Targeting CHK1 in cancer therapy is primarily based on the concept of synthetic lethality. Cancer cells, due to their aggressive proliferation, are heavily reliant on the DDR pathway. Inhibiting CHK1 can exacerbate DNA damage in these cells, leading to apoptosis. This approach is particularly effective in cancer types that already have defects in other DDR components, such as BRCA-mutated cancers, where CHK1 inhibition can lead to catastrophic levels of genomic instability.
