Good morning and welcome to the Artiva Biotherapeutics virtual event discussing the initial safety and translational data for AlloNK in autoimmune diseases. I am Fred Aslan, President and Chief Executive Officer of Artiva. We are excited to share the progress Artiva has made in advancing our lead product, AlloNK, through development in autoimmune disease. Sitting here today, we have dosed over 100 patients with AlloNK across oncology and autoimmune disease, a significant milestone for the company. Earlier today, we announced our Q3 financial results with $123 million in cash and runway into Q2 2027, and we believe our balance sheet provides us with the capital we need to advance AlloNK into the next stage of development. Before we begin, I would like to note that we may make forward-looking statements today, including about our product candidates and development programs, data from ongoing clinical trials, regulatory interactions, market opportunity, and cash runway. Forward-looking statements are subject to a number of risks and uncertainties that are discussed on this slide and in our filings with the SEC. Actual results could differ materially, and we undertake no obligation to update forward-looking statements. In addition, our product candidates have not been approved for marketing, we have not conducted any head-to-head studies, and you should use caution when comparing data from different studies or publications due to differences in study designs, patient populations, and endpoints. We have learned from the Auto-CAR-T experience that a deeper B-cell depletion could offer transformational treatments in autoimmune disease. Like the wave of targeted therapies, including the TNF inhibitors and JAK inhibitors that are today's largest categories, the deep B-cell depletion space across all modalities has the potential to wash over every indication in autoimmune disease. Auto-CAR-Ts have shown dramatically better efficacy than biologics, but that efficacy comes with some drawbacks. It has toxicities, it can be cumbersome to administer and monitor, it has scalability limitations for large indications, and it is expensive. Our vision is to combine the higher efficacy of cell therapy with the favorable safety and convenience of biologics, with the opportunity to provide durable responses to patients with only five or six visits to a community rheumatology infusion center. We have selected RA as our lead indication because our therapy is scalable and can be given in community clinics. We are pleased with the momentum and enrollment we have seen thus far. Today, we will report initial safety and translational data in 32 autoimmune patients already treated across our autoimmunity studies and indications. On today's call, we will review AlloNK's mechanism of action, we will remind you of why AlloNK plus monoclonal antibody has the potential to drive Auto-CAR-T-like deep B-cell depletion, and we'll discuss the regimen so you can understand the ease of use in a community setting. Subhashis Banerjee, our Chief Medical Officer, will then walk you through the initial safety data to support the understanding of the ease of use in a community setting. Next, Heather Raymon, our SVP of Research and Early Development, will share our translational data, which will demonstrate the consistency of our B-cell depletion data, both using conventional methods as well as with a higher sensitivity assay that offers even more confidence in our ability to deplete B-cells deeply. Finally, we will close with how we are thinking of tackling the refractory RA market with AlloNK plus rituximab, how we are defining where the unmet need is that we are pursuing, and what bar we're setting for AlloNK. I will start with a review of AlloNK's mechanism of action and treatment regimen. AlloNK is a non-genetically modified NK cell therapy. Because we don't engineer in a CAR, we use monoclonal antibodies for targeting B-cells. We can use any IgG1 monoclonal antibody, and thus far, we have focused most of our efforts on rituximab to target CD20 on B-cells. The mechanism is ADCC via the CD16 receptor on AlloNK cells. The CD20 monoclonal binds to CD20 on the B-cell, the Fc portion of the monoclonal antibody binds to CD16, this activates the NK cell, and the NK cell kills the B-cell. Our experience in B-cell lymphomas, which I will briefly review in a moment, has demonstrated the power of the approach. The advantage of not engineering the NK cell is that it makes the manufacturing process highly scalable. We source our NK cells from umbilical cord units, and from one umbilical cord unit, we can make thousands of cryopreserved one billion cell vials like the one you see on the slide. The cells are vialed using an infusion-ready media, the shelf life is over three to four years, and when it's time for use, the vials can be thawed at the bedside in its 10 minute-15 minute infusion. Our experience in aggressive non-Hodgkin B-cell lymphoma gives us the confidence that we can achieve deep B-cell depletion. This chart shows that when we treated 14 patients with all but one having aggressive NHL with AlloNK plus rituximab, we were able to drive a 64% complete response rate. As of the last follow-up, we still have not yet met the median duration of response with a minimum of 19.4 months, which is in line with what commercial Auto-CAR-T achieves in aggressive NHL, and potentially better than what the best commercial TCEs can achieve in aggressive NHL. In addition, there are a number of other clinical trials in lymphomas using non-genetically modified allogeneic NK cells with B-cell targeting biologics that have demonstrated consistent activity. The first one we highlight here was an NHL study at the University of Minnesota with non-genetically modified NK cells plus rituximab, achieving nice durable responses, and the other two are non-genetically modified NK cells with a CD30 NK cell engager targeting Hodgkin's lymphoma B-cells, also with notable activity. These results across almost 80 patients highlight the activity of non-genetically modified NK cells plus a targeting biologic. As we will share later today, we are seeing consistent results thus far in autoimmune disease with uniform consistent B-cell depletion across patients treated with autoimmune disease, just like we saw in oncology. An important component of the AlloNK treatment regimen is the use of cyclophosphamide or CY and fludarabine or flu as conditioning agents. We use low doses of CYFLU. For CY, we use 1 gram per meter squared, which is half the exposure of the urolupus protocol, which carries minimal infection risk. For flu, we use 90 milligrams per meter squared, which was given in the 1990s in monthly doses over six months to rheumatology patients. In other words, six times the cumulative dose we are using, and it was found to be well tolerated but not very effective. We use CYFLU for two reasons. Number one, it allows our NK cells to persist and to exhibit a nice dose-dependent PK, as you can see on this slide. Number two, it reduces the number of B-cells and T-cells. The positive element of these effects is that it contributes towards efficacy, reducing the B-cell burden and potentially eliminating autoreactive T-cells. The negative element is that it creates a short window when patients are lymphopenic and neutropenic, though this can be managed with prophylactic anti-infectives. As we will show you in the safety section of this presentation, the AlloNK treatment regimen has been observed to be well tolerated as of the data cut off, despite the use of CYFLU, and the administration and management has the potential to be quite similar to IV biologics in outpatient settings. The AlloNK treatment regimen is designed for outpatient administration and management. In our autoimmunity trials, patients come to the outpatient infusion center on six days over a period of 20 days, and they can go home after their infusions. Patients receive their CYFLU conditioning on days one, two, and three, and then receive AlloNK on days six, thirteen, and twenty. Rituximab is given on two of these days at the same dose as in the label for the relevant autoimmune diseases and around 14 days apart. In the next section of this presentation, we will share initial observations of the safety and tolerability of this treatment regimen in the community setting. The AlloNK treatment paradigm is a little different than traditional biologics that need to be given with repeated doses. For example, Humira is given every two weeks over long periods of time. Our therapy is more similar to Auto-CAR-T in the sense that the first cycle has an opportunity to provide durable responses. In RA, we will use 24 weeks as the time point for regulatory purposes, and we will continue to generate data that will inform how durable a single cycle can be. We hope we can achieve median duration of responses in at least the 12-24 month range. Like a biologic, our treatment regimen can be given again if a patient relapses. We hope to also explore whether additional cycles can durably extend the clinical effects. It is important to take a step back and appreciate the bottom part of the slide. Patients receiving the first cycle have a 30-day window when they're more prone to infections due to the lymphodepletion and neutropenia with CYFLU. However, if they can tolerate this initial period with supportive treatments as needed, they have the potential to be weaned off all immunomodulatory drugs, including steroids. Outside of these first 30 days, these patients have the potential to have a lower infection rate than patients on chronic biologic and immunomodulatory treatments, including steroids. Now I will turn it to Subhashis to present the initial safety data for AlloNK in autoimmune disease. Thank you, Fred. Good morning. My name is Subhashis Banerjee. I'm the Chief Medical Officer at Artiva. I have been in the industry for over 30 years working in the immunology and inflammation space and have been involved in the development of many well-known RA drugs, including Humira and Orencia. In this section, we will review the initial safety data on the first 32 patients with autoimmune diseases treated with AlloNK in combination with anti-CD20 monoclonal antibodies. On the left side of the slide, we highlight the three ongoing trials exploring AlloNK in autoimmune diseases. We have a company-sponsored phase II BASCA trial enrolling patients with RA, Sjogren's disease, myositis, and cystic fibrosis. We are also exploring AlloNK in an investigator-initiated trial where patients with RA and lupus were enrolled. This trial has been conducted in a community rheumatology practice in Florida. Finally, we have a company-sponsored trial in SLE and lupus nephritis. The starting dose of AlloNK in all our trials is one billion cells per dose of AlloNK, and in our company-sponsored studies, it has escalated to four billion cells per AlloNK dose. We have previously shared that we have over a dozen active sites across these trials, and it's important to note that the vast majority of patients have been receiving the treatment regimen at community sites with no specialized oncology oversight or complex monitoring. We will share the initial safety and tolerability observations for 32 patients treated with AlloNK in combination with anti-CD20 monoclonal antibodies across RA, lupus, lupus nephritis, Sjogren's disease, and cystic fibrosis across 1 billion and 4 billion AlloNK cell doses as of the October 1 data cut off. As of the data cut off of October 1, 32 patients were dosed at either 1 billion cells or 4 billion cells per AlloNK dose in combination with a monoclonal antibody across autoimmune indications. As of the data cut off, there were no cell therapy-related toxicities for AlloNK. In particular, there was no cytokine release syndrome or CRS, no immune effector cell-associated neurotoxicity syndrome or ICANS, no graft-versus-host disease or GVHD, or hypogammaglobulinemia. This really stands out compared to other modalities in this category. There were no grade three or higher AlloNK-related treatment-emergent adverse events, and the safety profile we have observed as of the data cut was consistent with what one would expect from rituximab, obinutuzumab, or from the cyclophosphamide and fludarabine conditioning regimen. There was a low rate of infections with only one grade three infection, which we'll provide more detail on in the subsequent slides. Importantly, there were no discontinuations reported. There was only one dose-limiting toxicity as of the data cut off, which was due to a patient with persistent neutropenia beyond day 28, with the patient not receiving GCSF supportive treatment. The patient was asymptomatic, and the neutropenia resolved by approximately five weeks without the need for GCSF. On this next slide, we compare the safety and tolerability profile of AlloNK observed thus far in autoimmunity with the tolerability profile of Auto-CAR-T and BCMA-targeted T-cell engagers or TCEs in the academic studies conducted at Erlangen. We are encouraged by the favorable safety profile that we have observed as of the data cut. Again, we see no CRS, no tocilizumab use for CRS since AlloNK does not have the same potential to cause escalating CRS, and no ICANS. Importantly, there was a low rate of infections compared to these other modalities. While not shown on this slide, I will point out that ICANS have been seen in several patients with autoimmune diseases treated with Auto-CAR-T in other trials. Our rates of infection were in line with what's seen with approved biologics in RA, and this is despite the use of CYFLU as part of our treatment regimen. We also see no hypogammaglobulinemia requiring the use of IVIG. Turning to the next slide, we wanted to provide more color on the compatibility of the AlloNK regimen with community administration based on the experience thus far in autoimmune diseases. This slide highlights how low the rate of hospitalizations were during the window when patients are lymphodepleted. In this chart, each row represents a patient treated in our IIT and two company-sponsored trials for a total of 32 patients as of the October 1st data cut off. The columns represent the first 28 days when the first cycle is administered and when patients are most immunosuppressed. A light green box means that the patient went into the infusion center to receive the infusion and went home with no adverse events or AEs reported at all. As you can see, patients come in on days one, two, and three to get the conditioning regimen and then come back on day six, day 13, and day 20 for AlloNK. In addition, patients received two doses of our monoclonal antibody, first on day one and second approximately 14 days later. A blue box is a protocol-specified pre-planned overnight observation. As you can see, the first four patients were required to do this as per protocol and not due to AEs. Finally, an orange box represents a hospitalization day. As you can see, out of 32 patients, there was only one patient that required hospitalization for an AE. This patient may have had an infection at baseline, which was missed, but that infection in the patient's ear evolved into an abscess. This is determined to be an infection with actinomyces, which are skin bacteria, in a patient with a history of congenital preauricular sinus. The patient had to be hospitalized for three days to receive IV antibiotics and was discharged and went home with no sequelae. We highlight safety and tolerability observation during the first 28 days because that is the period when the patient is most immunosuppressed because of the CYFLU regimen. By day 30 post-treatment, we have observed that the neutrophils and the lymphocytes are mostly returned to normal values. Further, these patients may have added protection during the first 30 days by the use of prophylactic anti-infectives in many of these patients. This very encouraging safety and tolerability profile and the low hospitalization rate observed thus far suggests that the CYFLU treatment can be managed in an outpatient setting. This is, of course, very different from other deep B-cell depleting modalities, for example, CAR-Ts and T-cell engagers, where patients are being hospitalized for the administration of treatment and for the management of treatment-emergent adverse events. This slide attempts to summarize the potential similarities and differences of managing patients treated with the AlloNK treatment regimen versus rituximab alone. As you'll see, the AlloNK treatment regimen is a lot closer to what treating with a biologic is compared to the complexity of traditional cell therapies. When treating a patient with either rituximab or with the AlloNK treatment regimen, a physician pre-medicates the patients to minimize infusion-related reactions in a standard infusion center. Patients get to go home after receiving the treatment. There is no escalating CRS, no need to carry specialized medication at the clinic, and the physician only needs to send patients to the emergency room or hospital if there are concerning AEs that require more intervention. The only significant difference is that with the AlloNK regimen, there is a window of a few weeks when the patient is immunosuppressed. As we have shown you with the initial safety data and experience thus far in autoimmune diseases, the lymphopenia and neutropenia were short-lasting. The vast majority of patients are asymptomatic, and many infections can be prevented using prophylactic anti-infectives. In summary, I have been increasingly encouraged by AlloNK treatment regimens' ability to combine the potential efficacy of cell therapy with the scalability and convenience of traditional IV biologics. I will now turn it over to Heather. Thank you, Subhashis. Good morning. My name is Heather Raymon, and I am the SVP of Research and Early Development. I have been at Artiva for five years and have been working on drug development for over 25 years, most recently at Bristol Myers Squibb and Celgene. I'm excited to present the initial translational data for AlloNK in combination with monoclonal antibodies in autoimmune patients. This graph demonstrates that AlloNK plus anti-CD20 monoclonal antibody is able to drive B-cell depletion in all 23 patients who had sufficient follow-up as of the October 1st, 2025 data cut-off, regardless of baseline B-cell levels. In all patients, we see B-cell levels below the limit of quantitation by day 13, and we start to see B-cell reconstitution at around six months, consistent with the time to B-cell reconstitution seen in autoimmune patients on rituximab alone. Note that even though we were using a CD20 monoclonal antibody, the chart is measuring CD19-positive B-cells in the periphery. As I will show you momentarily, we had an opportunity to measure the B-cell subpopulations present in the four patients who experienced B-cell reconstitution. I will note that total immunoglobulin levels mostly remain in the normal range, as seen with CD19 Auto-CAR-T, and no patient has experienced hypergammaglobulinemia as of the data cut-off. On this next slide, we highlight work that has been published using a high-sensitivity B-cell depletion assay. We will be sharing B-cell depletion data from autoimmune patients from our ongoing trials utilizing our high-sensitivity B-cell depletion assay later in this presentation. The B-cell depletion data presented to date by different deep B-cell depleting agents, including Auto-CAR-Ts, allogeneic cell therapies, and TCEs, have mostly used a TBNK assay. The TBNK assay was used in data shown on the prior slide, and this is the assay that was used, for example, in the Blinatumomab or Blincyto study at Erlangen in RA patients. As you can see on the left side of the slide, the data suggests that complete B-cell depletion is achieved in at least a single time point. Using these assays, Rituximab alone can also look like it achieves B-cell depletion in most patients. This is because the limit of detection, or LOD, is in the five to 10 cells per microliter range. However, if you look at the chart on the right, one can use a more sensitive assay to measure B-cells with 10-50 times more sensitivity. Several papers have demonstrated that when you use these high-sensitivity assays, it becomes clear that one can still detect B-cells at the one to two B-cells per microliter range following the use of rituximab. What we are showing on the right panel is that in one series of N equals 60 patients treated with rituximab alone and looking at the B-cell depletion using a high-sensitivity assay, one sees one to two B-cells per microliter. We believe this is nice supporting evidence of the fact that rituximab shows incomplete depletion in highlighting the potential of ADCC enhancement through the addition of AlloNK to deplete deep B-cells deeply. On this slide, we share B-cell depletion data as measured by the high-sensitivity assay from a patient with autoimmune disease treated with AlloNK. As part of our clinical trial, we treated one autoimmune patient with AlloNK and CYFLU, but no rituximab. We believe that without the monoclonal antibody, the B-cell depletion is transient and not in line with Auto-CAR-T. As you can see on the slide on the far left at time zero, or cycle one, day one, this patient began their first cycle of treatment with AlloNK and CYFLU. As you can see, B-cells were quantifiable at all time points during the cycle, which was through week 26 using the high-sensitivity assay. This same patient then received the full regimen of CYFLU, AlloNK, and monoclonal antibody as their second cycle. As you can see on the chart, we observed complete and deep B-cell depletion in this patient through at least four weeks, supporting our conviction that the full treatment regimen of CYFLU, AlloNK, and monoclonal antibody is necessary to deeply deplete B-cells. Turning to the next slide, again using the high-sensitivity assay and leveraging published studies that have already been conducted with rituximab, one can ask the question, what percent of patients have non-quantifiable B-cells when using rituximab versus when one uses the AlloNK treatment regimen? The chart on this slide demonstrates that roughly 40% of autoimmune patients treated with rituximab in this 99-patient sample still had quantifiable B-cells, whereas based on the experience thus far for patients treated with the AlloNK regimen of CYFLU, AlloNK, and rituximab in autoimmune disease, we believe we can eliminate B-cells in all autoimmune patients. Finally, one of the hallmarks of the immune reset, as described by Shet et al. with CD19 Auto-CAR-T, is measuring B-cell subpopulations when B-cells reconstitute following deep B-cell depletion and seeing a preponderance of naive and transitional B-cells. The left part, leftmost part of this chart in this slide comes from Shet's manuscript in 2022, highlighting B-cell reconstitution in five patients treated with Auto-CAR-T. To the right of the five patients in magenta are the results from the four patients treated with AlloNK plus rituximab, where we have seen B-cell reconstitution and have had an opportunity to measure the B-cell subpopulations. As you can see, the B-cells from all four patients had a predominantly naive or transitional phenotype at reconstitution. I will now turn it back over to Fred. Thank you, Heather. Artiva has been enrolling patients across the different autoimmune diseases you see on the slide: RA, Sjogren's disease, lupus with or without nephritis, scleroderma, and myositis. We have selected refractory RA as our lead indication as we strive to play to AlloNK's strength with the potential to drive cell therapy activity with biologics-like accessibility and tolerability. RA is the autoimmune indication with the largest population of patients refractory to standard of care, with over 150,000 patients in the U.S. alone. In RA, probably more than in any other indication, there's a need for a deep B-cell depleting agent that is scalable and easy to use if the goal is to impact more patients. As we evaluate our other indications, we see that this need for scalability and community tolerability varies by indication. Sjogren's disease, for example, is another indication where scalability and ease of use in the community setting could be very important, whereas in other indications like myositis, severe patients are already concentrated in academic centers and because of disease severity may not mind hospitalization in a more complex care paradigm. We plan to speak with FDA in the first half of next year on the pivotal trial design and strategy in refractory RA, and we'll be making data-driven decisions on the next indication selection. RA is a complex disease with several approved agents. Over the following slides, we will frame refractory RA, the unmet need, and what we are trying to achieve through the lens of ACR 50, an endpoint which is commonly used for regulatory purposes in RA drug development. Key opinion leaders in RA describe a ceiling effect for what can be achieved with immunomodulatory drugs, considering the fact that RA is heterogeneous and many patients with RA may have underlying joint damage that cannot be reversed or may have other pain conditions like fibromyalgia that sometimes get misdiagnosed as RA. These underlying conditions will not be addressed with immunomodulatory agents. Several approved agents can achieve an ACR 50 response in approximately 50% of patients when treated in the earlier lines of therapy, for example, after failure of conventional synthetic DMARDs like methotrexate. However, as patients become refractory to approved medications and progressively fail multiple targeted therapies, it becomes increasingly difficult to achieve this high level of response. On the slide, you can see how ACR 50 response is declining as patients move down lines of therapy. If we look at the ACR 50 of TNF inhibitors and JAK inhibitors in patients who are naive to biologics or targeted mechanisms, it is close to the 40%-50% response I described earlier. As patients fail a TNF or a JAK, their ACR 50 response declines to around 30%-40%. As patients fail a subsequent targeted therapy, you know, think of a patient that has already failed both a TNF inhibitor and a JAK inhibitor, their opportunity for an ACR 50 response is significantly lower. There are very limited studies conducted in this late-line population, but looking at a real-world registry in the U.S. with hundreds of treated patients, the ACR 50 appears to be in the 10%-20% range in this refractory population. We see an opportunity for a deep B-cell depleting approach to drive 50% or more of patients who have failed multiple targeted therapies back to the types of responses that today are only achievable in TNF inhibitor naive populations. Said differently, if we could achieve 50% or higher ACR 50 response in refractory RA patients, we have the opportunity to bring the transformative potential of deep B-cell depletion to this population. RA is a very large market with the top five approved treatments alone accounting for greater than $25 billion in peak sales. Many of these products have reached patent expiry, with many pharmaceutical companies experiencing revenue declines and potentially looking for promising emerging therapies, especially in the refractory subpopulation. When we look at what products are in the later stages of development in RA, to our knowledge, there are currently no therapies in late-stage development in the U.S. with MOAs that have demonstrated ACR 50 responses in truly refractory patients, near 50%. For this reason, we're excited with AlloNK's potential to be the first deep B-cell depleting agent to initiate a pivotal trial in refractory RA. To close, we're excited to potentially break away from the rest of the field and to differentiate ourselves by having the first deep B-cell depleting agent to start a pivotal trial in refractory RA. RA is a very large market with one of the largest populations of patients refractory to approved drugs, and there are limited products in the late-stage development pipeline. The next six to nine months could be very exciting for us. As we have guided, we will be sharing clinical response data in over 15 refractory RA patients in the first half of 2026, many of them with six months or more of follow-up. We also plan to conduct interactions with the FDA on a potential pivotal trial in refractory RA. The enrollment in our autoimmune disease trials has been going well with at least 32 patients with autoimmune disease treated, and we will be making data-driven decisions about our next priority indication. Finally, we have a strong team with deep expertise in cell therapy and autoimmune diseases and a strong balance sheet with runway into Q2 2027. Thank you for your time today. We will now turn to questions. For the Q&A section of today's session, we'll be utilizing the raise hand feature. If you'd like to ask a question, click on the raise hand button at the bottom of the screen. Once prompted, please unmute yourself and begin with your question. As a reminder, we ask that you stick to one question and one follow-up. We will now pause a moment to assemble the queue. Thank you. Our first question comes from Tyler Van Buren. Please unmute yourself and ask your question. Great, guys. Thanks very much for the presentation. Great to see the remarkably clean safety profile. As we think about the RA clinical update next year and the potential for this deep B-cell depletion with AlloNK to drive ACR 50 responses in these refractory patients that have failed two prior lines, is the goal of 50% on ACR 50 that you're hoping to achieve based solely on the B-cell depletion data that you're seeing, or do you also have clinical response data that you've observed to date that you're taking into account when you think about this bar that you hope to achieve? Hi, Tyler. Thank you for the question. What we guided is that we'll be sharing clinical response data on 15 or more RA patients in the first half of next year. What we are trying to do in this webcast is really start giving insights to investors and the broader community as we feel we have enough in and enough follow-up, right? We are trying to de-risk the asset as we are moving it along in development. Today, you have a good understanding that the depth of B-cell depletion is actually quite consistent in a large number. You also understand that the safety of the product is actually quite attractive in a large number of patients. What we are hoping to do in the first half of next year is to show you the clinical responses in a more robust data set. As we have described, yes, we do believe that achieving 50% of the patients having an ACR 50 is a very good bar for us to set for ourselves because it is the type of response that you just can't get in these later lines of therapy after you have failed so many of the targeted mechanisms. As a follow-up, if I may, what sort of durability do you think is important here? I guess where do you derive your confidence in the potential to achieve durability? Is it the B-cell depletion across all patients that looks to kind of be moving along the floor all the way out to at least three months, or is it the sensitivity assay where it looks like it's hitting zero at four weeks? I would argue that this whole field really got started once we started to observe the durability that was possible with Auto-CAR-T in many of these autoimmune indications, right? Our thinking is we have seen with Auto-CAR-T across a variety of diseases that if you do deplete the B-cells quite deeply, you do have the potential to see these benefits and to see them be durable. What we've learned from our oncology experience is that when we do treat patients with aggressive B-cell cancers, we do see levels of activity that are very much in line with what we've seen with Auto-CAR-T in these aggressive NHL patients. I mean, I just want to remind you that out of the 14 aggressive NHL patients that we treated, now close to two years ago, we have around a third of them, a quarter to a third of them that are still walking around in a complete response, and now we're almost two years out. Because of connecting those two dots, one, we know that when Auto-CAR-T depletes these B-cells deeply, one has the opportunity for durable effect, and the fact that we've seen in aggressive NHL, which is a really good test case, that we can deplete these B-cells really deeply, we're confident that we can see the levels of durability that I discussed. What I mentioned is, you know, if we can drive durability in the range of like 12 months-24 months, that would be a big win for patients. I mean, remember that when you're on any RA drug, you're on it chronically, right? You're either getting an injection of Remicade every two months for a long period of time, or you're getting daily OOPA for years, or you're getting Humira every two weeks for years. What we are talking about here is that there's a three- to four-week period when you receive your lymphodepletion, so physicians have to look out for your neutropenia and lymphopenia, those recover, and then you're off of your medications. For that period of, in that 12- to 24-month period that I'm describing here, you have an opportunity to be spending most of that time off of drugs that actually immunocompromise you. That is a huge advantage compared to just being on chronic therapies, which are part of the standard of care. Wonderful. Thanks so much. Congratulations. Thanks, Tyler. Our next question comes from Yifan Zhu. Your line is open. Please unmute yourself and ask your question. Hey, congratulations on your progress, and thank you for taking our question. One quick question about B-cell depletion. Can you provide some insights about B-cell depletion in tissues as well as like plasma cell? Because some data at ACL suggests that the incomplete depletion of BCMA cells that would result in the relapse of disease. I'm wondering if you have some insights on this front. Thank you. I mean, I would first question your overarching conclusion, right? Because we have seen now plenty of data from CD19 targeted Auto-CAR-T showing that even though they do not deplete the plasma cells deeply, one can still see a pretty durable response, right? I think that that at this point is uncontroversial. It is true that when you use a BCMA, there you do have an opportunity to actually deplete the plasma cells in addition to the mature B-cells and the plasma blasts. As you know, when you're coming in with a BCMA approach, it's, let's say, it's a bigger hammer that you're using, right? At that point, you see that most patients develop hypogammaglobulinemia, so you have to give IVIG, and then you know that many of these patients have to be revaccinated, and they're slightly immunocompromised because of that removal of plasma cells. We are confident, based on the data generated on CD19-a uto-CAR-T, that when you are depleting the mature B-cells and some of the plasma blasts, and I will point out that when we show our B-cell depletion data, we're showing you CD19 positive B-cells and how those are depleted. We're fairly confident that if one can deplete these cells, that you do get, you could have the potential to drive durable responses like we've seen with Auto-CAR-T. Your final question, you asked about evidence in tissue. Evidence in tissue is hard because you can have anecdotally a patient or two here and there, but our best clues as to whether you actually are driving deep B-cell depletion today, a practical one, is by looking at periphery. We do think that unless you use a high-sensitivity assay, it's hard to get a clear picture as to whether you're depleting it deeply or not. We have not had the opportunity to secure a sample to show you what tissue depletion looks like. It's the only reason we're not giving you an example because if we had one, we would be showing it to you, but that's the challenge of trying to collect these tissues very broadly. Thank you. Our next question comes from Martin Fan with Wedbush. Please unmute yourself and ask your question. Hi guys, thanks for taking our question and congratulations on the data. We were curious about patient demographics that you're available to share the information for here because RA is going to be skewing towards an older patient population. Could you comment on what% of these patients were 65 or older? You know, I don't have the breakdown here, but can you expand a little bit on your question? Are you wondering about the tolerability of the therapy in patients that are older? Is that your question? Yeah, tolerability and also the infection rates. Granted, there was only the one infection, but still wanting to get a sense for how many of the patients were young versus old, especially as we start to consider expansion into the RA trial. Yeah, so look, I would say that there are three, we could break down the ages into three components that we often think about, right? The first one is people always raise the question of how tolerable and acceptable will lymphodepletion be in young females of reproductive age, right? One of the advantages of RA as an indication compared to, for example, lupus is the fact that most patients that have RA are already beyond that point, right? Part of what you're seeing with many of the other companies is that in order to pursue lupus and pursue it broadly, one needs to think deeply about how they're going to be using the lymphodepletion. This is part of the reason why we are focusing on indications where that is more tolerable. Now, to the second point about the patients being a lot older and more vulnerable, it's important to remind you that we have treated dozens of patients with aggressive NHL who had failed prior lines, and those patients were definitely in that older category, and that drug was actually tolerated, our drug was tolerated quite effectively in that population, if you recall, from all the safety data that we have presented in the past. So we feel that I think the majority of the patients here are somewhere in that middle category, with some of the patients perhaps being a little bit older, but we have not seen any signs that we have something specific to worry about in these age groups. Perfect, thank you. As a reminder, if you'd like to ask a question, please use the raise hand button at the bottom of the screen. Our next question comes from Gil Bloom with Needham. Please unmute yourself and ask your question. Thanks for presenting a very robust data set. One quick one on that chart of B-cell aplasia, how many of your patients are out to three months? You know we're not providing more details than what's on the graph, and not because I'm trying to keep something back, but just because I don't know exactly, and I'm not going to put Heather to kind of guess, but I think what you're seeing is just doing the math. We've treated 32 patients, we've analyzed samples from 23, and you saw that there was a handful of patients that were actually having B-cell reconstitution towards that like six-month mark. Everything else is pretty much like in between, right? We've had a pretty nice, even though our enrollment has been accelerating from where it was before, we've been driving forward at a good pace. Is there something more specific that I can answer? No, I think that's about what we can do here. My other question, and this is a little bit of a broader concept. In oncology, CRS, ICANS, and some of the side effects are a sign of the T-cell underlying activity. Is there any underlying additional translational data, let's say cytokine picture, to support that B-cell depletion is happening via the NK cells? Thank you. Via the NK cells. You know, when you think about if we lymphodeplete the patient and then they're receiving the monoclonal with our NK cell, I mean, that's really the only active cell that you have in the system to actually be driving that depletion. Your point about CRS is an important one because you see CRS is associated with efficacy. It's almost like a marker that the drug is doing what it's supposed to be doing when it's a T-cell, right? When T-cells expand and when T-cells kill the B-cells, that's when you see the elevation of specific cytokines that are the classic signature for CRS. That's the one thing that's really special about NK cells is that, first of all, they're not expanding once we're giving them to the patients, and when they kill B-cells, they do so without the elevation. Very specifically to address this, you know, as you know, if you have a fever in a cell therapy trial, physicians may want to call that CRS, right? In our oncology study, we had four instances where the physician saw the fever and they called it a CRS. We subsequently analyzed the samples to actually understand what that cytokine pattern was, and we did not see the elevations in the cytokines that one sees typically when CRS is taking place, which then drove us to reclassify those events as not being CRS in that oncology trial. Since then, we continue to monitor that closely, but we have very little doubt that one of the big advantages of NK cells and B-cell killing is that they do not drive that pattern that actually causes CRS. Great, thank you very much and congrats on really interesting results. Thanks, Gil. Our last question comes from Emily Bodnar at H.C. Wainwright. Please unmute yourself and ask your question. Hi, good morning. Thanks for taking the questions and congrats on the progress. I was curious if you could talk a bit about what a pivotal program in RA could look like given some of the CAR-T pivotal programs we've seen in other indications like myasthenia gravis and myositis, and also your current thinking about appropriate dosing going forward, given you've used the one billion and four billion cells. Thanks. Thank you. Thanks for the question. I'll take your second question first, which is all the data that you've seen, not all the data that you've seen, but most of the data that you saw was based on 1 billion cell dosing, right? One billion cells per dose, and we give three doses in this trial. Some of the patients that you saw, both in the B-cell depletion as well as with the safety, were at four billion, right? What we see from, particularly from the B-cell depletion work, is that even at a billion cells, we are getting very consistent and uniform B-cell depletion. We decided to escalate to four billion to see what that looks like, only because we can, you know what I mean? Our COGS are actually quite reasonable. We have not seen any safety signal differences when we were treating in oncology. In oncology, we did not see major efficacy differences between one billion and four billion, but we figured we would be thorough here and actually test out four billion. The good news is we are already starting with a dose that we deem to be quite active. You know I will remind you that this is a little bit different from other modalities. We know that Auto-CAR-T does have a simpler dosing regimen. Most of the doses that have been used have worked, but with TCEs, we know that there's a therapeutic index. We know that when Blincyto was used, everybody argues it's not very active, and that's why it was really safe. When Teclistamab was used, it was actually quite active, but then we saw that 80%+ of the patients needed IVIG or required Tocilizumab. The good news here is we already have an active dose, and it is actually quite safe, but more to come on the four billion. On the pivotal trial, what we guided is that we're going to be having discussions with FDA in the first half of 2026, so we'll be able to provide more details then. What I can share with you is, you know, one of the reasons why some of these very large trials, like the ones that are run in RA, are so large is because typically most of the new regimens that have come to market, they have a very small incremental benefit over whatever the comparator is, and that's the reason why they have to be hundreds and hundreds of patients in size. The size of the effect that we are shooting for, considering the mechanism, the type of therapy this is, should potentially give us an opportunity to actually run a trial more efficiently. Is it going to be the very small numbers that we have heard from Kyverna with SPS, or we've heard from Cabaletta with myositis? Probably not, since this is the largest autoimmune indication there is. Will you get away without using an active comparator? Unclear. We're going to learn more about that when we talk to FDA. The bottom line is we do not see this as a particularly binary event, or we feel that there is this big concern coming to these conversations because the level of efficacy that we are targeting, as we discussed, is actually quite robust, right? We are talking about trying to get around 50% of the patients to have an ACR 50 response when they have already failed one or two prior targeted mechanisms. Awesome, thank you. Appreciate it. Thank you. We have no further questions at this time. That concludes the call for today. Thank you for joining. You may now disconnect.