ATM Inhibitors in Cancer Radiotherapy: Mechanisms, Clinical Development, and Future Directions

<p>Ataxia-telangiectasia mutated (ATM) kinase plays a pivotal role in the cellular response to DNA damage. Under normal conditions, ATM acts as a tumor suppressor by regulating pathways that lead to apoptosis and cell cycle arrest via effectors like p53, p21, CHK1, and CHK2. Paradoxically, in...

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محفوظ في:
التفاصيل البيبلوغرافية
المؤلف الرئيسي: Raed.M. Al-Zoubi (22254577) (author)
مؤلفون آخرون: Khalil Garada (22254580) (author), Reem Al Huneidi (22254583) (author), Zaid M.H. Baddar (22254586) (author), Ayman A. Zarour (17917709) (author), Mai Elaarag (17807390) (author), Sally R. Al-Zoubi (22254589) (author), Ahmad R. Al-Qudimat (17337808) (author), Mazhar Salim Al Zoubi (18024364) (author), Abdelali Agouni (181926) (author), Khalid Alrumaihi (14779210) (author)
منشور في: 2025
الموضوعات:
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author Raed.M. Al-Zoubi (22254577)
author2 Khalil Garada (22254580)
Reem Al Huneidi (22254583)
Zaid M.H. Baddar (22254586)
Ayman A. Zarour (17917709)
Mai Elaarag (17807390)
Sally R. Al-Zoubi (22254589)
Ahmad R. Al-Qudimat (17337808)
Mazhar Salim Al Zoubi (18024364)
Abdelali Agouni (181926)
Khalid Alrumaihi (14779210)
author2_role author
author
author
author
author
author
author
author
author
author
author_facet Raed.M. Al-Zoubi (22254577)
Khalil Garada (22254580)
Reem Al Huneidi (22254583)
Zaid M.H. Baddar (22254586)
Ayman A. Zarour (17917709)
Mai Elaarag (17807390)
Sally R. Al-Zoubi (22254589)
Ahmad R. Al-Qudimat (17337808)
Mazhar Salim Al Zoubi (18024364)
Abdelali Agouni (181926)
Khalid Alrumaihi (14779210)
author_role author
dc.creator.none.fl_str_mv Raed.M. Al-Zoubi (22254577)
Khalil Garada (22254580)
Reem Al Huneidi (22254583)
Zaid M.H. Baddar (22254586)
Ayman A. Zarour (17917709)
Mai Elaarag (17807390)
Sally R. Al-Zoubi (22254589)
Ahmad R. Al-Qudimat (17337808)
Mazhar Salim Al Zoubi (18024364)
Abdelali Agouni (181926)
Khalid Alrumaihi (14779210)
dc.date.none.fl_str_mv 2025-09-12T09:00:00Z
dc.identifier.none.fl_str_mv 10.1016/j.ejmech.2025.118137
dc.relation.none.fl_str_mv https://figshare.com/articles/journal_contribution/ATM_Inhibitors_in_Cancer_Radiotherapy_Mechanisms_Clinical_Development_and_Future_Directions/30135574
dc.rights.none.fl_str_mv CC BY 4.0
info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Biomedical and clinical sciences
Oncology and carcinogenesis
Pharmacology and pharmaceutical sciences
ATM inhibitors
Radiotherapy
Cancer therapy
DNA damage response
Clinical trials
Translational
dc.title.none.fl_str_mv ATM Inhibitors in Cancer Radiotherapy: Mechanisms, Clinical Development, and Future Directions
dc.type.none.fl_str_mv Text
Journal contribution
info:eu-repo/semantics/publishedVersion
text
contribution to journal
description <p>Ataxia-telangiectasia mutated (ATM) kinase plays a pivotal role in the cellular response to DNA damage. Under normal conditions, ATM acts as a tumor suppressor by regulating pathways that lead to apoptosis and cell cycle arrest via effectors like p53, p21, CHK1, and CHK2. Paradoxically, in some cancers, ATM promotes tumor cell survival and metastasis, especially when aberrantly activated, linking it to therapy resistance and poor outcomes. Its involvement in both radiotherapy and chemotherapy has made ATM an attractive target for cancer treatment. Inhibitors such as KU-55933, KU-60019, and AZD1390 have shown the potential to sensitize cancer cells to radiotherapy by impairing DNA repair, thereby enhancing treatment efficacy. A key challenge remains the development of ATM inhibitors that can effectively cross the blood-brain barrier for use against brain tumors. Currently, none have gained approval from the FDA or EMA, but six candidates, AZD1390, AZD0156, ZN-B-2262, SYH2051, WSD0628 and M3541 are in clinical trials, often as adjuncts to radiotherapy or in combination with PARP inhibitors. Their safety and effectiveness, however, are still under investigation. This review synthesizes ATM's dual roles and the therapeutic promise of targeting ATM in cancer radiotherapy.</p><h2>Other Information</h2> <p> Published in: European Journal of Medicinal Chemistry<br> License: <a href="http://creativecommons.org/licenses/by/4.0/" target="_blank">http://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.1016/j.ejmech.2025.118137" target="_blank">https://dx.doi.org/10.1016/j.ejmech.2025.118137</a></p>
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identifier_str_mv 10.1016/j.ejmech.2025.118137
network_acronym_str Manara2
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oai_identifier_str oai:figshare.com:article/30135574
publishDate 2025
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spelling ATM Inhibitors in Cancer Radiotherapy: Mechanisms, Clinical Development, and Future DirectionsRaed.M. Al-Zoubi (22254577)Khalil Garada (22254580)Reem Al Huneidi (22254583)Zaid M.H. Baddar (22254586)Ayman A. Zarour (17917709)Mai Elaarag (17807390)Sally R. Al-Zoubi (22254589)Ahmad R. Al-Qudimat (17337808)Mazhar Salim Al Zoubi (18024364)Abdelali Agouni (181926)Khalid Alrumaihi (14779210)Biomedical and clinical sciencesOncology and carcinogenesisPharmacology and pharmaceutical sciencesATM inhibitorsRadiotherapyCancer therapyDNA damage responseClinical trialsTranslational<p>Ataxia-telangiectasia mutated (ATM) kinase plays a pivotal role in the cellular response to DNA damage. Under normal conditions, ATM acts as a tumor suppressor by regulating pathways that lead to apoptosis and cell cycle arrest via effectors like p53, p21, CHK1, and CHK2. Paradoxically, in some cancers, ATM promotes tumor cell survival and metastasis, especially when aberrantly activated, linking it to therapy resistance and poor outcomes. Its involvement in both radiotherapy and chemotherapy has made ATM an attractive target for cancer treatment. Inhibitors such as KU-55933, KU-60019, and AZD1390 have shown the potential to sensitize cancer cells to radiotherapy by impairing DNA repair, thereby enhancing treatment efficacy. A key challenge remains the development of ATM inhibitors that can effectively cross the blood-brain barrier for use against brain tumors. Currently, none have gained approval from the FDA or EMA, but six candidates, AZD1390, AZD0156, ZN-B-2262, SYH2051, WSD0628 and M3541 are in clinical trials, often as adjuncts to radiotherapy or in combination with PARP inhibitors. Their safety and effectiveness, however, are still under investigation. This review synthesizes ATM's dual roles and the therapeutic promise of targeting ATM in cancer radiotherapy.</p><h2>Other Information</h2> <p> Published in: European Journal of Medicinal Chemistry<br> License: <a href="http://creativecommons.org/licenses/by/4.0/" target="_blank">http://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.1016/j.ejmech.2025.118137" target="_blank">https://dx.doi.org/10.1016/j.ejmech.2025.118137</a></p>2025-09-12T09:00:00ZTextJournal contributioninfo:eu-repo/semantics/publishedVersiontextcontribution to journal10.1016/j.ejmech.2025.118137https://figshare.com/articles/journal_contribution/ATM_Inhibitors_in_Cancer_Radiotherapy_Mechanisms_Clinical_Development_and_Future_Directions/30135574CC BY 4.0info:eu-repo/semantics/openAccessoai:figshare.com:article/301355742025-09-12T09:00:00Z
spellingShingle ATM Inhibitors in Cancer Radiotherapy: Mechanisms, Clinical Development, and Future Directions
Raed.M. Al-Zoubi (22254577)
Biomedical and clinical sciences
Oncology and carcinogenesis
Pharmacology and pharmaceutical sciences
ATM inhibitors
Radiotherapy
Cancer therapy
DNA damage response
Clinical trials
Translational
status_str publishedVersion
title ATM Inhibitors in Cancer Radiotherapy: Mechanisms, Clinical Development, and Future Directions
title_full ATM Inhibitors in Cancer Radiotherapy: Mechanisms, Clinical Development, and Future Directions
title_fullStr ATM Inhibitors in Cancer Radiotherapy: Mechanisms, Clinical Development, and Future Directions
title_full_unstemmed ATM Inhibitors in Cancer Radiotherapy: Mechanisms, Clinical Development, and Future Directions
title_short ATM Inhibitors in Cancer Radiotherapy: Mechanisms, Clinical Development, and Future Directions
title_sort ATM Inhibitors in Cancer Radiotherapy: Mechanisms, Clinical Development, and Future Directions
topic Biomedical and clinical sciences
Oncology and carcinogenesis
Pharmacology and pharmaceutical sciences
ATM inhibitors
Radiotherapy
Cancer therapy
DNA damage response
Clinical trials
Translational