Hello, everyone. Welcome to our next Meet GSK Management event, Getting Ahead of Cancer. This is an interactive event with the presentation sent to our distribution list by email, and you can also find it on gsk.com. Please turn to slide two. This is the usual safe harbor statement. Please turn to slide three, and let me now hand the call over to Luke to share today's focus. Thanks, Nick. So, today, we hope you gain a better understanding of our material growth opportunities across our key areas of focus in oncology, hematology, gynecologic cancers, and other tumor types. We'll highlight the future potential of Blenrep, which we anticipate to be a multi-blockbuster asset that delivers a favorable benefit risk profile for multiple myeloma patients in need. We will also discuss our differentiated immuno-oncology combinations, primarily anchored to our anti-PD-1, Jemperli, as the backbone. And given our recent in-licensing of two ADCs from Hansoh, we will detail our future opportunity across solid tumors. And finally, we'll walk you through the near-term catalysts that will help us to achieve our stated growth ambitions. If we can go to slide four, please. You'll hear from myself, along with Tony Wood, our CSO, and Dr. Evangelos Terpos, to walk us through the most recent Blenrep data. For Q&A, we'll also be joined by Nina Mojas, Hesham Abdullah, and Monder Majdoubi. If we just go to slide five now. As a reminder, GSK focuses on preventing and treating disease in four therapy areas. We most recently spoke to you about our progress in respiratory, and today, we will cover the emerging oncology portfolio. Slide six, please. Now, I don't think I need to tell people on this call that oncology is an exciting area. We're confident that our oncology strategy, which we'll cover shortly, will contribute to our previously committed 2031 GSK ambition, and it has the opportunity to deliver transformative medicines for patients and value for shareholders. The growth of our competitive portfolio stems from the potential to achieve clinical outcomes in defined subpopulations. In the near term, from 2024 to 2026, we expect our in-line medicines to continue growth. We also anticipate a potential market entry of Blenrep in second-line multiple myeloma, and this represents upside to our current ambitions. In the latter part of this decade through to 2031, we expect a shift in sales composition to reflect potential Blenrep expansion, the emergence of immuno-oncology combinations, and the entry of our two ADCs across tumors. In a moment, Tony will begin our medicine spotlights with Blenrep and the recent practice-changing data presented at ASCO. Please now turn to Slide seven. GSK Oncology is focused and focused across three core areas: hematology, gynecologic cancers, and other growth opportunities in solid tumors. We've got several modalities, whether they are antibody drug conjugates, immunotherapy, or targeted small molecules that span these disease areas. Our hematology portfolio includes Ojjaara and myelofibrosis, and belantamab mafodotin, or Blenrep, in multiple myeloma, offering significant growth opportunity. Gynecological cancers will continue to be a cornerstone of our portfolio with Jemperli in endometrial cancer and Zejula in ovarian. We also have a strong opportunity to strengthen our gynecological impact with our recently in-licensed B7-H4 ADC from Hansoh. And lastly, we're gaining investment decisions to maximize these medicines in additional solid tumor types where they could deliver transformational efficacy, such as with colorectal, lung, and head and neck. I'll now hand it over to Tony on slide eight. Thanks, Luke. Please turn to the next slide. Multiple myeloma is a complex disease with new combination treatment options continuing to emerge. With each line of treatment comes accumulating toxicity and decreasing time until the next relapse. What's more, novel modalities often necessitate hospitalization or in-patient care, particularly for anti-BCMA agents. Importantly, for the 70% of first-line patients who receive lenalidomide, they only benefit from 12-28 months of progression-free survival in second line and beyond. With this in mind, future treatment options need to address unmet need, namely, extending overall survival and time in remission, lowering toxicity, broadening eligibility and treatment accessibility across sites of care. We're grateful that Dr. Evangelos Terpos, Professor of Hematology at the National and Kapodistrian University of Athens and a DREAMM-8 Principal Investigator, is able to join us to walk us through recent Blenrep data. Welcome, Dr. Terpos. Please turn to slide 10. I'm Evangelos Terpos, Professor of Hematology and Director of the Stem Cell Transplant Unit in the University of Athens in Greece, and I'm going to present you the data of the novel studies, DREAMM-7, DREAMM-8, and the newly diagnosed transplant-ineligible patients with multiple myeloma who received the combination of Blenrep, an investigator-initiated study. Next slide, please. This is the study design of the DREAMM-7, which included patients with one prior line of therapy and relapsed refractory multiple myeloma, and the treatment schedule included the combination of bortezomib and dexamethasone at the standard schedule. In the first arm, we had the addition of belantamab mafodotin at a dose of 2.5 mg/kg every three weeks, followed by, after nine cycles, 2.5 mg/kg every three weeks alone. Or in arm B, the addition of daratumumab at the dose of 16 milligrams per kilogram weekly for cycles one till three, then every three weeks for cycles four to eight, and then after cycle nine, we had daratumumab monotherapy. So we had a direct comparison between belantamab mafodotin and daratumumab as monotherapy after the eight cycles, so from cycle nine and afterwards. The primary endpoint was PFS. Key secondary endpoints, overall survival, duration of response, and MRD. We had stratification for prior lines of therapy, revised ISS, and prior bortezomib use. Next slide, please. Regarding PFS, you can see that the combination of belantamab, Velcade, and dexamethasone produced an impressive, more than three years median PFS of 36.6 months, versus 13.4 months of daratumumab, Velcade, and dexamethasone, with a hazard ratio of 0.41. So Blenrep VD demonstrated a statistically significant and clinically meaningful PFS benefit, with a median PFS that was 23 months longer than that of Dara-Vd. Next slide, please. Regarding overall survival, even with this median follow-up of 28 months, you can see that we have a median overall survival that has not been reached in both arms. But, the proportion of patients who are alive at 18 months was 84% in Blenrep VD and 73% in Dara-Vd, offering a hazard ratio of 0.57 that was statistically significant. So overall survival showed a nearly strong and clinically meaningful trend favor Blenrep VD, and of course, additional overall survival follow-up is ongoing. Next slide, please. And this is mainly because of the impressive overall response rate, which was 82.7% in Blenrep VD and 71.3 in Dara-Vd. But if we see the quality of the response, it was much more impressive with Bela-Vd, with at least a complete response in 35% versus 17% of Dara-Vd. And the MRD negativity rate in complete responders was 25% versus 9.6% in Bela-Vd and Dara-Vd, respectively, and the VGPR MRD negativity, 38.7% versus 17% in the two arms, respectively. Next slide, please. The PFS benefit was consistent in favor of Bela-Vd versus Dara-Vd across all the pre-specified subgroups, including patients with lenalidomide refractory or high-risk cytogenetic, and especially for those patients who are lenalidomide refractory. And this is a big number of patients now and an unmet need, you can see. Next slide, please. That Bela-Vd offered a median PFS of 25 months versus 8.6 months of Dara-Vd. In the non-lenalidomide refractory patients, the median is more than three years and 18 months in Bela-Vd and Dara-Vd, respectively. But you have also to appreciate that patients who are lenalidomide refractory were more heavily pretreated, with three or more prior lines of therapy in 42% of the patients in Bela-Vd, compared to 19% in the same arm for those who were not lenalidomide refractory. Next slide, please. Regarding high risk, also, you can appreciate that Bela-Vd offered a hazard ratio of 0.31 in those with high-risk cytogenetic, offering a median PFS of 33.2 months versus 10.5 only in Dara-Vd. For the standard risk patients, also, Bela-Vd continues to have a median PFS, which is 36.6 months versus 15.3 months in the Dara-Vd, with a hazard ratio of 0.44. Next slide, please. The DREAMM-8 study was a study that included relapsed refractory patients with one prior line of therapy, that all of them had been exposed to lenalidomide. So a more focused study on lenalidomide-exposed and refractory patient. In that study, bortezomib, pomalidomide, and dexamethasone, which is one of the standard of cares, was compared to belantamab mafodotin, pomalidomide, and dexamethasone. Pomalidomide and dexamethasone was given at the standard dose, like bortezomib in the arm B, while in belantamab, we had a very nice schedule with a dose of 2.5 milligrams per kilogram given at cycle one, only every four weeks now, and then followed by 1.9 milligrams per kilogram every four weeks from cycle two and onward. And there was stratification for prior lines of therapy, prior bortezomib, and prior anti-CD38 therapy. While the primary endpoint was PFS, and key secondary endpoints included overall survival, MRD negativity, and duration of response. Next slide, please. The median PFS has not been reached for the belantamab, pomalidomide, and dexamethasone arm, while the 12-month probability of a progression-free is 71% versus 51% in Pom-Vd. In Pom-Vd, the median PFS is 10.7 months. That is expected also based on the OPTIMUM study that gave approval to this combination. The hazard ratio is 0.52. Next slide, please. Regarding the different pre-specified subgroups in the PFS, we've seen benefit with belantamab Pom-Dex in all these pre-specified subgroups, including patients with high-risk cytogenetic, as you can see here, with a hazard ratio of 0.57, but especially to patients who are refractory to lenalidomide, with a hazard ratio of 0.45. Next slide, please. And patients who are refractory to anti-CD38 monoclonal antibody, either daratumumab or isatuximab, with a hazard ratio of 0.65. Next slide, please. The response rate was almost similar between the two arms. However, the quality of response was much better with Bela-Pom-Dex versus Pom-Vd. So CR or better was 40% versus 16%, and VGPR or better, 64% versus 38% in the two arms, respectively. Next slide, please. The MRD negativity was much higher, almost seven times better or five times better with Bela-Pom-Dex versus Pom-Vd. The CR negativity MRD rate was 24% versus 5% in the Pom-Vd, and the VGPR MRD negativity rate, 32% versus 5% for the two arms, respectively. Next slide, please. The overall survival showed a trend in favor of Bela-Pom-Dex, with a 12-month probability of survival of 83% versus 76% in Pom-Vd, and, of course, the data are not matured yet. Next slide, please. How about ocular adverse events, which is the most important side effect, and I would say one of the very few side effects of belantamab? You can see that, we are talking about the worsening of the best-corrected visual acuity, because this is, something that can impact the daily activity of the patients. And you can see that, 20-50 best-corrected visual acuity reduction happened in 34% of the patients, versus only 2% who had a 20-200 or worse. The time to onset for the first event was 73 and 105 days, respectively, and the improvement of, the, first event happened in 98 and 100% of the patients, respectively. First event result in 94 and 80% of the two groups of the side effects, respectively. Next slide, please. The median time between the doses increased the longer patients were on treatment, and the dose delays did not have any impact on the PFS. Blenrep VD patients with at least one dose delay of more than 12 weeks, the median PFS was exactly 36.6 months. 23% of the patients experienced 20/50 or worse events in the first three months, and the prevalence decreased thereafter, as you can see in the graph. Rate of treatment discontinuation due to ocular events were very low. Next slide, please. In the DREAMM-8, the respective number of patients with best corrected visual acuity reduction to 20/50 and to 20/200 was 34% and 1%, respectively. The first event resolved to normal baseline happened in 84% and 50% of the patients, but you can recognize that it was only one out of the two patients in the 20-200 group, and the first event improved in 92% in all patients, respectively. So visual acuity change that could affect activities of daily living were reversible in most patients for both studies. Next slide, please. So in summary, we can say that in DREAMM-7, the combination of belantamab, Velcade, and dexamethasone was 36.6 months, compared to 13.4 months in patients who received daratumumab, Velcade, and dexamethasone after a median follow-up of 28 months. The PFS was consistent across subgroups associated with poor prognosis, including patients with lenalidomide-refractory or high-risk cytogenetics. We have a strong and clinically meaningful overall survival and more quality overall response rate, and durability of response with Bela-Vd. In the DREAMM-8 study, the median PFS has not been reached yet with belantamab, pomalidomide, and dexamethasone versus pomalidomide, Velcade, and dexamethasone, which the median was 12.7 months after a median follow-up of 22 months. All the patients in this study had been exposed to lenalidomide, and the PFS consistent across all pre-specified subgroups, including patients with high-risk cytogenetics or lenalidomide or anti-CD38 refractory patients. We had greater response rates, including MRD negativity, with belantamab Pom-Dex versus Pom-Vd, and we had an early signal for overall survival advantage. Regarding safety and tolerability of Bela-Vd and the Bela Pom-Dex regimens in the DREAMM-7 and 8 studies, this was consistent with the known safety profile of the individual agents. With dose modifications that were effective in enabling patients with ocular adverse event to achieve PFS outcomes and low treatment discontinuation rates, consistent with that of the overall study population. Next slide, please. This study gave us the rationale to go to a phase I/II study in the newly diagnosed patients who are not eligible for transplant, and these patients were intermediate fit or frail. We randomized the patients to receive either 1.4, 1.9, or 2.5 milligrams per kilogram, but given every eight weeks or every two months, in combination with lenalidomide and dexamethasone. The primary endpoint was the safety, tolerability, and the dose that we are going to go for the phase II study. Secondary endpoints included a lot of data, as you can see here. Next slide, please. The overall response rate was 100% in all the subgroups, and we've seen that we had a slightly higher number of patients with complete response in the cohort 1 of the 2.5 milligram per kilogram, but we have very good responses in the two others, two other arms also. The progression-free survival was extremely good, as no patients after a median follow-up of 24.8 months, has progressed. However, we had some deaths because the study was run, especially at the time of the Delta strain of the SARS-CoV-2. That's why we had 4 patients who died because of COVID-19, and also we had two patients who died because of pneumonia, one because of intracranial hemorrhage and one sudden death. Don't forget that these patients were intermediate fit or frail, and the median age is 74 years of age. Next slide, please. Regarding the ocular adverse events, you can see that the vast majority of the patients had no or Grade 1 adverse events, and Grade 3 or more adverse events happened in very low number of patients. As you can see, for example, keratopathy, it was for the cohort 2 of the 1.9 milligram per kilogram every 8 weeks, which was the dose that we have chosen to go to the part two of the study, was only 0.3%. Importantly, the time to resolution of keratopathy was only one month. The time to resolution of the best corrective visual acuity change from baseline was almost two months in all the groups, and the time to resolution of meaningful BCVA decline was more than three lines drop in better seeing eye was between one and 1.5 months. The frequency in clinically relevant vision impairments happened in 10% in the cohort 1, with, more than or equal to three lines drop in the better seeing eye, to up to 13.4% in cohort 1 and 7.7% in cohort, 3. Next slide, please. Regarding ocular symptoms who have, impact on the activities of daily living, and you can see in the second part of the figure, you can see that, in the group of patients who received 1.9 milligram per kilogram every eight weeks, who had only 5.7% of the patients who had almost, most or half of the time, symptoms that impaired their clinical- their daily activity of living, while the 93% of the patients had not such symptoms. Next slide, please. And in order to achieve that, we had a schedule of, as we call it, appropriate belantamab dose administration. So if you see within red color B, which we call it inappropriate belantamab administration, is when the substantial ocular symptoms are present, and this can impact the quality of life of the patient and the daily living of the patient. So if we don't give belantamab at that time, then we avoid these side effects. Well, in the contrary, as you can see on the left, if you have an appropriate dose administration, we have a dramatic reduction in the visual acuity. On the contrary, if you see on the right, the appropriate dose administration diminished the visual acuity reduction based on the Snellen Chart. Next slide, please. So in summary, the extension of belantamab doses to every eight weeks or even 12 weeks, if we had any symptom, did not lead to reduced efficacy compared to previous study implementing the every three-week schedule. These results show that the efficacy of belantamab is maintained even when administering extending time intervals, as we've seen also in the DREAMM-8 study. Furthermore, the extended dosing schedule had only a minimal impact on vision-related functioning, with all or most of the time in the activity of daily living responses, recording less than 2.5% of assessments. Furthermore, the frequency of clinically relevant impairment in vision was low, as meaningful BCVA decline was observed in less than 10% of assessment with a rapid time to resolution. So thank you so much for your attention, and we are going to the next presentation now. Thank you very much, Dr. Terpos. We greatly appreciate your time and expertise in sharing the potentially transformative DREAMM-7 and DREAMM-8 second line data, as well as insights, from your clinical experience, with your, with your first-line data. As you just showed, that management of, eye-related side effects is important to help patients achieve desired outcomes. So let's... We're just gonna have a patient here who, has experienced and managed eye-related side effects while on Blenrep treatment. Please, if we go to slide 35. When I was first diagnosed with the myeloma, I was told that I probably only had 22 months to live, basically. So eight years down the line, and obviously the grandchildren are growing up, things that I thought at the time I was never gonna see are just normal now. Previous treatments that I've been on have really affected me with my sickness. Since I've started the belantamab, I must say I feel in better health than I have for a good few years. When I first started on the belantamab, I suffered with some eye-related side effects, which were mainly the gritty eyes to start with, and then almost immediately on the next one, I was suffering with blurred vision. And, yeah, I couldn't stand any colored lights, things like that. But once we discussed it with the consultant, he changed my treatment to a lesser dose and also extended the treatment time, and it almost improved immediately after that. Now, at this time, I can do all sorts of things. I can read... I can drive. I can even thread a needle, I can do sewing. I can do more or less anything that I could do before. On this treatment, where I go every six weeks, it makes life a lot easier for me. On previous treatments, I've been going every week, once a week. I do feel that this is giving me a much nicer lifestyle. I feel like I'm almost living again. So with the information you just heard from Dr. Terpos, and the patient who has received Blenrep treatment, you can get a sense that Blenrep has the potential to meet unmet needs in second-line multiple myeloma across both standard and heavily pre-treated populations. You can see on this chart, which provides information for each regimen regarding lenalidomide exposure, PFS within the intention-to-treat population, regimen constraints, and frequency of administration. For both the standard and heavily pre-treated populations in second-line multiple myeloma, the Blenrep triplet regimens have the greatest or equal lenalidomide exposure associated with the greatest PFS benefit, and the most convenient frequency of administration. So when we look at this, it's anticipated that Blenrep in both academic and community settings will be differentiated among the anti-BCMA class. And we expect filings in all major markets by the end of this year. So if we now go to slide 37. Given the complexity of the multiple myeloma market, patient treatment eligibility can be broadly mapped along a scale of age and fitness, from young and fit to old and frail. On the left-hand side of the chart, you can see site-of-care breakdowns, which are listed across a current standard of care, as well as future anti-BCMA agents. With the benefit risk profile of Blenrep, it's anticipated that Blenrep would serve patients regardless of age and fitness levels, as well as being available in both academic and community settings. And it's this confidence in this broad applicability that's given us the insight to further our Blenrep development program in earlier settings, which Tony will discuss on the next slide. We've just discussed Dr. Terpos' data in first-line myeloma and data from DREAMM-7 and 8, that show Blenrep combinations outperformed Daratumumab. These compelling data and broad potential patient eligibility support our investment decision to initiate DREAMM-10, a phase III study of Blenrep in first-line multiple myeloma. Please turn to the next slide. Now moving to Ojjaara, which was recently approved for the treatment of myelofibrosis with anemia. Please turn to slide 40. Myelofibrosis patients experience disease hallmarks of splenomegaly, constitutional symptoms, anemia, and thrombocytopenia. Nearly all patients become anemic over time, with worsening of anemia associated with decreased overall survival. One year after diagnosis, around 50% of patients require red blood cell transfusion, that severely impacts their quality of life. These patients need treatments that extend overall survival and address the spectrum of myelofibrosis manifestations. Ojjaara is the only JAK inhibitor to address symptoms, spleen response, and anemia, and Luke will share with us the recent launch success. Now, following the acquisition of Sierra Oncology in 2022, we accelerated commercialization and launched Ojjaara, Ojjaara in the U.S. and EU with line-agnostic labels. Ojjaara performance has been outstanding, very pleased to say, delivering the fastest U.S. launch uptake by a JAK inhibitor in myelofibrosis over the first two quarters post-launch. U.S. share has been significant across both first line and second line, with market research indicating about 60% of US ACPs, anticipating that they'll increase their use within the next six months. EU launches have also been successful in the UK and Germany, and Japanese approval is anticipated in the second half of 2024. And we're also exploring further indications of the overlap of oncology and inflammation with this target, and we continue to believe in the blockbuster potential of Ojjaara. Next slide, please. We're now going to talk about Zejula and the impact in ovarian cancer outcomes and promising new data in glioblastoma, which we're very excited about. Next slide, please. Zejula is another one of our key medicines and continues to deliver sustained growth in that first-line maintenance setting in ovarian. We've been able to more than double total sales over the last five years in a very competitive environment. Active surveillance in first-line maintenance of ovarian cancer remains high, despite evidence supporting the use of PARP inhibition in this setting, particularly within the BRCA wild-type subpopulation who respond well to chemo. Additionally, alongside anticipated readouts in endometrial, which is RUBY-2, and non-small cell lung cancer, which is the COSTAR Lung Study, Zejula is also being explored in unmethylated MGMT glioblastoma, in which no meaningful treatment improvement has been seen in over 40 years. Clearly, this is very important because, with a high unmet need, which is indicated by an alarming 2% five-year survival rate for glioblastoma patients, Zejula has the properties and the potential to demonstrate meaningful improvement. And Tony will now take you through the new data. Next slide, please. ... Zejula has a differentiated opportunity in glioblastoma. Unlike other PARP inhibitors, Zejula crosses the blood-brain barrier in preclinical studies, indicating a favorable brain tumor penetration. phase II data just presented at ASCO showed promising improvement in a single-arm study, which showed approximately a 15-month median PFS, versus five months for historical standard of care. These data give us confidence to imminently initiate a phase III supported collaborative study with the Ivy Brain Institute in newly diagnosed MGMT glioblastoma. Zejula will be studied against temozolomide as a standard of care. Study primary completion is anticipated in 2027. Next, we'll now cover Jemperli and the CD226 axis slide. So if we go to that slide, please. While Jemperli's strong foundation is anchored in dMMR endometrial cancer, it's also being explored in colorectal and head and neck cancers. Immuno-Oncology has shown transformative outcomes for dMMR endometrial cancers, while significant unmet needs still remain for the MMR-proficient subgroup. In colorectal, chemotherapy as the standard of care significantly impacts a patient's quality of life. So, new treatment options are needed to deliver greater clinical benefit, and the dMMR stratification is of clinical significance. For head and neck cancer, clinical improvement is also needed and has not been seen in more than 20 years in the locally advanced setting. While about 85% of patients are PD-L1 positive, the benefit of an anti-PD1 or PD-L1 therapeutic has not been seen in early-stage disease. The development of Jemperli across endometrial, colorectal, and head and neck gives us confidence on the potential of this product. If we move to slide 47. Jemperli's foundation is in first-line dMMR endometrial cancer, and in the first line, dMMR endometrial cancer, the statistically significant PFS benefits in the dMMR MSI high population of the Ruby trial was not reached at 30 months versus 7.7 months of standard of care. And this is what led to U.S. and EU approval in 2023. If we look on a revenue sense, Jemperli has delivered more than 250% growth year-on-year, 2023 versus 2024. This has been driven by the unprecedented data, coupled with strong execution on the ground. If we look at the uptake of Jemperli, it's achieved about a 33% new patient share in the U.S., and more than 35% new patient share in Germany, with a strong U.K. performance since the launch in March of this year. Building upon that first-line dMMR success, the Ruby one trial is also the only trial to show statistically significant overall survival in an all-comer population, with 44.8 months median overall survival versus 28.2 months. The first-line indication for all comers in endometrial has been accepted for FDA priority review with an August PDUFA date, and GSK will also be imminently filing with the EMA. The impressive data for Jemperli gives us further confidence in the future combination potential of Jemperli and our B7-H4 ADC endometrial. Jemperli is also being developed in other dMMR tumors, and Tony will walk you through our plans. Next slide, please. Jemperli has indeed been shown to have clinical benefit in other dMMR-driven tumors, such as rectal cancer. Recent ASCO data from a supported collaborative study with Dr. Cercek from MSK show unprecedented 100% complete clinical response in the 42 patients treated with Jemperli monotherapy. These responses are durable with no evidence of progression. Data from this study provide continued confidence in our AZUR program in colorectal cancer. AZUR-1 explores Jemperli monotherapy in locally advanced, unresected setting for dMMR rectal cancer. The study is designed to inform if Jemperli monotherapy could potentially replace chemo and surgery as a standard of care. AZUR-2 explores Jemperli monotherapy in a perioperative setting for dMMR colon cancer. This study also lends to Jemperli potentially replacing chemo as a standard of care. Data from AZUR 1 and AZUR 2 are expected beyond 2026, contributing to the more than GBP 2 billion asset ambition for Jemperli. Let's hear more from Dr. Cercek on the unprecedented findings, serving as the foundation for Jemperli development in colorectal cancer. The idea of the study was to see if we could use dostarlimab alone to potentially replace all three treatments that were considered standard of care, so chemotherapy, radiation, and surgery. We now have 42 consecutive patients treated with dostarlimab that have had a clinical complete response. So every single person that we've treated, the tumors disappeared completely with just six months of dostarlimab. Maybe even the more exciting part of the presentation this year is that we're reporting the durability of responses. And so now we have 24 patients who have had a complete response for more than a year after completing treatment. It's really never been seen before, where just one biomarker, mismatch repair deficiency, and one drug, dostarlimab, really leads to these types of responses. So the potential of dostarlimab in mismatch repair deficient early stage rectal cancer for our patients is huge. Standard treatments would have significantly altered their quality of life: infertility, sexual dysfunction, bowel and bladder dysfunction, potential for permanent colostomy. None of our patients on trial have needed any of those interventions. This data has really contributed to the AZUR program. Both the AZUR-1 and AZUR-2 are based on the efficacy of dostarlimab in early-stage mismatch repair-deficient colon and rectal cancer. The most impressive thing here on behalf of GSK is that this study is designed thoughtfully based on our trial, thinking about the patients and the patient outcomes with an endpoint of a clinical complete response, and not simply taking patients to surgery because that gets you the answer right away, and that shows how good the drug works. I think for science, it's incredible and it's rewarding, and it's amazing to see these types of responses, but for the patients, it's absolutely life-changing. These are truly impressive data, and we hope that patients continue to benefit from Jemperli monotherapy. Beyond dMMR tumors, Jemperli is also being investigated in locally advanced head and neck cancer. J three is a phase III trial that builds on development lessons in head and neck cancer, and explores Jemperli monotherapy as a new standard of care in a post-chemoradiotherapy setting. Two notable trial design elements are important here. Firstly, the selection of a specific, newly diagnosed and treatment-naive patient population, and secondly, a post-cisplatin-based CRT setting, allowing optimal potential for PD-L1 benefit. Jemperli is additionally being studied in non-small cell lung cancer combination with Belrestatug. The phase III program span for Belrestatug was gated and dependent on preliminary interim efficacy and safety data from the phase II GALAXIES study. Consistent with the recent iTeos disclosure, interim analysis from this study found that the combination of Jemperli and belrestatug exceeded predefined efficacy criteria with clinically meaningful tumor reduction at each dose. Data also indicated an acceptable safety profile. We expect to present these data in the second half of 2024. As such, GSK and iTeos will imminently initiate the phase III GALAXIES Lung 301 study in previously untreated PD-L1 high current or former smokers with locally advanced, unresectable or metastatic non-small cell lung cancer. This is the first registrational study for the belrestatug/Jemperli combination. Several elements provide confidence in belrestatug in this competitive setting. These are the molecule's optimized Fc engagement, greater potency, clinically proven T-reg depletion, and the proven anti-PD-1 profile of dostarlimab, as evidenced in our PERLA trial. Please turn to the next slide. In summary, our Jemperli development program spans multiple solid tumors as either monotherapy or as combination backbone, where we envisage differentiated outcomes relative to the class. We are confident in Jemperli as an IO backbone, and we'll develop Jemperli proprietary combinations across our portfolio. Moving now to ADCs on the next slide. Please turn to the next slide. GSK584 is our ADC with best-in-class potential in gynecological malignancies. B7-H4 protein is highly expressed across these malignancies and serves as a key immune checkpoint. Hanso presented clinical data at ESMO in 2023, showing an ORR of 33% and 27% at two different doses in triple-negative breast cancer patients in China for this molecule. GSK will develop 584 in novel combinations with proof of concept studies initiating later this year. Please turn to the next slide. GSK 227, targeting B7-H3, is our second in-licensed ADC from Hansoh. Antigen expression is broad across numerous tumors with high unmet need and presents exciting development opportunities. Clinical activity disclosed at ASCO in 2023 in small cell lung cancer patients shows a 63.6% ORR for this molecule. This broad clinical activity provides confidence in monotherapy use in relapsed and refractory disease, as well as combinations in earlier settings, particularly with dostarlimab. We believe that 227 has the potential to be first to market in several solid tumors. Now, handing back to Luke to conclude on slide 56. Next slide, please. To conclude, this slide shows peak sales potential for key assets and the material contribution oncology can have to GSK even before we add, we hope, the relaunch of Blenrep. Ojjaara continues to deliver strong performance, with physicians indicating a switch to Ojjaara treatment within the next six months, and we'll continue with geographic expansion in the near term. Jemperli is a critical backbone of our immuno-oncology development programs and further growth in endometrial cancer, with pending regulatory decisions and development beyond dMMR-driven tumors will drive growth. Belrestatug, our TIGIT inhibitor, and nilistatug, our CD96 inhibitor, and our PVRIG inhibitor can also contribute with doublet and triplet combinations focused in non-small cell and head and neck. We will also initiate GSK-sponsored clinical trials for our two ADCs, GSK 227, which is the asset targeting B7-H3, and GSK 584, which is the one targeting B7-H4. Our clinical development programs will combine each ADC with proprietary combinations with enormous potential. Finally, Dr. Terpos walked us through the impactful Blenrep data to showcase this important medicine and its potential to benefit patients significantly. And, we've excluded Blenrep from our long-term ambitions, but it clearly represents a significant upside opportunity for us, and we look forward to keeping you, updated on the progress of this asset. Turning to the last slide. As a reminder, here are the forthcoming catalysts that you should monitor to track our progress. Overall, we're very confident in delivering our three core disease areas in oncology, hematology, gynecologic cancers, and emerging tumor types, whether they're through the antibody-drug conjugates, immunotherapy, or targeted small molecule modalities. These medicines will significantly contribute to the delivery of our long-term ambition and continued momentum. So with that, thank you. We'll go back to Nick, and we'll open up to Q&A. Thanks, Luke. So as we move into the broader Q&A session with the team, I just want to remind everyone, if you wanna ask a question on Zoom, please raise your hand using the icon in the menu bar, and then we'll open your line, so that you can ask a question. If you did join Zoom using the telephone, please press star nine to register a question and star six to unmute. But can I also please ask everyone just to limit questions to one to two in the first instances, just to be fair to all participants? So thanks in advance for that, and we're gonna take our first question, please, from Mark Purcell at Morgan Stanley. So over to you, please, Mark. Yeah, thank you very much, Nick, and thank you for hosting the meeting. So just two questions. The first one, could you help us understand the competitive landscape for BCMA-targeted medicines? There are a number of other approaches out there, which I guess you highlight in the slides, but if you can compare any other ADCs in development, but also CARs, bispecifics, et cetera, and just provide some color where Blenrep sits relative to those. And then secondly, in terms of the greater than GBP 3 billion peak sales potential and risk-adjusted for Blenrep, can you help us understand how significant the second line setting in isolation is related to the first line ambitions? Thanks very much. Thanks, Mark, and good afternoon. So I think, on the first question, if we can go to Nina to cover the competitive landscape, and then I'll comment on the three billion plus ambition. Yeah, sure. Just checking if you can hear me okay? We can, Nina. Yeah. Yeah. Perfect. Okay, I will start. I would also probably ask Dr. Terpos, I think he's on the call, to add his perspective. From the landscape perspective, I think this is something that we continue to remind people. For U.S. specific, majority of the patients, about 70% of all the patients, are treated in the community setting. And this is, Mark, where your question is relevant comparing to other BCMA agents. So if we look at bispecifics, and particularly CAR Ts, these are agents or assets that are administered in the hospital setting, largely in the academic centers, both because of the administration, but also because of the management of adverse events. So that's the first part of the question. How does it compete? Keep in mind, community setting, physicians, it's communities, physicians who like to treat their, keep their patients. These are second line, relapse patients who do not prefer to be sent or spend significant amount of time in the, in the hospital, and then particularly are not very keen on managing those adverse events, through, you know, delivering the drugs or supportive care that requires hospitalizations. That's just on the convenience. On the efficacy, we have seen the data for CAR Ts and in second-line setting. For bispecifics, we have still—we still haven't seen the data in second line, so we will need to see where it goes. But comparing the efficacy of Blenrep versus CAR Ts, we are actually not too far. And then once we see the bispecifics, we will see if the efficacy that they deliver is going to be worth the process of hospital administration, significant infection risk, and management of other adverse events that, again, requires hospitalizations. I don't know if Dr. Terpos wants to add something as well from his own experience. I don't know if you hear me also. We can, Dr. Terpos. Okay. Very clearly. So the anti-BCMA treatment seems to be the fourth pillar of multiple myeloma therapy. For patients who have been exposed to both daratumumab and lenalidomide upfront, which is the vast majority of patients in both the U.S. and Europe, we can say that in second line, we don't have a lot of available options. For example, for now, if we talk for now, what it is available, not off-label, of course, what it is available in Europe, for example, for a patient who progressed on daratumumab and lenalidomide in the MAIA regimen, then you can see that the only, the only reimbursed, let's say, regimens, includes the old-fashioned pom VD, Sel-Vd, KD, and only in a very, very few countries, including, in my opinion, only Germany and, with specific, let's say, specifications in Switzerland and Austria, the cilta-cel can be given. So I think that we have an unmet need here, and the two studies, especially that of the belantamab with pomalidomide and dexamethasone, seems to cover this unmet need. Just to let you know that, especially in Europe, the cilta-cel is available in a vast minority of the patients who are eligible to receive it, even in countries like Germany, that is the most in use in Europe country for cilta-cel. And from what I've heard, the vast majority of patients also in the United States do not have the possibility to have the CAR T, because they are treated in the outside of academic centers. This is the one thing, but on the other hand, even if you see the efficacy, as Nina mentioned, of the belantamab and you compare it with the cilta-cel, which is the second line option that can be given to the patient, it's not far away. On the other hand, it is much more convenient. It can be given to intermediate fit and frail patients. That definitely is the majority of patients with myeloma. We have not to forget what is the median age of myeloma at diagnosis. In our center, for example, 69 years. In other countries, it's 71 or 72. So the standard myeloma patient at first relapse is not the patient that we see several times in clinical studies. So definitely is not 62 years of age or 64 years of age, is much, let's say, more elderly and, not eligible for receiving a CAR T in the vast majority of cases, not only because of age, but mainly because of comorbidities and frailty. So I believe that the both combinations will give the opportunity to our patients to have very good therapies. Bela-Vd has given the best efficacy in patients who have been exposed and are refractory to Lenalidomide, and also Bela-pom-dex, to me, offer a special attention for patients who have been given their tumor Lenalidomide, especially for those who are refractory to one or both of these agents. I don't say anything about the BiTE, because I want to talk about evidence. I am one of the authors of the guidelines of EHA, for example, for the treatment in myeloma, so I want to talk only based on evidence. We have no data at all for the patients of one to three prior lines of therapy with bispecific targeting BCMA. Although I have to say that, from the some of the data that are reported during ASCO and EHA for first line therapy, seems not to be, to me, extremely encouraging, especially for the side effect and the safety profile, and especially the infection rate. Thanks, Dr. Terpos. And Mark, I'll just cover your second question very quickly. Look, I think you should see that GBP 3 billion plus that we communicated a couple of years ago as a base. The bulk of that is the second line setting, and I think what hopefully is coming very clear to you from the experience that Dr. Terpos has discussed and Nina's answer, the analog that we're looking at is CD38, Darzalex, in that second line setting. So you can start to model the scale there. Of course, it's always subject to regulatory interactions and the ultimate first line design that we go through. Next question, please. Thanks, Mark. Thanks. Our next question is going to come from James Gordon at JP Morgan. James, over to you. Hello, James Gordon, JP Morgan. Thanks for taking my two questions. First question was Blenrep, and just noting you've reintroduced the peak sales forecast, but it isn't yet part of the guidance, even though the guidance does include some assets that are quite a lot earlier. So just why is that? Or when might you have the confidence to add it back in? Is it that you still need more mature OS from DREAMM-8 or more tolerability or something like that? Why being a bit more cautious than some of the other assets, where we seem to have quite a lot less data, but that seem less deepest? The second question was, IO in lung and competition from other approaches, so clearly bullish on TIGIT, but how does this compare in terms of your excitement to other approaches, both your own and competitor approaches? So I know, for instance, you've got a TIM-3, I think, reports next year, that wasn't on the guide or catalyst list. And there's also other people doing TIGITs, not just monotherapies, but like bispecific or even bispecific TIGITs combined with Trop-2 ADCs. So could it be that TIGIT's a good approach, but actually a bispecific approach is better, or even combining a bispecific with a Trop-2 ADC, could be even more efficacious? Sure, James, thanks. I mean, I think on the first question, essentially, we want to have a few more regulatory interactions, but I hope you, you get the sense, the amount of time that we've allocated, the thoughtfulness that we have spent around how to manage the, the benefit, risk of Blenrep. So we'll update in the future, all in good time. Hesham, maybe you could cover James' second question, please. Yeah, no, happy to do that. And James, thank you very much for the thoughtful question. I think probably first and foremost, it's important to highlight that we have a number of different immuno-oncology assets that we're currently evaluating or assessing across different tumor types. And you touched on, of course, TIGIT, but also dostarlimab, which is, which is our PD-1 inhibitor, and then, of course, TIM-3 cobolimab, as well. With that in mind, I'd also like to highlight that there's two other assets in that CD226 axis beyond TIGIT, which includes CD96, but also, of course, ... So TIGIT, CD96, and PVRIG as well, as well, too. With that in mind, what I would like to highlight is for TIGIT, it is probably when compared to other assets, it is a bit more unique. Of course, it's FC enabled. That's one. Two, we're actually looking at, of course, in this instance, combining it with a PD-1 inhibitor, dostarlimab, which we've actually benchmarked quite well to other leading PD-1s in the class. You may recall, of course, we had the phase II data from the PERLA study. This was a head-to-head study of dostarlimab plus chemotherapy versus pembro plus chemotherapy in first-line non-small cell lung cancer. And it actually demonstrated what appeared to be similar levels of clinical activity in the context of response rates, but also encouraging trends for key secondary endpoints that include progression-free survival and an overall survival as well, too, and the data was previously presented at ESMO most recently in 2023. With that in mind as well too, we feel that, of course, having this certainly TIGIT that is FC enabled, a really strong PD-1 backbone, and then, of course, some preliminary data that's emerging from our phase II platform study, where we've actually looked to explore different dose levels of TIGIT, specifically three different dose levels as well too, relative to the benchmark of a PD-1 inhibitor, our own dostarlimab, which again has behaved performed consistently as pembrolizumab, that at certainly at least at this stage the data is encouraging. It warrants us moving forward with a phase III investment. But beyond that, we're also thinking more holistically across our portfolio. So, you may have heard from the presentation that we also have access to now our own B7-H3 antibody drug conjugate. B7-H3 is expressed in non-small cell lung cancer, and we expect to actually be evaluating that as part of different combination regimens. So you talked about the role of TROP-2 ADCs may have to play in lung. I think B7-H3 will also be a key asset in that capacity as well, too. And we'll actually be looking to combine it with our TIGIT and our PD-1 inhibitor as well. Looking at that relative to, for example, what other competitors may be considering or evaluating as well. TIM-3, we're really positioning, of course, in this post-IO setting. So we have our ongoing phase III study, which is called COSTAR, looking at the combination of dostarlimab plus cobolimab plus docetaxel versus docetaxel plus dostarlimab versus docetaxel. It's a 3-arm study. It initially began as a phase II/III trial, graduated from phase II into phase III, based on some pre-specified thresholds for clinical activity that were met on certain key surrogate endpoints, and the phase III study is currently ongoing. Again, you may be aware, of course, that TIM-3 is expressed in non-small cell lung cancer and certainly is a key primary resistance mechanism to checkpoint blockade and specifically PD-1. We think the rationale makes, you know, makes sense from that perspective, and we know that the study graduated from phase II to phase III because it met some of the key, at least, efficacy criteria at that time, at that time point. All in all, what I would say is, we're looking at different ways to at least evaluate, assess a number of different agents that we have across our portfolio. They include different IO assets. They include sequencing. They include combinations with other therapeutic modalities, such as antibody-drug conjugates, and may include potentially looking at earlier stages of disease. Again, all based on data as it continues to emerge, and outcomes, as well, at that point in time. Thanks, Hesham. And I think, James, you've seen with the approach on TIGIT, internally, that we're very disciplined in terms... and, and Hesham made this point several times, very disciplined in terms of looking at the clinical profile and the evidence before moving, but when we do make a decision to move, we're gonna move in a very focused way, but we're gonna move with speed, when we see what we like. Next, next question, please, Nick. Our next question is gonna be from Matt Weston at UBS. Matt, over to you, please. Thanks very much, Nick. Two questions, please. The first is on DREAMM-10, and now, based on the readout using MRD, approximately when would you expect we'll see a readout of that trial? And then my second question is to Dr. Terpos, and it's about sequencing of drugs. So we now have some great data from Blenrep in second line from DREAMM-7 and DREAMM-8, and now the proposal is to take Blenrep into the front line. But really, we've got no idea what to do with a Blenrep patient after it's been used in the front-line setting. So as a clinician, I'd be really interested as to whether or not, if it were positive in front line, you'd be prepared to use the drug, not knowing what to use next, or whether really we should wait for overall survival data from DREAMM-10 before we can really understand the sequencing benefit of Blenrep in the earliest line? Matt, we just lost you. You still there? Am I back? Can you hear me? I can hear you. I think we've got... Yeah, I think we've got color. Dr. Terpos, I think what Matt was saying is- Yeah, I heard Matt. The options for the BCMA target. Yep. Great. Over to you, and then we'll come to you, Hesham. Over to you, Dr. Terpos. Can I, can I start? Okay. Yes, please do. Matt, you are right that if and the BCMA agent, especially belantamab, is approved in the first line, we don't know exactly what would be the sequencing, but what we discussed previously, exactly is happening in the treatment of myeloma. All the drugs are approved in that way. They are going first to the 1,000% unmet need, which is the very end of myeloma. Then they go to the early relapses, one to three prior lines of therapy, and then they go to first line. See what we are talking about today, we are talking for patients who are refractory to daratumumab first line, and the options that I offered, or at least the options that are offered to physicians, include, outside of the U.S., mainly POMVYD, the OPTIMIST study that included no patient who had been exposed, not only refractory, had been exposed to dara. CELVD, no patient, I think it's 11 patients who had been exposed to dara in the CELVD arm. KD, no patient had been exposed to Dara. And of course, we have also the cilta-cel that has now been approved and includes mainly lenalidomide refractory patients and very few who were exposed to dara. So it is difficult. And now we are having the first, let's say, very good regimen, like Bela-Pom-Dex, which to me it would be the second-line therapy outside of cilta-cel, when it's going to be available, and it's going to be for a minority of my patients. Bela-Pom-Dex, which is going to be for these patients, and there are data for this specific patient. So unfortunately, it is the same with all the drugs. You see that the T-cell engagers were licensed in the very end, myeloma, after the fourth line of therapy, and now they, we are having studies in first line. So what's going to happen next after them? We will, we will be obliged to have either the older, regimens, dara or isatuximab-based therapies, or the CAR Ts or the bites, while we know, for example, that the CAR Ts are not, are not doing so well after BCMA, but this happens at the very end. Will it be the same if we give belantamab upfront, using it every two or three months, and then to give cilta-cel second line? We don't know if the results will be, similar to, belantamab, in two plus refractory patients and cilta-cel after. So your question is extremely important, but I don't think that there will be any physicians who can give you an answer, because unfortunately, what you described is exactly what we are facing in our clinical practice, where all the drugs are first approved in the very late myeloma and then go slowly to one to three prior lines of therapy and then to first line. And at the time that they are approved at first line, the available options at second line, all these data are based on studies that they have not had any patients who have been exposed to the drug that now is in first line. I don't know if I've... I tried to answer your question. I know how difficult it is. We don't have any data. The data that we have in the very end stage myeloma, I don't think that they will be confirmed in the first or second line. So, then every time we need to create new data for what's happening with a specific combination after a new approved indication. Thanks, Dr. Terpos. Hesham, DREAMM-10, please. Yes, no, absolutely. And if it's okay, maybe we'll just to kind of touch on what Dr. Terpos was highlighting as well, too, in the question early on, you know, should we wait for survival data before, you know, before we start moving drugs into frontline? Well, what's interesting is probably, as we look at the existing data for CAR-Ts in second line, we haven't necessarily seen neither of the CAR-Ts actually demonstrate a statistically significant improvement in overall survival. What we have seen, at least in DREAMM-7, is a very narrow miss to demonstrate stat sig OS at the time of the interim PFS analysis, which was positive, of course. So the narrow miss was by 0.00012. And so we feel very confident that at the time of the next pre-specified interim OS analysis for DREAMM-7, we'll be able to demonstrate a statistically significant OS benefit. So that's the first point. The second, of course, for DREAMM-8, you see the hazard ratio is 0.77. I expect that to actually get better over time, especially given the duration of response that this drug can demonstrate, lenalidomide, that is. And so with more maturity of data and more follow-up, I think you'll see that change over time as well, too. Getting back to the question around DREAMM-10, I think everyone's well aware, of course, that there's been a recent advisory committee meeting that was held and convened by the FDA in the U.S., whereby there was overwhelming support, of course, for the adoption, the use of, MRD negativity as a surrogate endpoint in multiple myeloma. So with that in mind, and with the data and the meta-analysis that were generated, on the correlation of MRD to long-term outcomes, we're planning on incorporating this as a co-primary or a dual primary endpoint, in DREAMM-10, so both MRD negativity and as well, PFS. I think I would probably also call everyone's attention to the data that Dr. Terpos presented during the presentation, which actually showed, at least both in DREAMM-7 and DREAMM-8. In DREAMM-7, more than a twofold increase in MRD negativity rates, and then in DREAMM-8, actually a fivefold increase in MRD negativity rates. So that certainly gives us a lot of confidence, hope, as we think about DREAMM-10 and the potential for demonstrating that type of improvement. Now, again, I'd just like to highlight two things. One is, we're gonna continue, of course, to progress with our current filing plans globally for the second-line indications, including DREAMM-7 and 8. As Luke had alluded to in the presentation, those filings are planned for the second half of this year, and we will have filed in all major markets, regions by the end of the year as well. Of course, we've been in ongoing dialogue with health authorities, regulators, and we'll continue to at least get additional updates as we move into, of course, the latter part of this year. And that will certainly also continue to support our evaluation, our assessment of DREAMM, of DREAMM-10. In terms of timings for MRD negativity and when it could potentially read out, again, these are all, of course, time to event and really depend on extent of follow-up. But what I would say is maybe there is a range, you know, in the year of, probably in the, in the possibility of 2.5-three years that we could be looking at. So by late 2027 or 2028, but again, we'd have to look at and assess and evaluate where the thresholds are set for demonstrating and making a meaningful improvement in MRD negativity. Right. Thanks, Hesham. Nick, next question, please. Yeah, so our next question is going to come from Peter Verdult at Citi. Over to you please, Peter. Thanks. Peter Verdult from Citi. Just a few questions, please. Just to follow on Matt's question about timelines. I think, Hesham, at ASCO, you said three years. So we're looking at probably a launch of 2028, 2029. Could you remind us the IP situation on Blenrep, given the false start we've had so far? When do you expect, or what does GSK view the timelines in terms of major LOEs? And then just for Dr. Terpos and maybe the GSK team themselves, I mean, the discussants at ASCO were almost saying less is more and urging the company to almost explore lower doses, given how durable the responses have been. And although you've ameliorated the ocular tox, it still bothers them. So I'll be interested in Dr. Terpos' view about, you know, exploring, you know, longer dosing intervals, lower doses still, whether there's any appetite to do that at GSK. And then one cheeky follow-up, just for Tony on the ADCs. I mean, it was clearly a massive theme at ASCO. There's now hundreds in development. B7-H4 and B7-H3 are clearly hot targets. Every man, woman, and dog seems to have one. So can you help just triangulate for us whether you feel you're in the vanguard on these ADC targets or the rear guard? And is there any indications where GSK could be first to market? Thank you. Thanks, Pete. I'll answer your first question very quickly. 2032 for the primary patent in the U.S., the primary patent. Dr. Terpos, if we can turn to you, and then once you've concluded, Tony, I'll hand it over to you. Thank you, Peter. I think that what you mentioned is what I'm investigated. I mean, in the first-line therapy, as you have seen, my study in combination with lenalidomide and dexamethasone, I checked lower doses like 1.4 and 1.9 mg per kg, given every eight weeks, as well as the standard dose of 2.5 mg per kg, but again, every eight weeks. So we start with that, and we have now 66 patients with a median follow-up of more than 24 months. I can tell you that we had only one progression. And the majority, if not all the patients, if I am correct, now all the patients receiving now 1.9 mg per kg every 12 weeks, so every three months, which... And the efficacy is extremely good. All patients have responded to treatment. Of course, we talk about newly diagnosed patients, but I have to tell you that all my patients in this study have intermediate fit or frail, according to the IMWG Frailty Score. So they are patients that, I mean, they are really, they are not the fit ones. So we have extremely good results, suggesting that the drug is very well tolerated. The ocular problems that we have with this schedule is very low, and the efficacy is very high. I think that based on some of the preliminary data that I had, GSK used a different schedule in the DREAMM-8 that, to me, it was extremely important, starting from a higher dose, 2.5 mg/kg, and then to 1.9 mg/kg after the second cycle. So they lowered immediately the dose, and they give it every four weeks instead of every three weeks in the DREAMM-7, because they have recognized early that the efficacy probably is the same, given the drug every four weeks or even every eight weeks, because a good number of patients, I'm not in the position to say how many of them, in the DREAMM-8, are in the every eight-week schedule, and the efficacy is very good. So I believe that it is a very efficacious drug. One thing also that has not been published yet, but I can tell you from the analysis that we've seen, is that the higher the dose, the higher the ocular toxicity, the higher probably the response rate. I think for the relapsed refractory setting, I like this schedule of starting with a 2.5 milligram per kilogram, and then to immediately go and lower the dose to 1.9 every four weeks, and then to go from the 1.9 every eight weeks if the patient has ocular toxicity. I believe that, Peter, you have right, that in the real world, I believe that the majority of the relapsed refractory patients are going to have, after an initial dose, having the drug every eight weeks, for example, if it is with Pomdex, or every six weeks, if it is with Velcade and Dexamethasone. In the real world, the drug is going to be given every two or three months, offering very good results to these patients. Helpful. Tony? Yeah. Thanks, Dr. Terpos. Yeah, can you hear me? Yep, clearly. Great, thank you. So, just to sort of headline, as far as the two ADCs are concerned, I'd say- ... in the context of H4, very much competitive in the and in the leading pack. For H3, as Luke mentioned earlier, what we're focusing on there is generating differentiated data through the platform studies, and then when we have those data in hand, moving aggressively and quickly recognizing the competitive environment. A couple of things to stress on top of that. Obviously, unlikely that these agents will be administered in the context of a regimen outside of immunotherapy, and we're very competitive in the PD-1 and TIGIT spaces, as you've already heard, and having individual assets which will allow dose titration to achieve optimal effects there, as well as potentially optimized profiles, and of course, the growing position and understanding of Jemperli as a backbone therapy, not only in gynecological cancers, but in lung. Probably the other thing to sort of emphasize, since you asked the question of me, is, of course, we'll continue to allocate capital across the portfolio in terms of the principles that you've heard before from Luke and myself, and that is very much focusing on return on investment and the potential to drive long-term growth. So I think we're in great shape. We're certainly in a good position, and the decisions we'll take will be on the basis of differentiated data in the context of platform and building out on the strength of position we've got in gynecological cancers. Thank you. Thanks, Tony. Hesham, did you want to add anything? Just a quick build on what Tony highlighted as well, too. I think first and foremost, I would just highlight that one of the elements, of course, that's really important for antibody drug conjugates is really the not only the target, but the linker and the payload. And one of the things that we've done, at least in terms of looking at B7-H3 and B7-H4, is evaluate and assess you know, our belief in the behavior of the platform itself that we've gotten access to now through Hanso. And we believe that it behaves very consistently with the leading platforms in the likes of Daiichi Sankyo. So that's one. Two, actually combinations. Combinations are gonna be really important. They're gonna be very critical for the development of these types of ADCs, and certainly, that includes combinations with in-house assets like dostarlimab, PD-1, combinations with other targeted therapies that may synergize with the topoisomerase warhead. And those might include other agents that target DNA damage response. And then three, of course, existing standard of care. And then three, I would say we've built capabilities. You know, we've recruited a lot of great talent that has had experience with antibody drug conjugates, whether it be Daiichi, whether it be at AstraZeneca, or other certainly big biopharma, but then also moving with pace. Moving with pace, and continuing to assess any potential opportunities as they emerge. And then finally, what I would say is, strategy matters. I think if everyone recalls, of course, what happened with the PD-1, PD-L1 class, it wasn't always about being first. It's the right strategy, the right development strategy, the right tumor types, the right combinations, the right approach, and the right patient segments and biomarkers, that will be really critical to the success of antibody drug conjugates. So I just wanna, you know, highlight that, and then, and then just say that, stay tuned. Stay tuned. I think for anyone that knows me, knows that, you know, I do, I do try to just, you know, note things, and, and then, and then you guys can look at them in hindsight and, and reflect on whether or not I was, I was right or wrong. Thanks, Hesham. Mm-hmm. I have to say, some days when I come to work, I think I might have walked into my old Swiss employer or another U.K. company where I spent some time. So, but I think critically, we've been able to assemble a group of people on the back of this collection of products, as Hesham has said, that have a track record in picking opportunities, and there's a recognition that operating in oncology is different. Again, the theme of focus, discipline, and speed, and that balance is something that we are very quick to emphasize. And again, it's just the tip of the iceberg with the people that you see on the call today, in terms of the people that we've been able to assemble to support these assets. So that's very, very exciting. Shall we go to the next question? Nick, please. Tony, did you... I might have heard, misheard you, Tony. Did you say something? Yeah, just one very quick comment to cap off on Hesham's point there. We've also built significant manufacturing capability associated with Blenrep, and that's gonna be an important aspect of indication expansion in this area. Absolutely. Thanks, Tony. Thanks, guys. Okay, so Emmanuel Papadakis at Deutsche Bank, over to you, please. Thanks for taking the question. Maybe, question on Blenrep, just you thinking about the sophisticated complexity of Dr. Terpos's answer on the dosing algorithm. You know, one of the virtues of Blenrep's applicability is its ease of use in the community setting. Presumably, you need a well-defined dosing algorithm to avoid community docs getting lost on complexities and worrying about trading off efficacy for safety. So if DREAMM-7 and 8 are approved, what are you expecting to be labeled in terms of how they manage dose levels and frequency? And then in DREAMM-10, what are you planning to actually use as the dose regimen? And a quick one on Dara, you don't seem to have any additional clinical development plans. Are you planning or considering a combination study? How much of an impact do you think that's gonna have on the treatment landscape in the front line if that combination is approved? Thank you. Thanks, Emmanuel. I think, Hesham, if we can cover the expected label, and there's probably a link question to that that will come up, which is pricing. One of the, I guess, the positives of withdrawal is that we can reset pricing in the U.S. and Europe, so we'll need to think through that, but it's a nice problem to have. So, Hesham, over to you for dosing expected label. ... Yeah. No, thank you very much, Luke. Manuel, good question. What I would start out with and say is that I think what we've probably seen, at least from some of the additional analyses that, you know, we continue to generate, is it's really important to start with the 2.5 milligram dose. So, you know, that, that is really important and critical, especially in the context of a second line setting, where patients are coming in, they have existing disease, and getting that depth of response early on, for the first one to two cycles is quite important. With that in mind, I think everyone's well aware, of course, that the drug was used at a 2.5 milligram every 3-week schedule, at least per protocol, within both studies. So I think that will be probably the starting point, right? But there are also toxicity management guidelines that were implemented in each study as well, too. And we're hoping, of course, that, you know, at least as we engage the regulators, and we share, you know, the data, of course, within our submission, that being able to manage each individual patient based on those toxicity management guidelines and using the, dose reductions, the interruptions, as a, as a means of, of guidance, will be important. This is not new. It's not new to Blenrep, it's not new in oncology. It's been done across multiple assets before, where you dose each individual patient based on their level of tolerability to the drug, and you use, of course, the side effects that they're experiencing as a means of actually titrating the dose down, delaying it, and so forth. So again, you know, based on some of the data that, you know, that we're seeing within the study, I think, and you've probably heard from the patient as well, too, you know, dosing it every, you know, six weeks, dosing it every eight weeks, those are things certainly, again, guided by the individual patient, you know, experience, are things to think about or consider in that context. Thanks, Hesham. And Nina, if you could just cover the LCM thoughts for Ojjaara quickly, and then we'll go to the next question. Yes, definitely. So when we licensed the asset, we actually had some plans for combination therapies and, you know, combination assets that have been in development in myelofibrosis. Unfortunately, as for the last 10 years, it has been a graveyard of drug development, and many of those potential partners fell off. So, Navitoclax is not a candidate anymore. We still have to see what's going to happen with the BET inhibitor, with Pelabresib. Is this going to cross the regulatory line or not? If it does, there potentially is a space for the combination because both Ruxolitinib and Pelabresib are myelosuppressive, so potentially causing even more anemia and thrombocytopenia than the individual agents on their own, and Momelotinib would be a very good combination partner, but we first need to see what happens with Pelabresib. Beyond myelofibrosis, we are looking at additional indications where Momelotinib could have a very interesting role, and the mode of action would fit that gap. But we will announce once we initiate those studies, we will start talking about it at that point. Super. Thanks, Nina. Nick? So we're gonna take our next question from Graham Parry at Bank of America. So Graham, over to you. Great. Thanks for your question. So, quick question on DREAMM-10. It looks from the side that that's powered for superiority. I just wondered, is there a non-inferiority test in the design there, or is that just gonna be a straight shootout, where you need to show superiority? And then secondly, just regarding the opportunity for Blenrep, most KOL feedback has been that they would prefer CAR T if it's available in a large treatment center, but to your point, 70% of patients are out in the community setting. So could you just talk there to the practical management of liaising with ophthalmologists for managing the eye toxicity? And within that setting, do you still think it's gonna be more frail patients that would be getting this? So perhaps just help sort of narrow down that target population even more, roughly what percentage of of the second-line myeloma patients we're talking about there. Thank you. Great. Thanks. Thanks, Graham. Hesham, if you could please take the DREAMM-10, and then, Nina, you've done a lot of work in terms of the pathways in the U.S. And then, Graham, if I could just add, if you cover that, Graham, I might just build on your question. If we could ask Dr. Terpos at the end, if you had a patient in front of you that you were looking to initiate on this treatment and they raised ocular complications, would you- how would you explain that in layman's language to that individual around your treatment strategy and how you're gonna manage that? So Hesham, you first, then Nina, and then if we could ask Dr. Terpos. Yep. No, happy to. Thank you, Luke. So, so first and foremost, just in terms of what the potential design of DREAMM-10 could look like from a statistical analysis perspective, I would just start off by saying it's been great to see, of course, the emergence of a number of different therapeutic modalities recently, in multiple myeloma for patients. That is important. I think we have to acknowledge that just in terms of providing treatment options. But, but with that in mind, in order to continue to move the field forward, we have to also take into account that, you know, we need to provide at least potential therapeutic options that actually provide patients with a step change in treatment outcomes, and the potential for, you know, better therapeutic benefits. So if anything, the DREAMM-10 study design will be directly certainly looking at or focusing on demonstrating superiority to an existing standard of care regimen in frontline multiple myeloma. I think the DREAMM-7 data give us a lot of confidence in that. I think if you look at all of the different outcomes in the study, whether it be the primary outcome of the study, PFS, with a median of a little over 36 months versus 13 months on the Daratumumab-based arm. If you look at the key secondary outcomes, duration of response, depth of response, and certainly also, of course, overall survival, which is still preliminary at this point in time. They all give us a lot of confidence in what the DREAMM-10 outcome could look like, but more specifically, of course, in demonstrating superiority in that regard. And we have to, you know, certainly acknowledge that, you know, as you look at the number of different, at least existing therapeutic modalities that are available to patients that target BCMA, some have limitations, you know, in terms of their side effect profile. You know, we've talked about, you know, of course, the CAR-Ts, the potential for risk of early death, especially with bridging therapies, and so forth, and there was even an advisory committee meeting that was held around that for both for both assets. We see the infection rates, Nina spoke to those as well too, with bispecifics. Both, of course, require hospitalization and they're not available to patients in the community setting. So that's actually where 70%-80% of multiple myeloma patients go, and hence, that's where the unmet need currently exists as well, too. And of course, that's beyond, you know, what Tony highlighted around the investments that we're making in manufacturing, where we have, of course, CAR-Ts limited by manufacturing and supply chain challenges as well, too. The other piece I just want to touch on was actually around the types of patients, and Dr. Terpos will touch on this better than I can, of course, but I would just like to highlight that we've seen it at ASCO, data on subgroups presented from DREAMM-7 and DREAMM-8. So if we wanted to talk about how this drug works or in which subgroup of patients this drug works, actually it works in everyone, you know. And thankfully, it's able to provide a benefit, meaningful benefit, to patients that are high risk, patients that are standard risk, patients with extramedullary disease, patients that, that have received prior lenalidomide, lenalidomide refractory, patients that have received prior dara in DREAMM-8 as well, too. And I think that's really important. There was one slide that Luke presented, during the presentation, that shows, which types of patients actually Blenrep would, would actually be, good for. Certainly, what you could see is probably all types of second-line patients, irrespective of number of prior lines of therapy, irrespective of risk, and irrespective of fitness as well, too. Thanks, Hersham. Nina, and then we'll come to Dr. Terpos. Yes, so very briefly, a lot will really depend on the label and the REMS, or no REMS, or REMS requirements. If you remember our first Blenrep launch in the U.S., the REMS requirement was quite stringent and challenging, definitely. So what will be the requirement in the end will determine to which extent and how physicians, hematologists need to engage with the eye care professional. Is it going to be ophthalmologists specifically, or it's going to be potentially optometrists? How frequently and for how many infusions that interaction needs to happen? All of that will be quite critical and will determine, you know, to which how much of a pain or effort physician will need to go through to initiate patient successfully. What we do know in the meantime, because now we are talking, you know, after having hundreds and thousands of patients treated versus three, four years ago when we launched, when it was dozens of patients of treated, is what we know is that, you know, no patient went blind, no patient lost their eyes, no patient died because of ocular adverse events, unlike many of the other therapies that you are talking about. And what we do know also is that many physicians, after treating, more than one patient, they start to recognize how to treat the patients, and they start to be able to manage those ocular eye-related side effects on their own. And I'm not sure that there is anyone better to describe that than Dr. Terpos, who has a lot of experience with that. I will ask him to also answer the question. Thanks, Dr. Terpos. Oh, yeah. Thank you. I think that you touch now one of the most important aspects of belamaf. I believe that the ocular toxicity, although as Nina mentioned, is something that cannot kill you or nobody was blinded because of belantamab mafodotin. It is a toxicity that may create some problems only when the patient hear that you may have some eye problems. So when you have a patient in front of you, because that was the question, you have to explain to him what he has to, let's say, to expect from belantamab, not only of the efficacy, of course, that we all know, it's very easy to understand, but also of the safety. And the ocular problems are not so severe in the majority of the patients. The majority of the patients may have a gritty eye, a sore eye, maybe some pain sometimes. But, I mainly focus on the number of patients, that they may have a problem in their daily activities. If the patient cannot read, cannot see the tablet or the smartphone, cannot drive, or they have problems in seeing television, especially at night, these are real, important problems. And that's why one of my main intention is to manage to make the drug ophthalmology free, let's say, if possible. And in order to do that, in our study, we have a randomization between the reduction and the handling of the drug based only in the ophthalmology assessment. In group B, we have both the ophthalmology assessment and the OSDI questionnaire, that the first five questions are describing symptoms, while the other four, they describe activities of daily living, like reading, watching the television, or reading the tablet and the smartphone, or driving. I can tell you that in the dose that we used in the newly diagnosed multiple myeloma, with the 1.9 milligram per kilogram every eight weeks, there was less than 5% of grade of more than four hours, as we say, during the last five days, problems in the daily activities. This is the time that you have to stop the drug and then to restart when this has totally recovered. I want to tell you that we have several patients with the ophthalmology grading two keratopathy, and they have almost no problems at all. And till now, we, according to this evaluation, we had to reduce or to stop the drug administration. So I believe that we will be very soon in a position that we can say that for the vast majority of the physicians, possibly for one, two or three cycles at the most, we may have an ophthalmology evaluation. Because the physicians needs to be secure for what they are doing, and then based on the questionnaire, we are going to provide a very good tool, the anamnestic tool, in order to drive the decisions. Don't forget that we had initially bortezomib, for example, many years before with the peripheral neuropathy, that we gave it twice per week, and then we ended up with once per week, and the patients had electromyograms and everything, going to neurologists for the peripheral neuropathy. And now, of course, this peripheral neuropathy is very well managed by the hematologist. And I believe that this is also one of my tasks, to provide the tool to the hematologist in order not to need the ophthalmologist, or at least to need it, to need the ophthalmologist very rarely. One more thing that I want to focus on is that, seeing more than now than 300 patients under belantamab, one, especially the newly diagnosed patients, we have seen that there is ophthalmology- ophthalmological problems in a very high frequency in these patients. And I talk about newly diagnosed, because someone can tell you that the relapsed refractory patients have received probably a lot of dexamethasone that created these problems, and this pro- main problem is cataract. So initially, I have seen that almost all my patients, I mean, the elderly patients, had cataract in the study, and I, I wanted to check, let's say, what is the incidence of cataract in the, in, in, in, the real, I mean, in the healthy individuals? We've seen that above the age of 70, it was like between 65%-75%, the majority of the epidemiological studies. The cataract is a problem because why it is a problem? Because with keratopathy Grade 1, if you have cataract Grade 1 or 2, you may have no problems. You have no blurred vision, nothing there. But if you have keratopathy Grade 1 in a cataract Grade 3 and 4, then you may have a blurred vision and reduction in your vision acuity. I think that this is something that we have to take into consideration when we talk about ophthalmological toxicity. The toxicity that the Blenrep is creating is reversible in more than 90% of the patients within one month of treatment. That's why giving the drug every eight weeks, for example, or even every six weeks after the initial, but then you can have very good results. Another thing, another important issue is that we are doing in our study in the newly diagnosed, but I didn't see it yet in the DREAMM-7 and DREAMM-8, is that when we describe the number of patients they have an event, especially an ocular adverse event, then even if the patient had a keratopathy of Grade 2 or 3, let's say, during the first cycle and never in the future, then this is described as one event. I would like to see what we are having in our newly diagnosed studies, the number of ophthalmology visits with problems. Then you can realize there that the number of patients who continue to have a problem, probably after one event, may be 0 after, or it may be extremely less. So, in order to conclude, I believe that we have an ophthalmic toxicity of belantamab mafodotin, which is totally manageable, is totally reversible, very fast, and that's why the administration every six to eight weeks is extremely easy to happen. And my task, one of my tasks now, is to provide an anamnestic tool to the physicians in order to make them ophthalmology free. And I believe that we will make it, and we will transform belantamab, like bortezomib, that the physicians can do it after some time, of course. They do all the reductions and the alterations in the administration of the drug by themselves. Fantastic. Thanks, Dr. Terpos. I think a very practical outline and something that's gonna be utilized by community-based physicians. Nick, go to the next question, please. Yeah. So we've got three questions left. I'm gonna come to Richard Parkes at BNP Paribas. Over to you, please. Hi, Richard. We don't have Richard. Maybe we come back to Richard, and we go to- Yeah, that's okay. So we'll take Navid Malik from TLSD. So, Navid, over to you, please. You're on mute at the moment, Navid, so you will need to unmute. Sorry. Yes, Navid Malik from The Life Sciences Division. Quick couple of questions. On Zejula, in unmethylated MGMT GBM patients, can you tell us, in the phase II study, how many IDH1 mutations there were in treatment versus the historical control? And I'm kind of intrigued as to why you're not necessarily looking, right now anyway, at the MGMT methylated patients who could be evaluated in a separate trial. And the second question on Blenrep. For intermittent and low dosing, do you think that there's a possibility, although I don't think this is seen right now, but is there a possibility you could introduce- ... some degree of resistance or refractory to lenalidomide, because you obviously are not giving the dose in a consistent way, you're taking the patients off once they see these ocular side effects. Sure. Thanks, Navid. I think on the MGMT un- or methylated population, Hesham, if you cover that, and then Dr. Terpos, if we can just come back to you in terms of your thoughts of this, again, this resistance question. Thanks, Navid. Well, yeah. Let me start out first just about the going after the unmethylated patient population, and specifically, of course, I think everyone's well aware that this is a an area of you know, key unmet medical need, and typically outcomes you know, tend to be even you know, even worse in terms of prognosis. So why did we evaluate this patient population? That's really the reason, of course, that Dr. Sanai and I had actually assessed them in their study. So that's one. Two, I think probably also just highlight that the IDH mutations are typically of quite low prevalence, even in GBM as well, too. So, with that in mind, you know, we could certainly look into how many patients there may have been, but I expect to be very few, if any, that were a part of this, a part of this cohort that was treated in the investigator-sponsored trial as well, too. One thing to just highlight, specifically regarding your your second question, around resistance, of course, and Dr. Terpos will probably touch on this a little bit. I think as of now, at least, and based on the data that currently exists in the field, we're not necessarily seeing that that there's any BCMA antigen loss that's happening. Actually, that's not the case. And what I would also highlight is the discontinuation rate, actually, due to the eye-related side effects is actually rather low in both DREAMM-7 and 8. So it's actually less than 10% in both studies as well, too. So it's not necessarily why the patients are coming off treatment, but Dr. Terpos could certainly touch on the resistance question. Dr. Terpos? The resistance to the BCMA seems to be extremely interesting. I mean, in general, the resistance has two important pathways. The one pathway is the reduction in the BCMA expression in the surface of the plasma cell, that we believe that it was the main, but it seems that this is not the main and the critical point of the resistance. The critical point seems to be the BCMA, let's say, the change in the form of the BCMA, in the surface of the myeloma cell, in order the antibody cannot bind to its binding position. So there is a mutation there that makes the antibody not to bind in its position, and that's why we have the resistance. This is not only with the belantamab, is with teclistamab, with elranatamab. It has been shown, especially by the work of Nizar Bahlis from Calgary, several times. So I don't think that, if you give the drug every six or every eight months, this is going to increase the resistance. On the contrary, and even the clinical data suggests that, if this happened, as the majority of the patients will have, let's say, a bigger interval between the administration, they would have worse results, which is not happening. So I believe that, and that's why also when you go from the one on the BCMA agent to the other, the other can work. That's why I don't believe that it is the lower expression of the BCMA that creates the... That makes the difference. So probably there, the mutation status that creates the difference, and that's why probably after belantamab, another BCMA-based regimen, or, for example, Teclistamab may work, as we have seen, that it can work at a lower, of course, rate of response, but it can work. So, to me, I don't believe that if you give the drug at intervals of six or eight weeks, this will create any problems in the refractoriness of the disease, or the resistance to that, it may be even the opposite. Thank you. Okay, so I think we're up to the last question, which is Peter Welford, right? Yeah, Peter Welford. Peter Welford. Yeah. Hi, thanks for fitting me in. Just two quick ones. Firstly, just coming back to the DREAMM-10 design, if I can, and it is to say, possibly together with standard of care, just curious on your thoughts, and I imagine you've not yet determined this, but what the standard of care would be. And I guess, most relevant is Darzalex potentially being considered, i.e., a second, I guess, antibody base, or will this most definitely not be combined with the Darzalex regimen, in the first line? And then secondly, just coming to the TIGIT. You've talked about the phase II, obviously, triggering the go decision to phase III and being very disciplined on this. I wonder if you can just give us a bit more insights in terms of, firstly, is it based on response rates, or do you have any sort of measure of, of long-term sort of follow-up in terms of duration of response and, and then early survival curves in the phase II? And, and secondly, is there any with regards to the toxicity? I think there's, there's some in the field who have seen incremental toxicity when they're combining the two IO agents. Just if you could give any sort of comment at all on what you've seen with regards to the tolerability of your Jemperli belrestatug. That would be great. Thank you. Fantastic. Thanks, Peter. I think, Hesham, both of those to you, and then we'll go to close. Yeah. No, thank you, Luke. So I'll start out first, maybe with the first question really around the choice of the control arm regimen in DREAMM-10. And what I would say is, you know, we're like... Yeah, I mentioned this or touched on it earlier. We're planning on looking at or evaluating what is a CD38-based regimen in frontline as a control arm. So, you look at, for example, the MAIA study, which included, of course, DRd, but you also look at, for example, some of the recent data that's been emerging, including data from the IMROZ study with isatuximab as well. Again, I would say that there's maybe different patient populations. We know that the triplet versus quadruplet kind of based approach also has different trade-offs, at least for such a control arm with regards to, you know, potentially toxicity as well, as well too. But what I would say is, we're definitely going to be looking at a CD38-based regimen and based on the DREAMM-7 data, I think, you know, you can get a sense that certainly a DARA-based regimen, at least for a sponsored GSK study, you know, would potentially be a key, you know, one to consider as a control, as a controller. It's not to say that we wouldn't evaluate, at least through other mechanisms, generating data with quadruplets or generating data that compares us to quadruplets. That is also an option that we will consider and evaluate and assess as well, too. The second question, specifically around TIGIT, and the data that we've used at this time, preliminary data that we've used from an interim analysis from our, ongoing, randomized, platform study. It's actually, I would say, probably a combination of different surrogates that we're evaluating, we're assessing. Of course, the data is continuing to mature over time, but, it is certainly looking at a combination of response rates, looking at also, preliminary, at least, duration of response data, but also, depth of response through, molecular, response and circulating tumor DNA data as well, too. So it's a, it's a combination of all three, and again, we're gonna continue to follow that data over time as it matures. And I would just highlight that, of course, you know, we anticipate presenting that data at a future scientific congress, as well, as well, too. And to note, at least for the phase III study, we have appropriate gating criteria that we've built into it, to make sure that we continually assess, of course, the data that's emerging from the platform trial, relative to, also any measures that we've included in the phase III study as well, as well too. Thanks, Hesham. Look, I think with that, we'll conclude. I think if you look at this from a specialist perspective or a generalist perspective, the sense of progress that we're making in this very focused and disciplined fashion hopefully is apparent and justified your time today in joining us. And also a sense of the team behind this collection of assets. I'd also like to thank Dr. Terpos for joining us today out of his busy schedule. We're very grateful for the time that you've taken to inform people with an interest in the company. So thank you, and thank you to everyone who joined today, and appreciate the thoughtfulness of your questions and the time. Thank you. Thank you, George.