KPV”.

Hepatocellular steatosis, an early stage within the non-alcoholic fatty liver disease (NAFLD) spectrum, is characterized by excessive lipid accumulation and oxidative stress in hepatocytes. This study examined the protective role of Lysine-Proline-Valine (KPV), an endogenous tripeptide derived from &#x3b1;-melanocyte-stimulating hormone, against oleic acid (OA)-induced oxidative damage and lipid accumulation in hepatic epithelial HepG2 cells. OA treatment markedly enhanced hepatic lipid deposition by upregulation of fatty acid synthase (FAS) expression. Treatment with KPV (100&#xa0;&#xb5;g/mL) significantly attenuated OA-induced lipid accumulation and suppressed FAS expression without inducing cytotoxicity. Mechanistic analysis revealed that KPV reduced reactive oxygen species generation, thereby preventing activation of extracellular signal-regulated kinase. KPV also downregulated AKT p

Why linked: The title contains the resolved identity “Lysine-Proline-Valine”.

In this study, we analyzed the anti-inflammatory effects of alpha-melanocyte stimulating hormone (MSH)11-13 (KPV) in comparison with other MSH peptides in a model of crystal-induced peritonitis. Systemic treatment of mice with KPV, alpha-MSH, the core melanocortin peptide His-Phe-Arg-Trp, and the melanocontin receptor 3/4 agonist Ac-Nle4-c[Asp5,d-Phe7,Lys10]NH2 ACTH4-10 (MTII) but not the selective MC1-R agonist H-Ser-Ser-Ile-Ile-Ser-His-Phe-Arg-Trp-Gly-Lys-Pro-Val-NH2 (MS05) resulted in a significant reduction in accumulation of polymorphonuclear leukocyte in the peritoneal cavity. The antimigratory effect of KPV was not blocked by the MC3/4-R antagonist Ac-Nle4-c[Asp5,d-2Nal7,Lys10]NH2 ACTH4-10 (SHU9119). In vitro, macrophage activation, determined as release of KC and interleukin (IL)-1beta was inhibited by alpha-MSH and MTII but not by KPV. Furthermore, macrophage activation by MTII

Why linked: The title contains the resolved identity “KPV”.

Why linked: The title contains the resolved identity “KPV”.

Why linked: The title contains the resolved identity “KPV”.

The melanocortin system is essential for survival, with the melanocortin-3 and -4 receptors (hMC3R and hMC4R) regulating energy homeostasis and metabolism, and the melanocortin-1 receptor (hMC1R) controlling pigmentation and skin cancer prevention. However, achieving subtype selectivity among these receptors remains challenging due to their high sequence similarity. Here, we first systematically examined the impact of the α-MSH C-terminal tripeptide –Lys-Pro-Val (–KPV) on melanotropin conformation and receptor selectivity. Incorporation of –KPV enhanced binding affinity toward hMCRs and modulated receptor preference. We identified a selective hMC3R antagonist, peptide 5 ([CO(CH₂)₂CO-DNal(2′)-Arg-Trp-Lys]-Gly-Lys-Pro-Val-NH₂) and a selective hMC3R agonist, peptide 20 (H-DNal(2′)-c[Asp-Pro-DPhe-Arg-Trp-Lys]-Ala-Gly-Pro-Val-NH₂). Additionally, several hMC1R-selective agonists (peptides 9–11

Why linked: The title contains the resolved identity “KPV”.

Why linked: The title contains the resolved identity “KPV”.

Why linked: The title contains the resolved identity “KPV”.

Why linked: The title contains the resolved identity “KPV”.