I think, first and foremost, as we’ve seen from others, dystrophin will be a very important trigger for us in central filing, so getting that data is critical to us. What we have is the benefit, and I’ll let Anne-Marie comment on as we think about function is the availability as we follow these boys not just from where the biopsies are, but really continue that study, as we said, for about 24 weeks and 48 weeks. We have an opportunity to measure a number of different functional endpoints. And those don’t only include the ambulatory, they include ability to look at respiratory function and others. So Anne-Marie, I’ll pause and let you answer any additional questions on potential filing around DMD data. And then I’ll come back to HD.
Anne Cheung: Thanks, Paul. So as you know, there is a well-trodden regulatory pathway for filing with dystrophin data. So, we would expect that to be adequate. But of course, as Paul said, we’re running the study through 48 weeks. So we’ll, of course, be providing any of the functional data available for that filing. Back to you, Paul.
Paul Bolno: Great. And so on HD, on the call, we mentioned available data. I mean, the key is there’s no change. Actually, we’re excited that the multi-dose — I think that’s the update, is that the multi-dose is underway in HD. So I think our update is being able to have available multi-dose data while we have single-dose data would be the update. I think it’s very safe to say, we got initiated that we would not expect full multi-dose data in 2023, that’s going to be available, despite the muti-dose data is for human study.
Salim Syed: Got it. Just quickly, the Phase 1 trial — my question was on the Phase 1 trial design. Are we getting that this year for 006 — or is that something you also plan to share in ’24?
Paul Bolno: No, I mean, we’ll share the trial design once the study is initiated. So that — that will be 2023. So I think that if you think about imminent filing and new updates. I think, we’ll be able to share the clinical trial plan, which to your question, we’ll provide a lot more clarity as to the timing of data as that study initiates.
Operator: The next call comes from the line of Joe Schwartz from Leerink Partners.
Unidentified Analyst: Hi. This is Joori on for Joe. I was just wondering if you guys have commented on the stoichiometry of the AIMers or RNA editing and how that compares to your other legos for exon skipping or splicing, et cetera. I guess what I’m really trying to get at is, do you expect dosing to be in a similar range or higher, lower? And how does that influence? How you guys are thinking about therapeutic index and any likelihood of potential dose-limited toxicity?
Paul Bolno: Yes, I’ll take the beginning, and then I can turn some of that over to Anne-Marie. We’ll see how — I think as you mentioned, as we think about the stoichiometry, we just think about the pharmacology. I think is the better way of translational pharmacology of AIMer editing. It is a catalytic pathway, so that we are able to harness the catalytic mechanism within the enzymes. So to your point, we do see the advantages that come with that, both on being able to give smaller amounts of drug that then be able to stay. And that’s where stability becomes such an important component of the drug staying stable, not being degraded staying in the cell and able to exert its effect. So it is catalytic as are a number of the mechanisms that we’re utilizing.
I think, the other advantage as we think about AATD is by leveraging GalNAc, we’re getting — we think that there’s a lot like other potential siRNAs and approaches where you’re using GalNAc-conjugated oligonucleotide human hepatocytes for the catalytic machinery. So I think we’re seeing an act very similar to other catalytic oligonucleotides in development. So this wouldn’t be kind of — we like stoichiometric dose was you have to give more and more drug to try to exert an effect. So I think the catalytic efficiency of the enzyme is a huge advantage as we think about AIMers and we think about a lot like we do RNAi very much under this — other behavioral enzymatic features that you think about winning versus others, but –.
Anne Cheung: No, this is a foundational technology benefits, right, looking at how you can use these catalytic machineries to work to enable fast turnover kinetics. So that’s really the basis. And to Paul’s point, all these are looking at catalytic machinery non-stoichiometric.
Paul Bolno: And I think it’s important, too, as we think about extra-hepatic that we’re not having to give large volumes to drug, particularly as we think to about being able to dose subcu and other routes as we think about other tissues. So I mean I do think that ultimately, as we think about the AIMer platform, we should be thinking a lot like other silencing capabilities like RNAi.
Operator: All right. I’m showing no further questions at this time. I would now like to turn the conference back to Dr. Paul Bolno for our closing remarks.
Paul Bolno : Thank you, everyone, for joining the call this morning. We have made significant progress advancing our pipeline and driving forward our leadership position in RNA medicines in the second quarter. I am grateful to every Wave employee for their dedication and focus on our mission and on the patients and families we serve. Have a great day.
Operator: This concludes today’s conference call. Thank you for participating. You may now disconnect.
