The treatment landscape post-CDK46 is evolving dramatically. We tend to max out our endocrine therapy options. So we now have targeted therapeutic options for ESR1 mutant patients, PIK3CA mutant, AKT or P10 altered. And then for our non-mutant patients, we have other endocrine therapy options as well. Everolimus combinations, get a tolasib is coming down the pike. Once we’re sure that a patient’s no longer benefiting from endocrine therapy, we call them endocrine resistant...
The treatment landscape post-CDK46 is evolving dramatically. We tend to max out our endocrine therapy options. So we now have targeted therapeutic options for ESR1 mutant patients, PIK3CA mutant, AKT or P10 altered. And then for our non-mutant patients, we have other endocrine therapy options as well. Everolimus combinations, get a tolasib is coming down the pike. Once we’re sure that a patient’s no longer benefiting from endocrine therapy, we call them endocrine resistant. And at that point, we use chemotherapy or antibody drug conjugates. 90% of our patients are HER2 low or HER2 ultra low. 90% of our ER positive HER2 negative patients are low or ultra low. Those patients derive benefit from trastuzumab droduroxtecan either as the first or second-line chemotherapy. Patients can also benefit from chemotherapy like capecitabine, taxane. Then we also have two approved trope-2 ADCs, datopotamab-duroxtecan and sasituzumab, particularly for our HER2-truly-zero patients.
