DR CORTES: Because of this physiologic relevance of the FLT3 mutations and the prognostic implications that they have, there’s been a strong attempt at trying to develop FLT3 inhibitors. And this is a partial list, but it shows some of the drugs that are being developed or have been developed. Some of them have made it to Phase III. Some of them have actually died after Phase III, like “lestaurtinib” and others. We mentioned, like, midostaurin. Hopefully going to be approved, because the FLT3’s completed and read out and et cetera.

And there are many others that have unique features. Some of them are specific for the FLT3 ITD. Others may inhibit that point mutation, the D835. Crenolanib does that. The ASP2215 does that. Probably midostaurin hits that as well. So they have unique features in terms of how specific they are for just the ITD versus even the nonmutated FLT3.

Sorafenib, as we all know, it’s a drug that we use in other cancers. It’s a very good FLT3 inhibitor. It doesn’t work against the 835. It doesn’t work against the unmutated. But it’s a good FLT3 inhibitor. It’s not being developed as an FLT3 inhibitor, but it’s widely used when you can.

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