Hematologic Oncology Update, Issue 1, 2016 (Video Program)Novel investigational agents for FLT3-ITD mutation-positive AML, including gilteritinib (ASP2215)
1:57 minutes.
TRANSCRIPTION:
DR SMITH: There’s been nearly a dozen, probably 8 or 9 FLT3 inhibitors that have been developed by drug companies. And through our traditional drug development paradigm, they do them as a single agent, refractory patients. So this agent, ASP2215, this is an FLT3 inhibitor that has pretty significant single-agent activity. It’s been looked at in both refractory patients/relapsed patients. It’s been looked at in combination, and it’s been looked at in patients that don’t even have an FLT3/ITD mutation. And it shows activity, clinical activity, in all of those scenarios such that we’re hoping that that drug becomes available so that, with a patient who fails induction therapy, has primary refractory disease, that we can actually use a single agent, orally available drug, the ASP2215, to try to get them into remission and then be able to move them to an allogeneic transplant. DR LOVE: Globally, what fraction of patients with AML right now are thought to have FLT3 or even this high allelic FLT3? DR SMITH: Yes. So the majority of the ITDs do have a high allelic ratio. But it’s somewhere between 20% and 25% of all new-comer leukemias will have one of the forms of an FLT3 mutation. DR LOVE: So are you anticipating that midostaurin is going to become available? And if it is, are you going to use it? DR SMITH: I think everybody’s quite excited about it. And I do think that having this large data that, if this drug becomes available for this indication, that it will be used. And it will most likely replace sorafenib. Midostaurin is not a perfect drug either. It has toxicities associated with it as well. So we do have some work to do to refine our FLT3 inhibitors so we get better effects. |