Welcome everyone to the 41st annual J.P. Morgan Healthcare Conference. My name is Tessa Romero. I'm one of the senior biotech analysts here at J.P. Morgan. I'm joined by Taryn Healy and Amber Daugherty from the team. Our next presenting company is Atara, Speaking on behalf of the company, we have CEO Pascal Touchon. Before I turn it over to Pascal, I just wanted to highlight that post the formal presentation we will have a Q&A session. There is an Ask a Question button in the portal. For those on the webcast, please submit your questions, and I'm happy to ask them on your behalf. We will also be taking live questions, so bring your questions for the session here. With that, I'm gonna turn it over to Pascal. Pascal?
Thank you, Tessa, and thank you J.P. Morgan team for inviting us to present today. It's a real pleasure to be with you in this room that is protected from the weather. I hope we can have a good time together. In terms of my presentation, I will really highlight for you the key elements of our industry-leading platform and pipelines in allogeneic T-cell therapy. First of all, during the course of my presentation, I will make some forward-looking statements, and I refer you to our SEC filings in that respect. What is amazing about Atara over the last few months is our ability to deliver on promises of delivering on the transformative potential of allogeneic T-cell therapy.
In fact, what we have here is an amazing type of situation where we've had been the first company ever to get an approval for an allogeneic T-cell therapy in the world. That value has been approved in December 2022 in Europe by the EMA, and that's a very exciting moment for not only Atara, but very importantly for the patients that are being treated with this treatment and could now access that therapy in Europe. We have a very exciting partnership with our partner, Pierre Fabre, that's going to launch that product in Q1 of this year. There is also a very important aspect of last year, which has been our work with our potentially transformative therapy, ATA188, for multiple sclerosis.
This targeted therapy is uniquely targeting what we believe is the root cause of multiple sclerosis because there have been some landmark publication last year in Science and Nature showing that clearly MS is caused by EBV infection, by EBV latent infection. We are here with ATA188, the first-ever therapy to specifically target EBV infection in B-cell and plasma cell that is both the trigger and a driver of multiple sclerosis. Last but not least, we are developing actively a potential best-in-class opportunity with our next generation allogeneic CAR-T program. We have our first product in our pipeline, ATA-3219, which is a potential best-in-class CD19-targeting allogeneic CAR-T that will enter the clinic in Q2 of this year.
Clearly we have a lot of work going ahead and a lot of catalysts coming, but I would like to spend some time to highlight the approval in Europe of Ebvallo or Ebivarlo, the first-ever allogeneic T-cell therapy to be approved in the world. Ebvallo is a treatment of an ultra-rare cancer, which is called PTLD, or post-transplant lymphoproliferative disorder. This cancer is a very deadly one that is progressing very rapidly. We've been able to obtain that approval in Europe through an excellent work done from a clinical development, regulatory process and process development, and of course, having the ability now through that approval to transfer this market approval to our partner, Pierre Fabre, that is getting ready for the launch in Europe.
This achievement validates not only the work done on Ebvallo on tabelecleucel, but also validate the platform because it really shows that Atara is able to get an allogeneic T-cell therapy not only developed, but approved by a major regulatory authority. Very exciting time for the patients, for the company, and of course, for our partners as well. It's the first of several anticipated value-creating milestone for the company, and we are really taking that as a first step in a lot of milestone coming, a lot of catalysts coming from the company in the next few months. We have a pipeline that covers different type of disease, different type of targets, all around the same platform, allogeneic T-cell therapy, that are relying upon our EBV T-cell or Epstein-Barr virus T-cell platform.
We have product that targets specific cancer linked with EBV, specific autoimmune disease like multiple sclerosis that are associated with EBV, in fact caused by EBV, but also in enabling these cells to have another target for chimeric antigen receptors, the ability to address through values, CAR-T development, different type of solid and liquid tumors. Let's spend some time on tab-cell. Here you have a kind of summary of the key elements in terms of tabelecleucel or Ebvallo, our first-ever approved product. This has been approved in Europe, as we just say. At the same time, we are progressing with the FDA towards a clarity on the BLA pathways that we hope to get in Q1 of 2023.
This product benefiting from a BTD, a breakthrough designation in the U.S., we are very hopeful that we can get with the FDA an alignment on a clear path to regulatory submissions in the U.S. and moving forward to be able to get through the review and approval in the U.S. and launch it as well. Now, tab-cell is supported by an amazing type of clinical development. On one hand, we had this particular pivotal study, the ALLELE study, for which here you have the data we recently presented at ASH, where we show that in patients with this second-line PTLD situation, so they have been in a situation where they had diagnosis for post-transplant lymphoproliferative disorders, EBV positive type of lymphoma.
And in different type of setting, whether they come from bone marrow transplant or RCT, or they come from solid organ transplant, the level of response that we obtain on pivotal study is very significant, with 50% objective response rate in the setting of HCT and nearly 52%, 51.7% objective response rate in SOT. Very significant level of response. Once the patient are responding, not only do they respond very fast because the median time to respond is just one month, but there is a duration of response. I think the durability of this response, something very important, is very unique to our platform. I know that many other allogeneic platform are trying to develop also approach to treatment for an off-the-shelf way.
That here we are with significant durability, and in that case, for the pivotal study, we have duration of response that is a median of 23 months for responders. High level of response, duration of response, rapid response as well, and a very favorable safety profile with no CRS, no neurotoxicity observed, and no GVHD organ rejection that could be attributed to the treatment. This is also supported beyond the pivotal study by data we presented at ASH 21 related to previous studies with longer follow-up, where we were able to show a very nice impact on overall survival. These patients with second-line PTLD have just a few weeks to a few months to live.
Here we are in a type of longer-term follow-up in previous studies, up to 86%-87% overall survivals at two years, whether the patients were responding as a complete response or as a partial response. Again, very unique features of tab-cell, that even with partial responders, we have this long-term overall survival. Now, the median overall survival was about 55 months, which is very significant. Again, these patients are dying within a few weeks or within a few months. Here we have this long-term data showing the impact on long-term survival. Very clear data coming from that. And now we're getting ready. In fact, we are partnered with Pierre Fabre, who is a great partner, very collaborative, and very committed to the success of Ebvallo in Europe, is preparing for launch. That should occur in Q1 of this year, in Q1 2023.
They are working on a very detailed phase, country-by-country approach, depending on the pricing and reimbursement. They have also very committed to leverage that very significant commercial opportunity, not only in second-line PTLD, which is the first indication for which we got approval in Europe, but also for the work that we are doing on the multi-cohort label expansion study, the ability to expand the label of the product with time in the different countries, and therefore achieve the optimal potential of that product in different type of setting. The other aspect of the story is of course, around pricing and reimbursement. We think that what we have, and our colleagues at Pierre Fabre also committed to that, is really very supportive of proving the value of tab-cell, of Ebvallo in different healthcare system in Europe.
And therefore, having value proposal that is really very significant, the potential for significant pricing opportunity as well. That's really where we are today, and more about that over the next few months when we get into the launch phasing with our partner, Pierre Fabre. Let's move now to ATA188, our multiple sclerosis development. This product is also an allogeneic T-cell therapy relying on Epstein-Barr virus, and we are really targeting this product to address a very specific situation of the latent infection with EBV in MS patients. That means that we have very specific antigens that we are targeting the products towards that are really always present in MS patients. This product, this allogeneic T-cell therapy, is really a very, very specific product for MS and possibly some other autoimmune disease, but here we are focusing on MS.
We have two fast track designation from the FDA based on discussion we had with the agency in terms of two unmet medical need that are particularly important, one in so-called non-active primary progressive MS, the other one in non-active secondary progressive MS. And these two populations is basically the same disease. It's just about the way the medical need is covered today. There is absolutely no approved therapy in non-active secondary SPMS, there is only one approved therapy today in the U.S. in non-active primary. That active, that particular therapy is showing a modest effect at best. If you think about the evolution of progressive MS, this is about 40% of the total population with MS in the world, in the U.S. in particular, what's happening, you have a progressive decline in terms of their disability.
And what's happening to this patient that progressively they start to be not able to move around, they need canes, and they need a walker, hopefully end up with wheelchairs and sometimes being bedridden. This progressive decline is really something that is extremely debilitating for these patients. The current approved therapy in this pathology have only a modest effect. In fact, the effect that they have is just about a six months delay in the progression of the disease. You can see clearly on this visual that this is, of course, a positive impact for patient.
We're not saying it's not positive, but it's modest, and there is a lot of space to improve on that. There could be, of course, a possibility to further delay the progression, possibility to halt the progression, to have more stability in this patient for many, many years. Very importantly, the possibility to, in some patients, to have an improvement and a sustained improvement. What's important for this patient is to be able to know that they are not going to progress, and for some of them to be able to improve.
Now with our development of ATA188, we are really targeting this kind of high medical need about how can we show to patients that we can improve their disability? How many patients will be able to improve with the treatment with ATA188? Of course, we'll also look at other aspects of benefit for patients. Could be the stability, so the lack of progression thereof, or delaying the progression. The most important objective that we have is really to have significant opportunity to create value for the benefit that the product might bring to patients.
Ultimately, we are relying upon our phase I data, that I will detail in a minute, that are really amazingly interesting and encouraging in the sense that they are looking at the possibility in 20 out of 24 patients to show improvement or stability of the disease over a number of years. We are very encouraged by this data, and on the basis of this phase I data, we have built a very exciting phase II program that is going to read out in October of this year. The reason we are so optimistic about what we're doing and encouraged by data is that 2022 was a year marked by landmark publication.
And in fact, EBV as a trigger for MS has not only been proven by this publication, but has been recognized by Science Magazine as one of the top scientific discoveries in 2022. Two key papers, one in Science, one in Nature. The Science paper was really looking at the population of a lot, about 10 million people followed for 20 years. They were military personnel in the U.S. They showed very clearly that EBV is what initiate MS, what cause MS, with a risk that is increased by 32-fold after infection to get EBV.
That's a very clear situations where now it's proven that EBV cause MS. It's not the only factor that cause MS. There is a need for additional aspect from the environment and the genetic profile of the patient, but that's a starting point, and that's a very important starting point. The Nature paper looked more in details about how could that happen, what's the potential mechanism by which EBV could cause MS.
They were able to clearly identify the fact that EBV infection can cause MS at the molecular level by a phenomenon called molecular mimicry, where the immune system of patient will be in fact mistaken by the similarity between some part of the EBV various protein and some brain protein. Therefore, they will start to create an auto immunity against brain protein based on the reactivity that they developed against the EBV infection. Especially because this EBV infection is being immortalized for B- cells, and some of them being compartmentalized in the brain.
A very clear explanation from the Nature paper about how a EBV infection could indeed cause MS. ATA188 is in fact a product that is specifically developed to be addressing at the root cause MS, and therefore addressing that through the specificity for the EBV infection in the B-cell, in the plasma cell, that are really the trigger and the driver of the progression of the disease. We have, as we said, encouraging data from our phase I, and we have this phase II randomized study called the EMBOLD study that is running now, for which we expect to have a readout of the primary endpoint on improvement in disability at 12 months. In fact, not only improvement, but confirm improvement in disability at 12 months in October of 2023.
Now the evidence that we have, we believe is extremely encouraging right now, because coming from that phase I study we conducted over the last few years and the open label extension, we have a very encouraging support from that growing clinical evidence. Not only to prove that out of these 24 patients in a phase I, 20 either improved or were stable in terms of their disability, which means really that something is happening clinically in these patients. There have been also improvement in patient-reported outcomes like fatigue. Very importantly, when we look at this disability improvement or stability, these have been sustained for the long term. That's where we start to see something that is extremely unusual, even though it's a small number of patients, that the ability for the EDSS stability to be sustained for up to 41 months median duration.
With follow-up of the patient for 48 months, five months. The ability for the improvement when it occur to be sustained for up to 27 months median, and in total with 46 month-plus type of follow-up, shows that something not only is happening clinically in this patient, but at the same time, this improvement or this stability is maintained in the long term. Which is extremely unusual when you think about the natural history of their disease, if it is caused progressive MS for a reason. This patient clearly not only are not progressing, but they are in fact, for some of them, improving in the long term. That clinical evidence is, we think, extremely encouraging. Now this is backed by a number of work we did with experts worldwide on can we see any signal of what's happening in the brain of these patients.
And we were able to present in a congress, MS Congress called ECTRIMS, some very exciting data on, first of all, the myelination status in the brain of these patients. We're able to show very clearly for a particular imaging as a type of measure called MTR for magnetization transfer ratio, that these patients with disability improvement in our phase I study had significant increase from baseline of their MTR at 12 months. An increase in MTR means, we believe, remyelination. What's happening is that ATA188, we believe, is eliminating the infected B-cell and plasma cell in this patient, and that allows the brain to start to repair itself and have remyelination happening, which then ultimately leads to disability improvement.
Not only we have this data on MTR, but recently, last quarter, we presented at the ECTRIMS Congress in 2022 some MRI data showing less brain atrophy in a patient that are improving. Not only we have remyelination, but we see that we have some potential brain structural changes where these patients improving are improving for a reason. Again, it's not just because they had a good day in some of the clinical evaluation that they had. It's really in the long term, they improve, their brain is changing, there is less brain atrophy over 42 months longitudinal follow-up, and at the same time, there is remyelination.
Small number of patients, phase I study, open study, yes. The type of data we see here is extremely encouraging for our phase II program. What we are doing here is also now to build on that. In fact, if you think about it on that growing body of evidence, we're now moving to this phase II study, the EMBOLD study, this double blind versus placebo.
About 90 patients will be available for the primary analysis, and we will be disclosing the result of that primary analysis, at least the top line results, in October 2023, so in not so distant future. We think that the way we've seen the initial evidence from phase I, the way we designed that phase II studies, allows us to have the possibility to really unlock a lot of value potential for patients, for the company, and of course, for our investors and shareholders. Following that EMBOLD readout, we believe that there will be the possibility to move into other late-stage clinical development, hopefully phase III in non-active PPMS, non-active SPMS.
These are not small population. I mean, the vast majority of progressive MS patients are non-active. It's about 60%-80% of the population, which by itself is 40% of the MS population. It's very significant number of patients, and we are developing actively the product to be ready to go into further development after the EMBOLD readout. We'll benefit, of course, from fast track designations that we have with the FDA, and we'll be also discussing with other regulatory authorities. From a corporate strategy point of view, we plan to do all that further development with a partner, and we've seen significant interest from various companies into considering that type of partnering following the EMBOLD readout. Let me move rapidly on the CAR-T front, where we have been developing allogeneic CAR-T, again, leveraging the same platform, this allogeneic EBV T-cell platform.
We are really now well versed into how we can make robust process, high-quality product from healthy donors with this EBV T-cell platform. Here we have the possibility to improve on anything that exists today in terms of different features of this possibility to make CAR-Ts, not only of course with a specific binder that will address different type of targets in solid and liquid tumors, but very importantly also in maintaining the endogenous TCR, the EBV TCR, which is a survival signal for those cells, so increasing persistence, having an optimized costimulatory domain called 1XX that has been proven to have an impact on T-cell exhaustion and to be more physiological in term of its impact on the behavior of the T-cells.
And of course, to work in, especially in solid tumors, on adding additional features that allows this allogeneic CAR-T to be protected against the immunosuppressive environment of the tumor. In particular here, we have the capacity to add some PD-1 dominant negative receptors that function as a decoy that allows to for the CAR-T to be more resistant to the immunosuppressive environment, therefore to persist longer. The first product we are developing is ATA-3219. That's a product that should come to the clinic this year in Q2 2023. That's a planned IND. It's very exciting one because it's really combining all features that should lead to increased persistence and therefore hopefully durability of remission, which is today the main weakness of other approaches.
So we have very differentiated, unique approach that will benefit from our platform knowledge and of course, the approval of Ebvallo in Europe and the late-stage data that we have in terms of safety and efficacy. Think about it. We have treated more than 500 patients in total with our allo EBV platform. We have a lot of data, and leveraging that for the construct that ATA-3219 is based on, which is having 1XX as a co-stimulatory domain, as well as having a manufacturing process that allows to have phenotype that is more geared towards memory type of cells, is all designed to have better efficacy, good safety, and long-term persistence of the cells, enabling durability of remission. Of course, we don't have clinical data yet. It's coming.
We've, as you can say, optimized things, and recent data coming from other approaches have shown that that's where the medical need is. How can we get an allogeneic CD19 CAR-T, an allogeneic CAR-T in general, that will be durable, persistent, enabling durable remission? That's what we've built, we believe, with 3219. We have also developing a mesothelin CAR-T program that at this stage is called 3271. An allogeneic mesothelin CAR-T addressing aggressive solid tumors.
This program is ready to go soon in the clinic. We are waiting for some additional data coming from an autologous version that function as a proof of concept of the program that is resuming its study now for Sloan Kettering in New York. We expect to have some data coming over the next few months from that study, phase I study that is going to help us define better the potential benefit of our mesothelin allogeneic CAR-T ATA3271. Altogether, this platform is really here to deliver benefit, to deliver benefit for specific features that we've built upon, such as no TCR gene editing, which we believe is a key advantage for this type of allogeneic cells.
It's an off-the-shelf with relatively low cost of goods, a scalable manufacturing, and a very versatile platform, as you could see, addressing different type of disease from cancer to autoimmune disease. This allows us then to consider adding some unique benefits compared with other approaches in terms of trafficking, extension, persistence, and tolerability. We are not only a leading allogeneic T-cell immunotherapy company, but we are a company that is delivering approval with the first-ever approval of an allogeneic T-cell with Ebvallo, delivering clinical data with the data we presented at ASH and the phase I study from ATA188.
We are delivering also very important program like the EMBOLD study, this first-ever double-blind study in progressive MS, with the aim to really be a big game changer in MS and transform completely that part of the therapy in these patients that could create multi-billion dollars opportunities, and of course, the next-gen allogeneic CAR-T portfolio that I really briefly presented to you. All that supported by proven technical capabilities, state-of-the-art capabilities, and a real know-how and expertise about not only how to create, how to develop, how to get full regulatory approval, allogeneic T-cell therapy addressing many type of disease.
Very exciting time ahead for us in 2023 with key catalyst around the launch of Ebvallo in Europe, the ability to get through some clarity of the FDA about the BLA timing in the U.S. of Ebvallo, the possibility to find a partner in the U.S. that will be able to commercialize the product in the near future. Of course, in October 2023, a very exciting time in terms of readout of the EMBOLD study. Thank you very much for your attention.
Great. I'm gonna welcome the rest of the Atara team up on stage to join us to have a little chat here. [audio distortion] Great. Maybe it makes sense to have everyone on stage introduce themselves, then we'll get started.
I'm, Jakob Dupont, Head of Research and Development for Atara.
AJ Joshi, the Chief Medical Officer for Atara.
Utpal Koppikar, CFO of Atara.
Great. We've got about 13 minutes or so here to have a chat, so please wave your hand at me if you have any questions, but I'll just lead us here. I thought we'd start with tab-cell. Ebvallo was recently approved, and we know that Pierre Fabre will lead that commercialization. How should we be thinking about the European launch ramp over the next few years?
Yeah. I think everything is getting ready for launch, we know colleagues from Pierre Fabre is really excited and committed to that. It's going to be a typical progressive launch in Europe, country by country. You have to go through the pricing and reimbursement. A few countries you can launch first because you don't need to negotiate pricing and reimbursement initially, and that's usually Germany, Austria, in typical situations. Then progressively, you get through these launches over the first 18 months. That's the first part of the progressive launch. The other part is going to be the label expansion. As you know, we are working on this additional patient population we could target with Ebvallo. What is very exciting about it, that we already have data.
For each of the cohort we have in a multi-cohort study, we have already data that we presented in previous congress from other studies that have shown that the product seems to be effective and has a favorable safety in these populations. It's very de-risked from that point of view. It's not like we are exploring new indication. It's a new indication for which we have data already. We're just putting that into a multi-cohort study with this idea of going to the regulatory authorities asking for label expansion when we have enough patients and enough follow-up in this study. That will be progressive in terms of pricing reimbursement in the first indication, and then, of course, having label expansion coming over the next few years.
Mm-hmm. And what are the next steps here, Pascal, in the U.S.? You know, has the Type B clinical meeting and/or a pre-BLA meeting occurred at this point?
Jakob?
Absolutely. Thanks, Tessa. last year we made a lot of progress with the FDA, where we made certain proposals to the agency in terms of how we could provide more clinical information for the sake of driving towards a BLA filing. That led to a reversal of the FDA's position that we needed to conduct a new clinical trial with the intended commercial material. That was a lot of progress. After that, we had a Type A CMC meeting where we came to agreement with the agency on the contents of the module three of the intended BLA filing as well. That is the manufacturing module in the BLA. That was a lot of progress.
What the agency also recommended at that time is that we schedule a Type B clinical meeting to talk about the intended clinical content of the potential BLA filing. We've requested that meeting. The meeting's been granted, and that meeting is gonna be occurring within a few weeks' time. The purpose of that Type B's clinical meeting is to speak with the agency about the number of patients that we need in the BLA filing clinical data, and then what percentage of those patients will be treated with the intended commercial material.
Again, that was the topic of the Type A meeting. We've been treating patients in the clinic with the intended commercial material since late 2021. Again, coming out of that Type B clinical meeting, we should have a sense of the number of patients the agency wants to see, and also the timing of that BLA filing, and we intend to provide clarity on those topics at the next quarterly call.
We'll stay tuned for that. You know, how should we be thinking about price for tab-cell here in the U.S.?
Yeah. As you know, we have been working for the last two years very actively on preparing for the launch of tab-cell in the U.S. We had not only a very good medical information awareness, we know exactly where the patient are and what centers are the patients in need. There is a level of awareness as well of the physicians about the potential for tab-cell to address their needs. They don't know what to do with these patients because these patients are really helpless, due to the very rapid progression of the disease. It's an emergency from a neurology point of view. Here we have a product that has really shown data that are very encouraging in terms of addressing that need.
Now this means that we have the capacity to have significant value for the patient, value for the physician, value for the society, but very importantly, value for the healthcare system and the payers. The value that we're bringing is around transforming the life of this patient, basically improving their ability to have long-term overall survival, based on the long-term data that we have in previous studies and for the pivotal study, very clear evidence of response rate, duration of response, safety, and of course, rapidity of response.
We think all of this aspect allows us to think about the significant pricing potential. In fact, we've been discussing already at Atara with a lot of payers in the U.S., and there is an agreement and alignment on the level of price that will make sense from payer's point of view in that ultra-rare disease. We have to think about a value in the U.S., like in Europe, by the way, as a very transformative type of product that could bring value to the system and therefore could benefit from significant pricing potential.
Okay, great. Okay, great. Just because of the timing here, I thought we might switch gears and talk a little bit about ATA188. You know, I think it was this summer that you headlined your kind of findings from your interim analysis. I think it left a lot of us with some questions just because it appeared that the predictability requirement between six months and 12 months did not hold up in the small sample there. What underpins your confidence that the full analysis will be a superior result, including that your sample size is large enough?
AJ, do you wanna take that one?
Sure. Thanks, Tessa. Yeah, you're right. You know, as we did the planned interim analysis earlier in the year, earlier after, I should say, What ended up happening was, you know, we had actually, to your point, a bit of a small sample size for that analysis. We end up having about 15 patients at that 12-month primary time point. Now remember, that is the primary time point, primary endpoint for the study. 12 months confirmed disability improvement.
That predictability you were talking about, six months to 12 months, we just didn't have enough data to say whether there was predictability or not, and that's kind of where we landed. Because if you think about it, if you have 15 patients at a 12-month time point, that means half of them are on drug and half of them are on placebo. There's really not much to work with there.
Because of that, Since there just wasn't enough data to make any kind of a determination, the independent data safety monitoring committee basically made a determination that said, "You know what? Continue the study without any changes." We made our own internal assessment. We felt the same way. It makes sense to continue without any changes. Now, what gives us confidence going forward on this thing is really kind of the data that Pascal highlighted a little bit earlier, where, you know, we're looking at 20 out of 24 patients have either maintained stability or had disability improvement in the phase I study.
When you look at the durability of that, Pascal described that. You've got patients who've got stable disease who are now out to 48 months in follow-up. The disability improvers, you're now they're out to about 46 months of follow-up. That's not typical for MS. You saw that constant downward progressive trend for progressive MS patients. That's what should happen. We're seeing something that's not typical. You could argue, you know, it's a phase I study, it's clinical. Maybe it's an open label thing that you're just seeing randomly. Well, that's where all that MRI data come in. When you look at the MRI data, those people who had disability improvement, they're showing signs of remyelination.
That was a statistically significant difference between disability improvers and those who did not have disability improvement, where you saw signs of remyelination in chronic enhancing T2 lesions. Very atypical. You shouldn't see that. The next part that was really important was brain volume. We showed something very similar, where those who had disability improvement had less loss of brain tissue over time than those who did not. Now for MS patients, you generally have rapid brain atrophy over time compared to people who don't have MS. We did not see that. We saw a statistically significant difference with the disability improvement. What you're seeing now is structural changes in the brain that really support this disability improvement that we're seeing clinically. When you put all that together, that again is very atypical for an MS population.
It either argues you're just having to get all that by chance, which is highly unlikely, or the ATA188 is actually really doing something meaningful for these patients. That's what underpins our excitement about the upcoming primary analysis in October. Note that that primary analysis kind of readout is gonna come out in October. There's gonna be 90 patients that are eligible for that. I highlight the 90 patients, 'cause remember I mentioned 15 patients hit the primary time point for the interim analysis. It's, I mean, it's less than it's around less than 20% of that total number. Really, we need a much larger sample size, like the 90 patients, to be able to actually have the proper readout that we're expecting.
Okay. What should we be prepared to see in October in your primary? Is it just the analysis around the primary endpoint? What level of detail should we expect?
What we committed to is to disclose top-line data. We've not yet confirmed which format will be the disclosure. Because there is a congress, for example, in October. We don't know yet whether that will be presented at the congress or differently. We commit to present top-line data, and top-line data in a way that will allow the investors community to make up their own mind about the potential that will be hopefully unlocked by this data.
We'll also at the same time move ahead with our partnering strategy, which I alluded to earlier, which is that we want to make sure that we can accelerate and expand the development of that product following the onboard readout into not only hopefully moving to phase III progressively through an end of phase II meeting and scientific advice, but also to be able to go into other type of MS indication and MS patients through other phase II studies. We'll be ready to move on after the disclosure, not only with the development of the product, but also with partnering.
Are there any questions from the audience? Oh, we've got a couple here.
The 1XX came out of Michel's lab and. He reported data at ASH on the 1XX, I believe it was autologous. How does that inform on your program, and what's the crossover there? Do they have rights that you guys don't have or vice versa?
I think it's MSKCC decided to license non-exclusively 1XX to different companies. There's one company that presented data at ASH and ourself as well for the allogeneic. That data at ASH were autologous, it's very exciting we believe, because it's de-risking a product, because before you go to an IND, you have already data with the same co-stimulatory domain in the same population. That's very nice in terms of de-risking the IND. Beyond that, the data showed that 1XX is really behaving in-patient as Michel designed it, which is to have less T-cell exhaustion that allows to have lower dose.
I mean, they have only 25 million cells, and durability of remission and safety. We're very excited because what we do with ATA-3219 is to combine together three elements that independently in the clinic have proven to be better than the existing CAR-T. One being the EBV-T cells, which have been proven in the clinic with a small study done by Sloan Kettering to be leading to 83% CR complete remission in advanced B-cell malignancies with long durability, with more than 26.9 months of follow-up and good safety.
1XX has been de-risked by the data and very exciting data showing that it's really a new co-stimulatory domain leading to less T-cell exhaustion and more, and very good safety as well. There have been also work presented at ASH on how a memory phenotype in an autologous CAR-T could lead to high level of response and durability of response. Again, we believe that 3219 is really trying to address all what is needed to have a potential best in class.
I do have a question. First, thank you for your 1XX data because we waited until your ESMO talk and until J.P. Zha talk at ASH before we submitted ours. We got our 1XX IND approved in 29 days. That was very good. My question though is about your MS product, and I may not understand it, but is this particular to EBV-attributed MS, and what percentage is that? What about the molecular mimicry for different types of influenza? Do you have any plans to do a product for that which was reported on probably 20 years ago? Is that correct that you have to HLA haplotype match the donor and the recipient?
Yeah. AJ, do you want to address that?
Sure. In terms of the EBV question, The theory and all the Science papers and Nature papers tell you all of MS has to start with EBV. EBV is the necessary trigger for MS. As Pascal articulated, there are other things. You need to have a genetically susceptible person for it, and there are some other environmental factors. You can have all of those things, and if you don't have EBV, you don't have MS. There's no subsets that we really have to focus in on.
It's really then trying to say, okay, once you have the EBV-driven disease, how do you eliminate just the cells that are causing that auto-inflammatory reaction? That's what ATA188 is designed to do. Get after those EBV-infected memory B- cells and plasma cells that are driving the auto-reactive disease. In terms of influenza, not part of the overall pipeline. At this point, I apologize, I forgot your third question.
We might just have to take that off. We might just have to take that offline just to... This needs to conclude. Thank you. Thank you to the entire team. Thank you.
Thank you.
Thank you.