Before we start, I would also like to refer everyone to the press release on the data, as well as the slides for this webcast that were published earlier today. Both are available for download in the Investor in Media section of our website. As usual, our data releases contain a lot of details for you to dig through. This presentation also includes an extensive appendix, which provides further background information and data that will not be covered during the webcast. This presentation, as usual, contains forward-looking statements. Immatics is the global leader in precision targeting of PRAME, a target expressed in more than 50 cancers. We have the largest PRAME franchise with the most indications and modalities, spanning TCR, T cell therapies, and bispecifics. Today, our update will be focused on our PRAME TCR bispecific IMA402. Beyond our PRAME franchise, we will also share data on our MAGEA4/8 bispecific called IMA401. Both product candidates are off-the-shelf biologics with antibody-like properties related to immediate availability for patient treatment, manufacturing, scale, storage, and supply chain. Our TCR bispecifics provide the opportunity to reach a large patient population and have the potential to be administered in community settings without the need for specialized medical centers. In addition, they are very well combineable with other agents in early line settings. Years ago, we defined the target product profile for our bispecifics at the recommended phase II dose to achieve at least 20% confirmed objective response rate, according to RECIST, as a monotherapy and in last-line solid cancer patients, and this being the boundary to qualify for the next stage of development. With this, I would like to hand over to Carsten Reinhardt, Immatics Chief Development Officer, to present today's update. Thank you very much, Harpreet, and good morning to everybody dialed in. Before we get into the clinical data, I will give you all a quick overview of how our next-generation half-life extended TCR bispecific molecules called TCER are designed and how their proprietary format combines superior potency with a long half-life. These molecules are antibody-like off-the-shelf biologics that seek to leverage the body's immune system by redirecting and activating T cells towards cancer cells expressing a specific tumor target. We designed our TCER molecules to enable the target-specific activation of any T cell in the body to attack the tumor, regardless of the T cell's intrinsic specificity. They are engineered with two binding regions: a TCER receptor, in short, TCR domain, binding the target, and a TCER recruiter domain. The TCR domain is designed to bind with high affinity and specificity to the cancer target peptide that is presented by an HLA molecule on the cell surface. Immatics' proprietary low affinity TCER recruiter domain is directed against the TCR/ CD3 complex and recruits a patient's T cells to the tumor to attack the cancer cells. The low affinity recruiter enables an optimized biodistribution of the TCER, with enrichment of the molecule at the tumor site instead of the periphery. This is supposed to reduce the occurrence of immune-related adverse events, such as cytokine release syndrome at higher doses, and also has been shown in preclinical models to significantly improve anti-tumor efficacy, as shown in the appendix. In addition to the TCR domain and the recruiter domain, the TCER format also consists of an Fc- part conferring half-life extension with a half-life of one to two weeks, stability, and antibody-like manufacturability. One of the key takeaways today is that the phase I- A data demonstrates clinical proof of concept for both our TCR bispecific product candidates. We observed a favorable tolerability profile for both molecules, IMA402 targeting PRAME and IMA401 targeting MAGEA4/8, at the recommended phase II dose range, the RP2D, notable without any high-grade CRS or ICANS. In addition to tolerability, we achieved promising clinical anti-tumor activity. For IMA402, we observed a 30% confirmed objective response rate at RP2D across all indications, including melanoma and ovarian cancer. For IMA401, the data demonstrated a 25% confirmed ORR in head and neck cancer, 29% in melanoma, and promising early signs of clinical activity in squamous non-small cell lung cancer at doses of 1 mg and above. Both bispecifics have completed phase I dose escalation, and the data gathered support our intent to advance clinical development for IMA402 PRAME bispecific initially in cutaneous melanoma, gynecological cancers, and in combination with IMA401 MAGEA4 bispecific in squamous non-small cell lung cancer and potentially other solid tumors. In the next slide, we will take a closer look at the phase I- A dose escalation data for IMA402. The primary objective of this phase I dose escalation study was to assess the safety and determine the maximum tolerated dose and the RP2D for IMA402 in late-stage cancer patients with recurrent and/or refractory solid tumors that have a high likelihood of expressing PRAME. We followed a MABEL-based approach by starting treatment at very low doses, and according to our preclinical and viewable studies, these first cohorts up to 1.6 mg were deemed subtherapeutic doses. We then moved up in the dose escalation to higher doses until reaching what we consider the RP2D range. Each patient in the RP2D range received a step dosing of three lower doses before reaching the target dose. A biweekly dosing schedule has already been implemented for individual responders who have been treated for more than six months. Dose escalation has now been completed, and the maximum tolerated dose has not been reached at 30 mg. We have identified a provisional RP2D range between 10 mg and 30 mg, and dose expansion is ongoing at two distinct doses within this range. We also recently started dosing patients with a combination of IMA402 and a checkpoint inhibitor. However, IMA402 data presented here are all from the monotherapy cohort. The table here illustrates the demographics and baseline characteristics of the patient population treated with IMA402. This population includes a majority of patients with melanoma and ovarian carcinoma, both indications with a high prevalence of PRAME expression. Of note, all the patients were heavily pretreated with a median of three prior lines of treatment. In general, the treated patients reflect the population typically investigated in first-in-human studies, namely a significant number of previous treatments, relevant negative prognostic factors, i.e., high LDH levels, and a significant tumor burden. When looking at the baseline characteristics of the patients treated in different dose groups, we do not see any noteworthy differences. The appendix of the presentation contains more details on the baseline characteristics of the patients in the focus indications of melanoma and ovarian carcinoma. Notably, all melanoma patients were immune checkpoint inhibitor resistant, and all ovarian patients were platinum resistant. The safety of IMA402 was assessed in 80 patients across all doses. Overall, IMA402 shows a favorable tolerability profile across a broad therapeutic range, and tolerability in all patients was consistent with the tolerability in patients treated at the highest doses in the RP2D range. As you will see, the most frequent adverse events were expected and transient lymphopenia consistent with a mechanism of action of T cell margination and low-grade CRS. Only one patient reported a higher-grade CRS event, which occurred at a step dose of 18 μg. This patient had a previous medical history of pneumonitis after previous immune checkpoint inhibition. After switching to an optimized step dosing with a lower starting dose, no high-grade CRS events were reported anymore in the last more than 50 patients. In addition, no ICANS or IMA402-related grade 5 events were observed. As mentioned earlier, the maximum tolerated dose was not formally reached at 30 mg, and all in all, we conclude that IMA402 shows a favorable tolerability profile, enabling a broad combination potential with various standard of care therapies. Looking at the waterfall plot, we observe a clear dose-dependent relationship in the efficacy of IMA402, with only one unconfirmed response in cutaneous melanoma at subtherapeutic doses below 3 mg. An increase in the clinical activity was observed in the intermediate dose group, with more disease stabilizations, another unconfirmed partial response, and a confirmed partial response. At doses at the RP2D range above 10 mg, the response pattern is more evident, with a confirmed objective response rate of 30%, and all six confirmed partial responders showing prolonged and deep responses down to a 100% reduction of target lesions. All confirmed responses at RP2D range are ongoing as of data cutoff. Given the clear dose-response relationship, we decided to add expansion cohorts at two distinct doses within RP2D range to define the final RP2D going into phase II studies, and in this presentation, we focus further efficacy analysis on those patients treated in the RP2D dose range. In this spider plot, you can see deep and durable responses at the RP2D range. If you take a closer look, all ongoing responders and the patients with ongoing disease stabilizations are indicated with a black triangle. Some have a relatively long follow-up of up to one and a half years of continued confirmed partial response. As mentioned before, all six confirmed objective responses are ongoing as of data cutoff. These include two complete metabolic responses in cutaneous melanoma and uveal melanoma, which are ongoing at 8 and 18 months, and one confirmed partial response in ovarian carcinoma with a 100% reduction in target lesions. Across all patients dosed at the RP2D range, the data showed a confirmed ORR of 30%, with a median duration of response not reached. In addition, tumor shrinkage was observed in 55% and disease control in 65% of these patients with advanced disease and no available treatment option. If we look specifically at the melanoma group, we observed a cORR of 29%, and we also have two confirmed responders out of three treated patients with ovarian cancer. You can also see some white triangles on the slide indicating continued treatment, also in patients who have progressed. For some of these patients, the investigators requested to continue treatment because they saw other signs of clinical benefit, like a decline in tumor markers and/or a decline in progression kinetics prior to treatment, which indicates prolonged activity of IMA402 beyond RECIST-based responses. The data confirm the expected disease stabilization profile of TCR bispecifics with the added benefit of deeper and longer-lasting responses, in addition to promising early survival readouts, as I will show you in the next slide. On this slide, we see a snapshot of early promising progression-free survival and overall survival for patients treated with IMA402 at the RP2D range as compared to the two other dosing groups, again clearly indicating a dose-response relationship. While there are still a relevant number of sensitive events at the RP2D group, the observed median progression-free survival of 4.8 months and median IPFS and median overall survival, both not yet reached, are encouraging. We would like to conclude the IMA402 data overview with one example among various interesting patient cases. This patient presented on the slide is a 60-year-old woman with a diagnosis of cutaneous melanoma and multiple lines of prior checkpoint-based treatment regimens. Of note, the tumor was refractory to treatment with lenvatinib in combination with pembrolizumab prior to inclusion into the IMA402 trial. IMA402 infusions resulted in a significant reduction of all tumor lesions, and a recent PET scan revealed no residual activity, thus indicating a complete metabolic response. Further, the patient's brain lesions also completely disappeared. The patient has been receiving treatment with IMA402 for approximately one year now, and we are pleased to report that the response is still ongoing. Taken together, based on these promising phase I dose escalation data, we are excited to now evaluate our IMA402 PRAME bispecific across specific patient populations and in potentially synergistic combinations. Next immediate steps will be advancing IMA402 into phase I- B dose expansion at two distinct doses to determine the final RP2D, both as a monotherapy and in combination with an immune checkpoint inhibitor, with a focus on melanoma and gynecological cancers in 2026. Depending on the outcome of these phase I- B cohorts, we would seek to convert existing phase I- B cohorts into phase II trials, which will then have the potential to become registration-directed. We are also exploring the option to initiate additional phase I- B cohorts in 2026 to evaluate IMA402 in late as well as earlier treatment lines. Lastly, we are also considering the potential combination of IMA402 with IMA401 in squamous non-small cell lung cancer, and we will address the underlying rationale for this combination when looking at the IMA401 dataset in a moment. In the next slides, we will cover the data from a different phase I- A dose escalation trial evaluating IMA401, Immatics TCR bispecific targeting MAGEA4/8. MAGEA4/8 is a proprietary peptide identified by Immatics' industry-leading peptide HLA target discovery platform. As detailed in the appendix, it has not only been shown to be presented on the cell surface of cancer cells at a five-fold higher target density than the commonly used MAGEA4 target peptide, but also shows significant upregulation under inflammatory conditions such as T cell infiltration in the tumor. Starting with a trial overview for 401, similar to IMA402, the objectives of the IMA401 phase I- A dose escalation study were to assess safety, determine the maximum tolerated dose in RP2D, and assess pharmacokinetics in patients with recurrent and/or refractory solid tumors who tested positive for MAGAE4/8. In this trial, we enrolled patients with more than 15 different, mostly very difficult-to-treat tumor indications. Again, a MAGE-based approach was followed with very low starting doses, and most patients were dosed biweekly after reaching the respective target doses. Among the patients treated, nine were treated in combination with immune checkpoint inhibitor pembrolizumab. Also, in the case of 401, we observed a dose-response dependency with higher clinical activity starting at 1 mg. Although the maximum tolerated dose was formally not reached, three dose-limiting events were observed at 2.5 mg, as described on the next slide, which triggered the decision to define the RP2D range as 1 mg-2 mg. As of the data cutoff, 55 heavily pretreated patients with a median of four prior systemic treatments were treated with IMA401. A demographic and baseline characteristic table is included in the appendix. Across all doses, the most frequent adverse events were low-grade CRS observed mostly at the first step dose and expected transient lymphopenia as observed for IMA402. Furthermore, dose-dependent neutropenia, mostly transient, was observed. A few higher-grade cases of neutropenia triggered the decision to limit the RP2D at 2 mg, where we observe a favorable tolerability profile. Again, not a single case of ICANS was observed in this trial. The tolerability of IMA401 in combination with pembrolizumab was overall consistent with the tolerability of IMA401 as a monotherapy. Given the highly heterogeneous patient population treated in this dose escalation trial with patients in more than 15 different indications, we decided to focus the efficacy analysis on the few indications of interest, specifically head and neck cancer, squamous non-small cell lung cancer, and melanoma due to their high target density and prevalence. The data in this waterfall plot highlights that IMA401, like IMA402, shows proven clinical activity in different indications. You can see this demonstrated by the confirmed partial responses in head and neck cancer with a 25% confirmed ORR and in melanoma with a 29% cORR, including deep responses. We also observed early promising signs of clinical activity in squamous non-small cell lung cancer, with all three patients showing signs of clinical activity. Taking a closer look at the IMA401 data in the three focus indications at 1 mg and above, we also observed deep and durable responses. In this spider plot, you will see that the longest response is ongoing over two years in a patient with cutaneous melanoma after five prior lines of treatment. Also, in the case of IMA401, some investigators requested to continue treatment in patients who progressed because they saw overall signs of clinical benefit beyond RECIST-based responses, as exemplified here by the clinical course of the patient whose progressing target lesion was removed at 12 months and who is still alive on ongoing IMA401 treatment after 18 months. We would also like to take this opportunity to present one other patient case. Depicted here, you can see scans from a patient with a very advanced squamous non-small cell lung cancer who received four prior lines of systemic therapy and failed to respond to any of the immune checkpoint and/or chemotherapy treatments for metastatic disease. This patient received biweekly doses of IMA401 at 1 mg + 400 mg pembrolizumab every six weeks. The first scan post IMA401 treatment already showed a partial response with a -39% tumor reduction in all target lesions. Not only was the significant tumor shrinkage observed, but the investigator also reported additional clinical benefits, including improvement of quality of life. Very unfortunately, the patient died following complications of an interventional biopsy without progressing prior to that. This patient case nonetheless demonstrated an early but promising clinical signal in a heavily pretreated patient. As noted previously, disease control and tumor shrinkage were also achieved in two additional lung cancer patients treated with IMA401. These early and encouraging results, together with a high prevalence and target density of IMA401 in squamous non-small cell lung cancer, form the basis for Immatics' strategy to explore the development of IMA401 in combination with IMA402 for this indication. On the next slide on the top left, you can see the prevalence of MAGEA4/8 and PRAME assessed in squamous non-small cell lung cancer tumor samples. Based on this data, 90% of patients with squamous NSCLC are positive for PRAME and/or MAGEA4/8. Thus, a potential IMA402 and IMA401 combination treatment could provide broad treatment coverage for this patient population with an estimated 40,000 addressable patients with metastatic NSCLC in the United States and EU5 per year. In addition, approximately 60% of patients with squamous NSCLC are positive for both targets, which could boost anti-tumor activity as shown by the in vitro data below. Looking ahead, we see squamous NSCLC as a starting point for IMA402 combination with IMA401, with opportunities to expand into other solid tumors that express both PRAME and MAGEA4/8, representing an increased therapeutic potential. In closing, we would like to express our sincere gratitude to the patients participating in our clinical trials, their families, as well as our investigators and the study teams listed on this slide. Back to Harpreet. Thank you very much, Carsten, and thank you to the audience for joining our call today on our TCR bispecific clinical data and development opportunities. Carsten and I will now be happy to take any questions. Thank you. If you would like to ask a question, you may press the star key followed by the digit one on your telephone keypad. If you are joining us on a speakerphone, please make sure your mute function is turned off to allow your signal to reach our equipment. Again, if you do have a question or a comment, you may press the star key followed by the digit one. We'll take your first question from Jonathan Chang from Leerink Partners. Please go ahead. Hi guys, good morning. Thanks for taking my questions. First question on 402. Can you discuss how you're thinking about a potential go-forward dose and schedule? Looks like you have a few options here. Yes, I can take that question. As mentioned in one of the slides, we have defined the RP2D range, and we are now going forward testing two different doses in phase I- B expansion cohorts. These two doses will be pharmacologically distinct doses in the range between 10 mg and 30 mg. Currently, in the initial dosing, we have weekly dosing, but already intend to go to biweekly dosing, which is supported by the good pharmacokinetic data we have achieved so far. Does that answer your question? Development. You mean further development in specific indications? Yeah. Okay. Very clearly, we see for 402 this clinical activity, as pointed out, by 29% confirmed response rate in last line late-stage cutaneous melanoma patients. We will expand in this specific population to get a more robust estimate of the clinical activity in this late-stage cutaneous melanoma. Similarly, we have early data in ovarian cancer, two of three patients responding with confirmed responses, and would like to expand this population to get a more robust dataset in order to estimate the efficacy size and then, based on this, go to next steps. Jonathan, let me just jump in. As we discussed before, the default positioning of our bispecifics, we'd rather see in frontline settings. I mean, what we've demonstrated today is that this can be redosed high and still has very favorable tolerability. It is very combinable in contrast to many other TCEs and ADCs. This is a real strength of this molecule. This has clearly met our internal goal of 20% confirmed response rate. Should this response hold and be at that level, we can even envision continued development in a second line checkpoint refractory melanoma setting, which potentially opens up an avenue for a registration trial. These are now new opportunities based on the recent data that we have received. Got it. I guess my question on the cutaneous melanoma opportunity for 402, how should we be thinking about the potential timelines for these efforts in frontline and second line? Thank you. I'm happy to kind of give you some indication. What we've said also publicly is that we've started the phase I- B trial, basically, and this is going to continue predominantly the first half of 2026. We can envision, depending on the outcomes of the trial, that further trials, including potentially further phase II trials, could already start in 2026. Understood. Thank you. We'll hear from the next caller on the queue, Clara Dong from Jefferies. Hi, thanks for taking our question and congrats on the data. For 401 bispecific, you've mentioned that depending on the outcomes of the dose expansion cohort, you could convert the phase I- B into a registration-directed trial. Just wondering what efficacy and safety bar would trigger that registration strategy for 402, and have you had any regulatory dialogue on this pathway? Thank you. I'm happy to start. As I said before, the default pathway for us is to use this high efficacious agent, or at least from our perspective, high efficacious agent in a combination setting in frontline cancers. Melanoma is a focus indication. Another one is gynon cancers, including ovarian cancers, where we've seen a very early but very promising signal. Going into frontline setting with checkpoint inhibitors or into frontline settings in plaque-resistant cancers with actually standard of care is the kind of default pathway. To go there, the minimum bar we need to reach is 20%, which we believe now has been achieved. Given that this is going beyond, there is opportunity also to pursue this even in last line settings. We have not defined the bars for that last line setting to kind of further pursue that. If you look at the competitive landscape, we know that the best agent so far that's approved in checkpoint refractory melanoma, unfortunately, only has a response rate around, if we look at checkpoint inhibitors, so off-the-shelf drugs are often 20% or less than that, some even single digit. There's a cell therapy approved that goes up to 30%. Unlike the first line setting, there is actually a very relatively low bar existing for off-the-shelf agents in terms of response rate, but we have not yet guided towards any specific bar for that specific treatment avenue that we could pursue. Got it. That's helpful. Thank you. As a reminder, ladies and gentlemen, that is the star key followed by the digit one. If you have a question or a comment, we do say please limit yourself to one question. We'll hear next from Eric Schmidt from Cantor. Thanks for the call. Congrats. The data are quite remarkable, and I think one of the most remarkable things is the safety profile here. Obviously, you didn't hit any kind of MTD or DLT, but when you did see the dose escalation, was there any dose dependency to the AEs? Is there anything that you think we need to watch out for at the target doses? So, clearly, for IMA402, I mentioned that, and there's some data in the appendix as well. The safety profile for the RP2D range is very, very similar to the overall safety profile. So, there's no increase really in safety events or adverse events at the higher doses compared to the lower doses. I've mentioned the one grade 4 CRS event, which was actually at a high first step dose. We have rescheduled the dose steps since then and haven't seen any high-grade CRS in any of the patients treated over the past year. At the target dose, we haven't seen any additional toxicity events which are concerning. I fully agree. This is a super good tolerability profile for IMA402, which would allow, in our opinion, to combine this basically be it other immuno-oncology drugs, be it ADCs, or be it classical chemotherapy. For IMA401, I mentioned that we have seen DLTs in terms of higher-grade neutropenia at the highest dose, 2.5 mg. According to the study protocol, this did not qualify for an MTD, but we have, based on that event, defined the RP2D range to 1 mg to 2 mg, where this is well manageable. Other than that, also a very favorable safety profile here. Yes. When you think about IMA402 and frontline melanoma, I know you need some combination use with pembro to establish safety, but I would think you would feel comfortable. I do not want to put words in your mouth. Based on the second line activity or second line plus activity, I assume you don't need additional efficacy in order to feel good about a phase III trial in frontline disease, or that's something you'd also want to wait for? I mean, in principle, I can say we have, in fact, been surprised by this very high response rate in this last line cutaneous melanoma patients. We didn't expect to get actually close to 30%, which was a positive surprise. I agree. With that data in hand, you could make the jump kind of at risk and do a randomized trial in first line setting, as do some competitors of ours. They based this jump on a response rate which is much lower in the last line setting than our 29%. That is something you could in principle do. We are in internal discussions how the next steps would actually be in this early line setting. Absolutely. Thank you, Carsten. Moving next to Sebastiaan van der Schoot from Kempen. Please go ahead. Hi, team. Congrats on the progress, and thank you for taking my questions. The first one is regarding the combination with the checkpoint inhibitors in first line setting. I think that you already combined for IMA401 with checkpoint inhibitors in later lines. Are there any interesting safety or efficacy biological observations that you learned from that dataset that maybe informed the first line decision with IMA402? We have safety data from the combination 401 with pembrolizumab, and there is a slide in the appendix where you can look at the safety profile. These are patients who came into the trial relatively late, so we have not done any efficacy analysis as of today. From a safety perspective, no additional safety events compared to the monotherapy safety profile. Got it. You also mentioned the patients that do progress, they stay on treatment, or certain patients stay on treatment. Can you give a little bit more color on what leads physicians to decide to keep patients on treatment? Thank you. There are different patients, obviously. This is actually something which happened quite often that investigators came back to us as the sponsor of the trial, mentioning that they have seen formal progress according to RECIST criteria, but they clearly believe in the benefit of the treatment because they know their patients for a longer time. They have seen how the patients responded to previous treatment regimens. They know the growth kinetics of the tumor prior to the treatment, which we actually cannot get into our ECRF here. They know that, and they either see that there's a clear decrease in the growth kinetics. Even if you see some increase in tumor lesions, it obviously flattened out. Other reasons were that tumor markers in some cases significantly went down. I mentioned one of the squamous non-small cell lung cancer patients. This patient has developed a small new lesion. At the same time, existing lesions decreased in size quite significantly. There is clear clinical benefit even if the formal criteria suggest that there's a progressive disease. Great. Congrats again. Thank you. Thanks so much. Graig Suvannavejh from Mizuho, your line is open. Please go ahead. Thank you so much. Congrats on the data, and thanks for taking my question. You've got bigger pictures, I think, about the pipeline. An outstanding asset in IMA203 or cell therapy with good data both in cutaneous melanoma and uveal melanoma. Now you have this really exciting data for your bispecifics in melanoma as well. Can you just remind us again of how to think about your cell therapy efforts and your bispecifics and how we should be thinking about their positioning relative to one another, specifically in melanoma? Thanks. Right. Thank you, Graig. Principally, we think about cell therapies being the biggest gun in the shop. They have the highest response rate that we have observed so far, up to 60%, as we have shown also in recent data shown at the ESMO Presidential Symposium. Obviously, they are more tedious to apply, these autologous cell therapies with a complex patient journey, and they are typically restricted to specialized medical centers. The best way we think actually to position cell therapies is in late line settings as a monotherapy where classical standard of care with biologics or other off-the-shelf drugs basically has failed. With bispecifics, we think about different positioning, given that they are, as we've just demonstrated, so easy to combine and given their favorable profile and are easy to apply, they can be much easier positioned into frontline settings or even into the adjuvant or neoadjuvant settings. That is a natural separation that we can envision between these two drugs. That's a kind of default positioning. However, we do not exclude that bispecifics could also make it into late line settings. If you think about that, then there's a whole new optionality that could unfold, right? Think about also the BCMA CAR-T and BCMA bispecific market, right, where bispecifics are used both as bridging therapy while patients are waiting for their manufacturing slot or as maintenance therapy. Giving a living drug like anzu-cel, our sort of leading PRAME drug, as kind of a backbone and then maintaining further with IMA402 or bispecific may be also an option. There is a lot of versatility that we think we would have in our hands with two different modalities that can be also applied so differently. Okay. Thank you. And then just your interest in moving into the (neo)adjuvant and adjuvant settings? I'll break it. Carsten, please. Yeah. I mean, it's obvious that if you talk about and think about development strategies for immuno-oncology drugs, it's likely that the true effect is even bigger in earlier settings, earlier lines, because in the late stage settings, you often have very strong growth kinetics. As you know, we have to do some step dosing. Until the patient receives a high enough dose, some of these very aggressive tumors may actually already progress in the early lines. This includes, obviously, adjuvant and neoadjuvant. This is less of an issue. We have seen quite a lot of data coming out in the past years that treating neoadjuvantly, for example, so prior to removal of the tumor, this might be the sweet spot for a lot of the immuno-oncology development. That is something we look at very carefully and will be some of the discussions we will have internally with key opinion leaders and obviously with regulators over the next months to look how we can eventually go into these earlier lines and settings. Thank you. Moving next to Alec Stranahan from Bank of America. Hey, guys. This is Matthew on for Alec. Appreciate you taking our question. For 402, the DLT at 0.3 mg, curious if you can describe what that was and whether there was something specific about that case that gives you confidence that you're not going to see something similar at your RP2D. Thanks. We have seen a DLT at 0.3 mg. I think it was a patient who had grade 3 renal adverse events. There was a discussion whether that might be related to the target because there has been some mentioning in previous publication that there's very slight traces of PRAME expression in renal tissue. This patient had renal injury already prior to coming into the trial. It is really difficult to dissect it. What we have seen now is another 60 patients treated at doses much higher than the 0.3 milligrams and never seen that degree of renal changes any longer. I do not think that this is really something to the drug. It is more a patient-specific event we have seen, I guess. One thing that is important maybe to say is that this kind of CRS is rather something we observe at this very first step dose. Given after this event, we have adjusted that step dose down. Carsten mentioned that in the webcast before. That actually also contributes to actually lesser likelihood of this reoccurring. After this event, I think we've treated more than 55 patients with the optimized step dosing and never saw a high-grade CRS again. Yes. Thank you. We'll move next to Paul Jeng from Guggenheim. Hey, thanks for taking the question. And congrats on the really great updates today. I just wanted to follow up on the discussion on the different settings of melanoma. I see you had some IMA402 patients who had received prior TCR therapy. Just wondering if you have any early thoughts on how prior treatment with the TCR impacted either the safety or efficacy profile for 402. Secondly, were any of those prior treatments PRAME targeted therapies? How do you think about sequencing PRAME targeted therapies in melanoma and how that may or may not impact the clinical profile you achieve? I can maybe start with an answer. I think the number of patients treated with pretreatment TCRTs is too low to get to any conclusive statements here. I don't think we have seen something sticking out there that there's a lower or higher likelihood of response. From a safety perspective, we didn't observe any additional toxicities in there. Obviously, we have had a few patients who had prior IMA203 treatments and then went on to IMA402. That is a prior PRAME treatment. We haven't seen any safety issues there. For the uveal melanoma patients, all of those actually have been pretreated with Kimmtrak. Got it. Okay. Thanks very much. As a quick follow-up, just for 402, to what degree did the PRAME expression levels you were tracking correlate with any responses or depth of response at a given dose level range? Any plans to incorporate PRAME expression cutoffs for some of the future indications and focus? Thanks. Very good question. I mean, we have done some early analysis on that. We have not seen any clear significant correlation with the expression levels of peptide copies. We see some higher responses maybe in higher expressors, but it is not clear-cut. We see significant clinical activity, even responders in low PRAME expressors. I would not conclude from the data we have so far that we should optimize the cutoff. I think all melanoma patients will benefit from this specific treatment. Paul, a great test for the sensitivity of the molecules actually varied in cancer. We did not really pick this. Also, the reason is because there are relatively low copies compared to melanoma. This was something that was an open question. Is our bispecific also strong enough to actually really yield responders in a low PRAME, a lower PRAME expressing cancer like ovarian? We've treated, it's early data. We've treated two patients as a data cutoff and to observe the response. That is actually promising and principally shows it's possible also to go for these low copies. This is actually what's incorporated in the design. When Carsten and the team designed the molecule, it was a T cell receptor, is a T cell receptor, to really optimize to also recognize lower copies. We're very encouraged by this early data. That also opens up the breadth of this molecule to many other solid cancers. Maybe just to add on that, what Harpreet just said, specifically on the low copies, I think that's one part of the good thing that we have seen such a good safety profile and can go really high up with the dosing. We have seen in preclinical experiment that we can kill cell lines with very low copy numbers, like 30-50 copies of PRAME. If we go higher with a dose, so EC50 obviously gets a shift. This is what we can do here in patients as well. That's probably the background why we see even in those patients with lower copy numbers or indications with lower copy numbers like ovarian cancer, this positive clinical data, yes. Okay. Thanks very much. We'll move next to James Shin from Deutsche Bank. Good morning. Thank you for the question. Congrats on the data, guys. For 402, I recognize the slide state tolerability was consistent across all doses. Can you share some kinetics on the AE, like specifically whether the AE was primarily limited to 402's initial step dose? Secondly, for 402's platinum-resistant ovarian patients, it does not look like ELAHERE was listed as a prior regimen. Is it fair to assume these were mostly FR alpha negative patients or low patients? Thank you. I start with the second question. I do not think we have this data at hand for the FR expression, actually. I cannot answer this question at this point in time, but I can certainly follow up on this. On the other question with the dose relationship to AE profile, as mentioned earlier by Harpreet and myself, we see a clear dose relationship for the very first step dosing. That is why we backed up and went down with the initial step dosing to 30 μg. This has been shown in many, many patients to be very safe now. At the higher doses, the only adverse events where we have seen some dose relationship was arthralgia, but this was mainly low grade, easily controllable with COX-2 inhibitors, for example. It did not increase with the higher doses now. Not really any dose tolerability relationship here. Did any patients need any TOCI management or CRS management prophylactically, call it? All the patients do get prophylactic steroids similar to what, for example, talquetamab is in the label, 8 mg of dexamethasone for the first four doses, which we do not believe has any impact on the clinical activity and efficacy of this. This is standard of care for T cell engagers. Other than that, not really, no. Awesome. Thank you so much, guys. I'm also just mentioning for the audience that if you look in the appendix of the slide deck that's available for download on our website, you'll find for every patient basically a detailed table of the pretreatments. Have fun digging through that. At this time, there are no additional callers in the queue. I would like to turn the conference back over to your speakers for any additional or closing comments. Ladies and gentlemen, thank you very much for great questions, listening in, and wishing you all a wonderful day. Bye-bye. Thanks very much. Bye-bye. That does conclude today's call. Thank you for your participation. 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