Welcome to the Fate Therapeutics third quarter 2023 financial results conference call. At this time, all participants are in listen-only mode. The call is being webcast live on the Investors section of Fate's website at fatetherapeutics.com. As a reminder, today's call is being recorded. I would now like to introduce Scott Wolchko, President and CEO of Fate Therapeutics. Thank you. Good afternoon, and thanks everyone for joining us for the Fate Therapeutics third quarter 2023 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 September 30, 2023, 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 statements 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 September 30, 2023, 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 the 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. During today's discussion, we will cover several key milestones that we recently achieved for our iPSC product platform, including expanding the clinical reach of our iPSC-derived CAR T-cell platform to solid tumors, as well as beyond oncology and into autoimmunity. In reaching these milestones, we are now well positioned to achieve important clinical readouts in oncology and autoimmunity across multiple programs in 2024. We will also discuss our continued focus on controlling costs that has resulted in a significant decrease in cash utilization, which we believe enables us to extend our operating runway into the second half of 2025. Beginning with FT522, our off-the-shelf CD19-targeted CAR NK cell program, I am pleased to announce that our phase 1 study is open for enrollment in patients with relapsed refractory B-cell lymphoma, where we intend to assess FT522 with and without conditioning chemotherapy. FT522 is the company's first product candidate to incorporate our proprietary allogeneic defense receptor, or ADR technology, which is comprised of a synthetic engineered receptor designed to target 4-1BB, expressed on alloreactive immune cells and induce NK cell proliferation. In preclinical studies, we have shown that the engagement of ADR-armed CAR NK cells with alloreactive immune cells mitigated rejection, promoted NK cell proliferation, and increased antitumor activity. These preclinical data suggest that FT522 has the potential to drive clinical responses without administration of intense conditioning chemotherapy to patients. The phase 1 study includes two regimens. Regimen A, or the conditioning arm, which consists of 3 days of standard conditioning chemotherapy, 1 dose of rituximab, and 3 doses of FT522. Regimen B, or the no-conditioning arm, which consists of one dose of rituximab and three doses of FT522 without conditioning chemotherapy. Enrollment into regimen A, or the conditioning arm, has now been opened at the first dose level of 300 million cells per dose, and upon clearance of dose-limiting toxicities at this first dose level, enrollment into regimen B, or the no-conditioning arm, will commence at its first dose level of 300 million cells per dose. Each regimen may proceed with dose escalation independently. Today, conditioning patients with intense chemotherapy is a necessary component of the treatment course for cell-based cancer immunotherapy, including for both autologous and allogeneic cell therapies. Conditioning chemotherapy induces toxicities, limits patient access, and prevents combination with standard of care immunotherapies widely used in the community-based setting. We believe we have the opportunity to establish clinical proof of concept for our ADR technology and for our FT522 program without conditioning chemotherapy early in dose escalation. Turning now to our T-cell programs. We believe our multiplexed engineered iPSC-derived CAR T-cell product platform is uniquely suited to bring a constellation of antitumor mechanisms to the fight against solid tumors. I'm pleased to announce that we have established a new landmark in the field of cell-based cancer immunotherapy. Our IND application was cleared by the FDA to initiate clinical investigation of FT825 in patients with solid tumors. The multiplexed engineered iPSC-derived CAR T-cell program, which is being co-developed under our collaboration with Ono Pharmaceutical, incorporates seven novel synthetic controls of cell function that are designed to harness the potential of both innate and adaptive immunity, and to overcome the unique challenges in treating solid tumors. These novel synthetic controls include a CXCR2 receptor to promote cell trafficking, a chimeric TGF-beta receptor to redirect immunosuppressive signals in the tumor microenvironment, and a high-affinity, non-cleavable CD16 receptor to promote antibody-dependent cellular cytotoxicity. At the 2023 Society for Immunotherapy of Cancer Annual Meeting, we unveiled that FT825 incorporates a novel cancer-specific antigen binding domain targeting HER2, which was contributed by Ono to our collaboration. Preclinical studies presented at the meeting demonstrated that the binding profile of the cancer-specific CAR construct is unique and differentiated from that of trastuzumab, exhibiting similar potency with greater specificity toward HER2-expressing malignant cells. In subcutaneous xenograft models, FT825 demonstrated robust antitumor efficacy against HER2 high, as well as HER2 low-expressing tumor cells. Additionally, FT825 resisted TGF-beta-mediated suppression, maintaining robust cytolytic activity across multiple rounds of tumor challenge and suppressive levels of TGF-beta exposure, and showed potent migration to CXCR2 ligands, which are often expressed in solid tumors. With the clearance of our IND by the FDA, phase I study start-up activities are now ongoing at multiple sites. The dose escalation schema for the phase I study includes two treatment regimens. Regimen A, or the monotherapy arm, consists of a standard three-day preconditioning regimen and a single dose of FT825 as monotherapy. Enrollment into the monotherapy arm will commence at the first dose level of 100 million cells. Eligibility includes patients with advanced HER2-expressing solid tumors. Regimen B, or the combination arm, consists of a standard three-day preconditioning regimen and a single dose of FT825 in combination with cetuximab, where we seek to additionally exploit innate immunity by leveraging the product candidate's high-affinity, non-cleavable CD16 receptor to target EGFR expressed on solid tumor cells. Enrollment into regimen B will commence at the first dose level of 100 million cells upon clearance of dose-limiting toxicities at the first dose level of regimen A. Eligibility includes patients with advanced EGFR-expressing solid tumors. While we have made great strides in advancing our most innovative and differentiated clinical programs in oncology, we also remain committed to pursuing new therapeutic opportunities beyond oncology, where cell-based immunotherapies can have a profound clinical benefit for patients. Our initial clinical data are now emerging, indicating that CD19-targeted CAR T-cell therapy has the potential to durably deplete a patient's pathogenic immune cells, drive immune reset, and meaningfully improve quality of life across a wide spectrum of autoimmune diseases. We believe there is a very strong value proposition for off-the-shelf cell therapy in autoimmunity, where a relatively short-lived cell can deeply eradicate an aberrant B-cell population and enable rapid reconstitution of a healthy immune system, and where patient safety, convenience, accessibility, as well as cost and scale, will be a differentiating factor. To this end, I'm pleased to announce the clinical expansion of our iPSC product platform into autoimmunity. In July, the FDA cleared our IND application for clinical investigation of FT819, our off-the-shelf CD19-targeted CAR T-cell program, in patients with SLE, including for patients with active lupus nephritis or active SLE without renal cell involvement.... We have now initiated phase 1 study start-up activities at multiple sites. The phase 1 study in SLE is designed to evaluate the safety, pharmacokinetics, anti-B-cell activity of a single dose of FT819 administered following a standard conditioning regimen consisting of either CyFlu or bendamustine. Dose escalation will commence at the first dose level of 360 million cells. Importantly, we have previously presented clinical data of a single dose of FT819 at doses up to 360 million cells in the setting of relapsed refractory B-cell lymphoma, where we reported safety and clinical activity. Of the first 11 patients treated with a single dose of FT819 at up to 360 million cells, we observed a favorable safety profile with no immune effector cell-associated neurotoxicity and mild cytokine release syndrome. We observed antitumor activity in heavily pretreated patients, including 3 complete responses, and we observed CAR T cell expansion that peaked in the peripheral blood between days 8 and 11. The phase 1 study of FT819 in SLE allows for assessment of higher dose levels, each up to 3 times the highest cleared dose level, as well as for the opening of multiple dose expansion cohorts, each of which may be enrolled in parallel. We are pleased to receive a favorable re-review of our FT819 clinical protocol from the clinical experts of the Protocol Design Committee of Lupus Therapeutics, an affiliate of the Lupus Research Alliance. We also continue to watch with keen interest the emergence of additional clinical data in autoimmunity, and we are currently evaluating additional clinical expansion opportunities for FT819, as well as for FT522, where we think the potential to reduce conditioning chemotherapy and to target and complete B cells, plasma cells, and autoreactive T cells with an off-the-shelf ADR-armed CD19 targeted CAR NK cell offers a highly differentiated therapeutic profile. We have remained resilient during these challenging times and focused our attention on building a fully integrated operation that leads in the research, development, and manufacture of multiplexed engineered iPSC-derived cellular immunotherapies. As we look towards 2024, we are well positioned to achieve important clinical readouts in oncology and autoimmunity across multiple programs. Clinical activities are now ongoing for our two most innovative oncology programs, FT522 in B-cell lymphoma and FT825 in solid tumors, as well as for our first autoimmunity program, FT819 in SLE. We also continue to advance our phase 1 study of FT819 in B-cell malignancies, where we are enrolling patients in single-dose treatment cohorts at 540 million cells in BCL and at 360 million cells in CLL. As well as our phase 1 study of FT576 in multiple myeloma, where we are enrolling patients in three-dose treatment cohorts at 1 billion cells per dose as monotherapy and in combination with CD38 targeted monoclonal antibody therapy. Finally, our investment in innovation continues, including under our solid tumor collaboration with Ono, as we continue to advance new multiplexed engineered CAR T cell programs toward clinical development. We remain confident in our belief that our proprietary iPSC product platform is uniquely suited to create highly differentiated product candidates with the potential to deliver multiple mechanisms of action and therapeutic benefit to patients with cancer and autoimmune diseases. I'd now like to turn the call over to Ed to review our financial results for the third quarter. Thank you, Scott, and good afternoon. Fate Therapeutics is in a solid financial position to advance our pipeline. Our cash, cash equivalents, and investments at the end of the third quarter were approximately $350 million. In the third quarter of this year, our revenue declined to $1.9 million, compared to $15 million for the same period last year. As indicated last quarter, our revenue is now derived exclusively from our collaboration with Ono Pharmaceutical and specifically reflects research funding associated with the development of a second product candidate against an undisclosed target in solid tumors. 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 last year, we now account for that program's reimbursable expenses as an offset within our research and development costs. We recognized $2.1 million of contra R&D expense in the quarter. Research and development expenses for the quarter decreased by 57% to $34.3 million. The decrease in our R&D expenses was attributable primarily to a decrease in salaries and benefits, including share-based compensation expense, following the company's restructuring in the first quarter, and from lower clinical trial costs and lower demand for R&D materials and equipment. General and administrative expenses for the third quarter decreased by 12% to $18.9 million. The decline in our G&A expenses was attributable primarily to a decrease in salaries and benefits, including share-based compensation expense. Total operating expenses for the third quarter declined 47% to $53.2 million, which includes $10.1 million of 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-$150 per share. We assess the fair value of these contingent milestone payments, currently valued at $700,000, on a quarterly basis. In the third quarter, we recorded a non-cash $1 million non-operating benefit associated with the change in fair value. Our net loss for the quarter was $45.2 million, or $0.46 per share. Finally, we reiterate guidance for full-year GAAP operating expenses to be in the range of $265 million-$285 million, and that our year-end cash and investments will exceed $300 million. I would now like to open the call for questions. Thank you. If you'd like to ask a question, please press star one, one. If your question has been answered and you'd like to remove yourself from the queue, please press star one one again. Our first question comes from Yigal Nochomovitz with Citi. Your line is open. Hi, guys. This is Ashiq Mubarack on for Yigal. Thanks for taking my questions. I just have a couple. For FT522 in the phase 1, I'm just curious if you think if there's a certain threshold in drop-off in engraftment or maybe activity that you believe would be acceptable between patients who receive preconditioning versus those that don't? Or does there really need to be no drop-off for you to utilize a preconditioning free regimen in future studies? Thanks. Yeah, I don't... I think when we look at the data, I think the data is really gonna be driven by, at the end of the day, patient outcomes and responses. We're definitely interested in understanding the PK profile of FT522, with and without conditioning. And I think that will be help guide dose escalation, but ultimately, I think it's about patient benefit and driving patient benefit, potentially with no conditioning, as that being the important element of FT522, with respect to its unique profile. Okay, understood. We'll just have to see. I guess, for FT825, I know you have the cetuximab combo, but are you also planning to combine with trastuzumab or maybe trastuzumab deruxtecan, given the differences in binding dynamics you showed with SITC? I'm just curious if you think an ADC combo might be something that's actually viable from a safety standpoint, you know, given your comments around the HER2 low opportunity. Thanks. Yes, absolutely. We've started this study with combination with cetuximab, but we certainly think there's opportunity to broaden the clinical profile to include other monoclonal antibodies. There are several that we're looking at. One of those possibly is actually trastuzumab, since there does not appear, at least pre-clinically, to be competition between the binding domains. And in fact, we've actually seen, and I believe we've presented this publicly, we've seen quite nice synergy, in fact, with FT825 and trastuzumab. Okay, great. Thanks very much. Thank you. Our next question comes from Michael Yee with Jefferies. Your line is open. Hi, this is Jenna on for Mike. Thanks for taking our question. We wanted to get your latest take on the landscape. The CD19 CAR T is moving into earlier lines, and there are new players coming to the market, CAR T and going after post-CD19. So in the context of all of that, where do you see the next-gen CAR NK program, CD19, ultimately fit into that landscape? And secondly, are you able to comment on how you're doing on enrollment? Have you enrolled any patients, and how soon you think you may be able to start the no chemo arm? Thank you. Sure. I'm not gonna comment on enrollment other than to reiterate the comments we made on the call, where the study is open for enrollment. We've not announced the first patient. The first no conditioning patient, if you will, that patient could be as enrolled as early as patient 4. We are required to clear the first dose level in the conditioning arm before opening the no conditioning arm. So first, assuming no DLT, the first 3 patients would receive conditioning. ...Then two events can occur simultaneously. Number one, you can dose escalate the conditioning arm as well as open the no conditioning arm. And so the fourth patient could be a no conditioning patient. In terms of the landscape, completely agree. It's a super competitive landscape, and I think there, I think at the same time, there are multiple opportunities that can exist for an off-the-shelf cell therapy. I've talked extensively in the past that I absolutely believe there will be a line of therapy that is of allogeneic or off the shelf, that can exist and will exist post auto CAR T-cell therapy. I think there's significant need that exists, whether it be lymphoma or myeloma, in post-auto CAR T-cell patients. In addition, I think one of the exciting elements of cell therapy, again, to be explored, determined, is the potential, especially with NK cell, is to plug into standard, immunotherapy regimens, for instance, like in a R-CHOP or an earlier line regimen in myeloma. I think those opportunities exist. I think one of the challenges that exists with, whether it be autologous or allogeneic cell therapy, is today, those regimens bring cyflu along for the ride. So if you want to combine with an existing regimen and reach patients early, including in a community setting, one of the hurdles to overcome potentially is cyflu. That's one of the reasons we're very excited about FT522 and ADR and the potential to reduce, significantly reduce the dependency on conditioning and enable a more seamless combination with standard regimens that are used earlier in care in the community. Understood. Thank you very much. Yep. Thank you. Our next question comes from Tyler Van Buren with TD Cowen. Your line is open. Hey, guys. As we think about the next 6-12 months, what will the one or two major value-creating events be in your view? And what should investors expect from them? Yeah, I think the three that I think are worth just noting were on... I highlighted with my comments. I think we have an opportunity to develop, to demonstrate proof of concept with FT522, including in a no cyflu regimen. I think that's it can be a pretty game-changing potential if you can deliver cell therapies without conditioning chemotherapy. And essentially, for all intents and purposes, make a cell therapy look like a monoclonal antibody therapy in terms of how it can be delivered and reach patients. I think that's pretty game-changing if we can demonstrate that with FT522, with the ADR built in and no cyflu. Also very excited about FT825. FT825, as you are probably well aware, there's been a lot of challenges in the solid tumor setting with CAR T cells historically. I think there certainly have been toxicities of note, and I think the activity has been modest, at least compared to hematological malignancies. 825 being an 8-point edited cell therapy and what I'll just sort of consider to be a fine-tuned binding domain against HER2. I think early on in that study, given that we're starting at 100 million cells, we do have the opportunity potentially to show responses, and I think and safely show responses. I think that would be a significant breakthrough with respect to the use of off-the-shelf cell therapies in solid tumors. And then finally, I'll note, and I did note it in our call, moving into autoimmunity, I think, we are one of the first companies to pioneer an off-the-shelf strategy in autoimmunity. I realize we're all sort of beginning this journey at the same time, both autologous and allogeneic. I think the potential to show, for instance, what's been shown with the autologous programs in a small number of patients, that you can durably deplete an aberrant B-cell population, enable reconstitution of the healthy immune system and do that in a durable way, I think could be really powerful. Thank you. Our next question comes from Dana Graybosch with Leerink Partners. Your line is open. Yeah. I wonder if you can talk about for autoimmunity, why start with FT819 rather than going to FT522, and how you think about both of those products and their potential, ultimately in autoimmunity? Yeah, I think the FT819, obviously, and, you know, we've sort of alluded to this, has human clinical experience. To date, has a highly differentiated, what we, we consider to be safety profile. It's readily available off-the-shelf, and, there's certainly strong proof of concept for autologous CAR T-cell therapy. And as you know, we have shown antitumor activity, including complete responses with FT819. So I think there is a very strong rationale for off-the-shelf cell therapy in autoimmunity, and at least in the cancer setting, we've seen all the sort of safety and, and activity hallmarks that we believe can have a differentiated profile in autoimmunity. We've talked about FT522 and potentially the benefits of an NK cell, which again, has an exquisite safety profile in oncology. I think with FT522, there is potentially a broader therapeutic appeal, including, and especially if the ADR technology allows for reduction or elimination of conditioning chemotherapy, which I think is somewhat of a barrier, obviously in autoimmunity, or certainly more so than in oncology. And with FT522, as you know, we have the potential to combine with monoclonal antibody therapy. And I think with FT522, we're looking at, let's call it sort of a broader array of potential autoimmune diseases that we could target, given the multiple mechanisms of action that are built into 522 beyond CD19 targeting. So whether that be, for instance, targeting CD20 with a monoclonal antibody, CD38 with a monoclonal antibody, or potentially even targeting autoreactive 4-1BB expressing T cells. I think the FT522 profile has, the FT522 product candidate has potentially much broader reach than a CD19-targeted cell therapy. Great. Thank you. Thank you. Our next question comes from Michael Schmidt with Guggenheim. Your line is open. Oh, hey, this is Kelsey on for Michael. Thanks for taking our question. I guess specifically for 825 in HER2 solid tumors, I guess, what types of tumors should we expect in the phase one? I guess, what kind of efficacy benchmark are you thinking about as we kind of get those patients in? Thank you. Yeah, I think the efficacy is gonna be judged by the particular patients that we will ultimately enroll. There is a fairly broad enrollment or inclusion criteria in the study. It's not limited to, for instance, HER2 IHC 3. So we can certainly enroll patients that are both high and low expressers of HER2 into that study. Thank you. Our next question comes from Peter Lawson with Barclays. Your line is open. Great. Thank you, Scott. Thanks for the update. Thanks for taking my questions. Just on your solid tumor programs, and circling back on that, what were the learnings from your prior NK cells in solid tumor that kind of rolled over to the current program? So what were the learnings there? And then for your HER2-directed T-cell, where do you think that would fit in the treatment paradigm? Yeah, and so I think, you know, while we've shared some of the data that we've seen in NK cells with solid tumors, in the setting of solid tumors, including CAR NK cells, where with our most recent version in solid tumors with FT536, which was the CAR MICA/B product candidate, we certainly saw activity at 100 million cells per dose. So, I do think there is interesting, interesting activity that we've demonstrated in the past with off-the-shelf cell therapies. I think it would be premature for me to say, comment on, gosh, you know, what, what do we know with respect to an NK cell versus a T cell? I think they're just very different sort of cellular vehicles, if you will. So I don't necessarily think you can extrapolate what we've seen in a small number of patients with NK cells to the sort of T-cell vehicle, if you will. So we don't really do that sort of cross comparison between NK cells versus T cells, especially in a solid tumor setting, and knowing, quite honestly, all the incremental innovation that's built into FT825. Interesting. Then I guess the follow-up question was just on where you think this HER2-directed T-cell would be positioned in a- Yeah, I think it's too early to comment on that. I think, you know, as we look at the HER2 landscape, obviously, you know, what's being demonstrated with the ADCs are pretty remarkable. But I think what we're excited about at the same time is that, you know, again, you know, in a solid tumor settings, patients are relapsing. There's significant unmet need, and I think what we're excited about as well is, you know, there seems to be activity in HER2 expressing tumors that cover a breadth of different types of solid tumors. I think that we're now seeing HER2 starting to become validated, especially if you're able to target HER2 low, not in what you would think of just the traditional setting, for instance, of breast cancer. I think the opportunity for safely targeting HER2 in the solid tumor space is significantly expanding. Great. Thanks so much. Thank you. Our next question comes from Andrea Tan with Goldman Sachs. Your line is open. Hello, this is Talani on for Andrea. Thank you for taking our questions. Firstly, for FT819, would you mind just sharing a bit more about the rationale for choosing lupus as the initial autoimmune indication? And then secondly, if you could provide a bit more details around the clinical trial design for the phase 1 study. Thank you. Yeah, I think the rationale for starting in lupus is there's strong clinical precedent for CD19-targeted therapy, and there's significant enthusiasm from the lupus community in treating patients with cell therapy. So I think it's a terrific place, I think it's a terrific place to start. The trial design, I alluded to on the call, it's, you know, a pretty standard design with respect to a cell therapy that we're seeing, that others are exploring. It's a dose escalation study. We can treat at multiple escalating doses, stepping up at 3 times the previously cleared dose level. Each dose level, well, each and every dose level that clears DLT is able to expand and enroll 10 patients in expansion. So you can explore multiple different dose levels and multiple different expansions, assuming that that dose level has cleared DLT. We are able to enroll patients with lupus nephritis as well as patients with other organ involvement. Thank you. Our next question comes from Yannan Xu with Wells Fargo. Your line is open. Great, thanks for taking our questions. First, on the lupus study for FT819, I was wondering, I think you mentioned that lymphodepletion regimen is standard. I'm wondering, how does it compare with the German group's lymphodepletion regimen? And also, if you- Exactly. It's exactly the same regimen. Great. That's very, very helpful. Thank you. Another question on FT522. For the no lymphodepletion regimen, I was wondering, the 300 million times three, that dose regimen as a starting dose. What's your expectation in terms of, how much T cells can that dose remove? Do you think it's, it could be possible that that's enough to remove all the T cells, or you might need to dose escalate simply on the basis of clearing more T cells as opposed to, optimizing for antitumor activity? Difficult for me to answer that question today. We're certainly going to prioritize translational data in understanding the differences between the doses. Keep in mind that this is not all about, at the end of the day, it's not really about lympho-conditioning through ADR. It's about the ADR technology potentiating the NK cell. And so the mechanism of action is not necessarily here to condition and remove all T cells. Not all T cells express 4-1BB. In fact, only, for instance, the alloreactive T cell compartment is the primary expressor of 4-1BB. So this is not really a lympho-conditioning approach. It's meant to defend the cell from potential forces of rejection. It's also a receptor. It is a CAR against 4-1BB, so it potentiates the NK cell and provides an additional activating signal. At least in preclinical models, we've seen synergistic activity between NK cells and T cells and increased antitumor activity. Got it. That, that's very helpful. And then lastly, in terms of your consideration for FT522 for autoimmune disorders, I was wondering, what might be the catalyst that prompt that decision? Would it be the observation in this cancer study and see how the non-lymphodepletion regimen is doing, or is it something else? Thank you. Yeah, I think the FT522 study in oncology certainly can inform how we design the study in autoimmunity or study in autoimmunity with FT522. I think, quite honestly, at least as I sit here today, I could imagine a study with FT522 in autoimmunity that actually would test something very similar to what we're doing in oncology, plus or minus cyclophosphamide. Got it. Thank you very much. Yep. Thank you. Our next question comes from Etzer Darout with BMO Capital Markets. Your line is open. Great. Thanks for taking the question. Just a question here on the systemic lupus program. Are you generating the preclinical data that, I'm assuming, you've generated, when could we see the data there, if you are indeed generating that type of data? And then ultimately, just trying to get a sense of how you think that the platform here with FT819 compares to sort of some of the emerging data around other assets that are exploring sort of systemic lupus. Thank you. Sure. I mean, there is a slide, there's a slide in our presentation deck or investor deck. It's in vitro, but it does look at... And I'll let Bob talk to it a little bit. It does certainly look at, for instance, the B-cell depletion with both 522 and 819, compares them head-to-head against, for instance, a primary T cell, if I'm not mistaken. Yeah, so our initial study does in fact do that. We've taken samples from healthy patients or healthy donors, SLE patients, and rheumatoid arthritis patients, and we can clearly see very distinct and specific elimination of the B-cell compartment within those three populations. But I would also reference you back to Michel Sadelain, it's a collaboration publication that we've had about a year ago now in Nature Biomedical Engineering, where there's a whole slew of in vitro and in vivo studies showing the durability of the activity of FT819 in targeting B cell. ...And then the final thing that we talked, the other thing that we talked to in the past, which we've not presented yet publicly, but are looking for an opportunity to do that. In terms of clinical proof of concept, we have looked at cohorts of patients in both the 819 oncology study, as well as the prior 596 study in oncology, wherein some of those patients, we were able to detect B cells in those patients at baseline. And we were able to go back and look at, for instance, the kinetics and depth of the cell depletion in patients in oncology receiving 819 or receiving FT596. Great. Thank you for the color. Thank you. And our last question comes from Mara Goldstein with Mizuho. Your line is open. Great, thanks. So I just wanted to go back to the autoimmune question and really maybe to understand, not so much FT819 versus FT522, but FT819 versus the rest of the field of CARs. And it... But and then the other question is, do you think of FT819 as a bridge into looking at other constructs in autoimmune in the same way you went through that process with NKs? Yeah, I think it's, I think it's a little too early to know. I mean, the field is very enthused by the potential of taking cell therapies into autoimmunity. And in a small number of patients, and I would potentially say in a carefully selected number of patients, in some academic studies, we've seen some pretty remarkable results. I think it's really early for the field, and ultimately, what are the therapeutic requirements that best serve patients and induce long-term drug-free remissions, which I think is the excitement in particular about cell therapies. I think we're all gonna learn a lot about that, quite honestly, in the next three, six, 12, 18 months as we explore at least the first versions of autologous and allogeneic CD19-targeted CAR-T cell therapies. Just on the autoimmune study, how many sites are you gonna start in the U.S.? Yeah, we're working through that. I can think one of the strategies, quite honestly, with respect that we have heard, in speaking with folks in the field, is that they, in these early days, they really do like to partner as much as they can with an oncologist that has significant experience in CAR-T cell therapy. And so for us, as you know, we are running the FT819 study in oncology, and I think somewhere between 12-15 sites are open. And so as we think about, you know, how to most effectively get FT819 off the ground in autoimmunity, you know, we're excited to partner with some of those sites as an example, who are very familiar with FT819, are currently enrolling patients and provide that sort of partnering opportunity with the oncologist and the rheumatologist to treat patients. All right. Thanks, Scott. I appreciate it. Sure, sure. Thank you. That concludes the question and answer session. I'd like to turn the call back over to Scott Wolchko for closing remarks. Thank you, and thank you all for participation in today's call. Hope all of you make it out here for ASH in San Diego, and happy to sit down and spend some time with you. Thank you very much. Thank you. This concludes the program. Thank you for your participation. You may now disconnect. Everyone, have a great day.