Catalog No.S4159 Synonyms: BM 15075

For research use only.

Bezafibrate (BM 15075) is the first clinically tested dual and pan-PPAR co-agonism.

Bezafibrate Chemical Structure

CAS No. 41859-67-0

Selleck's Bezafibrate has been cited by 2 Publications

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Description Bezafibrate (BM 15075) is the first clinically tested dual and pan-PPAR co-agonism.
PPAR [1]
In vitro

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. [1] 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). [2]

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. [2] 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. [3] 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. [4]

Protocol (from reference)

Solubility (25°C)

In vitro

Chemical Information

Molecular Weight 361.82


CAS No. 41859-67-0
Storage 3 years -20°C powder
2 years -80°C in solvent
Smiles CC(C)(C(=O)O)OC1=CC=C(C=C1)CCNC(=O)C2=CC=C(C=C2)Cl

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Clinical Trial Information

NCT Number Recruitment Interventions Conditions Sponsor/Collaborators Start Date Phases
NCT02291796 Completed Drug: Bezafibrate Acute Myocardial Infarction Instituto Mexicano del Seguro Social January 2011 Phase 4

(data from, updated on 2022-01-17)

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