product name Gemfibrozil
Description: Gemfibrozil is an activator of peroxisome proliferator-activated receptor-alpha (PPARα), and used for the treatment of hypercholesterolemia and hypertriglyceridemia. The mechanism of action of gemfibrozil is as a Peroxisome Proliferator-activated Receptor alpha Agonist. The chemical classification of gemfibrozil is PPAR alpha. Gemfibrozil is a lipid-regulating agent that lowers elevated serum lipids primarily by decreasing serum triglycerides with a variable reduction in total cholesterol.
References: J Pharmacol Exp Ther. 2002 Jun;301(3):1042-51; Drug Metab Dispos. 2001 Nov;29(11):1359-61.
250.33
Formula
C15H22O3
CAS No.
25812-30-0
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 50 mg/mL (199.7 mM)
Water: <1 mg/mL
Ethanol: 50 mg/mL (199.7 mM)
Solubility (In vivo)
Synonyms
CI-719
other peoduct :
| In Vitro |
In vitro activity: 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 Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | 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. |
| Animal model | |
| Formulation & Dosage | |
| References | J Pharmacol Exp Ther. 2002 Jun;301(3):1042-51; Drug Metab Dispos. 2001 Nov;29(11):1359-61. |
