Good morning, ladies and gentlemen, and thank you very much for joining us for our webcast. Today, we will provide another interim clinical update on our ACTengine cell therapy, IMA203, with durability data exceeding one year, and share the first clinical data on our second generation cell therapy candidate, IMA203CD8, targeting PRAME and solid cancer patients. Before we start, I would also 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 Investors section of our website. This presentation also includes an appendix, which provides further background information and data on all cohorts. Speaking today will be Cedrik Britten, Chief Medical Officer at Immatics, and Dr. Martin Wermke, Coordinating Investigator of the ACTengine IMA203 TCR-T trial. This presentation contains forward-looking statements. Many of you will already be familiar with PRAME, a multi-cancer target that we consider to be one of the most promising and prevalent solid tumor targets. TCR-based therapies targeting this antigen have a large potential to address unmet medical need for a large population of patients with solid tumors. To target PRAME effectively, we have developed three TCR-based therapeutics currently in clinical development. These include two generations of our cell therapy, ACTengine IMA203, and our TCR bispecific molecule, TCER-IMA402. Together, both therapeutic modalities aim to leverage the full potential of PRAME by providing distinct product features and modes of action suitable for different patient populations and medical needs. Today's update, with a data cutoff of September thirteenth, provides interim data on all IMA203 cohorts. We will focus on IMA203 generation one cell therapy in melanoma patients who still face a high unmet medical need following treatment with checkpoint and BRAF inhibitors in earlier lines, and the first clinical update from our potency-enhanced second-generation candidate, IMA203CD8. With this, I would like to hand over to Cedrik, who will start with an overview of the key takeaways of today's presentation. Thank you, Harpreet. In today's presentation, we will share updated data on our IMA203 gen one monotherapy in melanoma patients at the recommended phase II dose. We're excited to report that IMA203 has shown durable and ongoing responses in some patients exceeding 12 and 15 months after treatment, while maintaining confirmed objective response rate of 50%. We further observed that IMA203 is well tolerated. We have recently defined the recommended phase II dose for IMA203 at 1-10 billion TCR-T cells. In addition, we are pleased to share that we can generate these cell doses within a 7-day expansion period, followed by a 7-day release at an overall manufacturing success rate of over 95%. Based on this data set and our recently obtained FDA RMAT designation, we now plan to progress IMA203 gen one monotherapy into registration-enabling phase II trial in melanoma in 2024. We look forward to providing the next update on the clinical development path in the first quarter of next year. In addition to IMA203 gen one, which comprises functional CD8 cells only, we're excited to share the first clinical data on IMA203 CD8, our second-generation, potency-enhanced version of IMA203, which contains functional CD8 and CD4 T cells. Based on the data to date, the tolerability of IMA203 CD8 appears to be manageable. IMA203 CD8 shows a confirmed objective response rate of 56%, with a durable response seen more than 12 months after treatment. 6 of 7 responses are still ongoing, including 2 unconfirmed responses with no subsequent scan available at data cutoff. IMA203 CD8 also demonstrates an enhanced pharmacology with a differentiated response pattern compared to IMA203 gen one, as you will see in the course of the presentation. Dose escalation is currently ongoing. Once completed, as our next development step, we plan to conduct signal finding studies, preferably in non-melanoma indications such as ovarian cancer, uterine cancer, non-small cell lung cancer, triple-negative breast cancer, and others. 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've completed this part of the trial and are currently investigating IMA203 gen 1 in cohort A at the recommended phase II dose. A total of 45 patients were so far treated with IMA203 in the efficacy population. Data from phase IA and all IMA203 cohorts can be found in the appendix. In cohort C, we're investigating the second-generation version, IMA203CD8. Today's update focuses on 13 melanoma patients treated with IMA203 gen 1 at the recommended phase II dose across phase I A and cohort A, and on 12 patients treated with IMA203 gen 2 in cohort C across 3 dose escalation levels. With this, I would like to hand over to Dr. Martin Wermke, who will present the clinical data. ... Thank you, Cedrik. Let me start with an overview of the patient characteristics and high-level clinical outcomes across cohorts. Overall, by now, 45 patients have been treated with IMA203 Gen 1 monotherapy, and 12 patients with IMA203 CD8 Gen 2, who have an available tumor response assessment post-infusion. As you would expect for a last-line stage four patient population, the number of prior treatments, baseline LDH levels, and tumor burden are high. During phase IA, patients were treated with lower doses using a previous manufacturing process and the typical phase I cohort patients with an above-average tumor burden. While responses in this cohort were initially short-lived, IMA203 Gen 1 and Gen 2 are now achieving higher objective response rates and better durability in cohorts A and C. Let's now take a closer look at the clinical activity of IMA203 Gen 1 in melanoma patients treated at the recommended phaseII dose across phase IA and cohort A. My observation is that IMA203 has been well tolerated in these melanoma patients, and the tolerability profile remained consistent over time, despite having treated more patients at the highest doses. Most frequent adverse events were expected grade 1 to 4 cytopenia associated with lymphodepletion. Looking at adverse events of special interest, mild to moderate cytokine release syndrome was the most commonly observed adverse event, with only 1 patient experiencing grade 3 CRS. No dose-dependent increase of CRS was observed. Further, only 1 mild ICANS and no IMA203-related death in any of the treated patients occurred. The full tolerability profile for all patients treated with IMA203 Gen 1 monotherapy, including non-melanoma patients, can be found in the appendix. Overall, IMA203 seems to be well-tolerated in heavily pretreated patients at the recommended phaseII dose of 1-10 billion TCR-T cells. The waterfall plot on this slide shows that IMA203 achieved a deep, confirmed objective response in cutaneous and uveal melanoma patients. The initial objective response rate observed is 62%, and the confirmed objective response rate is 50%. The spider plot is a visual presentation of the clinical response over time for each patient. Tumor responses were assessed approximately at week 6 after infusion, at month 3, and then every 3 months. Importantly, at the data cutoff, the longest responses were ongoing at 12 months in one patient and 15 months in two patients after treatment. Since most patients still have an ongoing response, a median duration of response has not been reached yet at a median follow-up of 14.4 months. IMA203's ability to demonstrate durable and ongoing responses beyond one year post-treatment is one of the most important messages and takeaways from today's data presentation. With maturation of the clinical data set, it becomes progressively evident for me that targeting PRAME with Immatics IMA203 TCR-T approach has the potential to provide a durable benefit for advanced stage melanoma patients while offering a manageable safety profile. With this, I would like to hand over to Cedrik to discuss the market potential of IMA203. Thank you, Martin. In addition to the attractive clinical features for IMA203, it is worth mentioning that IMA203 benefits from a short manufacturing process for providing the cell product to patients. The process begins with a leukapheresis as starting material instead of a surgery. We're able to generate the cell product with a short expansion time of 7 days, plus release testing of 7 days in order to provide the cell product to patients as quickly as possible. Following cell infusion, we use low-dose IL-2. In the U.S., every year, approximately 8,000 patients die from cutaneous and uveal melanoma, which highlights the urgent need for novel and effective therapies. Of these, up to 3,300 last-line patients are HLA and PRAME positive, highlighting the significant market potential of IMA203 in addition to the medical benefit. In addition to IMA203 Gen 1, where we are dedicated to making it accessible for melanoma patients as fast as possible, our other focus today is the second-generation product, IMA203 CD8, where we are excited to report clinical data for the first time. While IMA203 Gen 1 comprises functional CD8 T cells only, IMA203 CD8 Gen 2 is an innovative addition to our portfolio as it broadens the potential of IMA203 by adding functional CD4 T cells to the cell product through the transduction of CD8 alpha and beta subunits. CD4 T cells have been characterized as aiding other immune cells by releasing cytokines to mediate long-term durability and potentiate the antitumor activity or cell product. Overall, we believe the data demonstrate that the tolerability of IMA203 CD8 is manageable. As expected, for potentially higher potency cell therapy, more CS occurred at higher doses as compared to IMA203 Gen 1. However, no high-grade CRS, no neurotoxicity, and no DLTs were reported for the 4 patients treated at dose level 3 or the 4 patients treated at dose level 4A. In the higher dose level 4B, we observed DLTs in 2 of 4 treated patients. Dose escalation is currently ongoing at dose level 4A. IMA203 CD8 achieved an initial objective response rate of 58%, with a response in 7 of the 12 treated patients across different solid tumor indications. For 2 of these patients, the confirmatory scan was pending at data cutoff. Of note, 6 out of 7 responses were ongoing at the data cutoff, and all initial responses were confirmed when a subsequent scan was available. This leads to confirmed objective response rate of 56%. Interestingly, we saw a deepening of response from stable disease to partial response in 2 patients. This conversion from SD to PR over time is something we have not observed for IMA203 Gen 1 so far. When looking at durability, we have a shorter follow-up period available compared to Cohort A. Still, we see that IMA203CD8 can achieve durable responses, with the longest ongoing response exceeding 12 months after infusion. Since 6 out of 7 patients still have ongoing responses, a median duration of response has not yet been reached. The differentiated response pattern for Gen 2 compared to Gen 1 is one of the most important messages and takeaways for this data set. In line with the clinical data, when comparing translational data between Gen 1 and Gen 2, we observed an enhanced pharmacology for Gen 2. This is indicated by higher peak expansion of T cells, as well as higher initial activation levels, while higher activation is not followed by higher levels of the exhaustion marker PD-1 over time for Gen 2. Interestingly, with Gen 2, tumor responses were observed at lower infused cell doses, but in patients with higher tumor burden compared to Gen 1. We believe our second-generation cell therapy is exhibiting unique patterns in pharmacology, guiding our development efforts for Gen 2 towards other and potentially harder-to-treat tumor types, such as ovarian, uterine, lung, triple-negative breast cancer, and others. With this, I would like to summarize today's findings and provide an outlook on the development path. Today, we were able to show the targeting PRAME with our IMA203 monotherapy has the potential to provide durable benefit for advanced-stage melanoma patients. We have defined the recommended phaseII dose and received FDA RMAT designation in multiple PRAME-expressing cancers, including cutaneous and uveal melanoma. This data will serve as a foundation for future pivotal development. Alignment with the FDA on the patient population, the trial design, and CMC aspects is ongoing, with a goal to enter into registration-enabling phase II trial in melanoma in 2024. In addition, we reported our first clinical data set for the second-generation product candidate, IMA203CD8. The results shared today highlight a differentiated pharmacology that was achieved by equipping IMA203 T cells with a CD8 co-receptor. While the data is currently less mature compared to Gen 1, we are excited about the enhanced pharmacology and the differentiated response pattern already observable at this early stage. We're now proceeding to complete dose escalation and initiate further dose expansion cohorts with a focus on non-melanoma patients. Overall, we're pleased with the progress we've made to date on both our PRAME-targeting cell therapy generations and the positive clinical data generated so far. We look forward to continuing our effort in advancing our cell therapies for the benefit of patients with different types of solid cancer. 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 eight selected tumors. The black and gray dots represent PRAME expression in clinical responders across IMA203 Gen 1 and Gen 2. Based on this data, we believe that our cell therapy has the potential to target PRAME in a range of different solid tumor indications, including lung cancer and triple-negative breast cancer, which have similar expression profiles as ovarian and head and neck cancer. As confirmed responses have also been detected at or close to our PRAME threshold, there may even be the opportunity in the future to lower the threshold for some of these tumor types. The goal of our development and commercial strategies is to make IMA203 available to a broad population of patients suffering from cancer, with an initial focus on the U.S. market. To achieve this, we're pursuing a three-step development strategy to leverage this multi-cancer promise of PRAME. Step one will focus on IMA203 Gen 1 in melanoma, with plans to enter registration-enabling phase II clinical trial in 2024. In the U.S. alone, there are up to 3,300 HLA- and PRAME-positive cutaneous and uveal melanoma patients in the last line per year. Step two, conducted in parallel, involves dedicated dose expansion cohorts for signal finding in ovarian and uterine cancer, preferentially with IMA203 CD8 Gen 2. Enrollment of patients with these cancer types is already ongoing. There are up to 9,000 HLA- and PRAME-positive ovarian and uterine last line cancer patients per year in the U.S. Finally, step three aims at the development of a broader tumor-agnostic label in PRAME-positive solid cancers, including non-small cell lung cancer, triple-negative breast cancer, and others. This could leverage the full potential of PRAME across multiple solid cancer types and make IMA203 accessible to up to tens of thousands of HLA- and PRAME-positive patients per year in the U.S. Looking ahead, 2024 will be a catalyst for Immatics, with planned updates across the entire clinical portfolio, starting with a development update on IMA203 Gen 1 in the first quarter of 2024. Further planned updates include the next clinical data update for IMA203 CD8 gen two, as well as our two TCR bispecific programs, IMA401 and IMA402. IMA401 is targeting MAGE-A4 and MAGE-A8, and being developed in a phase I basket trial in collaboration with Bristol Myers Squibb. IMA402 is our proprietary TCR bispecific targeting PRAME, where our development efforts are initially aimed at a diverse set of six cancers that show prevalent expression of PRAME, such as ovarian, uterine, and lung cancer, synovial sarcoma, as well as melanoma. In closing, we would like to express our sincere gratitude to the patients participating in our clinical trials, the families, as well as our investigators and the study teams. With this, I would like to hand over back to Harpreet to conclude today's presentation. Thank you very much, Martin and Cedrik, and thank you to the audience for joining our call today on the interim clinical data update for our ACTengine IMA203 programs. Cedrik and I will now be very happy to take any questions from the audience. If you would like to signal with questions, please press star one on your touchtone telephone. If you're joining us today using a speakerphone, please make sure your mute function is turned off to allow your signal to reach our equipment. Again, at this time, if you would like to signal with questions, please press star one on your touchtone telephone. Our first question today comes from Kelly Shi with Jefferies. Congrats on great progress, and thanks for taking my questions. Firstly, on efficacy, we saw four very durable responses across gen one and the gen two, passing 12-month landmark at this moment. So from the translational studies, any correlation you could find on T cell dynamics to drive the deep and durable responses? And also, have you done comparison on disease control rates for gen one or versus gen two? And from the plot, it looks like gen two seems to have, like, a better disease control rate compared to gen one, or at least, like, a trending better. Just curious your thoughts on that. Thank you. Yeah, happy to take this one, Kelly. This is Cedrik speaking. You asked for, let's say, any correlative data explaining differences in the patients that had long landmarks or responses compared to those with shorter responses. And the answer is yes, we looked into this, but we didn't see a clear difference here. We see generally that our T cells engraft quickly to very high levels and then stay in the periphery for a long time. We also find that these T cells make it to tumors. We generally see that those patients that have deep, and then also the durable responses, are those that have most of the TCR T cells in the tumor microenvironment in post-infusion biopsies. But if you just compare those four patients with responses that were deep and going beyond a year, we don't see a particular T cell phenotype or particular PK profile that really sticks out as compared to those patients that have shorter-lived PRs or stable disease. So this was the first question. The other was the disease control rate, generally high if you look at all patients with PRs and stable disease. You mentioned a potential trend for a higher disease control rate for the second-generation product. I would say, it's too early to really compare the disease control rate between the two. We have observed this differentiated pharmacology and also this differentiated response pattern with SDs converting to PRs, and it also looks like for generation two, that PRs continue to deepen for longer times. For me, it would be too early to say whether the one or the other generation has a higher disease control rate. And, keep also in mind that we are comparing patient populations with a different subset composition and different characteristics, so there are still very many variables in these two patient populations. Does this answer your question? Thank you very much. Yes, it's very helpful- If I may add, Kelly. And, if I may just very... No, go ahead. No, Kelly, just wanted to add, I mean, remember we said earlier this year, we want to pick a winner by the end of this year. And with the data that we have as of today, actually, we believe we may have now two winners. Gen 1 to move now into pivotal trial in melanoma, and Gen 2 showing an enhanced pharmacology that, in our view, may be beneficial as we further target tumors outside melanoma, with the addition of CD4 cells, that actually could be required to keep additional pressure on these tumors. So based on today's data, we believe pursuing both Gen 1 and Gen 2 are in the best interest of patients and actually may serve different patient populations. ... Terrific, super helpful. If I may, just a very quick one on the PRAME screening. Can you talk about what screening method you use and how accessible across different study centers? Thank you so much. So I can answer this question, Kelly. What we use is a PCR assay. Initially, we started the trial with PCRs only from fresh biopsies, but we have recently moved to also allow PCRs on archival material and tissue that we get from tissue banks. And this is typically readily available, and so far, we also had a good take of patients that were able and willing to give these fresh biopsies. The PCR threshold is a very special one because we really defined it based on, yeah, lengthy studies in the past with RNA expression levels in cell lines and primary tumors and peptidomics. And we have really set a level of RNA expression detected by PCR that we believe predicts sufficient peptide density expressed on tumor cells. All our clinical data so far really indicate that the threshold that we have chosen is the one that is certainly sufficient to induce deep responses. There is one slide where we look for RNA expression, and you can see that we see these responses very close to our threshold. There's even a potential in the future to potentially go further down, in particular with our second generation product that has enhanced pharmacology. I can imagine that patients with low levels of PRAME below the threshold, which is very high, could still benefit from the treatment. Terrific. Congrats again. Thank you, Kelly. Our next question comes from Jonathan Chang with Leerink Partners. Hi, guys. Congrats on the data, and thanks for taking my questions. First question: What gives you confidence in the ability to address tumor types beyond melanoma with your PRAME-targeting programs? And second question: How are you guys thinking about your cash position? Thank you. Should I take the first one, and then, Hubert, the one on the cash position? Sure. What gives us confidence about activity beyond cancers? So first of all, we have followed PRAME expression levels across many cancers, and we see that we can find patients with a PRAME above our threshold across a multitude of cancers. We've also seen responses for first generation and second generation, and those during dose escalation and in phase IA across in many cancers, including very hot cancers with lots of mutations like melanoma, but also rare cold cancers like synovial sarcoma, with responses in ovarian cancer, head and neck cancer, mucosal melanoma. Which means the clinical data that we have seen across so many cancers indicates us that PRAME levels expressed above the threshold will work. Our second-generation product so far shows really an enhanced pharmacology, higher potency from what we see in terms of number of cells, being able to hit tumor lesions hard and also lead to durable responses with the follow-up we had. This makes us confident that this is not only a melanoma drug, but that one that can really reach into multiple cancers. The second-generation product, as Hubert says, we believe could be the winner that goes across many of those cancers, and the signal finding is already ongoing and will continue over the next months. Hey, Jonathan, your second question. We're very well capitalized. We have over $500 million of cash and cash equivalents, and that gives us a cash reach well into 2026 to reach multiple value inflection points. I mean, there are multiple actually already in 2024, obviously advancing gen 1 into a pivotal trial in melanoma, further advancing gen 2 outside melanoma. But we also have two fantastic bispecific compounds. IMA401, that's developed in joint collaboration with Bristol Myers Squibb against MAGE-A4, MAGE-A8, where we intend to show first clinical data next year from the ongoing dose escalation. But also IMA402, which is our other PRAME compound. It's a bispecific compound that we fully own and where we also expect first clinical data update from the dose escalation next year. Overall, we're very well equipped in terms of our cash to kind of get to multiple value inflection points over the next years. I'd also like to state that at this point, we do not intend to raise on this data release. Understood. Thanks for taking my questions. Our next question will come from Alec Stranahan with Bank of America. Hey, guys. Thanks for taking our questions. Just a couple from us on the melanoma data. So first, looking at the swimmer plot, it looks like the unconfirmed PR spiked back up from six-week and three-month scans. Any additional details you can provide on these patients, and do you expect they will remain unconfirmed? And then any additional color on the two responders that went off therapy, since it looks like they were doing pretty well on IMA203. Is this due to tolerability in these patients or maybe something else? And then lastly, just any comments on the DOR calculation. Is this really dependent on those three patients on therapy out to 12 months at this point? Thanks. So let's start with those patients with those responses that were initially found and then not confirmed at the second scan. So these were patients treated at high dose, but during dose escalation, which is still our recommended phase II dose, but at the lower level. So this is then, I think, a phenomenon of an effector-to-target ratio, so number of T cells that we infuse and achieve in the system by the tumor mass that have to be fought. And they're just two cases of high volume disease that proliferated quickly. Luckily, with increase of the dose, and we now regularly achieve 3 billion or more cells in our manufacturing process, we saw that those initial responses could all be confirmed. This is something which we may see in the future, but something which we have actually seen much more in the past, and we rarely see nowadays. This was the question on the unconfirmed responders. Then you had a question about patients that went out of the study. Can you specify which patients you mean? Because it's multiple patients shown here. Yeah, I'm just looking at the light green bars on the swarm plot. Yes. So these were- The level for... Yeah. Yeah, and these were the two patients that had an initial response and then progressed and went out of the study and into other subsequent trials or treatments from patients. Okay. And then just on the, the DOR calculation, I guess- Yeah, we used the reverse Kaplan-Meier curve, where we looked indeed in censored events that drive this, and then particularly with these small patient populations, there is quite some volatility, and the calculation changes depending on new incoming responses and the durability and whenever a patient progresses. In this particular data set, you're indeed right. The follow-up is skewed or also influenced significantly by those three patients that are now in PR for more than 12, or the two with more than 15 months since infusion. So this number may change, but I think if you compare this data set with the one that we had earlier this year, the number of patients in the denominator and the total follow-up of the population has significantly increased. And therefore, this data set gives us much more confidence and should have much less volatility, as compared to the much smaller and data set with shorter follow-up that we presented in April. We see this as a significant de-risking and clear maturation of the data set that now opens the door towards not only the discussions with U.S. FDA. They have seen the data and assigned the RMAT status to this first-generation product. And we are therefore hoping, let's say, hopeful that this will lead to discussions that will give us a clinical trial design for registration-directed trials to start next year. Alex, mathematically, all confirmed responders, so all 6 confirmed responders, regardless of their median of their duration of response, drive the overall median duration of response. Our next question will come from Eric Schmidt with Cantor Fitzgerald. Oh, hi. Thanks for taking my question, and thanks very much for all of the supportive data in the slide deck. Question is on potential differential activity in melanoma versus ovarian cancers. With generation one construct, you're obviously seeing very good durability in melanoma, and it seems like quite short durability, say, in the ovarian cancer subset. I know it's just two out of four patients, but why shouldn't we believe that melanoma is just what's special here, and that melanoma cancers have a greater propensity for durability versus other histologies, as opposed to, you know, thinking there's something you can do with the generation two construct that overcomes potential greater refractoriness of other tumor types? Yeah, I can answer this question. So for the... It's in the moment, it's difficult to compare the melanoma with the few ovarian cancer patients that we have treated. From those 4 ovarian cancer patients that had initial response and then did not have responses going beyond 6 months, reaching a year or so, we have clearly an, let's say, confounding factor here, which is that at least 3 of these 4 patients had very high volume disease, multiple targets, and even more non-target lesions that are not reflected by the tumor burden, high LDH, fast progression, very many previous treatments, one patient with 10 previous treatments, and overall, also sometimes a lower dose infused. So just by looking at the dose and tumor ET ratio, these four patients were really set up for, let's say, less successful outcome as compared to the overall population in malignant melanoma. Which means based on this patient bias, I don't think that you can make a final statement of what generation one could or could not achieve in ovarian cancer. I think if you would take similar patient populations with all patient characteristics, you may potentially get similar results. But you're right, that melanoma is special. It is special in at least two regards. In average, the PRAME levels are higher in melanoma as compared to ovary. It's slightly higher, and we know that melanoma has really been something like the, the model cancer for immuno-oncology, so it seems to be very, let's say, sensitive to immune manipulation and immune intervention. So it might indeed be the cancer that is the lowest hanging fruit, and therefore, we have decided to move the second generation, which adds the CD4 cells and all the crosstalk between CD4 and CD8 cells, to now, go into all cancers beyond malignant melanoma. We believe that the additional pharmacology, the enhanced potency, will certainly help. Thank you. I was pleased to hear that you're gonna be giving us the update on IMA401 next year with your partner, Bristol. Can you provide any more color on when and what we might see in 2024? Unfortunately, not any more color on the detailed timing and venue, so please just stay tuned, and we will provide the central data. Thank you very much. Our next question will come from Rajan Sharma with Goldman Sachs. ... Hi, thanks for the update, and thanks for taking my question. Just on safety, and I was just wondering, both in kind of the Gen 1 and the Gen 2, if there are any notable patient characteristics, and I guess with 2, 2 or 3 or Gen 1, were there any notable characteristics for the single patient who did experience ICANS? And then similarly for Gen 2, those patients who did experience CRS and neurotox, was there anything specific in the baseline characteristics, be that tumor burden or prior lines of therapy? And then secondly, just on the initial signal finding data for Gen 2 outside of melanoma, when could we expect to see that? Yeah. So in terms of the ICANS, so except for this one patient that I would talk about in a few seconds, we have generally seen very mild grade 1 or 2 ICANS in generation 1 and generation 2, which are typically treated with corticosteroids and typically reversible within 1-5 days. And they typically come very close to the peak of CRS. So these are mild grade confusion, so CARTOX scores of 9 or 8, so difficulties to count backwards or to write a sentence. So these are really mild versions of neurotoxicity that we have generally observed. And in terms of the patient's characteristics for those, it's difficult to say. There is the impression that it's patients with a higher tumor load and a higher cell dose, but generally, we cannot really map it to a specific patient characteristics. But luckily, these are manageable, and by all our treating physicians. There was then this one case of a grade 4 neurotoxicity, so this is the one patient that also developed a grade 4 CRS, and then also later, a macrophage activation syndrome. This was a patient that clearly had a high risk, a constellation at the get-go, so high tumor load, many lesions, highly proliferating, high LDH, so that very strong and stark disease dynamic. And we treated this patient with the so far highest dose for generation two that we have ever given, with a product that had product characteristics that were also characterized by very high T-cell transduction level. So we had a high dose of cells, very high transduction, and the patient here with a very high disease burden and strong proliferation and high LDH. And these are risk factors also for CAR T, for inflammatory events. And therefore, we believe that this is indeed a situation that at a very high dose of Gen two in high-risk patients, we could potentially encounter in the future. So this... The other question, can you repeat this one, please? Yeah, just in terms of if it helps, That was on 401. Yeah, no, sorry, it was on the second, on Gen 2 construct and when we may see some of the data from those signal finding studies outside of melanoma. I think the- So we are intending to provide actually data updates throughout the next year, but it depends also, obviously, on patient population. Sorry, Cedrik, go ahead. Yeah. No, I think you can expect, as Harpreet said, we are about to complete those escalations, and we will provide an update at the time point when safety has been cleared, when we have more mature data, and particularly more 6-month scans and more of the 3-month scans. We're continuing to now enroll other patients with their gynecological cancers and beyond. Therefore, we will over time mature the data set as the data come in. So you can expect one update for sure, and then we will see how quickly we can fill the different disease cohorts and de-risk IMA203 CD8 in gynecological cancers or other big cancers beyond ovarian, endometrium, and melanoma data that you've seen today for generation one. Okay, brilliant. Thank you very much. Our next question will come from Graig Suvannavejh with Mizuho. Hi, good morning or good afternoon. Thanks for taking my questions. I have 2. One, could you just remind us as it relates now with your decision to move Gen 2 into non-melanoma settings, how you're thinking about the positioning of Gen 2 versus IMA402? It would seem that they're at a high level kind of going after the same patient population. So I just want to get kind of the high-level view there. And then my second question, I guess we're still seeing, you know, pretty decent durability. But just wanted to get your thoughts on not only your perspective on the durability trends that you're seeing, but also I believe you've set an internal hurdle of seeing ORR rates of 40%, and you're above that now. But as we go further out in time, just wanted to get your view on kind of the profiles of the products that you have with respect to that. Thanks. Yeah. So So I think that regarding the positioning of first generation with the second generation, whether it's the bispecifics, I think the, the answer to give is that only data can guide this, because ultimately, we, we develop the drugs by the safety and, efficacy profiles that we observe in patients. And, as, as you probably appreciate, the IMA402 study has just started, so we are in the dose escalation part. We, we still do not have sufficiently robust and large enough data sets in different tumors with sufficient follow-up to really tell you whether this is superior, similar, or inferior, what's the response rate? What's the duration of response? Will we see patients with, long-term disease stabilization, like, like Kimmtrak and uveal melanoma, or deep responses that you can measure? And therefore, without... Having the medicine profile in hand, it's also not clear where that can be positioned. That's the question where we don't know where we will position it, but I think I want to mention that Immatics is the only company that can play both in both arenas, which means the cell therapy that may have potentially lower activation threshold, higher response rate, or can go deeper down, and the bispecifics, which are easier to supply. And we believe that we have a highly differentiated platform that can achieve high dose levels and a better and more comfortable dose regimen as compared to some of our competitors. And therefore, I think we're looking optimistic into the future. We have a de-risk target and have moved ourselves in a lead position, you know, for TCR engagers and the cell therapies for PRAME. Therefore, let's stay tuned, wait for the data, and then, and then find out what the best positioning is, whether we see coexistence or, let's say, a distribution for different tumor types for the specific modalities. Second question again, please? Yeah, just overall thoughts on durability and kind of what you're seeing with ORRs in light of, I believe, a key internal threshold of wanting to see at least 40%. Mm-hmm ... ORR rate. I think with the durability, we're actually really excited about seeing that these responses, as our dataset matures, sticks. So we have now this increased durability, in particular, 3 patients in gen one and the 1 patient gen two, that has durability, are going beyond a year and still ongoing. So let's see how far this can go and how much long-term disease control we can see. Regarding the response rate, we are now at, let's say, 50%-60% confirmed ORR for generation one and generation two. Everything above 40% is certainly medically meaningful, for sure, also differentiated as compared to alternative choices in the last line, and potentially also are so transformational that it may support trial designs that could lead to an accelerated approval within acceptable timelines. Therefore, I think, this mark puts us in a very good position to really think about the next step. Thank you, and congratulations on the data. Thank you. Thanks, Craig. And our next question will come from Sebastiaan van der Schoot with VLK. Hi, team. Congrats on the data, and thank you for taking my questions. I think that you mentioned that there's a difference in the deepening of response over time between gen one and gen two. Can you maybe expand on how that development in gen two specifically looks like? Does that continue on over the total duration of follow-up, or is that short-lived? Can you discuss that? So what we mean by this is a differentiated clinical response, particular to patients that started out with a initial stable disease, but then at their subsequent scans, showed further deepening and conversion from SD to PR. And you also may appreciate that those patients, that even those that were PR from the get-go, had continued deepening from day 42 to 2 months, 3 months, 6 months, the 1 patient, or 1 patient also between 3 and 6, which means, from this very small data set, and keep in mind that obviously this could change with more patients, we really have the impression that the contribution of the helper cells may lead to something like a longer durability or more activity or longer, let's say, burning of the product, so that the tumor cells continue to be melted away, and we see this deepening, and therefore, we see this initial data set as something that's super exciting. And regarding the future development of Gen 2, the goal obviously is to have a good safety tolerability and durability profile, to have deep responses, and we see that these responses go deep. You can see they go far below 30%, in a significant number of patients, also in those in dose level 4A, and we hope that we will see long duration of response and many of those responses then achieving landmark PRs go beyond a year. Got it. And then what speaks for we can actually achieve long durations is that 6 of these 7 response are ongoing, and we see beyond also these two SDs, some deepening in other ones. So this is encouraging, but still warrants, obviously, further follow-up. Got it. And then you also mentioned that you have a specific cutoff for the PRAME levels for the inclusion criteria. I'm just wondering whether you will let go of this cutoff already during signal finding for Gen 2, and maybe you can also discuss your view on the importance of PRAME levels on tumors for bispecific TCR approaches versus cellular therapies? Mm-hmm. So, the These, these cancers come in two categories. There are some cancers that nearly always express PRAME and always express PRAME at high levels. That's, that's certainly malignant skin melanoma, uterine cancer, could be synovial sarcoma, but also, uveal melanoma, which is a bit of an outlier because we find more than 91% of our biopsies being positive above the thresholds of very high PRAME levels, whereas TCGA databases that the screening of primary tumors and metastatic disease indicate, let's say, a different distribution. Which means for those cancers here, there's even the opportunity to not test patients and include them without, a PRAME test to companion diagnostics. For those other cancers where you have, let's say, only a part of the population, more than 50%, but also for head and neck, for example, lower than 50%, expressing PRAME, it certainly ensure that we need to test. We wanna make sure antigen is expressed before we expose patients to lymphodepletion, the potential CRS, and also the whole journey. And at this stage, we're not thinking about lowering the threshold. Our goal is to really, yeah, enrich maximum potency, and best activity, and I think, looking for a PRAME low patients is certainly a life cycle opportunity that could be addressed, in separate cohorts in the future. Regarding the PRAME levels, what we currently see is indeed that everything above our level is sufficient for PRs and confirmed PRs, and there is a slight trend towards those patients that have a higher PRAME at starting point, being those that have the confirmed PRs or the longer PRs. So there is a hypothesis that in addition to number of cells that you infuse and size of the tumor that you need to remove, that the PRAME level in between modulates the immune response, and more PRAME could certainly be helpful. But it's too early to really define a minimum level, and the good news is that everything above our threshold seems to come with a clear antitumor activity, and also a PK data and tumor infiltration data to the tumor that follows the mode of action and points towards a clinical proof of concept. Okay, got it. Thank you. Would like to signal with more questions, please press star one on your touch tone telephone. Again, that is star one if you would like to signal with questions, and we'll pause for just a moment. That does conclude the question and answer session. I'll now turn the call back over to you for any additional or closing remarks. Well, thank you very much for the great questions from everybody, and we're very much looking forward now to the next steps. Next year will be a very exciting year for Immatics, with more news on the clinical development in the first quarter, and then updates on Gen 1, entering this into pivotal trial melanoma, updates on Gen 2, both on cell therapy. But also, as Cedrik mentioned, we are actually agnostic towards the modality. We also have very exciting bispecifics that have half-life extended and offer better potency than what has been done in the past, and we also will provide updates on both our bispecific compounds. Next year, IMA401 against MAGE-A4, MAGE-A8, jointly with Bristol Myers Squibb, and IMA402, which is our PRAME bispecific. So please stay tuned, and there's much to come actually in the next months and the next 12-15 months. Thank you very much. Thank you. Enjoy the rest of your days. Well, thank you. you. Thank you. That does conclude today's conference. 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