Good morning or good evening. Welcome to Everest Medicines' Business Update Call on interim data from EVER001, phase I-B of a clinical study in primary membranous nephropathy. Please be advised that today's conference is being recorded. During the Q&A session, for participants who join the call through PC or app, please click the raise hand button at the bottom of the screen to queue up for voice questions or text your questions as messages. For participants who dialed in, please press star one to queue up for questions. And finally, I would like to hand the conference over to your speaker today, Ms. Leah Liu, VP Investor Relations for Everest Medicines. Please go ahead. Thank you, Operator. Good morning or good evening, everyone, and welcome to our call. Joining us today are Mr. Rogers Luo, Chief Executive Officer of Everest Medicines, Mr. Ian Woo, President and Chief Financial Officer, Dr. Jason Brown, Chief Business Officer, Dr. Jennifer Yang, Chief Scientific Officer, Sandra Zeng, Chief Medical Officer. Before we get started, I'd like to remind you that the speakers on this conference call today may make statements that constitute forward-looking statements, including descriptions regarding the intent, belief, or current expectations of the company or its officers with respect to the business operations, financial conditions of the company, which can be identified by terminology such as will, expects, anticipates, future intent, plans, beliefs, estimates, confidence, and such similar statements. Such forward-looking statements are not guarantees of future performance and involve risks and uncertainties, and actual results may differ from those in the forward-looking statements as a result of various factors and assumptions. The company or any of its affiliates, directors, officers, advisors, or representatives have no obligations and does not undertake to revise forward-looking statements to reflect new information, future events, or circumstances after the date of this conference call, except as required by law, and now I will turn over the call to Rogers to provide you with more details on our EVER001, phase I-B/II-A clinical results. Thank you, Leah, and hello to everyone. Thank you all for joining us on this call. Today, we are very excited to announce positive results in the interim analysis of phase I-B/II-A clinical trial of EVER001, a novel BTK inhibitor for the treatment of primary membranous nephropathy. Expanding our leadership position in renal disease is a core strategic focus at Everest Medicines, and we are committed to build a pipeline of innovative therapeutics against the most common glomerular disease. Our lead product in this therapeutic area is NEFECON, the first innovative medicine approved for the treatment of IgA nephropathy globally and the only one approved in Greater China, South Korea, and Singapore. NEFECON has been launched in China and Singapore this year, and it will be launched in South Korea and Taiwan next year. Just last week, we announced that NEFECON has been successfully included in the national reimbursement drug list in China for 2025, which will make the medicine accessible to more patients and significantly expand our investment in the renal disease ecosystem in China. EVER001 is the next clinical asset in our renal pipeline, and we believe that it has broad potential across a range of autoimmune-driven glomerular diseases. The first indication we are exploring is primary membranous nephropathy, or PMN. PMN is one of the larger orphan diseases in the U.S. with about 80,000-100,000 patients, and there are also a total of about 120,000 patients in Europe and Japan. However, PMN is not rare in China. There are about 2 million patients beyond PMN. We believe EVER001 has potential in other autoimmune renal diseases, including IgA nephropathy, lupus nephritis, minimal change disease, and focal segmental glomerulo sclerosis. These are diseases critical unmet medical needs, with a total addressable patient population of over 10 million in China and over 300,000 in the U.S., we own the global rights for the renal disease. Membranous nephropathy is one of the most common causes of nephrotic syndrome in adults without diabetes. PMN is an idiopathic disease and represents about 80% of the membranous nephropathy cases, and the remaining 20% of patients have a secondary form that is associated with an underlying disorder such as autoimmune disorders like lupus, infections, drugs, or cancers. PMN patients have building up of immune deposits on the glomerular basement membrane in the kidneys, leading to high proteinuria and low serum albumin. 80% of patients with PMN progress to nephrotic syndrome, which is a set of syndromes including swelling, high cholesterol, and low blood protein levels. Thus, the onset of disease is very evident and heavily felt by patients. Half of the patients using current treatment options continue to have nephrotic syndrome, while over 1/3 of the patients would progress to end-stage renal disease. The mean age of diagnosis is between 40 and 60. Next slide. In relation to severity of the disease discussed on the previous slide, there is also a significant number of PMN patients. Similar to IgAN, the disease prevalence is higher in each Asian population. In China, we believe there are over 2 million patients. In the U.S., it is a rare condition. Still, prevalence is about 80,000-100,000 patients. In Europe, there is also a prevalence of around 80,000 patients, and in Japan, about 40,000. We have also observed a clearly rising trend of illnesses in recent years. There is currently no approved treatment for PMN. Current treatments like cyclophosphamide, calcineurin inhibitors, and rituximab are used off-label and are associated with substantial side effects. Still, more than 30% of patients do not respond to the current standard of care, and even among those who achieved remission, approximately 30% will relapse. So there is an urgent need for more potent and safer treatments. Next, I will now hand over to Jennifer to talk to you about EVER001, our unique BTK inhibitor. Jennifer, please. Thank you, Rogers, so EVER001 is a reversible covalent BTK inhibitor that we are developing for autoimmune renal indications, the first being primary membranous nephropathy. EVER001 can selectively form a reversible covalent bond with cysteine 481 in the BTK kinase domain. It differentiates from other BTK inhibitors currently marketed for other indications. Those BTK inhibitors are either covalent irreversible inhibitors or non-covalent reversible inhibitors. The covalent binding mechanism of EVER001 ensures a strong BTK inhibition, while its reversibility presumably will lead to less off-target toxicity, thus reducing the risk of idiosyncratic toxicity caused by the permanent modification of those off-target proteins. We also believe that the relatively fast on rate and its high selectivity may further benefit the safety profile. If you look at the left-side table, you can see that compared to ibrutinib, EVER001 has similar potency against BTK, but it has much better selectivity over those off-target kinases such as LCK, SRC, LYN, etc. For EGFR, ITK, and TEC family kinases that are thought to be associated with an undesirable safety profile, EVER001 demonstrated a superior selectivity profile even compared to the more selective BTK inhibitors like zanubrutinib and acalabrutinib. We believe this excellent selectivity profile, combined with its reversible covalent mode of action, makes EVER001 extremely attractive as a treatment option for PMN patients who likely would need long-term treatment. For a disease like PMN, the disease occurs when B cells produce pathogenic autoantibodies such as anti-PLA2R antibodies. Those antibodies can then bind to podocyte, and the in situ immune complex formation can further activate the downstream complement pathway, leading to podocyte damage and proteinuria. As you can see in this disease pathogenesis, B cells play important roles, and BTK, which can modulate the B cell receptor signaling, is an important component of the BCR signaling pathway. BTK inhibitors can prevent maturation, proliferation, and differentiation of B cells, therefore reducing the pathogenic autoantibodies produced by these B cells. Unlike B cell targeted therapies, for example, rituximab CD20 antibody or anti-CD38 antibody or BAFF/APRIL antibody, which can only affect a subset of B cell population, BTK inhibitors can have a much broader effect. Beyond B cell, it can also modulate other immune cells in the system, therefore, has an immunomodulatory effect on the chemokine-cytokine network. Compared to B cell depleting antibody like CD20 antibody, the oral formulation of BTK inhibitors can also allow for more rapid recovery of B cell function upon treatment withdrawal when it's necessary, therefore further reducing the risk of severe infection of patients. Of course, this will need to be further tested in the clinical studies. With that, I will hand over to Sandra to talk about the ongoing phase I-B, II-A clinical study. Thanks, Jennifer. Today, I would like to share with you our preliminary result from our ongoing phase I-B, phase II-A clinical trial of EVER001 in PMN patients. We included, you know, Chinese patients with biopsy-proven PMN, positive anti-phospholipase A2 receptor autoantibody, and 24-hour proteinuria of greater than 3.5 g. The study was conducted in two dose levels. The low dose level cohort 1 starting with 100 mg QD for four weeks, followed by 100 b.i.d. for 32 weeks. It's off-treatment follow-up up to two years. The cohort 2 is a higher dose with 200 mg b.i.d. for 36 weeks treatment, and then off-treatment follow-up until two years. The primary endpoint is safety and tolerability. The second endpoint is the efficacy endpoint, including percentage change from baseline of 24-hour proteinuria, anti-PLA2R autoantibody level, UPCR, and EGFR. Also, we measured complete and partial remission of 24-hour proteinuria rate and also remission of anti-PLA2R autoantibody level. Then by now, we already enrolled a total of 31 patients, including newly diagnosed patients and also including the patients relapsed from or refractory to prior immunosuppressive treatments. By the data cutoff September 13, 2024, we have 11 subjects in cohort 1 have completed 36 weeks of treatment. Seven subjects in cohort 2 have completed 24 weeks of treatment. Let's look at the immune response. As we know, clinically, anti-phospholipase A2 receptor antibody is a very specific for PMN diagnostic biomarker, and with about 70%-80% of patients, PMN patients have exhibited a high level of anti-PLA2R antibody level. It also is an important prognostic biomarker. Look at our data. By the cut-off, EVER001 induced close to 100% anti-PLA2R autoantibody reductions in both treatment arms. The blue lines chart represent the low dose at 100 mg, and the red line chart represents the high dose level at 400 mg. For the cohort 1, over 90% of reduction in anti-PLA2R occurred as early as week 24. Then this result, I just want to point out, this result was maintained to 50 up to 52 weeks, which included off treatment follow-up period like about 16 weeks. Reduction in the cohort 2, which is the red line chart, of anti-PLA2R was more rapid in cohort 2, and over 90% of reduction was seen as early as week 12. Another thing I wanted to point out is the time course of PLA2R antibody under treatment is tightly correlated with clinical outcome. A decrease of PLA2R antibody predicting clinical remission, especially the immunological complete remission, the ICR. I'm going to share with you next slides. As literature is showing, patients with achieved ICR have a dramatic low risk of progressing to the end-stage renal disease. Those making immunological complete remission are a very key objective for treating PMN patients. So in our study, we did observe as early as week 4-8, the ICR was induced by EVER001. In the table, the blue bars represent the result from cohort 1, the low dose, and the red bar represents the high dose cohort 2. In cohort 1, by week 16, more than 50% of subjects already experienced ICR, and by week 36, as high as 90% of patients achieved the immunological complete remission. In the cohort 2, by week 8, 67% of subjects experienced ICR, and by week 24, all subjects, seven subjects achieved the immunological complete remissions. So, as we know, clinical response follows immunological response. Usually, we always observe immune response, then we followed by the clinical response. In our study, we did observe remarkable proteinuria reduction during the treatment period for both cohorts. In cohort 1, reduction in proteinuria from baseline was 78% at week 36, and with continued benefits of up to 52 weeks, including the off treatment period of 16 weeks. In the cohort 2, more than 50% of proteinuria reduction was seen as early as week 16, and by week 24, reduction in proteinuria from baseline was 74%. If we further analyze the clinical response and look at the proteinuria remissions, and we noted for cohort 1, eight out of 11 patients experienced proteinuria remission at week 28, and with one subject achieving complete remissions, and by week 36, we already see nine out of 11 patients actually experienced proteinuria remission, with two subjects achieving complete remissions. The median time to proteinuria remission was about 20 weeks. For cohort 2, six out of seven patients already experienced partial proteinuria remission by week 20, and by week 28, all four subjects achieved partial proteinuria remission. Median time to proteinuria remission was 16 weeks. Besides the 24-hour proteinuria, we know serum albumin decreasing with associated swelling are important clinical symptoms and signs. With the corresponding reduction of 24-hour proteinuria, serum albumin levels gradually increased. Now, for cohort 1, by week 36, serum albumin levels already returned to normal or near normal. And then in cohort 2, actually by week 24, and serum albumin levels already returned to the near normal range. And in addition, by the cut-off date, EGFR was stable with small fluctuations in both cohorts. I just want to summarize what we have been observed, the clinical efficacy. In conclusion, EVER001 induced early onset and high rates of immunological and clinical response. Let's talk about the immunological response. In cohort 1, as high as 90% of subjects achieved ICR at week 36. In cohort 2, and then all subjects reached ICR at week 24. And of course, if we look at the percentage change, close to 100% reduction in both cohorts by the date cut-off. And then if we look at the clinical response, in cohort 1 at week 36, 82% of subjects already experienced proteinuria remission. And then for cohort 2, by week 24, 86% of subjects already experienced proteinuria remissions. In addition, the serum albumin levels returned to normal or near normal range in cohort 1 by week 36, in cohort 2 by week 24. Besides efficacy, we also want to talk about the safety, which is very important for new mechanisms of drug in autoimmune disease. And then in general, for both cohorts, EVER001 treatment was well tolerated and safe. We did observe 48% of subjects experienced treatment-related AE, but most AEs were just mild, moderate, let's say grade 1 or grade 2, and also these AEs were transient. No clinically meaningful adverse events typically associated with BTK inhibitors, such as serious neutropenia, hemorrhage, and cardiac arrhythmias, have been observed. With that, actually, I want to say, based on our safety and the efficacy data observed from this analysis, and then we definitely this data shows EVER001 as a covalent reversible BTK inhibitor, has very strong target binding, high selectivity, and potential low toxicity. We are extremely happy with this result and look forward to completing the trial and collecting the long-term follow-up data. We anticipate presenting the final analysis of the study in the future scientific conference. The last one, I want to just do a little bit of data comparison versus the historical data of current standard of care, including rituximab, cyclosporine, and also cyclophosphamide. We list three major randomized studies on the right side, and then we reviewed the major efficacy data at week 24, including the immunological complete remission and also 24-hour proteinuria reductions. From numerical number, definitely our data looks favorable compared with the historical data. Obviously, there are some caveats because this is a cross-study comparison. Maybe there are slight differences in terms of population or maybe medical histories. We have to be cautious. So I think finally, as we think ahead for the future development, and then we plan to maximize the global needs and opportunities in the PMN, as well as other renal indications like Rogers pointed out, including MCD, FSGS, IgAN, and LN, which we believe EVER001 may also have a potential to benefit patients with these indications. Stop here. Operator, can you announce the Q&A information? Okay, thanks. We will now open for Q&A session. For participants who join the call through PC or app, please click the raise hand button at the bottom of the screen if you want to voice questions or text your questions as messages. For participants who dialed in, please press star one to queue up for questions. For participants who joined the call through PC or app, please click the raise hand button at the bottom of the screen to queue up for voice questions or text your questions as messages. For participants who dialed in, please press star one to queue up for questions. The first question comes from Goldman Sachs, please. Hey, we cannot hear you. Linhai, we can't hear you. Can you hear me now? Yes, we can hear you now. Okay, okay. Thanks. I think there are some tech issues. Thanks for taking my question. My name is Linhai from the Goldman Sachs Healthcare team. First, congratulations on the phase I, I-B data, and the preliminary data really looks inspiring. I think I have two questions. The first question is about the clinical trials itself. I saw that we have two dose level designs, and it looks like there are clear dose dependencies in terms of clinical responses and no major safety issues as well. Going forward, can you share a little bit more on the next steps for the clinical trials and also which dose level should we move forward? That's the first question. The second question is, I saw that for MN, the age of onset looks older compared to IgAN. How should we think about the real-world treatment rate for MN compared to IgAN? Especially, I noticed that for IgAN, many of the patients have the disease onset during their golden age at their cradle. And how should we think that for MN, the later age of onset, for example, like older than 50 years old, would that have a discourage on their treatment willingness? Thanks. Sandra, first. Yes. And then Ian, you ask the second question. Yes. I think I can start for the first question. I think that's a great question. That's actually one of the key things we have to do, just during our development plan, because which dose is the optimized dose for the next step for the later development. And as you pointed out, we definitely see the same things. The high dose brings us the early onset in terms of both immunological response and the clinical remissions. We see that the same things. But we currently cannot, it is in the evaluations. We are collecting long-term data, including up to like 1.6 years and 1.5 years or also like two years data to see how these two data will look like. But for sure, the higher dose gives us the early onset. And also, both those levels didn't have safety issues, but we just need a little bit longer follow-up to help us to make decisions. We will share with you guys in the future. Okay. Yeah. Thanks for the question, Linhai. I think for your second question, I think what we have seen is most of the patients with MN are actually diagnosed between 40 to 60. So I think many of the patients are still in the prime of their working age. And we believe the ability and the willingness to treat is very high. The other is that I think, as Rogers mentioned at the beginning, about 80% of the PMN patients actually have nephrotic syndrome. They actually see the symptoms more, sometimes even more visibly than IgAN patients, right, because they have very high proteinuria. I think when they see this level of proteinuria, I think we believe that most of the people will seek treatment, especially if there are safe and efficacious options and convenient options available to them. Yeah. Adding to our earlier points, I think because still, currently, there's no approved treatment. Even with those available treatments, over 50% of the patients will eventually progress to end-stage renal disease. That's still a very severe disease in the renal area. The failure rate, 30% of patients fail to respond to the current treatments. Even that 30% will also relapse. So still a very severe disease. And as Ian pointed out, it's very symptomatic. It's even more evident than IgAN. Back to you. Got it. Thanks very much for the answers. Thank you. For participants who joined the call through PC or app, please click the raise hand button at the bottom of the screen to queue up for voice questions or text your questions as messages. For participants who dialed in, please press star one to queue up for questions. Actually, we received a couple of questions online before the call. So I will go through a couple of them. So one of the questions was that, what are your clinical development plans going forward in terms of IND filing and global development plans? Yeah, Sandra. Okay. Yes. I just started that. Yes. As you know, we see these very encouraging, exciting data. And with these studies, we are still collecting long-term follow-up. Simultaneously, actually, we are working on the development plan for the coming sort of phase II/phase III study design. And then just like that's what we are currently to do. And we plan to have our global development plans and then so involve both Health Authority, FDA, and China Health Authority, CDE, and to discuss our coming just development plans. So I can just share right now for these ones, but definitely we are working on those ones for sure. But it's going to be a global development plan. So I just don't know if it's enough or you guys want to know more. Maybe I'll ask the next question as well. So I guess they want to understand why is there no current treatment approach for PMN? What is the difficulty in terms of developing this? Also, why haven't previous companies had an approved drug in this area? Yeah, I can start first, and the others can add. As you guys know, currently, there's no official approved drug for these indications. But current standard of care, all based on the evidence generated from the IIT study with small sample size, that's for sure. And then I think for approved medicines, one thing first, you need to have a prospective randomized study with large sample size to demonstrate the therapy is better than current treatment. That's one thing you have to do. Second, usually, you need to have sort of a new mechanism of actions with very, very, very good efficacious first and efficacious. And second, you need to have a very safety profile. And then third one, you definitely have to be sort of have other such as convenience. And then we believe just EVER001, NEFECON, NEFECON, maybe all these three prospective efficacious and the very safety, very safe profile. The third one is convenient medicines. Yes. Just so far, no prospective studies, randomized study has been completed in these indications to make any official drug approved in general. But others, you can add. Yeah. Ian, you want to add something? Maybe just one thing. I mean, I think it's just autoimmune-driven renal diseases, I think in general, right, as we have seen with IgAN, has seen a significant uptick in clinical activities over the last four or five years. There are a number of reasons, right? Part of it is FDA's regulatory pathways becoming easier. Part of it is just a recognition that these are not diseases that are very mild, right? These are actually very severe, debilitating diseases. I also like to think that whereas before, development may just be focused on sort of the U.S. and Europe where these diseases are rare, when you add Asia and especially our core territories with 5 million IgAN patients and 2 million membranous nephropathy patients, there's just a lot more motivation in providing good therapeutic options to all of these patients. I think for all of these reasons, the renal disease areas really have been quite a bit of interest from companies, physicians alike, and quite frankly, patient demand as well, right? I think that all adds to the level of activity and the enthusiasm that we're seeing in this space. Okay. For the questions. Operator, could you also announce again for the questions? Okay. So participants who joined the call through PC or app, please click the raise hand button at the bottom of the screen to queue up for voice questions or text your questions as messages. For participants who dialed in, please press star one to queue up for questions. I guess if we have no further questions, we can wrap up the call. I'd like to ask Ian to give a summary of the call. All right. I'll keep it short. Thank you very much, everybody, for joining. So we are truly excited about this data that we have seen so far in the phase I-B, II-A trial of EVER001 in primary membranous nephropathy. We really believe that the emerging product profile for this for EVER001 in PMN is potentially best in class. With no approved therapies and substantial medical needs globally, we look forward to moving aggressively to advancing EVER001 through clinical development. Now, in addition to PMN, we think that EVER001 can be explored more broadly across a range of autoimmune renal diseases. We intend to show that as well, right? Today's data release is also another important milestone for Everest because it is the first time that we have announced clinical proof of concept data on a therapeutic where we have global rights. We look forward to assembling the right and the best global expertise while leveraging our leading renal ecosystem in China to maximizing the potential of this asset. Thank you very much.