Jonathan Aschoff: Yes. I mean it seems to actually be fairly quick, whereas a lot of companies on those things kind of like they still have this COVID hangover or something.
Mark Kirschbaum: We didn’t have any of that. Fortunately, we €“ yes, I think partly because we’re oral and because the drug is very well tolerated. So the investigators have been very eager to put patients on.
Jonathan Aschoff: Thank you very much.
Spiro Rombotis: Thank you, Jonathan.
Operator: We will move next to Ahu Demir of Ladenburg. Your line is open.
Ahu Demir: Good afternoon. Thanks so much for taking my question. My first question is looking at the 101 and 102 studies of fadra. Do you see similar safety profiles in the patients given the populations that are very different?
Spiro Rombotis: Thank you for your question, Ahu. This is a question for Mark.
Mark Kirschbaum: Yes. There €“ we haven’t seen extraordinary problems in the leukemia study, been €“ we actually have no SAEs reported there. In fadra, it’s the €“ in the solid tumor trial, it is €“ we’ve been clean on them all the way through to the current dose level. So yes, I don’t see any difference between the two.
Ahu Demir: Thank you. My follow-up question is on the target engagement. Do you do any target engagement work? And are we going to see any data from those €“ both for fadraciclib and plogo?
Spiro Rombotis: We are certainly doing target engagement work. This is central to our understanding of both drugs. Obviously, fadra is more advanced, and I would like Mark to speak specifically of what type of studies we are doing to confirm exposure of the threshold, which is critical for such agents, but also is important for us as we build confidence about enrolling a successful Phase 2. I think many companies rush into Phase 2 without fully understanding pharmacodynamic exposure as well as effect of pharmacodynamic markers and then try to sort of step back from Phase 2 and see if they can correct the problem, if that becomes a quagmire. We are going to be patient and develop the target engagement information as it comes from different dose levels and therefore pick the optimal dose in Phase 2. Mark, would you like to specifically discuss target engagement methodology?
Mark Kirschbaum: If you want €“ well, I am not sure exactly what you mean, but target engagement was done from €“ before the study started. So, we have an established set of values for which we know that CDK2 and CDK9 are inhibited by the drug, which has been our benchmark against which we have been looking at our current PKs and PDs as we are moving forward. As far as PDs go, I think what you €“ what we are trying to get at is that we are now €“ particularly in these dose levels that we are at now, we are certainly seeing the targets being hit that we anticipate. And we believe that this drug is a MYC inhibitor and MCL1 inhibitor, and we are seeing that activity in the PD samples that are drawn on the current patients that are involved. Is that the answer to the question?
Ahu Demir: Yes. It is. My last question is for Paul. Paul, on the SG&A side, are we expecting a similar trend moving forward in the subsequent quarters?
Paul McBarron: Ahu, yes, we are. It will sit around the $2 million to $2.2 million on a quarterly basis.
Ahu Demir: Thank you very much for taking my questions.
Spiro Rombotis: Thank you. Ahu, let me just add as a segue to Mark’s comment that we are also seeing Cyclin E levels coming down, which is also an important target part of the CDK2 target profile of fadra. So, we are very pleased that we are seeing this level of confirmatory activity in patient samples. Thank you.
Operator: Our next question is from Jeff Jones of Oppenheimer.
