Good day, ladies and gentlemen, and welcome to Atara Biotherapeutics Quarter Three 2021 Financial Results Conference Call. [Operator Instructions] At this time, it is my pleasure to turn the floor over to your host Eric Hyllengren, VP, Investor Relations and Finance. Sir, the floor is yours.

Thank you, operator. Good morning, everyone, and welcome to Atara's third quarter 2021 results conference call. Earlier today, we issued a press release announcing our third quarter financial results and operational progress. This press release and an updated corporate slide deck are available in the Investors and Media section at atarabio.com. On today's call, members from the Atara executive team will provide an update on our financial results and operational progress and also review our upcoming key milestones and objectives. Joining me on today's call are Dr. Pascal Touchon, President and Chief Executive Officer; Dr. Jakob Dupont, Executive Vice President and Global Head of Research and Development; Utpal Koppikar, Chief Financial Officer; Dr. AJ Joshi, Chief Medical Officer; and Dr. Kristin Yarema, Chief Commercial Officer. We will begin with prepared comments from Pascal and Jakob then open up the call for your questions. We would like to remind listeners that during the call, the Company's management will be making forward-looking statements. Actual results could differ materially from those stated or implied by our forward-looking statements due to risks and uncertainties associated with the Company's business. These forward-looking statements are qualified in their entirety by the cautionary statements contained in today's press release and the Company's SEC filings. These statements are made as of today's date and the Company undertakes no obligation to update these statements. Now, I'd like to turn the call over to Pascal. Pascal?

Thank you, Eric and thank you all for joining us this morning. We continue to make meaningful progress across all three strategic priorities, tab-cel, ATA188 in multiple sclerosis, and our next generation allogeneic CAR T programs. Today, we announced for the first time positive top line data from our pivotal Phase 3 ALLELE study for tab-cel in EBV positive PTLD, which includes new analysis, additional patients and extended follow ups. These data confirm a strong objective response rate of 50% with clear durability of response and overall survival of 89% at one year in responders, while still demonstrating well tolerated safety profile in line with prior results. These data will be the basis for the imminent MAA submission in the EU and our plan BLA submission in the U.S. next year for patients with EBV positive PTLD. We are very excited to submit in the next few days of filing for approval in Europe and we were recently granted accelerated assessment, we anticipate a decision regarding EU tab-cel approval in the [second half] (ph) on of 2022. Additionally, in October, we were extremely pleased to announce our exclusive commercialization agreement with Pierre Fabre for tab-cel in Europe, Middle East, Africa and other select emerging markets for EBV positive cancers. We believe this partnership reinforces the commercial opportunity for tab-cel in these markets and maximizes the strategic and financial value of this potentially transformative therapy. On the U.S. regulatory front for tab-cel, we continue to make step-wise progress for type B meetings with the FDA. In particular, we have aligned with the FDA on comparability approach including the statistical methodology. Based on the new request from the CMC review team following our recent interactions, we will provide the agency additional analysis of CMC data we have already submitted. We plan to…

Thank you. Pascal. I like to add further color on the progress we made during the third quarter in advancing our three strategic priorities. As Pascal mentioned, today we announced the first presentation of new positive data from the pivotal tab-cel Phase 3 ALLELE study in EBV positive PTLD confirming a strong objective response rate or ORR durability of response and continued well tolerated safety profile which support the imminent European MAA submission and plan BLA submission. These data will be presented at an oral session at the American Society of Hematology Annual Meeting next month. In these data, we observe a 50% ORR as measured by independent oncologic response adjudication with the response of 50% at both PTLD following SOT and PTLD following HCT. This response includes both complete and partial responses. Importantly overall median time to response was 1.1 months, which is critical in this setting where patients are in urgent need of treatment as they only have a few months to live. Of 19 responders at this point in time, 11 have duration of response lasting more than 6 months with a median duration of response, not yet reached. The one-year survival rate was 61% overall, 57% for SOT, 67% for HCT. Those who responded had a longer survival compared to non-responders with a median OS not reached and one-year survival rate of 89% compared to 32% in non-responders. Safety findings were consistent with previously published data with no reports of tumor flare reaction and no confirmed evidence of graft versus host disease related to tab-cel treatment. Next month at ASH, we will present additional data on tab-cel through several abstracts, including a second oral presentation on long-term survival from Phase 2 and multicenter EAP studies in relapsed-refractory EBV positive PTLD showing median overall survival of 54…

[Operator Instructions] And our first question comes from Salim Syed from Mizuho. Go ahead.

Yes. Hi, thanks guys for all the color and congrats on the progress. So, a couple from me on ATA188. So Pascal, Jakob, when we get the data in the first half of 2022, historically in multiple sclerosis trials, I think, folks generally understand companies need two trial to file for regulatory approval. But progressive of multiple sclerosis there is also an unmet need. And I think it's pretty established that you guys will let us know if you're going to have a large increase in here or a smaller increase. And I'm just wondering, is a fair way to interpret this is that if you say, hey, we're going to increase this by a large n, that the P value you're seeing is less than 0.01 and you only need one trial and if it's a smaller increase, the P value is something like - you think you can get to a 0.05 or less? I’m just wondering if you can actually give us that P value when you disclose the data? And then the second question, just more around the limited disclosure that we're going to get in the first half of 2022. Can you just remind us is this being driven by the FDA, where they've asked you to limit the disclosure? Or is this more an Atara decision? And the reason why I ask is, I think, some investors would argue here that it's more capitally efficient to disclose more data. So I'm just sort of curious how conceptually you're thinking about that? Thank you.

Thank you, Salim, for your question, And I will ask AJ to start answering there. I’m starting with the second question, because that will give color to the first one there. AJ?

Sure. Thanks for the question, Salim. Again starting with the second question, maybe we can just give an overall kind of view on this perhaps. So, as you know, the IA for this randomized placebo-controlled Phase 2 study, we're going to hit both efficacy and safety criteria as well as some additional biomarkers. And as you know, when we do the IA, We’ll have a range of results, everything from people who have been study for well beyond a year or with people with higher data around the three-month timeframe. So it's going to be a fairly large data set for us there. And the objective, as you kind of alluded to is to adapt the sample size, which at this stage is 80, but we could certainly - the plan is to potentially adapt it to a larger size, depending on the trend we're seeing and possibly discussions with the FDA. And what we're seeing is, we are in an incredible form. We will communicate publicly after that IA is done both what we plan to do in terms of the adjustments and sample size as well as provide detail on the rationale that we're using based on those IA results. So we are going to provide some additional detailed rationale there. Now today, we won't get into the specifics of the actual data that we're going to share because to some extent, the actual data that we’d share will depend on the IA results, but we can't emphasize that the IA-based rationale for any adjustments we're going to make in EMBOLD study will remain clear. But we still have to maintain the integrity of that double-blind study and that kind of leads into our last question that you're asking. So maybe I can just give an example to…

Got it.

And again, Salim, the aspects related to the specifics, we cannot give you the specifics at that time or the actual information we’ll share, because the specifics will be depending on the results and our discussion with the FDA. But we do plan to communicate enough to make sure that there is a clear understanding from investor community in particular about how meaningful is this particular milestone of this interim analysis there.

Super helpful. Thanks so much, guys, and congrats on the progress.

And our next question comes from Matt Phipps from William Blair. Go ahead, Matt.

Hi, everyone. Thanks for taking my question. Just wanted to clarify some of the regulatory discussions around CMC. So any color on what the CMC team is focused on this point? Because you said on the Q2 call that you're aligned regarding comparability approach. And so just kind of curious what additional information you’re looking for. And then again, just to make sure I understand the sequence of events correctly, you're going to submit this additional analysis that the FDA requested and then discuss that in Q1. Will that be a type - another Type B meeting or something informal and then hold a pre-BLA meeting in Q2?

Thank you, Matt. Maybe I start and Jakob can chime in if needed there. As you said, we have reached agreement on the methodology. We’ve presented during the recent Type B in October this new compatibility analysis. And you may remember, we said in Q2, this is a new analysis based on analyzing all the batch manufactured by Atara, these 74 batches there. So that's a lot of data that we sent to the FDA there. And we believe and we've shown in our analysis that these set of data demonstrate comparability between the pivotal study process and the Internet commercial process version there. Keeping in mind, of course, as you may remember that in reality this process difference is between this manufacturing process version are minimal, they are really minimal there. But we analyzed all the batches presented all these data, an immense amount of data to the FDA. So what the FDA has asked is additional data analysis related to a few attributes there and we will provide them because the data - they have the data already, but they ask us to do additional analysis. So we’ll do this additional analysis. We’ll provide the FDA with this analysis for this data already submitted. And then once the FDA analysis we plan for further discussion, we are not commenting yet on the type of discussion, but Type B would make sense for sure there. And then once we've got to that level of discussion and alignment with the idea and agreement on the comparability, that's where, then we will go to a pre-BLA meeting to be able then to present all what we plan to submit, including clinical and all the other stuff and then we'll be able to file for BLA. So that's the sequence of events there that we are planning based on this discussion with the FDA. Does it answer your question?

Yes. Thanks, Pascal, so far. Then maybe on the kind of ASH data we'll see in the ALLELE study, maybe you can just - I don't think if you can say this yet, but maybe how many patients received like a switch in cell line and if that was included in kind of these response rates? Can you remind me on that?

Yes. Jakob, do you want to answer that one?

Yes. So, Matt, thanks for the question. So we haven't included that particular on detail in the abstract at this point in time. But what you can see here, and this is what we're reporting obviously is that we have a 50% response rate in all these PTLD patients and a 50% response rate in both HCT and SOT, and this is of course by independent oncologic and radiographic assessments, so this is really independently reviewed. And I will say that most of the responses were with the first therapy. But of course, we can switch slots, but those details were not included in the current abstract presentation.

But you can expect - it’s an oral presentation at ASH. So you can expect much more detail at ASH.

Great. Thank you.

And our next question comes from John Newman from Canaccord. Go ahead, John.

Hi, guys, good morning. Thanks for taking my question and congrats on all the progress, especially in Europe with tab-cel. The question I have - excuse me, in the past, FDA has tended to look at durability at six months for CAR T products or T-cell products. In your case, I think, you provided some additional durability data to the FDA. But I just wanted to ask - my understanding is that the median follow-up for the study at this point is very, very long. And the reason I'm asking that is because I'm assuming then at this point, the FDA may have all the data that they would want regarding the durability. But I just wondered if you could perhaps just comment a bit about the follow-up for the study. Thanks.

Thank you, John, for your question there. Jakob, do you want to take that one?

Yes, sure. Absolutely. Thanks, John. So, as you recall, last year we disclosed that the data cut that we provided the agency with the number of patients, this is in October of last year, was a reasonable number from the FDA perspective. But they wanted this six months duration of response data, which again is required for regulatory approval, which is why we did this most recent data cut. And so we do again have this durability of response data. As I mentioned earlier in my comments that we think are quite encouraging. And I think the 89% survival of responders at one year is quite encouraging. So that's for the ALLELE study now. I also mentioned that we have a second oral presentation at ASH, which is on our historical and supportive studies. And there, again, we have median of 56 months of overall survival in that circumstance, which again is of course a very profound result for these patients. So I think the totality of the data between the ALLELE study and then the additional supportive data that will also be presented at ASH again shows a long-term benefit for these patients, where you get high response rates, a rapid response, a durable response and an impact on overall survival for these patients that have a really lethal disease.

Okay, great. I have one additional question, just sort of a general question on ATA188. Just wondering if you could comment on the understanding that you have regarding the way the agency thinks about the potential for EDSS improvement versus simply slowing EDSS decline. I think the MS therapies that have been approved or progressive MS are simply slowing the decline. I'm just curious if you could perhaps provide some color on how the agency thinks about something like EDSS improvements?

Thank you, John, for your question. I'll start and AJ or Jakob, you might want to chime in. But I mean, that's why it was so important for us to have this dialogue with the FDA at the end of last year where we align on these primary criteria of EDSS sustained improvement at 12 months, which is having two consecutive time points for improvement and the last one being a 12 months there. That was very important, because as you say, it was not yet - no product has been approved and to our knowledge only one has tried to develop on the EDSS improvement for the Phase 3, that was a MedDay study there with - unfortunately that study failing there. So it was very important there that we talk with the FDA and we align with them and they did say that sustainability improvement is an important primary endpoint for progressive MS and they prefer to have EDSS improvement, that's why we change our primary criteria in the EMBOLD study to be sustained EDSS improvement. So that's the first, nobody else has done that, nobody else is trying to do that. Because even the few studies that are trying to go now in PMS, nobody is trying to look at this sustained EDSS improvement. So - but that's a first that has been in line with the FDA. Does it answer your question, John?

Yes. Thank you.

And our next question comes from Tessa Romero from JPMorgan. Go ahead.

Hey, guys, good morning. A couple of questions from me this morning on the CAR T programs if I could. So just thinking a little bit about the mesothelin CAR T program ATA2271 ahead of the updates coming up here at ESMO I-O in December. What are you looking to understand in this data update given what we know about from the prior MSK data and also your allogeneic program? What would be a win scenario in your view here? And then my second question is on that ATA3271 allogeneic program, what are the gating factors to IND submission at this point? Thanks so much.

Thank you very much for your question. Jakob, do you want to take the first one?

Yes, absolutely. So, Tessa, thanks for your question. So as mentioned, we're excited to announce that we have a mini oral presentation with our collaborators at Memorial Sloan Kettering for the autologous mesothelin program. And again, we think that our allo CAR T platform really is an exciting one and potentially best-in-class because we are leveraging technology like 1XX of next generation costimulatory domain and PD-1 dominant negative receptor. And of course, this first study is for the auto program and then we have the following allogeneic one using our EBV T cell platform. And again, we don't do gene editing. And we think that that's really important for the performance of the cells and to limit risk as well. So at ESMO I-O, our collaborators, Sloan Kettering, will present preclinical data for the program, but also clinical data from low-dose patients. So you'll see safety there, translational data as well as some potential early efficacy I will say, of course, these are low-dose cohorts. But again, I would say, safety is really important here of course as we move into these CAR T therapies for solid tumors. And then, I also think, these questions are persistence of the cells is really important. Turning on to the allogeneic program 3271, just one comment, we are having a presentation here at SITC very shortly with preclinical data, updated data for that allo mesothelin program. So that will be a poster presented at SITC. And then we are very much on track with the IND filing in the second half of next year. And I will say, as with any IND, you have to get all of your studies ready for the IND filing, including of course for this type of therapy, the manufacturing aspects with this type of program. But I will say everything is moving ahead very well with our partner, Bayer, here and again preceding that will be the IND filing for 3219, which is our allogeneic CD19 CAR T, which we think could be best-in-class and again we're targeting a Q1 IND of next year.

Tessa, maybe two additional points. We are very excited about this program. And so 3271, in particular, one aspect that is very unique to Atara - in fact, two aspects. First one is this 3271 is going to be made - is being made right now in stirred-tank bioreactor, that's a big first for an allogeneic CAR T or CAR T in general there. And I think that's why it's taking the time to put that together because that's a big first, but we have already evidence at some early stage that we can make this allogeneic CAR T into stirred-tank bioreactor, which is going, we believe, to change radically the manufacturing efficiency of allogeneic cell therapy manufacturing. So watch the pace there. The other aspect is the fact that we are maintaining TCR in 3271. We’re maintaining the EBV TCR there in our manufacturing process. We believe that's very important not only from a safety point of view as a recent example have been shown, but also we believe from an efficacy point of view. In fact, recently, a clinical study has been published in Nigeria using mesothelin CAR T cells that were edited to lose TCR PD-1 expression. And what was very interesting in the Phase 1 study is that the authors could not detect CAR T cells in 12 of the 15 patients and the only three patients after just a few weeks. And the only three patients in which we could detect where the patient for which they were, in fact, I think a few of TCR that were not gene edited. And there were the TCR positive CAR T cells that were there – that were present there. So for us, it’s a clear evidence that if you maintain the TCR, you have more persistent. If you delete the TCR, or you modify the TCR, the endogenous one for allogeneic CAR T through gene editing not only you create a risk in terms of having additional gene edition in terms of safety but you also limit the persistence of the cells that will stay only for few weeks. Does it answer your question?

Absolutely. Thanks so much for the color. Pascal and team, I really appreciate it.

And our next question comes from Phil Nadeau from Cowen and Co. Go ahead, Phil.

Hi, good morning. Let me add my congratulations on the real data. A few questions for us on - from us on tab-cel. Just first on the guidance for Q2 FDA filing. I'm curious how confident are you that you can complete the BLA in Q2? It does seem like the FDA and the CMC division in particular in dealing with cell therapies is kind of evolving its requirements on the fly. So appreciating that you have alignment. How confident are you that you know exactly what the FDA wants and that there is not going to be a newer request when you talk to the agency in Q1?

Thank you, Phil. I'll start and Jakob will chime in. I mean, first of all, I like to say, we are very confident that we are ready to file. I mean, as I said, we are filing in the next few days in Europe. And so we have a full file ready to go and on all aspects of this product. We believe we have invested and developed a product that is of high quality and with great data there and we're going to file in Europe in the next few days. Now in terms of the U.S. and the FDA discussion, I mean, it's true that the - it's a step-wise type of a process. So far, we have a lot of questions coming there and there is a lot of data also that we could do that. I mean we are discussing things that very often or more at the BLA review level and we're doing that in various Type B meetings that we have increased with the [indiscernible] team and we are making progress step-wise progress there. So we certainly are understandings their questions and we're going to put together this new analysis they are asking for and all the interactions with them. We cannot predict whether they will have other questions, but we think we have given them all the data that exists on the product and it's really around new analysis more than trying to create new data at this stage. Jakob, anything to add?

Yes. And just to maybe amplify that as well, I do think, as you see, we're making this step-wise progress. So, at the last quarterly call, we announced that we've got this clarity in agreement that the FDA wanted to see all of the lots that were manufactured in order to make this determination of comparability between pivotal and commercial material and the great news is we can do that. We have all those lots. So that was great clarity to get from the agency. And at this quarterly call, we can now announce that we've made further step-wise progress with that October Type B meeting where we've now come to agreement with the FDA on comparability approach, including the statistical methodology. So again, this was an area of much discussion and we came to agreement there and then the agency have now further focuses and said that they want additional analysis on certain data points here, which we’re now providing to them in advance of our next interaction with the agency in Q1 of next year. So again, I think there is clear evidence of progress here and I think we are confident in that progress. And Pascal said, it's really incredible as a pretty small company here that we are completing our first regulatory filing and submitting in Europe here, as Pascal mentioned, within the next couple of days. But the implications of that, is that we have a full regulatory filing that's been completed and we can leverage all of those documents. All of those analysis and all of that data in the BLA filing, so we're really ready to go. And so we've also of course shared clinical data with the FDA from the ALLELE study any other supportive studies as well and gotten guidance from the FDA in that clinical feedback that actually helps us to position the data in the BLA filing the type of information that you would get in a pre-BLA meeting. So again, I think very nice progress here. And again, very proud of the team here at Atara that's worked so hard on getting this regulatory filing together.

And maybe a follow-up to your second point there. In the past management suggested that if you thought you had perfect clarity on what was necessary for the FDA filing, you might be able to progress to the filing without a pre-BLA meeting. Today, it sounds like you think you need a pre-BLA meeting. So I guess we’re curious, what do you expect to learn at the pre-BLA meeting that you haven't already established from all the other Type B meetings that you've had?

Yes, maybe I can answer that one. I think it's really a step-wise aspect there that we need to have that final agreement on the comparability and that will lead also to the content of the model free. And then the pre-BLA will be just to align on the different aspects of the file in terms of content, because as we said, we have the file ready to go to EMA, but FDA is asking some different type of analysis and so on. So we want to make sure that the way we put together the file or we plan to put together the file for the BLA is aligned with the FDA there. So that's why a pre-BLA meeting, we believe and we discuss that with them will be necessary more for what I would call maybe the administrative part, which is to make sure that the way we put the data together that we have is aligned with their expectations.

Perfect. And then last question from us is on 3219. It sounds like the IND is on track for first quarter of next year. How long do you think it will take from the IND to actually dosing the first patient, I think, in for prior CAR T therapies that there was somewhat of a lag maybe six months or so. Will that apply to 3219? Or is it possible that you could dose a patient sooner than that?

Yes, we're not going to comment on that, Phil, at this stage. So we will do that comment at a later stage when we are reaching that point. But suffice to say that we are trying to get all the learnings we can and with a lot of expense in the company about total CAR T and CD19 CAR T about the best way to accelerate the timing from IND to first patient and to make sure that we have the right type of patient that study is there. So we're working on that activity as we speak, but sorry, but we cannot give details. It’s too early for that.

Fair enough. Thanks again for taking our questions.

And our next question comes from Jonathan Miller from Evercore. Go ahead.

Thanks, guys, for taking my questions. One on 188. I thought the MTR data you showed at ECTRIMS is very interesting and obviously went through it again, a little bit on the call today. But I understand that MTR declines are associated with clinical decline in MS broadly, but has the inverse ever been demonstrated? I mean, that is - has MTR stabilization been associated with disease stabilization or MTR increase associated with disease improvement? How much confidence do we have in this biomarker sort of being predictive in both directions, I guess, is my question there?

Yes. No, thank you very much for your question. AJ, do you want to take that one?

Sure. Yes, thanks for the question. I think the best way to look at it is this biomarker has been most utilized in the relapsing remitting space when you're looking at trying to make those correlations. And when you're thinking about the disability improvement or resolution of symptoms in MS, remember, this is all about myelination, right? So when you look at relapsing-remitting lesions that are active, you will see MTR having significant decline - I should say substantial decline. And then when those lesions resolve, you will see the MTR increase that’s by definition, that the disability that's associated with that lesion is getting better, right? So in RMS, there has been connections between MTR increase and presumably remyelination there and improvement in the clinical status of those patients. In progressive MS, as you know, no one has ever seem disability improvement and that's why, to the questions you've asked, it's not been shown in progressive MS. You see evidence of the MTR utilization for improvement in disability in RMS just hasn't been seen in progressive and that's why the data that we have are so unique. Because if you take a look at it, for example, in the chronic T2 lesions where they're generally considered very old and many of those lesions we consider almost dead lesions those lesions are where we're seeing statistically significant remyelination. And really importantly, that's associated when you see the remyelination, the patients who are having that remyelination are the ones who had disability improvement. So this is the first time that people are seeing that in progressive MS. And this is why the data are so important because hints of it and relapsing-remitting, but here, we're showing something really powerful in the progressive MS.

Thanks so much. That makes a lot of sense. So I guess one more on and that's franchise. Just following up on the color you gave to Salim earlier in the call. When you talk about maintaining the integrity of the study, obviously, the – even a smaller part of the study here is randomized and double-blind. Are we to assume that the blinding is going to be maintained throughout the interim analysis? And therefore, the amount of data that you actually have in-house is going to be limited by what the prespecified DSMB run analysis provides you with? Like you're not going to have a bunch of data that you're hiring from us, it is more about the maintaining the blind in the study and a limited amount of data being pulled out of the IA, is that fair?

Why don’t you start and I’ll chime in.

Sure. I think the best way to look at it is, we are, as you might imagine for any really robust randomized controlled trial work, putting in as many controls as possible to make sure we maintain a stronger blind as possible. So of course, the DSMB - the safety monitoring committee will see all those. The data monitoring committee will see all the data. There'll be very limited exposure to the data internally. So it's not like we're looking to hide any specific information. But again, the best way to look at is, this will be conducted robustly. So we maintain the blind as much as we can, so that way the power of the result at the end will be as strong as we can.

Yes. And again, Jon, I think, as we say, the specifics of what we can say are going to be clarified at the time of the IA, because that depends very much from the data. That depends very much on the status of best of the following discussion with the FDA. Could it be transformed into Phase III or not? I mean, there are many variables there. What we can confirm today is that these are not only will be very important milestone, but we'll be able to say - while preserving the integrity of the study to say, not only what we are deciding based on that, but why we decided to a certain extent in terms of detail.

Thanks so much, Pascal. That makes sense. Maybe switching gears for just a second to 2271, looking forward to seeing some of that early data at ESMO I-O, just to expand on what you said previously there, I understand this is from the lower dose cohorts. But can you tell us how many patients in total you're going to have there and whether we should expect meaningful dose response to continue beyond these cohorts we see at ESMO I-O?

Yes, I think we are not commenting at this stage on the how many patients and so on. You will have to wait for few weeks there. We’ll give full details at that time. But we said last time that it was really the lowest dose cohort. So on the cohort one and two only. So these are - I mean step-wise – remember, it was 1 million per kg for cohort one, 3 million per kg for cohort two, and these are the low dose there. So that's why we are really focusing on safety and transnational there. I think for us, one of the key aspects will be really the PK because I mean, we’ve seen data from this type of CAR T that are showing expansion. and then the CAR T starts to exhaust and there is no more CAR T or at least much lower level there. And if we could be able to see something different there that will really be some proof-of-concept for having 1XX and - as a co-stimulatory domain and PD-1 DNR, both of them having a role to play on persistence and we see defense mechanism against the immunosuppressive tumor microenvironment there. So I think that would be great if we could show that.

All right. Thank you very much.

And our next question comes from Salveen Richter from Goldman Sachs. Go ahead Salveen.

Thank you for taking the question. This is Tommie on for Salveen. Can you just remind us of the key points of differentiation on Atara’s mesothelin targeting CAR Ts compared to other competitors? Thank you.

Yes. Jakob, do you want to take that one?

Yes, sure. Absolutely. So for our mesothelin CAR T, just a reminder that this is a program that we partnered with Bayer and there are two programs in the franchise. There is the autologous program 2271, which is currently in the clinic, and that is the ESMO I-O presentation that's going to occur here in December. And then there is the 3271 program, which is the allogeneic program where we're heading towards an IND filing in the second half of next year. So firstly, what both of these programs have in common is the binder against mesothelin. So this is a binder that's already been derisked by an academic first generation program at Memorial Sloan Kettering. So we know from the first gen program that this is a safe binder and again we'll share data here coming at the end of this year at ESMO I-O. Additionally, what we have in our programs are the 1XX co-stimulatory domain. So this is next generation co-stimulatory domain developed by Dr Michel Sadelain at Memorial Sloan Kettering, where the idea is to innovate co-stimulation in the T-cells, so that you enhance in vivo expansion persistence and reduce exhaustion of those cells. So again, this is an important co-stimulatory domain. Additionally, both programs also have PD-1 dominant negative receptor constructed into the cells, where you do not - where the cells are not at risk for the tumor suppression from tumor PD-L1 expression. And so again, this is a unique feature that could also enhance in vivo persistence and prevent exhaustion as well. And so, the additional feature with the allogeneic program is that we're using our EBV - allogeneic EBV T-cells as the cellular foundation for that those allo CAR T. And I think what's really important here is that we have a…

No, I think you covered all the aspect there and it's a very unique and differentiated platform there. And also I think not only in autologous, but in allogeneic following very fast. It's very exciting indeed.

Thank you.

And our last question comes from Yigal - I'm sorry I can't pronounce your last name, Nochomovitz Yigal.

Hi, no worries. Hi Pascal and team. Thanks for taking the questions. Just curious, are there scenarios where at the interim analysis for ATA188, the study could either be stopped for either overwhelming efficacy or futility or is the interim analysis necessarily going to result in the sample size adjustment with the study continuing?

Yes. Thank you for your question. AJ?

Yes, there is - as with any other kind of robust interim, Yigal, we - there's always a possibility that you would highly unlikely event that you’d stop for futility. And our intent would not - there's always a possibility that you stop because you’ve got an amazing efficacy round. So it's a standard interim analysis where you have those possibilities, but the primary intent really here is adjustment in sample size that would be our expectation.

Okay. And then just a separate question, when are we going to get an update on the MATCH trial? And where would this be presented?

I think we don't have the MATCH trial anymore. When we merged the two trials, that became the ALLELE. So ALLELE is now the pivotal study. When we merged, remember, about three years ago, we merged that into one study only - one pivotal study only, I think, both SOT and HCT cohort.

Okay. Got it. Thank you.

Any other questions?

We have no further questions at this time.

Thank you.

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