Autolus Therapeutics plc (AUTL) Earnings Call Transcript & Summary

Okay. Good morning, everyone. Welcome to the 9:40 session of the Goldman Sachs Global Healthcare Conference. My name is Graig Suvannavejh. I cover European and U.S. biopharma for the firm. I've got the great pleasure of hosting Autolus this morning. And with us from the company are Christian Itin, Chairman and CEO of the company; as well as Andrew Oakley, who's the Chief Financial Officer of the company. So with that, thank you both for joining us.

Perhaps what I'll do is I'll just start from a very high level, and I'll start with you, Christian. CEO of the company, and you've been with the company from relatively early days. But if you could tell us kind of where the company is today relative to kind of the original vision of the company, and how do you feel you're executing on that success?

Well, good morning, Graig, and thanks for having us. Real pleasure to connect here. I think one of the things that we were looking to do with the company was to have -- build on a very strong technology base but really be focused on what are the critical clinical questions that we need to answer to get to significant clinical benefit in the indications that we're actually embarking on. And that has really been kind of the guideline for the company, is really to focus on clinical outcome and on the features that we believed mattered most in that particular indication that we were going after. I think that's been actually -- it's been staying in sort of the mainstay really in terms of the focus of the company. Obviously, we started this company about 5.5 years ago as a spin-off of UCL in London and have built it from scratch. So we're now at a point where we have our first program in pivotal stage and a second program shaping up very nicely and hopefully moving that as well into pivotal stage towards the end of this year, beginning of next year.

Okay. Very good. Maybe we can start at the high level because of CAR T space is a complex space in terms of the technology. There's a lot of competition in this space, various approaches. So maybe we can start out, for those who perhaps aren't as knowledgeable on CAR T, kind of where we are in the state of technology -- state-of-the-art, I mean, with respect to CAR T and how we can make sense of all the different approaches and how your approach is differentiated.

Yes. I mean there's sort of 2 key areas that -- on a -- from a technology perspective, people are focusing on. One is the source of the immune cell that you want to use to direct against the tumor. And there's a wide variety of immune cells that are currently being investigated. Obviously, the most knowledge we have about actual T cells, particularly patient-derived T cells. And that is also where we obviously have now the most significant clinical data to date that showed us transformational activity in B cell malignancies in a proportion of the patients and also in pediatric ALL. And what we're starting to see is also a very significant level of activity in multiple myeloma as well with 2 programs in particular. When we then look more broadly, there are obviously other cell types that are being investigated, whether this is different immune cells like NK cells or subsets of T cells, like gammadelta T cells. And there is also a drive to see whether you generate active immune cells starting from stem cells or iPSCs, a journey that's been tried for a long period of time. It's quite a complex journey but certainly with significant investigation. So there's quite a range of approaches here that look at various sources of cells. Fundamentally, we do know that the T cells, particularly the patient-derived T cells, are enormously potent. The other area is to actually look at what is it about tumors that may limit the activity of immune cells. And one of the hallmarks that we all learned over the last 20 years with tumors is that they have a remarkable ability to defend against the immune system. In fact, they need that to actually even be in a position to start growing out and start winning against the immune system. So there are layers of defense mechanisms. Obviously, the best described, the probably best known in the field are the checkpoint inhibitors. But there are actually many other mechanisms that tumors can deploy, and that is another area of development and technology development to actually counteract these defense mechanisms that the tumors are deploying. And so where we're actually focusing on is we start out with what we know at this point to be the most active immune cell we can use, and that's the patient-derived T cell and really deploy that technology to break through defense mechanisms that we know to be critical to overcome in order to actually get to significant clinical outcome. And that is sort of a series of technologies that we're deploying really tailored to the specific indication and, as we go from B cell malignancies towards solid tumors actually, are building an increasing level of complexity into our products to be able to address the more complex environment that particularly solid tumors are presenting.

Okay. I appreciate that. So we do have CAR T therapies that are on the market, others that have been submitted. What are the high-level challenges right now with existing CAR T?

If we look at the first generation of CAR T programs, I think the remarkable thing about the program is and has been and is today, is the fact that they can induce in leukemias and in lymphomas lasting responses. And in fact, when you look a leukemias, you look at the longer follow-up on diffuse large B-cell lymphoma patients, it looks like we actually managed to get a proportion of these patients into cure. So that's a very significant advancement, in fact, for those -- in those therapeutic settings. What that requires is obviously a very high level of clinical activity. And in fact, these products do have an enormous amount of clinical activity, but it also comes with a significant amount of adverse events. Typically, immunologically typed adverse events, and the 2 critical ones fall into the category of cytokine release syndrome and neurotoxicity, both of which do build as the activity builds in the patient. And it is not that easy to project how far an adverse event would actually go in intensity. And what that requires you to do is very carefully manage these patients and make sure you can actually interfere early on if you start to see the adverse event build and counteract, using products like tocilizumab or using steroids to sort of dampen the immune activation. And that has been sort of a hallmark of the first generation of products, that the amount of patient management required is quite substantial. And it also led to a predominant use of these products in academic centers' inpatient segments. Now when you're in an indication like acute leukemia, that is not that much of an issue because these patients because of their advanced stage of disease do require a lot of support, and they're typically treated in those centers as inpatients. It is a much bigger issue in indications like diffuse large B-cell lymphoma or follicular lymphoma, where, in fact, hardly any of the patients end up at the centers of excellence. Even in late-stage disease, they tend to be treated in nonacademic hospitals, in outpatient settings and in specialized oncology practices. But they're really treated in the periphery and not at the university centers. And that has actually been a challenge in terms of the market uptake of the products because they got limited to really a subset of the patients because of that need for intense management. The second area clearly is there is room for improvement in terms of efficacy. And so that is obviously a key area of focus as we move forward with the next-generation programs.

Okay. Maybe let's focus on your pipeline, and you referenced that you're in a pivotal trial with your most advanced asset, which is AUTO1. Maybe we could talk about what are the data that have been seen thus far for AUTO1? What gives you the excitement around its prospects for success in the pivotal study?

Right. So adult ALL is a quite challenging disease to tackle. It's a disease of bone marrow. It is very aggressive in terms of its growth, so it can grow enormously fast. And you'd often deal with patients that are elderly, that have had a previous exposure to high-dose chemotherapy as well as stem cell transplant. So they're actually quite beaten up in terms of their immune system and the fact that they've been exposed to a lot of toxicity. So it's a frail patient population, and that creates a very specific type of challenge because the disease requires you to have a product that is enormously active. Otherwise, you can't actually cope or catch up with the fast progression of the disease. The second thing is, because the disease has almost a stem cell like nature, you literally have to get every single one of these cells eliminated. If you'd have one left, the risk that actually the disease comes growing back is very, very high. So you need to actually have a very significant level of surveillance in this patient, the pressure on the leukemia to actually ensure that a response gets converted into a long-term remission and cure. And in fact, when we translate that into terminology typically used in the CAR T world is that it's usually referred to as persistence. It is the sort of the presence of your CAR T cells over time. And in fact, you would actually require those cells to be around for a year to 2 years in order to convert a response into a cure. The third element goes back to the fragility of the patients and the fact that they're -- have been exposed to a lot of toxicity. And that is that your product, despite having to be extremely active, also has to be safe. And that creates a very significant challenge in terms of actually getting that sweet spot right where you actually can come up with a therapeutic modality that can actually serve or create long-term remissions in these patients as a single-agent approach. And that is what we're designed in terms of the properties into AUTO1. And what we're seeing to date and what we have reported at the end of last year at an oral presentation at ASH is that we have very high level of molecular responses, very deep responses in these patients, above 80%. We also have seen that the event-free survival was twice as long as what you can induce with the standard of care, which is blinatumomab. And we've been able to get that level of activity without inducing high-grade cytokine release syndrome. The final bit, and that's the one that we're going to give an update on, in particular, at EHA in a few days, on Friday, in fact, this week, is, obviously, we're particularly interested in the longer-term follow-up on these patients. What we had seen is that we were able to see first patients reaching 1-year in molecular complete remission at the end of last year. Now obviously, what we are able to sort of report on is an additional 6 months of follow-up on these patients. And that starts to become very significant because there are very, very few therapeutic options that even give you any reasonable level of durability of effect. But frankly, to get patients into molecular remission that is sustained beyond the year is quite remarkable in that patient population. So we'll give an update on that data set with really a focus on durability of effect. And our view is that the program has an ability to be transformational. And this is exactly what we're pushing forward with the pivotal study.

Okay. And just for the audience to confirm that this update is on Friday. I think it had been rescheduled. So it is this Friday.

Right. So the data release at EHA was announced to be on Friday morning European time. And what we decided to do is to actually do our analyst call on Friday morning, Eastern Standard.

Okay, great. We'll be looking forward to the update there on Friday, but maybe we can -- a lot more attention seems to have been placed -- not placed, but attention is gathering on AUTO3. And Autolus seems to be talking about it more and more, about the opportunity for AUTO3 in relapsed/refractory DLBCL. I know you spoke about it a little bit earlier, but what do you think with AUTO3 makes it so interesting and so exciting from the Autolus perspective?

I mean what we were aiming to do with AUTO3 and the features that we wanted to design into the program were, on the one hand, addressing the challenge that we'd seen with the first-generation program that about 30% of the complete remissions that could be induced upfront got lost pretty much within 3 months. And so what we wanted to do is actually counteract that loss of CR. And what we did know from characterization that was reported on the first-generation programs, there was particularly 2 mechanisms that drove that relapse. On the one hand, it is the loss of antigen. So in essence, the tumor makes itself invisible to the therapy that we're deploying. And the second aspect is the upregulation of checkpoint inhibition on the lymphoma cells. And so what we designed is a dual-targeting CAR-T approach with individual CARs in each cell that have an ability to see either CD19 or CD22, each one optimized. And in fact, when you look at the molecular design we're using, it's different from anything that's been in the clinic, different in terms of binders, the way we activate, even the actual structure that we're using for the design of the CAR, particularly on the CD22 CAR side. So it's a very different design. And what we were aiming for with the design is obviously minimized the risk for antigen-driven relapse. But we were also interested to actually have a product that would actually give us a high rate of kill without secreting a higher level of cytokines at the same time. And so when we dig through the permutation and design work for the program, that was one of the key features we were actually screening for. So we knew the product had very low levels of cytokine release procured. And we were hopeful that, that would translate into a favorable profile from a cytokine release syndrome perspective. What we also were hopeful is that we might actually have a product that builds slightly more slowly to the full level of activity and would actually have less high of a peak but maybe a broader shoulder of activity. And one of the problems with adverse events, particularly immune-based adverse events, is that they're typically linked to the intensity, the peak of activity. So if you could actually curb that further down, we assumed and speculated that, that would actually give us even more advantage on the CRS but may also start help to us on neurotox. But that was the design principle. As we moved the program into development, we also added -- made the decision to add a cover with pembrolizumab for -- against the checkpoint upregulation. And what we're using right now is literally a single-shot of pembro a day before we actually dose the CAR T. So it's part of the conditioning regimen. What we did see on the efficacy side with the program is that, at that recommended Phase II regimen, we're reporting 63% CR rate, a protocol that was actually higher. But that is sort of on an intent basis. What we then also did actually, obviously observe was the points we were discussing related to the adverse events. In fact, we have no patient that actually has a grade 3 or higher cytokine release syndrome. And that is without make -- actually having prophylaxis in play. These patients are not being prophylactically treated to sort of curb the development of CRS. So no high-grade CRS. What we also did observe, and that was actually a quite unusual finding is that we have no neurotoxicity. It's not only no high grade, but we have no neurotoxicity. And when you think about the implication of having a low level of cytokine release and no neurotoxicity, actually, that addresses the 2 primary issues that you need to manage the patients for and that require you to really manage these patients in a sort of very controlled environment with the other programs. So what this opens up is now an ability to actually test whether this type of therapy could actually also be given in an outpatient setting. And we're currently running a 20-patient cohort to confirm that. So that's where we are with the program. So what we also have obviously is observation from their complete remissions we're able to induce. And with the exception of the first patient that reached a complete remission at the lowest dose and without pembro -- that patient had a relapse at month 12 -- there's no other patient that has relapsed to date, and we have seen no early relapses. So addressing -- it looks like, the technology we've been deploying, it has been addressing the fundamental principles that we were looking to improve on. And so what we now look to do is we'd like to confirm at the recommended Phase II dose the activity that we see at 3 months so that we understand at what level we're going to end up of a sustained CR rate in that population.

A recent development that the company has announced is this expansion for AUTO3 into the outpatient setting. I think it would be helpful to remind the audience, and you did touch upon it earlier, but how important that could be, particularly from the commercial opportunity for Autolus.

So I indicated before that the current programs that are active in DLBCL currently reach about 10% of the third-line DLBCL population. The hope is that some of these programs might get into the academic center outpatient portion that may give another 10%. So the max you sort of can get to is about a 20% of the market that you can actually address. What we believe that the profile for AUTO3 allows you to do is go substantially beyond that. And that actually allows you to start bringing this therapy actually where the patients are. And one of the things that we also obviously do observe is that if you then actually looked at early lines of therapy, if I go to second line, that actually becomes even more challenging. It's not 80% that are never going to be at an academic center. It's more than 90% that will never be at an academic center. So that ability to manage the product is incredibly important from a commercial perspective. And so what we want to marry up here is a best-in-class clinical activity, a sustained clinical activity with the best-in-class safety profile. And we believe that is sort of the key to be able to sort of break out of this rather narrow bracket where currently CAR Ts are confined to, to the place where actually the patients are being treated. And that is where the real opportunity is. And this is also why we're very excited about the program and the data as it shapes up.

Yes. And then, admittedly, as I'm learning more about the outpatient opportunity or at least where the patients are outside of the traditional academic centers and maybe extending that into the community, so to speak, there is still a level of sophistication out there in the community. So perhaps could you give us a color on the real-world perhaps uptake that you could see outside of the academic setting?

Well, I think what I'd like to start probably with is highlight actually that other than CAR Ts, all the other therapeutic options that are available to DLBCL patients are available to them across academic, nonacademic hospitals as well as specialized oncology practices. And that includes complex chemotherapies. It includes combinations with antibodies, combinations with antibody drug conjugates. And all of these therapies are complex to manage. They're not easy to manage. But these facilities can actually manage both the disease and the adverse events related to the disease as well as the complexity of rather sophisticated regimens that have to be administered with any of these other treatment modalities. That is sort of -- so when we talk about that, these are not clinics that are not focused or not sophisticated. They're actually sophisticated. But they may not have the level of access to a significant number of ICU beds, et cetera, that, obviously, academic centers have and may not have the exact same infrastructure that a stem cell plant -- transplant center, as an example, would have. But they're very sophisticated in terms of -- knowledgeable in terms of the patient population. And that I think -- and that is sort of, really, the places that we think that this type of a therapy can actually be delivered at and move to and should give us a significant opportunity in terms of market penetration beyond this very narrow set of academic centers.

Okay. With all of that momentum that you have with AUTO3, technically, you still have a go/no-go decision that you've been communicating. So maybe if you could just tell us, what are the key criteria that you need to see to feel comfortable with actually saying yes and giving the green light to the program?

I mean what we had indicated is that we're -- we want to see a sustained CR rate at 3 months of more than 50%. And that gives us sort of a pretty high hurdle, frankly. But at the same time, it will give us a very clear-cut profile to position the program as well. And that's what we're aiming for. So that's what we want to see. So we want to see kind of the 3-month follow-up on the patients that were treated with the recommended Phase II dose, and that will be sort of the key determinant for us to move forward. In parallel, we're running the outpatient cohort because, obviously, that information will be important to support then the design for the pivotal study as well, where the idea would be that we would also include centers that could actually treat in outpatient setting as well.

Okay. Well, we have been -- focused a lot of our time so far on your hematology, oncology interests, but there is the potential of CAR T in solid tumors as well, which is, I guess, a very exciting space not only for patients and companies but investors. Could you give us a sense -- I know you did an R&D Day last year, talking about the opportunity and why you think your technology is applicable. But could you give us perhaps a high-level view on how you think your technology can work in solid tumors?

Right. So this is obviously an area that we've been actually very focused on from a technology development perspective and an early development perspective as well. We actually will have updates on 2 programs at the second portion of the AACR conference, second half of June. And we'll have 2 programs that we'll present. One will be an oral presentation on a prostate cancer program. And the other one is an extension of the data that we had started presenting last year on our program AUTO6NG and, in fact, show the rationale and the -- for the use of this type of an approach in small cell lung cancer. Now what we've been doing is that we were choosing very carefully kind of the targets that we wanted to go after to sort of make sure we don't have -- that we're very clear about the complexity that we're actually tackling. And so what we did with the AUTO6 is actually tackling an antigen, which is called GD2, which is homogeneously expressed on neuroblastoma, Ewing sarcoma and gives us an osteosarcoma. And that gives us a very interesting opportunity to actually have an approach that allows us to sort of be very -- have a very good way of actually engaging all these tumor cells in that solid tumor and then to be able to focus on the immune defense mechanisms that the tumor might use against the CAR T cell and look to crack through that. In the first step, what we did is actually we derisked the targeting component that we're developing, CAR that we're developing against GD2. And what we're able to show is that we can actually induce -- in kids, at the 2 highest dose level, given we have 6 kids treated, 3 responded to therapy. And the important part is that they responded without actually having toxicity. And the toxicity of concern was neurotoxicity. It was toxicity for pain fibers. And that's a major issue in the first generation of antibodies that were developed against GD2 that developed the major pain syndrome in kids when we actually would give those to them. So we're able to actually have a very nice proof-of-concept for the GD2 CAR. And what we now did is we actually added to the product additional modules that act on the inside of the cell. There is one module that actually renders to cell insensitive to checkpoints, not just PD-1 but the family of checkpoints, by shutting down the signal transduction pathway on the shutoff signal, basically. And that is given on the inside of the cell. That module is called dominant negative SHP2. The second is we're shutting down the TGF-beta pathway. That's a very powerful pathway that sort of acts as a decoy and as a way to sort of actually prevent the T cells from even entering the tumor. And the second component we're adding is actually giving the cells a survival component. And that is a low-grade cytokine-like signal on the inside side of the cell. The beauty with that is that the cells actually keep going even if they're in a very challenging environment. They don't exhaust. They just keep going and keep working. And so this is the component that we've developed. We show actually the implication, the importance of that also in the lung cancer models. And it's a program we're gearing up to actually get back into the clinic with this much more sophisticated level of engineering in the first part of next year. So very excited about it, very exciting technology, and I think highly differentiated in terms of the way we actually have an ability to impact the tumor biology. And then on the prostate side, we're actually going one step further. And one of the challenges with prostate cancer is that it's sort of considered an immunologically cold tumor. Very little evidence that immunologically based approaches can make a dent in prostate cancer. So one of the things we're doing in that particular program actually is delivering locally in the tumor a low amount of Interleukin 12 that's produced by the T cell. And that actually changes that milieu, and it creates sort of a "immunologically hot environment." But it's done in a way that actually doesn't give you systemic toxicity, which is always a challenge with cytokines. And so this gives you just a flavor of some of the technology we're working on and how we're looking to impact the tumor biology, which is obviously more complex in solid tumors than what we typically find in hematological tumors.

Okay. You've got a broad portfolio of assets. We've just mentioned a couple of them, but you also have BCMA-targeting assets. And there's been a lot of investor excitement around some of the competitor programs that are perhaps non CAR T based but are using BCMA as an antigen. Maybe if we can just talk about BCMA and why that is so attractive as a potential target, and what are the initiatives that you have on BCMA?

Right. So BCMA has been around for quite a while. And in fact, we had -- in my previous company, we started a program back in 2010 that is now actually the Amgen BCMA program that's basically on the BiTE side. So it's been [ known for a ] while that the attractiveness of the target is really its selectivity. It's incredibly selective for plasma cells. The challenge is it can't be expressed at very low levels. And so you have to actually create an approach that gives you an ability to recognize cells even if they actually have very low expression levels of BCMA. But the selectivity, I mean, is quite exquisite for the antigen. And that's where the interest is. Obviously, we've seen some very nice data coming out of both Bluebird and Celgene as well as J&J and Legend which tell you that, indeed, this is a very potent approach, and it looks substantially actually more potent than what is today feasible with the bispecific approaches. And so what we're looking at is with the completely redesigned or newly designed program, is to see whether we're in a -- whether this actually would allow us to get substantially deeper responses, which is sort of the hallmark for long-term benefit in these patients. And that's one of the key questions we're asking. We're doing a lot of that work. As you pointed out, we have a lot going on. But there's also a good number of these programs that we are collaborating with academic collaborators and have exploratory translational studies that give us actually a very good and important information about the performance of these programs and give us a very efficient way to then actually determine which ones to take forward into later-stage development.

Okay. I'm getting this question a lot by investors on BCMA itself. And it's the ability of BCMA-based CAR T to be positioned or compete against BCMA bispecifics or non-CAR-T approaches. How should we think about the 2 fitting side by side, so to speak?

I think the way I would -- first of all, one of the things I learned the hard way in this business is that the only thing that matters for patients is outcome, and that holds true for physicians as well. Technology is irrelevant. What matters is outcome. And I think that's the way to look at all of this. When I look at the data that we have across these various types of technologies, the most compelling data at this point, I believe, we see from the J&J program, with very deep responses, very high response rates, almost 100%. And that gives you a very significant level of activity that will be challenging to actually beat with any technology, frankly. So I think we need to be guided by data. And it's the clinical data will tell us that. The -- a lot of the other approaches are -- clearly, they're there. They have some level of activity, but they're nowhere close in terms of activity at this point. That may change over time, but at this point, that's the way that field looks. And so it will be very interesting to see how it develops. I mean, I think the hope for a lot of the other approaches is to try to move very rapidly to early lines of therapy. But again, the options there are significant with the triple combos that are available, et cetera. So you get into very significant trials, very significant trial sizes to prove that, indeed, you're going to be superior to the current therapies. One of the interesting thing about this space is that it is enormously expensive from a therapeutics perspective because we have a lot of products that are on patent, and they are given in combination. And so one of the arguments that you may hear at times about the potential cost of the CAR T, I think, is actually very much offset by the current cost of therapy that we have on the current therapeutic options. So this is all about outcome in this population. And what we're seeing in the third-line setting at this point is quite remarkable on the CAR T side. And a lot of the other therapies, we probably need to see combination data of some sort to see whether they can get into a similar ballpark of activity.

I just want to, again, stay on this topic of you having very broad pipeline, and you guys highlighted number of assets. Are there any other assets in particular, perhaps 1 or 2, that you think, in the near term, investors should be focused on or perhaps paying attention to?

Well, obviously, the key drivers in the short term are really the most advanced programs, and those are the programs on the B cell side. Behind that, obviously, we're building out the activities and franchise on the T cell lymphoma side. One program in the clinic, the other one, we're also actually going to show an update on the preclinical work at AACR. So that's the next one that's coming up. And then there are several programs that are entering translational studies in the upcoming 6 to 12 months. So for now, the short term, very much driven off the B-cell programs. But I think we shouldn't lose sight of the fact there is significant opportunity on the pipeline side, which also actually creates opportunity also to collaborate going forward on some of these programs as well.

Okay. And given all the activities that are going on, I think the question has come up around partnership and what makes most sense for the company, where they should focus. So what are the current latest thoughts on partnership activity around your programs?

Well, one of the nice things at this point, of course, is that we have an unpartnered pipeline, so that gives us a lot of opportunity. And this is clearly an area that we're exploring, which makes -- as you would expect us to do. And it all will be driven off the opportunities that we can generate around them and whether those types of transactions will make sense or not. But that's -- obviously, these are ongoing conversations as we always have, frankly, over the years, had. And it gives us sort of an excellent way to sort of -- creating optionality for the business as we're moving forward. And very excited about where we are with our lead programs.

Okay. And we've got maybe several minutes left in our fireside chat this morning. And maybe I could touch upon some kind of more housekeeping questions on cash. Obviously, COVID-19. Early on, there was perhaps a concern that the company wouldn't be able to on find the opportunity to finance, but we see that that's not the case. But maybe just to revisit kind of where the company's current state of finances are. And maybe I'll turn this over to Andrew. As the Chief Financial Officer, [ what are your ] comments?

I mean, look, we had $243 million at the end of the March quarter. Our guidance is still the same, that we see that lasting into 2022, so get us through '21.

Fantastic. And then obviously, with a lot of -- you've got an event happening this Friday that investors will pay attention to. But maybe broadly speaking, just on upcoming milestones and catalysts. Just to recap, I know we've talked a lot about in this call what the next milestones are. So whether that's for Andrew or Christian, if you could comment, that would be helpful.

Right. So in terms of the upcoming milestones, obviously, very much this June actually ended up to be incredibly a data-rich month, probably the most data-rich month that we had in the history of the company with 3 conferences back to back. Obviously, we have EHA with the AUTO1 data and longer-term follow-up, which is important to understand the clinical benefit that we can induce in this population. We then have 3 presentations at the AACR meeting coming up on the big clinical programs: 2 solid tumors, 1 B-cell lymphoma program. And then obviously, we're gearing up for the end of the year, where we have an opportunity to a significant -- for a significant update, actually, on the AUTO3 program with a good number of additional patients, the outpatient cohort; but also additional patients at the recommended Phase II dose level; as well as longer follow-up, getting back to the point I was making before about the importance of sustaining CRs, not only inducing them but then sustaining them. So we think it's going to be a very important update that we're going to have at the end of the year at ASH. And then obviously, as we get into next year, a significant opportunity in the first half of the year on some of the translational programs, but obviously, continued updates on the current programs as well.

Okay. Great. And maybe with the very last question asked, and it's a very high level, and obviously, CAR T has been an area where there has been M&A activity, and it was very busy a couple of years ago with Celgene, Juno, Gilead Kite. But what's your sense of the temperature on large companies and their continued interest or not in the CAR T space and whether you think there will be additional CAR T deals?

Well, what's interesting about any technology, and you look at technology sort of go through cycles of excitement, often in the absence of data to data and then actually to a transition to prove you can translate it in commercial success. And as indicated upfront, we did very good in the first 2. The third one was somewhat of a disappointment because the expectations for the sales of the initial CAR T programs were substantially higher. Now it's very well explainable why we see the sales we see and what needs to be done. And I think we're at this stage where -- we're at the -- in the show-me phase, where we need to demonstrate that, indeed, we get the right profiles not only to actually get to very significant outcomes but also to actually get the products where the patients are and get them actually in a place where they can actually be treated. And I think that's the stage we're at now. And it's actually a very exciting phase because it looks like we're starting to cracking some of those fundamental challenges. And I think what that will do, as it always does with clinical data that moves forward and shapes up, is it creates a lot of new interest. So we're going through cycles as we do always with technology. And we've gone through, I think, a challenging phase as a space for the last probably 1.5, 2 years. But I think we're starting to come to kind of a place where we see very significant levels of activity and underlying -- addressing some of the underlying limitations that we were observing in the first products.

Okay. Well, thank you for that perspective. And thank you again, Christian and Andrew, for joining us in our fireside today. I look forward to our next call and also look forward to [ a successful conference ]. So thank you very much.

Excellent. Thank you very much. Thanks for having us.

Thank you.

Thanks.

Cheers.