Hello, and thank you for standing by, and welcome to Allogene Therapeutics' second quarter 2025 conference call. After the speaker's presentation, there will be a question and answer session. 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. At this time, all participants are in a listen-only mode. 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 Therapeutics 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 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. We are cautioned not to place undue reliance on these forward-looking statements, and Allogene Therapeutics 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 coalesce 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 two-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 1 data at ASCO 2025. This trial serves as a significant proof point for our Dagger technology 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 technology to support both robust expansion of CAR T cells and durable clinical responses in solid tumors. We have since aligned with the FDA on a pivotal trial strategy and are actively exploring partnership opportunities with several third parties to advance this program. In autoimmune disease, we opened enrollment in the RESOLUTION study, one of the first allogeneic CAR T trials in this space and the first of such to contemplate a new approach to lymphodepletion. We have designed both our AlloCAR T product and the trial itself with patient accessibility, not as an afterthought but as a priority from the outset. By simplifying or eliminating lymphodepletion altogether, we are testing both hypotheses grounded in strong science and clinical insight. This study reflects not only our ambition but also our readiness to challenge paradigms with data. Each of these advances is rooted in the belief that the breakthroughs are not born by chance; they are built. They emerge from a foundation of strong science, disciplined execution, cross-functional collaboration, and the agility to adapt and evolve when circumstances change. Nowhere is this more evident than in cell therapy, a field with a potential to transform how we treat disease and, in doing so, generate extraordinary value for those who invest in companies that have demonstrated the ability to navigate the terrain. While early optimism often fuels bold ambition, reality is often far more complex, especially in the unforgiving terrain of clinical development, where transformative ideas must be tested and refined. That's why many have started on this path, yet only a few have advanced beyond the early promise. Allogene Therapeutics stands among the few that have successfully persevered in this field. From the beginning, we have committed to these principles, not just in theory but in practice. Today, we are one of the last allogeneic cell therapy companies standing and the one with the most diverse and advanced clinical pipeline, and we take that position seriously. While the finish line in this field is neither fixed nor guaranteed, our continued progress reflects the depth of our platform, the strength of our team, and our unwavering commitment to doing the hard, necessary work that real innovation demands. As we look ahead, our near-term milestones are more than clinical achievements. We believe they are value-driving catalysts that reinforce our foundation and advance our vision of making allogeneic CAR T the standard of care. I want to thank the entire Allogene Therapeutics team for their passion and commitment and give a special thanks to Zach for his steady leadership in R&D. The choices we made this quarter really reflect our responsibility to move boldly and thoughtfully, always keeping patients at the center. With that, I'll hand it over to Zach. Thank you, David. I want to start with a personal reflection on ALPHA3 and the journey this trial has taken. 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 six 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'd always hoped would be the ultimate outcome, potentially optimizing benefit-risk and front-line consolidation and driving greater uptake in both the clinical trial and commercial settings. Following this selection, ALPHA3 is now proceeding as a two-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 from investigators to this design change has been quite positive, reinforcing our confidence that the path forward improves the safety and scalability of the study while significantly enhancing its appeal to participating centers. Accordingly, we remain on track for the planned futility analysis in the first half of 2026, which will assess MRD conversion rates between the two arms and provide a critical early signal of efficacy. This is the intersection of science, clinical design, and disciplined execution, and where meaningful progress is made. Turning to ALLO-316, our Phase 1b data presented at ASCO showed promising responses in a heavily pretreated RCC population. The strength of our Dagger technology supported exceptional CAR T expansion and persistence. As David noted earlier, following recent alignment with the FDA on a pivotal trial design, we're actively exploring partnership opportunities to advance the program. RESOLUTION, our study in autoimmune disease, is now open and actively screening patients. This trial represents a meaningful expansion of our platform into a new disease area and into uncharted territory for the field. It allows us to explore how we might fine-tune the levers of lymphodepletion with greater precision. By reducing or potentially eliminating lymphodepletion, we're taking a bold step toward reshaping what's possible in the treatment of immune-mediated conditions. If successful, RESOLUTION could serve as the foundation for a new therapeutic paradigm. We look forward to providing an update on the early clinical results from the RESOLUTION trial in the first half of 2026. Taken together, these programs reflect both the maturity of our platform and the clarity of our strategy. This is no longer conceptual. It's advanced clinical development moving forward because of the discipline, foresight, and steady execution by our team. We've entered a stage where conviction matters. As R&D leaders, we're called to rely on the strength of our science. In cell therapy, we must make complex decisions, but we are confident in the direction we're heading and even more so in the evidence that's pointing us forward. In the coming months, you will see us continue to advance these studies built on the momentum we've created and stay focused on delivering not only clinical value but a durable platform capable of changing how patients are treated across multiple diseases. With that, I'll hand the call over to Geoff. 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 non-cash stock-based compensation. G&A expenses for the second quarter were $14.3 million, including $6.1 million in non-cash stock-based compensation. Net loss for the second quarter was $50.9 million, or $0.23 per share, including non-cash stock-based compensation expense of $8.7 million and non-cash 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 non-cash 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. 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, one moment for questions. Our first question comes from Tyler Martin Van Buren with TD Cowen. You may proceed. Hey, thanks very much. Appreciate you taking the question and congrats on the progress during the quarter. As we think about the scheduled fertility analysis in the first half of next year, and since you announced that you plan to provide the rates of MRD conversion between the two 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? Hi, Tyler. Dave Chang here. Great question. It's something that we have been thinking about quite a bit here. We have been asked this question a few times, and we've been giving a rough estimate about 30%. Now that we are beginning to talk about the MRD conversion rate in a more concrete way, let me give you some reference points about where we are coming to about the delta of 30% difference in the MRD conversion rate being meaningful. 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. 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. In that data set, if you look at the delta in the complete remission rate, that was 27%. 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. In the follow-up, they also showed an overall survival benefit. 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%. Those are sort of the reference points that we are using 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. Thank you. Our next question comes from Biren N. Amin with Piper Sandler. You may proceed. Yeah, hi. Thanks for taking my question. 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? The second question is on cash runway guide to the second half, I see to 2027. Do you anticipate having cash to get to EFS data readout from ALPHA3? Thanks. Hi, Byron. Let me take the first question, and I'll pass to Geoff for the second part. The only thing that I ask from what I have responded to Tyler's question is if you equate MRD conversion to the CR, you know, the complete remission that you see, which I believe is a fair, you know, sort of assumption that one can make, you know, the answer to your question is yes. Let me ask Geoff to comment on the cash guidance. Yeah, so Byron, 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. Thank you. Our next question comes from Salveen Richter with Goldman Sachs. You may proceed. Hey, this is Mark on for Salveen. Congrats on the quarter, and thanks for taking our question. 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 FCA arm in any way impacting patient willingness to enroll and the enrollment cadence? Thanks. Yeah, 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. Discontinuation 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. 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. I think signs are pointing to a positive impact to the study. We look forward to being able to update you further at the time of the interim analysis. Thank you. Thank you. Our next question comes from Kelly Shi with Jefferies. You may proceed. Congrats on the progress, and thank you for taking my questions. 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. 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 set for the pivotal frontline consolidation study? Thank you. Hi, Kelly. I'm sort of smiling because that's a lot of questions and very insightful questions. 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 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. As for the MRD testing after Cema-cel treatment, we have been saying this occurs within about four to eight weeks after Cema-cel treatment is done. That is a similar time period to when one would carry out tumor assessment in a standard way. The timing of the MRD, I don't think it will significantly impact what we are doing in the ALPHA3 study. Yeah, 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. 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. 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. 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. We really are looking towards that second-line post-relapse setting to set the bar for what efficacy could be, and we think that bar is certainly achievable with this strategy. Thank you. Super helpful. Thank you. Our next question comes from Jack Kilgannon Allen with Robert W. Baird & Co. You may proceed. Great. Thank you so much for taking the questions and 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 the 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, you know, one-time cures here? Thanks, Jack. This is Zach again. 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. 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. Maybe can 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? 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? 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. Thanks so much for the call. Thank you. Our next question comes from Samantha Danielle Corwin with William Blair. You may proceed. Hi, congrats on the progress, and thanks for taking my questions. 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. 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 two arms. Looking at the ALLO-329 data, should we expect to see data from both lymphodepletion groups? Thank you. Yeah, so Sammy, 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 uses the event-free survival as the primary endpoint. In that sense, the MRD conversion is a secondary biomarker-based data. 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 whose only evidence of disease is MRD positivity. There are certain caveats, and we're trying to walk the fine balance. 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 the 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 on biomarker as well as early clinical data. As you know, the study is progressing in two different lymphodepletion regimens, starting with the cyclophosphamide-only lymphodepletion, which already is a reduced lymphodepletion compared to the standard fludarabine and cyclophosphamide. In addition to that, we are also testing no lymphodepletion in a parallel cohort. We'll provide more updates on exactly how much will be included in the first half of 2026 update as the study progresses. Great, thank you. Thank you. Our next question comes from Matt Biegler with Oppenheimer & Co. You may proceed. Hey guys, thanks for the update. I've had a lot of questions on MRD, but we haven't had any on cell expansion. I'm just wondering, 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? Looking back to 2022, your R&D event, the push for 647 really was that it improved cell expansion. I'm just trying to make sense of where we are now that we're in a different disease setting. Thanks. Yeah, Matt, Dave Chang again, let me take that question. I don't think it's really changing our thinking. As Zach had made a comment in his prepared statement, we knew that as we started ALPHA3 trial, you know, 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. 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. The conclusion that we drew at the time is that the approach that we have made in the relapse 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. That was how the genesis of the ALPHA3 trial, starting with the three arm, not only testing FCA, but also testing FC. 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. At this point, really, let's just stay tuned. I mean, we will know more in the next six months. Makes sense. Thank you. Thank you. Our next question comes from Samantha Danielle Corwin with Citigroup. You may proceed. I'm sorry for giving the question. I was pausing the last part that we had earlier this month. Kim, can you speak up a little bit? It's coming out a little bit muffled. Oh, apologies. Is this better? Yes. Perfect. Thanks for giving the question. I apologize for the call earlier this month that there was a protocol amendment to close the FCA arm. I'm wondering if that has been completed and as well as if you are able to continue enrollment into the FCA arm while that protocol amendment is underway. In my sense of the prior response to your question, you said that there's a defined period of MRD positivity where the patient could be eligible for enrolling in the study and I'm wondering if there's any overlap with that window and some patients might be missing it and not being able to enroll in the study. Thanks very much. 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. 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 that protocol amendment to be approved in the next few days. We anticipate very little, if any, disruption to the operations of this trial as a result of this amendment. Maybe you can ask the second part again. Yes, hopefully you're able to hear me now. Apparently, my speech is getting better. Much better, much better. Thank you. Bluetooth headphones were causing some issues. I think you answered most of the question. Just confirming that once this IRB approval comes through in a few days, all of the patients that were screened in the interim are still eligible to enroll into the FCA arm. Yes, absolutely. Understood. Thanks very much for the question. Thank you. Our next question comes from Luca Acey with RBC Capital Markets. You may proceed. Oh, great. This is Shelby on for Luca, and thanks for taking the question. 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 three deaths reported in multiple myeloma. I guess the question is, is this event going to slow down enrollment materially, or do you think this is a non-event for enrollment velocity? Any color there, much appreciated. Thanks. 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. The consensus was really quite clear that these patients, you know, you characterize them as relatively stable. I think the data would strongly indicate that these patients have chemo-refractory cancer. We know from the MRD data that these patients are going to progress and likely to progress very soon. The investigators, the patients who consider enrolling in 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 any clinical trial, this one included. 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. At that point, we really had the confidence that moving forward with the FCA arm would deliver the appropriate benefit risk for the patients in this particular clinical setting. All of us looked at the data, and we all think that this, investigators included, is worth pursuing. Got it. Thanks. Thank you. Our next question comes from Asthika Sarith Goonewardene with Truist Securities. You may proceed. Hey guys, thanks for taking the question. I probably want to just jog my memory here a bit. If I remember right, some of the earliest selective data showed that early reconstitution of the patient's T cells was what was correlated with poorer response. That was what rationalized the use of CD52 antibody back in the day. That was also in a leukemia setting as well as in a late line setting. 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 poorer response? I have a quick follow-up. Yeah, Dave Chang, let me give Zach a break and take your question. In terms of the early selective data, I think you are remembering it correct. I mean, certainly, in the relapse refractory setting, most of the data from selective is coming from the ALL study that was carried out. There was definitely an 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. 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 would have a lot of discomfort in limiting the lymphodepletion with FC alone. As we have said, MRD positive is a very unique clinical setting. On one hand, it clearly foretells that the patient will have a disease recurrence. 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. 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. As I said, that always has been one of our hypotheses as we are embarking on the ALPHA3 study. Thanks, David. The quick follow-up here is when you talk about the MRD conversion rates early next year, will you also be in the 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? Would that be too early to comment on that? Thanks. 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 because the futility analysis is based on 24 patients. Having said that caveat, we are trying to make that communication as informative to you analysts as well as the investors. Thank you. Our next question comes from William Pickering with William Blair & Company. You may proceed. Hi, thank you for taking my question and 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? How sensitive are those assumptions or criteria to the observed MRD conversion rate that you'll share early next year? Thank you. Hey, William, this is Zach. 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. We collect that test at that time, and then we analyze whether it's positive or negative. That's the data that we intend to share. Thank you. Thank you. Our next question comes from Reni John Benjamin with Citizens JMP Securities. You may proceed. Hey, good afternoon, guys. Thanks for taking the questions. With 329, I guess I'd love to get a better understanding and additional color on how you picked just the cyclophosphamide regimen. You know, and why not have maybe a three-arm study with FC, just cyclophosphamide, and then no lymphodepletion? What's leading you to this? 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, you know, other cell therapy players that have generated data in the autoimmune space? Thank you. Hey, Brian. David here. Let me take the first question about why we chose cyclophosphamide. In the autoimmune disease indication, we do believe that we have to think about it 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. Second, cyclophosphamide as a chemotherapy agent is something that many rheumatologists are very comfortable with since it often gets used to treat severe lupus or other autoimmune disorders. Embedded in your question is, is cyclophosphamide going to be enough? I would point you to the earlier studies that were published from Fred Hutch, where they have looked at a comparison of cyclophosphamide and fludarabine. 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. The durability comes from the addition of the fludarabine. For the autoimmune indications, the objective is to achieve deep B-cell depletion without prolonging it. From that sense, we felt cyclophosphamide alone would be a much better fit for autoimmune indications. 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? I think, ultimately, we will have to look at the clinical data. Leading to clinical data, there's a lot of good indicators. After all, the objective of at least the CD19 part of ALLO-329 is B-cell depletion. The degree of B-cell depletion, and more importantly, how they're returning B-cells, what are their phenotypes, I think those are very important information. Somewhat associated with that is the disappearance of autoimmune antibodies. Those are things that have consistently been observed with the autologous CAR T that have been tested in the autoimmune indications. That will give us a lot of information. 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. Got it. Thank you. Thank you. Our last question comes from Brian Cheng with JPMorgan Chase & Co. You may proceed. Hi, David. Thanks for taking our question this afternoon. 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're coming from the later line trials. 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 an earlier line? Thank you. Yeah, Brian, great question. The information that I cited is really coming from the second-line randomized study that was conducted with Yescarta and Breyanzi. 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 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, this is a really good reference point for ones to think about. Certainly, the ultimate test is the outcome of the ALPHA3 study. 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. As we reflect on this past quarter, it's clear that Allogene Therapeutics 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 the FDA on the pivotal trial path, an important step for what we believe is the most advanced allogeneic CAR T program in solid tumors. With ALLO-329, we've officially launched the RESOLUTION trial, 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. 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 Therapeutics' 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 month 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.