＞98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

吉非luo齐；CI-719

白色粉末

DMSO : 47 mg/mL (187.8 mM)

Ethanol : 47 mg/mL (187.8 mM)

PPARα

Gemfibrozil exerts a minimal inhibitory effect on CYP3A-mediated simvastatin hydroxy acid (SVA) oxidation, but does inhibit SVA glucuronidation in dog and human liver microsomes. Gemfibrozil markedly inhibits M-23 formation, with a K(i) (IC(50)) value of 69 (95) mM, whereas inhibition of M-1 formation is weaker with a K(i) (IC(50)) value of 273 mM in human liver microsomes. Gemfibrozil strongly and competitively inhibits CYP2C9 activity, with a K(i) (IC(50)) value of 5.8 (9.6) mM. Gemfibrozil exhibits somewhat smaller inhibitory effects on CYP2C19 and CYP1A2 activities, with K(i) (IC(50)) values of 24 (47) mM and 82 (136) mM, respectively. Gemfibrozil, a lipid-lowering drug, inhibits cytokine-induced production of NO and the expression of inducible nitric-oxide synthase (iNOS) in human U373MG astroglial cells and primary astrocytes. Gemfibrozil induces peroxisome proliferator-responsive element (PPRE)-dependent luciferase activity, which is inhibited by the expression of DeltahPPAR-alpha, the dominant-negative mutant of human PPAR-alpha. Gemfibrozil strongly inhibits the activation of NF-kappaB, AP-1, and C/EBPbeta but not that of gamma-activation site (GAS) in cytokine-stimulated astroglial cells.

Gemfibrozil treatment significantly reduces (2-3-fold) the plasma clearance of SVA and the biliary excretion of SVA glucuronide (together with its cyclization product SV), but not the excretion of a major oxidative metabolite of SVA in dogs.