C17H15ClO4 Fenofibric Acid Aphrodisiac Powder CAS 42017-89-0

Fall hematic fat statins ANTI-DETECTION AND APHRODISIAC Lipoprotein

1, Product title:Fall hematic fat statins ANTI-DETECTION AND APHRODISIAC Lipoprotein

2, Product parameter table:

3, Product Description:

The activated form of lipid-lowering drugs, also an agonist of PPARα, has the effect of raising HDL. Fibricacids enhance catabolism of fatty acids and decrease lipid levels, mainly triglycerides. It upregulated the expression of ABCA1 and the HDL production mediated by APOA-I. Fibricacids exert their role on ABCA1 expression by enhancing the transcription of the LXR-dependent ABCA1 gene.

4, Fenofibrate acid biological activity:

Description Fenofibric acid is the active metabolite of fenofibrate and a PPAR agonist. The EC50 values ​​of PPARα, PPARγ and PPARδ are 22.4 µM, 1.47 µM and 1.06 µM, respectively; Fenofibric acid can also inhibit the activity of COX-2 with IC50 value of 48 nM.
Related categories
Research Fields >> Metabolic Diseases
Target
PPARδ: 1.06 μM (EC50)

PPARγ: 1.47 μM (EC50)

PPARα: 22.4 μM (EC50)

COX-2: 48 μM (IC50)

In vitro studies Fenofibric acid is a PPAR activator. The EC50 of PPARα, PPARγ and PPARδ are 22.4μM, 1.47μM and 1.06μM, respectively [1]. Fenofibric acid (10, 25, 50, 75 and 100 nM) inhibits COX-2 enzyme in a dose-dependent manner with IC50 of 48 nM [2]. Fenofibric acid (500 nM) can reduce the abundance of AOX1 protein in HepG2 cells [3]. Fenofibric acid (100μM) can reduce the phosphorylation level of JNK1/2, c-Jun and p38 MAPK, and can prevent the accumulation of reactive oxygen species, endoplasmic reticulum (ER) stress and blood retinal barrier (BRB) destruction. High glucose (HG) and hypoxia in ARPE-19 cells. Under HG conditions and hypoxia, fenofibric acid (100μM) activates the survival signaling pathway mediated by IGF-IR / Akt / ERK1/2 in ARPE-19 cells [4].
In vivo study Fenofibric acid (1,5,10 mg/kg, po) showed anti-inflammatory activity in Wistar rats with acute inflammation induced by carrageenan [2].
Cell experiment ARPE-19 cells were cultured for 18 days under normal blood glucose (5.5mM D-glucose) or hyperglycemia (25mM D-glucose) conditions at 37°C, 5% (v/v) CO 2 in medium DMEM/F12 Supplement 10% (v/v) fetal serum (FS) and penicillin/streptomycin. Using ARPE-19 cells, change the medium every 3-4 days. The test conditions are: (1) Maintain control cells in 5.5mM D-glucose (normal glucose) for 18 days. (2) Cells cultured in 5.5 mM D-glucose treated with 100 μM fenofibric acid for 72 hours (days 16, 17 and 18; administration once a day). (3) Cells cultured as in (1) or (2) and undergo hypoxia (1% oxygen) in the last 6 or 24 hours. (4) Cells were maintained in 25mM D-glucose (HG) for 18 days. (5) Cells cultured in 25mM D-glucose treated with 100μM fenofibric acid for 72 hours (days 16, 17 and 18; administration once a day). (6) The cells cultured in (4) or (5) undergo hypoxia (1% oxygen) in the last 6 or 24 hours [4].
Animal experiment The anti-inflammatory activity of fenofibric and its active metabolite fenofibric acid was evaluated by injecting 0.1 mL of a 1% carrageenan solution prepared in saline (under the sole of the foot) into the right hind paw of rats. The rats were divided into 6 groups with 6 animals in each group. The first group was used as a negative control and received 1% Tween-80, 10 mL/kg body weight in distilled water. Groups 2 and 3 received a single dose of fenofibrate and the standard drug diclofenac 10 mg/kg body weight, while groups 4, 5 and 6 received 3 doses of Fenofibric acid, 1, 5 and 10 mg/kg, respectively body weight. All drugs were administered orally using gavage 60 minutes before the injection of 0.1 mL of 1% carrageenan via the subplantar route. A plethysmograph was used to measure the edema volume of the test group and the control group at 0, 1, 2, and 3 hours after the induction of inflammation [2].

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