Mike Ulz: That’s helpful. Thank you.
Chris Anzalone: You’re welcome.
Operator: One moment for our next question. And our next question comes from Ellie Merle with UBS. Your line is open.
Ellie Merle: Hey, guys. Thanks for squeezing me in. Just in the past, on RAGE, you had mentioned a subcu program, I guess just what’s the latest on the status and timelines there, and just the focus of that program. And then just on a related note, as you think about planning a larger Phase 1 study in asthma, what are the considerations there and the design and what you’re looking to see in the high FeNO cohort later this year, and just what everything from the subcu program, perhaps the plans and some of the considerations and the design? Thanks.
Chris Anzalone: Sure, so the subcu programs we said we were seeing not — we are seeing RAGE knockdown. That’s the good news. We just weren’t seeing as deep a knockdown as we’ve seen with the inhaled. And so we are really focusing our future development on the inhaled. But again, but it did work. It just was not as strong as the inhaled version. James, you want to…?
James Hamilton: I don’t have anything to add to that. I don’t think it will play into our Phase 2 plans though.
Chris Anzalone: So what’s the second question about asthma again? Can you repeat that one?
Ellie Merle: Yeah, just the timeline for the Phase 2 start and the design considerations. And like what you’re looking to see from the high FeNO cohort, and how that might inform some of the design decisions. Thanks.
James Hamilton: Yeah, so we’re tossing around and thinking about a lot of different designs right now. I think with the design we would certainly want to be able to study both the high type two and the non-type two patients in a single design. And I think that the FeNO readout, Q3 may inform on which patient population, we want to favor one more than the other. But I think we’ll want to — plan to study both.
Chris Anzalone: Yeah, and keep in mind, with the FeNO, data, look, we’re looking forward to seeing that, of course, but it really only reflects moving a single pathway. As James mentioned in his prepared remarks, RAGE, we expect RAGE to move a number of different cytokines and FeNOs, only really detecting movement of one of those. And so while it’s helpful, it’s certainly not the only important data point.
Ellie Merle: Got it? Thanks. That’s helpful.
Operator: One moment for our next question. And our next question comes from Maury Raycroft with Jefferies. Your line is open.
Maury Raycroft: Hi, thanks for taking my questions. I was going to ask one about RAGE too. So for the higher dose PD asthma patient data that you’re collecting, can you clarify if you’ll do a public update on that at the end of this quarter on those data? And will that only include knockdown? Or will that include cytokine and other PD biomarkers as well.
Chris Anzalone: So it will include knockdown for sure. And I’m not sure if there’s going to be a good venue in the near term to report those. I can tell you that, that what we’ve seen so far, it’s still an incomplete data set. What we’ve seen so far is consistent to what we said in the past, which is what we’re seeing in knockdown in patients is really mapping on top of what we have seen the knockdown profile in healthy volunteers. And so that continues. Once we have a full dataset, given that again, I expect that to continue. I don’t know that we’ll rush out and have a press release based on that. I think we’ll probably have that as part of some presentation that — at a conference or what have you. But to be honest, we really haven’t put much thought into how we’re going to disseminate those data. Because again, we expect the knockdown in patients to be quite similar to healthy volunteers. That’s we’ve seen so far. Jim do you have anything else to add?
James Hamilton: No.
Maury Raycroft: Got it. Okay, that’s helpful. And then maybe one follow up just for DUX4, or DM1, could you potentially have data updates from either of those programs this year?
Chris Anzalone: Yeah, I think that’s depending on how enrollment goes. We could have some early data by end of the year, but very enrollment contingent.
Maury Raycroft: Got it? Okay. Thanks for taking my questions.
Chris Anzalone: Thanks, Maury.
Operator: One moment for our next question. And our next question comes from Prakhar Agrawal with Cantor Fitzgerald. Your line is open.
Prakhar Agrawal : Hi, thanks for taking my question. So number one on INHBE. Preclinically how does your candidates profile differ versus some of our competitors Alnylam and [indiscernible] in terms of the level of knockdown you’re seeing? I think you had mentioned 20% weight loss in DIO [ph] models. So maybe if you can compare and contrast that? And then I had a follow up?
Chris Anzalone: Sure. Yeah. I think that that level of differential in weight gain between the control animals and the animals receiving drug is similar to what others have reported. And in that study, we were seeing 90-plus, I think 96% knockdown in that that obesity mouse model, which is I believe, more than what others have reported. I think that’s probably the best I can tell you.
Prakhar Agrawal : Got it. And on the CV side, what are the key questions do you need answers from the FDA to make a decision on which CV asset to move forward into the outcomes trial for the broader population or is it just mostly an internal decision at this point?
Bruce Given: Yeah, I mean we haven’t gone to the — it’s Bruce Given again. We haven’t gone to the FDA at this point on that. At some point, we will of course go to the FDA. We can’t start a trial like that without their input. But we’re not at the point yet that we’ve engaged them in the discussion.
Prakhar Agrawal : Okay. Thank you for taking the questions.
Bruce Given: Sure.
Operator: One moment for our next question. And our next question comes from David Lebovitz with Citi. Your line is open. David Lebovitz, your line is open.
Unidentified Analyst: Hi. Can you hear me now?
Operator: Yes, we can.
Unidentified Analyst: Hi. This is Vibhanjana [ph] on for David. Thanks for taking our questions. So maybe it’s regarding the FPS readouts of last year. And you mentioned that the last patient is scheduled for the visit in second quarter. We were wondering if you could give us a little more color in terms of the data readout timeline. And maybe what data points can we expect to see at the readout?
Bruce Given: Well, I think, we would again be looking to present, I would think in a meeting. I actually haven’t spoken with Chris on this. Maybe we would top line in some way, once we did that, but we’d want to do that in such a way to not present a fulsome presentation in a in an academic meeting at some point. I think it’s kind of the same sort of question — the same answer we had before. At this point, it’s hard to predict, you know, what meaning that would be and when that would occur. But yeah, I suspect we would, in some way, get some top line information. But most of the fulsome data would come out later, I would expect.
Unidentified Analyst: Thank you. And just one follow up. Assuming that zodasiran and plozasiran are both approved, how do you think clinicians would choose between the two therapies?
Bruce Given: It’s hard to answer that question in a setting where actually we don’t have the comparative results of the two agents at this point on either efficacy or safety in the SES population. So it’d be wildly speculative at this point to try to make a call on that.
Chris Anzalone: Yeah, I don’t think we I don’t think that we’ve seen triglycerides levels in, from that Phase 3 yet. When we look at the available data from their Phase 2 versus our Phase 2s, we are comfortable that our dosing interval will be longer. And it appears at least according to the Phase 2 data appears that our APOC3 knockdown is greater and our triglyceride lowering is greater. But again, as Bruce says, we don’t know what the Phase 3 looks like on their side or on our side, frankly.
Unidentified Analyst: Thank you. That’s helpful.
Operator: And our final question comes from the line of William Pickering with Bernstein. Your line is open.
William Pickering : Hi, good evening. Thank you for taking my question. You’ve estimated the addressable FCS population at 70,000 to 100,000, which sounds like a pretty large population to get approved based on a single 75 persons study. So can you just remind us of your agreement with the FDA on the exact definition of that FCS population for which they agreed to accept just a single trial? Thank you.
