Welcome to the Fate Therapeutics Third Quarter 2020 Financial Results Conference Call. At this time, all participants are in listen-only mode. This call is being webcast live on the Investors and Media 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..

Regimen A as a single dose starting at 90 million cells, Regimen B as a single dose starting at 90 million cells with IL-2 cytokine support, and Regimen C as three fractionated doses starting at 30 million cells per dose. I'm pleased to announce that we have successfully completed GMP manufacture of FT819 at Fate Therapeutics.

And we are currently conducting product release testing to support the initiation of our landmark Phase 1 clinical trial in the fourth quarter of this year. Finally, we're looking forward to the ASH Conference next month.

In keeping with our tradition, we plan to host a virtual Investor Event to highlight the unique therapeutic features and functionality of our novel high-affinity, non-cleavable, CD16 Fc receptor. CD16 is a potent activating receptor, naturally expressed on NK cells that recognizes, binds, and kills antibody coated tumor cells.

However, CD16 expression in NK cells is often downregulated and cleaved in the tumor microenvironment which can significantly impede NK cell functionality and cytotoxicity. We have engineered our novel CD16 Fc receptor to prevent its downregulation and cleavage, and it's binding - and improved its binding affinity to antibodies for enhanced ADCC.

We think there is significant promise in the off-the-shelf combination of engineered NK cells and standard of care monoclonal antibody therapy to restore innate immunity in patients with cancer. It is now my pleasure to introduce Ed Dulac, who joined Fate Therapeutics in August as our Chief Financial Officer.

Ed comes to Fate from Celgene Corporation, where he has most recently served as VP Business Development & Strategy. And we're pleased to have him here with us. Welcome Ed..

Thank you, Scott. Turning to our financial results, revenue was $7.6 million for the third quarter of 2020 compared to $2.4 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 2020 were $30.7 million, compared to $23.2 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 the facility lease for our new corporate headquarters.

General and administrative expenses for the third quarter of 2020 were $8.4 million, compared to $6.3 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 third quarter of 2020 were $31.2 million net of $7.8 million in non-cash share-based compensation expense. In the third quarter, we recorded a non-cash $27.6 million non-operating expense associated with the fair value of contingent milestone payments under our license agreement with Memorial Sloan Kettering.

In the event a certain clinical milestone is first achieved, 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 on a quarterly basis, and changes in the fair value will be recorded in our earnings as non-operating income or expense. The company ended the third quarter of 2020 with $502 million of cash, cash equivalents and investments.

Common stock outstanding was 87 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 call up to any questions..

And thank you. [Operator Instructions]. And our first question comes from Yigal Nochomovitz from Citi. Your line is now open..

Hi, this is [Samantha] on for Yigal. Thanks very much for taking the question. And I apologize, I think I've missed a bit of your prepared remarks in the beginning, I'm switching back and forth your call. So I'll just ask sort of a big picture question to start off.

I believe you've talked about potentially sequencing therapy between first with NK cells and then followed by T-cells and potentially even combining both NK and T-cell therapies into a single infusion.

So when you think about your clinical pipeline and your products, or do any stand out as being best suited for these combinations, and do you have any plans to test this in the clinic in the near term?.

Alright, it's a really good question. And I think it's one of the unique advantages associated with our platform and our ability to develop both off-the-shelf NK cells as well as off-the-shelf T-cell therapies. I think we're learning a tremendous amount about the safety profile and the activity of off-the-shelf NK cells.

Clinically, we are just getting ready to begin our evaluation of off-the-shelf iPS-derived CAR T-cells. So before we obviously explore any unique combinations between NK cells and T-cells, we certainly want to see the independent activity of NK cells and T-cells in the clinical setting.

And that said, pre-clinically, we have absolutely done some pretty interesting work in combining NK cells and T cells. And we do believe and see synergistic and complementary effects. But there is no immediate plan to combine it..

Okay, and do you have any plans to present some of that pre-clinical data over the next 12 months or so?.

Yeah, I'll turn that over to Bob Vaamehr..

Hi, we just recently published today in Science Translational Medicine, the concept that you're addressing or alluding to. Basically showing that iNKs synergize with T-cells, they activate each other, they synergize an anti-tumor activity. And when combined with combinational agents such as checkpoint blockade therapy, you see an additive effect.

So take a look at that paper just came out today..

Perfect, I'll definitely do that. Thanks very much for taking the question..

Thank you..

Thank you. And our next question comes from Matt Biegler from Oppenheimer. Your line is now open..

Hey, guys. Thanks for taking my questions. Congrats on the progress. Scott, Dan, so just curious to hear your thoughts on the requirement for reconditioning patients prior to treatment. I'm not sure if you saw there was Nash abstract from one of your competitors that's also working with Jeff Miller's Lab.

And it appeared that there were some tumor regressions following repeat dosing and but I don't believe those patients were reconditioned, so just curious kind of on your thoughts on that?.

Yeah, I think it's I think it's a super interesting question. And obviously, we're exploring the potential to give, for instance, a single lympho-conditioning regimen, followed by multiple doses of NK cells. And we are doing that in the FT500 study without lympho-conditioning.

I think if you look, and again, I don't - I'm hesitant to compare the world of T-cells and NK cells. But in any event, if you look at, for instance, the data that's been generated in the T-cell space, including for instance, referencing Kite's data with Yescarta. I think it's really important to achieve a deep durable kill within the first 30 days.

I think the best way to achieve that deep durable kill within the first 30 days is to give multiple doses of a cell therapy.

And the cells change profoundly within the body upon administration, and I have - we've always maintained that we do believe giving sort of a continuous wave of cells over a relatively short duration can lead to the most profound responses. I do not necessarily believe that all that lympho-conditioning has to be repeated, though to achieve that..

Got it, fair. And maybe I can sneak one more in about your clinical trial strategy and site selection. Obviously, you've got some products that might compete for a given patient population, so, for example, 516 and 596, 538, 576.

How do you ensure that one product isn't cannibalizing recruitment efforts for another product?.

Sure, that's a great question, something we think a lot about.

And, Wayne, if you're on the line, do you want to address that?.

Yeah, sure. Thanks for the question. I think it's a really good question. It's and it's a very and it's an issue that, we address every day with our programs.

I think what we try to do is we try to have an optimal mix of sites and programs where select sites, given their operational capacities in terms of numbers of patients that they see in competing trials.

We would - they would provide opportunities to participate in multiple trials, largely to leverage their larger patient population, and also to leverage some of the efficiencies that we can get from opening up multiple trials at a single institution.

But we're also cognizant of the fact that trials can compete against each other, especially at sites that may be of more moderate size, or more modest size.

And in those instances, we work very hard to ensure that the numbers of trials participate in those sites are limited so that we're not putting ourselves in a position where we're competing against ourselves..

Cool. Makes sense. Thanks, guys..

And thank you. And our next question comes from Michael Schmidt from Guggenheim Security. Your line is now open..

Hey, this is Kelsey on for Michael. Thanks for taking our questions.

Regarding FT596, and specifically the ASH presentation, I guess, what type of cell expansion data might one expect relative to typical expansion data that we see with CAR T-cells? And kind of how should we think about that PK data to be presented? And then specifically for the trial protocol, I guess, what kind of data do you think you'll need to generate in order to have an amendment approved where all patients could get multi-dose? Thank you..

Sure, they are two really good questions, Kelsey. So with respect to cell expansion, of the product that we may say, and this is where again, I want to hesitate, I - we can't assume that NK cells and T-cells are going to behave the same.

So some of the rules of the road that have been written for CAR T-cell therapy, I'm not necessarily sure apply to NK cells. I mean, so we're going to be cautious about making assumptions based on all the literature in the T-cell world. That said, we have disclosed that the first - that patient two, to be clear.

Patient two that we're speaking about, did show PK in the blood, and showed expansion within the blood door and which peaked about day eight or nine, if I recall correctly, and then started to degrade over a period of the next 14 days.

And so, interestingly enough, that's one of the things we're going to look at with respect to the second dose, how does the second dose compare in with respect to the first dose with respect to its behavior, both in terms of PK expansion, immunogenicity, and then obviously look at outcomes of the patient.

So I think that's super, I think that's super interesting. With respect to the ability we want to get to a multi-dose paradigm. And I sort of articulated that that I think that's important just generally in the field.

So I think quite honestly, the data that we're generating for FT500, as well as for FT516, which are both multi-dose paradigms, right off of that, can be very helpful in working with the FDA in a collaborative manner to get to a multi-dose paradigm. As you probably can appreciate right now, we do have the ability to give a second dose.

We actually did do give a second dose to patient too. But we worked with the F - right now for 596, we're working with the FDA on a case-by-case basis.

I do expect us in the coming months to have a conversation with the FDA, including presenting the data that we have on FT500 and FT516, to try and transition and move to a multi-dose treatment paradigm, much like we have with all our other products, including FT538 and even FT819..

Got it? Thank you, Scott..

Sure..

Thank you. And our next question comes from Peter Lawson from Barclays. Your line is now open..

Hi, everyone, this is Mitchell on for Peter. And thank you for taking our questions.

The first one we have is, about how many patients at ASH of FT596 data do you expect that you might have? Is it like - is it a few or you comment there? And then how many may have had the second dose administered? And then how has your interaction been with the FDA on re-dosing and how many total doses could you potentially go up to with FT596? Thank you..

So with FT596, the Ash Presentation is going to be a case study on patient two only. So that --hat will be the FT596 Presentation at ASH. Our current protocol for FT596 is single dose administration. And then we're able at the end of that first cycle, which is a 30-day cycle, to engage with the FDA to re - to potentially re-dose patients.

That's a - obviously a protocol where we re-engage the FDA to support a second dose. All our other product candidates that are currently in the clinic, the protocol by design, as approved by the FDA already has multi-dosing in it. So for instance, FT500, has up to six doses, FT516 has up to six doses.

So I do believe ultimately with a little bit of safety data across our pipeline, which regenerating including 50o and 516, we'll be able to have an engagement with the FDA and discuss the potential to multi-dose FT596, just like we do for all our other product candidates..

Great. Thank you very much..

Thank you. And our next question comes from Ben Burnett from Stifel. Your line is now open..

Hi, guys. Thanks for taking my question. This is Neil on for Ben. Regarding the FT596, investigator sponsored study in the relapse prevention after transplant setting.

Can you shed any light on whether enrollment is underway? And then just give us your thoughts on how you would leverage any positive data that came out of that program?.

Sure, Wayne, you want to you want to take that?.

Sure. So as far as the study status, that study is open at the University of Minnesota. We have not enrolled patients on that study yet. However, we have identified candidate - potential candidate patients that if things go well, we could see first treatment on that study in the coming weeks or month or so.

To your second question about the data value, I think, as was alluded to before, I think we get we will get a lot of information from that study with respect to the pharmacokinetics of FT596 in the setting of a situation in a post-transplant where patients have been subjected to high dose chemotherapy which have been lympho-depleting and then understanding the pharmacokinetics, the proliferation and persistence of FT596 in that setting.

And it kind of goes to that broader question that Scott mentioned before around the ability of a variety of different regimens to serve as conditioning therapy to support our iPSC NK cell products.

So I do see value not only from the clinical situation where we can hope to enhance the anti-tumor activity and survival following autologous transplant lymphoma.

But we will also have the opportunity to learn important biology questions around our iPSC NK cell proliferation and persistence in other lympho-conditioning settings besides fludarabine and cyclophosphamide..

Okay, thank you guys..

Thank you..

Thank you. And our next question comes from Daina Graybosch from SVB Leerink. Your line is now open..

Awesome, thank you. Congratulation guys on all the science at SITC and ASH, it's quite exciting. And one abstract that caught our eye at ASH was the one that confirmed the NKG2A is quite effective at educating the iPSC NK cells.

And you also had some really interesting in vitro data showing that the HLA expression when you increased it, and cell line the K562 is going to actually reduce the cytolytic capacity of the NK cells.

And I wonder if you have any mechanistic hypothesis for why you're not seeing that HLA inhibition? And how translatable do you think these in vitro assays are to the human situation?.

So I'll take that question. Thank you for reading that abstract. And it was a, it was a beautiful collaboration with [Kelly Mabergeth], he's one of our premier individuals out there on NK biology.

So we went into this not knowing how the NK cells will develop with NKG2A or with KIR, because obviously, we're doing this in a P3 dish, this is not in the body. And what we found was very interesting that during development, the NK cells ended up using NKG2A to basically educate themselves.

And so traditionally, HLA expression is basically use with KIR to educate the cells. Here we found out that NKG2A was used and through the ligand-expression of activating receptors and NKG2A, we saw that the cells actually learned to use NKG2A. So when you express HLA-E, that should enhance their performance.

And so from that perspective, we saw that, in fact, it was the additive effect with HLA-E on CAR activity or just innate activity.

Does that answer your question?.

Well let's do or maybe just a follow up.

So you're licensing it, you see the additive effect, but doesn't then if you have a high HLA-E on a cell that you're recognizing, doesn't that also inhibit when you are ligands do that, but you didn't really see that? And I was wondering, why you didn't see that?.

Yeah, that's - so that we're looking at that and the poster or actually the presentation will shed some light on all the different signaling mechanisms that are upregulated. So we see that NKG2A whether its base level expression of HLA-E or super physiological expression of HLA-E.

It actually helps maturation and so it is compromises over for KIR expression. So we're just saying that NKG2A actually supports maturation, so we're investigating exactly why. But even when we go to higher levels of HLA-E, this maturation continues, and then we still maintain the anti-tumor efficacy..

That's helpful. Thank you..

Sure..

And thank you. And our next question comes from Biren Amin from Jefferies. Your line is now open..

Yeah. Hi, guys. Thanks for taking my questions. Scott, for the FT596 program, you announced that you're moving this into refractory CLL. But when you look at the autologous CAR T, CD19 CAR Ts, we haven't really seen much success in CLL.

So can you, I guess, provide what the rationale is on this? And I guess it is objective in looking at CR rates, because I'm going to assume most of these patients have failed BTK. And you're seeing, I think, very low rates of complete responses in these patients.

And would you also, I guess, require patients that have failed a Bcl-2 or PI3K inhibitor?.

So I'll let Dan talk a little bit about the findings in T-cell - in the T-cell world and why we're excited potentially about an NK cell, an iPS-derived NK cell. And I'll let Wayne then talk a little bit about the study protocol..

Hi Biren, this is Dan. So CLL is one of the areas that we're specifically excited about, because one of the findings in that patient population is their T-cell compartment is beat up and really not ready for the manufacturing and has shown very variable and poor performance in a CAR T setting.

And this is one of the huge advantages of using a healthy off-the-shelf approach. And specifically, our iPS manufacturing process really gets around this limitation. So this is one of the reasons we're very excited about developing, off-the-shelf products for the CLL population.

And Wayne, you want to take the next one?.

Yeah, sure. So regarding the question around eligibility for patients with relapsed refractory CLL, for this part of the study, patients will be required to a failed prior BTK inhibitor as well as a prior Bcl-2 inhibitor. So patients who have to received and failed on both a Bruton and venetoclax to come on to this part of the study..

Got it. And then I -.

Yeah, and as you said, the other thing I'd add to that is, again, I'm not going to read too much into small numbers of patients. But if you do go back and you look at the data set from MD Anderson and out of Dr.

Rezvani's Lab, that was published in New England Journal of Medicine earlier this year, actually, I think more of those patients, and we're dealing with small numbers of patients, I understand, but more of the patients actually had, I believe had CLL than they had DLBCL in that dataset.

So there is some interesting proof-of-concept there, albeit in small numbers of patients for a prior NK cell therapy..

Okay, that's helpful. And then on the DLBCL side, you mentioned that patient two had received a second dose, would that be the same number of cells as the first dose? Can you talk about that? And -.

It was..

Go ahead..

Well, I was it was the same as the first dose. So the patient received 30 million cells as a second dose..

And as you go higher in dose escalation, let's say 300 or 900 million cells, is the thought that if the patient requires re-dosing it would be at the same level, or could you re-dose at a lower 30 million or 100 million cell level?.

Yeah, so that's a really interesting question we have we have not yet done inter-patient dose escalation, we just have not gone there yet, in thinking about how we dose patients. But you - we potentially could..

And interestingly enough, and again, I don't want to, I don't want to read too much into it. But you know, the FT516 COVID experience, it's a clinical trial that we're running, actually does have interpatient escalation where we start out at 900 dose one, then go to 300 dose two, and then go to 900 dose three.

So we are actually learning a little bit about this in the COVID setting with that FT516..

Got it. And then - and then maybe just one last question. There seems to be I guess, you know, some speculation that patient two has achieve a complete response with the second dose.

Can you confirm that?.

No, I can't confirm what how patient did or did not respond to the second dose..

Great. Thank you..

And thank you. And our next question comes from David Nierengarten from Wedbush Securities. Your line is now open..

Hey, thanks for taking the question. I have maybe a little bit different one on the 819 and T-cell side of things.

Have you considered or and hanging out in the research works a system where you have your modifications, and then you add in a plus minus kind of effector signal for solid tumors, so to achieve greater efficacy with less toxicity depending on the antigen presentation by the tumor cells? Yeah, there's been I know, some work in the field on that.

And I was just curious if you guys were thinking about that on the solid tumor side on the T-cell side? Thanks..

Hi, this is Bob. Yeah, logicating, I think what you're referring to, it makes a lot of sense and especially in the heterogeneous tumor world. So we're definitely working on not just as Scott mentioned earlier, the CD16, where it gives you the multi-antigen components. We're also working with dual CAR strategies, and also TCRs.

And so at ASH you'll see a slew of concepts coming, where we're targeting multiple antigens in multiple different ways, whether it was CD3 engagement, CD16 engagement, TCR engagement, and CAR engagement. And now we're working, as you're suggesting, and having them be dependent on each other, so one has to turn on before the second one turns on.

And so through that kind of multi-antigen targeting modalities combined with logicating, I think it gives us a unique perspective. Because also, a lot of people are creative, as I mentioned, in some of the things we're doing, but when it comes to engineering, is very limited.

So this is what a platform has given us the ability to publish, for example, 12 abstracts at ASH because we get to do a lot of cool things at the single cell level and get access to a lot of different effector cell to play with..

Yeah, got it. Thank you..

And thank you, and our next question comes from Mara Goldstein from Mizuho Securities..

And then Scott and Dan, I'll just - I have a question here on the prior lympho-depletion.

What are your scientific efforts so far on other methods of innovation for your iNK therapies and if that may even be needed for the subsequent doses at all?.

Yeah, so I mean, we've looked at Cy/Flu. And we're actually in clinical studies. We're looking at different Cy/Flu regimens for instance, the FT500 Cy/Flu regimen, is not the same regimen that we use for 516 and it's not the same regimen that we use for 596. Its two days of outpatient lympho-conditioning in the FT500 setting.

I - like I said, I mean, I think one of the really interesting things about the FT500 data set, and it's why we ran the experiment, is I do believe that what we've seen from the data so far, does support the fact that you can give a single conditioning regimen, and then follow that up with multiple doses over at least a period of 45 days.

Keep in mind that the FT 500 study, when we went and started cycle two, to give three more doses, we did not repeat condition.

And so I do believe and I think the data support so far that there is a window, whether that's, two weeks, three weeks, four weeks, but certainly we've gone out to six weeks now, where we have yet to see rejection programs emerge against the cells we're delivering.

So I certainly think there's the opportunity to support a single conditioning regimen, including lighter conditioning regimens, followed by multiple doses. I also think this is a really interesting thing. And we will talk a little bit more about this at the event at ASH, as Wayne alluded to.

There are many standard of care regimens that are used in early line that provide degrees of conditioning. I mean, let's look at R-CHOP or O-CHOP, right? The CHOP at some level is a form of conditioning. And this is where I think FT596 or FT576.

I mean, there's an opportunity for - to move those products, again, with clean safety profile, to move those products to earlier line of therapy. I don't think there's anything unique about Cy/Flu that requires it to be the conditioning regimen for use with our cell therapies.

And I would add to that the fact that I think that's, potentially reinforced by the fact, once you engineer the cytokines support into the cell itself, like for instance, FT538 where you have the IL-15 receptor fusion engineered into it..

Okay and just one real quick question here. And I apologize if I missed this earlier in the prepared remarks.

Will the company be holding the traditional analyst meeting around the ASH meeting?.

Yeah, we're going to do an event and we won't - unfortunately, it won't be our - the traditional event that we like to hold. But yeah, we will probably do a - we will do a 60 to 90-minute call on the Friday before ASH..

Great, thanks a lot. I'm looking forward to that..

Thank you. And our next question comes from Alethia Young from Cantor Fitzgerald. Your line is now open..

Hey, guys, thanks for taking my questions. Congrats on all the progress.

Can you just talk a little bit about is 596 a function of kind of the number of patients before you go back to the FDA to kind of have the conversation around reducing or is there something else you are looking for? Because it seems like in the early, other clinical programs you've had a fair amount of success with those things? I guess I'm just trying to figure out what the plan is there.

And can you just talk a little bit about the strategy and thought behind the COVID study, which you just started, I think the ISG study? Thanks..

Yeah, absolutely. I'll let Wayne talk a little bit about the COVID study. It's early on in that study, but I'll let Wayne talk a little bit about that.

With respect to re-dosing, look it's a safe assumption to assume that when we first approached the FDA with the potential to take FT596 into clinical study, that we had a study design that was more similar to FT500 and FT516, providing multiple doses over multiple cycles.

The reality is when we started the FT596 study, we did not have obviously any data with FT596. And we had very little data with FT500 and FT516. So we did not yet have the precedent data set that we do today with FT500 or FT516 to support the discussion with the FDA.

As a result I think and the fact that it's a three-point edited cell therapy, it's a first of kind from that perspective. The FDA recommended we be a bit cautious in proceeding with a multi-dose paradigm and asked us to proceed with a single dose with the ability to give a second dose upon their consent.

I do think now, obviously, we're generating data with FT596 and showing it safety, even if it's just single dose safety. And we have certainly reduced at least one patient which we've discussed. And we're generating a tremendous amount of data now with FT500 and FT516 that provides up to six doses to patients. So I don't think we're quite there yet.

The FDA asked us to generate some data specifically with FT596. But I think we're getting to the point where we could potentially have that conversation with the FDA to support a multi-dose paradigm. Anything could happen, but I feel fairly confident that we will be able to move to that type of paradigm.

Keep in mind, we did file the IND for FT538 after FT596. And FT538 is a multi-dose paradigm. We also filed the IND for FT819, the first T-cell, after 516, and FT819 has a multi-dose treatment arm. So I believe we're getting there..

And then on the COVID?.

Then Yeah, so regarding the COVID study, this is a FT516. This is an investigator-initiated trial at the University of Minnesota where patients with documented SARS COVID 2 infection, as determined by PCR and who have, a clinical presentation that is, kind of that medium between completely asymptomatic and very sick.

Patients would come on to the study and they would receive 516 in a way that the dose escalation is designed for the study is kind of modeled along this intra-patient dose escalation. So the first dose level patients would be given a single dose of FT516 at a low dose of 90 million cells.

And then in the absence of any dose limiting toxicities, the next dose cohort would be that same dose on day one and then an additional day four dose of 300 million cells. And then the third dose level is basically the day one and day four dose and then the addition of a third day seven dose at a dose of 900 million cells.

And so this trial is open, it has enrolled at least two patients so far. And because these dose cohorts are essentially single patient cohorts, we've been able to rapidly clear dose escalation and so we're now still in the midst of dose escalation at the highest dose level.

As you can probably imagine, given all the advances in the standards of care for the treatment of COVID, it's I think finding patients for that fit the profile, as defined by the study has been a little bit challenging but it's not for the lack of the availability of patients or the enthusiasm for the study. So -.

Awesome, great. Thank you.

And Scott, this stuff will color on kind of the dynamics behind the timing of 596 relative to other things?.

Yeah, I think that was actually a pretty important dynamic that drove this at the time, right? We filed three INDs in pretty rapid succession. And we did not actually have a lot of data with an iPS-derived paradigm at the time we even we filed the FT596 IND..

Got it, very helpful. Thanks..

Thank you. I would now like to turn the call back over to Scott Wolchko, President and CEO of Fate Therapeutics for closing remarks..

Terrific. Thank you, everyone for attending today's call and all the great interactive discussion. And absolutely look forward to speaking with some of you at the SITC conference and then the obviously ASH event and the ASH Conference. It should be a really exciting couple of weeks here. Thank you very much and be well..

Thank you. Well, ladies and gentlemen, this concludes today's conference call. Thank you for your participation. You may now disconnect..