A – TolgaTanguler: I mean, I think one of the points that we really need to make it clear is innovation really rules the day. And AMVUTTRA has been a game changer already in polyneuropathy, and I believe – we believe very strongly based on our research, AMVUTTRA’s availability in cardiomyopathy is going to be important, especially if you look at our track records in price sensitive markets where actually tafamidis is available in Europe for polyneuropathy, we’ve been able to actually build an attractive business tablet versus infusion, tablet versus then subcutaneous and be able to build that business not just by net patients, but also with switches. Now in the U.S., which is similar to sort of the profile that you alluded to in terms of how we would actually think about in combination is our business is already built with the mixed phenotype patients, about 30% of our patients already on tafamidis granted we’re indicated for polyneuropathy and tafamidis is now indicated for cardiomyopathy.
Obviously, for us to be able to really elucidate how the positioning is going to work out, we need the HELIOS-B data that’s going to be really important and that will obviously inform the best way we’re going to position this and the best way we’re going to engage with the payers. But again, just to give you a sense about the unmet medical needs, if you look at the early access program that we have, we’ve already been able to enroll 200 patients because patients do progress and we believe this is going to be an important alternative.
Christine Lindenboom: Thanks, Tolga. That was a kind of great answer. With respect to your final question about KHK, we’re obviously trying to avoid taking multipart questions in the call to give everybody a chance to ask the question and respect to KHK. We look forward to seeing more data, as Pushkal explained at the end of the year. Next question, please?
Operator: Thank you. One moment for our next question. Our next question comes from David Lebowitz of Citi. Your line is now open.
David Lebowitz: Thank you very much for taking my question. You spoke earlier about talking that HELIOS-B can allow for a very differentiated profile versus the other therapies in the space. And my question is regarding to some extent linked to some of the earlier questions. Given the trial differences, they have different populations with different levels of severity. Their endpoints are slightly different from each other with slightly modified statistical analyses. How easy is it going to be to actually demonstrate to physicians that a profile is actually differentiated? And what aspects of the data would you focus upon?
Yvonne Greenstreet: I think maybe you can start off by maybe also reflecting on some of the data we’ve seen already from APOLLO-B and the 24-month data that demonstrated actually sort of stabilization of disease in many patients.
Pushkal Garg: Yes, absolutely. Thanks, Yvonne, and thanks, Dave, for your question. Look, I think it’s important to acknowledge, first of all, there aren’t any head to head data in this field, right? So what we’re looking at, though, is a field that’s evolving fairly rapidly, right, with because of the growing recognition of the unmet need and, for the benefit of patients multiple therapies coming forward. And you’re right to point out that everyone is using there are some variations, for example, in the way that endpoints and statistical analyses you’ve done. But I think what you have to do is think about it from the way that the clinician thinks about it when they step back and they look at a patient who’s coming in and they’re progressing with this.
They present with this disease at a various stages. It’s marked by dyspnea, by exercise, fatigue, poor quality of life, and you’re seeing a decline over time. Their echocardiographic parameters are worsening, their heart is thickening, their NT-proBNP is rising, they may develop arrhythmias, et cetera. And that’s what clinicians are looking at. And when they look at clinical data, I think what they’re looking at then is, I believe, is looking at all of the data that are coming forward in terms of how are these various drugs affecting the disease process. And I think, as Yvonne was alluding to, I think what we’re starting to see coming out of APOLLO-B really indicates the potential for a very unique profile when you silence TTR upstream using an RNAi mechanism of action, where we are seeing really favorable effects across all of these different parameters that we’ve looked at.
