Welcome to the Fate Therapeutics Fourth Quarter 2022 Financial Results Conference Call. At this time, all participants are in a listen-only mode. This 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 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 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 the market today as well as the risk factors included 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 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 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. Finally, we will highlight our financial results for the fourth quarter of 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 multiplexed 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 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 that novel synthetic controls integrated into 522 broaden the program’s potential therapeutic application to include both hematologic malignancies and autoimmune disorders. In the first quarter of 2023, we have reduced our workforce to approximately 220 employees in order to provide the necessary cash runway to achieve key clinical milestones across our prioritized iPSC-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 and 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, 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 sublicense 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 are $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 to $150 per share. We assessed 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 5 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 a 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 to $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 the 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. And 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 multiplex 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 1 clinical data from the first nine patients treated with a single dose of FT576 as monotherapy and in combination with a 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 rolling 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 one 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 CD90 targeted CAR NK cell program, referred to as FT522. Leveraging our unique ability to create multiplex 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 leverage 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 integrate with standard of care regimens, including those that contain targeted monoclonal antibody therapies. Importantly, we also believe the novel synthetic controls integrated into 522 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 iPSC-derived CAR NK cells resist host mediated rejection, and in fact, expand, persist and maintain anti-tumor 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 anti-tumor 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 1 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 targeting CAR T-cell therapy to induce drug-free remission in patients with certain severe autoimmune diseases. We believe this specific functional element integrated into 522 may have the potential to engage and suppress the broad array of destructive drivers of autoimmune disease pathology, including auto-antibody secreting T cells expressing CD19, auto-antibody secreting plasma cells expressing CD38, and autoreactive and helper T-cells expressing 4-1BB. We are also excited about the progress of our iPS-derived CAR T-cell pipeline for the treatment of hematologic malignancies and solid tumors. Dose escalation is continuing in our landmark Phase 1 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. We continue to believe a meaningful portion of the B-cell malignancy patient population will be unfit for autologous CAR T-cell therapy for numerous reasons, whether that be due to logistical barriers, prior therapy or disease aggressiveness, and these patients will require effective off-the-shelf therapeutic alternatives. At the 2022 ASH Annual Meeting in December, we presented interim clinical data from our ongoing Phase 1 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 naïve 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 cell 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 and efficient CAR T-cell trafficking to the tumor and an immunosuppressive tumor microenvironment. Our multiplexed engineered iPS-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 on a multiplexed engineered iPS-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 1 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 continued to be challenging times 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. And 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. Our first question comes from Tyler Van Buren with Cowen. Your line is open.

Hi, guys. This is Cara on for Tyler. So just wondering if you guys can tell us when you plan to present the next dataset for 576 and 819. Would that be at ASH or you thinking 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 are 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 will be able to give a specific update with respect to the timeline for a data disclosure, whether that be at ASH or an investor event.

Our next question comes from Yigal Nochomovitz with Citi. Your line is open. My apologies.

Hi, this is Carly on for Yigal. Thanks for taking our questions. 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 of the bar from an efficacy perspective? And you mentioned you started to enroll in the multi-dose cohorts 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 have 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. And so 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. So this year, we certainly believe we will be dosing at a more optimized NK cell – optimized treatment schedule for NK cells using three doses and at higher doses. Importantly, we are assessing the potential to combine with daratumumab which we have seen released in early translational data that we have seen sort of the dampening if you will of the alloreactive T-cell compartments when delivered in combination with the monoclonal antibody. I think in terms of the competitive landscape, look, I think what we have 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 the BCMA is emerging. It appears to be a more durable target. So I do think there will be multiple lines of BCMA targeting therapy. That said, I think what's unique about an off-the-shelf platform is the promise of being able to reach patients early on in care in the community setting, where most myeloma patients are treated and ideally to deliver and plug into a standard monoclonal antibody regimen with CD38 without intense chemotherapy conditioning. And so ultimately, our objective with 576 is to develop a highly differentiated product candidate that synergizes with CD38-targeted monoclonal therapy that can be delivered early and often to patients as part of the standard chemotherapy regimen.

Thank you. Our next question comes from Daina Graybosch from SVB Securities. Your line is now open.

Yes, I wonder if you could talk a little bit more about the 4-1BB targeted ADR for FT522, you say through several conferences last year published a lot of other interesting stealth edits, some passive, some active. And 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 at a high level, I mean, there are three different programs that we have looked at primarily with respect to, let’s just call it, sort of an ADR platform. There is the potential to target 4-1BB expressing alloreactive immune cells, which happened to include both T and NK cells, importantly. And so, 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 that 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 have 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 alloreactive cells, whether they be NK cells or T cells expressing CD38. So 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 in a differentiated approach. The third strategy, I’ll let Bob talk about that is the CD54 CD58 knockout and we think that’s an interesting approach. So 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. Importantly, it doesn’t provide an activating signal in its current form as well.

That’s right, Scott. Just to follow up on what Scott is mentioning, 54/58 knockout comes into play when knocking out B2M and that was an experiment that we worked with our collaborator, who serves as the solution for our B2M knockout strategy where we feel strategies such as CD47 overexpression or HLAE come up short. So in this perspective, 54/58 does play a role, but just to echo what Scott said earlier about ADR and our current focus is I really, really believe, as Scott outlined, ADR is a true replacement of Cy/Flu. It helps protect against allorejection. It helps potentiate and also create space. And these are the steps that we believe Cy/Flu brings to the table. And so we feel that ADR is the focus, but other strategies are there and we will continue to pursue our self-program in such a manner.

Thank you. Our next question comes from Michael Yee with Jefferies. Your line is open.

Hi, good afternoon. It's someone on for Mike. I have two questions, one regarding the actual pipeline and the other about financials. For the pipeline, could you share the expectations for efficacy for both 576 and 819? What benchmarks are you aiming for? Secondly, regarding financials, will the $12 million to $16 million be a one-time expense for Q1, and can we expect overall expenses to decrease afterwards? Please discuss this and the potential for combining or sequencing therapies.

Yes. With respect to the 576 program and the bar we are looking for, obviously, it’s a competitive landscape. And we are trying to develop a differentiated therapy. Part of the differentiation that we are 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. And so we do believe that we can, number one, develop a cell therapy that can plug into a standard of care regimen. Number two, because it is an off-the-shelf cell therapy, potentially reach patients earlier and in an outpatient setting. And number three potentially reduce the intensity of chemotherapy conditioning that is delivered to patients. So we do think we can have a very differentiated safety profile and deliver significant clinical benefit to patients. And again, I think that’s relevant across lines of therapy as there are no curative therapies for myeloma. With respect to financial, let’s turn it over to Ed.

Yes, the majority of the $16 million, as I outlined in 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. So 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 this continued 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. And so 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. So, 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. 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? And if so, which of the programs that you have spoken about could be up for updated data this year? Thanks.

I think the guidance that we will give with respect to data disclosures, we will probably give that guidance at the May call. We obviously are just getting our feet under us with respect to executing on our 576 and 892 studies. And so I think in the May call, we will be in a better position to outline the cadence with respect to the data updates for those clinical programs.

Thank you. Our next question comes from Michael Schmidt with Guggenheim. Your line is open.

Good afternoon. This is on for Michael. Thank you for taking our questions. What insights did you gain from your experience with solid tumors in the 538 and 536 studies? What improvements do you believe are necessary for success in treating solid tumors? Additionally, do you have greater confidence in T-cell based therapies or NK-cells in solid tumors following your initial experience? Thank you.

So, 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. And we have limited patient experience. I do believe NK-cells will play a very important role in solid tumors. We have – in any solid tumor experience with our CAT NK-cell programs we have seen anti-tumor activity in the clinic, but as we have 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 were 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. And I would also note that our FT825 product dose include and is one of the first five candidates that I can think of does actually include while being a T-cell, it also includes our high affinity non-cleavable, CD16 receptor. So, 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. So, 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 is about what we think is a multitude of functionality that is going to be required to successfully have profound impacts in solid tumor.

Thank you. 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 576 program here, do you plan to go to higher than a three-dose treatment regimen? And I am just trying to get a sense for how you are thinking about the dosing schedule. And if you feel that, the dosing schedule has been explored sufficiently here in this indication, multiple myeloma?

Well, certainly in 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 576, sorry, with 516 in lymphoma, and obviously, with 596, we progressed from one to two to three doses. I think given just sort of the biological properties of NK-cells and how they are different from T-cells, including their relatively short half life, and their inability to expand like a T-cell, I think a more high-dose treatment schedule is important. And I think in multiple myeloma, we are excited to start the three-dose treatment schedule. We are starting at one billion cells, and the protocol certainly allows us to continue to dose escalate beyond one billion cells.

Thank you. 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 would become solely an iPSC derived T-cell company instead?

Yes. I think honestly, with respect to NK-cells, I think what we have learned is that if you again, I do think NK-cells have significant activity. We have 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 and 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. And I think you potentially will, ideally with an off-the-shelf cell therapy need to begin to differentiate one of the modes of differentiation as well as moving away from intense chemotherapy conditioning. To the 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 unique and differentiated safety profile, which allows you to reach into the community setting. But I do think you need to – that will require a multiplexed engineered solution. And it will require the delivery of multiple mechanisms of action. And at the highest level, there are some of the decisions that we need to favor our multiplexed engineered product candidates that can synergize and combine with monoclonal antibodies that can be given earlier in care, and that potentially do not require intense chemotherapy conditioning as part of the treatment regimen.

Thank you. Our next question comes from Ben Burnett with Stifel. Your line is open.

Hi. Good afternoon. This is Karolina on for Ben Burnett. Thank you for taking our question. With regard to your next-gen CD19 CAR NK-cell program FT522 will give you confidence on the level of translation of the enhanced anti-tumor activity and persistence you have observed with your ADR technology and preclinical studies.

Yes. I mean the benefits – learner benefits that we have and again, it’s preclinical data. But one of the benefits we have is that an iPSC platform allows you to create very homogeneous consistent product. And so we are able to raise multi-generation product candidates against each other for instance, 516, 596, 522. We can do literally head-to-head studies of multiple different product candidates against each other. And I think part of the confidence, as I mentioned, when we had to make the difficult decision with respect to 596, 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 522 has some very unique features that allow for that differentiation. But certainly all the preclinical experimentation we have done over the past 18 months, raising 516 against 596, against 522 in some very difficult and stringent models, including models that are designed to promote our reactivity, really gave us the confidence to make the decision in advancing 522. I don’t know, Bob, if you have anything to add to that?

No. That’s right, Scott. I mean if you split it between potency and avoiding cell rejection. On the potency front, 522 leverages the 538 backbone, which 596 did not. And then on the survival factor of an allo environment as Scott mentioned, ADR gives you it a unique ability that other NK cells don’t have.

Thank you. 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 your competitive edge in multiple myeloma in the near term by using both 576 and 819 to clear up plasma cells and CD19 progenitor cells while harnessing the best in both?

So, we absolutely have preclinical models where we have combined NK-cells and T-cells. We are not prepared to discuss publicly our strategy for first launching combinations of NK-cells and T-cells. I do think there is significant value in being able to, let’s just say unite, I mean adaptive immunity. And it is the strategy for instance, that we have embedded into, for example, FT825, where we have combated – where we have engineered the high affinity CD16 receptor into the backbone of the T-cell. So, I would say based on our experimentation preclinically, we certainly are excited about the potential to unite and innovate in adaptive immunity. We think there are multiple ways to accomplish that. But certainly given the off-the-shelf nature of our product candidates, creating a defined composition of both cell types, we are delivering for instance, a T-cell followed by an NK-cell vice versa. Both are strategies that I think we can pursue.

Thank you. Our next question comes from Mara Goldstein with Mizuho. Your line is open.

Great. Thanks so much for taking the question. Just, I have a question on FT819 and not so much on 819, but really kind of the state of the world right now. And given what we are seeing from data and registration, with respect to bispecifics, and how you think about advancing 819. And then just on FT522, can you talk a little bit about what the rate limiting issues that are there for getting – for initiating an autoimmune program?

So, with 819 to begin with, look, it’s the first iPSC derived for T-cells. 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, where 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. So, understanding the activity level of 819, I think it is really important. That said, like I said, I absolutely believe that there will continue to be room for efficacious CD19 targeted therapies. Even in the phase of engagers, I mean we don’t fully appreciate the sequence of events, or sequencing of treatments, for instance, that will exist in the lymphoma space. We may find that there is already data coming out in other areas that bispecific engagers, when delivered aggressively into progression, CAR is for instance, and exhaustion on the T-cell compartment over time. That may not bode well for an autologous CAR T-cell therapy, and off the shelf T-cell therapy may be required for those patients. We also know for instance that and we have seen as you know, most of the patients we treated in our Phase 1 study are actually post-CAR T-cell therapy. And we certainly have looked at those patients that baseline CD19 expression. We have seen responses, down line of patients that have been previously treated with CAR T-cell therapy. So, I continue to believe that a safe and effective off-the-shelf CD19 targeted therapy will absolutely have its place. And 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, so definitely committed to 819 and that understanding. As it relates to 522, look 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. And so from our perspective, it may be a pathway where we treated a couple of patients, established safety of the novel ADR receptor and its ability to function and then move into autoimmunity.

Thank you.

I think there just to finish, I think there is 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. So, keep in mind 522 because it has the CD38 knockout, can be combined with daratumumab in order to target plasma cells. And 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 alloreactive and T helper cells. So, we think there is potentially a really unique three-pronged attack with the FT522 product in autoimmunity.

Thank you. Our next question comes from Matthew Biegler with Oppenheimer. Your line is open.

Oh, hey guys. Scott, any plans on disclosing the remaining 596 and/or 516 data because I think you mentioned in the past that you thought the data were either compelling or competitive? So, just kind of want to get your thoughts on that. Thanks.

Yes. I mean we are going to work with the investigators on the study. I think there is – I think there is desire on the part of these 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 516 and 596 studies because we do have patients that are continuing in response. And so yes, I do think we internally at Fate are not going to prioritize the 516 and 596 data windup and then presentation, but we will absolutely work with investigators to enable that. I think it’s – I think we will wait until all patients have reached the one-year follow-up since we have committed to follow patients for one year to get a sense of durability responses.

Thank you. I am not showing any further questions at this time. I will turn the call back over to Scott Wolchko for any closing remarks.

Thank you all for your participation in today’s call. Do well.

Ladies and gentlemen, this does conclude today’s presentation. You may now disconnect and have a wonderful day.