Hello, colleagues. My name is Sunao Manabe, CEO of Daiichi Sankyo. Thank you for joining our briefing session focused on the key highlights of the data presented at ASCO this year. As slide four show today's agenda, first, I will update our five-year business plan for sustainable growth. Ken Takeshita, our Global R&D head, will present a summary of R&D progress and our updated R&D strategy. Mark Rutstein, our Head of Global Oncology Clinical Development, will show you the highlights of our presentation at ASCO this year. Let's move on to slide five. This slide illustrates the position of our five-year business plan for ensuring sustainable growth. Our five-year business plan, that covers fiscal year 2021 through fiscal year 2025, is a plan designed to achieve our 2025 goal of being a global pharma innovator with a competitive advantage in oncology, and to shift towards a growth stage geared to realize our 2030 vision. Next, please. Slide six shows the financial targets for fiscal year 2025 and the strategic pillars for our five-year business plan. The financial targets for fiscal year 2025 are consolidated revenue of JPY 1.6 trillion, of which the revenue from oncology will be more than JPY 600 billion. Core operating profit ratio before R&D expense of 40%, and ROE of 16% or more. We have adopted dividend on equity, DOE, as a KPI for shareholder returns, and the target is DOE of 8% or more in fiscal year 2025. Out of four strategic pillars for our five-year business plan, there are two pillars which are highly related to R&D. The first strategic pillar is to maximize 3 ADCs. We will continuously maximize ENHERTU and Dato-DXd, and through our strategic alliance with AstraZeneca, HER3-DXd will be maximized by ourselves without a partner. We will efficiently keep expanding our development capabilities and supply capacity, depending on changes around the product potential. The next strategic pillar is to identify and build pillars for further growth. From the projects running in early clinical stage and from the multiple modalities entering clinical phase during the five-year business plan, we will identify the post pre-ADC growth drivers and select promising post DXd ADC modalities. Today, I am happy that Ken Takeshita will be presenting a new R&D strategy, which will ensure our successful and sustainable growth. Next slide, please. Slide seven shows our current expectation on oncology revenue. The oncology revenue in fiscal year 2025 is expected to reach JPY 900 billion or more, mainly driven by the revenue growth of ENHERTU and Dato-DXd, exceeding the initial plan. This graph shows an image of oncology revenue growth during the five-year business plan. As for ENHERTU, we expect strong growth in breast cancer market based on DESTINY-Breast03 and DESTINY-Breast04 study results that exceeded our original assumptions. In addition, the acceleration of the studies for indication expansion such as DESTINY-Breast09, will contribute to increased revenue from product sales and development milestone payments. As for Dato-DXd, we expect higher sales compared to the initial plan, and the target patient population at launch is anticipated to be broader than the original assumption. Any SCLC patients with actionable genomic alteration, AGA, has been added to TROPION-Lung01 study, which was originally designed for patient without AGA. Therefore, we expect that we can deliver Dato-DXd to more patient compared to the initial plan. Furthermore, the acceleration of the studies for indication expansion, such as TROPION-Lung08, will also contribute to increase revenue from product sales and development milestone payments in fiscal year 2025. Next, please. Slide eight shows our well-balanced investment for growth and shareholder returns. Considering the higher revenue growth, mainly driven by ENHERTU, the source of cash allocation during the five-year business plan is expected to increase by approximately JPY 300 billion compared to the initial plan. To realize sustainable growth, we will increase R&D expenses and capital expenditure, which is an investment for further growth. We will, of course, continue to consider the best balance between investment for growth and shareholder returns. As for R&D expenses, during the five-year business plan period, we will increase by JPY 300 billion to approximately JPY 1.8 trillion, prioritizing the investment for the DXd ADC, including the projects, which Ken Takeshita will explain, later. As for capital expenditure, we will increase by JPY 100 billion to approximately JPY 600 billion, mainly to enhance ADC supply capacities. Next, please. My last slide shows our current expectations around achieving fiscal year 2025 KPIs. We expect that our consolidated revenue will reach JPY 2 trillion, exceeding our target by JPY 400 billion, mainly driven by the increase in oncology revenue. As for core operating profit ratio before R&D expense, we will continue to aim for our target of 40%, as we expect an increase in SG&A, along with the revenue increase. Since we launched our five-year business plan, we have continuously obtained positive data from the DXd ADC clinical trials, including the data which Mark Rutstein will explain later. To realize sustainable growth, we will actively invest in R&D to maximize our product value. Last but not least, we will continue to commit to shareholder return that we promised by increasing dividends in line with profit growth and by flexibly acquiring own shares. We continue to aim for a DOE of 8% or more in fiscal year 2025. This is all from me for today. Thank you. I will hand over to Ken Takeshita. Manabe-san, thank you very much. Next slide, please. I'm Ken Takeshita from R&D, and I'm going to go over with you in a few slides, a general overview of what we are doing in R&D and our overview of our strategy, specifically. I think many of you are very, very familiar with the content of this slide. This illustrates really our the clinical trials that are part of the five-year plan that Manabe-san just talked about. Many of them are the breast cancer trials from the DESTINY programs and ENHERTU programs. We also have the lung and breast cancer programs, MODETO and HER3-DXd lung cancer programs. We are right in the midst of all these clinical trial programs during this five-year plan. I have to say that I think we're doing quite well in accomplishing all the goals that are listed here in the five-year timeframe. Next slide. I do want to make sure to introduce you to two additional antibody drug conjugates that we have in our pipeline. The first one is called DS7300. This is also based on the original DXd ADC technology, but it targets a new antigen called B7-H3. We are fairly early in stage in understanding the clinical spectrum of this ADC. We have already seen very good signal in small cell lung cancer, and we are well on our way to having a registration program leading to approval in this particular indication. Next slide. Another new ADC is called DS6000. It targets an antigen called CDH6, cadherin six. Here again, even though we are fairly early in the program, we are seeing very good activity in ovarian cancer. We anticipate, of course, a new registration program for this compound in ovarian cancer. Both of these, 7,300 and 6,000, still have a long way to go before we fully understand the potential of these two ADCs, beyond the two indications that I just mentioned. We are very, very hopeful that we'll see a lot of interesting clinical signals as these programs move forward. Next slide. Here again, I want to make really a very important announcement here, which is that on the left-hand side, you'll see what we used to call our program 3 ADC and Alpha. That's what we used to call our program. Because of the addition of these two new ADCs, we are calling our entire development program 5 DXds and Next Wave. The 5 DXd ADCs are listed here, the original 3+ the two new ones. Next Wave refers to additional assets we have in our pipeline that are not DXd ADCs, that will really contribute to the longer-term goals of this company. Next slide. Here's really an illustration of how we think about our R&D strategy and really how our pipeline fits into our strategy. It's simplest to describe this as an expand and extend strategy. Expand means really a focus on the DXd ADCs and really to maximize the value of these 5 ADC assets. In many indications, not just breast, not just breast cancer and lung cancer, but of course, many, many other indications, for which these ADCs are active. For example, the pan-tumor data that you saw earlier today, at ASCO, with their ENHERTU program. Of course, this expand strategy really refers not just to the ADs, these ENHERTU, but every single DXd ADC that we have. I also want to make sure to mention that, as part of our extend strategy, we have many other drugs coming up through our research pipeline into our clinical pipeline. These include next generation ADCs, second, third, and fourth generation ADCs, as well as very interesting drugs that are not ADCs. What we want to do, of course, is to develop each of these individual assets as they're on their own, as an independent asset. Interestingly, some of these assets, some of these new drugs with a very different mechanism of action compared to a DXd ADC, show very strong synergy in animal models to our existing ADCs. That really generates a whole new set of development strategies in which we can combine these newer, research-stage assets with existing ADCs. This is very important for us in order to maintain our presence in important cancers such as breast cancer and lung cancer. Next slide. Here again, a summary of what we're doing. We had the 3 DXd ADCs. now we have added two more to our group of ADCs, we have 5 DXd ADCs. more, most importantly, for the long-term future, we have our Next Wave strategy to extend our growth to address remaining unmet medical needs in oncology. now I'm going to ask Mark to come up and review our highlights. Ken, thank you so much, and it's my pleasure to be here. My name is Mark Rutstein, and I lead Oncology Clinical Development. What we're going to do now is walk you through the key data from ASCO and the recent ESMO Breast Meeting. It wouldn't be surprising, based on what Ken presented, that we have a very active pipeline, and we're proud to have presented a number of posters, presentations, at both the ESMO Breast 2023 Congress and the ASCO 2023 Congress, and you can see multiple oral presentations as well. If we can move to the next slide. What we'll first do is we'll give some updates of data in HER2-positive metastatic breast cancer and HER2-low breast cancer, areas where ENHERTU has transformed the standard of care. Now we'll show some data in patient subgroups, clinical subgroups, molecular subgroups, some quality of life data, as well as some updated safety in our HER2-low population from study DESTINY-Breast04. If we move to the next slide, please. Here we look at age subgroups. This is very important to think about elderly patients who represent a relatively underserved patient population, who may have suboptimal outcomes in oncology clinical trials. We've done a pooled analysis in DESTINY-Breast01, 02, and 03. These are the pivotal studies for HER2 positive metastatic breast cancer, looking at age less than 65 and greater than 65. You can see on the bottom of left, across these three studies and across those two age cuts, there's a consistent progression-free survival. The same is true on the right side with respect to overall survival. Similar outcomes, regardless of those age categorizations. If we would move, please, to the next slide. Continuing, this age subgroup analysis in our HER2-positive metastatic breast cancer trials, we turn to overall response rate on the left, and we can see across the three trials, similar response rates according to those different age cutoffs of less than 65 and greater than equal to 75. Of course, we want to characterize both benefit and risk, and on the right side of the slide is a representation of safety according to these age subgroups. What you can see is that the safety is very similar. In some AE categories, adverse event categories, there are some modestly higher rates in the greater than equal to 65 population. However, overall, we can see consistent positive benefit risk profile regardless of these age subgroups. If we could now move to the next slide, please. This is an important slide which looks at patient quality of life from our DESTINY-Breast02 pivotal trial in HER2-positive metastatic breast cancer. Of course, when we conduct the trials, we look at safety and efficacy, but it is certainly important that we look at the patient experience and patient reported outcomes measures. What's shown on the slide is a time to definitive deterioration analysis in patient reported outcomes measures. You can see various scales, including physical functioning, emotional functioning, pain and symptoms, etc. What you see for ENHERTU compared to chemotherapy arm, the TPC arm, you can see consistent improvement in time to definitive deterioration in these outcomes favoring the T-DXd or ENHERTU arm in each case. Very important and confirmatory of a favorable benefit-risk profile to understand that patient quality of life was maintained longer within HER2 and was favorable in this time to definitive deterioration analysis, which is consistent across both the DESTINY-Breast02 and the DESTINY-Breast03 trials. If we could move now to the next slide. Now we shift to a hormone receptor subgroup analysis. This is in our DESTINY-Breast04 HER2-low metastatic breast cancer trial. We looked here at estrogen receptor subgroups. In a subanalysis of these subgroups, we can see that compared to a TPC arm in chemotherapy, patients with HER2-low ER-negative, that's IHC 0, for the estrogen receptor and HER2-low, ER-low, that is IHC 1 to 10% for the estrogen receptor. Across these subgroups, patients benefited in terms of the overall survival analysis that you can see in the Kaplan-Meier below. This is important that these patients who are ER low, represent a poor prognostic subgroup, and therefore, it was important to demonstrate and look within this population and to confirm the benefit here. Overall, we can see that in this subgroup, consistent efficacy with the rest of the patients studied in this HER2-low study. We move to the next slide. Now we look at the safety side, and so to complement the efficacy, we look at the safety profile in this subgroup of estrogen receptor low expressing or zero expressing. We can see, compared to from an ENHERTU compared to the chemotherapy on the TPC, a consistent safety profile with the entire patient population treated with ENHERTU in the DESTINY-Breast04 trial, therefore confirming a positive benefit risk profile in this hormone-based subgroup. Now, if we would move to the next slide. Here we shift to molecular subtypes. Instead of clinical subtypes, we look at some biomarkers, and we look again here within the HER2-Low population of the pivotal trial, DESTINY-Breast04. What we see is that regardless of intrinsic subtype on the bottom, ESR1 mutation, PIK3CA mutation, or CDK4/6 inhibitor resistance markers, that we see consistently an improved overall response rate over the TPC arm across the board. If we could now move to the next slide. Now we look further beyond overall response rate in these subgroups that I've mentioned, these molecular subgroups, now toward the time to event endpoint. Here we can see, regardless again, of intrinsic subtype, PIK3CA mutation status or ESR1 mutation status, we can see longer progression-free survival in the ENHERTU arm compared to the TPC arm, thereby showing a consistent benefit across the subgroups. If we would move to the last slide in this molecular subgroup analysis. Here, we look at patients who have been treated with prior CDK4/6 treatment on the left, on the bottom, and patients that have not been treated with a prior CDK4/6 inhibitor treatment. They're broken out by whether or not they have these CDK4/6 resistance markers.... Across and within, across both of these subgroups and within, the considerations of whether or not patients have these CDK4/6 resistance markers or not, the benefit of ENHERTU over the TPC arm is maintained. If we move to the next slide. The last slide in this section now, again, providing an overview of patient subgroups, quality of life, and molecular subgroups in our in our hormone receptor set, in our HER2-positive metastatic settings, pivotal trials, as well as HER2-low, is an update of a detailed safety analysis of our DESTINY-Breast04 HER2-low metastatic breast cancer trial. Here, what we've done is engage in exposure-adjusted incidence analysis of adverse events. This is important because the duration of therapy on ENHERTU is longer than it is on the TPC arm or chemotherapy. Exposure adjustment helps to provide a clearer analysis of the safety. Here what we can see in these exposure-adjusted analyses are the rates of anemia, neutropenia, alopecia or hair loss, and fatigue are lower in the ENHERTU arm. Whereas nausea, vomiting, thrombocytopenia, and interstitial lung disease were higher compared to the chemotherapy arm. Very importantly, on the right side of the slide, we have a look at the ILD, interstitial lung disease, and we can see the majority of cases were low grade. This further look into the safety confirms the overall positive benefit-risk profile of ENHERTU and its approved indication based on the DESTINY-Breast04 data in HER2-low advanced metastatic breast cancer. If we move to the next slide. This is the summary of our first section, and what we conclude is the data that we present continues to support the benefit of ENHERTU in patients with both HER2 positive and HER2-low metastatic breast cancer. Again, places where ENHERTU has been approved and has transformed the standard of care for patients. In HER2 positive breast cancer, ENHERTU is an effective treatment option with a favorable benefit-risk profile in elderly patients, and data continue, importantly, to show improved quality of life in patients treated with ENHERTU. In the HER2-low setting, the benefit of ENHERTU is observed across baseline subtypes of HER2-low metastatic breast cancer, and a detailed safety analysis continues to support ENHERTU as a standard of care in this setting. Now we're going to shift from breast cancer to the pan-tumor or multiple tumor type setting beyond breast cancer. If we could move to the next slide. I'm excited to present data that we've just presented at this ASCO as well, that relates to colorectal cancer. Here we have a DESTINY-CRC02 study, which is a randomized study in a global multicenter study in patients with metastatic colorectal cancer. These patients express HER2, they're HER2 positive, and importantly, we enroll patients regardless of RAS mutation status. RAS wild type or mutant. They were BRAF wild type and they were centrally confirmed for HER2 status. You can see they were randomized to two doses initially, and that is 5.4 mg/ kg Q 3 weeks, versus 6.4 mg/ kg Q 3 weeks. You'll notice that in the 5.4 mg/ kg group, there was an additional stage. Additional patients were enrolled to take it up to approximately 80 at that lower dose, the primary endpoint being response rate. If we move to the next slide, please. Here we see the key data, the primary endpoint. What you can see is evidence of clinical benefit in both, on the left side, the 5.4 mg/ kg group, with a response rate of 37.8%, or on the right side, with the 6.4 mg/ kg dose, a response rate of 27.5%. Both subgroups experiencing benefit, but with a greater numerical benefit in the lower dose group. If we move to the next slide, please. I had mentioned importantly, that this study enrolled patients regardless of RAS mutation status, you can see here, as highlighted in red, that there is benefit regardless of RAS mutation status. Even patients in that poor prognostic group with RAS mutation status, have evidence of benefit. Another notable aspect of this trial relates to the HER2 status subgroups. As you can see, the response rate in the IHC 3+ group was significantly higher than the response rate in the IHC 2+, ISH plus, lower HER2 expressing subgroup, 46.9% versus 5.6%. You can see consistent benefit across the remainder of the subgroups on the slide. If we could move to the next slide, please. Now, we've presented the efficacy data, and now we present the safety data. What we see overall, regardless of patients in randomized to the 5.4 mg/kg group or the 6.4 mg/kg group, is that the safety profile is consistent, you know, with what we know about ENHERTU. However, if we look at the adverse event rates, we can see some of the rates are higher in the 6.4 mg/kg group compared to the lower dose group. Therefore, we would conclude, along with the response rates that I showed you as well, that the benefit risk is more favorable in the 5.4 mg group, the lower group, compared to the 6.4 mg/kg group. This is a very interesting data set for us because it represents, again, extension beyond the existing indications in which ENHERTU is approved, which includes, of course, breast cancer, you know, lung cancer, and gastric cancer. Now we've continued to look beyond even colorectal cancer. If we look to the next slide. Early this morning, we saw the presentation of DESTINY-PanTumor02, and this is an interim analysis, and this is a very exciting result for us to present. This is an open-label study in HER2-expressing advanced solid tumors. Importantly, we've enrolled many patient type, tumor types into this study, which really don't have available anti-HER2 targeted therapy, and these patients aren't even typically tested for HER2. This is an opportunity to potentially extend the clinical benefit of ENHERTU into additional tumor types and continue to potentially transform and change the standard of care. This is a second-line-plus population. These patients were tested either locally or centrally, and they had to be IHC 3+ or 2+. Prior HER2-targeted therapy was allowed. All the patients received 5.4 mg/ kg Q3 weeks, approximately 40 patients per cohort, each of cervical cancer, endometrial cancer, ovarian cancer, biliary tract cancer, pancreatic cancer, bladder cancer, and other tumors. Overall response rate per investigator was the primary endpoint. If we could please move to the next slide. Here we have the key efficacy overall response rate data, and I must say that there's evidence of very clinically meaningful responses as well as durability of response, and both aspects are important as a manifestation of benefit. Across the entire population, the overall response rate was 37.1%. In the patients that were IHC 3+, the response rate was 61.3%. You can see the overall response rates on the far right side of the slide, where even we show the IHC 2+ with a 27.2% response rate. On the bottom of the slide, we see the durability for all of these three groups. In all patients with a response, the median duration of response was 11.8 months. In the IHC 3+ cohort, the median duration of response was 22.1 months, which is quite prolonged. In the IHC 2+, a median duration of response of 9.8 months. Though I will not walk through all the individual response rates for all the individual tumors, you can see some of those response rates are quite high. Considering the fact that these patients have failed standard of care or don't have a standard of care available, and don't have certainly a targeted anti-HER2 therapy available and represent an unmet need, we're very pleased to see the level of the height of response in some of these very hard-to-treat tumors. If we move to the next slide, please. Here's just another look at the durability, and we've already cited the median durations of response. What I'd like to point out on this slide is the dashed vertical line in the middle of the slide. What it shows is that for those who responded in this trial, approximately half of them remain in response at 12 months. Again, a manifestation of durability across the patient population that's been enrolled and responded. If we could then move to the next slide. Here now we look at the safety, and so that we can frame the benefit risk profile. Very fortunately, the safety profile was consistent with what we know about ENHERTU. You can see on the left, there was adverse events leading to discontinuation in only 8% of patients. There was serious related adverse events in 12% of patients. Overall, the statistics that we have here and the metrics are largely consistent with with a favorable benefit risk profile that we know of ENHERTU, and when considering the response rates, is certainly again favors benefit over risk. Here, you can see on the right side the most common adverse events, which reflect what we already know about ENHERTU. Overall, evidence that ENHERTU can provide to benefit to patients beyond that where ENHERTU has been approved. We're very excited to have presented that data and to be able to provide evidence that that additional tumor types and high unmet needs can be addressed. If we could move to the next slide. This next study is an investigator-initiated study out of Japan called HERALD/ EPOC 1806, and instead of selecting patients for enrollment and treatment with ENHERTU, according to immunohistochemistry, here we have HER2 amplification using the Guardant360 assay to select patients according to circulating cell-free DNA, excuse me. a representation of HER2 amplification. Importantly, this testing is part of the nationwide cancer genome screening project in Japan, the so-called GOZILA study. You can see, again, a range of tumors that represent high unmet needs, patients that aren't normally tested for HER2, and patients that aren't typically treated with anti-HER2 agents. What you see here, is that patients with esophagus, pancreas, urothelial, cervix, endometrium, ovarian, salivary, head and neck, and others, very similar actually to the DESTINY-PanTumor02 data set in terms of the patient populations enrolled that I showed previously. Still getting 5.4 mg/kg with an overall response rate by investigator primary endpoint. Now if we can turn to the next slide, please. This is the efficacy data. Here again, you can see across these tumor types, a very high unmet medical need, clear evidence of anti-tumor effect and efficacy, promising response rates. As well, on the left, you can see an overall response rate in the whole population of 56.5%. You can see the waterfall plot in each of those tumors. For each of those tumors, very favorable with downward trajectory in the measurements representing tumor shrinkage. On the right side, you can see the durability. Here again, just using a different selection method, a biomarker selection method, cell-free DNA and HER2 amplification, we can see that we can select patients and show benefit. If we could move to the next slide, please. Here's the safety as well, and overall, the safety is again consistent with what we know about ENHERTU. I can see that there was an ILD rate of 25% in the study. Uh, grade three was very low, and importantly here, this was per investigator, whereas typically we would, uh, perform adjudication centrally in our studies, but it's an investigator-initiated study for which we assessed, um, ILD per investigator and overall, uh, consistent profile, uh, with what we have seen, uh, in other studies. Uh, and then I'd like to move to the next slide, please. So what can we say about additional tumor types? And so the potential is show-- is, is really, uh, starting to be fulfilled at this point, to, uh, look beyond, uh, breast cancer, gastric cancer, and lung cancer and addition- additional tumors, which show promising efficacy and manageable safety in HER2-positive, uh, colorectal cancer. We see, uh, potential to be a new treatment option based on DESTINY- Pan Tumor02 in multiple HER2-expressing tumors. We see using HER2 mutation or HER2 amplification, excuse me, to select patients using a cell-free DNA assay, demonstration of promising efficacy and manageable safety profile. Exciting time for us as we continue to look and expand the use of ENHERTU. I'd like to move to the next slide, please, and this would be the next section. We know that Dato-DXd program, our TROP2 ADC program, is very advanced in both breast and lung cancer. Here, and based on the data presented at ASCO, we're going to focus on the non-small cell lung cancer updates. If we could please move to the next slide. At this ASCO, we've presented an update to TROPION- Lung 02. This is a phase Ib study where we combine Dato-DXd plus pembrolizumab with or without platinum chemotherapy in advanced small cell lung cancer. This is a patient population that does not have known actionable genomic alterations. You can see the key eligibility. It included both patients that are frontline, but it also did include some up to two prior lines. There's a mix of patients here, and I think we'll focus in some of our analyses on the frontline population. You can see the cohorts there. They pair Dato-DXd with pembrolizumab, with or without platinum, and there are two doses of Dato-DXd that were tested in each case, the 4 mg/ kg and the 6 mg/ kg. We'll focus here, you know, with the data in these cohorts. The primary endpoint was safety, and the secondary endpoints included looking at efficacy. If we could move to the next slide, please. Yes, what we see here are the waterfall plots and the response rates for all patients on the left and then the subgroup of patients that were enrolled in the trial that were frontline patients, so frontline non-small cell lung cancer patients. What you can see on the left in all patients is the overall response rate in the doublet regimen of 38%. The overall response rate in the triplet, which again represents Dato-DXd plus Pembro plus platinum chemotherapy, is 49%. In the frontline population on the right, we can see overall response rate of 50% with the doublet and 57% with the triplet. Overall, in looking at this data, it's preliminary, but it is certainly encouraging. Of course, we're very happy to see how the data is evolving in support of our ongoing frontline pivotal trial program with both TROPION-Lung07 and TROPION-Lung08. If we could move to the next slide, please. Here's the safety data, no new safety signals were observed. The most frequent adverse events that you can see on the right were stomatitis, nausea, anemia, and fatigue. What you'll notice in terms of the difference in the adverse event profile and the triplet versus the doublet relates mostly to hematologic AEs, which isn't a surprise with the addition of platinum in the triplet regimen. Overall, a manageable safety profile and suggesting the evolution when we consider the response rates and the efficacy of a favorable benefit risk profile as we proceed with this study. If we would move to the next slide, please. Now we look at some of the adverse events of special interest in this TROPION-Lung02 study. We can see oral mucositis and stomatitis, most common adverse event of special interest, predominantly Grade one, two. Importantly, there were no Grade five adverse events of special interest of any type, and there were no Grade four or five adjudicated ILD or pneumonitis events. Now I would like to move to the next slide. I'd like to level set us to the lung cancer program for Dato-DXd in terms of the pivotal trial program. As we have mentioned, TROPION-Lung01, the phase III second-line trial with Dato-DXd versus docetaxel in the second- and third-line setting, we expect readout in this Q1 fiscal year 2023, with a potential first-to-market indication and with the potential first TROP2 targeting agent in non-small cell lung cancer. Now, I presented to you the TROPION-Lung02 evolving data set, which again, is encouraging, although preliminary, and it does indeed support the ongoing trials in the frontline setting that we have, which include TROPION-Lung07. That's a frontline trial in the PD-L1 less than 50% population, and that's with Dato-DXd and pembrolizumab, with or without platinum chemotherapy. TROPION-Lung08, this is in the PD-L1 greater than equal to 50% population, and that's with Dato-DXd and pembrolizumab. We're very pleased that the TLO 2 results continue to support our frontline pivotal trial program. If we could now move to the next slide. Here we're going to talk about HER3-DXd, and really, what we're talking about across the ESMO Breast 2023 and ASCO Breast 2023 data here is really focused on our most mature and late-stage ADCs that are in pivotal trials, and that includes HER3-DXd. Indeed, we're going to focus here on the updates in breast cancer. If we could move to the next slide, please. This is an ongoing phase II study, BRE-354, in collaboration with Sarah Cannon, which is a partner academic research organization. This is a study of our HER3-DXd in patients with metastatic breast cancer. It has multiple components. What we'll look at here is specifically the part A, which is in the HER2 negative metastatic population presented at ASCO 23 2023. I want to point your attention to the bottom right of the slide, because even though I don't have the data to show you right now, that's a part of the study called Part Z, and that's where we're actually looking at sequencing HER3-DXd at its 5.6 mg/kg dose after patients have been treated with an HER2 that are HER2 positive. We'll be able to answer multiple questions in this study, and we await the results of Part Z, though we'll show you today the results of Part A. If we could move to the next slide, please. Certainly, this data continue to support the potential of the HER3-DXd asset in the metastatic breast cancer setting. We can see in Part A, in this HER2 negative population, which is heavily pretreated, we can see the response rate of 35%. Importantly, what the data on the left shows is that these responses occur across a range of HER3 expression. When we develop these targeted agents, we certainly look to see whether or not the target expression of the ADC could potentially predict response. Here in this small set, what we can see in a preliminary fashion is that this drug appears to be active across the range of HER3 expression. There's the safety profile on the right side. Overall, quite manageable, consistent with what we've previously presented for HER3-DXd, and overall, an evolving favorable benefit-risk profile here. If we could move to the next slide, please. This is another study with an academic partner, this time with the Institute Gustave Roussy in Paris. This is an ongoing phase II trial called ICARUS-BREAST01. These are interim results. This is in hormone receptor-positive, HER2 negative metastatic breast cancer. Again, these patients have been pretreated, and the overall response rate here at three months, preliminary here, data, early data, is 28.6%. Importantly, a low rate of adjudicated ILD, with only 1.8% being Grade one, an evolving manageable safety profile. What I want to mention about this trial, and that we can present at further meetings, is the richness of the biomarker data in this trial. If you look at the schema, what you'll notice is there's the potential for sequential biopsy in this trial. This is an exploratory biomarker analysis that may allow us to answer key translational mechanisms about the HER3-DXd and the HER3 biology. We look forward to future presentations of the data. Already, what's been presented in terms of biomarkers is circulating tumor cell analysis, and we can see in the study so far, preliminarily, we see reductions in total in HER3 circulating tumor cells after the first cycle of the drug. More to come from a biomarker standpoint on this one. If we could move to the next slide, please. This is the last slide I'll show for the HER3-DXd, and now we shift to the early-stage setting. The previous two studies I mentioned focused in the metastatic setting. Here we focus on the primary disease setting. This is the SOLTI TOT-HER3 trial that's being done in collaboration with a group there in Spain. These are patients who are basically candidates for surgery. We're giving HER3-DXd or HER3-DXd plus letrozole, the anti-hormonal agent, or standard chemotherapy in a randomized fashion. The patients are having surgery. What we see here from the preliminary analysis is that after a single dose of HER3-DXd, there's a 30% response measured by ultrasound. This isn't pathologic response, but this is a first assessment of overall response. This is encouraging after a single dose of HER3-DXd. There's also some biomarker work that's interesting being done in this study. It's called the CelTIL score, and that's looking at the influence on cellularity and immune infiltrate after the administration of HER3-DXd. Indeed, the CelTIL score did go up, again, representing immune infiltrate and cellularity going up after one dose. The toxicity profile was more favorable in the lower dose tested. They tested both 6.4 and 5.6. There's more correlative work ongoing here. Again, a rich biomarker study. I want to mention on the bottom of the slide is that there's another ongoing trial called SOLTI-2103 VALENTINE. That is also in the neoadjuvant and primary disease setting and, again, a hormone receptor-positive, HER2-negative population. What we'll be able to see from that trial is pathologic assessment. When we start to think about efficacy in a neoadjuvant setting, it'll be in the VALENTINE trial that's ongoing, for which we'll be able to determine HER3-DXd's ability to improve pathological outcomes and to look at, like, pathologic complete response. If we could move to the last slide for HER3-DXd. We continue to look at HER3-DXd in breast cancer. We can see that there's a clear efficacy signal in the advanced metastatic setting. We're also exploring opportunities, as I've explained, in the post in HER2 setting, and that's in that Sarah Cannon trial. Then in the early breast cancer setting, in combination, excuse me, in collaboration with the SOLTI group in Spain. New data continue to support the potential of this asset in metastatic breast cancer, and we'll wait for the data in part Z of that Sarah Cannon study to show us the sequence of HER3-DXd after ENHERTU. We'll wait for the VALENTINE trial to get a further understanding of efficacy of HER3-DXd in early breast cancer setting. Now I'd like to move to our last section of the presentation, and this is on combinations. I think as we think about combinations, I want you to recall that, you know, Ken had presented a framework in which we both expand in our R&D strategy. That is, we take, we take our DXd ADCs, and we expand, we look for new indications or earlier lines of therapies and also extension, which is we take our DXd ADCs, and we combine them with new assets in our pipeline that may have a longer LOE and may have promise in terms of rational combinations. If we could move to the next slide, please. This is an overview of the combinations where we're looking to expand our DXd ADCs opportunities. I won't list, I won't explain all of these individual trials. In fact, I think we've presented them in one way or another in prior presentations. The key is to say that we're doing various studies in breast cancer and lung cancer on the top half of the slide with checkpoint inhibitors. That includes combinations with pembrolizumab, both in the phase II and also the phase III setting. That includes combinations with durvalumab, also in the phase II and the phase III setting. That's the PD-L1 inhibitor, pembrolizumab, of course, being the PD-1 inhibitor. At a poster, a trials and progress poster at this ASCO, we show TROPION-Lung04, which is in a non-small cell lung cancer advanced population, where we combine AZD2936 or MEDI5752 with Dato-DXd. These are our partner, AstraZeneca's, bispecific antibodies that are PD-1, TIGIT or PD-1, CTLA-4. Certainly, a number of opportunities, including for expansion into earlier lines of therapy, again, that expansion theme, with combinations with immunotherapy. There are targeted therapies, and we do have studies ongoing with pertuzumab. Of course, our flagship, frontline, HER2-metastatic positive breast cancer trial, DESTINY-Breast09, with pertuzumab in combination or with ENHERTU monotherapy. We also have tucatinib, another anti-HER2 agent. We have combination with capivasertib. This is an AKT inhibitor from our partner, AstraZeneca, that's being tested in DESTINY-Breast08, and we have combinations with osimertinib. Osimertinib, which was also profiled in some key data presented at this congress. Here we have combinations with either Dato-DXd in combination with osimertinib, that's the ORCHARD trial, or HER3-DXd in combination with osimertinib, and that's the ETUDE-103 trial. Beyond these combinations at the top of the trial, it's important for us to point out that we are doing combinations with our own pipeline agents, right? That's important that when we think of this extension as part of our R&D strategy, that we have two ongoing combinations with ENHERTU. The first is with our EZH1/2 inhibitor, small molecule, ENHERTU low metastatic breast cancer. That's an ongoing trial in collaboration with MD Anderson Cancer Center, MDACC. We have ENHERTU in combination with a SIRPα antibody. That's also going to be planned for disease states, including breast cancer, and that's the first subject dosed in this fiscal year, first half of 2023. Importantly, we have additional agents. Our scientists are hard at work in our preclinical pipeline, you'll see in the coming presentations, in the coming times that we gather, we'll see more combinations that leverage our pipeline with our extension strategy. If we would move to the next slide. Here's an example of those combinations and one that I mentioned. This is DS-1103. This is an anti-SIRPα antibody. As I've mentioned, we've engaged in a combination trial with ENHERTU, and we plan to test on the bottom right, an expansion trial in ENHERTU low advanced breast cancer. The SIRPα pathway is an important pathway. It's so-called the don't eat me signal. Fundamentally, what we have here is DS-1103 would block the SIRPα CD47 axis, and that is on the presence in macrophages and in dendritic cells, and by blocking this pathway, releases macrophages and phagocytic cells to attack the tumors. Basically overcoming a don't eat me signal. We have very promising preclinical data, where we. when we combine DS-1103 SIRPα antibody with ENHERTU, and this is the basis by which we have then moved into the clinic to look at what we think is a very exciting combination, which again, is just one example of what we hope to show you in the time to come. I'd like to move to the next slide, please. In conclusion, we do have plans, we have ongoing plans, extensive plans for combinations with our DXd ADCs, both assets that are external to our organization as well as with our internal assets. We do have the combination with ENHERTU and our EZH1/2 inhibitor, as HARMONIA. We have a combination with ENHERTU with a SIRPα antibody, and further combinations are in planning and are on the way. Now I'd like to close the session, and if we could move to the next slide. I appreciate your attention for a lengthy presentation. Certainly, I hope you would agree with me, based on seeing the data and what we know about our DXd platform, the approval of ENHERTU in multiple indications, the extension of ENHERTU into now different tumor types and meeting additional unmet needs, the evidence that we have a deep pipeline for which we're now able to combine our late-stage DXd ADCs, like ENHERTU, with our own internal pipeline agents, that indeed, what we seek to do is serve patients. That is the very reason we get up in the day, and that is very much what we serve to do and what I hope I communicated to you today as evidence of what we do. Thank you so much, and I appreciate your time. What we'd like to do now is answer any of your questions. Thank you. We'll now take questions. Yeah, thank you for the presentation. This is Tony Ren from Macquarie Capital. I wanna ask you about your TROP2 asset. It is, you know, some people describe it as a fancy chemo, right? Because it doesn't have a biomarker. That being said, in the press release this morning, AstraZeneca and you guys said that you guys are doing a study called, I believe it's called AVANZAR study, right? Where you are going to use a TROP2 assay to identify patients who can benefit from that. Just wanna get some sense from you on that assay selection. You know, is it gonna be a, at the current thinking, is it an IHC? Is it a next-generation sequencing? Is it tissue? Is it liquid? You know, just wanna get some understanding about how to target that. You know. You know, I believe it's nearly ubiquitously expressed surface antigen, right? That's my first question. The second question, which I posed at the AstraZeneca event just earlier as well, is that the TROPION-Lung02 study, you know, there's literally a 20% interstitial lung disease, right? It is pretty high. I mean, I think, you know, we're hoping to see it below 10%, but most of the time, it's below, you know, it's around 10-15. 20% is a bit higher than what I had expected. Just want to get a sense, you know, did you guys apply your mitigation for this study? That's on the ILD in TROPION-Lung02. In terms of activity, right? You know, I know it's small sample, but I noticed over time, from WCLC in 2022 to the ASCO abstract and to the data today, I noticed sort of a mean reversion or trending down of the doublet activity, but the increases in the triplet activity. Just want to get some understanding why that is taking place. I actually do have a few other questions, but I think I'll probably just stop here and get back into the queue. Yeah. Thank you. Yes, I'm glad to start with your three questions. In terms of the AVANZAR study and the endpoint structure, where AstraZeneca will look at TROP2 expressing patients, that's actually a study that they're independently conducting. In terms of questions about that study, we would need to relate those questions to our partner. We, of course, are interested in TROP2, and we have not disclosed an assay strategy, but certainly, you know, in our trials, we'll look in an exploratory fashion and are considering translationally, you know, different approaches. Of course, we have not in our trials to date, and certainly not in our pivotal trials, we have not selected patients, you know, nor, you know, based on this assay. At this point, TROP2 is exploratory for us. As you said, TROP2 is expressed at a very high rate in non-small cell lung cancer. Indeed, that approximates 90%. When we enroll that patient population, the majority of patients should express the target. You commented on the ILD in the triplet. Indeed, we see a 22% response rate of ILD. I think very importantly, there was a low rate of Grade three ILD. ILD is important to us. Fortunate that there's, you know, there's been just Grade three and no Grade four and Grade five. I think it's early here. We have a dose modification guidance in the protocols. We're watching this very carefully as we go, and we do think this is a manageable toxicity for us. Of course, ILD has been observed in pivotal trials that we've run, and the key is that we need to weigh both benefit and risk. Overall, with what we see here preliminarily, we believe the data is encouraging. We believe the data is headed in the right direction. With the majority of the ILD being low grade, we think the evolving benefit risk profile is favorable. You also asked about the response rates. Certainly, it's preliminary data. I don't think we can make conclusions regarding the comparison of the response rates in either the doublet or the triplet cohorts, at this time. It's a bit early, and also, the study is not designed to compare efficacy between these two arms. What we see in the 57% versus the 50%, is directionally encouraging, and we believe this is supportive of our ongoing frontline pivotal trial program, TL07 and TL08. Indeed, as you suggest, the response rates may evolve over time, and indeed, the data can be considered preliminary at this point, and we're not able to draw a conclusion based on the efficacy data to date, only that it's directionally supportive and encouraging to us. Hi, this is Yamaguchi from Citi. I have two questions. The first question regarding your HER2. You disclosed the DESTINY-CRC02 data and also pan-tumor data, both of which is pretty good. What's gonna happen on the filing process of those things? Especially that the pan-tumor, I think that Aditya Bardia, who was talking about the potential tissue tumor-agnostic approval, I mean, pan-approval on HER2. Can you give me the strategy for those things, first of all? That's the first question. Second question, regarding more general questions. I see so many ADCs showing early results at this ASCO. I don't know. They're saying 140 ADC are in the clinical trial, and you are ahead of our competition, I understand that. Can you give me some comments, how are you gonna keep this lead? Also, global companies sometimes are very quick at the development. Are you going to change your strategy to speed up, especially at the 7,300 and 6,000, which you don't have a tie-up at this moment? Thank you. Yes, thank you for your two questions. You've asked about the regulatory strategy based on DESTINY-PanTumor02. At this point, we're not disclosing the regulatory strategy. We're certainly very encouraged by the data and its potential. We will and are planning to engage the regulatory agencies, and that could potentially lead for us to come back and share a strategy with you. At this point, we're just encouraged by what we see. We're excited by the capability to discuss with the agencies, but do not have a submission plan to discuss now, nor to discuss a particular regulatory strategy. We'll come back to you as soon as possible with this. You asked, Your second question. I'm sorry, can you remind me? ADC. The ADCs. Certainly, at this ASCO, a prominent theme was the fact that we saw many ADCs being developed. Of course, our DXd platform has been a leading platform and has led to substantial changes in the standard of care, not just increments, but true changes in the evolution of the standard of care. We believe we continue to have a leading technology. We are aware that there's competition. We are aware that the competition continues to grow. As a result of that, we will certainly maintain our vigilance. We will certainly continue to enhance our pivotal trial execution capacities. When we also design pivotal trials, we will do so in an efficient manner, with a design that can produce results as soon as possible, in considerations of the various designs we can consider. Both with respect to trial design, efficiency, and also operational efficiency, we're focusing on both these aspects, understanding that we are not alone in this race to help patients. Want to add? I may add some comment to your second question. through the partnering with AstraZeneca, Daiichi Sankyo's R&D burden and also R&D budget have been reduced. The remained budget and data capabilities can be allocated to the following ADCs other than HER2 and Dato-DXd. At this moment, we believe we can maximize following ADC alone. In the future, if we may consider it is very difficult for us to maximize alone, we may look for a partnering opportunity, maybe or might be. Wakao-san from JPMorgan Securities. If you are on Japanese channel, please switch to English channel and please ask your question in English. Hi, this is Wakao from JP Morgan. Can you hear me? Yes. I thank you for taking my question. I have two question. Firstly, about HER3-DXd HER3-negative breast cancer data. As for HER3-DXd, it has been effective regardless of HER3 expression level. Do you think this is due to high activity of HER3-DXd, or is it due to some scientific feature of HER3 receptor? What do you think is the future positioning of HER3-DXd in HER3-negative breast cancer? This is the first question. Second question is about TROP2 antibody competitive landscape. First-line data was very encouraging, and I'd like to know your thought on the competitive landscape for TROP2 antibodies. I think data on SKB264 Merck TROP2 antibody was presented at this conference. How did you view this SKB264 data? Do you think it's it poses a threat to that DXd? I think, you are clearly ahead of SKB264 in terms of data accumulation and speed of development. I'd like to know your thought on the superiority of that DXd in light of this SKB264 data. Thank you. You want me to start? Yeah, okay. To the first question, thank you, regarding HER3-DXd and your observation that there was expression across the range of... there was efficacy across the range of HER3 expression. We're still trying to understand the biology of HER3. Indeed, the cohort that you saw is relatively small, so we probably can't draw a conclusion that HER3-DXd is effective regardless of HER3 expression status. We may need to have a larger data set to draw that conclusion, even if this early preliminary analysis in a limited set of patients may suggest that the HER3 expression does not predict efficacy. We cannot claim based on that data set, we cannot draw that conclusion. We would need a larger data set and probably to have a randomized trial and a control arm. Now, I think you've asked a good question about HER3 biology and how that could influence HER3 expression as a biomarker. This is something that we seek to understand. We don't, at this moment, have the answers. As you saw with those trials, both the one at the Institut Gustave Roussy and with the Sarah Cannon, which produced the analysis that you're asking about. There is additional biomarker work to be done, including sequential biopsy, that may help us, and that's in the Gustave Roussy collaboration study, that may help us very much further answer the question that you asked. The second question that you asked, I believe, and please clarify I'm wrong, is: what is our impression of the data from the Kelun-Biotech, and Merck, TROP2 ADC that was presented at the ASCO, and what do we think about this data? If I understood correctly. Yes, that's right. Yes. The data, what we can see, the TROP2 ADC is active, but it's very early. It's very early. The overall responses that we see certainly demonstrate activity, but it's too early to draw any conclusions regarding that asset versus our Dato-DXd. That's primarily because we have a lot more data with our Dato-DXd, and this data is very early and emerging. At this point, I don't think we can draw any conclusion regarding any type of differentiation because of the size of the data set that we have there, and that includes also the subgroup analyses that they show in both EGFR wild type and EGFR mutation-positive patients. It's hard to conclude across these subgroups and draw any conclusions. What I would say is, what I believe that you alluded to, is that we're certainly now at a more advanced stage than this asset. We do understand there's the intent for those parties to move the asset forward very quickly. Of course, we already have an ongoing pivotal trial program in the frontline. We are about to read out soon, as you know, the randomized pivotal trial in the second and third line with Dato-DXd. There is definitely a time difference in these two for these two programs. What I can tell you is, based on the presentation of that data today, we will certainly be continue to be vigilant. We will certainly continue to execute with efficiency in our ongoing and what is very large pivotal trial program for Dato-DXd. Okay, thank you. I'm looking forward to success of TROPION-Lung01 trial. Thank you. Next question is from Miki Sogi from Sanford C. Bernstein. Please go ahead and ask your question. Thank you very much. I have 1 question regarding the observed efficacy of ENHERTU in CDK4/6 treatment, the recent marker-negative and positive populations. I was wondering, this observed efficacy, what is the implication for the first-line potential of ENHERTU in HR positive and HER2 low population? Yes, I think that's a good question. I mean, the analysis was done to understand if ENHERTU is going to be active, certainly, you know, in patient populations that either have received prior CDK4/6 or have resistance markers. We have not disclosed any further study of ENHERTU in HER2-low metastatic breast cancer. Of course, what we have stated is, you know, we have an ongoing study, DESTINY-Breast06, which is in a HER2-low population that is chemotherapy naive. However, as we continue to explore in HER2 and look at those subgroup populations that you cite, we can certainly think of how such data could inform additional potential study. We're not able to disclose at this point, what studies we may do further, that relate to, you know, that relate to, additional lines of therapy or in relation to any CDK4/6 inhibitors. Thank you. I have a quick additional question. What's the percentage of population in the HR-positive and HER2-low with the positive CDK4/6 resistant marker? Yeah. I don't know that I have that information now, we may need to get that back to you. You're asking within that subgroup analysis, you're asking the HER2 status across the different CDK4/6 subgroups. Is that correct? Exactly. That's right. Yeah. I will check now, but I don't think we have that data with us here. Thank you very much. Next question is from Muraoka-san, from Morgan Stanley. Here on Japanese channel, please switch to English channel and ask your question in English. Thank you. It's Shinichiro Muraoka. Can you hear me? Yes. Great. Thank you. The first question is about the pembrolizumab, the filing strategy. Of course, I understand that it's a bit preliminary right now, but is it possible you do just in terms of filing or reviewing just focusing on IH3, IHC 3+, or excluding some non-effective tumor type, like pancreatic. Also, please guide me that your outlook going forward. The second question is the page 64, the maybe mostly the last page of your presentation. In 2024, yeah, it will be a question to maybe Manabe-san. In 2024, you have many more robust data readout events, like ENHERTU for Breast09, for first line, and data for TNBC, HER3 Lung02 studies as well. Is it possible that you are expecting more exciting days in 2024? It's a rough question, but if you can share your views, it would be pretty helpful. Thank you. Okay, well, let me try to answer those two questions. The first question I think was concerning with the filing strategy for the DESTINY-PanTumor02 data, particularly with respect to the IHC staining pattern. Right. Right. At the moment, we have not disclosed our regulatory filing strategy. I do want to remind you of the data which says that, yes, the activity is certainly very good in the 3+ IHC, but also certainly in IHC 2+, but also in certain other types of tumors that are listed on that slide. The drug is quite active in the 1 plus category as well. It's a very interesting set of data for which we require further regulatory discussion. I think the second question was about the all the data coming out that's listed in slide 64. Is that correct? How we view these data? Right. Yes, yes. As with last year, when we had very large amounts of phase III data coming out, as well as new phase I and phase II data, I think that pattern of a data-rich oncology development program that we have will continue for this year. I think the most interesting one that's coming up very soon is the data on lung cancer TL01. Really followed that quite soon by breast cancer data from a data program and many other data that you see here, so. I do think that the data TL01 is a very important one for us. I guess I would just add that, in addition to that, you know, we're also talking about in 2023, the DESTINY-Breast06 trial, right? Which is, I had alluded to that earlier, the HER2-low, phase III, advanced, you know, breast cancer study, where patients are naive to chemotherapy. These are the 3 key readouts that we look at for 2023, and very look forward to sharing that information with you. Thank you. We'll take one last question from the floor. Please wait for the microphone. Thank you very much. Yeah, I just want to ask you about your assays for HER2-low. We know that Dr. Modi, who presented your DESTINY-Breast04 study at the last ASCO, she talks about a quantitative assays quite a bit. Also, I know that Dr. Bardia talks about the spatial arrangements of the HER2 receptors on the surface of the tumor cells. Just so I just want to understand how are that coming along? I suspect that would have some impact to your future programs in targeting HER2-low and HER2-null. If I could just add one more, you know, just going back to what Mark said earlier about the lead, you guys have in TROPION studies, your TROP2 ADC against Kelun's and Merck's ADC. My estimate is that you guys are about three or four years ahead. I just want to see if that's your understanding as well. Please. You want me to start? Yeah, sure. In terms of assays, I mean, we remain very diligent in our translational medicine organization. We do understand that, of course, HER2-low metastatic breast cancer, the assay is established, right? I think as we look to additional ADCs in their development, certainly, and I won't get into any specific ADC, I think we haven't disclosed the translational strategies for some of our the ADCs that are in the earlier stages. Certainly, we look with any targeted agent, including our ADCs, to determine whether or not we can find analytes using different modalities, different assays, that can predict, potentially response. Certainly, immunohistochemistry is a prominent assay, and we can see that in the ENHERTU program. We are indeed, and as you alluded to, interested in looking at beyond immunohistochemistry and additional modalities, whether that be pathological or genetic, whether it be quantitative. I would say in a general sense, we have a very comprehensive translational medicine program to optimize the use of our ADCs and benefit risk profiles. Nothing specific that I could share at this point regarding any specific ADC and how we're going beyond, you know, immunohistochemistry. Of course, you're aware that ENHERTU is also approved in mutation-positive, non-small cell lung cancer, so that's another example of another type of, you know, a genetic-based assay. Yes, and for your... Remind me of your second question, I'm sorry. Your question about your lead time. Oh, the lead time, right. You asked if it's three to four years lead time. Well, I really, it would really be difficult for me to indicate, and that's simply because whereas I know where we stand at Daiichi Sankyo with our programs, of course, it's difficult to say, you know, where a competitor may stand. Whereas a competitor may present data, but they may present data, and then we still can't tell how far they're along, right? It's difficult to come up with a, I would say, a precise estimate of the lead that we may have. I would say that we have... All that we can confidently say is that we have a lead, we have a significant lead, we have a program that's in already moved into pivotal trials, well into pivotal trials, versus a program that, as far as we know, is in the dose finding in the early stages. That's about what we could add. I'm not sure if, Ken, you'd want to add anything else? Yeah. We would only be speculating about the timelines and the time difference between us and other companies. Just I think we can only probably conclude that we are ahead, but by how much, it's hard to tell. Like TROPION-Lung01 study, right? From start to the clinical trial on that, right, it's about three years, right? Yeah, your TROPION-Lung01 study, right? If I look at ClinicalTrials.gov registry, right? From start to a preliminary data readout to the final readout, it's about three-four years, right? Do you think a competitor would have speed this up a little bit? Because in the second-line lung cancer, you would be looking at a progression-free survival of about, let's call it 10-12 months, right? You need time to recruit, and the FDA will not approve something without an overall survival benefit. I would imagine a competitor cannot really speed it up, right? Yeah, I mean, I think it's, as you mentioned, the landscape may very well evolve. We hope with TL01, we hope for a positive trial. Of course, we don't know. That could change the standard of care potentially for patients. If that happens, then, maybe, the way that a competitor may approach, the second-line space may change. It may become more challenging, as an example. Again, difficult for us to know what their development plan is, so, and including, like, which line of therapy they could start with, they could initiate trials. The extent to which we would be ahead would depend, on where they may even, which line of therapy they may entertain starting a trial. Okay. Thank you. We've now come to our ending time, so we'll now conclude Daiichi Sankyo's ASCO 2023 highlights. Thank you very much for joining today.