Welcome to the Fate Therapeutics Fourth 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. As a reminder, today’s call is being recorded. I would now like to introduce Scott Wolchko, President and CEO of Fate Therapeutics..

FT536, which incorporates a CAR targeting the stress-induced proteins MICA and MICB overcome prominent mechanisms of immune cell elevation; and FT573, which incorporates a CAR targeting B7-H3 and is designed to uniquely target the metabolic profile and metastasis of discern.

In addition, we are also developing multiplexed-engineered CAR NK and CAR T-cell product candidates for solid tumors, alongside our two partners, Janssen and Ono.

I am pleased to announce that the first patients have been treated in our Phase 1 study to assess three once-weekly doses of FT538 in combination with monoclonal antibody therapy for advanced solid tumors.

The clinical protocol includes combination with each of four monoclonal antibodies, EGFR-targeted cetuximab, HER2-targeted trastuzumab, PD-1 targeted pembrolizumab and PD-L1 targeted avelumab.

Each patient is eligible to receive up to two FT538 treatment cycles, and additional FT538 treatment cycles may be administered to patients that achieve initial clinical response.

While the eligibility criteria enable the assessment of FT538 antibody combinations in a broad array of solid tumor indications, we are particularly interested in assessing various combinations in non-small cell lung cancer, given its immunological features, including that many tumor subsets express targets of interest for NK cell-based therapy.

We are also preparing to initiate a multi-center Phase 1 clinical trial to assess a multi-dose, multi-cycle treatment schedule of FT536 as monotherapy and in combination with monoclonal antibody therapy for advanced solid tumors.

FT536 is the company’s off-the-shelf, multiplexed-engineered iPS-derived NK cell product candidate, which incorporates a novel CAR targeting the proteins MICA and MICB.

High expression of MICA and MICB proteins, which is induced by cellular stress, damage or transformation has been reported on many solid tumors, although the proteolytic shedding of the alpha 1 and alpha 2 domains of these proteins is recognized as a common tumor escape mechanism.

The clonal master iPSC bank for FT536 was created from a single iPSC engineered with four functional elements, including the novel CAR, which uniquely targets the alpha 3 domain of MICA and MICB and is designed to overcome tumor escape mechanisms mediated by loss of the MHC Class 1 expression and protolytic shedding.

We look forward to providing an initial update on our FT538 and FT536 solid tumor programs as we advance through dose escalation. I would now like to turn the call over to Ed to highlight our fourth quarter financial results..

Thank you, Scott, and good afternoon. Fate Therapeutics is in a strong financial position to advance our pipeline. Our cash, cash equivalents and investments at the end of 2021 were approximately $717 million.

In the fourth quarter of 2021, our collaboration revenue derived from our partnerships with Janssen and Ono Pharmaceutical increased by $1.2 million to $17.1 million, compared to $15.9 million for the same period last year.

Research and development expenses for the fourth quarter increased by $30.5 million to $69.5 million compared to $39 million for the same period last year.

The increase in our R&D expenses was attributable primarily to investments made in equipment and materials; increases in employee headcount and compensation, including share-based compensation; and in expenses associated with R&D fees and third-party professional consultants.

General and administrative expenses for the fourth quarter of 2021 increased by $6.6 million to $16.9 million compared to $10.3 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 talent acquisition and facility-related fees. Total operating expenses for the fourth quarter were $86.4 million, which includes $14.6 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, in the third quarter of 2021, 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 paid in the fourth quarter. Up to two additional milestone payments may be owed to MSK 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 $24.2 million, on a quarterly basis. In the fourth quarter, we recorded a non-cash $0.5 million non-operating benefit associated with the change in fair value. Our net loss for the fourth quarter of 2021 was $69.3 million or $0.72 per share.

And finally, we expect to end this year with at least $400 million in cash, cash equivalents and investments. This does not include potential success-based milestone payments from our collaborations with Janssen and Ono Pharmaceutical. And with that, I would now like to open the call to questions..

Thank you. [Operator Instructions] Your first question comes from the line of Michael Yee from Jefferies. Your line is now open..

Hey, Scott, thank you for the update. Appreciate that. We think that solid tumor updates later this year could obviously be pretty important as you expand the power of the platform.

Could you just maybe comment on how to think about the ongoing 538 study in combination with antibodies? And how to think about what that could show in terms of efficacy? And since you did comment that you’ve obviously now about to start the 536 MICA/B study, would you have enough data later this year to talk about that in a solid tumor update? Thank you..

Sure. So I mean, we’re early in the 538 study. But obviously, there are four different escalation cohorts that are enrolling concurrently and independently.

So we do believe we’re going to get a very good early look here with respect to FT538’s potential in combination with four different monoclonal antibodies, again, across several different solid tumors, but with an emphasis on non-small cell lung cancer.

We can talk a little bit more about when we think that update will be, but we’re striving to continue to work through dose escalation in the 538 study and then provide an update, which we think can be in the second half of this year. That’s what we’re targeting currently with dose escalation.

With FT536, the IND has obviously cleared with the FDA, super excited about that. Another multiplexed-engineered product that’s pretty sophisticated, that we cleared the IND in 30 days. And we expect to begin dosing the first patients in that study in the – probably in the middle of this year.

I think what’s important about the 536 study is it all – in addition to combination with monoclonal antibody, it includes a monotherapy arm. And so the monotherapy arm will kick off first. We will start at 100 million cells. We will start at multiple doses of that monotherapy arm.

So we think this will be an interesting first look at the CAR MICA, MICB construct and its ability to target certain solid tumors. So we’re relatively early with respect to the development of the solid tumor franchise, but look for – look to provide an update as we work through dose escalation..

Thank you..

Your next question comes from the line of Yigal Nochomovitz from Citi. Your line is now open..

This is Ashiq Mubarack on for Yigal. Thanks for taking my questions.

In the – for the post-CD19 CAR-T expansion study that you’re initiating in B-cell lymphomas later this year, I guess, what are some of the key factors you’re considering in choosing between 516 and 596?.

Yes, there is a multitude of factors that will come into play. I think the two that I would highlight is, number one, we’re obviously continuing to generate data with both FT516 as well as FT596. So we will make – we will certainly make a data-driven decision. We’re also having conversations with the FDA with respect to clinical study design for that.

So input from the FDA will also impact our decision with respect to what product candidate we will ultimately select. I think the one thing to note is, certainly, FT596, were doing a little bit more work with respect to its dose and schedule.

And we’ve indicated that we potentially will even do a little bit of dose-escalation work still with FT596 and go to 1.8 billion cells. We think that’s prudent. It makes absolute sense.

As I think we will make the decision ultimately probably in the second half of the year based on a multitude of factors, we will be – we are prepared to move forward with either product candidate..

Okay, thank you very much..

Sure..

Your next question comes from the line of Tyler Van Buren from Cowen. Your line is now open..

Hi, guys. This is Tara on for Tyler. So I want to focus on the bendamustine combo that you’re currently enrolling for 516 and the R-CHOP cohorts for 596, which haven’t been talked about too much yet. So first, what proportion of patients, are being treated in the community sending, at least – setting, at least for the benda cohort.

And when can we expect data from that? Should it come along with the longer term Phase 1 data in August or at ASH and if so how many patients? And where can we set expectations? Thanks..

Yes. So I think in future updates, we will provide clarity on when we might be able to provide data on both 516 or R-Benda as well as 596, obviously, in combining with R-CHOP. But I’ll let Wayne talk about our strategy a little bit with 516 and 596, and our outreach into the community..

Sure. When we think about these combinations of 516 and 596, as Scott mentioned, we’re highly interested in the ability to use these cell products without Flu/Cy conditioning. And so the rationale for combinations with R-Benda and then R-CHOP are essentially twofold.

One is to take a standard immunochemotherapy regimen that’s used for the treatment of lymphoma and see whether or not by having complementary mechanisms of action, we can – that can translate into greater clinical benefit.

The second question is really about the ability of regimens such as R-Benda, R-CHOP to also serve themselves as conditioning regimens that can facilitate 516 or 596 pharmacokinetics. And so the purpose of doing both of these investigations is really to hone on those 2 different concepts.

And with respect – specifically with respect to rituximab plus bendamustine, R-Benda is a standard therapy that’s used in a broad array of B-cell malignancies, both aggressive lymphomas as well as indolent lymphomas.

And data from the University of Pennsylvania has demonstrated that single-agent bendamustine could actually serve also as conditioning therapy for autologous CD19 CAR T. So our intention to combine FT516 with R-Benda is really to extend that concept.

And then certainly, the same principles hold true when looking at combinations of FT596 with R-CHOP, right.

And the implication there, of course, is that if you can demonstrate additive activity as well as the ability of R-CHOP to serve as a conditioning regimen for cells, then that has significant implications with respect to how we treat patients with newly diagnosed disease.

Your next question comes from the line of Daina Graybosch from SVB Leerink. Your line is now open..

Yes. I want to ask a follow-up to, Wayne, what you just said on the R-CHOP in particular.

And can you talk about how you might design the trial to understand both of those goals over conditioning? And is there any other data in the community or in academic settings that talks about or shows how the CHOP part of R-CHOP could be a conditioning regimen for cell therapy?.

So I’ll take the first part of the question, and then I’ll turn it to Wayne. So Daina, I think it’s a little bit early for us to talk about what our development strategy is with respect to R-CHOP. Obviously, we do have one, and we’re thinking it through very carefully.

I think the one thing that we are interested in demonstrating off the bat is there – do we see in the first couple of patients, anything that is disqualifying. And so for instance, we – obviously, this has not been done before. Almost all cell therapy has been delivered in conjunction with Cy/Flu.

And so, we will be looking carefully at the translational data, both safety and translational data that would suggest or support the ability to deliver FT596 without Cy/Flu in combination with R-CHOP, where R-CHOP can provide the necessary sort of background for the cells to flourish and have potent activity.

I think I’ll turn it over to Wayne to answer the second part of that question..

Apologies.

Can you just repeat that second part of the question so that I’m clear?.

I just wondered if like bendamustine, there is anything combined in cell therapies with CHOP that you can lean on or gives you confidence of your strategy?.

Yes. So as Scott mentioned, this is the first time that we’re kind of embarking on this with respect specifically to CHOP. So I think the question is still a very valid one until we start generating clinical data. I would say that conceptually, it’s similar to that of R-Benda.

And I think the key question is whether or not CHOP when you give it – especially when you give it multiple cycles over six cycles, whether or not that can achieve the same conditioning effect as what we typically see with Flu/Cy. It may be very different, and that’s what the intention of this study is, to really start interrogating those questions..

I mean I think I’ll pick up on that. I mean I think it’s a very different – the idea of combining with R-CHOP or R-Benda is a very different paradigm than, for instance, the Cy/Flu paradigm, right. So obviously, standard-of-care R-CHOP, standard-of-care R-Benda are given in multiple cycles.

And for instance, with R-CHOP, the cycles are literally, I think, correct me, 21 days apart. So we’re talking about being able to add 596 to each cycle of R-CHOP and assess, obviously, the cells’ performance. So very different paradigm than what’s currently utilized for cell therapy..

Great, thank you..

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

Hey, this is Kelsey on for Michael. Thanks for taking our question. On FT596, I guess you’ve noted you’re treating patients in multi-dose multi-cycle.

I guess how many cycles are you planning to give there? And then regarding the decision in the second half of the year for pursuing either 516 or 596, I guess, is that specifically for the post-CAR-T patient cohort? Or are you choosing the go-forward product more broadly? And then will early 819 data inform that decision at all? Thanks..

Wow. There is a lot in there. That’s okay. That’s okay. That’s okay. Look, the decision around the development of a lymphoma strategy is obviously multifactorial. There are lots of, obviously, considerations. But we are very comfortable that at the end of the day, there may in fact be a multiproduct franchise in lymphoma.

There are plenty of targets, plenty of opportunities, patients to serve in lots of different settings. So we’re very comfortable with the fact that there may be a multiproduct franchise in lymphoma. How we make that decision, I’m not going to get into it necessarily on the call, but it’s certainly multifactorial.

I don’t know, Wayne, if you want to add anything to that?.

The only thing I would add to that is – and it’s just to emphasize the fact that while we are aggressively pursuing a potential fast-to-market strategy in a specific population of patients, who progressed or relapsed on prior CAR-T our clinical investigations for all of these products extend well beyond that.

We are looking at other patient populations in parallel with this potential fast-to-market approach. And so I would imagine – I think it’s safe to assume that the broad development strategy will be reflected on what data we get from these other patient populations for all of our products.

So you have not only multiple product candidates, but you have a multitude of B-cell indications in which these products can operate optimally..

Now with all that said, I will continue to maintain that we are big believers in multi-antigen targeting. We think that will add significant value to patients. And so I will continue to maintain that at the end of the day, we believe FT596 is a best-in-class NK cell product candidate, and that includes with respect to FT516.

We got to generate more data. We are certainly now looking at the first multi-dose, multi-cycle experience with FT596. But today, we continue to maintain FT596 as a best-in-class product candidate.

And if that becomes, for instance, our lead CD19, CD20 targeted strategy in lymphoma and our best-in-class way to engage rituximab, I am not going to apologize for that at the end of the day..

Okay. Thank you..

Your next question comes from the line of Nick Abbott from Wells Fargo. Your line is now open..

Good afternoon Scott Wolchko and thanks for updating as always. Maybe just starting on this post CAR-T, clearly, the data you have shown to-date, the activity in patients who – primary failures is less durable than those sort of are not primary failures. And I acknowledge these are still relatively low doses.

But as you go forward here, do you look at both of these populations as one population or as discrete populations? And then I have a follow-up. Thanks..

Yes. So, I think that’s a fair question. I think it’s one of the reasons I talked about continuing to generate data with both FT516 and 596. We certainly are looking at patients down line of CAR T-cell therapy that have previously responded to CAR-T. And we are certainly looking at patients that are refractory to CAR-T.

And so as we think about crafting ultimately our registration strategy and the pivotal trial design, we will continue to be guided by data..

Okay. And then I know there has been a couple of publications recently of patients who have failed CD19 CAR T following a CD19 bispecific. And it’s pretty clear that, that sort of epitope coating that’s preventing that.

So, given the likely uptake of CD19 bispecifics, is that a population that you think you can access with rituximab combo while the old CD19 washes off?.

Yes. I mean I will let Wayne talk, too, but I think that’s one of the value propositions that we bring to the table with either 516 or 596. CD20 seems to be a very durable target throughout the lines of treatment. We certainly have seen terrific synergy between our hnCD16 receptor and rituximab.

And so including, as you mentioned, demonstrating complete responses down line of CD19-targeted therapy. So yes, I continue to think the CD20-targeting strategy in combination with rituximab is definitely differentiated..

Only thing that I would add is specific to your question around T-cell engagers that – where the target is CD19, just keep in mind that most of these CD19-targeting T-cell engagers have relatively short-half lives, because they are not of an antibody format that’s similar to some of the CD20 engagers, which are more full-length antibody structures.

So in that context, there is still a possibility for the use of a CD19-targeted cell therapy with a relatively lower washout from prior 19 engaging antibodies..

Great. Thanks. And then just a last one for me, and that is just going back to AML. That was kind of the first therapeutic franchise update you gave last year, Scott, around midyear. And so do we take it from your comments that you sort of completed the 516 dose escalation now, perhaps some expansion.

But the data there are not compelling enough to move forward. And then, have you considered looking at this in high-risk MDS, being as that’s sort of considered less aggressive than refractory AML? Thanks..

Yes, I think our strategy has not changed at all. At the end of the day, we don’t plan on advancing more than one product candidate in the relapsed/refractory AML setting. We are making development decisions and bets on what we think are our best-in-class product candidates.

And we were always in the development mode, if you will, where we said we wanted to complete dose escalation with FT538, including up to 1.5 billion cells, and then make a further development decision. And nothing has changed there..

Thank you..

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

Okay. I actually wanted to ask a follow-up on the prior AML question, and it might be philosophical at this point.

But do you think that NK-cell therapy can be curative on its own, or is it always going to need to be consolidated with a standard of care stem cell transplant? And if it’s the case where you do need a stem cell transplant, have you guys considered exploring 538 or one of the other products in an earlier treatment setting? I guess this kind of gets to what the broader corporate strategy is.

But maybe looking at AML and like the MRG positive space post induction, but pre-transplant? Thanks..

Yes. We are so – we are doing a lot of work internally on a next step with respect to the development of the AML franchise. I think as you are alluding to, there are multiple development opportunities that exist in treating patients earlier in care.

Treating multiply relapsed or refractory patients is obviously a difficult space given how sick these patients are, given the frailty that many of these patients are with respect to age and lines of treatment that they have gone through, given the fact that usually multiply relapsed/refractory patients also, the bone marrow has been permanently damaged.

So, I think the curative potential in AML, I think you have to intervene earlier. And I ultimately believe that most likely, if you want to deliver cures in AML, you are probably best suited by a targeted strategy. One of the challenges in AML, obviously, is with targets.

We are obviously really interested in what we are going to see here with FT538 in combination with daratumumab. But certainly, I do think targeting leukemic blasts in the bone marrow and intervening earlier in care provides the best chance of a curative outcome.

I don’t know, Wayne, if you want to add up on that?.

No, just exactly as Scott said. I think the value of going in early line is to try to provide some form of therapy, where you can give it before the bone marrow gets totally obliterated by repeated rounds of treatment. So, that – we are always cognizant about opportunities to go into earlier line. And of course, that’s not just AML.

That’s B-cell malignancies, you can make a similar argument in that regard..

And obviously, in order to pursue that strategy, one of the concerns with AML is the frailty of patients. So, you have to have a pretty exquisite safety profile to enable that..

Thanks..

Your next question comes from the line of Mara Goldstein from Mizuho. Your line is now open..

Hi. This is Gabriel for Mara. Thank you for taking the questions. My question is on FT819, can you expand a little bit on the rationale behind the different cohorts exploring lower IL-2 and specific dosing.

And related to that, with its unique design, perhaps the treatment regimen, do you expect 819 to be differentiated from other allogeneic CAR-T in development, particularly on the durability? Thank you..

So, thank you for the question. So, regarding FT819, the way I would look at FT819 is – the nice thing about that study is that it is an opportunity to exploit a lot of the features of iPSC-derived CAR T-cells that – with the end goal of having a better therapeutic index or better clinical activity than current-generation CD19-targeting CAR-T.

And so the reason for the – each of the different regimens in that study is to address specific components regarding the efficacy and safety of FT819. So, for example, the addition of IL-2 is to really explore the value of that cytokine to promote T-cell persistence and function.

We know from multiple T-cell based therapies that – of the importance of IL-2. So, we believe that assessing the addition of IL-2 is an important clinical experiment.

Equally as important is the ability to take advantage of the off-the-shelf, on-demand features of a cell product like FT819 and see whether or not the flexibility around dose and schedule offers an opportunity to improve the clinical risk-benefit profile of the product.

And so the purpose of the multiple dose regimen, where FT819 is given on day one, day three and day five of each treatment cycle, is not only to evaluate the ability of multiple doses to drive deeper responses, but also to see whether or not flexibility with respect to individual day dose can lead to a better safety profile.

And this is exemplified by the experience from the University of Pennsylvania, where they were able to use a multiple dose cycle – or sorry, multi-dose cycle of their autologous CD19 CAR-T product to actually improve the safety outcomes in patients with relapsed/refractory ALL.

So, we are looking at that as an opportunity to do the same thing here with FT819..

I would also say just with respect to other programs, look, this is pretty novel. Sure, it’s a CAR T-cell and you can think about it that way. And you could say, gosh, it’s going to look like an autologous CAR T-cell or a donor-derived T-cell.

But there are some substantial differences here with respect to the targeted insertion of a CAR into the TRAC locus, with respect to the CAR construct we are using, which is a novel CAR construct, 1XX, with a perspective that we are making a fairly homogeneous patient – cell type with – that is majority of cells are of a memory phenotype.

And so we do think that the outcomes with FT819 do have the potential to be very differentiated. I think one of the challenges associated with, let’s call it, even patient-derived CAR T-cell therapy, but certainly donor-derived CAR T-cell therapy, is the cells do go through an extensive period of manufacturing and processing at the T-cell level.

And that can cause T-cell exhaustion. I mean even in the patient-derived CAR T-cell world, there is a desire to significantly reduce manufacture time. And that certainly has to do with vein-to-vein time to reach patients, but it also has to do with the potency of the cells, the T-cells themselves.

And so I think one of the unique features of our iPS-derived cell product is we create significant numbers of T-cells without actually, for any significant time, expanding the T-cell population. And so we think we are creating a very potent T-cell that has very low expression markers of exhaustion.

And that can be – potentially be very differentiating..

Got it. Thank you..

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

Hi. Thanks guys and thanks for the great update. So, I guess one small one, probably a stupid question, and a bigger one. So, for the 596 dose escalation to 1.8 billion, I know before you talked about 900 million times two, and then maybe a third dose.

Can you just clarify, when you are dose escalating to 1.8 billion cells, would that be 1.8 billion at day 1 and day 15, or are you talking about like another round of dosing? And then the second question, which is broad, is that I think last year, in oncology in general, not just say we are all plagued by expectations being so high.

Everyone wants to be very – more complete insights with longer durability. And you have got – you have said you are going to get some updates in the second half of the year on a couple of programs with, I think a huge focus on your 536 program.

Have you set any changes in your internal bar as far as like what you will release or disclose, and to say, at some point, we won’t disclose data unless it’s this mature? Given the environment we are in and given last year’s debacle, I think, with all of oncology, shifting how much data is required for investors to make an assessment if something was real or not? Thanks..

So, the first one is pretty easy. So the first one, we are doing two doses of 900 million cells, day 1 and day 15. We have the ability, obviously, to do two cycles now of day 1 and day 15 at 900 million cells. And actually, we have the ability to do more than two cycles as well with FT596 under the protocol with the FDA.

Certainly, with a couple of patients showing safety, we are able to expand that treatment schedule. And while we are expanding, we will very likely explore a higher dose, where the dose, to be clear, is 1.8 billion at day one and 1.8 billion at day 15. And again, we could give a second cycle of that or even more than two cycles of that.

So yes, we are going to do a little bit more dose escalation here and go to 1.8 billion cells delivered on day 1 and day 15. With respect to sort of the broader environment, look, I am a – we are doing something at Fate Therapeutics that is incredibly novel.

And I am going to continue within all reason to be as transparent as possible with respect to what we are doing and what we are seeing, just my philosophical perspective..

Thank you. That’s helpful. Thanks so much..

Your next question comes from the line of David Dai from SMBC..

Hi. Thanks for taking my questions. So, my question is on the FT516 plus R-Benda or R-CHOP without Cy/Flu conditioning. So, we have seen – we have increasingly seen, based on allogeneic CAR-T data, that we need intense attrition in order to see CAR-T expansion.

Could you just provide some color as to what gives you the confidence that FT516, R-Benda, or R-CHOP could expand in the absence of such? Thanks..

I think I will let Wayne talk to it, but I think it’s one of the reasons we are doing the study. I mean certainly, we have seen different environments that – where cells can perform under.

I think if I speak specifically about Cy/Flu or we R-CHOP – we are not so sure with R-CHOP yet, but R-Benda, certainly, when you start thinking about delivering cells in multi-dose cohort – or sorry, multi-dose treatment schedules, the reality is that, for instance, when you look at R-CHOP or you look at R-Benda.

Those treatment schedules the window for instance, that might exist with respect to lympho depletion is only, for instance, 20 days. So for instance, you give R-CHOP, and then 21 days later, you give R-CHOP again. And then 21 days later, you give R-CHOP again. So, we are not looking actually to achieve long-term persistence of a cell.

We are looking to plug into multi-dose treatment schedules, including standard of care that exists for early line patients. The treatment paradigm we are pursuing is not with an NK cell, is not necessarily a patient-derived CAR T-cell paradigm of one dose – persistence of one dose.

And quite frankly, I am not even sure the persistence of a CAR T-cell, a patient-derived CAR T-cell is correlated with long-term outcomes. There is a tremendous amount of data to suggest that long-term, durable responses have nothing to do with long-term persistence of cells.

It’s all about the killing capacity and potency during the first 14 days, 21 days, 30 days..

Thank you. Very helpful..

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

Hi. Thanks Scott. Just a follow-on question from David’s question.

Just kind of how many indications do you think you can use iPSCs, where you can kind of skip the conditioning regimen? Should we be thinking about those as any indication that has things like R-CHOP or R-Benda?.

I mean we are going to take – we get a first look. I mean right now, it’s all – it’s a speculation at some basic level.

We are certainly encouraged by the fact that when we have looked at Novartis’ data with respect to use of bendamustine with a not Cy/Flu, certainly, I think we have seen sort of evidence that you can move away from Cy/Flu and use R-Benda. I will also say – I mean keep in mind, and this is really important.

A big part of what Cy/Flu does is actually about cytokine spiking within the patient. So, if it was about, for instance, immunogenicity or alloreactivity, patient-derived CAR T-cell is delivered with Cy/Flu.

It’s delivered with Cy/Flu or it’s delivered with bendamustine because the cells that are being adoptively transferred love to go into a cytokine-rich environment. Our cell therapy, starting with FT596, have cytokine support engineered into them.

So, they are less reliant, we believe, and less dependent on the conditioning regimen spiking cytokines, because our cell therapies have cytokine support engineered into them..

Great. Thank you so much..

There are no further questions at this time. I would now like to turn the conference back to Scott Wolchko..

Terrific. I want to thank everyone for your participation in today’s call and all the great questions. Look forward to providing you updates in the coming months. Be well. Take care..

This concludes today’s conference call. Thank you for participating, and have a wonderful day. You may all disconnect..