Yeah, so in FLT3 targets like, say, Gilteritinib, Quizartinib, Midostaurin, you’re targeting only FLT3-mutated cells. This is a completely different approach here. This is a BiTE that’s targeting FLT3. You don’t have to be mutated FLT3 to have expression of your FLT3, 80% of myeloblasts express it. So you could target these patients even if they are wild-type FLT3...
Yeah, so in FLT3 targets like, say, Gilteritinib, Quizartinib, Midostaurin, you’re targeting only FLT3-mutated cells. This is a completely different approach here. This is a BiTE that’s targeting FLT3. You don’t have to be mutated FLT3 to have expression of your FLT3, 80% of myeloblasts express it. So you could target these patients even if they are wild-type FLT3. So it’s completely different. And it’s a phase one, early phase, but we saw some great responses in patients including p53. So we know p53 patients have actually the worst outcome, they’re so resistant to chemotherapy. And our last step-up dose cohort, we went to a high dose of 12 micrograms per kilogram. We had 50% of the patients with p53 mutation. And we saw 50% of these patients achieving CR and CRh. It’s an early phase, it’s just starting, but it looks like you can overcome even the toughest type of AML in this drug. So the future looks promising. I think in general, we’re understanding more about AML, we’re understanding the best way to approach and how to target it. But, you know, combination therapies and adding a BiTE to combination therapy, I think it could be a big, big potential for the future.
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