# ATR and CHK1 inhibitors

Source: https://onco.cc/technologies/atr-chk1-inhibitors/  
OnCo record `atr-chk1-inhibitors` (Technology). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

Drugs that disable the checkpoint cancer cells use to pause and repair DNA under replication stress, pushing tumours with faulty DNA repair into collapse.

## Summary

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.

## Fields

- Kind: Technology
- Status: phase-2
- Last checked: 2026-09-04
- Principle: ATP-competitive kinase inhibitors block ATR or CHK1 signalling so that cells with damaged or under-replicated DNA enter mitosis and die.
- Strengths: Exploits synthetic lethality with ATM loss and replication stress; Combines with PARP inhibitors and radiotherapy
- Limitations: Haematological toxicity; Biomarkers still being defined; No approval

## Sources

- Wikipedia: https://en.wikipedia.org/wiki/Ataxia_telangiectasia_and_Rad3_related
- Wikipedia: https://en.wikipedia.org/wiki/Ataxia_telangiectasia_and_Rad3_related

## Connected records

- cancers: [Non-small-cell lung cancer](https://onco.cc/cancers/nsclc/), [Ovarian cancer](https://onco.cc/cancers/ovarian/)
- fronts: [Targeted Therapy](https://onco.cc/fronts/targeted-therapy/)
- technologies: [PARP inhibitors](https://onco.cc/technologies/parp-inhibitor/), [Synthetic lethality approaches](https://onco.cc/technologies/synthetic-lethality-approaches/)
- targets: [ATR](https://onco.cc/targets/atr/)

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