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Drugs that disable the checkpoint cancer cells use to pause and repair DNA under replication stress, pushing tumours with faulty DNA repair into collapse.
ATR and its downstream kinase CHK1 halt the cell cycle when DNA replication stalls. Tumours with ATM loss, high replication stress from oncogenes or defective homologous recombination depend on this checkpoint, and inhibitors such as ceralasertib, camonsertib and berzosertib have shown activity in these settings and in combination with PARP inhibitors, chemotherapy and immunotherapy. Anaemia and neutropenia limit continuous dosing, so intermittent schedules are used; no agent is approved yet.
ATP-competitive kinase inhibitors block ATR or CHK1 signalling so that cells with damaged or under-replicated DNA enter mitosis and die.
Query for this technology: (TITLE:"ATR and CHK1 inhibitors" OR ABSTRACT:"ATR and CHK1 inhibitors") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about ATR and CHK1 inhibitors, not a curated reading list.
Shares ATR, Synthetic lethality approaches, PARP inhibitors, Ovarian cancer.
Shares ATR, Synthetic lethality approaches.
Shares Synthetic lethality approaches, PARP inhibitors, Ovarian cancer.
Shares Clear cell ovarian cancer, Ovarian cancer.
Shares PARP inhibitors, Ovarian cancer.
Shares PARP inhibitors, Ovarian cancer.
Shares PARP inhibitors, Ovarian cancer.