Good day, and at this time, I would like to welcome everyone to the Poseida Therapeutics P-BCMA-ALLO1 Clinical Data Conference Call. All lines have been placed on mute to prevent any background noise. After the prepared remarks, there will be a live question-and-answer session. If you would like to ask a question, please press star one on your telephone keypad. Today's call is being recorded. Lastly, if you should need operator assistance, please press star zero. Joining us on the call today are Kristin Yarema, President and Chief Executive Officer at Poseida, Syed Rizvi, Chief Medical Officer at Poseida, Dr. Bhagirathbhai Dholaria, Associate Professor of Medicine at Vanderbilt University Medical Center, Dr. Thomas Martin, Associate Director, University of California, San Francisco Myeloma Program, and Johanna Mylet, Chief Financial Officer at Poseida. It is now my pleasure to turn the call over to Alex Chapman, Senior Vice President, Investor Relations and Corporate Communications at Poseida. You may begin your conference. Hello, everyone, and thank you for joining us. 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. With that, I will turn the call over to Dr. Kristin Yarema, President and CEO, to kick off today's program. Kristin? Thank you, everyone, for joining us today as we review the data for our lead allogeneic CAR-T program, P-BCMA-ALLO1, which is partnered with Roche. Just yesterday, we presented interim clinical data at the International Myeloma Society 21st Annual Meeting in Rio de Janeiro, Brazil. Today, we're delighted to have Dr. Bhagirathbhai Dholaria from Vanderbilt University, who's an investigator on the phase I study of P-BCMA-ALLO1 in relapsed refractory multiple myeloma, review the data shared yesterday at IMS. Then, Dr. Syed Rizvi, our Chief Medical Officer, will have a fireside chat with Dr. Dholaria and Dr. Thomas Martin of UCSF to discuss the current treatment landscape for multiple myeloma and the significant unmet need for patients fighting relapsed refractory multiple myeloma. Following that, I'll make a few concluding remarks and then open up the call for Q&A. To get started, I'd like to briefly introduce Poseida. Poseida is, at its core, a platform technology company using a core proprietary and fully non-viral set of genetic engineering tools and other technologies to produce allogeneic CAR-T therapies to treat cancer and autoimmune disease. We are a clinical-stage company with three CAR-T programs in phase I. The strength of our platform has attracted leading global biopharma partners. We're privileged to have collaborations with Roche on some of our liquid tumor programs and with Astellas in certain areas of solid tumors. We are also using our same genetic engineering toolbox to develop in vivo genetic medicines for rare disease. Why do we believe the future of cell therapy is Allo? Well, in simple terms, we think the right kinds of Allo off-the-shelf CAR-T can be highly efficacious and safe, and they have the potential to expand patient access and enable treating patients sooner. While autologous cell therapies have benefited thousands of patients to date, still, only a small fraction of patients who are eligible for CAR-T therapy are able to receive it, given capacity limitations for manufacturers as well as hospitals. In addition, the process requires invasive apheresis procedures, significant waiting times, meaning additional bridging chemotherapy is needed in the interim, complex supply chain logistics, and some uncertainty as to whether a given patient's cells can be successfully made into CAR-T at times. All of this complexity and single patient, single batch manufacturing means autologous CAR-T is also costly to produce and administer, and difficult to scale up to meet the needs of tens of thousands of patients per year or more. And consider this. In our P-BCMA-ALLO1 trial, we're seeing a similar amount of time from treatment decision to clinical response as it takes for autologous CAR-T to complete CAR-T manufacturing. In a setting where every hour and day you can get ahead of a patient's cancer may be meaningful, we think this is an incredibly compelling time advantage. Poseida has a vision, which is shared by our partners, that all patients who can benefit from the transformational power of cell therapy will someday be able to do so. And It is our mission to make this vision a reality through allogeneic CAR-T. We are differentiated by our proprietary genetic engineering toolkit, which uniquely enables a TSCM-rich CAR-T approach, that right kind of Allo CAR-T, and our in-house GMP manufacturing, which is scalable and efficient. This has enabled us to create a high-potential, multi-asset pipeline and become a partner of choice for top pharma companies. We believe that Poseida is ideally positioned to break through the cellular engineering and manufacturing challenges that have historically been a roadblock to bringing allogeneic CAR-T to patients. Our proprietary tools for transgene insertion of CARs and other features, gene editing to avoid alloreactivity, and to support manufacturing at a high scale, work together as a system to deliver CAR- Ts that are uniquely rich in stem cell memory type. This is important because stemness has been shown to correlate with product efficacy, depth, and durability of response, specifically in CAR- T. So by using the T stem cell memory cell as the basis for our CAR- T, we are engineering in product differentiation from the very beginning. Furthermore, our non-viral system is able to engineer multiple different functions and genes into our cells efficiently, giving us the ability to produce multi-targeting CAR-T and also leading to several potential safety benefits. And we have proven that our manufacturing is scalable, positioning us to deliver lower-cost CAR-T products. We are proud to say that we are manufacturing all of our investigational Allo CAR-Ts in-house at our own GMP facility, including P-BCMA-ALLO1. We utilize a proprietary booster molecule, which enables up to 100 doses per batch in terms of cell yield. The P-BCMA-ALLO1 data you will see in just a moment includes patients treated with seven different manufacturing lots, produced from six different supplier-qualified donors. And we store finished products in inventory, so it's ready on demand. Production at scale will be needed to fully unlock the multiple myeloma opportunity for CAR-T therapy. Because multiple myeloma remains a relatively common and still incurable blood cancer, patients can and do move through many lines of therapy. As many as 85 thousand 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. As we think ahead to earlier lines of therapy in the future, ample opportunity for an off-the-shelf Allo CAR T also exists there. Already, it's estimated that well over 50,000 U.S. patients per year are receiving second-line or later treatment, and with the approval of multiple myeloma regimens in frontline care containing proteasome inhibitor, IMiD, and CD38 with steroids, not only are patients likely to receive BCMA-targeted therapies earlier in their patient journey, but also the population of BCMA-experienced patients will grow, and we have been generating data in that population. P-BCMA-ALLO1 is the most advanced allogeneic CAR T in clinical development for multiple myeloma. It is T stem cell memory rich, uses a novel single VH binder against the BCMA protein, and incorporates multiple safety features typical of our platform. We've been pleased to announce a couple of weeks ago that the U.S. had recognized P-BCMA-ALLO1 with RMAT designation for multiple myeloma patients receiving three or more prior lines of therapy, including a proteasome inhibitor, IMiD, and anti-CD38 antibody. We have also entered the phase I- B expansion phase of this study, which is partnered with Roche. Now, I'd like to hand it over to Dr. Dholaria to share with you the interim phase one data for P-BCMA-ALLO1. Hello, everyone. I'm Bhagirathbhai Dholaria, Associate Professor of Medicine at Vanderbilt University Medical Center in Nashville, Tennessee. I'll be presenting some interim results data from a phase I clinical trial evaluating the safety of P-BCMA-ALLO1, a non-viral allogeneic BCMA-directed CAR- T cell therapy in patients with relapse or refractory Multiple Myeloma. P-BCMA-ALLO1 is a novel non-viral CAR- T cell therapy manufactured from healthy donor T-cell. This technology allows gene transduction in a T cell in a resting phase, so majority of the CAR- Ts manufactured in this process are T-cell memory phenotype and less differentiated, with the idea being more anti-tumor effect and less side effects. This CAR- T also has a drug-resistant gene, which permits selection of the CAR- T gene, and hence, most of the product which is being delivered to the patient has CAR- T gene inserted in it. This manufacturing technology also allowed a rapid ex vivo expansion of the T cells, so multiple doses of CAR- Ts can be manufactured from a single donor. This phase I trial followed a simple three plus three dose-escalation schema, with the primary objective to evaluate safety and assess the maximum tolerated dose of P-BCMA-ALLO1 in the patients with relapsed or refractory multiple myeloma. This trial allowed patients with three or more prior lines of therapy or patients with triple class refractory multiple myeloma. This study does allow patients with prior BCMA-directed therapy, including currently FDA-approved autologous CAR- T cell therapy. Different dose level of P-BCMA-ALLO1 were evaluated in this trial, as you can see here on the slide, starting with cohort arms A, B, and C. Two million per kilogram cell dose was evaluated at different lymphodepletion regimen, with escalating doses of cyclophosphamide, 500, 1000, and 750 mg/m² for three days, along with fludarabine, 30 mg/m² for three days, to evaluate the safety and understand the in vivo kinetics with a different lymphodepletion and the intensities. At present, the phase I-B study is enrolling in Arm C lymphodepletion. This slide is showing the baseline characteristics of 72 patients treated so far on this clinical trial. As you can see here, these patients are high risk. The majority of the patients have high-risk cytogenetics. A quarter of the patients has including extramedullary disease, and several of these patients have prior anti-BCMA CAR- T-cell therapy, bispecific therapy, and including handful of patients who had talquetamab bispecific therapy before coming onto the trial. Median prior lines of regimen was six in this cohort. Given the rapid manufacturing and off-the-shelf delivery of this therapy, all enrolled patients 100% received the BCMA-ALLO1 infusion. No patients needed a bridging therapy despite having a very aggressive relapsed or refractory multiple myeloma. No prophylactic steroid tocilizumab was required in any of the patients treated on this trial so far. The median time from enrollment to the start of lymphodepletion was just one day. Here again, these patients were heavily treated, with 43% with prior BCMA therapy, with almost 70% with high-risk cytogenetics. Looking at the safety profile of this drug, so far, no patient has developed grade three or more CRS or ICANS events, and all CRS and ICANS events have been grade one or grade two. No patient has developed graft-versus-host disease, hemophagocytic lymphohistiocytosis, and also no patient so far has reported to have parkinsonism or movement disorder or isolated cranial neuropathy, which have been reported with other currently FDA-approved BCMA targeting CAR T-cell therapies. There were a few patients who had grade 3 or more infectious complications. Cytopenias were the most commonly reported side effects, which was thought to be related to lymphodepletion chemotherapy. Cytopenia was reversible by week four or six in majority of the patients. Looking at in vivo similar kinetics here, we can see with increasing intensity of cyclophosphamide and lymphodepletion, we saw better in vivo expansion and persistence of BCMA-ALLO1. Next few slides will cover the overall response rate, and impact on the myeloma disease burden after BCMA-ALLO1 infusion. Looking at here, arms S, A, B, and C, patients who received enhanced lymphodepletion with higher dose of cyclophosphamide, 500 milligrams per square meter or more, had a higher overall response rate and increased depth of response compared to patients who received standard lymphodepletion. Focusing particularly on Arm C, which is currently enrolling, 21 patients were treated. Here are the baseline characteristics of these patients, including 62% received prior anti-BCMA therapy or talquetamab therapy. Several of these patients had autologous BCMA CAR T-cell therapy and bispecific antibody therapy, including 29% of the patients who had both prior BCMA and talquetamab therapy. Majority of these patients had prior autologous stem cell transplantation, and a good number of them had extramedullary disease. None of these patients, again, in this Arm C cohort so far, have required any bridging therapy. Looking at the overall myeloma response rate across the different subgroup of patients treated in Arm C, here a total of 23 patients treated, overall response rate 91%, majority being complete remission or very good partial remission. Looking at patients who received prior one or more prior BCMA therapies, overall response rate was 86%, with a few patients with CR and VGPR. Among the nine patients who were BCMA naive, a 100% overall response rate was observed. Here, the waterfall plot, you can see a majority of the patients who received FL/Cy for depletion had some degree of reduction in their myeloma burden. Focusing on the duration of response, since the follow-up on Arm C is relatively short, we decided to focus on pooled data from Arm A and Arm B. Here, looking at 11 patients who had any response after BCMA-ALLO1 CAR T-cell infusion, the median duration response was 232 days. We are going to review some of the example cases in the next few slides. Here is a patient who is a 71 year old with triple-refractory multiple myeloma, who, after a single infusion of P-BCMA-ALLO1, had a dramatic reduction in extramedullary disease in the liver, breast, and lymph nodes, as you can see here in a baseline PET-CT scan and a day twenty PET-CT scan. This patient has ongoing very good partial remission five months after the cell infusion. Here is a second patient who had prior four lines of therapy, including prior BCMA therapy, with remarkable response in extramedullary disease after a single infusion, and this patient has ongoing partial remission at month three. Here is an interesting case of a seventy-three-year-old patient with prior 20 lines of therapy, heavily treated, including CAR- T-cell therapy, stem cell transplant, and both teclistamab and talquetamab and CELMoD therapy on the trial. This patient received two infusions of P-BCMA-ALLO1, which was allowed on this trial. Patient didn't have a significant in vivo expansion after the first infusion, and had minimal response to multiple myeloma. However, the second infusion of CAR T-cell therapy after a couple of months had a robust expansion and persistence, including deep myeloma response. This patient is in complete remission currently, so in summary, P-BCMA-ALLO1 is an autologous cell allogeneic T-stem cell memory CAR T-cell therapy derived from healthy donors. And this phase I clinical trial, 100% of intention-to-treat populations underwent lymphodepletion and an infusion called P-BCMA-ALLO1. Several of these patients were treated in a completely outpatient setting. So far, the safety profile looks quite compelling, with no grade three or more CRS or ICANS events, and majority of the CRS and ICANS were grade one or grade two. No graft-versus-host disease has been reported, and no evidence of movement disorder or Parkinsonism has been reported so far. Cytopenias were reported as expected, especially in enhanced lymphodepletion cohort. But fortunately, 82% of the patients had cytopenia down to grade two or less by day 30 from P-BCMA-ALLO1 infusion. A longer follow-up is needed to further characterize the safety profile. Looking at the antimyeloma activity of P-BCMA-ALLO1, despite enrolled in such a heavily pretreated, high-risk multiple myeloma patients, the overall response rates were quite impressive, especially in enhanced lymphodepletion cohorts. In Arm C, 100% of all response rate was reported in the BCMA-naïve patient populations, and 86% patients had some response even after prior relapse from BCMA therapy or talquetamab therapy. Study is ongoing and currently enrolling in Arm C and flu depletion. Recently, FDA has also assigned an RMAT designation for this therapy. I would like to thank all the co-investigators and study staff and patients. Thank you, Dr. Dholaria, for sharing the clinical data presentation on P-BCMA-ALLO1 in relapsed refractory multiple myeloma. We are very excited by the results shown today, and I'd now like to hand over the call to Dr. Syed Rizvi, our Chief Medical Officer, for a discussion with both Dr. Dholaria and Dr. Tom Martin, two of the leading voices in multiple myeloma today. Syed? Dr. Martin, Dr. Dholaria, thank you both for joining us today. I wanted to sit down with you both to talk about not just what you are seeing in the current treatment landscape for multiple myeloma, but also what you are seeing continuing unmet medical needs for patients and how you see the treatment landscape evolving. So Dr. Dholaria, before we dive in, could you please take a moment to introduce yourself and talk a little bit about your experience? What kind of patients do you see in your center, and where are your patients typically in the course of disease? Yes. No, thank you, Syed, for invitation today. I'm a professor, Associate Professor at Vanderbilt, and I work in the Cell Therapy and Transplant division here. And I see patients with relapse refractory multiple myeloma, who are seeking novel therapies, including CAR T-cell therapy or other novel immunotherapies. Most of my patients I see in my clinic are heavily pretreated. Many of them have seen majority of the FDA-approved outpatient therapies by the time they see me. Dr. Martin, could you take a moment to introduce yourself and, talk a little bit about your experience? Hi, I'm Dr. Thomas Martin from the University of California, San Francisco, and I practice in a multi-specialty group, an academic practice, and I see only myeloma patients, and I treat patients that are newly diagnosed all the way to the, when they're relapsed and refractory. We use clinical trials, we use autologous transplant, we use CAR T-cells, and I help actually get patients to those therapies and through those therapies, so I see basically a broad spectrum of myeloma patients. Because we're a tertiary center, we actually tend to see more relapse and refractory multiple myeloma patients, although we see quite a few autologous transplant patients too, so we do have autologous transplants, and then we do CAR T-cell therapies and offer patients a broad variety of CAR T-cell clinical trials, as well as bispecific T-cell engager clinical trials. Dr. Dholaria, could you also talk a bit about your experience treating patients in this phase I trial of P-BCMA-ALLO1, and, did you see any differences, especially in responding patients, you know, in regards to the prior therapies? Right off the bat, I was very impressed with the rapid responses we saw in a couple of initial patients we treated, including several patients of my colleagues who had failed other standard therapies, including significant amount of extramedullary disease. Within four to six weeks, the disease melted away with the clearance of bone marrow. The other thing I was very happy to see as it was the safety of this therapy, where compared to other CAR T-cell therapy, we are seeing severe CRS and ICANS, including prolonged cytopenia. The overall incidence of CRS was quite manageable, and the severity was so low that now we are treating most of our patients on this trial on a completely outpatient basis. We have very few patients actually who even requiring the facility lab nowadays. So that was another important thing for me when I treated my patients on this trial. ... Excellent. Excellent. Thank you so much. So I think the obvious next question would be that how would you compare immunotherapy patients with P-BCMA-ALLO1 to that of earlier studies? Yeah, so we talked a little bit about the safety aspects of it, and I would like to also add that so far, we haven't seen any movement disorders or craniopathy, which has been reported with other autologous BCMA-directed CAR- T cell therapy, such as cilta-cel and ide-cel. And we haven't seen such with the BCMA-ALLO1 infusion. Compared to the autologous CAR, of course, there is obviously a selection bias. When you are evaluating somebody for autologous CAR, you automatically tend to cherry-pick the patients who don't have exploding myeloma, because of the slot availability and the manufacturing issues, and the delay it takes. Like, for example, even as of now, it's taking at least six to eight weeks from the time I make a decision to somebody to receive autologous CAR till they actually get CARs, and many of our myeloma patients, including majority of who were treated on this Phase I clinical trial, would have not been able to stay stable for that long, so I think this is hard to compare the efficacy of BCMA-ALLO1 with this autologous CAR, because really, the patients who are being treated on BCMA-ALLO1 trial are vastly different, with a more aggressive BCMA phenotype, more extramedullary disease, compared to what has been treated on a pivotal trial with cilta-cel and ide-cel. And as well as even what we are doing in the standard of care arm, because we are certainly not treating the patients with such a direct disease with autologous CAR. They are going for bispecific antibody therapy if they're not able to go on a trial. In terms of efficacy, like I said, in my presentation, the overall response rates were quite impressive, including the patients with prior BCMA and talquetamab exposure. So, Dr. Martin, one more question from my side is: What's your perspective on the median duration response and the patient population that you've seen in other trials? Look, the patient population in the trial was actually quite an advanced patient population. This patient, especially in Arm C, had basically received. 62% of them had received prior BCMA. 62% of them had high-risk cytogenetics, and over 35% of the patients had EMD, extramedullary disease. This is a very tough patient population. I was very impressed with the overall response rate. The overall response rate in the patients who are BCMA naive was 100%, and the overall response rate in patients who are BCMA exposed was 86%. Even in the seven patients who had exposure to BCMA and talquetamab or GPRC5D, the overall response rate was 86%. That's quite impressive in this, in fact, quite refractory patient population. The duration of response is also quite impressive, so between five and 10 months. I think in any other clinical trial, if we look at patients who have EMD, high-risk cytogenetics, prior exposure to immunotherapies, that high-risk patient population, perhaps those patients, you know, may have a duration of response, so in the order of perhaps three to six months, three to nine months, maybe at the longest. Those patients, again, are an unmet need, and I was quite encouraged by the preliminary data as shown by the the BCMA. So, you know, as we know that the BCMA-ALLO1 study have included heavily pretreated patients, with more than 40% of patients receiving prior BCMA-targeted therapy and some even receiving talquetamab on top of it. What's been your experience treating BCMA-exposed patients in this trial, and do you think this drug could potentially fulfill an unmet medical need in the BCMA-exposed patient population? Absolutely. I think that's where I see the biggest role of this therapy, given the rapid availability, and overall safety and the responses which we have seen so far. I really have no tool to manage this patient after they have failed both the BCMA CAR and talquetamab, or teclistamab both, and we have seen the responses even in this type of patients. Of course, there are other competing trials. Current therapies are being investigated, such as different CELMoD model and combinations. However, a more data is really needed to compare BCMA-ALLO1 with other novel therapies, but I think that's definitely something I'm really excited to use this drug. Great. Thank you, Dr. Dholaria. So we know that you have treated several patients in this study in outpatient setting, and you just mentioned a little bit about that. So how has your experience been managing the toxicity profile in outpatient setting, and how do you think the potential for safe outpatient administration could set BCMA-ALLO1 apart from other approved CAR- Ts? Yeah. So, we are a bit spoiled with our program in the sense that we have a complete outpatient allogeneic and CAR T program. So even our autologous CAR Ts are being infused in outpatient setting. So that's the same approach you know we took with this product. In our experience so far, patients do get fever anywhere from 24-48 hours after P-BCMA-ALLO1 infusion. It's fairly predictable, I would say, and it follows the CRS pattern. Sorry, CRP increase in the blood. So we can almost predict sort of that when the patient's going to get fever, and most of the patients do respond to just Tylenol, and occasionally a patient has required tocilizumab for grade one CRS. So I think if this therapy moves forward and become commercially available, I certainly advocate using this in an outpatient setting and even oral low-grade kind of CRS and potentially like rapid reversal. And another thing to keep in mind is that the neurotoxicity, I have not actually seen in any of our patients treated in our site. That's certainly can be scary sometimes, and we have seen some severe neurotoxicity after autologous BCMA CAR-T cell therapy. So that also is an advantage of this product. One more question is that, you know, when we speak with myeloma physicians, we always talk about some of the challenges with autologous CAR-T. So if you can kindly share your experience at your center, I mean, that'd be great. Yeah. So there are, again, very significant challenges to autologous transplant. The biggest... Sorry, autologous CAR-T cell therapy. The biggest is it's not an off-the-shelf product, and so the timing is really, a difficult scenario. And when you first have a patient to, think about a CAR-T cell therapy to when they actually can, you know, put out their arm and have apheresis done, and that's the timeframe that we're calling brain to vein. When you think about it, to when you actually can get them a slot to get the apheresis is too long. It's very challenging. It's challenging at our individual centers. Our centers are, honestly exploding with the number of CAR-T cell therapies that we're doing for, autologous CAR-Ts, for myeloma and lymphoma and leukemia, and actually getting a chair at our centers to do apheresis is difficult. So that's really a significant challenge. The second is, patients are not equal, especially in the relapsed refractory setting, and whether or not we think they actually are going to be able to collect an autologous CAR-T cell product. These patients have undergone significant therapies to try to get them back in remission. Sometimes we have to do, you know, high doses of chemotherapy, like cyclophosphamide or alkylator-based therapy. Those patients, we've had a significant challenge in terms of actually collecting adequate lymphocytes that can expand during manufacturing and can produce an adequate product. Initially, when we started to do an autologous CAR-T cell therapy, we had a lot of out-of-spec products, products that would return, and they wouldn't actually meet specifications. And you know, we've become better at actually selecting patients and really better at telling patients, "Listen, I don't think you're gonna be a CAR-T cell candidate. I don't think we're gonna collect cells, so we have to go a different route. Let's try a bispecific T-cell engager." So a lot of patients actually can't get to CAR-T cell therapy. Now, what I heard at SOHO just recently is that in the U.S. for myeloma, there's been about a thousand CAR-T cells in the last year, and autologous CAR-T cell therapies performed, and that's a standard of care. And honestly, I would estimate that probably, you know, anywhere between 5000- 10 000 patients, maybe more, should be eligible for CAR-T cell therapy. So in fact, it's probably in the order of, you know, 10%-20% of people that are eligible or actually get moving forward with CAR-T cell therapy. So still significant hurdles for us to jump over. Great. Thank you so much, Dr. Martin. I think this is really, really insightful. So another question here is that, you know, given the treatment landscape in multiple myeloma, so where do you think the gaps still remain for patients? And, how do you think new therapies could fit into this treatment paradigm? We still are not curing patients with multiple myeloma. That is for sure. And so we, there is an I would say an open space for patients in the relapsed refractory setting. Patients who have had prior BCMA-directed therapy, when the patients relapse after prior BCMA-directed therapy, that's a, in my mind, an unmet need. That's a population we really need novel and new therapeutics for, or we need therapeutics that work well in that, in those patients. We also have the patients who have very high-risk disease, high-risk disease based on either having extramedullary relapse, having high risk, cytogenetic or FISH testing, in the relapse setting, or having what we call a functional high-risk disease. They get initial therapy, and within 12 or 18 months of initial therapy or transplant, they already have relapsed disease. Those patients really have, in my mind, a bad form of multiple myeloma, and those are are are our toughest patients, and that's our unmet need at the current time. Great. Thanks so much, Dr. Martin. And then, when do you start thinking about using CAR-T for your multiple myeloma patients, and when do you start thinking about, these bispecifics? So any opinions regarding sequencing of these agents? Yeah, so that's the hot, the hottest topic right now in myeloma therapeutics. In fact, the CAR- T cell therapy and the bispecifics were initially both approved in the later line setting, so patients had to receive four or more prior lines of therapy. And so it was, you know, difficult to decide after they've had four or more prior lines of therapy, what would be next. More recently, we've had two large phase III trials, randomized trials, of CAR- T cell therapy versus standard triplet therapy in the earlier line setting. And both trials, using both available and approved CAR- T cell products right now, showed an advantage to CAR- T cell therapy earlier in their line, lines of therapy versus a standard triplet. So now when we try to think about CAR T-cells, we are thinking about CAR- T cells in early relapse. So at first relapse or second relapse, you know, is that patient a candidate for CAR T-cell therapy? And my personal opinion is, you know, that is probably a better space to do CAR- T cell therapy because you have more time potentially to plan for CAR -T cell therapy, and, you know, patients aren't as ill, and hopefully their disease isn't as rapidly progressive. Now, bispecifics are still only available at the late line setting, so four or more prior lines of therapy. And so we typically would do a CAR -T cell therapy first, and then we would do a bispecific after the CAR- T, after patients relapse, after CAR -T cell therapy. In select patients who maybe already have had four lines of therapy, and when we decide, you know, okay, what's next for them? Is it a CAR or is it a bispecific? There's many things that go into that decision tree, and I think the first and foremost is what the patient wants, because CAR T-cell therapy requires a much bigger caregiver, you know, group for the patient. They have to come to the treatment center. They have to stay there for four weeks. They can't drive for eight weeks after they initiate therapy. They're at significant risk for infection for the first, you know, four to six weeks. In contrast with bispecifics, you know, they drive into the center. They spend the first, for us, the first week or 10 days admitted to look for CRS in the first cycle of therapy while step-up dosage is happening. But after that, they can drive themselves in for their visit, and it's a subQ injection, and they'll come in and get their therapy, and then they'll go home. So the patient actually, in my mind, has one of the biggest roles in terms of what, you know, direction to go to. But then the second is the disease. The disease has a big role because, bispecifics are off the shelf, and usually off-the-shelf products we can essentially give to anybody, no matter what their disease looks like, and no matter how fast their disease is progressing, we could take that therapeutic off the shelf and administer them usually within seven to 14 days. An autologous CAR T-cell therapy is much different. We need at least four to six weeks to get an apheresis slot and another six to eight weeks weeks for that CAR-T cell to be manufactured and to be able to give back to the patient, so it's a much bigger deal. Thank you very much, Dr. Martin. So another question is that, in regard to infection risk for bispecifics versus CAR- Ts and the safety profile of our CAR- T that you have seen, the P-BCMA-ALLO1. So, any feedback, any insights? I'll start off with bispecifics and standard of care CAR- T cell therapies. What we've seen is the bispecifics, especially the BCMA-targeted bispecific therapies, have had significantly increased incidence of grade 3 or 4 infections and infections while they're on therapy. So if you are continuously receiving a BCMA therapeutic, the patient is not gonna recover their B-cells for sure. And most of those patients are going on to receive intravenous gamma globulin as replacement-based therapy. Those patients are on significant risk, continuous risk for developing you know infections while they're getting therapy over time. We try to mitigate that by having them on prophylaxis and by giving them intravenous gamma globulin, but they still have a significant risk of grade three and four infections, and especially viral infections that can become severe. COVID infections, metapneumovirus, RSV, et cetera. All of these actually are very challenging in that patient population. With autologous CARs, you know, the infection risk tends to be higher in the first three months, maybe in the first three to six months. And then it tails off, because at that point in time, they do start to have recovery, some B-cell recovery. Now, the data that I've seen for, you know, P-BCMA, the data actually looks quite good in terms of the infection risk. So it's a very low incidence of grade three and four infections. I think the incidence was less than 20%. So those data are actually looking very positive. Certainly, allogeneic CAR T-cell therapy had been, you know, been associated with higher risks of infection when we were using much higher doses of cyclophosphamide and also anti-CD52-based antibody therapy to try to produce immunosuppression to allow the CAR T-cell expansion. But it looks like in your LD therapy with P-BCMA, that actually the infection risk looks quite favorable. ... I think the safety is. Let me put it in two ways. In terms of CRS, it's fairly comparable to bispecific, I would say. In fact, the overall incidence is lower compared to teclistamab or talquetamab, where almost everybody gets grade one CRS. The long-term safety, I think, is better than bispecific in my experience with this, because especially with the teclistamab, where patients get prolonged cytopenia sometimes or ongoing immunosuppression requiring IVIG and some recurrent infection episodes. We have not seen that with P-BCMA-ALLO1, because most patients do have a rapid recovery of their cytopenia, and there is no prolonged immunosuppression. At least we have not seen serious infection once the patient is beyond one month from the P-BCMA-ALLO1 infusion. So I think the safety, the immediate typical CAR-T related toxicities are comparable to bispecific, but the long-term toxicity is, I think, favorable with the P-BCMA-ALLO1 compared to bispecific. And then, another question is that, you know, with BCMA, auto CAR- Ts, and bispecifics, you know, moving to earlier lines, how are you thinking about treating patients who potentially relapse following treatments on products like Carvykti or Abecma? So that's a really important question, 'cause now what we're finding is that, you know, there doesn't seem to be a plateau at the current time with autologous CAR T cell therapy, so over time, patients continue to relapse, so we do have to have therapeutics for them when they relapse. When, you know, our current strategy is when they relapse from whatever immunotherapy that they're currently receiving, whether it's BCMA or GPRC5D, we do try our best to switch up the, you know, the target on the plasma cell. So if they got a BCMA-targeted therapy, we have basically gone to GPRC5D as our next. If we had GPRC5D, then we go to BCMA. And really, the reason we've done that is because with our currently approved therapeutics, we're really not seeing great data when we go from one BCMA therapy right to the next BCMA therapy. So I think that space is open. It's open if there is a, you know, a BCMA CAR- T cell therapy or off-the-shelf therapy that can show a, you know, a significant improvement, overall survival and improvement in PFS or duration of response, that therapeutic would, you know, obviously be used in that setting. That in my mind, would meet an unmet, you know, unmet scenario that we have, and that is post-BCMA therapy. I do think that post GPRC5D, going to a BCMA therapy is actually quite a is quite a good regimen for us to go to. It's only recently patients have started to receive GPRC5D first and now getting BCMA second. So we don't know if the sequence is better, BCMA first, GPRC5D second, or whether it's GPRC5D first and BCMA second, or how to sequence these things. Autologous CAR, bispecific, allogeneic CAR really is gonna be, in my mind, the next two to five years. That's gonna redefine how we sequence therapies. Thank you, Dr. Martin. Great feedback, Dr. Dholaria. So turning to manufacturing a little bit. So one of our biggest focuses in CAR Ts, especially with allogeneic cell therapy, has been the ability to manufacture hundreds of doses of products from a single healthy donor, and that can be delivered to patients on demand. How are you thinking about that compared to the current auto CAR T therapies on the market? If an off-the-shelf or on-demand therapy was available, how do you see them, that impacting the patients you are seeing and potentially even the outpatient setting? Yeah, no, I think that's definitely a huge advantage, and it will allow me to treat patients who really need this therapy, like aggressive patient, relapse patient, [uncertain], patients who have failed bispecific therapies. And really there is no good way to give them autologous CAR- T, because after the prior T-cell engagement exposure, the quality of autologous CAR Ts, as we know, is not as robust and the response rates are low, and the duration of response after Carvykti and Abecma has been suboptimal at least for the patients who have been exposed to other T-cell engagement therapy, so I think this therapy, being off the shelf, readily available, can certainly be quite advantageous for this, our patient. Given the fact that these cells are delivered cryopreserved to the site and can be potentially delivered in an outpatient setting, I think even the smaller academic program or community practices can potentially use this in their office, as long as they have immediate availability of support on demand. Now before we close, let me ask you this. What are you hoping to see from future CAR-T therapies, and what do you think the bar is for success? Especially, you know, thinking about the patient population who may be BCMA naive versus BCMA exposed. Yeah. So in the BCMA-naïve,I would you know, it would be really great if we can get to that plateau effect. And so my my recommendation has been, you know, CAR- T cell therapy as a one-and-done phenomenon works very well and gives a significant progression-free survival, but patients relapse. Would it be possible for us, after the CAR- T cell therapy, to do some maintenance-based therapy? Can we give three to six months of a CEL MoD? Can we give three to six months of a bispecific or a year of of maintenance-based therapy? And would that enhance our, you know, our progression-free survival? Would it enhance our duration of remission? Would it provide that plateau? In the patients who receive basically, CAR- T cell therapy and then have, relapsed, and we're doing a second BCMA therapy, I think in that, group of patients, we should be thinking about combination. What is the best combination therapy? Or can we do subsequent or, more than one infusion, especially with allogeneic CAR- T cell therapy, can we give subsequent infusions? Can we give one infusion and three months later, can we give a second infusion and enhance the duration of response and enhance the overall response rate in the PFS? You know what, what do we need to do to provide a longer and a deeper effect? I think that those are the strategies that I think are gonna, again, be what provides us with the next level of remission duration in, multiple myeloma therapeutics. We're doing well, for sure, but we certainly can do a lot better. Yeah, that's certainly a moving target because our therapies keep getting better, and now with the bispecifics and autologous CAR- T moving in an earlier line of therapy, we are increasingly seeing the patients who have seen this therapy before they get referred for the clinical trial. However, going forward, if I have to design an ideal gold standard CAR- T cell therapy, I would say it will be something which is readily available, safe, can be given in outpatient setting, with deep responses and durable responses. Dr. Martin, Dr. Dholaria, thank you for your responses and your feedback and your support. We are really excited about this P-BCMA-ALLO1, its development, and especially the RMAT designation that we recently received from FDA. And I am so, thank you once again for all the support and spending time with us today. Thank you. Thank you, Syed. We believe the IMS data presentation and additional commentary from Dr. Dholaria and Dr. Martin that you have just heard clearly supports the strong value proposition of P-BCMA-ALLO1, and we are enthusiastic about continuing its development together with our partner, Roche, using the Arm C lymphodepletion for the phase I-B study. The data show that P-BCMA-ALLO1 is a highly potent agent in a refractory and difficult-to-treat patient population, with both BCMA-naive and BCMA-experienced patients responding. We also see a compelling emerging safety profile and are demonstrating the ability to treat all eligible patients reliably and quickly without bridging therapy and offering a positive patient experience, so how do we think this might fit within the treatment landscape? We think P-BCMA-ALLO1 could be an attractive option for healthcare professionals and patients, particularly when comparing to the existing treatment landscape for BCMA-targeting autologous CAR-T and T-cell engagers, and we will highlight this comparison over the next few slides. First, the P-BCMA-ALLO1 phase I population included patients that were more difficult to treat than the patients in the corresponding pivotal studies of ide-cel, cilta-cel, and teclistamab, which are listed from left to right in the first three columns of the table. When looking at baseline demographics, we can see that P-BCMA-ALLO1 patients are older and have somewhat poorer performance status. We have successfully treated patients up to 85 years of age on this study, and we've given as routine prophylaxis, only Tylenol and Benadryl. We've also studied a racially diverse population in the phase I study, which is important, as patients of color have historically had poorer clinical outcomes. Moving down the table, our patient population also can be seen as high risk and possibly more frail. Looking at the disease manifestation in our patient population, you can see that almost seven of 10 patients overall, and more than three in five Arm C patients, had one or more high-risk genetic abnormalities, which tend to correlate with poor prognosis. Also, almost 40% of our Arm C patients have extramedullary disease, which could be extensive, as we saw in some of the patient scans. Lastly, our patient population is highly refractory, with patients having received a median, but up to 22 prior lines of therapy, and over three in five patients in Arm C had at least one prior BCMA-directed therapy. Nearly two in five of those same patients had multiple novel therapies, with 29% having failed both a BCMA auto CAR-T and a BCMA bispecific, and another 29% failing both BCMA and GPRC5D-directed therapy, so our patient population for this study really stands apart in our view, as among the most difficult-to-treat patient populations ever studied in myeloma. Our Arm C data is still relatively early and needs time to mature. However, the early efficacy is impressive. In this table, we're looking at data from commercial BCMA auto CAR-Ts and teclistamab that's taken from their pivotal clinical trial publications. Remember, these trials studied all BCMA-naive patients, and their patient populations were lower risk and easier to treat, as we just saw. Looking left to right, there are two columns for each of the CAR-Ts, one with the data published for patients who enrolled in the study and were actually treated with the CAR-T, and next to it, a column looking at response rates as analyzed for the total intent-to-treat population. Because some patients were unable to receive CAR-T due to disease progression before infusion, manufacturing failures, or other reasons, the ORR in the ITT analysis for these agents is lower. For teclistamab, a bispecific, no such correction is necessary. Looking across the table at ORR, we can see that the overall response rate for P-BCMA-ALLO1 in Arm C is higher than the reported data for the commercially available therapies, and the P-BCMA-ALLO1 ORR is not in any way inflated or augmented by the use of bridging therapy because we didn't use any, unlike autologous CAR-T. Looking at the depth of responses, CR and SDR rates are similar to Abecma and Tecvay, lower than for Carvykti. If VGPR or better rates are indirectly compared, P-BCMA-ALLO1 appears better than Abecma, but not as high as for the others. However, it should be noted that the median duration of therapy for Arm C is only three and a half months, and we will be watching to see if responses may deepen over time. When we recall that the P-BCMA-ALLO1 patient population is so very different from the patient populations in these other studies, we find this data even more impressive. P-BCMA-ALLO1 also is emerging as distinctly differentiated in terms of its safety. Looking again at data from our study in indirect comparison to data from competitor pivotal studies, we see lower rates of CRS, neurotoxicity, and infections, as well as no use of bridging chemotherapy, which has been associated with substantial toxicity as well as increasing the response rates. All CRS and ICANS have been grade one or two, and grade three or higher infections were uncommon even in arms with higher lymphodepletion. We have also seen no signals of parkinsonism or secondary primary malignancy in this study or our other clinical trials of T stem cell memory rich CAR-T, which in total have included over two hundred patients by now. Importantly, the safety profile observed was consistent in both BCMA naive and BCMA-experienced patients and across all the study arms. We're excited about the possibilities for patient treatment that a safer, off-the-shelf CAR-T could offer. We've treated some patients entirely in the outpatient setting already and could see P-BCMA-ALLO1 potentially being given at more sites of care and used more often in the outpatient setting, which brings convenience benefits to the patient and physician, as well as simplifying reimbursement and improving market access. So in summary, we've been very excited to share this interim data summary with you. We were able to treat 100% of the intent-to-treat population with P-BCMA-ALLO1, our investigational off-the-shelf allogeneic CAR-T, without waiting. Our patients received infusion of CAR-T cells one week after enrollment on the study, and they've underwent no invasive apheresis, no bridging therapy, and we were able to include treating patients in an outpatient setting. We're seeing a compelling emerging safety profile in our diverse, heavily pretreated, refractory, and high-risk patient population. We've seen an overall consistent safety profile across all the arms, which use no steroid or tocilizumab prophylaxis, and we've seen no DLTs, no GvHD, no HLH or macrophage activation syndrome, no Parkinsonism or cranial neuropathy. We've seen low rates of CRS and ICANS, all grade one or two, and low infection rates with rapid recovery of cytopenias in those cases. Importantly, we've seen exceptional clinical activity in our optimized lymphodepletion Arm C, including both BCMA-experienced and BCMA-naive patients. Arm C is our largest but least mature cohort, where we saw a 91% overall response rate, including 100% response in BCMA-naive patients and 86% response rate in prior BCMA and/or GPRC5D auto CAR-T and/or T-cell engagement-exposed patients, and many of those patients had seen multiple of those agents. Arms A and B were smaller but somewhat more mature, and we saw response rates of 42% and 70% overall, respectively, and we were able to see a median pooled duration of response estimated at five to 10 months, with patients with at least six months of follow-up. In those arms, the median time to response was only 16 days, for a total median physician treatment decision to patient response time of about three and a half weeks. This study is ongoing and currently enrolling patients in the phase 1B expansion using Arm C lymphodepletion, and P-BCMA-ALLO1 has been recognized by the FDA with RMAT as well as orphan drug designation. We are excited to be continuing the development of P-BCMA-ALLO1 in partnership with Roche, and the phase 1-B study is ongoing and currently enrolling. We have more data ahead for our other programs as well, including data updates in the fourth quarter for our other two clinical-stage allogeneic CAR-Ts and a cell therapy R&D day in November, where we will take a closer look at our earlier pipeline. In our non-viral genetic medicines area, we will be giving updates, including a distinguished oral presentation at the ACAAI conference in October, and we remain on track for at least one IND filing in 2025. We are also very pleased to announce today that P-BCMA-CD19-ALLO1, which is one of two Roche optioned programs in hematologic malignancies, has returned to Poseida. This program is at the IND-enabling stage, and we look forward to developing it in hematologic malignancies as well as autoimmune disease. Taking a brief look at this BCMA-CD19 allo CAR-T, we are excited to take this fully owned program forward, given that BCMA and CD19, both alone and in combination, are of high interest for heme malignancies as well as various autoimmune diseases. We have also incorporated a number of improvements into this program that we believe could enhance its potency. For example, these CAR-T cells carry two full-length CARs each. The BCMA-directed CAR also has a tandem binder, and we have further engineered the intracellular domain. This program uses our core non-viral technology suite, so it also has all the standard features of our program, such as being T stem cell memory-based and including our safety switch. In closing, we believe that our proprietary, validated, non-viral platform positions Poseida very well for leadership in allogeneic cell therapy. You've just seen our unique T stem cell memory-based cell platform, which we've used to produce P-BCMA-ALLO1 and the data you've just seen. Poseida also has the pieces in place to successfully navigate forward clinical development and commercialization, with scalable manufacturing and strong partnerships in place for our partnered assets, including P-BCMA-ALLO1. And our partner on this program, Roche, has outstanding global capabilities to ensure eventual commercial success. Poseida's growth potential is vast, with a rich early-stage pipeline in allo CAR-T and non-viral genetic medicines, which is backed by an extensive IP portfolio, and we welcome additional partnership opportunities. With that, I'd like to thank you very much for your time today and open the call for Q&A. Operator? Thank you. And a this time, we will conduct a question-and-answer session with our speakers. If you would like to ask a question, please press star one on your telephone keypad, and we will take our first question from Jennifer Kim with Cantor Fitzgerald. Please go ahead. Hi, thanks for hosting this presentation and to Dr. Dholaria and Martin for their thoughtful comments. Maybe my first question is just on the last update you guys gave. For the BCMA CD19, is there any color you can give on, I guess, the the decision from Roche's part, maybe not to exercise the option? And in terms of your prioritization over multiple myeloma and autoimmune, how are you thinking about the strategy there? And then I have a follow-up. Yeah, thanks very much, Jennifer. So, you know, we can't comment a lot on Roche's portfolio decision-making, but I think you've just seen, you know, P-BCMA-ALLO1 is a tremendously exciting lead asset. Roche is clearly partnering with us and in full support. The decision to move to the phase 1-B study was of course taken in that partnership and in concert, and that triggered another $20 million milestone for us. So I think, you know, we are all very enthusiastic about the bright future ahead for P-BCMA-ALLO1. In case people listening on the call today are not aware, Roche also has an R&D day coming up in just two days, on Monday, 30th September. And you know, we don't know entirely what they will say about the partnership and the program, but you know, it's a lengthy R&D Day, and historically, they've used that opportunity to really you know take you know take their folks through their entire portfolio. So I would encourage people to maybe pay attention to that. And in terms of how we see P-BCMA-CD19-ALLO1, well you know we think it has great prospects in both autoimmune disease as well as potentially multiple myeloma. And the premise behind that combination of targets is a little bit different, but quite strong in both areas. In autoimmune disease, we know that there are some autoimmune diseases where long-lived plasma cells appear to be the culprit driving the disease. And so the ability to cover kind of an end-to-end spectrum of B cells, which you get from that combination of two targets, is quite appealing, and others have been looking at that combination with, you know, autologous products already. ...In multiple myeloma, you know, the theory there would be that BCMA is a fantastic target, as we're well aware, but there may be some progenitor cells, that for which a CD19-based moiety might be particularly, effective. So you know, we're, as you've seen, excited about that program. We've put in some additional improvements with tandem binder and other things. So we'll be looking at multiple opportunities, to take that forward. But, again, to conclude, BCMA ALLO1, you know, we are very excited about that. We believe our partner, Roche, is very excited about that. And of course, the CD19 combination is further upstream. Okay, that's helpful. And then going back to the IMS data, in terms of the, or looking at the CRs that you're seeing in Arm C, is there any color you can give on, how many or, like, MRD negative, any color around that? And then in the more mature arms, like Arm B, can you say anything about the duration of response that you're seeing in patients who have stringent CRs? Is there longer duration that you've seen with those patients? Thanks. Yeah, absolutely, Jennifer. So, you know, we our MRD analysis is not mature yet, but maybe I'll ask Syed to try to bring some more color and answer your question. Yeah. Thank you very much, Kristin. So that's exactly right. And this is something that we are also very, very keen to look into, and that evaluation is ongoing, and we do plan to share this at a future venue. So we do understand that how important it is and- Okay. And then if I could squeeze one more in. I think in yesterday's press release, you said that the ongoing trial, you're using the Arm C lymphodepletion across two dosing cohorts, and there's still some dose optimization going on. Can you talk more about that dose optimization work and the strategy there? Thanks. Yeah, absolutely, Jennifer. Thanks for the question. So, you know, I think what we've just seen here is, you know, we have a very potent allogeneic CAR T here, in terms of the response rates. And at least as impressive as the efficacy is also the safety profile. So, you know, we are very happy with what we're seeing at, this current, what we call the cohort two dose, but, you know, there could be room to go higher as well in terms of the absolute number of cells. So, you're quite correct. The arm I- B study has multiple arms, and we are looking at a higher cell higher cell dose, excuse me, as well. Okay, thanks again. Congrats, guys. Bye. Thanks, Jennifer. Thanks. Thank you. And we will take our next question from Arthur He with H.C. Wainwright. Please go ahead. Hey, Kristin and team. Congrats, and thanks also for Dr. Dholaria and Dr. Martin to join us for these events. I had a couple of questions regarding the data-wise. So, Doctor, so I know you treat a couple, a number of patients in an outpatient setting in this trial already. I'm just curious, for the future, if when you're looking at this therapy or any other additional therapy for the outpatient setting, what are kind of the adverse events you're gonna focus on to be qualify this therapy as an outpatient setting? Yeah. Thanks, Arthur. Okay, so that's a question for Dr. Dholaria, who's here with us. So, Dr. Dholaria, please feel free to answer. Yeah. So, in our experience, except the first few handful of patients, vast majority of the individuals in our center is in an outpatient setting heavily. We do have a long-standing outpatient cellular therapy program at our center, so we can help them with this transition. But, I think if this therapy becomes widely available, it's feasible to this, even at its relatively size, for some reason. Number one, the overall frequency of CRS is half of what we see in the first time, and the severity of the CRS and quite low. Very few patients, in my experience, now get steroids. Actually, I don't even recall giving any patient steroids now, because most patients receiving tocilizumab have had complete response to their cytokine release syndrome fairly quickly. A handful of patients did require more than one dose of tocilizumab, but none of our patients did get to go to the ICU or require IV pressors. So that speaks to the overall safety of this agent and ability for this to manage from outpatient setting. Thank you, Dr. Dholaria. We've heard that maybe that answer wasn't wasn't entirely able to be heard. So just to briefly summarize, you know, Dr. Dholaria was saying that after the first few patients, they've really been treating essentially all of their patients in the outpatient setting at Vanderbilt. And the safety profile that's emerging here is very favorable for outpatient use because the rates of CRS and ICANS were about half what you were seeing with tocilizumab, sarilumab, and the severity also less. So, you know, those are some of the key AEs being looked at when evaluating if it's suitable for outpatient use. So yeah, hopefully that that summarizes your thoughts accurately, Dr. Dholaria. We've got a lot more, but okay. And Arthur, did you have another question? Yeah. So yeah, thanks, Kristin, and thanks to the doctor. So I had a second question is regarding the. I know you you show the overall patient baseline characteristics and the Arm C. I just want to see, could you give any color regarding the the arm, both Arm A and B versus Arm C regarding the patient baseline? Sure. And thanks, Arthur. So I'll ask, Syed to take that question. Yeah, thanks very much. So in regards to the patient population in different cohorts, what we have seen is that over time, as we are really enrolling patients in Arm C, Arm C patients seems to be more of a sick patient population. And the reason is that if you see overall patients who have received prior BCMA in our trial is about 40%, but if you look into Arm C, it's 60% or more. Then the seven patients have also received not just one BCMA, but several BCMA prior therapies, and on top of it, GPRC5D, which is teclistamab, a treatment as well. Patients seem to be more sicker, and I think it's it's the way really multiple myeloma treatment paradigm is evolving, where patients are able to, you know, get bispecific and other treatments more readily available than earlier. So this is definitely a more sicker patient population as we are really honing towards Arm C and moving towards our phase I-B. Great. Thanks, Syed. I'm back on the queue. Thanks. Thank you, and we will take our next question from Sami Corwin with William Blair. Please go ahead. Hi, congrats on the data, and thank you for taking my question. I have one for Dr. Dholaria. Given that bispecifics and BCMA-ALLO1 are built off-the-shelf therapies, if they were both commercially available, would you be inclined to use one over the other, or do you think some patients would be better suited for one versus the other? And then a question for the company is, did you see responses deepen over time at all in the arms that did have a longer duration of follow-up, so S, A, and B? Thank you. Yeah, thanks. Thanks, Sami. So, Dr. Dholaria, would you like to answer? Yeah, I think this is a difficult question to answer because we don't really have long-term follow-up of this cohort, although the earlier responses are quite promising. To answer your question more definitively, we really need to see the duration of response and MRD clearances. Your question was raised so to pick which is the better of Tecvay versus the BCMA-ALLO1. But if we assume that both have similar clinical efficacy, there are certainly patients who would benefit from BCMA-ALLO1, and I would probably favor this versus Tecvay. Patients such as individual who wanna do time-limited therapy instead of teclistamab, which is an ongoing treatment. Patients with a history of severe recurrent infections, we tend to come across this individual more often nowadays in the era of quad and transplant. Somebody with history of fungal infections and viral reactivation, I would be definitely hesitant to give the teclistamab, given its track record of significant opportunistic and severe infection, versus, so far, BCMA-ALLO1 does not appear to have that high infection risk. Thank you, Dr. Dholaria, and Syed, can you take Sami's second question? Yes, go ahead, Sami. Yeah, can you please repeat your second question, Sami? Yes. Yes, it was if you saw responses deepen over time in the arms that did have a longer duration of follow-up, so arms S, A, and B. Great question, I would say. So I would say, you know, what we have seen on the autologous side, we're very, very excited to see that we are seeing the same phenomena here in allogeneic CAR- T, where we are seeing deepening of responses over time. And I think this is part of the cell that we are really creating with our CAR- T, the stem cell memory T cell, and it's coming along quite nicely. Thank you, and we will take our next question from Justin Zelin with BTIG. Please go ahead. Thanks for taking our questions, and congrats on the data. For Dr. Dholaria, I understand the data here is still maturing, and I wanted to ask you, what what duration of response would you like to see for an allogeneic therapy like BCMA-ALLO1? And my second question is for Syed. You showed a case study here for a patient who had a retreatment. Could you comment on how many patients in the study have been retreated, in total thus far? Thanks. Yeah. So I think, as we earlier noticed this, we are looking at the highest patient population. Half of them had other prior BCMA targeted therapy and other bispecific. So, if if that's the background patient population we're looking at, I mean looking at the standard treatment option- ... I would say if a patient is going through an intensive therapy, such as P-BCMA-ALLO1, I would put in that category given the high degree of [audio distortion] inflation and the monitoring required away from patient's home. Patient would expect at least six to eight months of duration of remission, at minimum, in my opinion, before committing to such therapy. Thank you. Syed? Yeah, thank you so much, Dr. Dholaria. Thank you, Kristin. So, just to add to your question that how many patients have so far been retreated? So, there are five patients who have been retreated. So we have 72 patients who are unique, 72 patients, but if you count those retreatment, we have 77 patients. And I think this really talks about allogeneic cell therapy, where you have that CAR-T available in a hospital freezer whenever the patient shows up and whenever that's required, you don't have to go through resources, using therapies and unnecessarily wait for manufacturing time. And that's really the beauty of allogeneic, and we're really seeing that the future lies with allogeneic cells. Thanks, and if I could just ask one more question just on the infections, if you could give a little bit more color, if these were able to be managed with best available care and, just you know, qualifying that, that would be helpful. Thank you. Yes, absolutely. So first of all, the infection rates are very, very low, and all the infections were completely, you know, taken care of by routine antibiotics. So we did not have any major issues. So, you know, very, very manageable profile here. Great. Thanks for taking my questions. Thank you, Justin. Thank you, and it appears that we have reached our allotted time for questions. Dr. Yarema, we will now prepare to conclude the call. Yeah. Thanks, thanks so much. Everyone's been very generous with your time today. So, thank you, and look forward to further communications with you on this exciting topic.