Abstract

<div>Abstract<p>AZD4625 is a potent, selective, and orally bioavailable inhibitor of oncogenic KRAS<sup>G12C</sup> as demonstrated in cellular assays and <i>in vivo</i> in preclinical cell line–derived and patient-derived xenograft models. <i>In vitro</i> and cellular assays have shown selective binding and inhibition of the KRAS<sup>G12C</sup> mutant isoform, which carries a glycine to cysteine mutation at residue 12, with no binding and inhibition of wild-type RAS or isoforms carrying non-KRAS<sup>G12C</sup> mutations. The pharmacology of AZD4625 shows that it has the potential to provide therapeutic benefit to patients with <i>KRAS</i><sup>G12C</sup> mutant cancer as either a monotherapy treatment or in combination with other targeted drug agents.</p></div>

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