Great. Good morning, everyone. My name's Jess Fye. I'm a large-cap Biotech Analyst at JP Morgan. And we're continuing the 44th Annual Healthcare Conference today with BeOne. First, you're going to hear a presentation from the company, and then we're going to go into a little Q&A. If you are in the room, you know, raise your hand, we can pass you a mic. And if you're listening online, you can always submit questions to the portal. But with that out of the way, let me pass it over to the company's Co-founder, Chair, and CEO, John Oyler. Great. Thank you so much, Jess, and thank you all for being here. It's interesting, 44 years. I think I've been coming for about 25. I really want to say how proud I am of the industry that it's made such an impact in our fight against cancer. Over this time, across a broad range of cancers, the impact on overall five-year survival has been meaningful and dramatic. You can see that here. Now we see critical new therapeutic modalities that were once met with skepticism, and they're just beginning to become very important in treating cancer and other diseases. We're only seeing the tip of the iceberg right now. This is what makes me really excited about the real impact we can have for patients, but with that said, there's still a lot to do. 10 million people across the world are dying from cancer every year. 10 million, and that's the reason I'm here. It's the reason I wake up early in the morning. By the way, those of you here early in the morning, thank you for waking up early in the morning to join us in our fight against cancer and fighting for life in this industry. We're really committed as a company to doing this. It's why we changed our ticker to ONC, to ONC. It's why we're relentlessly focused on innovation and on speed. Cancer's an incredibly formidable foe, but we're not going anywhere. Together as an industry, we're here, and we're how the world stops cancer, because we must. I'd like you to note our customary disclosures. I'd like to start today with a brief look back at 2025. This was an incredible year of inflection for BeOne. From a financial perspective, we made important commitments at this conference last year: significant product revenue growth, GAAP profitability, and meaningful cash flow generation. And we delivered on every one of them. And we're just getting started. 2025 saw our foundational BTK inhibitor, BRUKINSA, become number one, both in the U.S. and globally. That's not just a commercial achievement. It's a scientific one. Our long-term data has now raised the bar and set a new standard for efficacy and safety in CLL treatment, which we'll explore further today. And our pipeline made incredible progress in 2025. In hem, Sonro, our foundational BCL-2 inhibitor, received breakthrough designation and priority review in the U.S. for relapsed MCL. And recently, it received its first-ever regulatory approvals. Sonro had four regulatory approval submissions in total in 2025. And we also initiated five phase three trials across a broader Heme franchise. In solid tumors, we saw positive top-line results for the Tisli-Zani triplet combo in first-line HER2-positive gastric cancer, which showed a clinically meaningful improvement over the standard of care. Six assets achieved proof of concept across four modalities, and five new molecules entered the clinic. These accomplishments set us up incredibly well for 2026 and beyond. So let's talk about CLL. CLL's a $12 billion and growing market today due to the tremendous therapeutic innovation and improvements in patient outcomes over the past 15 years. But it wasn't always this way. And it wasn't this way when I started coming to this meeting. As recently as the mid-2000s, patients with CLL received fixed-duration chemo. And the results were poor. In fact, the median progression-free survival for front-line patients taking chlorambucil was less than one year. This chart shows six-year overall survival on the x-axis and six-year PFS on the y-axis. Only roughly one out of five patients with CLL survived six years, and one out of ten did not see their cancer progress. In 2008, bendamustine was approved, and the use of bendamustine plus rituximab became widely used in early 2010s, and it provided substantial benefit over the first chemo regimens. As you can see, six-year PFS increased to 32%, and nearly half the patients survived six years, so this was better, but still not great. In 2016, the FDA approval of ibrutinib for front-line CLL marked the first chemo-free option in CLL, and it was a seminal innovation for patients. Anchored by data that were superior to chemo, the field switched away from fixed-duration therapy to continuous BTK treatment, and this was because it provided the best long-term outcomes for patients. You can see ibrutinib's six-year progression-free survival and overall survival, approximately 61% and 77%, respectively. At the same time, the field was beginning to explore fixed-duration treatments that were enabled by the discovery of BCL-2 inhibition and the approval of venetoclax. These ven-based approaches greatly improved upon historic chemo-based fixed-duration regimens, and they began to approach, albeit with a 10% negative delta, in the six-year progression-free survival, the level that we could see in the long-term benefit of continuous BTK. However, the VI regimen was not approved by the U.S. FDA, and the addition of obinutuzumab to ven has significant safety challenges, which I'll touch on later. As impressive as continuous use ibrutinib was on efficacy, the molecule was not optimized for selectivity, and it showed cardiac tox-related issues. The second approved BTK inhibitor, Acala, was designed to address this and to be more selective than Ibrutinib and to have a very short half-life, just about an hour, with the hypothesis that these changes would translate to a more favorable safety profile, including fewer cardiac adverse events. In that respect, Acala achieved its goal. It demonstrated statistically significant improvement in AFib in the ELEVATE-RR study. However, in that same study, Acala demonstrated non-inferior PFS compared to Ibrutinib. Interestingly, as shown on this chart, Acala's six-year PFS and overall survival of 62% and 76% is nearly superimposable on Ibrutinib in terms of efficacy and long-term patient benefit. The field didn't remain static. The bar set by the first two continuous treatments was to be raised yet again by a differentiated foundational medicine. Enter BRUKINSA. BURKINSA was designed from inception to be both more potent and more selective than ibrutinib, with complete and sustainable 24/7 target coverage. We took that preclinical hypothesis into the clinic, where BURKINSA demonstrated both superior efficacy to ibrutinib and a more favorable safety profile in head-to-head global phase 3 trial. At ASH 2025, BURKINSA set a new bar for long-term outcomes for patients with CLL. Here you can see six-year progression-free survival and overall survival of 74% and 84%. If you adjust for COVID, those are 77% and 87%, respectively. With these data, BURKINSA has established the foundational standard against which all future regimens must be compared, and the long-term outcomes for patients and physicians should expect and demand these types of results. As I'll discuss later, we really do believe in the promise of fixed-duration treatment, but not at the expense of PFS, of OS, and of safety. These data are the data that every oncologist, every healthcare professional, policymaker, and patient should see and discuss when they're facing a treatment. At BeOne, we're relentlessly focused on developing innovative medicines that develop the best long-term outcomes for patients. Because behind each one of these data points actually are lives. This is Lynn. I had the privilege of meeting her last year. Lynn was diagnosed with CLL six years ago. Her specific type is 17p deletion, which is high risk, which traditionally had meant much poorer outcomes prior to BRUKINSA. Over half of all CLL diagnoses are considered high risk. And for these patients, fixed-duration treatments have not shown to be as efficacious as continuous therapy. Lynn is thriving today, thanks to continuous BRUKINSA. She's a loving partner. She's a mother. She's a grandmother. And from my perspective, she's a real force to be reckoned with. Her journey reminds us that behind every innovation, our real people and their lives and the lives of their families are changed. Lynn's gratitude and resilience continues to inspire the team every day and it's because of her and thousands of patients that are similar that we get up early every morning and we fight with all we have for every improvement possible against this disease, against progression, and against side effects. Lynn's story is why we all do what we do. At BeOne, we believe true innovation comes from improving upon the best. Here on the left, you can see the Kaplan-Meier curves from the ALPINE trial of BRUKINSA versus ibrutinib. It's in relapsed-refractory, BTK-naive CLL patients. In the ALPINE trial, BRUKINSA separates from ibrutinib and remains separated with a hazard ratio of 0.69 and a p-value of 0.001, which demonstrates statistical superiority over PFS. When we presented this initially, the early cut of this data to the CLL community, the universal feedback was nice data, but we need longer follow-up. And there were two important scientific reasons for that. First, ibrutinib was known to have tolerability issues that could potentially influence patients' ability to stay on therapy during treatment. And secondly, the ELEVATE-RR study, acalabrutinib showed some early PFS separation from ibrutinib, but that separation was not sustained. As you can see on the right, Acala crossed over and became numerically worse than ibrutinib at roughly 33 months. ELEVATE-RR ultimately reported a hazard ratio of one. And its last reported data cutoff was September 15, 2020. While early separation was an encouraging signal, the CLL prescribers wanted to see sustained separation with longer follow-up to be convinced. And you can see that in ALPINE, BURKINSA'S longer follow-up showed exactly that. After these data were presented, the adoption of BRUKINSA began in earnest. We continue to present data from this study, including the six-year follow-up at ASH in December, a month ago. That brings me to Pirto, a non-covalent BTK inhibitor, which recently reported data from its head-to-head trial against ibrutinib in CLL. On the right, we see the curves from the relapsed refractory BTK naive cohort of BRUIN 314, and this comprises two-thirds of the patients enrolled in that trial. Importantly, the curves shown here for both studies were all assessed by Independent Review Committee, or IRC, and this is the global regulatory standard for all oncology trials. It's the global standard because it corrects for potential bias associated with investigator-assessed outcomes in an open-label study such as these. In both studies, the IRC assessed PFS was also the predefined key secondary endpoint to demonstrate superiority over ibrutinib. You can see that with Pirto, with only 18 months of follow-up, it does not show meaningful early separation versus Ibrutinib. There's a hazard ratio of 0.845 and a p-value of 0.41. Just look at the data. With the caveat of cross-trial comparisons, there was roughly a 12% separation at 24 months for Zanu and ALPINE, which was sustained, roughly a 5%-6% at 24 months for acalabrutinib in ELEVATE-RR, which was short-lived, and roughly 3% for Pirto at 18 months in BRUIN 314, so we certainly need longer-term follow-up data for BRUIN 314, but based on the minimal early separation in these short-term curves, Pirto may face quite an uphill battle in showing statistical superiority to Ibrutinib on PFS. Let me switch to safety, because part of the hypothesis around this molecule was a safer molecule. From a safety standpoint, the data are similarly underwhelming. Despite their hypothesis, Pirto did not show a meaningful safety difference versus Ibrutinib across clinically important metrics, such as infections, cytopenias, and AEs leading to treatment discontinuation, and Ibrutinib is the least selective of all the covalent BTKs. In contrast, as you see below, BRUKINSA has consistently shown long-term safety benefits versus Ibrutinib. Taken together, the efficacy and safety data do not support moving Pirto beyond the relapse setting, where it currently does play a much-needed role for patients that have progressed on covalent BTK inhibitors. We do believe the next chapter of CLL innovation will continue and will come from options that address unmet needs and deliver on the best long-term outcomes for patients. There's a clear desire from patients and physicians for fixed-duration first-line options that will provide a break from treatment. For fixed-duration therapies to change the treatment paradigm, they must elicit a deep response, demonstrate sustained progression-free survival, be safe with only minimal infection risk over continuous BTKI, and be convenient to administer, and we would argue they must now be compared to the foundational CLL medicine, BRUKINSA. These criteria are not being met by the current fixed-duration options. Existing ven-based BTK regimens have liabilities that have limited their uptake and approval. These include underwhelming efficacy, as demonstrated at ASH 2024 with the AMPLIFY trial, where the AV combination actually had inferior depth of response, uMRD, to its comparator, chemo, and which may result in patients being treated for much longer than one year. In this respect, the absence of longer-term data from AMPLIFY at ASH this year was quite noteworthy, and similarly, with respect to safety, the VI regimen contains ibrutinib, which is cardiotoxic. As a reminder, neither AV nor VI regimens are approved in the U.S. Lastly, ven has a convenience challenge due to its long half-life and TLS risk, which requires cumbersome patient monitoring. At the highest level, the primary benefit of fixed-duration therapy is the treatment-free interval, during which patients are not exposed to the potential side effects of ongoing therapy. In CLL, this means avoiding continuous BTK agents that suppress rapid B-cell expansion, allowing for immune expansion and a reduction of risk of infection. So fixed-duration therapies should lower infection risk over time, not raise it. The CLL 17 trial presented at ASH this year studied fixed-duration VO and VI versus continuous Ibrutinib and was presented last month. The chart on the left shows this trial data, which tells a clear and quite concerning story. First, after one year of VO, there was roughly a doubling of severe infections. These continued to climb for three years, even while the patient was off treatment. It's seen in blue. These infections are serious, often requiring hospitalization and IV antibiotics. Second, even after four years, severe infections were still higher with VO than with continuous Ibrutinib, despite the three-year treatment-free period. This is potentially because obin, a CD20-directed monoclonal antibody, has shown to cause prolonged depletion of both B cells as well as some populations of T and NK cells. And thus, it may severely impact the overall immune function. In contrast, rather than destroy the B cells, the BTK inhibitors prevent the B cell proliferation by blocking BTK, a key signaling node in the cell activation pathway. The VO arm also showed 67% nominally increased risk of death versus Ibrutinib. These findings, they're quite consistent with data from other recent studies, such as AMPLIFY. In our view, that profile stands in direct opposition to what patients want and what patients deserve from a fixed-duration treatment. In contrast, in ALPINE, BRUKINSA demonstrated two-thirds the rate of grade 3, 4 infections versus ibrutinib. If you now look at the table on the right, for the highest-risk patients, IGHV unmutated or 17p deletion, roughly over half of all CLL patients, VO shows notably lower PFS. In summary, the risk-benefit profile of VO simply does not justify a shift away from established continuous BTK therapy. We do believe the next innovation in frontline CLL will come from combining our best-in-class foundational medicines, BRUKINSA, plus a better-designed, more potent, and selective BCL-2 inhibitor, sonrotoclax. As you can see in this slide, this combination checks all the boxes. It's poised to be the first regimen that delivers truly on the promise of fixed duration. Our confidence in ZS is based on the totality of clinical data. But there's key aspects of the data that we find exceptionally compelling. Here you can see the undetectable MRD rates and time-to-blood MRD from our phase one trial, which was presented at ASH last month. All of the data from our Heme franchise is generating. These might be the most compelling when they're shown to KOLs with whom we meet. Let me explain. First, the combination of ZS can drive very high rates of deep response. Secondly, and perhaps most impressively, it does so exceptionally quickly, with kinetics previously unseen in any other trials of drugs targeting similar mechanisms. This type of deep response is what we're looking for in fixed-duration regimen to give physicians and patients the confidence to stop therapy and to still achieve positive long-term outcomes. The CLL landscape is roughly split evenly into patients who receive BTK inhibitors and those who receive some form of fixed-duration treatment, whether ven-based, CD20, chemo, or other. We believe that ZS will fundamentally change the treatment paradigm for patients who want effective therapy without lifelong treatment. This will enable BeOne to access a segment of the market that we previously have had no presence in. Therefore, we view this as a market-expanding opportunity relative to continuous BTK BURKINSA. Innovation in frontline CLL is vital, but we must also address the growing unmet need in relapse setting. While Pirto has been successful in addressing the C481 mutation, over time, we've learned this is just one of many potential mutations that can occur. Therefore, we've pioneered fundamentally a new modality, our first-in-class BTK CDAC, to address this important patient unmet medical need. This CDAC is both first-in-class and best-in-class, and it leads the way in the next novel foundation modality related for relapsed CLL. Regarding its potency, as shown on the left, we observe similar DC50 and 90 values for our BTK to the nearest competitor molecule in head-to-head BTK degradation assays in both human and whole blood B cells. We also have shown complete target degradation at one-fourth of our moving-forward dose, and we believe that our BTK CDAC holds a clear mechanistic advantage in terms of BTK mutation coverage, which is shown on the right. The robust clinical activity that we see with this molecule in heavily pretreated patients is extremely exciting. In our phase one trial, the BTK CDAC demonstrated an overall response rate of 86% with a median follow-up of 18 months, and the 12-month PFS is now mature at 79%, a very favorable profile compared with Pirto in a similar patient population. These data form the base of our confidence in our ongoing phase three head-to-head trial versus Pirto in relapse setting, and we believe this program can redefine what's possible for patients who relapse after BTK therapy. In summary, BeOne is the only company offering potential best-in-class foundational medicines for every CLL patient type and will continue our relentless approach to fighting CLL and other heme malignancies. 2026 promises to be a milestone-rich year for our foundational Heme franchise. We expect phase three data from the BURKINSA -MANGROVE trial in frontline MCL. We're really excited about that. And the first U.S. approval in relapsed MCL and initial global launches for Sonro. We expect accelerated approval submission for our potentially pivotal phase 2 BTK CDAC trial in relapsed CLL. And in addition, we're planning new phase 3 trial initiations and multiple exciting new molecules will enter the clinic. The BeOne story starts with CLL because it's an illustrative example of how our capabilities have come together to create significant patient impact. CLL is just the first case. But I'm here to tell you the next wave of BeOne innovation, it's already here. In the last decade, we've become a scaled, proven, and highly efficient R&D powerhouse. Our R&D team now comprises of about 4,800 people, making us one of the largest oncology-focused teams worldwide. We have deep expertise in designing small molecule inhibitors and biologics and are emerging leaders in protein degradation, bi and tri-specific antibodies, and ADCs. The sheer output of our research organization is remarkable, and it places us among the most prolific in the industry, irrespective of market cap. For example, in the last 18 months alone, we put 15 new molecular entities in the clinic. But it's not just numbers. Each molecule has differentiated therapeutic hypothesis with best-in-class and first-in-class potential. And with our capabilities now at scale, we have the ability to deliver between 8 to 10 NMEs into the clinic each year. I'm frequently asked, what's the part of the BeOne story that's not yet widely appreciated? And for years, I'd say it's the huge competitive advantages and capabilities that we're investing in and building. But now I think that's much more understood when people see our speed, our cost, our productivity. But today, it's certainly the untapped potential value of our pipeline. This chart helps illustrate that point. We believe that BeOne is punching well above its weight from a pipeline productivity perspective. In our Q3 earnings call, we highlighted four solid tumor programs achieving proof of concept in 2025. These include the CDK4, B7-H4 ADC, PRMT5, and GPC3 4-1BB. Today, I'm happy to add a fifth program, our CEA ADC. Each of these programs has achieved clinical proof of concept with key potential differentiation, and they're moving rapidly into late-stage development. Each represents a significant market opportunity, and each will have external data catalysts this year. At BeOne, we aspire to become the world's leading oncology company, and in our relatively short 15-year history, this lofty goal is becoming a reality before our very eyes. BeOne was purpose-built to discover, develop, and deliver breakthrough medicines to more patients faster and to do so sustainably and at scale. We analyzed each step of the drug development ecosystem, optimizing for speed, cost, quality, and scale. It wasn't easy. It took a tremendous amount of capital and human effort. But it certainly was worth it. Because today, our fully integrated in-house model is a truly unique strategic advantage, both for our internal innovation and also for our external partners and collaborators. We call this capability the BeOne Global Development Superhighway. When you consider that clinical trials comprise the vast majority of the time and cost to develop medicines to patients, it's very surprising to me that the traditional industry model outsources clinical development to CROs. We took a different approach. From the beginning, we believed that this and manufacturing should be a core capability, not something to be outsourced. So we built an integrated global organization of nearly 6,000 colleagues across clinical development and manufacturing. What's the secret? How do we accomplish it all? It's that we have people that are dedicated and motivated and driven to action. It's that we're delivering innovation at a pace that is comparable to the largest MNCs in the industry. It's that we're able to have fast proof of concept, which is the most important value inflection point in our industry. It's that we're able to be decisive and prioritize the most impactful and differentiated medicines that we have. And it's that being internal, we can move fast, we can employ technology, and enroll patients at a speed few can. The results overall are unquestionably incredible. These are a few examples of how the Global Superhighway enables industry-leading execution across development and registration. Over the past two years, we completed 200 dose escalation cohorts with a median time of 1.5 months per cohort. We've spoken a lot about the exciting data being generated by Sonro. Well, we enrolled 700 patients in the phase three CELESTIAL trial in just 14 months across 20 countries. And we achieved the U.S. Sonro filing in record time, two months from data cutoff and one month from the top-line data. I'm often asked, how can we enroll patients so fast? This slide shows our global infrastructure that enables geographically diverse patient enrollment at greater speed. The trials enrolled are with global intent and are designed to meet specific agency requirements such as the FDA's Project Optimus. This is one of the many areas we've optimized that leads to time advantages compared to traditional CRO-based model for drug development. And from a financial perspective, we're in a strong position. We generated over $350 million in free cash flow in Q3. We have a solid balance sheet with over $4 billion in cash. We've proven we can scale globally and that we can do it profitably. From a capital allocation standpoint, we'll continue to invest in commercial assets across geographies that drive profitable growth. We'll continue to fully invest on our prolific and innovative pipeline to maximize long-term value for patients and shareholders. We'll continue to pursue value-creating business development, including opportunities that leverage our global development superhighway. I started my presentation today with how proud I am to be part of an industry that's made such an impact in its fight against cancer. Yet, I think all of us can agree it's simply not enough. That's why at BeOne Medicines, 2026 isn't just another year on the calendar. It's another promise. A promise that we'll keep pushing boundaries, we'll keep relentlessly innovating, and we'll deliver therapies that can truly transform lives. Every breakthrough, every trial, every molecule in our pipeline is a step closer to a world where cancer is not a life sentence, but it's just a challenge which we can overcome. For the sake of all patients like Lynn and the 10 million more who simply want to be, we must all fight together as one. Thank you. Great. Can I sit next to you? You can. Yeah, go ahead. I'd rather sit next to you. Yes. So considering the breadth of the company's pipeline, what's the framework that you use to make decisions regarding what to resource? I think that one of the things we're trying to do is have a very, very robust early set of opportunities that we can prioritize from. Because it's hard when you're a smaller company to prioritize and stop programs that are initiatives. From that perspective, we invest heavily in the early stage of research and development, which most of the industry does not. And then we try to apply a much higher hurdle rate. That hurdle rate is the traditional things that companies think about: the commercial opportunity, the patient opportunity, the competitive landscape. But in all of those frameworks, I think having many more things to prioritize, you do stop a lot of things, but it lets you set an incredibly high bar, which has led so far to assets in the clinic that are very, very compelling. And maybe kind of related to that kind of prioritization, right? With the company transitioning to profitability, from here, how should investors think about the potential for margin expansion and kind of what's the time frame over which BeOne could achieve margins on par with other global large caps? My exceptional CFO doesn't provide long-term guidance, but has communicated very clearly a dual mandate of the company. One is growth, but the other is margin expansion over time. I think although in doing that, we do have the benefit of a time with incredible breakthroughs, all of these new technologies. We have this incredible team and this advanced and advantaged global superhighway. We want to think about the right ways to create long-term value with that. Those are things we bear in mind, but we're committed to those two concepts in the framework of let's help patients and let's do the right thing for the long term. And then you spent a lot of time in the presentation talking about kind of the data in CLL. But what if we were just thinking about the kind of the volume opportunity for the BTKIs in CLL? Kind of what does that look like from here? Well, I think we've talked about the industry currently being $12-$13 billion and growing. I think we do see as fixed duration options come to market, which we believe ZS will be, that actually do meet the requirements, that can be a much larger share. We think this is a very unique combination that is likely to have data that so far no one has any data that looks anything like it. So from that perspective, that expansion into that setting where there's a lot of fixed duration treatment right now that probably isn't as efficacious, that probably isn't as high-priced, there's a real expansion opportunity there. At the same time, I think in the fundamental continuous BTK therapy space, we still are the number one player, but we're sharing the market with two other major players. We've crossed over and will continue in our mind, given the data, to expand in that segment too. And then just thinking about kind of Sonro and how it fits into your CLL strategy and the pie chart you showed that was kind of like half fixed duration, but a quarter is sort of other. Do you need Sonro and a fixed duration combo to crack into that half of the market? Or is that only accessible with a fixed duration option, or can you get there with mono BRUKINSA? Look, I think mono BRUKINSA looks different as we showed with the long-term data than the other continuous BTKIs. I think that data alone, if you didn't have Sonro, it starts to raise some questions about some of the fixed duration treatment that you've seen in the past. There's reasons why you'd make that choice over an Ibrutinib. If the cardiotox isn't there, if the PFS and OS long-term looks better, I think it does, again, change the bar, and it may change that decision-making process. It certainly would in my mind if I were a patient. So yes, I think there's continued opportunity there. Okay. Let me switch gears a little bit. What gives you the confidence to pursue a frontline trial for BGB-43395? The reason that we have that confidence, I think, is the data that we have collected and generated in the first-line setting. We haven't presented that data because it was too immature yet at a scientific meeting, so it's what we're seeing from that perspective and the conversations we're having with KOLs. As we've said, we're going to share that data at a scientific meeting in cancer as soon as we can, but I think we have the confidence to tell the investment community we're moving in that direction. All right, so something to watch out for, and it looks like we are out of time, so we're going to stop right there. Thank you, guys. Thanks, everyone, for coming early. Appreciate it. Thank you. Thank you.