RANKL-IN-2

RANKL-IN-2 (compound 3w) (1 μM; 4 days) inhibits RANKL-induced osteoclastogenesis in RAW 264.7 cells with potent activity at 1 μM^[1].
RANKL-IN-2 (0.0625-2 μM; 5 days) inhibits RANKL-induced osteoclastogenesis in BMMs dose-dependently with an IC₅₀ of 0.577 μM^[1].
RANKL-IN-2 (0.5-2 μM; 7 days) suppresses RANKL-induced F-actin ring formation and bone resorptionin by BMMs in a dose-dependent manner^[1].
RANKL-IN-2 (0.5-2 μM; 5 days) inhibits RANKL-induced expression of osteoclast marker genes and proteins in BMMs dose-dependently^[1].
RANKL-IN-2 (0.5-2 μM; 5 days) regulates ROS signaling in BMMs by inhibiting ROS production and promoting antioxidant enzyme expression^[1].
RANKL-IN-2 (0.5-2 μM; 48 h) suppresses RANKL-induced intracellular and mitochondrial ROS production in BMMs dose-dependently^[1].
RANKL-IN-2 (1 μM; 6 h pretreatment, 0-60 min RANKL stimulation) inhibits RANKL-induced MAPK and NF-κB signaling pathways in BMMs at 1 μM^[1].
RANKL-IN-2 (0.5-2 μM; 7 or 21 days) does not affect osteoblast differentiation or mineralization in MC3T3-E1 cells^[1].
RANKL-IN-2 is stable in PBS and rat plasma for at least 12 h^[1].

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