Roughly how many patients with mixed lineage leukemia rearranged (MLLr) relapsed/refractory (R/R) acute leukemias do you currently manage?

On a scale from 1-10 (10 being extremely excited) where would you rate your level of excitement for Revumenib (SNDX-5613)?

What percent of your patients with acute leukemia are MLLr or mNPM1, and what percentages in the relapsed/refractory setting specifically?

Please explain the Menin-MLL1 pathway as it relates to MLL fusion proteins and what role this plays in acute leukemias?

What should the proposed activity of SNDX-5613 (blocking interaction of MLL1 and menin) accomplish in leukemic cells to combat the disease?

What can you tell us about genetic testing in acute leukemias? How routine is it, are these specific mutations/rearrangements being looked for, and how successful at finding them if they are there?  

Since no drug for MLLr specifically, do they still look for this?

In the 3 settings of MLLr ALL/MPAL, MLLr AML, or mNPM1 AML do you expect the drug to work equally well, or are there differences in how it should work in each?

Updated data in Phase 1: ORR 55% (n=28 of 51), and 31% MRD-negative rate (16/51).   ORR in MLLr = 61% (23 of 38) and NPM1c 38% (5 of 13). Overall 24% CR/CRh rate with mutations, and no discontinuations   (23% and 24% CR/CRh in the two mutation types) 50% having longer than 6 months response. What is your interpretation of these data? Is this exciting? So-so? Not good enough?

Median of four prior therapies, including 42% who received a prior stem cell transplant and 59% who received prior venetoclax, were dosed: How does the efficacy look within the context of this patient type?  

On safety, they saw >5% SAEs of QT prolongation, anemia, and differentiation syndrome - And at RecommendedPhase2Dose, 7% had QT prolongation: Can you explain these in terms of acute leukemias and are these common side effects of effective drugs in this space, or is this unique to this drug or otherwise something to be hesitant about that might prevent the drug's usage if it should eventually be approved?   How much do these side effects matter in the context of AML and developing this drug further including in more upfront settings?

Can you explain the difference between response rates on CR/CRh (24%), CRp (14%), and CRi/MLFS (18%) and how important the non-CR/CRh responses are?

Phase 2 pivotal portion of this trial has CR/CRh as primary endpoint with DOR and OS secondaries. What is the bar for FDA approval on these endpoints? And what is the bar on these metrics as something you would be excited about?

Future direction: planning to develop in frontline in combo with venetoclax + azacitodine. Does this have potential in your view?

Competition: Another menin inhibitor, Kura Oncology's KO-539, had a clinical hold based on a patient death. Is there any important ways in which these two molecules differ from each other? Any other menin inhibitors being developed that look interesting?

Big Pharma has not pursued this target to this point? If not, why not? Could this data from SNDX-5613 get them interested in this menin inhibitor arena?