A prostacyclin analog that is orally active with prolonged availability in vivo, having a terminal half-life in plasma of one hour inhibits the pro-inflammatory actions of certain leukocytes, suppresses cardiac fibrosis, and blocks mitogenesis of
A prostacyclin analog that is orally active with prolonged availability in vivo, having a terminal half-life in plasma of one hour inhibits the pro-inflammatory actions of certain leukocytes, suppresses cardiac fibrosis, and blocks mitogenesis of
An orally available, selective inhibitor of ALK (IC<sub>50</sub> = 1.9 nM) that also inhibits F1174L, R1275Q, and L1196M mutants of ALK (IC<sub>50</sub>s = 1.
An orally available, selective inhibitor of ALK (IC<sub>50</sub> = 1.9 nM) that also inhibits F1174L, R1275Q, and L1196M mutants of ALK (IC<sub>50</sub>s = 1.
A potent, cell permeable inhibitor of PKC (IC50 = 660 nM) also inhibits BclXL function (IC50 = 1.5 &muM), inducing apoptosis in several cancer cell lines can have PKC-independent effects, activate p38 and JUNK signaling pathways, and induce
A potent, cell permeable inhibitor of PKC (IC50 = 660 nM) also inhibits BclXL function (IC50 = 1.5 &muM), inducing apoptosis in several cancer cell lines can have PKC-independent effects, activate p38 and JUNK signaling pathways, and induce
A synthetic analog of retinoic acid that binds to retinoic acid receptors with similar efficiency as retinoic acid (Kis in the nM range) yet does not display affinity for cellular retinoic acid-binding protein (Ki = 540 µM).
A synthetic analog of retinoic acid that binds to retinoic acid receptors with similar efficiency as retinoic acid (Kis in the nM range) yet does not display affinity for cellular retinoic acid-binding protein (Ki = 540 µM).