Hello, thank you for standing by, and welcome to Allogene Therapeutics Second Quarter 2021 Conference Call. At this time, all participants are in a listen-only mode. After the speakers' presentation, there will be a question-and-answer session. [Operator Instructions] I would now like to turn the call over to Christine Cassiano, Chief Communications Officer. Ms. Cassiano. Please go ahead.

Thank you, operator, and to all on the line. Welcome. We will continue to limit questions to one per person, so we can get to as many as possible during the hour. After the market closed today, Allogene issued a press release that provides a corporate update and financial results for Q2 2021. This press release and today's webcast are both available on our website. Joining me on the call today are Dr. David Chang, President and Chief Executive Officer; Dr. Rafael Amado, Executive Vice President of Research and Development and Chief Medical Officer; and Dr. Eric Schmidt, Chief Financial Officer. During today's call, we will be making certain forward-looking statements. These may include statements regarding the success and timing of our ongoing and planned clinical trials, including the timing and ability to advance our ALPHA2 trial to phase 2, data presentations, regulatory filings, future research and development efforts, manufacturing capabilities and 2021 financial guidance among other things. These forward-looking statements are based on current information, assumptions, and expectations that are subject to change. A description of potential risks can be found in our earnings press release and latest SEC disclosure documents. You are cautioned not to place undue reliance on these forward-looking statements and Allogene disclaims any obligation to update these statements. I'll now turn the call over to David.

Thank you Christine, and good afternoon. We launched Allogene in the second quarter of 2018 with a bold mission. To create and lead the Next Revolution in cancer treatment by delivering to patients the first AlloCAR-T therapies for blood cancers and solid tumors. Three years later, we have made a giant lead for both Allogene and the field of cell therapy as data from our lead program bring us one major step closer to realizing our goal of commercializing a first-in-class and best-in-class off-the-shelf cell therapy. As we enter a new stage in our lifecycle, our focus turns towards advancing our lead development candidate ALLO-501A into a pivotal phase 2 trial for relapsed refractory non-Hodgkin's lymphoma by the end of 2021. Following initial data presented at our CD19 forum in May and ASCO in June, we are increasingly confident in the safety and efficacy profile of ALLO-501A and its path forward. As we shared during the CD19 forum, the ALPHA trial demonstrated that ALLO-501 can achieve deep and durable responses in patients with relapsed-refractory non-Hodgkin's lymphoma, who are CAR-T naive with an overall response rate of 75% and CR rate of 50% and the six-month CR rate of 36% in patients with large B-cell lymphoma histology, which is the patient population of our first pivotal trial. The safety profile was also very encouraging. No dose limiting toxicities or graft versus host disease and limited eye cause and cytokine release syndrome observed. I have been involved in the development of CAR-T therapies from the early days and the available efficacy and safety profile of ALLO-501 and ALLO-501A clearly show that all the key principles that we learned from autologous CD19 CAR-T therapies are holding true in our allogeneic CAR- T therapy. Setting aside the limitations of drawing a cross trial comparison,…

Thank you, David. As you might anticipate our research and clinical teams have been increasingly focused on advancing our portfolio of AlloCAR-T therapy. As David mentioned, we are on track with our plans to initiate a pivotal phase 2 trial for ALLO-501A in non-Hodgkin's lymphoma. Review the data that we reported in May for the ALPHA trial, including a 36% complete response rate at six months in large B-cell lymphoma as a sign that we are on the right track and look forward to exploring whether the use of consolidation therapy might lead to even greater promise. Across all non-Hodgkin's lymphoma histology, ALLO-501 demonstrated an overall response rate of 75% and a CR rate of 50% across histologies in CAR-T naive patients. At the time of the data cut off, the longest ongoing complete response was at 15 months in both last T-cell lymphoma and follicular lymphoma. Importantly, given our intend to move ALLO-501A into our pivotal study, we were also able to demonstrate that ALLO-501A, which eliminates the rituximab recognition domains in ALLO-501 to allow for use in a broader patient population has comparable safety and efficacy to ALLO-501. As we look to find ways to maximize all levers afforded to us by the nature of our allogeneic platform, one area of distinction for us is our lymphodepletion platform, which supports consolidated dosing. During our CD19 day, we also highlighted the initial data on consolidation therapy, which leverages the unique attributes of the off-the-shelf allogeneic cell therapy and our proprietary lymphodepletion regimen. We are highly encouraged by the results, especially the tolerability of consolidation and observed conversion of initial PR to CR. Pending additional follow-up, we plan to incorporate consolidation into our pivotal study we assigned. Our approach to consolidation dosing is not currently available for autologous therapies or…

Thank you and good afternoon. And so I open my portion of the prepared remarks, I'd like to highlight progress made in our joint venture with Overland Pharmaceuticals to develop and commercialize our AlloCAR-T therapies in Greater China, Taiwan, South Korea and Singapore. In June, we announced the appointment of Dr. Shuyuan Yao as CEO of Allogene Overland Biopharm. Dr. Yao has over 15 years of experience in cell therapy and was most recently the Chief Scientific Officer and Head of Research and Technology Development of WuXi Advanced therapies at WuXi AppTec, where he led new technology acquisition, development, translation and application. We are delighted to welcome Dr. Yao to the team and are already seeing his presence translate into meaningful activities as we seek to bring the promise of allogeneic cell therapies to individuals with cancer in Asia. In the second quarter of 2021, our research and development expenses were $52.3 million, which includes $10.5 million of non-cash stock-based compensation expense. General and administrative expenses were $18.8 million for the second quarter of 2021, which includes $10.6 million of non-cash stock-based compensation expense. Our net loss for the second quarter of 2021 was $70.9 million or $0.53 per share, including non-cash stock-based compensation expense of $21.1 million. As David and Rafael mentioned, we're on track to support five clinical trials during 2021, including the initiation of a pivotal trial for ALLO-501A towards year-end. We're also looking forward to initiating manufacturing at Cell Forge 1, our Newark manufacturing facility. Overall, we continue to expect our full-year 2021 operating expenses to be between $300 million and $330 million, implying a meaningful ramp in expenses during the second half of the year. This includes an estimated non-cash stock-based compensation expense of $80 million to $90 million and excludes any impact from potential business development activities. With that, we will now open the call for your questions.

[Operator Instructions] Our first question comes from the line of Michael Yee from Jefferies. Your line is now open.

This is Dennis staying on for Mike. I just have a quick question around the lymphoma data coming at year-end. Can you just comment on what type of data we will get in specifically for consolidation? Can you help us kind of set expectations for that data relative to what we've seen at ASCO? Thank you.

Hi, this is David Chang. I usually take a lot of questions, but much of today's discussion, I expect to be around CD19 and I'm going to ask our Chief Medical Officer, Rafael to comment on the expectations of what data we will be presenting at the year-end.

Sure. So at the ASCO time point, we have 10 patients that have received consolidation and we were pretty encouraged by what we saw, 80% of patients are responding with seven out of the ten in complete response. And more importantly, we saw some conversions from PR to CR. So, that gave us impetus to continue to accrue and investigators have been very enthusiastic about the ability of consolidation to actually boost up complete response rates, which may be a surrogate to longer durability. So, when you may expect towards the end of the year is longer follow up on those ASCO patients as well as more patients have been continued to accrue both on ALPHA and ALPHA2 and follicular lymphoma and diffuse large cell lymphoma, the durability will be variable obviously that at least will include those patients that we present that at ASCO, and I think, there will be sufficient to obviously make adjustment as to the merits of consolidation. So I can't give you an exact number, but it will be obviously more volume of what we shared at ASCO, because we've continued this approach.

Our next question comes from the line of Salveen Richter from Goldman Sachs. Your line is now open. Pardon me Salveen Richter from Goldman Sachs. Your line is now open. Please check your mute button. Our next question comes from the line of Marc Frahm from Cowen & Company. Your line is now open.

And thanks for taking my questions. I guess, on your comments about defaulting to using the consolidation dosing is kind of, you're going to default assumption. Would you expect the pivotal trial is going to be just a single dose? Do you think that single-arm or you might the FDA require a kind of a randomized trial for the consolidation piece of it to kind of definitively establish the utility of that second dose, and then I guess related to that, as you evaluate the early data that's coming out of the trial? Just what's your latest thoughts on kind of minimum difference in durable CR rate that you need to see to justify that second dose?

Yes. Frahm, I think those are very good questions. I mean in general, the fact that one gives more than one dose of a product doesn't necessarily lead to a mandate from regulators to test single dose in a randomized fashion. Obviously the agencies, negotiations need to happen, but just a keen to what may happen with the vaccine or with the product that requires periodic dosing where there is every two weeks or five weeks or dosing for a year or dose until progression et cetera, the sponsor establishes the regimen and proposes that the regimen to go forward. So I don't foresee that there will be a mandate for us to actually establish whether consolidation is better than single dose or not. It will be up to us to decide whether we believe that is the case, which leads me to the second part of your question. The evidence would be a composite of the high CR rates, the durability of the responses and we are accumulating more and more months on some of these patients as I mentioned before and also some of the surrogates like minimum residual disease, and then the ability to continue to expand and observe persistence of the CAR positive cells, which we've already seen after the second dose. So far we're excited about what we're seeing and that's why we believe that it's likely that we will incorporate consolidation in our pivotal trial, but will continue to observe the data prior to making a decision.

And Mark, this is Dave Chang, if I can add on to that, I think there will be a lot of questions about the study design that we will go forward with that in the FDA meeting. And I kindly ask you to stay tuned and then certainly we have to have the FDA discussion, and as we come out of it, we will clarify exactly what will happen for our pivotal study.

Our next question comes from the line of Luca Issi from RBC. Your line is now open.

hanks so much for taking my question and congrats on all the progress. Maybe a quick one. I think Sage Therapeutics is planning to show some for the first time I think clinical data for CD19 CAR-NK cells in the next weeks, I'm wondering if you can comment on what are your expectations getting into that data and a maybe bigger picture, what's your latest thinking on the debate between CAR-T cells versus CAR-NK cells? Thanks so much.

Yes, Luca. Thank you very much for that question. Certainly, our focus now is really advancing our allogeneic CAR-T program ALLO-501A into the pivotal study. We have treated number of patients and we have a good understanding coming from the large number of patients, the emerging data we have from the 501 were most of the single dose experience are coming from, as well as the consolidation dosing, which we are very interested in. As you know, the allogeneic cell therapy field is a very active place. I think a lot of companies give the promise off-the-shelf therapy with the potential providing a very deep and durable responses and companies are taking different approach, we believe in the CAR-T therapy especially therapy that leverages T cells and we eagerly wait to see what other companies, especially those leveraging the NK cells will provide in their data update. So let's have another conversation after the data presentation, which I believe is planned for some time in August.

Our next question comes from the line of Salveen Richter from Goldman Sachs. Your line is now open.

Just two questions here. Could you talk about CD70 and what you would see as a clinical bar here and first data with your CAR-T program and then, on the BCMA side, do you have an understanding here of the optimization levers required to get you closer to the autologous profile?

Yes. Salveen. This is Rafael. So on CD70 that program has begun not that long ago and as you know, we have to treat patients and observe them before we can go through the dose escalation. We are treating patients that have failed all pathway directed therapies, also that is step point inhibitors and angiogenesis inhibitors, many of them are progressing I think come into the study. So, we hope to get some early evidence of potential activity that we can show next year. In terms of the bar, I think it's premature to talk about it, but many of these patients are already refractory. And, as you know, the data in solid tumors with CARs still needs to mature and progress, but I think thirdly any complete responses or partial responses will be of interest, and we will follow the field very closely. And there is a number of surrogate markers that we're also looking at that will help us with other targets in solid tumors by just trafficking into the more tumor microenvironment effect, persistence et cetera. In terms of BCMA optimization, we have continued dosing. As you know, we were in the deal for, we have finished dose escalation. We'll continue to follow patients. We are starting consolidation as well and we were very glad to see the RMAT designation being awarded to the product and that was in recognition for the effect of the product, but also the ability to treat very quickly and to avoid bridging therapy, which are two important features that you don't see in the autologous setting. But, we clearly want to get closer to the autologous bar. There is no question that still the cell has set a pretty high bar, and so we are continuing with consolidation the use for Nirogacestat and obviously the TurboCAR that we've referred to in the prepared remarks that we just started. So, it's a matter of thing on seeing what these potential optimizations result on.

Our next question comes from the line of Michael Schmidt from Guggenheim Securities. Your line is now open.

This is Kelsey on for Michael. Thanks for taking our question. Maybe building on the multiple myeloma side, I guess, what should we be expect to get ASH in terms of when you implemented the consolidation regimen? Will there be a meaningful amount of patients that we can interpret single agent versus consolidation and would we see any initial data points from the Nirogacestat combination. That's it from me. Thank you.

Yes. So on the consolidation Kelsey this started relatively recently. So there will be patients, but there may not be long follow up. There will be more follow-up on the higher doses, which we've already noted that we're more effective than the lower doses. So we treated NDA-3 and NDA-4 and so we will have more patients on those as well as longer follow up. Nirogacestat are going well, but we will need to have sufficient patients and sufficient follow up and so we believe that will probably 2022 type data, really just like 605. So most likely it will be much more mature data with higher doses on 715 that we will present towards the end of the year.

Our next question comes from the line of Jason Gerberry from Bank of America. Your line is now open.

Thanks for taking my questions. Another BCMA question, just heading into ASH. Obviously, as you guys had mentioned autologous to set a high bar your data last year, ASH were immature for the 480 million cell dose, so just curious, do you think you might be at a point at ASH to determine whether or not a single dose is the right path forward or whether you need to shift the focus to gamma secretase or TurboCAR programs or dose consolidation, just sort of curious if you feel like the data might be mature enough for single dose to make that pivot or prioritization. Thanks.

Thank you, Jason, and thanks for great question, I mean, I think you're asking all the right questions. I mean certainly from the beginning, we set up the BCMA program slightly different than the way we set up our CD19 program. I mean, yes, there are different levers that we can test, including higher cell dose and more stronger lymphodepletion leveraging what we have specifically ALLO-607 and consolidation and all these are the parameters that we tested in the CD19 program and we have a lot of knowledge about how to best utilize different levers to optimize the benefits of ALLO-715. Also, we have taken in a sort of somewhat unusual step concurrently developing the next generation ALLO-605 that utilizes the TurboCAR technology. So, in terms of the question about when we will know about what to do with our different BCMA approaches that we are making, we got to take all different informations that we are generating and in all these trials are ongoing and enrolling patients and we are in a pretty good position. I believe that sometime in 2022 though we have convergence of data that will help us to map out the path for the BCMA program.

Our next question comes from the line of John Newman from Canaccord. Your line is now open.

Thanks for taking the question. Follow-up on the last question actually, just curious for ALLO-715 in terms of combining with Nirogacestat. I'm wondering if you're considering giving multiple doses of Nirogascestat sometime in the future. Yes, it may be beneficial to dose initially in combination with ALLO-715 and ALLO-647, and then maybe after that to give another dose or two. Just curious if that's something that you're considering for the future. Thanks.

Hi, Joe. This is Rafael. Yes, good question. I mean we haven't gone into how we're dosing Nirogacestat for competitive reasons obviously, but I can tell you that we don't just give one dose and our intent is to try to maximize the benefit of BCMA expression that Nirogacestat can afford. So, we will be testing the dose potential and it may take the form of several doses and this is something that is currently under exploration, so stay tuned for the results.

Our next question comes from the line of Mark Breidenbach from Oppenheimer. Your line is now open.

Thanks for taking my question. Just a quick one from me, I know the main focus of the upcoming pivotal trial will be on large B-cell lymphomas. But, I'm wondering if you have plans to continue development of ALLO-501A in follicular lymphoma or is that off the table for now?

Yes, Mark. I mean this is something that we are cross team right now, which is a comprehensive program that includes a suite of studies across various lines of therapy as well as histologies. As you know, there are second-line results that have gone come up and we are thinking about follow on trials that would address that need with the allogeneic 501A therapy and likewise to follow along with follicular lymphoma and potentially other histology, so right now, we are very focused on the third line histology and in discussions and preparations to get that study started, but there will be a lot of activity around ALLO-501A to really form a comprehensive program.

Our next question comes from the line of Reni Benjamin from JMP Securities. Your line is now open.

Thanks for taking the questions and congrats on the progress. Just one from me when we go to ALLO-316, can you just remind us why RCC as opposed to let's say any other solid tumors and when I think about RCC, I always think about in combination with checkpoints and I guess I'm curious as to where you guys are in the development of evaluating these allogeneic cell therapies in combination with checkpoints whether it's with RCC or any of the other indications are in the 501 test kitchen that you guys have?

Ren, great question. As you are pointing out with our ALLO-316 targeting CD70, there are several different development opportunities. CD70 as a target, it is very attractive in both heme as well as solid tumor indications. Certainly, renal cell carcinoma and are going to why we chose to renal cell as well as other types of tumors solid tumors and also there is a lot of interest and we are certainly getting a lot of inbound interest in advancing 316 in the AML indication, where there is a some earlier proof of concept coming from using antibody alone for the treatment of AML. So, we have many different options to consider. at the end from the corporate perspective, we wanted to advance Allogeneic CAR-T into the solid tumor, which is the reason that we chose the renal cell as the first indication. And, as a part of your question, I mean, is there an opportunity to combine CAR-T therapy with a checkpoint inhibitor. I mean, that's definitely CAR-T therapy that has been explored in other CAR-T settings as well. We will be considering that once we sort of generates the safety and efficacy data from the single agent treatment of ALLO-316 and also at the same time, as we get more proof of concept from ALLO-316, stay tuned, we will be advancing that program into other indications as well.

Our next question comes from the line of Raju Prasad from William Blair. Your line is now open.

Thanks for taking the question. I wanted to get your thoughts on the ZUMA-7 trial and transform results as it relates to how the B-cell landscape might change by the time ALLO-501 goes through its pivotal trial, just curious to hearing his thoughts on CAR-Ts moving into earlier lines of therapy, given the CAR-T naive data that you've shown today. Thanks.

Raju. Thanks for that question. I personally was involved in the ZUMA-7 study and I have to say that all of us really and the preliminary data came out and certainly that highlights what the CAR-T therapy can do, I mean there are a lot of questions about, is the CAR-T therapy going to be just for the relapsed-refractory setting or can it move back to the earlier line? I think the ZUMA-7 study that's a clear example that the CAR-T therapy can be more effective and work better in the earlier lines of therapy and we see that as an opportunity for the allogeneic to follow what was set by the autologous CAR-T therapy. Having been involved in both autologous and allogeneic CAR-T therapy, as I said in the prepared statement, what we are seeing in the allogeneic CAR-T therapies are coming out of the ALLO-501 and ALLO-501A data is so many consistencies with what we saw in that collateral CAR-T. I mean that's one of the reasons that we are very I guess somewhat bullish and confident about the future of ALLO-501A and the future collateral 501A will not start in the relapsed refractory setting. We will definitely advance that into other indications, especially in the earlier line as Rafael has earlier alluded to.

Our next question comes from the line of Dane Leone from Raymond James. Your line is now open.

Hi, thank you for taking the questions. Congrats on all the progress and looking forward to some of the updates later this year, one question for me. Just wanted to focus on the primary inbound that we get in terms of your data set in aggressive B-cell lymphoma right now and that's really focused on understanding the infection risk profile. I guess maybe a multi-part question here, sorry. One, could you just remind everyone how the lymphodepletion works for the consolidation regimen that you're now using that we should see more data on later this year. And then two, maybe comment on your expectations for infection rates for that consolidation regimen relative to maybe what we saw recorded around ASCO between the 90 milligram of ALLO-647, which seem to be a bit higher than the 60 milligram dose and then lastly, how that could play into discussions with FDA about clinical trial design if you do go forward with the consolidation dose or not. What they would want to see in terms of maybe patient numbers to understand that infection risk potentially relative to other salvage line therapies for those patients. Thank you.

Yes, thanks for the question. And this is a complex question and I'll do my best to do objective. So just to start with consolidation, we give dose intensity that is the same as the 90 milligrams that you've seen with the single dose and that we did 60 milligrams in three doses upon the first infusion. And then on the second infusion, which is down after day 28, I'll give 30 milligrams. So the total dose intensity is the same but is split into two doses. We've been incredibly pleased with the tolerability of both the initial and the consolidation infusion. What we hear or what we see is that particularly with consolidation, patients do fine. There has been really no class effects and tolerability has been quite good down to the point that we're considering whether it could be done as an outpatient. The overall infection risk, I mean, if you look at the USPI of the three products that are approved in the autologous setting, means it's is very clear that it is similar to the infection rates that we see, which is in that 20. It ranges between 19% to the mid-20% in terms of Grade 3 plus infection rates. And that's really what we see. So we do not believe that the way that we're using on a six or seven is leading to a higher rate of infection. And it's really a common feature, which is really highlighted by the guidelines of how to treat these patients and prophylaxes, and it is possible that the split dosing may lead to even lower rates. But this is something that we really have to wait and see. But even with the single dose, the rates have not been higher than what we see on your side.

And Dave, if I can just add on to that. As a clinician and as somebody who has been involved in the CAR-T study. I mean, I can understand some of the concerns that have been raised by about infection rate. But now, we have treated over 100 patients across different programs with our allogeneic CAR-T, AlloCAR-T, 501, 501A and 715 and I think at this point, the clinical data speaks for itself in terms of the infection rate that we have seen and I have to say that in 100 patients that we have treated despite some of the concerns that have been raised. I mean the data doesn't really indicate that the infection rate is any higher than what has been reported in those AlloCAR-T therapy.

Our next question comes from the line of Ben Burnett from Stifel. Your line is now open.

This is Catherina on for Ben. Thank you for the questions. For your solid CAR tumor program with ALLO-316, how should we think of cell expansion data and what time points can we expect to be supported by tissue biopsy data?

So, we in 316 follow cell expansion the same way that we doing in the rest of our programs, which is pretty closely early on and then obviously we've stated out time goes on, but we continue to follow until we seek to see cell expansion. But not our premature and we haven't obviously share any data with 316 yet. But we've seen cell expansion or cell persistence, although way out to six months and beyond. There is one feature of 316 as we've mentioned in the past, which is that it is expressed in activated T-cells. So we believe that the ALLO reactive T-cells may express CD70 and may be susceptible to actually cell killed by the allogeneic CAR bearing cells. So, it is possible that the persistence may actually be even superior and this is something that we are looking at and taking a look very closely. So, in terms of the tissue, we definitely want to see what's happening in the tissue particularly in migration of the CAR positive cells to this tissue and we do biopsies very early on. I don't entry into the study and then within the first 10 days, we look for CAR presence, we look obviously for CD70, PD-1, PD-L1 and other markers to tell us what's happening with the tumor microenvironment. So far the data are premature, but we are accumulating these results and he will be part of what will be presented into the diameters.

So, stay tuned.

Our next question comes from the line of Asthika Goonewardene from Truist. Your line is now open.

Just want to follow back up on ALLO-705 plus, you're going to see persist inhibitor. Pretty, you did mention that you might see the state in early 2022 and I just want to check if that early part is still in place here. And if not, could you maybe give a little bit more granularity as to when and then related to that, I guess the size response rates MRD level soluble BCMA levels, et cetera. What other measurements and data can we expect in the first look of this combination that will help support the rationale for putting these two together? Thank you very much.

Yes, I mean we haven't said exactly when this data will be shown. I mean, we said it will be at 2022 and I think, we will make the decision once we consider that we have a meaningful data set. So stay tuned. All I can say, running these two excellent team is that approval is not been a problem, and the execution continues actually on a very brief update. So, hopefully, we'll accumulate data as soon as possible and be able to share with you. Yes, I mean, obviously, we're looking at BCMA expression in the plasma cells, we're looking at soluble BCMA, we're looking at MRD, we're looking at persistence, we're looking something that is important than in this field also which is extramedullary disease and the ability to prevent relapses outside of the bone marrow. But, perhaps the most important factors is the mechanistic reason for giving the Nirogacestat, which we actually see meaningful increase in BCMA and that result in a better in-house activity of the CAR-T ALLO-705 and that's what we're focused on, but we're doing all the right biomarkers that you mentioned.

Our next question comes from the line of Kalpit Patel from B. Riley Securities. Your line is now open.

Yes, hi, thanks for taking the question. Maybe one for David or Rafael in the study for renal cell, obviously safety is the priority first. But, at what those level should we expect to see some signals of clinical activity based on your preclinical PK-PD modeling. And then, can you remind us if the lymphodepleting doses that you're using in renal cells are essentially the same as what you use in your liquid tumor trials. Thanks.

Yes, let me those cell dose question. From the preclinical to clinical, we all learn that in the CAR-T field, it is not as predictable. So, in terms of what is to see in clinics, I mean, it really has to be done in carefully planned clinical study, which is currently being done. So stay tuned, I mean it could happen in the first dose level or it could happen in the second, I mean the plan dose is three dose levels in the 316 study. The second question…

The administration of…

The lymphodepletion for the solid tumor versus heme malignancies. For different reasons, I apologize for not answering the question. We are trying to remain relatively silent on the lymphodepletion strategy that we are making. So, just wait for the data presentation and as we've said in the prepared statement, we expect 316 data presentation to occur in 2022 next year.

Thank you. That concludes our question-and-answer session. I would like to turn the conference back over to management for any additional comments.

Thank you. It's an exciting time for Allogene as we look ahead to two near-term events that begin the journey towards commercialization, the planned initiation of our first pivotal trial and taking control of our manufacturing with Cell Forge 1, our first world-class facility. With that, thank you for joining us today and for taking part in our journey to define the future of Allogeneic cell therapy. Operator, you may now disconnect.

Thank you. Ladies and gentlemen, thank you for your participation in today's conference. This does conclude the program and you may now log off and disconnect.