product name Bezafibrate
Description: Bezafibrate is the first clinically tested dual and pan-PPAR co-agonist. Bezafibrate is an agonist of peroxisome proliferator-activated receptor alpha (PPARalpha) with antilipidemic activity. Bezafibrate is a fibrate drug used for the treatment of hyperlipidaemia. Bezafibrate decreases triglyceride levels, increases high density lipoprotein cholesterol levels, and decreases total and low density lipoprotein cholesterol levels. It is commonly marketed as Bezalip.
References: Mol Endocrinol. 1997 Jun;11(6):779-91; Diabetes. 2001 Aug;50(8):1883-90.
361.82
Formula
C19H20ClNO4
CAS No.
41859-67-0
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 72 mg/mL (199.0 mM)
Water: <1 mg/mL
Ethanol: 18 mg/mL (49.7 mM)
Solubility (In vivo)
Synonyms
BM 15075
other peoduct :
| In Vitro |
In vitro activity: Bezafibrate is a lipid-lowering fibric acid derivative. Bezafibrate binds to xPPARβ with EC50 of 5 μM. Bezafibrate transcriptionally activates the PPARβ of Xenopus with EC50 of 1 μM. Bezafibrate exposure to rat primary culture of adipocytes for 24 h increases the mRNA levels of crucial genes involved in peroxisomal and mitochondrial β-oxidation. The mRNA levels of the peroxisomal β-oxidation rate-limiting enzyme acyl-CoA oxidase and of the muscle-type carnitine palmitoyl transferase I (M-CPT-I) increases by 1.6-fold and 4.5-fold, respectively. Bezafibrate induces an increase in the transcript levels of the uncoupling protein-2 (UCP-2; 1.5-fold induction) and UCP-3 (3.7-fold induction), mitochondrial proteins that reduce ATP yield and may facilitate the oxidation of fatty acids. Furthermore, Bezafibrate increases the mRNA levels of the fatty acid translocase (2-fold induction). Bezafibrate causes a 1.9-fold induction in 9,10-[3H]palmitate oxidation. Moreover, Bezafibrate reduces the mRNA expression of several adipocyte markers, including PPARγ (30% reduction), tumor necrosis factor-α (33% reduction), and the ob gene (26% reduction). The reduction of the adipocyte markers causes by Bezafibrate is accompanied by an increase in the mRNA levels of the preadipocyte marker Pref-1 (1.6-fold induction). Kinase Assay: Cell Assay: |
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| In Vivo | Bezafibrate treatment is able to induce increasing mRNA levels of M-CPT-I (4.5-fold induction), fatty acid translocase (2.6-fold induction) and Pref-1 (5.6-fold induction) in epididymal white adipose tissue of rats. Similarly, increases. Bezafibrate feeding causes a significant increase in liver weight in wild-type and PPARβ-null mice compared to controls, while liver weight is unchanged in Bezafibrate-fed PPAR-α null mice. Gonadal adipose stores are significantly smaller in wild-type and PPARβ-null mice fed Bezafibrate than in controls (2.8-fold less and ~2.6-fold less, respectively), and this effect is not found in similarly fed PPARα-null mice. Bezafibrate is able to cause changes of mRNAs encoding lipid metabolizing enzymes (such as AOX , cytochrome P450 4A (CYP4A), LPL, ACS, and LCA D) in wild-type, PPARβ-null mice and PPARα-null mice compared to controls. Bezafibrate is able to induce UCPs expression, and modify energy homeostasis by directly inducing aco gene expression (14.5-fold at 7 days) and peroxisomal fatty acid β-oxidation in white adipose tissue of rats. Further, Bezafibrate significantly reduces plasma triglyceride and leptin concentrations, without modifying the levels of PPARγ or ob gene in white adipose tissue. |
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| Formulation & Dosage | |
| References | Mol Endocrinol. 1997 Jun;11(6):779-91; Diabetes. 2001 Aug;50(8):1883-90. |
