Welcome to the Fate Therapeutics Third Quarter 2021 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 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 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 a 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 IPS 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 1 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 an 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 1 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 1 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 and 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 1 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 cutoff date of July 7 2021 from our dose escalating Phase 1 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 the 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 treatments cycle. Five of the 11 patients maintained their response without further therapeutic intervention, with follow up ongoing between 4.6 and 9.5 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 three or greater adverse events were observed. And 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 1 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 1 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 relapsed 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 1 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 a peer-reviewed journal, we showed that FT538 exhibits enhanced serial killing, antibody dependent cellular cytotoxicity and functional persistence compared to peripheral blood NK cells. The superior anti-tumor activity of FT538 was attributable to the biological effects of its novel IL-15 receptor fusion and CD38 knock-out, which were shown to improve metabolic fitness, increase resistance to oxidative stress and induce a protein expression program that enhanced NK cell activation and effector function. The Phase 1 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 IPS 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 1 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 IPS derived NK cell therapies to play a foundational role in the treatment of patients with AML. We are encouraged by our initial Phase 1 clinical data from our FT516 and FT538 programs, which have indicated that IPS 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 IPS 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 1 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've also commenced enrollment in an investigator initiated Phase 1 clinical trial of FT538, in combination with daratumumab in patients with relapsed refractory AML. A therapeutic strategy designed to exploit the product candidates' proprietary high affinity non-cleavable CD16 receptor and CD38 knock-out 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 1 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 relapse refractory AML as we generate additional dose escalation data with FT538, including duration of response, so we are able to fully compare the safety antileukemic activity and durability of response of both programs. Turning to our solid tumor franchise. We are looking forward to the Citi conference next week, where FT536 CAR NK cell program will be featured in an oral presentation. FT536 is our off-the-shelf multiplexed engineered IPS 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 1 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 IPS 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 multiplex 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 or multi-armed Phase 1 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 inhibitors and in combination with tumor targeting monoclonal antibody therapy, including those that target the tumor associated antigens, EGFR, HER2 and PDL-1. And 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 1 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 PD-1 PDL-1 checkpoint inhibitor therapy. Our Phase 1 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 4 melanoma that have progressed or failed PD-1 PDL-1 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 in expenses associated with third-party professional consultants and clinical trials. General and administrative expenses for the third quarter of 2021 are $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 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 maybe owed to MSK based on subsequent trading values of the company's common stock, ranging from $100 to $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’ve recorded a non-cash $11 million non-operating benefit associated with a 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.

Your first question comes from Michael Yee from Jeffries. 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 516 versus 596? Obviously, you've already presented some 596 data. So would we be able to get a pretty good picture about how that is shaping up at ASH given 596 and also higher doses? That's question one. And 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 in the context? I mean, responses are good. What would you expect to see and what's the read through? Thank you so much.

Sure. Regarding your first question about the durability of 516 versus 596, we will have an opportunity at ASH to compare the durability of both. We intend to present swim lane plots for both therapeutics. If you remember from our lymphoma update in August, we shared a swim lane plot for 516. The data cut for that was likely late June or early July, and now we will be able to fast forward that plot and include patients treated with 900 million cells. There were seven patients dosed at that level with FT516. For FT596, we previously noted that 10 to 14 patients responded at the second and third dose levels, and we will be able to present the duration of response for those 14 patients, along with adding a couple more patients who were dosed at the 300 million cell level. Overall, we have treated about 30 patients, including around 12 to 15 at the 900 million cell level. We will provide at least an initial response for those patients, though durability may not be fully assessable yet due to the early stage of their treatment.

But you'll be able to compare this one box and make inferences as you're pointing and see what 596 is doing. That's your point.

That's correct. We will have a swim plot for FT596. That is correct. Good.

Okay. And then on just quickly to solid tumors.

Yes, with respect to solid tumors. I mean, most of what we will present at Citi 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. And I think that's consistent no matter what therapeutic modality you're looking at, whether it's small molecule biologic or cell therapy. And so really, as we think about our solid tumor franchise, we're focused on multiplex 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 IPS derived NK cell therapy, you should have pretty modest expectations 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 within NK cell therapy in solid tumors. And 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. But again, your expectation should be pretty modest with these first generation NK cell product candidates.

Got it. Thank you very much.

Your next question comes from the line of Alethia Young from Cantor. Your line is open.

Your next question comes from the line of Michael Schmidt, from Guggenheim Securities. Your line is open.

Hey, this is Calci on for Michael, thanks for taking our questions. I think just two from us. First on 596, I guess, are we still thinking about 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 and then kind of following up on that, as you build out the solid tumor franchise, I guess kind of what you based on what you've seen with 500 and 516? Is 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.

With FT596, we have maintained one dose per cycle and now have the option to administer two cycles. Initially, we were restricted from providing a second cycle without FDA approval, but we can now proceed with two cycles of FT596 without needing further consent from the FDA. Therefore, we plan to continue dosing patients at one dose and will now introduce two doses in each cycle while still providing two cycles. We intend to revise the protocol to allow re-intervention with FT596 if a patient experiences a relapse. Currently, we are focused on one or two doses per cycle across two cycles and are also adding the possibility of re-intervention upon relapse. For our solid tumor franchise, the approach is quite similar. We are administering multiple doses in a cycle, specifically with FT538, which is being dosed for solid tumors in conjunction with a monoclonal antibody. This is a multi-dose treatment across several cycles, and we have the capacity for re-intervention if a patient relapses. We are considering the potential to retreat patients if they progress.

Okay, great. Thank you so much.

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 knock-out you sort of highlighted that modification as providing some improved metabolic fitness. So, I just curious for 596 I noticed you don't have that modification there. So I guess two questions. Number one, why not? And number two, are you considering potentially adding that in the future?

Certainly. We've developed our platform progressively over time. When we were working on FT596, we didn't fully recognize the therapeutic benefit of the CD38 knock-out. Initially, we viewed the CD38 knock-out as a functional step aimed specifically at myeloma to prevent fratricide when combining therapy with daratumumab. However, we have since come to understand and see publications highlighting the broader therapeutic value of the CD38 knock-out. We are now integrating this into all our product candidates going forward, including those for solid tumors. Additionally, we retain the option to further develop 538 for lymphoma.

Got it, that makes sense. And then maybe just a quick follow-up. With respect to ASH, you did a good job of outlining what to expect for 516 and then 596, as well. But is there any other data sets that we should be focused on at ASH?

So we're going to hold an investor event on Tuesday, we'll spend most of the time I think, on that investor event discussing lymphoma. And 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, your line is open.

Hey, guys, thanks for taking my questions. Sorry, I was on mute. I want something about 538 and your choice of using the in combination with daratumumab maybe versus some of the other maybe venetoclax, and some of those others. And just kind of your perspective there on that seems kind of differentiated? Thanks.

Sure. Wayne, do you want take that question with respect to 538 in AML, and thinking about combining with dara versus venetoclax?

Sure. So the combinations of FT538 in daratumumab and AML was based on evolving emerging evidence about CD38 expression on AML cells. And so as we've discussed in one of the engineering features of FT538 is the high affinity non-cleavable CD16. And so, given the availability of daratumumab, and given the data around CD38 expression at AML, it's a 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 cells, is an experiment moving forward. And that is something that's being done, as part of our IIT collaboration with the University of Minnesota. As far as combinations of 530 with other agents like venetoclax, we remain very interested in those combinations, obviously, not in the context of ADCC. But understanding really more about how combinations of things with BCL 2 inhibitors can have an impact on ourselves in the context of these diseases. And so these are concepts that are continuing to be under consideration. And at some point, 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.

Your next question comes from the line of Peter Lawson from Barclays. Your line is open.

Thanks for taking the questions. So on multiple myeloma, just how much data could we see at ASH and what's the appropriate value you think and is it current CAR T? And, just details around that and how you think about 538 versus 576 in that space?

Sure. So again, I'll make a comment. We’ve continued to build out our pipeline in a very methodical way and building off of multiplexed engineered backbones, to add additional features, which we believe will add incremental therapeutic value. So building off of our FT538, we built 576, adding a CAR against BCMA. And again, in combination with daratumumab, we believe allows for multi antigen targeting against both CD38 and BCMA. So much like lymphoma where we think 596 is a best-in-class product candidate, we believe the same for multiple myeloma in 576. 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, and that kind of approach can absolutely overcome tumor heterogeneity that exists both in lymphoma and myeloma.

Do you think we get enough data by ASH, or this kind of ends of twos and threes that we should be thinking about for?

Yes, I think 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, and obviously, it will take some time for the durability of response to mature such that we can be absolutely certain in our belief systems that we have based on preclinical data.

And then just a comment on one of the questions you asked about the modest expectations around solid tumors. Is that a case that you've kind of, you're not expecting to see any kind of responses? Or is it cytokine levels, as you're kind of looking at or influx of cells? What's the success for you for 505?

Yes, this is the first time that IPS derived NK cell therapies have been administered in solid tumors. The dose escalation for FT516 and the expansion for FT500 began some time ago. Our goal was to demonstrate that we could deliver multiple doses of an engineered NK cell in solid tumors, ensuring that the multiple dose paradigms would be safe and well tolerated. Additionally, we aimed to observe some level of tumor control and gather translational data to build upon as we develop our multiplex engineered pipeline.

Thanks so much. Thanks for taking the question.

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 cells of the dose range, whereas other NK cell companies are giving multiple billions of doses. And 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?

Sure, so I'm chuckling on the second question. With respect to going higher on doses, look, we reserve the right to go higher on doses. Absolutely. And 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 today very safe. So I don't think it provides us a lot of flexibility with respect to can continuing to explore higher doses and alternative dosing schedules. That said, I mean 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. And so we do believe it is worthwhile. And we do think there's significant development opportunity to move forward at the 900 million cell level and for instance, expansions and we plan on doing that. But again, given the safety profile and the flexibility we have with our platform certainly reserve the right to continue to do a bit of exploration as part of our Phase 1 studies, including with respect to 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. And so 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.

Your next question comes from the line of Robyn Karnauskas from Truist Securities. Your line is open.

Hey, this is Kripa stepping in for Robyn. Thank you for taking my question. I noticed a poster at ASH discussing modifications to current T cells to evade allo rejection. Could you elaborate on other strategies you might be exploring to keep these cells undetectable? Additionally, regarding the candidates you've mentioned, you've noted low levels of allo rejection so far. From conversations with several key opinion leaders, there's some confusion about how you demonstrate the absence of allo rejection. Can you explain what assays are being utilized and what feedback you've received from the KOL community about their confidence in the low occurrence of allo rejection? Thank you.

Sure. I mean, we're going to talk about this more, for instance, at solid tumor investor day, we will 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 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 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, so for ASH, we are presenting 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. So the cloaking strategy, which is a manuscript we're drafting right now with Kelly Malburg focuses on complete disruption of the interaction between T and NK cells with our product. So this is basically T or NK cells will not be able to recognize our product. I don't want to get to details with that. I think I want to respect Kelly's publication. But here, this goes beyond just thinking that one leg in 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. So that's cloak. Eliminate, which is what's on ASH is our unique strategy of using daratumumab to get rid of all the activated T and NK cells that are surrounding ourselves through the engagement of hnCD16 front on our cell with the anti CD38 mAb, targeting to activate a cell to come nearby. And 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 may go into more progenitor populations to induce lympho conditioning or lympho depletion. And lastly, what we're very excited about is attack and potentiate. And so, this is an idea where the cell, the product itself has the unique ability to not only target our reactive cells that come near it, but also to utilize that attack to proliferate and potentiate itself. So this is the strategy that's been published in Nature Biotech last year, by Max where allo defense receptor is used to target to allo reactive cells and CAR T-cells, but also through the signaling domain, add additional signal to the product itself to proliferate. So this becomes a very unique, timely induction of propagation. So we can use ADR in situations such as elimination of sigh flu conditioning, or creating space for our product.

On your second question, with respect to the assays that we use, I mean, honestly, we develop the assays with a bunch of KOLs with respect to how do you assess allo reactivity 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.

It’s actually great. Thank you. I appreciate the color. Thank you very much.

Your next question comes from the line of Matt Biegler from Oppenheimer. Your line is open.

Hey, guys. I'll be quick, just one for me. Just kind of question I 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 was pretty exciting, albeit early. So 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. 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 can be leveraged outside of oncology. I would also say just generally speaking, yes. I mean, we certainly closely watch the whole IPS 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 IPS derived cell therapy. I think you and I've talked about it, I think it's going to be the platform of the future for cell therapy. And certainly, we will look to play broadly in the field of IPS derived cell therapy over time.

Great. Thanks, guys. Congrats.

The next question comes from the line of Ben Burnett from Stifel. Your line is open.

Hello, this is Catalina in for Ben Burnett. Thank you for taking our question. On your B-cell lymphoma programs, you have 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 596 at 900 million cells per dose?

Sure, so 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 and 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. FT596 has in a single dose essentially we've shown it has functional persistence over about a 14 to 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. So for us, we started the experience 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 coding tumors. And again, I think this gets back to the point of, 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. Maybe it's a bit of an oddball question. But with respect to presentations at ASH, sorry, 516 presentation at ASH and 596. One's an oral and one is a poster. And should we read anything into that?

No. Don’t read anything into this. No.

All right. Well, I had to ask.

That’s okay. Yeah, no, don't read anything into it.

And then 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 could talk about that a little bit or if I’m incorrect in my assumptions?

No, that's fair. So we were a little delayed in getting out of the first dose level with FT538. And it wasn't because we saw any toxicity. We were only open at a single site. And so the single site was the University of Minnesota. So we launched the FT538 experience at the University of Minnesota. And yeah, we ran into some struggles early on at that single site with essentially patients meeting the enrollment criteria. And 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. So, it seems significant pickup now that we've been enabled to open it multiple sites.

Okay. All right. And then if I could just ask you, since you recognized some revenue, that's attributable to the 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, so I mean, the Janssen collaboration has continued to go very well. And 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. So, 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, Scott, I apologize if you provided some commentary on 819. But you've dosed some patients now. Is it too early to comment on experience with that and how that compares to memorials extensive experience with autologous products?

Yeah, sure. I can comment on it and 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 the patient ALL, we’ve dosed patients in lymphoma. We've not yet dosed if I'm remembering correctly in CLL. So starting at 90 million cells, which, depending on what data sets you look at, in the allogeneic space, CAR T-cells, 90 million cells 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.

Thank you.

Sure.

Your next question comes from the line of Ted Tenthoff from Piper Sandler. Your line is open.

Great. Thank you. I think most of my questions have been answered. But maybe just one about 819 and sort of what you're doing with T cells. And is there any work being done looking at macrophages or anything along those lines in terms of IPSC CEL line?

Sure. I'll turn that over to Bob. Bob's 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 multi potent, so it does give rise to not only NK and T cells, but also the myeloid lineages. And so, we're actively looking into other cell types within that sub lineage. 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 adventure planning.

Great. Thanks.

Your next question comes from the line of Rob Burns from H.C. Wainwright. Your line is open.

Thank you very much for the update here. As you've commented on presenting preclinical data in the past, and that you’ll also showed greater activity. Considering the incremental data regarding NK cells and solid tumors, could you perhaps clarify the strategy/investigational route that you shall pursue in solid tumors?

Sure. In solid tumors, and 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 engineered 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. And 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 down regulation of MHC class one. 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 up regulation of stress ligands, like MCA, MCB, which is, for instance, expressed on many solid tumors. Our 536 product candidate has a CAR engineered into it obviously, which can key on the MCA, MCB receptors. So, 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 Citi. Take care.

Ladies and gentlemen, this concludes today's conference. Thank you for your participation and have a wonderful day. You may all disconnect.