ALLO

Hello. Thank you for standing by, and welcome to Allogene Therapeutics first quarter 2026 conference call. After the speaker's presentation, there will be a question-and-answer session. To ask a question during the session, you will need to press star one one on your telephone. You will hear an automated message advising your hand is raised. To withdraw your question, please press star one one again. Please be aware that today's conference call is being recorded. I would now like to turn the call over to Christine Cassiano, Chief Corporate Affairs and Brand Strategy Officer. Ms. Cassiano, please go ahead.

Thank you, operator, and welcome everyone to Allogene's conference call. After the market closed, Allogene issued a press release that provided a business update and financial results for the first quarter of 2026. This press release and today's webcast are available on our website. Following our prepared remarks, we will host a Q&A session and will aim to keep the call to under an hour. I'm joined today by Dr. David Chang, President and Chief Executive Officer; Dr. Zachary Roberts, Executive Vice President of Research and Development and Chief Medical Officer; and Geoff Parker, 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, the safety and efficacy of our product candidates, commercial market forecasts, potential treatment settings, and 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 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 move through 2026, next generation cell therapy is shifting from promise to proof. The field is increasingly being defined by differentiated clinical evidence rather than platform ambition alone. At Allogene, our lead program, cema-cel, is built around the clear objective to establish a differentiated development path. That strategy is now translating into data that provides support for our approach. Our second program, ALLO-329 in autoimmune indications, is built on the same principle of product differentiation enabled by our understanding of CAR T design and the biology of allogeneic rejection. While these two programs are at different stages of development, the evidence emerging to date is consistent and aligned with the design principles behind each.

Starting with ALPHA3, we have taken an innovative approach of treating patients with cema-cel in the first-line consolidation setting for large B cell lymphoma with a primary goal of improving the cure rates. The key to achieving this goal is democratizing access by breaking the barriers that have historically limited the use of CAR T therapy and by enabling cema-cel to be delivered in the outpatient setting. We are very pleased with what we've seen in the recently announced interim futility analysis from the ALPHA3 trial. In this 24 patient analysis, cema-cel achieved a 58.3% MRD clearance rate compared with 16.7% in the observation arm, representing a 41.6% absolute difference. While preliminary, this differential exceeded threshold of MRD clearance reported in other trials that led to groundbreaking clinical outcomes.

We also observed a rapid and substantial reduction in circulating tumor DNA or ctDNA in the cema-cel arm, while the opposite trend was seen in the observation arm, where the ctDNA levels increased. Together, these early findings provide evidence consistent with the biological activity of cema-cel in the first-line consolidation setting as we advance ALPHA3 towards the next key milestone, the interim EFS analysis in mid-2027. Importantly, as we consider use in the outpatient community setting, this early biomarker efficacy signal was accompanied by a favorable safety profile. We observed no CRS, ICANS, or treatment-related hospitalization, enabling the majority of patients to be managed in the outpatient setting. These results reflect the trial that was designed to lead, not follow.

Under Zach's leadership, ALPHA3 was built around MRD testing as a point of intervention rather than passive observation, an approach that moved beyond conventional trial design. We set out to test that forward-looking thesis, and these early data reaffirm my conviction that we are not only in the right path but ahead of the curve. Taken together, we believe these data provide compelling support for a different paradigm. One where cema-cel can be used earlier, made readily available, delivered broadly, and potentially integrated into routine care beyond specialized centers. Turning to ALLO-329, the program is progressing through early clinical development in autoimmune indications with the RESOLUTION basket trial advancing efficiently through dose escalation. This progress embodies the same discipline and forward-looking development approach that underpins ALPHA3. ALLO-329 incorporates the Dagger technology, which is designed to overcome premature rejection of allogeneic CAR T cells.

This technology has previously been validated as part of our ALLO-316 program in the metastatic solid tumor setting. However, autoimmune disease represents a fundamentally different clinical context with distinct biology and a different threshold for safety and tolerability. With that in mind, we designed a structured and stepwise clinical approach, beginning at a conservative dose level to establish clear understanding of tolerability before progressing to therapeutic dose levels. Patients treated to date are within this initial dosing range as we evaluate both dose and lymphodepletion strategy. Our focus is on characterizing how the therapy behaves in patients by establishing a tolerability profile that supports continued development while also assessing early signs of activity. Within this framework, we are very pleased with the pace of enrollment and are beginning to observe initial signs of clinical activity coupled with favorable tolerability.

While still early, these findings are highly encouraging and have important implications for the overall dosing paradigm, which includes not only the dose of Dagger-enabled ALLO-329, but also the required lymphodepletion regimen. As the program progresses, we expect continued dose escalation and patient follow-up to further establish the activity, tolerability, and mechanistic profile of ALLO-329. We look forward to providing a further update in the fourth quarter. With that, I will turn it over to Zach to walk through the data in more detail.

Thanks, David. I'll start with ALPHA3 and then turn to ALLO-329. ALPHA3 was designed around a clear clinical hypothesis that intervening at the point of molecularly detectable disease before clinical relapse can meaningfully alter the course of disease. When we initiated the study, MRD was emerging as a prognostic tool in LBCL. Our objective was to move MRD beyond risk assessment and into a treatment decision point. Across oncology, we are now seeing the shift in approaching a potential breakout moment. A case in point is the IMvigor011 trial, which evaluated TECENTRIQ in muscle-invasive bladder cancer. In the trial, patients who were in remission but remained MRD positive after the standard first-line procedure of complete surgical resection were randomized to TECENTRIQ or placebo, with TECENTRIQ demonstrating improvement in both disease-free and overall survival.

The results of this trial could establish MRD as a clinically actionable endpoint following standard first-line treatment. If approved for this indication, TECENTRIQ would become the first therapy for which treatment initiation is guided by an ultrasensitive ctDNA MRD assay rather than clinical progression, a defining moment for the field. Against this backdrop, ALPHA3 is positioned at the forefront of how this new paradigm could evolve in large B cell lymphoma as the first pivotal trial designed to use MRD positivity as the trigger for CAR T therapy. The ALPHA3 study is enrolling patients who have responded to first-line therapy but remain MRD positive and therefore at high risk of relapse. Patients are randomized to treatment with cema-cel or observation. We partnered with Foresight, now a wholly owned subsidiary of Natera, to utilize their CLARITY MRD assay, enabling a highly sensitive and dynamic view of disease burden over time.

This enhanced sensitivity, detecting disease at or even below one in 1 million or 10 to the minus 6, is central to the design of ALPHA3 study and how we interpreted our interim futility data. At the interim analysis, we evaluated the first 24 patients enrolled in the ongoing two arms, a single dose of cema-cel versus observation. We observed a 58.3% MRD clearance rate in the cema-cel arm compared to a 16.7% in the observation arm, representing a 41.6 percentage point absolute difference. We also saw a rapid and substantial reduction in circulating tumor DNA. At the day 45 time point, the median ctDNA level decreased by nearly 98% in the cema-cel arm, while the median ctDNA level increased by more than 26% in the observation arm.

The ALPHA3 interim futility analysis rests on the assumption that MRD clearance foreshadows clinical benefit. This hypothesis is supported by a growing body of evidence in various clinical settings, including in LBCL, linking MRD clearance in the range of 25%-30% with meaningful reductions in EFS events. The magnitude of the difference we just announced exceeds that range. While these external data sets support the relationship between MRD clearance and clinical outcomes, the impact on EFS and durability will ultimately be determined through our planned interim and primary EFS analyses. From a safety and treatment administration perspective, we observed no CRS, ICANS, or treatment-related hospitalizations, enabling the majority of patients to be managed entirely in the outpatient setting. We believe this encouraging tolerability profile is a function of treating patients earlier when disease burden is low, which is inherent to the ALPHA3 design.

If the safety profile observed in the interim futility analysis bears out in the study overall, it could mark an important shift towards outpatient CAR T administration and enable cema-cel treatment in community practices where most patients with LBCL receive care. As ALPHA3 progresses, interest in the study is growing. First and foremost, we are seeing robust engagement from existing clinical sites resulting in high rates of patient screening. At the same time, new sites are expressing significant interest in joining the study, further reinforcing its momentum. From an execution standpoint, the trial continues to scale. We are now enrolling across more than 60 sites with global expansion underway. We recently announced regulatory approval in Australia and South Korea, where site activations and patient screening have begun. We anticipate the Asia-Pacific region to expand the study footprint to over 80 sites worldwide. These are not incremental additions.

Australia and South Korea offer established clinical research infrastructure, experienced investigators, and highly efficient healthcare systems. This expansion reflects both strong global investigator interest and the operational discipline required to execute at scale. We are also seeing meaningful participation from community cancer centers, which contributed approximately one-third of screening and cema-cel treatments in our interim futility analysis. This is an important early proof point up for the feasibility of broader administration as we look to move beyond specialized centers and into broader clinical practice. Let me now turn to ALLO-329, which as a first-in-human phase I trial, has a different objective at this stage of development. The program is supported by robust preclinical data recently published in Nature Communications, supporting the design of ALLO-329. These data demonstrated an optimized CD70 CAR engineered to protect allogeneic CAR T cells from rejection by eliminating alloreactive host T cells.

In those studies, co-expression of CD70 and CD19 CARs drove sustained CAR T cell persistence, elimination of pathogenic B cells, and activated CD70-positive T cells in humanized SLE models and corresponding reductions in autoantibody production. Importantly, the Dagger technology, which eliminates alloreactive host T cells, has been clinically validated by our third clinical program and first CD70 targeting program, ALLO-316, with recently reported outcome data further supporting the approach and reinforcing our plans to advance the program in the near future. At this stage of development, our focus for ALLO-329 is to define a tolerability profile that supports continued dose escalation while generating early evidence that ALLO-329 can achieve meaningful biological activity in autoimmune disease consistent with its differentiated dual targeting mechanism. The RESOLUTION Basket trial, which includes patients with systemic lupus erythematosus with and without nephritis, scleroderma, and inflammatory myositis, continues to progress through dose escalation.

Nine patients have already been treated since the study started enrollment in November 2025, with three patients at dose level 1 of 20 million cells and three patients at dose level 2 of 40 million cells, both following lymphodepletion with cyclophosphamide, and three patients at dose level 1 with no lymphodepletion. Importantly, the doses evaluated so far are substantially lower than those being explored in other CAR T approaches in autoimmune disease, including autologous programs testing approximately 100 million cells and some allogeneic approaches evaluating doses above 1 billion cells. Even at these lower doses of ALLO-329, both with and without cyclophosphamide, investigators have reported signs of clinical activity. While these observations are preliminary and dose exploration continues, investigators have been very encouraged by these early signals, facilitating strong patient interest in participating in the study. This reflects a consistent approach across our programs.

In ALPHA3, we designed the study to intervene earlier in disease treatment based on MRD. With ALLO-329, we are applying that same forward-looking discipline to autoimmune disease, prioritizing mechanism, durability, scalability, and long-term usability from the outset. As we continue dose escalation and patient follow-up, our goal is to build a data set that integrates clinical activity with mechanistic understanding and supports a path towards durable outcomes. We expect to provide a comprehensive update in the 4th quarter. Across both programs, our focus remains consistent, designing studies with clear hypotheses, executing with discipline, and allowing the data to define the role of allogeneic CAR T. With that, I'll turn it over to Geoff.

Thank you, Zach. As we execute against our key clinical milestones in 2026, we remain focused on maintaining a strong financial position that supports continued progress across our portfolio. As of March 31st, we had $266.9 million in cash equivalents, and investments. In April, we strengthened that position through a public offering that generated approximately $200.4 million in gross proceeds, extending our cash runway into the first quarter of 2029. R&D expenses for the first quarter were $32 million, including $2.7 million of non-cash stock-based compensation, reflecting continued investment in our clinical programs. G&A expenses for the first quarter were $14.1 million, including $5.6 million in non-cash stock-based compensation.

Net loss for the first quarter was $42.6 million or $0.18 per share, including non-cash stock-based compensation expense of $8.3 million. Based upon our current forecast for the overall timing of the ALPHA3 program, we are modestly increasing our guidance for operating cash expense in 2026 from approximately $150 million-$165 million. GAAP operating expenses are also expected to slightly increase.

From approximately $210 million-$225 million, including estimated non-cash stock-based compensation expense of approximately $35 million. These estimates exclude any impact from potential business development activities. Overall, we believe we are well-positioned to execute on our strategy with the capital and flexibility needed to reach our next set of milestones. We'll now open the call for questions.

Thank you. As a reminder, to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile a Q&A roster. Our first question comes from Michael Yee of UBS. Your line is open.

Hey, guys. Congrats on the progress to date and the updated autoimmune update. Maybe two quick ones. One is, can you talk a little bit more specifically about some of the initial signs of activity or B cell reductions? What does that mean? To what degree, maybe there are differences in B cell reductions for the lymphodepletion cohort compared to any of the different cohorts with different lymphodepletion. If I may get a question on, obviously, the lead DLBCL program. Since the announcement of your MRD negativity interim, how have you seen perhaps enrollment, engagement and feedback and things of that nature? Maybe just talk a little bit about how things have progressed since that positive interim. Thank you.

Hey, Mike, Zach here. Thanks for the questions. On the ALLO-329 question, we'll be saving the details pertinent to your question until the Q4 update, other than to say that the encouraging signs that we refer to are coming from the cohorts that we've highlighted in, both with and without LD. We will be continuing to enroll patients according to the protocol design with and without cyclophosphamide and expect to show a more complete update in Q4. So far so good, and we're really thrilled with the patients coming into the study very briskly. The second question around has the Phase 1a results stimulated increased activity in ALPHA3? I will say that they have.

It in these early days, these first couple of weeks since the announcement went out, that has come in the form of new sites coming and asking to participate in ALPHA3. Even sites that said early on that they didn't have room in their portfolio before the Phase 1a data was available. They're coming back and saying that they really do wanna participate. That kind of qualitative change is already underway. We will be watching very carefully for a quantitative uptick in the screening and enrollment pace. Except, I will say that, you know, that has been going very well in the last few months. We're optimistic. So far we're pretty happy with the way things are going.

Great. Thank you.

Thank you. Our next question comes from Tyler Van Buren of TD Cowen. Your line is open.

Hey, guys. Congrats on the progress. I have a couple, ALLO-329 questions as well. Since you mentioned favorable tolerability, can you discuss conceptually what sort of safety profile you hope to achieve with ALLO-329 over the long term? With respect to the update in the fourth quarter, can you give us any sense of what that might entail and kind of help put goalposts around what we should expect with that update?

Hey, Tyler, thanks for those questions. You know, the safety profile in autoimmune indications, I mean, you know, we want this to be, you know, as clean as, you know, one can get to. I mean, I think that's really the patient population that we're dealing with. I mean, you know, we have seen in ALPHA3 study, even in oncology, in the right clinical setting, you know, CAR T therapy can be well-tolerated. You know, that's kind of profile that we're trying to mirror, where, you know, the treatment can be given as an outpatient and patient can be managed as an outpatient. That's really the safety profile that we're looking for.

So far, you know, after, you know, completing, you know, both 20 and 40 million cell dose levels with cyclophosphamide lymphodepletion, you know, I feel very encouraged that, you know, if the, if the safety profile, you know, holds out, this can be very interesting finding. With respect to your second question about, you know, how to set up the expectations for the fourth quarter. I mean, so far, let's keep in mind in terms of the pace of enrollment that Zach had talked about. We dosed first patient, back in, you know, November of last year and May, so, you know, within six months. You know, dose escalation study where we have to wait about 1 month, you know, after first patient is dosed before we can fill up the rest of the cohort.

Even with that kind of, sort of, you know, preset barriers in how fast we can enroll, we enrolled nine patients. That is a, you know, pretty remarkable support that we are getting from various, you know, physicians involved in the autoimmune trial. We are highly encouraged.

You know, this, you know, autoimmune, obviously, you know, the way that the clinical responses are being measured is different than in oncology. When the investigators are calling us and telling us that they're seeing that they would not have expected to see, in any setting, I mean, that I would view as a highly encouraging early signs.

Thank you. Our next question comes from Biren Amin of Piper Sandler. Your line is open.

Yeah. Hi, guys. Thanks for taking my questions. Maybe just to stay on ALLO-329. Given your reporting data in Q4, should we expect data across the 20 and 40 million cell doses in the fourth quarter, or could we get higher cell doses? That's the first question. Second question, what would be the patient composition across SLE, inflammatory myositis, and scleroderma in the Q4 update? Lastly, on the trial itself, recently in April, I think there was a change that was recorded on ClinicalTrials.gov where you increased target enrollment to 66 patients from 54 patients. Could you maybe just talk about that change and what drove that? Thank you.

Yeah, Biren, as to your first question, I'm also realizing that was Tyler Van Buren's question, which I did not fully answer. In the fourth quarter, obviously, at this point, we have completed in 20 million and 40 million, and we are continuing the dose escalation by the fourth quarter, you know, update comes, you know, included patient in that will be more than just 20 million and 40 million. We're hoping that we can include, certainly the next dose level and possibly even, you know, higher dose, depending on how the pace of enrollment is maintained. When I'm talking about the cell dose levels, certainly, I'm talking about both with Cy and without cyclophosphamide. Zach, maybe you can cover the patient composition.

Yeah. Biren, we're seeing patients come from all of the indications that I listed previously, lupus, inflammatory myositis, and scleroderma. It's still too early to say whether the early signs of efficacy that we're seeing is segregated to 1 patient group or another. We're not gonna be making any changes to the basket style design of the protocol. As we continue to enroll patients, we expect a mix, and that mix will be presented in Q4. The ClinicalTrials.gov change that occurred, I actually have to say, I don't know why we made that.

It's a administrative change.

Administrative change. Sometimes we have to go through, and we have to make little clerical changes to ClinicalTrials.gov. There's not been any changes to the study design that would have warranted that change.

Thank you. Our next question comes from Salveen Richter of Goldman Sachs. Your line is open.

Good afternoon. Thanks for taking my question. For cema-cel, could you speak to the feedback you're hearing from the community practices to date, post the recent data? For the ongoing ALLO-329 RESOLUTION study, can you expand upon progress on site activation and patient enrollment and how that's playing out, just given some competition in the field for other autoimmune CAR T programs? Thank you.

Salveen, it's Zach. As far as how the community practices are reacting to the interim data from cema-cel, I would echo what I said a moment ago that the feedback has been really overwhelmingly and uniformly positive. As just to give another little anecdote on that, in the couple of literal days after that announcement was made that same week, we were on the phone with a couple of large community network practices that have already a couple of sites on the study seeking to expand their footprint within their practices and add additional sites. We believe that the interim analysis data is being viewed by the community practices and academic practices alike as potentially something very interesting and practice-changing.

Yeah. Also, I would say it makes a lot of sense. When you think about, you know, this is giving the community physician something to offer to patients rather than referring them to a tertiary or cell therapy centers. Two, I think, you know, during the course of treating patients, they are realizing that treatment is relatively hassle-free.

You know, what we have shared, you know, with the interim futility findings is the early safety profile. It was very clean, which also makes, you know, managing patient after the CAR T infusion extremely smooth. I mean, these are definitely early findings, but these are the things that, you know, I believe is making the community physicians being quite interested in participating in the ALPHA3 study.

Your second question, Salveen, about site activation and enrollment in 329. We are approaching the target number of sites that we sought to activate for ALLO-329. I can't say exactly what the number is on CT.gov, but we expect that to be completed here very shortly within the next few weeks, maybe a couple of months. That's gone very well. We've actually ended up getting quite a bit more traction even in that competitive space that you highlighted. We've got some really excellent marquee sites already listed on ClinicalTrials.gov and a few more in the can ready to come out. They are really being super productive on the patient screening and enrollment as we highlighted previously. We could not be happier with how ALLO-329 is going operationally.

The mixture of the patients in this basket study is, you know essentially it, you know, is excellent.

Yeah.

Thank you. Our next question comes from Samantha Semenkow of Citigroup. Your line is open.

Hi, good afternoon. Thank you very much for taking the question. Another one on ALLO-329. I'm wondering if you could just talk a little bit about your thoughts on dosing going forward. You know, you mentioned some early clinical signals that you're seeing in these first nine patients. I'm wondering, do you think the 20 million dose is too low or subtherapeutic? Curious your thoughts there. How are you thinking about dosing going forward? Are there any adjustments you're planning to make to the dose escalation? Thanks very much.

Hey, Sam. So, with respect to the question around the doses that we've tried so far, you know, we in the tenets of a phase I dose escalation study, you're really gated by safety. I wanna echo what David said a moment ago, that safety is paramount here, and we wanna make sure that we maintain the safety profile that would make this therapy attractive to patients and doctors with autoimmune disease. We're gonna keep going up until we start to bump up against that, the toxicity that we think would be prohibitive. So whether you call it subtherapeutic or room to go, I'm more of a room to go type of guy. We're gonna keep dose escalating. Then your other question is, do we see any need to make any adjustments?

At this point, we do not. We still have some doses to go up, and we're hopeful that we'll start to see, you know, really compelling activity here in these next dose or the dose after that, and we can maintain that safety profile. Look forward to that Q4 update.

Thank you. Our next question comes from Roger Song of Jefferies. Your line is open.

Hi, this is Cha Cha on for Roger. Thanks so much for taking our question. I have two. One is, can you just give us some more color on what your current cash runway covers? On my second question is on ALLO-329. Can you tell us more about the decision factors that are driving the optionality for the fludarabine addition? I know you mentioned with the option of adding this. Can you just explain the gating factors for why we add or why we don't? Thanks.

Hi, this is Geoff. On the cash runway, as we discussed in the script, our current cash runway, based on the addition of the capital added in the recent financing, the $200 million financing, takes us into the first quarter of 2029. During that time, you know, we intend to complete the ALPHA3 study. As you know, we anticipate finishing enrollment at the end of 2027. We anticipate an interim analysis on EFS in mid 2027, primary analysis in mid 2028 with the filing of the BLA as quickly as possible, based on the results of those interim or final analysis.

It really is focused on covering ALPHA3, as well as completing this phase I RESOLUTION study for ALLO-329, as we indicated, having the comprehensive data set in the fourth quarter of this year.

Yeah. Let me take the question on the optionality of fludarabine. I think this is just, you know, how, you know, we try to make the, you know, protocol as flexible as possible, you know, without, you know, predefined, you know, idea about when to kick in these optionality. I mean, it's really looking at the data and then, you know, making the decision. Right now, based on the data, our primary focus is continuing the dose escalation.

I'll just add one other piece of color on that. Honestly, in part, this would be driven by the demand to come into the study. By opening additional cohorts, it would allow us to park some patients and to allow patients into the trial. That is another factor that could come into it. Nothing has changed at all about our belief in the Cy or no Cy possibility here. We are continuing with that primary goal.

Thank you. Our next question comes from Matthew Phipps of William Blair. Your line is open.

Good afternoon. Thanks for taking my question. You know it's going to be on ALLO-329 as well. There's obviously been a lot made about B cell reset after, you know, CAR T with CD19. I was wondering if from your experience with ALLO-316, what the T cell kind of repopulation might have looked like after treatment, if you looked at that. I guess, do you expect maybe some ability to have an immune autoreactive T cell reset following ALLO-329 treatment? Will you have any data on that by Q4? Thank you.

Matt, a great question. Really insightful and I think right on point in terms of our understanding of the mechanism of action of ALLO-329. We are really focused on how the B cell and the T cell repertoires will change, and, you know, whether we achieve the reset as defined as just absolute B cells going all the way down to zero, or whether there's some editing of the repertoire on both the B cell and the T cell side. Now, obviously, B cells, we expect the chances of those cells going very low or to zero to be higher because, you know, we're targeting a pan-B cell marker. In the case of CD70, you're absolutely correct. It's only a subset that are gonna be CD70-positive.

Of course, there's going to be a population of alloreactive cells that we expect to be depleted through the Dagger effect. There is also known to be CD70 positive pathogenic AID-causing T cells, so clonal populations with specific TCRs that also express CD70. That has actually been one of the main reasons that we designed ALLO-329 the way we did, was try to wipe out that set, that clone or set of clones that may be driving the pathogenesis. We will be analyzing the T cell repertoire as part of the ALLO-329 study. If we've got something to share in Q4, we'll share it.

Thank you. Our next question comes from Jack Allen of Baird. Your line is open.

Great. Thanks so much for taking the questions, and congrats on the progress. I'll keep the theme going with the ALLO-329 question to start, and then I have one on cema-cel as well. On ALLO-329, I was just hoping you'd provide some additional color as it relates to how many doses you could escalate the study in and, you know, what the next step up might be. I guess logically it looks like 60 million would be a realistic target for the next dose, but how high could you go in that trial? On cema-cel, I just wanted to ask about the interim EFS look in mid-2027 and any additional color you can provide around the powering there.

Jack, great question. The next dose level that we're gonna be looking at is not 60, it's actually 80 million cells. That cohort is enrolling now, following Cy, and then the no Cy cohort is close behind. I'm gonna hold off on saying exactly how many cell doses that we plan to go up, and we'll sort of reveal that at Q4 'cause I do think that we'll be in that zone by the time we give that update, so stay tuned. Eighty million is the next dose cohort that we're working on now. As far as cema-cel, we talked quite a bit about this with the fundraising and the ALPHA3 allocation for the [IA2].

You know, we have not gone into specific detail. The method that we used to allocate the alpha was the O'Brien-Fleming spending function, so that will give you some general understanding of the fraction of alpha that's allocated to the phase II. I will take the opportunity now to reiterate, though, that, you know, the results of the interim analysis one does give us the possibility of having a positive outcome in phase II. That is something we are looking forward to and, of course, working feverishly to enroll the study and deliver on those timelines.

Awesome. Thanks so much for the color.

Thank you. Our next question comes from John Newman of Canaccord Genuity. Your line is open.

Hi, guys. Thank you for taking the question. Also have one on ALLO-329. The question is, do you expect that the Dagger technology that's targeting CD70 positive T cells could actually give you maybe differential efficacy in some of the cohorts that you're enrolling versus lupus, for example, scleroderma and myositis, where it's sort of theorized that there's more T cell activity? Thanks.

John, great question. As usual, thank you for the insight. The answer is yes. Not just within these rheumatologic disorders where T cells are known to play a role, and there's literature on it, but of course, there are lots and lots of papers and understanding about other therapeutic areas which are even thought to be more dependent on T cell biology. Just to throw out a couple, multiple sclerosis and type 1 diabetes are thought to be, you know, primarily driven by pathogenic T cells. Not only within this initial set do we think we could have some differential efficacy, as you put it, but we also believe it will give us a more plausible pathway into other therapeutic areas where T cells are known to play a larger role than just a straight CD19 product.

Great. Thank you.

Thank you. Our next question comes from Reni Benjamin of Citizens. Your line is open.

Hey, guys. Thanks for taking the questions. Maybe just starting off with the interim analysis. Now that you've been able to, you know, kind of sit on the data with the futility analysis, do you feel that this delta that you're seeing increases the chances of a successful interim mid-2027 versus, you know, what you were thinking when you first started the study? If so, does it make sense to potentially modify the trial design to allocate a little bit more alpha and increase your chances of success there? Then regarding ALLO-329, as we kind of look at the landscape, look at autologous therapies and bispecifics, can you just guide us as to what is the clinical sort of efficacy and safety benchmarks you're hoping to hit, hoping to meet so that you can move this program forward?

Does this program move forward ideally with a partner, or do you think you do this on your own? Thanks.

Hey, Reni. On the interim analysis, you know, EFS analysis, you know, without a question, after looking at the MRD clearance differential, we believe the probability, I mean, or the powering for the interim analysis, you know, has gone up quite a bit. I mean, that really, you know, goes down to we have said that, you know, study was designed to demonstrate, you know, the hazard ratio of 0.5, but the MRD clearance, as we extrapolate, based on the existing data, you know, leads us to a potentially the hazard ratio being much lower than 0.5.

If that turns out to be true as we continue to enroll the study, the probability of interim analysis, as Zach has pointed out, you know, leading to a statistical significance is very significant. We'll just have to wait and see. Your second question about, you know, you know, would we consider amending the protocol. You know, I think that probably is not something that would be, you know, that's needed or that would be good to do at this point. I mean, I think the best course is just us sticking with the original study plan.

The question around where does this fit in the evolving landscape? We actually feel really good about that. Right now, that landscape in the front line is really been focused for a long time on increasing intensity of those regimens and looking directly at the bispecific-based regimens that are being studied, that really do add a lot of complexity and toxicity to those newly diagnosed regimen, the patient regimens.

We actually feel really good that, you know, no matter what happens upfront, an MRD positive result at the end of frontline treatment could trigger a cema-cel infusion and to be able to administer that, even in centers that we believe actually may not ever engage fully in frontline bispecific regimens because of the complexity and toxicity, that those centers could administer cema-cel in a consolidation setting. We actually feel like we have threaded the needle very well with ALPHA3 and are somewhat insulated from all of that competition in the early lines.

Reni, does that answer your question, or was the question on ALLO-329?

That last one that Zach answered was on ALLO-329 in particular.

Okay. That's what I thought.

Just trying to get it clear. Yeah. Sorry about that.

Let me, let me just answer, you know, the question on the ALLO-329. The profile that we are looking for is something that can be administered as an outpatient and patient managed as an outpatient. You know, plus that on top of that, the nature of the, you know, cell, you know, CAR T is that, you know, this will be a, you know, one-time treatment with a, you know, possibility of redosing, you know, several years down the line if the symptoms were to come back. You know, that is the, you know, profile that we believe will remain very competitive when you think about other emerging modalities that's coming, you know, in the T cell approach towards the autoimmune indications.

Thank you. Our next question comes from Brian Cheng of JPMorgan. Your line is open.

Hi, guys. Thanks for taking our question this afternoon. Just a quick one from us. Can you talk about the rationale of updating the autoimmune RESOLUTION data updates from June to 4Q? Is that decision data-driven or are there other considerations? Thanks for taking our question.

Yeah, Brian, let me take the question. I think our intent is provide data update in a very meaningful way. In terms of the maturity of the data and what we have now, I think what we can say is enrollment is very robust. Also there is, you know, very sort of interesting signs of clinical activity. I don't think, you know, definitely I think this is for now and as we dose escalate, I mean, keep in mind, we intentionally started the study with very conservative dose to ensure the patient safety. 20 million, I think there was an earlier question about whether that may be low. In my view, it probably was lower than what was necessary.

As we dose escalate, and certainly we are going to the dose levels that in other programs that we have done, you know, 80 million or 120 million is sort of the range that we have seen activities in programs like ALLO-316 or cema-cel. We're getting to that dose range, and, you know, as we update the data in fourth quarter, we will have patients treated at the dose that may be more in the right range. You know, definitely, we are enrolling this study rather briskly, and we'll have a lot to talk about in fourth quarter.

Great. Thank you.

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

All right. Thank you. We said at the onset that this would be in a year of defining proof. The ALPHA3 interim analysis represents an important first step. The signal we see today must be validated through EFS. It provides early support for a fundamentally different approach to CAR T, one that is earlier, more accessible, and potentially scalable. Our focus now is execution, completing ALPHA3 enrollment, advancing ALLO-329 through dose escalation, and continuing to generate the data needed to define the role of allogeneic CAR T across oncology and autoimmune disease. We believe we are well-positioned to do that. Thank you for your continued support. 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 log off and disconnect.

Hello, and thank you for standing by. Welcome to Allogene Therapeutics, Inc. Fourth Quarter 2025 Conference Call. After the speakers' presentation, there will be a question-and-answer session. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star 11 again. I would now like to turn the call over to Christine Cassiano, Chief Corporate Affairs and Brand Strategy Officer. Ms. Cassiano, please go ahead.

Thank you, Operator, and welcome, everyone, to Allogene Therapeutics, Inc.'s conference call. After the market closed, Allogene Therapeutics, Inc. issued a press release that provided a business update and financial results for the fourth quarter and year-end 2025. This press release and today's webcast are available on our website. Following our prepared remarks, we will host a Q&A session and will aim to keep the call under an hour. I am joined today by Dr. David Chang, President and Chief Executive Officer; Dr. Zachary Roberts, Executive Vice President of Research and Development and Chief Medical Officer; and Geoffrey Parker, 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, the safety and efficacy of our product candidates, commercial market forecasts, and 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 press release and latest SEC disclosure documents. You are cautioned not to place undue reliance on these forward-looking statements, and Allogene Therapeutics, Inc. disclaims any obligation to update these. I will now turn the call over to David.

As we close 2025 and enter what we expect to be a defining year for Allogene Therapeutics, Inc., the environment around us is shifting. Cell therapy has entered a phase defined by evidence, where progress will be measured not by speculation and promises, but by data and disciplined execution. That shift plays to our strength. Our focus in 2026 is straightforward: delivering meaningful clinical milestones with rigor and speed. This is a year of critical proof points—proof points that could validate our allogeneic platform not merely as an alternative but as the imperative path to making cell therapy scalable, accessible, and deliverable at biologic-like scale. First, with SemiCell and ALPHA-3, we are asking a bold but important question that could redefine the management of large B-cell lymphoma. Can we intervene earlier, making CAR T truly accessible in the community setting, meaningfully improve outcomes, and alter the course of disease without disrupting the physician's practice? The goals of this study are not about incremental improvement in a late-line setting. It is about shifting the paradigm in the first-line treatment and demonstrating that SemiCell can reduce the risk of relapse and improve the cure rate. Importantly, it is about expanding access to community cancer centers that historically have been excluded from offering CAR T—bringing advanced cell therapy to where most patients are treated, off-the-shelf, at biologic-like scale. Second, with ALLO-329, we are extending the promise of allogeneic cell therapy to autoimmune disease. ALLO-329 is a purpose-built, dual CD19/CD70 CAR designed specifically for immune-mediated conditions, incorporating our Dagger technology to potentially reduce or maybe eliminate traditional lymphodepletion. We expect to report proof-of-concept data in June 2026, and assuming continued progress, another clinical update by the end of the year. We are entering this execution-focused period from a position of financial strength, having extended our runway into 2028. That gives us the ability to advance ALPHA-3 and RESOLUTION with focus and discipline. We have built a broad and innovative clinical pipeline, but we recognize we cannot advance everything at once. Discipline requires prioritization. Today, we are concentrating our resources on the programs where allogeneic CAR T has the greatest potential to demonstrate what this modality can achieve when developed around its inherent advantages: scalability, accessibility, and ultimately, the potential for durable cure. At the same time, we believe that as the field recognizes that allogeneic CAR T can deliver at scale with rigor and practicality, it will unlock new opportunities to expand the platform into additional settings and indications. With that, I will turn it over to Zach to walk through the clinical progress in more detail.

Thanks, David. As David outlined, the second quarter is defined by two key programs: SemiCell and ALPHA-3, and ALLO-329 in RESOLUTION. I will concentrate on the clinical execution behind these studies, and what we expect to learn in the months ahead beginning with ALPHA-3. ALPHA-3 is the first randomized study in lymphoma designed to test whether early MRD-guided consolidation with an allogeneic CAR T can prevent relapse. Patients who achieve remission after standard first-line therapy undergo highly sensitive ctDNA testing. Those who are MRD positive and therefore at high risk of relapse are randomized to observation or treatment with SemiCell. In April, we plan to report results from the interim futility evaluating MRD clearance in 24 patients—12 each in the SemiCell-treated arm and the control observation arm—along with early safety data. We will also outline the anticipated timeline and key inflection points as the study progresses. We have anchored expectations around what we and many clinicians believe would be a meaningful threshold at 25% to 30% absolute delta in MRD clearance between arms. Achieving that outcome would have the potential to alter disease and meaningfully improve the rate of cure of large B-cell lymphoma in the first-line setting. At the upcoming analysis, we also intend to provide preliminary safety data and additional perspective on how the use of SemiCell is being implemented in community settings. We now have over 60 active sites across the U.S. and Canada, with engagement with health authorities and clinical site start-up activities underway in Australia and South Korea. The level of real-world integration of SemiCell as consolidation into routine practice across both academic and community centers underscores what we believe is a core advantage of the off-the-shelf model and its potential to expand access beyond traditional CAR T delivery hubs. I will now spend a few minutes on ALLO-329, our first-in-class, dual CD19/CD70 allogeneic CAR T therapy designed specifically for autoimmune disease. ALLO-329 was engineered for this setting from the outset. It targets CD19-positive B cells and CD70-positive activated T cells, both of which contribute to autoimmune disease. Our Dagger technology is designed to endow the cells with a kind of built-in lymphodepletion to enable optimal cell expansion and persistence while potentially reducing or eliminating the need for conventional cytotoxic lymphodepletion. The Phase 1 RESOLUTION trial is a 3+3 dose-escalation study enrolling patients across multiple rheumatology indications, including systemic lupus erythematosus, lupus nephritis, scleroderma, and inflammatory myositis. The study is evaluating several dose levels beginning at 20,000,000 CAR T cells in two parallel dose-escalation cohorts—one that includes cyclophosphamide only and one without any traditional lymphodepletion. Twenty million cells is a small number, but one that we selected based on our conviction that the Dagger technology in ALLO-329 could drive meaningful in vivo expansion. For context, competitive programs in autoimmune disease are evaluating doses of autologous CAR T cells that are up to five to 10 times higher than our starting dose, and other allogeneic cell therapy programs are exploring cell doses nearly 50 times higher. In June, we expect to report initial proof-of-concept translational data as well as early clinical signals from the first dosing cohort with and without lymphodepletion. As an off-the-shelf allogeneic CAR T product that does not require any degree of patient HLA matching, ALLO-329 persistence in patients treated with minimal or no lymphodepletion at this low starting cell dose would be a strong validation of the Dagger effect in autoimmune patients. Assuming continued enrollment and follow-up, we anticipate providing an additional clinical update later this year. The opportunity in autoimmune disease could be significant. But success in this space requires tolerability, outpatient feasibility, and scalability, particularly as treatment moves into rheumatology practices. ALLO-329 was engineered with those requirements in mind. Across both programs, our focus remains on disciplined execution, with the goal of generating data that clearly define the role of allogeneic CAR T in earlier-line oncology and in autoimmune disease. With that, I will turn the call over to Jeff.

Thank you, Zach. As we prepare for multiple clinical catalysts in 2026, our financial position is aligned with our strategic priorities. We have been deliberate in concentrating our resources behind ALPHA-3 and RESOLUTION while maintaining balance sheet strength and operational flexibility. As of 12/31/2025, we had $258.3 million in cash, cash equivalents, and investments. In February, we received an additional $23.7 million previously held in escrow related to Servier's favorable arbitration outcome with Selecta. We have also made prudent and opportunistic use of our ATM equity facility, and have raised an additional $20.7 million year to date. As a result of these actions, we have extended our cash runway into 2028, which we believe covers the time frame we currently estimate is needed to complete enrollment in the ALPHA-3 trial. R&D expenses for the fourth quarter were $28.6 million, including $2.5 million of non-cash stock-based compensation. For the full year 2025, research and development expenses were $150.2 million, which includes $12.9 million of non-cash stock-based compensation expense. G&A expenses for Q4 2025 were $13.8 million, including $5.6 million in non-cash stock-based compensation. For the full year 2025, G&A expenses were $56.8 million, which includes $24.7 million of non-cash stock-based compensation expense. Net loss for the fourth quarter was $38.8 million, or $0.17 per share, including non-cash stock-based compensation expense of $8.1 million. For the full year 2025, net loss was $190.9 million, or $0.87 per share, including non-cash stock-based compensation expense of $37.6 million and non-cash impairment of long-lived asset expense of $2.4 million. Guidance for operating cash expense in 2026 is expected to be approximately $150 million. GAAP operating expenses are expected to be approximately $210 million, including estimated non-cash stock-based compensation expense of approximately $35 million. These estimates exclude any impact from potential business development activities. With pivotal data from ALPHA-3 approaching in April, proof-of-concept data for ALLO-329 expected in June, and cash runway now extended into 2028, we believe we are well capitalized to execute through these important inflection points. Our focus remains clear: advance high-impact programs, manage capital responsibly, and position Allogene Therapeutics, Inc. for long-term value creation. We will now open for questions.

At this time, please press 11 on your telephone. If your question has been answered and you wish to remove yourself from the queue, please press 11 again. Our first question comes from Tyler Van Buren with TD Cowen. Your line is open.

Hey, guys. Thanks for taking the question and looking forward to both data updates next quarter. Could you elaborate on the safety parameters you will be looking at with the data update next month and what the bar is to support broad uptake in the community setting, and perhaps more importantly, how investigators in the community setting have already responded to incorporating SemiCell as a seventh cycle of treatment in the frontline?

Okay, thank you very much. I will ask our CMO, Zach, to elaborate on the safety aspect.

Hey, Tyler. Thanks for the question. We plan to provide some high-level safety information—enough for everybody to understand how well this is being tolerated. It is unlikely we will go into very, very minute detail, but certainly serious adverse events in both arms, the sorts of adverse events that would lead to hospitalization—those sorts of things—which absolutely feeds into your second and third questions. What is the bar that we need to hit for safety? We believe that this is best delivered as an outpatient. Therefore, this needs to be a therapy that can be delivered as an outpatient and does not lead to rehospitalization due to adverse events. And finally, can this be done in the community? Absolutely, it is being done in the community currently, and we look forward to sharing all of the safety aspects that are allowing this to be taken up in the community by physicians.

Next question comes from Biren N. Amin with Piper Sandler. Your line is open.

Yes. Hi, guys. Thanks for taking my questions. I wanted to focus on the recent ZUMA-7 MRD analysis that were published last month, where ExaCell observed a treatment difference of 20% on MRD negative, which translates to about an EFS benefit of around 27 months versus the control group. Given you are expecting a 25% to 30% difference on MRD conversion, what read-throughs do you have from the ZUMA-7 data and your confidence on stopping at your interim EFS analysis? And on the interim EFS analysis, if you could maybe just walk us through how many events you need and what are the assumptions on hazard ratio that could lead to an early stoppage. And lastly, when can we expect interim EFS data? Thank you.

Hey, Biren. Thanks for pointing out that recent MRD data analysis coming from a subgroup of patients who were involved in the ZUMA-7 study. We view this study to be very consistent with how we have been looking at the MRD clearance and its correlation to the clinical outcome. Besides the study, an earlier study that we have been talking about is INVIGO 11, where MRD clearance difference of 11% led to a very meaningful clinical difference. So what has been reported with ZUMA-7 is very consistent, and I believe it validates the guidance that we have been providing, which is 25% to 30% MRD clearance difference at the futility interim analysis that we project to share in April. This is highly consistent, and we do believe that 25% to 30% is going to translate to very meaningful clinical difference in the outcome. With respect to your second question—how much can we speculate or model out about how the MRD clearance may translate to the EFS interim analysis—I would say it involves too many assumptions and speculations, and it is a little bit too early to talk about it. But internally, we are constantly reviewing the data and our functions. So stay tuned.

Great. Thank you.

Our next question comes from Michael Yee with UBS. Your line is open.

Yes, guys. We have two questions. One was your thinking—first question is your thinking around the interim analysis and what would define whether you took that interim analysis on EFS. In other words, if the MRD conversion is super high, is that what would drive your thinking to take the EFS? So that is the question number one. And then question number two is on autoimmune. We wanted to understand target product. When you get your data coming up, is this to be a low lymphodepletion, a no-lymphodepletion type program? What are you trying to envision with the profile of that product? Thank you.

Yes, two great questions. In terms of this being somewhat similar to what Biren was trying to get at, one thing is that there is not enough data out there to see how MRD clearance relates to clinical outcomes such as event-free survival—whether this is a linear relationship, meaning that if there is a greater difference in the MRD clearance, there will be a greater difference in the clinical outcome. That kind of data, while plausible, is—there is such paucity of the data—so we cannot really establish that other than saying it is possible that if we see greater MRD clearance difference, that may translate to greater clinical benefit. To the point about how that may put us in the timing of interim EFS analysis: interim EFS analysis is an alpha-spending analysis. It is the primary endpoint analysis at a smaller event rate, and there is always the possibility that interim may cross the statistical boundary. That is part of the reason that we do the interim analysis—not just us; everybody who does interim analyses faces this. But let us stay tuned. Our focus right now is the MRD clearance that we promised to communicate in April. With the second question on the target product profile with the autoimmune program, our CD19/CD70—as Zach has covered in his prepared statement—this is a highly differentiated program that is endowed with a Dagger that may enable ALLO-329 to work at low or no lymphodepletion. So in the ongoing study, the baseline case that we are testing is low lymphodepletion, which is essentially using cyclophosphamide only. Standard lymphodepletion involves both cyclophosphamide and fludarabine. We took out the fludarabine altogether, and we lowered the cyclophosphamide dose to only one day infusion. That is the baseline case that we are testing. Also, we are testing, as part of the study, no lymphodepletion. The target product profile we are trying to get to is providing a meaningful B-cell depletion that is leading to reset of the immune system at cyclophosphamide alone. We think that will be the base case, and we will see if we can get to that without any lymphodepletion. That would be a great win—not just for the field, but for patients and everything that people are trying to do with B-cell depletion in the autoimmune space.

Thank you. One moment for our next question. Our next question comes from Salveen Richter with Goldman Sachs. Your line is open.

Good afternoon. Thanks for taking my question. On the overall SemiCell market opportunity and commercial positioning, CD3 bispecifics move to the frontline. This could influence MRD positivity rates or directly exclude patients from SemiCell eligibility. Just curious to get your thoughts on the evolving LBCL landscape and how you see SemiCell positioned long term? Thank you.

Hey, Salveen, this is Zach. Great question. It has been an interesting few years as these bispecifics have been approved in late lines and now are moving into frontline. I think if the early Phase 1 data in untreated patients is consistent with the overall Phase 3 readouts, there is a likely outcome that a certain percentage of patients may be cured with these very intense upfront regimens. So there is a possibility that there will be fewer MRD-positive patients. However, I think we very much need to wait for those final data before we begin to consider how the market opportunity may evolve—and not just efficacy, but also safety and the pace at which these complex and expensive regimens are taken up in the community. Our initial feedback is that not everybody is going to be lining up to be giving these very, very complex regimens that often require hospitalization for step-up dosing and so forth. We are watching this space very carefully, but we believe that the MRD positivity rate is largely going to be unchanged for the next many years.

Thank you. One moment for our next question. Our next question comes from Matt Phipps with William Blair. Your line is open.

And the update on timeline staying on track. When you look at that Foresight CLARITY data that looks at rates of MRD positivity post R-CHOP, are there any patterns around high-risk baseline characteristics such as double-hit, triple-hit genetics or, you know, IPI in the 4s, or something that you see in those patients that do not reach MRD clearance? And maybe you can remind us how SemiCell performed in those types of subgroups in your previous last-refractory trial? Thank you.

Great question. This is Zach again. Absolutely, there does appear to be differential MRD positivity rates according to the baseline risk, which is of course no surprise. MRD positivity at the end of treatment is an extremely high risk for disease progression, and it is precisely disease progression that was used to generate those risk stratification tools. So it is very consistent that if you have high-risk disease at the time of diagnosis, you are more likely to be MRD positive at the end of frontline treatment, and of course then you are more likely to experience a relapse. The beauty of ALPHA-3, however, is that there are lots of examples out there where patients who even have low-risk disease turn out to be MRD positive at the end of treatment. These are the patients that keep oncologists up at night because you think that the patients are going to do very well, and then they end up experiencing relapse. One of the things that we find so exciting about ALPHA-3 is that everybody gets a shot at upfront cure, and we do the risk stratification at the end of treatment and then escalate care accordingly with a consolidation dose of SemiCell. Looking back at our Phase 1 experience, we definitely saw good activity across the risk spectrum. So we do not anticipate there being gross disparities in the risk profile of these patients in the context of ALPHA-3.

Thank you. One moment for our next question. Our next question comes from Samantha Semenkow with Citi. Your line is open.

Hello? Hi. This is Ben on for Sam. Thanks so much for taking our question. Can you talk about expectations for the observation arm in the ALPHA-3 study? What is the expected rate of spontaneous MRD conversion, and if there is any data you could help us to triangulate this? Thank you.

Hey, Ben. This is Zach again. Great question. We get asked this one quite a lot. We have long assumed that the number of patients who are clearing MRD without further treatment will be a nonzero number. We have modeled it at about 20%. So in the 12-patient arm that we will be revealing next month, we are talking about two to three patients that we expect to potentially have an MRD conversion from positive to negative. This comes back to the fact that no test in medicine is perfect. There are false positives and false negatives with every single test that you can perform, including PET scan. In fact, one of the reasons that MRD is so exciting and we believe will transform care of these patients is because the false positive and false negative rates of the MRD test are significantly better than they are for PET scan. This is why when we are talking about the efficacy that we hope to see next month in April, it is relative to the spontaneous clearance rate. So when we talk about 25% to 30%, we expect that improvement over the baseline clearance rate because patients, of course, are eligible to spontaneously clear in both arms. So we should expect that 20% distributed in both arms.