Hello everyone, and welcome to the Adicet Webcast. Participants are currently in listen-only mode. Following formal remarks from the company, the call will be opened up for Q&A. This call is being recorded. I'll now turn the call over to Chen Schor, CEO of Adicet Bio. Please go ahead. Good morning, everyone, and welcome to today's conference call to discuss the data we announced this morning from our Phase 1 study of ADI-001, demonstrating very promising safety and efficacy results in patients with LN and SLE. I'll start the presentation with a few remarks before turning it over to Dr. Julie Maltzman, our Chief Medical Officer, who will summarize the clinical data to date. After that, we'll be joined by Dr. Blake Aftab, our Chief Scientific Officer, to walk us through the data demonstrating clear evidence of immune reset that we observed in the study. And then Nick Harvey, our Chief Financial Officer, will join us for Q&A. Next slide, please. Before we start, please note that today's call may include forward-looking statements based on our current expectations. These statements represent our judgment as of today and inherently involve risks and uncertainties that may cause actual results to differ materially from the results discussed. Please refer to our filings with the Securities and Exchange Commission for more information. And now, without further delay, let's get started. We're excited to share with you that the key takeaway from Phase 1 study we are sharing today points to potentially unequivocal success for patients with autoimmune diseases and for treating physicians. We believe this dataset highlights the potential of ADI-001 to become a transformational, paradigm-changing approach to treating patients with autoimmune diseases. This preliminary data checked all the boxes in terms of the efficacy and safety results that we had hoped to see at this stage. Let's take a moment to revisit our aspiration for this trial. Previously, we laid out what good readout from the trial would be. First, we said that the data would hopefully demonstrate favorable safety profiles suitable for outpatient administration. We clearly have that, with no SAEs, no CRS events greater than grade one, and no ICANS. We believe this lays the groundwork for ADI-001's potential advantage of being used as an outpatient therapy and available to many patients with autoimmune diseases. We also said we wanted to achieve remission or halt disease progression, and we did, as you will see in the clinical data we present today. All patients, which includes five LN patients and two SLE patients with a follow-up ranging from two to nine months, experienced rapid and sustained reductions in their SLEDAI-2K and Physician Global Assessment, or PGA scores. Next, we wanted to show preserved or immune kidney function with a complete renal response, or CRR, rate of at least 40%, which is what regulatory authorities signaled to other companies as the bar for success in single-arm pivotal studies with B-cell-depleting cell therapies for the treatment of LN, and indeed, kidney function improved in all five LN patients, including three complete renal responses, which were also DORIS remissions, and two partial renal responses. We also wanted to see immune reset and emergence of B-cell repertoire that will support a one-time therapy, and we clearly did, which Blake will present shortly. We hope to see a discontinuation of immunosuppressants and discontinuation or reduction in the corticosteroid doses to physiological levels. That box was clearly checked. Finally, we wanted to see the potential for ADI-001 to become an off-the-shelf therapy with no need for leukapheresis, and we have that as well. In summary, with all these boxes checked, today's data are a clear win for LN and SLE patients. These data exceeded our expectations. The totality of the data suggests that ADI-001 has the potential to be an off-the-shelf, one-time therapy available for autoimmune patients in an outpatient setting with an impressive efficacy profile and favorable safety. Such a profile may enable rapid execution of our clinical development plan, and if ADI-001 is approved, significant commercial potential. Given the data we're presenting today, we plan to request a meeting with the U.S. Food and Drug Administration, or FDA, in the first quarter of next year to inform Phase 2 pivotal trial design, with a study anticipated to commence in the second quarter of next year. Precedent Phase 2 pivotal trials with B-cell-targeted cell therapies in LN, or SLE in LN, suggest that a relatively small single-arm pivotal study may suffice given the transformational clinical benefits observed with immune-resetting cell therapies. Next slide, please. The autoimmune program with ADI-001 is quite robust. We have seen a nice uptick in the number of sites interested in enrolling patients. We continue to enroll LN and SLE patients and recently also started systemic sclerosis patients. We expect to enroll patients with RA in the very near future and also see interest from sites in enrolling patients with myositis and ANCA Vasculitis. ADI-212 are optimized next-generation gene-edited and armored clinical candidates designed to enhance potency in solid tumors and deliver multiple anti-tumor mechanisms of action to the tumor microenvironment. ADI-212 is expected to enter the clinic in the first half of 2026, but today we'll be focusing on the data from Phase 1 trial in LN and SLE. Next slide, please. Given the strength of the data we are sharing with you today, we expect our ADI-001 program to generate a number of meaningful milestones throughout 2026. We will review these milestones in more detail shortly. With that, let me now turn the call to Julie to walk you through the clinical data in more details on the next slide. Okay, thank you, Chen. Good morning, everyone, and thank you for joining us. I'm pleased to be here today to share these preliminary results from Phase 1 study of ADI-001 in patients with LN, lupus nephritis, and SLE, systemic lupus erythematosus. This slide here just summarizes the data that I'll be showing you today. It includes seven patients in total, five LN and two SLE, as of August 31st data cut. I'm very pleased to report that we saw a rapid and sustained reduction in the SLEDAI-2K and PGA scores across all patients. You will also see that all LN patients had a reduction in proteinuria. Three patients achieved a complete renal response, or CRR. These same three patients also achieved a DORIS remission. The other two patients fit the protocol definition of a partial renal response, or PRR, which is defined as a drop in proteinuria by greater than 50% from baseline. ADI-001 was very well tolerated with no CRS greater than Grade 1, no ICANS, and only one Grade 1 infection. There was clear evidence of an immune reset that Blake will walk you through in a bit. And all patients discontinued immunosuppressants and tapered steroids to zero or below five milligram equivalents of Prednisone daily. So next slide, please. You know, in the interest of time, I'm not going to go into great detail on this slide other than to remind you that there is a major unmet medical need for LN and SLE. Most patients get treated with chronic triple therapy that is two immunosuppressants and a steroid. More recently, there is even a suggestion of adding on a biologic treatment. All these therapies carry significant toxicities in these young patients. There's a clear need for a one-time therapy with a favorable safety profile that can deliver flare-free remissions without the need for these chronic therapies. Next slide, please. Here's a quick review of our trial design. This is Phase 1 study with a three-plus-three basket design, which includes several autoimmune indications that you can see on the bottom left of this slide, and then a dose expansion that is indicated on the bottom right. The patient's journey begins with signing consent, a screening period, conditioning regimen, cell infusion, a 28-day DLT, dose-limiting toxicity evaluation period, and then follow-up. Patients are considered enrolled when they start conditioning. Next slide, please. Primary endpoints Phase 1 studies are always safety and tolerability, and our study is no exception. Secondary and exploratory endpoints focus on pharmacodynamic endpoints, including B-cell depletion, reconstitution, and immune reset, and the clinical efficacy endpoints are specific to each disease as outlined on the bottom right of this slide. Next slide, please. Well, this is the baseline characteristics of all five LN patients and two SLE. They have follow-up ranging from two to nine months. You can see they're primarily young women that have been living with their disease for quite some time, ranging from two to 22 years, and this reflects the typical demographics for SLE and LN. Their baseline SLEDAI scores were in the mid-teens, and all LN patients had over a gram and a half of protein in their urine. Patients had anywhere from three to seven prior therapies, and overall, these patient baseline characteristics are consistent with other datasets from company-sponsored clinical trials with B-cell-depleting autologous cell therapies. Let's go to the next slide, please. So let's look at safety. ADI-001 was extremely well tolerated in these patients, with no SAEs reported, no ICANS, and no CRS events greater than grade one. We had two patients with grade one CRS, which, of course, is defined by the American Society of Transplantation and Cellular Therapy as a fever of over 38°C, which is about 100.4°F. We also had one patient with a grade one upper respiratory tract infection that happened about three months after cell infusion and resolved quickly without the need for antibiotics. Most notably, we did not have any neurotoxicity, no ICANS, no HLH, no GVHD. Let's go to the next slide to see how ADI-001 data compares to other therapies in development. So, you could see in the blue box on the left, ADI-001 safety profile compares favorably with autologous alpha-beta CAR-T therapies in autoimmune patients. We believe this profile gives us the potential opportunity to dose ADI-001 as an off-the-shelf product in the outpatient setting. We were so encouraged by these results that we plan to speak to the FDA to see if we could administer ADI-001 as an outpatient therapy in clinical trials going forward. This would be a huge win for patients in our studies, and if approved, it will eliminate a major burden on the healthcare system by making this therapy more readily available. So please stay tuned for more information on that. Let's move on to the next slide, please. This slide shows the efficacy data for our LN patients specifically. You could see all five LN patients that received ADI-001 achieved a renal response. That's a wonderful outcome. In the bright blue, you can see three complete renal responses and DORIS remissions for patients LN1, LN4, and LN5. Two LN patients achieved a partial renal response, which is defined per protocol as a drop in proteinuria by more than 50% from baseline. As far as we know, all these responses are ongoing at this time. We're also pleased to observe that the complete renal response rate shown here exceeds 40%. 40% is what regulatory authorities have signaled to other companies as a bar for success for a single-arm pivotal study for cell therapies in lupus nephritis. Let's go to the next slide, please. Well, this is a summary of all the SLEDAI-2K scores for all patients. We're extremely pleased to see that patients had a brisk and durable reduction in their symptoms as defined by the SLEDAI. You can see SLEDAI scores from these patients start out in the mid-teens and have a nice decline. If you draw your attention to the orange triangle on LN1, LN4, and LN5, these are the patients that achieved a complete renal response and are also in a DORIS remission. The asterisk on this slide highlights three patients that were missing biomarker data, either anti-double-stranded DNA antibodies or complement levels at these particular visits. So we just assumed that they were positive to show the most conservative data for the SLEDAI 2000. All right, next slide, please. This shows the PGA scores. This slide shows a rapid and sustained reduction in the Physician Global Assessment, or PGA, across all patients, which further highlights ADI-001's impact on overall disease activity. The bright blue line that you see represents the mean PGA for all patients. If you draw your attention for a moment for this orange line, mustard color, you will see the data for patient SLE2. You could see that their PGA score decreased from two to 0.6 by month three. On the last slide, I showed you that this same SLE2 patient had a clinical SLEDAI score of zero, so it's kind of important to highlight that this patient missed a DORIS remission cutoff by 0.1, and we're anxiously awaiting for this patient's next visit to see if they become a DORIS remission if all continues. Next slide, please. All patients discontinued immunosuppressants, and you see on this slide that all patients tapered their steroid use to zero or below physiologic levels, which is considered five milligram equivalents of Prednisone daily. Four of seven patients discontinued all steroids, and the remaining three tapered their steroids to five milligram equivalents or less of Pred. This is a tremendous result for patients given that current therapy includes chronic treatment with immunosuppressants and steroids that are associated with significant toxicity. Long-term corticosteroid use, of course, leads to cataracts, diabetes, bone loss, easy bleeding, not to mention psychological issues. These treatments negatively impact quality of life for patients and their ability to live independent lives. In summary, we're very excited with this dataset. Patients want a single treatment with minimal side effects that could lead to disease remission and prevention of organ damage. We will continue to follow these patients and enroll additional LN and SLE patients on the study, and of course, advance enrollment in all other cohorts. And with that, I'm going to turn it over to Blake to summarize the data in immune reset. Blake. Thanks, Julie. Let's go to the next slide, please. These robust clinical responses are particularly compelling and are further supported by biomarker evidence of an immune reset. We see multiple levels of evidence supporting this reset, with the loss of B-cell clones presenting at baseline and the emergence of a new, less antigen-experienced B-cell repertoire. Specifically, we saw evidence of deep and broad B-cell depletion. That is the first step in a reset. Then we saw reconstitution driven primarily by naive and non-class switched B-cells. At the genetic level, we also observed depletion of clonally dominant and potentially pathogenic B-cell receptor clones. This was followed by the emergence of a new B-cell repertoire associated with previously undetected antigen receptor sequences. So we've checked the box here on all of these. Let's now go to the data and take a closer look. Next slide, please. Looking generally at B-cell depletion, we can see that every patient experienced deep and broad B-cell depletion, all with multiple time points where B-cells were undetectable in the first month after treatment. This initial period of deep depletion was followed by reemergence of B-cells within a one- to four-month window. This is very much in line with the dynamic seen with autologous CD19 CAR-Ts. With ADI-001, we are clearing the field and allowing new grafts to grow. Next slide. This slide provides an initial look at what these shoots are like with respect to B-cell phenotype and the degree of antigen experience associated with those B-cells. Here, we show the spectrum of B-cell experience and maturation ordered from left to right, starting with the less antigen-experienced naive B-cell on the left and running through the most antigen-experienced plasma blasts on the far right. Here, we see that the reconstitution of B-cells was primarily driven by naive, transitional, and non-class switched B-cells, which is exactly what we want to see. And this is again in line with what has been previously seen with autologous CD19 CAR-Ts. These data are consistent with the current level of definition of an immune reset as reported by others. However, this doesn't objectively tell us about how these B-cells are engaging with their antigens. To get a more objective view of this, we turn to deep sequencing of B-cell receptors, which is how these cells recognize and engage autoantigens. Let's go to the next slide. This slide shows our insights from deep sequencing in three patients from whom samples are available and demonstrate that dominant B-cell receptor clones that were seen at baseline were broadly eliminated after treatment with ADI-001 and were largely not detectable in reemerging B-cells. Sorted from top to bottom are dominant B-cell clones, each expressing a unique B-cell receptor, and the relative abundance of these clones is depicted by the depth of color. In the right column for each of these patients, we see that these clones were broadly eliminated in B-cells that reemerge at the six-month and three-month time points following treatment with ADI-001. Using deep sequencing, we can see that we are clearing the field and initiating an immune reset at the B-cell receptor level, at the level where these cells engage with antigens. We can use this same analysis to evaluate whether the grass that grows in its place is in fact new. Let's go to that on the next slide. Here, we expand the view a bit, looking again at the dominant B-cell receptors seen at baseline, now shown in pink for each of these patients. Following these tracks, we can see that these were largely eliminated and no longer detectable in B-cells reemerging following treatment with ADI-001. Similarly, in blue, we have highlighted B-cell receptor sequences that were not detected or present at baseline. We can see that these patients' B-cell repertoires are largely repopulating with completely novel B-cell receptor sequences, suggesting that these patients have experienced an immune reset at the antigen receptor level, representing a new B-cell repertoire. This depth of view for the immune reset is very much a story of out with the old and in with the new. Let me pass it back to Chen. Thanks, Blake. Next slide, please. This slide shows the sustained reductions in SLEDAI scores across industry-sponsored clinical trials with autologous CD19 alpha-beta cell therapies. As you can appreciate, the sustained reduction in SLEDAI with ADI-001 is overall consistent with these data. Importantly, Obe-cel, on the top right, observed three CRRs out of six LN patients, or a 50% complete renal response rate. Rap-cel, on the top middle chart, presented a very robust dataset at EULAR just a few months ago. The dataset included 12 LN patients and nine SLE patients, and on the next slide, we can see the percentage of patients that resolved the proteinuria. Next slide, please. As you can see on the top right of this slide, the percent of patients with proteinuria dropped from approximately 70% at screening to 35% by month 12, suggesting approximately a 50% complete renal response rate, so we have two examples of company-sponsored clinical studies with autologous CD19 alpha-beta CAR-T in LN patients demonstrating an approximately 50% complete renal response rate, and these data are very consistent with the CRR rate we are observing with ADI-001. ADI-001 has the advantage of being off the shelf and generally well tolerated, hence potentially optimal for dosing in an outpatient setting. Next slide, please. As Julie mentioned earlier, regulatory authorities have signaled to other companies that the bar for success in single-arm pivotal studies with cell therapies in LN is a complete renal response rate of 40%. This slide shows the pivotal studies underway in LN and SLE and LN with autologous CD19 alpha-beta CAR-T product candidates. Let's go to the next slide. There are two key takeaways from the data we presented today. One, this clinical data supports the potential of ADI-001 as an off-the-shelf immune resetting, one-time, well-tolerated therapy that could be used in the outpatient setting. And two, we believe that a product candidate with this product profile could enable treating physicians to provide patients with LN or SLE with a potential one-time therapy that leads to disease remission or halt disease progression while patients discontinue the use of chronic immunosuppressants and reduce the dose of corticosteroids to zero or below physiological levels. This could be a transformational treatment for many patients with autoimmune diseases. Next slide, please. We have now activated over 25 clinical sites globally, which is a testament to our team's focus and excellent execution, as well as demonstrating investigators' interest in ADI-001. The pace of enrollment we are now observing reinforces our confidence in our timelines for future milestones. Next slide, please. We believe there is a significant market opportunity in front of us and that ADI-001 has the potential to change clinical practice across multiple autoimmune indications. In addition to the six indications we already have underway in our phase one program, we have recently opened enrollment for a new phase one study for the treatment of RA. This trial will explore the use of ADI-001 following Cy/Flu versus Cy only Conditioning. With these trials underway, we are poised for a number of milestones in 2026, as outlined on the next slide. We plan to request a meeting with the FDA in the first quarter of 2026 to inform phase two pivotal trial design in LN or in LN and SLE, with a study anticipated to commence in the second quarter of 2026. Precedent phase two pivotal trials with B-cell targeted cell therapies suggest that a relatively small single-arm pivotal study may suffice given the transformational clinical benefits observed with immune resetting cell therapies. Stay tuned for these updates. SLE and LN patient enrollment to the ongoing phase one is expected to continue until the phase two pivotal study is open for enrollment. The phase one program is now open for enrollment of with systemic sclerosis, myositis, Stiff Person Syndrome, ANCA Vasculitis, and RA. We expect 2026 to be a year with many meaningful milestones. In the first half of 2026, we expect the following milestones: a clinical update in SLE and LN with more patients enrolled to our phase one study and longer follow-up. We expect to announce alignment with the FDA on the pivotal study design in LN or in LN and SLE. We expect to announce the initiation of a pivotal study in LN or LN and SLE. We expect a clinical update systemic sclerosis and a potential clinical update in other autoimmune indications. In the second half of 2026, we expect to provide the following milestones: a clinical update in SLE and LN, a clinical update systemic sclerosis, clinical data from our study in RA that we recently opened for enrollment, and a potential clinical update in other autoimmune indications. We also have an ongoing program with ADI-212 in metastatic prostate cancer. We plan to file an IND for the program in the first quarter and clinical data potentially in the second half of next year. With that, let's open the call for Q&A. Operator. For the Q&A section of today's session, we will be utilizing the raise hand feature. If you would like to ask a question, simply click on the raise hand button at the bottom of the screen. Once you've been invited to, please unmute yourself and begin with your question. If you have dialed in by phone, please press star nine to raise hand and star six to unmute. We will now pause a moment to assemble the queue. Our first question will come from Jenna Li with Jefferies. Please dial star six to unmute and ask your question. Hi, good morning. This is Jenna joining for Clara at Jefferies. Congrats on this data and thanks for taking our questions. We have two questions, if we may. The first one is, can you help us understand if there were any notable trends in LN2 and LN3, both of which had complete B-cell depletion? Are you observing anything that could suggest they may advance towards complete remission with longer follow-up? And specifically on the SLEDAI chart, noticed that for both of these patients, the last month had a star on it, and it looks like there were some unavailable samples and some assumptions. If you could just elaborate on that and how that could change or evolve over time. Thank you so much. Sure. Let me start and then perhaps Julie can add. So first of all, what success looks like? If we in 50% of the patients, if we can see a complete renal response and they stop taking their immunosuppressants and reduce corticosteroids to zero or below five mg equivalent of Prednisone, that's a huge win. Keep in mind that otherwise these patients will continue to be immunosuppressed and tend to die in their 50s from kidney failure. So that's a big, big win. Regarding the question of LN2 and LN3, Julie, perhaps you can share some background. I think patient two had many years of disease, if I recall. Yes, Chen, thank you. That is correct. Patient two had disease for 22 years. She's our longest duration. These two patients are the ones that had a partial renal response that decreased their proteinuria by greater than 50%. As Chen said, this is still a major win for them that they're off immunosuppressants and off steroids or nearly off steroids with less than five milligram equivalents. You hadn't said there was a second question. Can you remind us what was the second question? Oh, the asterisk. Yeah, you asked about. Yeah. Yeah, essentially, so for example, LN2 and LN3, we just wanted to get you guys the best update as of August 31st. So for example, for LN2 and LN3, we brought them to unscheduled visit. And in that unscheduled visit, we got their clinical SLEDAI, but we didn't have the sample to analyze for dsDNA or for C3 and C4, so we just assumed they're positive for the most conservative view of the SLEDAI-2K score. I've got it. Thank you so much, and if I may, how would this data inform your thinking on next steps, potential design for registration, patient selection, baseline dose, etc.? Yeah, absolutely. You know, they say the work of the holy ones is done by others, so first of all, other companies like BMS or Autolus or Novartis have moved to potentially pivotal studies after datasets along the number of patients that we provided, the same duration of a follow-up. What we know, based there was a slide here in the deck, what we know is that these studies tend to be single-arm, number of patients in the 30-90 patients, and the endpoint is a complete renal response, and the bar is at least 40%. So what's the design? It's kind of out there, and we expect to follow what others have established in the field. The only question that we have is the pivotal design in LN or in LN and SLE, or maybe start with an LN and then expand to an LN and SLE, and we'll discuss this with the FDA in the first quarter of next year. Great question. Got it. Thanks so much, and congrats again. Thank you. In the interest of time, please limit to one question. Our next question will come from Yatin Suneja with Guggenheim. Please dial star six to unmute and ask your question. Hey guys, can you hear me? Yes. Perfect. Can Julie and the team? Thank you so much for the presentation. Excellent results here. Obviously, very impressive in terms of both efficacy and safety. So the question I have is around durability. Could you maybe talk about your view on the durability? How should we think about that? Maybe contextualize some of the immune research results that you are seeing in that regard. So that's sort of the first question. And then the second, which is a quick question, is could you just let us know what was the lymphodepletion doses that you use? Was it similar to what we are seeing with other CAR-T auto designs? Thank you. Sure, absolutely. We're very happy with the durability. What's nice to see is generally immune resetting therapies show very nice durability. As you can see, just as an example, LN1 had a complete renal response at month one and has a follow-up of nine months. Generally, all the patients as of August 31st, we've seen very nice responses. I can confirm to you that as of now, we're not aware of any relapse. If we're aware of anything, then patients continue to improve. We're very, very happy with what we're seeing here. The data in terms of the number of patients and follow-up of patients is completely consistent with what other autologous cell therapy companies had before they started their pivotal studies. That was one question, and you had another question. Oh, lymphodepletion. The lymphodepletion regimen here is very consistent with autologous cell therapies that are going into pivotal studies. There is nothing too unique about it. Very good. Congrats to the team for the data. Oh, absolutely. Thank you so much, Yatin. Our next question will come from Asthika Goonewardene with Truist. Please dial star six and ask your question. Hi, this is Karina for Asthika. Thanks for taking the questions and congrats on the data. I guess you mentioned like on baseline characteristics, but how would you compare the baselines to other LN trials? And I guess more specifically, is it more similar to GSK's baseline characteristics? Absolutely. So first of all, thank you for asking. What we're not comparing, we're not comparing to baseline characteristics of ISTs. What we are comparing is generally to baseline characteristics of other company-sponsored studies, but even if compared to GSK, it might be the same. Overall, when you look at the age, it's approximately the same. If you look at the duration of disease, you know, two to 22 years is very much the same. If you look at the SLEDAI score, our mean was 14. If you look at Novartis, which is the largest industry-sponsored study that was presented so far, their mean SLEDAI at screening was, guess what, 14. If you look at the UPCR above 1.5, this is definitely an LN patient. We confirmed all LN patients with a recent biopsy. If you look at the number of prior line therapies, 3-7 is very consistent with other studies, and if you look at the corticosteroid levels, they all were on steroids. So bottom line, if you compare our dataset to the dataset presented by small companies like BMS or Novartis and also Autolus, very consistent with their dataset. If you look at our SLEDAI reduction, very consistent. If you look at the baseline characteristics, very consistent, and if you look at the complete renal response, very consistent. So we're very happy with this data. Okay, that's helpful. Thank you. And I guess another one is regarding pivotal study. Would this potentially be single-arm similar to obe-cel and BMS? Or how are you thinking about the pivotal design? Again, can you repeat the question? I just want to make sure I understand it. Yeah. On the pivotal design, are you thinking about doing potentially a single-arm study similar to Autolus and BMS? Or how are you thinking about the design? Yeah, absolutely. So we know that the clinical benefit that we see with these studies are so transformational that the pivotal studies here are expected to be single-arm, relatively small, with an endpoint that's relatively short in the six-month range. And the endpoint is complete renal response, or it might be in some cases, it might be DORIS remission if it includes SLE. So yeah, absolutely. We expect a relatively small single-arm pivotal study, and we'll discuss this with the FDA in the first quarter of next year and hopefully start the study in the second quarter. Okay, thank you so much. Absolutely. The range is approximately 30-90 patients based on what we've seen from other companies. Our next question will come from John Newman with Canaccord Genuity. Please dial star six and ask your question. Hi guys, good morning. Congrats on the tremendous amount of hard work that you guys have put into this study and all the programs. It's a really great day for lupus patients and autoimmune patients. Just had two quick questions. So just following on to one of the earlier questions, we saw with Novartis's data for rapcabtagene, they saw a very rapid decline in a lot of the SLEDAI-2K items, including proteinuria. Importantly, that proteinuria, even though it didn't go to zero, it continued to drop over time. My question is, is it reasonable to expect that in patients, I believe LN2 and LN3, we could still continue to see some improvement in terms of the proteinuria as patients continue to be followed? Yeah, let me try to address it. If Julie has something to add, that's great. Keep in mind that gamma delta 1 T cells have tissue tropism, including to the kidneys. By the way, we did confirm this in our RCC study with a different gamma delta 1 T cell therapy where we saw significant exposure in the kidney. What does that mean? If you look actually at Novartis datasets, they saw a 50% reduction in the percent of patients with proteinuria at month 12. What we saw, three out of five, i.e., 60% of the patients with complete renal response at month six. So this only may suggest that patients might get better sooner on their lupus nephritis components, or very, very happy with that. Regarding the continued improvement in the kidney function, it's something that we have seen, and I can tell you that today all the responses are ongoing or even getting better. The other point I might mention to you, there was one slide that we presented that showed the Rapso data. I discussed the right side of the slide where I showed this 50% reduction in proteinuria. I want to point your attention to the left side of the slide where actually Novartis outlined in blue the reduction with SLEDAI in the SLE patient, and in green, the reduction in SLEDAI in the LN patients. And as you can see, the reduction in the LN patients, there is like a little bit of a plateau around four. And based on the data that we see, you can see that this is a more persistent proteinuria. So overall, our data compare very well to Novartis, if only maybe you see a faster resolution of the proteinuria in patients. Great question, John. Thank you. And then just one quick follow-up question. Can you comment on how you taper the immunosuppressants before treatment with ADI-001? And also importantly, how does this compare to an autologous CAR-T where patients may be off of immunosuppression, may need to be off of immunosuppression during manufacturing, just in terms of ease of use for both the patient and the physician? Yeah, yeah. Let me walk you through the journey because it's very different. So generally, with autologous cell therapies, you want patients to discontinue immunosuppressants, let's say months before the leukapheresis because you want to get their cells with good fitness. So you stop immunosuppressants for a month, then you need to schedule a leukapheresis chair and fight for the resources in the hospital because there's not a lot of leukapheresis chairs in terms of capacity. Then you get the leukapheresis. Then you wait approximately a month before starting the treatment. So the patient needs to be for approximately two months off immunosuppressants before they start the study. Then you need to schedule time with HemOnc because these are autologous alpha beta T cells, and you never know who's going to get the high-grade ICANS, right? It's a, you know, it's a, you just never know. We see these events of grade three and grade four ICANS with autologous cell therapies. So they need to get resources from HemOnc to really watch over these patients and manage all of their toxicities. In our case, it's very simple. Patients get into screening. Screening is 28 days. During the screening, they take off their immunosuppressants, and then they come, and after three days of conditioning, they get a single dose of ADI-001, and you know, it's very well tolerated. Very, very well tolerated. No ICANS and just two cases of CRS, which were just grade one and, you know, simple fever. So very, very different. And in our case, you just stop immunosuppressants during screening and start the treatment. Much, much, much, much simpler for the patient and for the treating physician. Excellent. Thank you. Thank you, John. Your next question will come from Robert Driscoll with Wedbush. Please dial star six and ask your question. Morning, guys. Some really nice data here. I'm just wondering if there is a way to kind of characterize which patients may have more severe existing kidney damage at baseline, just in terms of maybe Predicting which of those kind of lupus nephritis patients kind of may have those more persistent proteinuria scores following treatment. Julie, any feedback you can provide here? I think the field is really young in trying to define who will respond and who will not. Yeah, I tend to agree. In clinical practice, when you do biopsies, you look at chronicity and activity scores, but none of that has panned out to really correlate exactly with outcome. Yeah. But Robert, I would just add to you, having three CRRs out of five is amazing. But also two, if two of the patients are at partial renal response, it's also great because keep in mind those immunosuppressants and corticosteroids have such significant toxicities. And in many cases, patients with LN die in their 50s, in many cases because of an infection, because they have been immunosuppressed for decades. So if you can give them one treatment and only halt the disease progression and they stop taking these chronic immunosuppressants and high-dose steroids, that's still an amazing outcome. Like we want to halt disease progression and further organ damage in these patients. So even if you can Predict who is going to be a partial renal response, still, it's great help for these patients to be able to stop their chronic immunosuppressants and steroids. Yep, yep. That makes sense. Maybe just sneak one more in. Just on the dose going forward, how are you thinking about that? Sure. So, you know, we're very, very happy with the efficacy that we're seeing and the safety per protocol. We're increasing the dose to a 1E9. We already started dosing the 1E9 dose. But based on the data so far, we expect the recommended phase two dose to be 38. We can see us improving efficacy more. This is as good as it gets when you compare it to all the autologous cell therapies. So that's currently what we expect with the recommended phase two dose, 38. Got it. Thanks, and congrats again. Thank you, Robert. Your next question will come from Reni Benjamin with Citizens JMP. Please dial star six and ask your question. Hey, good morning, everyone. Can you hear me okay? Yes. Hey, Reni. Good morning. Hey, good morning. Congratulations to Chen and team on the data. A couple of questions for you, I guess. One, any thoughts on potential redosing of these patients, especially the partial renal responses? And as you think about the 25 sites that are now activated and kind of the current enrollment trends, as we think about the next update that's coming in the first half of 2026, how many more patients do you think we might see? And in terms of durability, what do you think is the ideal kind of durable response rate? Reni, you got to start. You asked three questions, so let's go one by one. So the first one, can you repeat? Let's just go one by one. Yep. Any thoughts on redosing? Oh, yes. No, we don't have right now any thoughts about redosing. This is a single-dose treatment, and it's produced great data so far. We certainly have the ability to redose. This is an off-the-shelf product, and there's no prevention for people to redose in the future. But right now, this protocol is a single administration. So that was one question. And then the next question was regarding sites. So currently, we actually have more interest from more sites that are interested in joining the study. So we expect to continue to increase the number of sites. We see increased enrollment, increased interest in enrollment to the study. Patients, or sorry, investigators that provided one patient to the study very quickly come with their second patient with LN or SLE or with patients systemic sclerosis. and now we see patients interested with myositis and ANCA Vasculitis. So this process, once you have a drug that's off the shelf, well tolerated, and provides this type of efficacy, it just kind of feeds itself. And you see more and more interest from patients and from physicians and from sites. So we're actually very optimistic about the pace of enrollment here. I can tell you that, you know, if you told me that three patients per month, let's put it this way, as of now, enrolling three patients per month wouldn't be something that wouldn't be normal for the company. But we have not guided for how many patients we'll have in the first half of next year's update. But I believe that this data that we're presenting today de-risks the pivotal study in a very significant way. And next, in the first half of next year, following the discussion with the FDA and the additional patients that will present, the pivotal study will be completely de-risked. But, you know, we'll see that in the very near future. So that was your second question, and there was a third, if I remember. Yeah, thanks. Thanks for the attempt. You know, as we think about the competitive landscape, the fact that there are registrational studies kind of ongoing right now, how do you see ADI-001 maybe threading that needle in a world, right, not just for clinical execution, but in a world where, let's say, there's multiple cell therapies approved, right, in something like LN? Reni, we don't need to thread the needle because the tolerability that we see here should enable us to dose in outpatient settings. This opens the universe to so many sites that are interested in joining these studies, but just so far don't have the capabilities because, you know, they don't have the leukapheresis bed, and they don't know how to manage these CRS and ICANS. So from a clinical execution, we see a great potential. In clinical practice, we would expect the same advantage to continue because if you're a patient, why would you stop immunosuppressants for two months? And, you know, you might flare, then do the leukapheresis, and then be concerned about CRS and ICANS if you can just take something that's available off the shelf and, you know, is safer and doesn't require all the hustle around the autologous cell therapy. So we believe that this actually positions us for great success with an off-the-shelf and differentiated product. Excellent. Thank you very much, and congrats again. Thank you. Your next question will come from Soumit Roy with JonesTrading. Please dial star six and ask your question. Good morning, everyone, and congrats on the durable data, especially the robust immune reset. A quick one on the CRR eGFR definition. Is it going to be in line with Cabaletta or Autolus type cell therapy names where greater than 60 mL/min, or is it Roche and GSK, they are doing it at 85-90 mL/min? Is that something still up in the air and needs to be sorted out with the FDA, or? No, I don't think so. And Julie might correct me here. The complete renal response, that definition that we're using, is the one that's applicable for pivotal studies. Essentially, proteinuria needs to go to below 0.5, and eGFR needs to be stable. I don't want to see a reduction of more than 15% in the eGFR. That's the definition in pivotal studies. That's the definition that we're using. And separately, eGFR above 60 is considered in the normal range, but that's unrelated to the definition of complete renal response. Julie, anything that you would correct here? No, that's absolutely correct. Everything above 60 is normal. I'm sorry. One quick one is the dose level for the patients two and three. If you can remind us, was this three million, or was it lower versus one, four, and five patients? Yeah, yeah. It's actually on the first slide. The dose for the first three patients with LN was 1E8. That's 100 million CAR T cells. And the dose for the next two patients was 3E8, which is 300 million CAR T cells. Got it. Thank you so much, and congrats again. Thank you. Our final question will come from Robert Burns with H.C. Wainwright. Please dial star six and ask your question. Hi, guys. Thank you for taking my question, and congrats on the data. Just one from me, if I may. So given the strength of the data set, as well as the allogeneic differentiation for 001 relative to the autologous competitors, how are you seeing potential BD opportunities for 001, both in the U.S. as well as ex-U.S.? Thank you. Yeah, absolutely, Robert. Well, certainly, I can tell you that there is generally interest in BD, but, you know, we're going to be opportunistic when it comes to BD. We absolutely want to make sure we maximize shareholders' value. We believe that the valuation of the company, and that's reflected in the program right now, is completely not even remotely close to the zip code where it should be. But, you know, we'll be listening to BD opportunities. But again, we want to execute, build value, and generate the right returns for patients and progress aggressively with this program. We have the sites engaged. We have more sites engaged. We know what a pivotal study looks like. We can execute on a pivotal study. So, Robert, we want to run. Awesome. I love hearing that. Thank you, guys. Thank you, Robert. We have reached the top of the hour. This concludes today's call. Thank you for joining.