RXRα Inhibitor, K-80003-Calbiochem

C₂₃H₂₃FO₂

350.43

A cell permeable, Sulindac analog with IC₅₀=2.4 µM for RXRα binding, and unlike other NSAIDs, is inactive toward COX2 and COX1 even at 1 mM. The compound displays potent inhibition of RXRα dependent AKT Activation in both PC3 and A549 cells, and is RXRα but not RXRγ expression dependent as shown in PC3 cells. It is further shown to inhibit the interaction of RXRα/Δ80 with p85α either in the absence or presence of TNF-α. Induces PARP cleavage and caspase-8 activation at 50 µM when used with TNF-α. Furthermore, it almost completely suppresses colony formation of HeLa/RXRα/1-134 and RXRα/Δ80 cells at 25 µM in vitro, and exhibits potent inhibition of tumor growth in vivo when dosed at 60 mg/kg.
A cell permeable, Sulindac analog with IC₅₀=2.4 µM for RXRα binding, and unlike other NSAIDs, is inactive toward COX2 and COX1 even at 1 mM. The compound displays potent inhibition of RXRα dependent AKT Activation in both PC3 and A549 cells, and is RXRα but not RXRγ expression dependent as shown in PC3 cells. It is further shown to inhibit the interaction of RXRα/Δ80 with p85α either in the absence or presence of TNF-α. Induces PARP cleavage and caspase-8 activation at 50 µM when used with TNF-α. Furthermore, it almost completely suppresses colony formation of HeLa/RXRα/1-134 and RXRα/Δ80 cells at 25 µM in vitro, and exhibits potent inhibition of tumor growth in vivo when dosed at 60mg/kg.

Toxicity: Standard Handling (A)

Following reconstitution, aliquot and freeze (-20°C.

Zhou, H., et al. 2010. Cancer Cell17, 560.

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

100

≥95% (HPLC)

solid

Calbiochem^®

OK to freeze

yellow

DMSO: 50 mg/mL

wet ice

2-8℃

10 mg in Glass bottle

11 - Combustible Solids

WGK 2