Extracellular signal-regulated kinase 1/2 (ERK1/2) occupies a pivotal position as the distal effector in the intricate RAS-RAF-MEK-ERK signaling pathway. Remarkably, ERK1/2 exhibits a substantially lower frequency of mutational events in comparison to its upstream counterparts, namely RAS, RAF, and MEK. This inherent genetic stability confers distinct advantages upon ERK1/2 as a therapeutic target. Although ERK1/2 inhibitors have yet to receive approval for clinical use in cancer treatment, the industrial and scientific community is actively engaged in the development and evaluation of 14 distinct ERK1/2 inhibitors in various stages of clinical investigation, seeking to harness their potential for novel and efficacious cancer therapies.
