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Covalent targeting of noncatalytic cysteine residues at the ATP-binding site of kinases has since proven to be a successful approach to overcome competition by the native substrate [9,10], as illustrated by clinically approved covalent Bruton’s Tyrosine Kinase (BTK) inhibitors [11,12,13] and covalent (mutant) EGFR inhibitors [14,15,16,17]
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