Fate Therapeutics, Inc.
Q3 2021 Earnings Call Transcript

Published: 5 Nov 2021

[Operator:]

Welcome to the Fate Therapeutics Third Quarter 2021 Financial Results Conference Call. At this time all participants are in a listen-only mode. This call is being webcast live on the Investors section of Fate's website at fatetherapeutics.com. As a reminder, today's call is being recorded. I would now like to introduce Scott Wolchko, President and CEO of Fate Therapeutics.

[Scott Wolchko:]

Thank you. Good afternoon, and thanks everyone for joining us for the Fate Therapeutics third quarter 2021 financial results call. Shortly after 4

[Ed Dulac:]

Thank you, Scott. Turning to our financial results, revenue was $14.2 million for the third quarter of 2021 compared to $7.6 million for the same period last year. Revenue in the current quarter was derived from our collaborations with Janssen and Ono Pharmaceutical. Research and Development expenses for the third quarter of 2021 were $53.1 million, compared to $30.7 million for the same period last year. The increase in our R&D expenses was attributable primarily to an increase in employee headcount and compensation, including share-based compensation, and in expenses associated with third-party professional consultants and clinical trials. General and administrative expenses for the third quarter of 2021 are $15.7 million, compared to $8.3 million for the same period last year. The increase in our G&A expenses was attributable primarily to an increase in employee headcount and compensation, including share based compensation, and an office and computer supplies including software licenses. Total operating expenses for the third quarter of 2021 were $55.3 million net of $13.5 million in non-cash share based compensation expense. Note that in connection with the treatment of the first patient with our off the shelf IPSC derived Car T-cell product candidate FT819 we achieved the clinical milestone set forth in our amended license agreement with Memorial Sloan Kettering Cancer Center. This clinical milestone triggered a first milestone payment in the amount of $20 million to MSK, which we plan to pay in the fourth quarter. Up to two additional milestone payments maybe owed to MSK based on subsequent trading values of the company's common stock, ranging from $100 to $150 per share. We assess the fair value of these contingent milestone payments, currently valued at $24.6 million on a quarterly basis. In the third quarter, we’ve recorded a non-cash $11 million non-operating benefit associated with a change in fair value. The company ended the third quarter with $804 million of cash, cash equivalents and investments. Our common stock outstanding was 95 million shares, and preferred convertible stock outstanding was 2.8 million shares, each of which is convertible into five shares of common stock under certain conditions. I would now like to open the call to any questions.

[Operator:]

Your first question comes from the line of Michael Yee from Jeffries, your line is open.

[Michael Yee:]

Hey, Scott, thanks for the updates. I had two questions. One is on the updates coming later this year at ASH and obviously the abstracts are out today. Can you compare and contrast how you think durability would play out for 516 versus 596? Obviously, you've already presented some 596 data. So would we be able to get a pretty good picture about how that shaping up at ASH given 596 and also higher doses? That's question one. And then question two, I think you just laid out some nice commentary around your solid tumor update. I know these are in super heavily pretreated patients. How should we put that type of data you'll present in the context? I mean, responses are good. What would you expect to see and what's the read through? Thank you so much.

[Scott Wolchko:]

Sure. So and with respect to your first question with respect to durability of 516, versus 596. Yes, I think at ASH, we will be able to do a first look at comparing durability of both 516 and 596. We plan to present swindling plots for both 516 and 596. If you recall from our lymphoma update, in August, we did present a swindling plot for 516. The data cut for that I think was late July or -- sorry, it was probably late June, early July, we'll be able now to fast forward that swim lane, as well as add patients that were dosed at 900 million cells. And I believe I've mentioned there were seven patients dose that 900 million cells with FT516. With respect to FT596. Recall, we had 10 or 14 patients that had responded in the second and third dose level, we will now be able to present duration of response on those 14 patients, including adding a couple additional patients that were dosed at the 300 million cell level as backfill. We've also now I mentioned, I think we've treated about 30 total patients, including probably about 12, pay 12 to 15 patients at the 900 million cell level. We will at least be able to give a response first response on those patients, although durability may not yet be meaningful. Just given how immature the patients are.

[Michael Yee:]

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

[Scott Wolchko:]

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

[Michael Yee:]

Okay. And then on just quickly to solid tumors.

[Scott Wolchko:]

Yes, with respect to solid tumors. I mean, most of what we will present at Citi will be a go forward look at our R&D in the emerging pipeline. I think we've always maintained at the end of the day cracking the solid tumor nut if you will has proven to be much more difficult than treating hematologic malignancies. And I think that's consistent no matter what therapeutic modality you're looking at, whether it's small molecule biologic or cell therapy. And so really, as we think about our solid tumor franchise, we're focused on multiplex engineered product candidates that can attack the tumor from multiple different angles, we're looking at FT500, and FT516 literally as just a first experience with an IPS derived NK cell therapy, you should have pretty modest expectations with respect to what we think these product candidates can drive on their own with respect to solid tumors. It's really just getting our feet under us within NK cell therapy in solid tumors. And we think we've done that with FT500 and FT516 we'll certainly be able to look at safety data, we'll be able to look at, obviously clinical responses. But again, your expectation should be pretty modest with these first generation NK cell product candidates.

[Michael Yee:]

Got it. Thank you very much.

[Operator:]

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

[Unidentified Analyst:]

Hey, this is Calci on for Michael, thanks for taking our questions. I think just two from us. First on 596, I guess, are we still thinking about now that you're kind of moving from one cycle to two cycles? Is there still any flexibility there to maybe increase that further? Or is that kind of where you think you'll end up and then kind of following up on that, as you build out the solid tumor franchise, I guess kind of what you based on what you've seen with 500 and 516? Is you know adding additional cycles for the upcoming next gen products. Is that something that you would consider? Or are you still kind of thinking about three cycles as the max? Thank you.

[Scott Wolchko:]

Sure. So with FT596, we have continued to dose at one dose per cycle. And we now have the ability to give two cycles. If you recall, when we initially advanced our FT596 program, we were gated on giving a second cycle with FDA consent. So we're now able to give two cycles of FT596 without going back to the FDA. And so we will continue to dose patients at one dose, giving two cycles. And now we will -- we will now add two doses in each cycle and continue to give two cycles. We are planning on amending the protocol so that if patients relapse at some point, we could re intervene with FT596. And so right now we're sticking to one or two doses per cycle giving two cycles, and now adding the ability to re intervene if a patient later relapses. So that's where we're headed with FT596. With respect to our solid tumor franchise, very similar. We are giving multi doses in a cycle, as an example FT538 is a product candidate that we're now got dosing with solid tumors in combination with monoclonal antibody, it's a multi dose treatment and we are giving multiple cycles and we do again if a patient later relapses, we have the ability to re intervene again. So we are now looking at the potential to retreat patients upon progression.

[Unidentified Analyst:]

Okay, great. Thank you so much.

[Scott Wolchko:]

Sure.

[Operator:]

Your next question comes from the line of Mike Ulz from Morgan Stanley, your line is open.

[Mike Ulz:]

Hey guys, thanks for taking the question. Just a quick question on the CD38 knock-out you sort of highlighted that modification as providing some improved metabolic fitness. So, I just curious for 596 I noticed you don't have that modification there. So I guess two questions. Number one, why not? And number two, are you considering potentially adding that in the future?

[Scott Wolchko:]

Sure. So for FT -- I mean, we've built out our platform over time in a very sort of methodical stepwise fashion. And at the time, when we were building out FT596, we did not fully appreciate the therapeutic value of the CD38 knock-out. And initially, we thought of CD38 knock-out as a step that we would take a functional step that we would add, that would be unique for myeloma, knocking out CD38 to prevent fratricide when delivering the therapy in combination with daratumumab. Obviously, we've come to appreciate and there's been publications on the therapeutic value of the CD38 knock-out more broadly, we certainly are incorporating that into all our product candidates on a go forward basis, including our product candidates for solid tumors. And certainly, we've reserved the right obviously, to continue to build off of 538 for lymphoma.

[Mike Ulz:]

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

[Scott Wolchko:]

So we're going to hold an investor event on Tuesday, we'll spend most of the time I think, on that investor event, discussing lymphoma. And I think that's going to be the significant focus of ASH, as well as the investor event. We're continuing to generate data across all our programs, obviously. And we look forward to providing updates.

[Mike Ulz:]

Got it. Thank you.

[Operator:]

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

[Alethia Young:]

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

[Scott Wolchko:]

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

[Wayne Chu:]

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

[Alethia Young:]

Great, thank you very much.

[Operator:]

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

[Peter Lawson:]

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

[Scott Wolchko:]

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

[Peter Lawson:]

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

[Scott Wolchko:]

Yes, I think for that to play out overtime, multi antigen targeting best-in-class approach, you're not just looking at response rates, you're looking at durability of response, and obviously, it will take some time for the durability of response to mature such that we can be absolutely certain in our belief systems that we have based on preclinical data.

[Peter Lawson:]

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

[Scott Wolchko:]

Yes, I mean, it's the first -- at some level, it's the first time keep in mind right this first time IPS derived NK cell therapies have been delivered in solid tumors. So and the FT500, dose escalation in 516, -- sorry, dose expansion and FT516 dose escalation started, some time ago. And so for success for us was just again, demonstrating that we could deliver multiple doses of an engineered NK cell, and then a first engineered NK cell in the setting of solid tumors and that they would the multiple dose paradigms, multiple cycle paradigms would be safe and well tolerated, and that we could potentially see some control of tumor activity, and that we will be able to look at translational data that we could continue to build off of as we build the multiplex engineered pipeline.

[Peter Lawson:]

Thanks so much. Thanks for taking the question.

[Operator:]

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

[Daina Graybosch:]

Thanks, I, too, have two questions. The first is it seems like you're expanding a lot of your products in the 900 million cells of the dose range, whereas other NK cell companies are giving multiple billions of doses. And I wonder if you could speak to why at 900, and why not go higher, especially since you're not seeing any maximum tolerated doses? And the second question is, can you discuss your rate of genetic abnormalities in an IPSC products, simply from cell division? And how that might compare to let's say, a donor derived product?

[Scott Wolchko:]

Sure, so I'm chuckling on the second question. With respect to going higher on doses, look, we reserve the right to go higher on doses. Absolutely. And I'm not suggesting we won't continue to potentially explore higher doses and alternative dosing schedules, because we do believe we have an incredibly flexible platform, to your point that has proven to be at least today very safe. So I don't think it provides us a lot of flexibility with respect to can continuing to explore higher doses and alternative dosing schedules. That said, I mean we're quite pleased with what we're seeing both with FT516 and FT596, with respect to response rates, including CR rates, as well as the durability of response. And so we do believe it is worthwhile. And we do think there's significant development opportunity to move forward at the 900 million cell level and for instance, expansions and we plan doing that. But again, given the safety profile and the flexibility we have with our platform certainly reserve the right to continue to do a bit of exploration as part of our Phase 1 studies, including with, as I mentioned, alternative conditioning regimens, and earlier line, combining with standard of care regimens. With respect to how we characterize our master cell banks and how we release our product candidates, I'm not going to sort of get into any details around that other than to say, we assess for genetic abnormalities at multiple points in the process of selecting our single cell, which we use to make a master cell bank. And so again, our master cell bank is based on the selection of a single cell, which we do exquisite characterization around to select that single cell, and then again, use that to make a master cell bank. That master cell bank goes through extensive testing and qualification in order for it to meet FDA sort of guidelines and recommendations for use as a master cell bank.

[Daina Graybosch:]

Okay. Thank you very much for both of those.

[Scott Wolchko:]

Sure.

[Operator:]

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

[Srikripa Devarakonda:]

Hey, guys, this is Kripa on for Robyn. Thank you so much for taking my question. You have one poster of ASH that talks about modifications you're making to current T cells to evade allo rejection. Can you talk about other strategies you may also be working on or considering to ensure that this cells stay in stealth mode? And related question, with the current candidates that you have you talked about the absence or at least the low levels of allo rejection you're seeing, at least within the timeframe that you've observed there seems to be -- we've talked to a bunch of KOLs, and there seems to be a level of confusion in terms of how you show that there is no allo rejection? Can you talk a little bit about what assays are used in? What sort of feedback have you gotten from the KOL community in terms of the comfort level that there is little to no allo rejection? Thank you.

[Scott Wolchko:]

Sure. I mean, we're going to talk about this more, for instance, at solid tumor investor day, we will certainly talk more about this at ASH. I think, you know, again, there's been a lot of discussion about the value of stealth engineering. I think one of the things that we focus on, again, we don't believe there's much value in a long-term persisting cell, if the functional activity of that cell has significantly degraded. There's no point in a cell persisting if it doesn't have functionality. So we focus on functional persistence. And one of the ways to drive functional persistence is certainly through editing. Although I'm not sure stealth editing, to be fair, is a way to drive functional persistence. Multi dosing strategy is one way to create functional persistence, albeit through multi dosing strategy. I'll turn it over to Bob here to talk a little bit about sort of the three approaches we think about, as it relates to maximizing functional persistence.

[Wayne Chu:]

Sure. Thanks, Scott. Robyn, so for ASH, we are presenting one of our strategies, and Scott mentioned we have three. Let's categorize them into cloak that's one. Second is eliminate, and third is attack and potentiate. So the cloaking strategy, which is a manuscript we're drafting right now with Kelly Malburg focuses on complete disruption of the interaction between T and NK cells with our product. So this is basically T or NK cells will not be able to recognize our product. I don't want to get to details with that. I think I want to respect Kelly's publication. But here, this goes beyond just thinking that one leg in on the cell will overcome the hundreds of inhibitory and activating receptors that are found on NK cells as others are trying to do. This is more about going to the heart of the interaction between T and NK cells. So that's cloak. Eliminate, which is what's an ASH is our unique strategy of using daratumumab to get rid of all the activated T and NK cells that are surrounding ourselves through the engagement of hnCD16 front on our cell with the anti CD38 mAb, targeting to activate a cell to come nearby. And keep in mind that because our product is CD38 negative, this becomes a very unique lympho conditioning strategy that's better than other strategies that are using mAb for this because daratumumab is safe, and only targets activated allo reactive T and NK cells, unlike other strategies that may go into more progenitor populations to induce lympho conditioning or lympho depletion. And lastly, what we're very excited about is attack and potentiate. And so, this is an idea where the cell, the product itself has the unique ability to not only target our reactive cells that come near it, but also to utilize that attack to proliferate and potentiate itself. So this is the strategy that's been published in Nature Biotech last year, by Max where allo defense receptor is used to target to allo reactive cells and CAR T-cells, but also through the signaling domain, add additional signal to the product itself to proliferate. So this becomes a very unique, timely induction of propagation. So we can use ADR in situations such as elimination of sigh flu conditioning, or creating space for our product.

[Scott Wolchko:]

On your second question, with respect to the assays that we use, I mean, honestly, we develop the assays with a bunch of KOLs with respect to how do you assess allo reactivity or rejection. I'm happy to have a conversation with you offline based on the feedback you're getting versus the feedback we've gotten from our KOLs that we've used to develop these assays.

[Srikripa Devarakonda:]

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

[Operator:]

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

[Matt Biegler:]

Hey, guys. I'll be quick, just one for me. Just kind of question I left field, but just wanted to get your thoughts on the use of the platform outside of oncology applications. If there's any plans there, I'm sure you've seen some recent data on a stem cell derived therapy for diabetes. That was pretty exciting, albeit early. So just kind of wanted your thoughts on that. Thanks.

[Scott Wolchko:]

Sure, absolutely. We absolutely think we have a platform that can be broadly applicable. We have certainly focused initially on cell based cancer immunotherapies. We certainly believe there is opportunity for the cell types we make today, including NK cells and T cells. Those could be used outside of oncology. And we're doing some of that work internally at Fate Therapeutics. We certainly don't talk about it publicly yet, but certainly exploring the use of NK cells and T cells in areas where those can be leveraged outside of oncology. I would also say just generally speaking, yes. I mean, we certainly closely watch the whole IPS derived cell therapy space, including with respect to areas that we would consider to be regenerative medicine type of applications. Excited about all the opportunities that are emerging in IPS derived cell therapy. I think you and I've talked about it, I think it's going to be the platform of the future for cell therapy. And certainly, we will look to play broadly in the field of IPS derived cell therapy over time.

[Matt Biegler:]

Great. Thanks, guys. Congrats.

[Scott Wolchko:]

Sure.

[Operator:]

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

[Unidentified Analyst:]

Hello, this is Catalina in for Ben Burnett. Thank you for taking our question. On your B-cell lymphoma programs, you have mentioned in the past the need of delivering a certain dose of cells to see activity with the hnCD16 construct. For how long would you expect to have hnCD16 activity in combination with rituximab or other when you administer 596 at 900 million cells per dose?

[Scott Wolchko:]

Sure, so we give a single dose of rituximab and that single dose of rituximab we think provides tumor targeting availability. If you look at the traditional rituximab PK curves and receptor occupancy data with respect to rituximab and tumors. We think there's ability to engage a single dose of rituximab over a multi week period. Let's call it three to four weeks. We have certainly shown, I think a little bit of data with respect to FT596. FT596 has in a single dose essentially we've shown it has functional persistence over about a 14 to 21-day period. We are certainly looking forward to giving a second dose of rituximab where we think that second dose can still engage rituximab during that multi week period to continue to add therapeutic benefit. So for us, we started the experience with FT596as a single dose. We're certainly excited about adding a second dose of FT596 on day 14, to exploit that, let's call it that second window of rituximab’s availability in coding tumors. And again, I think this gets back to the point of, we really focus on the idea of functional persistence. And there's multiple ways to achieve functional persistence, certainly through engineering approaches, but a multi dosing approach can really add functional persistence by giving again a second dose that can have a day one experience.

[Unidentified Analyst:]

Understood. Thank you.

[Scott Wolchko:]

Sure.

[Operator:]

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

[Mara Goldstein:]

Thanks very much. Maybe it's a bit of an oddball question. But with respect to presentations at ASH, sorry, 516 presentation at ASH and 596. One's an oral and one is a poster. And should we read anything into that?

[Scott Wolchko:]

No. Don’t read anything in this. No.

[Mara Goldstein:]

All right. Well, I had to ask.

[Scott Wolchko:]

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

[Mara Goldstein:]

And then I wanted to ask on the AML program, it just seems that perhaps that is evolving a little bit slower than the B-cell lymphoma. Maybe you could talk about that a little bit or if I’m incorrect in my assumptions?

[Scott Wolchko:]

No, that's fair. So we were a little delayed in getting out of the first dose level with FT538. And it wasn't because we saw any toxicity. We were only open at a single site. And so the single site was the University of Minnesota. So we launched the FT538 experience at the University of Minnesota. And yeah, we ran into some struggles early on, at that single fight with essentially patients meeting the enrollment criteria. And we had a couple screen failures in a row, which was just unfortunate. We've now opened the study at multiple sites, and we've seen significant pickup in activity where I think I mentioned we've enrolled about 10 patients now with FT538 and AML. So, it seems significant pickup now that we've been enabled to open it multiple sites.

[Mara Goldstein:]

Okay. All right. And then if I could just ask you, since you recognized some revenue, that's attributable to the Janssen collaboration, maybe you can talk a little bit about where you are there and what we should be thinking about as potentially next public disclosure on that program.

[Scott Wolchko:]

Yeah, so I mean, the Janssen collaboration has continued to go very well. And obviously, as you can tell from the revenue that continues to increase, we continue to increase the resources under the collaboration. I think we've disclosed in the past that the collaboration started with two antigen targets, one in hematologic malignancies, one in solid tumors. A third antigen target has now been added to the collaboration. And Janssen reserves the right to add a fourth target to the collaboration. So, collaboration is moving forward. We're really pleased with it. I think we'll be able to give a little bit of visibility on the first product candidate at the solid tumor day, although we may not be able to disclose the target quite yet.

[Mara Goldstein:]

Okay. Thanks a lot. I appreciate the time.

[Scott Wolchko:]

Sure.

[Operator:]

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

[Nick Abbott:]

Hey, thanks for taking my question. I know it's getting late, so I'll just ask one quick one. During the call, Scott, I apologize if you provided some commentary on 819. But you've dosed some patients now. Is it too early to comment on experience with that and how that compares to memorials extensive experience with autologous products?

[Scott Wolchko:]

Yeah, sure. I can comment on it and you're the first one to ask about it. So, no one had asked about it before. The study is up and running. I think we're up and running at three or four sites now. We've certainly dosed patients in more than one disease area. Remember, it’s a three disease area study, so we've dosed the patient ALL, we’ve dosed patients in lymphoma. We've not yet dosed if I'm remembering correctly in CLL. So starting at 90 million cells, which, depending on what data sets you look at, in the allogeneic space, CAR T-cells, 90 million cells may be on the verge of being an active dose. It's a little bit early, we're still early dosing the first couple patients here. We've not yet escalated to the second dose level, but making good progress.

[Nick Abbott:]

Thank you.

[Scott Wolchko:]

Sure.

[Operator:]

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

[Ted Tenthoff:]

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

[Scott Wolchko:]

Sure. I'll turn that over to Bob. Bob's obviously leading the effort on research and development and the exploration of alternative cell types in the hematopoietic lineage other than NK and T.

[Wayne Chu:]

Thanks, Scott. I'll just be quick and say that our CD34 node is multi potent, so it does give rise to not only NK and T cells, but also the myeloid lineages. And so, we're actively looking into other cell types within that sub lineage. And I think we're making great progress. And we hope to give some updates when Scott allows us to do so.

[Ted Tenthoff:]

Thanks, guys. Looking forward to all the data readouts and the different adventure planning.

[Scott Wolchko:]

Great. Thanks.

[Operator:]

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

[Rob Burns:]

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

[Scott Wolchko:]

Sure. In solid tumors, and we will talk about this, there are certain mechanisms of action where we think at least with respect to an NK cell chassis, where NK cells can be advantaged. We're certainly looking at areas for instance, in non-small cell lung cancer, as an example, where we think NK cells can actually be valuable and be therapeutically relevant in patients that have progressed or failed checkpoint inhibitor therapy. Now, treating those patients with an engineered NK cell may not be the optimal approach. But certainly patients that have progressed or failed checkpoint inhibitor therapy, there are definitely challenges and mechanisms of resistance, where T cells may no longer be effective. And some of those mechanisms of resistance to T cells are opportunities to engage those tumors, for instance, with an NK cell. As an example, one of the mechanisms of resistance in non-small cell lung cancer is down regulation of MHC class one. That is a cell type that an NK cell can absolutely recognize, target and kill. Another example, for instance, in an array of solid tumors, is when tumors are undergoing escape mechanisms associated with T cells. There's oftentimes up regulation of stress ligands, like MCA, MCB, which is, for instance, expressed on many solid tumors. Our 536 product candidate has a CAR engineered into it obviously, which can key on the MCA, MCB receptors. So, we're looking at certain mechanisms where we think NK cells may be advantaged, and where there are mechanisms of scape in play with respect to T cells.

[Rob Burns:]

Great. Thank you.

[Scott Wolchko:]

Sure.

[Operator:]

This concludes our question-and-answer session. I would now like to turn the conference back to our President and CEO, Scott Wolchko.

[Scott Wolchko:]

Thank you. Thank you for everyone for participating in today's call. Be well and we look forward to speaking with you at Citi. Take care.

[Operator:]

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