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Hello there, I’m Swami Iyer from Houston. I'm here to give you a one-minute highlight on the AML program that happened here at SOHO in September 2016. It's a very exciting time to be in AML. For many years, you've seen this disease, which is so complex. Because of advances in biology and the new drugs, and also trying to combine them together to personalize the right treatment for the right patient, we now have a slew of targeted agents. You can see that today's approaches have changed quite a bit.
Before we get to that, I want to show you what we’ve done very well in the last 40, 45 years. One very good story that should always be told is about acute promyelocytic leukemia, where the first targeted therapy was used, with ATRA and arsenic. Now you have a survival curve that looks parallel to the x-axis and it's fantastic. You can see the five-year survival rate is almost 100%.
How have we done with the rest of the acute myelogenous leukemia? It's been 45 years since the inception of “7 plus 3,” the 45th anniversary since it was first studied. Since then lots of modifications have been done. What I will show you, though, in a particular type of AML, that there's the core binding factor for patients less than 60 years in comparison with the historical data at MD Anderson. We’ve done much better about making the three-drug regimen for tarabine, cytarabine, and idarubicin. For all the young patients, that's probably the best way to go.
Outside of that, I think we have to resort to targeted therapies. I'll talk about, or at least highlight, four of the targeted therapies that are discussed at this meeting. There's a resurgence of the anti-CD33 antibody drug conjugate, which is of importance. This is a slide on the gemtuzumab ozogamicin meta-analysis of five AML randomized studies. Despite the US study, which was a negative study, there are four additional studies in Europe which showed an improved survival advantage. This is making a resurgence with the SGN 33 compound and the AMG 330. You will hear more about this and, very likely, midostaurin might get a re-approval very soon.
The second exciting target is FLT3, and RATIFY was a plenary session at ASH last year. One of the reasons for that is midostaurin, in combination 7 plus 3, showed a survival advantage compared to placebo. One point I want to highlight here is that all these patients had FLT3 mutation status, whether it's internal tandem duplication or TKD. It appears that the patients with the TKD had a favorable outcome with this combination. This drug, again, might get an approval early next year for AML.
The third targeted therapy, which is very exciting, is the IDH2 inhibitor. It's seen in about 15 to 20 persons of all AMLs, but this is data presented by Dr. Etyan Stein and Dr. Courtney DiNardo. We can see that about 200 patients have the R140q mutation or R172k mutation; the response rates are pretty impressive at 17 persons. These patients have achieved what’s called a clonal remission, which means you still see the mutation but have obtained CRs at other levels.
Finally, I want to stop with this very important slide. You heard the story of the PD1 inhibitors in melanoma and non-small lung cancer; this survival code is very similar. This is a study comparing azacitidine with nivo and patients with AML with a historical control. You can see the blue code, which is the nivo code. Median response rate is about 9.3 months. Far better than the historical controls, perhaps we’ll start seeing patients who will not achieve the CRs but yet have a longer survival, as was reported with the PD1 and other malignancies.
These are some of the highlights of targeted agents in the context of chemo therapy and acute myelogenous leukemia. It’s an exciting time, and I thank all of you for this opportunity to present these highlights.