Autolus Therapeutics plc
Q1 2021 Earnings Call Transcript

Published: 10 May 2021

[Operator:]

Hello, ladies and gentlemen, and welcome to the Autolus Therapeutics First Quarter 2021 Financial Results Conference Call. As a reminder, this conference call is being recorded. I would now like to turn the conference over to your host, Mr. Andrew Oakley, the company's Chief Financial Officer. Please go ahead.

[Andrew Oakley:]

Thank you, Rebecca, and Good morning or good afternoon, everyone and thank you for taking part in today's call on the financial results and operational highlights for the first quarter of 2021. I'm Andrew Oakley, the Chief Financial Officer. And with me today is Dr. Christian Itin, our Chief Executive Officer.

[Christian Itin:]

Thank you, Andrew and good morning to all of you. And thank you for joining us. I'm pleased to review our progress for the first quarter of 2021. First and before we get to the update on our programs, we're very pleased to see the progress in the US the UK and the EU with the COVID vaccinations and seeing gradual decline of the case numbers. This bodes well for the conduct of clinical trials as we move through 2021 and into 2022. With the expected opening of travel for vaccinated people between the US and Europe, we also expect flight operations to start to gradually normalize, which will relax the pressure on logistics. We continue to work hard with our supply chain and logistics teams as well as our clinical centers to ensure timely continental and transatlantic deliveries of leukapheresis final products and samples for analysis in order to support our clinical trials and ensure timely data availability and integrity. While we feel optimistic about the developments, we continue to monitor them very carefully with a particular focus on patient safety.

[Andrew Oakley:]

Thanks Christian. If we move to Slide 14, it's my pleasure to review our financial results for the first quarter of 2021. So starting with our cash position, cash at March 31, 2021, totaled $239 million as compared to $153.3 million at December 31, 2020. In January of this year, the company sold 1.7 million ADSs under its open market sales agreement, resulting in net proceeds of $15.3 million. And in February '21, the company sold 16.4 million ADSs representing 16.4 million ordinary shares in a follow-on public offering, including the exercise informed by the underwriters of their auction to purchase an additional 2.1 million ADSs at a public offering price of $7 per ADS yielding net proceeds of $106.9 million.

[Christian Itin:]

Thanks Andrew. And let me conclude this part of the management discussion on Slide 16 with a recap of the major messages from today's call. The company is in a good position and combined with our cash on hand we feel well poised for success. We're very excited about the AUTO1 program and continue to enroll into the FELIX study in adult patients with ALL and expect to report data in 2022. We started the Phase I program for the AUTO1/22 product in pediatric ALL patients at the end of last year and expect first data to read out in Qq4 of this year. Additionally, we expect first data from the ALLCAR extensions program at EHA to give us first data on patients with non-Hodgkin's lymphoma. We're also planning to expand AUTO1 to primary CNS lymphoma with a CAR cell study, which is actually expected to start imminently. As indicated in our business outlook in January this year, we have announced a renewed focus on the AUTO1 program while intending to partner AUTO3 for the treatment of DLBCL patients. Additionally, we expect Phase I data from our AUTO4 program for the treatment of patients with peripheral T-cell lymphoma later in the year and expect multiple next generation development candidates to enter clinical development over the course of 2021 and in 2022. Finally, with our successful recent race, we are in a position to strength the cash runway into the first half of 2023. We're now happy to take questions. Operator?

[Operator:]

And your first question comes from the line of Maura Goldstein.

[Mara Goldstein:]

Great, thanks so much. I'm wondering if - since we're expecting data on both the ALL programs, starting in the fourth quarter of this year, and then obviously the FELIX program in 2022. If you could maybe just sort of wrap some color around what we should be anticipating in terms of number of patients' duration of treatment. And then secondarily, on the AUTO8 program, you're going into BCMA direct CAR and I'm just curious as to what your thoughts are from a competitive landscape perspective, given the development in that space and whether or not AUTO8 may, to some degree suffer the same fate as AUTO3 in terms of your prioritization and how you think about developing that?

[Christian Itin:]

Thanks Mara. I appreciate the question. So first, with regards to the work we're doing in the ALLCAR study to sort of explore the activities in the non-Hodgkin's indications as well as the CAR cell study for patients with primary CNS lymphoma. Those are exploratory studies. So we're basically having a part of the ALLCAR extension. We're having cohorts of approximately 10 patients each in each of the sub indications. And that is what we're expecting to actually report on at the end of the year. So it gives us a - overall will give us a nice additional set of patients and I think will give us a good feel for the performance of the product that we're seeing across those various indications. On the pediatric study, with the AUTO1/22 program, obviously, that's a classical Phase I study as well. And we expect the study to be enrolled by the end of this year and data available by - for the - for all of those patients. In terms of follow-up I'll say the follow-up will be limited because most of these patients are being enrolled and treat into the course of this year. So we're looking at typically at a few months of follow up for these patients on average. The third question or area that you were touching on is the AUTO8 program and basically the competitive environment in the multiple myeloma space. Now obviously, with the approval of hydrocele, but also the J&J program actually getting close to market as well. So what we're doing with this program, and again, this is a program we're running, first to an exploratory Phase I study on the academic side, is to actually evaluate whether Indeed, we can actually induce high degree of deep responses in patients and whether we do see a good level of persistence of the product. Both I think we believe are characteristics that are important to actually provide a product that has an opportunity for a differentiated profile. You're absolutely correct in asking the question, what about the profile that you actually need to meet. And clearly, we do set a very high hurdle for a multiple myeloma program, given where the standard of care is. Not just from a CAR T perspective, but overall, the standard of care, obviously, is. Has been moving quite significantly over the last few years and we clearly would need to actually see a good probability of inducing true long-term remissions in these patients, which is still being the challenge to induce with frankly, any modality at this point in time.

[Mara Goldstein:]

Okay, thank you. And if I could just ask, Andrew, can you remind us on the ATM program, what is less outstanding on that program?

[Andrew Oakley:]

Yes, Mara I can. It's around $80 million.

[Mara Goldstein:]

Okay. Great. Thank you very much.

[Christian Itin:]

Thanks.

[Operator:]

Your next question comes from the line of Matt Phipps.

[Matt Phipps:]

Hi, guys, thanks for taking my questions. Christian, I guess first EHA, which I abstracts would be coming on next week. Should we expect some data across all three cohorts from that ALLCAR trail or that just mainly going to be indolent assays beyond the four patients at ASH?

[Christian Itin:]

Thanks for joining Matt. The update will be focused on the indolent cohort.

[Matt Phipps:]

Okay, thanks. And then kind of following up on AUTO8, I guess, UCL posted the trial of a BCA CD19 dual CAR for BCMA or for multiple myeloma. And just wondering if you're - that's when we can talk about the decision to use CD19 here versus maybe some of the newer targets like bispecifics have shown such as DDRC 5d .

[Christian Itin:]

So the way we're thinking about the AUTO8 program is that the program is anchored in - with –on - through the BCMA CAR. The CAR that we designed there actually has a very - quite a different binder to - in terms of properties as well to what has been - worked so far in the space, and also use of the different actual design in terms of structural design that we're using for the receptor. So it's a significant change to certainly what we've have initially in our AUTO2 product, but also what we're seeing across the current programs that have been moved forward. So that's the anchor basically and what we're looking to get to is, as indicated, responses, which is really the hurdle that the program needs to take first to be sort of be moved forward. The next layer of questions that I think we need to address in this space is do you actually get to a long level - an extended level of persistence, which has been actually quite challenging in multiple myeloma where you look at the common programs that the data that's reported - has been reported so far. So what we're looking to actually add is an element that actually gives us an extended persistence with the program. And the third area actually will be to address the quite heterogeneous as well as challenging microenvironment that we find in multiple myeloma. The reason why this is still a disease study is basically we can buy time, but we have a hard time getting to a cure. So there's still remnants of tumors that we can't get to and there's situations that were clearly very challenging to sort of actually for anyone illogical, and frankly, any other approach to currently crack. So those are the three layers that we're basically working on. And so in terms of the target antigen that we're using, there is a - an importance there is to actually drive persistence, which is a key aspect of it, and potentially actually support some of the driving cells that we see in multiple myeloma to be able to actually get up those, which may actually, in part carry BCMA but also maybe in part BCMA negative.

[Matt Phipps:]

Okay. I mean, you kind of touched on this, but I mean, especially with the J&J product, I mean, the CR rates are extremely high. Do you think you can meaningfully -

[Christian Itin:]

Correct.

[Matt Phipps:]

Or I guess is their ability to meet or beat that as opposed to just want it - the real thing here is to drive better persistence to get that improved PFS beyond is meaningful beyond the year for PFS.

[Christian Itin:]

You're right in pointing out that obviously, the CR rate per se is very high. But I think the more interesting part of the data is that the depth of the CR rate actually is correlated with the length of outcome. And what you need to drive towards are very deep responses, very stringent molecular CRS. And that is actually where you start to see differences, also differences between hydrocele and the J&J program. And that is the area that you really need to actually drive. So it's actually to look at a very high level of stringency with regards to the molecular CRS that you're actually looking at. And that gives you an early readout. And then you're right, the next level is very clearly that you need to actually drive for persistence and have an ability to actually keep the product active over an extended period of time. And the third aspect as proceeding with the - in the space is certainly also related to the overall safety profile that we're seeing as well.

[Matt Phipps:]

Great and kind of last broader question, given kind of what we've seen with AUTO1 on the level of expansion and persistence and safety. Do you keep that in mind as far as using a lentiviral system with this construct, and just maybe with different scFvs in programs going forward or how you manage kind of the different backbone, so to speak of programs?

[Christian Itin:]

I think in indications where persistence is important to sort of actually get to long-term benefits. We're clearly do you see a benefit of using the lentiviral pro - lentiviral backbones. And that's obviously what we're using in the context of the - obviously, leukemia as well as multiple myeloma you'd be also be looking at a lentiviral backbone.

[Matt Phipps:]

Okay. Thanks Christian.

[Christian Itin:]

Thanks a lot Matt.

[Operator:]

Your next question comes from line of Gil Blum.

[Gil Blum:]

Everyone good morning, thanks for taking our questions. So within focus of manufacturing in the UK, it does offer some logistical issues in treating patients in the US.

[Christian Itin:]

Well, thanks a lot for joining Gil and a very good question. Obviously, we do it - we actually manufacture for our clinical trials currently out of the UK, out of the manufacturing site that's located north of London in Stevenage. And we've been able to actually serve all the various geographies within the US, obviously, as well as across Europe, within the timeframe required to actually shape not only frozen leukapheresis, but also fresh leukapheresis. So we can actually manage the logistics very well. Even - and we're able to do that even during the most limited flight patterns that we had during the course of last year. So we don't think that actually that adds a significant component here in terms of either time or risk from a logistics perspective.

[Gil Blum:]

Okay, thank you. And maybe a little bit about AUTO6NG here. So neuroblastoma in children is a relatively small market. Could you kind of remind us what the specialized features of AUTO6 engine? How those might translate across your solid tumor platform and learnings that you could have from a study in relatively small indication.

[Christian Itin:]

Right. So the AUTO6 program AUTO6 started out with a chimeric antigen receptor targeting GD2. Was first asked the question, can we actually generate an adequate therapeutic window targeting GD2, understanding that there is a low amount of GD2 also present in pain fibers. And that basically, that question was answered through the first trial. That was the publication that we had at the end of last year in Science Translational Medicine. The next question, however, is then once you have an ability to target is to actually address the challenges that are derived from the microenvironment that is present in neuroblastoma and frankly for that matter in most solid tumors. What we're doing with the program is actually building quite significant level of resilience into the cells, into the CAR T cells and we do that in three different ways. On the one hand, we're actually rendering the cells insensitive to checkpoints, or checkpoint signals by using an intracellular available dominant negative version of SIP2, which is a protein that transmits normally the signal from a checkpoint onto a T cell receptor and the chimeric antigen receptor, the dominant version of it have shaped to actually abolish a STAT signal transduction and with that, basically renders the cells insensitive to that negatively to that negative set of signals coming checkpoint receptors. The second element is TGFBeta, which is certainly one of the ways and have tumor cell actually defend and fend off T cells and other immune cells with this over distance. Here, we're rendering the cells insensitive to actually transmit the TGFBeta induced signal into the interior of the CAR T cell. We're using, again, the dominant negative version of a receptor sub chain that is part of the TGFBeta receptor. And the third element that we're adding is constitutively active IL-7 signal actually using a receptor that sort of actually gives you an IL-7 like signal on a constitutive basis. And what that does is actually - it actually helps the CAR T cells to keep activated. And actually, even if they receive negative signals from the environment, keep overcoming those. IL-7, just as a as a reference is, also, what we're inducing when we actually do the conditioning regimen, the phimostretch up from any of the CAR T therapies, it's actually tendocel IL-7 and IL-15. And obviously, with the very same reason to actually help the CAR T cells actually pay cold at that point. And in the case of actually having this signal engineered into the cells to actually keep them going, even if the environment actually is difficult to manage. Now these three components are just talked through, obviously, are components that are relevant for any program, we believe in the solid tumor setting. And hence actually the data that we're going to be generating in neuroblastoma will be important not just for neuroblastoma, but across our various programs also, that we've been working on towards other tumor entities as well. So I think that is sort of the important part. The reason why we're actually exploring these modules in neuroblastoma, first, is because in neuroblastoma we have homogeneously expressed target antigen, the case of GD2, which actually takes one of the elements of variability out that you often have with a tumor associated antigens, which often are highly variable in their expression, think about HER2 or EGFR as an example, which are - have a wide range of expression across cells within a given tumor sample. And that obviously creates a lot of challenges, in fact, and if you try to interpret results you actually generate. So here we have a homogeneous background. It's a high medical need setting, it's a pediatric indications. There's obviously a very good fit with the pediatric work we're doing in ALL from a center perspective, from a commercial perspective as well. But it also gives us a very good background and clean background to actually establish those additional modules and their utility in the solid tumor setting.

[Gil Blum:]

It was very helpful. And last one on the indolent lymphoma program. Could you remind us how important is having a safer lower CRS CAR T product in this patient population, maybe with a look at competitive programs here? Thank you.

[Christian Itin:]

Thanks Gil. It's a very important question because obviously, when we look at the CAR T experience so far that we have through the initial programs that reached the commercial stage, is that we - although we expected the CAR Ts to go where we brought in a lot of their indications, DLBCL first, but then also, now with approvals in follicular mantle cell that we should be able to reach a large proportion of patients. And the reality is we haven't been able to do that. The fundamental reason why that didn't happen is that actually managing the CAR T therapy in centers outside of highly specialized transplant centers has been really difficult. And it's difficult from a handling perspective, from an infrastructure perspective, from a cost perspective. And so the adverse event profile and in fact and the logical adverse event profiles of the product actually has significantly limited their commercial use, and frankly, have limited their ability to actually reach the majority of the patients in those disease settings. Now, if you go into a disease setting, like in follicular lymphoma, or also mantle cell lymphoma, or CLL for that matter, is that those patients very often are treated much more into the periphery, even more so than what we're seeing in DLBCL as an example. And that actually creates a very significant need for an excellent safety profile so that indeed, the therapy can be managed outside of the highly specialized academic centers. And that's really what is the core and what is needed in terms of the commercial translation of these of this therapeutic approach to reach a broader range of patients in the respective indications.

[Operator:]

Your next question comes from the mind of Eric Joseph.

[Unidentified Analyst:]

Hi, good morning. This is Rahul on for Eric and thanks for taking the questions. Just a couple from us, firstly, on AUTO1, how do you assess its potential in the earlier line settings and adult ALL? I mean what kind of response and durability would be seen as clinically meaningful relative to the existing treatment landscape? And then is it safe to say that the initial approval would likely be in the third line setting, followed by a potential label expansion based on the continuity PSP study?

[Christian Itin:]

So thanks a lot for joining. And thanks for the questions. Obviously, where we're starting with the development for AUTO1 in ALL is the last line setting. The challenge at that point that the patients have is that they've already experienced an enormous amount of cytotoxic agents and as a consequence of that are both highly immune suppressed, but also are overall in a rather poor condition because of the high level of cumulative toxicity they've been exposed to. So in that sense, it's actually a very difficult population to deal with both from a safety perspective, but also from a disease perspective, but obviously, because obviously with every line of therapy, you keep selecting the source that withstand, obviously, that particular line break through, and actually at that point, obviously are more difficult to treat. And so starting at the last line setting and actually showing a significant level of activity in this last line setting bodes extremely well in terms of the potential of the product in an earlier line. This was also exemplified very nicely by the experience in adult ALL patients with blinatumomab or Blincyto, where the last line or third line data was showing a complete remission rate of approximately 42%. However, in frontline consolidation in patients who actually have gone through front line induction chemotherapy constipation cycle one, and at that point still have minimal residual disease, which was obviously was resistant to chemo. In that patient population, Blincyto actually showed 78% complete remission rate. So in other words, what we're seeing is that as you move up - and this is obviously also T cell mediated activity, as you move up, we would expect actually that the activity we're seeing and the benefit that we're seeing induced in the third line patients to substantially improve as we go into early line of therapy. And that is what we would expect to see and clearly, in terms of the settings that you can think about is similar to what I just said with regards to frontline consolidation of high-risk patients is one setting you might want to go. Or you could also contemplate a more practical second line setting either in patients that are ineligible for transplant or patients that are eligible for transplant. Those are the basic settings that you can choose to actually move the product into an earlier line of ALL therapy.

[Unidentified Analyst:]

Thanks. Thanks for the color. And then on AUTO3, can you maybe clarify of the Phase I/II ALEXANDER study is a store for additional data readouts and useful in 2021 such as survival follow up and safety data from the outpatient cohort?

[Christian Itin:]

Right, so on the on the AUTO3 program, we're in the process actually of writing up the data in a publication. Given that we obviously had four oral presentations of that last year, we feel it's the right time to actually now show the full picture of the data, which is only possible in a limited way in 10-minute presentations. And hence we're moving to a publication, which we're hoping to publish during the course of this year.

[Unidentified Analyst:]

Great, thanks for taking the questions.

[Christian Itin:]

Thanks a lot. Appreciate it.

[Operator:]

Your next question comes from the mind of Kelly Shi.

[Kelly Shi:]

Good morning. Thank you for taking my questions. I have a question regarding AUTO4 in T cell lymphoma. So what kind of patients do you enroll on his trial? And what does the competitive landscape look like? Also for the ASH update as of this year, should we expect to see meaningful advocacy laid out? Thank you.

[Christian Itin:]

Thanks. Thanks a lot Kelly, for joining. So the patients we're enrolling in the AUTO4 Phase I trial are patients with peripheral T cell lymphoma that have failed, obviously, not just the frontline therapy, but typically three lines of therapy before they actually get onto our trial. So these are very advanced patients that we're enrolling into the trial. What we're expecting to see towards the end of the year is obviously, we're going through the dose escalation with the program and we expect data from currently, but we would assume data from three dose levels that point in time, potentially a bit more than that, but that's sort of the ballpark that we're looking at. So we're looking at the dose escalation and obviously, the readout related to that. In terms of the data that we expect to see as obviously safety data as well as tumor assessments in those patients and pharmacological pharmacodynamic type of data, which would give us a good understanding of the performance of the product in that setting. From a competitive perspective, at this point, I would say the competitive environment in PTCL late-stage setting is rather limited. There's obviously the subset of patients that are CD30 positive which are eligible for brentuximab, which is unfortunately only a small portion of the patient population. For the patients that are not eligible for brentuximab obviously, the current opportunities are predominantly actually to participate in clinical trials. So in that sense, there is not there from a commercial perspective or therapy perspective on the market. There is a very small sort of set of agents that are currently available, predominantly related to high dose chemotherapy, potential transplant and if your CD 30 positive printout.

[Kelly Shi:]

Thank you very much. Also have a follow up for AUTO6. I'm just wondering so far, the safeties which incorporated in CAR. At what juncture would a physician be allowed to trigger the safety switch?

[Christian Itin:]

So when we designed the original AUTO6 program, obviously, the question that we had was really the question around the safety of the product and whether indeed, we could get access to clinical activity without inducing significant neurological toxicity, in this case a very major pain syndrome. And because we couldn't predict whether or not our hypotheses around design actually would be working out, obviously, we did put an off switch into the product, which would allow the product to be eliminated, should that become a necessity. With the product actually having gone through the initial exploration in Phase I in neuroblastoma patients without actually inducing that type of toxicity, I would expect that it's quite unlikely that a physician would actually want to use the switch and certainly we didn't have a need to use it. I think in general, when you actually offer switches built them into your product, it's really the physicians decision. And it's the physicians call in the end whether or not to actually, frankly, abort the therapy, which is what it is, right. In this case, you would be providing a dose of rituximab, which would take out the CAR T cells, at which point you'd literally abort the therapy. So you do that clearly if you have indication of a significant level of toxicity that you have a heart controlling. And - but this is ultimately the decision of the treating physician that - where that - frankly that station has to decide.

[Kelly Shi:]

Thank you very much.

[Christian Itin:]

Thank you.

[Operator:]

Your next question comes from the line of Asthika Goonewardene.

[Asthika Goonewardene:]

Hi, guys, thanks for taking my question. I got a couple of AUTO8 if I may. Can you - Christian, can you talk about the design features of the CAR that could help you get more of those stringent CRS or more patients into MRD negativity? And then what items in your toolkit are you incorporating that could help AUTO8 overcome some of the suppressive factors in the tumor microenvironment? And then I have a follow up on AUTO1.

[Christian Itin:]

Okay, well, thanks Asthika for joining. What we're really were working towards and what the design work that we've done with receptors actually was Tier 2, is to get to a very high level of cytotoxic activity of the product against multiple myeloma cells that express very low amounts of BCMA. What we had published earlier is that the range of BCMA expression can vary quite a bit in these patients. I can be as low as 10, 20 receptors per cell, up to - in below four receptors per cell. But in general, it's an order of magnitude, two orders of magnitude below of what as an example 19 would be. So the real challenge is, how do you get to these cells that actually express very low amounts, and to sort of be still be very active on those cells. And that is really the test that we applied. And we did actually test a range of different types of pagers, as well as designs on the receptors that choose to - for exactly that ability to give us a very high level of activity against those multiple myeloma cells that express at very, very low levels of BCMA and it still has to work there. That's really the optimization that really was driving the selection for those features on design, et cetera that will give you exactly that outcome. So it was a series of designs tested for that particular outcome. And that is actually how that - how we sort of actually addressed the fundamental question that we believe is at the heart of the improvement that needs to be done. With regards to the toolkit, I think what I just went through with regards to the key elements that we're using, as an example for the ATO6NG program, actually, those elements all we believe would be relevant as well in the context of multiple myeloma. The exact composition we haven't disclosed at this point, but I think any of these modules actually would be we believe supportive in terms of activity and then - and drive further activity in that setting.

[Asthika Goonewardene:]

Great, Christian. And then - yeah, so just over to AUTO1 here, so there's data that suggests that deep upfront response may be a driver of durable or maybe durability in DLBCL. Do you think this data in the public domain does suggest that this also is the case with indolent lymphoma? Or is persistence something that's more important in this setting? Kind of to put the question another way, I'm trying to figure out, how does AUTO1 do better than let's say Axi-cel, which also generates some data in interval?

[Christian Itin:]

Right, so it's an interesting question, actually, in terms of depths of response. I think the best data and also correlative data with outcome that we have across the B cell malignancies is actually in ALL, where we have excellent data sets that actually show the impact of molecular responses, and the importance of reaching molecular responses to outcomes. Whether you're looking at patients who do receive subsequent transplants, or whether you look in the context, obviously, of other therapeutic modality. But getting to a molecular response is critical for a chance to actually have a long-term outcome. If you don't achieve that the disease will come back very, very quickly. The data set that we're seeing in multiple myeloma starts to point quite similar way, as we talked about before, and I think is sort gives us a very similar picture. I think that that we're starting to gain more information around non-Hodgkin's lymphoma more broadly. But the data sets are probably not quite as strong yet in terms of the correlation between the molecular remission as well as the long-term outcome with the data that is still actually being generated. But in general, I think there's a sense that getting to very deep responses matters, obviously in a significant way, in this disease settings. With regards to follicular lymphoma, I don't think there is enough data to use it as a guide quite yet. But I guess we're looking into the next two or three years, I would expect the field will start generating much more substantive data sets that will get much more conclusive answers around the correlation of molecular remissions and durability of response in those settings as well.

[Asthika Goonewardene:]

Great, thanks, Christian.

[Christian Itin:]

Thank you.

[Operator:]

Your next question comes from the line of Robert Burns.

[Unidentified Analyst:]

Hey, everyone. This is Jay on for Rob. My first question is on AUTO8. So thanks for the color on the optimized design. And do you think that would potentially help in eliciting lower CRS and neutropenia than something like J&Js asset, which showed pretty high rates in Phase I study? And do you think the field has evolved to manage some of these toxicities? In other words are these a major barrier to adoption? And a quick question on AUTO1 allogeneic program, can you provide like an update on when you're potentially going to initiate a study and type of patients and maybe even the target? Thanks

[Christian Itin:]

Thanks a lot for joining Jay. The question related to sort of multiple myeloma and the type of safety segments that we're seeing, I think that what we're obviously having multiple myeloma is a disease that actually is present - similar to ALL its present in the bone marrow, and it has significant impact on the onset of the health of the bone marrow of the patients. And that obviously, can drive - ultimately has an impact on cytopenias et cetera and prolonged cytopenias, of course, as well. So I think it is - we have an element here that's intrinsic to the disease, we then obviously, working with therapeutic approaches that actually are highly active and have to be highly active in the marrow and can drive significant levels of cytokines in these patients in the marrow as well, which can have actually a negative impact on the bone marrow's ability to regenerate. I think what we what we'll have to see and we probably need a bit more data on that in general in the field is at which point does the marrow actually start to recuperate and sort of actually start to compensate - basically rebuild its ability to properly function. It is - that is something I think that we just need more data on and I'm not sure there's a good lead at this point that will give you a sense around design premises et cetera, that you need to actually look at to improve the outcome with regard to these types of toxicities. Second question that you raised was related to the activity that we're doing having on the allogeneic side that - the program that you're referring to is also one. Obviously, that is in collaboration with our academic partners. And we expect that program to actually get going towards the middle of the year and we'll report at that point in time and give an update kind of where we're going with the program. So we'll still need a bit of time here to actually before we're going to start talking about it in more detail. But that program is obviously, on track to be initiated during the course of this year and down the clinical side.

[Unidentified Analyst:]

Thanks.

[Christian Itin:]

Thank you

[Operator:]

At this time, there are no further questions. Do you have any closing remarks?

[Christian Itin:]

Well, first off, thanks a lot for joining. Really appreciate your continued interest and support. And we're looking forward to keeping you updated. Obviously, next few updates for us will be at EHA. All right, thank you very much. Have a great day.

[Operator:]

Thank you for participating. This concludes today's conference call. You may now disconnect.