By Annemarie Hanekamp, our Chief Commercial Officer, so with that, I'm excited to hand over to Ugur and welcome him to the stage to talk to you about our unique approach to innovation. Thank you, Doug. Thank you. Yeah, good morning, everyone. I would like to welcome you also on behalf of my colleagues here in the Times Square. What we would like to do is, before going really into the details, we would like to discuss, give you a status quo of the company, and discuss the scientific concept, the medical concept, and how we translate that and execute on that, and it will be a data-based presentation today, and you will have the opportunity at the end of the presentation to ask questions, so this is just an updated company slide. We are a multi-platform oncology company with more than 20 ongoing clinical phase II and phase III trials. We have an infectious disease pipeline, and we have capabilities that we build around drug development and AI manufacturing and research. After the COVID pandemic in 2023, we pivoted back to oncology. This is our original focus. We are driven by the fact that oncology can still be one of the biggest challenges in healthcare. The challenge is depicted here in a very simple manner. We are, in principle, in drug development, dealing with two types of challenges. One is the inter-individual variability. Every patient is different. The second challenge is the intratumoral heterogeneity, which resides often in patients responding for a certain time to the treatment, objective responses, sometimes complete responses, that then the tumor relapse thereafter because of pre-existing tumor cells, heterogeneous tumor cells. The concept that we are addressing here is based on using, exploiting the power of the immune system via combination treatment, addressing complementary, potentially synergistic modes of action. We have a class of molecules, immunomodulators, for which we focus on critical IO pathways. Here, the idea is to target complementary pathways in cancer immunity cycle that promote durable anti-tumor effect. The second element is our targeted therapies, particularly ADCs. Here, the goal is to have a precise and potent approach to kill tumor cells without harming healthy tissues, and the emergence of third-generation ADCs allowed us here to make enormous progress, not only us, but also the field, and we started with well-defined targets for targeting tumors, but in the meantime, we are extending beyond the current targets with our own approaches, and the last piece in this concept is mRNA cancer immunotherapies, and here, the concept is, regardless of what kind of treatment is done, residual tumor cells will stay, and even if these residual tumor cells are just a million of tumor cells, they will result in relapses. The concept of personalized vaccines or cancer immunotherapies based on mRNA vaccines is to induce a polyspecific immune response that can deal with this heterogeneity and enable removal of the residual tumor cells. Let's start with immunomodulators. Our focus is critical IO pathways. Today, I will really discuss about the PD-1, PD-L1 pathway, and anti-CTLA-4 pathway. The question is, of course, if you go with PD-L1 and anti-CTLA-4, where's the innovation? I would like to show you how the engineering of the molecules can help to exploit an existing pathway and do something completely different or significantly better. The two molecules that I would like to discuss today are bispecific VEGF and gutistobart, our anti-CTLA-4 molecule. You are all aware about the bispecific PD-1, PD-L1 VEGF antibody class. Here, several candidates are existing that combine VEGF neutralization with PD-L1 blockade. These are actually two well-characterized targets. So PD-1 pathway and VEGF. So it's about the VEGF pathway is not only inhibition of neovasculature, but it is also an immune modulator. VEGF is an immune suppressive molecule. And by targeting VEGF, we can reduce hypoxia, we can increase immune infiltration, then leukocyte maturation, and Treg activity. And the activities of PD-1, PD-L1 are well known. So this bispecific, of course, has these two functions. On the one side, neutralization of VEGF in a dose-dependent manner. And on the other side, checkpoint blockade, PD-L1 blockade, and thereby accomplishing T-cell activation. So the antibody BNT327 for both arms has very high affinity so that even with low doses, we can accomplish complete inhibition. And this, of course, translates into immune activation. So we measure T-cell expansion, cytokine secretion, tumor cell killing, activation. In all functions, we see a robust activity of pumitamig. The question here is, is pumitamig just the combination of two antibodies? Our statement is very clear. Pumitamig is more than the sum of two monospecific antibodies. We have, on the one side, a VEGF function, anti-VEGF function. We have, on the other side, an anti-PD-L1 function. Pumitamig has certainly both. It has, in addition, functions that are not mediated by the monospecific antibodies. This is the link function or the conditional function by combining the VEGF binding and the PD-L1 activity. This is a slide showing we know that VEGF is, in natural configuration, a dimer. That provides the opportunity to form immune complexes. Immune complexes are dose-dependent. If we have a high concentration of the antibody and low concentration of VEGF, we have antibody alone. If we have a ratio of one to one, we have maximum complex formation. And if VEGF concentration increases disproportionately, we have more antibodies bound to VEGF, but forming less complexes. And this is an assay actually measuring VEGF pumitamig complexes. So what happens if we form complexes? What we observed is the formation of a complex of pumitamig with VEGF increases the on rate. You can see that on the left graph here. This is a faster on rate. And it reduces the off rate of the binding. And improved on rate and reduced off rate translates into a much higher binding and a lower dissociation constant. So we see here in the optimal concentration, a more than 32-fold increase of binding affinity of pumitamig to immobilized PD-L1. So this is one side of a bispecific antibody. Let's continue with that. The second is that this not only translates into a better binding, but a dramatically increased internalization of pumitamig. So this is an experiment on a cell line which expresses PD-L1. It's a tumor cell line with PD-L1 expression. This is a variant of our antibody in which we replace the anti-VEGF-A arm with a control. And here, the internalization of the antibody is visible by cells becoming red-colored. And you see here, even with longer incubation, we don't have internalization with a PD-L1 binding antibody alone. But if we take now the original molecule, then we see rapid internalization of PD-L1 and of the antibody within a few hours. And this is also depicted here. So we believe that the improved activity that we are seeing here for the antibody is mediated in part by the increased binding, the lower off rate, but more importantly, by the stronger internalization of PD-L1 mediated by VEGF PD-L1 complexes. So this is one differentiation factor. And this differentiates a bispecific antibody from the sum of two monospecific antibodies. But there's another differentiation factor. So anti-VEGF or VEGF and PD-L1 are both tumor antigens. They are increased in the tumor microenvironment. And this is a staining with anti-VEGFA of the tumor microenvironment. These are samples from non-small cell lung cancer, very strong VEGF staining in the tumor microenvironment. And this is PD-L1 staining. So we are now targeting with our bispecific VEGF PD-L1 antibody with both arms in the tumor microenvironment. And this means that we have the opportunity to target PD-1, PD-L1 to VEGFA high tumors. Or, you can see it also in a different way to target VEGF-A neutralization to PD-L1 high tumors. So, if you sum that up in a simple table, then what we observe is here, pumitamig has following function: blocking of PD-1, PD-L1 signaling, neutralization of VEGF. And this is something that is accomplished by other bispecifics as well, as well as the monospecifics or the sum of combination of anti-VEGF and anti-PD-L1. Then we have the cooperative effect of linking and VEGF binding. And this is not accomplished by combination therapy with monospecific antibodies, but it is also a feature of the other members of this bispecific class. And then we have the mechanism of tumor microenvironment targeting by anti-PD-L1, which is specific to the PD-L1 bispecific class. So we believe that this is one of the key reasons why we observed with this antibody immune responses in tumors independent of PD-L1 expression. So we see response in PD-L1 high tumors, PD-L1 low tumors, and even PD-L1 negative tumors. And clinically, this provides the opportunity that BNT327 has the potential to become a backbone independent of PD-L1 expression and for the ability to introduce IO into different patient populations. And this is an observation that we made in TNBC. And we are making similar observations in other tumor types as well. Here is the example for EGFR mutant non-small cell lung cancer, second line tumors. Here again, strong objective responses in PD-L1 high, PD-L1 low, and PD-L1 negative tumors. So this opens up the opportunity to bring this IO, to use BNT327 as an IO in the existing PD-1, PD-L1 positive space. That means replace pembrolizumab and other existing molecules and then also expand beyond into indications in which IO is not yet approved. Our clinical strategy for doing this is based on a three wave approach, so we already started the first wave. It's the foundational registration trials in three priority indications. Özlem, Ilhan and Michael, we'll talk about this. The next wave is expanding this combination into multiple other cancer indications in combination with standard of care, and the last step is to combine Pumitamig with novel combinations and we will hear today about what kind of combination trials can be executed, so this is a mode of action summary for Pumitamig. Next year, we will provide more details why we believe or how the action of Pumitamig is accomplished in PD-L1 negative tumors. The presentation provided a mode of action, but not really an explanation why PD-L1 negative also works. This will be part of the presentation next year. So there's a motivation to come also next year. I would like to now talk about CTLA-4. And this was the first IO target and was introduced as checkpoint blockade. Cotista Varg is an antibody monospecific antibody with an optimized Fc that targets CTLA-4. But the main function is not just checkpoint blockade, but depletion of tumor infiltrated regulatory T-cells. It is currently evaluated in multiple cancer indications, either alone or in combination with anti-PD-1. We have a running phase III clinical study. And I will provide information about what we are evaluating here. And we have also clinical studies running in indications that are usually not responding to checkpoint blockade. So anti-CTLA-4 is target for cancer immunotherapy. What is new? Why our mimetic is new? So the prevailing view on anti-CTLA-4 is checkpoint blockade. So the idea is depicted on the left side. An antibody inhibits the interaction of CTLA-4 with its ligand and thereby enables that T-cells can be activated. And the prevailing view is that this happens in the lymphoid tissues. And this activation of T-cells, so that means inhibition of Treg activity, results in an anti-tumor response. The problem with that is that this anti-tumor response is intrinsically linked to concomitant autoimmunity with a constrained therapeutic window. And there are dozens of clinical trials that tried to identify some sort of a therapeutic window for ipilimumab by having different dose schemes, by trying to identify better timing. But more or less, all these clinical strategies ended up either by lowering the efficacy or by having the same efficacy but the same toxicity profile. The concept of gotistobart, an antibody that we partnered with OncoC4, is a different one. Here, the idea is not that much to block CTLA-4. It is more used to use an anti-CTLA-4 effector with an effector-mediated mechanism to deplete regulatory T-cells and do it in a way that is tumor selective, so idea, depletion of regulatory T-cells in the tumor microenvironment, and this provides an opportunity for better therapeutic index, and this mechanism was one of the key reasons why we partnered this antibody, and so how is this accomplished with gotistobart? It's a little bit complicated, and this slide has been presented many times, and I would really like to show you the mechanism, which is really interesting. Because the mechanism that the antibody wants to accomplish is via the improved Fc receptor function to induce lysis by ADCC and by ADCP to remove Tregs in the tumor microenvironment. The problem is that the antibody still binds and inhibits CTLA-4, which would then be expected to induce autoimmunity. And this is solved for this antibody by a pH-sensitive binding. So that means when the antibody with the CTLA-4 complex internalizes, it is in the lysosome, the antibody, the CTLA-4 molecule, the antibody stops binding. And CTLA-4 can recirculate to the cell surface. And thereby, the antibody does not reduce the CTLA-4 expression on Tregs, but still accomplishes depletion. So the antibody is designed to allow regular recycling and enrichment of CTLA-4, thereby due to the Fc receptor function to selectively kill Tregs in the tumor microenvironment, improve their therapeutic index thereby. By improving the therapeutic index, the argument is not that it is safer, but it provides a therapeutic index so that it can be dosed higher. So that means the side effects that we are observing are very similar to the CTLA-4 class. But the dose that we can provide to patients is much higher. And we can provide this dose in a prolonged fashion. So that's the way how this works. That means it allows prolonged and repeated dosing. So this is supported by preclinical studies in mice where Cotista Varg has improved therapeutic efficacy as compared to controls. And it also results in a higher, stronger activity of immune cells recognizing it. These were preclinical data. In the meantime, we have unpublished clinical data in which we clearly see that the antibody does what it should do in patients. So that means reducing the Treg density, increasing CD8 T-cells, reducing the amount of Tregs in the total population of CD3 T-cells, reducing the amount of Tregs in the total CD4 population. And most importantly, and this is a factor really shown in many biomarker studies, increasing the CD8 to Treg ratio. So we have a running phase III clinical trial in patients with squamous and non-small cell lung cancer. The study started with an initial part where both patients, squamous and non-squamous non-small cell lung cancer, were treated. And the control is in second line squamous non-small cell lung cancer or non-small cell lung cancer as well is docetaxel. And we have now, based on the data, already started the stage 2 of the pivotal trial, which is currently recruiting well. What we will do is we will present from data from this initial study, which is randomized in December this year. In a which congress is that? North American ASCO. December 7, right? In Chicago. We look forward, of course, in presenting the data. Coming to the first part, mRNA cancer vaccines, I will keep it short because Özlem is going to share more information on that. The mechanism of action that is desired is here to eliminate residual tumor cells. As you know, we have both mRNA technology toolbox and reported in the recent years a number of clinical trials, including antibody-encoded monoclonal antibodies, bispecific antibodies, cytokines. But here, I would really like to focus more on the nanoparticulate mRNA vaccines. We have the mRNA LPX technology. Sorry for that. For the mRNA LPX technology. And here, we can take several antigens encoding shared tumor antigens and encapsulate that in lipoplex nanoparticles. And we have shown that this approach, particularly when injecting the nanoparticles intravenously, results in lymphoid targeting of the mRNA and expression of the mRNA in lymphoid tissues. And this is associated with two key mechanisms of action. One is the release of cytokines, type I interferon. This is the innate immune response. The innate immune response is dose-dependent. So you see here a study where we treated an individual patient with increasing concentrations of the RNA lipoplex. So this is week one, week two, week three. So this is weekly increasing dose. And what you can nicely see is that this is associated with pulsatile secretion of interferon alpha that is starting in the first two hours and going down within 24 hours. And this is pretty consistent. So this is the innate immune response. And we, of course, know that innate immune responses can improve the outcome of cancer immunotherapies. But this is a transient approach. And then we have a second function, which is the induction of T-cell-specific immunity. And this does not happen in the first hours or first days. But this is something that, for de novo immune responses, is requiring a time frame of six weeks to come to a maximum level. And then, by repeated vaccination, these immune responses can be kept high. So we described the full mode of action in our study in 2016, in which we really evaluated also what happens if we use RNA LPX with relevant antigen or with irrelevant antigens. You can download the paper and check for what kind of controls have been done. The key aspects here is the mechanism is driven by TLR7, is driven by type I interferon. We have shown that this is something that can be universally applied to any type of antigen. ADCs. ADCs don't require much introduction. What I would like just to state is that we focus in licensing our first set of ADCs to ADCs with a newer linker technology, allowing us not only to get potent anti-tumor activity but also bystander activity. We, in parallel, started to work with our own targets, generate antibodies, and generate ADCs against these targets and ensure that we use the ongoing innovation cycle. Because what we believe is ADCs are just emerging technology. We will see a number of improvements in the coming years with regard to their potency, their selectivity, and their immune effects. And we built an in-house ADC capabilities aiming to improve linker technology but also aiming to come up with new modes of actions. So this is the list of currently addressed targets. So we started with HER2. We have a B7-H3 ADC, TROP2, HER3. One of our new ADCs is CA19-9. It's a special antibody with an incredibly high affinity against CA19-9. And we also generated recently in-house an EGFR HER3 ADC with our own linker approach. So aiming here is combining target tumor cell killing, bystander tumor cell killing, immunogenic cell death, and the opportunity to synergize. So what kind of synergies are we addressing? So one obvious way to ask for synergy is combined pumitamig with the different ADCs. And these are all preclinical studies, either in xenograft models or in syngeneic mice. In any model evaluated, we see a synergy. That means the combination of the ADC with pumitamig results either in a complete tumor rejection or improved tumor control over time. So this is a slide that should come later. But it's okay. I will come back to that. Yes. This is the combination treatment with pumitamig and ADCs. But as you know, we have also other immune modulators. Ongoing studies also address the synergy of our bispecific anti-4-1BB anti-EpCAM antibody, which BNT314 or GEN1059, which is partnered with Genmab. Here, we see a clear increased activity of T-cells, improving beyond pumitamig's activity with regard to cytokine secretion and tumor control. We have our bispecific ADC anti-EGFR HER3 with a topoisomerase inhibitor linker technology. Here, as well, we see a very strong synergy of pumitamig with our ADCs. And this was all supported last year already with preclinical studies. Now, we are in clinical evaluation of our next-gen IOs with ADCs, pumitamig, and ADCs targeting different entities. We combine pumitamig with next-gen IO. These are IO-IO combinations, combinations in different indications. We combine our anti-CTLA-4 and our bispecific also with mRNA vaccines. These are running clinical trials. And last but not least, we do also combination trials where we combine mRNA with ADCs. And these are all addressed by the concept of identifying different types of synergies of these different treatment approaches. So the vision remains the same. This is aiming to combine our capabilities on IO, ADCs, and mRNA therapeutics for a personalized treatment approach. And ultimately, not only address off-the-shelf drugs but also proceed to the personalized space with tailored on-demand immunotherapies. We are combining that with capabilities in automated in-house manufacturing and our AI capabilities to support drug design, new antigen prediction, as well as manufacturing. So 2026, the key areas of focus is to use the combination therapy momentum. This will be a year of combination therapies where we will generate data and share, end of this year, data from multiple indications. And Ilhan and Michael will show you the ongoing clinical trials. We want to proceed, and we started to do that from just modalities to really disease areas. That means the optimization approach is now ongoing for specific types of tumors. And Özlem will provide and share the concept how we are doing this to get really the best type of combination therapy in disease areas. And of course, 2026 is also a year of late-stage acceleration, aiming to start a number of additional registration trials. So I would like to ask Özlem to come here and continue. Thank you. Also, a heartfelt welcome from me. It's a pleasure to see so many new faces and also friends who have been accompanying us for quite a while. Ugur has shared with you our vision. He has shared with you our science, which typically defines the boundaries of the space within which a company can generate innovation and value. What I will do in my part is that I want to describe our strategy from getting from one to the other, from what we have in terms of value foundation to our vision. This is about our clinical development strategy for our pipeline. You all know that over the past decade, the treatment paradigm for many tumors has shifted towards combining two modalities, IOs, immune modulatory molecules, with highly cytotoxic agents, meaning chemotherapies. This approach, without doubt, has brought progress. However, it has also shown that it is still limited by short durability of responses by limitations in depth and resistance mechanisms. The next paradigm is already unfolding in front of our eyes, and this next paradigm is based on improving both components of this duo, so what we see happening is that next-generation IOs are developed, and compounds with higher cytotoxicity, with higher precision, are being developed. Our deliberate strategic decision here is that we want to do both with our pipeline, and our multi-modal, our multi-asset pipeline allows us to do exactly that. This is also the reason why we have immune modulators, and you can also count, actually, mRNA vaccines or immune therapies as immune modulators on the one side and, on the other side, have brought into our pipeline over the last two years ADCs as highly precise and potent cytotoxic agents. The IO we have chosen for positioning as a pan-tumor backbone is pumitamig. And our pipeline and our strategy is anchored in this molecule. As Ugur has already pointed out, it is also a design choice for our strategy that our ambition is to develop pumita broadly, deeply, and fast, meaning across indications, disease areas, and across lines. We do this in three ways, which are shown sequentially here. However, in principle, they are happening in parallel. And I will talk about the way we execute in a couple of minutes. One part of this three-wave strategy is that, because speed is important for us, we are conducting foundational registration trials in combination with standard of care chemotherapy, which is well known to clinicians and well established in three indications: in non-small cell lung cancer, small cell lung cancer, and TNBC. So indications with large market size. You also have heard in our earnings call that we are adding two more indications, first-line CRC and first-line gastric cancer. And we will talk more about this in a couple of minutes. Then the second, in parallel, conducted wave is that we are extending into additional indications, which are listed here, and with registrational intent, but also with a large number of signal-seeking trials across indications to ensure that our next decisions towards registrational intention and our selection of indications is well informed. And the third line and the third wave, and Ugur already talked about that, is very close to our heart, namely novel combinations in sort of first initial wave with our in-house ADCs, but also beyond. And you already see this happening, that we are also starting to combine with our IOs. And Ugur has shown some of the preclinical data for this. This is the immunotherapeutic part of our innovation strategy. Then we have a second part in this duo. As I said, we also want to improve and optimize the cytotoxic component in the IO cytotoxic agent duo. And for this, we have built an entire panel, an entire portfolio of ADCs. These are all topoisomerase inhibitors with specific linkers, which also deliver bystander activity. We have diverse targets, which we are addressing here. And the reason is very clear. There is not the situation that you can address all biologies, all disease areas, all indications with one single target. And what we want to make sure is that we select for each indication the right target and the right ADC. And these targets, which we have selected cumulatively, as you can see on the bottom of this slide, cover with their expression and also with their biology, all these multiple indications we are interested in. As you can see, we have, on the one hand, targets like HER2, which means we have an ADC here, which addresses an already very well-entrenched target-defined market. We also have, with TROP2, an ADC which I would say is more semi-entrenched. So there are already approved TROP2s. But the market is not as well-defined. And then we have newcomers, B7-H3, HER3, where there are no approved ADCs around yet. And the way we have to develop them forward in order to make them fit for purpose for our novel combinations will also differ a bit with this entrenchment, which is given. So what about the execution? The last 24 months were actually only about execution. I would like to summarize on the next slides what we have done and what we have achieved. This shows you the studies and the settings in which we have tested pumitamig as a single agent and pumitamig in combination with standard of care chemo. This is data which is worth more than 1,400 patients and was essential for us in order to define across indications the safety profile, to inform those decisions, and to understand with our signal seekers the mono and also chemo combo activity in these different indications. As you can see here, and this is also a design choice, we are interested in all these disease areas: lung cancer, breast cancer, women's cancers, GI, and GU cancers, and have created data in all these indications. This data set has led to decisions to activate our three Rosetta trials in non-small cell lung cancer, small cell lung cancer, and in TNBC, and recently in the next wave with first-line CRC and gastric cancer. This is the execution which happened for our ADCs, where we tested single-agent activity of all our ADCs again to understand the safety profile, to inform dosing, and to prepare for novel combinations again across indications. And as you can see here, these are massive data sets, which really allowed us to understand which indications are the best, which settings are the best for each of these targeted ADCs. Just for clarification, the primary aim is not to develop these ADCs as monotherapies or in combination with standard of care, but to combine them as early novel registrational pathways with pumita. However, that does not mean that we are not pragmatic. Should we see in any of these indications compelling single-agent activity? And should it make sense due to commercial opportunity and other factors to proceed in this mono setting? We would do that. And admittedly, there are a couple of signals which make us think. Then we have already expanded based on this mono data or single-agent data from our ADCs in combinations with pumita. And you can see here all the indications we have selected for individual ADCs. This was, again, informed by the single-agent activity. In some of these indications, as you can see, for example, non-small cell lung cancer, EGFR-negative, we have still three of our ADCs in the game. And these early novel combo studies will define which one of those, for example, in this indication, to proceed with. So this is the execution which is going on. As Ugur has already said, this year will also or next year will also be about moving modalities, the modality-centric view into the disease area view, and this also starts to unfold, and here we are benefiting from the fact that with this ADC pipeline, with this ADC panel, and with pumita as a pipeline and a product opportunity, we have created optionality, and this, again, allows us to think broadly of those disease indications we are interested in, so this, for example, means we are not in the situation that we have only one ADC, and we have to drag it across all the lines in a certain indication. We can ask a question: which ADCs, which targets make sense for this disease, and also diversify across settings, lines, and, for example, subsegments of that disease. We are pretty strong in lung cancer. You can see the individual assets we are exploring or developing in lung cancer. I will not go too deep into our disease area canvases because you will hear on a very granular level from Michael and Ilhan about each of these boxes which are shown here. For lung cancer, you can see that we are active in all of these segments which are depicted here. We have registrational trials in first-line non-small cell cancer without EGFR very broadly. Histology-wise, all comers and also all PD-L1 scores, which we are addressing here with our Rosetta Lung 02 trial, pumita plus chemo. In small cell lung cancer, Rosetta Lung 01 combined pumita with chemo as well. Both phase III trials are recruiting patients. However, we already prepare for the next step. We have tested our ADCs here: non-small cell cancer, all three, B7-H3, TROP2, and HER3-free ADC in second-line plus settings, which, as you know, is the sandbox to address and understand single-agent activity, and that already has informed us and motivated us to start proof-of-concept trials of pumita with each of these three ADCs because all of them look compelling in the first-line metastatic setting to inform the next step. What I also would like to highlight is gotistobart. Ugur has already mentioned that positioned here in the second line, plus metastatic setting of non-small cell lung cancer. This is a very dire post-PD-1, heavily pretreated patient setting, and typically in this setting, patients have resistance mechanisms such as high Treg levels in the tumor microenvironment, MHC loss, and this is a perfect place to position Treg killer, gotistobart, in this case. We are also building our canvas for breast cancer. These are the assets we are testing here. Pumita plus chemo in our global Rosetta Breast 01 trial is addressing the segment of patients who are not served with first-generation PD-1, PD-L1 compounds, namely CPS lower than 10. We have an ongoing China phase III, which looks into all-comers in TNBC. As you can also see in the second-line metastatic setting, we explore pumita again with different ADCs in the HER2-low, HER2-expressor segments together with our new HER2 ADC TPAM. This will also be depicted in more detail by Ilhan and Michael. This is our GI cancer pipeline, which we are also building with multiple assets which are positioned here. You will hear about our Rosetta trials, pumita plus standard of care in CRC first-line and in gastric first-line. But also here, we are already combining with ongoing trials, BNT327 with ADCs or other IOs. And in the adjuvant setting, we have positioned in CRC and NSCLC our individualized vaccine, autogene cevumeran, with ongoing phase II potentially registrational trials. So with this, let me quickly wrap up our strategy. We think that we have a number of differentiation factors which are the tailwind to the strategy which I have described. One is the molecule itself. And Ugur has pointed out the differentiating factors on the molecular level, having the PD-L1 versus the PD-1 component. The other is the convergent and deliberate development of both BNT327 as well as our ADC portfolio as a platform. The third is our clear pan-tumor aspiration. We think that with the tailwind of a strong cash position and of having a partner who shares our vision for pumita, we are set up for success here. With this, I would hand over to Michael and Ilhan for more details on the studies. Thank you, Özlem. Good morning. Good afternoon. Good evening. My name is Ilhan Çelik. Together with my colleague Michael Wenger, we will guide you through this section in going into more details about our pipeline and our indications. As already introduced by Ugur and Özlem, in an overarching approach, we want to share with you where are we at the moment in conducting these trials, results which we can share with you, and giving you a perspective on what is next coming. We start with thoracic cancer. And as you already have seen on this slide, we will talk about some of the modalities in thoracic cancer, starting with our immune modulators, but also not only with Pumitamig, but also with gotistobart. So we have an ambition to establish a broad presence in lung cancer by introducing multiple new standard of care changing regimens across both NSCLC and small cell lung cancer stages and subtypes. We will begin to build that through the ongoing pivotal trials listed here, focused on introducing new checkpoint inhibitors either as a monotherapy or in combination with chemotherapy. These trials will form a basis for our novel combinations in lung cancer that we think will position us well against other competitive agents being developed in lung cancer. Zooming now into non-small cell lung cancer. This is a tumor type with significant incidence and where the majority of patients are diagnosed with already late-stage disease leading to poor long-term survival despite the treatment advances of checkpoint inhibitors. This slide summarizes all the data we have generated in non-small cell lung cancer so far as proof-of-concept trials in different indications and lines of treatments in EGFR positive and negative indications, and also looking into the perspective for future combinations with chemotherapy and ADC. All this data we have already presented at ASCO 2024 or ESMO 2024. Of note, on the right-hand side, you can see some data in EGFR mutant second line NSCLC, which I want to point out specifically, which is the efficacy you can observe here independent of PD-L1 expression level. Even in the PD-L1 negatives, you can see here encouraging data. And overall, this setting is known to be not sensitive to IO checkpoint inhibitor treatment. This is our ongoing phase II/III trial for BNT327 plus chemotherapy in first-line NSCLC EGFR-negative. We are testing this against the current standard of care, pembrolizumab plus chemotherapy. Since the beginning, and this is really something which I want to emphasize clearly, we have two independently powered sub-studies for squamous and non-squamous histologies. The phase II dose optimization portion of this study has fully enrolled, and we are recruiting the pivotal phase III portion now. We expect it to publish the phase II data next year. With that, I hand over to Michael. Yes. Hello. Good morning. Quick refresher on squamous. You heard squamous now a few times. What is squamous versus the other non-small cell lung cancers? Most of the others are adenocarcinomas. Squamous make up roughly 30%. In some areas, it's actually a little more. Squamous cell carcinoma usually develops due to some exogenous noxes, such as smoking or asbestos or things like this. It's a pretty nasty tumor. What it means is that not many patients make it out to second, third, fourth line treatment. Actually, most of the studies stop at second line, and that's also the case with our trial, that most of the data will be in second line. It's also a high medical need tumor, right, so the standard therapies, IO therapies, are usually given in front line, and in second line, doctors usually resort to chemotherapy, and it has been named the number one medical need for lung cancer, primarily as the existing treatments are so bad. Most patients, as I said, get either pembro or nivo in front line, but for second line, there's really, really not much. Now, you heard a lot already about gotesidasi b, so I keep this fairly short now, mode of action, etc. But important to understand is that from our phase I, we actually saw a nice signal that was conducted mostly by OncoC4 alone and the later stages with a little bit of help from our side, and again, for squamous, it shares some similarities with small cell lung cancer in that you do see some responses, but then patients relapse fairly early on, and the signal we saw here in this phase I was quite substantial prolongation of the responses with monotherapy, right, which is paclitaxel, which is not the most fancy drug, as you can imagine, that has been used in this setting. Now, you also saw this slide already from Ugur on the phase III. And I'll get a tiny bit more into detail here, what you're going to see also at the North American ASCO in case you're interested in a few days from now. The study had a two-stage design, in part because that was discussed with the FDA on the Project Optimus side that two doses were tested. That's what you see on the left-hand side. And this is also the data that we will be showing in a few days. The results from this also prompted the continuation of the study, which is on the right-hand side. And you heard Ugur saying that this study is recruiting. It's actually fairly advanced in recruiting. So we actually will hope to see some results early to mid of next year internally. And then we'll see what we'll do with this. Importantly, again, it's one of these rare cases where phase II data is almost done in an almost identical setting as the following phase III. You probably are all aware that the main reason why phase III failed for positive phase II's is that something changed between the phase II and the phase III. Usually, the indication was broadened or maybe a standard of care changed or prior treatment changed or stuff like this. This is done with the same sites, the stage one, almost at the same time as stage two, right? So we think we pretty much de-risk that stage two. Again, data will be shown in a few days from now. We're quite excited about this, and yeah, we can't show you a glimpse right now, but you hear from this. With this, over to you. Back to me. Thank you, Michael. We want to close this cycle for lung cancer and looking into another important indication of high unmet medical need, which is small cell lung cancer. Small cell lung cancer remains a challenging immunological cold disease in which responses to immune checkpoint therapy tend to be very short. Nearly two-thirds of patients who are diagnosed with small cell lung cancer have extensive stage disease, which means surgery, for instance, is not possible any longer. As you can see, these patients face much worse prognosis than those with limited stage disease. Based on data from a single arm trial, phase II in China, we started a global phase II dose optimization trial last year to help identify the right dose for the pivotal development. Patients were randomized to receive either 30 milligrams per kilogram or 20 milligrams per kilogram, as indicated on the slide, pumitamig every three weeks in combination with standard of care chemotherapy, so this was a fast way to justify the optimal dose for the pivotal already ongoing trial in first line and in second line small cell lung cancer. The data from the global phase II trial were presented recently at the World Conference on Lung Cancer some weeks ago, confirmed that the data which we have generated earlier from the China trial are also valid in a global population and helped us really to pick the dose for the now ongoing and enrolling global phase III, Rosetta Lung 01 trial. You can see the waterfall plots and overall response rates for both doses on the right-hand side of the slide. And an overview of data we have generated across our studies in small cell lung cancer on the left-hand side. And again, the confirmation of the data generated in China and also in the global patient population is very encouraging. In addition to the waterfall plot and the overall response data, I want to share with you also the data regarding duration of response and the PFS. Both indicates also here we have encouraging data with a median duration of response of 4.9 months and a median PFS of 6.8 months. We look forward to continuing observing this data as it matures and to get more insight and additional insight of the potential of pumitamig in first line small cell lung cancer. So this is the study design of our ongoing enrolling phase II three extensive stage small cell lung cancer trial. As already mentioned, the part one of this study, the dose optimization part is completed, data were presented, and the stage two part is ongoing. So as you can see here, we are randomizing in two arms against standard of care, Atezo plus chemotherapy. And in the treatment arm, we have pumitamig 1500 mg flat Q3W plus chemotherapy. With that, I want to hand over again to Michael for the next part, sharing with you some data which we are generating in proof of concept trials in combination. Okay. Strategy again. Strategy is rather simple, right? You heard Özlem talking about it earlier. For lung cancer, we're doing large head-to-head studies against checkpoints, right? Backbone of chemotherapy, that's the current wave. Now, what we're doing with the ADCs is basically preparing for the next wave. We add the ADCs to pomalidomide, assuming, of course, pomalidomide is going to make it. And we'll replace then the chemotherapy, hopefully, right, with these studies. So basically, the first wave is replacing the checkpoint. The second wave, if successful, would be replacing the chemotherapy. And ADCs are already replacing chemotherapy with checkpoints, right? And we're just coming from the other side. So it actually makes a lot of sense to prepare for this. And in the next couple of slides, I'll show you where we are with this and which agents we favor right now from the ADC portfolio. So the first one is B7-H3, right? Interesting target. Why is it interesting? Well, it's so broadly expressed on so many tumor types. You see them listed down there on the left. And I would say 60%-70% or so match with the expression of PD-L1 and VEGF. So this makes an ideal combination partner for a drug that is so broadly expressed. Now, why was it so late in drug development? You're aware there's not so many B7-H3s out there. That's a relatively simple explanation. First, the ligand for B7-H3 wasn't really known. It's still not really known. There's some hypothesis what the ligand is. And then in the early experiments, when B7-H3 was targeted, it had both lymphoproliferative and lymphodepleting effects, right? So it was a bit confusing. But we're over this right now. So it's now an established target again for many of these tumor types. And we have, specifically for lung cancer, a nice program both for non-small cell and for small cell. But I don't want to miss out on showing you all these other indications that we have phase I studies planned or ongoing as a monotherapy. And again, to emphasize what Özlem said, we're not necessarily planning for a massive single agent program for approvals, right? There may be pockets here that are quite interesting, but typically, we think this is also a combination play. Notable exception is CRPC, and I'll come to this after the break because prostate is a disease that wouldn't make a lot of sense to use a checkpoint inhibitor. Anyways, we've done together with our partner, Duality Bio, a typical phase I with extension cohorts and already found a broad therapeutic index for this drug. The data for squamous and non-squamous looks encouraging, but perhaps not super outstanding for many of the other agents that are in this field, such as TROP2 or others, right? It's clearly competitive, but it's not massive in that sense that you would jump to a phase III alone with this drug alone. And also, notably, squamous is always a little worse than non-squamous for the reasons alluded to earlier. Now, it gets more interesting with small cell. Again, what I alluded to earlier, you can throw at small cell lung cancer pretty much everything and get a response. But the responses are usually very short-lived. And when we see something that has responses of three months, four months, five months, or even longer, then it becomes interesting. And that's exactly what you see here on this slide. What you also see is that between six and nine mg per kg, where we had these expansion cohorts running, there's not a ton of differences from the efficacy side of things. So it wouldn't make a lot of sense to go further. And one of the clearly differentiating factors for this particular B7-H3 is that it's very safe. Why is that? You see the numbers of grade ones and twos here in the light colors. This is for six mcg per kg. This is a dose we'll go forward in most or perhaps all indications. This is a dose of nine mcg per kg. You see a little higher hematologic toxicity. But generally, it's really well managed. So again, ideal combination partners for doublets. We also dream already of triplets that could also be done in our pipeline with a molecule like this. Now, where are we? With the monotherapy, with a single agent, we've done a lot of experiments. You just saw some of the small cell and non-small cell data. We have in several other indications, also data, of course. This is now the combination with pomalidomide. While it may look a little complicated, you'll see similar schemas for many of the other combinations with pumitamig. Need to remember, this is a novel combination. So it's not with chemotherapy. So there's always the question of, is it safe? And what dose do you use? And you can imagine that the agency, the FDA specifically, is asking us to also run randomized comparison of different doses relative to Project Optimus. So this is what we're doing here, both in the EGFR-negative front-line and the second-line small cell. Then we have several cohorts for pretty much addressing all the relevant indications in lung cancer that can be targeted with this agent. So again, from our point of view, the play in lung cancer for this molecule is not necessarily the monotherapy, even though the data that you've seen are competitive. But really, to make a difference, we want to combine it with pumitamig. We're finishing up the part one right now. So we'll move to the second part very soon. And then it's not static like you need to complete this step to start the next step. We have at any point in time also the ability to talk with the agency and go to phase III right away. Yeah, I think that's for the ADCs in lung. Now, Özlem also talked about the mRNA vaccines. You are aware that. Oh, I'm sorry. This is no, this is the other one still. 326, HER3. HER3 ADC also falls in the bucket of ADCs. There are some, but not so many like for TROP2. Again, why is this? Same or similar idea. HER3 targeting isn't so super easy. The initial HER3 antibodies didn't work so well also because HER3 only works through dimerization, right? It only works if it's bundled with another member of the HER family, either EGFR or HER2 or something else. So creating an antibody, not super easy. What we did for this beautiful molecule in license from MediLink, DAR8, topo one toxin, so also very modern, is just a standard phase I. These are the results for patients with advanced disease. Most of these bars here are in lung cancer. You see it down here. Some are in breast cancer, and I'll come back to the same slide when we talk breast cancer after the break, but what you also see here, we went up to dose of 5.5, but we don't have to because we have quite nice activity around two and three mg per kg. Main tox of this molecule is also hematologic, specifically neutropenia, and so we need to pay attention when giving this molecule. But I think we learned how to do this now, also the course of last year with the help of G-CSF, if required, for providing a safe dosing of this molecule. For lung cancer, specifically, we are having expansion cohorts in second- and third-line EGFR-mutated and in squamous and non-squamous NSCLC. We go through the dose levels just as you would in any normal dose-finding experiment. I'll stay on this slide just a moment. Again, it looks complicated, but it really isn't. It's quite logical. We start here with the combination. Remember, same as before, HER3 ADC alone probably would be fine for a small indication or so, or where checkpoints really don't play a role, but we're in here for the combo with pembrolizumab. And so we'll start the combo studies right now. So far, so good. Couple of patients treated. No particular safety issues seen. And from this, we'll move on to the dose expansion and later dose optimization and contribution of component, right? All the things that the agency typically wants us to show. And this is designed in a way that we would both have the individual contribution component solved as well as contemporaneous control, which is standard of care, which would give us an idea of the efficacy relative to the control and potentially could be even expanded to a larger study with registrational intent. We're still here, right? So next year, we will basically move this program to here and potentially to here and hopefully be able to show then that the drug together with pomalidomide can be standard of care. This runs in parallel to the three to four efforts, as said. At any moment in time, we can pick the winner from one of these programs in case we choose to, in case we feel comfortable something is outstanding. Yeah, mRNA, last point here on the lung cancer tour de force. You heard Özlem talking about our mRNA vaccine BNT116. Just as a recap, because we talked about this a few times before, the idea of the fixed vax is it's off the shelf. It's readily available, can be used to get chemotherapy or as its own drug. It doesn't require a person's RNA or DNA to be processed, and interestingly, also the agencies were happy with this approach thus far when we run these studies, right? We are able to demonstrate with preclinical, not the clinical data. The study will actually do months. I don't have a patient before a study. We have one big study ongoing. It's called LuCa-MERIT. We constantly make this study cohorts of 20 or 30 patients. In gray, you see the part that is complete and also that we have reported to with our friends from Regeneron. We started these experiments. Some of these cohorts have sugemalimab as a second drug. We're currently repeating some of the more interesting data that we found with pomalidomide. Same idea, right? We think pomalidomide is probably better in this setting than also the checkpoint inhibitors. But we want to be sure, and so we repeat some of these experiments, even though the experiments with sugemalimab were quite nice. I'll show you some of the data we had. This was a very first entry into human cohort on the very left-hand side that was monotherapy vaccine. And if patients were interested and fit enough, the sugemalimab was added. You again see this pattern. You see a response, and then it becomes durable, right? This is what you want to see. Obviously, you want to see a lot more patients responding. But if you can keep patients in response, that basically shows you the vaccine works. Now, there was a lot of skepticism that you can pair the vaccine with blunt chemo. And the experiment with docetaxel changed this for us and for perhaps also the scientific community. But it's not that the chemotherapy affects not at all the generating T-cells, but not to a way that would be detrimental to the success of the experiment. So same thing. We saw some nice efficacy. Later study where both the vaccine and sugemalimab were given upfront together. The two most recent published data we have were in frail patients. Remember, about 10% or so of lung cancer patients either don't want to receive any type of chemotherapy or are simply not fit enough for that. It's a tough regulatory pathway, but it's also a pathway that is wide open. There's a few approvals at ESMO in Europe, for example. But otherwise, it's pretty open. Then there's earlier stages, stage three. After resection and radiotherapy or without the possibility of getting resection, but after chemo and radiotherapy, we also saw the vaccine showing some nice results. Anyway, this concludes the vaccine section. Over to you. Thank you. Okay, I want to summarize this section regarding thoracic cancer with some take-home messages regarding our development in non-small cell lung cancer, small cell lung cancer with the different modalities. Overall, we want to execute the initial pivotal trials to establish the presence in multiple thoracic cancers and tumor types and treatment settings to enable future combination studies. So this is our aim. And with that, we are generating now a break for you after all the science information, a lot to digest. And after the break, be curious and stay with us for the further indications. And we will move on with breast cancer after a 15-minute break. Thank you to our session. As mentioned before the break, we will move on with the breast cancer indication and share with you the different modalities which we are developing in the breast cancer indication. And so this is, again, our diverse breast cancer pipeline. And as you can see, we will talk about the immune modulator, pumitamig, and some of our targeted therapies. So this slide was already presented by Özlem in the beginning. And again, a short recap indicating that we are developing pumitamig in TNBC first-line metastatic with two trials. One is a trial in China in all comers in combination with chemo. The other one is the combination with chemo in CPS less than 10. By definition, this is the PD-L1 negative population with the highest unmet medical need. And in addition, we are developing hormone receptor positive HER2 -low. And regarding this, Michael will share with you some data. So in looking into the TNBC indication, these patients are facing problems due to limited therapeutic options. As you know, the majority of the patient population is in stage three and four. And the treatment option, depending on the PD-L1 expression level, is either chemotherapy or above 10 in combination with pembrol. Still, the treatment outcomes vary, and they are limited. And so the requirement for additional and innovative treatments is high. This slide, again, summarizes the data which we have generated in TNBC with pumitamig in combination with chemotherapy. These are data from our proof of concept China trial. And as you can see here, this is already presented several times. And last time, you have seen the data, which indicates, again, as already mentioned for the EGFR mutant second-line setting, that pumitamig in combination with chemo is effective independent of the PD-L1 level. And this is nicely summarized on the table on the left-hand side. And you can see different PD-L1 levels in the ITT population and encouraging median PFS of 13.5 months. On the right-hand side, you can see here the interim overall survival. And for the different PD-L1 levels and the ITT population, you can see that we are ending up in a range of 20-24 months. Important to note is that compared to the benchmark data in chemo in the below 10, you can see that we are really meaningfully above what we see with median overall survival, 15.2 months, and median PFS of 5.6 months. So based on the data from China, which I shared with you before, we have initiated a dose-finding study also for this indication. So this is a study which we have started last year in summer to investigate different doses of pumitamig in combination with different chemotherapies. And the cohort one is going to be presented. Data out of this cohort one will be presented in a few weeks at the San Antonio Breast Cancer Conference. We are investigating also other chemo combination treatment choices. As you know, in TNBC, it is different depending on the region and the preferences. So this is our study design from the combination trial in TNBC first-line, TNBC PD-L1 negative. And so this study is open and well on track recruiting patients within 2025. With that, I hand over again to Michael to give you more details about our combo. This clock says zero. I don't think I have any time left. But maybe that can be changed. Anyways, so for breast, our main play, at least in the next few months and perhaps year, is trastuzumab deruxtecan or short TPAM, perhaps also known by some of you under its old code, BNT323. This was a molecule that was the first of the ADCs that we've in-licensed from our partner, Duality Bio, in China and was back then also the most advanced, so what Duality did was a typical phase I, phase I two study exploring different dose levels, and you see here also two cohorts in HER2 -low and in HER2 positive disease in breast cancer, and this is the outcome of this phase I of these phase I data, a fairly large sample for phase I, different doses. And there's perhaps two things to take note or to take away from this. One, the higher doses yield better responses, unsurprisingly. And number two, we also saw some really nice efficacy at the lower expression levels at HER2, at IHC1+ specifically. We went up to 10 mix per keg, then went down to eight and to six, and had a discussion, or I should say, Duality had a discussion with the agency. And eight mix were taken forward to this phase III study. Now, before I go through where we are with the phase III study for TPAM, just to note that this molecule is pretty much de-risked in a way that, number one, some of the studies have been modeled after existing studies from other companies. But more importantly, if you've heard the press release from Duality recently, the HER2 positive study was positive, right? So they declared the study that was conducted in China, which was a randomized phase III study just in China, was positive in HER2 positive disease for this drug. Now, why is HER2 positive not our phase III study? Very simple. You probably all know this. T-DXd is approved in most countries. We couldn't do a study against chemo as Daiichi did in China. Again, point being that our drug versus chemotherapy in HER2 positive was positive. Data have not been released or published yet. We know they're positive also from Daiichi's press release. In parallel to that study, a global study was started. This is this study in HER2 -low. I guess in FDA speak, this study is well underway. We will need to wait for results, perhaps a few more months, to know what it would like. It's a very simple design and with a PFS endpoint. Now, coming to the assets that are a little earlier. Same theme, right? Like we're doing for pumitamig plus chemo phase III trials. Now we're exploring in parallel pumitamig plus ADCs. And for doing this, we first need to know what the single-agent activity of the ADC is. Is it even sensible to do combination with pumitamig? And if so, then do the combination rather quickly. This is basically what this slide shows. So we'll start, as you would for all novel combination later line setting. And we do this with TPAM first. So again, TPAM plus pumitamig in a variety of starting doses here. But as said, for BNT323 or TPAM, we know a lot about the dose. And we don't think we'll run into too many challenges with the combination of pumitamig, again, for the reason that, one, pumitamig is a fairly safe drug, more than 1,200 patients by now treated. So we know the safety profile very well. And number two, there's also a ton of combination data already. And so we still need to do this. But we do this fast. And we move quickly also then to the expansion cohorts, which would then address the same segments that you know from other breast cancer studies. So TNBC, but we will also look, of course, with TPAM targeting HER2 and everything between HER2 ultra low to HER2 -low to HER2 positive in an effort to really think if data are outstanding relative to existing data, that we would be able to replace existing HER2 ADCs, right? So this is the goal of this. And again, similar to what you saw for HER2, sorry, for HER3 and for B7-H3, we're at this part, dose escalation right now. But this one should be open kind of summerish or so that we will be able to get into tangible data sets for efficacy and safety. Yeah. With this going on to BNT326, this is, again, our HER3. You heard about it already in the setting of lung cancer. HER3, by the way, is not as broadly expressed as B7-H3, but it's expressed in the biggest tumor types that are out there, right, specifically in breast cancer and in lung cancer, so where HER2 targeting ADC wouldn't work, TNBC, because TNBC is obviously then HER2 negative, HER3 ADC could very well work, so that is what we're doing right here. We're having cohorts, again, as monotherapy in a variety of indication and then move fast to the combination, and we started the combination now with HER3 and osimertinib. Early days, right? I alluded to this in the lung cancer part, but again, in about six to nine months, we hope we have something that can guide the way whether we go into several or some of these breast cancer indications. And these data here from the combination will help us to show that w ith this. So also wrapping up this section for breast cancer. So again, the take-home message for you is we want to execute our initial pivotal trials to establish our presence in multiple breast cancer subtypes and treatment settings. So grow presence through novel combination. This is our aim. And so this is a theme overarchingly in all indications with all the ongoing trials we are following. So it's a central piece of our strategy. And with that, I want to move on into the gynecological cancer types. Handing over to Michael again. I hope you don't get too nervous about this swapping all the time. But yeah, bear with us. Okay. Gyne cancers. One of the features is that checkpoints play at least questionable role, but are definitely not ingrained that much in gynecological cancers as they are in several of the other tumor types, right? You might have heard the results of the B96 study in ovarian recently, which was after, I think, 11 failed studies in ovarian cancer for various applications of checkpoints and various checkpoints was the first one that was positive, and now the community is debating whether that's actually real or not and whether that will be a major success or not. Don't want to go into this, but for us, we're following a very simple strategy, right? We basically have our ADCs that will work most likely on their own. I'll show you some data in a second in ovarian, cervical, and also endometrial. But if we can, and we are very ready to take a little bit of a risk here, we'll combine them with pumitamig. Same idea. Pumitamig is not your run-of-the-mill checkpoint, right? It has also the VEGF effect. And we know already from the early days of pumitamig that it works also in PD-L1 negative patients. All right. So several combination studies in several disease indications you see on the left, cervical, platinum-resistant ovarian, and endometrial cancer. Starting perhaps with the most obvious one, TPAM or BNT323 in endometrial cancer. This slide we've been showing now for two-plus years because it's the only published data we have on BNT323. Rest assured, we're going to change this. We'll have data presented at a conference in half one, or I should say maybe even Q1 next year on a much larger sample than these handful of patients here. This was, again, the drug that we in-licensed from Duality as a first. And back then, the idea was there's nothing out there for endometrial cancer that is HER2-positive. And we wanted to jump on that idea and generate some single-agent data. And once we did that and also had this much larger sample size, we also embarked on a phase III study. So just before I show you the phase III design, we occasionally get the question, "What's happening with your HER2 ADC? Is it still alive?" Well, it's very alive and kicking. We have one positive phase III. This is the China study that I alluded to earlier. We have one phase III study that is nearing completion on HER2-low. And we have this study that we started fairly recently in endometrial cancer, right? So this is the third phase III study we're doing for this very efficacious resensitization step. Here we are investing in single-agent chemotherapy and advanced endometrial cancer. All these patients need to have a modern frontline therapy. The early mAbs that were approved one or two years ago in this setting. And so when discussing the design with several agencies, we came to the conclusion that it would be best to single out this particular group of patients that have received frontline treatment with a checkpoint inhibitor. Because once this study reads out, it needs to be relevant for the, specifically the U.S. population. And we always see a very high uptake of first-line both in the MMR high and MMR low patients. So all of these patients will be treated after failure of the first-line checkpoint plus chemotherapy treatment. We hope to be able to report on these results a couple of years down the road from now. As said, the study has just started. And part of a potential accelerated approval, as you all are aware of, for the single-agent study that I just alluded to earlier, is that the confirmatory trial needs to be well underway or even better fully enrolled or near fully enrolled. And so that's why we are currently making a lot of efforts to get this study recruited. We talked much during this few hours about one of the ADCs that is also in our pipeline for a while, BNT325 or TROP2. Why is that? Well, quite simple. Waiting for therapy to be the single-agent therapy. We have some double-agent randomization. And also, this is also an area that is interesting for TNBC where we have combined this as our first ADC with sacituzumab. So hopefully, we'll have advanced and mature data of this drug together with sacituzumab and TNBC around mid next year. So this is also quite exciting for us because, as you saw for the HER3 and for the B7-H3, we're just starting these experiments. And we don't have a ton of data to present. But for the earliest cohort that we started, which was 325 or the TROP2 plus pumitamig. W e will have some mature data in TNBC as said, like around mid next year. For the monotherapy, this is what we had, right? So nice response rates. Also, duration of response in ovarian is interesting. But we also admit that the space of ovarian cancer is super competitive with several TROP2s ahead of us. So I don't think we will pursue the monotherapy necessarily here based on these data. But as you heard earlier, this is anyway not our play. We think the combo specifically with 327, but perhaps also with other agents, is the most interesting thing that we can do. Now, very briefly, in smaller or not smaller indications, cervical cancer is, as you know, the biggest women's cancer of them all. It's just small in a sense in Western countries due to the prophylactic vaccine. It's a little bit less prevalent these days, thank God. But we're generating a little bit of data in cervical for this drug, actually also for 326, not depicted here. So for the HER3, that looks interesting. And we have some more data in other indications that are not women's cancer. We just didn't find another place in this presentation. So again, for 325, this is what I alluded to earlier. This is the early data we had, but we will have with quite a few more patients mature data on this combination soon. So this will be the most mature data of one of our ADCs plus pumitamig. Don't want to oversell this, right? So the individual drugs also still have their own individual toxicities. But at least for us, it validates our strategy that combining the ADC with pumitamig is feasible, that the additional toxicity is manageable if it's even relevant in the case of pumitamig, and that it gives us enough line of sight to decide if we pursue this further or follow a different path. And we do this strategy with all of our ADCs and pumitamig, as you probably have figured by now. So this concludes the section on gynecologic cancer. I think, well, I'm sorry, the cervical cancer and the PROC, we still have a few experiments ongoing. I tend to forget these because they are not relevant, but because we're typically talking a lot more about ovarian than about other indications. Now, in ovarian, as I said earlier, if I go back for a second, in ovarian, as I talked earlier, it's a super competitive field, right? So for us to pursue monotherapy in this area would require outstanding data. We may have some data that is really interesting. If it's outstanding, also it's a function of the duration of the responses that we're seeing. So we're not quite there yet declaring anything. But for pumitamig as monotherapy, you see here quite some nice responses. And also the duration of response is interesting. Remember, B96 is really the first study that validates or that suggests, I should say, that a checkpoint can work. Also, VEGF, many studies in this field in ovarian cancer have plus minus bevacizumab, right? So bevacizumab is not fully entrenched in ovarian cancer. It's used by some, not loved by many, also because of bleeding complications. For us, these data are clearly encouraging for ovarian cancer, for pumitamig alone, in the sense that it could be a valuable addition to an ADC or to plain old chemo. But we want to see these data mature further to take a decision because, as said, super competitive field. Similar things apply to cervical cancer. As we said before, it's still a very important and very prevalent cancer, mostly in formerly called Third World countries. But from a pure incidence, it's even still quite interesting. If you talk to people that work in the field, it's still a sizable problem in the United States and in other countries, other Western countries. These are our data in cervical cancer. We think, again, from a combination perspective, this drug would easily lend itself to combine with the little data that you saw for HER3 or for B7-H3. This is probably a path we will be thinking about further over the course of the year once these data mature a bit more. That concludes the gynecologic cancer section. Again, from a take-home message, if you wish, we have mature data for single-agent TPAM. We haven't shown you these data because they're not published, but they are mature. We're very confident on the data that we know both the side effect profile and the efficacy profile. We had discussions with the agency, and we have started the potentially confirmatory phase III trial. For this to mature a bit further and have a few more patients enrolled, we'll also determine if and when we will file the single-agent data. Now, for sacituzumab and ADCs, not much data with the combination of ADCs in these particular indications, cervical, ovarian. We're working on this. We want to see the individual data mature to know if we want to play in these areas, specifically ovarian competitive, cervical not so competitive, and could be something for us to think about more. Yeah, with this, we'll get to GI. Thank you, Michael. Yeah, as mentioned by Michael, so again, our take-home message is clearly we want to execute and accelerate the work on the monotherapy and combination data in the proof of concept trials, but for the next section, so we want to focus on GI cancer, and on this slide, again, we repeat what we are going to talk about, so we will talk about pumitamig data. We will talk about a combination with a bispecific antibody, which was introduced by Ugur already at the beginning, bispecific, which we are developing with our partner Genmab, some data with ADCs, but also with our messenger RNA cancer immunotherapies, so this is, again, our canvas indicating in which settings in GI cancer we have studies ongoing, and as you can see, again, the solid line boxes indicate in which indications we have registrational trials announced and open. So in colorectal cancer, MSS, and in gastric cancer, the dotted line boxes indicate really that these are proof of concept trials ongoing either in monotherapy or in combination with pumitamig or with an adjuvant setting with our individualized vaccine treatments. So MSS CRC. So this is a significant global incidence of colorectal cancer with an unmet high medical need and the requirements really for new therapies. And as you can see, again, on the left-hand side, so the majority of patients are in late stage, stage three and four. Important to note that only 3.5%-5% of stage four colorectal cancer are MSS high, so sensitive to checkpoint inhibitor treatment. The majority is not sensitive to that. And so especially the MSS, CRC indication requires additional treatment option despite the established standard of care, as you can see on the right-hand side. Currently, Cetuximab plus chemotherapy is the standard of care with 30 months of overall survival and a five-year survival rate of 15%-25%. Is this enough? Most likely not. And therefore, some treatment options increasing this level are highly required and demanded. So this is a brief introduction into what we are doing in colorectal cancer. This is a phase II study, signal-seeking trial, which we are running 40 patients in total. We want to generate data for safety and signal-seeking with different chemotherapy regimens. And so this is an ongoing trial, and data are not yet available and will be shared in time. In parallel, as you have seen, most likely announced recently, we have really initiated our phase II/III study with pumitamig in combination with chemotherapy in colorectal cancer first-line. This is a study schema, phase II part for dose optimization followed by a phase III part. The other indications I mentioned already for the GI section of importance is gastric cancer. Also here, again, you can see that there is a high unmet medical need for metastatic gastric cancer patients as long-term survival outcomes are very poor and treatment options remain limited to chemotherapy in biomarker-negative patients. As you can see in the CPS less than one, the chemotherapy option is leading to 12.5 months median overall survival. In the above one, you can see in combination with nivo and chemo, median OS is 13.8 months. Also, this indicates really clearly the need here for better treatment options and additional treatment options to elevate the efficacy of treatment and the perspective for patients in need. Again, I want to share with you also our study design of our phase II/III study, pumitamig in combination with chemotherapy in first-line gastric cancer, similar approach of phase II dose optimization part followed by a phase III registrational part. These studies are open and will enroll in due time. In colorectal cancer, you have seen in the scientific, in the preclinical section, the combinations which we have really investigated with also an IO drug, which is a bispecific drug which we are developing with our partner Genmab. It's 4-1BB. In this setting, also MSS, CRC, we want to see the additional contribution of this bispecific in a dose escalation part, which is ongoing, as you can see on the left-hand side. Then we want to do a dose optimization part in second line and in first line MSS, colorectal cancer, followed by a pivotal study in phase II, which will come a little bit later in the sequence. One of the most difficult to treat indications in the GI area is pancreatic cancer. You know that the life expectancy of pancreatic cancer patients is low. The treatment options at the moment are chemotherapy, leading to really absolutely low numbers in median overall survival and 24 months overall survival, for instance, with different chemotherapies as indicated here, are with 10% only. The five-year survival rate is 3% only. No need to really indicate here that there is a high unmet medical need, and therefore, we are also focusing on this indication and want to really develop treatment options with pumitamig in first-line TDEC patients. So this is a signal-seeking proof of concept trial, which we have initiated, testing different chemotherapies as indicated here with sunitinib. And we believe that this will be the foundation for combination trials in this indication, also with ADCs and all the other treatment options which we have in our pipeline. So this is, of course, really absolutely needed to indicate. So the combination with chemo is not the only thing we should evaluate. So there is also a need to combine with ADCs. And we have developed an ADC, which is based on the known expression patterns of CA 19-9. Most of you know this is also known as a tumor marker, usually Sialyl Lewis A. And you can see the expression of this target is very high in different GI indications, in pancreas, in bile duct, in colon, in ovary, in endometrium. This is a perfect target to be really investigated with our CA19-9 ADC candidate, which we will move into the clinical dose escalation setting soon. We will investigate different dose levels followed by expansion cohorts for PDEC, focusing on second-line PDEC here and a basket trial in gastric, colorectal, and others. I'm summarizing here also again. We want to really execute again here, execute and accelerate our first pivotal trials to establish pumitamig, so in colorectal cancer, in gastric cancer, which is really in focus for us in the GI cancer space. We want to also further evaluate and investigate as fast as possible combination with novel approaches, either with bispecific antibodies or with ADCs. Moving to GU. Okay. GU cancers, as indicated on this slide, again, you will see some data for the immune modulators, sunitinib and cabozantinib, but also for our ADC B7-H3. Do you want to do that? Yeah. So for sunitinib, there will be data or there are data from renal cell in China, both for the clear cell and the non-clear cell. And for prostate, as you just heard, we have some data for cabozantinib and for the B7-H3, both of which would not necessarily be with PD-1 or PD-L1 because they simply don't work in prostate cancer. Maybe I'll let you talk about sunitinib first, and then I'll continue. Yeah. So these are data from our clear cell and non-clear cell study conducted in China, first line and second line. In 53 patients, sunitinib was investigated either in Q2W or Q3W regimen. And the results of this are indicated on this slide. So we see for the clear cell population, second line plus, overall response rate of 25%, disease control rates over 80%, median duration of response 19.6. All this is very encouraging in line with a median PFS of approximately 11 months. So this is definitely encouraging enough to further investigate sunitinib in combination with additional novel approaches with ADCs or other drugs out of our pipeline. Same, you can see here in first line, non-clear cell, RCC, across subtypes, same pattern, high overall response rates for this disease, disease control rate over 90%, 25 months duration of response, and 15 months of median PFS. Now this is your part, Michael, to talk about the ADC. If you're wondering how many other disease areas we're going to show you, this is the last one. But you're not quite done yet. There's a few other slides from Özlem and, of course, from Ramón. Okay. So three to four or our B7-H3 again, right? If you remember the expression patterns, there was probably somewhere in the middle or a little higher than the middle. So pretty highly expressed in this space. And again, not to hammer home that message because most or all of you know this anyways, but here we would for once not do combination with sunitinib for the simple reason that neither VEGF nor PD-L1 plays a role. And while we're bold in many of our clinical experiments, we're not so bold that we combine things that really don't make any sense. So we have for BNT three to four several cohorts ongoing as a monotherapy in this setting. Why? Well, it's a slightly confusing area, at least for me, how this field develops with the radioligand therapies, Pluvicto specifically, but there's also newer ones, how they come into various states, first line, second line, behind or together with the newer anti-hormonal therapies, etc. Our approach, again, is relatively straightforward because we don't know exactly where this field is developing. We started off by multiple refractory patients, third line plus, right? That's where our initial data are. And that's where we saw also that this drug as a single agent works better than any other available chemotherapy therapies that are out there, at least if you believe the published literature. But we also think this is such a high area of need where also very or relatively benign therapies in terms of their toxicity profile and also therapies that are easy to give are off the shelf and don't require special institutions or shielding or anything like this would find its role. So this is our initial data from BNT324. Again, this is a third-line plus area, right? So these patients have exhausted all the available hormonal therapies and have either one or two, and in many cases, more than that, treatments received from the chemotherapy spectrum. And what you also see is here from the endpoint, it's rPFS, right? So r is the radiographic progression-free survival. So it's basically what we need to see is that the tumor doesn't progress. We obviously also look at the PSA and other factors in the blood, but this is the established standard for these types of patients. And similar to what you saw before, six and nine mg per kg, both work fine, and they don't seem to have big advantages over each other, which also then paves the way for a potential phase III trial that we're thinking of. So we're currently actively discussing what to do with these data, and we think there's some really interesting potential avenues both in these later line settings where these data were generated, but perhaps also in an earlier setting. Yeah. So this is the last slide of our little part here, and I would hand back to Özlem to drive us home before Ramón. The mic is not working. No? Now it works. So you have heard about our disease area strategy, and in some disease areas, we are more broader, in others, a bit leaner. And you might ask, what is the reason for covering all these disease areas? And the answer is pretty clear. With having the pipeline and the product opportunity with pumitamig, we can go into all these disease areas. You have clearly seen that pumitamig triggers this opportunity, but not only because we can, but also we must. If we look into other development architectures, for example, of first-generation PD-1, PD-L1 compounds, it's very clear that those development streams which have gone broad and fast have been the successful ones. And having created the opportunity with our ADC portfolio to match the multi-disease area strategy given by pumitamig, we are even more encouraged to do that. With this, we now move to the next modality. We have discussed this morning a lot about PD-1, PD-L1 blockade. The mode of action for first-generation PD-1, PD-L1 checkpoint inhibitors is that they reinvigorate T-cells directed against tumor mutations, tumor antigens, which are already around. So they do not induce new specificities. They reinvigorate those which are already there. And in tumors which have a high tumor mutational burden, the diversity, the multi-pronged nature of these T-cells is higher than in tumors with low tumor mutational burden. And this is also why checkpoint inhibitors work better in tumors like non-small cell lung cancer and melanoma because you have this diversity of pre-existent T-cells there very broadly. In principle, and this is a hallmark of cancer disease, the efficiency of spontaneously generating T-cells against tumor antigens is very poor. So you find only low numbers of tumor antigens recognized by spontaneously occurring T-cells. And here is where this new next modality comes in, namely cancer vaccine-type immune therapies, which have a purpose of generating a new diversified polyepitopic T-cell pool. And on this T-cell pool, checkpoint inhibitors can act again to reinvigorate. This is also the reason why, in principle, in patients which are checkpoint inhibitor refractory and resistant, the combinations of checkpoint inhibitors with vaccine-type immune therapies work because you have created a novel T-cell pool. So the purpose of this type of immune therapies is to generate new T-cells. And one of immunology tells us that in order to proficiently generate T-cells against tumor antigens, which is not trivial at all, you need two critical components. One component is the very antigen, the tumor antigen against which you want to generate these T-cells favorably or preferentially. These are multiple tumor antigens for a multi-pronged approach, so it's the antigen, but what you also need is an innate immune signature, innate immune modulation and activation, which ensures that, activated by the tumor antigen, the right T-cells have been selected and start priming. Priming, expansion, differentiation of these T-cells is supported by interferon type I dominated innate immune signatures. This is actually one of the reasons why when we, the scientific founders, started our journey, we selected the mRNA platform as our core vaccine-type immune therapy strategy because mRNA, because mRNA as a format, as a chemistry, comes with an intrinsic innate immune stimulatory activity. And this also explains some of the data you might have seen last year at ASCO and more prominently this year at ESMO from our friends out of MD Anderson, which shows that in tumors with high tumor mutational burden, non-small cell lung cancer and melanoma, adding the SARS-CoV-2 vaccine, which does not bring the antigen, the right antigen here, but which brings the innate immune stimulatory property of mRNA, leads to a significant overall survival benefit. So what this in principle shows is the proficiency of mRNA to bring the second component of inducing potent immune responses, namely the innate immune signature. That means what you see here in principle as an effect is like combining a checkpoint inhibitor with a TLR agonist on steroids, but it does not address another important component, namely the right tumor antigen. So our mRNA platform, which we use for our cancer vaccine-type immune therapies, is using mRNA in a nanoparticulate form. The specific platform version we are using in our ongoing clinical trials is based on uridine mRNA, which has a higher propensity to bring in the innate immune stimulation and interferon type I effects. These are nanoparticulate mRNA formulations based on lipoplexes, which you can administer intravenously, and they target specifically to lymph nodes, compartments where immune responses are primed and triggered and bring the antigen and the innate immune signature to the right place. We are using this platform for two purposes. We deliver tumor-associated antigen mixtures, which are indication-specific. These are off-the-shelf vaccines, our fixed vaccine to patients. The other version of this is our iNeST, our individualized approach, where we use neoantigens based on cancer mutations, not tumor-associated, but cancer-specific antigens, which are unique to every individual and therefore require true individualization and on-demand production. This platform has been extensively tested in both variations. We know from studies we have already published and preclinical work as well that both components of proficient immune antigen-specific T-cell response induction are delivered. The pro-inflammatory innate immune signature, which you see on the top from one of our studies with all the cytokines, and Ugur has also reported that delivered in a parenteral manner, and also high-magnitude T-cell responses against the encoded antigens on the bottom, including self-antigens, which shows the propensity to also break immune tolerance. This is the summary of ongoing and recently completed clinical trials. On the FixVac vaccine side, we have at the ESMO reported that our BNT111 trial, which is a melanoma off-the-shelf vaccine, has met its primary endpoint in PD-L1 refractory and resistant melanoma. The primary endpoint was objective response rate of the combination of BNT111 with cemiplimab Regeneron PD-1 compound, and this combination showing an objective response rate, which was significantly above historical control, which is 10%. We have observed 18% objective response rate, with 60% of these responses being complete responses. Duration of response was not evaluable yet, and we will get this data later next year. We have an ongoing clinical trial with our BNT113 FixVac vaccine, which is being conducted in HPV-16 positive, PD-L1 positive head and neck cancer. This is a phase II trial for which we will see a first readout in 2026. This is a randomized trial where we compare in first line BNT113 in combination with a standard of care pembrol against pembrol alone. Then we have BNT116 ongoing. Michael has extensively talked about this compound. You have seen that we are very broadly looking into different settings in non-small cell lung cancer and segments and combination partners, and the plan is that next year to identify the right setting. On the iNeST side, which is our individualized vaccine called autogene cevumeran, we have three clinical trials in the adjuvant setting ongoing, randomized trials, which the adjuvant setting is the one in which we see the best positioning of iNeST, of our individualized vaccine. The reason is that in this early setting, tumor burden is low. We have minimal residual disease, and a vaccine-based approach where you induce T-cells is in principle a man-against-man fight. So on the cellular level, which means that low tumor burden is of benefit. This is also a setting where immune suppressive mechanisms by the tumor disease are not established yet. Tumors are not heterogeneous, but clonal, and immune proficiency of the patient is still intact. The colorectal cancer trial where we have selected the CT DNA post-surgery positive stage two high-risk stage three population, and where we compare iNeST to observation only after standard of care surgery and standard of care adjuvant treatment has finalized enrollment of patients. And we will have readouts next year in 2026 with the final readout expected at the end of 2026. The two other trials in adjuvant setting of pancreatic cancer and bladder cancer are more early in their patient enrollment status and are ongoing, both as well potentially registrational trials, which are phase II and randomized. What I would like to do on the next couple of slides is share with you some insights from another trial, which is also on this slide, our first-line melanoma trial with BNT111, where we have compared BNT111 in combination with the standard of care or one of the standards of care pembrol in comparison to pembrol alone. This was a study which was not positioned in our favored indication simply because, as you know, the drug development paradigm is that you start with advanced settings before you with a new compound can work yourself into earlier settings or adjuvant settings. This trial read out and has been presented at ESMO a couple of weeks ago. As I said, this is a phase II trial in patients with first-line melanoma, unresectable, locally advanced melanoma, and metastatic melanoma who have not received treatment for the advanced setting yet. We have compared against pembrol, have combined in the investigational arm iNeST with pembrol. The key findings are that this trial did not meet its primary endpoint of significant improvement in PFS. We have observed in the pembrol arm PFS, a median PFS of 7.9 months, which is a bit lower than expected from benchmarks, and in the combination arm 8.3 months. What we, however, have observed is a difference in the 12- and 24-month OS rates in favor of the combination. This data is confounded by the fact that we allowed crossover of patients from the pembrol arm only into the combination, and one quarter of the patients used this opportunity. We have observed good safety. The vaccine was also, in combination with pembrol, well tolerated and in line with what we see in general also in other trials with this platform. Immunogenicity was strong and showed that the vaccine in principle, also in this metastatic setting, does what it is expected to do. We achieved multi-antigen or multi-neoepitope immune responses in the majority of patients. Immune responses were of high magnitude in the 10%-15% of circulating T-cells range, and immune responses were also of durability. We looked closer into the PFS data in a retrospective analysis in order to generate insights from this study. What we observed was, and these are Kaplan-Meier curves for PFS, where we distinguish or stratify patients who have a narrower or broader breadth of immune responses, meaning patients who have developed an immune response against only one or two or three or more of their vaccine antigens or their mutations. What we have observed for the combination arm was that a trend of incremental PFS improvement in patients with higher neoantigen response breadth, which indicates that optimizing the breadth of immune responses and of the capability of our vaccine to induce these will benefit the outcome in our clinical trials. Another observation is shown on this slide. As I pointed out, the secondary endpoint overall survival showed numerical trend of favoring the combination for the 12-month and 24-month OS rates. This was a secondary endpoint, and no formal testing was performed. However, we looked into markers which might correlate with better OS. We made two observations here. One observation was a trend of improved OS in patients with immune cell PD-L1 high as compared to immune cell PD-L1 low. Interestingly, this was only the case for the combination arm, not the pembrol arm only. And interestingly, the tumor cell PD-L1 status did not play a role in terms of predictive value for both arms. This again indicates that our vaccine might benefit from combination treatments which increase the hotness of the tumor microenvironment and create also in tumors which are per se not PD-L1 positive or high a situation where we can trigger the effect here. Another observation we made was that a trend of improved overall survival in patients with tumors with low mutational burden treated with a combination versus the pembrol arm, which again shows that tumors which basically don't benefit from checkpoint inhibitors are the ones which could benefit most from combining with vaccine-type immune therapies. And this again supports our choices we have made for our adjuvant setting with tumors like PDAC, pancreatic cancer, and colorectal cancer, which are more on the very low to low-middle tumor burden side. So, with this, to summarize our ongoing and next steps for our mRNA cancer immunotherapies in terms of autogene selvemeran, our individualized vaccine, our goals are all about bringing it home in the adjuvant setting. The next readouts to look out for will be 2026 for our colorectal cancer adjuvant trial. The other two trials in pancreatic and bladder are going on, and here it is about accelerating the enrollment. With regard to FixVac, Michael has already pointed out all our activities with BNT116, which we are combining with different compounds, novel ones, and also assessing in different lines and subsegments of non-small cell lung cancer. And you will hear more about data from these efforts also next year. And then for our BNT113 head and neck trial, we expect data next year from our phase II/III trial. So this year was silent for the COVID vaccine and iNeSTs, but next year you will hear more. Thank you. Thank you, Özlem. Let's see if this works. Can you guys? Yeah, you can hear me well. Thank you very much, Özlem. I'm very happy to be here with you guys. And despite the fact that I haven't been with the company for long, it's great to see several familiar faces amongst you with all the interactions we have had over the last months. So we will start this morning with our mission, translating science into survival. And if you think about it, this puts the patients at the center of everything that we do. And I do believe that value creation delivery is exactly having the same starting point. So today, I will be covering mainly three topics where we have been executing this year, the principles and financial levers that we are applying on the R&D part of our P&L, and hopefully exciting you about what's to come for 2026 and the years to come. So 2025, I think, has been a year where we have successfully defended our COMIRNATY franchise. We enjoy very healthy market shares, stable pricing, strong brand recognition, and I think that has been reflected into our results that we talked about in the last quarter. As we advance our key oncology, pan-tumor, and clinical execution, you have seen already from Özlem, from Ugur, Michael, and Ilhan, we have more than 20 phase II and phase III oncology trials ongoing and more than 30 novel combination cohorts across tumors. If we talk about M&A, business developments, and collaborations, I think this has been quite a good year. So earlier in the year, we completed the acquisition of Biotheus. Then, towards the summer months, we completed as well what I would say a foundational partnership with BMS to maximize pumitamig. And as we speak, we are in the process of closing the acquisition of CureVac that we are aiming to close till before the end of the year. And then finally, as we strengthen our financial position and continue to drive innovation, for all of you that were listening to our earnings call last week, we have increased our revenue guidance to EUR 2.6-EUR 2.8 billion from EUR 1.7-EUR 2.2 billion that we had at the beginning of the year. And also, we have further solidified our cash position. We closed last quarter with EUR 16.7 billion in cash and cash equivalents, and that is, of course, supporting all of the scientific efforts that we have been hearing from my peers, but also keeping optionality for us to keep moving forward. As we drive impact and innovation, I am very encouraged to see that we are expanding our later stage oncology pivotal trials. As you've seen in the last three years, we have significantly increased the number of trials from 10 in 2023 to more than 20 in 2025, and all of that being done with more or less the same levels of R&D. Can you hear me, or do I need a mic? Yeah, but can you hear me or? Oh, perfect. Thank you. And we have done this more or less with the same R&D level of spending. So 2023, EUR 1.8 billion. We are going to be closing this year around EUR 2 billion-EUR 2.2 billion. Now, if you ask me, because I know that most of you will already be asking, "So what is going to be the guidance for 2026?" so we are still working on that. I think it is too early to tell you if we are going to be more or less having the same levels of expanding. I think as we expand our phase III trials and widen our net of targets, this might change a little bit, but anyways, I think this has been good financial steering of the company, so we have these three levels that I want to be talking about. So first is, of course, active portfolio management and strategy, where we are really resource allocating our resources on programs that have the potential to really make a difference for patients and deliver value for stockholders. Then, as I was mentioning before, innovative tailored partnerships that will not only help us to advance the programs, but will also help us to widen our efforts and at the same time strengthening our P&L. And I'm going to be talking about it a little bit more in details later on. And then we are in an innovative company. We are an innovation engine. And to do that, I think that our lead optimization, early science, and discovery programs, they also need to be properly funded. And for that, we have now visibility and dedicated budgets for all of them. And we are always on the lookout for opportunities in terms of in-licensing or out-licensing agreements that will not only support the science, but of course, support our financial position. So if we talk a little bit more in detail about how important the collaboration with BMS is for us, so I think it's not only allowing us to accelerate and maximize pumitamig, but it's also strengthening our P&L and our financial footprint in the short term and in the long term. So we are advancing more than 10 trials, including registrational studies and plans, I would say very ambitious plans on CRC and gastric cancer. Most importantly, all of these so this is a 50/50 relationship. How this translates now is that before going commercial, so all of the efforts that we are investing on pumitamig and all of the combinations that my peers have been talking about, so all of these expenses and investments are on a 50/50 basis. Then finally, of course, with the anniversary payments and the upfront of $3.5 billion and thereafter potential milestones of up to $7.6 billion as we hit registrational and/or commercial milestones, I think this really bolsters I think two things. Bolsters our R&D efforts, but also it's kind of like a boat of confidence on how solid our platforms and our science is. That's the path to value creation, right? Strategic portfolio management, now shifting towards later stage de-risk programs that have, as I was saying, the potential to really change the course of BioNTech. My peers here will not allow me to say anything that is not correct. Optimizing productivity and efficiency is very close to my heart, and I have been having deep conversations with them on how we can better allocate our resources to be faster, better, and more efficient, all with the intent of, of course, elongating our cash runway, giving us optionality as we move along, and hopefully be in as good a financial position as we currently are once pumitamig hits its commercial stages, and then again, finally, this will, of course, allow us to be fast, to be efficient, and readily scalable by the time we are hitting the market and hopefully reaching as many patients as we can, so if 2025 has been exciting, I would say 2026 has the potential to be even more exciting as we gain momentum in our combination strategy. We shift from modalities to disease areas, as has been very professionally outlined by my peers, and then we gain acceleration into late stage programs. I'm not going to end up here quoting more scientists because we already have heard from very bright minds from Ugur, Özlem, Michael, and Ilhan, but I would maybe mention a management scientist that you guys all know, Peter Drucker. He says, "The best way to predict the future is to create it, to influence, to shape it." And I believe we at BioNTech are just doing that. So with that, I would like to open up for our Q&A panel and invite my peers to join me here, as well as Annemarie Hanekamp, our Chief Commercial Officer. Thank you very much for your time, for your engagement, and also for your analysis and questions that are always challenging, interesting, and will always help us to be better and improve. So with that, we'll open up for Q&A. Mike, you need the microphone. Are we doing one or two questions? Just your thing. Okay. I have two. One, on your ADCs, you're still focused on Topoisomerase I while you're innovating on the target. And I wonder why, particularly given the MMAE payloads have some additional immune stimulatory benefit or any other novel payloads. And then I'll ask another one. So I think the topoisomerase payloads come with an additional selectivity. Particularly, topoisomerase is a target which is expressed in proliferating cells. So that means all the side effects are focusing on proliferating cells. Thereby, we are getting two types of specificity on the one side based on the target, the second based on the proliferative index of the cells. We believe that this is, at the moment, the better strategy for developing safe and effective combination therapies, and we are working on novel payload approaches that follow the same logic. Dana had a second question. We took away her mic. Okay, one more. I just came from SITC, and we know what's happened this year in vivo approaches for CAR-T, and in some ways, I think you guys were leading with the LNP and your various approaches of either making RiboCytokines or T-cell engagers or CAR-T, and it's not on the priority, and I wonder how you think about nurturing some of that really exciting innovation where you were leading sort of from a corporate strategy perspective. Please go ahead. You go ahead. No, you are right. So we have indeed a portfolio of in vivo approaches. But the limitation is not the technology itself, but coming up with a viable approach, multi-target approach. And we see at the moment really the focus in our core strategy with IO ADCs plus mRNA vaccines. This is something which will go with, I would say, the first wave of personalization, where this type of in vivo approaches can be really combined with multiple targeting approaches. At the moment, the limiting factor is there are not that much CAR constructs targeting tumor-specific antigens. The TCRs are too segmented in too many sub-indications. That means HLA restriction plus the target expression. So this is something which has a great potential, but we think it's too early to drive that with full energy into the clinical application. Yeah, I would echo that. There is a lot of space for improvement in the technology, further optimization space as well. This is work we are continuing. Sometimes it's good to wait until you move the most optimized version of your iteratively improved technology into clinic. Oh. Okay, so hi to Tazeen Ahmad from Bank of America. Let me ask maybe one question on pipeline and one finance question. For pipeline, you've talked a lot today about upcoming data. For those of us who've been on this journey with you since IPO, it's good to see that we're going to see a lot of data sets coming through starting next year. You specifically focused on ADCs. This is a class that some might consider to be an older class, but I think Ugur, you yourself said that's still in the early innings of looking at ADCs. So I maybe wanted to ask about the upcoming pumi plus ADC GYN data that you've guided to expect to see next year. Can you just give us a little bit of color on what exactly we're going to see and what decision-making processes will occur as to which ones you may choose to move forward? Just for modeling purposes, we'd like to get a sense for that. And then the finance question, I'll just go ahead and ask that now. So the process that the company has talked about in terms of maintaining a strong balance sheet while looking for good external opportunities has been followed through since the IPO. As the company moves forward, you do have a very large cash balance. How do you balance out your increasing R&D expense, let's say, with increasing data sets coming internally versus the desire to continue to look for external assets outside? And would your threshold for what you want to pay increase relative to what you were doing before? Thanks. I can take the first question. So our approach is really assessing single compound activity for pumita in multiple indications and single compound activity for our ADCs. We see as a general pattern for pumita that we have increased objective response rate. We have prolonged PFS. And for our ADCs, we identify particularly doses that are safe but still are associated with a prolonged PFS. We believe that the combination of both will not only have an improved response rate but particularly help us to further increase the PFS and translate into OS. That's our strategy. And I think on the finances, so I think you're right. The way I think about how to really preserve our financial strength is relentless priority on what we are doing. So every time that we are talking about resources, how much these are going to be costing, what are the clinical trials that we are going to be starting, particularly early science and thereafter, it's like they really have to be bolstering and underpinning our strategic priorities, which I think they have been very clearly outlined by my peers. Then on your second question, if I think this is giving us the firepower to look after even bigger opportunities, I would say yes. I think if there is anything that is strategically aligned with what we are pursuing that will give us further insights and ways to get into this market in a way that will even prepare us better for commercialization stages or further expanding our pipeline, we will always be looking after this and very interested in analyzing them. Is there an upper limit on how much you'd be willing to spend right now? Not really. Thank you. Hello. This is Cheng Li with Dales at Oppenheimer. Thank you for hosting the event and taking the questions. Maybe I can have two questions from us. First, I'm just wondering about the BNT327. It seems like it's like some interesting data from the squamous non-small cell lung cancer, but just wondering why you haven't started the combination with pembrolizumab, whether it makes sense to combine those two agents. And second question is on your dose selection from the small cell lung cancer. The lower dose is selected. Just want to confirm that the FDA has agreed on this decision and how to think about other ongoing phase II through trials on which dose maybe makes more sense and also the dose for your ongoing ADC combination. Thank you. So I can try to answer the first question on gotistobart and pumitamig. It's an intriguing combination for sure, and we would love to pursue this. We probably will, but we are, through certain historical reasons, restricted with the collaboration with our partner Regeneron. So we may or may not be able to do this fast to an approval. Otherwise, data generation will be something we will certainly do. For ADCs, sorry, what was exactly? The pumitamig part or the ADC part, for example? Maybe Ilhan takes the first. First, the pumitamig part, and then you ask also regarding the ADC dose, so you ask regarding the selected dose for small cell lung cancer, and the answer is yes. This is discussed and aligned with the FDA. How do you think about the dose for other non-small-cell lung cancer that you've been seeing? Will the dose selection be significant for ADC? We are looking constantly in the data evolving and will make really data-driven decisions about the dose selection. I shared with you also the designs of the new trials which we are generating, which has a dose optimization part still included, and this will drive. With regard to the published data, you might have seen that 20 and 30 milligrams per kilogram for pumitamig is very similar with regard to the safety profile. We are still assessing whether 20 to 30 milligrams makes a difference in the objective response rate and PFS. This is something that will provide us additional information. Updated data for TNBC are coming in a few weeks, right? Yes. Yeah. Okay. Questions from this side of the room? Hey, thanks so much. So can you talk about B7-H3 and why this seems to be your kind of preferred agent instead of the TROP2 for not just small cell, but also NSCLC? And maybe it's working in squamous, non-squamous. But I think the other question is really, do you have any responses to some of the data we saw at ESMO from Merck and Kelun with the sac-TMT drug, right? You're seeing on the low end of four-month OS benefit. It looks like it's trending to six to 12 months. So I think the question is, your B7-H3, you guys talk about safety, but could you have an efficacy signal that would look like that? So maybe first to say for non-small cell lung cancer, we have several options, right? So B7-H3 is one of them. TROP2 is another one, but actually probably the least data we have, but also the most promising is on the HER3 side. So taking the competitive landscape into account, when I showed the data on non-small cell, I think I said something like, this looks interesting and perhaps competitive, but there's others that are ahead of us with other moieties such as TROP2. And from a place where we want to win this, we want to see single-agent activity that is superior, right? So for B7-H3, the NSCLC data is good, but it's not outstanding. Small cell, perhaps, yes. So small cell, also, as I alluded to, the duration looks quite interesting. NSCLC, we'll see the data mature. We'll take an informed decision. We do the combination with pumitamig. But assuming that we will not see anything magic with B7-H3 and pumitamig in non-small cell, I think we have better options. Maybe just to put that. So if you were to guess right now what your novel combo would be in first-line NSCLC, what would those two agents be and when would we see that combo get initiated? Part of when we need to see that combo initiated is when we will have also a more mature pumitamig data, right? Because we will not start a phase III with pumitamig without knowing where pumitamig is actually heading towards, right? We have the phase III started, but we still want to see that mature. Also, we don't want to have a year after a successful phase III, another phase III, which would basically not be very cost-efficient to doing this. I think we still will see on our three ADCs which one is the best. When exactly, I don't know. It will be probably during the course of the coming year, probably more towards the end of the year for taking an informed decision. If so, which one to take in combination with pumitamig. Okay. Terence next. Thanks, Doug. Terence Flynn, Morgan Stanley. I had a two-part question on iNeST. Özlem, you mentioned that based on the phase II melanoma data, you were thinking about optimizing the breadth of immune responses as that could benefit the outcome in these trials. And so are there any plans to update the algorithm you're using in the antigen selection process? And how dynamic is that during clinical trials? And what does that require from an FDA input perspective? So that's the first part of the question. The second has to do with manufacturing scale-up and turnaround time for iNeST. Just anything you can provide in terms of an update there in terms of where that stands and how quickly you could expand that if successful in phase II. Thank you. The first part of your question, we are constantly working on optimizing our algorithm. Also, given the fact that with the data we generate in our clinical trials, we also generate the opportunity with the use of AI to reflect these new insights into the ways how we predict our new epitopes. There is very limited opportunity to introduce innovations in the algorithm into an ongoing trial, obviously. There is some wiggle space, which we discuss and get support from regulators, but changing the algorithm entirely during an ongoing study is not feasible. So this is something which then comes with new studies. What was your second question? Scale-up. For iNeST. Yeah. We have a manufacturing time depending on trial around 40 days, and there are also trials in the adjuvant setting where you can deliver the vaccine in six weeks or eight weeks because the patients can stay longer. For pancreatic cancer trial, we try to stick to 40 days where the patients have only a limited window. Okay. Up next, Bill. Hi, Bill Maughan, Clear Street. So early in the slides, you had preclinical data that put pumitamig on the same graph as an ivonescimab analog. And six out of six, it looked more potent. So just are you comfortable making the claim that you believe you may have that you likely have a more potent molecule? And then secondly, just to get Annemarie involved here, you've talked before about building a commercial organization to support the endometrial launch that can then be leveraged for future oncology launches. So can you just kind of list out your priorities on your to-do list for 2026 and how you can start to set that foundation? I take the first question, Annemarie. So we use, of course, different positive control. With IVO being one control, it's indeed consistent that the affinity appears to be differentiated. Whether this translates in any way into a differentiated clinical thing, we cannot make a statement here. It's a quantitative difference of the two molecules, but that might not play a role in the concentrations of the antibodies applied into patients. To your second question, yes, we've guided to endometrial for TPEM as a strategic launch. I'm very pleased that we're working towards establishing the commercial footprint in the U.S. We have a team of well-rounded professionals from both big pharma, small pharma with a lot of deep experience. We're out in the field right now compliantly to ensure that we have the right metrics in place for when we have that strategic launch and that foundation. Very excited also about this BMS partnership to just throw that in as well because the opportunity with pumitamig is such that we want to make sure that when it plays out, patients across the globe have the opportunity to get access to pumitamig. Now, we're very mindful that, of course, building a commercial-stage organization just from scratch may be a little bit to chew off in one go. This partnership, which is also a co-commercialization partnership, will allow us to focus on predominantly the U.S., where in oncology, 60% of your revenue comes from, followed by the markets that we're getting ready for today as well. Other big markets like the EU4, the U.K., Japan contributing to another 20% of commercial value, and then making sure that the other markets in our initial startup phase can be accessed by a partner like BMS for pumitamig. And as we're then building to our novel, novel combinations where we will have a leverage, we can slowly, gradually, but with focus, build up that commercial presence. Hi, this is Jae Park from GIC. I have two questions, please. On small cell lung cancer, we have clearly seen a good translation of Chinese response rates into U.S. response rates. Every cancer is, of course, different. So if you could just talk to us about your confidence level in kind of Chinese to global translation in other cancer settings as well. And I have a second question after this. So do you want? Yeah, sure. So the data presented and which you have seen is indicating really in small cell lung cancer, definitely it is confirmatory, right? So we are seeing same levels even in global, a little bit better from the response rate and duration of response. We believe there should be no difference in other indications, but this, of course, is the reason why we are running POC trials, signal-seeking trials in both regions, global and in China, and so this will be, again, guided by the data, but there is no reason to believe that there are significant differences regarding the response and the efficacy. Safety, by the way, is also very similar. That's great. Thank you. My second question is, I think on early ELCC data, TROP2 ADC plus pembrolizumab looks very combinable, looks very safe. Obviously, we don't have other, say, 324 plus pembrolizumab combination data just yet, but is there anything that you see from 324 monotherapy data that makes you think that it could be maybe as combinable as 325 or other ADCs for that matter? Thank you. Actually, based on the large portfolio of indications that we assessed with pumitamig and with our ADCs, we know the side effect profiles of the compounds, and so far, we clearly see that the ADCs have a different side effect profile associated, for example, with dose-dependent neutropenia, which is not a challenge for pumitamig. pumitamig itself has a very low rate of adverse events, immune adverse events. We don't expect any influence here, so based on that, what we are seeing so far in the early studies, this looks very good, and we don't expect added toxicity, but of course, this is the game: go into the combination therapies, assess the safety of the combination, identify the right dose, and then go for phase III clinical trials. Hi, Malcolm Hoffman here for Evan Seigerman from BMO Capital Markets. In metastatic CRC, can you talk about why pumitamig may be differentiated versus other PD-1 VEGF bispecifics? I know Pfizer recently highlighted the plan to start their phase III in first-line trial next year, and at the start of the presentation, you highlighted the potential benefit of tumor microenvironment targeting with PD-L1 versus PD-1 bispecifics. Is this something that we should be anchoring on when thinking about the potential relative benefit, or is this more just mechanistic theory at this point? Thanks. I think it's early in this indication for CRC to predict any differentiation of the PD-L1 VEGF class versus the PD-1 class. It's a colorectal cancer. It's an interesting indication since at least the microsatellite stable indication is so far not open for anti-PD-1 treatment, and this is definitely something where we would like to see the signal. We would like to see the PFS, the response rates, and that's also the reason why we are assessing different doses in this indication to ensure that the findings that we got now in one indication can be transferred into another indication. It is quite possible that the dose identification could become even a differentiation factor for the response rate and durability. Appreciate it. Thanks for taking my questions. Asthika Goonewardene from Truist. I want to tag on to Daina's question. So some payload optimization has been described in the literature to increase the potential for immunogenic cell death. I think some groups have been able to show increased DAMPs expression, etc. Has any of this work done with your payloads, just given that you have such a broad assortment of ADCs to combine with? And then how would you compare your payload versus DXd and MMAE on immunogenicity? Yeah. See, we are doing that intensively, and we clearly see, and I have shown you data also in syngeneic tumor models where we clearly see that this is not only additive but synergy-based. The immunogenic cell death is mediated by a release and a number of well-characterized factors, so there is no difference with regard to the ADCs, so at the end of the day, it's a cell death that is mediated by necrosis, by release of intracellular cellular signals, DAMP molecules. This is happening independent from the ADC class, but the question that we have with regard to the innovation is, can we go beyond this classical cell death mediated immunogenicity approach? And this is something where we believe in the next two years we will see innovations coming. And we are working ourselves in-house on some pathways to further enhance this immunogenicity. KP on the IO team here. PD-1 historically has not shown great data in MSS CRC, but there's obviously a lot of interest in pursuing this with the PD-1 VEGF bispecifics. I'm guessing the effect there is more driven by VEGF component, but have you done any work internally to show that there might be some immunological activity as well? Microsatellite stable colorectal cancer. You know there are publications and clinical data of combination treatments in MSS CRC, including, for example, anti-CTLA-4 and anti-PD-1 treatments, combination chemotherapies. So no tumor is actually immunologically silent. CRC has a special aspect to ensure that this immunological silence is not broken. But biologically, for example, if you look to microsatellite stable tumors and unstable tumors, you will not find a different biology. It's just more mutations. So at the end of the day, it's a way to enable T-cell infiltration into tumors and get the things running. And I'm sure that we will make in the next years great progress in making colorectal cancer MSS CRC as a highly immunogenic tumor type suitable for cancer immunotherapy. Thanks. And the question is also that the PD-1s have not been successful in colorectal cancer just means that there was in sufficiently powered studies not a statistically significant difference, right? But you do see in clinical practice that there are MSS CRCs that this has also been shown in the studies, which seem to have an effect. So the question is, what happens if you concentrate the blocking via targeting via VEGF into the tumor microenvironment and thereby change the milieu there? And that means we should not shy away from indications in which we don't see PD-1 effects, but would like to try this bispecific. It is a nice bridge to what Ugur showed at the beginning. pumitamig is more than the combination of the monospecific parts of this equation. What you see before in combining PD-1 and VEGF, for instance, in colorectal cancer is not indicating what you can expect here from this bispecific with an enrichment in the tumor microenvironment. I think that's an important part. Okay. We have time for one more question. No question. Hi. Will Zhang from Wells Fargo. Thanks for taking our question, so we saw competitor data at ESMO that showed basically a diminishing treatment effect as you increase PD-1 expression in subgroups, and just wondering a response on your end to that, and also, can you give us some color on how BioNTech is thinking about a potential treatment effect in checkpoint inhibitor indications versus non-checkpoint indications? Thanks. Yes. I think this is an observation, a trend that we are also seeing, and this needs to be translated into the clinical strategy, how to deal in these indications to have a better hazard ratio also in these indications which are high PD-1 positive. Okay, so that concludes this Q&A panel and our event today. Thank you very much to everyone for attending, and we'll now open for a networking event, which will be just through here in the lobby.