Unidentified Analyst: Got it. Thanks again for the color.
Operator: One moment for our next question. The next question comes from Ananda Ghosh with H.C. Wainwright. Your line is open.
Ananda Ghosh: Hey, hi, thank you. The first question is probably what are some of the advantages of iADRS over CDR-SB and the rationale behind choosing iADRS over CDR-SB for the ALTITUDE study? And the second thing is there has been a lot of correlations made based on how much of plaque reductions you were seeing and what’s the probability of success in terms of some of these anti-A-beta immunotherapy trials. Are there other associations, which has been done with other biomarkers such as TAU 181 or 217, where at least some modeling-based studies can tell you to what extent you might need to see a change in these two biomarkers so as to kind of have an impact in either CDR-SB or iADRS? Thanks.
Eric Siemers: Yes, I can try to take that one, too. As far as the use of the iADRS versus the CDR Sum of Boxes, one of the things that was interesting in the recent draft guidance was that they no longer called out the CDR Sum of Boxes. And they’ve actually presented it at public meetings, the idea that in the previous draft guidance where they did mention the CDR Sum of Boxes, they didn’t mean to endorse that as sort of the only scale. But what they did say in this most recent draft guidance is that a scale that’s a composite of cognitive measures and functional measures may have real utility. And that’s what the iADRS is. It’s a combination of cognitive measures from ADAS-Cog and then functional measures from a scale called ADCS-ADL.
So we think that it’s very positive actually in terms of our use of the iADRS. I would assume that [indiscernible] the trailblazer studies, that’s their primary. They were happy to see that. So yes, I think that’s a really good clarification from FDA in terms of that — those kind of scales. In terms of correlations between plaque reduction and clinical benefit, I think what’s really becoming a consensus opinion now is that you actually have to get plaque below a certain threshold. And this is something that we at Acumen been saying for a long time is that if you’re going to target plaque, you have to basically get rid of it. And so the goal seems to be based on existing data that you want to get below 25, say — or at most 30. So if you want to — if your target is plaque, that’s what you need to do.
But again, our target is not plaque. Our target is oligomer. So it will be interesting to see what effects we have on plaque. But with our differentiated mechanism, that’s really not the construct of our development plan.
Ananda Ghosh: Thanks.
Operator: I show no further questions at this time. I would now like to turn the call back over to Alex Braun for closing remarks.
Alex Braun: Thanks, Michelle, and thanks for everyone for taking the time to tune in today. We are always available at the company. For any follow-up questions, please be in touch and have a great day. Thanks.
Operator: This concludes today’s conference call. Thank you for your participation. You may now disconnect.
