Good morning, ladies and gentlemen, and thank you for joining us today for our webcast to provide an interim clinical update on cohort A of our phase Ib clinical trial, exploring our ACTengine IMA203 TCR-T monotherapy candidate targeting PRAME and solid cancer patients. Before we start, I would like to refer to the press release on the data as well as the slides from this webcast that were published earlier today. Both are available for download in the investor section of our website. This presentation also includes an appendix which provides further background information and data on today's announcement. This presentation contains forward-looking statements. In the past months, we have steadily continued to execute on our goal to deliver novel and better treatment options for solid cancer patients with very high unmet medical need. The data presented today marks another significant step towards reaching this goal. While the data is still early, the observed response rate, coupled with more than 9 months of follow-up, demonstrates that IMA203 can generate durable responses and has the potential to deliver a meaningful clinical benefit in a range of solid tumor types, including cutaneous and uveal melanoma, ovarian cancer, synovial sarcoma, and head and neck cancer. Speaking today about the data will be Cedrik Britten, Chief Medical Officer at Immatics, and Martin Wermke, Coordinating Investigator of the ACTengine IMA203 TCR-T trial. With this, I would like to hand over to Cedrik, who will introduce you to the PRAME multi-cancer opportunity and our therapeutic approach. Thank you, Harpreet. Let me recapitulate the key characteristics of the PRAME peptide that we target with our ACTengine IMA203 cell therapy. Using our mass spectrometry-based XPRESIDENT platform, we identified an HLA-A or two presented peptides derived from the cancer-testis antigen PRAME. We consider PRAME as being one of the most promising solid tumor targets with the potential to address an unmet medical need for large patient populations. It is highly prevalent across multiple solid tumors and shows a high target density as well as homogeneous expression. It is cancer specific, and targeting PRAME has already delivered clinical proof of concept. Taken together, these features make PRAME an ideal target for TCR-based therapies independent of tumor type. To efficiently target PRAME, we have generated a high affinity TCR designed to recognize the peptide with high specificity tailored for its use in autologous cell products. In our view, there are five key pillars to be successful with an autologous TCR-engineered cell therapy, namely favorable safety, deep and broad antitumor activity, long durability, robust supply of a product with high-quality attributes, and the ability to reach broad patient populations. We will show you in today's update that IMA203 monotherapy targeting PRAME addresses all these key pillars. IMA203 demonstrates manageable tolerability at doses as high as approximately nine billion CD8-positive TCR-T cells and a high confirmed objective response rate of 67% at month three. We further show, for the first time, durability of tumor responses elicited by our IMA203 TCR product candidate exceeding 9 months after treatment. The median duration of response has not yet been reached at the median follow-up time of 8.5 months. We are also able to quickly generate high numbers of IMA203 TCR-T cells within an expansion period of only seven days at an overall manufacturing success rate of 94%. Finally, we observed confirmed objective responses in a range of solid cancer types at low, medium, and high levels of PRAME above our threshold, supporting a broad reach and multi-cancer opportunity of PRAME. Before we dive into the clinical data, let us have a quick look at the trial design. The clinical trial to evaluate IMA203 in patients with solid tumors started with a phase Ia dose escalation cohort. We have completed this part of the trial and are currently investigating IMA203 in three phase Ib dose expansion cohorts. In Cohort A, we test IMA203 TCR-T as monotherapy in the last line setting. Cohort B is focused on generating safety data for potential further investigation of IMA203 in combination with a checkpoint inhibitor as a frontline therapy. In Cohort C, we introduced a potency-enhanced version of IMA203 TCR-T called IMA203CD8, in which functionally engineered CD4 T cells are added. IMA203CD8 is currently being explored at the lower end of dose level 4. Today's data update with a data cutoff April 4th focuses on 11 patients in Cohort A that received IMA203 TCR-T monotherapy. With this, I would like to hand over to Dr. Martin Wermke, who will present the clinical trial design and outcomes. Thank you, Cedrik. Let me start with an overview on the patient journey and trial. It consists of three phases. In the first phase, we screen patients, and the manufacturing of the cell product is initiated. In the second phase, we treat patients and monitor them for 12 months. The third phase is the long-term follow-up. The screening phase includes HLA genotyping for HLA-A*02:01 from a sample of the patient's blood. This is followed by PRAME target confirmation using Immatics' qPCR-based biomarker test IMADetect. Patients that have passed the test positive proceed to leukapheresis, which is the starting point for manufacturing your autologous engineered T-cell product by Immatics'. Immatics' has developed a proprietary rapid manufacturing process to provide the T-cell therapy to patients as fast as possible. This includes a 7-day cell expansion and an expedited 7-day release testing process, which Immatics' has recently transitioned from the previous 14 days. Patient treatment is initiated by lymphodepletion with fludarabine and cyclophosphamide for 4 days prior to IMA203 T-cell infusion at day 6, followed by low-dose IL-2 for 10 days to enhance T-cell activation and expansion. Let us take a closer look at the patient population treated in the phase Ib cohort A. At cut-off date, 11 patients were treated with IMA203 TCR-T monotherapy across dose levels 4 and 5. Overall, patients were heavily pretreated and had relapsed over refractory from 1 to 10 lines of previous systemic treatments. The table on the left provides information on the baseline LDH levels and tumor burden. As you would expect for a last line patient population, these numbers are very high. The T-cell dose administered to patients ranged from 1.3 billion to almost 9 billion CD8-positive TCR-T cells. The graph on the right shows the cell dose of 5 patients treated at dose level 4 and 6 patients treated at dose level 5. Dose level 5 was recently cleared for safety, and the updated provisional recommended phase II dose now includes dose levels 4 and 5. Immatics' improved manufacturing process introduced in phase I B includes monocyte depletion and has a success rate of 94% to reach this provisional recommended phase II dose. The final recommended phase II dose will be defined at the end of the phase I B trial prior to starting the clinical phase II trial. IMA203 has overall been well-tolerated, we did not observe any differences across the dose levels as we continued to treat more patients with higher cell doses. Most frequent adverse events were expected grade 1 to 4 cytopenias associated with lymphodepletion. When we look at adverse events of special interest, we observed low to moderate cytokine release syndrome in almost all patients, which is of course expected in an active cell therapy. We were pleased to see no high-grade CRS in 11 patients treated in cohort A and no dose-dependent increase of CRS. Further, we did not observe any ICANS in these 11 patients. The full tolerability profile of the 39 patients treated with IMA203 TCR-T monotherapy thus far, including the data generated during dose escalation and recorded last October, can be found in the appendix. Overall, IMA203 monotherapy continues to be well-tolerated in heavily pretreated patients at dose levels of up to 9 billion TCR-T cells. Let's take a closer look at the clinical activity of IMA203. The waterfall plot shows that IMA203 achieved a high rate of deep confirmed objective responses across a variety of different PRAME-positive cancers, such as checkpoint refractory cutaneous melanoma, platinum-resistant ovarian cancer, uveal melanoma, synovial sarcoma, as well as head and neck cancers. We see an initial objective response rate of 64% at week six and a confirmed objective response rate of 67% at month 3. Initial responses at week six were confirmed for all 6 responders with available subsequent 3-month scans. Importantly, partial responses were observed independent of tumor type. It is worthwhile to mention that the one ovarian cancer patient who showed a progressive disease at the initial 6-week scan and highlighted in orange on this slide did not only have five target lesions summing up to more than 200 millimeters diameter, but also had 20 additional non-target lesions with an estimated diameter of more than 600 millimeters. With such an extremely high tumor burden, this patient is an outlier compared to all other patients enrolled into IMA203 so far. This final plot is a visual presentation of the clinical responses over time for all 11 patients. Tumor responses were assessed approximately at week six after infusion at month 3 and then every 3 months. What you can see here is a rapid onset of all initial responses which were confirmed at the 3-month scan. This stands in contrast to previous observations during the phase Ia dose escalation when we saw a significant fraction of responses that were rather short-lived. This was also prior to the monocyte depletion step, being introduced into the manufacturing process. Notably, at data cut-off, five of seven responses were still ongoing, three of them exceeding durability of six months. Since most patients still have ongoing responses, a median duration of response has not yet been reached, or in other words, is still ongoing and cannot be calculated at the median follow-up of 8.5 months. The ability to demonstrate durable and ongoing responses to IMA203 treatment across different tumor types is the most important message and takeaway from today's data presentation. While more patients and longer follow-up time will be required to fully assess the long-term durability of the IMA203 product candidate, this new data set further increases the confidence that IMA203 may deliver a high rate of durable responses across multiple cancer types. This slide shows in more detail key patient characteristics and outcome of selected clinical readouts. I do not intend to go through the entire slide, but I want to focus your attention on the fact that the patient population treated in phase Ib cohort A consisted of heavily pre-treated patients who have exhausted all available standard of care options. It also becomes clear that deep and confirmed RECIST responses could be achieved over a wider range of different doses of induced TCR T-cells. Finally, it is very encouraging to see that IMA203 is able to provide clinically relevant responses in patients suffering from multiple types of cancer with different origin and biology. I'm looking forward to seeing the data mature as the trial further progresses. I would now like to hand back to Cedrik to discuss the translational data and the development strategy. Thank you, Martin. To assess biological activity of the infused IMA203 T-cells, we continue to monitor T-cell engraftment and persistence in the blood and infiltration into the tumor. In the graphs on the left and in the middle, we show robust T-cell engraftment and persistence, which is significantly higher in patients in cohort A following increase of cell dose and switch to the monocyte depletion process. It is reassuring to see that this improved PK profile nicely matches with our RECIST readouts and the finding of a higher rate of confirmed and more durable responses in patients. When looking at the data obtained from post-treatment biopsies, the figure on the right, we see that IMA203 T-cells were detectable in all available post-infusion tumor samples. This indicates that migration of T-cells into the tumor microenvironment can be achieved across a variety of different tumors. Furthermore, a high level of IMA203 T-cell infiltration was significantly associated with the observed objective responses, supporting the proposed mechanism of action for IMA203. Overall, we continue to see that the translational data in this trial is consistent with the clinical outcome. This figure shows the PRAME expression profile for all 11 patients infused with IMA203 in cohort A. Focusing on the Y-axis, it becomes clear that confirmed objective responses could not only be detected in patients with a very high expression of PRAME in their tumors, but likewise occurred in patients with PRAME just above our mass spec-guided RNA expression threshold, shown as dotted red line. It becomes clear from the data that clinical responses were irrespective of PRAME expression levels above the threshold and agnostic of tumor type. This data is in line with results presented earlier and confirms our position that IMA203 may be able to deliver a meaningful clinical benefit in all PRAME-positive patients with high, medium, and low PRAME expression. The data shown here highlight the multi-cancer opportunity of PRAME in the light of other tumors beyond the ones treated in our trial so far. The slide shows PRAME expression profiles derived from the TCGA database for nine selected tumors. The black dots represent PRAME expression in the seven responding patients in cohort A. Based on this data, we believe that IMA203 has the potential to target PRAME in several different kinds of cancers, including lung cancer and triple-negative breast cancer, which have similar expression profiles as ovarian and head and neck cancer. There may even be the opportunity in the future to lower the threshold for some of these tumor types. We therefore take the position that the data shown here highlight the multi-cancer opportunity for PRAME. I would like to summarize our findings and highlight our PRAME development strategy. Today marks a significant step towards bringing our ACTengine, IMA203 monotherapy, to patients with solid tumors. We present, for the first time, longer-term clinical data demonstrating a high number of deep responses with evidence of durable responses reaching beyond 9 months post-infusion, while demonstrating an acceptable tolerability profile. We show that these responses are agnostic of tumor type, and that IMA203 achieved objective responses at all PRAME expression levels above our threshold. We were able to generate these high doses of transduced engineered T-cells with a process that only uses 7 days of ex vivo manufacturing while achieving a 94% manufacturing success rate. In March, we significantly shortened the sterility QC release from 14 to 7 days, which now enables us to speed up turnaround time and treat patients 7 days earlier moving forward. This improved turnaround time is not only a clear differentiator when compared to other cell products manufactured by our peers, it also has the potential to further improve safety and increase clinical activity in this last line patient population where every day counts. The data further increases our confidence in the success and broad potential of targeting PRAME and our product candidate, IMA203 TCR-T. We plan to announce details of our development strategy later this year after further alignment with regulatory agencies. Today, we are happy to provide first insights that our clinical development plan will be based on two pillars, namely a fast to market approach for the first one or two indications and a broader signal finding in other cancer types. The initial indication for late-stage development will focus on cancers with high prevalence of PRAME and may include cutaneous melanoma and/or uveal melanoma or ovarian cancer. The highly flexible and scalable manufacturing facility we are building is designed to enable commercial supply and thus supports our fast to market approach. Our goal is to start the first phase II trial in the first half of 2024, with the ambition to make this trial registration-directed. We further plan to fully leverage the potential of PRAME through continued signal finding in the phase Ib trial across additional PRAME-positive cancers such as uterine cancer, lung cancer, breast cancer, and head and neck cancer. We will provide a clinical update on all 3 IMA203 cohorts and more details of the clinical development plan in the second half of this year. I would like to finish by emphasizing the potential of targeting PRAME with our TCR-based therapeutics. Immatics has achieved a leading position by targeting PRAME with 2 therapeutic modalities, namely ACTengine cell therapy and T-cell bispecifics. Both approaches have unique features, are differentiated, and bear the potential to provide innovative treatment options for a variety of cancer patient populations. The choice of therapeutic modality, ACTengine or T-cell or both, will be driven by clinical data and other factors. 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 their study teams. Thank you very much for joining our call today on the interim update for our ACTengine IMA203 TCR-T monotherapy cohort A data. We will now be happy to take any questions from the audience. Thank you. Dear participants, as a reminder, if you wish to ask a question, please press star one one on your telephone keypad and wait for a name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster. This will take a few moments. Once again, if you wish to ask a question, please press star one one. We're going to take our first question. The question comes from the line of Jonathan Chang from SVB Securities. Your line is open. Please ask your question. Hi, guys. Congrats on the update. Thanks for taking my questions. First question, with these data on hand, what is your latest thinking on what drives durable clinical responses? Jonathan, I'm happy to take this question. Obviously, we don't have the final answer, but we have, like, clinical data and biomarker that really match. What we have seen over time when we moved from dose escalation through the different dose levels to cohort A, we saw that the increase of the cell dose administered and the ability to generate cells that can expand in vivo and achieve high peak persistence is what made the biggest difference. If you compare the cell numbers administered over time, they went up. We believe that there's good reason to assume that the effect of the target dose, so number of trigger-happy cells, is what, now leads to this marked difference between dose escalation and what we now see at cohort A. I think we have now found the sweet spot where we give enough cells to hit the tumor hard, but also cells that if administered to patients lead to a manageable tolerability profile. In addition to Cedrik's point, we've always said the numbers game, and we feel now that's truly the case. In addition to your question, Jonathan, there's a background slide in the backup of the deck that's also published on our website that actually gives a little more detail on some of the functions of these T cells in vitro and how they translate in vivo. It looks like that actually our latest manufacturing enhancement that we introduced prior to starting phase Ib, the so-called monocyte depletion, also added additional quality to these patients. We think the quantity, the number, plus that additional enhanced phenotype that also Martin mentioned very briefly in his presentation, are actually adding to this persistence. This persistence now translates into significant durability than what we've seen compared to what we've seen in early doses in dose escalation. Got it. Second question, in terms of the tumor types activities being achieved in, do you think this is primarily a function of enrollment at this time, or are there other reasons why certain tumor types would be more susceptible to IMA203? This is just a question of enrollment and the patient populations and referring sites that our PIs have. It's typically phase I units which have a great catchment zone and can include and enroll a diverse set of patients to our trials, which means we get the patients that are typically enlisted by our PIs. We're now moving into a much more tailored approach where we really design our clinical footprint and our clinical trial in a way that we really get a systematic datasets, which means we are reaching out to lots of melanoma docs who can enroll in skin and uveal melanoma. We're now building also relationships to GYN onc experts that could address ovarian, endometrial and triple-negative breast. We are planning to set up another cohort for this broad signal, finding the sites that really have ability to enroll head and neck and diverse lung cancer patient populations. Which means we're now really moving from dose escalation phase I centric basket trials to really a focused approach where we can, yeah, on one hand push forward to a late-stage trials, confirm more signals in GYN onc and then broader signal finding. We do believe PRAME has a very broad activity. Obviously, more data still needs to be delivered to kind of provide evidence for that. Slide 16 that also, Cedrik showed us actually that activity happens in various different types of tumors at various levels of PRAME, even levels that are actually also present in tumor types that have lower PRAME levels. That really encourages us that this has a very broad activity based on this biomarker data and based on the association of response with low, medium, and high PRAME levels above our defined threshold. Understood. Last question, if I may. How do these results with cohort A impact your thinking across your other efforts targeting PRAME? This, of course, includes your second gen cell therapy, the combination strategies and the bispecific program. PRAME is a fantastic target, and it's so good that we actually really wanna go with everything we have against this target. We have what we call first generation IMA203. It's actually more like generation 1.5, if you consider all of these manufacturing enhancements we've implemented. We have our second gen, which is the co-transduced with CD8. We have our bispecific against PRAME. At this point, the data in cohort A looks very promising. This could actually be already a drug candidate that we could take for even into registration directed trials. At this point, cohort C, so the second gen, presents pure upside for us, and we're very much looking forward to the data from our bispecific IMA402. We've just filed, according to plan, the clinical trial application in Europe. That's the equivalent of the IND, which really gets us to start of this trial of hopefully early in the 2nd half of this year. We hope to have data also then from our bispecific modality next year. Our current hypothesis is that these two modalities, cell therapy and bispecifics, may have complementary activity. We think that cell therapy, as we have seen today, can act actually very effectively even in very late-stage disease, patients with high tumor burden that need that kind of debulking. While bispecifics, obviously with the lower cost of goods and lower logistics, may be more adaptable to a mass market, but may need a slightly earlier patient population. Whether that's the case or not, we'll see. we're really well equipped at Immatics to really serve all these cancer populations with different modalities that we have at hand. Got it. Thanks for taking my questions, and congrats again on the progress. Thank you, Jonathan. Thank you. The next question comes from line of Kelly Shi from Jefferies. Your line is open. Please ask your question. Thanks for taking my questions and congrats on the great progress. First, for the fast-to-market strategy, you will go for uveal and the cutaneous melanoma and ovarian cancer with monotherapy approach. I think previously you highlighted 5 initial tumor types to pursue. For the broader cancer types, how would you choose among monotherapy CD8 or PD-1 approach? Thank you. I'm happy to take this one. First of all, the PRAME, we have matured our thinking on the late-stage strategy. Before closing details, we wanted to have one more loop. The regulators to get alignment from the end of phase I meeting to really then share news with you, which would then, let's say, be at low risk for any changes. What we're happy to disclose today, indeed, as you said, that the primary indication will include high prevalence tumors. Most likely this could be skin melanoma, potentially even in a bundle with uveal melanoma or ovarian cancer. These are the three cancers with highest prevalence, are the ones where we have most of the data, and we are getting into a position where our clinical footprint will allow a significant ramp up in enrollment, which is required to really execute upon late-stage trials pretty quickly. As a second stage, we will then trigger, we plan to trigger a broad signal finding, which will then include the other cancers like lung, head and neck, or other gynecologic cancers like triple-negative breast cancer that also show high prevalence for PRAME. Don't expect a lot of these data this year because these are cohorts which we want to establish as soon as possible. They're not up and running. Thank you very much. I also have a follow-up, if I may. On which aspect CD8 and the PD-1 approach will further improve the treatment and efficacy respectively? Can I hypothesize that a CD8 could have been even faster outside of tumor killing and a deeper response because this approach increased CD8 T cell portion? Does CD8 and the PD-1 approach actually overlap efficacy? I assume it's not, so is it possible to combine to maximize the efficacy outcome? Thank you. Look, there's lots of hypothesis that we have, and there's early emergent data that plays into our hypothesis. Today, we don't feel comfortable to come up with a final answer because we still need to generate more data. Obviously, there is the chance, and Harpreet mentioned it, that generation 2 or combos could be seen as an upside with more activity and incremental benefit or significant benefit. We will actually give an update on all cohorts before end of this year, so in the second half of this year. Let's not speculate. Generate enough data to make firm claims, and then that data speak can answer your questions. A little bit more patience, please. Okay. Lastly, for the data update in second half, will cohort A and the B and C be presented together or separately? Thanks. We have not fully decided how to do the release. That will be most likely in the fourth quarter. The best guess at the moment is that we will do this together for cohort A, B and C. Okay, thank you very much, and congrats again. Thank you, Kelly. Thank you. Now we're going to take our next question. Just give us a moment. The next question comes from line of Alec Stranahan from Bank of America. Your line is open. Please ask your question. Hey, guys. Thanks for taking our questions and congrats from us as well on the strong data. The first question I had is on the correlation between PRAME expression and response that you're seeing in the clinic. It seems that, you know, once patients reach a certain threshold in expression, that's what it takes to get them into the response. My question is, how do you approach this in terms of designing your phase two, in terms of patient selection, and how do you see this ultimately feeding into your registration strategy? Thanks. I think the good news is that the level of PRAME that we have set for our clinical trials now gives us the confidence that this level is sufficient to drive confirmed and deep tumor responses that are durable, which means this level of PRAME expression is right. We can use this level not only to confirm the prevalency and therefore predict our enrollment rates, but we can also move forward with the patient population where we can be really confident that there will be a fruitful interaction with our T-cell receptor. There is obviously, from this data now, a potential lifecycle opportunity to go even further down to lower levels of PRAME. We have still not defined how exactly we would get there. One thing that one could conceive is that we now accelerate with the validated level that we have, which we can now move forward and open an extra cohort of patients with low PRAME and potentially with such an extra cohort that expand the patient population to patients with PRAME above our threshold and maybe even patients below our threshold. We haven't defined how to deal with the opportunity of patients that have even lower PRAME levels as the ones that we have selected because this threshold really looks right. Does this answer your question? Got it. Yes. Yep, that's helpful. One more, if I may. You know, given the data is still maturing from the study, looking at the totality of evidence you have for 203, you know, how do you guys feel about your asset versus other PRAME-directed assets that are in development that have had clinical data? Do you want me to start, Harpreet? Yeah, sure. First of all, what's great for patients is that their PRAME now, I think, has been firmly constituted as a clinical validator. That's the most important news for today. There are very few clinical-stage PRAME assets. As I mentioned before, I do see room for both bispecifics and cell therapy approaches, and this will be all data-driven. Let's today really celebrate this as another step forward for cancer patients that are really suffering from solid cancers where there are very, very few therapeutic options, something that Martin can dearly confirm to you from his day-to-day practice. Yeah, absolutely. I can really say that this drug is a game changer for the patients we've treated so far. I do also see room for bispecifics as well as T-cell receptor engineered T-cell therapies. They both have their pros and cons and are suitable maybe for different patient populations or can even be used together or in sequential fashions. I really appreciate that we have more than one agent being in development for this kind of patients. Okay. Just lastly, on manufacturing, I guess where are you at currently? Are you comfortable with that 94% at the billion cell dose? What would you need to do to scale for phase II and potential commercial ramp? Would the goal to be to do this all in-house, or would you outsource some parts of that process? Yeah, 94% is a good rate for phase Ib. We're happy about that, but our ambition is high. We wanna get to 97% plus, actually, then for commercial phase, ideally, already in registration director trial. This is the time now to really think about how to bring this potentially into registration director trials and further. To that extent, we have actually decided to build a commercial stage GMP manufacturing facility in Houston, Texas. We already have a phase I facility, which can also deliver material for phase II that we're currently entertaining that's fully in-house on our own, and we're building our in-house commercial stage facility. This is a facility that's built in a very scalable, modular, and cost-efficient way, basically a warehouse. We can then build module after module in a way that you don't have to spend all the money up front. We feel that's the kind of right way to build that over time. Getting ready now for the next stage but doing this in a kind of cost-cautious way is very important to us. Good. Thanks. Congrats again on the progress. Thank you. Thank you. When we take our next question. The next question comes from line of Rajan Sharma from Goldman Sachs. Your line is open. Please ask your question. Hi. Thanks for taking my question. First one just on the manufacturing capacity. What do you expect kind of capacity to be when the facility is operational in 2024? I realize it's kind of modular, but I guess when it first comes online, what are your expectations for capacity? Just a second question on IMA402, the bispecific. Obviously you've kind of filed for your CTA. I was just wondering if you could provide any more color on what that trial may look like in terms of dose levels and potential tune type. Thank you. I'll start with the manufacturing, and then I'll hand over to Cedrik on the 402 trial that you asked. I guess this was on the bispecific. On manufacturing cell therapy, the capacity that we're currently building, we have not disclosed yet. Those kind of numbers we will provide once this gets closer to opening. Already the facility that we currently have can serve our ongoing phase I trials as well as a future phase II trial. Obviously the new facility will be able to do that as well, plus more. Very importantly, the facility will be also designed to include initial commercial supply, which will then be the supply beyond BLA filing and beyond potential market approval. On the bispecific 402 question, I'll hand over to Cedrik. Yes. We have so far not disclosed many details about IMA402, and this is a session to really appreciate the cell therapy. What I'm happy to disclose to you today is that we have submitted our CTA, so we are on track with the timelines. We expect clinical data from our bispecific programs, both from the MAGE that is part of the BMS, but also from the non-partnered PRAME program. Because of good relationship with our agencies, I think we've been able to come up with a design that allows a fast and adaptive approach to dose escalation to reach pharmacological active doses as soon as possible, balancing safety for patients. Regarding the scope, we are prepared to not only deal with cancers that are, let's say, restricted to melanoma and highest prevalence, but we are from the get-go are looking at those cancers with high prevalence and those with high biological rationale and those with the highest commercial potential. You will see an aggressive approach that will lead to an early de-risking and signal finding to describe, let's say, the value and define it for us and others as soon as possible. Clinical data will be expected to be published next year, not this year. Thank you very much. Thank you. Now we'll go and take the next question. The next question comes from line of Graig Suvannavejh from Mizuho. Your line is open. Please ask your question. Hi, this is Avantika on for Greg. I just, congrats on the data. I just had two quick questions. My first one was: What will the deciding factors be to choose the recommended phase II dose between dose level 4 and 5? Oh, that's an easy one. Look, when we initially started this trial, we were, let's say, orienting us towards the, let's say, a benchmark from the field that you need to generate at least 1 billion TCR-T cells. Then we saw three things. First of all, we saw high activity, then we saw good tolerability, then we saw that our manufacturing ability to manufacture high doses increased over time with CMC innovation, which means we can now robustly supply much higher doses. Based on the great clinical signals and the good safety and the ability to just generate high doses, we just opened up to around the maximum of cells we can achieve within only 7 days of ex vivo expansion. We think it's important to keep this period short, to have fit cells with early phenotypes. Pre-clinically this really leads to a higher potency. What you can see here is really then a mixture of, Driven by clinical data and moving the boundary of what we can manufacture and supply robustly and safely within seven days. We now have a wide range of, let's say, doses we can administer. We see that within the whole range shown on this slide, on the right-hand slide, we can hit the tumor heart and lead to durable responses, which means we now need to only generate a little bit more data and experience, and then can lock in the final recommended phase II dose before we amend the protocol and kick off the phase II trial part. Great, thank you. Another just 1 follow-up. On slide 11, you have something in the notes section mentioning about an ovarian cancer patient that was erroneously given 1 dose of nivolumab. Can you talk about what you mean by the patient being part of an intent to treat population? This was a patient who was treated in a site that had treated many patients in cohort B. For whatever reason, this patient who was in the monotherapy received a single dose of nivolumab, so was treated like a cohort B patient. This was immediately detected, reported and changed, which means we don't believe that this 1 dose of nivolumab has, let's say, changed the clinical course. We don't know. It's a confounding factor that we didn't, let's say, want to introduce in cohort A, which means in a clean analysis intent to treat, this patient would not be, let's say, counted because this patient has not been treated for protocol, but had, let's say, the minor, let's say, additional deviation of receiving 1 single half dose of nivolumab. In other words. Thank you so much. We have shown here the full ITT analysis. The response rate that you see here is really based on the ITT. There's no slicing down of these numbers, so the response rate includes ovarian cancer patients. Got it. Thank you so much. Congrats again. Thank you. Thank you. Dear participants, as a reminder, if you wish to ask a question, please press star 1 1 on your telephone keypad. Now we're going to take our next question. The question comes from the line of Sebastiaan van der Schoot from Van Lanschot Kempen. Your line is open. Please ask your question. Hi, team. Congrats on this update. Thank you for taking my questions. I was wondering, in your latest communication regarding cohort B, you mentioned prioritizing IMA203 monotherapy in a last line therapy setting, but we're also considering further investigation of a combination with nivo as a frontline therapy. Can you give us some color on what led to that specific decision to go into frontline and whether that is still explored and what we can expect from that in Q4? Good. First of all, the decision to de-emphasize the nivo cohort is just driven by our wish to define a winner as soon as possible, which means either the generation one monotherapy in the cohort A or a second generation IMA203 CD8 product. If you fill three cohorts with full speed, you just delay all of them. Now focusing on A and generation two to really find the winner is just what gives us the key answer for us as quickly as possible. Obviously, the generation data with the nivo as a combo gives us additional safety data. You're probably aware, as we all are, that checkpoint inhibitors have become your standard of care in first line across many, many cancers. We see that our cell therapy may have a positioning in the future which is not only in the last line when everything else has failed, but may work, may even work better in earlier lines when patients are less heavily pre-treated and cancer comes with, let's say, lower disease burden. The safety data that we now have will allow us to move into earlier lines as a second step and then combine cell therapy on top of standard of care. We have not disclosed a detail of the technical development beyond last line, therefore we have to wait until we disclose when and in which cancer we want to take the liberty to initiate the trials where we go into checkpoint-naïve populations and combine with the checkpoint. Okay, got it. Thank you. I was also hoping that you could maybe provide some color on the data readout in Q4 for the other two expansion cohorts. Specifically regarding the tumor types, have there been patients enrolled with other tumor types or another focus than we have seen for cohort A so far in those specific cohorts? Most of the patients that we currently enroll are indeed focused on those five cancers of special interest that we recently introduced, those that have a high prevalence of PRAME. We continue, and the protocol allows to also enroll other types of cancers. You shouldn't be surprised if by end of the year the data set will include the one or other patient with a different cancer. Broader signal finding. Just as a caveat, any decision shouldn't be based on a small number of patients, which means, yes, additional cancers will come. Systematic data sets with patients in lung cancer or head and neck cancer or other gynecological cancers shouldn't be expected with larger ends this year. Great. Thank you very much. Congrats again on this great result. Thank you. Thank you, Sebastiaan. Dear participants, as a last reminder, if you wish to ask a question, please press star one one on your telephone keypad. Dear speakers, there are no further questions at this time, and I would now like to hand the conference over to all of you for any closing remarks. Ladies and gentlemen, it has been a real pleasure today to be able to present to you the data on cohort A of the IMA203 trial. Very much looking forward to also engaging with the audience, with investors, analysts now in the next days. See you then. Bye-bye.