argenx SE (ARGX) Earnings Call Transcript & Summary

Welcome to the first day of the 44th JPMorgan Healthcare Conference. I'm Richard Vosser, European pharma analyst at JPMorgan. It's my great pleasure to introduce argenx CEO, Timothy Van Hauwermeiren. Just a few housekeeping rules. We will take questions from the room after Tim's presentation and/or you can submit those into the portal. So with that, Tim, welcome to the conference.

Thank you, Richard. Thanks for having us. It's great to be together and kicking off this fantastic week at JPMorgan. Very warm welcome, by the way, ladies and gentlemen, to the argenx presentation. And let me kick it off with an important question each biotech entrepreneur should ask himself. The question actually is, who would miss you if you wouldn't exist? And in our case, that question is leading us straight to our patients on VYVGART. And I couldn't be more pleased to bring Sam today to this meeting. We're going to listen to a 30-second video from our patient, Sam. [Presentation]

And Sam is not the only person who undergoes a transformation when he's on VYVGART. By the way, Sam is now on PFS, and he's traveling the world. What happens is the transformation of a patient life. And the way that happens is by offering breakthrough science to our patients. We're an immunology company. We think we're just at the beginning of our understanding of human immunology. And therefore, we think that the opportunity in front of us as bio entrepreneurs is infinite. Patients are also central to Vision 2030. We have the bold mission to impact 50,000 patients by 2030. We would love to do that through 10 labeled indications. And because we're in the business of building a sustainable biotech company, we have the ambition to have 5 new molecules in Phase III by 2030. I'm very proud to tell you today that we are well on track. Actually, we have 19,000 patients on VYVGART today. We're running 10 registrational trials in 2026. And last year, we advanced 4 new pipeline molecules. I'm very proud of this. When patient transformation happens, financial success follows. I couldn't be more proud of the commercial team, which gave us such a strong Q4 in 2025. We sold about USD 1.3 billion, which is 14% up from last quarter. And that means that we almost doubled the business in 2025 compared to 2024. Last year was also the first year where we reached structural profitability. So I believe we're in a position of strength to execute on Vision 2030. Let's look at our strategic priorities for 2026. We have 3 of them. First, we want to impact more patients with VYVGART. Second, we want to shape the long-term future of FcRn. And third, we want to deliver on the next wave of innovation. In my presentation today, I will be unpacking each of these priorities step by step. Let's talk about impacting more patients with VYVGART. Our playbook in the indications where we are is very clear. First, we redefine biology, then we redefine the treatment paradigm and then we redefine patient outcomes. For example, in myasthenia gravis, we have redefined biology. Regardless whether you're seropositive or seronegative, we have proven for once and for all, this is an IgG-mediated disease. In CIDP, after 30 years of no innovation, for the first time, we have shown this is an IgG-mediated disease and potentially a subset of patients with an IgM mediated disease. I'd like to believe VYVGART is not just first-in-class, but also best-in-class. When it comes to redefining treatment in MG, we have changed the bar. The bar used to be at, "Oh, my patient is doing fine because the patient is not hospitalized." That's not good enough. We have established a whole new gold standard, which is called MSE, minimum symptom expression. That means that these people can live a life with no or minimum symptoms. 60% of VYVGART patients in the real world achieve MSE. In CIDP, as we could see from Sam, we can see in the subset of patients a spectacular regain of function. Sam is not the only patient who's sending me his step counter through FaceTime or WhatsApp. Many patients are doing that. I would also like to applaud the commercial excellence of the team. Our secret power is market access. We made a promise not to leave any patient behind. I can assure you that we're serving the broadest possible population of MG patients and CIDP patients. And then we redefine patient outcomes. We constantly out-innovate competition. We're announcing today that we are in combination studies in MG. I will explore that later in this deck with you. But we're also bringing a second mechanism of action into the CIDP space. Raising expectations also means that you delight your customer with your product presentation. Sam is traveling the world with his prefilled syringe. Many people are enjoying the prefilled syringe. And actually, the PFS has been a real driver of growth in 2025. What that results into is that VYVGART is the #1 prescribed biologic in MG. It's driving 60% of the biologic growth in MG. We continue to penetrate the treatment paradigm. 70% of the patients are coming straight from orals. So we get earlier and earlier and VYVGART becomes the go-to therapy for a newly diagnosed MG patient. In CIDP, we already achieved blockbuster status in Q3 of last year, and we continue to penetrate the prescriber base. I'm very proud of the fact that now there are more than 4,700 active prescribers here in the United States, which is a 20% growth year-on-year. Playbook in MG is crystal clear. We landed in a TAM of 17,000 refractory patients, and we have articulated clear stepping stones to move into that 60,000 patient TAM. First of all, the seronegative patients. We made a promise to them, which we kept. We run the biggest ever seronegative trial, strong data, and we believe we are on track for a potential approval and launch second half of this year. The next data cart to turn is ocular MG. That data point is around the corner. It will happen in Q1, and we're going after significant unmet need in these ocular MG patients. And then we continue to build the market by generating real-world evidence. We have pretty spectacular data in terms of steroid sparing. We have pretty impressive data in terms of eliminating hospitalizations and dramatically reducing stays in the hospital. And we continue to innovate with things like, for example, the auto-injector and the combination trial, which is now public. Also in CIDP, there is a clear path of growth. There's no reason VYVGART should stay in the 12,000 refractory patient population. Actually, we're already entering in the 24,000 patient population of people who are currently on steroids and/or IVIg. We do a ton of translational work unraveling the biology behind the disease. That is why we're bringing a second mode of action into the disease with empasiprubart going complement after complement C2. And based on the regain of function data, the real-world evidence data, we think there is upside potential into that 42,000 CIDP diagnosed patients. Guys, I couldn't be more excited about rheumatology in 2026. First of all, autoimmune myositis. This is no longer idiopathic myositis. It's an autoimmune disease. We know it is driven by pathogenic IgGs. And actually, today, the fingerprint of your pathogenic IgGs is determining the subtype of myositis you suffer from. We had solid Phase II data with significant improvement in muscle strength on the TIS score. Sjogren's disease, 2 independent Phase II trials have shown for once and for all that pathogenic IgGs and the circulating immune complexes they form drive this disease. Pretty remarkable impact in systemic disease activity. And what both rheumatology indications share is these are both sizable patient populations in very high unmet medical need with treatment toolboxes, which are virtually empty. Let's talk about priority #2, shaping the long-term future of FcRn. Today, we're in a position of strength. We have a very clean, very powerful IV product. We already have 2 subcu product presentations, one HCP administered, one self-administered. They have a unique formulation, thanks to the exclusive partnership we have at Halozyme, and we continue to innovate on the product presentation side, not just with a one-of-its-kind PFS, but also with the first of its kind auto-injector, which is well on its way for launch in 2027. And as I said, we're venturing into the combination trial, which is public on clinicaltrials.gov. That's not enough. Tomorrow, we will be advancing ARGX-213, our first next-gen FcRn, which I will showcase later in this presentation. We have a second next-gen ARGX-124, which is currently in Phase I clinical trials, and we are building more molecules in typical argenx fashion, which means in close collaboration with the best out there with whom we partner. We also believe there is more combination potential in the pipeline of argenx. Combination therapy has been the standard in oncology. It will become the standard in autoimmunity. Priority #3, the next wave of innovation. Guys, this is the year of MMN. We spoke about it multiple times. This is an underdeveloped market. It's already a blockbuster market today, driven by the plasma fractionators. These patients are in bad shape. There are about 12,000 patients in our key markets, difficult diagnostic path. Lots of misdiagnosis. These patients are getting the diagnosis of ALS, sometimes the diagnosis of CIDP. There is 0 targeted therapies out there today. 60% of these patients progress despite being on the highest dose of IVIg, 20% of patients ending up in permanent disability. I couldn't be more excited about the opportunity which is waiting for us to transform the life of MMN patients. A couple of data. This would not be an argenx presentation without data. 2 panels on this slide. The left panel is the randomized controlled portion of the Phase II ADAPT trial. The right-hand part of the slide is new to you. This is the first time we're showing the open-label extension data from this study. Remember, on the left panel, we randomized MMN patients at their best on IVIg onto empasiprubart in blue, 2 different doses or placebo in yellow. What you see is the immediate jump in functionality, the improvement in grip strength. This is a dramatic gain in function, similar to what we have shown with VYVGART in CIDP. And now comes the cool part, when these guys roll over into the open-label extension, you see again the same jump for the placebo patients, then enjoying the same instant effect of empa. And the blue curve show you that the longer you stay on drug, the more function you recover. Guys, what you're seeing is a remarkable ability of the human peripheral nervous system to recover function when you take away the toxic pressure of these pathogenic IgM autoantibodies. So we spoke about efgartigimod, which is being developed in more than 15 indications. I now spoke about empa, which is being developed in more than 3 indications. Adimanebart had its little moment of glory in a mini R&D Day in Boston, not such a long time ago. I will not talk about it today, but it's advancing into Phase III for CMS, and it is currently in Phase II for ALS and for SMA. I want to spend a few minutes on ARGX-213, our next-gen FcRn, the first of many and ARGX-121, our IgA sweeper. What I brought to the presentation today are PD data. So on the left-hand side, you see ARGX-213. The ask to the scientist was make a molecule, which with a single monthly subcu push can replicate the PD effect of weekly efgartigimod dosing. The child can see that the curves overlap. This is the outcome of the healthy volunteer study. We are ready to go into advanced clinical development. The curves overlap mission accomplished. On the right-hand side, we see ARGX-121, our IgA sweeper. This is a single subcu push, which is instantly and completely eliminating IgA selectively, including all the pathogenic forms of IgA. There are many of them. This molecule can grab all of them. And you can see that it would be easy to achieve monthly dosing, if not less frequent dosing. This molecule has successfully completed Phase I, clean safety profile, ready to venture into a number of IgA-driven diseases, including IgAN. In the press release this morning, we also spoke about a deal, which we did with Tensegrity. You know our formula of innovation. Our innovation engine is constantly looking for novel biology, typically in the hands of strong translational biology labs in academia. We started to open up the aperture and started to work with biotech companies. The Tensegrity deal is the first of many, and that basically means that we are pushing 3 new molecules into the pipeline, ARGX-118 going after Galectin-10, ARGX-125, a bispecific antibody against undisclosed targets and then TSP-101 targeting FM14 in muscle regeneration. All of this is summing up into a pretty exciting pipeline. Today, we have 10 molecules in clinical development. We have 4 molecules in Phase III development, and we have built an engine, which can crank out INDs at a cadence of about 1 new molecule per year, each time going after pretty cool biology with black belt antibody engineering. The news flow for the next months, the next quarters is going to be busy. That's why we only limit this to the Phase III readouts. But for efgartigimod, we are waiting now for the ocular MG data, which will come on back in the first quarter of the year, followed by the myositis data in the third quarter of the year, followed by ITP in the fourth quarter of the year. And of course, Sjögren's is well underway to give us data in the second half of 2027. For empa, we're waiting for the MMN data to come out in the fourth quarter of 2026, and the first CIDP data will start to emerge second half of 2027. And I can confirm today that we did submit the sBLA for the seronegative MG patients. We are on track, we believe, for a potential approval second half this year. Where this leaves us is a company, which I think is a sustainable innovator. We have this wonderful IIP machine, this engine, which is cranking out these waves of innovation. Very proud of the new programs entering the clinic, very proud of the advanced clinical development assets being empa and [ AbbVie ] and of course, the FcRn franchise, which we're building out as the leader in the space. And with that being said, I would like to open the floor to questions with the panel, but I would like to ask Karen to join us on the podium. Thank you.

So are there any questions from the floor? If not, I'll start. Welcome to the panel, Karen. Thanks, Tim, for the presentation. Maybe we can start just from -- we've just seen '25 results, but how are you thinking about -- or '25 results for VYVGART? How are you thinking about the growth of VYVGART into '26? Where are we? How do you think about that?

Thank you. Happy to take the question. From my perspective, we're still at the beginning of the growth journey with VYVGART. And I think that is incredible 16 quarters since the launch that we continue to see double-digit growth quarter-on-quarter. And when you look at the underlying fundamentals for MG, for CIDP, for the PFS launch, what we see is consistent momentum, consistent patient growth and really strong performance across the board. When I look forward to 2026, I think you continue to see MG growing. We have opportunities with seronegative that Tim just referenced. We have ocular MG as another market expansion. potential. And of course, we continue to grow the biologics market with VYVGART and MG. And at CIDP, we're very much at the beginning of the launch story. And what's exciting in 2026 is that we start the journey into rheumatology with the first data readout in autoimmune myositis. So I think it's clear to say that -- or it's clear to me that VYVGART is at the beginning of the growth journey. And certainly, our FcRn leadership is also at the beginning with the exciting molecules to come.

And when you mentioned the ADAPT SERON data that is going to be filed and come to -- come on the label in the second half of '26. Are you already seeing a change in the way physicians are and the competitive profile? I mean one of your competitors had a slightly broader label, which may have let them into the market a little bit. Are you already seeing a benefit from that in MG for VYVGART?

Yes. I mean, obviously, we don't promote off-label, and we don't see broad use off label in terms of payer restrictions. But what we do hear is a lot of questions and a lot of unmet need in seronegative. I mean the study enrolled very quickly. By the way, that's the same for ocular MG. The study enrolled very quickly. And I think that's a really good sign of the unmet need that is out there. And we received a lot of questions and a lot of excitement from the community. I think it's important to note that we had positive data in seronegative from our pivotal trial, and we made the commitment to the patient community that there will be no patient left behind. We're going to go back and do a study and pursue the approval for seronegative. And I'm really proud that we're so close to delivering on that promise to patients.

And on ocular MG, 2 questions really. One, if we think about the ADAPT trial, the ADAPT trial, I think, had some patients in there. What can we learn from that in terms of the readout and the confidence in the success? I think, Tim, you had -- you breeded confidence on the readout, but just some thoughts there. And also in terms of commercially, are you seeing some use already on the back of ADAPT and how broad -- how much of a broadening could ocular -- the readout bring?

I'll give the second part of the question to Karen, but this is a database company, and we're marching on the back of strong data. So there is a peer reviewed publication from Vera Bril, the leading MG authority in Canada, which did a post-hoc analysis of the ADAPT data, where actually she was looking at the impact of VYVGART for each individual muscle domain. And what we saw is that the impact of VYVGART is equally strong on the eye muscle domain as it was on all other muscle domains. It's a post-hoc analysis, but the data are pretty clear. There are also stories reaching us from the real world where physicians report to us a pretty spectacular improvement in ptosis and diplopia. So now the question is, can you prove that in a controlled trial in a way that is convincing to regulators. Typically, we precalibrate with the FDA and the regulators on trial design, on endpoint. So I think this experiment is marching on strong data, has been very well designed. But of course, there's always intrinsic risk in any clinical trial. Maybe, Karen, you can comment on commercial.

Yes, happy to. I mean our strategy in MG is to get the broadest label in MG. So we updated the addressable market from 17,000 at launch to 60,000. And a big driver of that is ocular MG and getting the expanded label in ocular MG. We do hear to your question, from neurologists that -- of course, they're not using VYVGART off-label, and we're not promoting it. But in generalized MG, they see the impact on ocular on the eye symptoms. And so they're excited given the fact that there's no other treatment options, no other than steroids for these patients. And what you hear from patients is that ocular MG is a devastating disease and that often they're not taken seriously enough. So the impact on the health care system is large. These patients have trouble working. They have trouble driving. They can't use a laptop. So the patient impact is big. And for us, the real opportunity is, can you imagine in the future that you can treat ocular MG with VYVGART and these patients never progress to generalize. They never experience the symptoms of generalized MG. And we won't know that from the data that we get in Q1. What we'll see is the impact on the eye domain. But we'll follow these patients with open-label extension. And I think that's in the style of argenx to see how do we provide -- demonstrate the long-term benefit of our treatments.

And we saw last year a third FcRn get approved, but it doesn't seem to have done anything to really affect your momentum with VYVGART at all. I think you've already broadened the opportunity in terms of patient number once maybe a couple of years ago now. Just is this evidence that there's a broader opportunity for FcRns? What do you think about competition from other FcRn?

Yes. I mean I think what we see in -- whether it's MG, and I think we'll see it in the future indications that we're in as well is a few different things. The indications that we go into as argenx are white space indications where there's significant unmet need for patients. You're talking about MG, and we've seen how we transformed outcomes there. In CIDP, we entered there had been no innovation in terms of mechanism of action for 30 years. And so with that comes growth in the market and the ability to transform patient outcomes. And I think in these white space indications, there is room for multiple different mechanisms and medicines because what we're trying to do is transform patient outcomes. Within that, I think we've demonstrated that VYVGART is not just first-in-class, but I believe, like Tim, best-in-class in terms of how we -- what we deliver to patients, whether you look at the efficacy, we've redefined the standard of efficacy in MG, establishing MSE and then more broadly looking at steroid reduction and disease control. More -- the breadth of our safety data and the consistency of the safety data and then out-innovating the competition, bringing the first the butterfly execution, then prefilled syringe, we have auto-injector coming. So I think you can see in our playbook that we raise the bar, we out-innovate, and that allows us to grow these markets, build these markets and certainly be #1 within those markets. And I think that will continue.

You touched on the expansion of the CIDP market. How is patient retention going? How is that rollout going? And maybe just generally?

Yes. We're definitely at the beginning of the launch curve for CIDP. And what we're seeing in the real world is actually mirrors what we saw in the clinical trial. So we had a 70% response rate for CIDP in the clinical trial, and we had data where in a subset of patients, you see functional improvement. And we heard that from the patient earlier today. And I'd say that's what we're seeing in the real world. So we see patients starting on VYVGART. We see generally a similar response rate to what we saw in the clinical trial. And then they want to stay on VYVGART, especially because they're seeing the efficacy. But most importantly, with prefilled syringe for self-injection, they're not tethered to the infusion chair any longer. They can go out and get back to living their life and being with their loved ones and doing what they love.

Maybe we could pivot to the myositis data and that's upcoming. The placebo response in Phase II was a little bit higher than we've seen in IVIg trials. Just maybe you could talk through what you've seen in the Phase II and why that gives a little bit more color than earlier on why that gives confidence into that readout later this year.

Yes. Thank you for the question. Of course, it's very difficult to compare between trials and the IVIg trial was a very short trial and was just done in dermatomyositis. So we're running a longer study in Phase II or we have been running a longer study, and we did a basket trial. So actually, we looked at different subsets of myositis, IMNM, ASyS, DM. And what is important, I think, is the efficacy, which emerged from that study. We hit that primary endpoint with a very convincing p-value. But what gives me even more confidence is actually then when you look at the this 20, this 40 to 60 readout, where actually you just blow placebo out of the wall. So I think that this for the proof-of-concept study, mission accomplished. It's not a Phase III, but it's pretty strong and gives us conviction that we have a winning Phase III clinical trial design. So I think we're ready for success. Every clinical trial, of course, involves some intrinsic risk. We cannot exclude it.

I should ask any questions from the floor? Yes, we've got one question. Go ahead. We have to wait for the mic these days blindly.

Congratulations, tremendous talk and just all the innovation, very impressive. My question is about just following up on the immediately prior discussion. If you have anything you can share so far about early data or if you've had a look at the data so far from the Phase III myositis with regard to the TIS, the steroid sparing as well and any toxicity data as well and how that compares to IVIg and toxicity in this population?

Yes. Thank you for the question. It's too early to tell. So there is no early look at data in this trial. It was a seamless -- operationally seamless Phase II, Phase III. We can monitor in a blinded fashion, the steroid tapering protocol. I think steroid tapering is important in these patients. The steroid burden across autoimmunity, I think, should no longer be tolerated. I think we have to actively work on it. So now we have to wait, of course, for the unblinded data. But I think the sterotyping protocol is carefully watched and I think it's being implemented according to the protocol. From a safety point of view, blinded look at the data, we don't see any emerging safety signal. We now have a safety database, which is very sizable. And actually, across indications, we see the same consistent safety pattern. So nothing really standing out. But again, let's wait for the unblinded data. Thank you for the question.

Any further questions from the floor? Maybe moving to ITP. There was some mixed data, I think, in previous trials. Maybe you could just give an idea of the learnings that went forward into the design of the upcoming Phase III that's going to read out and what we should read into that?

I will take the responsibility for that, Karen. You're right. We had 2 registration trials, one with the IV product, one with the subcu product. The IV product was a clear win. The subcu product was flat. We published on it. There's a bit of speculation about what really derailed that study, but the IV study was a clear win. Remember, we are on the market in Japan now for quite some time with IV product. I personally visited the physicians dosing the product to the ITP patients. It's pretty interesting. The efficacy in the real world is spot on as what we have seen in the clinical trial. This is a very refractory patient population, 50% response rate. And the 2 things which stand out and which really differentiate VYVGART and ITP is the speed of onset and secondly, the clean safety profile. So this is a later line drug also because it is IV administered, but it's clearly finding its place in the treatment paradigm. What we have learned in the clinical trial is that we have to pay attention to the use of background medication, how it is used, when it is used. There are certain rules on how you can change the dose for the TPO receptor agonist, et cetera. There were also some geographical biases. So we have taken all these learnings into account in the Phase III trial design. I think the FDA gave us a much more powerful endpoint, cumulative platelet count and this weird construct of the earlier primary endpoints. So I think this company is investing in a responsible way in ITP IV, and we can now wait for the data.

Makes sense. Maybe moving to empa in MMN. You recently changed the primary endpoint there. Maybe you could talk through -- I mean, you showed strong data just now. But maybe you could talk through the reasons for the change, what that brings to the study and how we should think about that.

Yes. Happy to. I'm excited for empa for this year. It's a pivotal year for empa in MMN. So the change to the endpoint was relatively straightforward. It was in partnership with the FDA. Actually, they requested the change to the endpoint. And we were very happy to do that given the fact that, that was our Phase II endpoint, and you saw the data that Tim shared earlier, not just short term, but long term with grip strength being a good endpoint for empasiprubart. So pretty straightforward from that perspective. From an MMN perspective, I'm excited for -- to see the data. It should be coming in Q4. And I think this is really another opportunity like MG, like CIDP, where we can truly transform outcomes for patients.

And I think you touched on the combination in CIDP as well with VYVGART and empa together. What's behind that decision? Maybe give us a bit of color to what we can think about the additivity of the 2 mechanisms, et cetera.

So when we venture into an indication, we really do a lot of bet to bench research. So we do a lot of translational biology work, also trying to write or rewrite the textbook on immunology for these indications. No one has done that in CIDP. And we have actually presented a poster at PNS last year where you see a pretty sizable cluster of autoantibodies of the IgG type going after a certain type of autoantigen on the myelin sheath, but we also saw a distinctly different cluster of IgM autoantibodies against their own auto antigens. So we believe there could be opportunity for a complement blocker to push the efficacy envelope above and beyond the 70% Karen just mentioned. So let's first see what empa can do as monotherapy in CIDP. Then we will be able, based on the serology of these patients, determine whether this is an overlapping patient population or a different one, and that will then set the strategy going forward to develop in CIDP.

Makes sense. Makes sense. Maybe on 119, I think we've got -- maybe I'll characterize it as high risk, but in ALS. I think there is a Phase II readout this year as well. Maybe you could talk about the mechanism and how that reads into ALS and what you could see in this disease, what it's trying to do.

Yes. This is a high-risk area, don't get us wrong. But we're moving in there again in a database fashion, I think in a responsible fashion. We're working with the world experts as we always do on this target, MuSK. It is remarkable what knowledge we're tapping on the MuSK in biology, and there seems to be a mechanism involved when you activate MuSK, you enhance the communication between the muscle cell and the nerve cell, which is important for the innovation. Now the first step in ALS is the denervation, the nerve cell and the muscle cell decoupling, which is the beginning of the disease process. And we believe based on the preclinical work we did is that by activating MuSK, we can keep the 2 together longer. So this is not a curative approach. It is an approach where maybe you can slow down the disease in a significant fashion. And we feel confident moving into a proof-of-concept study also based on some precision measurements we're doing, which are way better equipped to measure the effect of the biology than that endpoint, that typical ALS clinical endpoints. So eyes wide open. It's a high-risk, high-reward indication, but we will be looking at the data in this year and make a decision that we continue to expand the Phase II clinical trial or not. Stay tuned.

And do you ensure -- I mean, patient selection presumably is going to be very, very important in terms of having early enough stage patients that you can slow down the disease. That's presumably built in.

That's built in. It's a proper study. It's placebo-controlled. It's dose finding. We have been very thoughtful about inclusion/exclusion criteria with the world experts on ALS. So I think this is a high-quality experiment, but we need to manage our expectations.

Maybe one final question for me, maybe a slightly more boring one than the pipeline. But the pipeline and the burgeoning pipeline has implications, financial implications on costs. So maybe how should we think about R&D costs going forward for argenx?

Yes. I would say, as you say, you can see with that pipeline slide that Tim shared how our late-stage pipeline is growing and also the early-stage pipeline. And it's really exciting. And they're all pipeline in a product opportunities. So what you can expect is as we advance those pipelines -- those products through the pipeline that our investment in R&D will continue to increase. And that's part of our strategic agenda. We're a growth company, we're an innovation company, and we're going to continue to invest to fully develop our pipeline.

Fantastic. There's maybe 1 minute left for a question in the room? And if not, I'll say thank you very much to Tim and Karen. Thanks very much. Thank you for presentation.