Hello, everyone. Welcome to BeOne Medicines' 2025 Investor Research and Development Day. My name is Liza Heaps. I'm Senior Director of Investor Relations at BeOne. We are very excited to host our investor event today, both in person in New York City and online for our global attendees. Thank you all very much for joining us. This is truly an exciting time at BeOne, and we are thrilled to walk you through recent progress to date and provide a sneak peek of what lies ahead. I would like to remind all participants that during this presentation, we may make forward-looking statements regarding, among other things, the company's future prospects and business strategy. Actual results may differ materially from those indicated in the forward-looking statements. You can find more details in our filings with the SEC, Hong Kong Stock Exchange, and Shanghai Stock Exchange. I'm delighted that joining us to present today are John Oyler, our Co-Founder, Chairman, and CEO; Dr. Lai Wang, Global Head of R&D; Dr. Remus Vizon, VP of Hematology Clinical Development, to take us through our BCL2 program; Dr. Jacob Soumerai from Massachusetts General Hospital, who will share Sonrotoclax data; Dr. Amit Agarwal, also our VP of Heme Clinical Development, walking us through our BTK degrader programs and early research assets; Dr. Mark Lanasa, Chief Medical Officer for Solid Tumors; Dr. Shom Goel, who came in from Peter MacCallum Cancer Centre in Australia to share the latest on our CDK4 clinical development data. At the conclusion of the slide presentations, our speakers will be joined by Aaron Rosenberg, our CFO and moderator for today's Q&A session. Now, please, let's welcome John Oyler, BeOne Co-Founder, Chairman, and CEO. Thanks so much, Liza. If you didn't notice, there was a small break in the middle, which probably will make all of you happy in about 45 minutes. You know, I just really want to thank everyone for joining us. You know, we know that everyone's very busy. There's, you know, time and energy taken to try to understand our company. We really appreciate all of the effort that you have, you know, made to date in helping us in this fight against cancer. We really, really appreciate it. This is our first investor meeting under the name BeOne Medicines. I think our company BeOne, it was never simply about making one medicine to fight cancer. A lot of biotechs are. We were not. It was about trying to entirely transform the R&D process, to do that, to be able to make medicine more affordably and more accessibly for cancer patients here in the United States and all around the world. We also believed in doing that. We had to fight cancer, do it in a better way to improve the R&D process, and thirdly, provide superior returns to investors so that we'd be able to continue to fund the next generation of medicine for cancer patients. I think you'll see we're well on our way in all of those areas. The name BeOne, likewise, is very purposeful. B is because the singular goal of any cancer patient is simply to be. One, because we all need to work together as one, and no patient, no family, no clinician, no hospital, no company, no policymaker, no country can fight the formidable cancer enemy alone. We all need to work together. We need to change the process to be better at what we do. Of course, within one in red, you can see onc. And this represents our commitment to oncology, which I think we wanted to reiterate to the world, because right now, given some policy that's occurred, given, you know, success in other areas like diabetes and weight loss, some companies are pulling away from cancer. We're not. We were built to fight cancer. We will be here fighting cancer with patients, with clinicians, you know, forever. That's what we're here to do. We were built differently from day one. We remain mission-driven. We remain founder-led. We have a tremendous sense of urgency in everything we do. I think that will flow through in what you see today. We're fighting cancer through scientific innovation, unquestionably, and that's what you will see today. We're also fighting it through R&D business process innovation. We're doing that because we really want to drive broader accessibility again here in the U.S. and around the globe. We want to be able to provide superior returns in an industry that's struggled to do that to any investment dollar that's coming in so we can continue to make great oncology medicines for the future. It's great to have a noble vision, and it's great to have one that's really hard. Success isn't about a vision. It's so much more. It requires incredible people. I think you'll see some of those from our team here today. It requires tremendous teamwork because this is one of the hardest things you can possibly do. There are so many different areas of expertise that need to work together to make a medicine. Of course, it requires a lot of hard work, some of which is not glamorous at all, to get things done that need to get done. I think you'll see we're an organization that isn't afraid to roll up our sleeves and do that work. Sustainable success also requires building strategic competitive advantages. Since day one of this company, we've been investing very heavily to build these. It has now been 15 years. The simple and biggest example is clinical development. Clinical development is the vast majority of time and the vast majority of cost associated with making an oncology medicine. Yet it's largely been outsourced and is not a core competency of most oncology companies. We have built this internally over 15 years, and we now have this spectacular global team of over 3,700 people that is operating largely CRO-free. They're doing the hard work and the heavy lifting that you will see the results of here today in what we're able to do as an organization, which I think will shock you at the speed and the quality of what we're doing. We also have incredible internal manufacturing and research teams. They enable us further cost and speed advantages. Each of these capabilities, strategic advantages are incredibly hard to build. They took every penny that we ever generated in this company of revenue, reinvested, or upfront licensing fee or financing that we raised to build these capabilities. It also took every penny we ever pinched, and we pinched a lot of pennies so we could spend it building capabilities and running programs. This only exists, these capabilities, because of the tremendous efforts of the people that are here today and here with our company today and that have collaborated with us, and also those who have previously worked at BeOne, who really built these through brilliance, through dedication, and through hard work driven by their commitment to fighting cancer. Today, BeOne has already helped 1.7 million patients, 1.7 million patients and their families fighting cancer. You know, to me, that's something that makes me unbelievably proud, grateful, and thankful that there's such a wonderful group of people within our company and around us working with us to help have that impact for patients. What I can say unquestionably is this is just the very beginning of BeOne. It goes without saying that if you want to build a sustainable business, it's critical to continue to be sustainable. It's critical to have the right core values and have them across your organization. We have that. We simply live our core values. With that, we always strive to have positive influence in every environment in which we're working. We strive to work cooperatively with all elements of the industry. What are we going to share today? First, we're going to share how our unique R&D model has already proven that we can deliver quality, speed, and cost-sustainable advantages. We can do that in a manner that provides superior returns to investors so we can continue to build the medicines for the future. From that perspective, you know, this is core to everything we're doing. I really think you'll see a wealth of information today that gives you the confidence to have that true belief. Our goal is to be the most impactful oncology company in the world. I think when you see what we're doing, we're well on the way to that. Secondly, we're going to talk about hematology. We have built a hematology franchise over the last decade. We have three incredible medicines that can be combined to create the solutions for patients not only today, but in the future, for the next five years and the decade beyond. We are sure that we can continue to grow into the hematology leadership we already have in CLL and that it's highly sustainable and that we do have the right medicines for the future. We can build more broadly in hematology outside of CLL and some of the other indications we're already approved in to become a broad hematology leader. Third, in solid tumors, although it took us a decade to build this franchise in hematology, we believe now we have several opportunities to build franchises that are similar in solid tumors and that we can do so in roughly half the time. We are very excited to share this information with you, the data associated with some of these programs, which in their own right, if they were not in BeOne, if they were in a small biotech company, I think there would be huge excitement and a lot of value attributed to them. We are glad to share some information about them. With that said, I think that you will see there is new data being presented too, and that is highlighted on the right-hand side of the slide. I know you come, you want to see new things. There's new programs that are disclosed here and a wealth of new data. I know you want to get to that. I think that the magnitude of what we're about to share, you know, to me is honestly a bit overwhelming. I think as you can see, it's tremendously exciting. It has the potential to be massively impactful for patients all around the world. We really should get to the heart of things. With no further ado, I think Liza said we should see what lies ahead. I'd like to introduce, you know, Lai Wang, who's a good friend of mine. He's also well known for being BeOne's second biggest Dallas Cowboys fan. Here he is, Lai. Thank you, John. Good morning. It's really nice to see the turnout. Thanks for coming. I'm really excited to share that the BeOne R&D is at a pivotal moment in its journey. Over the years, we have built strong research, global clinical development, and manufacturing capabilities from the ground up, allowing us to deliver, develop, and discover novel oncology medicines much quicker and more cost-efficiently than industry standards. The strategic advantages, capabilities are now scaled and fully functional across R&D. This inflection point signifies the dawn of a new era for BeOne, where our commitment to excellence and the pursuit of scientific breakthroughs will enable us to profoundly impact the field of oncology. Since 2019, we have transformed from a middle-sized setup into a scaled and highly efficient research powerhouse. Our discovery team now comprises over 1,200 research scientists, making us one of the largest oncology-focused discovery teams in the world. We have made substantial investments in the variety of the modalities, including protein degrader, we call it chimeric degradation activation compound, CDAC, bispecific, trispecific antibodies, antibody drug conjugates, and the cell CRPs. As illustrated on the graph on the right, our new era is marked by a significant increase in preclinical programs and the diversified modalities. CDAC and the complex biologics, including bispecific, trispecific, and antibody drug conjugates, now constitute the majority of our portfolio. Typically, it would take two to five years to progress from target identification to a new molecular entity entering clinical trial. With our recent investment, we observed a substantial rise in the number of AMEs entering the clinic, especially starting from the second half of 2023. In 2024 alone, we had 10 new molecular entities entering clinic, really functioning as a strong testimony about how strong and how productive our discovery team is. At BeOne, we prioritize quality over quantity. The rigorous innovation approach we have applied to Brukinsa is now being used across multiple programs. We focus on conducting the crucial experiments and only move high-quality molecules into the clinic, stopping any programs that do not meet our standards. Over the last three and a half years, we have terminated 60 programs that did not make the cut. This disciplined approach ensures that only the best candidates move forward. For instance, Sonrotoclax was designed to be more potent and more selective than Venetoclax and also addressed Venetoclax's associated inconvenience issue by designing a short half-life molecule. This will be easier for ramp-up. The FGFR2B ADC has the potential to spare ocular toxicity associated with Maurotuzumab by preserving ligand signaling. Additionally, IRAK4 CDAC can achieve complete target degradation in tissues by facilitating a very fast ternary complex formation involving IRAK4, CDAC, and E3 ligase. Next, I would like to highlight some of the technology platforms in which we have heavily invested in recent years, beginning with protein degraders. We currently have 23 degrader programs in our pipeline, including three in the clinic: BTK, EGFR, and IRAK4, which are designed for hematologic malignancies, solid tumor, and autoimmune disease, respectively. Preclinically, we have 17 small molecule programs, including two we're introducing today, the CDK2 and the KRAS. In addition, there are three degrader antibody conjugates, DACs, at the discovery stage. Our dedication to protein degradation is evident in the scope and the depth of our pipeline. The biology underlying the CDAC platform is fascinating. As illustrated in these circular diagrams, CDAC provides many unique advantages across multiple dimensions, some of which we did not foresee, we did not see at the beginning of exploring these modalities. Later in our discussion, we will dive into strategies such as increasing potency, enhancing selectivity, reducing on-target resistance, and impairing scaffolds with specific examples. For now, I would like to briefly highlight two additional advantages. First, targeting undruggable protein is conceptually straightforward. As long as the CDAC molecule can bind to the target, it has the potential to degrade the target protein. The binding does not need to neutralize the protein function. Secondly, by utilizing a tissue-specific E3 ligase, we can potentially minimize the degradation in the normal tissue, therefore enhance the safety profile. Now, let's turn to ADCs. We currently have 25 ADC programs, including four already in the clinic. Today, we will provide updates on a couple of those programs. Our initial wave of ADC assets consists of mono TAA ADCs. The second wave, starting from the end of this year, we're going to bring a set of the bispecific TAA ADCs into the clinic, although still using the topo isomerase as the payload. Moreover, this mono TAA, as well as bispecific TAA antibodies, can serve as a building block for future novel payload ADCs, including DACs. Our investments in the technology platforms go way beyond just degrader and ADCs. We believe that technology is fundamentally tied into innovation in our industry. Since cancer is such a complex disease, it requires a multifaceted approach to targeting various pathways, as well as many different targets within that pathway. Choosing the right modality for each target is vital. To create a perfect drug and then to create a deep portfolio for a certain disease area, you really need to draw from a diverse range of technology platforms. Our journey with CLL began in 2012 when we started our BTK program, followed by BCL2 in 2017 and BTK degrader in 2019. We are anticipating the first CLL approvals for Sonrotoclax and the BTK CDAC in at least one of the major markets within the next two years. For the CLL franchise, we leveraged only two technology platforms: our traditional small molecule inhibitor and the protein degrader platforms. This journey, spanning 15 years, is a tremendous success by any industry standard, but we feel it is long. Now, with our expanded discovery capabilities in both people, team, and the technology platforms, we believe we are in a much better position to build a similar franchise across our disease area of focus, which I'm listing here. More importantly, we can do it much faster. Our goal is to create a deeper pipeline by introducing eight to ten new molecular entities for each of those areas over the next three to six years. For example, I'm going to use the breast cancer and the gynecological cancer franchise as the example. Our first molecule, a CDK4 inhibitor, which we're going to give you some updates today, entered the clinic at the end of 2023, so only 18 months ago. Take a guess. By the end of this year, how many molecules will we have in the clinic for this franchise? Eight. We will have eight new molecular entities in the clinic just for this franchise in just two years. This is what now we can do. Certainly, you will hear a whole lot more about our breast cancer and gynecological cancer franchise in Markh sections. The competition in oncology has heated up in the past 10 years. For almost any target you pick, there are so many competitors working on it. We firmly believe the future of oncology really relies on innovative combinations. Our deep pipeline empowers us to develop unique and proprietary combinations that address our mathematical needs in cancer treatment. This slide presents several examples we will discuss throughout the presentation. Using Brukinsa and Sonrotoclax as examples, I strongly believe this might become the best treatment option ever for CLL patients. You will hear a lot more about this in the later sections. This strategy enables us to maximize the potential of our assets and ultimately enhance the patient outcomes. Our philosophy of rigorous scientific innovation, combined with our skill and a sense of urgency, sense of urgency is really important, has led to an industry-leading pipeline. This slide showcases our extensive portfolio ranging from proven therapies like Brukinsa, Tivembra, to very promising early candidates in early-stage development. Our pipeline reflects our unwavering commitment to advancing transformative medicines and improving patients' lives worldwide. Currently, we are executing 96 trials, ongoing trials involving 30 assets across various phases, modalities, and disease areas. This slide illustrates the breadth and depth of our clinical portfolio. I will spend the next few minutes also to share with you how we are building our clinical development capability to handle this large and growing clinical portfolio. Building our global clinical development organization has been a significant undertaking. It is hard. The timeline highlights our journey from inception in 2013 to our current state and beyond. We began laying the groundwork in 2013, and from 2017 to 2024, we are concentrating on establishing our global capabilities. Today, after streamlining and optimizing our process over the past few years, we are not only operational but thriving. In addition, we have an ongoing plan to further enhance our efficiency through the integration of AI and automation. Our global clinical team consists of over 3,700 professionals, covering a wide range of functions to drive our efforts. Each skill on the slide represents a different function within our team. Recruiting specialized talent and assembling this formidable team of clinical developers is no trivial task. This visualization highlights the collaborative and the integrated nature of what we do. At BeOne, we harness our internal global clinical capabilities to drive speed, cost, quality, and site access. We will showcase some speed examples in the upcoming slides. When it comes to cost, CROs typically charge you about 30% additional money. By eliminating the need for CROs, we can cut the CRO fees. Additionally, our internal model has led to enhanced trial quality. Over the past 10 years or so, we have successfully undergone over 100 inspections by 15 different health authorities in more than 10 countries, and all this without any critical findings. This is a remarkable achievement. Also, direct interaction between the investigator and the sponsor provides enormous value, as the investigator strongly prefers working directly with the sponsors over dealing with the CRO. Our patient enrollment strategy emphasizes diverse regions, highlighting our commitment to global representation. We ensure broad global enrollment across various regions, with increasing representation from emerging markets. This strategy helps us gather valuable data and insights from a wide range of populations, and in certain cases, the access to hard-to-reach patient populations, which I will touch on later. It is worth pointing out that our China enrollment in 2025 only accounts for a quarter of our total enrollment globally. All the examples I will share with you later really represent our global capability, not just the China capability. At BeOne, we are dedicated to streamlining the drug development with a focus on excellence. On this slide, you will see metrics from our fast-to-prove concept efforts, and we are applying across all early programs. I truly believe this is important for our success. For instance, if you look at the middle column, we hold a safety monitoring committee meetings only two to four days after the last patient finished their dose-limiting toxicity evaluation. Our median time to complete a dose escalation cohort is only about seven weeks, slightly over a month and a half. This is well below industry standards. This speed can save us more than one year with dose escalation alone. In the drug development, time is truly of the essence. To further illustrate our efficiency, let's look at the CDK4 inhibitor program as an example. We have enrolled over 300 patients and evaluated 22 dose cohorts, including both mono and combo in just 18 months. Do you know how quickly we initiate the first-line letrozole combination in CDK469E patients after completing the DLT evaluation combo in the second-line patients? I have the answer here. You already see it. It's just 13 days. This is remarkable, seriously, if you think about it. We accomplished this by strategically opening sites in regions with very limited CDK4/6 access, including Brazil, Malaysia, Moldova, and Thailand. Also, for the BTK CDAC, we successfully enrolled over 600 patients in the last few years. A lot of people are comparing us to another small biotech company. We entered the clinic only about six months ahead of the other company, but now we are way ahead. We effectively used the backfield and the safety expansion cohort to gather dose response data. Remarkably, it took us only four weeks to go from the recommended dose for expansion. Basically, it's the time you pick a few doses to expand. Only four weeks from that time point to start our pivotal phase two trial. Now, this CLL phase two has already enrolled more than 100 patients. I hope I have demonstrated to you that we have made significant strides in our pursuit of operational excellence through our internal operational model. I firmly believe the next wave of efficiency will come from the integration of AI and automation. Such advancements are not attainable using a CLL model. Clinical trials are essentially a data journey. By incorporating cutting-edge technologies into our process, we can streamline the operations, reduce manual labor, and boost accuracy. This approach not only accelerates the clinical development, but also ensures we deliver the highest quality results. Here are a few examples to give you a flavor of how much efficiency we have already gained. This is what we have already done with our AI and automation. BeOne's R&D strategy is anchored in four foundational principles. This really sets us apart from probably our peers in this industry. Number one, we are leveraging our diversified technology platforms to build a robust pipeline in targeted disease areas for synergistic outcomes. Number two, accelerating the development of molecules toward value inflection points and achieving clinical proof of concept to inform data. Data, keep in mind, data-driven decisions. Number three, initiating proprietary combination therapies early to maximize the potential for our assets and enhance patient outcomes. Number four, exercising discipline by advancing only transformative medicine into late-stage clinical development. Our industry, however, on the other hand, especially some of the large pharmaceutical companies, often falls short in terms of investing sufficiently in discovery and early development and by lacking principle in late-stage development, typically driven by commercial interests rather than data. In contrast, we focus on strengthening early development while being highly selective in late-stage investment. Our strategies are supported by our highly productive discovery capabilities and our CLL-free clinical operational model. We are committed to pursuing these principles urgently and with a firm resolve to challenge the status quo. Next, let us update you on our hematology portfolio. Over the years, we have witnessed remarkable advancements in CLL treatment. Key FDA approvals for therapies like Gazyva, Imbruvica, Venclexta, Calquence, Brukinsa, and Jaypirca have truly revolutionized our approach to treat CLL. The market for CLL is not only substantial, but still rapidly growing. However, it is important to note, despite the effectiveness of Brukinsa, it only addresses a fraction of the available treatment opportunities. Despite this significant advancement, there remains a considerable unmet medical need for new treatment options in CLL. There is a clear demand for fixed duration treatments, particularly for treatment-naive, young, and fit patients. Current phenetic-based fixed duration regimens often fall short due to various challenges, including efficacy, safety, and inconvenience. Additionally, the increasing number of patients relapsing after first-line treatment underscores the necessity for innovative treatments in a relapse refractory setting. BeOne stands out as the only company with fully owned, potentially best-in-class assets across three foundational MOAs in CLL. This provides a unique opportunity to comprehensively address the medical needs of patients across all lines of therapy and in the different subpopulations, using both monotherapy as well as our unique combinations. We are strategically positioned to tackle the unmet medical needs in CLL treatment with our wholly owned portfolio. While Brukinsa currently serves a portion of patients, we aim to develop regimens that cater to all patient segments. We are dedicated to relentlessly pursuing best-in-class options from frontline to late lines of therapy with both continued use as well as the fixed duration treatments. Now, move on to Brukinsa. Brukinsa continues to deliver exceptional value for patients around the globe. As the best-in-class BTK inhibitor, it serves as the cornerstone of our CLL franchise. In the U.S., Brukinsa leads in new patient starts for both frontline and relapse refractory CLL and across all approved indications. It boasts the most comprehensive label of any BTKI, and it is the only BTKI shown to offer superior efficacy and safety in a head-to-head trial against ibrutinib. With approvals in 75 markets, including recent launch in Japan, Brukinsa has successfully treated over 200,000 patients globally. From its inception, Brukinsa was designed to provide best-in-class 24/7 BTK inhibition. Our hypothesis was achieving complete and sustained BTK inhibition, with a result in a superior therapeutic profile. Notably, Brukinsa is the only BTKI that maintains serum concentrations significantly above its IC50, I should say only covalent BTKI, while exposure for acalabrutinib and ibrutinib remains well below their respective IC50 for the majority of the treatment period. You know, we actually had this data about 10 years ago, and we shared it with a lot of people. We said, "This is the best-in-class BTK inhibitor." Nobody believed in us. We took the hard road and did the experiment. We did this experiment in trying to demonstrate in a head-to-head fashion, this is a better BTK inhibitor based on science, based on the design. Brukinsa's superior target coverage translates into exceptional clinical efficacy. In the Alpine trial, Brukinsa exhibited sustained superior progression-free survival efficacy alongside low cardiac toxicity when compared head-to-head with ibrutinib. In the intended treated population, the PFS ratio was 0.66, with milestone PFS of 64% for Brukinsa and 53% in ibrutinib at the 42-month mark. The treatment effect is even more pronounced in high-risk Delta 17P population, where the HES ratio was 0.48, and the landmark PFS at 42 months was 59% for Brukinsa and 32% for ibrutinib. This result underscores the efficacy of Brukinsa and its potential to improve outcomes for patients with relapse refractory CLL. Maybe just add another commentary. When we began to show ORR superiority, people still do not believe this can be a better one, not until we show the PFS. So we have demonstrated to you once we can make great molecules and design the right experiments. Hopefully, next time you will believe in that. In the treatment-naive settings, Brukinsa has demonstrated impressive PFS outcomes for patients regardless of their del(17p) status. The presence of del(17p) is associated with significantly higher risk of mortality due to CLL. The graph presents PFS curves in the SEQUOIA trial from two separate arms of the treatment-naive CLL patients with or without del(17p). Both arms were treated with Brukinsa monotherapy alone. In arm C, which represents the largest prospective cohort of uniformly treated patients with del(17p), Brukinsa achieved a remarkable 60-month PFS, five-year PFS rate of 72%, comparable to the 76% in those without del(17p). The success of Brukinsa reflects our rigorous approach to drug development. We focus on creating superior molecules and are not afraid of conducting head-to-head clinical trials when necessary. We are now seeing us doing that also with Sonrotoclax and BTK degrader. These efforts have placed Brukinsa in a strong market leadership position in the U.S. within just two years of its launch in CLL, despite being nine and three years later than ibrutinib and acalabrutinib, respectively. Best drug wins. Now, I will hand the presentation to my colleagues, Remus, who will share insights on Sonrotoclax and our option for fixed duration treatment. Thank you, Lai. Good morning, everyone. I am Remus Vizon, Vice President of Clinical Development at BeOne, and I'm very excited about the opportunity to share with you our clinical development plans for our next-generation BCL2 inhibitors, Sonrotoclax. Fixed treatment duration is emerging as an important therapeutic modality in CLL, and our company is dedicated to addressing this important issue for patients and physicians. In our view, the fixed treatment duration should meet a few essential characteristics in order to be ideal for patients and give the confidence to patients and physicians to stop therapy. One, this essential element should have the capacity to achieve high efficacy, demonstrated in high rates of responses and measured by deep uMRD levels. Two, it should have the capacity to achieve long progression-free survivals, at least at the level of the BTK continuous therapy. Three, it is also important to have a favorable safety profile with minimal added toxicity, no TLS, and low rates of high-grade toxicities, and very important, no increase in death events. Four, it should be able to address the convenience factor, being an all-oral regimen with no requirement for hospitalizations and minimal number of clinical visits for TLS monitoring. All this would allow for this medicine to be accessed by most of the CLL patients. Venetoclax is currently the only BCL2 inhibitor approved and represents an important therapeutic agent for CLL patients. However, there are significant limitations with Venetoclax, and these limitations are very often being cited by the healthcare providers and even more pronounced in the community settings where access to fast laboratory results and hospital beds is limited. These limitations with Venetoclax are mainly due to the intrinsic clinical pharmacologic profile of this product. Venetoclax has a long half-life, over 24 hours, therefore accumulates in blood, and it takes a long time to achieve a steady-state level. These characteristics translate into a labor-intensive TLS monitoring due to the ramp-up and to achieve the target dose, and that you see represented here in the image. The frequent lab checks, like five to seven clinic visits, including a 24-hour time lab check for the first two dose levels, and this is in the low-risk patients, and even more frequent visits and requirement for hospitalizations and serial lab checks for high-risk patients really significantly limits the use of this product. In conclusion, we believe that a next-generation BCL2 inhibitor that could overcome these important limitations and would be able to be used by the broad CLL community is highly needed. As I showed, Venetoclax has important limitations, and more than half of the CLL patients cannot access this medicine. More so, the vast majority of patients treated in the community setting cannot access this medicine due to the safety concerns and the feasibility around the ramp-up. Despite these challenges, Venetoclax has a blockbuster drug status with multi-billion dollar annual revenue and with opportunities to further increase in annual sales over the next few years. Now, imagine the clinical and commercial value of a next-generation BCL2 inhibitor with superior clinical activity, better safety, the ability to be accessed by the broad CLL population, including in the community setting, but also with a broader label and more indications. Sonrotoclax, our next-generation BCL2 inhibitor, has key characteristics that position this product to be best in class with superior efficacy and a more favorable safety profile. On one hand, the higher potency, 14 times the increased potency in preclinical models versus Venetoclax, may translate in superior efficacy with much deeper and longer responses. On the other hand, the improved selectivity, shorter half-life, and no drug accumulation in the blood can offer a more favorable overall safety profile with less treatment-associated adverse events. Also, very important, it offers the opportunity for a shorter ramp-up, a shorter and safer and more patient-friendly ramp-up that can be used by all the CLL patients, including in the community setting. These important elements give Sonrotoclax the potential to be a superior product that could be used by the broad CLL population. Now, I'm honored to introduce you to Dr. Jacob Soumerai, Assistant Professor of Medicine, Harvard Medical School, hematologist-oncologist at Massachusetts General Hospital, a key opinion leader in CLL and the BCL2 malignancies, and also a principal investigator in multiple Sonrotoclax clinical trials. Dr. Soumerai is going to walk you through some of the most recent data with Sonrotoclax in combination with zanubrutinib and will share his perspective on this product and its results. Dr. Soumerai? Thank you very much. BTK and BCL2 inhibitors have distinct and complementary mechanisms of action. Besides the anti-proliferative effects of BTK inhibitors in patients with B-cell malignancies, we know that BTK inhibition interacts with multiple important cellular functions. For instance, it impairs the homing of malignant B cells to lymphoid tissues, where they are normally receiving growth signals and other supportive signals from the tumor microenvironment. This results in the migration of malignant B cells into the peripheral blood, where we know that BCL2 inhibitors can more effectively induce apoptosis and kill. Indeed, combinations of BTK and BCL2 inhibitors have demonstrated synergistic activity in preclinical models, and importantly, the combination of BTK and BCL2 inhibitors also results in synergistic efficacy when used in patients with B-cell malignancies. Now, BGB-11417-101 is a global phase I-II open-label study of Sonrotoclax alone or in combination with zanubrutinib and/or obinutuzumab in patients with B-cell malignancies. Multiple combination dose expansion cohorts have been completed, and today I'm going to review recently updated data, including data presented at EHA in CLL and mantle cell lymphoma. Starting with the Sonrotoclax and zanubrutinib combination in treatment-naive CLL, safety outcomes are shown here on this slide. No cases of laboratory or clinical tumor lysis syndrome occurred on study. Most treatment-emergent adverse events were grade I or II. Few grade III or IV treatment-emergent adverse events occurred. The most common treatment-emergent grade III-IV adverse event was neutropenia, with grade I-II neutropenia in 7.9% of patients and grade III or IV neutropenia in 27.9% of patients. Importantly, this was transient, did not lead to higher rates of grade III or worse infections, and no cases of febrile neutropenia occurred on study. GI toxicities, which are an important class effect of BCL2 inhibitors, were relatively infrequent and predominantly grade I. No fatal treatment-emergent adverse events occurred on this study. In the recently updated analysis, no new safety signals were observed with longer follow-up with Sonrotoclax and zanubrutinib in treatment-naive CLL. Measurable residual disease, or MRD, outcomes are shown on this slide for patients with treatment-naive CLL receiving Sonrotoclax and zanubrutinib. We observed high rates of early undetectable MRD at a threshold of 10 to the minus four, or uMRD4, including in high-risk patients such as those with an unmutated IgHV and deletion 17P. The median time to undetectable MRD4 was 7.1 months for patients with unmutated IgHV and 7.2 months for patients with mutated IgHV. This includes a three-month lead-in with zanubrutinib alone and is significantly more rapid than what one would expect based on previous data. 92% of patients with this combination achieved undetectable MRD4 at week 48 of the combination. Now, these data are particularly encouraging given previous evidence that more rapid MRD responses have been associated with prolonged progression-free survival outcomes among patients with CLL receiving BTK-BCL2-based combinations. Progression-free survival, or PFS, outcomes for patients with treatment-naive CLL receiving Sonrotoclax and zanubrutinib are shown on this slide. With a median follow-up of 25.5 months, the median progression-free survival has not been reached. No progression-free survival events have occurred in the 320 milligram Sonrotoclax cohort, and one patient in the 160 milligram Sonrotoclax cohort had Richter's transformation, adiel BCL, which occurred at eight months of the combination. Now, importantly, an important feature of this study was that it allowed for elective treatment discontinuation at week 96. Thirty-five patients have reached the week 96 time point and elected to stop therapy. All remain in an ongoing remission with a median of three months off therapy, with some at 12 months off therapy. Sonrotoclax and zanubrutinib was also evaluated in relapsed to refractory CLL, and safety outcomes are shown here on this slide. Importantly, these data are very consistent with what was seen in treatment-naive CLL, with no new safety signals observed in the relapsed or refractory setting. Measurable residual disease and progression-free survival outcomes are shown on this slide. 80% of patients treated at the recommended phase II dose of 320 milligrams of Sonrotoclax with zanubrutinib at the approved dose achieved undetectable MRD4. Looking to the PFS curves, responses appear durable. At a median of 19.6 months of follow-up, the median progression-free survival has not been reached. Two PFS events have occurred. These were both progression events on active therapy in patients with deletion 17P CLL, one at the 40 milligram dose and one at the 320 milligram Sonrotoclax dose. Like in the treatment-naive setting, this protocol allowed for treatment discontinuation electively in patients reaching the 96-week time point. 13 patients have elected to stop therapy after 96 weeks of the combination, and all remain in an ongoing remission after a median of four and a half months off therapy. Sonrotoclax and zanubrutinib was also evaluated in relapsed or refractory mantle cell lymphoma, where we currently do not have an FDA-approved BCL2 inhibitor. Safety outcomes for this combination in mantle cell lymphoma are shown here, and were again consistent with what was seen in CLL, notably with no cases of laboratory or clinical tumor lysis syndrome. An MTD was not reached up to a sonrotoclax dose of 640 milligrams, and 320 milligrams of sonrotoclax was selected as a recommended phase II dose for sonrotoclax when used in combination with zanubrutinib in patients with mantle cell lymphoma. We observed deep and durable responses in patients with relapsed or refractory mantle cell lymphoma treated with sonrotoclax and zanubrutinib. At the recommended phase II dose, the overall response rate was 82%, and the complete response rate was 67%. The median duration of response was not reached with a median follow-up of 17.7 months, and 84% of patients remain in an ongoing response at 24 months. Importantly, of 18 patients who achieved a complete response, 16 are in an ongoing complete response at a median follow-up of 13 months. Sonrotoclax and obinutuzumab was also evaluated in treatment-naive CLL. Now, these data have not previously been reported and are planned to be presented at the upcoming ASH annual meeting. Sonrotoclax and obinutuzumab was well tolerated with a safety profile that's consistent with the individual agents, suggesting no additional combinatorial toxicity, and demonstrated promising efficacy in treatment-naive CLL. 87% of patients achieved undetectable MRD4 by week 36, and 90% of patients achieved UMRD4 by week 60. In summary, the all-oral combination of Sonrotoclax and zanubrutinib is a very promising fixed-duration treatment combination for patients with CLL and mantle cell lymphoma. Now, this combination is associated with a favorable safety profile, with the potential for a significantly more convenient ramp-up. Additionally, Sonrotoclax and zanubrutinib demonstrated very promising efficacy in treatment-naive and relapsed or refractory CLL, and in mantle cell lymphoma in the relapsed refractory setting. In CLL, we observed high rates of early uMRD4, including across molecular risk factors. This combination has the potential to become a new standard in CLL and mantle cell lymphoma, and I'd like to just take a moment to thank all of the patients and their families who participated in the studies, and of course, my co-authors and co-investigators. Thank you very much for your attention. Thank you, Dr. Soumerai. As you just heard, the impressive results observed with Sonrotoclax in combination with zanubrutinib really positions this combination to offer the best-in-class fixed-duration regimen in CLL. When we look across the currently available limited-duration treatment options, Sonrotoclax plus zanubrutinib really demonstrates the highest level of deep responses of efficacy, with deep responses of over 90% uMRD rates, unmatched PFS for the respective follow-up, but also a favorable safety profile with less high grades of adverse events, and importantly, no deaths. In contrast, the currently available fixed-duration therapy shows limitations either from efficacy or safety perspective. In regards to safety, it is important to mention a few safety concerns, like the infusion reactions observed with the infusion of obinutuzumab, the toxicity, the cardiac toxicity, and cardiac deaths associated with the use of ibrutinib, but also the high rates of grade III or higher toxicities, like infections or other treatment-emerging adverse events leading to deaths or treatment discontinuations. From an efficacy perspective, there are some important deficiencies, like the low rates of undetectable MRD observed with acalabrutinib plus venetoclax combination, where only 34% of patients achieved uMRD at the end of treatment, but also the underwhelming three-year PFS rate of near 77%. This is despite the very fit population that was studied with this combination. For the Sonrotoclax plus zanubrutinib combination, in addition to the superior and the favorable safety profile, I would like to remind you that we did not observe any clinical or laboratory TLS, and we are continuing to optimize the ramp-up schedule for Sonrotoclax. We are very optimistic that for the vast majority of patients, only one clinical visit is going to be required after the zanubrutinib lead-in. In conclusion, we believe that this therapy has the potential to be a game changer as a fixed-duration treatment for CLL patients. The Sonrotoclax plus zanubrutinib combination showed the highest level of uMRD, but not only that, they also achieved this uMRD in a very short time, and this element is a further testament or evidence to the potency and superior clinical activity of these two products. The fast kinetics in achieving the undetectable MRD were observed with the Sonrotoclax zanubrutinib combination, regardless of the high-risk features, like the mutated or unmutated IgHV status, something that was not observed with other venetoclax-based combinations, like ibrutinib-venetoclax data that was recently shared from the FLAIR study, where the patients with a mutated IgHV seem to have a slower and lower MRD. Now, looking ahead to our clinical development plans for Sonrotoclax, currently we have few important phase III registrational studies that I would like to highlight here. Celestial Treatment-Naive CLL 301 study is a global phase III study that is designed to demonstrate the superiority of Sonrotoclax zanubrutinib over venetoclax obinutuzumab. This is currently the only registrational study designed to investigate the superiority of a fixed-duration regimen against the current standard of care. This study completed enrollment of almost 700 patients in less than 14 months, and this achievement is a testament of the high interest, trust, and excitement of investigators in this combination, but is also a testament of the unique capacity of BeOne Medicines to run large phase III clinical trials at the highest standards. The same combination of Sonrotoclax plus zanubrutinib is currently being investigated in mantle cell lymphoma. Celestial Relapsed Refractory MCL 302 is an ongoing phase III trial that is looking to demonstrate the superiority of Sonrotoclax plus zanubrutinib over zanubrutinib plus placebo. In this trial, Sonrotoclax is given for two years, and the zanubrutinib is given to progression or intolerance, and the primary endpoint of this study is in the PFS by Independent Review Committee. This trial is also currently enrolling. We received high interest for this trial, and we anticipate a very fast enrollment. We are pursuing also other combinations of Sonrotoclax, like with the anti-CD20 antibody. In the relapsed refractory CLL setting, we have a phase III study that is currently ongoing, Celestial Relapsed Refractory 303 study, that was developed and is running collaborations with the German CLL study group. This is an important phase III study that is designed to demonstrate the PFS superiority of Sonrotoclax either plus obinutuzumab or rituximab versus venetoclax rituximab, which is the current standard of care in this setting. This study provides also the opportunity to run a head-to-head comparison of Sonrotoclax versus venetoclax, and we are very confident that it will demonstrate the superiority of Sonrotoclax as a next-generation BCL2 inhibitor. While CLL and MCL remain our priority indications, we are moving aggressively to expand the clinical opportunity of Sonrotoclax and maximize its clinical potential. Multiple myeloma represents an indication, an important indication, and a vast market, and patients with a translocation 11-14 represents about 20% of these myeloma patients. Venetoclax was evaluated in this indication at the higher dose levels, however, failed to show significant clinical benefit due to toxicity and limited efficacy. The combination of Sonrotoclax plus dexamethasone has demonstrated very compelling clinical data with high response rates of 78% across all dose levels and over 80% at the 640 milligrams of Sonrotoclax, data that compares favorably with the previous venetoclax results in this indication. Building on these promising results, a study of the triple combination of Sonrotoclax, daratumumab, and dexamethasone is currently ongoing with positive preliminary safety data, and a pivotal phase III study in the second-line multiple myeloma of Sonrotoclax triplet is also being currently planned. Here we are presenting an overview of the broad clinical development plan and clinical studies with Sonrotoclax that are designed to maximize the clinical and commercial value of Sonrotoclax, but are also designed to further increase the clinical opportunities with our other internal assets. It is worth highlighting that we have multiple registrational studies ongoing that offer the opportunity to register Sonrotoclax in multiple indications, either as a single agent like MCL, CLL, or Waldenstrom, but also other various combinations. Also important to note, market applications for Sonrotoclax were already initiated in China based on the preliminary results from two studies, relapsed refractory CLL and relapsed refractory MCL, and the applications were accepted by the regulatory authority in China. Also, a global filing for Sonrotoclax in relapsed refractory MCL indication is planned for the second half of 2025, and we are very excited about this potential first global submission and potential approval. I hope you are as excited about Sonrotoclax as we are, and I would like to hand it over to my colleague Amit to provide you an overview of our BTK-CDAC program. Thank you. Thank you, Remus. Good morning, everyone. My name is Amit Agarwal, and I'm a VP of Clinical Development here at BeOne Medicines. It is my great pleasure to share with you an update on BGB-16673 and also walk you through why we believe this asset has the potential to be a cornerstone of our hematology pipeline. Let's start with the why. Despite many advances, CLL still remains incurable, and there is an enduring unmet need for these patients. As the treatment landscape evolves, more patients will have received the current generation of therapies in the front line. There is an important need to develop drugs with novel mechanisms that can overcome resistance when these patients progress. In this context, we're developing BGB-16673 to be the potential first-in-class BTK degrader. This drug is fundamentally different than traditional small molecule inhibitors. This is a first drug from our proprietary CDAC platform. Think of it as a molecular machine that not only blocks BTK, but completely removes it. This mechanism has several advantages. The first is because of a catalytic action, a single degrader molecule can actually degrade thousands of the target protein, which makes it much more potent. The second is that the mechanism allows for being able to not only overcome existing mutations, but also delay the emergence of new mutations. The third is that the degrader is able to remove the entire protein scaffold and shut down both the kinase-dependent and independent signaling, which traditional small molecule inhibitors cannot do. We have seen evidence of all three aspects of this MOA translate into meaningful clinical benefit. This is just a better mousetrap. We have tested this drug in a global phase I-II study called the Cadence 101 study across B-cell malignancies. Most of the data that we have shared comes from the phase I portion of the study. The cohorts that I will present today include the relapsed CLL, Waldenstrom's, and indolent lymphoma histologies. I will point out that we are also enrolling patients in the phase II part of this study, and in particular in the relapsed CLL cohort, we have enrolled more than 100 patients now that we could file with in 2026. Let me talk about the types of patients we've enrolled on this study so far. The study has enrolled heavily pretreated patients who've seen multiple lines of prior therapy. In case of CLL, we have patients with a median of four prior lines of therapy, including a BTK inhibitor, a BCL2 inhibitor, and other treatments. We have several patients who've also received a non-covalent BTK inhibitor like pirtobrutinib before coming onto this study. An important aspect to point out here is that of the patients who've received a BTK inhibitor, most of them, 90%, got off that BTK inhibitor due to progressive disease. This is important context when we look at the efficacy in this group in a minute. Let me start with the safety first. The safety profile here is consistent with on-target BTK degradation. The most common adverse events we've seen include cytopenias, with neutropenia being the most common. There are some adverse events associated with platelet dysfunction, like contusion and bruising, and we do see some infections in the form of COVID-19 and other infections. The rate of drug discontinuations due to adverse events in this lateline population is less than 5%. What we have not seen are off-target BTK-directed side effects like arrhythmias, and again, we think this is an attribute of the program as well as the mechanism. With some patients now continuing on treatment for more than two years, we're building long-term safety data on this molecule. Moving on to efficacy, for the relapsed CLL cohort at the 200 milligrams dose, which is the dose that we're moving forward into the phase III study with, we see that the overall response rate is 94%. This includes some complete responses, which are rare with the BTK-directed treatment. These responses occur relatively quickly and typically at the time of the first disease assessment. In terms of some key subgroups, you can see on the right, responses are consistently noted regardless of prior exposures or mutations. In the patients who are the so-called triple-exposed patients, meaning that they've received a covalent BTK inhibitor, a non-covalent BTK inhibitor, and a BCL2 inhibitor before coming onto the study, we see response rates of 75%. These patients truly have no treatment options left, and a 75% response rate in this group of patients is highly encouraging. With longer follow-up, we have seen that these responses are also durable. In the graph on the left, you can see that in the Cadence 101 trial, the durability looks very promising. On the right-hand side, you can see the Bruin 3-1 results for pirtobrutinib. With the normal caveats of a cross-trial comparison in place, you can see that in this group of relapsed and refractory patients, there is a strong reason to believe that the degrader offers a much better mechanism than an inhibitor for these patients. These results give us the confidence to launch a head-to-head study against pirtobrutinib. Relapsed refractory patients will be randomized to receive either 16673 or pirtobrutinib monotherapy. We have engaged several health authorities for this trial and have an agreement on the design and the dose. We're planning to start the study later this year. We're also seeing a strong signal in other B-cell malignancies. For Waldenstrom's, in a group of heavily pretreated patients, we have seen an impressive response rate of close to 85%. Interestingly, the responses occur quickly and also deepen over time. We now have VGPRs in almost a third of these patients. The responses are seen in particularly hard-to-treat populations based on both the types of prior treatments that they've received, but also genetic risk factors. As you can see in the PFS curve on the right, these responses also appear to be durable. We have now opened enrollment on the phase II expansion of the Waldenstrom's cohort and are planning the next steps for registration in this setting. Moving to other indolent lymphomas, in this study in follicular and marginal zone patients, we're seeing meaningful responses, including complete responses. As a single agent, this activity is very promising and could allow us to develop this drug in these diseases, particularly as a combination. Finally, I'm going to share a clinical vignette from this trial that illustrates what this drug can do. This is a 69-year-old gentleman who was diagnosed with CLL in 2009 and received multiple rounds of standard treatment. In 2024, his disease progressed and he was diagnosed with Richter's transformation. Richter's represents a serious, often fatal complication in progression of CLL. He initially received standard treatment of R-CHOP for this, but had no response. He came onto the study in early 2025, and you can see he had significant disease burden at the time of study entry. This is the response after being on the trial for three weeks, three weeks of an oral treatment. You can see that his lymph nodes have dramatically reduced. This case nicely highlights the transformative potential of this drug. We have a broad clinical program designed to establish BGB-16673 as a foundational therapy. You heard earlier from Lai. We're moving fast with this program. This is driven not only by our own conviction in the drug, but also great enthusiasm that we've seen from our investigators on these studies. We plan to file for an accelerated approval in 2026. We already have ongoing registration studies as a monotherapy, and the head-to-head against Jaypirca will start later this year. We're also looking at the combination of the BTK-CDAC and Sonrotoclax as a fixed duration for CLL. In the front line, we have started some work looking at the monotherapy as well as combination settings for proof-of-concept data that will inform our frontline strategy. Beyond CLL, we're also actively assessing other indications, both as a monotherapy as well as combinations. We believe that 16673 has the potential to reshape the treatment landscape of B-cell malignancies. Now, let me take a moment to recap where we are and where we are headed. We've built a comprehensive registrational program that spans the full spectrum of CLL, from the treatment naive to the relapsed and refractory settings. In the frontline setting, Brukinsa has already established itself as the leading BTK inhibitor with this best-in-class profile. With the combination of Brukinsa and Sonrotoclax, we're now advancing what we believe will be the best-in-class fixed duration regimen. For relapsed patients, we will bring forward several options, both as a continuous monotherapy as well as in combinations. Our BTK degrader should become a foundational therapy in this setting. We're also advancing fixed duration regimens, including CD20 antibody and Sonrotoclax, and evaluating the CDAC plus onro combination as a potential next-gen option. This program is designed to offer patients important options throughout their CLL journey and make BeOne Medicines the leader in CLL. You've heard the details of our oncogenic signaling cluster of drugs that will provide near-term value. Now, I want to zoom out and talk a little bit about our research efforts. We are focused on developing several novel modalities. We're developing modalities that have orthogonal mechanisms and should allow us to make a broad impact on B-cell malignancies. I would like to talk about the T-cell engager cluster and our cell therapy platform. We're developing three different T-cell engagers: a CD19 by 20 trispecific, a BAFFR CD22 trispecific, and a CD79 with an undisclosed target trispecific. We're also developing co-stimulatory drugs with CD20 by CD28 and CD20 by 41BB, the leading drugs. Often, the cause for disease progression in the context of bispecifics has been the loss of tumor antigen. To obtain broader coverage with the initial response and to avoid antigen loss, we're developing trispecifics that will bind to distinct tumor antigens. To complement this approach, we're also looking at co-stimulatory drugs that have shown significant synergy with the T-cell engagers. As shown here, our CD19, CD20 trispecific, and the CD20, CD28 co-stimulatory drug have compared favorably to the competitor molecules and also demonstrated great synergy together in preclinical models. The CD19, CD20 trispecific is on target to enter the clinic in 2026, and the CD20 by CD28 drug in early 2027. Finally, I want to introduce our cell therapy platform. We all know that autologous cell therapies have made a major impact on the outcomes in hematologic malignancies, but have faced several challenges that have limited their wide adoption. Initial efforts to address some of these challenges with allogeneic cell therapies have not been successful. We're developing an IPSC-derived platform that we believe will address some of these challenges. The platform has been developed to address CMC issues around differentiation and expansion, and there are several key genetic changes that provide hypoimmunity, prolonged survival, as well as potency. A unique aspect of this platform is a proprietary signal converter that provides these cells with significant potency. I'll show a little bit of the impact of a signal converter with the experiment on the right. What you can see in blue is what would typically happen in a preclinical killing assay with some of the older generation of allogeneic cell therapies. With the signal converter on board, as well as our entire platform, you can see that we see continuous killing of these cells without any evidence of exhaustion. We think that these are optimistic changes, and if successful, this will lead to a highly differentiated cell therapy solution, which we're planning to enter the clinic with in 2026. To summarize, we're not just building a pipeline, but rather systematically building a franchise. We're doing it with a sense of urgency, scientific rigor, and a clear focus of delivering impact for patients and value for investors. With that, I thank you for your attention. I think next on the agenda, we're going to take a 10-minute break. You'll want to come back because Mark has some very exciting updates on the solid tumor portfolio as well. Thank you. Okay, great. Welcome back, everybody. My thanks as well for joining today. Come for hematology and stay for solid tumors. My name is Mark Lanassa. I'm the Chief Medical Officer for Solid Tumors at BeOne Medicines. Today I will be providing an update on our solid tumor portfolio, focusing on our progress and future plans. Indeed, Lai and I were chatting before today's session, and we were commenting on how, since our last R&D day two years ago, about essentially everything that I'm about to share with you is new since our last R&D day. Our pipeline includes diverse modalities and mechanisms across three franchises: breast and gynecologic cancers, lung cancer, and gastrointestinal cancers. Today, I am extremely excited to share updates from each of our core disease area franchises, with a focus on emerging data, new targets, and exciting in-portfolio combinations. Let's begin with our breast and gynecologic cancer franchise. We are establishing an innovative approach to these cancers with several promising candidates in our pipeline, most notably our potent and selective CDK4 inhibitor. We are committed to advancing research and bringing new treatments to market for breast and gynecologic tumors. It is important to recognize that breast cancer has been a clinical area of focus for BeOne Medicines for only approximately 18 months. In each of our franchises, the research organization focuses on both established and novel targets that enable in-portfolio combinations that can maximize patient impact. In these overview slides, these areas of focus are highlighted as clusters. Key to our breast cancer programs are the investigational molecules in the cell cycle cluster, including our CDK4 selective inhibitor, our clinical stage CDK2 targeting small molecule, as well as our novel CDK2 targeting CDAC that will enter the clinic by the end of this year. There is also a growing body of work in our estrogen receptor cluster, where we are exploring agents that can bring benefit in combination with estrogen blockade, including a novel BCL2 inhibitor and a selective CAT6AB molecule. ADCs are also an important modality across the portfolio, with our B7-H4 targeting ADC being most advanced, with additional multi-specific ADCs progressing through preclinical development. While not a focus of today's presentation, we recently achieved the first human dose of our CALODN6 by CD3 bispecific, which is our first internally discovered clinical stage CD3 conjugated T cell engager. I'd like to begin with our CDK4 selective inhibitor, which is the foundational molecule in our breast cancer franchise. CDK4/6 inhibitors are one of the largest commercial markets in solid tumor oncology, valued at approximately $13 billion and continuing to grow. One of the primary issues with CDK4/6 inhibitors is hematologic toxicity, which leads to dosing interruptions, resulting in suboptimal target coverage. Additionally, there are safety concerns due to off-target inhibition. In an effort to address these limitations, we developed a selective and potent CDK4 inhibitor designed to address the limitations of current CDK4/6. It aims to provide superior therapeutic benefits by reducing hematologic toxicity and off-target inhibition. The bar graphs on the right panel of the slide show the potency and selectivity of 43395. In a preclinical cellular assay, our CDK4 inhibitor more potently inhibits proliferation than any of the approved CDK4/6 inhibitors. It is approximately four-fold more potent than Pfizer's CAT6AB. This potency conveys a 38-fold 4 versus 6 selectivity, almost twice as selective as CAT6AB. Although we were second to enter the clinic, we have moved very quickly through phase one development, enabling first-in-class potential. We have closed the development time gap with Pfizer's CAT6AB from three and a half years from first human dose to less than 18 months to a phase three start in frontline hormone receptor positive breast cancer. Today, we are honored to have Dr. Shom Goel, a key opinion leader in breast cancer, presenting the CDK4 data update. Dr. Goel is an Associate Professor and clinician scientist at the University of Melbourne and the Peter MacCallum Cancer Centre. He serves as the global PI and translational PI for four randomized clinical trials in breast cancer and has over 60 publications, including recent works in high-impact journals such as Nature, Cancer Cell, and Nature Cancer. We're excited to hear Dr. Goel's insights on our selective CDK4 inhibitor and its potential impact on breast cancer treatment. Dr. Goel. Good morning, everyone. It's a pleasure to be here. CDK4/6 inhibitors, in a nutshell, they work by inhibiting the CDK4/6 enzymatic complex, and this leads to prevention of phosphorylation of the RB tumor suppressor protein. Ultimately, this stops cancer cells from dividing, leading to cessation of tumor growth and, over time, tumor regression. We have three approved CDK4/6 inhibitors, but each comes with toxicity issues and also the problem of resistance, which ultimately emerges with ongoing treatment. Common side effects include neutropenia with all the drugs and diarrhea with some, and hematologic toxicity as well, which is thought to be largely driven by inhibition of CDK6. BGB-43395, which is a potent and selective CDK4 inhibitor, aims to provide this select inhibition of CDK4, minimizing toxicity and preventing the emergence of resistance. I would like to start by sharing with you the study design for the first in-human study of BGB-43395, the selective CDK4 inhibitor. As of June 9th, this phase I A study has enrolled a total of 284 patients, with 178 of them treated in one of three dose escalation arms: the CDK4 monotherapy, or combination with fulvestrant, or combination with letrozole. A fourth arm, combining this medicine with elacestrant, will initiate soon. The remaining 106 patients have been enrolled into combination dose optimization arms. Based on PK and PD data, which I'm going to share with you, we've selected three dose levels for that dose optimization: 240 milligrams, 400 milligrams, and 600 milligrams orally twice a day. I'd also like to point out that this is truly a global study with France and the U.S. leading enrollment. BGB-43395, here I'm showing you the PK, and it has shown favorable PK characteristics. The panels at the bottom show dose-proportional and linear pharmacokinetics within the dose range of 240-600 milligrams twice a day. The mean elimination half-life is 13 hours. Importantly, exposures are not impacted by co-administration of either fulvestrant or letrozole. Also, there were no notable differences in exposures observed between non-Asian and Asian populations. On this slide, we present some pharmacodynamic data. We observed a dose-dependent and durable reduction in TK1 activity. This is a biomarker of cellular replication at doses 240 milligrams twice a day or higher. That is what led us to select the 240, 400, and 600 milligram twice daily doses for the dose optimization. I highlight the dose-dependent nature of this PD effect, with less TK1 inhibition seen at doses below 240 milligrams, and that this PD effect is sustained with no rebound observed at cycle two, day one. In the bottom right panel, early CT DNA decrease, which is another potential response biomarker, was also observed starting from the 240 milligram dose level in the fulvestrant combination. Both the TK1 data and the CT DNA data suggest that doses of 240 milligrams twice a day and above are biologically active, making these the doses for further development, for focus on for further development. Here I'm showing the safety data for almost 100 patients who received BGB-43395 in combination with fulvestrant during both the dose escalation phase and dose optimization. The safety data I'm showing you are again limited to those three dose levels, which are under consideration for further studies. Overall, the tolerability is excellent, with related grade 3 or higher events observed in approximately 20% of patients, and only a single patient in each study phase discontinuing due to a related adverse event. When we look at some specific adverse events, diarrhea was frequent. However, these events were predominantly low-grade and straightforward to manage with once-daily administration of loperamide. None of the cases of grade 3 diarrhea observed in the dose optimization phase resulted in a dose reduction or discontinuation. When we look at the heme toxicity, the rates of hematologic toxicity are very favorable in regards to any grade of anemia, neutropenia, or thrombocytopenia. These rates compare favorably to the rates of hematologic toxicity with the approved CDK4/6 inhibitors and to atiromicinabin. These hematologic AEs are important because they can result in dose interruptions, dose reductions, and thereby ultimately reducing effective CDK4 target coverage. Here we're presenting the tumor burden change from baseline in patients treated in combination with fulvestrant during dose escalation. Please note that we are only sharing efficacy from the dose escalation phase here rather than the dose optimization phase, because that latter data, the optimization data, is still quite immature and will be used to identify a recommended phase three dose. The data that you can see on the screen here shows preliminary anti-tumor activity in extensively pretreated dose escalation patients. During this dose escalation phase, 37 patients, including 29 with breast cancer, were treated with the fulvestrant combination at doses from 240 up to 600 milligrams twice a day. Now, during that dose escalation phase, breast cancer patients were permitted to have bone-only metastatic disease, and therefore 10 of those patients are not response evaluable. It's a heavily pretreated group of patients, as you can see. The median number of prior lines of therapy in the metastatic setting was four. All patients had received prior chemotherapy or an ADC, as well as prior endocrine therapy. The median follow-up at the moment is limited at three months. Given the cytostatic mechanism of action of these drugs, the response rate may improve over time. The objective response rate was 11% amongst the patients with breast cancer and 15% in the full cohort. Time to event endpoints such as PFS are immature at the moment and will be presented at a future meeting. It is important to note that, in my opinion, the response rate is also immature at this point. This is a class of drugs where traditionally median times to response sit somewhere between three or five months. With our median follow-up of only three months, we may expect the response rate to change over time. Nonetheless, what we can see here is that among this advanced patient population, heavily pretreated, the results show that BGB-43395 in combination with fulvestrant does show meaningful anti-tumor activity. In summary, these data show that BGB-43395 has a strong pharmacodynamic effect across a range of well-tolerated doses. The safety data show a potential best-in-class hematologic safety profile with low-grade and readily manageable diarrhea. Emerging evidence also shows clinical efficacy in extensively pretreated post-CDK4/6 patients at those doses with pharmacodynamic activity. This positions BGB-43395 as a promising candidate for further development. We are excited about the clear path forward towards registration-enabling studies and look forward to initiating these studies within the next 6 to 12 months. I would like to thank the study patients, my co-investigators on this phase I 101 study, and I would like to pass the presentation back to Mark. Thank you. Thanks so much, Shom. Next, I would like to share an update for our promising B7-H4 targeting ADC. B7-H4 is frequently expressed in breast and gynecologic cancers. As you can see in the lower right panel, B7-H4 has minimal expression in normal tissue. This high tumor versus normal selectivity makes B7-H4 an attractive ADC target. Additionally, the drug linker design enhances the therapeutic profile of this ADC, while the non-PGP substrate and non-PGP substrate payload with a DAR of six yields strong bystander effect, contributing to its efficacy. We recently made the initial data disclosure at ASCO. Today, I will share updated data and new analyses. These data indicate a favorable safety profile and compelling emerging efficacy. Here, we're sharing data across selected dose levels. The most frequently reported adverse events include low-grade nausea, neutropenia, and fatigue. Neutropenia and thrombocytopenia were the most common grade three or greater AEs. The dose-limiting toxicities were principally hematologic and were observed at the higher dose levels. However, there have been no related AEs that have led to study drug discontinuation. Overall, the early clinical data indicates a favorable safety profile as monotherapy across a broad range of dose levels. Here, we are showing the updated efficacy data as of earlier this month for our B7-H4 ADC, showing its promising anti-tumor activity in breast and gynecologic cancers. A total of 95 patients were treated across nine different dose levels with a median of four prior lines of therapy. This waterfall plot is limited to the 68 patients with breast, endometrial, and ovarian cancer. These are currently the target tumor types for subsequent lead development. The confirmed objective response rate is 24%, and the unconfirmed response rate is 29%, with 14 out of 20 responses ongoing. We observe an emerging dose-response relationship. For example, if the analysis is limited to the 6 milligram per kilogram dose level, the confirmed response rate increases to 43% and unconfirmed to 48%. We also observe an association between B7-H4 expression and efficacy. Among the enrolled breast and GYN patients, the unconfirmed response rate overall is 29%. If we limit to the half of patients with higher B7-H4 expression, the response rate increases to 42.4%. In conclusion, our B7-H4 ADC shows favorable safety and compelling early efficacy. Dose optimization expansions and biomarker selection for breast and gynecologic cancers will initiate in the third quarter, and planning is underway for phase three study starts in 2026. I'd next like to present BGB-68501, a potent and selective CDK2 inhibitor. CDK2 is an important target in breast cancer because CDK2 activation may convey resistance to CDK4 inhibition. Preclinically, BGB-68501 shows strong potency and selectivity, which may lead to improved efficacy and safety profile. Forty-nine patients with pretreated solid tumors were recently presented at ASCO. These data indeed reveal a favorable hematologic toxicity profile with no dose-limiting toxicities. Common adverse events included nausea, vomiting, and fatigue. Nausea and vomiting are mitigated with scheduled antiemetics, and a food effects study is ongoing, which may further improve nausea. The preliminary efficacy results show a 6% unconfirmed response rate and a 39% stable disease rate, which supports our core development intent for combinations and breast cancer. Our breast cancer franchise will soon add two additional innovative molecules that promise improved patient outcomes in hormone receptor-positive breast cancer: a CDK2 CDAC and a CAT6AB inhibitor. Both molecules will begin clinical studies prior to the end of this year. This is our potential first-in-class CDK2 selective CDAC. We believe that this CDAC has three potential key advantages over a small molecule inhibitor of CDK2. First, the catalytic mechanism that you heard about from Amit conveys superior target inhibition. Preclinical potency of our CDK2 CDAC is 30 times that of Pfizer CDK2 and 5-10 times that of our first-generation CDK2 small molecule inhibitor. Second, because of the target binding geometry, our CDK2 degrader has much greater selectivity for CDK2 over CDK1 compared to any small molecule inhibitor. The IC50 for CDK1 inhibition is greater than 10 micromolar, a greater than 4 log difference from the IC50 for CDK2 inhibition. Finally, this molecule is anticipated to have a longer half-life than small molecule inhibitors, which will enable more continuous target coverage with relatively flat PK, which may in turn further improve safety. To conclude the update on our breast cancer franchise, BGB75202 is a potent and selective CAT6AB inhibitor. In the upper right figure, we show greater potency than the Pfizer CAT6AB against the number of different hormone receptor-positive breast cancer cell lines. Importantly, BGB75202 also has a greater than 10-fold higher selectivity for CAT6 over CAT7, which is anticipated to improve the hematologic toxicity profile when compared to Pfizer's molecule. In just 18 months, we've made significant strides establishing an innovative breast and gynecologic franchise with an initial focus on hormone receptor-positive breast cancer, growing to eight clinical molecules by the end of this year. Just to reinforce the point that Lai made earlier, eight molecules in less than 24 months: CDK4, CDK2, CDK2 CDAC, CAT6AB, BCL2, B7-H4, our CD3, or Clon6 by CD3, and MUC1 by CD16 bispecific antibodies. The emerging data for our CDK4 inhibitor shows a differentiated hematologic safety profile with a promising benefit-risk balance as we move towards phase three trials. The B7-H4 ADC shows substantial efficacy with manageable toxicity, and we are planning subsequent registration-intent studies in ovarian, endometrial, and breast cancer. These lead molecules, along with CDK2, CAT6AB, and BCL2, provide unique development opportunities in breast and gynecologic cancers. Next, I'd like to provide an update on our emerging lung cancer franchise. I'm excited to share our vision for building a truly industry-leading lung cancer franchise. We are dedicated to advancing the field and improving outcomes for patients with lung cancer, featuring innovative and intentionally designed molecules. Our current focus is on three driver mutation populations in innovative ADCs. The three biomarker clusters include, first, targeting tumors with MTAP deletion; second, targeting EGFR mutations with our EGFR-targeting CDAC; and third, oncogenic KRAS mutations. I will present our MTAP cluster and the EGFR-targeting molecules in this section, and we'll cover KRAS as part of the GI franchise overview. We also believe that the full potential of ADCs has not yet been met in non-small cell lung cancer. We have a lot of specific ADCs in clinical development, including a B7-H3 and CEA-targeting ADC, and we have additional candidates with multi-targeted ADCs and, in the future, ADCs with novel payloads. We are very excited to show the early progress of our MTA-cooperative PRMT5 inhibitor and MAT2A inhibitor. First, let's discuss our potential best-in-class PRMT5 inhibitor. This compound has demonstrated superior preclinical potency and selectivity when compared with essentially all clinical-stage competitor molecules. I will provide our first clinical update for this molecule today. MAT2A has mechanistic synergy when combined with PRMT5 and induces robust efficacy in animal models. Both of our compounds are highly brain-penetrant, which is an important characteristic for lung cancer and other tumor types that unfortunately have frequent brain metastases. Let's begin with the emerging data for our PRMT5 inhibitor. Here are the initial pharmacodynamic data for our PRMT5 inhibitor. The left panel shows serial biopsy of a metastatic lesion of esophageal squamous cell carcinoma that has spread to the lung. In the middle of the figure, the change in SDMA between screening and cycle two-day-one is shown. By cycle two-day-one, the tumor cell SDMA score has dropped to zero, indicating effective target engagement at the first tested dose level. On the right, we also observe rapid plasma SDMA reduction in the first two patients enrolled in the study, the first two patients enrolled at dose level one. Taken together, the pharmacodynamic data for our PRMT5 inhibitor demonstrates potent target inhibition as detected in both tumor and plasma. Although we achieved our first human dose in only January of this year, just five months ago, the phase one study is progressing very well with 27 patients enrolled to date. Regarding the safety profile, the most common treatment-related adverse events are nausea and anemia. Importantly, we have observed no significant hematologic toxicity, no dose-limiting toxicities, no serious adverse events, and no AEs leading to discontinuation or treatment modification. For efficacy, we have achieved target efficacious exposure at only the second dose level due to a better-than-anticipated clinical PK. Despite the short follow-up, we have already observed three objective responses in three histologic distinct tumor types at the second dose level. In summary, the early clinical data and efficacy data for 58067 are very promising, which support its potential as a best-in-class brain-penetrant PRMT5 inhibitor. Our PRMT5 and MAT2A are a strongly synergistic combination, and we are currently the only company with both clinical-stage PRMT5 and MAT2A. We will begin enrolling patients to the PRMT5 and MAT2A combination as early as the third quarter of this year. In light of the encouraging early safety, PK, PD, and efficacy data we are observing with our PRMT5, we will also start testing standard-of-care combinations in various tumor types. Next, I will share our EGFR-targeting molecules, starting with our EGFR CDAC. This first-in-class compound has a truly differentiated mechanism of action designed to completely and selectively abolish EGFR signaling. It is highly potent against all typical primary and resistance mutations in EGFR, while sparing wild-type EGFR and demonstrating excellent proteomic selectivity. The EGFR CDAC is currently in monotherapy dose escalation, and we have again observed a strong pharmacokinetic profile with good oral absorption and a very long elimination half-life. The emerging safety profile is consistent with the EGFR wild-type sparing design. There have been no skin or GI toxicities reported to date. Dose escalation is in the early stages, and we're planning to start a combination study with a third-generation TKI in the second half of 2025. In summary, the EGFR CDAC is a highly promising compound with a unique mechanism of action, strong preclinical efficacy, and encouraging early progress. Next is our EGFR by MET by MET tri-specific antibody. This compound has best-in-class potential with a unique design that offers superior and optimal MET inhibition through a biparatopic MET antibody construct that is, again, EGFR by two different epitopes of MET. T187 has demonstrated stronger efficacy than amivantamab and MET-driven in EGFR TKI-resistant models. Importantly, T187 was also designed for lower EGFR on-target skin toxicity due to weaker killing of primary keratinocytes when compared to amivantamab. Regarding the clinical progress, T187 is currently in monotherapy dose escalation, and we're planning to initiate dose escalation with subcutaneous formulation by the end of the third quarter of this year. In summary, T187 is a highly promising compound with a unique design and mechanism of action, strong preclinical efficacy, and potential for clinical differentiation. Having a focused and deep portfolio in specific tumor types and specific oncogenic drivers naturally creates the opportunity to develop potentially synergistic in-portfolio combinations. Here I'm sharing preclinical combination studies for the two molecules that I have just shared: our EGFR CDAC and our EGFR by MET tri-specific antibody. On the left, the combination of the CDAC and T187 yields near-complete and sustained reduction in tumor volume in an EGFR TKI-responsive tumor model. On the right, this combination also yields deep and sustained tumor volume reduction in an EGFR TKI-resistant with superior activity when compared to the combination of amivantamab and lazertinib. Planning is underway to test this combination clinically. Our growing and comprehensive lung cancer portfolio features a diverse and differentiated array of molecules designed to address lung cancer segments with substantial residual unmet medical need. Our PRMT5 and MAT2A are foundational molecules for an MTAP-deleted non-small cell lung cancer and other MTAP-deleted tumors. Early data support their differentiated and best-in-class profiles, highlighting their potential to make a significant impact in this area. Next, we have the EGFR cluster. Our differentiated and first-in-class molecules provide substantial opportunities for patient impact through in-portfolio combinations and through combinations with third-generation tyrosine kinase inhibitors. Finally, multi-specific ADCs have the potential to broaden the eligible patient population and improve the therapeutic window. With novel payloads, we aim to further advance tumor selective targeting. In summary, our lung cancer portfolio is built on a foundation of innovation and differentiation. We are committed to advancing the field and improving outcomes for patients with lung cancer. Okay, I will conclude the solid tumor section with a discussion of our GI franchise with a specific focus on innovation for patients with KRAS mutation. Hang in there, sort of last lap. A lot of information in this section. For this final disease area franchise, I will focus on KRAS targeting, which is mutated in virtually all cases of pancreatic cancer and almost half of the cases of colorectal cancer. While I will not revisit the specific molecules, MTAP, EGFR, and MET are also important targets for GI cancers. MTAP deletion is present in approximately 20% of pancreatic cancers and up to 10% of esophageal and gastric cancers. Similarly, EGFR is an established target in RAS wild-type colon cancer, and MET biology is relevant in both colon and gastric cancers. We are also excited about the development potential of our ADCs and immune cell engagers, including our potential first-in-class FGFR2B-targeting ADC for gastric cancer and the GPC3 by 41BB bispecific antibody for hepatocellular carcinoma. KRAS plays a crucial role in cell signaling pathways. KRAS cycles between two states: the inactive GDP-bound off-state and the active GDP-bound on-state. While there have been advancements in developing small molecules to target specific KRAS mutants, challenges remain due to the presence of undruggable mutants and the emergence of secondary mutations. Given these challenges, we are taking a multi-progress approach to hitting RAS to maximize clinical benefit through new modalities and rational combinations. Our first KRAS-targeting molecule, BGB-53038, is a non-covalent inhibitor of both the on and off-states. This molecule is progressing well through early dose escalation. We will build upon this molecular framework by developing a second-generation KRAS CDAC, which will both improve potency and likely also have a long half-life, thereby improving target coverage. We are also actively working to deliver RAS-on targeting molecules from discovery to the clinic. The most advanced molecule is an internally discovered, potent brain-penetrant RAS-on inhibitor. We are also planning to use this molecule as a non-cytotoxic drug-antibody conjugate to improve tumor targeting with the intent of reducing systemic toxicities associated with broad RAS inhibition. Finally, we're also progressing a G12D-specific RAS-on inhibitor through preclinical development. This slide provides more detail regarding the KRAS CDAC and RAS-on inhibitor. In the left panel, the KRAS CDAC shows high and improved potency across various KRAS mutations while retaining strong selectivity for KRAS over H and NRAS. The pharmacological properties suggest that it can be dosed daily, which is a significant advantage for patient compliance and may improve the safety profile by delivering constant exposure. The brain-penetrant RAS-on demonstrates impressive potency. The panel on the right shows similar preclinical efficacy to RMC6236 at 1/25th of the dose. The middle panel shows that dual RAS inhibition via concurrent blockade of both the off and on forms delivers substantial preclinical synergy. Both these molecules are scheduled to enter the clinic in the second half of 2026, again providing a unique opportunity for in-portfolio combinations to maximize patient benefit. The final compound I would like to present today is BGC-137, an FGFR2B-targeting ADC that has the potential to be first-in-class with a best-in-modality design. BGC-137 has shown stronger efficacy in xenograft models when compared to bemarituzumab, an unconjugated monoclonal antibody. The safety profile of BGC-137 is designed to be differentiated. Bemarituzumab causes ocular toxicity as an on-target effect that is due to the blockade of the interaction between FGFR2B and its ligands. The parent antibody of BGC-137 spares ocular toxicity by binding a unique epitope with much weaker ligand blockade. Our FGFR2B ADC is progressing very well through early dose escalation. With over 20 patients enrolled, there have been zero ocular adverse events reported to date, including at dose levels where we are observing early evidence of efficacy. We are encouraged by the early clinical progress of BGC-137 and are likely to begin the dose optimization prior to the end of this year. We are committed to developing multiple differentiated pathway-targeting therapies to address KRAS mutations, which are prevalent in several GI cancers. Our goal is to develop innovative therapies with the potential for synergistic in-portfolio combinations and improved patient outcomes. Next, the MTAP-deleted cluster presents an important combination opportunity with PRMT5 and MAT2A in MTAP-deleted pancreatic cancer. Finally, we have multiple first-in-class and best-in-class ADCs. Our FGFR2B ADC is emerging with a superior safety profile and has the potential to be first-in-class in gastric cancer. To conclude the solid tumor section, we have completely reshaped the clinical stage solid tumor portfolio over the past two years with almost 20 new clinical stage molecular entities designed and selected to enable in-portfolio combinations, which we believe is critical to making the next step change in solid tumor oncology. This innovation continues with the intent to bring two to three additional clinical stage molecules per year into each of our three disease focus areas. Through our internal delivery model, we are progressing our portfolio with unparalleled speed, with multiple phase three starts in planning for 2026, including CDK4 and B7-H4. In the light of very encouraging early data, PRMT5 and FGFR2B ADC may also be on an accelerated path to registration-intent studies. Our approach highlights our commitment to improving patient outcomes by driving innovation in solid tumor oncology. Thank you. With that, I'd like to hand back to Lai. Thank you, Mark. Before I conclude, I'm squeezing this slide because I do want to also talk about some data. Just have a chance to talk about data at my on-day day. I'd like to share an update on our IRAK4 CDAC program. BGB-45035 was designed to achieve faster and more profound target degradation compared to KT-474, a molecule developed by Sanofi, while also avoiding the cardiovascular risks associated with KT-474. You might have heard from Sanofi just, I think, yesterday. They will no longer advance KT-474, instead to focus on a new molecule, which will not be in the clinic until next year. Now our molecule is not only potentially best in class, but also first in class. The clinical program has advanced smoothly with the successful completion of both single ascending dose escalation and multiple ascending dose escalation studies. We are currently conducting our phase 1B in patients with PN and AD. A notable feature of 45035 is extended half-life in humans, ranging from 60-96 hours, leading to sustained IRAK4 degradation. Please look at the top graph on the right, the green line. That is the second dose. We tested in the SAD. Seven days after just a single dose of 45035, you can observe, we still observe complete IRAK4 degradation in the blood. We're anticipating initiating the phase two in the second half of this year, and with the proof of concept of the IRAK4 degradation in the tissue expected by the end of the year. In summary, I remember two years ago, we made a promise that we would deliver 15 new molecular entities in 18 months. I just counted when I was listening to my colleagues. We actually, the promise we made, we succeeded. We delivered 18 molecules at that time point in 18 months. I do believe BeOne's oncology is truly a pipeline, is truly a game changer in the industry. First, our unprecedented research output and the clinical advancements underscore our leadership in R&D. I hope that what we have presented today has convinced you that we are at an inflection point where the capabilities we have diligently built are now converging. Our historical performance does not define our future productivity. We're not simply following the trends. We're piloting both first-in-class as well as best-in-class therapies. Second, Brukinsa is a cornerstone asset for our strategy for CLL. Now, with Sonrotoclax and BTK CDAC, we're expanding treatment options for all CLL patients across all segments, offering both continuous treatment as well as fixed duration therapies. Third, our approach to solid tumor reflects our successful strategies in hematology, emphasizing continuous innovation and the proprietary combination to build the breast, GYN, lung, and the GI cancer franchises. It is indeed a very exciting time for BeOne Medicines. Finally, I'd like to highlight a few key milestones within our pipeline. We have successfully achieved all critical goals we set at the beginning of the year, with some complete ahead of schedule, such as the CLL MCL filing for Sonrotoclax in China. In the later half of this year, we anticipate several significant milestones, including phase three readouts from the Mangrove study, which is a frontline mantle cell lymphoma for Brukinsa, and also the global filing for Sonrotoclax in mantle cell lymphoma. Turning to our early stage pipeline, as you have heard, we have a number of proof of concept catalysts expected for our early stage pipeline across multiple modalities and the disease franchises. We look forward to sharing more data with you in the future updates. With that, I'd like to hand over to Aaron. Thank you. This morning, we're really looking forward to a great Q&A. While we set up the stage, we're going to get some chairs set up for our panelists. Let me ask participants in the room and online for some quick feedback. If you look at the screens, you'll see a QR code on the slide. What this will be is a quick four-question survey. It won't take more than one minute. The team told me 30 seconds, but I guarantee it won't take more than a minute. It's anonymous. This session is to provide valuable information to our investors. We really would like feedback so we continue to improve as we move forward in future settings. There is one very interesting bonus question at the end, and we definitely want your feedback on that. We're going to get the room set up. As we do so, let's just do some housekeeping items. For the guests in the room, if you want to ask a question, please just raise your hand. We have people walking around with microphones. Ask your question after you have the microphone. If you're joining us virtually, feel free to submit your questions using the Ask a Question button on the top right corner of your screen. While we'd love to take a variety of questions, today is an R&D meeting, if you didn't notice. We'd love to spend the time maximized on our R&D portfolio. We please ask you to stay on topic and ensure questions are related to R&D. When you do ask a question, please start by sharing your name and company. Please limit your questions to one to two so we can get to many questions from around the room. I think we are all set. Let me just pull this back and let's open it up to questions. Hello? Yep, I got you. Andrew Barrons, Lynch Partners. Thanks for hosting this. Very helpful. Just a couple. The CDK4, did you guys actually declare a dose yet? And then can you also give some color on your combination strategies? It looked like fulvestrant in the second line, but what would the frontline combination strategy be? And then on the fixed dose combination strategies, would you be looking, do you think that it will be in patients that have relapses, will they get retreated with a fixed dose combination or move on to something like potentially the degrader? And then any color on the NCCN efforts to get endorsed there for the compendia? Mark, do you want to go ahead? Sure. Thank you very much, Andy. To start with CDK4, we have not yet selected a dose. We have this dose optimization phase that is ongoing both in combination with fulvestrant as well as in letrozole. Each of those cohorts is randomizing 60 patients across three dose levels. Those data are maturing. We hope to share those data in the not-so-distant future and declare a dose. That is the key gating event that will enable phase three studies. Insofar as combination, as you heard from Shom, we are combining with fulvestrant, but we're also about to start combining with alisertib or alisertinib, which could also enable novel combinations in the second line. In the frontline setting, we're going to combine with an aromatase inhibitor, which is why we're combining with letrozole in the phase one study. I can take on the fixed duration questions. In terms of the fixed duration, I think you're referring to Sonrotoclax plus zanubrutinib. Certainly our one-on-one study, we plan to test retreating the patients if they relapse. That study is going to take a while, unfortunately, because almost nobody progressed. It will be a while before we can really be challenging any of the patients. Certainly, I think that will be one of the options. As you heard today, besides the SC combination, we're also exploring potentially Sonrotoclax plus our degrader. If you think about it, the Sonrotoclax plus degrader can potentially be an even better fixed duration treatment in the relapsed refractory setting because even for patients who had a continuous BTKI in the frontline, you can potentially get on this type of fixed duration treatment. We do believe rechallenge data is critical. As for your question about NCCN, I think you're referring to our R&D in our SEQUOIA study. We're certainly working very actively in that front. We'll keep you updated. Thank you. Great. Thank you, Justify, JP Morgan. A couple more on CLL. For Sonrotoclax, I think there was a comment that you're continuing to optimize the ramp-up. What specifically are you optimizing and where could you improve there? For the Celestial 301 frontline study for the fixed duration combo, with that completing enrollment earlier this year, when should we be thinking about top-line data? Lastly, maybe just following up on the last one, for the BTK CDAC, which you're looking at in combination with Sonrotoclax for fixed duration treatment, it sounds like you're kind of positioning that for relapsed refractory setting right now. Could that one day move up and be the frontline fixed duration regimen? I love all those questions. It's a definite grade. Maybe just initially in terms for your first question, what are we optimizing? I was prohibited by our lawyer to share too much because we are still in the process of filing our IPs. What I can share with you, we have tested various different ramping up in our phase one as well as actually in the phase three. We used two different regimens. And we actually, based on everything we have seen so far, that gives us the confidence, which Remus has mentioned during the presentation, that we are very optimistic. In the end of the day, patients take on Sonrotoclax, we only need one clinical visit. We're not saying that lightly. It's because based on everything we have seen, we have the confidence we'll be able to achieve that. Now, in terms of the readouts for Celestial 301, it's an event-driven study. I hope I can predict exactly when that will read out, but it's going to take a little bit of time. Certainly in that study, we also have uMRD as a point, which we're going to take a look at. Hopefully, we'll be able to share the data earlier than the PFS readout. In addition to that, I think your question is another fascinating question about taking the degrader and the Sonrotoclax combination potentially into the frontline. I'm sure someone is going to ask another question associated with that, about degrader itself going to frontline. I assure you, I've been getting that question almost on a daily basis. This is an amazing drug, and it's truly amazing. This is one drug I never need to spend a minute to convince PI it's good. Just everyone was telling us it's a good drug. We're definitely contemplating about degrader going to frontline and either in a mono or in a combination format. We're accumulating data. Go to frontline is now the bias is already high, very high. If you look at our Zanubrutinib, continue to use three-year PFS, COVID adjustment is 86%. That's really high. The fixed duration today, you have seen our combination of the 320 dose level plus Zanubrutinib plus the Sonrotoclax, that's the ES regimen. We haven't had a single disease progression yet. We have 86 patients treating that cohort. We will see how the data pan out, but that certainly will be an option for BeOne. Rosy Liao with Guggenheim. A couple of questions on the solid tumor franchise. First one on CDK4. In the frontline, CDK4 or 6 naive setting, how are you thinking about the bar for efficacy in terms of making a phase three go decision down the line? I know we've seen some data from Pfizer in that frontline setting, so curious how we should be thinking about benchmarking there. Then separately on B7-H4, regarding your phase one trial, can you comment on whether those patients have previously been treated with another topo 1 ADC? I'm just curious on potential cross-resistance and whether that's a factor that you're considering for the phase three planning. For the second question first, these patients, my understanding is that all of them are topo 1 ADC naive. We want to understand what this molecule would look like in a topo 1 naive patient population because that's fundamentally our development intent for the molecule. For CDK4 in frontline, certainly the frontline standard of care with the CDK4 inhibitors is quite high. It would be virtually impossible to run a conventional randomized phase two study. Therefore, we've enrolled this cohort of 60 patients. We are going to follow those patients closely for surrogate endpoints that will help us to inform that decision in terms of response rate, CT DNA reduction, tolerability, discontinuations. It will be holistic based upon that body of evidence to give us sufficient confidence to proceed to phase three. You're done, I think. Okay, hi. Thank you. Can you hear me? Yigal Dov Nochomovitz here. Two sort of big picture questions for John and Lai, and then one specific one for Mark. You mentioned AI, Lai, and you mentioned using it for data prep and visualization and efficiencies. Are you actually using it for drug discovery projects in terms of optimizing molecules at the preclinical level? That's the first one. Yes, we definitely are embracing this. This is a game changer. Just to be on the practical side of it, I think that things will take step by step in terms of where you can apply AI for discovery. I do believe, my personal belief on the large molecule side of it, that the application will be probably even more advanced compared to the small molecule side of it. Because at the end of the day, AI has to do the deep learning from whatever is available out there. We're already definitely starting doing those types of works. Obviously, you have basically every modality there is for drug development, small molecule, large molecule, biospecifics, ADCs. You mentioned cell therapy again. The one that seems to be missing or intentionally you're not pursuing is radiopharma. Just wondering if you've given any thought to that and whether radiopharma could feature in the development scheme at some point? You want me to answer the question? Please. Yeah, good question. I get that question quite a bit as well. We have been thinking about that. I'm not saying we're definitely not going to do it. As you know, there are certain things associated with radiopharmaceuticals, which is due to the transportation, preparation, and all the things you have to associate with that. It is not an easy task. One of the fundamental questions is, can you do something else achieving the same effect with all the hassles? I think that's a critical question for that particular field. If you do not have a choice, certainly that's an option. If you have another more convenient choice, maybe that's not the best option. Right now, we do not have that. I'm not saying for sure we will not do it. Okay. Quickly for Mark, the argument on the 600 milligram versus the 400 milligram data for the CDK4, I'm assuming the point there is that you potentially do not have enough durability to really be able to show responses at 600, or is there potentially some bell-shaped dose response? Could you just clarify? I noticed with the CT DNA was consistent with the response data too. Yeah, we are disclosing data today from our dose escalation phase. I would highlight that these are very small cohorts. Part of this also is statistical power and wanting to have more patients that are, shall we say, more homogenous, treated in the same way with contemporaneous randomization to inform that decision. We just think that it is primarily related to the fact that these are late-line patients in a limited data set. There is the possibility, as you heard from Dr. Goel, that this data set could continue to evolve in a favorable way over time. Thank you. I just wanted to comment on your AI question. You asked specifically about discovery. If you actually look at what you saw today, we are using the tools, but our issue is not really, can you make a molecule that completely degrades something? Or can you make a really good inhibitor or a really good ADC? We are quite good at that. The cost of doing that is quite small, and we do it pretty quickly. Will AI make us better in that area? Are there certain areas where it is very hard to make something that maybe the industry can be better? Perhaps. The huge problem, again, is clinical development. This is the huge area of opportunity for applying this technology. Because the industry is so cut up in the way we do clinical trials, because most companies are outsourcing this, and most companies have five or six different platforms, a clinical operations platform, a safety platform, an EMR platform, it's very, very hard to have that information in high quality in a place in a system that you can use these incredible tools that are now available to optimize the system. I think this is where our company is very uniquely positioned because we don't have all the legacy nightmares of a big pharmaceutical company, but we have the breadth, and we're doing everything internally. I think from our perspective, we're really looking at how can you apply this to be infinitely better in the area, which is 75%-90% of the cost and 75%-90% of the time, and in which we're incredibly uniquely positioned to move in that area. I think Markello is here. If he is, he can wave. He's come on board as our CTO and is certainly helping us look and drive forward in that area. I think that's a place where five years from now, we have the potential to be game-changingly different than most organizations. There's a lot of promise there. We're certainly investing in that area. I also want to add one comment on the CDK4 questions. We certainly don't believe there's a hook effect. The CT DNA should correlate with somewhat the tumor. That's not really a truly pharmacodynamic PD biomarker. It's more of like an efficacy PD biomarker if you think about it. The TK1 is one truly pharmacodynamic PD biomarker. We don't see hook effects. So far, the 600 milligram is well tolerated. I think that's, like Mark said, it's just small sample size, the heterogeneous kind of population we have enrolled. Yeah. 600 is certainly still in play for selection. Leo from RBC Capital Markets. I wanted to stay with the CDK4 program for a minute. I've got two questions. I guess you mentioned that follow-up's still early, and that's sort of why it's hard to maybe judge response rate. I guess as you have longer follow-up, is it possible that you're going to have some of the AEs compound, see more of the neutropenia over time? I guess how confident are you that the safety profile is going to continue to hold up and discontinuations are going to remain low? Maybe looking ahead to the commercial market and positioning, I guess, do you think a win on safety is going to be enough to convince physicians given that competitor drugs have survival data? Or do you need to show a win on efficacy and safety? Thanks. Maybe I'll start. I think that as I began the CDK4 section, the whole hypothesis behind this molecule is that it is more potently inhibiting CDK4 than any of the approved molecules and with greater 4 versus 6 selectivity. This was designed to have more continuous target coverage, deeper target coverage, and therefore better efficacy. That is the objective for the program. In terms of your question about safety, my understanding of our safety experience is that most of the AEs that we're observing do emerge early in the patient's treatment course. This is a great opportunity for Dr. Goel to share his personal experience on the safety and certainly any comments you have on efficacy as well. Yeah, certainly. Actually, to the first point about safety, our clinical experience from this study, and certainly my experience taking care of patients on this study, is that the adverse events I described do tend to come on early. Overall, we found the safety profile of the drug over time, and there have been many patients on the study for a considerable length of time, even though the median follow-up was short, has been very favorable. I think time will tell. The data will tell. I think the chances that a number of new adverse events would emerge later on is, in my opinion, quite low. What I think does have a greater chance of changing over time is the response rate. I think this is a really important point to make. If you think about what we know about CDK4/6 inhibitors as a class, if we think about the big randomized phase three studies that we look at, the median time to response in many of these studies is several months, 3.6 months in MONARCH 3, up to 4.9 months in the RIGHT Choice study with ribociclib. Now, our median follow-up is three months. I think I'm encouraged because, as Lai said, the CT DNA data certainly shows very encouraging signs of efficacy. As for response, I think we just need a little more time to get a full impression on that. Good morning. Thanks for the presentation. Sean M. Laaman from Morgan Stanley. My question relates to venetoclax versus sonrotoclax. And if you have some suggestions around the stratification of venetoclax use, and then I think you said on slide 16, approval of sonrotoclax, file for approval for sonrotoclax next year. How do you see, with respect to the ramp, the evolution of the Venn diagram of overlap of use over time? Yeah, I can start. Maybe Remus can also add. In terms for our molecule, again, I just want to emphasize probably a couple of points here. From day one, we were trying to figure out how to solve the issue with venetoclax. We're not saying venetoclax is not a good drug. Venetoclax actually is a very powerful drug, has clearly shown great activity in the clinic. The problem with venetoclax lies in two. Number one, it is very difficult to use it during a ramp, as you pointed out. We are working extremely hard on that. Maybe Remus can chime on that. I just want to add one more point about venetoclax issue. It's a pretty large small molecule. Molecule weight is big. When you're dealing with a large small molecule, you're going to deal with a big PK variation between patients. The larger you get, usually absorption is worse for a small molecule drug. Venetoclax does have a lot of PK variation in the clinic. The patients who absorb well, probably hitting target okay. There are a significant portion of patients who don't absorb that well. The PK will be low. When the PK is low, you don't hit the target hard enough. When we designed sonrotoclax, this drug is 14-fold more potent than venetoclax. We uplift everybody. In a way, even for patients who probably have low absorptions, you still can achieve enough BCL2 inhibition. End of the day, about doing small molecule is about hitting the target. We're definitely hitting target really hard. We're seeing that now in the clinical in term of the UMRD rate. If you say maybe it's not apple to apple comparison, SZ versus VI or SZ versus AV, that's a different BTK inhibitor. We also have our internal SZ versus SV data. We have our ARMD Sequoia data. You clearly see, even when you combine with same BTKI, sonrotoclax is hitting the target harder, which is leading to deeper UMRD and also quicker UMRD. Maybe Remus can chime a bit more on that. I would just add that we have currently over 1,600 patients treated with this molecule in a single agent or in combination. We have a very good understanding of the safety profile. As we look across a single agent or combinations, we consistently see a better safety profile in addition to the efficacy that Lai was mentioning. We see some rates of neutropenias, maybe or cytopenias, but consistently, the GI toxicities are much lower than what we see the adverse events with venetoclax. This gives us the confidence that this is a much tolerable molecule. We can combine it with our internal assets so we can address multiple indications. I may just add one more point about ramp-up mechanistically. Why can it be easier for us versus venetoclax? Venetoclax has a half-life of 26 hours. For a drug with a 26-hour half-life, it usually takes four to five half-lives to get to your steady state. So venetoclax naturally will take a longer time to get to steady state. This is why you need to monitor patients more intensively while the drug level goes up. Because when the drug level goes up, the TLS risk comes. Our drug is a much shorter half-life. It's five hours. This story is very different from zanubrutinib's story, which for us, for the zanubrutinib, was about more sustained target inhibition there. Here, actually, you'd be able to clear out the drug a little bit faster. It's better for your ramp-up. The reason why this in this fashion works is because this is not like a kinase inhibitor. Kinase inhibitor is like hitting the brake. You have to constantly hit the brake. Otherwise, the kinase signal goes on, cells survive. This just induces apoptosis. It's not like hitting the brake. Once you hit a target, cytochrome c will release from mitochondria. Once cytochrome c releases from mitochondria, cells will die. It's a very different mechanism of action. This is actually really beautiful, kind of scientifically putting together. Yes, you are able to hit it hard, but you don't have to hit it constantly. In a way, you're able to induce cell death. This is why our ramp-up requires much less monitoring. We believe at the end of the day, patients only need one visit to the hospital to do a pre-dose check, then probably four to six hours after-dose check on day one of taking Sonrotoclax. That's it. Maybe you want to chime in? Yeah, let me just chime in a little bit. The 101 data is clearly very exciting that we see a favorable safety profile, and we see high rates of early uMRD that appear quite durable. Obviously, the hope is that this holds up in the celestial phase three study. The biggest barrier to patients receiving and achieving deep remissions to BCL2-based therapies right now is actually feasibility. The truth is that I use quite a bit of venetoclax, but most patients are not treated by me. They're treated in the community where the feasibility of venetoclax-based strategies has been really quite limited. It is really the minority of patients who actually are able to achieve this type of therapy. Safety and efficacy is crucial. I'm looking at that. That's absolutely critical for comparing the sonrotoclax and ibrutinib data against the existing landscape. It's the feasibility that I think is really the key linchpin here in the future about getting BCL2-based therapies into patients. Great. Thank you. If I can have one pretty high level. As investors, ultimately, the true measure of R&D success is commercialization and success there. If you think about your research and development efficiency and benchmarking, where would you say you sit compared to Global Pharma? Where do you think you sat a few years ago? I do not want to tell Lai that he is truly outstanding. His research team is exceptional. I think what my co-founder, who's a real scientist, not a CEO, would say is you're always striving to be as good as you possibly can be and as successful as you can be. There is no best because whatever you do, there are other people that are also trying to compete. No matter what, we always have to strive to be the absolute best we can. I think what I can say is I'm known for being super critical and having an unbelievably high standard and setting unrealistic expectations that people strive for. What our R&D team is known for is actually achieving those. They actually achieve those. I think to all of our amazement, this is a team that's able to do things that are truly extraordinary. I think that speaks a lot to the passion and the energy and the commitment. It also speaks to the group of people and the way they're able to work together as a team to really deliver on things. I feel incredibly proud of where we are at this point in time. It certainly was aspirational, but probably viewed by most people as impossible five years ago. I think that I can tell you we're setting just as high standards for ourselves to improve and be better five years from now. Our goal is to come back and do this meeting in five years and have all of you say, "I never could have possibly imagined that, but you actually did it." That is who we are and what we're trying to do. I think that it is not luck. It is not entirely brilliance. It's a lot of hard effort by a lot of people that are really committed and trying to fight cancer. Great. Yarun, and then we probably have time for one or two more after if there's others in the room. Go ahead. Thank you. Yarun Werber from TD Cowen. I have just maybe a few questions. The first one, 18 drugs into the clinic in 18 months. That's pretty good. I guess the question is, how much bandwidth do you have, especially R&D-wise, as you, I mean, you're ramping revenues very nicely, but as you go into late-stage development? And then on CLL, what's the Sunral dose that you're taking forward for 301 and 303, the celestial studies? And is 303 fixed duration? I'm going to have a quick follow-up. Maybe the second question first. The dose we're taking to the 301, which is the treatment naive CLL, that's a fixed duration for 320 milligram. That's for basically the combination is only for one year with up to three months of the lead-in for zanubrutinib. So the 303 is the phase three study in the relapsed refractory CLL. In that study, we're testing a two-year combination with either obinutuzumab or rituximab. There is an interesting cohort which we are going to do is look at after one year if it's uMRD negative a patient will be able to stop treatment. That's not really a registration cohort. That's also fixed duration. To your first question about how can we handle such a big pipeline, first of all, thank you to all of you, the investor support. We appreciate it. I think to go back to our philosophy, we're going to be very disciplined in terms of which one we move to late stage. I truly believe the industry made a lot of mistakes in the past, which is they investing based on how big the market is and how close the drug is to the finish line, not based on data. This is why during the presentation, we emphasized twice or three times about data. To be able to really make a database decision, you have to move to clinical POC. I think maybe in this world, and also thanks for that question asking John about it. It is on the record now, John. We are pretty efficient in terms of getting from target all the way to get the critical data points in the clinic. That is actually what is important. If you can do this well, you will be able to sit in a position to really pick the winner, the ones. The others, maybe you are not so sure. You still can partner. There are many different opportunities there. We are very excited about this potential problem because that is a great problem to have. On the EGFR MET, just given the data with Amy, how are you thinking about tox, especially rash, scalp tox, insecticide reactions? You have a lot of phase one data, probably at ESMO or toward the back end of the year. Some of them are going to be v ery early kind of phase one looks, and some are more mature. Which ones are going to be a little bit more mature where the data is going to be a little bit more telling? We will have relatively limited phase one data at this year's ESMO, just the sequence and the cadence of the molecules entering the clinic. A lot entered in the fourth quarter last year, and we've already passed the abstract deadline. Most of the phase one disclosures in terms of new data will actually be in the first half of 2026. For EGFR MET, it's very, very early days. I believe we have fewer than 10 patients enrolled. As I mentioned, it was designed to mitigate skin tox, which is an important toxicity associated with the class. Including imivantamab, we are hopeful that we will see mitigation of that. We are going to focus the development based on subcutaneous administration to mitigate infusion-related reactions. We are hopeful and look forward to sharing the data. We think that molecule has a lot of potential given the impact that we're seeing with imivantamab. Maybe I just add a little bit more mechanistically side of it. Part of the hypothesis behind that was maybe similar to VGF PD1 bispecific idea. The idea over there, at least, is not proven. The hypothesis was the antibody, the bispecific half-life is a little bit shorter. Therefore, you do not have as much circulating times, but more you get it concentrated in the tumor tissues. This is somewhat a similar idea here. We probably do not have as much kind of the systematic kind of the rash, this kind of toxicity due to the EGFR inhibition. We also did some of the screening during the preclinical looking using a particular cell line to screening for that. Please. Kelly Shi from Jefferies, and thanks for great presentation and the discussion. I have two questions. First, on CDK4 inhibitor, besides the development strategy that you have elaborated, I have a question on how to better understand today's clinical data, especially on efficacy front while we're looking at ORR and stable disease rate, and also with the patient baseline characteristics that are with all post-chemo endocrine and also CDK4/6 inhibitors Yeah. This is a really important question because when we are talking about the phase three study start in a second-line population, that would be a true second-line patient population that would be patients would be post-CDK4/6, but they would not have had such extensive prior treatment, which is an important point. I think our efficacy data need to be interpreted in the context that the target population for development is earlier line than the patients that we're showing today, in addition to the maturity that Dr. Goel mentioned before. I don't know if there's anything more that you would like to add in that context. No, I think that's good in terms of interpretation. For ADC, following the promising ORR from this first clinical data, what are the key questions for next step of development in your consideration for achieving best-in-class position among all the B7-H4 agents? Yeah. I think what I shared today is that we're seeing efficacy that we're very excited about across a range of doses. Now we need to simply expand that experience to help us refine our final dose level selection for future studies. We need to get into our dose optimization phase. The other point is thinking about the patient selection. I showed you a simple, if we just cut patients into high-low, what does that look like? Refining the biomarker for optimal patient benefits. I think those are the two critical questions that we're working to address for that program to engage registrational intent studies as early as the second half of next year. Great. I think that rounds out our Q&A. Thank you to the panel. Our panel is going to make their way off the stages now. In the meantime, it's a great opportunity, if you haven't done the survey, to take the 30 seconds to complete. I will hand it over to John for some closing remarks. Probably people know which choice I'd make on the survey for the last question. I hope you all did. Look, I want to thank you again for all your time and energy today. I know it's a lot, and it's a lot to digest, but there are a couple of takeaways at the highest level. First of all, our pipeline and our company is really at an inflection point. There are 20-plus near-term milestones in the next 18 months for our company. It is a lot to digest. In short, though, it is incredibly exciting. It is a great time to be here at B1. It is a great time to be in the oncology field. The data that we are seeing looks incredibly promising, and that is a great thing for patients. We also believe it is a great thing for the company and for investors. Absolutely, I think it is a tribute to the group of individuals we have that are working on this internally in the company and the collaborators that we have working with us. I really want to thank them all. It is great for you to have some exposure to them here today. Again, huge thank you to everyone. Massive thank you to our esteemed guests and collaborators, Dr. Soumerai and Goel. Please join us again next year when Lai will, with his R&D team, truly amaze us at what they're able to accomplish. Thank you all so much.