Good day, ladies and gentlemen and welcome to the Fate Therapeutics First Quarter 2021 Financial Results Conference Call. This call is being webcast live on the Investors section of Fate Therapeutics website at fatetherapeutics.com. [Operator Instructions] I will now turn the call over to Scott Wolchko, President and CEO of Fate Therapeutics. Scott, you may begin.

Thank you. Good afternoon and thanks everyone for joining us for the Fate Therapeutics first 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 March 31, 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 March 31, 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 Bob Valamehr, our Chief Research and Development Officer. Today, we will highlight our clinical progress and plans for each of our disease franchises, including our plans to share interim clinical data for off-the-shelf IPS-derived NK cell programs…

Thank you, Scott. Turning to our financial results, revenue was $11.1 million for the first quarter of 2021 compared to $2.5 million for the same period last year. Revenue in the current quarter was derived from our collaboration with Janssen and ONO Pharmaceutical. Research and development expenses for the first quarter of 2021 were $44.9 million compared to $29.3 million for the same period last year. The increase in our R&D expenses is attributable primarily to an increase in employee headcount and compensation, including share based compensation, and in expenses associated with clinical trial costs. General and administrative expenses for the first quarter of 2021 were $12.5 million, compared to $7.7 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 first quarter of 2021 were $44.4 million, net of $13 million in non-cash share based compensation expenses. In the first quarter, we recorded a non-cash $0.7 million non-operating benefit 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 or are currently owed to MSK. We will re-measure this liability currently valued in the aggregate at $47 million on a quarterly basis, and changes in the fair value will be recorded in our earnings as a non-operating income or expense. In January, we completed a public offering of common stock, whereby we issued 5.1 million common shares. In addition, in lieu of common stock, we issued 257,000 pre-funded warrants. The net proceeds from the financing were approximately $432 million. The company ended the first quarter of 2021 with $888 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. I would now like to open the call up to any questions.

[Operator Instructions] And we do have our first question from Robyn from Truist Securities.

It’s Robyn Karnauskas. Thanks for taking my question and so much on the call. So with this is sort of next week, and then you have a lot of data coming, you talked that – you updated on the call, you talked about how you updated on FT516 and FT538. Maybe give us some color about the patient baseline. How many patients will we see, how many doses will be treated with? And how do we think that your strategy in AML. And sort of big picture, how do you digest this data? And how do we set the expectations for? Thanks.

Sure. So Robyn, I mean, we will have a fairly comprehensive event from now. I think its next Thursday. So eight days from now, we will have a fairly comprehensive event. We will walk through what has historically been done with respect to NK cell treatment in AML. We will provide some detail on the preclinical results that we have seen for instance with FT538, including comparing FT538 to FT516. And then Wayne will spend a significant amount of time walking through the history of the patients that we have treated. You will see patients – on a patient you will see detail on a patient-by-patient basis. So, we plan on providing the detail for each and every patient. And you will see baseline characteristics. You will see whether that patient is relapsed or refractory. You will see most recent therapy. You will see that for instance risk profile associated with each and every patient. And then importantly, you will obviously see anti-leukemic activity and responses associated with each and every patient. So, there will be a tremendous amount of detail. There will be – it will be very transparent on a patient-by-patient basis. And we expect to include in that about in total…

And strategy in solid tumors, I mean going forward that’s the big one for you with more clarity there, I am excited about that?

Strategy in solid tumors, absolutely, I mean clearly we think there are multiple monoclonal antibodies that are improved in solid tumors, for instance, whether it would be Herceptin, Erbitux, avelumab or others. And part of their mechanism of action is dependent on antibody-dependent cellular cytotoxicity ADCC. And we think NK cells play a really important role there. We actually think there is plenty of evidence to suggest that ADCC today is not being optimized that the NK cell compartment essentially that exists within patients is checked or compromised. And that by coming in with a wave of NK cells that are designed to synergize with the monoclonal antibody, we think we can substantially augment responses. That’s step one. And we are started to initiate that obviously, with FT516, which obviously, increasing our investment based on our conviction in ADCC, by moving FT538 now into solid tumors across a fairly broad set of monoclonal antibodies in solid tumors. Ultimately, though, as you know, we think of that as a stepping stone. What we are doing for instance in lymphoma, what we are doing in myeloma, where we are utilizing for instance CD16 in addition to engineered CAR functionality. We are doing the same exact thing in solid tumors, while we have product candidates emerging in the second half of this year, building off of the FT538 backbone, engineering CARs for instance, our first IND will be engineering a CAR against MICA/B stress ligands. We recently presented data where we have engineered in a CAR into the FT538 backbone against B7H3 as a solid tumor targeting strategy. And in addition, we expect that the first IND, actually under the Janssen collaboration will be a core NK cell product for solid tumors.

Alright. Thanks, guys. Again, you have mind blown me about how many different products you have to focus on. I am writing them all down. But thank you so much. I appreciate it.

Sure.

And we do have our next question from Ted Tenthoff from Piper Sandler.

Hi guys. Thanks so much for taking the question. I want to follow-up a little bit, appreciating that we are going have the event later this year, and more datasets. With all these different approaches on the solid tumor side, how do you ultimately envision this playing out? Do you expect that there will be certain cell types that may be played better in different kinds of cancers with different kinds of therapeutic combinations? Do you ultimately see an ultimate product like the MICA/B, give us a little bit more color on sort of where your thinking is at? Thank you.

Sure. I mean I think it’s early for us to have a definitive strategy in solid tumors with multiplexed engineered cell therapy since we are breaking new ground. I do think generally, there are certain solid tumors that may actually be more amenable to an NK cell therapy. We have talked in the past for instance, that there are various mechanisms of resistance that solid tumors utilize to escape recognition of the immune system, whether it’s T cells or NK cells. One of the more significant mechanisms of resistance is actually where the tumor works to down-regulate MHC class 1. And there is loss of antigen presentation through that down regulation of MHC class 1. Because of that T cells can no longer recognize those tumors. That’s the exact cell type that an NK cell can in fact recognize. And often times the cells, the tumor cells that down-regulate MHC class 1, or high expressers of stress ligands. Again, these are for instance, cues for NK cells to recognize an attack. So, I think that is one area of solid tumor biology that we are really interested in with respect to NK cells. And in particular the CAR MICA/B product candidate, since it’s designed to key in on stress ligands and even overcome resistance that exists with down-regulation of stress ligands or shedding of stress ligands. But in addition, I also think, there is going to be a fundamental role for combination with monoclonal antibody. I mean, monoclonal antibodies are used early and often successfully, clearly solid tumors. And part of their molecular mechanism action is ADCC, and NK cell dependent. And so we are really excited for instance, with respect to FT538, and being able to combine that with monoclonal antibody therapy against a broad array of solid tumors.

Excellent. I am excited to the events coming up and more data this year. Thank you.

And we do have our next question from Alethia Young from Cantor.

Hey, guys. Thanks for taking my question and congrats on all the progress looking forward to next week for sure. I guess I just wanted to maybe it’s a philosophical and practical question, just how important that durability after kind of a single dose or understanding that or having a kind of a perception of that and like this data set and other upcoming datasets as well. And then also, can you talk a little bit about is it the PDL1 that’s kind of a better target versus PD1, I am just curious about…?

Sure. I will start with the last question. I mean, we are obviously early in exploration with respect to combination of monoclonal antibodies and solid tumors. We started with avelumab. It doesn’t mean it was the right place to start. But we started with avelumab, because obviously PDL1 is up-regulated on the tumor itself. So we thought at least it provided a means by which the NK cell could target in combination with avelumab, a target expressed on a tumor as opposed to PD1. With respect to durability of the doses, I mean, again, this is something that we are exploring and we are experimenting with different treatment regimens, and schedules to begin to tease out the differences that might exist between treatment schedules, whether that’s one dose, whether that’s for instance, up to six doses. I think it’s too early to know the answer to that question. I think, fundamentally, we believe two things that there is a period of time, especially for aggressive cancers, where you need to hit the tumor hard. And that may be the first two weeks, maybe that’s the first four weeks, maybe that’s the first six weeks. But there is a period of time where we believe a therapy really needs to aggressively attack the tumor to lead to deep durable responses. And I would also say, our belief system today is that the best way to drive that deep durable kill going that window, again, whether it would be two, four or six weeks, is through multi dosing. And the reason for that is because when you administer a cell into a patient, I think there is lots of data emerging, that that cell profoundly changes with respect to its function, properties, anti-tumor killing ability, going that window of kill. And so our belief is that to really maximize activity, and because the cells administered to patients do change within the patient, that a multi dose strategy is likely going to be the best strategy. And I would say finally, similar to that, we believe a multi targeting strategy is going to be the most effective strategy.

Okay. Thanks. That’s helpful.

And we do have our next question from Yigal Nochomovitz from Citi.

Hi. Thank you very much for taking the question. Following your prepared remarks on AML, you mentioned that – alluded to are being correlated with improved overall survival and obviously some of the more recent approved therapies for AML targeted therapies such as FLT3 and IDH inhibitors were approved based on the narrow measure of CR CRH. So I was just wondering, is there any specific reason with respect to cell therapies, the focus should be on ORR as opposed to CR CRH as in the case for the targeted therapies and have you had any discussions with the FDA on this nuance?

Now, we have not had any discussions with the FDA at this point. We are using what we believe to be an updated criteria using 2017 ELN. We think it is the gold standard. We can have an interesting discussion. And maybe Wayne can jump in with respect to CRH versus CRI. We actually believe under the 2017 ELN criteria, CRI is a higher bar than CRH. CRI requires either full recovery of neutrophils, or platelets. CRH does not require full recovery of either. So under the 2007 ELN criteria, we actually believe CRI is a higher bar than CRH. And Wayne, I don’t know, you may want to comment on that.

So just one comment, I mean, I think, yes, I mean we are certainly assessing our responses objectively, based on the 2017 ELN criteria. We are very aware of some of the recent approvals, for example, with some of the IDH inhibitors where the approval was based on composite CR and CRH. And I think it’s important to emphasize that, as we are in – because we are only in early Phase 1 study, early part of Phase 1 dose escalation, we are not holding fast to specific endpoints like CR CRH as the path to registration. We look at the responses as early indicators of activity that might confer clinical benefit. So, I would caution just a little bit about committing to a particular response criteria at this early stage of the game. But certainly, as our data set matures, and we get more data, then understanding some of the relationships, between response and durability and even survival as we get enough patients, will allow us the opportunity to further refine some of these relationships when we apply other criteria like CRH.

Okay. Thank you very much. I just had one other question. Maybe you have commented on this in the past. But if you could remind us, can you just explain why the starting dose for 538 in myeloma is 100 million cells, whereas for 516 and 596, its three-fold lower at 30 million cells, and also what is going to be the expected starting dose for 576?

Yes. I wouldn’t read too much into it other than just time and experience. If you go back, obviously, the initial experiences with FT516, we are talking about an IPS derived therapy, FT516 at the time that was engineered with CD16, very little clinical experience. And so we started and proposed to start at 30 million cells per dose. As we have gotten more advanced and build up clinical experience over time, we have gotten comfortable with the safety profile quite honestly of what we are seeing with our IPS derived NK cell therapies, including at much higher doses and so when we submitted our protocol for FT538, as well as FT576. Now, given all the safety history, we do have with our platform going back 2 years, we opted to start at a higher dose 100 million cells per dose. And the FDA was comfortable with that.

Great. Thank you.

Sure.

And we do have our next question from Michael Yee from Jefferies.

Hi, Scott. Congrats on the progress. We had two questions. One was going back to expectations on AML. You have previously said 20% to 30% cure rate has been seen. In literature, you have talked about the various I guess limitations for some of those programs. Is that the right bar to think about for 516 and how to put that into context with the fact that you will have some 538 data next week as well. So maybe just compare and contrast those programs versus the expectations you have laid out. And also how important is durability? So that question one is on AML. And question two is similar and that is with lymphoma in the summer, we know the data at ASH and I think you had two prior CRs. Durability seems to be a question that would be important. Can you just help us understand expectations around a durability given there is only 2 CRs, but CAR T is 33% to 50% durable CRs, so maybe make some comments around durability? Thank you.

Sure. So, yes, obviously, I think starting in AML, I think there is going to be a lot of interest in trying to compare, for instance, FT516 with – or FT538 with the historical experience with donor derived NK cell therapy. And I do think donor derived NK cell therapy, as I have mentioned in these sort of single center academic studies have shown 20% to 30% – 35% response rates. I understand the natural desire to do that comparison. I think there are significant differences that have existed with donor derived NK cell therapy versus the paradigm that we are pursuing. And I have touched on some of them. We have talked about just right off the top the lymphoconditioning regimen is significantly different. We have a lighter conditioning. We give – we deliver the product outpatient. Historically, the paradigm for donor-derived NK cell therapy has been transplant like significant lymphodepletion such that patients are hospitalized. So I do see – I do understand the natural comparison, I think there is differences. That said, the reason I am focused on 20% to 30% is not the comparison with donor derived NK cell therapy is because I think that’s the right bar to determine whether or not we actually potentially have a product. Going back to my comments that I made on some recent approvals in AML given the unmet need, there have been multiple approvals in the past 2 or 3 years, where the response rate has been about, let’s call it, somewhere between the high-teens and the mid-20. And so when I focus on response rate of the 20% to 30%, I am not actually looking at that in the context of gosh, donor-derived NK cell therapy, I am looking at it in the context of – do…

Thank you. Great.

And we do have our next question from Peter Lawson from Barclays.

Hey, Scott. Thanks so much for all the detail. Just I guess going back to Mike’s question around the response rate or the bar for AML, are you focused on CRI or CRH at response rate that 20% to 35% response rate in AML or is that more of a just ORR umber?

It’s the number that I have described is a composite of CR CRI mLFS. There is just a very interesting paper that was released and published of venetoclax actually in relapsed refractory AML where the data that I referred to and the reference I made was a comparison of patients using the 2017 ELN criteria that achieved CR, CRI, mLFS versus patients that did not, there is a clear survival benefit between those two groups, CR CRi mLFS versus non-responders, clear survival benefit, statistically significant that extends out over 30 months.

Got it. Would you be, I guess more content with a high CRi versus high CRH, I am just trying to gauge…

CRH is not part of the 2007 ELN criteria. It’s part of the criteria that originally existed in 2003. I agree there are paths forward where approvals have been achieved based on CR CRH. There is also paths forward where products have been approved on CR CRi. There are two different response criterias. Both of them are very viable.

Good. Thank you. And then just your comment around not using Cy/Flu that really appealing to – are you thinking of other ways to deplete the bone marrow through other methods or…

Yes, yes. I think this comes down to a question, a philosophical question and scientific question on what is the purpose of Cy/Flu? I think that’s an open question. There is, I think, a lot of speculation around what the purpose of Cy/Flu is, but I don’t think there is any magic to Cy/Flu and cell therapy, where Cy/Flu has to be delivered with cell therapy. Cy/Flu has a biological effect. It is probably multi-factorial. One of those biological effects is, for instance, significantly increasing cytokines within patients as a result of the Cy/Flu. And so I do think as we look forward and think about what is the ultimate cell therapy paradigm for patients, I think looking at ways, for instance, where we can significantly reduce Cy/Flu is important and we are very interested in exploring that and it’s actually one of the reasons why we are engineering in cytokines support into ourselves.

Great. Thank you so much. Much appreciate it.

Sure. Sure.

And we do have our next question from Tazeen Ahmad from Bank of America.

Tahseen, are you on mute?

Sorry, can you hear me now?

I can. Yes.

Excellent. Sorry about that.

No problem.

Thanks for taking my questions. For 516 and 596, I just wanted to drill in a little bit into the pursuit of DLBCL as an indication. Over the last year, there has obviously been a number of companies that have had drugs approved in the space from Seattle Genetics to MorphoSys to most recently, ADC Therapeutics. They are all different mechanisms, obviously, from what you are pursuing, but I wanted to get your thoughts about how you view the opportunity overall in DLBCL and where you see NK cells potentially fitting into the treatment paradigm? And then the second question is more of in general, what’s your strategy for re-dosing NK cells and how many doses could a patient potentially receive? Can you just remind us with the highest number of doses any patient has received across your program so far? Thanks.

Sure. So I will tackle the last question first. So, the most doses that we have – the maximum number of doses that we have administered to a patient is 6. And this goes back to first started with actually FT500, where we – and was actually the reason we sort of ran this experiment with FT500. We gave 2 days of outpatient lymphoconditioning, followed by doses of FT500 on Day 1, Day 7, Day 14 and the patient was off therapy for 2 weeks and we did a safety assessment. And then we actually re-dosed the next month, Day 1, 7 and 14 without lymphoconditioning. And so that was essentially you could think about it as 6 doses over 45 days following light outpatient lymphoconditioning and the entire experiment at some level initially was setup to assess whether or not a patient could tolerate multi-dosing in that form, for instance, would there be mechanisms of profound immune rejection that would arise. That was one of the very early things we were looking at. Would there be, for instance, a form of CRS that would emerge, because you would administer essentially a cell unmatched to a patient and that the patient would be building up allo reactivity to that cell? We did not see that with FT500. And we have not seen that with FT516. FT516 has been dosed up to 6 doses. And we have not seen that with any of our other product candidates to date. Now, FT596, we have given a single dose and then they can repeat that single dose cycle. But generally speaking, we feel really confident about our ability to re-dose and I am certainly demonstrated our ability to re-dose safely with tolerability up to 6 doses over a 45-day period. With respect to where we think NK cells fit within sort of the B cell lymphoma DLBCL landscape, I think there is lots of opportunity here. I mean, clearly, we have started out in a position where we are – you can think about it as sort of third line where patients have failed multiple lines of rituximab and we are really excited about what we have seen in that setting where we have combined FT516, for instance, with rituximab in patients that have either relapsed or failed rituximab. We think there is a great opportunity there given the response rates that we are seeing with FT516. And additionally, like we discussed, we actually think if the product candidate really does synergize, effectively with rituximab, and if it really does continue to show a differentiated safety profile compared to T-cell therapies, whether they are being engagers or CAR T cells, we think we have a terrific opportunity to go very early line with FT516 or FT596.

Okay, thank you.

Sure.

And we do have our next question from Michael Schmidt from Guggenheim.

Hey, guys. This is Kelsey on for Michael. Thanks for taking our question. First, I guess how quickly can the protocol for 596 be approved and implemented? And I guess is there any chance you could provide some insight into maybe the number or proportion of patients to-date that has gotten the second dose? In other words, I guess, could we read into the fact that you are now at the point that you can file this amendment that there is maybe more than just that single case study patient? And then secondly, could you possibly provide an update on where you stand kind of in launch or in Phase 1 trial for 819 and what maybe still needs to be done there before you start treating patients? That’s it. Thank you.

Sure. First question first. So with respect to the protocol amendment, the protocol amendment, we believe can be IRB approved and active, let’s call it by the end of June. It’s submitted. We are giving the FDA an opportunity to comment on that protocol. We are taking that protocol to multiple IRBs. And we think by the end of June we maybe in a position to begin to implement a multi-dose treatment schedule with respect to FT596. I think one of the reasons and I have alluded to this in the past that we have taken some time to file that amendment is we clearly wanted to get experience with administering more than one dose of FT596 and clearly the patient that we disclosed at ASH of last year did go on to a second cycle. We have had lots of experience now with patients in lymphoma receiving multiple cycles of FT516 and yes, there have been other patients that have been retreated with FT596. That I think was your first question. Your second question with respect to 819, we actually have just recently completed two additional manufacturing runs with 819. And we believe that those manufacturing runs will be released shortly and we will be in a position to treat patients with FT819 quickly upon release. And so, yes, in the next call it weeks to months or next weeks, we’ll – I think we will be in a position to treat patients with 819.

Okay, perfect, Scott. Thanks so much.

Sure.

Thank you. And we do have our next question from Daina Graybosch from SVB.

Hi, thanks for the question. Two for me. One is a follow-up on the moving away from Cy/Flu, I guess wonder why you are starting with – I think you said a FT516 cohort given that it doesn’t have the membrane ground IL15 that could reduce dependence on Cy/Flu impact on cytokine? And then the second question is on durability of response and you have many, many trials in cohorts, I wonder which one do you think is most likely the first give the best opportunity to test your ability of response? Meaning it won’t have the complexity of many patients going on to transplant after you get them in a CAR or PR?

Yes. So last – your last question first, I think FT516 in lymphoma is a perfect example to test durability of response. I just don’t know if we are far along with – I don’t think we are far along enough with respect to time on study. We are certainly not clear the entire dose escalation to answer the question in an informative way with respect to durability of response. But I think the FT516 study is a really great study to judge durability of response. I continue to believe FT596 given it is dual antigen targeting will show improvement over and above 516, but that remains to be seen. I think FT596 is a best-in-class product candidate, super excited with what we are seeing with 516, but I do believe that FT596 is a best-in-class product candidate. But I do think the first sort of benchmark with respect to durability response can be assessed using FT516 plus rituximab absolutely. With respect to Cy/Flu and where we are starting with that and why 516? 516 is given being administered with IL-2, keep that in mind, 538 is not, but 516 is. And so even though we may, for instance, significantly reduce Cy/Flu or move to a different form of conditioning, we will likely still administer with some degree of cytokine support for 516.

Got it. So, I guess what’s your opinion on that the depletion removes the IL-2, I think that’s the other idea, not that it just increases cytokines, but all those cells that you don’t deplete them will suck up all the IL-2 you administer?

Yes. No. So, that’s why the experiment needs to be done. I think it’s a fair question, because I think that is one of the things that Cy/Flu may do as well is while it provides in a better field for competition for the adoptively transferred cells. And so I think that will be an interesting observation with FT516, because there maybe competition there. Obviously, with FT538, it doesn’t need to fight that fight, because it has its own cytokine support building.

And we do have our next question from Mara Goldstein from Mizuho.

Great. Thanks for taking the question. Hey, on FT538 in multiple myeloma, we are – I think we have seen peripheral neuropathy emerge as a potential issue, Pfizer just announced a pause on its bi-specific and I believe, Amgen’s AMG 420 had a few reported Grade 3 incidences, and of course, CAR T studies targeting BCMA have reported this. So, I understand that multiple myeloma patients were likely to have been treated with neurotoxic prior therapies. But I am curious as to your thoughts in this setting for 538, what you would anticipate with respect to peripheral neuropathy for that work? And then also if I can just ask on the J&J payment was that tied to any achievement of any specific milestone or was it just clinical R&D work?

So, on the last question that J&J is just revenue. We did not trigger any milestone with J&J this quarter that contributed to revenue. So, the revenue contributors from J&J were sort of typical recognizing upfront. The allocation of the upfront as well as J&J does fully fund all of the work under the collaboration. So, we obviously get paid for the work that we do and that gets recognized as revenue. With respect to FT538 myeloma, I mean, I will let Wayne comment on that. I mean, the one thing I will say right off the bat, the initial experience with FT538 is obviously in combination with daratumumab and daratumumab has a well-established history with respect to [indiscernible], but I’ll let Wayne comment on that.

No. I mean, I think that’s a really good question. And we have been following the peripheral neuropathy plus some of these more T cell based therapies, I guess, one hypothesis that we hope to address with the 538 study in myeloma is whether or not a different effector cell, i.e., an NK cell, even one that’s combined with daratumumab may have a different safety profile than what’s been observed with some of the more T cell directed therapies like bi-specifics and the CAR T. It’s a clinical experiment that we obviously will need to conduct.

Right. But there is no exclusion criteria based on prior peripheral neuropathy in case those patients are treated. Okay. Alright, thank you.

Yes.

And we do have our next question from Do Kim from BMO.

Hi, this is James on for Do. Thanks for taking our questions and congrats on the progress. I guess it’s a two part question. Given the MD Anderson data using NK cells combined with NK cell engager in Hodgkin’s lymphoma, how do you view that combo regimen versus your CAR iNK cells? And do you think there is any merit in doing a preloaded iNK cell with an engager using something like FT500? Thanks.

I think today our strategy has been to leverage our CD16 receptor in combination with a variety of well-established FDA approved modalities. And I think that will continue to be our strategy. I think the idea of being able to promote ADCC with FT516 or FT538 and synergize with agents that are used early and often in both hematologic malignancies and solid tumors, I think it’s an exciting opportunity to leverage CD16 and ADCC and that’s the strategy that we are pursuing. People can have different belief systems or what around what they think is more productized or is has better patient reach. I personally believe in off-the-shelf cell therapy combined with a monoclonal antibody that is also delivered if you will, off-the-shelf, or in fact engineering an NK cell to target. For instance, an antigen is a much better strategy than manufacturing a product patient by patient that requires us essentially combinations, cryopreservations and construction of products through a manufacturing paradigm. That’s a personal belief.

Great, thanks. That was incredibly helpful. Thanks again and looking forward to the update next week.

And we do have our next question from Nick Abbott from Wells Fargo.

Hi, good afternoon and thanks for taking my questions. I missed the beginning of the call, but personally I would like to see Dan I don’t know if you are on the call, but you will be missed going forward. And then a couple of questions, Scott, you’ve mentioned this sort of light outpatient lymphoconditioning regimen a few times. So, can you compare firstly rates of regimen, the lymphoconditioning regimen related Grade 3/4 tox and in tox versus what has been reported a standard for conditioning regimens? And then I have a follow-up. Thanks.

Yes. I honestly I don’t have those figures off the top of my head or fingertips. So I would not want to provide those, but I would say just generally lymphoconditioning does have toxicity associated with it. And I do think where the field will go and we have to recognize this is that the better therapies will be therapies and a better experience for patients will be therapies that have lighter conditioning regimens and therefore less toxicity as opposed to cranking up on the conditioning. And I think the field needs to recognize that and I think it’s one of the things that we are very focused on.

Great, thanks. And then…

I mean, if you want to – for instance, if you want to go early line therapy, whether it’s hematologic malignancies or solid tumors, there is no way you are conditioning patients, putting them in the hospital or significantly increasing the risk of, for instance, infection and it’s just not going to happen. I don’t think that’s the way to maximize patient reach or benefit.

Great. And then you listed a trial of inotuzumab with 516 and so can you talk a little bit about the genesis of the trial and why 516 or 538, is this de-risking for 573 or B7H3?

Sorry about the – are you talking – are you referring to the ovarian study?

Yes, the Minnesota trial, yes.

Okay. Yes, okay. So, I wasn’t aware it was public to be honest with you, but okay, yes, to be fair, we are starting with FT516 as a monotherapy. I suspect the trial will transition from FT516 to FT538 as a monotherapy. We will likely with progress begin to combine locally with a B7H3 engager. However, as you know, we are developing a product candidate that is in fact engineered with a B7H3.

Okay. Thanks a lot.

Sure.

And we do have our last question from Robert Burns from H.C. Wainwright.

Hey, everyone. This is [indiscernible] for Rob. I just have a couple of very quick questions. One is on FT538 and please excuse me if you have provided guidance in the past, but on clinicaltrials.gov, you also have avelumab as one of the potential combination arms, are you still evaluating their arm or are you just focused on daratumumab? And the last one on the FT500, can we still expect further datasets in patients who are anti-PD1s in tumor types like non-small-cell lung cancer? Thanks.

Yes. So, your last question we will be providing a solid tumor update likely in the second half of this year, probably sometime in the third quarter. We will discuss what we are seeing in solid tumors with FT500, FT516 in combination with avelumab and also we will be providing an update at that time with respect to our broader solid tumor strategy as it relates to, for instance, CAR MICA MICB. We just discussed B7H3 as well as the J&J product, first time under the J&J collaboration, which is solid tumor targeted. So in the second half of this year, we will provide a fairly fulsome update on our solid tumor efforts. Sorry, what was your first question?

So, on clinicaltrials.gov you also have the...

Yes, sorry. Yes, now we are very focused on combining with daratumumab. They are different regimens and the regimen that we are focused on today is the combination with daratumumab.

Okay, great. Thank you.

Sure.

And I am showing that there are no more questions at this time.

Perfect. Thank you everyone for your time today. We look forward to providing a full update on our initial clinical observations with FT516 and FT538 next week.

Thank you, ladies and gentlemen. This concludes today’s conference. You may now disconnect.