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Bezafibrate PPAR agonist

Cat.No.S4159

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

Batch: Purity: 99.78%
99.78

Solubility

In vitro
Batch:

DMSO : 72 mg/mL (198.99 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 60 mg/mL

Water : Insoluble

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In vivo
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Chemical Information, Storage & Stability

Molecular Weight 361.82 Formula

C19H20ClNO4

Storage (From the date of receipt)
CAS No. 41859-67-0 Download SDF Storage of Stock Solutions

Synonyms BM 15075 SMILES CC(C)(C(=O)O)OC1=CC=C(C=C1)CCNC(=O)C2=CC=C(C=C2)Cl

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Mechanism of Action

Targets/IC50/Ki
PPAR
In vitro
Bezafibrate is a lipid-lowering fibric acid derivative. This compound binds to xPPARβ with EC50 of 5 μM. It transcriptionally activates the PPARβ of Xenopus with EC50 of 1 μM. This chemical 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. It 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, this compound increases the mRNA levels of the fatty acid translocase (2-fold induction). It causes a 1.9-fold induction in 9,10-[3H]palmitate oxidation. Moreover, this chemical 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 it is accompanied by an increase in the mRNA levels of the preadipocyte marker Pref-1 (1.6-fold induction).
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. This compound feeding causes a significant increase in liver weight in wild-type and PPARβ-null mice compared to controls, while liver weight is unchanged in similarly fed PPAR-α null mice. Gonadal adipose stores are significantly smaller in wild-type and PPARβ-null mice fed this compound 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. It 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. This chemical 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, it significantly reduces plasma triglyceride and leptin concentrations, without modifying the levels of PPARγ or ob gene in white adipose tissue.
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/11216866/

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2025-08-27)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT06443606 RECRUITING
BPC; Non Optimal Response to UDCA
Assistance Publique - Hôpitaux de Paris
2025-03-27 PHASE3
NCT02481245 COMPLETED
Bipolar Disorder; Depressive Episode
Massachusetts General Hospital
2018-01-11 PHASE2
NCT06488911 TERMINATED
Primary Biliary Cholangitis
Intercept Pharmaceuticals
2024-07-01 PHASE3
NCT04594694 TERMINATED
Primary Biliary Cholangitis
Intercept Pharmaceuticals
2019-10-02 PHASE2
NCT05239468 COMPLETED
Primary Biliary Cholangitis
Intercept Pharmaceuticals
2022-03-21 PHASE2
NCT04997811 UNKNOWN
Myelodysplastic Syndromes (MDS)
Prof. Janet Dunn
2021-12-21 PHASE2

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