Thank you, operator, and welcome, everyone, to Allogene's Third Quarter 2025 Conference Call. After the market closed, Allogene issued a press release that provided a business update and financial results for the third 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 the 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. This quarter has been about conviction, conviction in our science in the path we have chosen and in the future we are building for patients. We are aware of the shifting conversation in the field. Every new modality brings excitement and speculation about what the future might hold. But true innovation isn't about chasing what's next. It is about delivering what patients need now. And if a platform can safely, effectively and at scale deliver curative therapies, it doesn't just shape the future. It redefines it. At Allogene, our focus has never wavered. We are advancing the platform we believe is not only essential to making cell therapies accessible and scalable, but one that could fundamentally alter the current paradigm and even the one others are still imagining by making the promise of curative, one-time, off-the-shelf cell therapy a reality today. And that's exactly what allogeneic cell therapy represents. It's not a bridge to something else. It is the foundation. Allogeneic technology delivers the scalable backbone needed to democratize access, reduce the overall cost of care and bring transformative and potentially curative treatment to far more patients than ever before. We expect allogeneic therapy to be central across oncology and autoimmune disease because it combines the precision and power of autologous with a flexible, efficient and commercially viable model that no other approach can. Its capacity for multiplex gene engineering allows the creation of future platform products within a single cell, an advance that we believe will be critical for addressing complex cancers, including solid tumors. This is incremental progress. It's a leap forward that reshapes what's possible. We have done the hard work to make the future real. Our leadership in manufacturing, translational science and clinical development positions Allogene to endure and lead, setting the standard for how cell therapy can be delivered at scale and with impact. Each of our programs, cema-cel, ALLO-329 and ALLO-316 reflects that strategy to make cell therapy scalable, practical, successful and in some cases, curative. At Allogene, we are not waiting for the future of cell therapy. We are creating it with conviction, with data and with a platform built for lasting impact. As we move into next year, we are preparing for what we expect to be a defining moment with pivotal interim data from cema-cel in the ALPHA3 trial in first-line consolidation and proof of concept from ALLO-329 in autoimmune disease, both milestones that we believe will shape the next era of cell therapy.

Thanks, David. Our programs this quarter continue to demonstrate the conviction David spoke of, conviction in our science and our execution and the discipline required to advance truly innovative medicines. Across ALPHA3, Resolution and Traverse, we're driving forward a portfolio that spans earlier line lymphoma, autoimmune disease and solid tumors. Each is a distinct challenge, but together a unified demonstration of the strength and versatility of our allogeneic platform. In ALPHA3, our pivotal trial of cema-cel has now been streamlined into a 2-arm randomized study comparing treatment after standard Fc lymphodepletion versus observation. This structure balances efficacy, safety and scalability, which are critical for translating CAR-T therapy into earlier lines of treatment. We are now at more than 50 active sites across the U.S. and Canada with expansion into Australia and South Korea expected early next year. The planned futility analysis focused on MRD conversion remains on track for the first half of 2026. A positive outcome would not only demonstrate disease modification in earlier line lymphoma, it would also mark a key step toward a potential BLA submission. As we look ahead to the upcoming futility analysis and the questions we often get about what success looks like at this stage, there are 2 key benchmarks worth keeping in mind. The first is the pivotal POLARIX study, and the second is the recent IMvigor-11 trial in bladder cancer, which is highly analogous to what we're doing with ALPHA3. The POLARIX study, which evaluated polatuzumab plus chemoimmunotherapy in frontline DLBCL demonstrated a modest 7% improvement in progression-free survival over standard treatment. That result alone underscores how much opportunity remains for meaningful progress and the transformative potential of ALPHA3. While ALPHA3 is the first study of its kind in LBCL, the concept of consolidating remission in patients at high risk of relapse has guided adjuvant trials in solid tumors for decades. Highly sensitive MRD tests are emerging as powerful tools to identify patients at greatest risk of progression. The recent data from the IMvigor 11 trial in bladder cancer is a powerful illustration of this approach. Patients with no evidence of disease after definitive frontline treatment, in this case, surgery, underwent a ctDNA-based MRD test. Those who were ctDNA positive while in remission were randomized to immunotherapy or placebo. Notably, ctDNA clearance differed by only 11% between arms at cycles 3 or 5, yet both the primary endpoint of disease-free survival and the key secondary endpoint of overall survival were statistically significant, representing a potentially practice-changing advance. While every study is different, the new IMvigor 11 data provides a valuable analog for illustrating the potential impact of this kind of approach. Achieving an approximately 30% delta between cema-cel and observation would represent the largest improvement in lymphoma outcomes since the approval of rituximab. Given these reference points, we believe our study is well positioned to deliver a highly meaningful difference and the potential for a successful trial outcome. Together, these insights reinforce our confidence in the strength of the ALPHA3 program and its potential to meaningfully advance lymphoma treatment. As we look beyond cema-cel, our Dagger technology continues to demonstrate its value across indications. In the TRAVERSE trial, the Dagger technology enabled ALLO-316 to produce durable responses in nearly one-third of patients with metastatic kidney cancer and high CD70 expression. These responses following standard Flu/Cy and a single infusion of ALLO-316 highlight the built-in lymphodepletion advantage of the Dagger technology, enabling best-in-class CAR T cell expansion in solid tumors. The TRAVERSE trial provided important insights that helped shape the design of our dual CD19/CD70 construct in autoimmune disease. Rather than repurposing a construct from another indication, we set out to create something truly fit for purpose designed from the start with a long-term application in mind for autoimmune disease and the patients who would be treated. We were the first to engineer CAR specifically for this setting, pairing dual targeting with our Dagger technology to achieve intrinsic built-in lymphodepletion through selective immune modulation. ALLO-329 is a first-in-class allogeneic CD19, CD70 dual CAR T product designed to target both CD19-positive B cells and CD70-positive activated T cells, which are key drivers of autoimmune disease. This approach is intended to simplify administration, improve tolerability and extend the reach of CAR-T therapy to a much broader patient population. If successful, it could represent a step change in the treatment of immune-mediated diseases. That is what we aim to achieve in the Resolution study, our Phase I basket trial in autoimmune disease, which is now enrolling for lupus, myositis and scleroderma. We expect to report translationally important biomarker and early proof-of-concept data in the first half of 2026. Dave and I spend a great deal of time in the field with investigators. Their enthusiasm remains strong because they see how these studies could fundamentally change the accessibility of cell therapy. By enabling treatment delivery within community networks where most patients receive care, we are aligning with how these institutions operate clinically and economically. This model reduces referral barriers, simplifies logistics and supports sustainable integration of advanced therapies into routine practice. Clinical development is complex. We compete for patients, particularly in autoimmune indications and face both scientific and operational challenges. But each challenge strengthens our understanding and sharpens our execution. That is the nature of innovation: iterative, demanding, and grounded in data. Collectively, our programs underscore that allogeneic CAR T is not an iteration. We believe it is the foundation upon which the next generation of cell therapy will be built. The science continues to advance. The early signals remain strong, and our focus is on turning that progress into real-world impact for patients. With that, I'll hand the call over to Geoff.

Thank you, Zach. The operational and scientific progress that David and Zach described is backed by a strong financial foundation and disciplined capital management. Our focus remains on advancing our clinical priorities while maintaining flexibility to capture long-term value for shareholders. As of September 30, 2025, we had $277.1 million in cash, cash equivalents and investments. Our disciplined approach to resource management continues to support a cash runway that extends into the second half of 2027. R&D expenses for the third quarter were $31.2 million, including $2.8 million of noncash stock-based compensation. G&A expenses for Q3 2025 were $13.7 million, including $5.9 million in noncash stock-based compensation. The net loss for the third quarter was $41.4 million or $0.19 per share, including noncash stock-based compensation expense of $8.7 million. We continue to expect a 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. The impact of our allogeneic platform extends well beyond our disciplined cost structure. By manufacturing product in advance and at scale, we lay the groundwork for a more efficient and sustainable model for the broader healthcare system. Allogeneic therapies have the potential to meaningfully lower the overall cost of care for cell therapy, expand access beyond specialized centers and make transformative cell therapies available to patients in a way that is both clinically practical and economically viable. With important clinical catalysts on the horizon and a solid financial foundation, we remain confident in our ability to execute and deliver on the opportunities ahead. We will now open the call for questions.

For the futility analysis in the first half of next year, could you see any data beyond MRD conversion? And can you just expand on the 30% bar that you commented on? And then just remind us how enrollment is progressing for ALPHA3 and whether you've seen any changes post discontinuation of the FCA LD arm earlier in the year?

Zach here. For your first question, regarding any additional data beyond the MRD conversion, we are currently focused solely on the MRD conversion. This will not involve an interim analysis where we might allocate alpha. We're concentrating on the MRD conversion instead of the primary efficacy endpoints. Regarding the 30% benchmark we mentioned, we believe achieving that would be a significant success for cema-cel in the trial. This belief is based on the POLARIX data, which showed a 7% improvement in progression-free survival in frontline lymphoma. Additionally, recent data from a similar trial in bladder cancer showed an 11% MRD clearance in that context while still achieving significant primary endpoint wins in disease-free survival and overall survival. Therefore, we view 30% as a strong outcome for the MRD clearance rate of cema-cel. As for your question on enrollment, I want to emphasize that we are on track for our interim futility analysis scheduled for the first half of next year. In terms of the study's conduct changes after the grade 5 event last summer, switching from a three-arm to a two-arm design has generally pleased investigators, as they prefer a regimen they recognize as standard in CAR-T without the need for an additional component like the CD52 antibody. This adjustment seems to have slightly improved patient screening for the trial.

This is Sam on for Tyler. Just for the over 50 U.S. and Canada active sites, what percent of these have made it through that initial internal setup period and are now able to start actively enrolling patients?

Sam, this is Zach again. We have gotten a lot better at forecasting how long that internal setup takes as well as sort of incorporating that into our timelines. So I would say that of the over 50 that are active, it's going to be close to all of them that are open to enrollment. Only the most recently activated sites might still have a few remaining things that they need to do before they switch on. But for the most part, all 50 of those 50-plus are actively screening and enrolling patients.

Congrats to the team on the progress made over the course of the quarter. I guess I'll ask one on the autoimmune program with 329. It seems like that's starting to get off the ground here, and you're going to have an update in the first half of next year. I just wanted to hear any updated thoughts you have around the size and breadth of the dataset we should expect next year from that program.

Chad, this is David Chang. Let me take that question, giving Zach a little bit of a break. In terms of the scope of that data communication, as we have previously said, there will be a handful of patients where we can show biomarker as well as the early clinical responses. So that's the extent of it. And frankly, what we have seen with autologous programs is a handful of patients are sufficient to really understand what's going on with the CAR-T therapy. So we are hoping that the initial communication in the early first half of next year will be a very meaningful communication.

On the progress I'm curious how many patients have consented for MRD testing now in ALPHA3 and if you're seeing the expected rate of MRD positivity that you initially theorized you'd see?

Zach mentioned that since the update earlier this year regarding the number of patients who consented, there haven't been regular updates on that information. He noted that the rate of consenting has remained steady since the beginning of the year, indicating growth in numbers. Additionally, the rate of MRD positivity is consistent with their initial assumptions.

So Caribou recently reported that their allogeneic CAR T product derived from younger donors demonstrated improved durability. Have you observed similar associations in your experience?

Carina, let me take that question. Yes, we follow Caribou and in terms of their recent announcement of the result, it looks pretty encouraging. But in terms of the material, I mean this is something that we have been following pretty closely, and we have a good way to identify the exciting materials that will result in very potent and consistent products.

Another one on the autoimmune program. I'm wondering, there's some recent data in the autologous space in pemphigus where there was no lymphodepletion in that trial that showed some pretty encouraging results. I'm wondering if there's any read-through that you can take into your program. Obviously, you have the CD70 CAR as well. But I'm curious if this increases your optimism on showing pretty robust efficacy without lymphodepletion.

Samantha, Dave here. Thanks for that great question. I have to say that what we are seeing in both autologous CAR-T therapy, so obviously, autologous and allogeneic, there are different issues. But what we have seen just gives us even higher confidence that ALLO-329, this is a CD19 dual CAR that has built-in lymphodepleting capability that ALLO-329 in the low-volume setting, such as in the autoimmune disease setting where it targets essentially the resident B cells and activated T cells, it will work well without the lymphodepletion. Obviously, we have to show that. And just as a reminder, in the ongoing study, we will be testing two different cohorts, one with reduced lymphodepletion. So this is just with cyclophosphamide alone. And the second cohort will be without any lymphodepletion.

So David, given that 329 is pretty unique in that it targets both B cells and activated T cells, I'm wondering, in the initial data readout, will you be able to get a look at the phenotype of the remaining T cells, just to see if perhaps there's anything left after you hopefully wipe out all the CD70-positive T cells.

John, that's certainly something we are considering. It raises nuanced questions about how CD70 is functioning. We have examined the fraction of CD70 positive versus CD70 negative T cells. It's important to note that most plasmatic T cells are CD70 negative and are not impacted by ALLO-329. There is a significant advantage in removing activated T cells, particularly those that may be contributing to the autoimmune disease, as well as our reactive T cells. Regarding the data we will share when we present the proof-of-concept results in the first half of 2026, I won't go into too much detail, but your question is very pertinent, and we will definitely analyze both CD70 positive and CD70 negative fractions.

Also for ALLO-329, when you talk about the biomarker data, David, are there any in particular that would alert you to achieving a B-cell reset? And when we get those results, will the results be robust enough that it can help you, help us as analysts and decide which indications you might move forward with?

Yes, great question. I mean, there are two parts to your question. One is whether the biomarker data will give us a lot of insight about how ALLO-329 is working. Having seen most of the data that's coming out in this space from CAR T, I do believe that the biomarker data will be very meaningful. But also, we intend to show some early clinical responses depending on how long the patient has been followed up. So when we communicate the proof-of-concept data in the first half of 2026, it will be more than just a biomarker. There will be early sort of clinical responses that may corroborate with what we see in the biomarker data. The second question to me is probably the most fascinating one. And if anything, I believe that we have probably very broad indications that we can potentially consider. The fact that 329 targets both CD19 and CD70 really allows us to not just think about those autoimmune disorders that are heavily B cell-driven, but also autoimmune diseases that are very T cell-dependent or have a big T cell component. So essentially from the rheumatology indications to neurology indications such as multiple sclerosis or even metabolic indications such as type 1 diabetes could be considered. So stay tuned.

Can you talk about your level of confidence in the MRD conversion to event-free survival? And then when you said around 30% MRD conversion as the bar, can you clarify a bit on the time point that is going to be meaningful for LBCL? And then how soon after dosing do you think we can reach that level of conversion? Zach, do you want to take that question?

Yes, I can take that question. So Ron, I may need to have you repeat one or two of them. But I think the first question was how confident are we in the prognostic value of MRD conversion as it relates to the study endpoints? I would say we're pretty confident, high confidence actually, given everything that we know about the performance of this assay after frontline, which was recently published in JCO, as well as after CAR-T has been shown at ASH a couple of years in a row. The test seems to be pretty good and actually correlating with long-term outcomes. Can you repeat the next two questions? I heard the second one, but I didn't hear the third one.

Yes, of course. Sorry. When you said the bar you said of 30% MRD conversion, can you clarify a bit on the time point that's going to be meaningful for LBCL? And then how soon after dosing do you think we can reach that level?

I understand. So regarding the 30% MRD conversion we've discussed, we have already provided some reasoning for choosing that number during this call. One way to view it is that it is comparable to or perhaps even slightly better than the results seen with rituximab added to CHOP. If MRD conversion is indeed a good predictor of clinical outcomes, which I believe it is, it would represent a significant success, possibly even a home run. As for the timing, we haven't gone into specifics about when we will be measuring these MRD results. However, I can mention that it is a dynamic test that shows rapid increases and decreases. Thus, we can evaluate MRD fairly soon after CAR-T infusion. While we haven't defined the exact timing, we are quite confident that the timing we have chosen will be predictive of clinical outcomes.

This is Catia on for Luca. Congrats on the progress this quarter. And if I can push on the last question on the timing of analysis for MRD. Is the futility study for stopping the trial as MRD is below your bar of 30%? And I think you mentioned the last time the 30% MRD bar is partially based on other autologous CAR-Ts objective response rate. And correct me here, if I'm not understanding this correctly, but that is from a potentially much longer follow-up. So is there a chance that you see insufficient MRD at your futility analysis first half next year, but we'll probably just have to give it more time. Any color there much appreciated.

Yes. Let me address that question. There are still some uncertainties regarding what would be ideal for the study. Regarding the MRD conversion, which is the key reference point for our futility analysis, we are confident in the assumptions we are making. These assumptions are supported by various data sources, including information from autologous CAR T therapy and new data from other MRD-based studies. Therefore, we feel quite assured about how we will conduct the futility analysis in the first half of next year.

This is Katie on for Rob. My question is about any recent interactions with the FDA and whether the movement towards greater flexibility in CAR-T oversight might provide accelerated pathways or lessen obstacles for you to reach the market.

Yes. We have a lot of ongoing communications with the FDA. And so far, it has been very timely and very productive. And the question that you are raising is a very interesting one. I mean, I think we will have to see when the time comes, but all the indications that we can make from what the FDA has said is that a single-arm approach with CAR-T therapy, that path is still wide open. And the FDA is carefully reviewing the other side of the BLA requirement, what is needed on the CMC side. So we view this to be very positive for what we are doing.

I apologize for the technical issues. I have one question. How are you managing variability in the MRD assay sensitivity across different sites? What measures are you taking to ensure consistency in MRD conversion assessment for the futility analysis?

Claire, that's an easy one. The MRD test is all being done centrally by Foresight Diagnostics. So all the sites are doing is collecting the samples and then sending them into the central lab. So we don't expect there to be any kind of technical variability in the test performance.

Thank you, operator. Let me close out by saying that everything we have built over the past 7.5 years has led to what's ahead in 2026. There are many ideas about where cell therapy is headed, but progress depends on staying focused on what is real and achievable. At Allogene, we kept our focus on building therapies that are scalable, reproducible and ready for patients. In the first half of 2026, we expect two major milestones: interim futility data from ALPHA3 with stem-cell in first-line consolidation and proof-of-concept results from ALLO-329 in autoimmune disease. These will not be theoretical advances. If successful, they will mark true clinical validation of the allogeneic platform, shaping our company's trajectory and building broader confidence in the potential of allogeneic CAR T therapy. The opportunity ahead is significant. We are entering 2026 with conviction, clarity and momentum and are excited for what the coming months may hold.

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