Hello and welcome to Genmab's 2024 R&D update and ASH Data Review. I'm Jan van de Winkel, President and CEO of Genmab, and I'm delighted to share with you some of the highlights for Genmab in 2024, as well as data from this year's ASH meeting. As always, we have a busy agenda, so let's jump right in. Next slide, please. As a reminder, this presentation may contain forward-looking statements and, as such, may contain certain risks and uncertainties. Let's move to slide three. Genmab is a science-anchored and innovation-focused culture. Collaborations and partnerships have always been part of our DNA. During today's presentation, we will reference some of the products being developed under these strategic collaborations, and this slide acknowledges those relationships. Let's move to our agenda on slide four. We will begin with a review of the progress we made this year as we advance toward our 2030 vision. Central to our achievements are the significant advancements for Epkinly and Rina-S. To provide a comprehensive understanding of these developments, our Chief Medical Officer, Tahamtan Ahmadi, will deliver an overview of both the Epkinly and Rina-S programs, highlighting key milestones and near-term plans. Following Tahamtan's presentation, we are excited to share a prerecorded presentation by Dr. Elizabeth Lee. She will discuss the latest Rina-S data that was showcased at the European Society for Medical Oncology Congress in September, and next, we will review some of the pivotal Epkinly data presented at this year's ASH meeting, and for this, we are very pleased to have a presentation with Dr. Martin Hutchings. Looking ahead, we will provide a brief overview of some of the key events we are anticipating for 2025. To conclude, we will open the floor for a lively Q&A session. But first, let's explore some of the highlights from the past year that have set the foundation for our continued success. Next slide, please. This has been a landmark year for Genmab, marked by significant milestones that advance our mission to bring innovative medicines to patients. We and our partners successfully submitted and obtained multiple regulatory approvals for both Epkinly and Tivdak. These approvals are pivotal in making these therapies accessible to a wider number of patients. And with its strong performance in markets like the U.S. and Japan, we are confident in our ability to grow the footprint for Epkinly to reach even more patients. We will also accomplish two additional indications, and I'm pleased to note that there are currently five phase III trials ongoing for Epkinly, including frontline trials in both diffuse large B-cell lymphoma and in follicular lymphoma. While Epkinly was our primary focus at the beginning of 2024, we have now expanded our late-stage development pipeline to include Rina-S and acasunlimab. All three of these programs, Epkinly, Rina-S, and acasunlimab, have the potential to drive significant future growth. Rina-S was a key factor in our acquisition of ProfoundBio, the first major acquisition in our 25-year history. This acquisition enhances our pipeline and positions us for long-term success. Our partnerships continue to validate our innovation and technology, and notably, both Darzalex and Rybrevant received multiple additional regulatory approvals this year. A particular note is the relatively recent submission by J&J for regulatory approval of subcutaneous daratumumab in both the U.S. and Europe for high-risk smoldering multiple myeloma, and if approved, this would be the first treatment option for these patients, providing a novel approach to treat people at risk before the onset of active disease, so let's move to the next slide to explore the impact of these milestones. The acquisition of ProfoundBio has been a significant milestone, enhancing our capabilities with next-generation ADC platforms. This strategic addition, combined with our diverse existing next-generation antibody technologies, positions us to accelerate the development of world-class therapies. With two 50/50 partnered medicines successfully on the market, we are building the necessary infrastructure and expertise to bring medicines directly to patients ourselves, and now these capabilities can be leveraged with our wholly owned programs, Rina-S and acasunlimab. These product candidates, along with Epkinly, exemplify our focus on developing best-in-class therapies, and we will continue to develop our novel clinical stage assets while also making strategic decisions to prioritize high-potential programs, ensuring our pipeline remains focused and impactful. Before we move to today's data presentations for Rina-S and Epkinly, I would like to introduce our Chief Medical Officer, Tahi Ahmadi. Tahi, the floor is yours. Next slide, please. Thank you, Jan, for this kind introduction. If we just move on immediately to the next slide. Let's start with Epkinly. We just come out of an exciting ASH where we had a significant presence with more than 20 abstracts for our presentation, really highlighting the quality of data across a spectrum of data that we've been generating, focusing on the efficacy and the durability of the efficacy, the safety profile as well, the versatility and the ability to combine with a variety of backbones, which to us is a key component of the development strategy for Epkinly as we move it along the lines. As a note, Epkinly is the first and only bispecific approved for both indications, diffuse large B-cell, and for follicular lymphoma in third line. On this slide, you have the five phase III that Jan highlighted. This is a very robust program this early in the development stage for any product in lymphoma. We're very proud of our achievements together with our colleagues at AbbVie. I should note that the frontline diffuse large B-cell study in combination with R-CHOP versus R-CHOP is already fully accrued, way ahead of the initial projections, a testament to the excitement of both patients and investigators. The same is true for the second line follicular lymphoma study in combination with R-squared. We have a phase III in combination with lenalidomide in the second line diffuse large B-cell that is now actively ongoing. The frontline follicular lymphoma study is also moving very rapidly. Very excited about these phase IIIs and expecting readouts on these phase IIIs, particularly on the ones that are fully accrued in the foreseeable future. As we transition to the next slide, the expansion of our pipeline to the acquisition of ProfoundBio, Jan highlighted the key component of that is Rina-S. Again, we're moving very rapidly into expanding our development program. We have an ongoing phase I study that has multiple cohorts. It has expansion cohorts both in endometrial as well as in ovarian, but also combination data that's being generated with carbo, with Bev, with PD-1, and really intended similarly to what we've done on Epkinly, to very early generate data in combination to then allow us to move into earlier combination settings and earlier lines. Phase III, as we already discussed on the Q3 call, in folate receptor alpha, our high population product is open and is ready. It's rolling. We're excited about the acceleration of our registration enabling program here in this program as well. With that, I hand it over back to Jan. Thank you, Tahi, for that excellent overview. It's now my pleasure to introduce a video by Dr. Elizabeth Lee. Dr. Lee is a faculty member within the Department of Medical Oncology and the Division of Gynecologic Oncology at the Dana-Farber Cancer Institute in Boston. In September, she presented the promising Rina-S data at ESMO. And we are grateful to have Dr. Lee provide us with a review of the data again today. Please play the video. Move to the next slide, please. And then the video. On behalf of my co-authors, it is my pleasure to present data from the phase I/II study evaluating rinatabart sesutecan or Rina-S in patients with advanced ovarian or endometrial cancer. These are my declarations. There continues to be a significant unmet need for the treatment of patients with ovarian or endometrial cancer. Folate receptor alpha or FR alpha is a validated therapeutic target that is overexpressed in multiple solid tumors, including in ovarian and endometrial cancer. Rina-S is an investigational antibody-drug conjugate or ADC that is directed at FR alpha with a novel hydrophilic cleavable linker and carrying a topoisomerase I inhibitor payload. Additionally, Rina-S features a high homogenous drug-to-antibody ratio of eight. We conducted a study evaluating single-agent Rina-S administered once every three weeks for the treatment of advanced solid tumors regardless of folate receptor alpha expression, which was only tested retrospectively. From part A dose escalation, we evaluated patients with heavily pretreated ovarian and endometrial cancer treated with Rina-S 100 or 120 milligrams per meter squared. Cohort B1 of dose expansion involved 42 patients with heavily pretreated ovarian cancer who were randomized one-to-one to receive either Rina-S 100 milligrams per meter squared or Rina-S 120 milligrams per meter squared. These patients received a median of three prior lines of therapy and almost all have platinum-resistant ovarian cancer and had received prior bevacizumab. Additionally, 20% of patients received prior mirvetuximab soravtansine or Mirv for short. In dose escalation, Rina-S showed encouraging anti-tumor activity in patients with ovarian and endometrial cancer with a confirmed objective response rate of 30.8% and a disease control rate of 88.5%. As shown on the waterfall plot on the right, treatment with Rina-S led to meaningful reductions in target lesion size for both ovarian and endometrial cancer patients. The median duration of response was 35 weeks, as was the median on-study follow-up. At the time of data cutoff, three patients had ongoing responses. In patients with ovarian cancer from dose expansion, treatment with Rina-S 120 milligrams per meter squared led to an encouraging confirmed objective response rate of 50%, including one complete response. Treatment with Rina-S 100 milligrams per meter squared led to an objective response rate of 18.2%. In addition to a superior response rate, treatment with Rina-S 120 milligrams per meter squared led to deeper and more meaningful tumor size reductions as seen in the waterfall plots on the right. At the time of data cutoff, the median duration of response was not yet reached. As shown on the swimmer plot, responses with Rina-S 120 milligrams per meter squared were observed as early as six weeks. At the time of data cutoff, all confirmed responses with 120 milligrams per meter squared were ongoing, and most patients with stable disease had not yet progressed. Of note, responses were also observed in patients who had received prior mirvetuximab soravtansine. Responses with Rina-S were observed in tumors with FR alpha expression of PS2+ at both cutoffs of greater than or equal to 75% and less than 75%. In exploratory analyses, we also observed clinical activity with Rina-S at FR alpha expression of PS1+ at a cutoff of less than 25%. In cohort B1 of dose expansion, the safety profile was similar between the two dose levels. The most common treatment emergent AEs were cytopenias in grade one or grade two gastrointestinal events. Grade three or grade four neutropenia occurred in approximately 45% of patients. Treatment emergent AEs leading to dose reduction or treatment discontinuation were similarly low. Prophylactic G-CSF was used in 32% and 50% of patients treated at the 100 and 120 milligrams per meter squared dose levels, respectively. There were no signals of ocular toxicities, interstitial lung disease, or neuropathy observed in this reported patient cohort. In conclusion, single-agent Rina-S given once every three weeks showed encouraging anti-tumor activity in patients with ovarian and endometrial cancer. In dose expansion, treatment with Rina-S at 120 milligrams per meter squared resulted in a confirmed objective response rate of 50%, including a complete response in patients with heavily pretreated ovarian cancer. All responses were ongoing at data cutoff. Responses were observed regardless of FR alpha expression levels, as well as in patients with prior mirvetuximab exposure. Rina-S was well tolerated with manageable treatment emergent AEs. Based on these findings, further evaluation of Rina-S is ongoing as a single agent and in combination with other agents. On behalf of the authors, we'd like to thank the patients, study investigators, and site personnel for their participation. Let's move to the next slides. Next slide, please. Turning now to the epcoritamab data at ASH, I would like to introduce Dr. Martin Hutchings. Dr. Hutchings is a Hemato-Oncologist at Rigshospitalet in Copenhagen, Denmark. He's a world-class expert in the treatment of malignant lymphoma and a key investigator on the phase I/II study of epcoritamab. We very much appreciate Dr. Hutchings being with us once again to review some of the epcoritamab data presented at this year's ASH. Martin, please go ahead. Thank you very much for the introduction, and I think you just need to tell me whether I share my slides or whether I can ask for the next slide. Yes. Next slide, please. We can see your slides. Yeah. You can see the slides. So thank you very much for the opportunity to give a fresh brush-up on a truly exciting ASH, which finished just yesterday. So I completely agree with Tahi that there was a lot of action also on epcoritamab, really exciting and clinically useful data. And I will try to give you a brief update of the most important points that have been made over those last three, four days. So next slide, please. A little bit of technical issues here. Are you displaying my slides? Here we are. So we'll begin with the pivotal NHL1 trial. And this trial was or is a trial of looking at single-agent epcoritamab therapy in the treatment of relapsed and refractory large B-cell lymphomas with two or more prior lines of treatment. This is a situation for which until just a few years ago, there was actually no standard of care and outcomes of conventional therapy were generally very poor. Since then, we've had the introduction of CAR-Ts in third-line therapy, much improving outcomes for those patients with access to such treatment, and then more recently, approval of the bispecific antibodies, including Epkinly. This is an update of the pivotal study that led to the approval of Epkinly in this very indication. This is an overview of the study design. You can see that the patients who were led into the study had what we call large B-cell lymphomas. There are several subgroups of those with different characteristics and risk profiles. They needed to have a reasonable performance status, so general status and organ function, and they needed measurable disease. Epcoritamab was given in the step-up fashion, so with a small initial dose, a slightly higher intermediate dose after one week, and then from cycle one day 15, so that's two weeks into treatment, the full dose of 48 milligrams of epcoritamab given weekly for the first three cycles, that's 12 weeks, then biweekly for the next six months, and then every four weeks, and until progression or unacceptable toxicity. The primary endpoint of this study was overall response rate, but key secondary endpoints included complete response rate and, of course, the survival analyses, particularly duration of responses and progression-free survival. So what was presented here at ASH, unfortunately, just in a poster, were the quite mature follow-up results at a mature follow-up of almost three years, including not only the efficacy parameters, but also a long-term look at safety. Next slide, please. So to cut a long story short, the overall safety profile is consistent with what has been reported and also published recently. So, of course, the primary acute toxicity of the bispecific antibody is cytokine release syndrome, long over with in all these patients and already reported, and really quite manageable and generally of low grade in the majority of patients. So at this point, more interesting is it perhaps to look at the more long-term side effects, which are dominated by the slightly increased risk of infections, which is brought about by the long-term B-cell depletion. So it's encouraging to see that almost three out of four patients who were on treatment for more than two years, and these are perhaps the worry because of the long-term suppression of B-cells, three out of four of those, 73%, did not experience a serious infection as defined by grade three or higher. We do see cytopenias, so drops in blood counts among patients, mainly seen to a high degree during the first couple of months of treatment. And then later on, these reduced rates of both platelets and particularly white blood counts go back to normal, except, of course, for the B-cells that I mentioned, they keep being low and depressed as long as we treat the patients because it goes with the territory of B-cell depletion. Next slide, please. Looking at the long-term efficacy outcomes, the overall response rate for the overall population remains stable at 59% with 41% of complete responses, so 41% with a complete disappearance of the signs of disease on the PET scan, which is the used method, preferred method for response assessment in this disease. Now, for patients who were on treatment for a long time, prolonged time, over 12 and 24 months, we see that very few of those patients actually lose their response. Patients come off treatment during the first year, a few due to toxicity, more due to progressive disease. For those patients who are on prolonged treatment beyond one and particularly two years, we see very rare cases of loss of response, which is really encouraging and to some extent supportive of the treatment until progression, at least in some patients. Next, please. So this is a take on the durability of the complete responses. 41% of the patients responded completely, and they are really the meaningful responses. And I think this chart is really a testament to that clinical meaningfulness. You can see that for the overall group, the median duration of a complete response was 36 months. That is three years, so three years of maintained complete responses in a disease situation where, like I said, until five, six years ago, there was no real meaningful treatment. And this durability is more or less the same regardless of which of the subgroups of large B-cell lymphomas that we are looking at. At the bottom, you can see a statement saying that this suggests a curative potential. That was criticized and discussed a little bit during the ASH meeting because how can you say that something is curative if you keep giving the drug? But I think the suggestion is strong enough. But of course, it's clear that clinicians need guidance on how long to treat patients and if treatment until progression is really relevant, at least in a subgroup of patients. Next slide, please. Looking at the overall survival, again, a testament to the clinical meaningfulness of this great therapy. You can see that at three years of follow-up, 75% of the complete responders had not initiated a new anti-lymphoma therapy, and that is because they were still alive and progression-free at the time of the most recent follow-up. You will see that for the overall group of large B-cell lymphoma patients at three years, the overall survival, 63%. Next slide, please. In conclusion, long-term safety consistent with previous reports and no new important safety findings, which is really encouraging because it's a concern when you keep B-cell depleting your patients for several years, but really no serious long-term signals. About efficacy, the complete response rate is maintained. That's not a big surprise, but the durability, that was really the big news from this year's ASH with a median duration of complete response of 36 months, three years, median progression-free survival, more or less the same, 37 months, and the median overall survival, as I just showed you, is not reached. Long-term remission support to some extent, treatment until progression, at least for subgroups of patients in this heavily pretreated patients with at least two prior lines of treatment, and in the eyes of the beholder, suggesting a curative potential at least for some of these patients. Next slide, please, which is where we move on to another important study also presented, and this time as an oral session. This was the phase II study of fixed duration epcoritamab+ R-CHOP in previously untreated patients with diffuse large B-cell lymphoma. And this was one of many cohorts of the important EPCORE NHL-2 trial, which had a lot of different cohorts where epcoritamab was combined with several different standard therapies in various indications and various treatment lines. But here we're looking at the combination of epcoritamab and R-CHOP in first-line treatment. Next, please. So the background for this is that we have a very well-established standard of care in first-line treatment, unlike third-line treatment. R-CHOP has been used for 20, 25 years and has not very often been successfully challenged by new regimens. But that doesn't mean that there isn't an unmet need because with R-CHOP, we actually only cure approximately two-thirds of patients, and also there are many patients who cannot tolerate R-CHOP. We have initial data showing safety when looking at the combinability of epcoritamab and R-CHOP, and here we present long-term outcomes with more than two years of follow-up for this combination in the first-line treatment of large B-cell lymphomas. Next, please. So this is the study overview. Patients could be included if they had large B-cell lymphomas newly diagnosed, and they needed, and this is important, an IPI score of three to five. What does that mean? That means that they need to be among the approximately 50% of worst prognosis patients in order to be included in this study. R-CHOP was given in the usual three-weekly doses times six. Epcoritamab added weekly for the first four of those doses, then every three weeks, so once together with each of the two last of the R-CHOP doses. And then in this study, every four weeks after the completion of chemotherapy until up to one year of total epcoritamab treatment. The primary objective of the study was the anti-tumor activity as assessed by the overall and complete responses, and also with MRD negativity as an important secondary endpoint using the AVENIO ctDNA assay. The median follow-up for this analysis, importantly, just over two years, 27 months. Next, please. So here you see a rough overview over the safety profile, actually very similar to what has been presented previously. And I would say that the safety profile of the combination really is in keeping with the contributions of the individual elements. So looking at R-CHOP on one side and then epcoritamab. And it's important to look at the cytokine release syndrome, which is the bar number three that is brought about, of course, by the epcoritamab mainly during cycle one and early in cycle two of this treatment. And we see that both frequency and severity in keeping with epcoritamab monotherapy, very rarely CRS of grade three or higher. Next, please. So this is a very active combination. We're not surprised to see high responses because we see high response rates to R-CHOP as well, but it's still quite encouraging to see a 100% response rate in the efficacy evaluable population of 46 patients. That's actually all patients except one that made it to the first response assessment and could be included in the efficacy evaluable population. So 100% response rates. As you can see, and this is just as important, very high complete response rates in the range of 80%-90% depending on the subgroup studied. Next, please. These responses are really quite durable. These Swimmer plots are a little bit busy to look at, but what you will see is that for the patients who end their treatment, finish complete their treatment, not only the chemotherapy, but also the Epkinly maintenance up to one year, you will see that all these patients at some point, most of them very early during treatment, some of them later during treatment, reach complete responses. And in the vast majority of patients who are still being followed, these complete responses are maintained. That is actually the fact for all patients finishing treatment and complete response except three. So really durable responses and promising a high cure rate in these difficult-to-treat patients with high-risk features. Next, please. And that is, of course, reflected by the both survival curves and in this case, the curve showing the durability of complete responses. Time is here counted from the time of the first complete response observed in the patients. And you can see that for those patients who reach a complete response at some point, the durability of that complete response is very, very high. The median, of course, far from being met, 83% at 21 months, which is the median follow-up for that part of the population. Next, please. And that is, of course, reflected in equally impressive progression-free survival. I just told you before that for the overall group of patients with large B-cell lymphoma, the cure rates are among just around 60%-65%. Of course, this is not cure rate. We're looking at progression-free survival, but still it's encouraging to see 82%-83% progression-free survival rates at almost two years, considering that we are thinking about a high-risk group of patients. Next, please. And overall survival increasing and just equally encouraging at 87% for the overall population and 83% for the high-risk group of patients with double or triple hit lymphomas, those that we also call high-grade lymphomas. Next, please. So the conclusion from this important update was the fixed duration epcoritamab with the standard R-CHOP chemotherapy induced remissions in the vast majority of patients and in the majority of these patients with responses, also highly durable remissions as we can see with this long-term update. No safety signals observed, and this is really quite important, particularly because these patients are, of course, all the majority of them will be cured. Long-term safety signals are particularly important here. We believe that these findings compare favorably with R-CHOP alone. Of course, that is a historical comparison so far, but as Tahi Ahmadi already told you, the phase III study of R-CHOP+ or minus epcoritamab in the first-line treatment of large B-cell lymphoma has been ongoing, accrued very quickly, and has, as I understand it, completed accrual earlier this year. Next slide, please. Then we move on to another abstract, which also made it to the oral sessions. It was the single-arm study of epcoritamab monotherapy in elderly and/or frail patients over the age of 75 years with previously untreated large B-cell lymphoma, excellently presented by my colleague Franck Morschhauser a couple of days ago. Next slide, please. So this is a completely different population because generally the cornerstone of curative treatment or curative chemotherapy for large B-cell lymphoma is the anthracyclines, usually doxorubicin. But this is not an easy drug to tolerate, particularly for elderly patients. So the majority of patients over 75 or 80 years, they cannot tolerate a full course of R-CHOP. Sometimes we reduce the doses of the chemotherapy, then we call it our mini-CHOP, but many patients cannot even tolerate reduced doses of these quite intensive chemotherapies. So about 10% of newly diagnosed patients are ineligible for anthracycline treatment, low or full doses. And of course, as you can imagine, they are highly concentrated among patients who are elderly, both because of general frailty and particularly because of cardiac or other comorbidity. This trial looked at patients who were old, elderly, older than 75 years, and for many, in many cases, had relevant comorbidities preventing them from accepting or tolerating anthracycline-based curative intent chemotherapy. Next slide, please. This is really a population of patients that we struggle with in the clinic. They are not easy, and as the median age at onset of large B-cell lymphoma is around 65 years, you can imagine that this is actually a relatively high group, a prevalent group of patients that we see every day. Patients could be included if they had newly diagnosed large B-cell lymphomas, a reasonable performance status of zero to two, and then, like I said, ineligibility for anthracycline-based cytotoxic therapy defined as either an age over 80 on its own or an age over 75 with a well-predefined comorbid condition, and that could be cardiac comorbidity, but also other comorbidities, and patients should have measurable disease, so this was, in fact, a randomized study, but no randomization results were presented in this analysis, so you can regard the data that I show you here as a kind of single-arm study of single-agent epcoritamab because no data have yet been presented regarding the other side of the randomization, which is the combination of epcoritamab and lenalidomide in the same patient group. Next, please. This is just a quick overview to give you a taste or a feel for the comorbidity status of these patients. This is actually a slide that really caught attention because you can see there was a lot of comorbidity. 78% of patients included had hypertension. 71% had elevated cardiac enzymes. That means there is some kind of strain on the heart, not necessarily symptomatic, but still a clear signal that these are patients where you should be very careful with anthracyclines or probably not give them at all. Then you can see a long list of other comorbidities with relevance, particularly for the vasculature of the patient. Next slide, please. Despite these patients being previously untreated, which means that they have a relatively intact immune system, they actually tolerated treatment quite well with less cytokine release syndrome than some of us had perhaps feared or anticipated. You will see that frequencies of cytokine release syndrome are a little bit higher than, for example, in the groups of patients treated for relapsed refractory disease. CRS was seen there in approximately just under half of the patients. And here you can see that cytokine release syndrome is seen in just over 70% of patients. Not a surprise because this is a single agent given to patients who have not had their immune system suppressed by previous chemotherapy. But the good news is that the majority, the vast majority, in fact, of patients experiencing cytokine release syndrome did so at low grade. 39% with grade one, that is just fever, and 27% grade two fever accompanied by either hypoxia and/or hypotension, manageable in a standard hospital setting and generally of relatively short duration and easily manageable in a regular hospital clinic. Eight patients experience serious infections. We call that grade three to four infections or serious adverse event infections. This was to some extent dominated by COVID-19 because many of these patients were treated during the height of the COVID pandemic. Neutropenia was relatively rare. We do see neutropenia in the context of epcoritamab treatment, but usually quite transient and rarely very deep. That's probably the explanation why none of these neutropenias led to febrile neutropenia. Five patients had fatal treatment emergent adverse events and mainly of infectious character, two caused by COVID-19, one by CMV virus reactivation, one tumor hemorrhage, and one case of tumor lysis syndrome early during therapy. ICANS were reported in seven patients. ICANS is a complex of central nervous system phenomena that is seen in association with cytokine release syndrome and immune effector cell therapies. I would cast doubt on whether these were in fact real ICANS. We are talking about elderly patients who develop a high fever in a hospital environment. Confusion and related phenomena are actually expected in patients even if they are treated just with chemotherapy or without any immune therapy. This is conservatively reported and still quite encouraging. Next slide, please. Another take on the cytokine release syndrome, like I said, just over 70% of patients experience cytokine release syndrome at some point. The vast majority of those of low grade, fortunately. And you can see on the right that the pattern of first occurrence of CRS is just like we've seen it with monotherapy in a later line setting, which is that most of the cases of cytokine release syndrome occur after the first full dose of epcoritamab, which is two weeks into treatment. And quite predictably, the majority of cases of CRS occur within the first 24 hours of that first full dose. And in the vast majority of cases, quite easily manageable and resolving within typically two to three days. Next slide, please. So quick look at efficacy. For the full analysis set, which is 45 patients, all of the patients, including patients who were not response evaluable, the overall response rate was 69%. And if we look only at patients who made it to their first response evaluation, the overall response rate was 78%. And among those, the vast majority reached complete responses in the efficacy evaluable set. That's 70% of all patients, which is regarded as relatively good in such a difficult-to-treat population. Remember, these are patients who are not candidates for real effective chemotherapy. So they would be candidates otherwise for what we would consider more or less palliative chemotherapy. You can see in the subgroup analyses, which are, of course, hampered by the relatively low number of patients, there are no real clear signals as to which patients benefit less or more than others. But it's actually comforting to see if you look at the age that patients included over 80 years of age, which was the majority of patients actually had the same good response rates as the overall population and perhaps looking at the mere numbers a little bit higher even. Next slide, please. And here we look at the swimmer plot showing the individual patient's fate in order to give us a little bit of a taste of the durability of these responses. And you can see that many of the patients reaching complete responses, and that was again the vast majority of patients, they remain in remission with a complete response at the most recent data cut. Suggesting not only effective anti-tumor activity at the time of treatment and early thereafter, but in fact suggesting high cure rates in these patients, even though, of course, that should be said with caution because the follow-up is relatively short. Next slide, please. So here again, you have another take on the durability of the responses. 82% for the overall population of at least six months of response. And you will agree with me that the follow-up is really short, but it's still nice to see that patients stay in response well beyond the completion of their treatment. Next slide, please. And here we have the progression-free and overall survival. And you will probably notice that this looks not quite as good as in the previous demonstration of the efficacy of R-CHOP+ epcoritamab. And this is what we are used to seeing in the elderly patients. First of all, they more frequently die of other things than lymphoma. They are more frequently subject to fatal adverse events that are not lymphoma-related, but still seeing progression-free and overall survival and not reaching 50% within the first year of observation is actually quite encouraging. The median follow-up here is too short to really make firm conclusions. 8.1 months for the analysis of PFS and 9.5 months for the analysis of overall survival is, of course, only very preliminary data. Next slide, please, so this actually caught quite a lot of attention, and the audience generally seemed to be agreeing with the conclusion that epcoritamab, which in this case was given up to one year, so not until progression, what seems to have a role in this difficult-to-treat and hard-to-reach population of elderly and/or comorbid patients ineligible for anthracycline-based first-line chemotherapy. CR rates in the evaluable population of 70% and 89% of the complete responses ongoing at the most recent data cut, which admittedly is quite soon after completion of treatment with the very short follow-up. Also, something that I didn't stress, MRD negativity, as we have observed, often is reached in the younger population, is also seen in this elderly population, and it's another surrogate for the benefit of the treatment and a surrogate for later cure, at least in some patients. Safety, quite encouraging. The perhaps feared high rates and severities of cytokine release syndrome in an immune-naive and previously untreated group of patients was not confirmed, even though CRS was seen more frequently than in cohorts of patients with heavily pretreated disease. Again, the vast majority of cases of CRS were grade one or two. So this is really regarded as quite promising, and there was a lively debate after this presentation. So next slide, please. Perhaps the most talked about, at least of the oral abstracts that I attended involving epcoritamab, was this one. Another set of results coming out of the NHL2 study with the many different cohorts. And in this cohort, it was patients with a newly diagnosed follicular lymphoma treated with the combination of epcoritamab and bendamustine rituximab. Next slide, please. So this is a group of patients where we have had many standard treatments for many years. And the most commonly used standard nowadays is the combination of rituximab and bendamustine chemotherapy. And that leads to response in the vast majority of patients. This CR rate of 30% is from historical data before the introduction of PET-CT. So you should take that with a very big pinch of salt. But still, the point is that we induce responses even with standard chemotherapy in the vast majority of patients. The problem is that all these patients eventually will relapse and have a need for new treatment. And the whole idea behind first-line treatment of follicular lymphoma is to make that relapse-free period as long as possible. So that's the background for the combination of bendamustine rituximab with epcoritamab in this very treatment setting. Next, please. So patients could be included into the study if they had a newly diagnosed follicular lymphoma with a treatment need according to the GELF criteria and a good general status and organ function. So they were treated with the classical schema of rituximab-bendamustine, which is six four-weekly cycles. And for the first three of those cycles, epcoritamab was given weekly. For the next three, every two weeks, and then every two weeks for another three cycles of Epkinly, and then every four weeks from cycle 10, day one and onwards, and until up to two years after beginning of treatment, with overall response rate as the primary endpoint, and again, secondary endpoints such as complete response rate and durability of complete responses, progression-free and overall survival as important secondary endpoints. Next slide, please. Again, here safety is important because we are talking about newly diagnosed patients with a very good treatment already available. So it's important that in order to perhaps increase efficacy anti-tumor activity a little bit, we should not compromise safety. Fortunately, again, that was not apparently the case because what we saw of side effects or toxicity signals were really in keeping with the individual contribution of bendamustine on one side and epcoritamab on the other side. In this case, cytokine release syndrome was not the most commonly reported adverse event that was seen in the majority of patients, but exclusively of grade one to two. But due to the timing of this study, the most frequently occurring adverse event was really COVID-19, which, as you can see, was recorded in the vast majority of patients. Fortunately, not of a fatal character in the majority of these patients. One patient had a grade five COVID-19 event. Next slide, please. So cytokine release syndrome, we look at that again focused here. You can see, like I said, no cases of grade three or four CRS occurred. The majority of the cases of cytokine release syndrome, once again, occurring after the first full dose of that drug, which is two weeks into the first cycle of treatment. Again, occurring quite predictably within two days of the first full administration of glofitamab and usually quite transient resolution within a median of two days, although there were some cases of more prolonged cytokine release syndrome in a few patients. Next slide, please. Overall responses, 96%. All of those 96% of responding patients, which is all but one of 25 evaluable patients, had complete responses. Of course, you can't really compare that with historical data because back in history, PET-CT scans were not used. The comparator is a little bit tricky, but still, this is really encouraging. I wouldn't say that in the clinic we expect 96% of patients with newly diagnosed follicular lymphoma to reach a complete response. So the median follow-up for this patient group is two and a half years, 13 months. You can say that looks like a long time, no. In follicular lymphoma, indeed, two and a half years is a short time. Follicular lymphoma is a disease where benefit is measured more rather in decades than in years. So these are just really preliminary data, but I must say they're very encouraging. And as you can see, that the durability of the responses on the right looks very, very promising indeed. Next slide, please. This is another take on the durability of responses and the clinical benefit for the patients. All the green dot means that patients at their regular assessments are in complete response. Many of them make it to the end of the two years of treatment. That is the blue diamonds, the complete treatment. And you can see that the complete responses extend beyond the completion of this fixed duration treatment. Next slide, please. And that leads to a progression-free survival, which is at two and a half years estimated at 83%. And of course, the median very, very far from reached. And you can discuss whether, in fact, the median progression-free survival will be reached because I know that we generally look at follicular lymphoma as an incurable disease, but perhaps the introduction of the T-cell engagers will change that dogma. Next slide, please. Overall survival, a testament to the high efficacy of the treatment, but also the natural history of the disease itself, 96% at two and a half years. Next slide, please. Generally accepted conclusions, they were not really debated during the presentation, is that the combination of bendamustine rituximab+ epcoritamab leads to very, very deep and durable responses, even though the follow-up is still relatively short in the context of newly diagnosed follicular lymphoma. Safety profile manageable, consistent with previous reports from the study and also consistent with the individual components of the combination, and you can discuss whether the comparison with a historical CR rate of 30% is meaningful, but I think the data just can stand for themselves. CR rate of 96% is really, really high even in this setting. Next slide, please. Another study in follicular lymphoma has been presented several times before is another cohort from the EPCORE NHL-2 multi-arm study, and in this case, it's the combination of epcoritamab and R-squared. That's the same as rituximab lenalidomide, which in this part of the study was given for patients with relapse or refractory follicular lymphoma. This has been presented several times before, but still an important and interesting update of the efficacy and safety from this cohort. Next slide, please. So R-squared, as I call it, rituximab lenalidomide has been used in many years, and it is a standard of care for patients with follicular lymphoma, sometimes used in first line, sometimes in second or in later lines of treatment. So that is based on the data from the AUGMENT study in relapse refractory follicular lymphoma, where the overall response rate was 78% and CR much lower, but again, based on CT-based determination of responses. So this is the standard that this study would look to improve by combining R-squared with epcoritamab. And in the case of this study, next slide, please. The treatment is given again in a fixed duration, so with lenalidomide up to one year of treatment and with epcoritamab for up to two years of treatment and rituximab only in the beginning of the lenalidomide induction. So patients could be included if they had follicular lymphoma with a treatment need and relapse disease and at least one prior line of treatment. Next slide, please. So again, looking at the safety profile first, very consistent with what we have seen so far. And this is important because both lenalidomide and epcoritamab lead to some immune suppression. So the long-term safety is really important to follow in these cohorts. Again, we see cytopenias. That is mainly the contribution of lenalidomide. And we see other constitutional symptoms that are very commonly seen with lenalidomide: diarrhea, fatigue, constipation. But the contribution of epcoritamab is mainly seen with cytokine release syndrome in approximately half of the patients and in the vast majority of grade one, which is very encouraging. Next slide, please. So responses have already been reported previously. A staggering overall response rate in this relapse refractory setting of 96%, including 87% with complete responses. And I never cease to enjoy looking at these response rates because it's really quite high, even in comparison with effective existing therapies such as R-squared. On the right, you can see that these very high response rates are consistent across various subgroups, including the high-risk populations of primary refractory patients and those with progression of disease within 24 months of completion of first-line treatment, those that we call POD24. Next slide, please. So you can look at the durability of these responses, really quite high. So for the overall group of patients, 96 patients, we see the durability of complete response rate with 86% having durable complete responses at 21 months. Why 21 months? When that was the median follow-up. And there was some debate whether it's fair to show a durability curve like this with so many patients still at risk at the far end of the survival curves. And perhaps that is a tip for future demonstration of these impressive data that it's actually fair to even show longer follow-up, even of the patients that are way beyond the median follow-up. So next slide, please. That's the progression-free survival. And you can see that because of the durability driven by the complete responders, which is the vast majority of patients, we saw for the overall group of patients, progression-free survival at the point of the median follow-up of 24 months of 80%. Really, really impressive and durable benefit of this combination treatment. Next slide, please. This is really the important curve when you assess the benefit of a treatment for follicular lymphoma. It's the time to the next treatment because you can have a slow relapse of follicular lymphoma and perhaps not even need your treatment yet. The really important determinant for the benefit of a treatment is the time to the next treatment. You can see that at 24 months, and this is looking at all patients, responders as well as non-responders, 85% of patients had not made it to their next initiation of the next treatment, which is really encouraging for this combination treatment. Next slide, please. That, of course, leads to an excellent overall survival for the overall population of 90%. Not a surprise to any of you that such high response rates, of course, leads to a very high overall survival, albeit overall survival is a tricky endpoint in follicular lymphoma, which, like I said, is a disease where benefit is measured over decades rather than years. Next slide, please. So we see confirmed safety findings and efficacy findings from this study. Overall survival maintained at 96%. CR rate maintained at 87%. MRD negativity rate showed, so that's the clearance of MRD as measured by the AVENIO ctDNA assay in 88% of patients. So that's either during or after completion of therapy. And this correlates very well with progression-free survival, as you would expect. Next slide, please. No, former slide, sorry. Because it's important to note that these are the next slide, please. Thanks. So just direct your attention to the last bullet point on this slide, which is that, of course, such impressive results need to be followed. And I direct your attention to the ongoing and I believe recently completed phase III trial of this very combination in comparison with the standard R-squared in patients with relapse refractory follicular lymphoma. Highly interesting study, and we're eagerly awaiting the readout from that randomized study. Next slide, please. Which is the last one for me. So already now, I have to thank you for your patience. This is the important study of epcoritamab as a single-agent therapy in patients with relapse refractory CLL. This was presented by Alexey Danilov from California. He was on his own home turf when he presented this excellent study report. Next slide, please. So now we're shifting to a completely different disease, patients with refractory CLL. They are not so easy to treat. They have been exposed to chemotherapy usually. And also in order to be included in this study, because these are standard treatments, they should be exposed to both a Bruton's tyrosine kinase inhibitor, BTK inhibitor, and a BCL-2 inhibitor, usually venetoclax. These are great treatments. They keep the patients alive for many years in many cases. The problem is when they relapse and the majority eventually do, they are very difficult to treat. And at that point, they have a poor prognosis and usually a relatively limited time span. So we need desperately new treatments for these patients. And we have already seen encouraging results from this study of epcoritamab as a single agent in this patient population. So what we saw at ASH was really both of the safety and particularly the efficacy from this treatment. Next, please. This is the design of the study. And it's important to note that the first patients, what we call the expansion part of this study, were treated with the usual epcoritamab step-up dosing. There was an optimization core at a slightly lower number of patients, 17, where an extra step-up dose was introduced. Between the intermediate and full dose, there was another dose of three milligrams of epcoritamab in order to harness cytokine release syndrome, which, as I will show you in a second, was done quite successfully. Patients could be included into the study if they had relapsed refractory CLL, but they also needed at least two lines of systemic therapy, which in the vast majority of cases included both a BTK inhibitor and venetoclax or another BCL-2 inhibitor. Next slide, please. So here you can see the safety findings, more frequent toxicities than in the lymphoma populations, which is not a surprise. It has to do with the nature of the disease, the prior treatments, and also the way that epcoritamab reacts in a patient with a systemic blood-borne disease rather than a solid lymphoma. You can see that the vast majority of patients had cytokine release syndrome, 96%, but fortunately, the vast majority of those with low grades of CRS and reasonably manageable CRS as well. Very commonly did we see cytopenias, which goes with the territory of CLL treatment, and then also the other constitutional symptoms, which are very commonly seen in studies of this disease. Next slide, please. So this is important. You can see that cytokine release syndrome was particularly commonly observed in patients treated at the normal schedule of epcoritamab. This is what I just showed you before. But shifting to the optimized delivery of epcoritamab, where another step-up dose was introduced after two weeks, this really dramatically changed. So first of all, the overall frequency of CRS went from 96% down to 82%. But perhaps more importantly, all the relatively commonly occurring cases of CRS of grade three completely disappeared. So with the optimized dosing schedule, all cases of CRS, albeit still quite frequent, were of grade one and two and thus quite manageable. Next slide, please. Responses were really encouraging in this study. 61% of patients responded, and 39% of those had complete responses, which is actually a relatively rarely occurring outcome phenomenon in relapse refractory CLL. So very encouraging efficacy results. That's the depth of the responses occurring usually quite early during treatment. The challenge, of course, is to maintain these responses. Next slide. As you can see, there are in this swimmer plot, which of course is a relatively short follow-up, quite a lot of patients who either discontinue treatment because of adverse events, but particularly because of loss of the response. Next slide, please. That leads you to progression-free survival curves, which are perhaps not what I made you used to see when we talked about the lymphomas. These patients do both die, and they also have loss of response of their epcoritamab treatment, but still a highly, highly active drug in this very tricky-to-treat space. Next slide, please. That's the conclusions. Just to reiterate that this single-agent subcutaneous epcoritamab led to very deep responses, more than 60% and 39% complete response rate, and the undetectable MRD ratio in 75% of evaluable patients with a response. So that's really a testament of at least long-term durability in some of these patients. And very importantly, with the optimized delivery schedule of epcoritamab, cytokine release syndrome, which in the beginning of this study was a problem, has really been harnessed, lower overall frequencies, and most importantly, lower grades of CRS after a slightly extended step-up dosing. So with this, I ask for the next slide. And thank you very much for your attention. I hope I stayed within my allotted time, but I'm not entirely sure about that. Absolutely. You definitely stayed within your time, and this was fascinating. Thank you very much, Dr. Hutchings. Let's move to the next slides. Next slide. And thank you also to all the other inspirational speakers for a really excellent presentation. So let's now move to some of the key pipeline events we are anticipating for next year. Next slide, please. Genmab has an established track record of being able to select and develop innovative and differentiated therapies. We're able to do this because we are deeply rooted in science, and we follow the data derived from our clinical programs. And here you can see some of the key pipeline events we are anticipating as part of our continual development. Let's start with HexaBody-CD38. Here, I will reiterate what I said already during our third quarter results call. We are well on track to submit the data package to J&J by the end of this month. The opt-in period of 60 days is expected to start in the beginning of January, which means that we anticipate a decision from J&J no later than the first quarter of 2025. We will inform the market via press release when J&J has made their decision, and this release will include relevant clinical data. To support the integrity of J&J's review process, we will not disclose this information before the official release. Looking beyond this event, next year, we are anticipating additional regulatory decisions for both Epkinly and Tivdak, as well as additional data for both acasunlimab and Rina-S. For Rina-S specifically, the expansion data and endometrial cancer will also inform next steps for that indication. And then finally, for Gen1042, we look forward to providing you with an update on our next steps for the program in frontline head and neck cancer. In 2024, Genmab made significant strides by investing in our pipeline and technologies, with a strong focus on prioritizing late-stage development and expansion for Epkinly, Rina-S, and acasunlimab. As we prioritize investments in these key programs, 2025 will serve as a key stepping stone on our path towards our 2030 vision of fundamentally transforming the lives of people with cancer and other serious diseases. Our strategic focus ensures that our pipeline remains robust, impactful, and aligned with our long-term goals. Let's move to the next slide, please. So now it's time for our Q&A session. And I'm pleased to note that we also have members of our executive committee to answer your questions, our Chief Development Officer, Judith Klimovsky, and our Chief Medical Officer, Tahi Ahmadi, who you already heard speak, in addition to Martin Hutchings, who will also contribute to the Q&A. So we will begin by taking questions from those of you participating in the teleconference. To ask a question over the webcast, simply click the Ask a Question button, type in your question, and then click Submit. Let's move into the Q&A. For the Q&A section of today's event, we'll be utilizing the raise hand feature. If you would like to ask a question, please join the teleconference by clicking the button in the top right corner of your browser. Once you've joined the live Q&A line, click on the raise hand button at the bottom of your screen. Once prompted, please unmute yourself and begin with your question. We will now pause a moment to assemble a queue. Thank you. We'll take our first question from Jonathan Chang. Your line is open. Please feel free to unmute yourself and ask your question. Great. Thanks for taking my questions. First, maybe just to clarify, is Dr. Lee available for the Q&A session? No. Dr. Lee is not here for the Q&A. Got it. So then maybe for the Genmab team, how are you thinking about potential opportunities for Epkinly beyond DLBCL and follicular lymphoma? What do you need to see before advancing Epkinly for CLL in later-stage development? And also, what are the considerations for potential autoimmune disease applications? Thank you. Thanks, Jonathan. Excellent questions. And I will hand them over to Tahi. Tahi can definitely give us our thinking on, for sure, expanding epcoritamab into other indications. Tahi. Yeah, thank you for the question. So yeah, in follicular lymphoma, just to remind everybody, there's a phase III in combination with R2, Martin alluded to. I mentioned this also in my presentation in second line on relapse refractory follicular lymphoma. That's already fully accrued. So we're waiting for that data to read out. There is a frontline study that is very well actively enrolling already, comparing an R chemo regimen versus a combination with R square as well, so from a registration point of view, these are our big committed studies. There is a broad data generation package beyond that, also interrogating monotherapy in frontline. I think epcoritamab, generally speaking, is a very active drug. This mechanism of CD3 CD20 is a very active mechanism in follicular lymphoma. In CLL, yeah, Martin, I think, also shared a little bit the enthusiasm. The data that was generated in this patient population has to be understood, and this patient population, I think, is significant. It has the potential for really transforming CLL because for the first time, you're getting actually deep CRs, not only CRs, but also deep MRD negativity in patients who rarely even achieve a CR. And so we're actively working with our partner, and there will be indeed significant next steps on the development of epcoritamab in CLL coming up in 2025, more to come on that end. On autoimmune disease, without a doubt, there is an increased awareness of the potential of deep B-cell depletion in certain autoimmune diseases. And we are fully aware of this. And these are also things that we are interrogating with epcoritamab or outside of epcoritamab. Thank you very much, Tahi. Thanks, Jonathan, for the questions. Let's move to the next question, operator. Our next question comes from Yaron Werber. Your line is now open. Please ask your question. Great. Thanks so much for the questions. I have a couple of questions. First of all, when the CLL data is really intriguing, we did a KOL event at ASH, and they were definitely highlighting that as one of the highlights in CLL. When you're looking at the OPT1, you're reducing the CRS nicely, so you don't have grade three anymore. The CR rate was lower, though. It was 10%. Is that just a function of an early follow-up in that specific cohort or anything we should be thinking about? And then maybe just secondly, when we looked at the data, it was the data for the first-line follicular. The data is really compelling, but there was a lot of dropouts in that cohort. I think nine patients dropped because of tox, seven because of COVID. Did that sort of happen later on, or how should we think about tolerability? Thank you. Thank you for the questions. I'll ask Tahi to start, and then maybe Martin can also step in because I think you can also add further perspective, Tahi. Well, I so totally agree with your enthusiasm of the CLL. I think there's a number of commentary out of the community that highlights an incredible opportunity that now exists with the ability to redirect T cells. I think it was important as we think about the development for epcoritamab and CLL to figure out the CRS because in the initial standard approach, at least as monotherapy, the CRS rate was uncomfortably high, to be very frank. And so it is now, and Martin showed the data, converted into basically 70% of the patients having grade one, which is fever, completely different safety profile. But the safety with completely different safety risk. The CR rate is truly a follow-up issue. So there's some conversion that happens a little bit later. More importantly, I would also say that now we're actually starting to generate combination data, and the CRS issue is actually almost non-existing once you go into combination. So you have another mechanism that helps address the CLL burden, particularly the circulating component of that burden. The combination CRS rates are, and we're going to have the ability to share that data next year, I'm sure, already in a very, very low rate. So that is why we are now actually able to make decisions on moving forward on CLL. I believe your question on follicular lymphoma in frontline was related to the bendamustine rituximab cohort. I don't want to sound defensive, but there was a period of time around Omicron where, generally speaking, the conduct of clinical trials was difficult. Martin can also speak maybe from his perspective on that. A lot of this was really in the midst. It just so happened that this particular cohort was opened right in the midst of this massive wave. It's not something that we've seen, for example, with the R-squared epcoritamab cohort in frontline. So it was somewhat a unique situation for that particular data set. Thanks, Tahi. Martin, maybe you can jump in and then give further perspective if you want to. Yes, I want the CLL. Yeah, yeah, it's a good observation with the CR rates in the optimization cohort. It's a low number of patients, and I didn't even mention the CR rate. It's not because I was trying to hide anything. It's a really, really short follow-up for that particular cohort. So I think it's probably not really fair to assess or compare indirectly efficacies. I think for me, the important thing here is really to look at the dynamics of cytokine release syndrome, which really was a successful optimization. So at least we've not seen, we can try and extrapolate from other experiences with the bispecifics. And delaying by one week the arrival at the first full dose has not, in any other examples, led to less efficacy in patients. I would be very surprised if it had any negative impact on the efficacy in this particular setting. Thanks, Martin. Let's move to the next. And about the bendamustine combination, I mean, the fact that it was possible to carry these studies through during the height of the COVID pandemic, not only the bendamustine, which is perhaps particularly tricky, but generally, all these studies is just only possible due to a high level of confidence from patients and their relatives and a great collaboration between sponsors and investigators because this has really been tricky. And I can only dream about how results would have been if we had done this five years earlier when we wouldn't have had all of these COVID-related events. Thanks, Martin. That's really helpful. Let's move to the next question. The next question comes from Paul Jeng. Your line is now open. Please feel free to unmute yourself. Hey, this is Paul on for Michael Schmidt in Guggenheim. Thanks for taking our question and thanks for the helpful call. For Dr. Hutchings, it would be great to get your view on the recent data for tafasitamab+ R2 in second line follicular, which showed, I think, around 22-month TFS. How does that sort of data impact the bar for Epco and R2? And how do you and your peers plan to sequence assuming both regimens might be approved in this setting? Thank you. Martin? Yeah, so that's a good question. The question refers to the data presented in the late-breaking abstract session of yesterday at ASH, a combination of R squared and tafasitamab. So yes, it looks like an active treatment, and it's a novel concept in early line treatment of follicular lymphoma to combine two different B-cell targets. I think it looks quite attractive, and the safety profile that we got presented, as you would perhaps expect, looks quite encouraging. So it's definitely going to be one standard that we need to talk about. The durability is still something that we need to see, of course. That's always the case with the first presentation of data. And now I'm just giving you my personal subjective impression. I alluded earlier to a transformation, at least a mental one, of follicular lymphoma from something which we have regarded as incurable and chronic. I do not believe the tafasitamab combination is transformative in that respect. I have confidence that the CAR-Ts and the bispecifics will. This is subjective, so it's only my personal view, but that is my strong conviction. Thanks, Martin. Operator, let's move to the next question. The next question comes from Eric Yang. Please unmute your line and ask your question. Hi, this is Eric on for Matt Phipps from William Blair. Just two questions. First, Eric asks where you saw activity in folate receptor alpha high and low expressors at that 75% cutoff. I was just wondering, was there activity in FR alpha patients such as those FR alpha negative patients, such as those with weak or no folate receptor expression that supported the no FR alpha requirements in phase III? And then on the second question, just on the long-term follow-up of the EPCORE NHL-1 trial, in patients who did relapse, have you looked more into the cause of relapse? Could it potentially be a loss of CD20 expression or some sort of T cell exhaustion mechanism? Thanks. Thanks, Eric, for the questions. So the first question, can we have that handled by Judith Klimovsky? And then the second question, Tahi and Martin can definitely give perspective on that one. Judith? Yeah, so for Rina-S, thank you for the question. For Rina-S, as Dr. Lee showed in the presentation, we saw responses in the CAT that we did based on the approved companion diagnostic, which is above 75% and below 75%, and responses were consistent. We did an exploratory analysis, which was mentioned in the presentation as well, in patients even below 25%, and we saw activity across the board in the very low. This is why in the phase III, we are enrolling patients regardless of folate receptor expression, and it's not a new phenomenon for a disease when they have a potent payload and a good linker that ensures a lot of intratumoral payload. As I said, we are enrolling regardless of folate receptor, and we saw activity in very, very low folate receptor expression patients. Of course, data is being gathered as we speak. Great, Judith. Thanks a lot. I'll move to Tahi for the relapses with the epcoritamab studies. Oh, yeah, thank you, Yaron. And maybe if I just am allowed to add one more comment on what Judith said. I think I mentioned this, I think, in our Q3 call. To some degree, the concept of negativity is a function of the sensitivity of the assay, how capable the assay actually is accurately to determine whether there is folate receptor. And these IHC assays are not completely 100% accurate. So there is a space there where patients have very low folate receptor alpha expression. And that's the explanation why we also see the activity, as Judith was saying. And that's why we are designing the study as we're designing it. On the question of why patients are relapsing in CR to CD3, CD20 therapies, of course, like everybody else, we've been looking into this. It's a little bit of a hodgepodge in our hands, in our data. You do have cases where CD20 loss has been observed, although I would say the loss of CD20 is not a phenomenon similar to the loss of CD19. So it might just very well be easier for bispecifics to drop CD19 or CD22, and CD20 is a little bit more relevant. There are increased mutations in the p53 pathway that also render the tumor cells unresponsive to T-cell-mediated killing. They certainly play a role. Some T-cell exhaustion at times. It's really all over the place. It's not necessarily one phenomenon. It's also a relatively rare phenomenon if you look at the numbers. So once patients actually are exceeding the CRs for a period of time, you don't have that many patients. Martin showed that in the curve. And sometimes, actually, what ends up in the event as a curve is not even progression. It's actually the death of the patient to some other cause. Life in the end is finite. So there is actually not that much data right now for a conclusive statement of how to mitigate that, which is the main reason for us to look into this to understand how to then potentially mitigate the occurrence of late relapse in these patients. But it does occur. Thanks. Thanks, Tahi. And maybe Martin, some further perspective on what can happen with relapse patients under pressure of T cell engagers? Yeah, so I completely agree with Tahi that here we're talking about patients who lose their response relatively late, and they are rare and far between. Furthermore, when the patients come to clinic and they have gotten used to a benefit, and then they suddenly lose it, they are usually not happy about that, which is totally understandable. Top of their mind is not to deliver a new fresh biopsy unless they get something out of themselves. We do, at our site, biopsy all our patients at every relapse, if at all possible. I must say that in probably a small majority of the patients who lose a deep response to Epkinly, we see either complete CD20 negativity or a very reduced expression of CD20 in these patients. But again, it's a small number of patients. I'm not even suggesting that loss of CD20 is a mechanism of resistance. Maybe it's just something that goes along and is driven by an underlying mechanism. We actually presented some data from our group on NOTCH1 mutations to be a potential driver of resistance. And that's just one little contribution to a field which is really ongoing. I think in a few years, we'll learn a lot more about mechanisms driving response and resistance. But I think overall, it should be said that targeting one antigen is, of course, weaker than going broader. Thanks, Martin, for that perspective. And that should give you some food for thought, Eric and Matt. Let's move to the next question. Our next question comes from Yifeng Liu. Please unmute your line and ask a question. Thanks for taking my questions. I've got two for acasunlimab. In 2025, there'll be a data update for phase II. Could you maybe share some colors on what to expect in that update? Secondly, on this upcoming phase III study, and just wonder if there's any plans to test progression-free survival in the interim? Thanks. Thanks for the questions. Judith, why don't you start with the questions, and then Tahi can add to that if needed. Judith? Yeah, thank you. The update on 2025 is the update on the time-to-event endpoints, which is the most relevant in this setting and disease. Basically, the data that was presented at ASCO in this year will be updated with more follow-up. With regard to the phase III, it's from the regulatory point of view, the endpoint for second-line in small-cell lung cancer is overall survival. There is no benefit on another endpoint. We are following the registrational intent of the study with overall survival as the primary endpoint. Thanks, Judith. I don't know whether you want to add anything, Tahi. I think this is exactly how it is. Exactly. All right, let's move to the next question then. There are no further questions at this time. This concludes the Q&A section of the call. I would now like to turn the call back to Jan van de Winkel for closing remarks. So thank you all for the questions and for the lively interactions. Let's move to the next slide.