Aptose Biosciences Inc (APTO)

[dcaf7]

I am not sure about the role of each of these individual mutations in a whole context of AML. With Gilteritinib as monotherapy, you can see many CRs in patients with Flt3 and these co-mutations although Gilt is not considered as multi-kinase inhibitor. BTW, from what I can see in latest presentation, Tusp targets NPM1 mutations only in patients with Flt3 co-mutations. No responses in NPM1/Flt3 WT group. Actually, very important piece of information would be a mutation profile of non-responders. To me, for AA most obvious patient population is previous Flt3i failures. TP53 is potentially another indication for AA but more data is needed.
As for DoR, I remember discussion and proposal to count time from response to progression regardless of HSCT. Like HSCT is not a next line of therapy.