Ladies and gentlemen, thank you for standing by. Welcome, and thank you for joining the top-line results MANIFEST-2 study. Throughout today's recorded presentation, all participants will be in listen-only mode. The presentation will be followed by a question and answer session. If you would like to ask a question, you may press Star, followed by One on your touchtone telephone. Please press the Star key, followed by zero for operator assistance. I would like to turn the conference over to Julia Neugebauer. Please go ahead, madam. Ladies and gentlemen, good afternoon and good morning. Thank you for joining us. It is my pleasure to welcome you to our conference call today, where we will be presenting the top-line results from our phase 3 MANIFEST-2 study of pelabresib in myelofibrosis, following yesterday's announcement. You can find our press release and the slides from today's call on the investor section of our website. Before we begin, I'd like to remind you on slide 2, that some of the statements made during the call today are forward-looking statements, including statements regarding our expectations for the commercialization of our products, our development plans, and expectations for the compounds in our pipeline, as well as the development plans of our collaboration partners. These forward-looking statements are subject to a number of risks and uncertainties that may cause our actual results to differ materially, including those described in MorphoSys' Annual Report on Form 20-F for the year ended December 31, 2022, and from time to time in other SEC documents of MorphoSys. It is important to keep in mind that our statements on this webcast speak as of today. Today's call will be led by our Chief Executive Officer, Jean-Paul Kress. Joining Jean-Paul will be our Chief Research and Development Officer, Tim Demuth, and guest speaker and myelofibrosis medical expert, Dr. John Mascarenhas, Director of the Adult Leukemia Program at the Tisch Cancer Institute at Mount Sinai in New York. Lucy Crabtree, our Chief Financial Officer, will be available during the Q&A session. With that, I now turn the call over to Jean-Paul. Good morning and good afternoon, everyone. Thank you for being here with us today. Yesterday was an exciting day for the myelofibrosis community and the entire team at MorphoSys. We announced strong top-line results from our phase 3 MANIFEST-2 study of pelabresib in first-line myelofibrosis. We are very pleased with the data, as these are the most impressive results we have seen in clinical studies of patients with myelofibrosis. MANIFEST-2 achieved its primary endpoint. pelabresib, in combination with ruxolitinib, demonstrated a statistically significant and clinically meaningful improvement in SVR35 at week 24, nearly doubling the SVR35 response rate. This is a critical endpoint, as studies have shown, which reduced spleen size, which is linked to survival. The key secondary endpoints assessing symptom reduction, TSS50 and absolute change in TSS from baseline at week 24, showed significant improvements for intermediate risk patients, the vast majority of patients in this study. Strong numerical improvements were shown for the overall population. Further, the pelabresib and ruxolitinib combination showed a clinically meaningful anemia improvement versus placebo and ruxolitinib. The safety results of the pelabresib and ruxolitinib combination were consistent with previous clinical trials, with no new significant safety signals observed. Bottom line, while this was not our scenario A, these results underscore the potential for pelabresib to shift the treatment paradigm for this debilitating disease. Looking ahead, we will soon share detailed MANIFEST-2 findings in an oral presentation at the 2023 ASH annual meeting. We also look forward to continuing our conversations with regulatory agencies. Based on these strong results, we intend to file in the U.S. and in Europe in the middle of 2024. With that, I will hand the call over to Tim for a detailed discussion of our exciting top-line results. Good morning and good afternoon, everyone. MANIFEST-2 is a global, multicenter, double-blind phase 3 study that randomized a total of 430 JAK inhibitor-naive myelofibrosis patients. It is one of the largest myelofibrosis studies conducted to date, representative of the disease population. The primary endpoint was the proportion of patients achieving at least a 35% reduction of spleen volume, or SVR35, at week 24. The key secondary endpoints were the proportion of patients achieving at least a 50% reduction in total symptom score, or TSS50, and the absolute change in total symptom score, or TSS, at week 24. Absolute change in TSS was added as a key secondary endpoint to directly measure change in the average TSS from baseline to week 24. It is a continuous endpoint that provides a meaningful, detailed assessment of symptom score reduction, thereby enhancing precision in estimating the magnitude of symptom burden reduction in patients with myelofibrosis. This endpoint was added to the MANIFEST-2 clinical trial protocol following a Type C meeting with the FDA in September 2023. MANIFEST-2 is also assessing several other important clinical endpoints, including progression-free survival, overall survival, and duration of the splenic and total symptom score responses, among others. This is a comprehensive data set, and it will support our regulatory filing and inform clinical practice. Now let's examine the results, starting with the primary endpoint. We are thrilled to report that the pelabresib and ruxolitinib combination demonstrated a statistically significant and clinically meaningful improvement in spleen volume reduction across all patients. In MANIFEST-2, 66% of patients receiving pelabresib in combination with ruxolitinib achieved SVR35 at week 24, versus 35% of those receiving placebo and ruxolitinib, nearly doubling SVR35 response rate. Both key secondary endpoints assessing symptom improvements, TSS50 and absolute change in TSS, showed a strong positive trend favoring the pelabresib and ruxolitinib combination. For patients classified as intermediate risk, constituting more than 90% of patients in MANIFEST-2, the combination therapy demonstrated significant improvements in both key secondary endpoints. For TSS50, the P value was less than 0.05, and for absolute change in TSS, the P value was less than 0.02. TSS was reduced by 15.99 points at week 24 from 28.26 at baseline in the pelabresib and ruxolitinib treatment arm, and it was reduced by 14.05 points from 27.36 at baseline in the placebo plus ruxolitinib arm. In intermediate-risk patients, TSS was reduced by 15.18 points at week 24 from 28.20 at baseline in the pelabresib and ruxolitinib treatment arm, versus a 12.74-point reduction at week 24 from 27.53 at baseline in the placebo plus ruxolitinib arm. This result was significant, with a P value of less than 0.02. TSS50 was achieved by 52% of patients in the pelabresib and ruxolitinib treatment arm at week 24, compared with 46% in the placebo plus ruxolitinib arm. In intermediate-risk patients, TSS50 was achieved by 55% of patients in the pelabresib and ruxolitinib treatment arm at week 24, compared with 45% in the placebo plus ruxolitinib arm. Surprisingly, we did not see the same symptom reduction benefit in high-risk patients. This is an anomaly we need to better understand, and we're looking into it. The pelabresib and ruxolitinib combination was well tolerated in the MANIFEST-2 study. At the time of this analysis, the safety of pelabresib and ruxolitinib was consistent with the previously observed safety profile of the combination therapy, with no new safety signals observed. Importantly, anemia adverse events were reported less frequently with pelabresib and ruxolitinib than with placebo and ruxolitinib. We are looking forward to presenting the detailed findings from this study during an oral session at the 2023 ASH Annual Meeting on Sunday, December 10, the perfect stage to showcase these compelling trial results. I would now like to turn the call over to Dr. John Mascarenhas, who will provide an overview of myelofibrosis in clinical practice and his thoughts on these clinical results. John? Okay, Tim, thanks very much. Thanks, MorphoSys team, for inviting me to join you today on this call, which I'm truly thrilled to be a part of. As an investigator that is dedicated to this space and has been involved in multiple studies and the evaluation of novel therapies, I'm really thrilled to see pelabresib continue to move forward in a very positive direction and build upon the phase 2 data that we've developed and presented and eventually published in JCO this year. And I think this data really represents a wider, more comprehensive approach to treating patients with myelofibrosis. And just to remind the listeners today, myelofibrosis is a chronic, progressive hematologic malignancy. It is derived at the level of a stem cell, and it is a very serious disease that holds multiple aspects in consideration, including cytopenias and anemia, extramedullary hematopoiesis, driving splenomegaly and hepatomegaly. That also adds to symptom burden, and then a disorganized bone marrow with bone marrow fibrosis and egress of normal hematopoiesis. Ultimately, these patients suffer significantly due to inflammatory cytokine expression that drives systemic symptoms, fevers, night sweats, bone pain, profound fatigue, and debility, which eventually contributes to poor outcomes of patients with these terrible diseases. The bulk of patients that we see with myelofibrosis are, in fact, intermediate-risk patients when looking at the DIPSS score, IPSS score, or in fact, any scoring system. And the disease is progressive, so even patients who are low risk at diagnosis or intermediate risk will eventually progress. And the survivals are rather poor as the disease moves on. In the intermediate-risk group, the survival can range between 4-15 years, and that highlights the heterogeneity and variability in the patient presentation and clinical course, which is dictated by the complex biology underlying this disease. Patients with high risk have even worse survival, with an estimated overall survival of approximately 1.5 years. So this is really a poor prognosis, chronic progressive hematologic malignancy in need of effective therapies that can control spleen symptom and ultimately provide durable benefits, progression-free survival, and overall survival. And that's what I'm most excited to see unfold with the MANIFEST-2 data. I'll move on to the next slide. I want to bring home a couple of points that we've recognized over the years. Regulatory endpoints for approval of drugs in myelofibrosis typically constitute reduction in spleen and reduction in symptom burden. This was set over a decade ago by the evaluation of ruxolitinib, excellent and important advance forward, for the treatment of myelofibrosis. We recognize, after multiple analyses, that there's value to reducing spleen volume, and this is one example, that was published, more than a decade ago by Dr. Verstovsek and colleagues, looking back at the open-label, single-arm, phase I/II results of patients treated at MD Anderson, making the correlation importantly between depth of reduction in spleen, at least here, measured by spleen length reduction and overall survival. Looking at spleen reduction as not simply a regulatory endpoint, but importantly as a clinical biomarker for an eventual outcome measure that truly matters to patients, and that is survival. So this was the first documentation of a correlation between spleen reduction and survival. In the next slide, I want to impress upon the participants in this call that this has played out in multiple aspects. So what I'm showing you here is the RR6. This is a prognostic scoring system when treating patients with ruxolitinib to determine overall survival within the first 6 months of treatment of ruxolitinib. And I've highlighted in red, one of the independent prognostic indicators with ruxolitinib treatment, and that is spleen reduction of 30% or less by palpation at 3 months and 6 months, is an indicator ultimately of poor survival in patients treated with ruxolitinib. Meaning that, again, the deeper the spleen response, the better the outcome of the patient ultimately. Spleen response as a biomarker, a clinical biomarker for improved outcomes such as survival. So the next slide highlights why I think the MANIFEST-2 provides some of the most important data release that we've seen in recent years. One, we've known now for a number of years, based on excellent preclinical modeling done by Ross Levine's lab and Kapil Bhalla's lab, that BET inhibition is rational, and it's supported by preclinical modeling, both in vitro and in vivo models. And we've now seen that play out in the clinical arena with combination pelabresib first in class, I would say best in class at this point. Pan BET inhibitor in combination with ruxolitinib is clearly clinically active. We saw this in the phase II study. This was now replicated and duplicated here in the top-line data from the phase III study, with very significant and clinically meaningful reduction in spleen volume over the entire population that was evaluated in this trial. With also strong numerical improvement in symptom reduction and serious symptom improvement in intermediate-risk patients in particular. And I want to stop on this for one second just to make a very important point. Ruxolitinib is an excellent drug by itself, monotherapy, very effective in reducing spleen and symptom. We can see with the addition of pelabresib, it is even more effective in reducing, in a greater number of patients to a greater degree, the spleen, volume. But also importantly, adds to symptom improvement, does not detract from symptom improvement, for a drug that already has benefit from symptoms. So we get both benefit from spleen and symptom with the combination of pelabresib without the addition of concerning toxicity. This was a well-tolerated therapy. We saw it in a phase II, and we'll analyze and look more closely at the toxicity profile at the ASH abstract in December. I look forward to looking in more detail with everyone. I would also point out that we even have an early signal of correlative evidence of biologic disease modification in terms of anemia improvement. This group knows that anemia is a very significant component of myelofibrosis. It's prevalent, worsens with disease course, is an adverse prognostic factor for survival. So improving anemia has been a large focus of drug development in myelofibrosis, and here with the combination of pelabresib, we see not only offsetting therapy-related anemia, but the potential for improving disease-related anemia, and durable benefits will be viewed over time. I do believe that the combination of pelabresib and ruxolitinib, for the first time, demonstrates with strong clinical data, a paradigm shift to combination therapy. I would even make the argument that one, particularly given the abundance of intermediate-1 risk patients in this study, one would consider treating patients earlier on in the clinical course with a combination therapy in order to optimize JAK inhibition and downregulation of NF-kappa B, and to maximize spleen reduction, symptom improvement, and ultimately, the secondary endpoints that we all look forward to evaluating in this trial, which is prolongation of progression-free survival and overall survival for our patients with myelofibrosis. So I'm in summary, I'm really impressed by the benefits that we see with the combination. I'm excited to see this continue from phase 2, phase 1, phase 2 to phase 3. I'm really thrilled about this outcome at this point. I'll turn it back over to MorphoSys. Again, thank you for your attention. Thank you for allowing me to participate today. Thank you very much, John, for sharing these great insights to contextualize our results in clinical practice. This is invaluable. In MANIFEST-2, the pelabresib and Rux combination demonstrated strong reductions in spleen volume and symptoms over Rux monotherapy. These are the most impressive benefits seen in clinical studies of patients with myelofibrosis. Based on these results, pelabresib presents us with a multi-billion dollar market opportunity in myelofibrosis. We believe we have the best new molecule to treat this disease, and as John said, the paradigm shift opportunity. We are very pleased with this positive outcome, and we will continue our conversations with regulatory agencies with the intention to file for approval in the US and Europe in mid-2024. We are committed to bringing this novel therapy to patients as soon as possible. With that, I'd like to open the call for questions. Operator, please open the line. Thank you. Ladies and gentlemen, at this time, we will begin the question and answer session. Anyone who wishes to ask a question may press star, followed by one on their touchtone telephone. If you wish to remove yourself from the question queue, you may press star followed by two. If you're using speaker equipment today, please lift the handsets before making your selections. Anyone who has a question may press star followed by one at this time. The first question is from Mr. Jason Butler, JMP Securities. Please go ahead. Hi, and congrats on the results. Maybe first of all, just on the symptom score data from the high-risk patients. Obviously, you've only just got the data, but can you give us any more color about what you think might have happened there? Is it something to do with the patient population or how data were evaluated, or just any insights into why you're seeing an unexpected result there? Thanks. Jason, this is Tim. As I said in the prepared remarks, this is really an anomaly, and we are investigating the data together with Dr. Mascarenhas and some of the other investigators, and we'll come back with more details on that in due time. Okay, great. And then can you just walk us through what your plans are ahead of the NDA, planned NDA submission in terms of interactions that you'll have with FDA and EMA? I mean, how quickly do you plan on sharing the data with regulatory authorities? Thanks. Yes, yes. So, Jason, thanks. This is Jean-Paul. You know, as mentioned in the call, you know, we're very, very pleased with the results, and we think we have a very strong data package here, probably one of the strongest ever in myelofibrosis. So based on this, we look forward to continue conversations with the agencies. We intend to file definitely mid-2024 in the U.S. and Europe, and we will follow the standard filing procedure here, and we'll update you in due time. Okay, great. And then just one more, if I could squeeze it in for this physician. If you could put into context for us the anemia effects and how important you think that those benefits of the drug are with pelabresib in terms of how you would use the drug? Thanks. So for me, the benefits of alleviating anemia with any drug is both there's usually a symptomatic aspect tied into it, but importantly, and sometimes underrecognized, you remove patients from the transfusion suite, which is a major burden for patients and family members in the healthcare system in general. And that's a huge improvement for quality of life. So addressing anemia has significant benefit to the patient. But I also believe that anemia is in itself a marker of poor disease and poor outcome. So addressing anemia has the additional benefit of potentially improving outcomes like survival. And that's been shown with, for example, momelotinib. So I'm very excited and intrigued by the fact that the addition of pelabresib has the potential in patients to alleviate not only the therapy-related anemia that's characteristic of ruxolitinib, but potentially the disease-related anemia that's characteristic of progressive disease. I would love to see, as we follow the data, whether that also translates to improvement in progression-free survival and overall survival. So- ... The combination of pelabresib and ruxolitinib in not exacerbating anemia, but in blunting anemia, particularly early on when Rux is used, and ultimately improving anemia, is likely to benefit the patient over the long run, and we'll have to look at the data as it matures. But that's where I see the excitement and the benefit. It would be a huge benefit to our patient population, if we are able to develop effective therapies going forward that induce these deep responses and do not worsen the cytopenias that classically occur as we develop treatment. So this is really a positive finding. Great. Thanks for taking the questions. The next question from James Gordon, JP Morgan. Please go ahead. Hello, James Gordon, JP Morgan. Thanks for taking the questions. I've got a couple. One was on the stats. So, you've gotten p-values for absolute TSS and TSS50 at intermediate- and high-risk subgroups, but are you adjusting for multiplicity, as in you're asking multiple questions post the primary? And was that something that was pre-agreed with FDA? Second question, the Type C meeting, was this something that the FDA suggested or requested or something that you suggested? And did the FDA agree that absolute TSS was an approvable co-primary endpoint, or was it more just something that MorphoSys thought would be interesting, but wasn't necessarily something that the FDA were keen on? And did you discuss a scenario like today's outcome with FDA and get any comments from them? And then, two other quick ones. Filing plans seven months away, is it because you need PFS and OS, and what do you need to show here? And then just finally, funding. I think you've got cash till about early 2025, but even if all goes well, pelabresib probably won't be approved by then. So how are you thinking about addressing the funding shortfall, please? Thanks, James. Tim will take the medical and scientific questions, and we see the cash. Hey, James, this is Tim. So, as we said, the overall population achieved very strong benefits in SVR with a significant p-value. TSS benefits in the INT-1 and INT-2 patient population, the intermediate risk patient population, surprising findings in the high-risk patients. That's a small subpopulation in the MANIFEST-2 study, as well as overall of the myelofibrosis population. The study stratified 4 risk categories, and that's how the data was analyzed. With regards to the FDA interaction, MorphoSys reacted to a recent development by FDA, where they put out a draft guidance on patient-focused drug development, and as a science-focused organization, we took the opportunity to proactively reach out to the agency in the form of a Type C meeting, to discuss exactly the content of that patient-focused drug development, that is looking at patient-reported outcomes as continuous variables to enhance the precision and the detail derived from such outcome measures. Subsequent to this meeting, we decided to update the MANIFEST-2 clinical trial protocol to include absolute change into the testing hierarchy. Filing plans. Filing plans are, as stated, mid-next year. We will submit the dossier and the regular steps, that everybody takes between top-line data, primary analysis, are taking place, which is nothing out of the ordinary and very well established. There will be a more detailed presentation on the data, as we mentioned, at ASH, on the tenth of December, where we will have the opportunity to share this rich data sets with the scientific community and, gain further insights. We are confident we can secure approval based on our strong data package. Lucy, on the cash question? Yep. Thanks, James. So as you know, we had approximately EUR 640,000,000 of cash at our Q3. You know, this is more than 12 months of cash. Our guided runway is cash into 2025, and we'll continue to evaluate all options, both dilutive and non-dilutive. Importantly, I will say there are levers and options, you know, we've spoken previously about the value in our partnered programs, from the legacy business. And so that represents opportunity on the non-dilutive side, and we'll update accordingly, James. Thanks. The next question, please. The next question from Derek Archila, Wells Fargo. Please go ahead. Hey, good morning, and thanks for taking the questions. Just a few from us. I guess first, in terms of the stuff that you'll show at ASH, the additional data, I mean, will you show depth of SVR35? So that's one question. And second question, in terms of the safety, I don't know if you have any color in terms of, like, discontinuations in the study or, if you'll be offering that today. And then maybe one for the physician, you know, I guess, was there anything from a baseline perspective, I guess, in the high-risk group patients in the study that, like, would impact the TSS and, maybe, you know, cause this type of anomaly that we've seen in the trial? Thanks. Hey, Derek, this is Tim. Regarding data at ASH, the data that will be presented is currently under embargo by ASH, so we cannot comment on any more details of the presentation beyond what you've seen in the abstract. So stay tuned for the December tenth presentation. John, you want to take the medical question? Sure. So from my perspective, I'm unclear as to why pelabresib would not have the same, you know, synergistic or added benefit, as we saw with intermediate-risk patients in this high-risk population. Now, the only thing I could say, this is a relatively small number, 30 patients, compared to the larger 430 patients. And I for the life of me, I'm not quite clear why it would perform in a different direction. So I'm eager to get into the weeds to understand whether there were particular baseline-related aspects that might explain why the response was such. We didn't see this in the MANIFEST-2 phase 2 study in combination Arm 3, so it was unanticipated in the high-risk patient population. Biologically, I can't quite explain it. I do think that perhaps, you know, there may be issues with high-risk patients in terms of the advanced nature of the disease, perhaps more potential for cytopenias and dose modifications, perhaps. To me, it may, again, read into the concept that as a treating community of physicians, it is likely the best benefit to start therapy and to provide, you know, most effective therapy, in this case, a combination approach earlier on in the treatment, and not to wait perhaps for patients to be more advanced in disease. But for me to feel super comfortable in saying that repeatedly, I really need to have the time and the luxury to go through the data with the high-risk patients, so that it's yet to be determined why they perform differently. It's a little bit odd. Understood. Thank you so much. The next question from Xian Deng, UBS. Please go ahead. Hey, thank you for taking my questions. Apologies if those has already been addressed. I got cut off earlier on during the call. So just one question- two questions, please. So the first one is on the high-risk group data for TSS50. So just wondering, you know, is there sort of anything that you could potentially point towards in terms of what could be the possible reason here? Is there anything you could comment on in terms of safety, any sort of potential imbalance that you could comment on that might potentially be a cause of this? The second question is that during your September meeting with the FDA, of course, you mentioned that the TSS change has been made to a key secondary. So just wondering if you could comment on alpha hierarchy here, and also just wondering, what are the other suggestions that FDA has made to you in terms of endpoint? For example, have they ever suggested to make SVR TSS endpoint as a co-primary? Thank you very much. Hey, Xian, this is Tim. Good morning. On the surprising findings, as Dr. Mascarenhas called them in the high-risk population, as we said in the prepared remarks, we, we have to look into this. This is totally unanticipated. We did not expect to see this based on the MANIFEST-2 Arm 3 results, and we will come back with more details in due time when that evaluation is completed. That goes to the baseline characteristics as well as any potential imbalances on the tolerability profile that you asked about. With regards to the FDA meeting from September, that was a meeting that MorphoSys requested proactively in response to the recent guideline on patient-focused drug development, where we discussed a continuous measure of symptom score in myelofibrosis. Following the meeting, we made the decision to update the MANIFEST-2 clinical trial protocol. On the testing hierarchy, the hierarchy is SVR35 as the primary endpoint, followed by absolute change, followed by TSS50. Got it. Thank you very much. As a reminder, if you wish to register for questions, please press Star and One on your telephone. Star and One. The next question is from Rajan Sharma, Goldman Sachs. Please go ahead. Hi, thanks for taking my question. So firstly, just if you could provide some kind of additional color on the filing strategy. So I guess you've been clear throughout collaborative development that the regulator's bar for approval is statistically significant improvement in both SVR35 and TSS50. So if you could just kind of clarify what specifically changed in your view to give you confidence on a filing and an approval now? And then secondly, are you specifically seeking an approval in the intermediate-risk patients? And again, just to be clear, is that, in your view, likely to be an accelerated or conditional approval, which then may need a confirmatory trial, as we've seen with another recently approved drug in the field? And then finally, do you know what the average dose of ruxolitinib was in intermediate-risk patients versus high risk? Rajan, this is Jean-Paul. Thanks for the questions. The strength of the data is such here that we believe we are confident that we can secure approval of pelabresib. You know, I mean, it's a mix of things here. One of them is the fact that we've seen, you've seen also that the regulators have approved some products recently based on, you know, way more mixed data than ours. Our datas are very strong. Dr. Mascarenhas just reminded us how much we are addressing the unmet medical need here. The comments in the past on the TSS, 15 needs and everything are probably from the past. That's our impression, based on conversations with the different stakeholders and including the regulators. We have a very strong data package. We intend to file mid-2024. We have a path forward for that. We're not deviating from that, so we'll update you in due time. Now, on the question on the rux dose, team? Yeah, Rajan, Rux dose analysis is not available for the top line release, and we will share that with the scientific community as the data become available. Okay, thank you. And then, sorry, just to follow up on the first one. Are you seeking an approval in intermediate-risk patients, or are you looking for kind of a broad approval at this point? John, we actually think we have a very strong case for all comers here. You know, I mean, just besides this anomaly, unanticipated anomaly in the high-risk patients, which was very well described by Dr. Mascarenhas. And also the fact that on these high-risk patients, our SVR-35 is very strong. We have a very strong results on the SVR-35 on these patients, and these patients are the ones who need the most their OS to be improved. They have a very short life expectancy, as John said. So no, we are definitely going for the broad all comers label. Okay, thank you. Once again, if you wish to register for questions, please press star and one on your telephone. There are no more questions at this time. Would you like to conclude the conference call? Yes. Ladies and gentlemen, this concludes today's conference call. If you'd like to follow up, MorphoSys Investor Relations team is available for the remainder of the day. Once again, thank you for joining. Have a great day and goodbye. Ladies and gentlemen, the conference is now concluded, and you may disconnect your telephone. Thank you for joining, and have a pleasant day. Goodbye.