gemfibrozil

Gemfibrozil (CI-719) interacts with peroxisome proliferator-activated receptors (PPARalpha) resulting in PPARalpha-mediated stimulation of fatty acid oxidation and an increase in lipoprotein lipase (LPL) synthesis. Gemfibrozil is a fibric acid derivative with hypolipidemic effects. This enhances triglyceride-rich lipoprotein clearance and reduces the expression of apolipoprotein C-III (apoC-III). The reduction in hepatic production of apoC-III result in the subsequent reduction of serum levels of very-low-density-lipoprotein cholesterol (VLDL-C). In addition, gemfibrozil-mediated PPARalpha stimulation of apoA-I and apoA-II expression results in an increase in high-density lipoprotein cholesterol (HDL-C).

Gemfibrozil-d6 is intended for use as an internal standard for the quantification of gemfibrozil by GC- or LC-MS. Gemfibrozil is a peroxisome proliferator-activated reporter α and PPARγ agonist. In vivo, gemfibrozil reduces serum total cholesterol, triglyceride, and LDL levels in a rat model of high-cholesterol diet-induced hyperlipidemia. Gemfibrozil reduces atherosclerotic plaque area, superoxide production, and expression of the genes encoding the NF-κB subunit p65 and chemokine (C-C) motif ligand 2 (CCL2) in ApoE-/- mice. Formulations containing gemfibrozil have been used in the treatment of high cholesterol.

Gemfibrozil 1-O-β-Glucuronide, a metabolite of Gemfibrozil, is a potent and competitive inhibitor of P450 (CYP) isoform CYP2C8, with an IC50 of 4.07 μM.

AH057 is a novel JAK inhibitor, effectively blocking the JAK/STAT pathways by directly inhibiting JAK1/2 kinase activities, and leading to compromised cell proliferation and invasion, increasing apoptosis, arrested cell cycles, and impairing tumor progression in vitro and in vivo