Hello everyone, and thank you for joining us. My name is Alex Chapman, and I'm the Head of Investor Relations and Corporate Communications here at Poseida. Before we begin, we'd like to remind listeners that today's call will include forward-looking statements that are based on current information, assumptions, and expectations that are subject to change. Actual results could differ materially from those stated or implied by our forward-looking statements due to potential risks and uncertainties that can be found in our press releases and latest SEC disclosure documents. These statements are made as of today's date, and the company undertakes no obligation to update these statements. During today's call, you are welcome to type questions into the chat window, which Poseida Management will address, as time allows, during the Q&A portion of the agenda. At the conclusion of the call, a recording of the program, including speakers and presentation slides, will be posted to the investor section of Poseida.com. With that, I'll turn it over to Dr. Kristin Yarema, President and CEO, to kick off today's program. Kristin? Thank you, Alex, and thank you everyone for joining us today. It's my great pleasure to welcome you all to Poseida's first-ever R&D day dedicated to our allogeneic cell therapy pipeline in oncology and autoimmune diseases. We have a packed agenda today. After I give an overview of our company's platform technology, visible pipeline, and high-level cell therapy strategy, we will go much deeper into each of three therapeutic areas. Following that, we'll have a fireside chat on the power of partnerships with special guest Peter Sandor from Astellas, and take a look at Poseida's in-house GMP manufacturing capabilities. We will then conclude and take Q&A. Poseida is a company built on a set of proprietary non-viral genetic engineering tools that we have used to generate a rich and rapidly advancing pipeline of products. We have two areas of focus: allogeneic CAR-T and non-viral in vivo genetic medicines. We had an R&D day in April of this year for genetic medicines, while this session today is dedicated to cell therapy, including clinical stage programs, preclinical, new platform tech, and cell therapy manufacturing. We believe our highly differentiated tools and technology, which are now being validated in the clinic and with our own GMP manufacturing, put Poseida in position as the emerging leader in allogeneic CAR-T, and that we will be able to create value and deliver transformational therapies with what we call a capacity to cure, where other companies relying on older viral technologies have struggled. Poseida stands apart in using a non-viral system of genetic engineering tools and supporting tech, including a unique gene editor and transposon technology rather than viral vectors. We use these tools to engineer and manufacture allogeneic CAR-T from healthy donor cells for our allo-CAR-T business. We are also using the same tools for in vivo gene editing and/or gene insertion, which is our non-viral genetic medicines business. So altogether, we really have extraordinary familiarity as well as versatility with our toolbox. Turning to cell therapy, we continue to believe that allogeneic CAR-T, where products are manufactured from healthy donors, manufactured at high volume and low cost, and stored frozen in inventory to be immediately ready for patients, is what is needed to unlock the opportunity and is the ultimate future of cell therapy. We also think you need the right type of cell to do this. Our vision is that our T stem cell memory-rich allogeneic CAR-T will enable all patients who can benefit from transformational cell therapy to be able to do so. With this in mind, we are now working in three therapeutic areas: hematology, where despite a small handful of autologous CAR-T approvals, access to therapy remains constrained and additional safe and efficacious options are needed, solid tumors, a much larger patient population with significant unmet need, where success with CAR-T has remained elusive and we do not yet have approved CAR-T, and finally, autoimmune disease, a new and burgeoning area offering the exciting possibility that CAR-T might be able to simply reboot the immune system with a single treatment in many highly symptomatic and grievous autoimmune diseases. Vast numbers of patients today are treated chronically, often with expensive therapies that do not provide full levels of disease control. Designing, developing, and commercializing allogeneic cell therapies is not easy because a company needs to have answers for four things simultaneously. First is the selection of cell type. Unlike other companies that use virus-based technology and/or an assortment of immune cell types, Poseida's non-viral technology enables us to produce CAR-T very rich in T stem cell memory cells. Stemness has been shown to be correlated with depth and durability of response, and T stem cell memory cells in particular are persistent, self-renewing cells that are expected to deliver a better safety profile in the clinic. Second is a safe, reliable, and cost-effective gene insertion technology to put in the CAR transgene. Poseida's non-viral transposon delivers the T stem cell memory cell phenotype and the ability to insert multiple genes in a single step, which allows us to produce products with multiple CARs while also conferring safety and product purity traits. Thirdly, a strategy to avoid allo-reactivity, graft versus host and host versus graft interactions, must be used. Poseida uses its own high-fidelity Cas-CLOVER gene editor to do this, which is able to edit resting T cells and maintain the T stem cell memory phenotype. Finally, the great promise of allogeneic cell therapy is providing many, many doses from a single production batch to dramatically lower manufacturing costs and eliminate wait time to the patient. We have our own GMP facility right on site in La Jolla, and we are achieving high yields reliably for all our clinical stage products. This slide provides a closer look at our suite of technologies that enable us to address the four key areas I just described. I'd like to emphasize that this fully non-viral toolbox has been designed and developed over many years to work together as a system. For example, we accomplish the gene insertion and gene editing together in one single production step for efficiency. We also have developed enabling technologies such as a proprietary booster molecule and a selectable marker that we use in purification to deliver consistent and high-purity products. All of these tools are unique to Poseida and are well protected with an extensive Poseida IP estate. Here's a look at our current visible pipeline for all Poseida programs, with cell therapy programs appearing to the right of the blue box. In heme malignancies, our lead program, P-BCMA-ALLO1 for multiple myeloma, is in phase 1b and is partnered with Roche, as is our other phase 1 program, P-CD19CD20-ALLO1 for B-cell malignancies. Roche has also recently nominated a new dual CAR-T program coming out of our research collaboration for heme malignancies, including multiple myeloma. We also have two programs that we will be introducing today. First, our wholly owned dual allo-CAR-T directed against BCMA and CD19, which is an exciting asset for a range of autoimmune diseases and heme malignancies as well. We are also advancing P-CD70-ALLO1, which could be useful in both AML and solid tumors such as renal cell carcinoma. Roche has an option on this program. In solid tumors, our internal program, P-MUC1C-ALLO1, is in phase 1 with a data update coming at ESMO IO. We also have an internal PSMA allogeneic CAR-T program for prostate cancer. And finally, we have a partnership with Astellas in solid tumors for convertible CAR-T that we'll hear more about today. In the gold color, we have our two preclinical non-viral in vivo genetic medicines programs, including our gene editing program using Cas-CLOVER, P-KLKB1-101, and our non-viral gene insertion program for hemophilia A, P-FVIII-101, which uses transposon technology. We believe that we are poised to become the leader in allogeneic cell therapy with a roadmap to value creation for our shareholders and for patients. Until recently, we've been working in the first of the three growth horizons depicted on this slide, Validate Platform, which is foundational work directed at validating our allogeneic T stem cell memory-based CAR-T platform through delivering clinical data across multiple programs led by P-BCMA-ALLO1, which is enrolling in a focused phase I B study and has received RMAT designation in multiple myeloma. We expect this program to continue to move rapidly toward registration-enabling data generation. Importantly, we also see as foundational our establishment of our partnerships with Roche and Astellas, which help us fund the company as well as support our technology and the programs. As we said many times, advancing cell therapy manufacturing in lockstep with clinical development is also critical to maintain program speed and lower risk. We are very proud to have been manufacturing in-house exclusively for over two years now. Now we've entered the second horizon, Drive Value, in which we're extending our work into new areas such as autoimmune disease, deepening and extending our pharma partnerships, which continue to provide funding for the business while further building our manufacturing and donor pool competencies. We are also highly focused on growing the proportion of our pipeline made up of Poseida wholly owned assets to create further value, and we are working on next-generation tools and technologies that will help us crack the toughest problems and biggest opportunities in cell therapy, such as solid tumors. What is our ultimate aspiration and destination? We will not stop until we reach our third horizon, deliver for patients. We believe our allogeneic cell therapies can disrupt and set new standards for care in the diseases we work in. Because we have worked hard to develop a system of genetic engineering tools and manufacturing processes that consistently and reliably deliver product candidates, we believe we will have a product engine generating wave upon wave of products and will be able to produce them at volumes that meet the needs of many, many thousands of patients at low production cost in a wide range of diseases. These products will incorporate the technologies you will hear about today, such as our CAR-TCR platform. With a product engine in place, there are many paths to commercialization, and we look forward to the future commercialization of our partnered and our own internal products. With the advantages in efficacy, safety, cost, and patient experience that we believe are accessible using T stem cell memory-based allogeneic cell therapy, we foresee excellent value propositions for these products that will drive uptake in the market and make our bold vision for allogeneic CAR-T a reality for patients. Now, I'd like to turn things over to Syed to kick things off with heme malignancies. Thank you, Kristin. I'm Syed Rizvi, Chief Medical Officer at Poseida, and I'm thrilled to be here today to talk more about our most advanced assets in heme malignancies, a recap of the interim data we recently shared at the International Myeloma Society annual meeting in September, and a look at our broader heme pipeline and upcoming data milestones. When we recently presented the data at IMS, not only our investigators who have put their heart and soul in the study, but also many of the key opinion leaders were really, really intrigued and impressed with the data, so let's first talk about multiple myeloma. Multiple myeloma is a serious and incurable disease in which malignant plasma cells proliferate in the bone marrow, giving various symptoms to the patients. Patients suffering from this incurable disease can go on to be treated for many years or even decades. Unfortunately, sooner or later, every therapy fails, and the patient faces progressive disease. For this reason, many different classes and choices within classes of myeloma therapeutics are needed. Use of drugs in combination is also common in myeloma and considered a standard of care. Despite recent advancements, access to approved auto CAR-T cell therapy strictly is still highly limited, with only a small percentage of patients actually receiving the potentially life-saving therapy. To fully unlock the multiple myeloma opportunity for CAR-T therapies, production at scale will be needed. As many as 85,000 multiple myeloma patients may be starting new therapies this year in the U.S. alone, of which roughly 16,000 may be starting their fourth line of therapy or more. It is also estimated that well over 50,000 U.S. patients per year are receiving second line or later treatment. With the approval of multiple myeloma regimens in front line, patients are likely to receive BCMA-targeted therapies earlier in their treatment journey, and the population of BCMA experienced patients is growing. In our myeloma study, we are generating data in both BCMA naive as well as BCMA experienced patients. Not only this, but we are generating data in patients who have received more than one prior BCMA-targeted agents as well as have received prior GPRC5D-targeted agents. Autologous cell therapies have been transformational for myeloma. Yet, only a small fraction of myeloma patients are able to receive it, given various limitations and challenges with auto CAR-Ts, such as auto CAR-Ts require invasive apheresis procedures to collect patients' own cells for manufacturing, significant manufacturing waiting time, complex supply chain logistics, and need for bridging chemotherapy to keep a patient's myeloma in check, resulting in potential adverse events. Even with all these challenges, there is always some uncertainty as to whether a given patient's cells can be successfully made into CAR-T or not. All of this complexity and single patient, single batch manufacturing means autologous CAR-T is costly to produce and administer, and difficult to scale up to meet the needs of tens of thousands of patients per year. We believe the future of cell therapy is allo. In simple terms, we think the right kinds of off-the-shelf allo CAR-T can be highly efficacious and safe. They have the potential to expand patient access by enabling rapid treatment to patients. Our allo CAR-Ts are made from healthy donor cells and not from patients' own cells. Poseida CAR-Ts are manufactured in bulk and way in advance. They are available in the freezer of a medical center when a patient shows up for treatment. In our P-BCMA-ALLO1 trial, we are seeing only about 3.5 weeks total time from treatment decision to measured clinical response compared with months for autologous CAR-T. In a setting where every hour and every day matters for a cancer patient, it is very meaningful to provide the treatment as quickly as possible and without any delays. We think this is an incredibly compelling time advantage. P-BCMA-ALLO1 is the most advanced allogeneic CAR-T program in clinical development for multiple myeloma at Poseida. We are developing it with our partner, Roche. P-BCMA-ALLO1 is currently being studied in open-label phase I dose escalation trial in adult patients with relapsed refractory multiple myeloma to evaluate safety and anti-myeloma effect. Patients must have received at least three prior lines of therapy, which should include an IMiD, a proteasome inhibitor, and an anti-CD38 antibody, or they would be triple refractory. The study includes patients who have been previously treated with BCMA-targeted therapy and/or GPRC5D-targeted therapy. The study employs a 3+ 3 dose escalation design to test multiple doses of CAR-T from multiple product lots manufactured from different donors. Several lymphodepletion regimens are being investigated to enable optimal CAR-T expansion. The lymphodepletion regimen consisting of cyclophosphamide 750 milligrams per square meter per day and fludarabine 30 milligrams per square meter per day given for three consecutive days in Arm C is the chosen lymphodepletion for phase I B. The study is actively enrolling patients. The overall response rate in Arm C was 91%, including five patients who achieved CR or stringent CR, six patients who achieved VGPR, and 10 patients who achieved PR. The overall response rate was 100% in BCMA naive patients and 86% in patients who previously received BCMA-targeted therapy. The overall response rate of 86% was maintained in the subset of seven patients who received prior treatment with agents targeting both BCMA and GPRC5D. The overall response rate was 82% in 11 patients that had received prior therapy with a bispecific T cell engager. This is a growing area of high unmet medical need with poor outcomes and with no established therapies. First, the P-BCMA-ALLO1 phase one population included patients that were more difficult to treat than the patients in the corresponding pivotal studies of different agents, and these are listed from left to right in the first five columns of the table. When looking at baseline demographics, we can see the P-BCMA-ALLO1 patients are older and have somewhat poor performance status. We have successfully treated patients up to 85 years of age in this study, and we have given as routine prophylaxis only Tylenol and Benadryl. We have also studied a racially diverse patient population in the phase 1 study, which is important because patients of color have historically shown poor clinical outcomes in myeloma. P-BCMA-ALLO1 is also emerging as distinctly differentiated in terms of its safety. Looking at data from our study and doing an indirect comparison to data from competitor pivotal studies, we see lower rates of CRS, neurotoxicity, and infection, as well as no use of bridging chemotherapy. All CRS and ICANS have been grade one or two. Overall, grade three or higher infections were uncommon, even in arms with higher lymphodepletion. We've also seen no signals of Parkinsonism, cranial nerve palsies, or secondary primary malignancies or SPMs in this study. Importantly, the safety profile observed was consistent in both BCMA naive and BCMA experienced patients and across all study arms. We're excited about the possibilities for patient treatment that a safer off-the-shelf CAR-T could offer. We have treated some patients entirely in the outpatient setting already and could see P-BCMA-ALLO1 potentially being given at more sites of care, including community sites, bringing significant convenience and benefits to the patients and physicians, as well as improving market access. Although the ORR data is still relatively early and need time to mature, the early efficacy is impressive. In this table, we are looking at data from commercially available auto CAR-Ts that's taken from their pivotal clinical trial publication. Remember, these trials enrolled only BCMA naive patients. We know that auto CAR-Ts enrolled an ITT population, which was larger than the patients who actually received the CAR-T. This was because some patients were unable to receive CAR-Ts due to disease progression before infusion or manufacturing failures or other reasons. This is why auto CAR-Ts report their response in modified ITT population and not the entire ITT. However, if we analyze the overall response rate in the ITT population for these CAR-Ts and for these agents, it is lower. Looking left to right, there are two columns for each of the CAR-Ts. First column shows the response data published for patients who enrolled in the study and were actually received the CAR-T, and the next column shows the response rate for the total intent to treat patient population. The benefit is clear. Similarly, here we are comparing commercially available bispecifics: Talvey, Tecvayli, and Elrexfio. Early safety and efficacy data from P-BCMA-ALLO1 Arm C looks very promising. The overall response rate higher than the approved bispecific looks great. We will be looking to see if responses from Arm C will continue to deepen over time. We believe there are many factors that contribute to the activity of P-BCMA-ALLO1 in a heavily pretreated patient population, most notably the robustness of stem cell memory T cells that our CAR-T produces. In addition, the CAR utilized by P-BCMA-ALLO1 has potent activity against wild-type BCMA and clinically identified escape mutants, which may contribute to the efficacy we have observed in BCMA experienced patients. Patients across all optimized lymphodepletion ARMCs A, B, and C are shown here, with the waterfall indicating the responses by disease markers. This was the data that was presented at the International Myeloma Society meeting earlier in September. Impressively, the median time to response for the most mature cohorts of ARMCs A and B was only 16 days. The median duration of response reported for patients with at least six months of follow-up at the time was 232 days. We are enthusiastic about continuing the development of P-BCMA-ALLO1 together with our partner, Roche. The data shows that it's a highly potent agent in a refractory and difficult-to-treat patient population. It was great to see that BCMA naive patients as well as BCMA experienced responded, including patients who received prior bispecifics, which were BCMA-directed and GPRC5D agents-directed. We're also seeing a compelling emerging safety profile and are demonstrating the ability to treat all eligible patients reliably and quickly without bridging therapy. So how do we think this might fit with the available treatment landscape? We think P-BCMA-ALLO1 could be an attractive option for healthcare professionals and patients, particularly when comparing it to the existing treatment landscape for myeloma patients. We will highlight this comparison over the next few slides. A little bit more information about our phase 1b portion of the study, which has just started. The study is actively enrolling patients. The phase 1B has two dosing cohorts. One cohort will be evaluating patients who receive a dose of about 250 million CAR-T cells, and the other cohort will be evaluating patients who receive a dose of about 500 million CAR-T cells. The lymphodepletion in both cohorts will remain the same at 750 cyclophosphamide and 30 fludarabine. Around 40 patients will be enrolled. Key inclusion criteria includes patients who have received three or more lines of therapy, including a PI, IMiD, and an anti-CD38 antibody, or be triple refractory. Patients must have measurable disease and have an ECOG of zero or one. Key endpoints include overall response rate, safety, and tolerability. With RMAT in place, we will be advancing this program, working very closely with the agency. Changing gear and looking at our other assets and development. Our first dual allogeneic dual CAR-T in clinic is P-CD19CD20-ALLO1, which is currently enrolling patients in a phase one study in selected B-cell malignancies. This is the first allogeneic dual CD19, CD20 targeting CAR-T in our knowledge. Antigen escape up to 40% of relapse and progression is reported in B-cell malignancies. Early data indicates that a dual CAR-T may be more effective in this space. In addition, we believe our allogeneic approach would be convenient for both patients and providers alike. This phase one dose escalation study is currently enrolling patients with select relapse refractory B-cell malignancies. The study shows. I'm sorry, the study allows patients who received prior CAR-Ts or bispecific T-cell engagers. We are looking forward to share data updates in the future. Here we are showing in vitro and in vivo potency of P-CD19CD20-ALLO1 CAR-T cells against the Raji cell lines, which is a CD19 and CD20 dual positive B-cell malignant model. On the left panel, you see that P-CD19CD20-ALLO1 CAR-T cells show high potency across multiple effector-to-target or E:T ratios and multiple donors. Similarly, as shown on the right, our dual targeting product shows high in vivo efficacy, again, across multiple healthy donors and dose levels. As a next step, we then engineered Raji cells to express only CD19 or only CD20 and showed that, as envisioned, P-CD19CD20-ALLO1, which is dual targeting, can efficiently target cells that have gone through antigen loss and therefore prevent relapse. So in this experiment, we show that P-CD19CD20-ALLO1 is equally potent against primary B cells from patients with a variety of autoimmune diseases, including SLE, MS, and RA. CAR-T were incubated with PBMC, and equally potent B cell killing was observed across patient samples with about 90% B cell killing at a one-to-one effector-to-target ratio and 100% B cell killing at five-to-one ratio. So another asset in our pipeline is targeted towards CD70. CD70 has emerged as a very intriguing target for both hematologic malignancies and also solid tumors, most notably, I would say, AML and RCC or renal cell carcinoma. For AML, what distinguished CD70 from other targets is the lack of expression on HSC or hematopoietic stem cells, which has been a persistent toxicity problem for other AML targets. For RCC, CD70 has also emerged as safer and more specific than most solid tumor targets. P-CD70-ALLO1 uses our latest CAR-T platform technologies and, in this case, also uses shRNA knockdown of CD70 on the CAR-T to avoid fratricide. We have found that shRNA knockdown has potency advantages over knockout. CD70 is highly expressed in AML, including AML leukemic stem cells. CD70 is also expressed in other tumor types, including non-Hodgkin's lymphoma and RCC. The good thing is CD70 is not expressed on normal bone marrow and hematopoietic stem cells, as I indicated earlier. In addition, expression of CD70 on activated T cell enables its potential use as a target in autoimmunity and/or as a T cell shield to improve persistence of allogeneic CAR-T cells. Published data suggest CD70 knockout in the CAR-T can increase CAR-T potency by removing CD27-CD70-mediated checkpoint inhibition. Our CD70 targeted CAR-T uses robust shRNA-mediated depletion or knockdown of CD70. The benefit of 100% knockdown is reflected in higher in vivo potency. Robust in vivo activity of CD70 targeting CAR-T against AML model was also demonstrated. On the left here, we are showing the robust in vivo anti-tumor activity of P-CD70-ALLO1 against an AML model. For AML, what distinguished CD70 from other targets is the lack of expression on HSC, which has been a persistent toxicity problem for other targets in AML, such as CKIT and CD123. The experiment on the right shows when CKIT or CD123 CAR-Ts are used, they may adversely affect HSCs. However, CD70 is not expressed on HSC, resulting in a natural protection of HSC from P-CD70-ALLO1. With all this encouraging data on our CAR-T assets, we are thrilled to advance our programs in development. Now I will pass the presentation to Kurinji. Thank you, Syed. It is my pleasure this morning to tell you about our new wholly owned program, P-BCMA-CD19-ALLO1. This program targets two key antigens that are critical in autoimmune disease as well as in oncology. I'll highlight the opportunity in autoimmune disease, the gaps we see unfolding, and the opportunities for Poseida's platform and program. I'll also share exciting preclinical data that establishes proof of concept for this program across both areas. It's been a few years since Georg Schett and group ran a revolutionary study that showed that autologous CD19 CAR-T can drive severe, highly refractory lupus patients into a long-lasting remission. This has triggered a flurry of activity in the space, and we are learning a tremendous amount. We've seen that autologous CAR-T is able to drive an immune reset, and this has been validated by the new data that's emerged in the space. However, there have been safety events such as a grade four ICANS or neurotoxicity, a CRS, as well as early relapses that are raising a number of questions in the space. What are the right target antigens, the right diseases? What is the appropriate therapeutic modality as well as therapeutic approach? These are a few of the many questions in the space since this field is indeed nascent. At Poseida, we believe that cell therapy can and will play an important, even a transformative role in autoimmune disease. Instead of rushing into phase one of activity here, we're taking our time to develop a thoughtful approach of how and where to begin. Now, what is ultimately needed for success in autoimmune disease? Toward driving this immune reset and maximal efficacy, there's a question of the right antigen. CD19 targeting is what has been deployed by most today, but it appears there's good reason why BCMA targeting could also be very relevant. Given the role of eliminating the bad actors, this really covers a spectrum of B-cell and plasma cells. We believe that both antigens could be very important in B-cell-driven autoimmune diseases. CD70 is also an important antigen for T-cell-driven and autoinflammatory diseases. Poseida's platform is clinically validated with the data we shared in oncology. In addition, we have a platform and a transposon-based technology that is capable of delivering many of these antigens singly or in combination, which we have access to. On safety, there's no doubt that this is paramount in autoimmune disease. Poseida's platform has been established to have a standout safety profile as well as additional elements such as a safety switch, a high-fidelity editor, and a non-viral platform that are all ideally suited for autoimmune disease. Additionally, the ability to scale and to meet patients where they are, which is the outpatient setting, is critical in autoimmune disease. We've seen that autologous CAR-T has posed challenges in terms of scaling as well as the cumbersome nature of the regimen. Poseida's off-the-shelf product is manufactured well in advance of patient need. We have successfully treated patients entirely on an outpatient basis and also have access to innovative lymphodepletion approaches, including triggered by methotrexate, an autoimmune-relevant agent. With a scalable manufacturing and a differentiated platform, we believe we have all the right elements to unlock opportunities in autoimmune disease and help patients in need of innovative and accessible treatment options. We are excited to be taking P-BCMA-CD19-ALLO1 into IND-enabling studies in both autoimmune disease and in oncology. You see here a schematic of the construct where key features include two CARs that have been developed and designed in an optimized configuration. These target CD19 as well as a dual BCMA CAR, which is in a tandem format. Additionally, these also have dual intracellular domains with the combination really to drive exceptional potency against cells that have either BCMA or CD19 or both. As described earlier, we believe this is a combination that is required to drive an immune reset in autoimmune disease. In oncology, in multiple myeloma in particular, these are also very important targets. BCMA, we know, is a well-established myeloma target. However, there's emerging evidence that myeloma precursor or progenitor cells do not express BCMA. Instead, they express CD19. Hence, this dual combination could be ideally suited for depletion of myeloma cells and precursors. We believe with this powerful tool, we are ready to drive into IND-enabling studies with both programs, and I'll share with you the preclinical proof of concept that establishes that. In addition to our own data, these targets in combination have been validated in the clinic in both autoimmune disease as well as in oncology across multiple myeloma and non-Hodgkin's lymphoma. This program, P-BCMA-CD19-ALLO1, is in IND-enabling studies, and we expect to file one or more INDs in 2025. To begin with the autoimmune data, we started by assaying P-BCMA-CD19-ALLO1 for cytotoxicity against B cells derived from primary patient samples, patients who had either rheumatoid arthritis, lupus, or MS. These were chosen as examples of disease with varying B and plasma cell contributions to the pathophysiology. Using two lots of P-BCMA-CD19-ALLO1 derived from two unique donors as well as donor-matched mock T cell controls, we observed robust depletion of B cells. You can see on the chart that the orange bars depict surviving B cells from the autoimmune patient-derived samples. You'll observe that the negative control T cells or mock cells did not kill the cells. However, the use of P-BCMA-CD19-ALLO1 resulted in very effective killing. Additionally, no cytotoxicity was observed against antigen-negative cells, which are the NK T cells and macrophages. To take these in vitro learnings a step further, our team leveraged a humanized mouse model. This was developed by engrafting cord blood-derived human CD34 positive cells into a NOG-EXL model. P-BCMA-CD19-ALLO1 or control was injected into the mice. On the left-hand side, you see the control cells that continue to grow over the four-week period that was assayed. In contrast, at different dose levels, deep depletion of B cells was seen from the range of 61%-83%. This was sustained up to four weeks queried at the higher doses. You'll note that most autoimmune CAR-T programs have been lifted and shifted over from oncology with little or no in vivo proof of concept. We may find that some of these lack potency in the context of lower number of target cells or lower antigen density, which one would expect in an autoimmune patient versus in an oncology context. In contrast, P-BCMA-CD19-ALLO1 is being designed for optimal potency in the context of both autoimmune disease and in oncology, as demonstrated here by this rapid dose-dependent depletion of B cells in a humanized mouse model. We believe that our differentiated platform and approach will lend itself to various autoimmune indication opportunities that could be significant, not only the areas that are seeing a deluge of activity today, but also well beyond. Mechanistically, there are several diseases that will require the targeting of BCMA or long-lived plasma cells in addition to CD19, an example being myasthenia gravis. There are large indications such as MS, where the scale of allogeneic will be important to address patient needs. There are also indications where the B cell targeting role has been well established. However, there is no systematic development of CAR-T today. While there are several areas to explore, we are being targeted and purposeful in our choice of disease area to develop it. Turning now to oncology, we have also explored the utility of P-BCMA-CD19-ALLO1 in tumor models. First of all, it's well known that BCMA is an effective antigen and expressed on the bulk of myeloma cells. However, as discussed earlier, progenitor cell populations do not express BCMA. In contrast, they express CD19. Now, it's been shown that patients having progenitor cells have worse outcomes in myeloma and are resistant to standard-of-care myeloma agents. Hence, it could be really the unlock to delivering deep and durable remissions as well as to wipe out these progenitor cells in addition to the bulk tumor. Our team began exploring the utility of P-BCMA-CD19-ALLO1 first in the bulk myeloma cells by testing against this population. You will see on the left-hand side panel the percentage of killing of both P-BCMA-CD19-ALLO1 as well as an anti-BCMA CAR-T, the blue and the purple lines. These are effective at eliminating the bulk cells. In contrast, an anti-CD19 CAR-T was not. Now, to shift to the key challenge we're seeking to address, which is really the progenitor cell elimination, we queried effectiveness in targeting this population by taking four patient samples derived from the bone marrow, which contained these precursor cells. The precursor cells were identified as CD19 positive, CD81 positive, but BCMA negative. We found that P-BCMA-CD19-ALLO1, as well as an anti-CD19 CAR-T, resulted in significant killing of this population. However, an anti-BCMA CAR-T did not. In summary, of the three CAR-Ts tested, P-BCMA-CD19-ALLO1 was the only configuration capable of eliminating the bulk myeloma tumor cells that are BCMA positive, as well as the myeloma progenitor cells that are CD19 positive, but BCMA negative. We are very encouraged by these results and believe that the ability to kill progenitor cells could underpin delivering deep and durable responses in multiple myeloma. To round out this data, our team also looked at our tandem CAR and what it was capable of delivering against escape mutants for BCMA. This is emerging as a possible mechanism of myeloma disease progression in BCMA-treated auto CAR-T and TCE patients, or T cell engager patients. There are several escape mutants that are now well characterized, including R27P, which is associated with treatment of teclistamab. We see here on the left-hand side that tandem BCMA binder had superior binding over BCMA monobinders to the escape mutant R27P. It also had equivalent binding of all BCMA-identified escape mutations. Cytotoxicity against this mutant was also evaluated in an in vitro assay with cells expressed in either wild type or BCMA mutant isoform. Potent cytotoxicity was seen against wild type as well as these mutant cells. With all of this encouraging data on hand, establishing proof of concept in autoimmune disease and in oncology, our team is rapidly advancing IND-enabling studies with the goal of one or more IND submissions in 2025. Shifting gears now to our development activity in solid tumors, I will hand it over to Dr. Devon Shedlock. Over to you, Devon. Good morning. I'm Dr. Devon Shedlock, Chief Scientific Officer, Cell Therapy at Poseida. I'm delighted to be here today to discuss our innovative approaches in the development of therapies targeting solid tumors. Let's dive in. Solid tumors have been notoriously challenging for CAR-T development. This is due to issues like antigen heterogeneity, high toxicity, difficulties with CAR-T cell trafficking and infiltration, and the hostile tumor microenvironment. As a result, there are currently no approved CAR-T therapies for solid tumors. Yet, overcoming these obstacles is essential. Nearly 90% of cancers originate in solid organs, leading to around 2 million new diagnoses and over half a million deaths each year in the U.S. alone. This represents significant and growing opportunity, with global revenues from oncology therapies now reaching $190 billion. At Poseida, we view these challenges not as roadblocks, but as opportunities to innovate. Our cell therapy platform is uniquely positioned to help us do this. Using our allogeneic transposon-based technology, we can not only create CAR stem cell memory-based CAR-T cells, but we can also insert multiple transgenes to engineer various functionalities into a single CAR-T cell. We think successfully tackling solid tumors will require hitting multiple antigens, addressing the tumor microenvironment, and optimizing CAR-T cell expansion, trafficking, and persistence. At Poseida, we're confident that our approach and technology positions us better to do this than many other companies. This slide illustrates our evolving approach to tackling solid tumors, which we categorize into three strategic waves within our solid tumor portfolio. Our first wave is led by our MUC1-C Allo program for epithelial tumors, which utilizes our foundational platform featuring stem cell memory T cells and optimized preconditioning regimens. To enhance CAR-T engraftment and potency, we're testing low-dose methotrexate, a compound that our CAR-T cells are engineered to resist to extend the therapeutic effects. We're also exploring multi-dose treatment options to improve outcomes. Our second wave in the middle centers on PSMA Allo program for prostate cancer, where we're integrating process and cellular engineering improvements based on what we've learned from both our autologous PSMA and allogeneic MUC1-C programs. We expect these advances to enhance cell viability, potency, and persistence, and this wave also explores dual CAR formats, optimized and mixed intracellular domains, and novel armoring strategies. Additionally, our second wave encompasses our work advancing our ConvertibleCAR stem cell memory T cell platform in collaboration with Astellas. Looking to the future, our third-generation programs are all about innovative targeting. These include our CAR-TCR platform designed to target both intracellular and extracellular tumor antigens by incorporating both a CAR and a TCR in a single cell. We've also shown that TCR expression can synergize with T-cell engagers, paving the way for a CAR-TCR-TCE combination approach. This strategy could not only broaden our targeting capabilities, but also enhance CAR-T's response to evolving heterogeneous or reemerging tumors. Our entry into allogeneic solid tumor treatments began with our first-generation MUC1 allo program, which enrolls patients with epithelial cancers who have exhausted standard treatment options. This therapy targets Mucin 1 at the C-terminus, a region uniquely exposed in malignant tissues. In clinical trials, MUC1 Allo has shown good tolerability, and we're seeing signs of activity. We'll be sharing an update on this program this December at ESMO IO. Through our research, we've learned that effective lymph depletion is critical for CAR-T success. Earlier this year, we presented data at AACR showing that patients with solid tumors, including those in our MUC1 trial, tend to be more challenging to lymphodeplete than patients with hematologic cancers. To address this, we're systematically exploring better lymphodepletion strategies and new conditioning drugs. Our platform selectable marker for genetically modified T cell purification offers us unique flexibility to use methotrexate in vivo as a conditioning agent alongside CAR-T treatment. This selective survival approach could enhance CAR-T engraftment, expansion, and persistence, significantly boosting potency. As shown on the right, increasing methotrexate concentrations selectively eliminates activated host T cells while sparing activated CAR-T cells. Importantly, low-dose methotrexate is already a well-established safe therapy, commonly used to treat autoimmune diseases like rheumatoid arthritis and lupus. Given these advantages, we're investigating methotrexate's use in the MUC1 Allo trial. This strategy is unique to Poseida, with potential applicability across all of our allogeneic CAR-T programs. Our allogeneic CAR-T therapy offers the unique ability to retreat patients, thanks to our platform's on-demand dosing capability. This flexibility is generally not available with autologous CAR-T, which require the need for manufacturing on a per-patient basis. Here, one compelling case is a patient with end-stage appendiceal carcinoma, a rare and challenging cancer with typically poor outcomes. This patient had previously failed all standard-of-care therapies. After receiving two doses of MUC1 Allo, the patient achieved a remarkable response with over 40% reduction in the size of a paraesophageal lymph node. Now, nearly one year after the initial treatment, the patient continues to experience stable disease without any toxicity from P-MUC1C-ALLO1. For patients with appendiceal carcinoma who have exhausted standard treatments, the median life expectancy is usually less than six months. This case highlights the potential for P-MUC1C-ALLO1 to offer meaningful clinical benefits in difficult-to-treat epithelial cancers. P-PSMA-ALLO1 is our second-generation approach, currently in preclinical development. Interest in PSMA as a target is growing, with increasing validation from treatments like the recently approved PSMA-targeted radiopharmaceutical Pluvicto and further exploration with modalities like T cell engagers. At Poseida, we see significant potential in PSMA-targeting cell therapy for prostate cancer. P-PSMA-ALLO1 builds on insights from our earlier autologous P-PSMA-101 program, which we've now adapted to an allogeneic format. In the autologous trial, we saw promising and durable responses in patients with skeletal and soft tissue metastases. Remarkably, two patients achieved remissions lasting over 12 months, with PSA declines of over 90%. This demonstrated that prostate cancer can respond to CAR-T therapy and that our stem cell memory-rich CAR-Ts have the ability to reach peripheral tissues, including the bone marrow. While solid tumors remain challenging, we're focused on enhancing cell health, viability, potency, and persistence of CAR-T cells to overcome these obstacles. P-PSMA-ALLO1 incorporates advanced innovations and platform technologies enabled by the large CAR capacity of our transposon system. Specifically, it features dual CAR format, with each CAR containing a different PSMA binder, optimized and mixed intracellular domains to enhance potency, and armoring strategies to support cell expansion and persistence. In our search for the optimal binder for P-PSMA-ALLO1, we designed and tested various heavy chain-only human VH, tandem, and dual CAR formats at a stress dose in a head-to-head in vivo study, as shown on the left. Through this process, we identified one dual CAR candidate that demonstrated superior efficacy. Consistent with prior findings, full-length dual CAR formats outperformed the same single-domain binders expressed in a tandem VH CAR or VHH CAR. Additionally, all tested tandem and dual CARs outperformed the P-PSMA-101 scFv CAR used in the autologous P-PSMA-101 trial. Importantly, integration of two full-length CARs into T cells was made possible by our transposon system's large CAR capacity, something not achievable with viral vectors. To increase potency further, we are also exploring the use of distinct intracellular domains within the dual CAR product, strategy we validated in our P-BCMA-CD19-ALLO1 program and hold a patent for. Given that several PSMA isoforms can be expressed outside tumors due to alternative splicing, we also evaluate P-PSMA-ALLO1's reactivity against cells engineered to express non-tumor PSMA isoforms, assessing any risks of on-target, off-tumor toxicity. As shown in the graph on the right, our lead dual CAR showed potent cytotoxicity against wild-type PSMA on prostate cancer cells, with no activity against non-tumor PSMA isoforms. In summary, these data show that the P-PSMA-ALLO1 dual CAR candidate is highly potent, surpassing the efficacy of our P-PSMA-101 CAR-T and predecessor, with a favorable safety profile and no off-tumor toxicity. Also, in our second wave of solid tumor programs, we're working on two programs that combine our proven allogeneic CAR stem cell memory platform with ConvertibleCAR technology from Xyphos, a subsidiary of Astellas Pharma. The ConvertibleCAR platform offers a unique convertible CAR system that uses a small, soluble tumor-targeted agent called a MicAbody. In this collaboration, instead of expressing a standard CAR, our CAR stem cell memory cells will express a convertible CAR or an inert NKG2D CAR. Here's how it works. Instead of a traditional CAR, the cells express the convertible CAR, a receptor that has been engineered to be inert. Once the MicAbody is infused, it binds both our CAR-T cells and the tumor antigen, thereby creating a bridge that enables the CAR-T cells to effectively kill the tumor cells. This system allows a single CAR-T cell chassis to target multiple tumor antigens by simply switching out different MicAbodies, making it a highly adaptable system for treating evolving solid tumors. Think of it like a screwdriver with interchangeable tips. Our CAR-T cell is the handle, and the MicAbodies are the different tips that enable it to target various tumor types. The partnership is designed to deliver two ConvertibleCAR programs. And since starting in May of this year, we've already nominated both targets, and the programs are moving forward quickly. I've shown you that preclinical studies have shown strong compatibility between our platforms and Xyphos, and we're moving rapidly towards the clinic. This partnership represents an exciting advancement in expanding the flexibility and precision of allogeneic CAR-T therapies for solid tumors. Herein, our Allo CAR stem cell memory T cells are both phenotypically and functionally distinct from typical cell therapies. So confirming their compatibility with Xyphos technology was a crucial step. In this proof-of-concept experiment, we tested two lead MicAbody versions, version one and two, targeting the same antigen in combination with two different versions of the convertible CAR. As shown here, when the MicAbody was combined with Allo convertible CAR stem cell memory cells, but not with MOC T cells, it effectively controlled tumor cell growth. This potency held consistently across a range of concentrations, even down to 10 picomolar of MicAbody. Importantly, the activity was highly target-specific, with no killing observed when using a non-targeting MicAbody control. These findings demonstrate a strong compatibility between the Poseida and Xyphos platforms, highlighting the potential for this approach. Looking ahead, Poseida is building on learnings gained from our BCMA Allo 1 clinical trial while systematically exploring next-generation improvements to tackle solid tumors. We prioritize a deep understanding of the unique biology of our CAR-T cells, focusing on key factors like stemness, trafficking, multipotency, viability, and metabolism. To combat immune escape in allogeneic CAR-Ts, we've found that optimized lymph depletion shows promise in improving responses. Beyond this, insights from our BCMA Allo 1 program are guiding our exploration of cell shields to reduce host cell-mediated rejection further. For armoring, given the lower CAR-T expansion typically seen in solid tumors, we are optimizing activation and survival strategies within the hostile tumor microenvironment. Finally, our strategy includes multi-antigen targeting to improve the depth and durability of responses in these highly heterogeneous tumors. The large CAR capacity of our transposon system allows us to integrate multiple targeting elements into the same transgene. This includes multiple CARs, as well as an alpha beta and/or a gamma delta T cell receptor for recognizing intracellular tumor and heat-shock phospholipid antigens. This flexibility also supports the use of T cell receptors in combination with a T cell engager for targeting additional antigens, which I'll detail shortly. Our third wave of solid tumor innovation goes beyond traditional CAR-T therapy, combining CARs and TCRs into a single-cell multifunctional therapy. We call this our allogeneic CAR-TCR technology. This platform expresses both CARs and TCRs within a single cell, allowing for the simultaneous targeting of both extracellular and intracellular tumor antigens. Thanks to our transposon system's large CAR capacity, this dual-targeting capability addresses the heterogeneity of challenging solid tumors, something that viral vectors cannot achieve. In preclinical studies, we've observed several key benefits of this CAR-TCR approach. Our platform process consistently generates CAR-TCR T cells with high stem cell memory frequencies, leading to effective tumor control across a range of models. Alpha beta T cell receptor CAR-T cells show dual targeting of tumor cells via either the CAR or the TCR, maintaining strong potency and metabolic fitness. Similarly, gamma delta TCR CAR-T cells exhibit robust targeting and proliferation, retaining their effectiveness in vivo. We've also shown that our activation-induced gene expression system technology can tightly control CAR or TCR expression with T cell activation. This ensures localized activity and/or minimizes the risk of on-target, off-tumor toxicity. Additionally, our TCR-expressing alloCAR-T cells can be paired with T cell engagers to amplify tumor targeting, which I'll explain in more detail shortly. Altogether, these advancements underscore the versatility and depth of our platform, offering a powerful approach to treat complex solid tumors with improved durability and precision. To assess the ability of CAR-TCR stem cell memory T cells to target both cell surface and intracellular antigens, we engineered MUC1-C CAR-Ts with either an NY-ESO-1 alpha beta TCR or a phosphoantigen-targeting gamma delta T cell receptor. We then tested the CAR-TCR stem cell memory T cells for cytotoxicity against tumor cells expressing either one or both antigens. The results showed robust potency, with the CAR-TCR stem cell memory T cells effectively killing both single and dual-antigen-positive target cells. Additionally, we observed distinct activation patterns when comparing CAR-TCR cells to traditional CAR-T cells. When activated by cells expressing both antigens, the CAR-TCR cells showed a higher percentage of poly-functional cells, or those cells expressing multiple cytokines, as measured by single-cell proteomics. This suggests that the CAR-TCR approach not only enhances cytotoxicity but also improves the functional response of the cells. In an exciting case study, we observed a late and dramatic re-expansion of our autologous stem cell memory-rich CAR-T product P-BCMA-101 in response to a T cell engager. This re-expansion led to a deep and lasting remission of the patient's myeloma. Molecular analyses confirmed that the patient's lymphocytosis was composed of P-BCMA-101 CAR-T cells, though initially it was unclear whether this proliferation was benign. However, further analysis revealed thousands of distinct transposon insertion sites with an average of two transposon copies per cell, confirming that the expansion was polyclonal in nature. Importantly, the lymphocytosis was benign and resolved spontaneously on its own. This patient remains in a stringent complete response off all therapy more than 10 months since the CAR-T reactivation event. This is the first known case demonstrating that a T cell engager can reactivate CAR-T cells years after the initial single-dose infusion of CAR-T. We believe the anti-myeloma effect from a brief one-week single therapeutic dose of talquetamab was significantly boosted by the secondary CAR-T activation and expansion. We hypothesize that this unique response is tied to the stem cell memory-rich nature of P-BCMA-101. This inspiring outcome has prompted us to explore how we can replicate this phenomenon in an allogeneic setting. Let's take a look at how we are making that possible. As we saw earlier, our CAR-TCR cell technology allows us to incorporate both a CAR and a T cell receptor into a single cell, enabling dual-antigen-targeting capabilities. But what's even more exciting is that this platform can also redirect CAR-TCR cells to target tumor cells that don't express either of the targeted antigens by leveraging a T cell engager. To explore the clinical mechanism, we conducted a preclinical proof-of-concept study in a tumor-bearing mouse model testing if CAR-TCR cells could be reactivated by a T cell engager. In this model, we targeted MUC1-C with the CAR and NY-ESO-1 with the T cell receptor, then added a T cell engager against a different antigen, CD70, during the second tumor rechallenge. What we found was remarkable. After initial tumor control, the T cell engager not only reactivated the CAR-TCR cells but also redirected them to target a second tumor with a different antigen, shown here in light blue on the graph to the right. Furthermore, we saw similar results when we used a gamma delta TCR CAR-T cells demonstrating the versatility of this multi-target approach. For gamma delta TCRs, they target heat-shock proteins and lipids, are MHC-independent, and avoid triggering alloactivity, making them ideal for allogeneic therapies with our CAR-TCR platform. By creating an allo cell therapy with knockout of endogenous TCR and beta-2 microglobulin genes, we can add both a CAR and a gamma delta T cell receptor to the same cells. Then we can redirect and potentially re-expand these cells using a T cell engager targeting a different antigen. This innovation suggests that T cell engagers would enable CAR-T cells to adapt to multiple tumor antigens, a strategy we're patenting to enhance not only commercial autologous CAR-T therapies but also new allogeneic TCR-positive products for heterogeneous and evolving tumors. Thank you for your attention. I hope you've enjoyed learning more about our unique approaches to tackling solid tumor therapies through our versatile platform technologies. Now, I'll hand it over to Karen and Peter to discuss the strength of our partnerships. Thank you, Devon. I'm Karen Basbaum. I'm the Senior Vice President of Business Development here at Poseida, and it is my pleasure to welcome Dr. Peter Sandor, who, as mentioned earlier, is the Executive Vice President and Head of Corporate Strategy at Astellas. Peter, we're honored to have you join us for a fireside chat to talk more about your focus at Astellas and, of course, to talk a little bit more about our collaboration. To start out, Peter, would you mind telling us a little bit about your role at Astellas and what you're focused on as the Head of Corporate Strategy? Sure, absolutely. Karen, thank you for having me for this short, fireside chat. I'm really excited to be here and talk about the exciting work that the teams are doing, between our companies. As Head of Corporate Strategy, my and my team's primary role is to define the mid and long-term direction of the company. Within this frame, we are mostly looking at options and ways how to deal with the highly dynamic environment, both economic and scientific, as technologies are becoming more and more complex and complicated, as well as the science is evolving very fast. We try to find ways to develop and build flexibility, agility in the organization to capture the best available options. Within these, we prefer to partner with companies who have developed the best science in the given area. That's how we ended up and landed with our partnership with Poseida as well to start to build CAR-T cells. Great. Now, as part of your strategy, Peter, I know you have established the focus area approach, and as I understand it, with four key areas. One of these is immuno-oncology, where you're working on multifunctional platforms, including oncolytic viruses, bispecific immune cell engagers, small molecules, and, of course, cell therapy platforms. Can you describe why Astellas selected cell therapy as one of its focus areas within immuno-oncology? And also, importantly, how do you see this modality fitting into the broader landscape? If you allow me to take a smaller step back and just to clarify what focus area approach means for us, we have defined our R&D strategy based on the right combination of the different modalities, disease areas, and underlying biology. And even if it sounds trivial, it is not easy to do to find the right approach to address a certain biology, which can change the course of the disease and deliver benefit for the patients. Specifically for immuno-oncology, we have realized very early in the work that we need so-called multifunctional modalities to address the disease because these are complex biologies under the tumor progress or driving tumor progress. Addressing these can be done by a combination of traditional modalities, but also we can build different technologies and approaches which combine different modes of actions into one modality. The reason why we like and are excited about cell therapy is because they can deliver multiple different functions and effects on the tumor at the same time. Even beyond this multifunctionality, they have the promise to deliver long-term benefit for the patients because these are living cells that can persist a long time and eliminate the tumor and keep the tumor from going back, growing back. Therefore, we believe it is a very important modality in the future to manage both hematologic malignancies and solid tumors as well. So, Peter, when you think about solid tumors and, of course, talking about complex biology, what opportunity do you see over the long term for cell therapy in solid tumors? Are there specific indications? Is there a specific line of therapy you're thinking of? Maybe even specific geographies? I mean, what opportunities are you seeing for cell therapy within solid tumors? The opportunities are endless, and the learning is endless as well, which leads us to results. After the early success with cell therapies in hematologic malignancies, it is clear by now that a lot to learn still about solid tumor biology. It is more complex. It is more difficult for the cells to enter in the tumor microenvironment or overcome the hurdles of what the tumor microenvironment means within the tumor. So this learning process is still ongoing. The first results and positive signals are already visible in this effort. Therefore, I believe that the long-term benefit of these cells will come in almost any type of the solid tumors. The real opportunity is with the allogeneic cell types, including CAR-Ts, where one of the biggest hurdles with the current patient-derived cell-based cell therapies is the delivery complexity, the production complexity. Even if these cells are tailored to the patient, it is more difficult to access these treatments and medicines. It requires specific background, both manufacturing and from a patient-handling perspective. So if we can get to a point where we can manufacture and deliver allogeneic cells, CAR-T cells, very similar to as we did with traditional pharmaceutical medicine, we will be able to address and reach patients in almost any geographies in the future. So you've talked a little bit about some of the challenges, the tumor microenvironment, some of the manufacturing challenges associated with autologous therapies. Peter, what do you think is one of the biggest hurdles? In other words, what do you think we really need to be able to break through and have CAR-T therapies be successful in solid tumors? We need further research and understanding and how these cells enter, get to the tumor, how do they enter in the tumor microenvironment, and how do they function long-term. One of the reasons why we got excited about the collaboration with Poseida very early during our discussions is the realization that the gene editing technology, what you use for cell editing and the resulting stem cell memory-type T cells, have the opportunity and potential to persist longer in the tumors or in the human body, which allows us to create long-term benefit, sustained benefit for the patients, means less cells, less repeated administration, and potentially better impact on the patient with less side effects. We'll talk a little bit about how this partnership was formed and what technologies do we combine. But combining these cells with the so-called ConvertibleCAR system allows us potentially in the future to prolong this effect even longer and tailor it how the tumor evolves in the future by changing the targeting part of the cells. We'll talk about it later or happy to cover it now. Yeah, no, thank you, Peter. Just as a reminder, it was in May of this year that Astellas and Poseida announced a collaboration in allogeneic CAR-T therapies for solid tumors, expanding on the strategic investment Astellas made in Poseida in August of 2023. As mentioned, Devon has just given us an overview of the science behind the collaboration. Peter, you shared some of your excitement behind this collaboration, and you've mentioned the advantages of us working together across platforms, the advantages of the allogeneic approach. I'm just curious, from a purely strategic standpoint, what would make this or what does make this a compelling collaboration for Astellas? It is about combining synergistic technologies, deep expertise in CAR-T technology, tumor microenvironment, and biology in a way that when we combine one technology, one team with another, it results into something completely different, which is much more impactful than simply adding one to the other and combining it. It is a rare partnership as well compared to many other work what we do with partners, partner companies, given that we both contribute to the know-how, the knowledge, and the technology, and we are building truly jointly within the teams a completely new convertible CAR-T system. It is palpable every day how well the teams work together, how good the chemistry is, and how excited they are about, again, combining the knowledge what they have built in the two companies over the years. Well, Peter, we share that enthusiasm. We now have two program targets nominated. We are thrilled with the strong progress we are making so far, and again, how we're bringing together technologies from both companies to create something that could be even more impactful for patients. It sounds to me, Peter, that this really is a novel approach when we think about collaborations and we think about sort of the larger strategy. Is there anything else about sort of this model that that excites you, or is there anything about this novel approach that is unique to Astellas and your vision going forward? I will start with the technology and talk a little bit about the teams and how the two companies work together. In terms of technology, it combines the stem cell memory T cell platform with a so-called convertible CAR system, which comes together from two pieces. One is a binding domain, which is inserted into the T cells, and the other part is an antibody ligand fusion protein, which can bind exclusively on one side to the T cell and the other side to the tumor microenvironment. The beauty of this technology and promise is that the cells can be preloaded with the binding by a specific type fusion protein and delivered to the patient as it would be a standard CAR-T therapy. But as the disease progresses, very often it changes either the antigen structure or the cells are losing their effector mechanisms. With the repeated administration of the antibody part only, the cells can be reinitiated. It can be retargeted. So the promise is that we can fully control how the activity will happen in the system. It can potentially even influence side effects profile as well by the frequency of readministering the bindings. That's what I meant earlier with creating something which is entirely novel and very different from both of the technologies separately. In terms of teams and how they work together, this is clearly a synergistic work. Both teams are excited. And maybe because of this, we are already seeing how fast the collaboration progresses compared to other work what we do either internally or in other partnerships. We would agree very much, Peter. We're, like I said, thrilled with the progress we've made so far. With that, Peter, I want to thank you for joining us today. We really appreciate you sharing your thoughts and perspectives. And so I will hand it over to my colleague, Loren Wagner. Loren? Thanks for that insightful fireside chat on the power of partnership. My name is Loren Wagner, and I'm the Chief Operations Officer here at Poseida Therapeutics. We're going to spend a little bit of time talking about our donor screening processes and how that sets us up for manufacturing success. Before we dive into our processes, we're going to spend a little bit of time talking about our manufacturing facility here. For the past two years, we've been fully self-reliant with our facility here in San Diego, which is co-located with our corporate headquarters. We have a relatively small facility with a modest investment in staffing equipment, and we are able to fully meet all of the requirements of our three allogeneic cell therapy products from this facility. We are tremendously proud of this capability. We are able to meet with other individuals from quality, from immuno-oncology, research and development, process development, manufacturing sciences, and solve almost any problem that comes up fully internally. By making use of these capabilities, we've been able to speed up our path to the clinic and to save on our costs and to make sure that we have maximum flexibility for anything that may strategically come up in our portfolio. Poseida has a number of gene editing tools that we've talked about at great length in the past. We've spoken about our non-viral gene insertion and editing technologies and the safety benefits that those tools provide. We've talked about our booster molecule and its ability to improve our manufacturing yield, but today, I want to talk about our healthy donor screening program and its ability to ensure that we have great starting materials to work with, and I also want to talk about our selectable marker that purifies any variability that we see from our donors. As we move forward over the next couple of slides, I'll give you an insight on how our donor screening program is constructed and some of the data that we've recently seen, so for the next few slides, I'm going to talk about our donor screening process. When we receive material from prospective donors, one of the first things that we look at is the cellular makeup of the leukapheresis that we see. In this particular slide, we're looking at three typical donors, and you can see the cellular makeup is very, very different from one donor to the next, but interestingly, the collections within a particular donor are very, very consistent. This really forms the basis of our donor screening program in that we can be fairly confident that when we recall a donor and ask for another collection from that donor, that is going to look very similar to what we've seen in the past. That gives value to the fact that we want to find the donors that work best in our process and use them as many times as possible. Secondly, after we're satisfied with the makeup of the cells, we want to see how they perform in our manufacturing process. As you can see from the data here, there's a tremendous amount of variability from prospective donors as they are run through our manufacturing process. We see donors that do not expand at all in terms of moving from the cells that were seeded to the cells that were harvested two weeks later. In some cases, we see explosive growth of 15-20 times the seeding density that was originally put into the flasks. So we want to go through these data and find the donors that have the best possibility of providing a successful, robust manufacturing output. Looking further into the growth, we also see that while individual donors tend to be very, very variable from each other, within a particular donor, there's a high degree of consistency. So for instance, as we look at these three typical donors, we would expect the collections we receive from donors one and donor two would generally have higher output than donor three. We take this into account as we schedule our manufacturing operations and determine what the best path is for each particular donor as we move through our research and development and GMP manufacturing operations. While growth is certainly important, the quality of the editing is equally important. We want to make sure that every cell has the best opportunity to deliver the effect that we are looking for. So one of the ways we measure this is through assessing the knockout of two different complexes. One is CD3, shown in the top panel, and one is beta2m, shown in the bottom panel. Again, we see a remarkable amount of consistency between donors, between collections, but individual donors will show a great deal of variability across these parameters. So we've talked a little bit about how the manufacturing will perform, how the editing will perform. Now we're going to talk a little bit about how the final product looks. As you've heard previously, we take a great deal of pride in the early memory phenotype cells. What we're looking at here is three different collections from the same three typical donors and the proportions of the cells that are available at the final product step. Again, you see very high concentrations of stem cell memory and central memory, but there are some differences. You do see, for instance, in donor one that there are some effector cells that are there that you don't see in donors two and three. Again, we take all of these parameters into consideration when we assess whether we want to move forward with using a donor in our GMP manufacturing processes. Lastly, we will look at the in vivo potency or the tumor control of the final product that is generated from these prospective donor cells. Again, we see even with successful manufacturing and successful editing, certain donors perform better than others in controlling tumor. Again, we have a number of different parameters that we look at as we assess our donors to create our donor pool that we will use for GMP manufacturing and further research and development activities. All of this data goes into improving our manufacturing processes and to put forward the best strategic development plan that we can. Now, as we turn back to our manufacturing process, we have previously spoken about the non-viral gene editing and the booster molecule. I would like to spend a little bit of time talking about our cell selection and how it affects the go-forward expansion from that point forward. Several days after the nucleofection, we will engage in a CAR-T cell selection that allows us to cull any cells that did not successfully go through the gene editing process and then further expand that purified cell culture. This ensures an exceptionally high CAR-positive process and ensures that the controls that we have take an inconsistent input and deliver a highly pure product. As you can see, we are exceptionally pleased with the fact that multiple donors were used during the phase one study, which delivered the tremendous results that we saw and presented at IMS 2024. Seven different manufacturing lots contributed to patients that were in that study, and of those seven manufacturing lots, they came from six different qualified donors. This represents that this is not a one-shot opportunity for Poseida. Each of our donors that goes through the screening is able to give us a consistent and efficacious product as we move forward, so as we look to the future, we are very, very confident in our donor screening capabilities. However, artificial intelligence may be a great mechanism for us in this data-rich environment to find faster and easier ways to select our donors. Secondly, in the manufacturing process itself, there are two major areas we can look for further improvement. Number one, we've noticed that gene editing is clearly the most critical element of success, both in terms of yield and for efficacy. There are new ways of performing that unit operation that are being developed and that we are assessing, and we will be looking for ways to implement that as soon as possible, and then secondly, Poseida has been manufacturing to date in static expansion flasks. While those flasks are excellent for providing the yields that we need right now, at some point in time, we will like to get to higher levels. Bioreactors offer a pathway for us to reach those levels, and we're excited to look at ways to get the cost of goods lower and to further increase the accessibility of these therapies. So all in all, we have a great program here from a donor screening and a manufacturing standpoint, and we're excited to see what the future holds, so without further ado, I will turn it over to Kristin Yarema, our CEO, for our closing remarks. Thanks, Lauren. To wrap things up, I'd like to come back to the idea of our three growth horizons, which have really been enabled by the approach we have always taken and continue to take with our partnerships. Our partnerships with Roche and with Astellas are advancing novel therapeutic options for patients while supporting us on our growth journey. Thank you to both companies for your partnership and support. I hope what you've seen today has convinced you that Poseida is well on its way to leadership in allogeneic cell therapy. As we work today within our second horizon, drive value, we are looking ahead with commitment to a future where we will disrupt the cell therapy field and deliver on our vision that someday all patients who can benefit from the transformational potential of cell therapy are able to do so. In closing, I'd like to extend a very heartfelt thank you to the patients we serve and who have joined our clinical trials. Also, thank you to our investigators and partners and to our dedicated Poseida teams who are making all our work possible. With that, I'd like to thank you once again for joining us today, and we will now open the Q&A, where I will be joined by Syed Rizvi, Devon Shedlock, Loren Wagner, Kurinji Pandiyan, and Alex Chapman. As stated at the top of the call, you are welcome to type questions into the chat window, and we will be happy to answer questions as time allows. Thank you, everyone. As a reminder, please input your questions in the chat window at the bottom of the screen. Our first question today comes from Ted Tenthoff for Piper Sandler. Considering the success of autologous BCMA CAR-T, how do you envisage allogeneic CAR-T being used on relapse as a bridge to auto? Thanks. Yeah, thanks for the question, Ted. I think ultimately we see numerous patient segments that will be candidates for P-BCMA-ALLO1. Certainly the data that we've been talking about today is where our program is starting in relapsed and refractory patients. And I would remind everyone that our RMAT designation from the FDA covers patients who are triple-class refractory and have received three or more previous therapies. We've shared what we see as highly compelling, very differentiated data in that segment based upon what you've seen from arms A, B, and C from our study within RC, a 91% overall response rate, and 100% response rate in BCMA naive patients, and an 86% response rate in patients who've received one or more prior BCMA and/or GPRC5D-directed therapies. You know, I think we would say incredibly differentiated and promising in that segment. But of course, our vision for this product does not end there. We are actively thinking about the lifecycle plan with our partner, Roche. It's a little bit early to talk about that in a fulsome way, but you can bet that we're thinking about it. And we think that there's great promise for this type of product in earlier line disease. So our vision at Poseida for allogeneic cell therapy is that every patient who can benefit from these transformational therapies has the opportunity to do so. And we think that in earlier line disease, the advantages of allogeneic therapy, such as our experience and ability to treat completely in the outpatient setting, to potentially reach centers beyond just a few accredited CAR-T centers today, and importantly, to produce at high scale and, you know, with a low target COGS, ultimately with no waiting time to the patient, brings an awful lot of advantages. Certainly the idea of a bridge to auto transplant is appealing to directly answer that part of your question, Ted. But I would say there are many different patient populations that we'll be thinking about over time. Our next question comes from Sami Corwin at William Blair. Based on your conversations with KOLs, what durability of effect would be meaningful with P-BCMA-ALLO1 in late line/BCMA experience patients? Yeah, so we've shared with you today data that we presented at the IMW conference in September, which is from arms A, B, and C of our P-BCMA-ALLO1 study, which has now entered a phase 1b, and of course, in partnership with Roche. So what we have heard and what we know is that today in this type of patient population, bispecifics are being used along with older therapies. The durability for the bispecifics that people are seeing is, you know, variable depending on the agent, but, you know, say six months plus, six months, you know, six, eight plus months. Traditionally, the expected median mortality for patients, you know, in fifth line or plus line of disease is only five months. So that, I think, is how people are looking at the options today. What we showed with the waterfall plot and the arms, the data from the durability data that we have from patients with six or more months of follow-up in arms A and B of our study, which I would remind you are not optimized. We're taking the arms C regimen forward into phase I B. So even without optimization of lymphodepletion or dose, we're already seeing in those patients a median duration of follow-up that's around eight months. With that backdrop, unsurprisingly, we're getting a great reception from the thought leaders in the community today regarding the product profile, all aspects of the product profile of this therapy. Our next question comes from Jennifer Kim at Cantor Fitzgerald. In the phase I B study for P-BCMA-ALLO1, it looks like you're exploring doses at three times 10 to the sixth cells per kilogram and six times 10 to the sixth cells per kilogram. What's the strategy behind exploring those doses? Yeah, thanks for the question, Jennifer. So, you know, the cohort two dose that we used in the 1a portion of the study, you know, is about that lower of the two doses. And I'll ask Syed Rizvi to comment in just a second. Why are we exploring that dose as well as a higher dose in the phase 1 B extension? Well, it's very simple. I mean, we're very encouraged with the product profile that we're seeing already. We don't know that we need to go to a higher dose. But our safety profile, as I hope you've seen, is differentiated when compared to published data for both autologous CAR-T as well as bispecifics. So, you know, we certainly, we believe, have the room to explore a higher dose. And so that's what we're doing. We really want to get dose and dosing regimen correct for this product, which I think is a hallmark of Poseida's approach. We've been more systematic in looking at all aspects of dosing, such as lymphodepletion and now cell dose. You know, we really want to make sure that's right. And I know our partner does too. Syed, anything to add there? No, thanks so much, Kristin. I think you summarized it very, very well. The only thing I would say from my side would be that, you know, this phase one study is really the right place to look at different doses. And especially if, you know, we could see, say, more durability over there, that would be wonderful. And the other thing is, I feel that as we are moving forward, and we know that, you know, looking at other cell therapy programs, usually the first study is your dose finding. The second study could be a registration phase II study. So we would like to really position ourselves where we have a very strong strategy about the dose that we are going to be bringing forward. Our next question comes from Justin Zelin at BTIG. How do you see BCMA- CD19- ALLO1 being differentiated for autoimmune disease and what are the benefits of an allogeneic approach? Yeah, fantastic. Thank you for the question, Justin. So let me start with the second part of the question, and then I'll take first. So I'll flip the order on you there, Justin. We believe that all of the benefits of our allogeneic T stem cell memory-based CAR-T platform that are being proven out in the oncology setting will be at least as powerful in the autoimmune setting. Why? Well, having spent a lot of time in autoimmune drug development and businesses myself, I'll tell you, the patient populations that we're looking at and the number of patients in a practice can be extremely large. And the patients tend to be treated more in a community-type setting. So you really want a product that can be produced at a reasonable cost, reliably at high scale in order to meet the needs of these patient populations. Moreover, you really want a product that has a favorable safety profile. And again, you know, we've spent time today showing you how we feel our safety profile, as expected from T stem cell memory cells, is developing in just that way. In autoimmune disease, we also don't really know what persistence of cells is necessary or even desirable. And with our platform, we feel we can really have this both ways. Our T stem cell memory cells do persist. We've seen that, whether it's from our auto case study by Thomas Martin that you heard, or some of the persistence data that we're seeing in the allo setting. But so we know that the cells persist, but they are allo. We also carry in every single one of our programs an embedded safety switch where we can turn down or turn off the cells within minutes, minutes to hours, by just administering a simple small molecule agent. If the premise in autoimmune disease is just to very quickly reboot the immune system and then clear the cells out, we absolutely have the ability to do that. There are a lot of advantages that we see to our platform, and we're very excited to be carrying it into autoimmune disease with this approach. Why the combination of BCMA and CD19? There's a spectrum of B cells ranging from the very naive all the way up to plasma cells. In some autoimmune diseases, it's actually the plasma cells that are implicated. In others, it's the earlier cells. With the combination of BCMA and CD19, you have a very nice end-to-end coverage of that spectrum of B cells. Some of the diseases that are examples that we're looking at that Kurenji talked about today are indeed programs or diseases where the plasma cells are thought to be quite important. Kurenji, anything you want to add there? You covered it well, Kristin. I would say that there are several indications where we believe that targeting both plasma cells as well as B cells will provide differentiated efficacy benefits compared to some indications where there are other players today with CD19 alone. We also think there are some that will be uniquely suited to plasma cell targeting. There are various options at play here that we are considering, and we'll guide on that at a later time. Sticking with BCMA CD19, for the next question, which comes from Arthur He at H.C. Wainwright, which indication do you plan to go for first for IND, autoimmune or blood cancers? Could you tell us more about the selection criteria for a good donor? Okay. So there's two questions in there, I think. So let's take the first one. You know, what we've shared with you is we think that there are a number of diseases where the BCMA CD19 allo1 could be very powerful. We have a short list. You know, we are in the process of finalizing the prioritization, and we'll, you know, in the future share with you exactly our plans as we move forward into the clinic, Arthur. So it's a little early to be that specific. Your question is a good one, though, because we do think that that combination could be beneficial, as we've showed you, in hematologic malignancies as well, so you know, everything is within scope, though we are particularly excited at this time about autoimmune disease applications. Second question is more about donor screening and what makes a good donor. You heard about that today from Loren Wagner, our Chief Operations Officer. Loren, what would you want to say to that question? Yeah, I think we covered a lot of it as we went through the presentation in terms of how different donors grow, how well their cells tend to be edited as they go through our process, and then finally what the phenotypes look like in the final product as well as what the response to tumors is going to be. I think the one thing I would add to it is there's also a human factor associated to it in terms of how recallable is the donor, how responsive are they. It's a very unique place to be where you're relying on human beings to provide your starting material. So you also have to take that into account. But realistically, we have to do what makes sense for Poseida's processes, which is why we look at the variables that we've looked at. And each manufacturing operation has a little bit different personality. And we're trying to find the donors that have the best match to that personality. Yeah. I'd also add, you know, it's been really exciting for us to share some of that with you today. We haven't really talked much about our donor screening or donor pool approach. But Poseida has been building this over years. This has been a long-term project for us, and we are very proud of the very rigorous system that we've put in place as well as the pool of Poseida donors that we have amassed. We see this, frankly, as an overlooked competitive advantage for us. Our next question comes from Jennifer Kim at Cantor Fitzgerald. With BCMA CD19 allo1, you're targeting one or more IND filings in 2025, and it seems like the prioritization here is autoimmune disease indications. You pointed to some opportunities, RA, SLE, multiple sclerosis. When will we get a better sense of your initial targets, and can you walk through possible timing of trials and initial clinical data? Yeah, I think we touched on that a little bit with the earlier question. You know, I would just emphasize that the data that we shared with you today are just a few select examples from those diseases. They certainly are diseases that we like quite well. But, you know, we have been doing a lot of work in this area. And so, you know, we will come forward with further guidance when the time is right. Our next question comes from Sami Corwin at William Blair. For P-CD70-ALLO1, would you focus on patients with a certain range of baseline bone marrow blasts and could bridge to transplant be a viable endpoint or clinical outcome? Okay. So this is a question about AML, acute myeloid leukemia, and the application of our CD70 allogeneic CAR-T in that setting. So, you know, AML is a terrible disease for anyone who may not be familiar with it. And it's one of the diseases where we've made the least progress in terms of reducing patient mortality. Five-year patient mortality in AML is still, you know, incredibly high, despite the fact that we have seen several new classes of therapies come forward. In AML, we always need new classes of therapies, though, because one of the hallmarks of that disease is relapse and progression through clonal evolution. So patients progress very rapidly, but they also go through, you know, could go through a number of lines of therapy. So certainly, you know, we see a place for CD70 in relapsed refractory disease. That might be a natural place to start. But there's also the potential, again, to move it earlier. And the idea of one patient population bridged to transplant certainly is interesting. You know, it's an appealing concept. Why? Because allogeneic cell transplant is considered the gold standard of care in AML because it has the potential to be curative. Unfortunately, many patients don't make it all the way to transplant or their disease is not in deep enough remission for transplant to lead to that successful cure. So many, many places we could go with this in AML. Thanks for the question. Our next question comes from Justin Zelin at BTIG. What should we expect from the P-MUC1C data update at ESMO.io? Yes. Well, thank you. The data is embargoed until ESMO.io. So we certainly look forward to sharing it at that time. As we've said before, we intend that to be a fulsome clinical update. And, you know, we look forward to sharing that with you in December. Our next question comes from Sami Corwin at William Blair. For the CAR-TCR platform, will you focus on targets that have synergy or targets that are expressed independently of one another? In addition, how are you thinking about TCR HLA selection? Great. So thanks for the question. We are so excited about this new platform that we have introduced today, our CAR-TCR technology. And, you know, most companies working in the space will not find this easy to do. I just want to emphasize that this is really made possible by the cargo capacity of the non-viral transposon, where, you know, we can introduce all of these elements in a single genetic engineering step. So in terms of the targets and how we're thinking about that, as well as the HLA matching, let's hear from Devon Shedlock, our CSO. Thanks, Kristin. So the way we're thinking about this would be targeting antigens that are expressed independently of one another to give us the best amount of coverage. We think that's particularly important in heterogeneous and evolving solid tumors. And when thinking about HLA selection, you know, that's really addressed to the type of T cell receptor that's used in the therapy. So if it is an alpha beta TCR that is used, then the patient will need to be matched to the type of TCR that's being used. However, when using a gamma delta TCR, as I mentioned earlier, the gamma delta TCR is MHC independent and would allow us to treat any patient. So we believe that gamma delta TCR is particularly suited to treat a vast number of patients without the need for HLA matching. Our next question comes from Justin Zelin at BTIG. You've had successful progress with your current partnerships. What is the appetite for additional partnership opportunities? Yes. Well, you know, as we mentioned earlier, this model has been so successful for us. We've been very fortunate to have incredibly strong partnerships with both Roche and Astellas. You heard from Peter Sandor today, you know, really, really give his view on our partnership. And it's been fantastic for us to both, you know, work on and advance programs and validate our technologies with these partners, but it's also been a very important way for us to fund the company. You know, just to say it again, over the past three years, we have received over $400 million through external partnership payments, upfronts, and milestones. So, but we have a lot of technology, right? As you've seen, we have entire areas of technology and diseases that we haven't entered yet with a partnership of any kind. And today's R&D day is focused on cell therapy. But of course, we have our genetic medicines arm of the business as well, where we also don't have any current partnerships. So we are always interested to talk to people who might be out there considering opportunities for partnership. Very happy to do that. And we think there's plenty of space to continue that work as well as do the important work of advancing our own internal Poseida-owned assets. And we've received another question asking about the life of allogeneic CAR-T cells in the freezer. Yes. Okay. Thank you. So, Lauren, do you want to take that one? Yeah, absolutely. So we've seen very good stability with our products once they are at liquid nitrogen temperatures. And so far, our stability programs have allowed us to dose our products out to two years shelf life beyond the manufacturing date. Our next question comes from Dominique at Merlin Nexus. Can you please expand on the unique and proprietary technologies Poseida employs to produce high TSCM memory cells? What specifically are these technologies and how proprietary are they? Thank you. Very unique and very proprietary. It's the short answer. So, you know, this harkens back to the very opening of our session today, where I introduced our toolkit. So it's part about the toolkit and it's part about production. So our core tools are our non-viral transposon, which has the advantages, you know, of being non-viral, which brings, you know, safety advantages, some cost and reliability advantages. But its most important advantage is that it preferentially inserts transgenes into naive and stem cell memory, T stem cell memory cells. It also has that great cargo capacity, which enables us to build a tremendous amount of functionality into the cells. And it's a very simple cut-and-paste mechanism. It's one step to insert as many genes from the transposon as we want to use. Our gene editor is Cas-CLOVER, which is unique and proprietary to Poseida as well. We have actually run head-to-head studies versus Cas9, which people may be quite familiar with. And we believe Cas-CLOVER is about 25 times higher fidelity than Cas9. That's because it requires few guide RNAs to situate itself before making, you know, making any cuts and doing any editing. Importantly, the transposon and Cas-CLOVER work very well together. Cas-CLOVER can edit resting T cells. We actually do the gene insertion and the gene editing in one single process step. It's not a multi-step process. It's one step. So it starts there. But then the production, I would say, is equally important. For that, maybe I'll turn to Lauren to want to talk about that. Yeah, just briefly. We talked a little bit about, you know, all the tools that are available. And we've been able to engineer the manufacturing process to take full advantage of that. So even with the best donors and with the best editing, there are still going to be some cells that are not going to be edited. And that's why we talked a little bit earlier today about the selectable marker. After giving the cells a few days to rest following the editing that Kristin described, we're able to call out any cells that did not successfully edit, which puts us in a position where not only do we have this great T stem cell memory consistency to the product, but we also have extremely high CAR positivity as we move through the remainder of the manufacturing process. So again, when you combine all of these features together, it allows us to get the right phenotypes in a very high quantity, which is where we all want to be. And this is all covered by an extensive IP estate that Poseida has been building for years. Great. And we're at time. So this will be our last question, which is from Ben Mallett at Stifel. You have a number of ongoing clinical trials. How many more clinical programs can you handle with your current manufacturing capabilities before needing to expand? Yeah. Thanks for the question, Ben. So you've heard a lot from Lauren about what we can accomplish with a very small facility, you know, with a smaller footprint and lighter staffing than autologous facilities. You know, we can do more with the capacity that we have. We also will be looking ahead to tech transfer of some of the current programs as activities move forward with our, you know, BCMA program and eventually our CD19, CD20 program partnered with Roche. You know, those will move on from the Poseida facility to, you know, to Roche's facility. So we both have additional capacity with our own footprint. And we will also have the progression of some programs moving forward. Lauren, anything to add there? No, I think you covered it. And as our platform continues to improve and we're able to get more and more material from each batch, it improves the capacity of the facilities as well. So again, it's one of those situations where everything that we're able to transfer out provides capacity. Every improvement we make with our manufacturing process improves our capacity. So as long as we keep working on both of those variables, there's always more levers for us to pull. Right. And even today, I'll remind everyone that we're achieving cell yields that are up to over 100 doses from a single donor, single batch. So we've got a pretty good baseline to work from. And it's just scaling up further from there. And that wraps up Poseida's cell therapy R&D day today. We hope you enjoyed the event. Thank you very much for your questions. You can now disconnect.