Good afternoon, everyone, and welcome to the Vor conference call discussing the telitacicept China phase III short-term results. At this time, all participants are in listen-only mode. There will be a question-and-answer session to follow. I would like to introduce the company. Thank you, and good afternoon, everyone, on the call. Earlier today, our collaborator, RemeGen, presented a late-breaking poster at ACR Convergence on their phase III study evaluating telitacicept in primary Sjögren’s disease. Vor’s press release and presentation for today's webcast can be found on the Investor section of the company's website. Before we begin, please note that we'll be making forward-looking statements during this call. I refer you to slide two for the full disclaimer. On the call today, we have Jean-Paul Kress, our Chairman and Chief Executive Officer, Qing Zuraw, our Chief Development Officer, and Dallan Murray, our Chief Commercial Officer. We'll also be joined by Professor Ronald van Vollenhoven, the former Chair of the Department of Rheumatology and Clinical Immunology at the Amsterdam UMC, and Member Elect of the EULAR Executives. Sandy Mahatme, our Chief Financial and Business Officer, will also be available for the Q&A session following the prepared remarks. I will now turn the call over to Jean-Paul. Thank you, Sarah, and good afternoon, everyone. We are very pleased to speak with you today regarding the results from the primary Sjögren’s disease phase III study in China, evaluating telitacicept, our fusion protein therapy targeting BAFF and APRIL that we in-licensed from RemeGen and, importantly, the most advanced BAFF/APRIL inhibitor in the world. For this trial, not only were the primary endpoints and all secondary endpoints met, but we believe this data demonstrates that telitacicept has the potential to be best in disease in this indication, as well as myasthenia gravis. Now, before we jump into the Sjögren’s data, we wanted to highlight on slide four the oral presentation tomorrow at AANEM, highlighting the 48-week open-label extension data from RemeGen’s phase III study in China, evaluating telitacicept in generalized myasthenia gravis. Like the data we’ll be presenting today, we believe they are highly differentiated and have the potential to redefine how clinicians will treat myasthenia gravis. As a reminder, earlier this April at AANEM, RemeGen presented 24-week top-line data from this trial, demonstrating a historic sustained reduction in MG-ADL. Tomorrow, we believe the conversation will begin to shift. With telitacicept, we are demonstrating deep sustained improvement through 48 weeks. This represents a potential disease modification. I would also like to briefly mention the recent publication of the China phase III data in SLE in the New England Journal of Medicine, which further reinforces the differentiation of telitacicept’s dual BAFF/APRIL approach. For the first time, a therapy in a phase III trial is delivering more than double the clinical response seen with the current standard of care in lupus. This is with true B-cell modulation versus immunosuppression or immunoselective targeting. Now, let’s jump into the ACR data. What you are about to see represents an important moment for the field. For the first time in Sjögren’s, the therapy has shown clear statistically significant and clinically meaningful efficacy, demonstrated by placebo-adjusted ESSDAI reduction of 3.8 and ESSPRI reduction of 1.5, with a safety profile that was consistent with previous telitacicept clinical trials and vast commercial experience. Importantly, in this trial, the only background therapy allowed was hydroxychloroquine, a mild symptomatic agent that does not influence the core disease biology ESSDAI or ESSPRI. No DMARDs, no steroids, so what you see here is a true potential effect of telitacicept, a real signal of a placebo. Across both physician and patient-reported outcomes, telitacicept delivered consistent, statistically significant improvement through 24 weeks and 48 weeks, and did so with a favorable safety profile. In a space where global trials often rely on immunosuppressive background drugs, these results set a new benchmark for what meaningful efficacy in Sjögren’s disease could look like. If we turn to the next slide, what makes this data set so compelling is the alignment and the separation from placebo. Patients are feeling better faster; nearly 90% report improvement, while physicians confirm meaningful disease control in three out of four patients. ESSDAI captures organ-level disease; ESSPRI reflects fatigue, dryness, and pain, what patients actually live with day to day. The fact that patients are improving even beyond the ESSDAI signal suggests that the drug is reaching the core biology of this disease. Competitors have struggled to move both measures together. Telitacicept is demonstrating clear clinical activity, and importantly, these effects are observed without confounding background therapies. This represents a meaningful and measurable benefit for patients. Telitacicept is a fusion protein that targets both BAFF and APRIL, the two key survival factors for B-cells. By blocking these pathways, telitacicept does not deplete the immune system. It restores balance. It quiets the overactive B-cell signaling that drives autoantibody production while preserving normal immune defense. This balance is especially important in primary Sjögren’s disease, where unchecked B-cell activity not only drives autoantibody production but also contributes to an increased risk of B-cell lymphoma, highlighting the need for true B-cell modulation rather than simple antibody clearance, as with FCRN inhibition. The dual inhibition is what delivers the consistency we are seeing across every endpoint. What makes telitacicept unique is not only what it targets; it is also how it is built. Unlike engineered fragments or truncated constructs, telitacicept nearly preserves the full native TACI binding domains, the N-terminus and CRD1 and CRD2, enabling natural engagement with both BAFF and APRIL. We believe this design delivers stronger, more selective binding and contributes to the clean tolerability we have seen across thousands of patients. Telitacicept is a validated molecule with an established clinical foundation across multiple indications, with the potential to be a pipeline within product. In China, the therapy is already redefining success in autoimmune disease, with three commercial approvals in lupus, rheumatoid arthritis, and myasthenia gravis, and tens of thousands of patients have been treated in the real-world setting. The consistency of efficacy, the strength of the safety profile, and the scalability of manufacturing give us tremendous confidence in expanding the clinical development globally, starting with myasthenia gravis today and Sjögren’s next. Now, before we dive further into the data, I'd like to hand the call off to Professor Ronald van Vollenhoven, Professor of Rheumatology at Amsterdam UMC and Member Elect of the EULAR Executive, to provide a brief background of Sjögren’s disease. Hello, everyone. It's a great pleasure to be here. My name is Professor Ronald van Vollenhoven, and I'm speaking to you from Amsterdam in the Netherlands. It's always a pleasure to be able to connect over large distances, thanks to modern technology. Of course, it would be even nicer to meet you in person, and I'm hoping for maybe a future opportunity. Today, I would like to speak with you about Sjögren’s disease, and I will try to convince you that this is indeed a major unmet need, a disease that has maybe been underestimated in terms of the impact it has on people's lives. It's also a fairly common disease, and it's a disease with many medical repercussions, and hopefully, in the future, also more that we can do about it, better treatments. The next slide shows my disclosures, and then after that, I would like to give you a general introduction to Sjögren’s disease. In the short time we have, I can't do it full justice, so I just will give you the highlights, what I think are the most important points to take with us. It will be about Sjögren’s disease, but towards the end, I will also tell you that it has similarities to another disease, systemic lupus erythematosus, and how that has impacted also our understanding of the disease, but also in terms of our ability in the future, hopefully, to be better and better at treating patients and giving them the relief they deserve. On slide three, we see that Sjögren’s disease is indeed a multi-organ systemic autoimmune disease. We think of it as the disease with the dryness of the eyes and the mouth, but in fact, it has many other manifestations, and it occurs in the whole body. The cartoon drawn up here in the review article that was published seven years ago by Xavier Mariette from France and his colleagues actually shows that in detail. On the next slide, I'm going to take you on a little bit of a historical trip. This disease is named after Henrik Sjögren. He was a Swedish ophthalmologist, an eye specialist, and around 1950, he described a syndrome. I have worked in Sweden for many years. I'm from the Netherlands myself, but I've worked in Sweden many years, and my Swedish colleagues will never forgive me if I do not at least once tell you the correct pronunciation of the name, because it's not Sjögren. It's not Sjogren, and it is in Swedish different. Maybe you'll find it interesting because I do not speak, unfortunately, the language of China, but I've understood that it is a language where the level of the tone is important. This is actually the same in Swedish, and so it's not Sjögren, it's Sjögren. The name of the ophthalmologist was Sjögren. We don't say it that way because in English, that's not very practical, but that's correct. It was called a syndrome for many years, for decades. Now, people have said that it's maybe better to consider it a disease, that we should maybe speak about it as Sjögren's disease, and that's what I will do. After the initial description by Henrik Sjögren, that was already more than half a century ago, it became clear that this is a disease that's not so unusual. The incidence and the new cases are about 1 in 10,000. The prevalence in the population is almost 0.5%, going to some even more. That is a bit subject to how it is defined. In Sjögren's original description, the eyes were very important because as an eye specialist, he noted that there were patients with very dry eyes and also suffering the consequences of those dry eyes in the form of a keratoconjunctivitis sicca, meaning that the layers of the eye also get inflamed. He noted that these patients often also had a dry mouth, and he also described the arthritis that's often accompanying these symptoms. He also pointed out that there were many more women with this disease than men, and that has actually been borne out in study after study. It is among the autoimmune diseases with the very high female-to-male ratio, in some studies, 9:1. The disease can actually start at an early age, and it's correctly pointed out here in this slide that it can start already in the third decade of life, and then there's another peak in incidence around the time of menopause in female patients. The disease is associated with autoantibodies, particularly the ones that are also named after Sjögren's syndrome, SS, SSA, and SSB. They have also been identified as anti-Ro and anti-La. For this disease, there are criteria to help classification, and I'll get back in a moment on what they are. First, on the next slide, I want to point out that there is also a histopathology associated with this. The histopathology is found in the glands that supply the eye or the mouth, especially. Most of the studies are done for practical reasons on the minor salivary glands, in the lip, sometimes also on the major salivary glands, the parotid glands, and only very rarely in the lacrimal gland. In all these cases, what is found pathologically is a lymphocytic inflammation. It says on the slide inflammatorium, but it's, of course, inflammation, and that is characteristic and can actually be considered pathognomonic if it's very, very clear. This is a histopathology that suggests an autoimmune disease. There are other reasons that we think of it as an autoimmune disease, more of which in a moment. First, on the next slide, I want to point out that there are these criteria. I mentioned them already, the ACR EULAR criteria from 2016. Here you can see what they are. The biopsy with that particular histopathology gives you three points. The positive antibodies over the anti-Ro type, they give you three points. There are some other items, the eyes, that can give you one point, and the salivary flow can give you one point. That's how you get to the classification, but do not forget that the classification is not the same as making a diagnosis. The diagnosis is very much part of the medical thinking and medical skills. Sometimes the patient really does have the disease, but they do not meet the criteria according to the classification, and also the other way around. These can nonetheless be very helpful, these classification criteria, and of course, in clinical trials, they should be used. Now, on slide seven is an overview of all the autoantibodies that can be seen in Sjögren’s disease or Sjögren’s syndrome. Here, it's abbreviated PSS, primary Sjögren’s syndrome. Within a moment, I will also tell you why that name is not so good anymore. What you can see here is that many patients have the antinuclear antibodies. Many have the anti-Ro and anti-La antibodies. Maybe if you're very good, you will see that it can be higher, the percentage can be higher than for the antinuclear antibodies. You might say, "Wait, wait, how can the anti-Ro be positive and the ANA negative?" Because the Ro antigen is in the nucleus. It turns out you're right in most cases, but not always. Sometimes the Ro and La antigens can actually be found in the cytoplasm. If the suspicion for Sjögren’s is very high and the antinuclear antibody test is negative, it's actually worth it to ask the lab to specifically check for the anti-Ro and anti-La staining in the cytoplasm. Other antibodies that are found in patients with Sjögren’s disease are the rheumatoid factor in up to 75% of the patients. In some patients, cryoglobulins, but that would often be already in the transition to lymphoma, which is a serious long-term consequence. Antiphospholipid antibodies and then some other antibodies that are maybe found more in the experimental setting. There is also the absence of some antibodies that are more typical for other diseases. That is also illustrated here on the same slide where the antibodies are given for systemic lupus erythematosus. You can see that there are other antibodies such as anti-DNA and anti-SM that would not be seen in Sjögren’s. On the next slide, there is a little bit about terminology because, as I already said to you, it used to be called Sjögren’s syndrome. Now we really talk about Sjögren’s disease. It used to be called primary or secondary. The idea was that, "Okay, if you just have it, then it's primary. If you have rheumatoid arthritis and then you get it, or you have systemic lupus and you also get these typical symptoms, then it's secondary." That is so confusing because sometimes the one comes first and sometimes the other comes first, and sometimes they emerge at the same time. Nowadays, it's actually considered that you have or you do not have Sjögren’s disease. If you also have another rheumatic disease, then it's an overlap. Of course, in rheumatology, we know that there are many overlap situations. Many patients have more than one diagnosis correctly made. It would be an overlap between Sjögren’s and something else. There is also the important distinction between the glandular and the extraglandular manifestations. I've already talked to you about glandular, the glands of the eye, the lacrimal gland, the parotid glands, the minor salivary glands. They all contribute to the mouth and then to the dryness of the mouth if they are dysfunctional. There are also other exocrine glands that are involved. For this reason, sometimes Sjögren’s disease is described as an autoimmune exocrinopathy. There are also extraglandular manifestations. There are some manifestations that you really cannot attribute to a gland, for example, arthritis, which can be a feature of Sjögren’s disease, and also polyneuropathy. For these manifestations, it may not be so correct to speak of an exocrinopathy. Some have suggested, including [Skopouli], that it should be called an autoimmune epitheliitis because that's very distinguishing that the epithelium also is subject to the autoimmune attack. These terminology things are difficult because they reflect, to some extent, that we do not completely understand the pathophysiology sufficiently well to make a very definite comment on that. On the next slide, slide number nine, I will point out that there are these many symptoms, and many of them we have already mentioned now today. There are a few things that for the patients can be very important and that nevertheless are not always respected so much. The patients will often say that the worst thing about this disease is how tired they are, how they're chronically fatigued, and how they cannot think straight. Brain fog is something they sometimes say. There are many other symptoms. This is really from the perspective of the patient also on multi-system disease, a generalized disease, a disease that affects them in many ways, and it does make life very difficult. It's not deadly, although it can transition to lymphoma, which can be deadly. Sjögren’s is certainly a disease that has associated with it a very profound decrease in quality of life. The next slide also shows this in terms of the many symptoms that the patient can have, including, as mentioned, the fatigue, the mental fatigue, also pain in the joints, vascular dysfunction, etc., and the dryness symptoms. This makes it also difficult to do a proper assessment because how do you measure something that has so many different manifestations? It has been a concern because if you do a study, you have to be able to put it in numbers. For this reason, the task force many years ago devised something called the ESSDAI, and this is on slide 11. You can see that one of the members of the task force was Professor Hendrika Bootsma from the Netherlands, and the other learned colleagues were part of it. They decided that in the assessment of Sjögren’s disease with an activity index, it should be based on eight different organ systems. They are shown here in pictures. This led to the development of the ESSDAI, and it has stood the test of time. It's used in many studies and clinical trials, and it turns out to reflect very appropriately what's happening to the patient. On the next slide, you can see what those components are. Each of those components has a certain weight. They can be severe, moderate, or mild, and then they get three, two, or one point. You add up all the points to get the final ESSDAI score. This is a useful measure, and it can be used as the primary endpoint in clinical trials, as it has now indeed been done on a number of occasions with positive and convincing results. For the last part of my talk, I want to go to the next slide, which is slide 13. As I already mentioned, many rheumatic diseases can overlap, and there is certainly overlap between primary Sjögren’s disease and some other rheumatic diseases, including systemic lupus erythematosus. This may be relevant for the therapeutic future. If we go to the next slide, we see a little reminder that lupus is the disease that's characterized by the wolf, because lupus means wolf in Latin, but also by the butterfly because the butterfly rash in the face is one of the characteristic symptoms of lupus. Lupus is a multi-system disease. On the next slide, you can see that it has persistent disease activity, but it also has to be treated, and the treatments may also have side effects. All of this can lead to organ damage. In the end, what this leads to is a decreased quality of life. There is further damage that can be decreased work productivity. In fact, the patients may die earlier as a result, not so much of the disease itself, although that does happen, but also the consequences of the disease. In a very recent article that was published in the New England Journal of Medicine, just very recently indeed, we saw the results of a treatment for systemic lupus erythematosus that, from the perspective of someone like me practicing in Amsterdam in Europe, is still very novel. I understand in China it has already been used, and that is telitacicept. On the next slide, slide 16, you can see that the treatment with telitacicept was vastly more effective than placebo, which was statistically very clear, but also very meaningful and clearly expresses a very profound improvement for the patient thanks to this new treatment. We're now fortunate enough to see that this is also promising for Sjögren’s disease. Hopefully, for both of these diseases, the future will be better for our patients. On the final slide, I would like to conclude that Sjögren’s disease is a very important chronic autoimmune disease. It imposes a major burden on the patient's quality of life, and the treatment options for Sjögren’s disease have so far been very limited. Now there are new treatments that are emerging. They're based on our understanding of the pathophysiology that includes the B-cells, which are important in producing the autoantibodies, and it can be targeted with biologicals. Indeed, for lupus, which is a closely related disease, we now have recent data that support the efficacy and the safety of the BAFF/APRIL antagonist, telitacicept. Thank you very much. Thank you so much, Ronald, for your thoughts and time providing a background on Sjögren’s disease. Now, let's move forward to review the clinical data. If you look at slide 28, this was a robust double-blind, placebo-controlled phase III study conducted in China in 380 adults with primary Sjögren’s disease. Patients were randomized 1:1:1 to receive telitacicept 80 mg, 160 mg, or placebo once weekly for 24 weeks, followed by blinded extension through week 48. At week 24, if a physician felt that patients were not responding, they had the ability to move them to a different treatment arm. Only nonresponsive patients in the placebo arm were eligible to shift treatment arms. If they were already in the 80 mg or 160 mg arm, they remained in those arms. Importantly, no DMARD or steroid was permitted. The only background therapy allowed was hydroxychloroquine. That means the outcome we presented today suggests a clear and interpretable treatment effect. The primary endpoint for the trial was change from baseline in ESSDAI at week 24. Secondary endpoints include change from baseline in ESSDAI at 12 weeks, as well as change from baseline in ESSPRI and other measurements of disease activity at week 12, 24, and 48. The study was executed with exceptional consistency and patient engagement. Of the 380 patients that received treatment, nearly all completed the 24-week blinded period, and more than 90% entered into the extension phase. Importantly, completion rates were balanced across all arms, a reflection of both strong tolerability and the patients' confidence in treatment. Turning to baseline characteristics, the study enrolled a well-balanced and representative patient population across all treatment arms. Patients were predominantly female with an average age of 46 and a mean disease duration just over 21 months, reflecting a demographic we've typically seen in Sjögren’s. Baseline ESSDAI and ESSPRI scores were 10 and 5, respectively, indicating moderate systemic and symptomatic disease activity at entry. Importantly, hydroxychloroquine use was consistent across groups, and the key serological markers, such as immunoglobulin levels and B-cell count, were evenly distributed. Together, these factors provide confidence that any differences observed later reflect the potential effect of telitacicept. Now, we are incredibly excited to share these slides. What you see here is a deep and a durable reduction in disease activity measured by ESSDAI, the gold standard for systemic improvement in Sjögren’s. By week 24, patients on telitacicept 160 mg improved by more than four points versus 1.4 placebo, a seven-fold difference. That benefit continued to deepen through week 48. Importantly, this was achieved without DMARD and steroid, indicating that these results reflect the drug's direct effect. The trajectory and the separation here are consistent, sustained, and clinically meaningful, demonstrating the strength and the biological precision of this mechanism. When we look at clean ESSDAI, which excludes the biological domain, the improvement remained virtually identical to ESSDAI, 4.6 versus a 4.5-point reduction. This tells us that the benefit isn't driven by serological change alone, like what you're seeing in FCRN therapies. We are seeing true clinical improvement, organ level and symptom level control, consistent with the therapy that is rebalancing immune activity rather than just lowering biomarkers. While reducing ESSDAI is important, the goal for the physician is to get a patient to low disease activity below ESSDAI 5 points, the point where patients move from living with the disease to living beyond it. In Sjögren’s, this threshold represented minimal systemic involvement, fewer flares, less fatigue, clear function across organs that were once chronically inflamed. Here, more than half of patients on telitacicept reached this state by week 48, compared to just 12% on the placebo arm, nearly a five-fold difference. For context, this represented one of the most robust demonstrations of disease control reported to date in this indication. It signals durable immune stabilization from telitacicept and brings us closer to what remission could look like in this disease state. Now, I want to focus on patient-reported outcomes in Sjögren’s with ESSPRI, which captured what patients actually feel and function: fatigue, dryness, and pain. These are symptoms that dominate daily life and drive treatment dissatisfaction. What stands out here is the magnitude and the persistence of the response. By week 48, patients on telitacicept reported an average nearly 2.6 reduction, a level of improvement that exceeds what's considered clinically meaningful by nearly double. For context, most therapies in development have struggled to move ESSPRI meaningfully, even when ESSDAI scores improve. The fact that patients feel this benefit sustained over a year tells us telitacicept is not just changing biomarkers; it has the potential to change how patients live with this disease. Let's turn to MFI-20 score, which evaluates fatigue, one of the most debilitating and difficult-to-treat symptoms of Sjögren's. It is what patients describe as the constant weight of the disease and where most therapies have failed to make a difference. MFI-20 is a valued measure for fatigue, ranging from 20- 100, where 20 score represents no fatigue and 100 represents maximum fatigue. With telitacicept, we see a 12-point or 21% reduction on the MFI-20 scale by week 48, which corresponds with patients moving from moderate fatigue that interferes with the patient's daily activity to mild fatigue that is noticeable but manageable by the patient. In practical terms, this means patients report being able to complete a daily task, concentrate longer, and rely less on rest periods. That kind of a shift isn't just statistically significant; it suggests a real, felt improvement in daily energy and motivation, suggesting telitacicept's potential to improve overall functioning. Now, this slide brings the story full circle. These are the symptoms patients live with every day: dryness, fatigue, and pain defined by the burning of Sjögren's and are notoriously resistant to treatment. Here, we see the improvement across all domains, including a 2.2-point reduction in dryness, a symptom most drugs fail to meaningfully impact. That's the dual BAFF/APRIL mechanism at work. With its potential to restore normal glandular function and reduce systemic inflammation, translating biology into day-to-day relief for patients. Turning to our exploratory endpoint, STAR, combines the measurements that matter most: systemic disease activity, patient-reported outcome, serological markers, and glandular function. Of the five-domain measures, STAR puts more weight on systemic disease activity and patient-reported outcomes. What we're seeing here is a coordinated improvement. By week 24, nearly 75% of the patients on telitacicept met the STAR response threshold, compared to just over 20% on placebo, more than a three-fold difference. This composite view is critical because it reflects the disease as a physician and the patient actually experiencing it. What underpins the clinical result we were seeing is a clear biological coherence. Telitacicept produced consistent, proportional reduction in immunoglobulin, IgG, IgA, and IgM, as well as circulating B-cells, without excessively depleting or rebound. These patterns suggest the dual BAFF/APRIL mechanism is doing exactly what it's designed to do: normalize overall B-cell signaling and antibody reduction while remaining balanced. It is this biological precision that underlines the sustained clinical improvement observed across multiple endpoints. Finally, safety. This is what telitacicept continues to demonstrate its strength. Across 380 patients in this trial, average event rates were comparable to placebo, with no new safety signals and no opportunistic infections. This profile is consistent with tens of thousands of patients and years of experience across multiple indications. This consistency across diseases and time gives us confidence that the immune balance observed with telitacicept could be both effective and sustainable. With that, I'm turning the call over to Dallan. Thank you, Qing. With this latest phase III data now in hand, we are positioned for global success with best-in-disease data in two compelling indications. Firstly, as a reminder, in myasthenia gravis, we started discussing the telitacicept phase III data just a few months ago with a compelling advantage at week 24 on the gold standard efficacy scale in MG, the MG ADL. As you can see on the left-hand side here, telitacicept delivers a two-fold improvement versus the entire competitive field on the relative difference versus placebo on this MG ADL scale. The magnitude of effect is compelling. Just this week at AANEM, we've added to that magnitude of effect new durability data. That's what you see on the right-hand side of the slide here, an increasing magnitude of effect that is sustained out to 48 weeks. Sustained symptom control is of critical importance to prescribers, as in some cases, such as myasthenia crisis, these symptoms can be life-threatening. Now, with the Sjögren’s data just presented by Dr. Zuraw, we are replicating the results of our smaller phase II Sjögren’s study and showing a similar efficacy advantage as measured by the relative difference versus placebo on the ESSDAI scale. You can see on this slide the magnitude of effect shown in these telitacicept trials compared to the entire competitive field. We believe that the dual targeting of telitacicept to both BAFF and APRIL is what is behind the compelling efficacy and safety results that you are seeing across studies and across indications. While we initially had spoken at length about the compelling commercial opportunity in MG, we believe this Sjögren’s opportunity is even larger. Looking only at the diagnosed Sjögren’s patients and looking only at the key markets, as you can see from this slide, there are well over 800,000 diagnosed, identified Sjögren’s patients in the key global markets today. There are currently no approved therapies for these patients, and we believe the rate of diagnosis will increase rapidly with the onset of approved therapeutic options for these patients. In short, it's a huge opportunity, and Vor Bio is in the best position to win the number one position in these key markets that you see on this slide. There is, of course, a strong desire from the community for any approved therapeutic options we can get for Sjögren’s. Telitacicept provides real hope for these patients and checks the boxes of important attributes for a therapeutic option for Sjögren’s. The foundational attribute is, of course, demonstrating efficacy. You’ve now just seen the magnitude of efficacy on the primary outcome of ESSDAI, along with the key secondary and exploratory outcomes, which are all positive in this study. Secondly, and perhaps the most important attribute for patients, is safety. Since these patients are already suffering from the devastating complications of Sjögren’s, it’s important to deliver a clean safety profile. It can’t be overstated how important this is and how important it is that the safety data that you saw today in Sjögren’s disease is consistent with what has been presented in other indications studied with telitacicept to date. Thirdly, patients and prescribers would ideally like to see long-term real-world data. On this front, we’re in a uniquely strong position due to the wealth of clinical and commercial experience with telitacicept. Finally, targeting Sjögren’s disease at its source, the upstream targeting of B-cells with telitacicept provides dual targeting of both BAFF and APRIL to modulate B-cells and decrease pathogenic autoantibodies with the goal of long-term disease modification. It’s an exciting time for patients with Sjögren’s disease, for the rheumatology community here at ACR, and for us at Vor Bio. Thank you for your attention. With that, I’ll hand it back over to Jean-Paul. Thanks, Dallan. What you have seen here today is more than just a data set. Telitacicept is not a single-asset story. It is a validated pipeline in a product redefining how we think about autoimmune disease. With a mechanism that has been proven, a safety profile that is consistent, and efficacy that is reproducible across indications, telitacicept stands as the most advanced BAFF/APRIL inhibitor worldwide. For myasthenia gravis, we have the potential to become the first disease-modifying therapy. In Sjögren’s disease, it is delivering results that no other agent has achieved. In both indications, we have the potential to be best in disease in a matter of a few years. These data mark the beginning of something bigger, a new standard for B-cell modulation, and a future that extends beyond a single disease. Thank you for your time today. I would now like to open the call for questions. Thank you. At this time, we'll conduct the question- and- answer session. As a reminder, to ask a question, you'll need to press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster. Our first question comes from the line of Jack Allen of Baird. Your line is now open. Great. Thank you so much for taking the questions, and congratulations to the team on the presentation of the data. I guess my first is for the company, but I also wanted to ask if the KOL, Dr. van Vollenhoven, is also around for questions as well. Maybe just first to the Vor team, I know you mentioned the lighter background treatments that are given in the Vor study in China as compared to some of the competitor studies. I'd just love to hear a little bit more about your thought process as you move towards a Western patient population, and if you would allow for additional background therapy in that sort of setting, or is it your understanding that studying the product in a space where maybe there aren't as many background therapies provides you a more clear imprint on the therapeutic effect as you're outlining today? Yeah, Jack, thank you very much for your question. By the way, the KOL is not on the phone with us. He had a conflict. Qing will answer your question on the background therapy. Oh, okay. Jack, thank you for your question. The background therapy in the China study, we're only allowed to have hydroxychloroquine, no DMARD, no steroid. I mean, to your point, the global study did include steroid and methotrexate. What is really important when you have no background therapy is it provided opportunity to show the drug effect. What is really meaningful is the placebo-adjusted efficacy endpoint. That is what's clinically meaningful. With well-designed and well-balanced treatment arms, we will expect this for the global study will be a comparable result. Our timing is good because we now have the opportunity to review the data and all the lessons learned from the other trial, and then we will apply those lessons learned to our global trial going forward. Got it. That's great color. I guess as it relates to expectations for the phase III study, I'd just love to follow up and maybe understand how you're thinking about the design of the phase III study. Do you plan to bring one or multiple doses forward? Would you allow for those background therapies? I know you mentioned maybe that you'd expect a similar delta even in light of having those background therapies. Is that how you'd be framing up expectations for phase III, maintenance of treatment effect over a greater placebo response? What kind of patients would you look to enroll in a Western phase III study? It's a bit early to be specific on the phase III study. Actually, we wanted to learn from the data this confirms from other products, including Novartis, obviously, and J&J. Now we have a set of data we can benchmark and compare. We are obviously positioned in a very favorable way. We will be learning from their experience in the Western studies. In terms of the dose, we are planning to have only one active dose, 160 mg, which you remember in the China study, we had two doses, 160 and 80 mg. 160 makes perfect sense for efficacy-safety ratio. Got it. That's great. Maybe one last question. I totally hear you that Sjögren’s is a large opportunity here with some estimates being as many as 1 million patients in the U.S. alone. I saw some data from ACR outlining that. I guess have you done any preliminary work on the severity of those patients and trying to understand how many of these diagnosed patients maybe would be looking to receive a biologic therapy as compared to maybe an earlier line treatment? Yeah. Dallin? Yeah, thanks, Jean-Paul. Yeah, we have actually. The estimates do range, but it's a large group. It's the patients, for the most part, that fit our trial criteria of ESSDAI greater than or equal to 5. Those are the patients with systemic involvement, and that ranges, depending on the EPI estimate, between 30% to upwards of 50% of the patient population. As you mentioned, there is a large estimated prevalent population. There's about 300,000 diagnosed patients, and you can say anywhere between 100,000- 150,000 that are in this moderate to severe category. It's really, by far, the largest unmet need, untapped opportunity in autoimmune diseases. Got it. That's great. Thanks so much for all the color today. I'll jump back in the queue with any further questions. Thank you. Thanks. Thank you. One moment for our next question. Our next question comes from the line of Stephen Willey of Stifel. Your line is now open. Yeah, good afternoon. Thanks for taking the question and for the call, grabbing some of the data. I know we've received a lot of questions from investors just regarding the relatively muted placebo response that's been observed in this trial, I think, compared to some of the other phase II data sets that have been presented and published. I know your commentary would suggest the absence of background therapy is likely having an impact here. Curious if you've interrogated any of the individual ESSDAI components to see if the placebo response, or I guess lack thereof, appears to be concentrated or driven within any specific domains. Qing will answer the question. Yes. We did look at the ESSDAI domain. Thinking this patient population is moderate to severe that we use as a study entry, when we look at the ESSDAI domain, they are consistent with this patient population. For example, they are mainly driven by the constitutional, lymphatic system, and articular, and so forth. When we look at the response and we don't see this particular domain driving the placebo response, it's well balanced within the study. It's a really important point you see in our poster. If you see those patients who are in the placebo arm, once they cross over to the active arm, they actually were able to reach the same result as the 24-week data. That really gives us confidence in the reliability of the placebo response. I would add that actually, you know, I mean, it's pretty intuitive that with background therapies, steroids, and in many cases, immunosuppressants like methotrexate, you have a profound effect on the ESSDAI components and on the symptoms as well. When you don't have those, you basically have the patients, the role patients, and the role placebo subjects as well. It's obvious there is a difference here. If this, as we are looking at the balanced effect between the two arms, the thing would actually be the same in the global study if you would do without background therapies. Okay. Understood. Just with respect maybe to piggyback off Jack's question, I think the clinical definition of severe Sjögren’s is a baseline ESSDAI of greater than 14. I was just curious how many of those severe patients were enrolled into this study, and should we assume that there's no differential efficacy between those patients who are either moderate or severe? I believe we have around 50% of the patients with more than 10 ESSDAI score and around 50% with less. Actually, Qing, do you want to comment if we see any difference here? Yeah, that's correct, Jean-Paul. I think our baseline is the mean is around 10, right? We have about 50% of patients that are greater than 10, and it's a pretty even distributed amount of disease. Okay. I believe there's going to be the presentation of the phase III China high-gain data in a couple of weeks. I was just kind of wondering if you could provide a little bit of an expectation framework and perhaps what you think investors should be focusing on ahead of that data. Thanks. Yeah. It's a great question. I think we're preparing actually a PR for that. I don't recall if the abstract is already out, but Qing, you can comment on that and how it's a great proxy for reproducibility of the China data in the global setting. Qing? Yes. Yes. I think the China data, I think it's, I mean, first of all, the study results really are driven because based on the well-designed study, right, and a robust SQL study. If you look at our high-gain study from the phase II data and then compare it with the global studies, for example, the virus, it's the same mechanism actually in the same class, right? You see the results are comparable. That is really a validation to see the Chinese data versus global data. It's reputable. Also, we will have the Phase Three result presented at ASN on the 8th. I think, I mean, we have not disclosed the, it's currently still under embargo. We have not shared the specific data, but we are expecting excited to present the data will be consistent with what we have seen in the phase II. All right. We're looking forward to the presentation. Thanks for taking the questions. Thanks. Thank you. One moment for our next question. Our next question comes from the line of Geoff Meacham of Citi. Your line is now open. Oh, great. Hey guys. Thanks so much for the question and also congrats on the great data. I just had a few quick ones. The first one is looking at the screenout rate from the trial. Maybe talk about what the main trends were there and does that have any commercial relevance as you look to a launch? I'll follow up with the next one. Jeff, you were breaking up a little bit on the first part of the question. Apologies, can you repeat? Sorry. Looking at the screenout rate from the trial, what were the main trends and does that have any commercial relevance as you look to a launch? Qing and Dallan? Yeah, Qing can comment, but Jeff, I think that was really reflective of all the other studies out there, Jeff, that about 90% or so were antibody positive. The antibody negative, we're factoring that into our estimates of the market size. There wasn't any, from my estimates of the market potential, there wasn't anything surprising that would cause me to increase or decrease my estimates. Qing, I don't know if you have any more details on the screenout in the Sjögren’s. Yeah, I think Sjögren’s in general, the ESSDAI certainly has some limitations, right? It’s pretty good nowadays. Typically, you screen patients, you will see, especially in central laboratory, you will see about 30% of patients will be negative. For our study, we did not include any negative patients. I think you’ve seen some of these studies include up to 10% patients being negative as part of exploratory. Okay. Thank you. That's helpful. My follow-up is when you look at BAFF/APRIL, it does look to be among the most potent mechanisms. I wasn't sure if you guys have done direct comparisons or have a view, but I would just maybe ask you to stack up BAFF/APRIL as a mechanism in Sjögren’s relative to, say, FCRN s or anti-CD19 s. We get this question a decent amount. Thank you. Yeah. Let me give it a try here, Jeff. This is a great question. We believe we have the most compelling mechanism with BAFF and APRIL because we are actually addressing the two most important cytokines modulating the B-cell lineage. These are actually on the upstream and on the downstream. BAFF is more on the upstream, targeting the B-cells upstream, and APRIL is mostly on the downstream with the plasma cells. With that, we have two shots at the goal, not in a depletion mode, which we don't target and kill the B-cells, but we modulate them. We actually normalize them, especially on the hyperactivated clones, which are at the origin of the autoimmune diseases. These clones activated by autoantigens become hyperstimulated, and they secrete the pathogenic autoantibodies. They are at the origin of the disease. We normalize these clones, and we actually are pretty selective in some ways because normalizing these hyperactive ones, we kind of spare the B-cells which are used for fighting infections or anything else, which would be bad for the health. This is extremely compelling. We believe that we have the best of both worlds, the upstream, which is amplified by, for instance, anti-CD19 therapies, but also the downstream, which are right now owned by very downstream mechanisms or modalities like FCRN therapies, which address in a narrow way the on-and-off production or at least recycling of autoantibodies. That actually is probably the explanation. You cannot draw too many conclusions, but the explanation of our very compelling and consistent clinical activities across a series of autoimmune diseases in a very consistent way, but also for the safety profile. To make a long story short, we believe we have the most compelling modality here. We've demonstrated that through this series of phase III that we are communicating on these weeks. Jean-Paul, if I may add, based on the buzz that was here at the ACR meeting, at our poster today, it was just swarming with people. Yesterday, there was a presentation on the role of APRIL in Sjögren’s disease, and the presenter really flagged our poster as being of major interest. I think the BAFF/APRIL mechanism, as you were talking about, really is starting to have its moment. It was really a big part of this ACR meeting this week as well. Thanks, guys. Thanks, Jeff. Thank you. One moment for our next question.