ATM mutations occur frequently in cancer cells. Inherited ATM deficiency leads to ataxia–telangiectasia, a genome instability syndrome characterized by neurodegeneration, immunodeficiency, radiation sensitivity, and cancer susceptibility. Thus, ATM has a clear role in the maintenance of genome stability, cellular and tissue functioning, and cancer prevention.1,2
Upon detection of a double-stranded break (DSB), ATM is recruited to the break site. Following activation, ATM triggers a signaling cascade resulting in cell cycle arrest and DSB repair. It can also trigger apoptosis or senescence if necessary.3-5
ATM activity is dispensable for cellular viability, yet necessary for maintaining genome integrity. It plays a pivotal role in DNA double-strand break signaling and repair.3-5
M4076 is an investigational orally administered, potent, selective, ATP-competitive ATM inhibitor. It is designed to block ATM activity in cells leading to increased double-strand DNA breaks that cannot be repaired and drives tumor cell death.6
A phase I, open-label trial evaluating M4076 in patients with advanced solid tumors.LEARN ABOUT COMPANY SPONSORED CLINICAL TRIALS LEARN ABOUT ALL CLINICAL TRIALS
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ATM, ataxia telangiectasia mutated; ATP, adenosine triphosphate; ATR, ataxia telangiectasia RAD3-related; DNA-PK, DNA-dependent protein kinase.