Welcome to the Fate Therapeutics third quarter 2021 financial results conference call. At this time, all participants are in 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 third quarter 2021 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, 2021 was filed shortly thereafter and can be found on the Investors section of our website under Financial Information. Before we begin, I would like to remind everyone that except for statements of historical facts, the statements made by management and responses to questions on this conference call are forward-looking statements under the Safe Harbor provisions of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements. Please see the forward-looking statement disclaimer on the company's earnings press release issued after the close of market today, as well as the risk factors included in our Form 10-Q for the quarter ended September 30, 2021 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 Senior Vice President of Clinical Development, Ed Dulac, our Chief Financial Officer, and Dr. Bob Valamehr, our Chief Research and Development Officer. Today, we will highlight our clinical progress over the past several months with our off-the-shelf iPSC-derived NK cell programs and discuss our plans to share clinical and preclinical data from certain of these programs in connection with the Society for Immunotherapy of Cancer Annual Meeting in mid-November and the American Society of Hematology Annual Meeting in mid-December. Beginning with our B-cell Malignancy Franchise, autologous CAR T-cell therapies targeting CD19 have delivered remarkable results for patients with relapsed/refractory B-cell lymphomas. However, there remains a significant need to develop off-the-shelf cell-based cancer immunotherapies that can bring transformative outcomes to more patients. Over the past several months, we have made significant clinical progress in advancing our FT516 and FT596 product candidates, including expanding clinical investigation of these off-the-shelf iPSC-derived NK cell programs to broader patient populations. We continue to be very pleased with the early clinical data we have observed from our phase I studies of FT516 and FT596 in relapsed/refractory B-cell lymphoma, where interim clinical data have shown the potential to drive response rates that are comparable to those achieved with autologous CAR T-cell therapies while maintaining a substantially differentiated safety profile that not only supports administration in outpatient setting without requiring hospitalization, but may also enable combination with standard of care treatment regimens used in earlier line community settings. FT596 is our off-the-shelf iPSC-derived CAR NK cell product candidate designed to target multiple B-cell antigens, both through its CD19-targeted chimeric antigen receptor and through its high-affinity non-cleavable CD16 Fc receptor in combination with tumor-targeting antibodies. In our dose-escalating phase I study, FT596 is being assessed as monotherapy as well as in combination with rituximab, a multi-antigen targeting approach that we believe may hold best-in-class potential in addressing tumor heterogeneity and antigen escape. In August, we announced that as of the data cutoff date of June 25, 2021, 10 of 14 patients treated with a single dose of FT596 achieved an objective response, including seven patients that achieved a complete response in the second and third dose cohorts of 90 million cells and 300 million cells, respectively. Importantly, four of these 14 patients had previously been treated with autologous CD19 CAR T-cell therapy, two of whom achieved a complete response with a single dose of FT596 in combination with rituximab. Treatment with FT596 was well-tolerated and showed a differentiated safety profile to that commonly observed with CAR T-cell therapy. With only two reported low-grade adverse events of cytokine release syndrome and no reported adverse events of immune effector cell-associated neurotoxicity or graft-versus-host disease. We have now enrolled approximately 30 total patients in the second, third, and fourth single-dose cohorts of 90 million cells, 300 million cells, and 900 million cells, respectively. Earlier today, we announced that updated clinical data from our FT596 phase I study will be featured in an oral presentation at ASH on Monday, December 13. The presentation is expected to cover safety, tumor response, and duration of response for all patients treated through the third single-dose cohort of 300 million cells as monotherapy and in combination with rituximab. In addition, we plan to hold an investor event on Tuesday, December 14, to further supplement the ASH presentation, where we expect to present safety and tumor response data for those patients treated in the fourth single-dose cohort of 900 million cells. We continue to believe that one significant advantage of off-the-shelf cell therapy is the potential to deliver multiple doses over multiple cycles, and that such a treatment paradigm will confer best-in-class outcomes for patients. To that end, having observed that a single-dose treatment cycle of FT596 was well-tolerated with no dose-limiting toxicities, we have now increased the frequency of FT596 dosing and initiated enrollment of a two-dose treatment cycle, with FT596 administered on day one and day 15 at 300 million cells per dose, with the potential to dose escalate to 900 million cells per dose. Patients showing clinical benefit following the first two-dose treatment cycle are eligible to receive a second two-dose treatment cycle. Additionally, based on the positive interim clinical data we have observed with FT596 in relapsed/refractory B-cell lymphoma, we have broadened our clinical investigation of FT596 to include treatment of other B-cell malignancies in our ongoing phase I study. I'm pleased to announce that we have initiated enrollment of FT596 in combination with obinutuzumab for the treatment of patients with relapsed/refractory CLL and have treated the first patient at 30 million cells per dose. Turning to FT516. In August, we also announced positive interim clinical data as of the data cut-off date of July 7, 2021 from our dose-escalating phase I study of FT516 in combination with rituximab for the treatment of relapsed/refractory B-cell lymphoma. Eight of 11 patients achieved an objective response, including six patients that achieved a complete response in the second and third multi-dose cohorts of 90 million cells per dose and 300 million cells per dose on day 29 of the second FT516 treatment cycle. Five of the 11 patients maintained their response without further therapeutic intervention, with follow-up ongoing at between four point six and nine point five months, indicating that FT516 has the potential to drive durable responses. The observed safety profile of FT516 was favorable and is differentiated from that of T-cell-based therapies. No FT516-related serious adverse events or FT516-related Grade 3 or greater adverse events were observed. No events of any grade of cytokine release syndrome, immune effector cell-associated neurotoxicity, or graft-versus-host disease were reported. We have now completed the dose escalation stage of our FT516 phase I study, having enrolled seven patients in the fourth multi-dose cohort of 900 million cells per dose. Earlier today, we announced that updated clinical data from our FT516 phase I study will be featured in a poster presentation at ASH on Monday, December 13. The presentation is expected to cover safety, tumor response, and duration of response for all 18 patients treated at the second, third, and fourth multi-dose cohorts. In addition, we plan to further supplement the ASH presentation with updated FT516 data at our investor event on Tuesday, December 14. Having completed dose escalation, we have now initiated dose expansion at 900 million cells per dose to further assess the clinical activity of FT516 and are intending to enroll patients into three disease-specific cohorts, including one, third-line diffuse large B-cell lymphoma in patients that are naive to autologous CD19 CAR T-cell therapy, number two, third-line follicular lymphoma in patients that are naive to autologous CD19 CAR T-cell therapy, and three, patients with relapse refractory B-cell lymphomas whose disease has progressed following autologous CD19 CAR T-cell therapy. We believe assessing the clinical activity of FT516 in patients whose disease has progressed following autologous CD19 CAR T-cell therapy addresses a growing market segment with significant unmet need and may offer a potential fast-to-market development opportunity. In addition, because FT516 may be administered in the outpatient setting and given its favorable safety profile observed to date, we have also initiated dose expansion of FT516 in combination with bendamustine and rituximab and without Cy/Flu chemotherapy conditioning to explore its potential to combine with standard of care CD20-targeted regimens that are used in earlier line community settings. Importantly, in these four dose expansion cohorts, we intend to include sites that serve patients in the community setting. Turning to our Multiple Myeloma Disease Franchise, I'm pleased to announce that we have treated the first patient in our dose escalating phase I study of FT538 in combination with CD38-targeted monoclonal antibody daratumumab. Our FT538 product candidate builds off of our FT516 backbone and is engineered with three functional components to optimize innate immunity. In addition to a novel high-affinity non-cleavable CD16 Fc receptor, FT538 incorporates an IL-15 receptor fusion and the deletion of the CD38 gene. In preclinical studies recently published in the peer-reviewed journal Cell Stem Cell, we showed that FT538 exhibits enhanced serial killing, antibody-dependent cellular cytotoxicity, and functional persistence compared to peripheral blood NK cells. The superior antitumor activity of FT538 was attributable to the biological effects of its novel IL-15 receptor fusion and CD38 knockout, which were shown to improve metabolic fitness, increase resistance to oxidative stress, and induces a protein expression program that enhanced NK cell activation and effector function. The phase I study of FT538 is designed to assess three once-weekly doses in combination with daratumumab for the treatment of relapsed/refractory multiple myeloma. The first patient was treated at 100 million cells per dose. Similar to our approach in lymphoma, where we are developing FT516 and FT596, we have further modified our FT538 product candidate to create FT576. Our off-the-shelf iPSC-derived CAR NK cell product candidate designed to target multiple antigens, both through its high avidity BCMA-targeted chimeric antigen receptor and its high-affinity non-cleavable CD16 Fc receptor. We have initiated enrollment in our dose-escalating phase I study of FT576 to assess both single-dose and multi-dose treatment regimens as monotherapy, as well as in combination with daratumumab, an approach that enables targeting of both BCMA and CD38 antigens, which we believe may hold best-in-class potential for the treatment of multiple myeloma. Patient dosing will begin with FT576 as monotherapy in the single-dose treatment cohort at a dose of 100 million cells. Turning to our AML disease franchise, we continue to be excited about the potential of iPSC-derived NK cell therapies to play a foundational role in the treatment of patients with AML. We are encouraged by our initial phase I clinical data from our FT516 and FT538 programs, which have indicated that iPSC-derived NK cells are well-tolerated and can induce objective responses with complete clearance of leukemic blasts from the bone marrow. Importantly, these clinical outcomes were achieved with iPSC-derived NK cells administered off-the-shelf, and in the outpatient setting. Over the past three months, we have made significant strides in opening our dose-escalating phase I study of FT538 at additional clinical sites, and our rate of enrollment has accelerated accordingly. We have now enrolled approximately 10 patients with relapsed/refractory AML in the first and second multi-dose cohorts of 100 million cells per dose and 300 million cells per dose, respectively. No dose-limiting toxicities have been reported, and treatment with FT538 continues to be well-tolerated. We have also commenced enrollment in an investigator-initiated phase I clinical trial of FT538 in combination with daratumumab in patients with relapsed/refractory AML. A therapeutic strategy designed to exploit the product candidate's proprietary high-affinity non-cleavable CD16 receptor and CD38 knockout to recognize, bind, and kill leukemic blasts expressing CD38 through antibody-dependent cellular cytotoxicity. We have also completed the dose escalation stage of our FT516 phase I study in relapsed/refractory AML, having enrolled seven patients in the third multi-dose cohort of 900 million cells per dose. The maximum tolerated dose of FT516 was not established, and treatment with FT516 was well-tolerated. We will look to provide an update on our FT516 and FT538 programs in relapsed/refractory AML as we generate additional dose escalation data with FT538, including duration of response, so we're able to fully compare the safety, anti-leukemic activity, and durability of response of both programs. Turning to our Solid Tumor Franchise. We are looking forward to the SITC conference next week, where our FT536 CAR NK cell program will be featured in an oral presentation. FT536 is our off-the-shelf multiplexed engineered iPSC-derived NK cell product candidate that incorporates a novel CAR targeting the alpha-3 domain of the pan-tumor-associated stress antigens MICA and MICB. IND-enabling preclinical data for FT536 will be presented on Saturday, November 13, and will highlight the novel binding domain of FT536, which is specifically designed to overcome tumor escape mechanisms mediated by loss of MHC class I expression and by shedding of MICA, MICB. We expect to submit an IND application for FT536 in the fourth quarter of 2021 for the treatment of advanced solid tumors, including in combination with monoclonal antibody therapy to exploit multi-antigen targeting. In addition, on Monday, November 15, we intend to host a virtual 90-minute investor event to highlight our emerging pipeline of off-the-shelf multiplexed engineered iPSC-derived NK and T cell product candidates for solid tumors. During the investor event, we plan to discuss the following. Our multiplexed engineered preclinical candidates for which we intend to submit IND applications during the next 18 months, the unique mechanisms of action that our product candidates seek to exploit in attacking solid tumors, our proprietary multiplexed engineering and single iPSC selection platform, as well as new innovative features and functionality that we are currently assessing for integration into our solid tumor product candidates, our multi-arm phase I study of FT538 in solid tumors, where we have initiated enrollment of FT538 in combination with checkpoint inhibitor therapy in patients with resistance to checkpoint inhibitor and in combination with tumor-targeting monoclonal antibody therapy, including those that target the tumor-associated antigens EGFR, HER2, and PDL1. We also plan to disclose clinical data from our first-generation product candidates for solid tumors in patients that have progressed or failed checkpoint inhibitor therapy. Our phase I study of FT500 has enrolled approximately 10 patients in dose expansion at 300 million cells per dose and includes heavily pretreated patients with non-small cell lung cancer or classical Hodgkin lymphoma that have progressed or failed PD1, PDL1 checkpoint inhibitor therapy. Our phase I study of FT516 has enrolled approximately 12 patients in dose escalation, ranging from 90 million cells per dose to 900 million cells per dose, and primarily includes heavily pretreated patients with stage four melanoma that have progressed or failed PD1, PDL1 checkpoint inhibitor therapy. I would now like to turn the call over to Ed to highlight our third quarter financial results. Thank you, Scott. Turning to our financial results, revenue was $14.2 million for the third quarter of 2021 compared to $7.6 million for the same period last year. Revenue in the current quarter was derived from our collaborations with Janssen and Ono Pharmaceutical. Research and development expenses for the third quarter of 2021 were $53.1 million compared to $30.7 million for the same period last year. The increase in our R&D expenses was attributable primarily to an increase in employee headcount and compensation, including share-based compensation and expenses associated with third-party professional consultants and clinical trials. General and administrative expenses for the third quarter of 2021 were $15.7 million compared to $8.3 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 in office and computer supplies, including software licenses. Total operating expenses for the third quarter of 2021 were $55.3 million, net of $13.5 million in non-cash share-based compensation expense. Note that in connection with the treatment of the first patient with our off-the-shelf iPSC-derived CAR T-cell product candidate FT819, we achieved the clinical milestone set forth in our amended license agreement with Memorial Sloan Kettering Cancer Center. This clinical milestone triggered a first milestone payment in the amount of $20 million to MSK, which we plan to pay in the fourth quarter. 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 $24.6 million on a quarterly basis. In the third quarter, we recorded a non-cash $11 million non-operating benefit associated with the change in fair value. The company ended the third quarter with $804 million of cash, cash equivalents, and investments. Our common stock outstanding was 95 million shares, and preferred convertible stock outstanding was 2.8 million shares, each of which is convertible into five shares of common stock under certain conditions. I would now like to open the call to any questions. Ladies and gentlemen, if you have a question at this time, please press star then the number one on your telephone keypad. If your question has been answered or you wish to remove yourself from the queue, please press the pound key. Once again, that's star then the number one on your telephone keypad. Your first question comes from the line of Michael Yee from Jefferies. Your line is open. Hey, Scott. Thanks for the updates. I had two questions. One is on the updates coming later this year at ASH, and obviously, the abstracts are out today. Can you compare and contrast how you think durability would play out for FT516 versus FT596? Obviously, you've already presented some FT596 data. So would we be able to get a pretty good picture about how that's shaping up at ASH, given FT596 and also higher doses? That's question one. Then question two, I think you just laid out some nice commentary around your solid tumor update. I know these are in super heavily pretreated patients. How should we put that type of data you'll present into context? I mean, responses are good. What would you expect to see and what's the read-through? Thank you so much. Sure. With respect to your first question, with respect to durability of FT516 versus FT596, yes, I think at ASH we will be able to do a first look at comparing durability of both FT516 and FT596. We plan to present swim lane plots for both FT516 and FT596. If you recall from our lymphoma update in August, we did present a swim lane plot for FT516. The data cut for that, I think, was late July. Sorry, it was probably late June or early July. We'll be able now to fast-forward that swim lane as well as add patients that were dosed at 900 million cells. I believe I mentioned there were seven patients dosed at 900 million cells with FT516. With respect to FT596, recall we had 10 of 14 patients that had responded in the second and third dose level. We will now be able to present duration of response on those 14 patients, including adding a couple additional patients that were dosed at the 300 million cell level as backfill. We've also now, as I mentioned, I think we've treated about 30 total patients, including probably about 12- 15 patients at the 900 million cell level. We will at least be able to give first response on those patients, although durability may not yet be meaningful, just given how immature the patients are. You'll be able to compare the swim plots and make inferences is your point and see what FT596 is doing. That's your point. That's correct. Yeah. We will have a swim plot for. Yeah. FT596. That is correct. Good. Okay. Uh. On solid tumors. Yeah. Yeah. With respect to solid tumors, I mean, most of what we will present at SITC will be a go-forward look at our R&D in the emerging pipeline. I think we've always maintained at the end of the day, cracking the solid tumor nut, if you will, has proven to be much more difficult than treating hematologic malignancies. I think that's consistent no matter what therapeutic modality you're looking at, whether it's small molecule, biologic or cell therapy. Really, as we think about our Solid Tumor Franchise, we're focused on multiplexed engineered product candidates that can attack the tumor from multiple different angles. We're looking at FT500 and FT516 literally as just a first experience with an iPSC-derived NK cell therapy. You should have pretty modest expectations what with respect to what we think these product candidates can drive, on their own with respect to solid tumors. It's really just getting our feet under us with an NK cell therapy in solid tumors. We think we've done that with FT500 and FT516. We'll certainly be able to look at safety data. We'll be able to look at obviously clinical responses. Again, your expectations should be pretty modest with these first generation NK cell product candidates. Got it. Thank you very much. Sure. Your next question comes from the line of Alethia Young from Cantor Fitzgerald. Your line is open. Alethia Young from Cantor Fitzgerald, your line is open. Your next question comes from the line of Michael Schmidt from Guggenheim Securities. Your line is open. Hey, this is Kelsey on for Michael. Thanks for taking our questions. I think just two from us. First on FT596, I guess, are we still thinking about, you know, now that you're kind of moving from one cycle to two cycles, is there still any flexibility there to maybe increase that further, or is that kind of where you think you'll end up? Then kind of following up on that, as you build out the Solid Tumor Franchise, I guess kind of based on what you've seen with FT500 and FT516, you know, adding additional cycles for the upcoming next-gen products, is that something that you would consider or are you still kind of thinking about three cycles as the max? Thank you. Sure. With FT596, we have continued to dose at one dose per cycle, and we now have the ability to give two cycles. If you recall, when we initially advanced our FT596 program, we were gated on giving a second cycle with FDA consent. We're now able to give two cycles of FT596 without going back to the FDA. We will continue to dose patients at one dose, giving two cycles. Now we will now add two doses in each cycle and continue to give two cycles. We are planning on amending the protocol so that if patients relapse at some point, we could re-intervene with FT596. Right now we're sticking to one or two doses per cycle, giving two cycles, and now adding the ability to re-intervene if a patient later relapses. That's where we're headed with FT596. With respect to our Solid Tumor Franchise, very similar. We are giving multi-doses in a cycle. As an example, FT538 is a product candidate that we're now dosing with solid tumors in combination with monoclonal antibody. It's a multi-dose treatment, and we are giving multiple cycles. Again, if a patient later relapses, we have the ability to re-intervene again. We are now looking at the potential to re-treat patients upon progression. Okay, great. Thank you so much. Sure. Your next question comes from the line of Mike Ulz from Morgan Stanley. Your line is open. Hey, guys. Thanks for taking the question. Just a quick question on the CD38 knockout. You sort of highlighted that modification as providing some improved metabolic fitness. I was just curious for FT596. I noticed you don't have that modification there. I guess two questions. Number one, why not? And number two, you know, are you considering potentially adding that in the future? Sure. I mean, we've built out our platform over time in a very sort of methodical stepwise fashion. At the time when we were building out FT596, we did not fully appreciate the therapeutic value of the CD38 knockout. Initially, we thought of CD38 knockout as a step that we would take, a functional step that we would add that would be unique for myeloma. Knocking out CD38 could prevent fratricide when delivering the therapy in combination with daratumumab. Obviously, we've come to appreciate, and there's been publications on the therapeutic value of the CD38 knockout more broadly. We certainly are incorporating that into all our product candidates on a go-forward basis, including our product candidates for solid tumors. Certainly, we've reserved the right, obviously, to continue to build off of FT538 for lymphoma. Got it. That makes sense. Maybe just a quick follow-up. Just with respect to ASH, you did a good job of outlining what to expect for FT516 and FT596 as well, but is there any other data sets that we should be focused on at ASH? We're gonna hold an investor event on Tuesday. We'll spend most of the time, I think, on that investor event discussing lymphoma. I think that's going to be the significant focus of ASH as well as the investor event. We're continuing to generate data across all our programs, obviously, and we look forward to providing updates. Got it. Thank you. Your next question comes from the line of Alethia Young from Cantor Fitzgerald. Your line is open. Hey, guys. Thanks for taking my question. Sorry, I was on mute. I wanted to talk a little bit about FT538 and your choice of using it in combination with daratumumab, maybe versus some of the other, you know, maybe venetoclax and some of those others, and just kinda your perspective there on that. It seems kind of differentiated. Thanks. Sure. Wayne, do you wanna take that question with respect to FT538, in AML and thinking about, combining with dara versus venetoclax? Sure. The combinations of FT538 and daratumumab in AML was based on, you know, evolving emerging evidence about CD38 expression on AML, on AML cells. As, you know, as we've discussed, one of the engineered features of FT538 is the high affinity non-cleavable CD16. Given the availability of daratumumab and given the data around CD38 expression in AML, it's a consequence, natural consequence that a clinical experiment would try to see whether or not combining FT538 with an ADCC competent monoclonal antibody against an antigen that is known to be expressed on AML, AML cells, you know, is an experiment moving forward. That is something that's being done as part of our IIT collaboration with the University of Minnesota. As far as combinations of FT538 with other agents like venetoclax, we remain very interested, you know, in those combinations. Obviously not in the context of ADCC, but, you know, understanding really more about how combinations of things with BCL-2 inhibitors can have an impact on our cells in the context of these diseases. These are concepts that are continuing to be under consideration, and, you know, at some point, you know, we would consider opening up a clinical experiment that looks at combinations of our cells with these other anti-leukemic agents. Great. Thank you very much. Sure. Your next question comes from the line of Peter Lawson from Barclays. Your line is open. Hey, thanks for taking the questions. So on multiple myeloma and just how much data could we see at ASH, and what's the appropriate bar you think, and is it, you know, current CAR Ts? Yeah, just details around that and how you think about FT538 versus FT576 in that space. Sure. Again, you know, I'll make a comment. We've continued to build out our pipeline in a very methodical way and building off of, you know, multiplexed engineered backbones to add additional features which we believe will add incremental therapeutic value. Building off of, FT538, we built FT576, adding a CAR against BCMA, and again, in combination with daratumumab, we believe allows for multi-antigen targeting against both CD38 and BCMA. Much like lymphoma, where we think FT596 is a best-in-class product candidate, we believe the same for multiple myeloma and FT576. Obviously, both statements need to play out in the clinic, but we're firm believers that multi-antigen targeting will lead to best responses, including durability of response. That kind of approach can absolutely overcome tumor heterogeneity that exists both in lymphoma and myeloma. Do you think we'd get enough data by ASH, or is this kind of ends of twos and threes that we should be thinking about for? Yeah, I think, I mean, you know, it's for that to play out over time, multi-antigen targeting best-in-class approach, you're not just looking at response rates. You're looking at durability of response. Obviously, it will take some time for the durability of response to mature such that you know we can be absolutely certain in our belief systems that we have based on preclinical data. Gotcha. Just a comment on one of the questions you asked about the modest expectations around solid tumors. Is that a case that you kind of, you're not expecting to see any kind of responses or is it, cytokine levels you're kind of looking at or, influx of cells? What's a success for you for FT500 and FT516? Yeah, I mean, it's the first time. Keep in mind, right, this is the first time iPSC-derived NK cell therapies have been delivered in solid tumors. So, you know, in the FT500 dose escalation in FT516, or sorry, dose expansion in FT516 dose escalation started, you know, some time ago. For success for us was just, again, demonstrating that we could deliver multiple doses of an unengineered NK cell, and then a first engineered NK cell in the setting of solid tumors, and that they would the multi-dose paradigms, multiple cycle paradigms would be safe and well-tolerated. That we could potentially see some control of activity. Of tumor activity, and that we would be able to look at translational data that we could continue to build off of as we build the multiplexed engineered pipeline. Gotcha. Thank you so much. Thanks for taking the question. Sure. Your next question comes from the line of Daina Graybosch from SVB Leerink. Your line is open. Thanks. I too have two questions. The first is, it seems like you're expanding a lot of your products in the 900 million dose range, whereas other NK cell companies are giving multiples of billions of doses. I wonder if you could speak to why at 900 and why not go higher, especially since you're not seeing any maximum tolerated doses. The second question is, can you discuss your rate of genetic abnormalities in an iPSC product, simply from cell division and how that might compare to, let's say, a donor-derived product? Sure. I'm chuckling on the second question. With respect to going higher on doses, you know, look, we reserve the right to go higher on doses. Absolutely. I'm not suggesting we won't continue to potentially explore higher doses and alternative dosing schedules because we do believe we have an incredibly flexible platform, to your point, that has proven to be, at least to date, very safe. I do think it provides us a lot of flexibility with respect to continuing to explore higher doses and alternative dosing schedules. That said, I mean, you know, we're quite pleased with what we're seeing both with FT516 and FT596 with respect to response rates, including CR rates, as well as the durability of response. We do believe it is worthwhile, and we do think there's significant, you know, development opportunity to move forward at the 900 million cell level, in for instance, expansions, and we plan on doing that. Again, given the safety profile and the flexibility we have with our platform, we certainly reserve the right to continue to do a bit of exploration as part of our phase I studies, including with, as I mentioned, alternative conditioning regimens and earlier line combining with standard of care regimens. With respect to how we characterize our master cell banks and how we release our product candidates, I'm not going to sort of get into any details around that other than to say we assess for genetic abnormalities at multiple points in the process of selecting our single cell, which we use to make a master cell bank. Again, our master cell bank is based on the selection of a single cell, which we do exquisite characterization around to select that single cell, and then again, use that to make a master cell bank. That master cell bank goes through extensive testing and qualification in order for it to meet FDA sort of guidelines and recommendations for use as a master cell bank. Okay. Thank you very much for both of those. Sure. Sure. Your next question comes from the line of Robyn Karnauskas from Truist Securities. Your line is open. Hey, guys. This is [Karplon] for Robyn. Thank you so much for taking my question. You have one poster at ASH that talks about modifications you're making to, you know, current NK cells to evade allorejection. Can you talk about other strategies you may also be working on, or considering to ensure that the cells stay in stealth mode? And you know, a related question, with the current candidates that you have, you've talked about the absence or at least low levels of allorejection you're seeing, at least within the timeframe that you've observed. We've talked to a bunch of KOLs, and there seems to be a level of confusion in terms of, you know, how you show that there is no allorejection. Can you talk a little bit about what assays are used and what sort of feedback have you gotten from the KOL community in terms of the comfort level that there is little to no allorejection? Thank you. Sure. I mean, we're gonna talk about this more, for instance, at our solid tumor investor event. We'll certainly talk more about this at ASH. I think, you know, again, there's been a lot of discussion about the value of stealth engineering. I think one of the things that, you know, we focus on, again, we don't believe there's much value in a long-term persisting cell if the functional activity of that cell has significantly degraded. There's no point in a cell persisting if it doesn't have functionality. So we focus on functional persistence, and one of the ways to drive functional persistence is certainly through editing. Although I'm not sure stealth editing, to be fair, is a way to drive functional persistence. Multi-dosing strategy is one way to create functional persistence, albeit through a multi-dosing strategy. I'll turn it over to Bob here to talk a little bit about sort of the three approaches we think about as it relates to maximizing functional persistence. Sure. Thanks, Scott. Robyn, for ASH, we are presenting our one of our strategies, and Scott mentioned we have three. Let's categorize them into cloak, that's one. Second is eliminate, and third is attack and potentiate. The cloaking strategy, which is a manuscript we're drafting right now with Kalle Malmberg, focuses on complete disruption of the interaction between T and NK cells with our product. This is basically T or NK cells will not be able to recognize our product. I don't wanna get into details with that. I think I wanna respect Kalle's publication. Here, this goes beyond just thinking that one ligand on the cell will overcome the hundreds of inhibitory and activating receptors that are found on NK cells as others are trying to do. This is more about going to the heart of the interaction between T and NK cells. That's cloak. Eliminate, which is what's in ASH, is our unique strategy of using daratumumab to get rid of all the activated T and NK cells that are surrounding our cell through the engagement of hnCD16 found on our cell with the anti-CD38 mAb targeting the activated cells that come nearby. Keep in mind that because our product is CD38 negative, this becomes a very unique lympho-conditioning strategy that's better than other strategies that are using mAbs for this because daratumumab is safe and only targets activated alloreactive T and NK cells, unlike other strategies that may go into more progenitor populations to induce lympho-conditioning or lympho-depletion. Lastly, what we're very excited about is attack and potentiate. This is the idea where the cell, the product itself, has the unique ability to not only target alloreactive cells that come near it, but also to utilize that attack to proliferate and potentiate itself. This is the strategy that's been published in Nature Biotech last year by Max, where allo defense receptor is used to one, target the alloreactive cells, NK or T cells, but also through the signaling domain, add additional signal to the product itself to proliferate. This becomes a very unique, timely induction of propagation. We can use ADR in situations such as elimination of Cy/Flu conditioning or creating space for our product. On your second question with respect to the assays that we use, I mean, honestly, we developed the assays with a bunch of KOLs. With respect to how do you assess alloreactivity or rejection, I'm happy to have a conversation with you offline based on the feedback you're getting versus the feedback we've gotten from our KOLs that we've used to develop these assays. That'd be great. Thank you. Sure. I appreciate the color. Thank you very much. Yep. Your next question comes from the line of [Matt Sagler] from Oppenheimer. Your line is open. Oh, hey, guys. I'll be quick, just one from me. Just kind of question out of left field, but just wanted to get your thoughts on the use of the platform outside of oncology applications, if there's any plans there. I'm sure you've seen some recent data on a stem cell-derived therapy for diabetes that looks pretty exciting, albeit early. Just kind of wanted your thoughts on that. Thanks. Sure. Absolutely. We absolutely think we have a platform that can be broadly applicable. We have certainly focused initially on cell-based cancer immunotherapies. We certainly believe there is opportunity for the cell types we make today, including NK cells and T cells, that could be those could be used outside of oncology, and we're doing some of that work internally at Fate Therapeutics. We certainly don't talk about it publicly yet, but certainly exploring the use of NK cells and T cells in areas where those could be leveraged outside of oncology. I would also say, just generally speaking, yes, I mean, we certainly closely watch the whole iPSC-derived cell therapy space, including with respect to areas that we would consider to be regenerative medicine type of applications. Excited about all the opportunities that are emerging in iPSC-derived cell therapy. I think you and I have talked about it. I think it's gonna be the platform of the future for cell therapy, and certainly we will look to play broadly in the field of iPSC-derived cell therapy over time. Agreed. Thanks, guys. Congrats. Sure. Your next question comes from the line of Ben Burnett from Stifel. Your line is open. Hello, this is Carolina Ibanez Ventoso for Ben Burnett. Thank you for taking our question. On your B-cell lymphoma programs, you've mentioned in the past the need of delivering a certain dose of cells to see activity with the hnCD16 construct. For how long would you expect to have hnCD16 activity in combination with rituximab or other when you administer FT596 at 900 million cells per dose? Sure. We give a single dose of rituximab, and that single dose of rituximab, we think, provides tumor targeting availability. If you look at the traditional rituximab PK curves and receptor occupancy data with respect to rituximab in tumors, we think there's ability to engage a single dose of rituximab over a multi-week period, let's call it three to four weeks. We have certainly shown, I think, a little bit of data with respect to FT596, that FT596 has, in a single dose, functional persistence over about a 14-21 day period. We are certainly looking forward to giving a second dose of rituximab, where we think that second dose can still engage rituximab during that multi-week period to continue to add therapeutic benefit. For us, you know, we started the expansion with FT596 as a single dose. We're certainly excited about adding a second dose of FT596 on day 14 to exploit that, let's call it that second window of rituximab's availability in coating tumors. I think this gets back to the point of, you know, we really focus on the idea of functional persistence, and there's multiple ways to achieve functional persistence, certainly through engineering approaches, but a multi-dosing approach can really add functional persistence by giving, again, a second dose that can have a day one experience. Understood. Thank you. Sure. Your next question comes from the line of Mara Goldstein from Mizuho. Your line is open. Thanks very much. Hey, maybe this is a bit of an oddball question, but, with respect to presentations at ASH, you have FT516 presentation at ASH and FT596. One's an oral and one is a poster. Should we read anything into that? Primarily- No. Okay. Don't. Yeah, don't. Don't read anything into it. No. All right. Well, I had to ask, and then I. That's okay to ask. Yeah. No, don't read anything into it. All right. I wanted to ask on the AML program, it just seems that perhaps that is evolving a little bit slower than the B-cell lymphoma. Maybe you can talk about that a little bit or Yeah. Yeah, sure. Am I incorrect in my assumption? No, no. no. No, that's fair. We were. I mean, we were a little delayed in getting out of the first dose level with FT538. It wasn't because we saw any toxicity. We were only open at a single site. The single site was the University of Minnesota. We launched the FT538 expansion at the University of Minnesota. You know, we ran into some struggles early on at that single site with essentially patients meeting the enrollment criteria. We had a couple screen failures in a row, which was just unfortunate. We've now opened the study at multiple sites, and we've seen significant pickup in activity where I think I mentioned we've enrolled about 10 patients now with FT538 and AML. It seems significant pickup now that we've been able to open at multiple sites. Okay. All right. If I could just ask, since you recognized some revenue that's attributable to Janssen collaboration, maybe you can talk a little bit about where you are there and what we should be thinking about as potentially next public disclosure on that program? Yeah. I mean, the Janssen collaboration has continued to go very well. Obviously, as you can tell from the revenue that continues to increase, we continue to increase the resources under the collaboration. I think we've disclosed in the past that the collaboration started with two antigen targets, one in hematologic malignancies, one in solid tumors. A third antigen target has now been added to the collaboration, and Janssen reserves the right to add a fourth target to the collaboration. Collaboration is moving forward. We're really pleased with it. I think we'll be able to give a little bit of visibility on the first product candidate at the Solid Tumor Day, although we may not be able to disclose the target quite yet. Okay. Thanks a lot. I appreciate the time. Sure. Your next question comes from the line of Nick Abbott from Wells Fargo. Your line is open. Hey. Thanks for taking my question. I know it's getting late, so I'll just ask one quick one. During the call already, Scott, so I apologize if you provided some commentary on FT819, but you've dosed some patients now. Is it too early to comment on experience with that and how that compares to, you know, Memorial's extensive experience with autologous products? Yeah, sure. I can comment on it. You're the first one to ask about it, so no one had asked about it before. The study is up and running. I think we're up and running at three or four sites now. We've certainly dosed patients in more than one disease area. Remember, it's a three disease area study, so we've dosed patient in ALL. We've dosed patients in lymphoma. We've not yet dosed, if I'm remembering correctly, in CLL. Starting at 90 million cells, which, depending on what data sets you look at in the allogeneic space, CAR T-cell space, 90 million cells, you know, may be on the verge of being an active dose. It's a little bit early. We're still early dosing the first couple patients here. We've not yet escalated to the second dose level, but making good progress. Great. Thank you. Sure. Your next question comes from the line of Ted Tenthoff from Piper Sandler. Your line is open. Great. Thank you. Actually, I think most of my questions have been answered, but maybe with just one about FT819 and sort of what you're doing with T cells. Is there any work being done looking at macrophages or anything along those lines in terms of iPSC cell line? Thanks. Sure. I'll turn that over to Bob. Bob is obviously leading the effort on research and development and the exploration of alternative cell types in the hematopoietic lineage other than NK and T. Thanks, Scott. I'll just be quick and say that our CD34 node is multipotent, so it does give rise to not only NK and T cells, but also the myeloid lineages. We're actively looking into other cell types within that sublineage, and I think we're making great progress, and we hope to give some updates when Scott allows us to do so. Thanks, guys. Looking forward to all the data readouts and the different events you're planning. Great. Thanks. Your next question comes from the line of Rob Burns from H.C. Wainwright. Your line is open. Hi. Thank you very much for the update here. As you commented on, you know, presenting pre-clinical data in the past, and that you'll also show data at SITC, considering the incremental data regarding, you know, NK cells and solid tumors, could you perhaps clarify the strategy slash investigational route that you shall pursue in solid tumors? Sure. In solid tumors, we will talk about this. There are certain mechanisms of action where we think, at least with respect to an NK cell chassis, where NK cells can be advantaged. We're certainly looking at areas, for instance, in non-small cell lung cancer as an example, where we think NK cells can actually be valuable and be therapeutically relevant in patients that have progressed or failed checkpoint inhibitor therapy. Now, treating those patients with an unengineered NK cell may not be the optimal approach, but certainly patients that have progressed or failed checkpoint inhibitor therapy, there are definitely challenges and mechanisms of resistance where T cells may no longer be effective. Some of those mechanisms of resistance to T cells are opportunities to engage those tumors, for instance, with an NK cell. As an example, one of the mechanisms of resistance in non-small cell lung cancer is downregulation of MHC class I. That is a cell type that an NK cell can absolutely recognize, target, and kill. Another example, for instance, in an array of solid tumors is when tumors are undergoing escape mechanisms associated with T cells. There's oftentimes upregulation of stress ligands like MICA, MICB, which is, for instance, expressed on many solid tumors. Our FT536 product candidate has a CAR engineered into it, obviously, which can key on the MICA, MICB receptors. We're looking at certain mechanisms where we think NK cells may be advantaged and where there are mechanisms of escape in play with respect to T cells. Great. Thank you. Sure. This concludes our question and answer session. I would now like to turn the conference back to our President and CEO, Scott Wolchko. Thank you. Thank you for everyone for participating in today's call. Be well, and we look forward to speaking with you at SITC. Take care. Ladies and gentlemen, this concludes today's conference. Thank you for your participation, and have a wonderful day. You may all disconnect.