DR CORTES: So quizartinib — it was formerly known as AC220 — is another FLT3 inhibitor. This one seems to be a little bit more specific. It inhibits fewer kinases. It seems to be more potent against FLT3, at least in the preclinical data. So this drug has gone through several Phase II studies — this is one of them — on patients that have, in this case, first salvage. So they’ve received 1 part of therapy, and they relapsed or didn’t respond. And this is a single-agent trial.

And it is a drug that is effective. It works in many of these patients. Now, as single agent, most of these drugs will give you more of what we call CRIs, complete remission with incomplete recovery of the neutrophils or the platelets, fewer true CRs, full recovery of both. So that’s what you get. If you add those to what we call the “composite” CR, it’s about 50%.

A couple of interesting things on this drug: One is there was some activity in the non-FLT3-mutated patients. The rationale for that is unclear. It could be c-KIT inhibition, whatever. Another aspect that’s important, the main toxicity for this drug has been QTC prolongation. No major arrhythmias or cardiac deaths or anything like that. But it’s a dose-dependent QTC prolongation. And actually, what the Phase I study gave us, an MTD of 200 in combination with using it all the way down to in the range of 30 to 60 mg, so a much lower dose.

Module 1: Current and future approaches to targeted therapy for acute myeloid leukemia (AML)

Module 2: Other clinical issues in AML management

Module 3: Case discussions