Hello, and thank you for standing by, and welcome to Allogene Therapeutics Second Quarter 2025 Conference Call. [Operator Instructions] 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 thank you for joining this call. After the market closed, Allogene issued a press release that provided a business update and financial results for the second quarter of 2025. This press release and today's webcast are available on our website. Following our prepared remarks, we will host a Q&A session. We recognize that historically, questions have been multifaceted, but note that we will endeavor to keep this 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 forecast 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, and welcome, everyone. This past quarter marked a period of significant advancement across our portfolio with progress that highlights how scientific excellence, rigorous decision-making and thoughtful planning and execution can call us into transformative momentum. We are seeing the power of this approach across our pipeline from cema-cel in first-line consolidation for large B-cell lymphoma to ALLO-316 in solid tumors and now ALLO-329 in autoimmune disease. Let me begin with cema-cel in the ALPHA3 study. The ALPHA3 study has been streamlined into a 2-arm randomized trial comparing treatment with cema-cel following a standard lymphodepletion regimen of fludarabine and cyclophosphamide in the active arm to observation in the control arm. This decisive move made in conjunction with the Data Safety Monitoring Board and Steering Committee reflects our unwavering commitment to patient safety. It also reflects our ability to act swiftly, balancing scientific judgment with agility to create and preserve the long-term value of our platform. I also would like to thank the review team at the FDA that provided prompt informal consultation and guidance. More than 50 sites are now activated across the U.S. and Canada and additional international expansion is underway. We remain on track for the planned futility analysis in the first half of 2026 and expect to share MRD conversion rates at that time. The changes to the protocol exemplify our vision to redefine CAR T therapy by prioritizing patient accessibility in every stage of development. Turning to ALLO-316, our CD70 targeted CAR T for renal cell carcinoma, we presented compelling Phase I data at ASCO 2025. This trial serves as a significant proof point for our Dagger platform and how this technology may define the future of off-the-shelf cell therapy. The results seen to date from the TRAVERSE trial underscore the potential for Dagger…

Thank you, David. I want to start with a personal reflection on ALPHA3 and the journey this trial is taking. The hypothesis that patients whose only evidence of disease was MRD positivity could be cured by cema-cel without the need to use enhanced lymphodepletion was always compelling. Standard FC is widely used, well tolerated and critically easier for doctors to give and patients to receive than a regimen that includes an additional infusion of an anti-CD52 monoclonal antibody. Furthermore, because these patients are just coming off 6 cycles of treatment, they are partially lymphodepleted already. For these reasons, we designed the study to test this hypothesis by comparing standard FC to the enhanced regimen that included ALLO-647, our anti-CD52 monoclonal antibody. While the recent developments in the trial required that we make a decision on lymphodepletion sooner than planned to ensure the safety of patients in the trial, the early biomarker and safety data emerging from the standard FC arm has given us confidence that the trial is moving ahead with the right treatment regimen. From the beginning, standard FC is the regimen we always hoped would be the ultimate outcome, potentially optimizing benefit risk and frontline consolidation and driving greater uptake in both the clinical trial and commercial settings. Following this selection, ALPHA3 is now proceeding as a 2-arm randomized trial comparing cema-cel after FC lymphodepletion versus observation. With more than 50 sites now open and incoming interest from new investigators globally, we continue to see a high degree of engagement from our sites and are continuing to add patients to the pipeline for MRD screening to support enrollment. For many sites, the simplification and streamlining of the study through the removal of the FCA arm is expected to boost participation and further strengthen engagement. In fact, the response…

Thank you, Zach. As David and Zach have outlined, our operational progress has been matched by disciplined financial stewardship. As of June 30, 2025, we had $302.6 million in cash, cash equivalents and investments. Our cash runway continues to extend into the second half of 2027. R&D expenses for the second quarter were $40.2 million, including $2.6 million of noncash stock-based compensation. G&A expenses for the second quarter were $14.3 million, including $6.1 million in noncash stock-based compensation. Net loss for the second quarter was $50.9 million or $0.23 per share, including noncash stock-based compensation expense of $8.7 million and noncash impairment of long-lived asset expenses of $2.4 million. We continue to expect 2025 cash burn of approximately $150 million and full year GAAP operating expenses of approximately $230 million, which includes an estimated noncash stock- based compensation expense of approximately $45 million. This guidance excludes any impact from potential business development activities. Let me conclude by highlighting that our allogeneic platform allows us to manufacture product well in advance and at scale, supporting trial execution while enabling cost reductions. With a refined strategy and strong clinical catalysts ahead, we remain confident in our position. We'll now open the call for questions.

[Operator Instructions] Our first question comes from Tyler Van Buren with TD Cowen.

Congrats on the progress during the quarter. So as we think about the scheduled futility analysis in the first half of next year and since you announced that you plan to provide the rates of MRD conversion between the 2 arms at the time of the announcement, what does good look like as you think about the bar for success with the MRD conversion rates?

Tyler, Dave Chang here. Great question. And it's something that we have been thinking about quite a bit here. And we have been asked this question a few times, and we've been giving rough estimate about 30%. But now that we are beginning to talk about the MRD conversion rate in a more concrete way, let me give you some reference point about where we are coming to about the delta of 30% difference in the MRD conversion rate being meaningful. So here, I would just ask you to sort of equate the MRD conversion to the remission, complete remission that you see with the CAR T treatment. And with that one assumption, take the reference point to the USPI of YESCARTA and BREYANZI, both of them are approved in the second-line setting in a randomized study that used event-free survival endpoint. In those studies, BREYANZI showed statistically significant and clinically meaningful event-free survival as well as progression-free survival benefit. And in that data set, if you look at the delta in the complete remission rate, that was 27%. Now if you take the same to the YESCARTA USPI, again, the ZUMA-7 study showed statistically significant and clinically meaningful event-free survival benefit as well as progression-free survival benefit. And in the follow-up, they also showed an overall survival benefit. And when you look at their initial indication of efficacy, which is really the response rate, the complete remission rate difference between the YESCARTA arm and the standard of care bone marrow transplant arm, that was 33%. So those are sort of the reference points that we are using and to sort of guide about a delta of 30% difference in the MRD conversion rate could potentially give us a statistically significant and clinically meaningful benefit demonstration of the ALPHA3 study.

Our next question comes from Biren Amin with Piper Sandler.

Maybe just to expand on the last question. How should we translate if we're able to see a 30% delta on MRD conversion, should we expect similar EFS benefit to what was observed with BREYANZI and YESCARTA in their respective trials in the second-line setting? And then second question is on cash runway guide to the second half -- excuse me, 2027. Do you anticipate having cash to get to EFS data readout from ALPHA3?

Biren, let me take the first question, and I'll pass to Geoff for the second part. So only thing that I ask from what I have responded to Tyler's question is, if you equate MRD conversion to the CR or the complete remission that you see, which I believe is a fair sort of assumption that one can make. The answer to your question is yes. And let me ask Geoff to comment on the cash guidance.

Yes. So Biren, as you stated, we do have cash into the second half of 2027. Whether that is sufficient to get to EFS readout on ALPHA3, frankly, depends on the pace of enrollment that we will see in the trial, and we'll be updating you on that once we have the futility analysis. As you recall, though, there is an interim analysis and a final analysis in the ALPHA3 study. And I would say second half of 2027 is going to be right in the ballpark as to when those events could occur.

Our next question comes from Salveen Richter with Goldman Sachs.

This is Mark on for Salveen. Congrats on the quarter. So kind of to expand on that, how is enrollment progressing for ALPHA3? You briefly mentioned this in the prepared remarks, but I was wondering if you can give any quantification. Is the discontinuation of the FDA arm in any way sort of impacting patient willingness to enroll and the enrollment cadence?

Yes. Thanks, Mark. This is Zach. I will say that the momentum that we described at the last quarter continues to this day. There's a lot of interest in patients coming into the study. It's a little soon still to see how the discontinuation of FC may impact -- sorry, FCA. Thank you, Christine. Discontinuing of FCA may impact the overall enrollment cadence. What I can say in these very early days post the discontinuation of that arm, we are generally getting positive feedback from investigators who are happy to be dealing with a regimen that they are much more comfortable with. And it's also -- they've told us that it's easier in the conversations with the patients. They don't have to spend as much time talking about this additional agent that can induce the immunosuppression that is associated with CD52. So I think signs are pointing to a positive impact to the study. So we look forward to being able to update you further at the time of the interim analysis.

Our next question comes from Kelly Shi with Jefferies.

Congrats on the progress. I'm curious actually whether you see the timing of capturing MRD-positive patients post R-CHOP have any impact on the MRD conversion rate after the treatment and also maybe also the impact on EFS as the endpoint? And the second question is, if we take a step back, can you talk about the clinical evidence from your prior studies or maybe other historical studies? Like how was the efficacy bar was set for the pivotal frontline consolidation study?

Kelly, I'm sort of smiling because there's a lot of questions and very insightful question. Happy to have you sort of covering us again. With respect to the timing of the MRD, in the clinical study, we are doing it in very similar to how the retrospective study was done. There is a defined window at which the MRD testing is done to make the patient eligible to the ALPHA3 study. And as for the MRD testing after cema-cel treatment, we have been saying this occurs within about 4 to 8 weeks after cema-cel treatment is done. So again, that is a similar time period to when one would carry out tumor assessment in a standard way. So the timing of the MRD, I don't think it will significantly impact the -- what we are doing in the ALPHA3 study.

Yes. And there's no data to just piggyback on David's point, there's no data, Kelly, to date to indicate that the timing of that MRD assessment will impact our ability to induce conversions. So -- and similarly, we don't expect that to influence EFS. Those are fairly tightly correlated MRD conversion and long-term disease control based on prior data from our MRD partner. And then I think the second question that you asked was around whether there's any prior data on MRD conversion and whether the bar that we are aiming for is aligned with that prior data. So I'll actually point back to David's answer to Tyler's question around what we think is going to be a clinically meaningful and significant outcome from ALPHA3, and that is around that 30% mark. There isn't really any data in large B-cell lymphoma, looking specifically at MRD clearance in a prospective way, ALPHA3 is really the tip of the spear on this. So we really are looking towards that second-line post-relapse setting to really set the bar for what efficacy could be. And we think that bar is certainly achievable with this strategy.

Our next question comes from Jack Allen with Baird.

Robert W. Baird & Co. Incorporated, Research Division Congrats again on all the progress. I guess I wanted to ask about how you're thinking about MRD conversion and its correlation with durability. I know a lot of the earlier stage data that you have from cema-cel included both the FC and FCA arm. How much confidence do you have as it relates to the durability of remissions that you maybe see on this MRD test playing out as onetime cures here?

Thanks, Jack. This is Zach again. So our belief and based rooted in the data that is now sort of growing in the field around this MRD assessment is that an MRD conversion going from positive to negative at the time point that we're performing the assessment is a very good correlate to long-term disease control. So that is why we analyzed this biomarker assessment to enable LD selection because we did believe that this was going to correlate tightly to EFS.

Robert W. Baird & Co. Incorporated, Research Division And maybe could I just follow up, are you going to look at any other internal metrics of durability other than MRD at the time of the interim? And then one brief follow-up on 329. I just wanted to think about the first half readout next year. What kind of patient numbers could you have there across the different diseases in the basket study?

So we will -- as promised in our materials and in our prepared remarks, we will be giving you some detail around the MRD conversion, and we'll leave it at that for now. With respect to the question on 329, we've also not given specific numbers on what to expect, except to say that the study is open to enrollment currently, and we do expect to have a meaningful amount of data to share in the first half of next year.

Our next question comes from Sami Corwin with William Blair.

Congrats on the progress. I know previously, when we've spoken, you guys were initially hesitant to do the MRD analysis with the futility analysis or share that information because you were concerned that sharing the MRD conversion rates could influence the behavior of treating physicians. So I guess I'm curious how your thoughts around that have kind of evolved and how that might ultimately impact the difference in overall survival between the 2 arms? And then looking at the ALLO-329 data, should we expect to see data from both lymphodepletion groups?

Yes. So Sami, David Chang here. The great question. Yes, we do have a lot of sensitivity in the amount of the efficacy data that we can share. The ALPHA3 study, it uses the event-free survival as the primary endpoint. So in that sense, the MRD conversion is a secondary biomarker-based data. And in the large B-cell lymphoma, yes, there are some data that seem to correlate the MRD conversion to the durability of the response, but that has not been prospectively tested, especially in patients who only evidence of disease is MRD positivity. So there are certain caveats, and we're trying to walk the fine balance. But from the fact that we are limiting the data communication at the interim futility analysis to MRD conversion, we believe that we can still maintain in a balanced way as we continue to enroll additional patients after the futility analysis. I think the clinical equipoise would not be compromised by sharing the secondary biomarker data on a limited number of patients. With respect to ALLO-329 data communication in the first half of next year. Let's just say that we are focusing a biomarker as well as early clinical data. And as you know, the study is progressing in 2 different lymphodepletion regimen, starting with the cyclophosphamide only lymphodepletion, which already is a reduced lymphodepletion compared to the standard fludarabine and cyclophosphamide. However, in addition to that, we are also testing no lymphodepletion in a parallel cohort. So we'll provide more updates on exactly what -- how much will be included in the first half 2026 update as study progresses.

Our next question comes from Matt Biegler with Oppenheimer.

I had a lot of questions on MRD, but we haven't had any on cell expansion. So I'm just wondering like has your thinking changed now that you're in a lower tumor burden setting on the importance of cell expansion? Is it not as relevant as it was in a higher disease setting? Because that -- looking back to 2022, your R&D event, the push for 647 really was that it improved cell expansion. So I'm just kind of trying to make sense of where we are now that we're in a different disease setting.

Yes. Matt, Dave Chang again. Let me take that question. I don't think it's really changed in our thinking as Zach had made a comment in his prepared statement, we knew that as we started ALPHA3 study, we are going into a different clinical setting of the extremely low volume disease setting, where the antigen target, which is really what triggers the cell expansion is at the lowest possible level that one can think about. So we had a very open-minded approach about in that kind of setting, what degree of cell expansion would be optimal to eradicate MRD positivity. And the conclusion that we drew at the time is that the approach that we have made in the relapsed/refractory setting. So these are the patients with the bulky disease where we felt cell expansion as well as persistence is really important. We cannot think the same way. And that was how the genesis of the ALPHA3 study starting with the 3 arm, not only testing FCA, but also testing Fc. So obviously, at this point, we have some idea as we have previously communicated through the unplanned data analysis, MRD conversion being seen in the Fc. So at this point, really, let's us stay tuned. I mean we will know more in the next 6 months.

Our next question comes from Samantha Semenkow with Citi.

I recall that you had earlier this month that...

Can you speak up a little bit? It's coming out a little bit muffled.

Apologies. Is this better?

Yes.

Perfect. I recall from the call earlier this month that there was a protocol amendment to close the FCA arm. And I'm wondering if that has been completed as well as are you able to continue enrollment into the FC arm while that protocol amendment is underway? And as to the prior response to your question, you said that there is a defined period of MRD and where is the MRD productivity and where the patient could be eligible to enroll in the study. I'm wondering if there's any overlap with that window and some patients might miss it enrolling in that study.

So sorry, Samantha, it was still quite muffled. I think I got the first part of your question, and I'll answer that and then maybe you can try to fix your connection and ask the second part because that one was a little harder to understand. The first question was around the status of enrollment as the operational implementation of the closure of the FCA arm is underway. So the patients are continuing to be screened for MRD. The protocol amendment that enabled us to close the FCA arm earlier than anticipated is with IRBs currently. We expect those -- that protocol amendment to be approved in the next few days. So we anticipate very little, if any, disruption to the operations of this trial as a result of this amendment. And then maybe you can ask the second part again.

Yes. Hopefully, you're able to hear me now.

Much better, thank you.

Bluetooth headphones were causing some issues. So yes, I think you answered most of the question, just confirming that once this IRB approval comes through in a few days, all the patients that were screened in the interim are still eligible to enroll into the FC arm.

Yes, absolutely.

Our next question comes from Luca Issi with RBC Capital Markets.

Great. This is Shelby on for Luca. Maybe circling back on a prior question on enrollment. We appreciate that the death that you guys reported a couple of weeks back was likely related to ALLO-647, which you're obviously no longer pursuing. However, this is also the first time you're reporting a death in the first-line maintenance setting for a patient that was otherwise relatively stable post R- CHOP versus, I believe, the other deaths that you reported in the past were in patients with much more refractory disease like the 3 deaths reported in multiple myeloma. So I guess the question is, is this event going to slow down enrollment materially? Or do you think this is a nonevent for enrollment velocity? Any color there much appreciated.

Thanks, Shelby. Good question and absolutely part of the analysis when we wrote the study and then in the immediate wake of this unfortunate Grade 5 event, we asked ourselves that very question. We discussed it with all of the external stakeholders like the DSMB, the steering committee and the FDA. And the consensus was really quite clear that these patients, you characterize them as relatively stable. I think the data would strongly indicate that these patients have chemo refractory cancer. And we know from the MRD data that these patients are going to progress and likely to progress very soon. So the investigators, the patients who consider enrolling this trial, see themselves not as in remission and likely to never hear from their cancer again. They actually, I think, appropriately see their situation as extremely high risk and worthy of enrollment into a clinical trial. That said, a Grade 5 event like the one that we observed is a significant moment in a clinical -- any clinical trial, this one included. And that was what prompted us to take a look at the overall safety data as well as that MRD conversion data that we referred to. And at that point, we really had the confidence that moving forward with the FC arm would deliver the appropriate benefit risk for the patients in this particular clinical setting. So all of us looked at the data, and we all think that this investigators included is worth pursuing.

Our next question comes from Asthika Goonewardene with Truist.

Truist Securities, Inc., Research Division A follow-on just to jog my memory here a bit. And if I remember right, some of the earlier Cellectis data showed that early reconstitution of the patient's T-cells what was correlated with poor response, and that's what rationalized the use of CD52 antibody back in the day. But that was also in lymphoma setting as well as in a late-line setting. So to ask the question again, but more focused on the endogenous T-cell population, is the earlier line setting and also post R-CHOP, does that change the dynamics here of what could predicate a poor response? And then I have a quick follow-up.

Yes, Dave Chang, let me give Zach a break and take your question. In terms of the early Cellectis data, I think you are remembering it correct. I mean, certainly, in the relapsed/refractory setting, most of the data from Cellectis is coming from the ALL study that was carried out. There was definitely indication that adding anti-CD52 antibody leads to a more prolonged cell expansion. Having said that, even with the FC regimen, there always has been some degree of cell expansion, and that's always something that we have known. So it's really trying to thread the right needle that fits the clinical indication that we are going after. If we are going after a bulky disease setting, I'll have a lot of discomfort in limiting the lymphodepletion with FC alone. But as we have said, MRD positive is a very unique clinical setting. On one hand, it clearly curtails that the patient will have a disease recurrence. But on the other hand, the level of disease that's in the patient's body is not detectable by conventional PET-CT scan. It is at the molecular level of disease burden, which is the objective of the ALPHA3 study, trying to eradicate that minimal disease. So this is a lot different clinical setting and the kind of cell expansion or persistence that most people are thinking about doesn't really apply. And as I said, that always has been one of our hypothesis as we are embarking on ALPHA3 study.

Truist Securities, Inc., Research Division And then a quick follow-up here is, when you talk about the MRD conversion rates early next year, would you also be in a position to give color on the mix of patients that came from community versus academic as well as those who are treated inpatient versus outpatient? Or would that be too early to comment on that?

I mean, certainly, in terms of patient distribution, I don't see any reason to withhold that information. It may be in a limited number of patients, I mean, because the futility analysis is based on 24 patients. So having said that caveat, I mean, we are trying to make that communication as informative to you analysts as well as the investors.

Our next question comes from William Pickering with Bernstein.

Congrats on the continued progress. For the interim analysis, are you able to share any of the quantitative criteria to run that, such as minimum number of events or minimum duration of follow-up? And how sensitive are those assumptions or criteria to the observed MRD conversion rate that you'll share early next year?

William, this is Zach. So we don't think that the MRD conversion rate that we intend to share is going to be terribly sensitive to some of those aspects that you highlighted. The protocol describes an MRD assessment at a specific time point. And so we collect that test at that time and then we analyze whether it's positive or negative, and that's the data that we intend to share.

Our next question comes from Reni Benjamin with Citizens.

With 329, I guess I'd love to get a better understanding and additional color on how you picked the just the cyclophosphamide regimen? And why not have maybe a 3-arm study with FC, just cyclophosphamide and then no lymphodepletion. So what's leading you to this? And then as a follow-up, what kind of proof-of-concept data do you think you need to see in order to move the program forward, especially given other cell therapy players that have generated data in the autoimmune space?

Ren, David here. So let me take the first question about why we chose cyclophosphamide. In the autoimmune disease indication, I mean, we do believe that we have to think about a little bit differently when it comes to the benefit risk profile, especially the risk profile. Taking away fludarabine provides a lot of additional safety benefit. And then second, cyclophosphamide as a chemotherapy agent is something that many rheumatologists are very comfortable with since it's not -- it often gets used to treat severe lupus or other autoimmune disorders. And sort of embedded in your question is, is cyclophosphamide going to be enough? This one, I would sort of point you to the earlier studies that were published from Fred Hutch, where they have looked at a comparison of cyclophosphamide and cyclophosphamide and fludarabine. So what was very clear from that presentation was that cyclophosphamide alone is good enough to give the cell expansion. However, the durability of cell expansion is not as great. Really, the durability comes from -- by the addition of the fludarabine. So for the autoimmune indications, really, the objective is to achieve deep B-cell depletion without prolonging it. So from that sense, we felt cyclophosphamide alone would be a much better fit for autoimmune indications.

Got it. And just as you see that data, that proof-of-concept data, what are you looking for in order to kind of get that go/no-go decision, make that go, no-go decision?

I think ultimately, we will have to look at the clinical data, but leading to clinical data, there's a lot of good indicators. After all, the objective of at least CD19 part of ALLO-329 is B-cell depletion. So the degree of B-cell depletion and more importantly, how they're returning B cells, what are their phenotype. I think that those are very important information. And somewhat associated with that is disappearance of autoimmune antibodies. And those are things that have consistently been observed with the autologous CAR T that have been tested in the autoimmune indications. Certainly, they will give us a lot of information. And ultimately, as we follow those patients, their clinical response, whether they continue to require other anti- autoimmune medications, whether their symptoms go away, I think all those things can be told relatively quickly.

And our last question comes from Brian Cheng with JPMorgan.

I just want to follow up on your bar for success in ALPHA3 earlier. The 30% delta reference, I think you and Zach mentioned, they seem to be coming from the later line setting. I think the trials that you quoted, they are coming from the later line trials. So how is this bar, the 30% conversion bar a fair translation in this consolidation line that you're shooting for after R-CHOP or R-CHIP? Shouldn't we expect a higher bar when you're looking into earlier line?

Yes, Brian, great question. Frankly, the information that I cited is really coming from the second-line randomized study that was conducted with YESCARTA and BREYANZI. And I think this is, in my view, a very good reference point as long as you equate MRD conversion to the CR that you can detect with a PET/CT, as long as you accept that premise, I think the sort of the analogy or the reference point about what bar would be sufficient to get to a statistically significant as well as clinically meaningful benefit on the EFS and PFS. I think this is a really good reference point for ones to think about. And certainly, the ultimate test is the outcome of ALPHA3 study.

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. As we reflect on this past quarter, it's clear that Allogene is entering a new chapter, one defined by operational clarity and growing clinical momentum. With ALPHA3, we made a decisive move to streamline the study, enhancing patient safety while preserving the trial's scientific integrity and simplifying the regulatory path. With ALLO-316, we've reached alignment with FDA on the pivotal trial path, an important step for what we believe is the most advanced allogeneic CAR T program in solid tumors. And with ALLO-329, we've officially launched RESOLUTION study, our first foray into autoimmune disease with a study that could redefine how cell therapy is applied in immune-mediated conditions. These are not incremental steps. We are -- they are true inflection points with each one accelerating our path towards a future where allogeneic CAR T is not only possible, but the standard of care. Our upcoming milestones are value-driving catalysts that have the potential to reshape the landscape of cell therapy and define Allogene's leadership in the field. Thank you for your continued interest and support. We look forward to connecting with many of you in upcoming meetings and events in the months ahead. Operator, you may now disconnect.

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