BMS-561392

BMS-561392 (10 nM; 1-2.5 h) potently inhibits recombinant human TACE (ADAM17) enzymatic activity by ~80%^[1].
BMS-561392 (10 μM; 1 h pre-incubation followed by 4 h LPS stimulation) effectively suppresses LPS-induced TNF-α secretion in RAW264.7 macrophage cells^[1].
BMS-561392 (1-100 μM; 1 h pre-incubation followed by 4 h LPS stimulation) dose-dependently inhibits LPS-induced p-IκB expression, and thus NFκB pathway activation, in RAW264.7 macrophage cells^[1].
BMS-561392 (1-100 μM; 1 h pre-incubation followed by 1 h LPS stimulation) inhibits LPS-induced p-NFκB expression in RAW264.7 macrophage cells^[1].
BMS-561392 (0.3-2.7 mM; 48 h) reduces viability of undifferentiated HOG cells in a concentration-dependent manner, with the greatest reduction (89.5-93.5%) observed at 2.7 mM after 48 h incubation^[2].
BMS-561392 (0.3-2.7 mM; 48 h) modulates viability of BV-2 microglial cells in a concentration-dependent manner after 48 h incubation, with a slight increase at 0.3 mM, 50% reduction at 1.3 mM, and 94% reduction at 2.7 mM^[2].
BMS-561392 (1.3-2.7 mM) induces apoptosis in BV-2 microglial cells, as shown by increased activated caspase-3-positive cells^[2].
BMS-561392 (2.7 mM; 3 h) increases membrane TNFR-1 expression in BV-2 microglial cells by >50% after 3 h incubation^[2].
BMS-561392 (0.3-2.7 mM; 3 h) modulates phosphorylated p44 MAPK levels in BV-2 microglial cells in a concentration-dependent manner after 3 h incubation, increasing levels at 0.3 mM and eliminating detectable levels at 2.7 mM, with no effect on phosphorylated p42 MAPK^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.