Sanofi (SAN) Earnings Call Transcript & Summary

[Audio Gap] It's really great to be here. As we said before, it's more of a way point. I think Paul actually used that terminology way point. Now again, you go back to what we said in immunology day. We have big ambitions in the immunology space to be leaders in that space. But it starts with what we're doing with dupilumab, kind of cross indications and so on and so forth. So we guided to more of a waypoint for $10 billion plus before. And then we -- our newest way point, I would say, so it's probably not a fair comparison to like consensus necessarily, but our newest way point is $13 billion plus, doesn't include COPD. Does it -- your question about does it take into consideration cannibalization -- no, not really. I mean, as we think about it, it's more about -- the fundamentals of this is more about the market growth. So if you think about all these indications that we've gone into thus far, atopic dermatitis being the first one, so let's just pick on that one. It's about that market growing. We have a bio penetration rate of just over 9% in the U.S. right now if you think about the atopic dermatitis space for adults. As you go in the younger age groups, we've just got an approval for down to 6 months of age. And we were ahead of physician tell me this the other day, I can give Dupixent to patients that I can't give cough medicine to. I mean, so the validation of what that does for the profile, but that patient population needs to grow. Physicians need to be prescribing this for a broader patient population. And that will grow over time. We've said to more like what psoriasis has done likely around the 30% bio penetration rate. So again, I think we'll be having these conversations for quite a while about what is that number. But if we're having those conversations, it's a good conversation because it means that this drug is growing exponentially as we've done kind of quarter-on-quarter.

And 9% is a global number, I think. But if you look at the U.S. at the moment, -- so we had Jonathan Silverberg from George Washington here yesterday. It's just standard of care in their sense, obviously, he was saying community centers, they felt there was still penetration to go. In fact, the pun he used was the fairly scratching surface. So the -- so if you can help us understand where you think you are on penetration in the U.S., both in sort of big centers and then in the community dermatology clinics. How much more upside is there for the U.S. opportunity?

I think Eva reminded me of this -- again, a lot of times when we talk about that, we talk about the U.S. first because it's our first market that we launched into. So we not talking about 9%, that's really U.S.-specific. You go to other markets like Germany, Japan, China, France, at least , you name it. The biopenetration rate advanced therapy is much less than that. You're typically talking 4%, 5%, 6% in some of those marketplaces. So again, it takes time to grow these marketplaces. We're seeing it develop faster than what psoriasis did because a lot of these prescribers had the experience of biologics, at least in the psoriasis space. But what's quite interesting, and I'm sure Jonathan, he's fantastic, by the way. So it's top-notch speakers to have here. In a practice like his, bio penetration is much greater because again, these are people that are really on the leading edge of science. They are the ones that are in a lot of the clinical trials, and they start using these agents really early on. But it is -- the bulk of the patients really sit with the in the community type of dermatologist community. And that reaching them is really what it's been taking for us as an organization. We spent a lot of time and a lot of resources on building that marketplace from those offices, quite frankly, by private practices in the U.S. where it's quite different in U.S., Canada, Australia versus more hospital settings like in France, U.K., Germany and so on and so forth. So yes, I would say the bio penetration rate, as you go into those clinics is very low single digits. But you go to like a Jonathan Silverberg's clinic, and it's much more where it probably should be, probably 30%, 40% already now.

Okay. So in terms of the competitive dynamics in the U.S., you've had tralokinumab launch earlier this year, lebri is coming. And maybe Dietmar got view on this as well, the lebrikizumab maintenance data at ESC, they're quite interesting is perhaps the way they'll look to try and differentiate that asset. So just perhaps help us understand how you think that competitive dynamic will shift into next year, in particular.

Yes. So you're absolutely right. We've seen a number of competitors come into the marketplace, whether it's the JAKs. We've also seen an IL-13 come into the marketplace already. So we've seen that in markets ex-U.S., and we've seen it in the U.S. And it's gone as we anticipated. Once you've been in the marketplace more than 5 years now and we continue to go younger and younger and younger in age populations, it just continues to build more and more trust. I didn't mention it, but we also hit a milestone that we announced really around EADV and ERS this past week. We have more than 500,000 patients on therapy around the world now. And so when you have that, it just builds trust in the general prescribing population that this is a therapy that they can use. So now back to the data, it wasn't really surprising to us. We've said for a long time that IL-13 is a really important target in the treatment of atopic dermatitis, but it's incomplete by itself. And the data continues to show that. Again, it's -- we have data that shows really good maintenance effect as well. But when you're missing that hitting of IL-4, what you're seeing is a little slower onset of action as far as age goes, which we would anticipate. And again, our continued clinical data in private nodularis is just another one of those examples where the IL-4 -- that is such an important part, I think, of the holistically treating the disease that's just missed with something like lebrikizumab. So all of that said, it's good news to have another company coming into the place. I never thought I'd say that, certainly not on a stage that we welcome competition. But when you have a bio penetration rate of 9% in the U.S. and even less x, you need more companies to come raise awareness to get patients treated so...

And just thinking about China. So you talked about potential this being a lot in China alone, launch now on the NRDL. Just perhaps an update on how that's going. What's the sort of price volume trade-off that you've had to make for the broad access? And do you still sort of maintain that kind of blockbuster potential ambition?

Yes. We definitely maintain the ambition. And I think China is -- it's a really exciting time there. It's to see that they're really sticky to this top track of innovation. Dupixent is a real validation of that, I think, to be -- to get approval on NRDL in 5 months, which in record time, normally it takes on average around 2 years to get NRDL reimbursement is a real sign that they're supporting innovation in China. And we've seen that now for the last 2 years. As we've been on NRDL, we've seen a really strong commitment to the community for prescribing this for patients. So we're still very bullish about Dupixent in China. Price volume trade-off, we had to go through the normal negotiations for NRDL. And again, it's -- obviously, it first starts with the science. It starts with the unmet medical need. And then it starts with, okay, what is the value in the marketplace. And as we said before, the teams did an absolutely amazing job of establishing a very good starting point for us. Now we'll have to continue to negotiate with the authorities as we bring new indications and so on and so forth as we go down in younger patient populations, but we're off to really good start more than 3,000 hospitals we have covered. You have to go to provinces. As you know, you have to kind of take on the whole marketplace and Sanofi's long-standing commitment to China, I think we're approaching our 40-year anniversary in China. And so that knowledge of the space, along with an innovative asset like Dupixent makes us really bullish about -- not only Dupixent, I think beyond with our pipeline with other innovative assets, I think, in China as well.

Okay. And then you recruiting eosinophilic esophagitis in May as well. So just update on launch progress sort of where you see the opportunity or how big do you see the opportunity as being in that indication.

Yes. I think, it's funny, last night, I was reading a success story that we just heard yesterday of a patient. I mean, it's just unbelievable patient that they go and get the scopes. And the mother was telling the story basically. So this is anecdotal a little bit, but the mother was telling the story about how she always dreads the scope the readout because she always knows it's going to be bad. And for the first time in her child's career -- in the child's life and the child has been on the feeding tubes actually for a big part of their life. The scope was completely clean of eosinophilic esophagitis, after 8 weeks on Dupixent. So again, that's 1 patient and 1 patient story, but it was posted to the patient support group actually that's out there for eosinophilic esophagitis. So I think it's a really exciting time for that disease. How big is the potential? I think like a lot of the diseases that we've gone into because of unlocking the science behind disease is driven by underlying type 2 inflammation. Likely, the patient population is bigger than we anticipated from the beginning, but we will see. It's still very early. But the community, I can tell you has really embraced it so far. We actually have -- we've had -- we're off to a very good start as far as number of physicians that have expressed extreme interest and so they have patients for the product so.

Okay. And you're filing prurigo nodularis as well. So just to perhaps give us an update on how you see that and the -- I guess there's more biologic competition in the wings there with things like nemolizumab as well. So perhaps just compare and contrast how you think that market will progress and how you're going to compare to perhaps more age-focused mechanisms.

I mean -- so we're currently -- I mean I was about to look at my watch when you said filing, we're -- so this is September, I think, right, so actually, we're in discussions with the FDA now. So we anticipate the end of this month, I think, is the current plan from a discussion with the FDA. So it could be any day now, quite frankly, as it relates to prurigo nodularis. As it relates to the competition, again, I think it goes back to the mechanism of the drug. I was just having a conversation with a gentleman. I think prurigo nodularis, again, really reinforces the importance of the target of IL-4 and IL-13. Prurigo nodularis is the most debilitating itch condition in dermatology. The dermatologists will tell you this over and over again. A lot of our patients had more than 100 lesions as well. So there's a lot of commonality between this and atopic dermatitis, but the itch is -- you hear patients talk about it. It is extreme. So as you see our mechanism of action, you saw it in both of the trials that we did, it validates, again, why this target really matters for a disease like this. So for us, we're quite optimistic about what this will mean for patients, assuming the regulatory bodies to get this approved and get it into patient's hands. And then we're quite bullish as it relates to competition. I think so bullish, I think, innovatively what we did from a development standpoint, you saw we went straight to Phase III. So you -- I think you mentioned nemolizumab, we actually were previously significantly behind them because of our bullishness with the product, we went straight to Phase III, and we've since passed them and likely will be ahead of them by a year or greater. So with our teams around the world, I wouldn't -- I would be extremely bullish of us versus any other asset.

Okay. And just regarding life cycle extension or actually more patent life extension, I guess. Paul has alluded to they're being a very talented IT team working on IP. So I think the sort of the basic patterns that we can see in the annual report of about [ 2032 ] but sort of perhaps just help us understand who is it you hired? What sort of the prior experience they have in this? And what sort of -- could we be thinking about this as actually being an asset that you could have until mid or the end of 2030s?

It always makes me nervous when you say Paul said, and so whatever he said is probably accurate. Again, I don't -- the team themselves, we've done an amazing job, I think, of hiring incredible talent across all critical subject matter experts or functions, if you will, to support brands like this. So no doubt that team is extremely talented and we'll do everything humanly possible between us and across the alliance to try and keep this product exclusive for as long as humanly possible. But I think it's hard to speak to what does that mean. Does it mean an extra year, next 2 years, or extra 5 years? Again, it's hard to speak to what we will be able to achieve. But I think the teams that we've hired around, I'd say, the brand and around where we're going actually immunology and even more broadly from an innovation standpoint in specialty care, we've got a lot of really talented folks that will help to navigate that. I don't know, Dietmar, you might know these folks a bit better than I do.

Yes, [indiscernible] the other really important that because you obviously prepare for LOE for Dupixent, right? So not only the life extension, it's also really the portfolio that we're building in immunology, right? We have no major loss of exclusivity in this decade. So we have some time, right? That doesn't mean we're waiting. That actually means, yes, we are really busy building a strong immunology portfolio, and we think we have that. And we really think about how do we apply that to atopic dermatitis, to asthma, to the other indications. We have studies in CSU, AD, asthma, et cetera already now and going with other mechanisms of action to really prepare for that event, right? And then [indiscernible] is not going to go away from one day to the other. So there will definitely be some growth opportunity there as well.

And any other commercial questions on DPO, I think we might shift into the pipeline. So perhaps then on -- if you look across the pipeline, you're starting to develop as the next phase OX40-Ligand is the -- and the tezepelumab is probably the most advanced. I guess, perhaps just help us to understand how you think this differentiates from Dupixent? What can you add? The Phase II data seems to show sort of very similar response rates to Dupixent so -- and there's possible unknown toxicity, I guess. So perhaps help us understand how you think that could be positioned and what data you need to show to make it successful?

No. Only to say that the next one is actually itepekimab, right? And that's our COPD medicine that is redeveloping that's already in Phase III, right, at this point in time, but picking up -- and we can talk about that as well. But picking up on amlitelimab, it targets the OX40-Ligand. We feel that's important. It doesn't target the receptor, right? The targeting the receptor means that you also take out the immunosuppressive cells that you want to maintain. That's why with competitor products that are targeting the receptor, you get these autoimmune effects, you get actually exacerbations of the autoimmune reactions. We don't see that. We think the Phase II data have been really encouraging, right? We need to obviously demonstrate that we can maintain that in Phase III. And then the question really becomes like are there different patient populations? Are there different segments? We hope that we can have extended dosing with amlitelimab as well. So really looking at the profile of the drug, I think there's a real potential that this enhances in the biologic space, right? And as Brian said, there's definitely plays for more than 1 molecule in this space. So we're really looking forward to do that.

So I think you talked about the [indiscernible] pathways as being something you can hit outside of just Th2 with OX40, but I guess if you were going to hit a broader number of patients wouldn't we have expected to have seen a different response to higher response rates on easier IGA scores in the Phase II?

That was a pretty small study, right, the Phase II. So we need to explore that more broadly. And we're doing that, right? We're taking it to asthma. We're evaluating there. We're also internally discussing our broader program, which we will obviously talk to you about once we're ready. But we think that OX40, especially targeting OX40-Ligand has -- is one of those immunological nodes that we're talking about. And we just need to generate the data to see how broad can we address that.

And do you see the mechanism is disease modifying potentially? I know the idea is if you go to the receptor, it could be because of T cell depletion, but has also got risks with it. Does going after the ligand give you potential for disease modification?

I think it absolutely does. Obviously, we need to demonstrate that. But it's -- when you target a specific pathway, right, that's where you get via the pathway, the disease modification. The difference between the receptor and the ligand is more really around the expression levels, right? Where is it expressed and that's where the expression of the receptor on the likes of regulatory T cells is really well, what we don't want to touch.

Any others on OX40, I might shift back to COPD, the Dupixent COPD first half. So we should get some data next year. You obviously started a second trial after you hit a -- I think it was a futility interim on the first study. Can you just help us understand what that interim was. So what did you need to show in order to start the second study? Was it based around the same endpoint that you're using for Phase III on COPD exacerbations or is it something else?

We never really spoke about the hurdle in that interim, right? And quite frankly, it wouldn't help you along because we don't know what the data are. The interim was looked at by a data monitoring committee. We put in a bar where we basically said, this is the bar that gives us confidence to move forward. And by design, we had those 2 studies, right? We didn't want to start the 2 Phase III studies at the same point. We said, let's derisk the program. We have some interesting reason to believe at this point. And let's start the program, start with one study to the interim hit that bar and then start the second study. The broader question, I think, is what reason to believe do we have at this point? And why are we confident? One is in the Dupixent studies in asthma, there are subpopulations of patients that have COPD like features, and we saw improvement in those patients. We've also looked at real-world evidence, and we looked at patients that are receiving Dupi and do they see an improvement in the exacerbation and we also saw that, right? And then we designed the studies in a way that we're really focusing again on a Type 2 population within COPD. So we're not looking at the overall COPD where many other drugs have failed. We're looking very specifically at the Type 2 defined by eosinophilia. So we feel that, that again increases our probability of success, right? So there's -- I'm actually optimistic, right, reading the study outcome. Obviously, we need to demonstrate that the first study is going to read out next year, right? And then we have as we said, right, we have this broader approach also to COPD with itepekimab that covers a different patient population.

And on the Dupi study, so I think you said one of them reason next year but I think both of them have primary completion during the course of the years, could we get both? And would you press release them separately? So if you hit on one, would you let the market know? Or do we have to wait until you get both studies?

Well, we'll have to see the data first, right? So let's wait for that. But what we've always communicated is that we're going to file in 2024, and that holds.

Got it. Okay. On itepekimab, we see Astra is also developing products in that space. You've gone for former smokers only, and that's where in your Phase II saw 40% reduction in exacerbations rather than 20 across [ 4 ] brands, current smokers. They're not doing that subgrouping, -- so they're just running in the Phase II, at least at the moment. The Phase III, this now just started there and in the Phase II studies, they didn't segment it down like that. So perhaps just compare and contrast their asset versus yours and why you think they didn't need to go into the subgroup?

Yes, I don't know whether they need to go into the subgroup, right? I cannot really comment on their decision. I mean I can only say that there have been various approaches to the IL-33 pathway. There is one. There have been others, right? Many of them didn't demonstrate the type of impact that we have seen in the former smoker category, which is this 42% reduction in exacerbations, which then led us to really follow the data, follow the science, follow what we've seen in the Phase II and really focus on that former smoker population. By the way, in the Phase III, we do have a smaller subgroup that also includes current smokers, right? And so that -- and that was done in discussion with regulatory authorities also so that if we see a broader effect, we absolutely have the upside. But the study is powered to really look at that former smoker population where we saw the best benefit. And based on the data that we saw, we felt that's the best path forward. That gives us between Dupi And Brian can talk to that better than I can. But between Dupi and itepekimab, if we had both biologics in COPD, would give us access to 80% of the COPD population, which we felt is really meaningful.

Okay. And I think on the Astra studies, they argue that they're hitting a non-ST2 [ pathway ] which also has an impact on fibrosis and epithelial changes. So is that something which you've looked at for itepekimab? Is that something which is a differentiated point between the 2 assets? Or do you think you're -- there's essentially no difference between them?

Yes. Well, the clinical data need to show that. We have not looked at other mechanisms outside of the IL-33 pathway, right? I mean that's something that definitely we can follow up on further. But at this point, we're following the data that we've seen in our Phase II.

Okay. And If I move on to rilzabrutinib, we've got Phase II data next year across atopic dermatitis, asthma, CSU. Just help us understand what the target profile is in each of those 3 potentially very large indications and where you think positioning of the asset would be if the data is as you expect?

And maybe I can start and then you can talk about the profile as well. So rilzabrutinib is a BTK inhibitor, right? And then it is differentiated by this concept of tailored covalency. And that means that the binding at the tyrosine kinase is different. And that we feel we can actually in a safe and effective way, which higher doses and have a larger impact, right? The first data that we -- or the most advanced data that we're going to see is actually going to be in ITP, immune thrombocytopenia, where we already saw Phase II data presented those at the ASH meeting, and we are also looking forward to those. In AD, asthma CSU, we've got these Phase II studies ongoing. The first studies are reading out next year. The profile in my mind is that basically of a safe oral in these categories. And we're doing that because really when you come from the disease course, for example, in AD, many of these patients go from a topical, go to an oral, then go to a biologic, right? And if you really want to cater for these patients and for the whole profile, you need to have these in your portfolio. And for AD, for example, we have a topical BTK that we're developing. We've then got rilzabrutinib as a same oral. And then we got the biologics. And we look at rilza as the safe oral opportunity in all of these, right?

I mean I think it's -- we're building, as we sit back to this leadership in immunology space, we're building this reputation as well in the marketplace where when you bring these other agents, you've got -- you're in a strong position to start to have discussions with physicians about where each of these drugs will sit. Now of course, it needs to be a safe and effective oral especially as you take it into a few of these indications. But whether it's atopic dermatitis, and I think this is a space where we haven't seen a safe oral yet. I mean look at what it did for psoriasis with and when Otezla launched into the marketplace, it didn't on the biologics, it really opened up that moderate space. So I think that's really the unmet need in the -- still remains in atopic dermatitis to really get to that advanced therapy penetration rate. You're going to need some safe orals to come into the marketplace. Clearly, the JAKs didn't do that. But the hope is with rilzabrutinib is that we can do that for atopic dermatitis, a safe and effective world there. It's quite similar in asthma as well, ironically enough. I mean still the advanced therapy penetration rate in asthma, there's most severe patients that are still on control on background therapies. You needed a safe world in that space as well. And so it's quite similar there. And I think you see it as well in CSU. And I would say, even more broadly, urticaria in general, this is an area we're just being done at EADV this past week of still real excitement. As we advance Dupixent in the space, not only with CSU, but also with [indiscernible] you still see the need for other targets and certainly safe oral targets as well as CSU. So I think all of them share some similarities of needing a safe and yet effective, but really important to get a clean safety profile as for these patients.

So on safety, receive BTKs in MS, we've seen evobrutinib some liver enzyme elevations, you've had the drug-induced liver injury, issues with tolebrutinib, certainly the physician feedback we've had is any kind of labs on an oral in for terms, just that curtains. So just talk us through what you know about the liver profile of rilzabrutinib and the level of confidence that this won't be an issue for rilza?

We -- for rilzabrutinib, we're coming back to that concept of tailored covalency right? And it's really -- tolebrutinib is a covalent binder, right, and that contributes. Rilzabrutinib is the tailored prevalence. And we believe that we can get to higher doses in a safe and effective manner. At this point in time, we have -- the studies are ongoing. We have not seen liver toxicity for rilzabrutinib. So we're confident that we can move that forward. Obviously, we're monitoring, right? Obviously, we're paying attention to that as we did for tolebrutinib as well.

Got it. Okay. And perhaps finish off on the immunology when we'll move on tolebrutinib. But then on the bispecific portfolio. So the -- I think the product, it seems to me that you're most excited about the IL-13,, OX40 combination as a possible sort of long-term son of Dupixent, if you like, or daughter. So if we're going to -- is that a fair characterization? And what is it about the combination, do you think it's important that you want to be able to do from just combining OX40 and Dupixent, for example.

It's really this question of when you hit 2 pathways that are obviously contributing to the disease from a pathological perspective, whether you can increase efficacy, right? That's really the question. And we brought 5 different nanobodies and bispecific nanobodies into the clinic last year in immunology. This is early days, right? So we're going to have to see what they show. We're basically in dose escalation at this point. But I'm excited about several of those, right? For exactly that reason, can you combine 2 therapeutic principles in 1 molecule that then addresses AD specifically or asthma specifically, right? We've also got the IL-13 T slip, for example, which is really interesting and could be a could play a key role in asthma, right? So there's really the broader potential here. And what's important really is that the toolbox that we have allows us to generate those combination, really allows us to come up with novel mechanism and addressing those key targets.

Yes, I'd say just one last thing on that is we were both at EADV and ERS, we were talking with the HCP community about our pipeline and what we're doing in the immunology space. What I can tell you is that the interest in the varying targets, it was more the platform that they were interested in whenever we started to talk about the antibodies because then they started thinking about all these variety of combinations, and it wasn't one that -- any one in specific that they leaned in on. I think that's kind of the way that we feel as well, although the -- when they recognize the target, they tend to get quite excited about like IL-13 TSLP, of course. But otherwise, they just like idea of being able to potentially combine targets to continually raise the efficacy bar for patients.

And perhaps shift on to tolebrutinib. So I think you said you're going to submit the additional info to the FDA by the end of September and hope to be of a partial clinical hold by fourth quarter. So just any updates there at all?

Yes. There's actually no update to that. Yes, we will submit by the end of September, FDA generally has about 30 days to react. So we're confident that in the fourth quarter, we will get their response. What we already take as a really positive sign is that FDA has asked us to have like a Hepatic Assessment Committee look at the cases, right? And the Hepatic Assessment Committee has done that. They're working very closely with the DMC. They are really linked to the data monitoring committee, and then they are coming up with a recommendation. That's the mechanics of it, right? And the Hepatic Assessment Committee has looked at the cases, has given their recommendation to the DMC and that's when they came back and said, "Yes, we agree to continue the studies, right? So that currently takes place. We're currently reopening the studies outside of the U.S., right? Because we have that supported by the DMC. Obviously, we have risk mitigation measures in place as you would find them for other drugs in MS, right, that demonstrates some liver injury. And that's also why we're confident when we send back the response to FDA. And I'm never going to give you a guarantee or something, but we're confident about the quality of the response because we already have the feedback from the DMC as well.

Okay. And then on the -- just perhaps to back track there. So why did the DMC decide to pause recruitment outside of the U.S. So that was a U.S. regulatory decision. The ex-U.S. regulators were seemingly happy to continue. And it was your own DMC that said, hold up. So what was behind that?

Well, there's several comments here. One is there was no new data. There's absolutely no new data. And the DMC before had decided differently. I think it was more the DMC is heavy in U.S. participants. So the FDA will count a lot for them as well. And the other factor is they said we have the HAC coming in. We have the Hepatic Assessment Committee coming in. They will look at all the cases that will give us more information. So let's wait for that, right? But there was no new data, no new data of concern or anything. It was literally this type of thinking that's behind that.

Got it. And to be clear, the Hepatic Assessment Committee has now completed that for given information to the DMC or reopening ex-U.S. and then you give updates to the FDA in September for fourth quarter, okay?

It will remain in place, right? They will also follow the patients throughout the study, which is very reassuring.

And in terms of the drug-induced injuries that you did see -- I think you said the majority were in patients with pre-existing risk factors, which are now excluded from the new protocol. But were there or how many were there that weren't pre-existing? So did you see drug-induced liver injury in patients that didn't have pre-existing risk access?

Very few. Very -- I cannot give you an exact number, but very few. The vast majority had other factors that were contributing either co-medications or pre-existing liver damage, right? And when we exclude those patients from the studies moving forward, that's what you generally do, it excludes low number of patients actually because liver damage is not very prevalent in MS, right, in MS patients.

Got it. Okay. Any others on tolebrutinib is, I think we perhaps just want to talk about this in the last couple of minutes is 2 launches next year. So efanesoctocog and nirsevimab. So just perhaps just help us understand your sort of route to market and how you see -- where do you see the biggest opportunities in efanesoctocog initially in terms of where the unmet need is still.

It's interesting when you look at the hemophilia market, we were looking at it as like gene therapy, nonfactor, factor, right? And we were actually thinking -- a lot of us were thinking that the factor is going to shrink a lot. In fact, there's still about 60% of patients that are on factor at this point in time. So the factor market has shown a I think, quite amazing resilience. And if you think about it, patients on nonfactor have to use factor whenever they undergo surgery, or whenever they have a bleed, right? Because what nonfactor actually does, it brings you back to kind of a mild-hemophilia state, right? That's where I think the real opportunity for efanesoctocog is that patients can lead a normal life for the majority of the week. And that's why I'm actually quite bullish on efa as we call it, because the data that we've seen, the prevention of bleeding is, in my mind, just unprecedented. And patients called up on this very quickly. When you go to these conferences, to the hemophilia conferences, patients are there, right? Parents are there. And because they look at what's the right treatment for my child. And when you have these patients that want more activity, then efa is a really important opportunity for them and a real point in treatment. So I'm thinking -- I'm actually quite confident for efa is going to play a key role because it just is the best factor that is out there, right? And the current factor market, there was really not a lot of innovation since Eloctate that was 10 years ago, right? So I think the -- just having a factor that normalizes bleeding for these patients, is going to make a real difference.

And nirsevimab, is that really going to be a sort of September launch to hit the season?

Yes. I mean the -- we're going to have to wait for the regulatory authorities act now, obviously. But I find nirsevimab also a really important new drug because basically, RSV infection, as you know, right? As we all know, is really the key reason for hospitalization even for death in these children, between zero and 1 year. And we believe that, that whole population will benefit from nirsevimab. We look at it like a vaccination in a sense, right? And the data is very strong. The unmet need is clearly there is protection for all children. So again, we're really bullish about nirsevimab as well.

Got it. Well, I think we're just about on time actually. So unless there's any other last questions in the room, we'll call time and say thank you very much to Brian and Dietmar today. Thanks for your time today. Thank you.

Thank you.