Jay Backstrom: Yes. So maybe I’ll start just talking about what we would expect to see in clinic with apitegromab and then following with SRK-439 and obesity. I think what we can say, which is, I think, very clear now and we’ve shown that, I believe, in the TOPAZ study is that targeting myostatin does result in preservation, if not increase in lean muscle mass. I think we’ve shown that functionally in TOPAZ. I think there’s consistent observation across. So myostatin is a very good target. And it certainly should be able to do that in the setting of obesity, where you have normal muscle. So I think that’s the case. The fact that there was up – that their signaling is high in myostatin, I think is interesting, but I do believe that we’ll have an opportunity to demonstrate that in this setting just as we will demonstrate it in the SMA setting.
Srikripa Devarakonda: Great. Thank you.
Operator: Our next question comes from the line of Etzer Darout from BMO Capital Markets. Your line is now open.
Etzer Darout: Great. Thanks for taking questions and congrats on the progress. How are you thinking about the development of SRK-439, I mean, given the size of the obesity indication? And I guess is the proof-of-concept data with apitegromab, the catalyst for an update, if you will, on development plans. And then maybe on SRK-181, just maybe next steps for the program, maybe a little bit more color on what you described earlier during opening remarks and maybe the opportunity for future programs to be in sort of in earlier lines of RCC, for example. Thank you.
Jay Backstrom: Yes. So let me start with 439 and proof-of-concept and sort of overall path forward. Again, I think we’re designed — we’ve shown to date at Scholar Rock that we can run randomized Phase 3 studies, we can run proof-of-concept trials. And so as I think about the cardiometabolic space, certainly to get Apitegromab proof-of concept, which will really, in my opinion, validate our approach. And as we report that out, we’ll then at the time, open up with 439 getting right into clinic really positions us to drive 439 rapidly forward also to that proof-of-concept. And so that’s our near-term horizon. Anything beyond that, I think, really, we’re still open for discussions around how we get the bigger, broader trials. But I think for what we can do in our hand, I think we can certainly drive value, if you will, for the company by driving the clinical data and their proof-of-concept setting.
So that’s really our thinking around. And what Mo laid out very beautifully about how we’re looking at both Apitegromab and 439. For 181, you know, the data that I shared on the way I try to put the color on it, this is really a tough group to treat. And to see this level of response rate in this heavily pretreated failed on checkpoint inhibitor, I think, really shows that proof-of-concept, which is why we reach those conclusions. But I think like in any therapy, particularly in immunotherapy, earlier lines of therapy are really the place to take any such treatment. If you really want to have a major impact because patients have been so beat up and progressed so much through these therapies that getting earlier makes sense. And so frankly, that’s the whole concept behind the end of Phase 1 meeting.
It’s really to engage FDA and review our data and then begin to work with them to kind of lay out what would be the next logical steps in any further development of 181. And as Ted said, right now for us today, really pleased with the way Dragon performed. I think it’s met its objective, it’s done its job, if you will. We’ll wind that down, reset, take a look at what’s happening with the FDA interaction. But in the meantime, in 2024, it’s really all on our focus is on our anti-mist [ph] stand programs.
Etzer Darout: Great. Thank you.
Operator: Our next question comes from the line of Andres Maldonado with H.C.Wainwright. Your line is now open.
