Jon Congleton: Yes.
Mohit Bansal: Okay, sorry about that. So I just wanted to ask about the kind of magnitude of benefit you want to see in the CKD proof-of-concept trials here, given the shorter treatment period here because – I mean, I think in the past, you talked about SGLT2 inhibitors could have 30% to 40% improvement in proteinuria. So can you talk a little bit about that? And how would you compare and contrast when the data come with and what is out there? And how would you make the [indiscernible] decision here? Thank you.
Jon Congleton: I think what we would anticipate, Mohit, and thank you for your question. In Target-HTN, again, we saw the 8 to 10 millimeter mercury placebo-adjusted drop in blood pressure with a really nice safety profile. The majority of that response was seen in about 2 weeks or with 2 weeks, we saw the beginning of the drop and the majority of it was at 4 weeks. So I think we’re comfortable that we’ll see that level of drop within systolic BP. As far as the renal benefit, I’d hate to extrapolate at this point in time. We know that the kidney benefit to a large degree, is derisked within ASI based on what the Beringer Ingelheim data that was presented last fall. We wanted to confirm that we see the same benefit with lorundrostat.
We think that, that UACR effect is likely driven from the reduction in blood pressure. And so that’s what we anticipate seeing from a BT standpoint of 8 to 10, and then we’ll be evaluating what we see from an UACR reduction standpoint. But again, our perspective is ASIs within CKD have been significantly derisked based on some of the other work with the class.
David Rodman: Jon, can I just talk a little bit to that?
Jon Congleton: Yes, sure.
David Rodman: Well, thanks for the question. It’s really a good question. First of all, we made blood pressure the primary because we have a very effective blood pressure drug. And if you just treat the metabolic piece of this and you don’t treat the hypertension piece of it, you’re still going to lose your kidney. And so you have to treat those and we think our drug is going to be particularly effective there. But flipping over to your question about proteinuria, which is a – UACR is what we’re measuring. It reads through to decreased decline in GFR over a year or 2, but you can’t measure that in a short study. And your point is, well, can you really wait for something in 4 weeks. The answer is yes. We’ve talked to many experts about it.
Will it be the maximum? It will be most of it. It won’t be necessarily all of it, but enough. But I want to caution you, everybody is going to come down on an SGLT2. This is going to be the benefit of our drug above SGLT2. We don’t think we need to do a monotherapy trial anymore because that’s already been – question has been asked and answered by BI and also AC is doing that. And so we just want to know what’s that increment above standard of care. So when you compare it, it’s got to be apples-to-apples. Make sure it’s not our addition of lorundrostat compared to the combination product, say, with BI or AZ, which starts from a lower baseline. It is only the comparison to what they get above the SGLT2. And we expect to see a similar magnitude of what they’ve reported in their prior trials for that increment.
Mohit Bansal: Got it. This is super helpful. If I may ask one more. I know I understand that you are approaching CKD or chronic kidney disease with hypertension angle. But there is a lot of activity in rare kidney disease space as well. And I mean the relationship between hypertension and kidney diseases is very much intertwined. Is there an angle which lorundrostat can play in those rare kidney diseases as well? Or I’m just too – like is more of a wishful thinking right now?
David Rodman: Well, that’s a really good question. We’ve been excited to see, for instance, the IgA nephropathy data. That’s a group of – it’s often children. It’s a bad disease, and now it has multiple treatments. We expect we can play in that space, not against IgA. We do have some ideas. Right now, we’re not at liberty to discuss them. But yes, the answer is I think there is an opportunity there for lorundrostat.
Mohit Bansal: Got it. Helpful. More work for us to do that. Thank you.
Jon Congleton: Thanks, Mohit.
Operator: There are no further questions at this time. Mr. Jon Congleton, please proceed with your closing remarks.
Jon Congleton: Thank you, operator, and thank you to everyone for joining us today. We’re very excited about the progress we’ve made thus far in 2024 in advancing our clinical programs and remain enthusiastic about the upcoming milestones for the rest of the year. We look forward to updating you as our pivotal program for lorundrostat continues to advance. With that, we’ll close the call.
Operator: Ladies and gentlemen, this concludes today’s conference call. Thank you for participating. You may now disconnect.
