Fenoprofen calcium hydrate is a non-steroidal anti-inflammatory drug (NSAID).
Storage Temp
Store at -80°C
Shipped In
Ice chest + Ice pads
This product requires cold chain shipping. Ground and other economy services are not available.
Action Type
INHIBITOR
Mechanism of action
Cyclooxygenase inhibitor
Product Description
Information
Fenoprofen calcium hydrate is a non-steroidal anti-inflammatory drug (NSAID). In vitro
Fenoprofen is a more potent inhibitor of collagen-induced platelet aggregation than either aspirin or phenylbutazone. Fenoprofen inhibits the formation of palmitoyl-CoA in both microsomal and peroxisomal fractions, and inhibits the beta-oxidation of lignoceric acid and cerotic acid in rat hepatocytes. Fenoprofen exhibits modest antiproliferative activity against HT-29, DID-1, and SW480 cells with IC50 of 240 μM, 300 μM, and 360 μM, respectively. Fenoprofen (0.1 mM) is an efficient activator of peroxisome proliferator-activated receptor gamma (PPARγ), activating the receptor to a degree comparable to that obtained with the PPARγ ligands BRL49653 and 15-deoxy-D12,14-PGJ2 and the peroxisome proliferator Wy14643. Fenoprofen is also an efficacious activator of PPARα, activating the receptor to a degree comparable to that obtained with the strong peroxisome proliferator Wy14643. Consistently, Fenoprofen treatment promotes lipogenesis in C3H10T1/2 cells. Although Fenoprofen displays only modest antiproliferative activity, Fenoprofen amides can potently induce cell cycle arrest at the G1 phase, as well as apoptosis, probably because of a greater lipophilicity and/or better cell uptake.
In vivo
Oral administration of Fenoprofen at 50 mg/kg potently inhibits thrombus formation by 47%, whereas a dose of 200 mg/kg of aspirin is required to reduce thrombus formation 21 %. Similar to indomethacin, adminstration of Fenoprofen inhibits prostaglandin synthesis. In rats with type II collagen-induced arthritis, Fenoprofen treatment at 40 mg/kg/day partially suppresses the paw swelling, but has no significant effect on humoral and cellular responses. Administration of Fenoprofen depresses the rebound contraction, thus transforming the brisk relaxant response, elicited by vagal stimulation or ATP, into long-lasting relaxation. Administration of Fenoprofen causes a strong and dose-related induction of peroxisomal palmitoyl-CoA oxidase, and of carnitine acyltransferase and acyl-CoA hydrolase activities in liver homogenates of mice fed diets. Hepatic catalase activity is significantly increased in mice fed the diet with 0.05 and 0.1% fenoprofen but not the 1% fenoprofen-containing diet. Cell Data
cell lines：
Concentrations：Dissolved in DMSO, final concentrations ~1 mM
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