Mo Qatanani: Yes. Thanks, Jay. I mean I’ll start with talking about SRK-439. SRK-439 is a novel molecule that we developed based on our extensive understanding of myostatin and the structure and the obesity space. It is highly selective, as we mentioned, it only binds myostatin utilizing our platform. It has attractive property. And from the get-go, we developed it to target this patient population. So it has very high in vitro affinity leading to potentially lower doses when you’re looking at efficacy with these. And we’ve seen that in the mouse models that we’ve done, and we continue to do in other models as well as we develop the molecule. It also amenable to high concentrations. Again, this is to support subcu profile, especially for this patient population.
So the overall, profile of SRK-439 was designed by design for this patient population to have higher affinity — efficacy with lower doses and concentration to enable subcutaneous dosing. From an IND-enabling studies, we’re going forward with the typical IND-enabling studies. We’re initiating all of the IND-enabling studies as we move forward into next year, as you see the Tox, the PK studies and all of these things as well as cell line developments, et cetera.
Allison Bratzel: Got it. Thank you.
Operator: Our next question comes from the line of Tessa Romero with JPMorgan. Please go ahead.
Tessa Romero: Good morning. Thanks for taking my question. Two questions from us this morning, if we could. First one is, how do you disclose the statistical test you are using and what the powering assumptions are for the SAPPHIRE trial around the primary endpoint of the main Hammersmith change from baseline at 12 months? If not, what can you tell us at this time as to how we should be thinking about this? And secondly, a related question. Will you consider disclosing the baseline characteristics before the top line result next year? Thanks guys.
Jay Backstrom: Yes. So this is Jay. I’ll take the questions. From the statistical powering assumptions, we’ve really not fully disclosed it, but just to kind of put color to that for the Hammersmith. We expected certainly be able to demonstrate a three-point change. By the way, we power the trial and we have adequate power to demonstrate that. And again, we’re doing hierarchical testing on that and then the following secondary endpoints. So I think we’re well positioned to – to replicate in SAPPHIRE what we saw in the TOPAZ study. And then with regard to baseline characteristics, Alli, we’re looking at that very critically as sort of our publication planning and data disclosure plans really, we try to do that time to important Congresses, as we think in conferences as we think about over the year. So more to come as we disclose that, but not likely to occur anytime in the near-term, given the cadence of the medical conferences.
Tessa Romero: Okay, great. Thanks for taking our question.
Operator: Our next question comes from the line of Srikripa Devarakonda from Truist Securities. Your line is now open.
Srikripa Devarakonda: Hey, guys. Thank you so much for taking my question. As you develop apitegromab and SRK-439 and obesity, I actually had a couple of maybe basic questions on myostatin and obesity. Some studies have shown that myostatin is upregulated in obesity. Just wondering, how well this dynamic has been characterized in patients, is there a lot of variability and how do you think that could potentially impact, how effective the drug could be in these patients, especially if you consider the background of obesity versus SMA where you’ve shown activity, and given that the studies show myostatin is also reduced as patients lose weight, do you think there’s an optimal window where you treat patients with antimyostatins? Thank you
