Olutasidenib is an IDH1 inhibitor, was very recently approved, and it’s approved as a single agent for refractory/relapsed acute myeloid leukemia that has IDH1 mutations. And the rationale for these sub-analyses is because many times patients, even if they have IDH mutations, we started on treatment with aza-venetoclax. One, because we know aza-venetoclax works in that subset of patients very well – even venetoclax alone has activity against the IDH1-mutated patients...
Olutasidenib is an IDH1 inhibitor, was very recently approved, and it’s approved as a single agent for refractory/relapsed acute myeloid leukemia that has IDH1 mutations. And the rationale for these sub-analyses is because many times patients, even if they have IDH mutations, we started on treatment with aza-venetoclax. One, because we know aza-venetoclax works in that subset of patients very well – even venetoclax alone has activity against the IDH1-mutated patients. And two, because from the practical point of view, you can give aza-venetoclax to any patient with AML that’s not suitable for intensive chemotherapy, you don’t have to wait for the mutation analysis. Whereas for example, ivosidenib, which is approved for frontline in combination with azacitidine, you have to wait for the IDH mutation. So in practical terms, many times patients received, as their first line therapy, venetoclax, so the question is: does olutasidenib work when patients have already received this effective therapy? And this is a small cohort of patients, but what we found is that it really works similar to any other patient that has been treated with any other modality of therapy, meaning about 35% of patients responded, about 30% of those responses are CRS. The responses can be durable. So it is good to know that whether the patient had received intensive standard chemotherapy, 3+7, for example, or they had received venetoclax or venetoclax-based chemotherapy, usually aza-venetoclax, they can still benefit from olutasidenib in the context of refractory relapse, this is of course, again with an IDH1 mutation.