Hey, good afternoon, everyone. Thanks for joining us here for Jefferies Global Healthcare Conference in London. My name is Clara Dong. I'm a Biotech Analyst here at Jefferies. It's my absolute pleasure to have the BeOne team here joining us here on the stage. We have the CEO of BeOne, John Oyler, Aaron Rosenberg, CFO, and Mark Lanasa, the Chief Medical Officer for Solid Tumors. Welcome. It has been a really eventful year for BeOne, I have to say, with your name change, achieving profitability, and BTK inhibitor, BRUKINSA, now leading the global revenue. I have to say, BeOne is probably among the fastest growing biotech companies today. For those who might be less familiar with BeOne, can you talk about what makes BeOne's strategy and development platform or infrastructure very unique for enabling those milestones here? Sure. Thank you for the question, and it's a pleasure to be here again this year. Very exciting times. We are a company that, from the beginning, decided to do things quite differently. We felt if we really want to transform the way medicine's made, have more attractive R&D returns, we needed to change the way we did things. The vast majority of the money spent to make an oncology medicine, and we fight cancer, is really spent in clinical trials, probably 75%-90% of the cost of the medicine delivered to a patient. As a result, we, from the beginning, had a plan to go out and build our own infrastructure. Today we have what we call the BeOne Global Superhighway, which is about 6,000 people all over the globe, 2,000 in manufacturing, 4,000 in clinical trials in 40-50 countries all around the world running our own trials. We are not working with third parties in the same way. That lets us be faster. It lets us go places they are less interested in or they are not. It lets us collect high-quality data quickly and cost-effectively. I think this is fundamentally very different than almost any company in the industry. It is very, very unique to us. From that perspective, we also have a strong research team. We are very science-based. We put 16 new molecular entities in the clinic in the last two years, and we expect that to be increasing, not decreasing over time. From that perspective, we have great products that are late stage in hematology, BRUKINSA, which is a wonderful commercial medicine already for patients with lymphoma, but then we are in earlier stages in solid tumor and doing a little bit in INI. So that is a little bit about our company. Since you mentioned the R&D capability, I mean, BeOne has built a really extended pipeline across multiple modalities, small molecules, degraders, ADCs, and anything I can think of across oncology areas. What gives you confidence that BeOne can remain highly competitive across all those areas? We are in a lot of the modalities, but not all. We have not been a major player in CAR-T or radiopharma or cell and gene therapy. Some other areas we have been less focused on, but clearly we have built with great scale in many of these areas. In protein degradation, I think we are probably one of the most prolific R&D companies in the world with three programs in the clinic and I think 20 pre-clinical programs at this moment. From the other perspective in biologics, as I had mentioned, we build our own manufacturing, which gives us the ability, as we are doing R&D and even R, to be able to leverage that and move quickly and cost-effectively. We learned that the hard way by working with third parties, and we really struggled to do that. It was slow, and it was very expensive. As a result, we're doing a lot in biologics, a lot of bispecifics, trispecifics, or ADCs. By ADC, it doesn't have to be a toxin. Your payload could be something else. It could even be a degrader. I think we do feel like we're able to do a lot in research in these areas, be very strong. In addition to that, when they move forward into the clinic, because we've built this BeOne Global Superhighway that has got cost and time advantages, we really can pursue these and understand what's working and what isn't and triage and wind up with some incredibly impactful medicines for patients. As a global company, you're operating in many, many regions, and your drugs are selling across the globe. Maybe could you break down the geographic diversity of your revenue base? What kind of efforts are you making to kind of further expand the company's global footprint? Great. Thank you for the question. And we're very proud of the financial performance for the company in 2025. We've talked about this being an incredible inflection point, and that's really showing itself across the financial profile. With respect to the globalization of our business, where we sit today, if you look at Q3 results, which we just announced, more than 50%, I believe it's 52% of our business is in the United States. We are growing significantly with our European business. That printed a 71% year-over-year growth and now accounts for 12% of sales. And we're growing even more rapidly in rest of world countries with 133% year-over-year growth in the third quarter. And many important markets like Japan just coming online earlier this year. So we continue to globalize, I'd expect, over the longer horizon. We will continue to have a profile that looks very much like any major biopharmaceutical that is in a mature phase. Maybe a relevant question is, maybe talk about your manufacturing scale across the globe as well. Sure. So we certainly have, as John mentioned, significant operations from a manufacturing perspective. We do follow a regional model that includes significant investments in the United States, where we have investments and partners for our small molecule production, as well as the investment that we made in our biologics facility just outside Princeton, New Jersey, where we invested more than $800 million. It'll be the future home of our production for Tevimbra, our PD-1 for the U.S. and other markets around the world. Great. Let's now talk about your CLL franchise, which is really a key pillar of BeOne's story here. Maybe could you provide a high-level overview of your CLL strategy and then what's your real ambition in CLL? What's your vision? I think in CLL, our vision is to make the best medicines and be able to provide the right treatment for any patient with any type of CLL at any stage. From that perspective, we have three important medicine or potential medicines in this space. Our BTK inhibitor, BRUKINSA, which is approved and which I think, as we mentioned, is the number one revenue-generating BTK in the world. It is a molecule that was designed to be in all disease compartments 24/7 a day with superior PK, high potency, high selectivity. The belief was, if you want to fight cancer, you're better off sustainably inhibiting at every moment and preventing that cancer from growing. That data is broad and impressive. Most recently, our ASH abstract published, which shows the six-year data and six-year follow-up for BRUKINSA. It's 74% milestone PFS, which is double digits better than results previously reported by any monotherapy BTK in this space. It's really impressive data. That's the PFS data. The OS data is quite similar. We're very excited to share that later this year, but it's consistent with everything we've seen. We've run head to head with ibrutinib. It showed superiority. One of the other BTKs ran head to head. It didn't. Actually, at the time the study was last reported, it was numerically worse. I think from that perspective, we believe this is the continuous therapy treatment of choice already. It's established from that perspective. There's a breadth of data, including the data we'll report at ASH, including lots of real-world data. The more you look at it, the clearer it is that that hypothesis was a strong one. From the other perspective with our BCL2, we've shared some data about its kinetics. Basically, when you look at its speed and depth of MRD negativity, so your inability to measure CLL in blood, what we've seen is a much faster and deeper response than we've ever seen with a Venetoclax set of combinations with a BTK. Roughly in a six-month period, you can see a deeper response than in 15 months with, say, AV or IV, for example. From that perspective, once you have a year's worth of treatment, the 15-month full course, you're seeing a much, much deeper response. It's not just in the mutated population, which traditionally is the population that the Venetoclax-based therapies have done well in. It's also in the unmutated population, which that has not been true for. From that perspective, it really looks like this is a combination that can do things that other fixed duration therapy has not. That is really important because right now, only half the patients are getting continuous therapy in first-line CLL, and roughly half of those patients, maybe a little less, are on BRUKINSA today. As we think about this combination, it really lets us broaden that. I think 20% of patients are on Venetoclax or combinations thereof in the first-line setting. It really is helpful to this franchise. More importantly, with the data, the way it looks, I think it is going to be very, very helpful to patients. The third piece of our CLL franchise is our BTK degrader. We are really excited about this because the covalent BTKs have similar mutations. They overlap. There are some differences. There is a non-covalent medicine, pirtobrutinib, that was developed to kind of try to address some of these mutations. It does not address all of them, but it addresses some. It is approved in the relapsed refractory setting. The beautiful thing about the degrader mechanistically is it looks like it has much broader applicability. We also have a lot of early data in the second and third-line settings from that perspective, which compares extremely favorably with the pirtobrutinib data. A year ago, almost a year ago, we announced we would be starting a head-to-head study against pirtobrutinib. That is in progress from that perspective. We are very excited about that for relapsed refractory patients. There are many other combinations from these. We're incredibly excited about the prospect for CLL patients and our ability to help them no matter what their subtype is or what their line of therapy is. I see you are talking about a fixed duration regimen here. I want to talk about your kind of clinical strategy for running phase III head-to-head trials versus standard of care with both BCL2's sole role and BTK degrader. Maybe just talk to us about why are you running those phase III head-to-head trials and why is this strategy so important? You know, I think we also ran BRUKINSA against ibrutinib. It's because the data supports it and because that's the fundamental question that matters to patients. We're not afraid of that. Of course, we analyze the risk, and we're not wild cowboys taking stupid risks. When you look at the data that exists and that is in hand, those are very warranted studies. We're running our BCL2 sonro plus BRUKINSA against BeOne. BeOne is good. Other people did not do that. We're running against that despite the fact it's a high hurdle. We're doing it. We're running against pirtobrutinib. I'm sorry, we're running against pirtobrutinib with the degrader. We're not afraid to do these studies because the data supports them. By the way, if you are successful in those studies, it ends all the questions. It ends all the nonsense about it. You've shown you're the best medicine. The commercial market's there, and it's clear for you. I think that we've done that historically in the company. You'll continue to see us do that where we find it warranted. We're excited and happy to be doing that. I think from the other perspective, in the CLL space, the only thing we ask is for people to look at the data. It's so clear when you actually look at the clinical data. There's been a lot of noise about fixed duration therapy. There was a lot of noise about the recent data. It's not that recent. The data that came out over a year ago, which was the combination of Acala plus Venetoclax, this is going to sweep the market. It's going to take the whole market. It was supposed to be approved six months ago. We're waiting on the data. We haven't seen the follow-up data. The approval in the U.S. has been delayed. In Europe, it was approved. In that study, the milestone PFS at three years, which is only 21 months off therapy, the first 15 months you're on therapy, it's pretty close to our six-year milestone data that I just mentioned. We're fighting cancer. Patients want efficacy when they have cancer. I think that all we ask is people look at the data. Clinicians look at the data. Patients look at the data. You all look at the data. We think it's, at this point, increasingly clear. Maybe if we can talk about the timeline for Sonrotoclax and BTK degrader to enter the market globally, and then how should we think about the CLL market in the long run? Do you think the BCL2 inhibitor and BTK degrader will actually expand the CLL market? Thank you, Clara. Yes. Our expectation is that we'll be presenting data at this year's ASH for Sonrotoclax. Our expectation is that will lead to initial approvals in the United States and globally for Sonrotoclax in 2026, and that we have potentially registrational cohorts that are enrolling for the BTK degrader that could enable a first market approval for the BTK degrader in 2027. These molecules will be coming soon. We think that, as John was saying, this will present an option for patients despite or regardless of what molecular subtype they have and regardless of where they are in their patient journey. Then beyond CLL franchise, you also have a very, very broad pipeline in solid tumors. I also want to talk about that. Across your solid tumor programs, I mean, we hear a lot of discussion on the CDK4 inhibitors. You did commit to initiating a phase III trial in the front line HR-positive HER2-negative breast cancer next year. Maybe just talk to us about what you've seen with your CDK4 inhibitors to support such a rapid development path. It is a very exciting time within the solid tumor portfolio. As John mentioned, we have brought 16 new molecular entities into the clinic over the past two years, the majority of them in the solid tumor space. At the earnings call that we just had, we highlighted four programs that we believe are progressing towards phase III study start, not only the CDK4, but also PRMT5, B7-H4 ADC, and our GPC3 by 41B bispecific. For CDK4 specifically, we have enrolled cohorts of patients in the front line setting as well as the second line setting. In front line, it is in combination with letrozole. What we are seeing in that patient population is a high response rate, higher than what one would expect for the approved CDK4/6 inhibitors. We think that that will pull through to ultimately have improved PFS. We are intending to start a phase III study for our CDK4 inhibitor in the front line in combination with a nonsteroidal aromatase inhibitor, which we believe will show superior PFS over the currently approved CDK4/6 inhibitors. That study will start by the end of the first half of 2026. You just mentioned the other preclinical and early-stage clinical products in your pipeline. Maybe talk to us about what's the differentiation of your PRMT5 inhibitor as well. For all of the medicines we bring into the clinic, our aspiration is to develop first-in-class and best-in-class medicines. To do that, everything that we bring forward needs to have what we believe is substantial preclinical differentiation that is reasonably likely to yield clinical differentiation. In the case of our PRMT5 molecule, what that means is that preclinically, we have the most potent PRMT5 inhibitor of any clinical stage asset. This greatest potency also leads to the greatest selectivity. Critically, it was designed to be CNS penetrant, which we view as a really essential characteristic, particularly in non-small cell lung cancer, where unfortunately, CNS metastases occur in about 30% of patients. That molecule is off to a great start. It's only been in the clinic for 10 months. Again, using our development superhighway, we've enrolled over 100 patients in approximately 10 months' time. We're seeing responses across multiple tumor types, including non-small cell lung cancer, pancreatic cancer, and other less common tumor types. Maybe we can also touch briefly on your BTK degrader platform. I mean, this platform is highlighted by the very promising data in BTK degrader. You also have a KRAS degrader and a EGFR degrader. Maybe talk to us a little bit about those two programs as well. As you heard from John, we're very excited about the data that's emerging from our BTK degrader. We've initiated phase III studies. We also have an IRAC4 degrader, which we recently disclosed has met its clinical proof of concept with high target degradation in target tissue of skin. We think that this is a potential first-in-class molecule for INI indications and recently started a phase II study in rheumatoid arthritis. We're very excited about degraders as an entity because of their catalytic mechanism of action that has advantages over small molecule inhibitors, which require a one-to-one stoichiometry to inhibit specific enzymes. As you mentioned, we have an EGFR degrader that's in the clinic that's progressing well. We've disclosed other targets. For example, we have a CDK2 degrader, which should enter the clinic by the end of this year and provides another opportunity to hit CDK2 in a differentiated way that can be combined with our CDK4. We also have a pan-KRAS degrader coming forward, which we think mechanistically is very attractive in KRAS because amplifications could be a mechanism of resistance. By actually removing the protein, you can prevent amplification. You can prevent conversion from the off-state to the enzymatically on-state. That was such a broad pipeline. Maybe a question to you, Aaron. How does BeOne invest in R&D and kind of balance your internal invest in R&D versus maybe outside asset acquisition or BD activities? Sure. Thank you. We are very pleased with how our financial profile and particularly our balance sheet has evolved over the course of the year. We continue to operate against two mandates. One is we are a high-growth oncology company. On the other hand, we will do so in a sustainable way. You see that in our financial performance. In the beginning of the year, we committed to GAAP operating income and cash flow generation for the year. If you look at our Q3 results with $125 million in net income and $354 million of free cash flow, I think we are well underway to achieve those goals. As we think about the longer- term, and I did not provide perspective on 2026 specifically, but in my prepared remarks in the third quarter, we did talk about how the pace of our margin expansion will be measured given all of the incredible opportunities that you just heard from Mark in terms of investment in more than 20 phase III trials next year. We continue to operate with discipline. I think to your first-order question, the key focus is making sure you are investing in the right programs, you are testing your hypotheses, and you have a very high bar that you do not sacrifice. With the depth and breadth of our pipeline and so many opportunities, we are able to maintain that high bar without question. In terms of capital allocation, I think our priorities around capital allocation are unchanged. It is about investing to grow the business. It's about investing in the pipeline. We will continue to be active on the business development side. Certainly, with our balance sheet position, we have additional strategic flexibility in that regard. We are really disciplined on prosecuting the wealth of opportunities we have coming out of our internal engine and looking for complementary assets related to those pipeline assets. Thank you. Got it. Maybe for the last minute or so, I also want to touch on AI. In the world of AI, maybe tell us how is BeOne leveraging AI in drug discovery and development? How do you expect this to have, what kind of impact would you expect on the efficiency and innovation across your pipeline? Sure. I think there's lots of areas in which it's being used in an Ad hoc fashion as a tool in research with structure folding and other things. We're certainly doing a lot of that in manufacturing. Same thing for process optimization and other areas. Those, I think, are very straightforward. I think we see a huge opportunity in the clinical trial side of things from that perspective. Overall, I think there's great promise, but it's hard. AI is very good when there's huge data sets and predicting what new ideas, new things could be. In the area of overall drug discovery, a lot of the data is very fragmented and not public. A lot of the data is not high quality and in legacy systems. It's a harder problem that just is going to take some time and energy. The system's only as good as the data that it's built upon. For overall drug discovery, predicting what's going to work in a disease state, that data needs some time and energy, and we need it to evolve a bit and probably have a system where we have more access. The real key to unlocking that would be tapping into real-world data, which right now is not high quality, unfortunately. Great. Thank you, everybody, for tuning in in person and online. That concludes our session here. Thank you.