Okay, welcome everyone to our next Fireside Chat. My name is Ben Burnett, analyst at Stifel. Pleased to have Atara Bio with us, and specifically we have, Pascal Touchon, President and CEO. So Pascal, thank you for doing this. Thank you, Ben. Pleasure to be with you today. Thank you for inviting us. Let's start with maybe if you, if you just give a brief overview of Atara and just highlight near-term events, and then we'll get into Q&A. Certainly. Atara is a leader in the field of allogeneic T-cell therapy for oncology and autoimmune disease. We are applying a very unique and differentiated type of technology, which is relying upon Epstein-Barr virus or EBV T-cells coming from healthy donors that we're able to manufacture, and then to possibly transform into allogeneic CAR-T, especially for oncology and autoimmune disease. But we are also the only company in the world having an approved product as an allogeneic T-cell therapy, and that's tab-cel or Ebvallo, the first ever allogeneic T-cell therapy approved in the world, that has been approved in Europe, and for which we have filed a BLA in May to the FDA. So we on one hand, we have a very exciting platform, on the other hand, we have the only approved product, which means a lot towards the scale-up and efficiency of our platform to deliver allogeneic cell therapy for oncology and autoimmune disease. In fact, we are now developing our lead program in terms of allogeneic CAR-T called ATA3219, that is right now in the first in human study for NHL, for non-Hodgkin lymphoma, and we're expecting to have some initial data at the end of the year. But at the same time, we're also developing that same product in autoimmune disease with a study in lupus nephritis, for which we have cleared the IND, and we are now busy organizing the initiation of the study very soon, with the hope to get the first patient treated by the end of the year. Not only do we have a cohort in lupus nephritis, but we also have another cohort in the same study that we plan to open in SLE, so systemic lupus erythematosus. The idea is to have the two cohorts in parallel, slightly different population of patients, one for which we are, in fact, using exactly the same protocol as the fascinating and exciting academic data from Dr. Schett that have been published in the New England Journal of Medicine recently, that have shown this profound impact on lupus nephritis patients with autologous CAR-T. So we have one cohort that is exactly the same protocol as that one, but with an allogeneic product that is very exciting. And then, at the same time, the other cohort will use no lymphodepletion to allow for a simpler treatment for the patient, less risk of side effects, and easy access. So we're very excited with this data that will come in 2025. The data in lupus nephritis in the first half of 2025, and the data in SLE without lymphodepletion in the second half of 2025. At the same time, we have also a second allogeneic CAR-T called ATA3431, which is a dual target CAR-T, targeting CD19 and CD20, for which we plan to have the IND filed in the second half of 2025. On one hand, one product that is already approved in Europe, going through the BLA right now, that has been partnered with Pierre Fabre for commercializations in Europe and in the US. On the other hand, an early stage, but very defensive, very unique type of allogeneic CAR-T, targeting CD19 for NHL and for autoimmune disease, and then another one coming soon to the clinic, targeting CD19 and CD20. Fantastic. Okay, you know, one thing that I think really separates Atara from kind of other other allogeneic approaches is the strategy of partial HLA matching. This is something I think you've implemented in all your programs in Tab-cel. I guess, why take that approach? What are the benefits of that? Yeah, you're right. We have treated more than 600 patients with this approach of partial HLA matching over the last few years, and that's a unique number. It's the most of any other companies that is using allogeneic T-cell therapy. And the reason we chose this approach is to be able to limit host versus graft immune reaction, to have to, more persistence, more fitness and persistence of the cells when they are infused into patients. So these allogeneic cells are less recognized, if I may say, as foreign, therefore, can persist for longer, and therefore, they can clearly have a better impact from an efficacy point of view. Now, this is the main reason why we chose this HLA matching. Now, the other reason is applicable to autoimmune disease, where we think for the same reason that the cells will persist longer when there is this partial HLA matching. We also believe that this will allow us to use a product in autoimmune disease without lymphodepletion, so without the need for pre-treatment. This is proven by the fact that the 600 patients we've treated with our allogeneic T-cell therapy, either tab-cel or ATA188 in multiple sclerosis, have all been treated without lymphodepletion, just with a 5-10 minutes IV infusion and followed by monitoring. So very simple administration with less risk for the patient. Now, we're going to apply that to our allogeneic CAR-T platform with the cohort that we're going to treat in SLE without lymphodepletion. So clearly, two key advantage: one is to have more persistence, the other one is potentially, not yet proven, but potentially not to, have the need for lymphodepletion for these patients. Okay, fantastic. Can you maybe walk us through kind of just the, kind of the logistics that a physician would go through with an HLA-matched program? You know, given your experience with tab-cel, like what is the perspective of a physician on a clinical trial? It's very simple. We ask the physician to provide us with information related to the HLA typing of the patient that he wants to treat with our product. We look at our inventory and we find the product that is best adapted to that patient in terms of HLA matching. We want to match 2 out of 10 HLA, and that's really required for this persistence and efficacy based on our experience with tab-cel and ATA188 in more than 60 patients. So we just need the HLA typing, we look at our inventory, we find the right product, we label and ship the product to the site, and then the patient can be treated. All that process in the U.S. can be done within 3 days, so very fast access for the patient to the right treatment for that patient with that HLA matching. The fact that we need to match HLA means that we have a bank, an inventory of product available for the different type of patients. But if you think about the patient with NHL or with lupus nephritis or SLE, we just need to have 4-6 lots or cell line to be able to treat 90%-95% of the patients in the U.S. and Europe. So very limited type of inventory, but the inventory that allows to treat 90%-95% of the patients within 3 days. 4-6 lines. Okay. Yes. Excellent. Okay, another, I think, unique feature of the 3219 allogeneic program is that, as I understand, you don't try to edit or break the TCR gene. Instead, you restrict that TCR receptor to Epstein-Barr viral epitopes. I guess, why take that strategy, and why is that better? We think that, this strategy is better because you, in fact, modify less the cells. You don't gene edit the cells. And what we do is to preserve the natural, the endogenous, the native TCR that is targeting EBV, and that means that the cells are, in fact, very close to an autologous CAR T, but they are allogeneic. And that, having this specificity for EBV on the native TCR, allows to avoid GvHD, so graft-versus-host disease. This plus the HLA matching, which avoids the host-versus-graft disease, allows the perfect balance between having an allogeneic cell, so foreign cell, that is accepted sufficiently by the immune system of the recipient, of the patients, and allows to be fully functional. It has been proven in a number of clinical studies that maintaining the native TCR, the endogenous TCR, allows for more not only persistent of the cells, but more fitness of the cells, more potency of the cells. That's something we're really very keen to get. We want to get a product that is allogeneic, that is off-the-shelf, with all the benefit of allogeneic in terms of, faster access for the patient, lower cost of goods, and also having a product that is really ready for use for the patient, and at the same time, maintain all the advantage of autologous CAR T in terms of efficacy and safety, and even try to improve on efficacy and safety with other type of features of our product. When you mention fitness, are you referring to T-cell phenotype? I guess what is sort of the phenotype you see in your kinda final product? When we have decided to develop ATA3219, we really discussed with a lot of experts to try to optimize all the features that will allow us to have a best-in-class. That was the goal. Because, as you know, the CD19 space is extremely crowded. There are a number of autologous CD19 CAR-T already approved in lymphoma. There are numbers being developed in autoimmune disease. There are many approaches that are being followed to address the allogeneic options for CD19 type of cells, being a CAR, an NK, or gamma delta T cells. What we're doing is very unique, is very different. What we're doing is really to optimize all elements of the sets. One is to have these EBV T cells as a chassis, as the backbone of our platform. As I said earlier, this allows to avoid GvHD, but also to have very fit cells that are not overly modified, gene edited, which creates a simpler manufacturing and allows the cells to be fitter for purpose. Second is to have a co-stimulatory domain called 1XX, which is a modification of the CD3 zeta domain of a CD3, CD28 type of typical, co-stimulatory domain. But that modification of CD3 zeta allows for less exhaustion, more fitness of the cells. So this is the second feature together with the native TCR, the EBV TCR, having this particular 1XX co-stimulatory domain that has been invented by Michel Sadelain from MSKCC, a luminary in the field, with the purpose of having less T cell exhaustion, allows our CAR T to be fitter for purpose, to be able to really express their potency at a very high level. I will explain later on how we can be certain on that based on clinical data. The third aspect is to have a manufacturing process that will allow to have a real phenotype towards the memory phenotype, so to allow for more persistence of the cells. Having more memory type of cells will allow that persistence and will allow, therefore, to have more efficacy. So these three aspects are key to start with, the EBV T cells as native endogenous TCR, to allow for no GvHD and more persistence. To have also the 1XX costimulatory domain and to have the memory phenotype are all towards one goal, which is to have a more potent product that is safe and effective at the same time. Now, to add to that, the HLA matching, you also increase the persistence of these very fit cells, which allow, we believe, for a potential to be best in class. Okay, fantastic. Talk about the NHL phase I study that you're running. I guess walk us through the study design and sort of the types of patients that you're enrolling, just given, I guess, maybe in the sense of sort of prior lines of therapy you expect them to be on. This is a typical first-in-human type of study, where we have dose escalation phase starting at 40 million cells, 40, and we think that's a dose that already could indicate some level of efficacy and persistence, because this is based on something I was mentioning earlier around the type of fitness we have of our cells and the features that we have introduced into our 3219, into our CD19 CAR-T. Have in mind that 1XX, this co-stimulatory domain I was mentioning, has already been used in a clinic by a product that was done through MSKCC in a study that they were conducting on behalf of Takeda. That particular product managed to get very high level of efficacy in NHL, with only 25 million cells per patient, so about 10 times less than a typical autologous CAR-T. That was an autologous CD19 CAR T with, as only difference compared with the other type of CAR T used, this particular co-stimulatory domain. So just in having that difference, you can already reduce by 10 the dose per patient, which mean that these cells are much more potent, much fitter for purpose in terms of addressing the needs of having the right level of expansion and persistence of the cells. On top of that, having the memory phenotype could also allow to reduce the dose compared with autologous CAR T. In fact, Novartis developed a product called YTB323, where they presented clinical data showing that only 12.5 million cells are able to achieve a very high level, up to 69% CR in NHL patients, with only 12.5 million cells per patient, so twenty times less than what is usually used for Kymriah, the original product. So having the memory phenotype, having 1XX, we believe allows us to have more potent cells, therefore a lower dose, and that's why we're starting at 40 million cells. Then we go to 80 million cells, and then we escalate. This study is really targeting patients that are either naive to a CD19-targeted therapy or have been exposed to a CD19-targeted therapy, including CD19 CAR T, but could benefit from a CD19 allogeneic CAR T with all the features I mentioned that allow us to have a potential best-in-class. That study is started, and we hope to have the first initial data at the end of the year. Do you have a line of sight yet as to how many patients you might have at that update? We, we're not going to comment on that at this stage, Ben, but what we can say is, the reason we think initial data will be interesting is really to look at few things. One, of course, is the efficacy and safety, but that will be limited follow on the patient. But very importantly, all the PK/PD data, especially the level of expansion and persistence of the CAR T, will be very important to confirm our hypothesis based on clinical data of the different features taken independently. When we put all that together, we think we should have the level of expansion and persistence that is needed for these patients. And then we'll have also the B-cell depletion in this patient data that will allow us to confirm our assumptions about the potential best-in-class type of platform for allogeneic CAR T. Okay, fantastic. And so, yes, you're looking for— So, it is fair to look at this update and apply some read-through to the lupus program in terms of cell expansion. I guess maybe that should be the question. Is it— Is cell expansion, is that a parameter that we should look at in terms of, you know, what we should expect for lupus? And also, does it inform on dose? Yeah. I think it would certainly inform on the dose, but more than the expansion, I think, so the B-cell depletion will be an important aspect there. How much can we deplete the B cell? Yeah. Of course, when you have a, a lymphoma patient, you have a tumor burden that means much more cells to, eliminate than in a lupus patients, much more B cells. But the level of B-cell depletion at the periphery, but also the fact that we know that all cells are penetrating, are trafficking into the lymph nodes, into the tissues, that is what's going to be important in autoimmune disease, where you want to eliminate the clone producing the, autoantibodies there. And that's really what we expect to get with our product. But it will be the read-through in terms of the dose and in terms of B-cell depletion, certainly. Now, one aspect that is important, I would like to mention as well, is we believe 3219 is extremely de-risked from the point of view of going to first-in-human, because each feature of the product has already been used in clinical trials, be it the allogeneic EBV T cells. We have treated more than 600 patients with a very specific allogeneic B cell T cell product, tab-cel and ATA188, with excellent efficacy and safety for tab-cel. We have also this data from other parties with 1XX, proving, as I said, that only 25 million cells can be very effective as an autologous CD19 CAR-T. And then we have the data on memory phenotype that shows also that this has led to more potent cells that are very effective and safe. And then the HLA matching is the fourth items of our product, the partial HLA matching, that is, going to increase the level of potency and persistence of the cells, leading hopefully to a good level of efficacy as well as a good safety there. So you see that we are bringing that product for the first time to the clinic, but the four key features of the product have already been used in many, many patients and have proven to be safe and effective independently. Here, we're putting all the four items, all the four features into one product, and that's why we believe that that could be the best in class, that physician and patient are really waiting for as an allogeneic T-cell therapy. Very cool. Okay. It may be kind of a similar question that we just asked, but with regards to the lupus nephritis study, what kind of patients do you expect to sort of be early enrollers into that study, just in terms of kind of the class or the staging of their kidney function? From a strategic point of view, we've decided to open two cohort in lupus. One will be lupus nephritis, and exactly the same type of patient that Dr. Schett, the academic that published in New England Journal of Medicine a few months ago, has selected for his study, which are lupus nephritis patient, class 3-4, ± class 5, and they are refractory patients, refractory lupus nephritis patients that have received one or more line of therapy at this stage. So that exactly the same type of patient. We also use exactly the same type of lymphodepletion with Cy/Flu that Dr. Schett has used. So we want to compare like with like. We want really to use exactly the same and see how different will be a product in the same condition, the same type of patient, the same type of pre-treatment there. And then the other cohort is in SLE, and in fact, they are not overlapping. They are slightly different patients in the same site, in the same investigational site, the clinical site, and that will allow to test the hypothesis that maybe we don't need lymphodepletion for our product because of the HLA matching and because of the fitness of the cell. That is, again, very, very different from any other approach that are being used today. So that's the two cohort we're using, SLE and lupus nephritis, with the same type of dosage, starting at 40 million, then moving to 80 million cells per patient, and then up to 160 million cells per patient. Okay. You know, it's interesting, so you mentioned you're testing a cohort in SLE without lymphodepletion, with kind of the hypothesis that HLA matching will buy you some persistence. I guess, are you worried about cell expansion, or do you need cell expansion for this to be an effective product? You know, we have a very clear experience with data with tab-cel. tab-cel is an allogeneic EBV T cell therapy that is addressing PTLD, post-transplant lymphoproliferative disorder, so lymphoma post-transplant that is specific to EBV. So these are B cells infected by Epstein-Barr virus that are proliferating. And using tab-cel without lymphodepletion, we've been able to show in patient an expansion of CTLP, the precursor of CTL, and the persistence long enough to get very high level of efficacy, because in our clinical data, we have up to 50% response rate, CR and PR, and very long impact with overall survival over several years in the patients that are responding. So we have this evidence that in patients that have a lymphoma who EBV-infected B cells, we can treat them without lymphodepletion, and we see an expansion of the product and the persistence of the product that is sufficient to get high level of efficacy and very favorable safety. So based on that learning, we believe that our allogeneic CD19 CAR-T, that in fact, we preserve this allogeneic EBV T cell platform with, on top of that, the memory phenotype and 1XX as a costimulatory domain to have very fit cells, might allow, we don't know yet, but might allow to be, to be used without lymphodepletion. That could be then a unique advantage, but also a unique benefit for patients, because we know that physicians in that are treating autoimmune patients, particularly lupus nephritis and SLE, are very reluctant to use lymphodepletion in these patients. The patient themselves, they don't want to take chemo. They don't want to be exposed to chemo. They're a relatively young patient in many cases, and they don't want to have the impact on infection, the impact on their, the ability, to have, an impact on the reproductive system, and so on, or MDS that could be linked with chemo. So if we propose to them a product that doesn't need chemo, doesn't need lymphodepletion, we think that could be a big winner and a big game changer in that space. We want to facilitate the treatment of this patient to make it as easy as possible, and having the possibility to get an allogeneic T-cell therapy that is immediately available without pre-treatment, with just a few minutes of infusion to get their treatment. And then, of course, depending on the safety that we see in clinical trials, we'll see how long they needs to be monitored. But with tab-cel, we have just one to two hours monitoring, and off they go. So that's really the type of vision we're developing for ATA3219 in autoimmune disease, to have a treatment that will be much simpler to administer to patients than the current autologous CD19 CAR-T. So you have two cohorts. You have the SLE cohort, you have the lupus nephritis cohort. What are you comping? Like, what should we comp efficacy to? Should the bar be the academic data, or is that a fair comp when thinking about kind of efficacy of a sort of a first-in-product study? We think that when we look at the most recent data, where we start to see the emergence of industry data in these type of patients, we see that the initial academic data have put the bar very high in terms of efficacy, with nearly 100% efficacy, long-term persistence, and long-term remission of the patient being drug-free, symptom-free for two years and more. This, of course, in that case, there is limit in terms of how can you improve on that. But at the same time, the industry data shows very clearly from other companies that have tried to treat more patients and maybe different type of patients, that the level of efficacy, of efficacy is not really at 100%, and you start to see some safety aspect that needs to be monitored, such as some ICANS, for example, with one of the product. So our aim will be, we are being this potential best-in-class to reach a highest possible level of efficacy with a safety that will allow to have an easy access for patient and easy treatment. But we think today, if you compare with Dr. Schett data, at least having that level of efficacy will be a big win. But if you compare with other companies, biotech and pharma, that have shown data, we may be able to show higher level of efficacy if indeed our product is proven to be in a clinic to be best in class. Okay, great. Let's talk about, just in the last couple minutes, so you're dual targeting CD19, CD20 CAR-T. I guess a couple questions here. Why those two targets? Why pair CD20 with CD19? And then what's kind of your vision for this, for this asset? Is this gonna be sort of an allogeneic-focused asset? Could it be, broad and include lupus as well? It's an asset we've developed because we think there is a need in lymphoma in particular, and in B-cell malignancies in general, because of evidence showing that some of the relapse or refractory patients to a CD19 treatment in general, not only CAR T, by the way, bispecific as well, is linked with CD20 and an escape on the antigen. So part of it is still CD19 positive, it's just that the treatment has not been persistent enough or effective enough. But part of the relapse and the refractory case are linked to CD20 type of lymphoma without, or with limited CD19 expression there. So I think that dual targeting makes a lot of sense from a scientific rationale point of view. Now, what is very important when you do dual targeting, to make sure that you are equipotent on both targets, and we believe we've shown that because we have tested pre-clinically our product compared with CD19 CAR T, and we are much, much better, but also compared with a benchmark CD19/20 that is already in the clinic, and we are even better than this one in pre-clinical study. So we think we optimize the structure of the dual CAR T for CD19, CD20 to be better than the existing. Now, why is that important? Because recently, the clinical data emerging on CD19 and CD20 dual CAR T are quite impressive in terms of the level of response. In fact, data presented at ASH by a company, Chinese company called AbelZeta, showed a 91% objective response rate in patient with lymphoma. These data are to be replicated, of course, in the U.S. setting, but we believe that shows that there is a unique benefit from dual target for an allogeneic product. There are very few allogeneic product trying to target both of them, and we have pre-clinical data showing that it is better than the autologous CD19, CD20 CAR-T. So that's why we're excited to bring that to the clinic and to have an IND filed in second half 2025, with the main objective being lymphoma, where we can be really a big game changer there if we can replicate this type of high level response with an allogeneic approach. Of course, we'll also consider exploring autoimmune disease, because CD20 is a well-known target for autoimmune disease, and maybe, we don't know yet, but maybe there will be, with emerging data from us and others, a need to address dual targeting in autoimmune disease. But first goal is going to be lymphoma. Okay. Okay, impressive. Let's just quickly talk about Ebvallo and tab-cel. Major milestone to get, you know, as you mentioned, the first autologous T-cell therapy approved, also submitted to the FDA. I guess, what are your kind of expectations around the commercial launch? So we hope the commercial launch will be as early as possible in 2025. As you know, we filed the BLA in May, so if the BLA is accepted in July, and with hopefully a priority review, if as we have BTD, we have breakthrough therapy designation for that product, all that might allow to have an approval early 2025, and the product could be launched immediately. Pierre Fabre, our commercial partner, has already recruited a lot of people, MSL and commercial leaders, to be able to launch the product. We have also done, at Atara, a lot of work to prepare for the launch. In terms of awareness, there have been 70 sites in the U.S. that have already used tab-cel for different studies and compassionate use, so there is really an awareness and experience with tab-cel that is existing in the U.S. Then we've also started to prepare from a pricing and coverage point of view, with the fact that tab-cel is already listed in DRG 18, which is a DRG for CAR-Ts, which mean that will facilitate coverage by Medicare. So all that means that the launch is well prepared, by us initially, now by Pierre Fabre, our partner, and we're very excited to see that product hopefully approved in early 2025, if everything works well with the agency, and then being launched successfully by Pierre Fabre. There are a few hundred patients in the U.S., but there is no approved therapy, there is no competition being developed at all right now at the level of efficacy and safety we've seen in our clinical trials. So we're very, very excited to see that launch that can treat many patients in need that are dying within a few weeks, a few months today because they don't have a therapy for their disease. Okay, so 70, 70 sites. Does the footprint at all overlap with the 3219 program, the clinical trials? Partially, yes. yes. Partially, yes, yes. Okay. That's why there is already some experience among this hem/onc with tab-cel that will facilitate their understanding of 3219, and the ability to use 3219 in a most optimal way. Okay. Okay, fantastic. Maybe just last question to squeeze it in here. Can you speak to the cash runway of Atara Bio? So with the current cash balance that we have, and certain anticipated payment from the expanded global partnership we've executed at the end of last year with Pierre Fabre, as well as some pre-funded warrants, ATM program, and operating efficiencies, all that together should allow to fund our plan operation until 2027. So 2027, that's the current forecast and estimate we have. Great! Well, we are out of time. Pascal, thanks so much for the time. Thank you, Ben. Pleasure talking to you.