Vikram Purohit: We had two. First on bullous pemphigoid, we’re just curious for the decision you’re contemplating internally. What are some of the key considerations at play right now? And what do you see as the potential scenarios that could result from the update you’re planning on providing us later this year? And then secondly, based on market research you might have done for MMN, I was curious to see how you segment this patient population and which segment of the patient base you think efgartigimod could be — I’m sorry, empasiprubart could be a viable therapy for?
Karl Gubitz: I’ll take question two on our MMN patients. For bullous pemphigoid, I think the data analysis is ongoing as we said. And the key consideration is going to be what is the impact of the background medication on the disease causing autoantibody and is there a clinical trial design conceivable where actually efgartigimod can still shine, because it is knocking down all the antibodies like health, but are you still able to show a delta over the background medication. And there is a thread and needle between what we want to achieve as a company and what regulators actually are going to see as a minimum background therapy. So I think we’re well advanced with the homework. We will do again consultancy with our experts during AAD in the coming weeks.
And I think we will be ready to think through couple of scenarios based on that feedback. So stay tuned. This is an important discussion internally for the Company. And we believe that unmet need in BP warrants is very thoughtful consideration.
Karen Massey: And on the topic of MMN, MMN is the type of disease, I think that we say that we like at argenx because it’s characterized by the fact that there’s an enormous unmet need in these patients. There’s been limited innovation, and these patients continue to progress, despite treatment, today. So they are of all of the diseases that we’re studying, we get the most calls from MMN patients that are asking for innovation to come to the market. So these are the types of diseases that we like because we think we can really raise expectations and reframe what patients can expect. And we think we’ll do that with empasiprubart. In terms of what the market research is telling us beyond that. We’re not breaking down our clinical trial design as yet, but beyond that, but rather just thinking about what’s the broadest patient benefit that we can create.
Karl Gubitz: Vikram, remember that in MMN at least 85% of the patients share that pathogenic autoantibody that are GM autoantibody against a GM1. We actually think that 100% of the MMN patients have that autoantibody the disease causing antibody is a sensitivity detection issue. We think that the underlying biology is pretty much unifying for all MMN patients. So, I think we’re in a good position.
Operator: Your next question comes from the line of Joel Beatty from Baird. Your line is open.
Joel Beatty: Are you seeing or anticipating any meaningful differences in the frequency of dosing between IV and subcu and then soon prefilled syringe and eventually auto injector?
Karen Massey: Thanks for the question. We are not seeing any differences between the formulations. It’s really about product presentation for patient convenience.
Operator: Your next question comes from the line of Danielle Brill from Raymond James. Your line is open.
Unidentified Analyst: Hey guys. This is Alex on for Danielle. If I recall correctly, it looks like you updated prevalence estimates for CIDP, which are higher than your previous projection. Just curious what factors you saw that are attributed to the TAM growth as it pertains to diagnosis treatment rates and potentially life expectancy? Thanks so much.
Karen Massey: Yes, I wouldn’t read too much into it. I think previously we shared a number from official sources specifically for U.S. and Europe. We now gave you the accurate number what we think is accurate for the key markets in which we play, but our view on prevalence actually has not really changed. We try to feed with as much accurate information as we can, representing the markets in which we play.
Operator: Your next question comes from the line of Simon Baker from Redburn. Your line is open.
Simon Baker: If I can go back to Sjogren’s please. I’m not sure if I missed the answer, but I just wanted to check if you did say what the form of the disclosure of that Phase 2 data would be. I’m guessing it would be an announcement that study has worked and you will proceed followed by disclosure at a clinical conference. But I just wonder if you could confirm that and suggest a potential conference where that would be disclosed. And just putting the cart before the horse a little and thinking about Phase 3 design. Tim, I think you mentioned the likely regulatory endpoint is changes in clinical SDI score. It also looks like 48-week duration looks like a typical length for Phase 3 study in the indication. From other studies, it looks like 300 to 400 patients is a typical size. Can you comment on the legitimacy of those assumptions? Thanks so much.
Karl Gubitz: Yes. Thanks for both questions. Yes, we’re looking for the signal. Of course, when we see it, we will share it with some level of detail surrounding the Go decision or the No/Go decision. And assuming a go decision, you’re correct in your understanding that then we would show more detailed data at the midterm medical need. So that that understanding is correct. From a Phase 3 assumptions point of view, I think you’re spot on. This is indeed what you can see from all the Phase 3 registrational trials in Sjogren. There are not many. But I think that’s going to be subject of the conversation with the FDA. With the data in hand, we will need to go with our proposal into an end of Phase 2 meeting and basically triangulate expectations for that Phase 3. For the time being, I would also build on your assumptions looking at the other registrational trials. Thank you.
Operator: Your next question comes from the line of Suzanne van Voorthuizen from VLK Kempen. Your line is open.
Suzanne van Voorthuizen: Hi, team. This is Susanne with Kempen. Thanks for taking my question. I wanted to ask if you can speak a bit about your early stage molecules, specifically the ones with the disclosed targets, the IL-6 target of 109 and FcRn target of 213. What can you tell us at this moment about these two molecules? And how do you think about development from here?
