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Similarly, in a series of imidazo[1,2-a]pyridine-based c-Met inhibitors, this scaffold, combined with fragments designed to occupy hydrophobic regions and the solvent-front region (the area near the entrance to the ATP pocket at the interface with the solvent), has yielded low-nanomolar c-Met inhibitors that selectively suppress c-Met phosphorylation and key downstream signaling nodes (AKT and ERK), thereby effectively limiting the proliferation of c-Met-dependent cancer cells [55]