Good afternoon, ladies and gentlemen. Thank you for standing by and welcome to the Allogene Therapeutics Tomaso di Vignano Oregon 2020 conference call. At this time, all participants are in listen-only mode. After the speaker's presentation, there will be a question-and-answer session. To ask a question during the session, you'll need to press star one on your telephone. Please be aware that today's conference call is being recorded. I would now like to turn the conference call over to Christine Cassiano, Chief Communications Officer. Ms. Cassiano, please go ahead. Thank you, Operator. To all on the line, welcome to our first afternoon conference call. As we look ahead to the rest of 2021, we will now be conducting these calls in the afternoon, and we will continue to limit questions to one per person in order to answer all of your questions during the hour. After market closed today, we issued a press release that provides a corporate update on corporate financial results for Q4 and full year 2020. 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, 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. As we head into our third full year as a company, we are pleased to provide an update on our progress in 2020 and a look ahead at what to expect in 2021. By any measure, 2020 was a standout year for Allogene Therapeutics. We have succeeded in building a company that is capable of highly efficient execution across all research, development, manufacturing, and GNA functions. Our strong corporate foundation underpins our ability to deliver meaningful clinical data sets at two major medical meetings in 2020, each of which demonstrated the potential of an allogeneic CAR T therapy and provided proof of concept for our proprietary lymphodepletion platform. We've delivered uninterrupted supply for all clinical trials and have now treated over 75 patients with our Allogene CAR T therapies. We believe our clinical experience in the Allogene field is unparalleled in scope, and we expect our leadership position to widen as we anticipate having five clinical trials underway in 2021. This goal would include four firsts for Allogene: the TRAVERSE trial, our first AlloTumor trial with Allo316 in renal cell carcinoma; the UNIVERSAL trial, where we now initiated our first combination arm exploring Allo715 plus nirogacestat in multiple myeloma; the IGNITE trial, our first TurboCAR trial investigating Allo605 in multiple myeloma; and the ALPHA2 trial, potentially our first pivotal trial with Allo501A in large B-cell lymphoma. Our ability to prosecute multiple clinical trials in parallel and the rational optimization strategy that we are pursuing gives us confidence in our ability to overcome hurdles inherent in the Allogene field. As we advance our increasingly broad allogeneic CAR T pipeline towards multiple industry firsts, we are also investing heavily in next-generation technologies designed to keep us at the forefront of innovation in the field. As part of these efforts, we have expanded our research to execute on novel strategies designed to increase cell potency, overcome tumor microenvironment considerations, and delay immune rejection. We have made a considerable investment behind TurboCAR, a highly innovative and proprietary technology with widespread application. Our initial TurboCARs, which we plan to introduce into the clinic beginning this year, have the ability to increase potency, improve T-cell fitness, and augment persistence via the addition of a cytokine stimulation domain. Meanwhile, next-generation TurboCARs are already being designed to overcome immunosuppressive factors in the tumor microenvironment, particularly in solid tumors by engineering T-cell stimulatory domains that are activated by certain factors such as PD-L1 and TGF beta that normally inhibit T-cell functions. Our focus on new technologies extends to the progress we are making in our partnership with Notch Therapeutics, directed at iPSC drive therapies. Notch is applying its scalable, engineered thymic niche platform to develop homogeneous and universally sourced stem cell drive therapies. They have assembled a world-class scientific team and are building a fully integrated, rigorously controlled platform for generating and editing immune cells from clonal stem cells to enable development of a range of T-cell therapeutics. While our current focus with Notch is to develop fully functional T-cell therapies for initial applications in non-Hodgkin's lymphoma, leukemia, and multiple myeloma, our agreement also gives us the rights to pursue natural killer or NK cell therapies should we opt to do so. Our work allows us to consider next-generation anti-rejection strategies that might complement our proprietary anti-CD52 platform. We are advancing preclinical programs based on what we call dagger approaches. For example, in concert with Baylor College of Medicine, we are exploring the use of alloimmune defense receptors, or ADRs, to recognize and destroy allo-reactive host immune cells that would otherwise be capable of rejecting the Allogene CAR T cells, thereby providing enhanced persistence to Allogene CAR T cells. In addition, we are advancing cloaking approaches that seek to hide Allogene cells from detection by the host immune system. We hope to advance one or more novel strategies into clinic by 2023. Based on the strong foundation we have created, we believe we are in a great position to broaden our reach, both in terms of pursuing new targets as well as expanding our geographic footprint. Let's first talk about new targets. We have previously spoken about our first foray into solid tumors with Allo316 in renal cell carcinoma. We believe this disease state is ripe for innovation as current therapies are based on a few mechanistic targets and complete response rates are low. Our goal is to deliver the potentially transformative impact of CAR T therapy to patients with kidney cancer. We are pleased last year to receive clearance for our IND and are now preparing to launch our TRAVERSE trial. We would expect to share initial data from this trial in 2022. Finally, as we look at both expanding development and our footprint, we are excited about the joint venture we announced late last year with Overland Pharmaceuticals named Allogene Overland BioPharm. This first-of-its-kind collaboration for an allogeneic cell therapy will focus on our candidates targeting BCMA, CD70, SPLT3, and DLL3. Not only will this joint venture give us access to a large and rapidly growing pharmaceutical market in China, but it may also give us the opportunity to accelerate clinical development of certain allogeneic pipeline candidates. Based upon my experience over the past eight years of developing successful and lifesaving cell therapies, the pursuit of a disciplined, methodical, and data-driven approach to the most challenging obstacles facing the field of this modality can sometimes be unheralded. However, I personally believe that a rigorous scientific approach is of critical importance to long-term success in the field. Only companies that commit to such scientific excellence and to rational decision-making will be able to make the necessary progress to reliably deliver radically transformative and durable therapies to patients. To accomplish such formidable tasks, one should surround oneself with a world-class team of scientists, clinicians, and cell therapy manufacturing experts. I am blessed to have Dr. Barbra Sasu, our Chief Scientific Officer, Dr. Rafael Amado, our Executive Vice President of Research and Development and Chief Medical Officer, and Dr. Alison Moore, our Chief Technical Officer on the Allogene leadership team, and I'm proud that the teams embrace these same principles. We greatly appreciate your support as we seek to make allogeneic therapy accessible to more patients with advanced cancer. I will now turn the call over to Rafael for further updates on our research and development activities. Thank you, David. I'd like to first discuss our CD19 program with Allo501 and Allo501A in non-Hodgkin's lymphoma as we look ahead to our next data presentation in a medical forum in Q2 of this year. While our policy has been to not get ahead of meeting announcements to alleviate any speculation with regards to timing, we're targeting ASCO for this update. At ASCO 2020, we presented initial data on 22 non-Hodgkin's lymphoma patients treated with Allo501, of which 19 were evaluable for efficacy. Updated Allo501 data from the ALPHA trial will reflect longer-term follow-up from those patients previously presented, as well as more recent data, which will include additional patients who received higher doses of Allo647. We will also examine biomarker results such as minimal residual disease or MRD status. As we expect to have a more meaningful data set, we also intend to provide information on patient subset. As you might recall, our Allo501A ALPHA2 trial was designed to potentially move into a pivotal phase should the data support it. As a result, this trial was designed to enroll a homogeneous patient population focused on relapsed refractory large B-cell lymphoma. As noted in our press release this afternoon, Allo501A was granted fast-track designation for the treatment of this population. The abbreviated phase one dose escalation portion of this trial was designed to recapitulate initial findings from the ALPHA trial with a modified construct where the rituximab recognition domains have been removed. Dose escalation was completed late last year, and as such, durability will be limited from the ALPHA2 trial when data are first presented. As we continue enrollment in this trial, much like the ALPHA trial, we're now focused on enrolling patients into the consolidation portion of this study. For each of these trials, consolidation consists of two infusions of 120 million allogeneic CAR T cells. The first infusion follows lymphodepletion with fludarabine and cyclophosphamide as well as Allo647, and an initial tumor assessment is performed on day 28. If a patient is in complete response, partial response, or stable disease on day 28, a second infusion is given approximately five to six weeks after the first infusion. Prior to the second cell infusion, a patient will be eligible to receive a modified lymphodepletion consisting only of Allo647. The consolidation protocol will evaluate whether an additional dose of cells can further improve the complete response rate and translate into durable complete responses. Approved autologous CAR T therapies have demonstrated a best overall response rate in the 70%-80% range. However, over half of these patients fall out of response. The intention of the consolidation protocol is to see if we can potentially induce responses in a higher proportion of patients over the long term. As the duration of follow-up from these consolidation protocols in both ALPHA and ALPHA2 will be short, we look forward to assessing the best course of action for a pivotal trial in the second half of the year. At ASCO in December 2020, we were pleased to present the initial data from our Allo715 program in relapsed refractory multiple myeloma. This was the first data set ever presented on an allogeneic cell therapy targeting BCMA. We were very pleased with the initial look at the UNIVERSAL trial and the proof of concept generated by allogeneic therapy in this indication. In this initial data readout, 31 patients treated with Allo715 were evaluable for safety, and 26 patients were evaluable for initial efficacy. As has previously been observed in multiple myeloma, higher CAR T cell doses were associated with an increased response rate and greater AlloCAR T cell expansion. In the DL3 cohort of 320 million AlloCAR T positive cells, the overall response rate was 60%, with 40% of patients achieving a very good partial response or better, which we refer to as VGPR plus. MRD was assessed in five of six patients with VGPR plus response, and all five were MRD negative. Approximately 90% of patients were treated within five days of study enrollment, and importantly, no bridging therapy was required. In terms of safety, there was no graft-versus-host disease or immune effector cell-associated neurotoxicity syndrome observed. Grade 1 or 2 cytokine release syndrome was reported in 14 patients and was manageable with standard therapies. The rate of grade 3+ infection events was similar to what has been reported in other advanced multiple myeloma studies. Grade 3+ adverse events reported as serious adverse events occurred in 19% of patients, which included the previously disclosed single grade 5 event related to progressive myeloma and a reduced intensity conditioning regimen. This proof of concept data was an important step forward in the field, as an on-demand option may be critical for patients with multiple myeloma, knowing that many either cannot wait for an autologous option or may need to be healthy enough to tolerate and respond to bridging therapy in order to receive autologous CAR T. The findings from the UNIVERSAL phase I dose escalation trial positions us to move on to the next steps in this study, namely optimizing cell dose, lymphodepletion, and potentially repeat administration of Allo715. Our plan is to provide an update on Allo715 later this year. We're also exploring Allo715 in combination with the gamma secretase inhibitor nirogacestat from our partner Springworks Therapeutics. We are pleased to report that we have now initiated this cohort, our first clinical milestone for 2021. Continuing in the BCMA program, we remain on track to submit our IND for Allo605 in the IGNITE trial, our first TurboCAR targeting multiple myeloma in the first half of the year. We continue to believe that the innovation behind TurboCARs represents a breakthrough, as this technology has the potential to overcome T cell exhaustion and expand allogeneic cell viability and efficacy while reducing CAR T cell dose requirements. These properties may enable CAR T to succeed in harder-to-treat hematologic malignancies and solid tumors and may enable us to raise the bar in multiple myeloma. Lastly, in what is one of our most exciting programs, we're eager to initiate our first solid tumor trial. The TRAVERSE trial with the anti-CD70 CAR T Allo316 in clear cell renal cell carcinoma is initially designed to explore Allo316 dosing at 40, 160, 320, and 480 million alloCAR T positive cells. The protocol will also evaluate components of the lymphodepletion regimen, including Allo647. The endpoints being assessed are safety, tolerability, depth and duration of lymphodepletion, cell expansion, and anti-tumor activity. Given the high prevalence of renal cell carcinoma and the lack of curative therapies for advanced disease, we look forward to working closely with leading kidney cancer centers and CAR T specialists in the innovative development of Allogene cell therapy for this disease. With three trials underway and two more on the horizon, we remain very enthusiastic about our alloCAR T platform and its potential for patients. I'd like to now turn the call over to Eric to review financials. Thank you, Rafael, and good afternoon. Before I provide a brief overview of our financials for the quarter and year-end, I'd like to spend a few minutes on some of our recent business development activities. In particular, at the end of the year, we announced the formation of Allogene Overland BioPharm, our joint venture with Overland Pharmaceuticals to develop and commercialize our allogeneic CAR T therapies in Greater China, Taiwan, South Korea, and Singapore. Overland, which is backed by Hillhouse Capital, owns 51% of the joint venture through its investment of $117 million. This investment includes an upfront payment to Allogene of $40 million, the majority of which we expect to book as revenue in Q1, and the commitment of $77 million in capital to support operations at Allogene Overland BioPharm. In addition to the upfront payment, Allogene, which owns 49% of the joint venture, will be eligible to receive approval milestones as well as tiered low to mid single-digit royalties on in-territory net sales. Overland will provide operational support, while Allogene will provide technical and manufacturing expertise. Now on to our financials. In the fourth quarter, our research and development expenses were $52.2 million, which includes $7.9 million of non-cash stock-based compensation expense. For the full year of 2020, research and development expenses were $193 million, which includes $31.3 million in expenses associated with non-cash stock-based compensation. General and administrative expenses were $17.1 million for the fourth quarter of 2020, which includes $8.6 million of non-cash stock-based compensation expense. For the full year of 2020, G&A expenses were $65.3 million, which includes $34 million of non-cash stock-based compensation expense. Our net loss for the fourth quarter of 2020 was $68.6 million, or $0.53 per share, including non-cash stock-based compensation expense of $16.5 million. For the full year of 2020, our net loss was $250.2 million, or $2.08 per share, including non-cash stock-based compensation expense of $65.3 million. As we look toward financial guidance for 2021, David and Rafael have noted that we expect to have five programs in the clinic, including a potentially pivotal trial for Allo501A. To support the advancement of these programs and to prepare for initial GMP production at our Newark manufacturing facility known as CellForge One, we anticipate that we will need to make substantial incremental investments in R&D. On the other hand, our focus on maintaining an efficient corporate infrastructure should enable more limited growth in G&A spend. Overall, we expect our full year 2021 operating expenses to be between $300 million and $330 million. This includes an estimated non-cash stock-based compensation expense of $80 million to $90 million and excludes any impact from potential future business development activities. With that, we will now open the call to your questions. Thank you. As a reminder, to ask a question, you'll need to press star one on your telephone. To withdraw your question, press the pound key. Please stand by. We compiled the Q&A roster, and we ask that you please limit yourself to one question. Our first question comes from Salveen Richter from Goldman Sachs. Your line is now open. Hi everyone. This is Andrea Ahn for Salveen. Maybe a question for you, David, or for Eric, just with respect to the Overland JV. Just can you provide additional color on your thinking here, why the structure was so appealing, and if you think this is a strategy you'll look to employ in other ex-U.S. geographies? Yeah, Andrea, thanks for that question. Obviously, we are very excited about the joint venture that got started, and Eric worked very hard on this. Let me ask Eric to explain why we did it the way that we have done with this joint venture. Eric? Yes, thanks. Thanks, David, and thanks, Andrea, for the question. We are very proud of what we've been able to accomplish here. I think that China is a little bit of a unique market, honestly. One thing that we really liked about China is it's a very large growth opportunity, and it's one where we think manufacturing on the ground can be a huge competitive advantage. The structure of this joint venture allows us, through our equity position of 49%, to really benefit from the growth in China while we use the influx of capital from our partners at Overland to support much of the build-out. For China, it makes a lot of sense. We'll see in other territories. Obviously, I should reiterate that our focus in the major markets of the US and Europe is really to keep rights commercially to all of our products. Got it. Thanks so much. Thank you. Our next question comes from Biren N. Amin from Jefferies. Your line is now open. Yeah, hi guys. Thanks for taking my question. Regarding the ALPHA2 trial and the consolidation dose of 120 million cell dose, is that strictly for dose level two, or would patients be eligible to receive consolidation at dose level three? Are you using a similar consolidation regimen for Allo715? Okay, Biren, thanks for that question. We have spoken a little bit about the consolidation, but let me just reiterate what we are trying to do with a consolidation regimen, which I think is a very unique opportunity that comes with the Allogene off-the-shelf cell therapy. This is not something that I can easily see that can be done easily within the autologous setting. As we have done throughout the development of 501, I mean, we are checking every possible levers to optimize and improve what we get with the Allogene XL therapy, starting with a cell dose, lymphodepletion, where we saw very positive findings as we increased the 647 dose. What is really left is the consolidation. The details, obviously, with the consolidation is a little bit complicated, and Rafael went through that, but let me ask Rafael to explain exactly what's being done with the consolidation in 501A. Yes, Biren. The consolidation, as I described in the opening remarks, is where we are enrolling at the moment in both ALPHA and ALPHA2. ALPHA2 is only large B-cell lymphoma. Patients are enrolled. They are treated with the usual lymphodepletion regimen, including Allo647. At day 28, they are assessed. The initial dose is 120 million, and the second dose is 120 million. We are not exploring any additional doses because we believe that the dose response that, for instance, tends to be observed in myeloma is not something that we have observed in lymphoma. That gives a dose of a total of 240 million cells in total. Here, again, as David mentioned, what we're trying to do is to see whether we can increase the responses, increase the durability, and we're looking at a variety of biomarkers to try to give us some surrogate information that this is superior to single dose. Great. Thank you. Thank you. Our next question comes from Mark G raham from Cowen & Company. Your line is now open. Thanks for taking my question. Just focusing back on the ASCO presentation from ALPHA. Maybe can you give us a little bit more granularity on how many patients you would expect to be at six months, and then just kind of the relative breakdown of new data in the abstracts versus the presentation itself? Which of those is probably the bigger event that we should be focused on? All right. Mark, you're going straight into data presentation that we plan to do targeting ASCO. I mean, we're getting pretty close, so in terms of what we will say is somewhat limited. Let me ask Rafael to recap what are the salient findings from the ASCO presentation and what has happened over the last, essentially, about six months since the data presentation, which will be sort of underlying the content of what is to be expected in 2021 ASCO. Rafael? Sure.So, Mark, you may recall that at ASCO, we enrolled 22 patients, and as I mentioned before, 19 were eligible for efficacy. We did see dose response with regards to Allo647, with 50% of patients seeing complete response when we used 90 milligrams. We believe that higher doses of Allo647 can cause better lymphodepletion and retard the recovery of endogenous lymphocytes in the patient, and therefore allow for a longer dwelling time of the donor cells. In the meantime, after that, of course, we have continued to follow those patients, so you can expect a longer follow-up of both the 39 milligrams and the 90 milligram patients. We have continued to explore the higher doses of Allo647 as a single dose. We have treated a number of patients at that dose. After that exploration, we commence the consolidation treatment. In ALPHA, we've enrolled both follicular and large cell, and in ALPHA2, as I said before, we've only enrolled large cell lymphoma. Just to make the point that the consolidation started much later, obviously, is the last thing that we started exploring. Therefore, the follow-up in those patients will be naturally shorter. You can expect longer follow-up from the initial patients from ASCO, additional patients treated with higher doses of Allo647, and some data on consolidation. Okay. Thanks. Thank you. Our next question comes from Tyler Van Buren from Piper Sandler. Your line is now open. Hey, guys. Thanks. Good afternoon. Just wanted to focus on the second dose specifically with the consolidated dosing regimen. Previously, at the last data update, you guys showed a lower CRS rate than the other therapies and no ICANS. I wanted to ask about the second dose and the propensity or the potential for it to potentially increase some of those safety events. I guess in the broader context of just using Allo647 and not doing conditioning again. Tyler, I'm trying to better understand the question. Rafael, as he stated, I mean, the second dose is the same as the first cell dose of 120 million cells. The question is around why 120, or I want to better understand exactly what you're asking. Oh, sorry. Does the second dose add new safety events or make tolerability worse based upon your experience of patients that you've dosed with the consolidated dosing regimen to date? Okay. I got it. My apologies. I think that's a relatively simple question, and let me take that. I mean, I think we are getting to have a growing information with the redosing, certainly in the days of early autologous CAR T, when we were redosing patients after first dose with Yescarta. And that's several months later. One thing that was quite noticeable at the time was the redosing was relatively well tolerated among the patients. I think not just us, others are seeing a similar trend where redosing is much better tolerated than the first time. We don't know what the reason is, but I think there are many things that we can speculate, but that's not important. The way we see it in terms of consolidation, it's more concentrated in terms of the time window between first and second dose. Overall, when we look at the data and based on all my experience, I feel pretty confident that redosing, as we're doing in the consolidation, will be relatively well tolerated. Certainly, we are testing that in a phase one setting, which is the right setting to really assess both safety and efficacy. Thanks for taking the question. Thank you. Our next question comes from Michael Schmidt from Guggenheim. Your line is now open. Hey, guys. I had a question on your Allo316 program that is now starting in phase one. I guess what type of efficacy safety profile do you think might be necessary for this in the solid tumor context, specifically in RCC, to ultimately be successful at a minimum? To what degree do you think this could be achieved with this product candidate already, or whether you think additional optimization may be necessary down the road, maybe similar to what we've been doing with 501? Thanks so much. Okay. Michael, thank you for those excellent questions. I mean, there are two parts to the question. I mean, one is really what are we expecting? I mean, in a solid tumor, we have to realize when you look at the renal cell cancer, despite all the advances that have occurred over the last decade, still complete responses are very rare. I mean, if you look at the history of how the solid tumor is currently managed, it's just buying additional time from one treatment to another and continuing that. What's to expect from the solid tumor trial with ALLO-316, which we're very excited about? I mean, I think time will tell. I think we are looking at more than just the response. Certainly, whether we get a complete remission in solid tumor, that will be very important information. The second one is really amongst those who get responses, how long does the response last? I think we have to factor many different elements of what we would consider as a meaningful clinical benefit, which we believe that the cell therapy can provide in solid tumors. Allo316 is one of the early and probably the first Allogene CAR T programs that is going into the solid tumor, so stay tuned. The second question is really an important question. What else can we do? Certainly, there is a lot of innovation that's awaiting to occur in the cell therapy space. TurboCAR is one of them. TurboCAR is actually a platform approach that we are making to make the Allogene CAR T cells work better. We have several different tricks that we are exploring in the preclinical setting that's almost ready to go into the clinic. Stay tuned, but we are definitely planning to continue to innovate from the first generation to second generation, always looking for the best. Thank you. Thank you. Our next question comes from John Newman from Canaccord. Your line is now open. Hi, guys. Thanks for taking my question. Question is regarding the Allo715 plus Nirogacestat cohort. I'm just curious, David, if you have an opportunity or if there would be perhaps a need to explore different dose levels of Nirogacestat in the future, or if it's more likely that you might simply continue to explore higher doses of 647. Thanks. Great question. That is why we are doing these things in a phase one setting where we have the option of exploring different things. The question of whether to explore different doses of gamma secretase inhibitor or different doses of cell therapy, that is really fundamental to any combination therapies being tested. I mean, the hypothesis for these combination studies is very straightforward. The way that the study is designed, it gives us optionality to explore different doses of gamma secretase inhibitors. We are very excited that we were able to clear the IND in record time and also in the process of activating the sites. These are the questions that we will know in the very near future, so stay tuned. Great. Thank you. Thank you. Our next question comes from Mark Vredenburg from Oppenheimer. Your line is now open. Hey, guys. Thanks for taking the question. I wanted to jump back to Allo316 for a second and the TRAVERSE trial. I'm wondering if you think you'll need to identify distinct lymphodepletion conditions that are very different from what seems to be working in hematogenous settings. Would you consider including IL-2 cytokine support given that IL-2 is already approved in RCC aside from a future TurboCAR approach? Yeah. I always get amazed about the sophisticated questions that you're asking. Let me ask Rafael to answer those very important questions. Rafael? Yes, Mark. I mean, we are definitely planning to follow a variety of translational parameters. Obviously, the initial information that we're seeking is tolerability, so it's a dose escalation trial. We will be looking at what happens to these cells. Do they traffic to the tumor? Do they encounter antigen? Do they expand? Do they eventually cause cytolysis to the tumor cells? We have thought about combinations. This is an immunogenic tumor, as you know. Whether it's IL-2 support or PD-1, those are things that may come in the future along with potential modifications of the construct itself, such as what David was referring to before. In terms of the lymphodepletion, that's an unknown, and we will be testing that in the phase one study. One thing that I would say is that CD70 is also in lymphocytes. It's actually a marker that was discovered in lymphocytes, and it's actually expressed in activated lymphocytes. It is possible that alloreactive lymphocytes may be susceptible to depletion by the CAR. Because of that, we are obviously starting carefully with doses, and then we will continue to escalate as we see that the program is safe. It's a fascinating question what kind of lymphodepletion we will need because of the biology of the target and as well as the biology of the tumor, what kind of partner perhaps we will need to be using with the CAR to make it effective and lead to complete responses. Yeah. I would just add, besides those, the patient's prior treatment history, that also influences patients' underlying basal conditions about their immune system, which is relevant as we think about the lymphodepletion. We rely a lot on our translational and clinical groups to find answers to these important questions as we are studying, taking a new path in solid tumors. Super. Thank you. Thank you. Our next question comes from Cory Kazimov from JPMorgan. Your line is now open. Hey, guys. Thanks for taking my question. This is Matthew on for Cory. Just a quick one from me. Can you remind us if you're looking at anti-CAR antibodies in your ALPHA and ALPHA2 studies and whether we might get some of this data at ASCO? Okay. Rafael, you want to cover that? Yeah. Just very simply, we are looking, and we plan to disclose a variety of translational markers, including anti-CAR antibodies. Great. Thank you. Thank you. Our next question comes from Luca Issi from RBC. Your line is now open. Oh, hi everyone. Great. Thanks for taking our question. This is Lisa Walter on for Luca EC from RBC. I just wanted to continue the conversation on the gamma secretase inhibitors. The gamma secretase inhibitor obviously induces the expression of BCMA. Do you think that it will just improve the response rate, but maybe not necessarily the duration of response? The reason why I'm asking is because we've seen some impressive data from Fred Hutch at ASH 2019, but we haven't seen an update on the data since then. Just wondering if you have any thoughts on this. Thank you. Lisa, let me take that question. What the field has seen, and I think this is something that we have seen from the early days in CAR T trial where others who generate the data find this similar pattern. One, cell expansion tends to correlate with the response. The response, especially the depth of response, tends to correlate with the durability of the response. One of the sort of underlying hypotheses that we want to test in the combination study is, as we increase the density of the BCMA on the multiple myeloma cells, can we get a deep response? Response, as you know, partial response, very good partial response, complete remission, stringent complete response, and also MRD status. I think all these are different levels of responses that we can look into. I think that will tell quite a bit. The question about the response and the durability, that are somewhat linked in the cell therapy in my experience. Excellent question. The second part to your question about updates from Fred Hutch, I do not know what is going on there. Hopefully, they will update sometime in the near future. This is a very interesting hypothesis, and this is a very interesting concept that we feel that we have to test as we advance our BCMA CAR programs in multiple myeloma. Great. Thanks for taking the question. Thank you. Our next question comes from Reni Benjamin from Citizens JMP Securities. Your line is now open. Hey, good afternoon, guys. Thanks for taking the questions. I guess one for me, just from a manufacturing perspective, CellForge One is going to be up and running. Can you just talk a little bit about how the products get integrated into the existing trials? Does it kind of just come on full blown with the pivotal study or slowly get integrated? How many facilities do you think? How many CellForges do you think you might ultimately have across the U.S. as well? What's the capacity? Eric, CellForge One, this is something that you've paid close attention to. Do you want to cover the answer about the capacity? Yeah, sure. I'm sure. I'll come back and cover the questions about integration. Okay. I mean, in terms of capacity, REM is a very large facility. I think as we've talked before, it's 120,000 sq ft. The construction is essentially complete. And we're now in a position where we can begin to activate and operationalize manufacturing in the facility. So a lot of effort, a lot of investment has gone into making this state-of-the-art facility. And we're very proud of its becoming operational this year. In terms of the capacity, we've spoken in the past about being able to commercialize on a global basis multiple products from this facility. It's modular in its design. So it's quite flexible and quite large and can certainly suit us for the foreseeable future. David, back to you. Yeah. The first question is a very important one, which is really rephrasing your question. Right now, we are making the cell product using the contract manufacturer. Now, you have the process going over to our own facility, CellForge One. How do you source the clinical studies with different site manufacturing? I mean, this is something that we have—I personally have a lot of experience having done that at Kite where we went from the contract manufacturer to our own manufacturing facility. In terms of how to do that and what's also required, part of which is being able to characterize your product, analytic assay capability, which we have been building internally within our tech ops group. A very important question, something that we have a lot of experiences in. I feel very confident that we will be able to handle this very smoothly. Perfect. Thank you. Thank you. Our next question comes from Ben Burnett from Stifel. Your line is now open. Hi. Good afternoon. This is Carolina Ibanez on for Ben Burnett. Thank you for taking our question. As a follow-up to the previous questions on Allo715 in combination with nirogacestat, can you provide additional details on the type of patients you are enrolling, whether or not you plan to test both low and high-dose Allo647? When do you expect to have initial data? Thank you. Rafael? Sure. The study is exploring Allo647 and also doses of nirogacestat as well. The cell dose is going to be relatively fixed. We'll study a limited number of cell doses because we have an idea from 715 of what doses are active. In terms of when we will have data on this, I mean, the study just started. As I said, there's some exploration that we need to do in dose escalation in a variety of parameters. We anticipate to have data probably not this year, but early next year. That's our projection. Thank you. Our next question comes from Jason Gerbery from Bank of America. Hi. This is Shahida Rahman on for Jason. Thanks for taking our question. For the CD19 update at ASCO, I know you started enrolling pretty recently. Can you talk about the pace of enrollment and give some idea on the number of patients we might see that are treated with both doses of the consolidation regimen? I'm trying to understand how meaningful the update could be and if there'd be enough patients followed at least a month after the second dose to gauge how response rates might improve compared to the single infusion. Excellent question. This is David. Let me take the question. As I've said, we're getting pretty close to ASCO time, so we're not going to go too much into the details. I would sort of look at our record study enrollment. We have highlighted the fact that since we started the clinical programs across CD19 and BCMA, we have enrolled 75-plus patients. We have an outstanding clinical team that is managing the enrollment and also patient follow-up issues. We are still enrolling, and we are hoping that we can provide a meaningful update as we have done in the past two presentations. Okay. Thank you. Thank you. Our next question comes from Dane Leone from Raymond James. Your line is now open. Hey, guys. This is Bowen on for Dane. Thanks for taking our question. Just one from us on Allo715. When we're talking about redosing patients, can you just give a little bit more color on the criteria you would be using there? Okay. Rafael, I would ask Rafael to respond to that question. Yeah. We have not yet started consolidation in the Allo715. That's why it wasn't mentioned in the opening remarks. We saw meaningful responses as well as VGPR plus, as I mentioned earlier, in the 60% and 40% respectively with 320 million cells. We have finished the dose escalation with the Allo647 as well as the cell dose. We started nirogacestat as we've been discussing today. We're looking forward to start 605. The next thing to explore in 715 is consolidation. That is something that we're looking forward to doing, maybe slightly different in design than the ALPHA studies due to the nature of the disease. Stay tuned to that in an upcoming update. Great. Thank you. Thank you. Our next question comes from Raju Prasad from William Blair. Your line is now open. Thanks for taking the question. There's been some discussion in the BCMA space on antigen escape and antidrug antibodies from some of the autologous data that's been analyzed. Can you maybe just talk a little bit about that aspect and how you anticipate nirogacestat and, more importantly, the TurboCAR to potentially help mitigate kind of some of those potential concerns? Thanks. Yeah. Let me take that question. I think the first question of the antigen escape, which is BCMA loss that I think you're referring to, if anything, I mean, I think this is something that the field has been looking for some time. I mean, also the data that was published in New England Journal of Medicine on the DV2121, it certainly tells you that the antigen escape is a relatively infrequent event in multiple myeloma. Obviously, we are learning about the biology of different tumors, but that's the status of it. We will continue to follow in our study about the occurrence of the antigen loss. The second question around the antidrug antibody, that is somewhat difficult to respond to because there are some variabilities in how different companies measured antidrug antibodies. This is something that we knew for some time from the early days of autologous CAR T therapy. In terms of whether the antidrug antibodies affect the response and all those things, I think at this point, there's no evidence that antidrug antibodies have any negative consequences. This is something that we will be testing in our own studies. We will look for any evidence of what the antidrug antibody, if it occurs, will do to the efficacy. Stay tuned. Thank you. Our next question comes from Asthika Goonewardene from Truist Securities. Your line is now open. Hi, guys. Good evening. Thanks for squeezing me in. I want to talk a little bit about expectations for homing and penetration with Allo316. I wonder if you can discuss what your preclinical experiments have shown you and how you set expectations for that. Also, what kind of persistence you expect based on preclinical data of 316 in the tumor microenvironment. Thanks a lot. Rafael, do you want to take that question? Sure. The product in preclinical studies performs incredibly well. We do a variety of in vitro assays as well as animal modeling. In in vitro assays, we obviously challenge the product with CD70 positive cells. We continue to rechallenge, and we continue to see killing. The cells diminish in terms of persistence until they get rechallenged again. Then you see again a resurgence. This is more pronounced in general in the case of TurboCARs, but it is seen also in 316. In animal models, we have done a variety of them, including TDX model that is immunocompromised animals that contain human tumors. We have seen penetration of the CAR T positive cells into the tumor, into the stroma, and disappearance of these tumors. These are not xenograft or cell lines. These are actual cells or tumors rather that come from metastases procured from surgical excisions. If the preclinical data is a good omen to what's going to happen in the clinic, we are pretty pleased with what we've seen thus far. Great. Thank you. Thank you. I would now like to turn the call back over to management for closing remarks. Thank you for joining us on our earnings call and for many outstanding questions. As we close out the call, I'd like to thank our team at Allogene Therapeutics and our many partners and collaborators who overcame the global challenges of 2020 to make the progress we highlight today possible. Operator, you may now disconnect. Thank you. Ladies and gentlemen, this concludes today's conference call. Thank you for participating, and you may now disconnect. Everyone have a great day.