Pete Stavropoulos: All right. Thank you. And for the changes in biomarkers that you showed today, was there any correlation between, let’s say, plaque reduction and changes in any of the biomarkers or levels of A-beta plaque or Centiloids levels with all those changes?
Eric Siemers: Yeah. Well, the correlations between target engagement in the biomarker changes were greater than the correlations with plaque reduction and those biomarker changes. So again, it’s not absolutely conclusive, it’s directionally — that’s the way the data turned out. But we think that’s very consistent with our hypothesis that the efficacy, in this case, the biomarker changes are related to binding to these A-beta oligomers more than related to plaque reduction.
Pete Stavropoulos: Okay. Thank you. Thanks for taking my questions.
Operator: Thank you. And our next question coming from the line of Paul Matteis with Stifel. Your line is open.
Unidentified Participant: Hey. This is Catherine (ph) on for Paul. Thanks for taking our question. On the Phase II/III, what do you expect to look at in the interim? And what would prompt a move into expanding the study? And then anything else you can say on when you might be interested in taking the interim? Thank you.
Eric Siemers: Hi, Catherine. Thanks for your question. So as we mentioned, we had a favorable interaction recently with the FDA on the Phase II/III design. I don’t think we’re going to go into details on the algorithms and elements that will inform the decision to scale from Phase II to Phase III. But as we get the meeting minutes, and get the study up and running, I think we have an opportunity, maybe share some additional information. But not in a position to comment today.
Unidentified Participant: Thank you.
Operator: Thank you. One moment for our next question. And our next question coming from the line of Colin Bristow with UBS. Your line is open.
Colin Bristow: Hey. Good morning and congrats on the progress. Maybe first one for Eric. Eric, I’m curious, what did you — in terms of the Leqembi subcu data that you saw at CTAD, I’m curious, like what were the key sort of learnings that you had from that and any surprises there? And then how will this change your approach to subcu 193? And then just secondly, more of a sort of administrative question, but how long do you think it’s going to take to enroll Phase II? Thank you.
Eric Siemers: Okay. Well, let me talk about the subcu first, and then we’ll take the other question afterwards with Dan. But anyway, in terms of the subcu, what was really interesting about that was there was this hypothesis that was pretty prevalent with a lot of researchers that ARIA-E was driven by Cmax rather than AUC. And so with the subcu formulation, you would have a lower Cmax and so you’d have less ARIA. And that just turned out not to be the case. It’s unusual in science to just have one experiment be so definitive. But I think in this case, it was pretty definitive that Cmax was not driving ARIA-E, and it was more related to AUC. And so we got an answer to that question. I think from our standpoint, having — well, and for other people in the field, actually, having a subcu formulation is more a matter of patient convenience, what people prefer, that sort of thing, there’s probably not going to be a safety benefit.
But it still means that it can be useful for people in terms of convenience and that sort of thing. So from that standpoint, we got a definitive answer to that question and — but subcu is still something we want to look at. So I’ll turn it over to Dan to talk about timelines.
