Good day, and welcome to the Immatics IMA203 Data Update webcast. Today's conference is being recorded. At this time, I would like to turn the conference over to Harpreet Singh, CEO. Please go ahead, sir. Thank you very much. Good morning, everybody, and thank you all for joining us for our webcast. Today, we are very excited to provide you another update on the clinical data for our lead cell therapy product candidate, ACTengine IMA203, targeting PRAME. IMA203 is currently being studied in a phase 1b dose expansion study with focus on PD-1 refractory metastatic melanoma, and is about to enter a phase III study later this year. Before we start, I would also like to refer everyone 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. The presentation also includes an appendix, which provides further background information and data. In addition, the data will also be presented by Dr. Martin Wermke, lead investigator of IMA203 phase I trial at the annual conference of the Society for Melanoma Research in New Orleans tomorrow. This presentation contains forward-looking statements. With that, I'd like to turn over to Cedrik Britten, Immatics Chief Medical Officer, who will present the data. Thank you, Harpreet. Let's quickly recap the key features of the PRAME peptide that we target with our ACTengine IMA203 cell therapy. Using our mass spectrometer-based XPRESIDENT approach, we identified an HLA-A*02:01-presented peptide derived from the cancer-testis antigen PRAME. We consider PRAME to be one of the most promising solid tumor targets with the potential to address unmet medical need for large patient populations. It's highly prevalent across multiple solid tumors, including melanoma, with high target density as well as homogeneous expression. All in all, these features make PRAME an ideal target for TCR-based therapies across multiple solid cancer types, including melanoma. To efficiently target PRAME, we have generated a high-affinity T cell receptor designed to recognize the peptide with high specificity, which is tailored for use in autologous cell products. Here's an overview of the patient journey in the phase 1 trial with ACTengine IMA203, in which we infused heavily pretreated last line patients in a basket trial for multiple PRAME-positive cancers. 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, patients are lymphodepleted, treated with the cell product, and monitored for months. The third phase is the long-term follow-up. Immatics has developed a proprietary rapid manufacturing process to provide the cell therapy to patients as fast as possible. This includes a seven-day cell expansion and expedited seven-day release testing process. Before we dive into the clinical data, let's have a quick look at the trial design on the left side of the slide. The clinical trial to evaluate IMA203 in patients with solid tumors started with the Phase 1a dose escalation cohort. We completed this part of the trial and are currently investigating IMA203 in the Phase 1b dose expansion cohort, with all patients treated at the recommended phase II dose. We specifically looked at all the melanoma efficacy population that consists of twenty-eight melanoma patients that were treated with IMA203 in the dose expansion phase of the trial. The overall safety population consists of seventy patients across all dose levels and all indications. The patient characteristics in the safety population, as well as the melanoma dose escalation and dose expansion populations, are depicted on the right side of this slide. As you would expect for a last line, Stage IV patient population, the number of prior treatments, baseline LDH levels, and tumor burden are high. During dose escalation, patients were treated with much lower cell doses using a previous manufacturing version compared to the dose expansion. IMA203 has been well tolerated in all enrolled patients, and the tolerability profile remained consistent over time, despite having treated more patients. Most frequent adverse events were expected Grade I to IV cytopenia associated with lymphodepletion. Looking at the adverse events of special interest, mild to moderate cytokine release syndrome was the most commonly observed adverse event, with eight of 70 patients experiencing Grade III CRS. Further, we infrequently observed ICANS, which all fully resolved, and no IMA203-related death occurred in any of the treated patients. The tolerability in the melanoma subset is generally consistent with a full IMA203 monotherapy tolerability profile, which can be found in the appendix of the slide deck that we are publishing today. Overall, IMA203 seems to be well-tolerated in heavily pretreated patients at the recommended Phase II dose of 1 to 10 billion TCR T cells. The plot on this slide shows that IMA203 achieved deep confirmed objective responses in melanoma patients. The confirmed objective response rate is 54%, with 7 of 14 confirmed responses ongoing at data cutoff. Twelve out of the 26 patients showed remarkably deep tumor responses, with target lesions tumor shrinkage of over 50% according to RECIST. The initial objective response rate is 62%. Eighty-eight percent of patients demonstrated tumor shrinkage, and disease control was achieved in 92% of patients. The spider plot is a visual representation of clinical responses over time for each patient. Tumor responses were assessed approximately at week six after infusion, at month three, and then every three months. The median duration of response is 12.1 months at a median follow-up time of 9.3 months, with two responses ongoing for more than two years, two other patients with responses over months, and several patients with responses at six, which are still ongoing. Notably, IMA203 demonstrates six months of median progression-free survival, with most patients still alive at data cutoff. The median overall survival has not been reached at a median follow-up of 8.6 months. As this is not a randomized controlled trial, we use the dose escalation cohort as comparator. These patients, who have been enrolled at the same sites and share comparable baseline characteristics stated in the appendix, received significantly lower doses of IMA203. Interestingly, we see a significant improvement when comparing progression-free survival and overall survival in melanoma patients treated in the dose escalation cohort, shown in red, versus the dose expansion cohort, shown in green. Median PFS increased from 2.6- 6 months, and while median OS of melanoma patients in the dose escalation cohort was 6.3 months, median OS in the dose expansion has not been reached yet. Of note, when looking at the right graph depicting the overall survival, we can see that all patients in the dose escalation cohort died, whereas 20 out of the 26 patients treated in the dose expansion cohort are still alive. These data highlight the potential of IMA203, given at relevant doses, to achieve long-lasting antitumor effects in melanoma patients. To generate more context for the observed PFS and OS data in the IMA203 phase 1b dose expansion cohort, we look at the IMA203 phase 1a dose escalation cohort with suboptimal doses of IMA203, two additional Immatics phase 1a dose escalation studies conducted in second-line plus melanoma, as well as other industry studies in second-line melanoma. Interestingly, PFS and OS data in IMA203 dose escalation seem to be consistent with other second-line plus melanoma cohorts, whereas IMA203 dose expansion plus longer PFS and OS not reach a data cut. Of course, while we should be aware of the limitations of cross-trial comparisons, we find the various datasets helpful in understanding the IMA203 data for melanoma patients. As mentioned earlier, of all melanoma patients in phase Ib, approximately half demonstrated a deep response with tumor reduction of 50% and more. This subgroup of deep responders show a median PFS of more than one year. Even the subgroup of 14 patients with less than 50% tumor reduction or even tumor size increase, shows a prolonged median PFS, which is more than twice as long for patients treated in the dose escalation cohort. Let's take a look at some other key features from this phase 1a trial. Translational data from our phase 1a and 1b trial reveal that IMA203 T cell dose and exposure seem to be linked to clinical responses. When we compared the infused doses for patients with confirmed responses to those with unconfirmed responses, stable disease, or progressive disease, it is clear that patients achieving confirmed responses receive significantly higher doses of IMA203 T cell. Additionally, there's a strong correlation between T cell dose and peak T cells observed in peripheral blood of patients, as shown on the graph on the right. The graphs on the left show PCR results to assess the decay from sampling peripheral blood in patients from the dose escalation and the dose expansion cohorts. After single dose, IMA203 T cells rapidly engrafted in all patients, demonstrating persistence for over two years. Notably, patients treated at higher doses during the dose expansion phase exhibited higher peak T cell levels and longer persistence at higher levels when compared to those in the dose escalation phase. Depicted on the right side, we also found that peak T cell levels and T cell exposure are associated with confirmed clinical responses. These results strongly reinforce the link between IMA203 dosing, in vivo expansion and persistence, and subsequent clinical outcomes. Let's conclude the phase I data update with a patient case. The slide shows results observed in a 50-year-old patient with cutaneous melanoma and a long history of cancer. After progressing following five prior lines of treatments, the patient was enrolled and subsequently treated with IMA203 at the lower end of the recommended phase II dose. Remarkably, after 50 months of treatment, complete remission was observed on PET scans, and as of today, the patient remains in remission over two years post-infusion, as shown by the CT images. The presentation by Martin Wermke tomorrow at the SMR conference will include two additional patient cases. Based on the promising data from our phase Ib trial, we are moving into a registration-enabling phase III trial. Following a Type D meeting with the FDA and a scientific advice meeting with the German Paul-Ehrlich-Institut, we have determined the recommended phase II dose and finalized the trial design and endpoint. Our phase III trial, named SUPREME, will enroll 360 patients with unresectable or metastatic melanoma who have already been treated with a checkpoint inhibitor. Patients will be randomized one-to-one to receive either IMA203 or the investigator's choice out of selected approved treatments in the second line or later setting. The primary endpoint for full approval will be median progression-free survival. We believe this to be the quickest path to seeking full approval in this patient population. Median PFS readout is expected to occur earlier compared to objective response rate, followed by substantial follow-up time. In addition, median PFS provides clinical benefit on the entire population, which we believe allows more attractive commercial position of this drug. We are on track to begin SUPREME phase III trial in December 2024, with enrollment forecasted to be completed by late 2026. A pre-specified interim analysis is planned after approximately 200 patients are enrolled. In summary, IMA203 has demonstrated a favorable tolerability profile over time, with mostly mild to moderate CRS, infrequent ICANS, and no treatment-related deaths. We observed robust antitumor activity with a confirmed objective response rate of 54%. The median duration of responses has been reached at 12.1 months, and ongoing responses were observed for over two years in some patients. One of the most important takeaways from today's data presentation is IMA203's ability to achieve a median progression-free survival of six months, with a significant subgroup of patients with deep tumor responses showing long periods of progression-free survival exceeding six months. Overall survival data are still maturing, with median overall survival not yet reached. Translational data further confirm that IMA203 T-cell dose and exposure are significantly associated with clinical responses observed in patients. RMAT designation has been granted for PRAME-expressing cancers, including cutaneous and uveal melanoma. We finalized our phase III trial design after dialogue with U.S. FDA, and the SUPREME phase III trial is forecasted to start in December 2024. With the continued maturation of the clinical data set, it's becoming increasingly clear that targeting PRAME with Immatics IMA203 TCR-T therapy has the potential to offer durable benefits for advanced-stage melanoma patients while maintaining a well-manageable tolerability profile. 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. Back to Harpreet. Thank you very much, Cedrik, and thank you to the audience for joining our call today on the IMA203 clinical data. Cedrik and I will be now happy to take any questions from the audience. Thank you. If you would like to ask a question, please signal by pressing star one on your telephone keypad. If you are using a speakerphone, please make sure your mute function is turned off to allow the signal to reach our equipment. Again, press star one to ask a question. We'll pause for just a moment to allow everyone an opportunity to signal for questions. The first question will come from Kelly Shi with Jefferies. Please go ahead. Yeah. Congrats on the progress, and, thank you for taking my questions. I have two. The first one is, regarding the pivotal trial design. Are you going to test the both dose level four and the five, in the pivotal trials? And also, you mentioned you have dose response, but curious at these two dose levels, do you see, like, a difference, on efficacy and safety? And also, will, lifileucel, the approved cell therapy in second-line melanoma, be allowed in your comparator arm for pivotal trial? I also have a follow-up. Thank you. Yeah, I'm happy to take this one. So in the past, we have indeed, during dose escalation, introduced multiple dose levels. We have since recently agreed on the recommended phase II dose, which is everything between one and ten billion transduced TCR-T cells. So that's the dose we are going to use moving further, so there will not be dose levels 4 a, 4b, or five in the future. Within this range, we typically give, yeah, all of the cells that we can manufacture from a patient, so we don't have to put any cells back. And from the data that we have generated, the safety profile within this range is rather similar. We never reached an MTD. The frequency and duration of CRS is similar. There is a small trend towards maybe higher severity of CRS in the higher and the upper threshold of this recommended phase II dose. But we also see, and we have shown the translation graphs, that more cells typically also have a higher chance to lead to higher peak expansion exposure, and we would predict that this would also lead to higher benefits. So the benefit-risk ratio is not skewed, even if you have a patient where we can manufacture six, eight, or up to ten billion cells.... Regarding the choices of the control arm, we. Yeah, does this answer your question on the dose? Oh, yes. Regarding the final choices on the control arm, we have, as of today, before the end of the year, and we'll disclose more of these details, and then we will be able to- Fantastic. And also, I have a question for the manufacturing. The process time is 14 days, but curious, what is the total, like, a turnaround time from the first doctor office visit to, like, infusion? And also, regarding the low interleukin-2 used for the preconditioning regimen, would you be able to share some color on the physician's experience in terms of like contrasting to high-dose IL-2 use? Thank you. Cedrik, I'm not sure you're still online. Hmm. Would you be able to take over? Yeah, sure. I'm sorry that Cedrik has some technical difficulties. He's actually in New York right now in a hotel. So let me take this over. So could you just repeat the question, the second part? Yeah, of course. Of course. So for the manufacturing, the process time is fourteen days. Curious, what is the total, like a turnaround time from the doctor, office visit to infusion, and also regarding the low dose interleukin-2 used, would you be able to share some physician's feedback, who's actually conducting the trials in contrast to, like, high-dose IL-2 use? Yeah, let me start with the second one. So this is low-dose IL-2. It's actually just 5% of the dose compared to what's typically given for TIL studies. So it can be easily applied in an outpatient setting, and it is very well tolerated, does not add actually any toxicity. So the post-infusion low-dose IL-2 is actually something that is very well manageable and does not add toxicity. On the turnaround time, it is indeed 14 days from the time when we receive a leukapheresis up to delivering this. The total turnaround time can vary. In the phase I trial, it varied quite a lot because we also did leukapheresis for some of these patients while they were still on previous therapies. In the upcoming phase III trial, this will be much more streamlined. So we're sort of expecting only a few days will be added before and later for logistics and leukapheresis. Thanks very much. Congrats again. Thanks, Kelly. The next question comes from Jonathan Chang with Leerink Partners. Hey, guys. Congrats on the update, and thanks for taking the question. I'm still on for Jonathan. So, for the phase III study design, are there any relative proportions of melanoma subtypes that you'd be envisioning to allow for a broad label approval? And then I just have one more follow-up after that. So, Cedrik, are you back online? Let's try it one more time. Yeah, I can hear. Let's see. So the question was, which melanoma subtypes we want to include? So we are allowing cutaneous melanoma, including acral melanoma and melanoma of unknown origin. We have decided to leave the mucosal melanoma and the uveal melanoma out to also satisfy the agency's wish for homogeneous patient population. So for the beginning, we start with this one, but rest assured, we are not forgetting about the rare cancers, and there's certainly ways to address those. We see a lot of encouragement from PI sides, but also signals from agencies that there will homogeneous patient populations, mucosal and uveal will come. Great. Yes, thanks so much. I guess just one follow-up. With the continued development of both PRAME cell therapy, bispecific, and the MAGE data that you just presented as well, how are you thinking about the relative positioning in the treatment paradigm with melanoma and then also potentially other tumor types as well? Thanks so much, guys. Yeah, happy to take this one. So we think actually very highly of both of our modalities, and we think that they can be positioned in a complementary fashion. So cell therapy, as you've seen, has actually unprecedented potency and really can deal also with large tumors. The patients that you've seen were not cherry-picked and had large tumors on average, more than 100 millimeter target lesions. And so this is a setting in the last line, or in this case, two L plus metastatic melanoma setting, where cell therapy can be easily positioned as a potential best-in-class therapy in a monotherapy, so simplified setting. Bispecifics is something where we have recently shown encouraging initial data for our first program, IMA401, against MAGE-A4/A8, which clearly shows that there's activity. We have to see what the ultimate potency and extent is, but from our point of view, bispecifics are much easier and better positioned in a frontline setting in combinations with checkpoint inhibitors. And here, our second generation, half-life extended bispecifics come into play because they, as like for IMA401, have a half-life of more than two weeks. They can be actually dosed in this commercial setting even every three or four weeks, making them ideal combination partners for checkpoint inhibitors. And that allows also very easy commercial positioning, even in the community setting. Perfect. Thank you. The next question comes from Eric Schmidt with Cantor Fitzgerald. Thanks for taking my question, and as always, appreciate all of the details, especially in the appendix of the deck. Maybe on manufacturing, it sounds like the changes you made a while back are really important in terms of producing superior product. Harpreet, can you talk a little bit more about this monocyte depletion, what specifically is going on there? And then in terms of the upcoming phase III study, whether you've got all your specifications set, potency assays, everything else you need to do to lock down that process to begin the trial. Thank you. Yeah. Good morning, Eric. Happy to take this one. So yes, we found actually that when removing the monocyte, so by enrichment of T-cells, can be done by plastic adherence originally, but now we do this through positive CD8/CD4 selection, we actually have a much more robust manufacturing platform. We can get to higher doses. Part of the reason is, and I'm an oncologist by background originally, that monocytes can be actually bad guys. They release certain anti-inflammatory cytokines that actually can really inhibit the growth of CD8 and CD4 cells, and hence, that removal of the monocyte fraction has actually provided a lot of benefits to really get to higher doses. We also saw a secondary effect, actually, that, and this is, displayed in the appendix of the presentation that Cedrik just provided, is that these T-cells now show a younger phenotype. We have a significantly higher fraction of naive T-cells, and we believe that this further positively contributes to the behavior of these T-cells, and that these T-cells then show enhanced persistence given that younger phenotype. And so, Eric, just remind me of the second question. More on the specification readiness for phase III. Yes. So we had multiple Type D meetings, and also these include meetings on the CMC package. So in contrast to TILs, these are very defined products, very similar to CAR T, and we have already aligned on all the relevant specs as well as the potency assay. This is very straightforward and very similar to what you know from CAR T. Thank you very much. Pleasure. The next question comes from Rajan Sharma with Goldman Sachs. Hi, thanks for taking my question. A couple. The first, just on the phase III, maybe Harpreet, if you could just talk about how you think about the relevant efficacy bar for the phase III trial, and not necessarily just from a regulatory perspective, but also from a clinical and I guess a commercial perspective, kind of given the costs associated with cell therapy. And I have a follow-up. I'm happy to start this from a kind of commercial and reimbursement perspective, and please, Cedrik, feel free to chime in. I mean, we know that cell therapies are tedious compared to biologics like our bispecifics, but they offer unprecedented, or at least what we've seen so far, unprecedented activity, and we were particularly encouraged by seeing a subset of patients, a substantial subset of patients, with these deep responses and very long PFS that we think will also translate into a very strong OS benefit. So when we make these people jump through hoops with cell therapy, and we try to make these hoops as big as possible and as simple as possible compared to other cell therapies, we really need to give back something to these patients. I think this is exemplified really by the data that we've shown. While our statistics that we have used to run the phase III trial are very conservative, obviously our ambition is to provide a substantial clinical benefit in terms of progression-free survival and down the road, also overall survival to these patients. The bar is actually set very low by the industry. As Cedrik showed in the table, the PFS in this patient population is very poor, 2- 2.5- 3 months, and so really, sort of raising that bar significantly in a very meaningful way for this patient is absolutely important. Okay, thank you. And then just my second point, question is sort of related there in terms of the phase III, the endpoint of no OS detriment, just kind of wanting to understand the rationale there as opposed to trying to show an OS benefit, particularly given the strength of the data. I'm happy to take this one. Look, this is the statistical framework, and for the agencies, for a PFS trial with primary endpoint, the minimum requirement is to show lack of detriment, which means this is the hurdle that we need to achieve to have, let's say, to reach our endpoint and have a successful trial. What you can see from our own data, that our ambition is not to show that we don't have a detriment, but we would expect a separation of OS curves, and in particular, as Harpreet mentioned, a significant fraction of patients, half or close to half of them, that have massive PFS shifts and that should translate into really also prolonged overall survival and long-term disease control. So don't use the statistical framework as indicative of our ambition. That's the statistical framework. The data that we have point towards a superiority about what is set in terms of the statistics for the clinical trial. Okay, that's very helpful. Thank you. And thank you for all the detail in the slides as well. The next question comes from Graig Suvannavejh with Mizuho. ... Good morning. Thanks for taking my question. Congrats on the data. I've got two questions. One is for clarification. Actually, they're both kind of for clarification. First, in the phase III trial design in terms of patients that you're enrolling, are you including or excluding uveal melanoma? You may have discussed it before. I just didn't pick up on it. And then my second question has to do with your Gen 2 product, and along the lines of a question that was asked earlier on, on the positioning of first-gen with bispecific. How now are you thinking about the Gen 2 product and where that might fit? Thanks. Maybe I can do the first, and Herbert, the second question. So the first is easy. I already mentioned it. We will keep uveal melanoma patients out for now. So this is not this trial is not going to include uveal melanoma, a patient population with different standard treatments, standards, and different biology. But we see that for both of these cancers, we can induce similar high response rates, similar PK. We have a similar safety profile, and we see similar expansion of PFS and OS data. So there is a strong rationale under this now or later, so the clinical data and the biology speak for that. And then, Graig, thank you very much. On the second question, positioning of gen two, so we will actually provide an update on our gen two dataset for IMA203 at the upcoming SITC conference, which is in November in Houston, Texas. What we have now with IMA203, which we also call gen one previously, is, from our point of view, an ideal product candidate for melanoma. We know that PRAME levels are very high in melanoma, and this works extremely well with high PRAME levels at a very good safety profile or tolerability profile that we've displayed. We also see other tumor types that are very interesting, such as GYN onc. This includes ovarian cancer, uterine cancer, triple-negative breast cancer, and squamous lung cancer, where PRAME is well expressed in terms of prevalence but comes at slightly lower PRAME levels. And for those, we would like to employ gen two, which shows higher firepower per cell. Last year, we showed some gen two data and also had an MTD at 1.5 billion. We've now managed to actually change the protocol in a way that we can now raise that MTD. That's a process that's currently ongoing, and that's still ongoing in melanoma patients, which then really allows us to increase the absolute firepower, and then we can unleash this increased firepower gen two on GYN onc and breast cancer and other patients once we achieve this. So this is ongoing, there will be an update at the SITC conference. Okay, thank you very much for that clarification, and congrats again. Thanks. The next question comes from Sebastiaan van der Schoot with Kempen. Hi, team. Congratulations on the, another strong update, and thank you for taking my questions. Two questions from my side. The first one is on the manufacturing process. I appreciate all the detail, but I was wondering, whether you can say something on whether experience also contributes to whether getting to the higher range in the dose, dose levels and whether you expect, during the phase III, to actually get, maybe a median dose level that is higher than you have seen so far in the phase II, in the phase I B, expansion. And then I have a follow-up. Cedric? Look, we don't want to speculate and look forward. We have observed, I think this we can disclose, that over time, as we go, again, more experience, as we optimize all parameters, we've been able to more robustly manufacture higher cell numbers. So there's a clear trend, and this has also translated into much improved clinical outcomes, as we have shown, and the biomarkers point in the same direction. Whether or not there is more we can do and whether the experience in the process will lead to even better results is something that only the future can show. But I'm optimistic that we will be able to robustly supply high cell doses, and I wouldn't exclude that there is a small opportunity to up the numbers and do even more. But again, let's not speculate. Let the trial run, and then we can share the data with you. Great, thank you. And then I was also hoping if you could provide some additional context on your TCR therapies, TCRTs for sure, bispecifics. Recently, you showed first data for IMA401 that showed clinical efficacy, whereas your TCRT, IMA201, against the same target, showed, let's say, modest efficacy. How would you put your results of today into the context of your bispecific, on which you're gonna report data later this year? And then I'm wondering whether there are any differences between your IMA201 product versus the bispecific TCR specifically. Yeah, the IMA201, which is a discontinued product, and actually employed a T cell receptor that, from today's point, we actually deemed as not having sufficient affinity. So what we found out, actually, for TCR-T is that there is a Goldilocks zone for affinity. If it's too low, like single- and double-digit micromolar, you won't have enough efficacy. If it's too high, so less than one micromolar, you'll actually have more activation-induced cell death and less persistence. So the PRAME TCR-T or the PRAME TCR is exactly in that Goldilocks zone and makes it an ideal program. This doesn't apply for bispecifics. So for bispecifics, the idea is always to maximize the affinity. This actually goes down to single-digit nanomolar affinity, and that's the case for both-... IMA401, our MAGE-A4/A8 program that actually has shown better data than the original cell therapy, given the kind of now high-affinity T-cell receptor, and that also is the case for IMA402, which also has a highly optimized T-cell receptor. Okay. Thank you so much. Thank you, Sebastiaan. The next question comes from Joe Catanzaro with Piper Sandler. Hey, guys. Thanks for taking my question. Thanks for the update. Yeah, maybe first one for me is a follow-up. Cedrik, I think you said that, but just wanted to get confirmation that when you cut today's data and look at just the phase III eligible patients, cutaneous acral, you know, the efficacy profile you see in those patients is comparable to what you're reporting here for the full 28 patients. Thanks, and I have a follow-up. I can confirm this. Okay, great. Yeah. Appreciate that. Maybe my second question relates to the correlation you're seeing between T-cell, PK, PD, and responses. I guess maybe interrelated, but are you seeing any correlation between the T-cell, PK, PD to duration of clinical benefit, or is it really just depth of tumor reductions that's the most predictive of prolonged clinical benefit? Yes, they are connected. We have shown that higher dose can lead to higher peak expansion, can lead to... is associated with deeper responses, and in this obviously, the maturing data set, we see that the depth of the response may potentially have a significant effect on PFS. I think for us, it was most striking that if we really move the response down to 50% or less, so really deep responses, that this cutoff puts PFS from this six months range to more than a year. So, we would argue that from understanding of our mode of action, these things are connected. At higher dose of more fit cells, can lead to a higher chance for deep responses, could potentially lead to a much longer PFS and hopefully also then long-term disease control and OS outputs. Okay, thanks. That's helpful. And then maybe just one last quick one for me. The interim analysis that's designed into the phase III, anything you can say on that, whether it's just futility or there'll be other opportunities there to look at the data? Look, it's primarily a futility, but it's certainly a data set that can lead to meaningful data readouts that we will be using for pre-BLA meeting with the U.S. FDA. Obviously, if there are spectacular data surprises or endpoints even being met at that time point, this could open the opportunity to have fruitful dialogue with the agencies to see how to translate this into further action. So I think there's a formal base, certainly an opportunity to look in the data and engage in dialogue and make sure that this innovation is developed at the pace that is adequate for the clinical results that we observe. Okay, great. Thanks for taking my questions. There are no further questions at this time. Mr. Singh, I will turn the conference back to you for any additional or closing remarks. Well, thank you very much. Ladies and gentlemen, thank you very much for listening and for your questions. Please accept my apologies for the technical details. This is a real-life webcast, so Cedrik's in New Orleans right now. Obviously, the internet is not as good there as here in Houston, but we still hope that we could sort of really show you what the potency of IMA203 and the opportunity here we're building for melanoma patients. Wishing you a wonderful day, and thank you again for listening in. Thank you, and goodbye. This concludes today's call. Thank you for your participation. You may now disconnect.