Welcome to the Fate Therapeutics Fourth Quarter 2022 Financial Results Conference Call. At this time, all participants are on a listen-only mode. This call is being webcast live on the investor section of Fate's website at fatetherapeutics.com. As a reminder, today's call is being recorded. I would like to introduce Scott Wolchko, President and CEO of Fate Therapeutics. Thank you. Good afternoon, thanks, everyone, for joining us for the Fate Therapeutics fourth quarter 2022 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-K for the year ended December 31, 2022 was filed shortly thereafter and can be found on the investors section of our website under financial information. Before we begin, I'd 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, including in our Form 10-K for the year ended December 31, 2022, that was filed with the SEC today. Undue reliance should not be placed on forward-looking statements which speak only as 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 Dr. Wayne Chu, our Chief Medical Officer, Ed Dulac, our Chief Financial Officer, and Dr. Bob Valamehr, our Chief Research and Development Officer. We will focus today's discussion on recent developments that have impacted the company and our employees, including the termination of our collaboration agreement with Janssen, as well as our reduction in headcount and operating expenses to extend cash runway. We will also discuss the outcome of our strategic review of our product candidate pipeline, where we elected to focus our resources on the advancement of our most innovative and differentiated off-the-shelf iPSC-derived CAR-NK and CAR T-cell programs. We will highlight our financial results for the fourth quarter 2022, as well as the key initiatives that we are prioritizing across our programs during 2023. As I highlighted during our last quarterly call in early November, we were poised at that time to achieve several key milestones under our collaborations with ONO and Janssen. Indeed, several days later at the SITC annual meeting, we announced that both ONO and Fate had exercised their respective options to co-develop and co-commercialize FT825, a multiplex engineered CAR T-cell product candidate for solid tumors. This triggered a $12.5 million option exercise payment to Fate from ONO. Under the Janssen collaboration, Fate was authorized by Janssen in November to submit an IND application for a multiplex engineered iPSC-derived CAR NK cell product candidate for the treatment of B-cell lymphoma. That IND was allowed by the FDA in December and triggered a $3 million milestone payment to Fate from Janssen. In addition, Janssen exercised a clinical development and commercialization option for its second antigen target, which triggered a $10 million milestone payment to Fate from Janssen. Given this positive momentum under the Janssen collaboration, we were disappointed to first learn in December that Janssen desired to significantly reduce its 2023 spending under the collaboration, as well as modify certain key financial and intellectual property terms of our agreement. Unfortunately, we were not able to align with Janssen for continuation of our collaboration on revised terms, and Janssen exercised its right to terminate the agreement in early January. As a result, all research and development of collaboration candidates are being discontinued, and we expect to complete the wind down of the collaboration in early April at Janssen's expense. As a consequence of the termination, we were required to significantly reduce our workforce and operating expenses. We also completed a strategic review of our product candidate pipeline and elected to prioritize the company's most innovative and differentiated product candidates having the potential to address large unmet clinical needs. This strategic review resulted in, most notably, the discontinuation of our first generation FT596 CAR NK cell product candidate for the treatment of B-cell lymphoma. While our clinical experience with a three-dose treatment schedule for FT596 was in its early stages. We made the strategic decision to prioritize the advancement of our second-generation CD19-targeted CAR and NK cell program, referred to as FT522. FT522 incorporates five novel synthetic controls of cell function designed to increase NK cell potency, enhance functional persistence, and reduce or eliminate the need to administer conditioning chemotherapy to patients. Taken together, we believe FT522 has the potential to improve safety and clinical benefit, reach patients earlier in care, including in the community setting, and seamlessly combine with standard of care regimens, including those that contain CD20 as well as CD38-targeted monoclonal antibody therapies. Importantly, we also believe the novel synthetic controls integrated into FT522 broaden the program's potential therapeutic application to include both hematologic malignancies and autoimmune disorders. In the first quarter of 2023, we reduced our workforce to approximately 220 employees in order to provide the necessary cash runway to achieve key clinical milestones across our prioritized iPS-derived CAR-NK and CAR T-cell programs. This was an exceptionally difficult and painful step, and we are greatly saddened to have had to move in this direction. Our employees continually demonstrated the highest level of dedication and commitment to our mission. We want to extend our deepest appreciation and wish them great success in the future. We are thankful that many of our employees have already found their next home within the thriving biotechnology communities of San Diego and San Francisco. Before I highlight the key program initiatives that we are focused on for 2023, I would like to turn the call over to Ed to discuss our financial results for 2022 and our expectations for the first quarter of 2023. Thank you, Scott, and good afternoon. Fate Therapeutics is in a strong financial position to advance our prioritized iPSC-derived CAR-NK and CAR T-cell pipeline. Our cash equivalents, and investments at the end of the year, including net receivables from success-based milestones achieved in the fourth quarter, were approximately $475 million. In the fourth quarter of 2022, our revenue derived from our partnerships with Janssen and ONO Pharmaceutical increased significantly to $44.4 million, compared to $17.1 million for the same period last year. We achieved multiple success-based milestones within our collaborations, which resulted in non-recurring revenue in the amount of $25.5 million in the quarter. Research and development expenses for the fourth quarter increased by $17.7 million to $87.2 million, compared to $69.5 million for the same period last year. The increase in our R&D expenses was attributable primarily to increases in employee headcount and compensation, including share-based compensation and expenses associated with license fees and the use of third-party consultants. General and administrative expenses for the fourth quarter increased by $4.7 million to $21.6 million, compared to $16.9 million for the same period last year. The increase in our G&A expenses was attributable primarily to an increase in employee headcount and compensation, including share-based compensation and legal fees. Total operating expenses for the fourth quarter were $108.8 million, which includes $19.4 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-$150 per share. We assess the fair value of these contingent milestone payments currently valued at $3.9 million on a quarterly basis. In the fourth quarter, we recorded a non-cash $5.2 million non-operating benefit associated with the change in fair value. Our net loss for the fourth quarter was $56.4 million or $0.58 per share. As we turn our focus to 2023, I want to share a few thoughts regarding the restructuring we announced on January fifth and how this will impact our GAAP financial results this year. In connection with the termination of the Janssen collaboration in the first quarter of 2023, we expect to recognize as revenue $41.2 million that currently sits on our balance sheet as deferred revenue. Additionally, expenses associated with closeout activities are expected to be reimbursed and will be recognized as revenue in the first quarter of 2023 as well. As previously announced, we have discontinued a number of earlier generation iPSC-derived NK cell programs. While we expect a more focused pipeline to generate significant cost savings and operating leverage, the anticipated cost savings from our reduction in force are not likely to be realized until the second quarter of this year. We expect to incur charges of approximately $12 million-$16 million for severance and other employee termination-related costs in the first quarter of this year. Additionally, we have many patients that remain on study for programs that have been discontinued. This includes patients who were enrolled in our FT516 and FT596 clinical studies and continue to maintain an objective response. We have elected to follow these patients for up to one year to assess durability of response. As a result, costs and support for these studies will dissipate over the course of the year. I would now like to turn the call back to Scott to discuss our key program initiatives for 2023. Thanks, Ed. As we look ahead to 2023, we have focused our operations on advancing our most innovative and differentiated iPSC-derived CAR-NK and CAR T-cell product candidates for patients with cancer and autoimmune disorders. We have substantially reduced our expenses with the intent of providing the necessary cash runway to achieve key clinical milestones across our programs. We are now enrolling multi-dose treatment cohorts with FT576, our multiplexed engineered CAR-NK cell product candidate for multiple myeloma. In addition to its novel BCMA binder, FT576 also incorporates our proprietary high-affinity non-cleavable CD16 Fc receptor, which is designed to augment antibody-dependent cellular cytotoxicity and enable combination with CD38-targeted monoclonal antibody therapy for dual antigen targeting of plasma cells. Importantly, the potential for enhanced clinical activity in combination with a CD38-targeted monoclonal antibody therapy is enabled through the knockout of CD38, which eliminates the possibility of CD38-mediated fratricide. Despite the recent launch of two FDA-approved BCMA-targeted autologous CAR T-cell therapies, we believe an off-the-shelf multi-antigen targeted product candidate that is uniquely designed to synergize with CD38-targeted monoclonal antibody therapy may offer an attractive and differentiated value proposition. At the 2022 ASH annual meeting in December, we presented interim phase I clinical data from the first nine patients treated with a single dose of FT576 as monotherapy and in combination with CD38-targeted monoclonal antibody. Clinical data from the single dose treatment cohorts in heavily pretreated patients showed encouraging clinical evidence of BCMA-targeted activity and a favorable safety profile, indicating the potential for administration in the outpatient setting. In particular, of the three patients treated with a single dose of FT576 in combination with CD38-targeted monoclonal antibody at the first dose level of 100 million cells, one patient achieved a partial response. Notably, translational data from this combination cohort showed rapid and selective depletion of activated host immune cells through the first month of therapy. This suggests that CD38-targeted monoclonal antibody may also serve as a conditioning agent to mitigate the risk of rejection of FT576 and potentially reduce the need for administration of intense conditioning chemotherapy. We are currently enrolling two dose cohorts as monotherapy and in combination with CD38-targeted monoclonal antibody therapy at 300 million cells per dose. Upon clearance, we plan to open and assess three dose treatment cohorts starting at 1 billion cells per dose. In keeping with our commitment to develop highly differentiated product candidates with the potential to address large unmet clinical needs, we are advancing our second-generation CD19-targeted CAR NK cell program, referred to as FT522. Leveraging our unique ability to create multiplexed engineered iPSC lines, FT522 incorporates five novel synthetic controls of cell function designed to increase NK cell potency, enhance functional persistence, and reduce or eliminate the need to administer intense conditioning chemotherapy to patients. Notably, FT522 is the first product candidate to incorporate our proprietary alloimmune defense receptor, or ADR technology. Our synthetic ADR receptor is designed to target 4-1BB expressing activated host immune cells, and upon target engagement to potentiate the cell product via CD3 zeta signaling. Unlike cell engineering approaches that are designed to passively evade the host immune system, which do not obviate the need for intense chemotherapy conditioning to induce cell activation and functional persistence, our proprietary ADR technology is instead designed to feed off of the host immune system to promote its activity. We believe the design of FT522 has the potential to improve safety and benefit, reach patients earlier in care, including in the community setting, and seamlessly combine with standard of care regimens, including those that contain targeted monoclonal antibody therapies. Importantly, we also believe the novel synthetic controls integrated into FT522 broaden the program's potential therapeutic application to include both hematologic malignancies and autoimmune disorders. At the 2022 ASH annual meeting in December, we presented preclinical data demonstrating that ADR-armed iPS-derived CAR NK cells resist host-mediated rejection and in fact expand, persist, and maintain antitumor activity in the presence of alloreactive T cells. These preclinical data provide proof of concept that ADR-armed cell therapies have the potential to persist and induce potent antitumor activity without requiring intense conditioning chemotherapy. We intend to submit an investigational new drug application to the FDA in mid-2023 to commence a phase I study of FT522 in combination with rituximab for the treatment of B-cell lymphoma, including without administration of intense conditioning chemotherapy to patients. We are also particularly interested in expanding our clinical investigation of FT522 beyond oncology to autoimmunity, where recent publications have highlighted the potential of autologous CD19-targeted CAR T-cell therapy to induce drug-free remission in patients with certain severe autoimmune diseases. We believe the specific functional elements integrated into FT522 may have the potential to engage and suppress the broad array of destructive drivers of autoimmune disease pathology, including autoantibody-secreting B cells expressing CD19, autoantibody-secreting plasma cells expressing CD38, and autoreactive and helper T cells expressing 4-1BB. We are also excited with the progress of our iPSC-derived CAR T-cell pipeline for the treatment of hematologic malignancies and solid tumors. Dose escalation is continuing in our landmark phase I study of our FT819 CD19-targeted CAR T-cell product candidate, which to our knowledge is the first ever T-cell product candidate manufactured from a clonal master iPSC line to undergo clinical investigation. FT819 incorporates several first of kind features, including the integration of a novel 1XX CAR construct into the TRAC locus, which is intended to promote uniform CAR expression, balance T-cell activation and exhaustion, and prevent graft-versus-host disease. These patients will require an effective off-the-shelf therapeutic alternative. At the 2022 ASH annual meeting in December, we presented interim clinical data from our ongoing phase I study of FT819, which showed a favorable safety profile and demonstrated objective responses in heavily pretreated patients, including in patients who were not eligible for or had previously failed autologous CD19-targeted CAR T-cell therapy. Of the eight patients with aggressive large B-cell lymphoma treated with a single dose of FT819, ranging from 90 million cells to 360 million cells, two patients were naive to CAR T-cell therapy, one of whom achieved a complete response, and six patients were previously treated with CAR T-cell therapy, two of whom achieved an objective response, including a complete response in a patient with DLBCL previously treated with seven prior lines of therapy and who did not respond to autologous CD19-targeted CAR T-cell therapy. Dose escalation is currently ongoing in single-dose treatment cohorts at 540 million cells in B-cell lymphoma and at 180 million cells in chronic lymphocytic leukemia. Although autologous CAR T-cell therapy has shown significant efficacy in treating hematologic malignancies, its application to solid tumors has been hampered by several factors, including tumor-associated antigen heterogeneity, inefficient CAR T-cell trafficking to the tumor, and an immunosuppressive tumor microenvironment. Our multiplex engineered iPSC-derived CAR T-cell product platform is designed to specifically address these challenges and enable the safe and effective treatment of solid tumors. Under our collaboration with ONO, we are conducting IND-enabling activities for FT825, a multiplex engineered iPSC-derived CAR T-cell product candidate targeting HER2 expressing solid tumors. The product candidate incorporates seven novel synthetic controls designed to enhance effector cell function and overcome unique challenges in treating solid tumors. At the SITC 37th annual meeting held in November, we presented preclinical data of FT825, which highlighted the differentiated targeting profile of the product candidate's novel HER2-targeted binding domain, as well as the functional activity of the product candidate's novel synthetic control, including to promote cell trafficking, redirect immunosuppressive signals in the tumor microenvironment, and induce T-cell activation. We expect to submit an IND application to the FDA in 2023 to commence a phase I study of FT825 for patients with HER2-positive solid tumors under our ONO collaboration. While it certainly has been a difficult two months and these continue to be challenging time for the biotechnology sector, I would like to conclude by thanking the employees of Fate Therapeutics. We are pioneers, the first to develop off-the-shelf iPSC-derived cellular immunotherapy. We are resilient, embracing uncertainty and forging ahead. We remain passionate and committed to leveraging our proprietary iPSC product platform and bringing highly differentiated product candidates to patients with the potential to transform outcomes and change lives. Thank you. I would like to now open the call to any questions. Thank you. Ladies and gentlemen, if you have a question or a comment at this time, please press star one, one on your telephone. If your question has been answered and wish to withdraw yourself from the queue, please press star one, one again. In the interest of time, we ask that you limit yourself to one question, and if you have further questions, feel free to get back in the queue. One moment for our first question. Our first question comes from Tyler Van Buren with Cowen. Your line is open. Hi, guys. This is Tara on for Tyler. I'm just wondering if you guys can tell us when you plan to present the next dataset for FT576 and FT819. Would that be at ASH, or are you thinking of an investor event? Thanks. Thanks for the question. I think it's a little too early for us to commit to the data update around both of those programs. We're currently working with the modified team at Fate Therapeutics to target and focus our enrollment on the dose cohorts that I specifically mentioned during our call. I think in a couple of months, we'll be able to give a specific update with respect to the timeline for our data disclosure, whether that be at ASH or an investor event. Thank you. One moment for our next question. Our next question comes from Yigal Nochomovitz with Stifel. Your line is up. Sorry. With Citi, your line is open. My apologies. Hi, this is Carly on for Yigal. Thanks for taking our question. Well, we wanted to ask about FT576 as well. We just wanted to get your updated thoughts on the competitive positioning. I guess, should we be thinking about the BCMA bispecifics as the bar from an efficacy perspective? You mentioned you've started to enroll in the multi-dose cohort, and I know it's still relatively early, but just curious when you think you may have enough data to really understand the profile and be able to make a go, no-go decision on a registrational pathway. Thanks very much. Sure. Sure. I think, as we've seen with NK cells with our other programs, I think a three-dose schedule of NK cells is going to be important to create the right area under the curve, if you will, with respect to cell load, to most effectively attack the tumors. We are completing a two-dose schedule right now with FT576 as a monotherapy and in combination with CD38 at 300 million cells. Once that dose, those dose cohorts clear, we will move to the three-dose schedule at 1 billion cells per dose. This year, we certainly believe we will be dosing at a more optimized NK cell an optimized treatment schedule for NK cell using three doses and at higher doses. Importantly, we are assessing the potential to combine with daratumumab, which we've seen, at least in early translational data, that we have seen sort of the dampening, if you will, of the alloreactive T-cell compartment, when delivered in combination with the monoclonal antibody. I think in terms of the competitive landscape, look, I think what we've seen so far is that unfortunately in multiple myeloma, there are no curative therapies. There will continue to be patients that will progress through multiple lines of therapy. I think, BCMA is emerging. It appears to be a more durable target. I do think there will be multiple lines of BCMA targeting therapy. That said, I think with an off-the-shelf platform, the full promise of an off-the-shelf platform is to be able to reach patients earlier in care in the community setting where most myeloma patients are treated, and ideally to deliver and plug into a standard monoclonal anti-antibody regimen with CD38 without intense chemotherapy conditioning. Ultimately our objective with FT576 is to develop a highly differentiated product candidate that synergizes with CD38 targeted mAb. It can be delivered early and often to patients as part of a standard chemotherapy regimen. Thank you. One moment for our next question. Our next question comes from Daina Graybosch with SVB Securities. Your line is open. Yeah. I wonder if you could talk a little bit more about the 4-1BB targeted ADR for FT522. You, Fate through several conferences last year, published a lot of other interesting stealth edits, some passive, some active. I wonder why go and prioritize the first clinical program with just ADR versus some of the other edits or a combination of edits. Sure. I mean, I can talk to you at a high level. I mean, there's 3 different programs that we've looked at primarily with respect to, let's just call it sort of an ADR platform. There's the potential to target 4-1BB expressing alloreactive immune cells, which happen to include both T and NK cells, importantly. With 4-1BB, we certainly think we are have the potential to address the complement of host immune cells that may mitigate rejection. Importantly, with that specific ADR technology, it sends a potentiation signal to the cell as well, which we also think is important and differentiated from the passive approaches. The other approaches we've looked at are certainly CD38 on developing a CAR against CD38. We think that's a very interesting approach. Again, similar to the 4-1BB strategy. CD38 will take out or be able to defend the cell against, activated allo-activated, cells, whether they be NK cells or T cells expressing CD38. We think that's a similar type of strategy that we also like, and obviously in the format of a CAR can activate and potentiate the cell, a differentiated approach. The third strategy I'll let Bob talk about, but is this CD54, CD58 knockout, and we think that's an interesting approach, but we think it's primarily interesting in the context of the cell defending itself against an NK cell therapy attack, which we do not think is sort of a prevalent mechanism of rejection, and importantly, it doesn't provide an activating signal in its current form as well. That's right, Scott. Just to follow up what Scott is mentioning, you know, CD54, CD58 knockout comes into play when you're knocking out B2M, and that was an experiment that we worked with our collaborator, Karl-Johan Malmberg, as a solution for a B2M knockout strategy where we feel strategies such as CD47 overexpression or HLA-E come up short. In this perspective, CD54, CD58 does play a role. Just to echo what Scott said earlier about ADR and our current focus is that really, we really believe, as Scott outlined, ADR is a true replacement of Spike Flu. It helps protect against an allo rejection. It helps potentiate, and it also creates space. These are the steps that we believe Spike Flu brings to the table. We feel that ADR is the focus, but other strategies are there, and we will continue to pursue our stealth program in such a manner. Thank you. One moment before our next question. Our next question comes from Michael Yee with Jefferies. Your line is open. Hi, good afternoon. It's Siddharth on for Mike. Just two questions, one on the actual pipeline and the second on financials. On the pipeline, can you kind of let us know what the bar is or what the expectations are on efficacy for both FT576 and FT819? Like, what are you looking for in terms of the bar? Secondly, on the financials, is the $12 million-$16 million going to be just a one-time incurring expense for Q1 and then we expect expenses overall to drop? Talk a little bit about that and the potential for, you know, combination or sequencing of therapies. With respect to the FT576 program, and the bar we're looking for, obviously it's a competitive landscape, and we're trying to develop a differentiated therapy. Part of the differentiation that we're looking to seek is essentially a cellular therapy that can be given in combination with monoclonal antibody therapy, which is used across multiple lines in treating patients with multiple myeloma. The monoclonal CD38-targeted monoclonal antibody therapy may serve as a conditioning agent as well. So we do believe that we can, number one, develop a cell therapy that can plug into standard of care regimen. Number two, because it is an off-the-shelf cell therapy, potentially reach patients earlier and in an outpatient setting. Number three, potentially reduce the intensity of chemotherapy conditioning that is delivered to patients. We do think we can have a very differentiated safety profile and deliver significant clinical benefit to patients. Again, I think that's relevant across lines of therapy as there are no curative therapies for myeloma. With respect to financials, I'll turn it over to Ed. Yeah. The majority of the $12 million-$16 million, as I outlined in my prepared remarks, will occur in the first quarter with respect to severance and other employee termination-related costs. Some of that will be covered by the wind down of the Janssen collaboration as well. That will also be occurring in the first quarter. What remains then is sort of the rhythm of the business afterwards, and as sort of we indicated, while we have discontinued a number of programs, or earlier generation iPSC-derived NK cell programs, we do have follow-up, particularly for patients that are ongoing in response to both FT516 and FT596. We will follow those patients for up to an additional year. That will require both human resources as well as financial resources to do that. A lot of that benefit from a financial leverage perspective, cost savings perspective, will come in the second half of the year and work its way through the remainder of 2023. Thank you. One moment for our next question. Our next question comes from Tazeen Ahmad with Bank of America. Your line is open. Hi, good afternoon. Thanks so much for taking my question. Pretty simple one for me. Should we expect any clinical updates to be presented at medical conferences this year? If so, which of the programs that you've spoken about could be up for updated data this year? Thanks. Sure. I think the guidance that we'll give with respect to data disclosures, we'll probably give that guidance at the May call. We obviously are just getting our feet under us with respect to executing on our FT576 and FT819 studies. I think in the May call, we'll be in a better position to outline the cadence with respect to the data updates for those clinical programs. Thank you. One moment for our next question. Our next question comes from Michael Schmidt with Guggenheim. Your line is open. Hey, good afternoon. This is Yigal for Michael. Thanks for taking our questions. What clinical learnings did you gain from your experience in solid tumors with FT538 and FT536? What type of enhancements do you think will be necessary to be successful in solid tumors? Do you have more confidence in T-cell-based therapies in solid tumors or NK cells after your initial experience? Thank you. Unfortunately, our experience with NK cells in solid tumors is fairly limited. We have dosed patients with both FT538 at low dose levels. We also in combination with monoclonal antibody. We also dosed patients with FT536, a CAR NK cell product, at very low dose levels. We have limited patient experience. I do believe NK cells will play a very important role in solid tumors. We have in the solid tumor experience with our current NK cell programs, we have seen antitumor activity in the clinic. As we've noted, if you look at, for instance, the product candidate FT825, which is a T-cell product candidate, that product candidate in addition to being a T-cell, has additional synthetic controls built into that, which are specifically designed to overcome some of the challenges with solid tumors, namely, for instance, homing and resisting the immunosuppressive signals in the tumor microenvironment. Those features were not built into FT538. They were not built into FT536. They are built into FT825, and we do think they are important features. As I mentioned, I do think that cell therapies can synergize with monoclonal antibodies in attacking solid tumors. I would also note that our FT825 product does include, and is one of the first product candidates that I can think of, does actually include while being a T-cell, it also includes our high affinity non-cleavable CD16 receptor. We do have the potential with our 825 product candidate to actually, through the CAR, target HER2, but also leverage monoclonal antibody content to achieve dual antigen targeting with our T-cell product candidate. In making some of the hard decisions that we were confronted with, we felt like advancing FT825 in solid tumors was the right approach given the specific and additional functionality built into FT825. It wasn't necessarily a decision about NK cells versus T-cells. It was about what we think is a multitude of functionality that is going to be required to successfully have profound impacts in solid tumors. Thank you. One moment for our next question. Our next question comes from Peter Lawson with Barclays. Your line is open. Hey, good afternoon. This is Alex on for Peter. Thanks for taking our question. Just one on the FT576 program here. Do you plan to go to higher than a three-dose treatment regimen? I'm just trying to get a sense for, you know, how you're thinking about the dosing schedule, and if you feel that, you know, the dosing schedule has been explored sufficiently here in this indication, multiple myeloma. Well, certainly, some of the dosing, some of the learnings we are taking from our lymphoma programs, where we have dosed, and typically dosed three doses, from patient one, starting with FT576, sorry, with FT516 in lymphoma. Obviously with FT596, we progressed from one to two to three doses. I think given just sort of the biological sort of properties of NK cells and how they different from T-cells, including their relatively short half-life and their inability to expand like a T-cell would, I think a multi-dose treatment schedule is important. I think in multiple myeloma, we are excited to start the three-dose treatment schedule. We're starting at 1 billion cells. The protocol certainly allows us to continue to dose escalate beyond 1 billion cells. Thank you. One moment for our next question. Our next question comes from Andrea Tan with Goldman Sachs. Your line is open. Good afternoon. Thanks for taking my question. Scott, maybe, just given the profiles you have seen to date with your NK cell programs and what's been going on with your competitors, can you help us understand your level of confidence in this modality? Do you see a scenario where you become solely an iPSC-derived T-cell company instead? Yeah, I think honestly with respect to NK cells, I do think NK cells have significant activity. We've certainly seen that across multiple NK cell programs. I think if you really want to develop a highly differentiated product though, especially in the context of competitive landscapes like lymphoma, like myeloma, you need a unique product offering. That unique product offering, I think, will require sophisticated and multiplexed engineering. I think you will have to include multiple functional elements. I think you will have to potentially deliver multiple mechanisms of action. I think you potentially will, ideally, with an off-the-shelf cell therapy, will need to begin to differentiate one of the modes of differentiation, as well as moving away from intense chemotherapy conditioning. With an off-the-shelf cell therapy, the promise of an off-the-shelf cell therapy is to reach patients early and often in care. With an NK cell therapy, I do think it has a unique and differentiated safety profile, which allows you to reach into the community setting. I. I do think you need to. That will require a multiplexed engineered solution, and it will require the delivery of multiple mechanisms of action. At the highest level, there's some of the decisions that we made to favor our multiplex engineered product candidates that can synergize and combine with monoclonal antibody that can be given earlier in care, and that potentially do not require intense chemotherapy conditioning as part of the treatment regimen. Thank you. One moment for our next question. Our next question comes from Benjamin Burnett with Stifel. Your line is open. Hi, good afternoon. This is Karina on for Ben Burnett. Thank you for taking our question. With regard to your next-gen CD19 CAR-NK cell program, FT522, what gives you confidence on the level of translation of the enhanced anti-tumor activity and persistence you've observed with your ADR technology and the clinical studies? Yeah, I mean, the benefit, one of the benefits that we have, again, it's preclinical data, one of the benefits we have is that, you know, an iPSC platform allows you to create very homogeneous, consistent product. We are able to race multi-generation product candidates against each other. For instance, FT516, FT596, FT522. We can do literally head-to-head studies of multiple different product candidates against each other. I think part of the confidence, as I mentioned, when we had to make the difficult decision with respect to FT596, we had very limited clinical data with a three-dose schedule at higher dose levels. I think one of the, essentially what gave us confidence, though, in addition to we think we need obviously to compete in a competitive landscape, you need a highly differentiated product candidate, and we think FT522 has some very unique features that allow for that differentiation. Certainly all the preclinical experimentation we've done over the past 18 months, racing FT516 against FT596 against FT522 in some very difficult and stringent models, including models that are designed to promote alloreactivity, really gave us the confidence to make the decision in advancing FT522. I don't know, Bob, do you have anything to add to that? No, that's right, Scott. I mean, if you split it between potency and avoidance of rejection, on the potency front, FT522 leverages the FT538 backbone, which FT596 did not. On the survival factor of an allo environment, as Scott mentioned, ADR gives you a unique ability that other NK cells don't have. Thank you. One moment for our next question. Our next question comes from Robyn Karnauskas with Truist. Your line is open. Hi, this is Bill On for Robin. Do you envision the possibility of bolstering a competitive edge in multiple myeloma in the near term by using both FT576 and FT819 to clear out plasma cells and any CD19 positive progenitor cells while harnessing the best of both worlds? We absolutely have preclinical models where we've combined NK cells and T cells. We're not prepared to discuss publicly our strategy for first launching combinations of NK cells and T cells. I do think there's significant value in being able to, let's just say, unite innate and adaptive immunity. It is a strategy, for instance, that we've embedded into, for example, FT825, where we've engineered the high affinity CD16 receptor into the backbone of a T cell. I would say based on our experimentation pre-clinically, we certainly are excited about the potential to unite an innate and adaptive immunity. We think there's multiple ways to accomplish that. Certainly given the off-the-shelf nature of our product candidates, creating, a defined composition of both cell types or delivering, for instance, a T cell followed by an NK cell or vice versa, both are strategies that I think we can pursue. Thank you. One moment for our next question. Our next question comes from Mara Goldstein with Mizuho. Your line is open. Great. Thanks so much for taking the question. Just, I had a question on FT819, and not so much on FT819, but really kind of the state of the world right now and given what we're seeing from data and registration with respect to bispecifics and how you think about advancing FT819. Then just on FT522, can you talk a little bit about what the, you know, with, how, what the rate limiting issues are there for getting for initiating an autoimmune program? Sure. With FT819, to begin with, look, it's the first iPSC-derived CAR T-cell, period. I think it's really important for us to advance that product candidate and understand its potential. Are we truly making iPSC-derived CAR T-cells? What does the activity level look like? Obviously, we have a very nimble and versatile platform which we can improve upon shortcomings, whether that be for hematologic malignancies or solid tumors. Mm-hmm. Understanding the activity level of FT819, I think is really important. That said, like I said, I absolutely believe that there will continue to be room for efficacious CD19 targeted therapies. Absolutely. Even in the face of engagers. I mean, we don't know, fully appreciate the sequence of events or sequencing of treatments, for instance, that will exist in the lymphoma space. We may find, and there's early data coming out in other areas, that bispecific engagers, when delivered aggressively into progression, cause, for instance, an exhaustion in a T-cell compartment over time. That may not bode well for an autologous CAR T-cell therapy and a off-the-shelf T-cell therapy may be required for those patients. We also know, for instance, that, we have seen, as you know, I mean, most of the patients we treated in our phase I study are actually post-CAR T-cell therapy. We certainly have looked at those patients at baseline, CD19 expression, and we've seen responses downline of patients that have been previously treated with CAR T-cell therapy. I continue to believe that a, that a safe and effective off-the-shelf CD19 targeted therapy will absolutely have its place. We need to understand what the potential for FT819 is in that context, as well as inform the development of our platform and other product candidates. I definitely committed to FT819. That, and that understanding. As it relates to FT522, our first commitment with FT522 is to file an IND in the space of B-cell lymphoma and combined with Rituximab. I do not believe we will need to wait for significant clinical data in oncology to move into autoimmunity. From our perspective, you know, it may be a pathway where we treat a couple patients, establish safety of the novel ADR receptor and its ability to function and then move into autoimmunity. Thank you. One moment. I think there's, just to finish, I think there's a unique opportunity in autoimmunity with FT522. I think FT522 could provide three axes of attack, essentially against the pathogenesis. We can absolutely target CD19 cell. Keep in mind,FT 522, because it has the CD38 knockout, can be combined with Daratumumab in order to target plasma cells. Then the 4-1BB ADR technology is actually really unique when it comes to the potential for autoimmunity because it can target, it will target, and it can actually eliminate autoreactive and T helper cells. We think there's potentially a really unique three-pronged attack with the FT522 product in autoimmunity. Thank you. One moment for our next question. Our next question comes from Matt Biegler with Oppenheimer. Your line is open. Hey, guys. Scott, any plans on disclosing the remaining five nine six and/or five one six data? I think you mentioned in the past that you thought the data were either compelling or competitive. Just kind of wanted to get your thoughts on that time. Yeah. I mean, we are gonna work with the investigators of the study. I think there's desire on the part of the investigators to complete the study and potentially publish the results. I think as Ed alluded to, we did make the decision to keep following patients in the FT516 and FT596 studies, because we do have patients that are continuing in response. Yes, I do think we are, we internally at Fate are not going to prioritize essentially the FT516 and FT596 sort of data wind up and then presentation. We will absolutely work with investigators to enable that. I think we will wait until all patients have reached the one-year follow-up, since we've committed to follow patients for one year to get a sense of durability response. Thank you. I'm not showing any further questions at this time. I'd like to turn the call back over to Scott Wolchko for any closing remarks. Great. Thank you all for your participation in today's call. Be well. Ladies and gentlemen, this concludes today's presentation. You may now disconnect and have a wonderful day.