Beneath the surface of Prexasertib’s clinical potential lies a complex and often overlooked story of molecular precision. Developed by Eli Lilly as a checkpoint kinase 1 and 2 (CHK1,2) inhibitor, Prexasertib operates through a finely tuned mechanism that disrupts tumor cell survival. By suppressing CHK1 and CHK2 activity, it downregulates Cdc25A, preventing cyclin-dependent kinase (CDC) phosphorylation. This destabilizes the replication fork and impairs DNA double-strand break repair, ultimately pushing cancer cells toward apoptosis. However, beyond its known effects, deeper mechanisms influence its resistance in non-small cell lung cancer (NSCLC). This article unveils the hidden intricacies of Prexasertib’s action and resistance, shedding light on the molecular pathways that shape its true impact.
