Hello everyone, this is Guido Oelkers, CEO of Sobi. We are delighted to welcome you to this call to discuss the NASP program after we have just received the acceptance of the filing package with FDA for uncontrolled gout. Please turn to slide two. We would like to remind you of the usual provisions on statements about expectations and projections of future events. With this said, please turn to slide three. I'm very pleased to have Dr. Herbert Baraf joining us today. He is Clinical Professor of Medicine at George Washington University, Associate Clinical Professor at the University of Maryland, and a Senior Clinical Advisor at the National Institute of Arthritis and Musculoskeletal and Skin Diseases at the National Institutes of Health in Bethesda, Maryland. Dr. Baraf was a founding member of Arthritis and Rheumatism Associates, one of the largest private rheumatology practices in the United States. He has served as a principal investigator on over 400 clinical trials, including several significant therapeutic gout trials. We are also joined by Dr. Rehan Azeem, who is the Medical Development Lead for the NASP program here at Sobi, as well as Matthew Winfield, our NASP Core Asset Team Leader at Sobi. Dr. Azeem has served in various medical research capacities on NASP, formerly SEL-212, for over seven years, while he's been present with Sobi and historically with Selecta Biosciences. Please turn to slide four. And here, let me start with a high-level overview of the opportunity and unmet medical need in uncontrolled gout. This executive summary lays out the key pillars of our story. There's still a high unmet medical need in uncontrolled gout, a condition that, while affecting a smaller subset of patients, carries a disproportionately high impact in terms of pain, complication, and mortality. Uricase therapy is a proven and effective option for these patients, offering rapid and meaningful relief. However, despite its efficacy, uricase therapy remains significantly underutilized with limited market penetration. Yet, even in its current state, the market already exceeds $1 billion, underscoring the potential of the market. NASP, our innovative investigational therapy, is hence a significant opportunity for Sobi. Its monthly two-component uricase regimen is designed to deliver robust efficacy with the need for oral systemic immune suppression. This sets the stage for a deeper dive into the science, the high unmet medical need, and the commercial opportunity. With this said, I hand over to Dr. Baraf. Thank you. Thank you very much, Guido, so I'll be discussing the burden of uncontrolled gout and its pathogenesis. Next slide, please, so gout is a disease that has sort of exploded with increased survivability around the world in terms of life expectancy. It is a chronic inflammatory disease caused by a buildup of monosodium urate crystals, the precipitating salt of uric acid in the blood. This precipitates in the soft tissues and in the joints, particularly in cooler and under-circulated places. Thus, the foot is the site of 50% of first attacks of gout, and over time, these attacks become more frequent. The global prevalence of gout is doubling every 30 years because we're living longer. People with kidney failure and heart failure are on diuretics, which raise serum uric acid levels, and so the prevalence around the world is increasing fairly rapidly. It's worse with age. As life expectancy expands, it becomes worse. The global prevalence of gout is 3.2 x higher in males than in females, but women who hit the menopause begin to have the same incidence of gout as men do, just that men begin sooner, and with the loss of estrogen at menopause, uric acids rise. Next slide, please. So why do these salts precipitate? They precipitate because the blood can only hold so much in solution of uric acid. Uric acid is the breakdown product of DNA, particularly the nucleic acids in DNA, and these break down to uric acid, and it's not particularly soluble, so over a blood level of 6.8 mg per dL, the serum uric acid can't hold onto what's floating around. It begins to precipitate. If you look at this graph, the light blue wedge really represents the accumulation of uric acid over time. To the far left, you have a period of asymptomatic hyperuricemia where the precipitates really go unannounced, but they develop over time. And then all of a sudden, the first attack occurs, and that's represented by the orange spike on the left. And over time, if the serum uric acid is not controlled, these spikes occur more frequently. They last longer. More joints are affected. And as you get all the way to the far right side, you begin to have chronic and persistent gout pain, inflammation in joints, and accumulation of lumps of monosodium urate that we call tophi. If we go to the next slide, please. What's happening physically in patients, it's on the far left side, you have these crystals that deposit. These are crystals seen under compensated polarized light microscopy recovered from a joint. And these crystals are there long before the first attack ever occurs. That central picture is a gout flare. Again, 50% of first flares occur in the big toe, but they can involve any tissue, and in fact, the flares can involve the fingers, the shoulders, the knees, the ankles, and then over time, these collections of monosodium urate become so great that they erupt under the skin. They become visible, so here's the hand of a physician who developed severe gout, uncontrolled gout, because he was on no medications to keep the serum uric acid low, so as long as the uric acid is above 6.8 serum level, it will be precipitating into the tissues. Let's move to the next slide, please. With age come comorbidities, and hyperuricemia is associated with a number of comorbidities. There's a higher incidence of cardiovascular disease. Hyperuricemia is seen in the metabolic syndrome. Whether it's cause or effect isn't clear. This syndrome includes obesity, diabetes, renal insufficiency, heart disease, hypercholesterolemia, and all of the comorbidities that those conditions are associated with, including renal failure. And gout is seen twice as often in patients with chronic kidney disease. And uric acid has adverse effects on the kidney. And the kidney, if not functioning, will cause the serum uric acid levels to rise because the kidneys can't excrete it. Let us go to the next slide. So this accumulation of crystals causes chronic joint pain, unsightly lumps in the patient with uncontrolled gout, social isolation, significant functional impairment, and pain. And here are some quotes on the right. I think the one on the bottom right, "Gout makes me feel helpless. I once had both hands swollen at the same time. Couldn't even pick up a toothbrush or a pencil, count change, button buttons. I had to depend on my wife for everything." And to the next slide, please. How do we treat hyperuricemia? For the most part, 95% of patients do just fine if properly managed with uric acid-lowering drugs, with oral uric acid-lowering drugs. The goal is to lower the uric acid to less than 6.8, to less than 6. In fact, the lower you get it, the more rapidly you can mobilize the deposits, which are the root cause of gout. With first-line therapy, we use xanthine oxidase inhibitors, particularly allopurinol or febuxostat. If that fails, even at maximal doses, we might add drugs that improve excretion of uric acid. Probenecid is the only drug in the U.S. that's currently approved. There have been others. In Europe, benzbromarone is also used. When these fail, both EULAR and the American College of Rheumatology have produced guidelines that say that's where a uricase would fit in, where a pegloticase or Krystexxa would be used. At the moment, that is the only uricase that's available on the market for patients with uncontrolled gout. Let's move to the next slide, please. Here's what uric acid does through the lifetime of the patient with gout. We'll say the lifetime of the patient who's properly treated ultimately with a uricase and then goes back on regular treatment. Uric acid remains high. Eventually, there are clinical manifestations, flares, persistent joint pain, tophi. Some patients don't respond all that well to oral uric acid-lowering therapies, or physicians don't administer them properly in sufficient doses to lower the uric acid, and the patient continues to have problems and they have uncontrolled gout, which brings us to that rough color area where uricase is employed. Now, whereas oral uric acid-lowering therapies will bring the uric acid down to five or maybe four and something, rarely three, uricase drops it to almost unmeasurable levels. Uricase, we know, one of the ways of mobilizing uric acid is to create a gradient between the solid deposits and a serum that has capacity to dissolve uric acid, and the greater that gradient is, the more quickly you may mobilize crystals, but uricase probably has a direct effect on monosodium urate where it's deposited, dissolving it into allantoin, a more soluble substance that's easily excreted. Uricase is given for a period of time until all these significant clinical manifestations of uncontrolled gout come under control. Then patients typically will come off of the uricase and will go back to oral uric acid-lowering therapies, which at that point may be much easier, may work easier to control serum uric acid and keep accumulations from recurring. Let us go to the next slide. By the way, those improvements are rather dramatic. Whereas tophi may disappear over five years with standard oral therapies, we've seen improvement at eight to 12 weeks in the clinical trial setting and as well as in the clinic. If uricase treatment is so efficacious, why is it underutilized? Because less than 5% of eligible patients, it's estimated somewhere between 100,000 and 200,000 patients in the U.S., would be classified as having uncontrolled gout. What limits it to just 5%? Because that's ostensibly the market that pegloticase currently has. Well, there are safety concerns. The word anaphylaxis appears in the pegloticase package insert 46 x. There were infusion nurses when the drug was first approved and marketed who refused to infuse patients for fear that the patients would be having severe unmanageable allergic reactions. The concern was a bit overblown. And over time, we learned that the way you could prevent these attacks is by learning whether or not the uricase was working and the uric acids were being dropped well below one or two. And if the serum uric acids had remained above six, that meant there were antibodies and the drug wouldn't be working. There's some reluctance among physicians when we learned that using immunosuppressants might suppress the development of antidrug antibodies, which then suppress the activity of uricase. There are some physicians who have been slow to learn that they can give standard immunosuppressants to make the uricase more tolerable, but also more effective. Twice-monthly dosing is difficult, particularly for patients who have to travel for care, which is the current prescribing recommendation for pegloticase. There's a shortage of rheumatologists and a shortage of rheumatologists who are familiar with and able to infuse uricases for patients with gout, and that's been an inhibiting factor. Insurance companies with prior-authorization requirements sometimes create an impediment, and some of these patients are just so damn sick from their other comorbidities, their heart disease, their renal disease, their pulmonary disease, that they're just not candidates for a more vigorous therapy, so these are some of the factors that have kept the numbers down, and some of them are clearly fixable, and some of them are structural and not fixable. But certainly, patients derive extraordinary life-changing, transformative benefits from a course of uricase therapy if they've got uncontrolled gout and are suffering all of the consequences of that. And with that, I thank you for your attention, and I move things on to Rehan. Thank you, Dr. Baraf. In the next few minutes, I will provide a higher-level overview of Nanoencapsulated Sirolimus plus Pegadricase, which I will refer to as NASP moving forward, its mechanism of action, and key clinical Phase 3 results. Next slide, please. NASP is an innovative investigational uricase therapy administered every four weeks through sequential infusions of nanoencapsulated sirolimus, which I will refer to as NASP moving forward, and pegadricase, a pegylated uricase enzyme derived from Candida utilis. Since humans lack the production of uricase, this leads to uricases being immunogenic, triggering antibody production, reducing the effectiveness and increasing safety risk. Therefore, it is vital to mitigate the antibody production. First, NASP is infused to provide targeted antigen-specific Treg immunomodulation by inhibiting anti-drug antibodies specifically towards the pegadricase without the need for additional oral broad immunosuppression. Following the completion of NASP infusion, the pegadricase is infused immediately in a sequential manner. Given the immunogenic nature of uricases in humans, pegylation has been added to further mitigate immune response and extend the uricase activity. Now, I will direct your attention to a short animation of mechanism of action of NASP. Next slide, please. Uricases are potent therapeutic agents used for treating uncontrolled gout by rapidly reducing urate levels and monosodium urate crystals. However, they are highly immunogenic, resulting in anti-drug antibodies, which can diminish efficacy. Nanoencapsulated Sirolimus plus Pegadricase, NASP, is an investigational two-component sequential infusion administered every four weeks that begins with the administration of nanoencapsulated sirolimus. Due to their virus-like size, nanoparticles selectively biodistribute to lymphoid organs where they encounter antigen-presenting cells. Next, the pegylated uricase pegadricase is infused, which circulates throughout the bloodstream, reducing urate levels. It also distributes into the lymphoid organs. The co-localization of these two components with antigen-presenting cells introduces pegadricase during a sirolimus-induced tolerogenic window occurring through mTOR inhibition. This is designed to provide targeted antigen-specific T regulatory immunomodulation of effector cells, inhibiting anti-drug antibodies specifically toward pegadricase. Given this proposed mechanism of action, including inhibition of pegadricase-specific anti-drug antibodies by nanoencapsulated sirolimus and reduction in serum urate by pegadricase, NASP is being evaluated as a potential treatment for uncontrolled gout. Thank you. The Phase 3 studies of NASP comprised of two studies, namely DISSOLVE I and DISSOLVE II. The objective of these robust, parallel, double-blinded placebo-controlled studies was to compare the efficacy and safety of NASP administered every four weeks in patients with uncontrolled gout. DISSOLVE I was a U.S. trial, while DISSOLVE II was a global trial. For today's presentation, I will focus on discussing the pooled data from these two studies. There were three arms in each study. The two active treatment arms received sequential infusions of either a high-dose NASP at 0.15 mg per kg or low-dose NASP at 0.1 mg per kg. Within 30 minutes of completion of NASP infusion, patients in both treatment arms received a similar dose of 0.2 mg per kg of pegadricase. Patients in the placebo arm received sequential infusions of normal saline. The primary endpoint in the DISSOLVE program was defined as maintaining sUA target for at least 80% of weeks 21-24. During my presentation, I will also cover key clinical endpoints, including mean sUA reduction, gout flare incidence, and reduction of tophaceous burden. Next slide, please. When looking at the primary endpoint in the overall study population, a statistically significantly higher proportion of patients in the NASP treatment arms maintained sUA control compared to those in placebo, with 51% and 43% of patients in the high and low dose of NASP, respectively, achieving the primary endpoint versus only 8% in placebo. Next slide, please. This graph demonstrates the trajectory of rapid and sustained reduction of sUA levels for those patients who were on treatment during each dosing period. The y-axis denotes mean sUA level in milligrams per deciliter, while the x-axis shows time in terms of study visits done to assess sUA levels. The dashed black straight line in the middle of the graph denotes sUA clinical goal level for guidelines of 6 milligrams per deciliter. In comparison to the placebo group in black, patients on high and low-dose NASP had a rapid and sustained reduction in sUA within one hour of the first infusion, corresponding to a 94% and 95% reductions in sUA from baseline, highlighting the potency of pegadricase. When looking at subsequent treatment periods, those who maintained an active NASP treatment were able to maintain the low sUA levels, while this was not the case in the patients in the placebo group, demonstrating the durability of NASP. Next slide, please. An increase in the incidence of gout flares is commonly reported by patients starting on urate-lowering therapies due to the mobilization of urate crystals. For those patients who were on treatment during each dosing period, the percentage of patients who reported at least one gout flare during the first 12 weeks was similar between the active and placebo arms. This finding suggests that NASP does not worsen disease burden. As the study progressed, there was a reduction in patients reporting gout flares in the high-dose or low-dose NASP arms as compared to placebo. This ultimately led to 95% and 94% of patients on high-dose and low-dose NASP being flare-free by the end of the study. Given that uncontrolled gout patients suffer from more frequent, painful gout flares, the possibility of a treatment that does not increase these events while reducing disease burden may be positively viewed. Next slide, please. To address the impact of NASP on progression of disease burden, we photographically examined changes in tophaceous burden as compared to baseline, specifically looking at clinically meaningful complete resolution of tophi which was defined as 100% reduction in the area or complete disappearance of the tophus without enlargement or any existing tophus or no new tophi. In patients who received six doses of treatment, 49% in high-dose NASP, 70% in low-dose NASP, and 5% in placebo achieved a complete resolution. This equates to roughly a 10 to 14-time complete resolution of tophi with NASP versus placebo. On the right side of the slide are photographs of hand and foot of an uncontrolled gout patient on high-dose NASP who received all six doses. As depicted at baseline, they have large visible tophi which are completely resolved after receiving all six doses. All the clinically relevant results presented here highlight that when patients are being responders to NASP, it is effective in reducing disease burden, including sUA, flares, and tophi. Next slide, please. Patients with uncontrolled gout have a twofold higher risk of developing CKD than those with controlled gout. When assessing response rates in the DISSOLVE subgroup of patients with stage 3 CKD, a significantly higher proportion of patients in the two active NASP treatment arms maintain sUA control compared to those in placebo, equating to 52% and 61% of patients in the high and low dose of NASP, respectively, achieving the primary endpoint defined as maintaining sUA target for at least 80% of weeks 21 to 24. When looking at the right side, overall stage 3 CKD patients on NASP treatment experience slight improvement in kidney function compared to a slight decline seen in placebo patients. Next slide, please. On this slide, I will be reviewing the adverse events of special interest. Notably, no difference was seen in gout flare incidence between NASP treatment and placebo groups. In addition, infections, hypertriglyceridemia, and stomatitis are known adverse events attributed to the sirolimus component of NASP. There was a slight imbalance in infections between high and low-dose NASP. However, given that the study was run during the COVID pandemic, you can see that there is no difference in the COVID-19 infections among the treatment arms in placebo. Also, the rate of hypertriglyceridemia was similar among the three study arms. As anticipated, the high dose had a higher rate of stomatitis compared to low dose. However, all events were mild to moderate in severity. Majority did not require any treatment, and none of these events resulted in treatment discontinuation. Low incidence of infusion reactions, 3.4% versus 4.5%, were observed in the high and low-dose groups, which reflects a total of seven infusion reactions across both treatment groups. These infusion reactions resolved after cessation of study drug and supportive therapy. None of these infusion reactions required intubation or hospitalization. This validates the rationale for choosing the specific doses of NASP. Finally, no major renal, cardiovascular, or hepatic safety signals or risks were identified with NASP therapy. Generally, NASP was a well-tolerated therapy. Overall, the innovative mechanism of action of NASP, combined with substantial improvements in key clinical outcomes and safety profile, offers a promising potential treatment alternative for people living with uncontrolled gout. With that, I will hand it over to Guido. Thank you. Thank you so much, Rehan. And please turn to slide 25. This slide outlines our strategic roadmap for NASP as we move from regulatory submission to launch readiness. It's a critical journey, and every step is designed to ensure that we maximize the impact and deliver value to patients and stakeholders. We have now completed the submission and received acceptance notification last week with a targeted PDUFA date of June 2026. This gives us a clear timeline to prepare for a successful launch and to ensure that we are fully prepared. We have identified four key areas of focus. First, we are working to highlight the significant unmet medical need in this space and the current underutilization of uricase-based therapy. This sets the stage for NASP relevance. Second, we are strengthening the belief in NASP efficacy and its unique clinical profile. Our data supports a differentiated value position, and we want to ensure that the message resonates clearly. We will continue to publish data and can even expect more data from pivotal programs at the upcoming ACR Congress in October. Third, we are actively addressing financial and logistical barriers to treatment. And finally, we are focused on optimizing the experience to customers, caregivers, and physicians. Altogether, this will pave the way for a successful launch and long-term adoption of NASP. Please turn to slide number 26. This slide illustrates the compelling market opportunity for uricase therapy in the treatment of uncontrolled gout. Despite the large prevalence of gout, uricase remains significantly underutilized, presenting both a clinical and commercial opportunity. In 2023, approximately 7.1 million people in the U.S. were diagnosed with gout. Of those, roughly 100,000 were diagnosed with uncontrolled gout and actively managed by specialists, which is critical for identifying candidates for advanced therapies. And finally, we arrive at the core addressable population of around 15,000 patients who are most likely to benefit from uricase treatment. These 15,000 patients represent the core opportunity for uricase-based interventions. Less than half are on treatment with uricase today. Just remember that this subset of patients creates a market exceeding $1 billion annually, with room for significant growth. Please turn to slide 27. Even though the filing is now complete and our goal is to ensure that NASP reaches its full potential clinically, commercially, and globally, we have a robust lifecycle management strategy in place, and we have significant opportunities for market expansion. In terms of lifecycle management, we are focused on enhancing NASP product profiles. This includes ongoing data generation that could improve outcomes. We are addressing the unique needs of several special populations with uncontrolled gout. Additionally, we are focused on optimizing the experience for both patients and providers. That means improving support services and ensuring that NASP is easy to access and administer. In parallel, we are evaluating market expansion opportunities. We see significant opportunities in countries such as Japan, Brazil, the Middle East, and Canada, and we are also exploring opportunities for Europe and other key markets moving forward. Please turn to slide 28. You will remember the slide form from our quarterly calls. NASP is an important growth driver for Sobi, and we are launching actually two major, we have two major launches in 2026: Aspaveli and NASP, showing you the unrepresented opportunity or the unprecedented opportunity for Sobi in the year to come. We are very excited to launch both products: first, Aspaveli in January in Europe, and then NASP during the mid of 2026. Please turn to slide 29. To close, we have reached an important milestone on the journey of NASP to deliver meaningful outcomes for patients while minimizing treatment burden in uncontrolled gout. NASP has demonstrated rapid and profound reduction in serum uric acid level, a critical therapeutic goal for uncontrolled gout. Beyond serum uric acid levels, NASP has shown significant clinical benefits. Patients experience less flares, reduction in tophi size, and overall improvement in quality of life. These outcomes speak to the real-world impact of NASP that NASP can have. This is delivered with a low treatment burden as NASP is administered in a sequential monthly infusion and does not require broad systemic immunosuppression. This simplifies the treatment regimen and reduces the burden for both patients and providers. We are targeting a U.S. launch, as mentioned, mid of 2026, and preparations are on the way, supported by a robust lifecycle management plan to maximize this opportunity. NASP represents a major advancement in the treatment of uncontrolled gout, combining efficacy, safety, and convenience. We are excited about this potential to transform care in uncontrolled gout and improve lives. So with this there, you can sense we are truly excited about this forthcoming launch. We would like to give back to the operator, and we will open the floor for questions. Thank you, sir. We will now begin the question- and- answer session. Anyone who wishes to ask a question may press star and one on the telephone. You will hear a tone to confirm that you have entered the queue. If you wish to remove yourself from the question queue, you may press star and two. Questions on the phone are requested to disable the loudspeaker mode and eventually turn off the volume of the webcast while asking a question. Anyone who has a question may press star and one at this time. Our first question comes from Gonzalo Artiach from Danske Bank. Please go ahead. Hi, and thank you for taking my question, Gonzalo Artiach from Danske Bank. I have two for Dr. Baraf. The first one is on the comparison between Krystexxa and NASP. We know that from a response rate endpoint perspective, the compared study did not show a statistical difference between the two drugs, but NASP patients showed lowering levels of serum urate maybe faster than Krystexxa. So how would you compare these two options? And the second question also for Dr. Baraf, it seems that on paper, Krystexxa combined with methotrexate, which is already approved, that combination hasn't improved the efficacy profile versus monotherapy. But you said there that there is some reluctance on the use of this combo in the clinic. In your practice, what proportion of patients eligible for uricase treatment would you put in the combination therapy and in monotherapy? What would be your go-to patient group, treatment-naive patients for NASP or patients that do not respond properly to this methotrexate combination? Thank you very much. Let me see if I can repeat all the elements of those two questions. In the comparative study, to me, what struck me, first of all, the comparison was between NASP and pegloticase without methotrexate. The primary endpoint was patients who achieved superior results in both the three- and six-month periods. NASP just missed superiority for the combination result, but at the three-month result was superior. If you look at the time of uric acid suppression in NASP, there was a superior outcome through probably the fourth month, and then the loss of efficacy of NASP came up to the same level as the loss of efficacy with pegloticase. At least that's how I interpreted it, and it's the difference in the two curves that probably would indicate that even if the patient didn't sustain a superior outcome at six months, I think it was numerically superior, that period of time of difference likely led to a significant difference in the amount of urate burden at the end of the treatment period, so my impression is that NASP performed superiorly in that setting. The practical question, who's going to get NASP as a first option and who's going to get pegloticase? I think pegloticase will still take the lion's share for a few reasons. One is that it's been in the marketplace and people are comfortable with it, and certainly in the first few years. But the advantages for a four-week versus a two-week are those of convenience. There's a maldistribution of rheumatologists in the United States, and in addition to that, there's an inadequate supply of rheumatologists. And these would be the people who would be administering the drug. So patients who have to travel a distance will find an every four-week option better than an every two-week option. It's conceivable that pegloticase will get an every four-week indication. And then how does it differ? I think the main difference would be, well, the initial difference would be, is the patient a good candidate for methotrexate? Does the patient drink? Is the patient reliable enough to take their co-therapy, their methotrexate, on a regular basis and not skip out on doses? NASP gives the doctor 100% control of the treatment end-to-end where you're relying. I don't think rheumatologists are at all worried about methotrexate, except for the compliance issue and for the occasional patient, not so occasional in the gout population with an alcohol problem or with liver function abnormalities, so I think that's how it will sort out, and overall, I suspect that having two drugs in the market (oh, and the last one) is that both drugs are immunogenic. Once immunogenicity is established, neither for either drug, the drug is no longer valuable, and although we don't have any data or any knowledge about cross-reactivity, we don't see cross-reactivity with other biologics that have similar mechanisms of actions. For example, TNF inhibitors. There's no cross-reactivity of immunogenicity with the monoclonal antibodies used to inhibit TNF. So I think there's clearly a niche for a new entry and a niche for an alternative, a niche for patients going from NASP to pegloticase or pegloticase to NASP that will probably be tested in the marketplace, not necessarily in the clinical trial world, but as a practical consideration. These patients are fairly desperate, and desperate patients require desperate measures. I hope that helps. Thank you very much. The next question comes from Mattias Häggblom from Handelsbanken. Please go ahead. Thank you so much. I have two questions for Sobi, I guess. And the first one is the platform input has never been manufactured in larger commercial volumes. Can you talk about your confidence in the CMC package and if you could remind me how and where you intend to manufacture NASP and the status of any FDA audits? And then secondly, in 2020 at the CMV in December, you described the peak sales potential of the project at the time called SEL-212 as SEK 3 billion-SEK 5 billion in dollar terms at the time, $350 million-$600 million roughly. Is that still how you feel about the opportunity five years later, or how would you describe it? Thanks so much. Yeah. Let me start with the easy one, Mattias. I think we see the opportunity probably in the higher end of that range. So if anything, we are more confident about it, and we feel that we have the manufacturing process under control. We spent extensive time. I mean, for me personally, the development of SEL-212 and now NASP has been. It was not an easy journey, but it was a very rewarding one because the team has done a spectacular job and spent a lot of time on clinics, but clinical development, but also on CMC development and worked with our partners. And this is at the end now to bring all of this together is very gratifying. I mean, maybe I ask Matthew who is the champion of NASP in our company, maybe how he sees the end-of-year situation and how confident is he that we can bring this product to the market. Yeah. Thank you, Guido, and thanks for the question. As Guido quite rightly mentioned, we have various partners globally that combined will help us pull not only the supply chain but obviously available products ready, in particular for the first half of next year when the anticipated U.S. launch could take place. Our technical operations team has been very close to our partnerships. We've got a very good relationship with all five. We've been looking at site inspections. We've also been staying very, very close to what those audits are reading out. From From a mock perspective, we feel very confident around the current situation that we're in. Clearly, now that we've initiated the BLA and we've heard positive feedback from the FDA, those audits will now start to take place. We feel ready for those. Our partners feel ready for those. Although obviously it's going to be a big ask, we remain very confident that the supply chain will stay robust and that we will be prepared, ready for that first-half launch in the U.S. Thanks, Guido. Thank you. Thank you so much. Very much. Thank you. May we move to the next question? The next question comes from Michael Leuchten from Jefferies. Please go ahead. Thank you very much. Two questions, please. One for Dr. Baraf. Just going back to phasing of products, just interested in the data that you showed on eGFR and the active versus control are quite compelling. I suspect whether that's a spot estimate or just looking at the eGFR slope, that's quite a strong argument to use the product earlier than existing alternatives. Just going back to your comment that pegloticase will remain as the first-line option, why wouldn't the data in and around the existing comorbidities push for early use already? And then I guess related to that, what's the clinical burden of proof now for these comorbidities? Does it require CV outcome trials, or do you think there's enough data to make that case for the comorbidities? And then question for Guido, just in terms of market access expenses, how do we think about the phasing of those as we head towards the June 2026 PDUFA? Yeah. Maybe we start with the first question. Yeah. Sorry. I'll tackle the first question. I think the central part of that question is why do I think pegloticase will take the lion's share? Certainly in the short term because of familiarity and comfort on the part of physicians who've already used it. That would be, and perhaps the response rate if you look at the two of them. But it's mostly familiarity. They're in the marketplace. Who would be adding to it? And the numbers are small. They may very well be significant. I'm a person who performs clinical trials. I don't write them or strategize which ones to support. So I can't tell you if the company would be doing a deeper dive there. I do know that the data was looked at with pegloticase because I was involved with that, and for that matter with febuxostat. And despite robust lowering of serum uric acid, there was no clear renal benefit demonstrated in either of those development programs. So I think mostly out of habit, you're the second entry into the market. It usually takes a bit of time to get established, particularly with a, almost called it a boutique-type therapy like this where there's a limited market and a limited number of specialists who engage in it. Yeah. Thank you. And maybe I just cover, we are building obviously a formidable team right now. We have already a core in place. We were waiting obviously for the confirmation on the BLA side. Now we plan for an appropriate launch. We will have the respective team size. You're looking at a team that is not dissimilar to what we have built up for Synagis at the time. And we think that for the kind of focus we will lay upon this product and the segmentation, we see a significant opportunity as Dr. Baraf was outlining in segments such as CKD patients, for instance, and others. And this gives a pretty large opportunity for us. Then there is this blue ocean of patients that could benefit from the product for many of the uricase cases but not getting it. In a way, increased noise level should help the class as well as us. Yeah. That's really how we are thinking about it. It's a significant undertaking. Hence, I just want to reiterate this because it was a bit misunderstood. We have tightened the belt this year in areas that are not as core to us as in the past to make sure that we can meet in a way earnings expectations as well as give proper justice to the investment into the product. Thank you. I want to just add one other thing. There have been studies with pegloticase in patients with renal failure and studies with pegloticase in patients with renal transplants. Those are patients who wouldn't be able to take methotrexate. Methotrexate's contraindicated in patients with severe renal disease. So that might be a group of patients that Sobi might focus on. I haven't had any discussions with Sobi, so I'm just sort of freewheeling here. But that would be an area where there'd be an advantage for NASP. Thank you. Next question, please. As a reminder, if you wish to register for a question, please press star followed by one. The next question comes from Kirsty Ross-Stewart from BNP Paribas. Please go ahead. Hello. Thank you very much for taking my questions. One for Dr. Baraf, just on kind of duration of treatment, I wonder if you could kind of just elaborate a little bit on the typical duration of treatment for uricase before going on to oral maintenance therapies and kind of the rate of patients who actually end up needing to go back on the uricase? Is that something that happens? Maybe a bit of color around that. And expectations maybe from Sobi's side on NASP, I know that you said you kind of fixed doses in the trial, but is there potential that the label allows kind of more doses than that? Is it kind of treat to a certain level of serum uric acid reduction? And then maybe just a question on the opportunity kind of outside of the U.S. You said that you're kind of evaluating the opportunity in Europe. Can you maybe talk to some of the considerations that you're making there and kind of what are the challenges and differences versus the U.S.? Thank you very much. So I'll address the duration and the retreatment questions. Duration-wise, when I was doing phase 2 trials for pegloticase about 15 years ago now, we reported two patients in a 12-week trial that had complete resolution of tophi. It was something that the company was looking at a high level of infusion reactions, about 40%, and they were looking at an 80% gout flare rate. And they were asking themselves, "What the hell are we doing with this stuff?" And then I sent them these two photographs from my Palm Zire 71, 1.2-megapixel camera before and after photos and showed tophi resolution at 12 weeks. My initial impression was that you really don't need this type of treatment for more. Maybe six months is the duration of treatment you need before you bring them back down to a controllable level with uric acid lowering therapies. Then I saw more severe patients who had more sustained tophaceous deposits. But it's rare that a patient with the most extraordinary deposits will need more than a year of treatment. So that's the duration question where you eliminate the clinical manifestations of the disease. At that point, remember, uric acid comes from two sources: diet, about 10%, and breakdown of DNA, about 90%. And uric acid is eliminated about 70% or 80% through the kidneys and maybe 10%-20% through the gut. So when a patient has tophi, where does the uric acid come from? It comes from the diet. It comes from the breakdown of DNA, body DNA, blood cells, lining cells, skin cells, but it also comes in the uncontrolled gout patient from the tophi themselves. So you've got three forces adding uric acid into the serum, and after you've treated patients and debulked them, you have two sources, so they should be easier to control. Oral therapy in gout management by primary care is terrible. We didn't talk about the untreated patient who comes to the uncontrolled gout physician or the undertreated patient. In truth, if xanthine oxidase inhibitors were given correctly, which they probably never will be, the size of the uncontrolled gout population would be much smaller, but now the patient's under the focus of the specialist, and once they achieve the clinical outcomes that the specialist is looking for, it's not that difficult to control the serum uric acid with oral drugs. So the next question, retreatment, once antibodies form against the drug, which may occur after the therapy has stopped, you don't get treatment responses back. Sobi hasn't examined this question. Savient then Horizon, now Amgen, has evaluated this question. Actually, originally, Savient and retreatment just doesn't work. Patients have antibodies. They tend to react to the drug. And you can't eliminate those antibodies once they're formed. So retreatment is not an option. And that's why if a patient needs retreatment, a switch to having an alternative may be not known to be, but may be a viable alternative. Thank you, Dr. Baraf. With regard to the questions related to the study, maybe Rehan, you want to comment? Definitely. Thank you, Guido. As far as the DISSOLVE I and DISSOLVE II studies were concerned, as I mentioned, they were mirror studies of each other. But the difference between DISSOLVE I and DISSOLVE II were the study durations. DISSOLVE II was a six-month study evaluating the primary endpoint, while DISSOLVE I was the same. However, it also had a six-month extension. So in addition to the initial six months of treatment, patients are followed up for an additional six months for safety and efficacy. So a total of 12 months duration. And both data for the six-month pooled data for DISSOLVE I and DISSOLVE II, in addition to the long-term extension, have been submitted to the FDA for their evaluation. Thank you. Thank you, Rehan. And with regard to Europe, I mean, first of all, our business case is built on a successful commercialization in the United States. And that basically prompted our guidance. The markets that we have indicated, singled out, are the markets where we clearly see a path forward already. With regard to Europe, we still have to do some more work with payers to basically understand whether we can get an adequate price, particularly in today's world where potentially price comparisons with other OECD countries may be performed. But it is not essential for the economic case of this product. Next question. Ladies and gentlemen, that was the last question. I would now like to turn the conference back over to Guido Oelkers for any closing remarks. Yeah. First of all, I'd like to thank Dr. Baraf for his comments and for his presentation. Obviously, it's an honor to have such a distinguished expert in the field as part of our presentation. And I'd like to thank everybody for their keen interest. But as you can see, there are quite a bit of opportunities for us. And we try, obviously, to make a significant impact. Whether we stay in a junior position or not, time will tell. But I can reassure you that the team is very excited and very motivated to make a difference in chronic refractory gout. On this note, I wish you a great day and look forward to staying tuned. Thank you.