AG 126 selectively inhibits the phosphorylation of ERK1 and ERK2 at 25-50 μM. It also acts as a cell-permeable inhibitor of lipopolysaccharide (LPS)-induced synthesis of tumor necrosis factor-α (TNF α) and nitric oxide in murine peritoneal macrophages. AG 126 blocks LPS-induced tyrosine phosphorylation of a p42MAPK/ERK2 protein substrate, as well as glucocorticoid-induced COX-2 activity in cells (IC₅₀ = 15.38 μM).