Fate Therapeutics, inc (FATE) Q2 2021 Earnings Call Transcript

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Fate Therapeutics, inc (FATE -5.80%)
Q2 2021 Earnings Call
Aug 6, 2021, 8:00 p.m. ET

Contents:

• Prepared Remarks
• Questions and Answers
• Call Participants

Prepared Remarks:

Operator

Welcome to the Fate Therapeutics Second Quarter 2021 Financial Results Conference Call. [Operator Instructions] This call is being webcast live on the Investors section of Fate's website at fatetherapeutics.com. [Operator Instructions]

I would now like to introduce Scott Wolchko, President and CEO of Fate Therapeutics. You may begin

Scott Wolchko -- President and Chief Executive Officer

Thank you. Good afternoon, and thanks, everyone, for joining us for the Fate Therapeutics Second 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 June 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 the 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 June 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 Bob Valamehr, our Chief Research and Development Officer.

Today, we will briefly highlight our clinical progress and plans for each of our disease franchises, with focus on our FT516 and FT596 programs for the treatment of B-cell lymphoma and our plans to share interim Phase I clinical data from these programs at our August 19 Investor event. I would like to begin today's conversation, though, marking what is a landmark achievement in the field of cell-based cancer immunotherapy. Our treatment of the first patient with the first ever off-the-shelf iPSC-derived T-cell therapy. FT819 is a first-of-kind, allogeneic, off-the-shelf CAR T-cell therapy that is manufactured from a clonal master-induced pluripotent stem cell line. The clonal master iPSC line is derived from a single iPSC, which is precisely engineered to insert a novel one timesX anti-CD19 CAR construct under the regulation of the T-cell receptor alpha constant or TRAC locus.

Preclinical studies have shown that this precise configuration optimizes T-cell effector function and antitumor activity, and completely eliminates T-cell receptor expression, abrogating the risk of graft-versus-host disease. Unlike the manufacture of patient and donor-derived CAR T cells, which require batch-to-batch sourcing and engineering of primacry T- cells, the use of a clonal master-engineered iPSC line serve as a renewable starting cell source and ensures mass production of uniformly engineered CAR T-cells in a efficient and consistent manner. Our GMP manufacturing run for FT819 produced over 25 billion CAR T-cells in a single small scale campaign, representing an implied yield of 250 doses at 100 million cells per dose. Release testing showed that the drug product is well defined and comprise of greater than 99% CD45+, CD7+ lymphocytes with greater than 99% CAR expression. The phenotype of FT819 exhibits high level expression of the activation marker CD25 and the trafficking marker CXCR4 and low-level expression of the checkpoint proteins PD-1, TIM-3, CTLA-4 and LAG-3.

In July, the first patient was treated with FT819, which is the first ever treatment of a patient with an iPS-derived T-cell product candidate. The patient, a 61-year-old male, with refractory acute lymphoblastic leukemia was treated with a single dose of FT819 at 90 million cells. The multicenter Phase I clinical trial is assessing dose levels ranging up to 900 million cells. Three FT819 dosing regimens are being tested. FT819 administered as a single dose. FT819 administered as a single dose in combination with IL-II and FT819 administered as fractionated doses on days one, three and five. Each dosing regimen is being tested for the treatment of B-cell lymphoma, lymphocytic leukemia and acute lymphoblastic leukemia. The advancement of FT819 into clinical development ushers in a new era for T cell-based cancer immunotherapy with the promise of multiplexed engineered functionality, off-the-shelf availability, on-demand treatment and greater patient accessibility. We have confronted countless obstacles on our five-year journey to the clinic, including some that seemed insurmountable at the time. We are certainly excited to have reached this landmark achievement in bringing iPS-derived T cells to patients.

I would like to thank the employees of Fate Therapeutics and our collaborators at Memorial Sloan Kettering Cancer Center, especially Dr. Michel Sadelain, who began this important work with us back in 2016, when the steps ahead were anything but clear. Turning to our off-the-shelf iPS-derived NK cell programs. We are very pleased with the progress and the early clinical data from our FT516 and FT596 programs for the treatment of relapsed refractory B-cell lymphoma. The ongoing Phase I study of FT516 is assessing up to two treatment cycles. Each cycle consisting of three days of cy/flu chemotherapy conditioning, a single dose of rituximab and three weekly doses of FT516 each with IL-2 cytokine support. At the ASCO Conference in June, we presented positive interim Phase I data, where eight of 11 patients achieved an objective response, including six patients that achieved complete response in dose cohorts two and three of 90 million cells per dose and 300 million cells per dose, respectively. Importantly, the two patients treated in dose cohort one of 30 million cells per dose had progressive disease, suggesting that cy/flu, rituximab and IL-2 may not be sufficient to induce clinical responses, absent clinically relevant doses of FT516.

The observed safety profile of FT516 was favorable and is potentially differentiated from that of T-cell based therapies, including T-cell engagers and CAR T-cell therapies. No FT516 related SAEs or FT16 related Grade three or greater AEs were observed, and no events of any grade of CRS, immune effector cell-associated neurotoxicity syndrome, or GVHD, were reported. Dose escalation in our Phase I study of FT516 is ongoing with enrollment in dose cohort four of 900 million cells per dose. We are currently planning to initiate multiple dose expansion cohorts to further assess the efficacy of FT516. These cohorts include third-line diffuse large B-cell lymphoma and third-line follicular lymphoma, both in patients that are naive to autologous CD19 CAR T-cell therapy. Additionally, since we observed complete responses in two of four patients in dose cohorts two and three, whose disease progressed following autologous CD19 CAR T-cell therapy. We plan to initiate a dose expansion cohort in patients with aggressive B-cell lymphomas that have previously been treated with autologous CD19 CAR T-cell therapy. We believe this dose expansion cohort in particular addresses a growing market segment with a significant unmet need and may offer a potential fast-to-market development path.

Finally, since FT516 may be administered in the outpatient setting with no mandatory hospitalization stays and given its favorable safety profile observed to date, we also plan to initiate a dose expansion cohort of FT516 in combination with bendamustine and rituximab and without cy/flu chemotherapy conditioning to explore its use with standard of care, CD20 targeted regimens in earlier-line therapy. In these dose expansion cohorts, we intend to include sites that serve patients in the community setting. We are also pleased with the progress in our Phase I clinical trial of FT596, our off-the-shelf iPSC-derived CAR NK cell product candidate designed to target multiple antigens through its CD19 targeted CAR, and its high affinity non-cleavable CD16 Fc receptor. Unlike the FT516 Phase I study, the FT596 Phase I study is currently assessing a single dose of FT596. Additionally, since FT596 incorporates a novel IL-15 receptor fusion for cytokine activation, FT596 is being administered without IL-2 cytokine support.

The monotherapy arm of the FT596 Phase I study is intended to evaluate the activity of our novel CD19 targeted CAR construct, which is optimized for NK cell biology and is comprised of an NKG2D transmembrane domain, a 2B4 co-stimulatory domain and a CD3 zeta signaling domain. The combination arm is intended to evaluate the potential of FT596 to target multiple antigens through its CD19 CAR and its high affinity non-cleavable CD16 Fc receptor, an approach that we believe may hold best-in-class potential in addressing tumor heterogeneity and antigen escape. A total of 20 patients, 10 in each arm, have been treated in dose cohorts one, two and three at 30, 90 and 300 million cells, respectively. No dose-limiting toxicities have been observed and dose escalation in both arms is ongoing with enrollment in dose cohort four of 900 million cells. As we have cleared the single-dose treatment schedule at 300 million cells in both arms, we are preparing to initiate a two dose treatment cycle under an amended protocol, with FT596 administered on days one and 15, beginning at 300 million cells per dose.

On August 19, we will host a 90-minute investor event to present interim Phase I clinical data for our FT516 and FT596 programs in relapsed/refractory B-cell lymphoma. During the investor event, we plan to share the following data: For FT516, we plan to present duration of response for the 11 patients treated in dose cohorts two and three of 90 million cells per dose and 300 million cells per dose, respectively. This will provide the first indication as to whether FT516 can effectively drive durable responses against CD20 positive tumors, including in patients that have progressed on autologous CD19 CAR T-cell therapy. For FT596, we plan to present safety and overall response rates for 10 patients in the monotherapy arm and for 10 patients in the rituximab combination arm, so 20 patients total. As a reminder, the FT596 Phase I study is open to patients that have previously been treated with autologous CD19 CAR T-cell therapy.

With respect to the monotherapy arm, since FT596 does not benefit from the addition of rituximab for CD20 targeting, we will look to these first 10 monotherapy patients to assess the potential of our novel CD19 targeted CAR to drive objective responses, especially in those patients that are naive to autologous CD19 CAR T-cell therapy. With respect to the combination arm, we also consider the first 10 patients to primarily be a test of the CAR constructs potency rather than a test of the multi antigen targeting potential of FT596. Recall, based on our dose dependency operations -- observations from our FT516 study, we did not see activity of the hnCD16 CAR -- sorry, hnCD16 construct until a dose of 90 million cells three times once weekly was reached. In other words, a cumulative cell exposure of 270 million FT516 cells. Therefore, at single dose levels of 30 million and 90 million FT596 cells, we would not expect the hnCD16 construct to be a major contributor to efficacy.

That said, in the combination arm, we would consider objective responses in patients that have progressed on CD19 CAR T-cell therapy as compelling demonstration of the dual antigen targeting functionality of FT596 and the product candidate's unique ability to address tumor heterogeneity and antigen escape. Additionally, patients with clinical benefit after the first FT596 treatment cycle are eligible to receive a second single-dose treatment cycle with FDA consent, and we plan to present safety and response rates after the second FT596 treatment cycle. Finally, we plan to share certain translational observations from both the FT516 and FT596 Phase I studies. Turning to our other disease areas for a brief update. We are encouraged by the interim Phase I clinical data from our FT516 and FT538 programs in relapsed/refractory AML that we shared at our investor event in May, which indicated that iPSC-derived NK cells are well tolerated and can induce objective responses with complete leukemic blast clearance in the bone marrow.

Importantly, these compelling clinical outcomes were achieved with iPS-derived NK cells administered off-the-shelf in the outpatient setting and without patient matching. This therapeutic paradigm has the potential to efficiently and effectively treat many patients with AML and overcome the significant challenges that have limited the clinical advancement of donor-derived NK cell therapy, which typically requires use of a transparent-like process, where patients are hospitalized, receive intense lymphodepleting chemotherapy and our administered donor NK cells that are specifically manufactured for and matched to the patient. Dose escalation for FT516 program as monotherapy is ongoing with enrollment in dose cohort three at 900 million cells per dose, which we expect to complete during the third quarter. No dose-limiting toxicities have been reported and treatment with FT516 continues to be well tolerated. Dose escalation for FT538 program as monotherapy is ongoing with enrollment in dose cohort one at 100 million cells per dose. No dose-limiting toxicities have been reported. However, we have not yet cleared dose cohort 1. Until recently, our FT538 Phase I study was open at a single clinical site only. We have now activated multiple additional sites for conduct of our FT538 Phase I study and expect to increase the pace of enrollment with these additional sites now open.

Upon clearance of dose cohort one, enrollment will also initiate in the investigator-initiated study of FT538 in combination with daratumumab for relapsed/refractory AML. We expect to report additional clinical data from the dose escalation stages of our 516 and 538 Phase I studies in relapsed/refractory AML at the American Society of Hematology Annual Meeting in December. At ASH, we also expect to report the first clinical data from our FT538 and FT576 programs in relapsed/refractory multiple myeloma. Similar to our approach in lymphoma, we are beginning clinical investigation in multiple myeloma by leveraging our high-affinity, non-cleavable CD16 Fc receptor. And we are combining FT538 with the CD38 targeted monoclonal antibody daratumumab to maximize antibody-dependent cellular cytotoxicity. We have activated multiple clinical sites for conduct of our Phase I study, and enrollment of FT538 in combination with dara will be initiated at 100 million cells per dose upon clearance of dose cohort one in the Phase I study of FT538 in relapsed/refractory AML. GMP production is underway for FT576.

Our off-the-shelf iPS-derived NK cell product candidate designed to target multiple antigens through its high-affinity, non-cleavable CD16 Fc receptor, and its high avidity BCMA targeted CAR, an approach that we believe may hold best-in-class potential for the treatment of multiple myeloma. The multicenter Phase I clinical trial is designed to assess both single-dose and multi-dose treatment regimens of FT576 as monotherapy and in combination with dara. The study will initiate upon completion of GMP manufacture and successful release of drug product. We continue to be pleased with our progress in building a deep pipeline of novel, multiplexed engineered iPSC-derived CAR NK cell product candidates for solid tumors. We are well positioned to exploit multiple mechanisms where NK cells may be uniquely advantaged, including targeting tumors with acquired resistance to PD-1, PD-L1 blockade resulting from loss of MHC Class one expression. Combining with standard of care monoclonal antibodies to maximize CD16-mediated ADCC and incorporating CARs and other synthetic receptors to directly target cell surface antigens and stress ligands. In the third quarter, we expect to initiate our Phase I clinical trial of FT538 in solid tumors.

The trial is a multi-arm study and will assess FT538 in combination with checkpoint inhibitor therapy in patients with resistance to PD-1, PD-L1 blockade and in combination with an array of monoclonal antibodies, including those that target the tumor-associated antigens EGFR, HER2 and PD-L1. In addition, we intend to submit INDs for three new product candidates over the next 12 months, including FT536 CAR MICA/MICB, FT573 CAR B7H3, and our first product candidate under our Janssen collaboration, for which we achieved a preclinical milestone in the second quarter. In the fall, we plan to hold an investor event to further discuss our solid tumor strategy, highlighting our multiplexed engineered pipeline and presenting Phase I clinical data from our FT500 and FT516 studies.

I would now like to turn the call over to Ed to highlight our second quarter financial results.

Edward Dulac -- Chief Financial Officer

Thank you, Scott. Turning to our financial results. Revenue was $13.4 million for the second quarter of 2021 compared to $5.5 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 second quarter of 2021 were $48 million compared to $26.7 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 equipment and materials. General and administrative expenses for the second quarter of 2021 were $12.2 million compared to $7.5 million for the same period last year. The increase in our G&A expenses was attributable primarily to an increase in headcount and employee compensation, including share-based compensation. Total operating expenses for the second quarter of 2021 were $46.9 million, net of $13.3 million in noncash share-based compensation expense.

In the second quarter, we recorded a noncash $8.7 million nonoperating expense associated with the fair value of contingent milestone payments under our iPSC-derived CAR T-cell collaboration with Memorial Sloan Kettering. In the event, a certain clinical milestone is achieved with an iPSC-derived CAR T-cell product candidate, up to three milestone payments may be owed to MSK based on subsequent trading values of the company's common stock, ranging from $50 to $150 per share. These milestone payments, in the aggregate, total up to $75 million, and no amounts have been paid as of the second quarter of 2021 to MSK. We will remeasure this liability currently valued in the aggregate at $55.7 million on a quarterly basis and changes in the fair value will be recorded in our earnings as a nonoperating income or expense. Note that in July, with the treatment of the first patient with FT819, the clinical milestone was achieved and the first milestone payment in the amount of $20 million is owed to MSK. The company ended the second quarter of 2021 with $845 million of cash, cash equivalents and investments. Common stock outstanding was 94 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.

And with that, I would now like to open the call up to questions.

Questions and Answers:

Operator

[Operator Instructions] And our first question comes from Yigal Nochomovitz from Citigroup. Please go ahead.

Yigal Nochomovitz -- Citigroup -- Analyst

Hi, great. Thank you very much. Hi, Scott, and thanks for taking the questions. Could you just clarify something about your high-level development strategy? Is it the correct assumption that you plan to select FT516 or FT596, the late-stage studies in B-cell lymphoma? And if so, are you more likely to select 596 for advanced development in BCL, given the additional engineered features in 596?

Scott Wolchko -- President and Chief Executive Officer

Sure. So I certainly believe FT596 is a best-in-class product candidate for reasons that we've described in B-cell lymphoma, given it has multiantigen targeting potential and can overcome, for instance, heterogeneity and antigen escape. That said, we're very pleased with the data we're seeing so far with FT516, and we think there may be some unique opportunities, for instance, as I alluded to, downline of CAR T-cell therapy, where we may be able to move very quickly on a path toward market with FT516. We will continue to be guided by the data from both studies in -- as we refine and further develop our development strategy. But right now, I would say, yes, FT596, I think is best-in-class product candidate. FT516, I think there's unique opportunities where we can move quickly, including downline of CAR T-cell therapy.

Yigal Nochomovitz -- Citigroup -- Analyst

And then on that point about the new cohort that you're planning to initiate in for 516 on patients previously treated with autologous CAR-T, are you stipulating that those patients had to have not responded to prior autologous CAR T or just their prior response on autologous CAR T not relevant to their enrollment?

Scott Wolchko -- President and Chief Executive Officer

They could -- as currently contemplated progressed or actually failed.

Yigal Nochomovitz -- Citigroup -- Analyst

Okay, great. Thank you.

Scott Wolchko -- President and Chief Executive Officer

Sure.

Operator

Our next question comes from Michael Schmidt from Guggenheim, please go ahead.

Michael Schmidt -- Guggenheim -- Analyst

Hey, it's God. Thanks for taking my questions. Congrats on all the progress and the detailed pipeline update. I just have a clarification regarding your FT596 update and future plans for that product in lymphoma. Could you clarify how many of these 20 patients that you're planning to present on have received a second dose? And then second to that, you are switching over now to a 2-dose treatment protocol in the study. I guess what is your confidence level that two doses is sufficient to generate durable responses and also maximize the potential additive effect of rituximab?

Scott Wolchko -- President and Chief Executive Officer

That's a tough question and answer 10 days in advance of a data disclosure. So with respect to the number of patients that have achieved -- have been administered a second dose. I mean we'll provide that data as part of the update. I will say that we have administered a second cycle with FDA consent to monotherapy patients as well as combination patients. I think I'll leave that first. I'll leave it at that. With respect to the single versus the 2-dose treatment regimen, we're going to run the experiment. I mean I think the reality is, we are now looking at response rates at single dose. At 300 million cells, we will escalate as we already have to 900 million cells, single dose. We will likely backfill patients at 300 million and 900 million to get a meaningful cohort of single dose patients, and we will compare that to the cohort at 300 million and 900 million under the 2-dose treatment. So I think, if you think about it at some basic level, we're going to get a cohort of, say, 12 to 20 patients looking at single dose and 12 to 20 patients looking at two doses at the highest dose levels, and make a decision from there.

Michael Schmidt -- Guggenheim -- Analyst

But it sounds like you're not leaning toward a six dose regimen like you have implemented in the 516 study. Is that correct?

Scott Wolchko -- President and Chief Executive Officer

That's correct.

Michael Schmidt -- Guggenheim -- Analyst

Okay. Super helpful. And then another question just on development strategy now with 819, the CD19 CAR T program in the clinic. I guess, how do you think about positioning that longer term relative to the 596 product candidate in terms of development strategy?

Scott Wolchko -- President and Chief Executive Officer

Yes. I think it's too early to know. I mean it'll -- we're just starting with T-cells. I do think -- clearly, NK cells to date, I do think have a differentiated safety profile so far. Obviously, we have not necessarily seen from Fate Therapeutics or any other company, response rates at higher dose levels as well as the durability of those responses. So I think it's too early in our development life cycle of both FT516 and FT596 to think about how we will advance these different product candidates, how an NK cell will compare with a T cell. That said, I've always said and it won't surprise me in the next, let's call it, 18 months, if there may be an investigator-initiated study where an NK cell is combined with a T cell. And I think to date, we're the only company that has the unique potential to exploit both innate and adaptive immunity in an off-the-shelf setting.

Michael Schmidt -- Guggenheim -- Analyst

Greg, thanks for the armed guard really appreciate it.

Scott Wolchko -- President and Chief Executive Officer

Sure. Sure.

Operator

Our next question comes from Alethia Young from Cantor Fitzgerald, please go ahead.

Alicia Young -- Cantor Fitzgerald -- Analyst

Hey, guys, thanks for taking my questions. Maybe just two for me. One, this is a big picture. You have so many products. And I guess -- and I know you were kind of talking about late stage, maybe 516, cell CAR-T. How do you think about -- do all the products seem to be blockbusters? Or is there kind of a strategy behind some being fast to market and some being blockbusters since you kind of have like a building platform? And then I guess my second question is, can you just talk a little bit about like kind of if you think we'll have enough duration by the time we get to ASH to kind of make head to tails of some of the activity here?

Scott Wolchko -- President and Chief Executive Officer

Sure. So I'll start with the second question. Yes, I mean at ASH, I think we will have even significantly longer duration of response with FT516, certainly. And I think we'll get our first meaningful view of duration of response with respect to 596. So I think ASH is going to provide us a lot of really good information with respect to both 516 and 596 durability of response, including understanding the -- with 596 monotherapy versus combination. We may not necessarily be at a point to tease out single dose versus two doses with respect to duration of response. As it relates to your first question, look, we're going to be really opportunistic. I've said it before, I think FT516 and its performance to date has surprised us pleasantly. We saw significant response rates at 90 million and 300 million cells, including patients down line of CAR T-cell therapy. I think that was a fairly unique observation, and I think it does provide a potentially very fast path to market. And even though I believe 596 is a best-in-class product candidate, I think the FT516 opportunity is there, and we want to move quickly up with it and take advantage of that.

Alicia Young -- Cantor Fitzgerald -- Analyst

Great, thank you.

Operator

Our next question comes from Michael Yee from Jefferies, please go ahead.

Michael Yee -- jefferies -- Analyst

Hi, thanks for the question. Scott. Thanks for the updates. I wanted to understand some of your comments, I guess, on 516 and 596. This data update coming up. How you would contextualize the data and CR rates for 516 versus what we would see for 596? How to think about those two from a CRA perspective? And most importantly, you just commented about durability much more clear at ASH, but I would like to understand in the handful of patients who'll get here coming up, how should we contextualize durability?

Scott Wolchko -- President and Chief Executive Officer

Okay. So durability. We will absolutely provide an update on durability of response with respect to the FT516 study, to be very clear about that. With respect to FT596, we are not far enough along to have a meaningful discussion with respect to durability of response. We will clearly provide response rates on 10 patients in monotherapy and 10 patients in combination. With respect to thinking about FT516 versus 596, I think it's an interesting first observation because at one level, the FT516 study is essentially about the potency, if you will, of the hnCD16 CAR construct. The FT596 study, while there is a combination arm, I don't think we're getting much tailwind yet in the combination arm from 516 -- from the hnCD16 receptor because of the dose -- the low doses and the single dose schedule. So I do think the 596 study at some basic level at these lower doses is a test of CAR potency. And so I think at some basic level, at this early stage of comparison, we're looking at FT516 at one level, assessing its -- the potency of hnCD16 with FT596, we're assessing the potency of the CAR construct, and obviously, we would love to be able to see potency from both those mechanisms of action because I think that would feed in to essentially the premise that we have a best-in-class dual-antigen targeted product candidate where both targeting mechanisms have the potential to drive meaningful responses.

Michael Yee -- jefferies -- Analyst

Perfect. And to clarify your comment on durability, do you believe or, let's put it this way, the street seems to believe that allogeneic CAR-T durability that's out there in the public domain is somewhat of the front runner in terms of having data. Do you believe that you want to be better than that in addition to the fact that you have an improved safety profile?

Scott Wolchko -- President and Chief Executive Officer

I clearly think that we need to compete on therapeutic profile. Absolutely. I've said this at a high level. Look, I do think safety can be a differentiator, but at the end of the day, I think you got to compete on therapeutic profile, which obviously is driven primarily by response rates and durability of response. I mean I've said this sort of flippantly before. The patient doesn't care where the cells came from. You have to deliver the patient the best product.

Michael Yee -- jefferies -- Analyst

Okay, thank you.

Operator

Our next question comes from Daina Graybosch from SVB Leerink. Please go ahead.

Daina Graybosch -- SVB Leerink -- Analyst

Hi, thank you for the question, too. For me. I wonder if you could talk about why you decided to do in the two dose regimen of 596 doses at -- two doses in the first cycle rather than doing one dose for two cycle as you initially did of this FDA approval? And the second question is, when should we expect to see more pharmacokinetic data from 516 and 596 in non-Hodgkin's lymphoma, both peripheral blood and tumor and overtime.

Scott Wolchko -- President and Chief Executive Officer

So we'll provide a translational update from 516 and 596, certainly at the investor event, and we'll continue to do that at ASH when we have additional discussions with 516 and 596 with respect to the lymphoma franchise. As it relates to why doses two in one cycle, and I think that just comes back to the fact that at the end of the day, we believe NK cells relative to T-cells are shorter lived. We also believe that -- I'll use the phrase, the kill window, if you will, to really drive deep durable responses occurs in the first 30 to 45 days. And we certainly want to basically maximize the therapeutic availability during that 30- to 45-day window. So our view is certainly that, especially with NK cells and the shorter life cycle is, to provide more than one dose -- in this case, two doses, during the first 30-day window and compare that, for instance, with the single dose cycle.

Daina Graybosch -- SVB Leerink -- Analyst

Thank you.

Operator

Our next question comes from Ben Burnett from Stifel, please go ahead.

Ben Burnett -- Stephen -- Analyst

Hey, thank you very much. I have to ask -- so I want to ask about the FT596 academic study, which I believe is at the University of Minnesota in the adjuvant setting. What's the status here? And I guess, do you have a sense for when this might reach a point of maturity in terms of having enough data to present publicly?

Scott Wolchko -- President and Chief Executive Officer

Yes. Yes, sure. Enrolling patients, I didn't provide an update on it. As you alluded to, it's an investigator-initiated study at the University of Minnesota. Still enrolling patients, absolutely. Probably provide an update, I suspect, probably not at ASH, given how crowded ASH will be with our updates, but maybe in the first quarter, for instance, at the TCT conference, as an example.

Ben Burnett -- Stephen -- Analyst

Okay. Excellent. And then just one quick question on 819. Apologies if I missed this, but this -- the program that you outlined, the clinical program is this and specifically patients that are naive to CD19 CAR-T.

Scott Wolchko -- President and Chief Executive Officer

With 819, no. So patients can have previously received CAR19 cell therapy.

Ben Burnett -- Stephen -- Analyst

Okay, OK. Thank you very much. Appreciate it.

Scott Wolchko -- President and Chief Executive Officer

Sure.

Operator

Our next question comes from Peter Lawson from Barclays. Please go ahead.

Peter Lawson -- Barclays -- Analyst

Hey, thanks for taking my questions. Just the data update that we get on the 19th, how many patients could we see in that post CAR T-cell setting?

Scott Wolchko -- President and Chief Executive Officer

Let's wait for the data. Let's wait for the discussion. I mean, as an example, we had -- in 516, we had four of 11 patients were post CAR T-cell therapy, I believe. Similar range, probably something in that range.

Peter Lawson -- Barclays -- Analyst

Perfect. And then how many patients do you think you'll need to try and file in a post CAR T-cell setting?

Scott Wolchko -- President and Chief Executive Officer

I think it would be pure speculation for me to give you a number. I think our -- what our plan is, and we'll discuss more of this at our investor event, is to complete dose escalation for 516 and pursue RMAT designation to have those conversations.

Peter Lawson -- Barclays -- Analyst

And then just as we think about the solid tumor readout, do you think 516 or 500 could be a viable long-term product in solid tumors? Or should we really be kind of focused around, I guess, for three sets of other constructs in solid tumor?

Scott Wolchko -- President and Chief Executive Officer

Yes. No, I think -- I think 516 -- I think 500 and 516 in the solid tumor setting at some basic level, proof of concepts, understanding sort of translational learnings and incorporating those into certainly, 538, and then even more complex engineered cell therapies that have direct targeting like the three products I alluded to, FT536, FT573 and the first Janssen product candidate. So I think the true test in solid tumors at the end of the day, while I think we can absolutely gain learnings from 500 and 516. I think the true test and to maximize patient benefit is certainly with a multiplexed engineered cell therapy in solid tumors.

Peter Lawson -- Barclays -- Analyst

Got you. So that update in the middle of the year or 3Q would be more focused around kind of biomarker work as opposed to PRs or deeper?

Scott Wolchko -- President and Chief Executive Officer

Yes. Yes. I mean yes, I mean, to put it in context, I don't think we're curing solid tumors with a nonengineered NK cell.

Peter Lawson -- Barclays -- Analyst

Gotcha. Okay. Thank you so much.

Scott Wolchko -- President and Chief Executive Officer

Sure.

Operator

Our next question comes from Matt Biegler from Oppenheimer, please go ahead.

Matt Biegler -- Oppenheimer -- Analyst

Scott, can you hear me?

Scott Wolchko -- President and Chief Executive Officer

I can. Thank you.

Matt Biegler -- Oppenheimer -- Analyst

Thank you. Okay. Great. Thanks for the question. I actually want to piggyback on that last question. Just about the overall solid tumor strategy. Given where your market cap is now, I'm just I'm kind of curious how important is success in solid tumors for your platform? And maybe if you could just point to any data, and it can be more broadly among the NK cell therapy space, that kind of gives you confidence that you can find success or at least, proof of concept in solid tumors. I think if I remember back to the year old APOLLO study, there is at least one partial response. So anything you could give.

Scott Wolchko -- President and Chief Executive Officer

Yes. No, actually, that was one of the references I was going to give you. I mean when we were advancing and you've been following Fate long enough to remember, when we were advancing actually a donor-derived NK cell therapy, which was partnered with the University of Minnesota, you have to go back now two or three years for this. We did run a very interesting study in solid tumors, specifically patients with recurrent ovarian cancer. And we -- it was a single dose of a donor-derived NK cell product. I think it delivered at close to maybe one billion cells, and it was delivered locally with IL-2. And in fact, in that small cohort of patients, I think six patients, there were several patients that had stable disease for a meaningful period of time. So duration of disease control is meaningful. And in fact, yes, you are remembering correctly, one of the patients actually did achieve a partial response. So I do think there is precedent clearly, where NK cells in certain areas may be advantaged, certain mechanisms that we do want to exploit. We've talked about in the past, for instance, patients that have progressed on checkpoint inhibitor therapy, where tumor mutations drive down regulation of MHC Class one. It's a perfect setting for an NK cell to potentially have unique activity compared to a T-cell as there's loss of function with respect to antigen presentation.

Clearly, we believe CD16 is an important receptor and can synergize with monoclonal antibody therapy, and we think that's supported by data that's been seen with respect to -- in the solid tumor setting in monoclonal antibodies. Folks walking around with the high-affinity CD16 flavor do better in outcomes with monoclonal antibody therapy in solid tumors. So I think there is certainly proof of concept out there. But yes, clearly, we are pioneering NK cell therapy in solid tumors. It's an important initiative to us. It's supported by investment in a significant pipeline. We've declared two product candidates already that are multiplexed engineered with CARs in addition of 538, MICA/MICB 7H3. And I would say, under our collaborations, both with Janssen and Ono, product candidates we're developing are against solid tumors.

Matt Biegler -- Oppenheimer -- Analyst

Yeah, that's exciting. Congrats on the progress, guys.

Scott Wolchko -- President and Chief Executive Officer

Thank you.

Operator

Our next question comes from Mara Goldstein from Mizuho, please go ahead.

Mara Goldstein -- Mizuho -- Analyst

Great. Thanks so much. Hey, Scott, I wanted to revisit something that you said around sort of candidate -- multiplex candidates and seeing activity as a function of duration of treatment? And can you talk a little bit more about that and what the kinetics behind that are?

Scott Wolchko -- President and Chief Executive Officer

Yes. I mean, ultimately, look, I don't think durable disease control is going to be sort of carry the day in solid tumors. I think, ultimately, it's about responses and driving responses. And so I think that's how we have to assess ourselves at the end of the day. It's about responses and driving responses.

Mara Goldstein -- Mizuho -- Analyst

Okay. And then also just with MICA/MICB from that perspective, where is the opportunity for therapeutic differentiation there?

Scott Wolchko -- President and Chief Executive Officer

Several different areas. I mean, I will -- we'll talk a lot more about this, obviously, at our solid tumor day. I mean I can turn it over to either Bob or Wayne to talk about the unique potential of MICA/MICB. But obviously, it's a pan tumor targeting strategy, if you will. Many tumors significantly up regulate stress ligands, specifically the MICA/MICB protein. And one of the main mechanisms actually of NK cell evasion -- mean people have talked about mechanisms of T-cell evasion, but one of the main mechanisms of NK cell evasion in solid tumors is shedding of the MICA/MICB stress proteins. And so we always like the idea of targeting stress ligands, but really wanted an approach that could overcome the mechanisms of NK cell resistance, which is why the MICA -- are specific MICA/MICB binding domain hits the alpha three region and is able to bind and kill even after MICA/MICB have been shed from the surface of a tumor.

Mara Goldstein -- Mizuho -- Analyst

Okay. All right. Thanks, God. Appreciate it.

Scott Wolchko -- President and Chief Executive Officer

Sure.

Operator

And our next question comes from Robyn Karnauskas from Truist Securities, please go ahead.

Unidentified Participant

Hey, guys, thank you so much for taking my question. This is [Indecipherable] for Robyn. Congrats on treating the first patient with your CAR T-cell, a year long wait after the IND was approved. So I have a question about that. So can you talk a little bit about what sort of safety concerns do you have? These cells -- you talked about how these T-cells don't exhaust because of their differentiated design. And also, I think you mentioned that 819 is a product comprised only of CD8 cells. So how do you monitor these patients for CRS and neurotoxicity? And also, given that it took a year from IND clearance to first patient treated, can you talk a little bit about what the key hurdles were and what lessons you've learned for future iPSC-based T cell therapies in the pipeline?

Scott Wolchko -- President and Chief Executive Officer

Yes. Sure. So I think we're going into this, expecting that 819 is going to bring us squarely into T-cell land. And what I mean by that is, obviously, with respect to CAR T cell therapies, CRS is a concern. ICANS is a concern. Neurotoxicity, certainly. And so I think we are thinking with respect to 819 that absolutely that if 819 is truly a T-cell, and we believe it is, that we will potentially face many of the challenges that have confronted the autologous and allogeneic CAR T-cell space. I think one of the things that we've done in this study, interestingly is, there's been some work done with autologous CAR T-cell therapy to suggest that lower dosing and multiple doses over a shorter period of time, potentially can drive responses, but mitigate some of the risks associated with CRS and neurotoxicity. And that's why one of the arms of our studies of this 819 study is actually the fractionated dose arm. Where essentially you give 1/3 of the dose, 1/3 of the dose and 1/3 of the dose spread out over a five day period. So that's one of the ways we're thinking about trying to optimize the potential of an iPS-derived T-cell therapy compared to, for instance, the autologous world, as an example.

With respect to your question of manufacture, it was really unique -- it was a unique situation. The reality was, we had kicked off a manufacturing campaign for 819, and we had completed that and that campaign was ongoing. And we are constantly investing in process development improvements, including scalability and consistency of product. And at the end of the day, while we were doing that first manufacturing run, we did discover and have some innovative developments where we wanted to more, I would say, slightly, but important -- but in some important areas, modify the manufacture of 819. And so what we decided to do since we did not treat the first patient, we decided to incorporate that into the manufacturing process, rerun the manufacturing process and then ultimately release the product. So it's very -- it's a pretty unique circumstance where there was a development -- in process development that we felt was important enough and given we hadn't treated the first patient, we elected to wait.

Unidentified Participant

Very helpful. And just a follow-up question on AML, are we still on track for readout around ASH timeframe?

Scott Wolchko -- President and Chief Executive Officer

Yes.

Unidentified Participant

Will you see updated data from 516 and 538?

Scott Wolchko -- President and Chief Executive Officer

Correct. Correct. At ASH.

Unidentified Participant

Do you think -- you had mentioned, I think, at the earlier data readout that 538 is in preclinical studies, more potent than 516. Do you think you'll have enough data this year to make a decision about which one to take forward in AML?

Scott Wolchko -- President and Chief Executive Officer

Yes. If we're not there quite at ASH, I think we'll be there shortly thereafter and sort of my expectation today, again, largely based on preclinical data that FT538 is going to be the product candidate we're going to pick moving forward in AML. But I'm happy to be surprised again with 516.

Unidentified Participant

Okay, great, thank you.

Operator

And our next question comes from Nick Abbott from Wells Fargo, please go ahead.

Nick Abbott -- Wells Fargo -- Analyst

Thank you, Scott, complements on a clear, comprehensive update today. Unfortunately, my questions probably will neither be as clear nor as comprehensive. But first one relates to 819. And you've discussed this a little bit, but you've designed a very broad and aggressive program. So this is clearly not just establishing proof of concept. So do you believe you can show superiority with currently in development or approved off-the-shelf -- sorry, in development off-the-shelf products? Or establish just a broad reference range for your own internal development of next-gen products? And then I have a follow-on.

Scott Wolchko -- President and Chief Executive Officer

Yes. I think from my perspective, look, I think -- and I've said this before, I think that the patient-derived CAR T-cell products have delivered revolutionary results for patients. And certainly, there are logistical challenges. Certainly, there are clinical complexities associated with the patient-derived products, but the results are fairly remarkable. And when I think about FT819, that's the bar. Quite honestly, I think that's the bar with 596 as well. That's the reality of what's out there. There are three CAR19 products now approved, and I think they're obviously being shepherded by very large established pharmaceutical companies, and they will continue to invest in bringing those terrific solutions to patients. So the burden is on us, if you will, to continue to be able to compete with that therapeutic profile. We think there is a lot of advantages to be really clear with an off-the-shelf iPS-derived strategy, a lot of advantages. But like I sort of alluded to before, look, at the end of the day, the patient doesn't care where the cells came from, you have to have a terrific therapeutic profile.

Nick Abbott -- Wells Fargo -- Analyst

Sure. And then just in relation to the new manufacturing facility, I mean can you talk about how that facility could be used? I mean, for example, could you be making thousands of doses for a single product and simultaneously, hundreds of doses of one or more products for...

Scott Wolchko -- President and Chief Executive Officer

Yes. Yes, absolutely. I mean it's -- we didn't give an update here. We'll probably give an update on the next call. We're right on schedule. We're actually in the midst of moving and occupying that headquarters. It's a 50,000-foot GMP footprint. We absolutely -- I think in there, maybe 12 different GMP suites. And so certainly, we have the capacity to manufacture multiple different product candidates at large scale, and we do think we potentially could launch, at least initially, commercially from that facility. It likely -- with continued success, it likely won't be our only manufacturing facility, but certainly, I think it provides us tremendous opportunity to advance multiple product candidates in parallel and accommodates initial launch, commercial launch.

Operator

We have no further questions at this time. I will turn the call over back to Scott Wolchko.

Scott Wolchko -- President and Chief Executive Officer

Perfect. Perfect. Thank you. Thanks, everyone, for participating in today's call and all the great questions. Definitely look forward to reconvening here, I think, probably maybe two weeks from today and providing a fulsome update on the FT516 and 596 programs in lymphoma. Thank you very much. Be well. [Operator Closing Remarks]

Duration: 63 minutes

Call participants:

Scott Wolchko -- President and Chief Executive Officer

Edward Dulac -- Chief Financial Officer

Yigal Nochomovitz -- Citigroup -- Analyst

Michael Schmidt -- Guggenheim -- Analyst

Alicia Young -- Cantor Fitzgerald -- Analyst

Michael Yee -- jefferies -- Analyst

Daina Graybosch -- SVB Leerink -- Analyst

Ben Burnett -- Stephen -- Analyst

Peter Lawson -- Barclays -- Analyst

Matt Biegler -- Oppenheimer -- Analyst

Mara Goldstein -- Mizuho -- Analyst

Unidentified Participant

Nick Abbott -- Wells Fargo -- Analyst

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