Everyone here in San Diego and to those on our webcast, welcome to Autolus Therapeutics Analyst and Investor Meeting to discuss the data that we presented yesterday here at the ASH symposium. I'm Rob Dolski, CFO of Autolus. With me today are Dr. Christian Itin, our Chief Executive Officer, and Professor Claire Roddie, Associate Professor of Hematology and Honorary Consultant Hematologist, Cancer Institute, University College London. As a reminder, before we begin, I just want to remind that during today's meeting, we will make statements related to our business that are forward-looking under federal securities laws and safe harbor provisions of the Private Securities Litigation Reform Act of 1995. These include, but are not limited to, statements regarding the clinical status of clinical trials, development or regulatory timelines, and expectations regarding our runway, our cash runway. These statements are subject to a variety of risks and uncertainties that could cause actual results to differ materially from expectations and reflect only our views as of today. We assume no obligation to update any such forward-looking statements. For a discussion of the material risks and uncertainties that could affect our actual results, please refer to yesterday's press release announcing the ASH data and our SEC filings, both available on our investor website. On slide three, you'll see the agenda for today. Christian will begin with a brief intro, and then we'll pass to Dr. Roddie to summarize the obe-cel FELIX data that were presented in an oral presentation yesterday. Christian will follow up with the pooled analysis from the ALLCAR19 and FELIX Ib studies, as well as initial data from the AUTO8 study, also presented yesterday. He'll wrap up with upcoming milestones and closing remarks. After that, we'll welcome your questions. We're going to start with questions from the room, and then we'll open those up to questions on the webcast as well. I'll now turn things over to Christian. Well, good morning, everybody. Fantastic to see you all here on a sunny morning in San Diego, and particularly on the Sunday morning of the conference. I know many of you had already a lot of engagements from Friday and Saturday, and some of you may have had long nights already on Saturday night. So the fact that you're actually showing up at 8:00 A.M. this morning is fantastic, and we really do appreciate it. I think we have a great opportunity today to actually walk you through the data in sort of a more measured pace than the typical format that we have at the conference. And it's fantastic to actually have Claire Roddie here, who's been instrumental in the program, in the obe-cel program. Not only with the FELIX study, but also with the Sentinel study, the ALLCAR19 study, and she'll talk about the update from both studies in this morning's session. One of the remarkable things about this field is that it's the collaboration that we have between the treating physicians and the companies tend to be very tight, probably tighter than you have in many of the other indication sets. We had this opportunity, my old team, when we developed Blincyto, where we had this very close relationship with universities in Germany as well as MD Anderson. And we now obviously have, with obe-cel, had this enormously fruitful relationship with UCL over many, many years. Obviously anchored with Martin Pule, our chief scientist, who has a dual role, both at the company as well as at the university. Obviously, the colleagues that Martin obviously assembled around himself, which is quite an eclectic group. And Claire, obviously, has been clearly one of the key drivers of this program, and fantastic to have you here today. So, just as a brief introduction, obviously, we have yesterday presented on two of our programs. The first, obviously, on obe-cel itself, with an updating analysis of the FELIX study, the pivotal study. And what we've done with this study is actually pooled all the data that we had from that program, which is different from what we have presented at ASCO, where we only looked at the morphological cohort. The reason why we're looking at a pooled data set and the entirety of the range of patients, is that that's actually reflective of the reality of what a physician will actually see in terms of the patients that are coming through the door. You have patients that have very low disease burden, you have patients that have extremely high disease burden. You may have patients that actually have disease that actually does not only originate in the bone marrow, but already has gone to another organ and actually forms so-called extramedullary disease, patients that actually typically are excluded from clinical trials. We had a specific cohort of where we included those patients, and it is that view across this entire range of patients, which is really where we believe the real value of this study ultimately is to physicians, because they can recognize their patients within the population of the patients that we're seeing. So we're excited to hear more about that from Claire today. The second aspect was a poster presentation, and what we were looking to do is pool together the ALL CAR 19 study together with this, the data from the FELIX Ib study, which gives us a median of follow-up in these patients of three years, and in fact, all the way out to five years of follow-up. That starts to give us a very interesting view on where we think the actual benefit, ultimate benefit for obe-cel will be as a standalone agent, not as an agent that gets consolidated or gets in combination, but as a standalone agent. I think what you'll see from the data, as Claire will go through it, is there is a remarkable overlap between these data sets, and that gives us the confidence we have in our program.... The third presentation that we gave, which is an oral presentation Lydia Lee gave also from UCLH, on a dual targeting program that targets BCMA and CD19, that was highly optimized for the use in multiple myeloma, and obviously also could be used in additional indications that I'll sort of talk about a little later. What we also will have tomorrow is a data set that we actually look at the manufacturing performance around obe-cel. And that manufacturing performance is really important. When we're running clinical reports now, there's a lot of that activity ongoing. This is also why we only have part of the team here today. There's a lot of other activities ongoing. But the first feedback we get actually from physicians is: Can we get access to product? That has been one of the real challenges that we have seen in the field, is that we've had, on the one hand, fantastic clinical data on programs, but then virtually no ability to get your hands on the product and your patients on the product. So that is really important. This is gonna be a focus of, on the presentation tomorrow night, which I, I would, I would encourage you to have a look at, because you'll get a sense for the robustness and the capability on delivery. And then, obviously, very recently, we did announce that we did, based on the FELIX study, filed for a BLA with the U.S. FDA. Just as a reminder, before we go into the presentation from Claire, just to a reminder of where obe-cel comes from and what we were looking to address with the product. What we did realize in the early programs that were in the space is that they had a behavior but that was not physiological. And it was a behavior that actually led the cells to attack the target cells, deliver the kill, but then getting stuck on the target cells. The cells could not dissociate easily, and that had a very significant impact in at least two different directions. One is, the cells actually got overactivated because they were in continuous cell-cell contact, and that overactivation actually is driving high cytokine release, and it drives a lot of the immunological toxicity that we're seeing with these programs. The second aspect is that it also actually slows down the activity because the T-cells cannot recycle and do another kill. They get actually held back. When we're looking at the behavior, what we postulated is that a product that would give you that level of sensitivity in terms of seeing and recognizing the target, but have then an ability to dissociate rapidly after delivering the kill, we would actually get a product that would actually have a higher level of activity, more CAR T cells formed in vivo, better persistence, and a better safety profile. That was the postulate, and this is really what was at the foundation of obe-cel. The product has a unique property in its binding. It has an ability to fast bind with a fast binding to the target antigen, but then also an ability to actually dissociate rapidly as a fast off-rate. That biophysical behavior is really what's fundamentally different about this product and at the core of the differentiation that we see in the clinical experience. So with that, it's my pleasure to introduce and obviously ask Claire Roddie up here for the presentation. Obviously, Claire's been instrumental in many of the studies that we've been engaged in. And one of the things that's really remarkable about Claire is that she did not only actually treat the patients, but on the ALLCAR study, she also manufactured the product for the patients. So she has the level of understanding of this field like very few people do, and it's a pleasure to have you here today. Thank you, Claire. Thank you very much, Christian. Very generous introduction. Let's move into the data. First of all, this is the FELIX pooled analysis. Yeah, we're looking at basically obe-cel for relapsed and refractory acute lymphoblastic leukemia in adults in the FELIX phase Ib/II study. Christian's nicely illustrated what obe-cel is. It's got this fast off-rate binding domain, which was specifically selected with the objective of reducing toxicity and improving persistence of the CAR T products. He's alluded to the fact that we have tested this in pediatric and adult ALL in phase I setting. We've also tested in primary CNS lymphoma. It's had a wide sort of range of different applications in the phase I setting at UCL. We're presenting initially these results from the FELIX phase Ib/II study as a pooled analysis of all of the patients that are treated to date with obe-cel, including patients with low leukemia burden at treatment. What that means or how that's defined is morphologic remission, that's less than 5%, bone marrow blast without extramedullary disease and as measured at screening and lymphodepletion. This is the study design, which you will probably all be familiar with. There is a leukemia burden-adjusted split dosing schedule here. I think what you can see is the fact that we do our bone marrow aspiration at screening before we recruit the patient into the study. Then importantly, we repeat the bone marrow aspiration prior to lymphodepletion. The reason that we do this is because we use a disease burden-based titration of the initial dose of CAR T-cells given to the patient. We use this Day -6 marrow to guide that decision making. You can see that the doses are split over day 1 and day 10. Here's where the decision rests. So if you've got bone marrow blasts of less than 20% on that Day -6 marrow, then you will receive a higher initial dose of CAR T-cells. That's 100 million cells. If you've got more disease, and the perception being that that might portend to more in the way of immunotoxicity and side effects, you then get a lower initial starting dose of 10 million cells. These patients are all followed up, and we look out for signs of immunotoxicity, but in the absence of significant immunotoxicity, we can then go on and give this top-up dose to reach a total dose of 410 million cells... So that's the kind of broad study schema. The efficacy and safety follow-up, the first analysis point for the impact of the drug is at day 28. In terms of the patient eligibility and endpoints, as you can see, we've split this study design into three main cohorts. You've got Cohort A, where we've got morphologic disease. That's more than 5% bone marrow blasts at screening. You've got Cohort B, where there's MRD level disease at screening, that is, MRD positivity, but less than 5% blasts. Cohort C is where we're treating isolated extramedullary disease. The endpoints, I think you can see here, and CR/CRi rate and duration of response, EFS and OS, and of course, importantly, MRD negativity, safety, and feasibility. So in terms of the patient disposition, 127 of 153 enrolled patients actually went on to receive obe-cel. That's 83% of patients. The table on the right-hand side of the slide illustrates reasons why patients may have discontinued and not received their infusion. The predominant reason here was death from progressive disease, and we know with acute lymphoblastic leukemia, the burden of infections that complicate bridging therapies and alternate strategies, it can be quite high. So that was the predominant reason for discontinuation. There were a few manufacturing-related reasons also, and very occasional other reasons, such as physician decision. Oh, sorry, and we'll just go back to that just to illustrate the point that, in terms of the patients treated on the study, the majority of patients infused were in Cohort A. That was 84% of all of the patients infused, 10% were infused in Cohort B, the MRD cohort, and 6%, on the extramedullary disease cohort. So in terms of the baseline characteristics, again, it's quite a detailed slide. The median age, of the infused patients here was 47. You can see that, we actually treated one patient who's 81 years old. So again, you know, the sort of safety profile of obe-cel coming into its own there. In terms of the nature of the patients, they were certainly very heavily pretreated, and you can see that there is a median of three prior lines and 35%. Most of the patients have had a prior allogeneic stem cell transplant, and most have been exposed to blinatumomab, inotuzumab. In terms of the disease burden, this is at screening. The median bone marrow blast percentage was 36%, with a significant number of patients whose disease burden was up at 100%, and there was a significant number of patients who had extramedullary disease, and this was a particularly poor risk group of patients. You can see there that that affected 23% of the total population. Now, with this in mind, and the fact that you've got this heavily disease burden patient group, it was actually all the more remarkable, I guess, that the manufacturing was as straightforward and robust as it turned out to be. The starting material, as you can see on the left-hand side of this slide, the CD3 T cell presence in the leukapheresis was fairly small for the majority of patients of the total sort of leukapheresis that arrived in the lab. But despite that, the majority of patients received a released product. The plot in the middle here is supposed to tell us a bit about the CAR expression in the cells, and you can see it's really pretty consistent and tight in around sort of 70%. And of course, importantly, the viability of the cells after thaw was really nice and high up at 90%. And a lot of the physicians who ask sort of their biggest request to us is to get a product to their patients quickly. And I think that was really nicely realized here, and you can see the median range or release time here was 22 days. So I think the point to make here is that there was really consistent manufacturing despite the leukapheresis from these patients, with not only really heavily pretreated, many of whom have had an allogeneic stem cell transplant, but also they had a lot of disease, meaning that these factors conventionally make it difficult to manufacture for patients. So then let's look at the remission rates and the depth of those remissions. So we saw high MRD negative remission rates across this study after infusion of obe-cel. And of all the 127 treated patients here, we've split it into morphologic disease versus no morphologic disease. And of the 98 patients who were in the morphologic disease bracket, 74% of them had a CR or a CRi, and 95% of those who were evaluated for a response were MRD negative. And in the no morphologic disease cohort, that was a smaller number of patients, 29, but 100% of evaluable patients were MRD negative when they were evaluated at day 28. So again, good responses seen in both of those cohorts. And then in terms of the CR/CRi subgroup analysis, essentially, we're looking here at a forest plot, and we're looking at the different subgroups treated with obe-cel, and I think we can agree that there are high CR/CRi rates just across all of the subgroups. And in particular, I think we can illustrate the fact that the Philadelphia-positive patients seem to be doing well. Even those patients who've had a prior allogeneic stem cell transplant, we might be concerned that those sorts of patients would not necessarily do so well with the CAR, but in this case, we're seeing really good responses. I think higher-risk groups, and I think we can expect this from the data, not just from our own study, but also from ZUMA-3, is that patients with very high disease burden, and by that I mean more than 75% blasts, it is a more difficult task to get those patients into deep remissions, but they, they represent a sort of a small number. And the extramedullary disease, again, illustrated the fact that this is actually a high-risk group, and again, they are a higher risk group, for, for CAR T cell therapy also. So if we look at the EFS in all treated patients, well, the twelve-month estimate of event-free survival here was 50%, and you can see this is nice in terms of this curve. There are patients dropping off, but there is, you're reaching a plateau. And the median follow-up time for this whole patient group was 16.6 months, but we've actually got patients as far out as 36.6 months. So we've got that nice and durable and long-term follow-up for some of these patients. Only 17% of the patients, the responders, proceeded to stem cell transplant in remission. And again, that's in contrast to approaches in some of the other CAR T-cell studies, where physicians prefer to consolidate their patients' remissions with it, with a transplant. And I think because of the durable persistence of the CAR T product on this trial, I think there were less patients that were referred on for this therapy. And in terms of the obe-cel persistence in responders, I think we can agree this looks quite familiar to us. This is a bit like what we saw in the phase I study. We've got this nice high initial expansion here, and this is sort of our, like, target of 100,000 copies per microgram of genomic DNA. That's when we look for the CAR by a DNA measure in the peripheral blood of these patients. That nice peak is happening sort of within the first 28 days, nothing before day 14, really. But I think what's really nice here is the fact that the persistence is actually plateauing out at around about 1,000 copies per microgram of genomic DNA. So we have got that persistent signal in our responding patients at last follow-up. In fact, CAR T persistence was detected in 72% of ongoing responders at last follow-up in this cohort. Now, this slide is basically to illustrate why we do the bone marrow aspiration prior to lymphodepletion, because, of course, we're making an important clinical decision at that point. We've decided we want to stratify patients first, still according to their disease burden. What this is trying to illustrate to us is that you can't predict disease burden at the point of screening on this study. You'll see here that we've got the patients here at screening. This is the bone marrow blast percentage, and this is at lymphodepletion. 93% of our patients received bridging therapy, and certainly, response to bridging was not universally successful. And I think if you follow these lines out, you know, a proportion of the 5%, patients with 5% or less disease, you know, they stayed at that level, but there were a number that went on to develop sort of this intermediate-level disease. That's between 5% and 75%, and there were even a proportion that ended up with more than 75% blasts. So again, we would be making the wrong decision to use this marrow aspirate result to guide our sort of first use in the study. And we can sort of see similar patterns really in this intermediate group between 5% and 75%. We see a proportion respond to bridging and go to less than 5%. A significant number stay right where they are, but you can also see some of them are falling into this very high-risk group, with more than 75% blasts. But interestingly, even with these patients with lots of disease at screening, and you can see that certainly some of them are pretty refractory to bridging therapy, and they remain at 75% at this point of lymphodepletion. But with some bridging therapies, we do have success in reducing burden. So for instance, the proportion here are going into this intermediate bracket, and a proportion are even going to less than 5% blasts. And anecdotally, there are some success stories within inotuzumab being used as a bridge. One can achieve deep but transient remissions and, you know, good disease control with the judicious use of that agent. So I think the point to make here is that the sort of the pre-lymphodepletion marrow is really important in terms of determining what treatments we give to our patients. And again, let's talk about this leukemia burden associated with the EFS. I think we maybe didn't dwell on this in lots of detail in yesterday's presentation, but it's important to look at these lines really sort of in a bit more detail. So this blue line at the top of the graph, these are the patients who had 5% or less blasts at the point of lymphodepletion. This green line is telling us about the intermediate cohort. That's between 5%-75%. And then we've got this line at the bottom here, which is telling us the patients with 75% or more blasts in the bone marrow at lymphodepletion. And I mean, it's really striking, isn't it? The difference between these curves and in fact, you know, it's obviously preferable for your long-term EFS if you have well-controlled disease at the point at which you come in for obe-cel. But actually, this sort of 5%-75%, the pattern is the same. You're getting this nice plateau coming off both of these curves. So these are not dissimilar, but there is something about having more than 75% blasts biologically that is difficult to deal with. It's. Presumably, it's just, you know, this is worse prognosis disease, and it's, it's a harder nut to crack, if you will. And I think, I mean, you can see that this is reflected even in the numbers at the bottom of the slide. If you look at the six-month EFS, and we look at our less than 5% blasts, you can see that the, the six-month EFS here is 83%. But if you follow that across to those patients with more than 75% blasts, you can see that drops to 48%. Again, this isn't really a surprise to us. This is exactly the same pattern that we saw on ZUMA-3, and this is it just represents a particularly difficult patient population to deal with. And I think the way that we move forward with this sort of thing is to try and figure out how we can reduce these disease burdens down, prior to giving CAR T-cell therapy. And again, let's talk a little bit about toxicity, because I think this is the piece that really sort of it really emphasizes the differences with obe-cel compared to other products. So there were really low rates of grade 3 or more CRS and ICANS on this study. You can see on the left-hand side of the slide here, this is the overall patient population, 69% overall CRS, 23% overall ICANS, but very low rates in the dark gray here of grade 3 or more events, and 2% CRS and 7% ICANS. And of course, when we then take that one step further and stratify that according to bone marrow blast percentage at lymphodepletion, well, you can see exactly how this pans out. It is high disease burden that portends to immunotoxicity, with the over 75% blasts representing the majority of the immunotoxic events in terms of CRS, but particularly in terms of ICANS here. You can see that the over 75% had 15% ICANS represented as a proportion of the total. You know, while this, you know, as a clinician, we don't like managing grade three events, I think this is not dissimilar to data that we've seen with the TOWER study and the use of blinatumomab. So we think on the whole, we have to emphasize the fact that the toxicity profile here really is a sort of almost best in class. And I think the other thing to note is that if we can control a patient's disease, you know, we're getting no grade three CRS, no grade three ICANS. This really does truly represent the kind of agent that would be safe to give in the outpatient setting. So I think that's the sort of, you know, like a flavor that we have amongst the clinical community, at least in terms of where obe-cel sits, and that's in the patients with less than 5% blasts at lymphodepletion. So I think that's a really sort of exciting direction of travel for us. Now, in terms of, you know, the patients that got CRS, there was a very few of them that had sort of severe phenotypes that required vasopressors. That was only in 2.4% of the patients. And again, that—I mean, it sort of stands up really when we compare it to our closest sort of competitor, I guess, with Tecartus, where there was a significant use of vasopressors, in those studies. So concluding, I think it's a really important point that obe-cel was successfully manufactured for so many patients. 95% of leukapheresis patients got a product, and that's despite the really low CD3 percentage in that starting material, those heavily pretreated patients. So I think that's a real sort of victory for the trial. There were high remission rates, which appeared to be independent of leukemia burden at lymphodepletion. So essentially, you can still achieve a remission, irrespective of how you come into the trial. The 50% EFS estimate at 12 months, again, is—it's just reflecting what we saw in ALLCAR19. So it's giving us that confidence that, you know, what we saw in the phase I is really drawing out into the phase I experience. And, you know, that is reflected in the fact that only sort of 17% of responders proceeded to stem cell transplant while in remission. So if we follow out that EFS curve, we're actually seeing the impact of obe-cel as a standalone therapy, and we're not sort of seeing the waters muddied by the presence of allogeneic transplant. And there was, again, a very favorable safety profile here, only 2% grade 3 or more CRS, and 7% grade 3 ICANS. So again, severe toxicity, as we saw in the previous slide, it's mostly in those patients with high leukemia burden, more than 75% blasts. So again, it gives us a feel for what patients we would be watching out a bit more closely and following infusion. And there really are durable remission rates on toxicity, but again, they tended to inversely correlate with leukemia burden at lymphodepletion. And so I think we'd emphasize again, how important that is to assess the leukemia burden at lymphodepletion in order that we accurately sort of risk/benefit stratify our patient cohort. So in conclusion, I'd say obe-cel is an effective treatment for relapsing and refractory adult ALL. There are better outcomes observed in patients with low leukemia burden at lymphodepletion. Of course, as we always, you know, caveat longer follow-up is required. You know, we want to follow these patients out, make sure these responses continue to be durable and patients continue to do well. But so far, it's really exciting data, and it's fantastic for us clinicians in the ALL space. And this is just a slide to emphasize the TEAE seen in the study, and I think it just again fits in, ties in with the immunotoxicity slide. Favorable safety profile, and only 15% of the patients were admitted to the ICU, which again contrasts favorably with other agents used in the space. And there were only two deaths on the study that were considered related to the therapy, and that was neutropenic sepsis and a case of ARDS and ICANS. So again, that's quite remarkable considering the numbers of patients treated. Of course, you know, I mean, we couldn't do this without our patients. They've been fantastic. They're all sort of warriors in and of their own right, their families and friends, and of course, all the authors and study investigators, all the staff who've helped to carry this off and deliver this study. So I think with that, we'll move quickly into the long-term follow-up in B-ALL. Again, we've got this pooled analysis from the ALLCAR19 and the phase Ib FELIX studies in B-ALL. So moving into that, I mean, some of this is reprising what we've already discussed. Again, you know, both of these studies are looking at adult acute lymphoblastic leukemia. One was phase I, one was phase Ib. And essentially, we've got nice long follow-up to talk about now. We're reporting the long-term obe-cel data from the pooled analysis, again, of ALLCAR and FELIX Ib patients. We'll also briefly mention the ALLCAR19 extension phase, which we extended out to include patients with non-Hodgkin's lymphoma and relapse and refractory CLL. The EFS and OS curve here is supposed to show us the median follow-up or the long-term follow-up in relapsed and refractory B-ALL in that shared cohort, that ALLCAR19 and FELIX Ib. The point again to emphasize here, the Holy Grail was always set out by the ELIANA study in pediatrics and young adults, where Shannon Maude showed the fact that there was a plateau, because everyone is seeking out the plateau in the EFS curve. As far as I'm aware, in the adult space, no one else has shown this. But I think we can confidently say that on this ALLCAR19 and FELIX Ib study, we are seeing a plateau in our patients. So when you get to a certain point, the relapses stop happening. And it's exactly the same with the OS. We're getting that nice plateau. So, you know, while there are some events happening up until about sort of Month 18 and so on, you're then seeing this sort of stabilization of the plot. And this is just telling us that potentially, obe-cel could represent a standalone and long-term solution for some cases of adult ALL. If we were to want to talk about the numbers specifically, so there's a censoring endpoint being made here. So, we're talking about EFS censored at stem cell transplant for new treatment and EFS with no censoring. And so, when we sort of take the stem cell transplants out, we can see EFS sits here just around sort of. You can see up here, it's sort of 45%, and without censoring, it's 36%. But I think what we can agree is the fact that we've plateaued out really nicely here. And in terms of the 36-month overall survival rate, again, that's top numbers here, that's 41%. And again, we just don't have other therapies that can deliver these sorts of results in these sorts of really high-risk patients. So again, this is, you know, really encouraging data for us. If you want to look at the individual patient dates, the swimmer's plot is often a good place to look. And I think, the point I'd make about this is the fact that, you know, we've got these patients up to month 60. So this is sort of five-year data, and a lot of these patients actually come through my clinic, and it's great to see them, you know, coming in, ongoing CAR T cell persistence in some and doing really well. So, you know, I think this is really sort of it. It's heartening for the clinical team to see these patients coming into clinic, but the point is, this can represent a long-term solution, for cases of the ALL. And in terms of the toxicity, again, this, you know, there were no new safety signals, no grade three or more CRS. And we know about the ICANS signal from the early days, 4 out of 36 got a grade three event, but certainly no new infective signals and so on to cause any concerns in this patient population. And the prolonged persistence we talked about with this product that was seen in most of the long-term responders here. And so you can see the ongoing CAR T cell persistence across this large number of patients. So it was 60.6% at 12 months, and 55.1% at 24 months. It's pretty comparable to persistence at 12 months, and that persistence is ongoing at 24 months. And, you know, we believe with this product that persistence is important to ongoing maintenance of response. So there is a bit here, I think, for Christian to talk about. Thanks, Claire. Fantastic presentation. I hope that the added color, I think, has been helpful because the, the challenge in a 10-minute presentation is it's basically boom, boom, boom, and there is really not much time for nuance. But I think the, particularly the view that, that actually looks what the patients look like at screening versus at lymphodepletion, that's really important. And it did resonate actually also yesterday, for those of you who were in the presentation, it did resonate with the treating physicians in the room because it's something they know, but it's normally not actually evaluated or looked at systematically in the trial. And we looked at it systematically because we made our dose, actually, this dosing decision dependent on it. And that's one of the great outcomes of the study. It's actually beyond just the study itself. I think it has actually much more ramifications for the actual way and how we manage these patients going forward. So what I'd like to do now is just really take a brief outlook for the program into the indications beyond ALL. But before we get there, just a brief reminder where we are on the journey with regards to obe-cel. We obviously filed the BLA. That is obviously, it was an important step. We expect to file an MAA with the European Agency during the first quarter of next year. And then obviously, we'll really be very busy, particularly Edgar's team and our manufacturing team, dealing with all the information requests that will come from the various agencies during the review process. So that's gonna be the primary focus for the team. There's obviously a lot of activities ongoing on the commercial side. There's enormous activity ongoing to get the clinical centers ready for the use of obe-cel once the product gets approved. That is a massive push, and we're aiming to have at least 30 centers open and available at the time of an approval for the product. So this is gonna be a very aggressive push, and we're going to go from there very quickly towards approximately 60 centers. That will allow us to capture most of the patients and reach most of the patients in the U.S., in that process. So with that, just a few words on SLE. For those of you who were yesterday in the session where Claire presented, there was a fantastic presentation from the University of Erlangen. Dr. Fabian Müller presented. He's part of the team from Georg Schett and Andreas Mackensen at the university. The data is really remarkable because they have now up to three years of follow-up on their patients. They see that they can reset the disease, which is a hypothesis that's been in the field for about 30 years. Resetting the B-cell compartment is an old idea. It was tested initially with rituximab, didn't quite work. So one of the key collaborators we're working with, also at UCL on the SLE side, actually was part of the original study that evaluated rituximab in SLE patients in the around year 2000 to 2002. So the idea has been out there, but we couldn't quite reach the depth into the compartment. Particularly, we couldn't reach the CD20 targeting agents, the plasma cells that were producing the autoantibodies. And the really remarkable finding from the team in Erlangen, actually, is that the plasma cells that are producing the autoreactive antibodies are CD19 positive. That's something we actually did not know. That is something we learned from that clinical experiment. So it's a quite remarkable outcome. Now, what we've seen yesterday is obviously a remarkable reset of the disease course. These patients go to baseline. We've seen in part actually with images of kind of what these patients looked like before and after treatment. What we didn't see, but actually are published in part, are actually the CT scans on these patients, where you can see fibrosis in their organs before and the fibrosis gone after therapy. And that is really important. You heard in the talk yesterday that these patients had typically one or two organs involved already at the stage of inclusion in this study. So we believe we're in a remarkably good spot. Why do we believe that? The product that was used in Erlangen is actually a product that is very similar to Kymriah. It has the same fundamental receptor, has a manufacturing process closer to the way we manufacture. And the product was initially used in pediatric ALL patients with very similar data as we had shown in our original CAR T study. What's important to know about that product is it's a product with a long persistence in pediatric ALL. So this is the nature of the product. That product is what they used then in the SLE setting, and they created and really showed these remarkable data out of it. This is the data from a long-persistent CAR T in SLE. We believe we're in a great spot because obviously, you've seen from Claire that we have an exceptional safety profile, an exceptional activity profile. What's going to be very important in that space is you have to be able to deliver product at scale and economically. And that is obviously one of the core focus was the core focus for us over the last few years, to actually establish this capability. I think that will become a very important part. In addition, we're obviously using the product that we already have experience in oncology in autoimmune. We have a known entity. We also have a lot of safety information, and we will be able to leveraging, obviously, the regulatory filing, and by the time we move into a pivotal study, hopefully approval, approved product, in our favor with regards to obe-cel. So that puts us in a very strong position, even different from the large pharma companies who move in with new products into the autoimmune space. They're not using their oncology products for that. So this is just as a brief outlook. We're starting a phase one study early next year. Expect the first patients to get dosed in the first part of next year, so that we should actually have data to guide us with regards to the design of the pivotal study, which will end at next year. Now, the way we think about the expansion of the obe-cel opportunity, there's sort of two directions or three directions we're going. One I just talked about, which is taking obe-cel into additional indications. One on Hodgkin's space that I'll talk about briefly, but then also obviously the autoimmune space. In addition, we looked at AUTO1/22, which was results from pediatric patients published in Blood about two months ago, which showed that we had a highly active product that also allowed us to be active in patients that were ineligible for Kymriah, which is the standard of care in that setting, including patients that have lost CD19 antigen. This program clearly is sort of a lifecycle management program when you think of it, to obe-cel on the oncology side, because it addresses, obviously, one of the routes of escape that we see with obe-cel, which is CD19 loss. Now, the second program, AUTO8, is one that we'll talk a bit about in a minute, which is targeting CD19 and BCMA, and that's obviously primarily initially designed for multiple myeloma. And the premise behind the program is to address, on the one hand, on the BCMA side, have a product that can recognize cells that have very low expression of target antigen, and on the CD19 side, actually provide an ability for persistence and sustained activity over time. And if you think back of what we just talked, what I just talked about with SLE, there's always been a hypothesis in multiple myeloma that the driving cell of multiple myeloma is an early plasma cell, which is likely CD19 positive. So that's on the upside, of the equation. That's been very hard to prove so far. It's been a hypothesis for 30 years. It's been unambiguous in terms of the data, but I think we have the way to test it. But of course, there's also a possibility when you think about autoimmunity, that you have actually disease that may be driven off plasma cells that are mature plasma cells. At this point, everything that was looked at in Erlangen and in all the indications would suggest it's CD19 positive population of plasma cells that actually are the culprits, but we do not know that for a fact, for many of the autoimmune indications. That's one of the areas we need to explore. But clearly, AUTO8 gives us an ability and a product design that allows us to go there, should that become necessary. Here's just a quick look in terms of our experience, also from the ALLCAR extension that Claire introduced before, with patients with non-Hodgkin's lymphoma and CLL. What we do have is very high overall response rates. You see CRs in the majority of these patients. What we do see is also very nice persistence in many of these patients, which is shown below, the table. When you look at the right-hand side, you can see the swim plots, and you can see that we have many patients out for quite extensive period of time. What's very encouraging, overall, obviously, the experience in DLBCL mantle cell, but also CLL starts to look very interesting in terms of the activity and the sustained nature of the activity. Important here, again, the safety profile is exceptional in these patients. They receive a single dose, and when you look at the profile, clearly will be supportive of our patient use in any one of these indications. Now, a quick word on AUTO8. So I mentioned the fact that this is a product that has two chimeric antigen receptors, one's for BCMA, the other one obviously being the CAR for obe-cel. And, on the right-hand side, you basically see some of the characteristics, and there was more detail shown yesterday on how we actually went about designing the BCMA portion. And importantly, what you do see is that the binder and the CAR that we were going for on the right-hand side actually had much more potency against low-expressing target cells than any other product, either from our side, whether it's BB2121, which is the equivalent of Abecma, or LCAR-B38M, which is the equivalent to Carvykti. So it is a much more potent CAR that we designed, and you saw, for those of you, you yesterday in the room, you saw it was both about the binder as well as the actual architecture of the CAR, which was different. We then actually took this in a study, which is the MCARTY study, that has two cohorts. We wanted to first actually establish the activity of the BCMA CAR alone so that we would know actually whether the CAR does what it was supposed to. And as we start to have information on that, then add the second CAR to it, obe-cel, basically to it. With that, then to look at do we have an impact on cellular kinetics, in particular in these patients, and whether we would have seen any other impact, particularly longer term, which obviously is something we're still in the process of observing. The initial data is very encouraging. All patients responded to therapy. Most of them have already achieved a CR. Typical in this space is that you go from a PR eventually to a CR, because you look at clearance of paraprotein, and depending on the nature of the paraprotein, can be very long-lived. And so you need to actually... This actually has usually a progression, but you see a remarkable level of activity where the BCMA CAR was used alone or in combination with obe-cel. The safety profile was very encouraging. We had no ICANS whatsoever in these patients, and we had no high-grade CRS either in these patients, although we had very high levels of clinical activity. One thing that was also shown yesterday was actually cellular dynamics. One of the interesting things we start to see is that when you add obe-cel component, the CD19 component to the product, that actually the persistence starts to build. There were some nice FACS plots yesterday shown by Lydia Lee, who presented, did the work and presented it yesterday, that actually really nicely illustrated the fact that indeed, you start to see very nice enhanced persistence by adding the CD19 component. Obviously, this is early days, more data to be generated, but a program we're excited about. So with that, obviously, there's been a lot of news flow that we had, particularly towards the end of this year. We expect to start our quite advanced engineered program in neuroblastoma, AUTO6NG. The study is open. We're enrolling patients on this program. This is a program that you may remember has five cell programming elements in it, and a program we're very excited about to see what the technology we've developed over the last few years can actually achieve. The study on that one is called MAGNETO. And then obviously, the SLE study starting early next year. And then I think in terms of the regulatory steps, the next key step will be the validation period through which is a 60-day time point after filing, where you know actually whether the filing is accepted, and you will also know at that point in time whether we get priority review or not, which frankly, at this point is difficult to predict. So with that, I think we're going to get close to the Q&A session. Just to remind you, obviously, we're in a great spot, we believe, with obe-cel. We're on track, moving forward towards the regulatory review process. And we are executing on the pipeline as well, as you've seen with a number of data sets that we shared with you. Overall, we're in a good position from a cash perspective, have an adequate runway with the business that allows us to get, you know, through the key regulatory steps and then obviously drive the program forward and the company forward from there. So with that, I think we're going to move to Q&A. Yanan? Thank you. Hi, Yanan Zhu, Wells Fargo. I was wondering about the response rate and yes, EFS from the pivotal cohort, i.e., what might appear in the product label. How would that look compared to the pooled analysis? And when might we see that data? That's the first question. And the question regarding to your comment about persisting CAR T in the SLE presentation in that kind of a setting, I thought they showed B cells began to come back after three months. So I was wondering, how does that sit with the kind of hypothesis of a persisting CAR T in that setting? Thanks. Very good questions. And so the first one is in terms of the activity for the patients with morphological disease, which are the patients that actually will go into a label. As you've seen in the data presentation, that the ORR for these patients is 74%. So that is very you know, similar, although we have slightly more patients in this analysis than the 76% that we had reported at ASCO, where we had the smaller, somewhat smaller data group. So it is, that's unchanged, and that's going to be, that's the range of ORR that we have with the product. In terms of the time-dependent outcomes, we expect those to be at the time of the label, similar probably to Tecartus, and that is mostly an impact of the time of follow-up. that we have with the, with the program at the time of, at the time of filing. What we did see, and this is the important part of what we presented today, is that when you look at the overall population, you look at the intent- to- treat population, where we clearly going to be, have a superior profile because we have more patients treated and we had overall, obviously, a very nice outcome, as you've seen today. What the physicians are, are looking at, and this is very interesting, is obviously what Claire presented. The physicians are going to look at the totality of the data, and they're also going to look at the, impact of the patients that were intended to be treated, because that's when you make the treatment decisions. It's screening, that's when you make a deeper treatment decision, and from there on, you're on therapy. That's also, and that's actually the key way on actually how the physicians are looking at it. That's interesting because there is a discrepancy there to some extent, between the way that the regulatory review will look at it and the way that the treating physician will look at the data. It's also actually different in terms of the agencies. The agencies are not actually homogeneous in the way they look at data. You have the, the FDA looks very much at the, at the patients in terms of, the disease burden at lymphodepletion. We'll look at that. That's the primary observation. And the European agency will look predominantly at intent to treat, because they're looking at it, at what's the decision that the physician is making and what is the outcome that it can generate. So even there, the regulatory authorities actually take different positions of what they think matters, but they run their analysis in slightly different ways. But overall, we are going to be in a very nice spot. The safety profile is remarkable, and the efficacy profile, in terms of the key parameters, will be similar, and certainly from a statistical perspective, given the size of the studies, we have no way to discriminate these outcomes on these point estimates. Mara? Oh, on the SLE. So on the SLE, the question on the persistence. And I also appreciate you asking the question because I sort of teed up for that question, I guess. But it's interesting when you look at it, the product, obviously, that was used in ELIANA as indicated in pediatric patients led to two-three years and maybe even ten times longer persistence in these patients, very, very similar to what we're seeing with obe-cel. Now, that persistence is substantially shorter in patients with SLE. The primary reason is that SLE patients or autoimmune patients have a normal immune system. They have an aberrant clone that's autoactive, but other than that, the immune system is pretty much a normal immune system. It's not immune suppressed as an ALL patient actually is. As a consequence, you do see substantially shorter persistence in these patients. But it doesn't mean that short persistence is what is needed. It's a long, persistent CAR that, in those circumstances, lasts for that period of time, and that drives the outcome we've seen. We don't know if you could generate these outcomes with a short-lasting product. That's why I'm raising-- I was raising the point, because that was one of the things that I think that must have been short in the communication, in the field for that. Thank you. [Mara]? Sorry. Great, thanks so much. So I wanted to ask a question. Maybe this is appropriate for Dr. Roddie, but you alluded to the different approaches that the regulatory agencies take, as it, you know, in terms of looking at different, the patient populations within a clinical trial. And so I'm curious, from Dr. Roddie's perspective, how readily that will be incorporated into practice, even if, you know, the only data that's on the label is the morphological group data, but you've got, you know, these other cohorts published. And then secondarily, maybe if we could also talk a little bit about understanding sort of sequencing of obe-cel relative to blinatumomab, for patients from a practical perspective. Yeah, very good. I'll, I'll start, Claire, and then I'll, I'll hand off. I think what's very interesting is, in this field, is that the treating physicians are a very small group of physicians. We're talking, as I mentioned before, somewhere in the range of 60 centers treating at least 90% of the patients in the U.S. In those 60 centers, you may have somewhere in the range of key physicians, three or four physicians treating these patients. So it's a very small group of physicians, and all of these physicians are very similar to Claire, physician scientists. And that is very different from many of the other, many of the other settings, which is that that group is driven by actual clinical data, and much less by what the label will state, because they look at the data, they evaluate the data, they interpret the data as well. Is this a real-world situation? Is it not? Does it reflect what my patients look like or not? And that's why this is a very different space, where in fact, the, the published data, the actual clinical data, has a different weight. But Claire, please chime in on the, how you actually make decisions and how you inform yourself. I mean, the label will be really important because, I mean, I can only speak to the UK experience, where the access to CAR T is driven by a sort of a centralized panel through NHS England. So it's all sort of overseen and funded through NHS England. And so they have a stipulation for what criteria the patients need to meet in order to qualify for eligibility. And if the label says you have to have 5% or more blast, then that will be the criteria that we'll need to meet in order to get that patient access to the product at the point of screening. But again, if the patient gets a good response to bridging, for instance, you know, and they end up with an MRD negative response to bridging, that will not preclude administration of that product. I think we'll struggle to get extramedullary disease in at the point of screening, unless it emerges sort of post-screening, and we treat it as part of a sort of larger ALL piece. And I guess we'll have to leave it to Christian and the team at Autolus to see whether or not those indications can be expanded on the label at some point in the future. And the second question was about sequencing with blinatumomab- Yes. Wasn't it? I mean, I think the reality with blinatumomab is that, and particularly in the U.S., everybody seems to be, you know, pushing towards using it as upfront as possible. And if you listen to Elias Jabbour, that's all he'll talk about is, you know, using blin and I know upfront, et cetera, et cetera. So I don't think we can ignore the fact that that's the direction of travel, for a lot of ALL. But I think the data that we have on sort of prior exposure to blinatumomab, you might remember the forest plot, and there was a sort of an inkling that perhaps prior exposure to blinatumomab potentially pushed you a little bit towards a lower ORR. But actually, when you separate that data out and you, you know, you categorize it according to blinatumomab followed by allograft versus blinatumomab non-responder refractory, it's a totally different picture because it's the refractory patients who are the ones who are doing worse, and that might be giving us a feel potentially for those are patients with perhaps some sort of impaired T-cell fitness or some, you know, maybe it's the heavily pre-treatment or whatever, but it, it's not across the board that blinatumomab is bad news for CAR T. It just, it's in those sort of refractory patients that's skewing that result. So I don't think the blinatumomab is going to sort of change the paradigm or going to impact upon the, the value of obe-cel. I think there will be a population of patients, and I think if you asked Elias Jabbour the same question, he would say the same thing. There are patients that we know who are likely to be refractory to all sorts of chemotherapies. People with TP53 mutations, people with MLL, people with complex karyotype. Those are populations who we know, for whom allograft won't be particularly effective, allogeneic stem cell transplant in ALL. You know, it, it's really predominantly, it has its impact through the high-dose chemotherapy rather than the sort of graft versus leukemia effect. So these are patient populations for whom and I sort of point to Christian and Edgar here, we would love to see a study where we could take those patients up front and put those patients into a CAR T. For the future, I think that's a sort of a population that would benefit. But on the whole, in terms of sequencing, I don't think we can get away from blinatumomab, and I think I would urge you to consider that blinatumomab does not mean that CAR T cell will not work for this patient population. Okay, thank you. And Christian, if I could just ask on the phase I, lupus trial, the SLE trial, will you be collecting data on, you know, you know, disease-modifying data on sort of organ fibrosis? Will you be looking at that? I mean, that type of data actually gets typically reported and also falls into the composite scores as well. So you have the totality of, you know, symptoms, changes in organ function, as well as if you look at proteinuria, as well as obviously fibrosis, which you can look at by imaging too, you know, the performance on alloreactive antibodies. So the disappearance or the change in the levels of double-stranded DNA antibodies, antinuclear antibodies, all of that, this part of the standard panel that you would look at in these patients. And maybe one add-on to Claire's point about the sequencing. What has been very interesting to see in the ad boards that we're running is that there clearly is a view that there is an interest in actually moving obi ahead of blin in the relapsed refractory setting. Obviously, as blin goes up into frontline and the patients are relapsing, the interest is to move obi up, particularly if there is a belief that indeed you can actually generate a long-term outcome as a standalone therapy, because everything else you do will require some form of consolidation as well. And that change in sequencing in the relapsed refractory setting was interesting to see pop up very early on in these interactions, and we expect that is certainly a feature and a theme that we're going to be seeing as well. Kelly Shi from Jefferies. So, one of the slide, it was noted that 15% of the patients on the FELIX trial were admitted to ICU. Curious, could you share more information on what triggered this ICU stays? And also, also curious, what is the ICU admission rate across other CD19 CAR products in adult ALL or in the broader, hem-onc, indications, and what are those numbers in what we also have for SLE. Thank you. Yeah, very good question. I'll start and then hand over to Claire. Also, the reasons for why patients go in ICU is actually manifold. One of the issues that you have with many of these patients, that they can actually develop infection and sepsis, and that often is a reason why you may actually have to put them in ICU. So there's a series of events that are disease-related, and there's a series that could be related to the therapy itself, and I'll let Claire talk about it. One of the parameters you may have seen is there are only 2.4% of the patients on vasopressors, which used as an indicator for why you would actually have to move a patient to an ICU because of a CRS. Okay, so that already I think links very nicely with Claire. Yeah, I mean, so the ICU, the admissions for immunotoxicity, that was about a third of the cases, was directly for the management of immunotoxicity. There was one patient who was transferred to ICU for more in-depth monitoring, so they needed more intensive blood pressure and heart rate monitoring, et cetera. So that was one, an additional reason, and as Christian says, infection. And actually, if you look across the board and even patients who are receiving non-CAR T therapies in the context of heavily pretreated ALL, this is not a surprising finding. You know, we see a lot of patients with quite significant infections because remember, they've all had conditioning chemotherapy, and they're all neutropenic by this point also, and so you see this across ALL. And then I think it compares favorably with what's been described in other studies, and certainly in the ZUMA-3 study, where a higher proportion of patients required intensive care support. And And there were certainly more patients that required vasopressors. So I think, you know, it speaks to the kind of toxicity profile that we've talked about, you know, quite extensively in this meeting, that this is a much better tolerated, and considering we're treating these, a lot of older patients as well, and a lot of patients with heavy disease, and we're definitely moving in the right direction with this product. So clearly on the vasopressor side, the corollary with 40 would be 40% on vasopressors, not 2.4%. And obviously, about 5% on our study, that would be related to the immunological toxicity. Thank you. Also for the AUTO8 CD19 BCMA dual CAR, you have showcased the first promising data yesterday in multiple myeloma. For other new indications, I'm curious regarding the CAR design. You mentioned you have a sensitive BCMA binder. So do you have concern for this increased binding to untargeted tissues such as CNS due to a sensitive BCMA binder for other new indications because the higher bar on safety, or should I think any, like, synergy between this sensitive BCMA binder with a faster off CD19, thanks. So there's a few things in there. One of the things was the concern around that you might actually induce neurological toxicity with these types of products. And I think part of that is that we've seen for one class of CD19 or BCMA CAR, we've seen Parkinsonism. With the other kind of BCMA CAR, there's no such data available. It doesn't seem to be happening. I haven't heard any data coming through the third developed product that is very far along or moving along, so it's not clear whether this is product-specific, the issue that was described for the one product or not. We haven't... We would think that based on the experience that's there with BCMA, bispecifics as well, who also can actually get into the brain, that it doesn't look like there is a general BCMA risk for that type of adverse event. But we'll have to see as more data is generated. In our own hands, as you've seen before, we haven't seen any ICANS whatsoever. And, I think that is sort of probably where we need to go by at this point in time. If this is the profile that we can see sustained, then I think it's a very attractive profile. Thank you. Asthika? Thanks, Christian. Asthika Goonewardene from Truist. I got a multi-part question on transplant to BCMA. So did the blast count, Dr. Roddie, did the blast count drive your decision to put a patient on transplant? And second, in that, below 5% and 5%-7% groups, could you estimate the frequency of, proportion of persons that went on transplant? And also, in these groups, did you and colleagues feel comfortable in making a decision to spare patients from going on to transplant? I mean, yeah, it's a multipronged question. So in terms of allogeneic transplants, it was 17% of the patients overall received transplant. And I don't have the breakdown in front of me as to, you know, what sort of groups that they fell into in particular. It certainly wasn't my decision to push them towards transplant. It was very much an investigator-driven decision, and a strong view with some investigators that CAR T cell should be consolidated. So I think it's quite hard to dissuade people from doing that. So those were decisions that were driven by the sort of local investigators. The majority of the transplants that were given on this study were first transplants, but five of the patients received a second transplant. And I think that those patients did particularly badly. I think there is no room for second transplant in this space whatsoever, and I've actively discouraged colleagues from that practice across the board. When we look at the outcomes per allograft compared with patients who didn't go on and have an allograft, actually, it's an interesting finding. You find that the sort of the EFS is slightly lower for those patients who had a transplant. So there's certainly an indication from this data that transplant is not enhancing these patients' outcome. You know, there's no substantial benefit to be gained from doing so. And from my understanding, it's not that there was some growth divide between the patients who went on to have transplant versus not, in terms of the demographics. So that's the information I have from the statistician on the study. In terms of, you know, what drives the decision to go to transplant, it's not that the patients lost persistence, because actually, the majority of patients who went on to receive a transplant actually had ongoing CAR T cell persistence. And you know, as we are all familiar with, in the realm, transplant has not only a high treatment-related mortality, but also there's an incidence of relapse. In fact, if you take a patient who's got an ongoing CAR T cell persistence with the obe-cel, they've got ongoing B-cell aplasia, representing a sort of like a functional engraftment of their CAR, and then you give them a transplant and you obliterate that CAR, you know, really, you're putting that patient at pretty high risk, potentially over relapse, and particularly in those patients with, as I say, the high risk, the TP53, the MLLs, the complex karyotypes, et cetera. Those are the patients who we know that won't benefit from a transplant anyway. So I think we have to sort of, you know... There's a bit of a paradigm shift here in terms of the role of allogeneic stem cell transplant post CAR T. I think we can acknowledge that sort of the over 75% bone marrow blast bracket is a tricky one to contend with, and I think as a standalone therapy, it's, that's a much more contentious point. Maybe you would have to counsel patients in that bracket that a consolidated stem cell transplant should be considered, but certainly not a second transplant. A first transplant, I think, would be the recommendation for transplant-naive patients. ... Christian, in fact, just a quick question on AUTO1. Can you talk to us a little bit about your plans to commercialize this product going forward, given that there's a, it's a competitive space. Do you feel the need to have a partner for this? And maybe what, what's your long-term strategic thoughts on that? Right. So when we look at the multiple myeloma space, we believe actually it makes a lot of sense to consider a partnership. This is, to your point, very competitive, but it also requires very substantial investment, because you will basically run a late line or late-stage study, give it a fifth-line study. But in parallel, you will have to also run a second or third-line study just to be able to actually move you know, sufficiently swiftly, through the development cycle and position your product. So that's certainly one of the areas we're looking into, and I think this would be attractive for us to consider that. Gil? Good morning, everyone. Gil Blum from Needham & Company. My question is kind of on the bridging aspect, 'cause we saw that graph that showed that on average, the type of bridging didn't really change the, you know, patient outcome when it comes to blast. As a clinician, you know, you get a patient with very high, like 75% blast count. What is your thinking about how you're gonna bridge that patient to get him a better outcome from the therapy? Well, I know... I mean, there's no hard and fast rules here. It's actually, and if you look across the different centers, the practice varies wildly between different clinicians. On the whole here, about 80% of patients received a chemotherapy-based bridge, plus or minus TKI, in some cases, plus or minus inotuzumab and others. My sort of like rule of thumb is that if patients have got a significant disease burden and they're positive for CD22, and it doesn't need to be, you know, strongly positive. You can have 5% or more, you know, so it's quite low. There's a sort of a low bar, but I would give inotuzumab in that setting, and I might curtail the dosing. So I might give one out of the three doses that would be recommended as sort of standard practice, with the objective of reducing down that burden, and both the immunotoxicity and potentially from the EFS perspective. For patients with lower burden disease, if a patient presents with maybe sort of less than 10% blasts, for instance, or you know, even sort of at the level of 5% blasts, I would probably use Blincyto, because it's well-tolerated and quite easy to administer an, you know, outpatient therapy. So that's the kind of hard and fast sort of rules that we use in our own center to try and manage the risk. Given the results from the MRD positive cohort and also what you've seen from transplant, this kind of suggests that maybe, you know, there's a path forward here. This is as a, let's call it a transplant replacement, that you can get the patients into MRD positivity, I should give them hope itself. That's a trial that needs to be done, isn't it? Looking nowhere in particular. There you go. I'm just looking for the checkbook. Yeah. That's up to you. But it is an important question. It's no doubt about it. Yeah. It's a key question to ask. Thank you. Okay, thanks. James? Hi, James Shin from Goldman Sachs. Sort of a nitpicky question here. What was the EFS for the phase Ib portion of FELIX? Assuming the 20 ALLCAR19 patients had an EFS of 20 months, I think that was presented at ASH 2021. It seems FELIX's phase Ib EFS was a little bit lower. By back-of-the-envelope math points to around 6 months to arrive at the pooled 9 months that we see today. Was FELIX's phase Ib EFS indeed lower, and was this lower EFS attributed to COVID? That's question one. Sorry for the length of it. Along that same vein, what was the EFS for the phase I portion of FELIX? It seems like the phase I portion of EFS was close to 12.5 months, which is more in line with the phase Ib that we saw in ALLCAR19. So that's a little bit. Thank you. So it's. I'm always amazed with the amount of reengineered data that you guys are going through. So first of all, hats off for doing the work. I think you're actually, I think from a trend perspective, I think you're looking at this the right way. The phase Ib portion of the FELIX study was a little bit below where ALLCAR19 came in, and we believe that actually had a lot to do with the challenges that we went through. I mean, this was 2021, where we got started. You know, during that period, just to give you a feel, UCL shut down as one of our key centers, and pretty much every center in the U.S. eventually shut down. So it was a very, very challenging period to go through. So the patients were in extremely poor condition, particularly during that phase and into the early part of 2022, and I think that actually clearly contributed to that slight difference. It wasn't a big difference. It was slightly reduced. And I think the trend that you sort of indicated, I think, is about right, with regards to the phase II portion. Matt? Thanks, Christian. Matthew, William Blair. I'll ask one more on SLE. How are you thinking about the criteria for your initial enrollment, your inclusion, exclusion criteria, as far as maybe patient age or time to diagnosis of anti-titers at baseline? And then when do you think you'll disclose any additional autoimmune indications? How are you thinking about those beyond SLE? Right. So think of the trial that we're planning to run as looking very, very similar to what Andreas and [Garrett] did in Erlangen. It's the same type of patients that we're looking to enroll. A wider patient, you know, age range that we would allow, but they tend to actually cluster more in that earlier, you know, teenage to mid-twenties and twenties range. So that's just a question of distribution of when you look at the severe or refractory patient pool in particular. So it looks very, very similar to the way that we actually designed the study. What we're doing differently in this study is that we're using a fixed dose. Obviously, our product, obe-cel in pediatric patients, is also dosed. There's 1 million cells per kilogram. Actually, we have a huge range of ages on the pediatric side, and also the currently ongoing study that we're running. You know, the youngest child that we had when we started looking at was a one-year-old, and you can have, but then you can have a sixteen-year-old at 100 kg. I mean, you can have this wide range, which is why you have this type of dosing. That, of course, doesn't make sense when you actually deal with adults, and so we're gonna use a fixed dose in this setting of approximately 50 million cells, total dose. And that also is very practically driven because it gives us a good volume, so it's easy to work with. If you're going to smaller doses, actually, the volumes get small, and it's actually more difficult to handle. And it also gives us, I think, plenty of activity. You've seen Claire talk about patients that have received 10 million cell dose with these astronomical levels of tumor burden that got into complete remission. So we know the product is hugely active, and we're, for very practical reasons, are picking a dose level that is easy to manage and easy to handle in a real-life setting. And then the second part of the question is, okay, when will we consider to move beyond the initial step we're taking? So step one is actually determining and establishing, confirming that dose. That's step one. Once you've established that, that's when we actually are considering to branch out. One direction goes towards pivotal study in SLE and/or lupus nephritis. On the other hand, we're considering running a basket study to explore the activity of the product across the range of autoimmune indications. We're still pretty small in terms of data sets across many of these indications and want to understand what the profile of the product is before we would make decisions into additional indications beyond the two or three that are very clear at this point. All right. So I think with that, first of all, I'd like to thank you all for coming. We slightly went over time. I'd like to thank Claire for a fantastic job and for your time, and sharing your insights with us, and really looking forward to keep you updated and continue the conversations. Thank you very much.