Aptose Biosciences Inc (APTO)

[dcaf7]

A few thoughts after reading recently published paper “Olutasidenib (FT-2102) induces durable complete remissions in patients with relapsed or refractory IDH1-mutated AML”
1. Patients who received HSCT were followed for DOR and OS as HSCT was not an event. Possibly, same approach will be used in Tusp study.
2. The CR+CRh reference rate of 15% was selected as the null hypothesis based on historical data in similar high risk patient populations, with rates of CR from 12% to 16%. Now I can see where CR of 13% in proposed Tusp trial came from.
3. Analyzing mutation profile of responders, the authors noticed that ORR was not significantly reduced in patients with receptor tyrosine kinase (RTK) pathway mutations as compared to patients without RTK pathway mutations, although the rate of CR/CRh was lower. And response rates tended to be lower in patients with concurrent FLT3 mutations. But a key point is that you can still see them. Question is why? Patients have Flt3 mutations, but they respond to IDH1 inhibitor. Olutasinedib is not a multi-kinase inhibitor, but it works like Tusp.