Welcome to the Fate Therapeutics first quarter 2024 financial results conference call. At this time, all participants are in listen-only mode. This call is being webcast live on the investors' sections of Fate's website at fatetherapeutics.com. As a reminder, today's call is also being recorded. I would now like to introduce Scott Wolchko, President and CEO of Fate Therapeutics. Please go ahead. Thank you. Good afternoon, and thanks everyone for joining us for the Fate Therapeutics first quarter 2024 financial results call. Shortly after 4:00 P.M. Eastern Time today, we issued a press release with these results, which can be found on the investors' section of our website under Press Releases. In addition, our Form 10-Q for the quarter ended March 31, 2024, was filed shortly thereafter and can be found on the investors' section of our website under Financial Information. Before we begin, I would like to remind everyone that except for statements of historical facts, the statements made by management and responses to questions on this conference call are forward-looking statements under the Safe Harbor provisions of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements. Please see the forward-looking statement disclaimer on the company's earnings press release issued after the close of market today, as well as the risk factors included in our Form 10-Q for the quarter ended March 31, 2024, that was filed with the SEC today. Undue reliance should not be placed on forward-looking statements, which speak only as of the date they are made, as facts and circumstances underlying these forward-looking statements may change. Except as required by law, Fate Therapeutics disclaims any obligation to update these forward-looking statements to reflect future information, events, or circumstances. Joining me on today's call are Ed Dulac, our Chief Financial Officer, and Dr. Bob Valamehr, our Chief Research and Development Officer. We will focus today's remarks on the data presented today at the American Society of Gene and Cell Therapy annual meeting for our off-the-shelf FT819 CAR T -cell and FT522 CAR NK cell programs, and discuss key program initiatives that we are pursuing to achieve therapeutic differentiation and improve patient outcomes. In addition, we will highlight clinical readouts that we are projecting to achieve in 2024 across our iPSC product pipeline for the treatment of cancer and autoimmune diseases. Finally, we will review our financial position, where our first quarter capital raise and strong cash balance have created operating runway into the second half of 2026. Beginning with FT819, our off-the-shelf CD19-targeted CAR T -cell program. Today, at the ASGCT annual meeting, we presented translational data from our FT819 phase I study in relapsed/refractory B -cell malignancies, which showed that a single dose of FT819 exhibited multiple mechanisms of action implicated in generating an immune reset in patients with B -cell-mediated autoimmune diseases. The translational data supporting these mechanisms included rapid, deep, and sustained CD19-positive B -cell depletion in the peripheral blood, patient case studies of primary, secondary, and tertiary tissue trafficking infiltration and activity with CD19-positive B cell elimination in tissue, and patient case studies of plasma cell depletion and B cell reconstitution with recovery of naive B cells and little to no recovery of activated memory B cells or plasma blasts. Notably, we also presented patient case studies demonstrating rapid, deep, and sustained B cell depletion accompanied by clinical responses without the use of fludarabine as a conditioning agent. Collectively, we believe these data support the disease-modifying potential of FT819 for patients with B cell-mediated autoimmune diseases. To that end, I am pleased to announce that the first lupus patient has been treated in our phase I autoimmunity study of FT819. This first patient, a 27-year-old woman with refractory disease despite having previously been treated with multiple standard-of-care therapies, received conditioning chemotherapy followed by a single dose of FT819 at 360 million cells. The patient was discharged after a three-day hospitalization stay without any notable adverse events. At ASGCT today, we also presented promising data from a first-of-its-kind translational assay using a sample of the patient's blood obtained prior to administration of conditioning chemotherapy, where we observed rapid and potent depletion of the patient's CD19-positive B cells in an ex vivo cytotoxicity assay with FT819. It is worthwhile to note that treatment of this first patient occurred within weeks of site activation. We believe this patient experience exemplifies the potential of an off-the-shelf cell therapy to overcome challenges that may hinder autologous cell therapies in reaching patients with autoimmune diseases, including the need for apheresis, complex manufacturing and treatment logistics, and extended patient hospitalization. Furthermore, since we have observed deep B cell depletion and clinical responses without the use of fludarabine as a conditioning agent in our phase I study of FT819 for B cell malignancies, we believe FT819 may have disease-modifying potential in autoimmunity using alternative conditioning regimens. We plan to amend the current clinical protocol for our phase I autoimmunity study in the second quarter of 2024 to enable FT819 administration with single-agent Cytoxan at the same dose used by rheumatologists for treatment of patients with autoimmune disease. We believe that an off-the-shelf add-on of FT819 to commonly used treatment regimens may contribute to a highly differentiating patient experience. Dose escalation in our FT819 phase I study in relapsed/refractory B cell malignancies has now completed, where 43 patients were treated with a single dose of FT819 at up to 1 billion cells without HLA matching. We observed clinical responses, including complete responses in heavily pretreated patients with aggressive disease, including in relapsed/refractory large B cell lymphoma patients that were previously treated with autologous CD19-targeted CAR T cell therapy. The safety and tolerability profile of FT819 was favorable, with no dose-limiting toxicities, no events of any grade of ICANS or graft-versus-host disease, and low incidence of only low-grade CRS. We believe the established clinical safety and tolerability profile of FT819 is differentiated and may also be of significant import for treatment of patients with autoimmune diseases. At this time, we intend to focus all further clinical development of FT819 exclusively in autoimmunity. Today, at the ASGCT annual meeting, we also presented data from our FT522 off-the-shelf CD19-targeted CAR NK cell program, which is the first product candidate emerging from our iPSC product platform that incorporates Alloimmune Defense Receptor technology. Today, the treatment course for administration of cell-based immunotherapies, including both autologous and allogeneic cell therapies, requires conditioning patients with chemotherapy. Conditioning chemotherapy can induce toxicities, prevent combination with standard-of-care treatments widely used in the community-based settings, and limit patient access and reach. ADR technology incorporated into FT522 is designed to enable effective treatment without administration of conditioning chemotherapy to patients, which we believe has the potential to redefine the cell therapy treatment paradigm. We have previously presented preclinical data using cancer cell lines demonstrating that the co-culture of ADR-armed CAR NK cells with alloreactive T cells promotes NK cell proliferation, enhances NK cell persistence, and increases anti-tumor activity, indicating that arming with ADR technology has the potential to enable effector cell function in the presence of an alloreactive system. Today, at the ASGCT annual meeting, we reported preclinical data using SLE diseased cells in a novel re-challenge assay using peripheral blood mononuclear cells from an unmatched SLE donor. FT522 uniquely drove rapid and deep depletion of CD19-positive donor B cells, eliminated alloreactive donor T cells, and maintained functional persistence with the ability to kill additional CD19-positive donor B cells upon re-challenge. In addition, we also presented initial translational data from the first two patients treated in our ongoing phase I study of FT522 in relapsed refractory B cell lymphoma. These data show enhanced persistence of 522 in the periphery compared to clinical data observed with FT596, our prior generation CD19-targeted CAR NK cell without ADR technology. Importantly, these data also show rapid, deep, and sustained B cell depletion in the periphery throughout the one-month treatment cycle. We intend to submit an IND application to the FDA in the middle of 2024 to expand our clinical investigation of FT522 for treatment of various B cell-mediated autoimmune diseases, including without administration of conditioning chemotherapy to patients. I'm also pleased to report that the first three patients in the conditioning arm of our phase I study of FT522 for relapsed refractory B-cell lymphoma have now completed safety assessment without any dose-limiting toxicities, and there were no events of any grade of CRS, ICANS, or GVHD. Dose escalation is now ongoing at 900 million cells per dose. In addition, patient enrollment has now been initiated in the no-conditioning arm at 300 million cells per dose, and we are poised to clinically assess the safety and activity of our ADR-armed FT522 CAR NK cell program without administration of conditioning chemotherapy to patients. Turning to our solid tumor initiatives, I'm also pleased to announce that under our collaboration with Ono Pharmaceutical, we have recently treated the first patient in our phase I study of FT825. Designed using the company's iPSC product platform, we believe FT825 represents an exciting new frontier in the field of cell-based cancer immunotherapy. The multiplex-engineered iPSC-derived CAR T cell program incorporates a constellation of synthetic anti-tumor mechanisms that are designed to harness the potential of both innate and adaptive immunity and to overcome unique challenges in treating solid tumors. These mechanisms include a CXCR2 receptor to promote cell trafficking, a chimeric TGF beta receptor to redirect immunosuppressive signals in the tumor microenvironment, a high-affinity non-cleavable CD16a receptor to promote antibody-dependent cellular cytotoxicity, and a novel cancer-specific HER2-targeted antigen binding domain, which has shown differentiated activity from that of trastuzumab in preclinical studies, including against HER2-low expressing tumor cells. The first patient in the phase I study was diagnosed with HER2-positive gastroesophageal junction adenocarcinoma, had progressed after receiving multiple lines of treatment, including HER2-targeted therapies, and was administered standard conditioning chemotherapy followed by a single dose of FT825 as monotherapy at 100 million cells. As we consider our strategic direction, we believe there is a strong value proposition for our iPSC product platform and off-the-shelf cell therapies in autoimmunity, where patient safety, convenience, and accessibility, as well as cost and scale, may be key differentiating factors. We believe our ADR technology can enable effective treatment with cell therapy without requiring administration of conditioning chemotherapy to patients, which has the potential to redefine the cell therapy treatment paradigm and patient experience for cancer and autoimmunity. We believe our multiplex-engineered iPSC-derived CAR T cell platform can deliver multiple synthetic mechanisms of anti-tumor activity with the potential to overcome unique challenges in treating solid tumors. As we look ahead into the second half of 2024, we are well positioned to reach and report on five key clinical milestones across our iPSC product pipeline for cancer and autoimmune diseases. Number one, we seek to demonstrate the disease-transforming potential of FT819 in B cell-mediated autoimmune diseases. Specifically, we expect to read out initial phase I clinical data for the first three to five patients treated with FT819 for moderate to severe SLE. Number two, we seek to administer FT819 without fludarabine and instead with commonly used treatment regimens for autoimmune diseases. Specifically, we intend to amend the current IND for our FT819 phase I autoimmunity study to include administration with single-agent Cytoxan and expect to read out initial patient clinical data. Number three, we seek to demonstrate the potential of our proprietary ADR technology to enable effective treatment of patients without administration of conditioning chemotherapy. Specifically, we expect to read out the first five no-conditioning patients treated with 522 in our phase I study for B cell lymphoma. Number four, we seek to broadly investigate 522 without conditioning chemotherapy for treatment of various B cell-mediated autoimmune diseases. Specifically, we expect to submit an IND application and, subject to IND allowance by the FDA, initiate patient enrollment in a phase I multi-indication study of 522 for autoimmunity. And finally, we seek to establish an initial clinical proof of concept for our multiplex-engineered iPSC-derived CAR T cell platform in treating solid tumors. Specifically, we expect to read out the first three to five patients treated with FT825 in our phase I study for advanced solid tumors. I would now like to turn the call over to Ed to review our financial results for the first quarter. Thank you, Scott, and good afternoon. Fate Therapeutics is in a strong financial position to advance our pipeline of iPSC-derived CAR T and CAR NK cell programs for autoimmune diseases and cancer. With the addition of net proceeds from the company's $80 million underwritten offering of common stock and $20 million concurrent private placement of pre-funded warrants in March, our cash equivalents and investments at the end of the first quarter were approximately $391 million. In the first quarter, our reported revenue of $1.9 million was consistent with the prior two quarters and reflects the research funding associated with the development of a second product candidate against an undisclosed target in solid tumors under our collaboration with Ono Pharmaceutical. As a reminder, after opting into a U.S. and European co-development and co-commercialization arrangement with Ono for FT825 in the fourth quarter of 2022, we account for that program's reimbursable expenses as an offset within our research and development costs. We recognized $800,000 of contra-R&D expense in the quarter. Research and development expenses for the first quarter were $32.1 million, essentially flat versus the fourth quarter of last year. Our expenditures in R&D were driven primarily by salaries and benefits, including share-based compensation, and from clinical trial costs and demand for R&D materials. General and administrative expenses for the first quarter increased sequentially by 16% to $20.9 million. The increase in our G&A expenses was attributable primarily to increases in legal-related fees. Total operating expenses for the first quarter increased by 7% relative to the fourth quarter of 2023 to $53 million, which included $11 million in non-cash share-based compensation expense. Note that in connection with the development of our off-the-shelf iPSC-derived CAR T cell product candidate, FT819, we previously achieved the clinical milestone set forth in our amended license agreement with Memorial Sloan Kettering Cancer Center, which triggered a first milestone payment to MSK in 2021. Up to two additional milestone payments may be owed to MSK based on subsequent trading values of the company's common stock, ranging from $100 to $150 per share. We assessed the fair value of these contingent milestone payments, currently valued at $2.7 million on a quarterly basis. In the first quarter, we recorded a non-cash $1.4 million non-operating loss associated with the change in fair value. Our net loss for the quarter was $48 million or $0.47 per share. Finally, as we consider the investments we plan to make this year, we expect our GAAP operating expenses, which includes non-cash items such as stock compensation expense and depreciation for the full year, to be between $215 and $230 million, and that we will end the year with more than $270 million in cash equivalents and investments. I would now like to open the call for questions. We will now begin the question-and-answer session. To ask a question, you may press star, then one, on your touch-tone phone. If you are using a speakerphone, please pick up your handset before pressing the keys. If at any time your question has been addressed and you would like to withdraw your question, please press star, then two. At this time, we will pause momentarily to assemble our roster. The first question comes from Michael Yee with Jefferies. Please go ahead. Thank you. We had a two-part question. Congrats on all the progress, Scott. On the autoimmune study that is enrolling, I know that was a bit slow to get off, but it sounds like you're going to have some good momentum and report patients. Can you just talk a little bit about how the plan to also allow single-agent Cytoxan would impact things and how you think about what that would show and how that would impact the design of the study? And then the second question is related to 522. I think it's exciting. You're now in the second cohort without lymphodepletion. Can you just talk about the results that you might see there and how you would read through and what you see there into the idea for autoimmune as well? Thank you. Sure. So in the autoimmunity study with FT819, the current study as designed has two different alternatives for conditioning. There is a standard 3-day conditioning cycle of Cy/Flu, which is commonly used in the oncology setting. So I believe it's 500 milligrams per meter squared times three days for cyclophosphamide and 30 milligrams per meter squared times three days for fludarabine. We also have a second, in the current study, we also have a second conditioning regimen that is permitted. The second conditioning regimen is a bendamustine-based conditioning regimen, and that is a 2-day treatment regimen with bendamustine. What we're contemplating doing, and this is based on data we presented today, we believe we have good proof of concept in our FT819 oncology study. So this is the study in B cell malignancies, where several of our patients in that study received bendamustine as a conditioning agent. So they did not receive Cy/Flu. They received the bendamustine-based conditioning regimen in the oncology study. We presented the data on those patients specifically today. We saw very deep B cell depletion in the periphery, which was maintained through the 30-day treatment cycle. And importantly, we saw clinical responses with the bendamustine treatment conditioning cycle or conditioning regimen. So we did not use fludarabine so in that regimen, we're not using fludarabine. So we saw activity with FT819 without fludarabine. And so that gives us confidence that we can amend the IND to add onto a Cytoxan-only regimen. We believe we can accomplish that efficiently through an amendment to the IND, essentially adding a third "conditioning regimen" for patients. And so the study would provide physicians' choice of Cy/Flu conditioning, bendamustine conditioning, or single-agent Cytoxan conditioning. And again, since Cytoxan and bendamustine are in the same class of molecule and given the activity we've seen in the oncology study, we feel confident in FT819's ability to perform in a Cytoxan-only regimen without fludarabine. Long answer, but I hope that was clear. Yeah. No, very nice. And then the read-through from oncology, because you're in the Cohort B without conditioning. Yeah. So with respect to FT522, obviously, we have a long history with NK cells. We have started the study with Cy/Flu conditioning. It provides us the opportunity to do some direct comparison with FT522 based on historical datasets that we have generated with FT596, our prior generation product. We presented data today where we believe in early small numbers of patients, obviously. We think we're seeing some differentiated activity with respect to persistence, which we're excited about. And so we are very excited now to essentially begin our clinical experiment with FT522 or clinical experience with FT522 with no conditioning. Preclinically, and I'll let Bob talk about it, we've done a tremendous amount of work with FT522 preclinically in allogeneic systems, both using cancer cell lines as well as now using donor SLE cells. And we presented the donor SLE preclinical data today. I'll let Bob talk about that because I think it does demonstrate the potential of FT522 to essentially thrive in an allogeneic disease system. Thanks, Scott. So just to talk about preclinical and also answer some of your questions about how the clinical data will play out for autoimmune. So in the preclinical, as Scott mentioned, having the ADR technology in 522 allows us to actually show activity and persistence even when there is an intact PBMC compartment. So in a Petri dish, we try to mimic what's happening in the patient setting by having the PBMCs, and they're all different types of cells from PBMC. And we showed that with 522, you can actually show functional persistence. And this is very unique to the ADR technology because if you have NK cells without ADR or autologous CAR T, you won't get this observation. And this observation is very specific because we can co-culture 522 with PBMCs and show that we can target, because there's a CAR19 in 522, the B cells in PBMC. However, we don't see an allo-reaction that's induced by the T cell compartment. Even though these cells have an intact HLA expression on their surface, our product, we are able to hold off the allo-reaction because we target foreign B positive population, which is the final stage of an activated cell. So we are able to hold off on that. And we can maintain activity through functional persistence because when we rechallenge the 522 co-culture with additional PBMCs, we can continue targeting the B cell compartment and maintain functional persistence. This is not seen with auto CAR T. This is not seen with NK cells. Moving to the clinical experience, I think one of the things that we're very excited about with our ability in translational on the 522 Cy/Flu arm, we're going to be able to look at ctDNA and see how the disease is modulated with each dose of 522 in an intact patient immune compartment and also look at the entire disease decrease over the treatment cycle. That's going to give us a hint of 522 activity without Cy/Flu conditioning. We'll also look at the endogenous immune compartment and see how that's modulated and also look at the PK in an intact immune compartment with very sensitive assays. So we'll hopefully see a lot of activity there and be able to parlay that into autoimmunity. Yep. Perfect. Thank you, guys. Thanks. The next question comes from Yigal Nochomovitz with Citi. Please go ahead. Hi, this is Alim on for Yigal. Thank you for taking our questions. We had a couple. First, on FT819, you mentioned patient case studies have shown secondary and tertiary tissue trafficking and infiltration. Are you doing tissue biopsies here? Sure. We do show primary, secondary, and tertiary activity. For the primary, we show that we have persistence in the bone marrow, and that correlates with reduction and elimination of CLL-positive cells. This is based on flow cytometry. We show persistence and infiltration in the bone marrow and clearance of disease. In our secondary, for the lymphoid, we have biopsies the lymphoid tissues, we have biopsies there, and we can show that the population is reduced. For tertiary, the example we use in our presentation is liver and PET score, which correlates to PK. We're able to, through different methods, whether it's direct detection of cells or proxy detection of cells, be able to show that we are able to have activity in both primary, secondary, and tertiary tissues. Okay. Great. That makes sense. And then a second question. It's more of a general question. Given your planning to file an IND for FT522 for autoimmune, how should we think about the expectations on the efficacy here? Are you hoping to see efficacy on par with CAR Ts, or is it the main focus is more like removing or lowering the preconditioning burden, maybe with a little bit of a cost on efficacy? Yeah. I think as we're going into this study, we acknowledge efficacy is really important. I think at the end of the day, what's been really exciting about cell therapy here in autoimmunity is the fact that, again, this is coming out of the German study. Single dose of CAR T cell therapy has been able to generate an immune reset in patients that have had disease and refractory disease for a significant period of time. And that's been quite remarkable. And I think folks are very excited about that. I think with respect to autoimmunity, efficacy is certainly going to be important. And we need to acknowledge that at some basic level, we need to be able to compete on efficacy. That said, autoimmunity is a very different setting than oncology. And I think safety is certainly going to be at a premium with respect to autoimmunity. I think one of the challenges that has already confronted the field is that Cy/Flu conditioning may not be well accepted by patients in the field of autoimmunity. And so I think safety is going to be critical. I think alternative regimens where you can add onto standard of care treatments is going to be critical. I think reaching patients where they live and breathe, which is not at the academic CAR T cell centers, is going to be critical. And so I think there are a multitude of elements here that are going to be important in autoimmunity that are different than oncology. And I do think an off-the-shelf cell therapy has significant sort of attributes that can be very appealing for these patients. Okay. Got it. Great. Thank you very much for taking our questions. The next question comes from Daina Graybosch with Leerink Partners. Please go ahead. Hi. So this is Jeff on for Daina. So we have two questions. The first was around a competitive landscape. There was some recently published encouraging data with the first-gen CD19 bispecific blinatumomab. What was your view of that data, and how are you thinking about T-cell engager competition overall for autoimmune disease, given that the modality addresses many of the same challenges of autologous CAR T that your off-the-shelf programs do? And then looking at kind of BCMA and your plans for a next-gen program there, do you expect to use the ADR modality there, and is that sufficient, or are you looking at other edits? And what do you think BCMA adds that you wouldn't already achieve with your CD19 program? Thank you. Yeah. So on your sort of general question around CD19 engagers, I think we're approaching the autoimmunity space eyes wide open with respect to the disruptive potential of CD19 engagers. And ultimately, as we're thinking about the development of the autoimmunity space, we recognize the benefits that can be brought to patients potentially in differentiating potential of the CD19 engager. We've obviously seen that play out in oncology. And as we think about it, we were thinking about essentially our target product profile going directly up against what the value proposition of a T cell engager is. And hence, that's how you will hear us obviously talk about, and we've talked about on the call today, how important we think it is to move away from Cy/Flu, to add on to standard of care treatments, to reach patients in the community setting, to minimize hospitalization, and to prioritize safety and efficacy. So I think we're going into this recognizing that T cell engagers will play an important role in treating patients with autoimmunity and developing target product profiles directly head-to-head against those. As it relates to BCMA, I think just generally and this is not a comment specifically to BCMA, but I think we're very excited about the ADR technology, both with respect to its first assessment with 522 clinically. I'll let Bob talk to it and correct me if I'm wrong, but I think any product candidate you're going to see emerge from Fate Therapeutics from this point forward will incorporate ADR technology. We absolutely believe that conditioning chemotherapy, intense conditioning chemotherapy, is a headwind for the field of cell therapy, and we need to move beyond that. We're excited to do that. We're excited to pioneer that. We think we've put a tremendous amount of work, both with respect to research and innovation, on how to achieve a new cell therapy treatment paradigm with off-the-shelf cell therapy. Great. Thank you. Actually, just a quick follow-up in the mitigating lymphodepletion. How does bendamustine only compare to Cyclophosphamide only in terms of relative potency? And would you expect the same degree of CAR T, FT819 expansion, in vivo in the same level of potency as you kind of saw with the bendamustine examples? Thank you. Yeah. I think there's some data on this, right? There's some data out there that certainly combines in the field of oncology and CAR T cell therapy that has done work comparing Cy/Flu conditioning to bendamustine. I think, generally speaking, it's been demonstrated that bendamustine can be an effective alternative treatment conditioning regimen for CAR T cell therapy. Bendamustine is in the same chemical class as cyclophosphamide. We do have experience, as I mentioned, with bendamustine as a standalone conditioning agent without fludarabine. So we're fairly confident that our programs, FT819, can perform with cyclophosphamide. Great. Thanks for taking our questions. The next question comes from Mike Ulz with Morgan Stanley. Please go ahead. Hi. This is Rohit on for Mike. Thanks for taking our questions. Can you just talk about what you've seen with the first lupus patient treated with FT819 and how safety compares to what's been seen in the autologous CD19 therapies? And then can you also talk about what other autoimmune diseases you would consider expanding to? Thank you. Yeah. I think I'll limit my comments to what we disclose to date. The patient is still the first lupus patient. It still is in the 30-day DLT assessment window. I can absolutely say that the patient was discharged after three days of hospitalization. So it was a 3-day hospitalization stay. It was uneventful, and there were no notable adverse events. The patient does still remain, though, in the 30-day DLT assessment window. With respect to expansion into other indications in autoimmunity, we are doing a fair bit of work assessing that opportunity. Obviously, one of the elements of assessment is looking where others have established, and this is primarily coming out of the German study, but also the field of allogeneic stem cell transplant, looking at where there's been success with other B cell-mediated diseases with either transplant or out of the German group in the early seminal datasets. I think I'll leave it at that. Thank you. The next question comes from Li Watsek with Cantor Fitzgerald. Please go ahead. Hey. Good afternoon. Thanks for taking the questions. Maybe just follow up on what other indications that you might go into. I mean, this is specific for 522. I know, Scott, you mentioned that you're looking at multiple autoimmune diseases. So just wondering, since it's quite crowded in the lupus space, so just wondering what are other indications that you might be considering, such as RA? And how do you think about 522 fitting with 819 in terms of which types of patients to go after? Sure. At this point, we are doing a lot of work. I'm not going to disclose our strategy at this point in time. We are obviously doing a lot of work in thinking about our expansion strategy in autoimmunity. We are looking at areas where there has been clinical precedent with cell therapies, whether that be in transplant or out of the first datasets that are being generated, both out of Germany as well as the initial sort of company initiatives or company programs. So not prepared to disclose today how we think about expanding our FT819 IND into additional indications or the initial multi-indication study that we plan to submit for 522. Okay. And then maybe just wondering if you can just comment on your expectation for the patient enrollment in the FT819 study. It seems like you can dose the patients fairly quickly. And then it seems like you're going to amend the protocol to allow some alternative conditioning regimens. So do you think that might drive sort of the traction with the site investigators? Yeah. So specifically, we have guided to three to five patients, an update on three to five patients in the FT819 study by the end of this year. We've also guided to and we've discussed it on the call that we are looking to utilize Cytoxan only as a third potential regimen for treating patients, so Cy/Flu or benda or Cytoxan only. We do think that and I think there's been discussion about this, that Cy/Flu potentially is a barrier to treating patients with autoimmunity. These patients aren't oncology patients. They don't deserve to be treated like oncology patients. And so I do think moving away from Cy/Flu as a conditioning regimen is going to be critical to really capturing the potential of cell therapy in autoimmunity, and we look to pioneer that. Thank you. The next question comes from Tara Bancroft with TD Cowen. Please go ahead. Hi there. This is Greg speaking on behalf of Tara. I'm wondering if you can give us any timeline for when we can expect clinical data in lupus for 819? Sure. In the prepared remarks, we've guided to an update on the first three to five patients with FT819 in SLE by the end of this year. Okay. Great. Thank you. Sure. The next question comes from Ben Burnett with Stifel. Please go ahead. Hi. This is Carolina Ibanez Ventoso on for Ben Burnett. Thank you for taking our question, and congratulations on all your progress. On the ex vivo data for 819, on the pretreatment sample from the SLE patient, what do the ET ratios shown imply about the necessary dose and cell expansion that you would need to achieve to get that deep B cell depletion at the end of the curve in vivo in the SLE patient? I'm happy to answer that question, and I'll use some math here, so please forgive me if I start getting a little hypothetical. So what we show in the data is that at 2:1 ET ratio, we effectively eliminated all B cells that were in the PBMC compartment from the patient. If you were to think about the disease burden in autoimmune, specifically SLE, we anticipate somewhere around 100-300 million diseased B cells residing within a patient. So if we're effectively clearing around almost all cells at 2:1, but pretty much over 95% at 1:1, our current dose at 360 million falls right smack in the middle of an effective dose that we see in vitro. To answer your question specifically, we are eliminating all B cells at 2:1 and over 90% at 1:1, and that should give us confidence that the current dose is basically on par to match that in the patient setting at 360 million. Okay. Very helpful. Thank you. You're welcome. The next question comes from Peter Lawson with Barclays. Please go ahead. Hi. This is Alex on for Peter. Thank you for taking the question. Just wondering if you could maybe just recap the data a little bit, the ASGCT data, when you look at the preclinical and translational data for 819 versus 522, so the CAR program versus the NK cell program, any notable differences you see in terms of tissue distribution, B cell depletion, or B cell reconstitution? Sure. I can answer that question. So FT819 and FT522 obviously are very different. FT522 not only has the ADR technology but also has the IL-15 receptor fusion. So preclinically, we see a very good biodistribution with FT522 because it very much doesn't need antigen for expansion, doesn't need cytokine for expansion. So we see very good biodistribution. Obviously, it has the ability to be combined with a monoclonal antibody, so we see that as well. Either we enhance activity against a specific cell, for example, targeting CD19 and CD20 at the same time, or going after other cell types that have eliminated the CD19 expression, and I'm only expressing, for example, CD38. So that multi-antigen perspective also comes in through with FT522. With FT819, having the 1XX CAR in the TRAC locus is a very potent CAR product, and so we see that when we go head-to-head against auto CAR T in preclinical studies. So we see very potent activity with FT819, as I mentioned earlier, as well. So those are the main differences in terms of behavior of these cells. We have a product that's ADR that does not need conditioning and can go multi-antigen targeting, and another product that's very potent against CD19. And I think one of the comments I would just add on to that is FT819, with respect to its manufactured phenotype, has high expression of CXCR4. And so we've seen very good sort of homing and trafficking and infiltration of secondary and tertiary tissue in preclinical studies. That's a good point. Okay. Thank you. I guess does that have any implications for which type of indications you could target in the autoimmune setting? Thank you. Yeah. Yeah. I mean, it's something we're looking at. I mean, we are still doing work on thinking about exactly how to expand and what indications are going to be prioritized with 819 and 522. We are prepared, and we are preparing to expand the 819 IND to consider additional indications. And obviously, we've discussed filing a multi-indication IND for 522. So a lot of work is going on. Stay tuned there on that front. The next question comes from Yanan Zhu with Wells Fargo Securities. Please go ahead. Great. Thanks for taking our questions. To follow up on a prior question about the recent literature, I'm just wondering, do you have a view on the depth of B cell depletion a bispecific antibody can achieve compared with cellular therapy? And do you foresee, for the bispecific, if it becomes a modality, would it be a repeat administration at a certain time interval? Could that be viable or competitive with cellular therapy? And lastly, for 819, do you foresee the potential possibility of additional doses at a certain time interval and whether that could be part of the product profile and whether you might even be considering looking at that in a current study? Thanks. Sure. So forgive me. I am not an expert on the bispecific engagers, and so I can't talk in an informative way about the depth of B cell depletion that's been seen or achieved with the B cell engagers. Obviously, in the setting of oncology, the T cell engagers have generated complete responses. So again, we are going into the field of autoimmunity, recognizing that T cell engagers can be an attractive modality and have the potential to drive an immune reset. Whether that's achievable, what the duration of that looks like, what the side effect profile of that looks like, how many doses, all of that's TBD. We're very early, I think, just generally in the field of autoimmunity. That said, I think one of the potential strengths of an engager is that it can be multi-dosed. I do think, from our standpoint as a company, we've always discussed the fact that an off-the-shelf cell therapy, we do think, has multi-dosing potential. I I think multi-dosing potential can be hindered by Cy/Flu conditioning. Hence, as we've discussed, we think it's important to think about both 819 and 522 being developed as add-on strategies to standard regimens that are used today to treat patients in the community setting with autoimmune disease. I think you will see us continue to move in that direction where we are thinking about delivering and dosing cell therapies as if they were a monoclonal antibody. Got it. Very helpful. Thank you. The next question comes from Bill Maughan with Canaccord Genuity. Please go ahead. Hi. Thanks for taking the question. So to follow up on this morning's 819 data, all the PK obviously was positive. But thinking about translating that from an oncology patient to an autoimmune patient when antigen-dependent expansion is a key part of the PK of a CAR T cell therapy, I'm just wondering how you think about being able to translate from one population to the next? Yeah. I think there's a lot we don't know with respect to how the two diseases are going to translate. I think what we have certainly seen with the PK is that we have seen CD19-mediated expansion that is dose-dependent. Certainly, the mechanism of action or one of the key mechanisms of action in autoimmunity is being able to recognize and target and eliminate CD19-positive B cells. So I don't necessarily presume that actually, the PK profiles are necessarily going to be the same in oncology versus autoimmunity. I think at the end of the day, what's obviously critical is the kinetics and depth of B cell depletion. Thank you. The next question comes from Ethan Markowski with Needham & Company. Please go ahead. Yeah. Hi. This is Ethan on for Gil Blum. Thank you for taking our question. So I'm just looking at the charts in the ASGCT data, and I think you guys clearly show that FT522 demonstrates deeper B cell depletion than FT596. But it looks like FT819's graph, at least the bar graph in depletion, is very similar to FT596 with some cells kind of coming back up in the mid to end of the cycle. So I was wondering first how important this complete response is and if some cells coming back at the end is clinically relevant. And then also just from a cost-savings perspective, I know you're no longer planning to move forward in multiple myeloma and B cell lymphoma. So I'm wondering if that has any impact in a positive way on near-term R&D spend. So thank you for taking our question. Yeah. So on the last question with respect to clinical development in multiple myeloma, obviously, there are patient costs associated with clinical development. While we are not advancing FT576 into dose expansion, we are in multiple myeloma. We are certainly expanding development in autoimmunity. And so in terms of changing cash burn, I don't think we're thinking about that as enhancing or savings or reducing burn. We're certainly investing in autoimmunity. As it relates to B cell depletion, I think keep in mind with both FT819 as well as FT522, we are seeing very, very low levels of cells in many instances, and I'll let Bob talk about it, below the lower limit of sort of detection. And so when we start getting into very, very low levels, you start to get into sort of a discussion about whether it is significant or not. I don't believe, at least we think, that we're seeing different levels of depletion with FT819 versus FT522. I'll let Bob comment on that. I will say, just to be really clear, the FT819 dataset is over a much larger dataset of patients. I think we used 23 patients with B cell lymphoma for that dataset. Some of those patients had relatively high B cell counts going into the study. In fact, we noted that there were certain patients that had superphysiological levels of B cell counts that we were able to deplete with FT819. The FT522 dataset is, I think, only on two patients, and their B cell counts generally were lower at baseline compared to the totality of the FT819 patients. I'll let Bob talk on that. But I think, generally speaking, what we've seen with respect to B cell reconstitution from the Schett data is B cell reconstitution actually can happen, for instance, as early as the third or fourth week and can happen as late as four months. But I'll let Bob sort of finish up on that if I missed anything. No. I think you well covered it. When discussing 819, as Scott mentioned, there was a large number of patients. But it fell pretty much in line with showing very good B cell depletion over the treatment cycle, and B cell recovery was seen in some of the patients. Now, keep in mind, this is oncology. So what's coming back up could be a lymphoma cell or something. So we're in a much more aggressive stage than what Schett showed. But as Scott mentioned, what Schett shows is that B cells do come back from 30 days to 180 days. So every patient treated, all 15 in Schett data, had, by I believe, day 180, full recovery of B cells. So 819 is very much in line with what Schett showed. Now, with 522, you bring up a very good point. And I think part of that has to do with the fact that it's being combined with Rituxan. So this is kind of the one-two punch that we're seeing. Again, two patients. I'm not going to sit here and speculate too much on it. But you are seeing the power of CAR plus hnCD16 in these settings. And I think both programs' data has been so far very encouraging. Ethan, I'll just pick up on Scott's comments. Qualitatively, I agree. The mix of the business will change through the course of the year. But if you look at the first quarter, we had roughly $52-$53 million in GAAP operating expenses and about $37 million in cash burn. That's been pretty consistent for the last couple of quarters. So even though we have one or two programs winding down, the hope is that now that we have first-patient dosed and we're beginning to clear dose levels in certain programs, that's going to pick up throughout the year. So I expect that those numbers I just quoted, the $53 million on the GAAP operating expense and the $37-$38 million on the effective cash burn for the quarter, to remain fairly consistent. I'm more than happy to invest behind these clinical programs. So if that ticks up to, call it, circa $40 million on a cash burn basis. But we feel pretty good about where we are. Just the mix of the businesses will evolve. But that's a pretty good number to work with for the rest of the year. Thank you. Very helpful. This concludes our question-and-answer session. I would like to turn the conference back over to Scott Wolchko for any closing remarks. Thank you. Thank you for everyone today for all your good questions on the ASGCT data. Appreciate all the input and thought. Speak to you soon. Thank you. The conference has now concluded. Thank you for attending today's presentation. You may now disconnect.