Welcome to the Fate Therapeutics Third Quarter 2019 Financial Results Conference Call. At this time, all participants are in a listen-only mode. This call is being webcast live on Investors & Media section of Fate's Web site 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.

Thank you. Good afternoon and thanks everyone for joining us for the Fate Therapeutics third quarter 2019 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 & Media section of our Web site under Press Releases. In addition, our Form 10-Q for the quarter ended September 30, 2019 was filed shortly thereafter and can be found on the Investors & Media section of our Web site 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 the market today, as well as the risk factors in the Company's SEC filings included in our Form 10-Q for the quarter ended September 30, 2019 that was filed with the SEC today. Undue reliance should not be placed on forward-looking statements, which speak only as of the date they are made as the facts and circumstances underlying these forward-looking statements may change. Except as required by law, Fate Therapeutics disclaims any obligation to update these forward-looking statements to reflect future information, events or circumstances. Joining me on today's call are Dr. Dan Shoemaker, our Chief Scientific Officer; Dr. Bob Valamehr, our Chief Development Officer and Dr. Wayne Chu, our Vice President of Clinical Development. Over the past three months, Fate Therapeutics has achieved a series of key milestones that have firmly…

[Operator Instructions] And our first question's coming from the line of Alethia Young from Cantor Fitzgerald. Your line is open.

Thanks for taking my questions and congrats as we move toward closer to kind of a readout your ASH. I guess two. One we saw the release from Allogene going after iPSCs today with Notch Therapeutics. So maybe just talk about points of differentiation that you perceive in that technology. And then also you are starting to add a notable amount of patients in FT500. So I just want you to talk about what it means from the safety that you're seeing and the implications around re-dosing and how we should make a read to the platform? Thanks.

So I'll talk about Allogene and sort of their initiative in iPSCs. Wayne should feel free to talk about the initial results we're seeing with FT500, which we are going to talk much more about at ASH. The group that Allogene did the collaboration with is led by an investigator, Juan Carlos Pflucker and so we are very familiar with Dr. Pflucker. We've had conversations with Dr. Pflucker quite frankly dating back for probably five years. And we're very familiar with his technology. Our read of his technology is that his technology primarily relates to maturation of T cells and maturing T cells to specific phenotypes. I know my conversations with Juan Carlos interestingly enough have never viewed him as someone who is an expert in iPS cell technology, quite frankly. So I think the technology is interesting as it relates to how you might mature a cell to a specific T-cell phenotype, but I did not -- and I don't think Juan Carlos necessarily views himself as an expert in iPS cell technology. I would say we've looked at that technology that is being used by that group and we are very comfortable with the technology we've developed under Memorial Sloan-Kettering collaboration on the phenotype of the T cells, we're generating and we plan to highlight some very significant in vivo data at ASH. I don't know Bob, if you have anything to add to that.

No, that's exactly right. We've been talking to JC for quite some time, as Scott mentioned. And his technology is associated with taking hematopoiesis down to T cell lineage, specifically microbeads that have expressing ligands DL4 and VCAM, which has been published a couple of years ago. He is amazing in T-cell development, but when it comes to iPSC culture, I think, as Scott mentioned, there is that we're still thinking, we have a differentiated platform that's not seen by JC's technology.

And then with respect to FT500, I mean, I'll turn it over to Wayne. He is obviously very closest to running the FT500 clinical study, and he can comment a little bit more on safety and that we're seeing with respect to the multi-dose paradigm. But really we're looking forward to unveiling a deeper dive on what we're seeing at our ASH investor event.

What I can say about FT500 as Scott mentioned earlier that, I think one of the key objectives of FT500 is demonstrating that safety and tolerability of giving multiple doses on demand of FT500 in patients. And I think one important point to remember is that all of these FT500 doses are administered on an outpatient basis. So unlike some of the other autologous CAR-T products that require mandatory hospitalization for monitoring, we do not have such requirement. And the patients that we have treated to-date with FT500 have all tolerated the FT500 quite well, really there has been no dose limiting toxicities or any related serious adverse events, as was mentioned before and really primarily reasons for not continuing to the full course of FT500 are really related to underlying disease rather than anything related to FT500. So it's still relatively early days, but we're very encouraged by what we've seen so far from a safety and tolerability perspective.

And our next question's coming from the line of Michael Schmidt with Guggenheim Securities. Your line is open.

This is Kelsey on for Michael. Thanks for taking our questions. I guess, kind of more bigger picture. Now that you kind of keep adding increasingly more edits, now up to three kind of in the clinic. I guess, how have you seen regulators respond to this increased complexity and do you see a ceiling for the number of edits that you could make to these cells? Thanks.

Sure. I'll touch lightly on this topic, because it has to do with regulators view of editing, I do think, as we talked about in the past, I do think we have a significant advantage when it comes to gene editing. And that is imparted upon us based on the specific nature of our platform. We're engineering iPS cells and we're selecting a specific clone where that and the engineered properties are locked in and they are uniform just by the very nature of selecting a single clone. And so I think that is very unique. I think in the world of patient derived cell therapy or donor derived cell therapy where you're engineering at a batch level, I believe, and our experience has been at least pre-clinically, it is very challenging to create homogeneous product and that there are significant off target effects associated with batch engineering, especially when you're trying to do two, three, four, five edits. I mean, Dan can talk a little bit about the work we're doing under our Ono collaboration right now, but we certainly have not stopped at three. Certainly, we'd stop there with FT596 in the clinic, but what we're doing under the Ono collaboration and the limits that we're seeing, I mean we're thinking about for solid tumors ultimately that we are exploring right now, four, five, six edits as part of a iPSC platform again where you have the benefit of one-time engineering, selecting a single clone and fully characterizing the elements associated with that engineering event. And then that translates all the way to the patient, because ultimately the patient is receiving a homogeneous cell product and quite frankly that homogeneous cell product has been that exact product with those engineering features has been thoroughly preclinically tested before seeing a patient and I think that's another unique difference we can do preclinical evaluation of all that editing and ensure that the patient is receiving that product and that is very different than batch engineering. I'll turn it over to Dan who'll provide more insight into the Ono collaboration.

Just a few thoughts here as we're really in the sense that their lead products now have three edits. It's really focused on dual targeting persistence and just sort of a function of the base CAR-T and CAR NK cell as we then look toward solid tumors, there is whole new realms of opportunity to make yourself better, stronger, faster with expected trafficking infiltration into the tumor overcoming the tumor microenvironment and recruiting other immune cells into the tumor to turn cold tumors hot. So I think the future is really going to take the shape of how are we going to build on this current generation of base products to overcome the challenge of solid tumors. And I think as we sort of assessed the competitive landscape of what different platforms are capable of doing, I think one of the unique strengths of our iPS clonal platform is the ability to generate these highly edited clonal iPS populations and performed extensive characterization to demonstrate all of the rigorous copy number variation and translocations and things that can happen. These are just part of our standard QC process that we think is a unique path to getting to these really extraordinary processes and this is one of the things we're most proud about.

Our next question's coming from the line of Ben Burnett with Stifel. Your line is open.

Just two questions and thank you for laying out so explicitly the FT500 updates at ASH that we can expect. But can you provide maybe just a little bit more color as to whether any FT516 data will be disclosed by their Dr. Miller at SITC or by Fate at the Company's event at ASH?

So at SITC, I can absolutely confirm that Dr. Miller is not going to disclose clinical data around FT516. His presentation at SITC is around FT500 and the preclinical data package around FT500, including the value of NK cells, synergizing with checkpoint inhibitor therapy, which has a publication that I think is currently in review around that. So he will be discussing that at SITC. At the ASH conference, we do have an ASH events or event. Obviously I can't speak to what abstracts will be unveiled tomorrow, but we will give an update certainly on FT500. I think it's a little too early for us to say definitively whether FT516 will be part of the clinical update or not. But certainly, we're very pleased with the fact that we've dose the first two patients; the first obviously being in the lymphoma arm in combination with rituxan and the second being in AML.

And maybe if I could just ask beyond ASH and into this year, what sort of the cadence of clinical updates for FT516, and I don't know if it's too early, but also FT596 that we can expect?

I think we will be happy to talk more about this at ASH.

And maybe if I could just squeeze one more on ProTmune then. If I recall, there were some discussion around the potential to use a day one 100 end point versus maybe waiting for data to mature and look at a longer. I think we talked about one year endpoint which could potentially inform on survival. I guess, can you just remind us sort of current thinking and when we can expect the ProTmune trial to readout and sort of what the endpoints are that you're looking at?

The primary endpoint of the study, you are correct, is a day one 100 endpoint. It's cumulative incidence of grade two through four GvHD at day 100. We are finalizing the statistical plan right now with respect to the primary endpoint. And we are looking very closely at also including a key secondary endpoint, which is a composite around freedom from chronic GvHD relapse and death at day 365. And we are going to discuss this more at ASH with our key investigators in the PROTECT study, but that key composite endpoint as we've thought about it and gotten feedback is important to at least consider that as a potential secondary endpoint given it does represent essentially the totality of the outcome of transplant.

Our next question's coming from the line of Matt Biegler with Oppenheimer. Your line is open.

Thanks for taking our questions, definitely a lot of progress, a lot to digest. A quick clarification on FT596's stage one. Is it only a single patient that will be enrolled in the monotherapy cohort and also on that Phase 1 is it all covers by design or will you be excluding patients who are CD19 negative?

Sure, I'll let Wayne answer those questions.

So for FT596, it will initially start as a monotherapy cohort but it will directly transition into an escalation that focuses on the combination of FT596 with the anti-CD 20 monoclonal antibody, specifically rituximab. So that initial cohort is a three patient cohort and adherence to three plus three dose escalation principle. So minimum three patients will need to be enrolled in that monotherapy cohort before being tested at that same dose, but in combination with rituximab and then dose escalation will proceed from there. As far as the types of patients to be enrolled, it's generally quite broad across multiple subtypes of non-Hodgkin's lymphoma with the goal of getting to the maximum tolerated dose or maximum assessed dose as quickly as possible and then at the point of dose expansion then we have the optionality of enrolling specific cohorts based on histology and other baseline characteristics, where we would then look at the overall safety, tolerability and anti-tumor activity in greater depth.

And then I was just wondering if we should expect any updated data from the NK100 programs. I mean I do realize that these programs have been discontinued in the focuses on the iPSCs going forward?

I think we are having discussions right now with the investigators that are involved in that study. With respect to whether they would like to publish that data or present data at various conferences, we're very open to that and I think actually at SITC, Jeff may provide a little bit of update on the ovarian study, quite frankly, I've seen a draft of his presentation. There is a little bit of an update on the ovarian study with NK100.

Our next question's coming from the line of Amanda Murphy with BTIG. Your line is open.

Just a question on 596, you've obviously done a good job with 505, 516 in terms of laying out what you view to be the comparable efficacy targets, I guess, or sort of bogeys. How do you think about that from the 596 perspective? I know there is not obviously easy comparisons that are already out there other than maybe MD Anderson slightly different. But just kind of thinking about what you're looking for in both arms and response and durability in theory, for that therapeutic?

So for FT596, because it has many of the features that we think are desirable to maximize efficacy against lymphoma. And based on what information that has released so far regarding NK cell-based therapies with a CD19 directed CAR. What we're expecting to see with FT596, quite frankly, is a level of efficacy that approaches level that's seen with other adoptive cell therapies. But potentially with its safety profile that is quite manageable in the sense that minimal cytokine release syndrome, minimal neuro toxicity, in totality, which still enables us despite the addition of these generic engineered elements to administer FT596 on an outpatient basis. And certainly, because of the flexibility with respect to multiple dosing and even flexibility with dose and schedule, one would hope that we would not only be able to achieve deep responses at a meaningful level of frequency, but also have these responses be durable.

Do you have the option to tweak the lympho depletion as well, or is that pretty much out of the frame?

I would say I mean Wayne can answer. I mean, basically I think our view is that, what we've seen and the conversations we've had with the FDA, the FDA is very amenable to protocol changes that are based on clinical data.

Yes, I think that certainly given this is still a relatively new area. I think that the lympho conditioning regimen that we specified for FT596, I would consider as a starting point. As we get more data regarding the persistence of FT596 maybe data around the pharmacokinetics of FT596 the safety, efficacy so and so forth. We have the opportunity to look into the possibility of modifying lympho conditioning, even if it means modifying lympho conditioning with the subsequent cycle compared to the first. There are a lot of different variables that one can consider, but we would need to generate that data before we would make a informed decision on that.

If I could just sneak in one about sort of longer-term question I guess and then answer maybe just wait for ASH, so that's fair. But I just was curious you've obviously made a lot of progress on the T-cell back on side as well. When you think going forward from here, how are you thinking of prioritization of the pipeline between, I guess with the [NQ] product you talked about BCMA CAR, CD38 knockout etc vis-à-vis a T cell backbone candidate?

So from my perspective, we're doing both. And we are completely committed to doing both. There may be we've talked about this a little in the past. There may be situations where T cells we think T-cells are particularly advantaged. There may be tumor types, for instance, we've talked about the solid tumor types where MHC class I has been down regulated where T-cells are clearly not advantaged and NK cells might be advantaged. And I have said this publicly before, it will not surprise me within, well, let's just give it two years. If a cell therapy is given that is comprised of both NK cells and T cells.

I could just simply add that in terms of prioritization of where to place individual products, I think they will be largely dictated by what we see in terms of the clinical data that defines the risk benefit profile for these products and then matching them with the individual disease because as many of us know lymphoma is a very heterogeneous disease and what works really well in one indication may not necessarily work well in another indication.

Our next question's coming from the line of Biren Amin with Jefferies. Your line is open.

Scott, on 596, what criteria would trigger redosing of patients in that trial and I guess how are you defining moderate lympho depletion, if you could just further characterize that a bit more?

Sure. I mean we could touch on that. So I mean actually I'll let both Bob and Wayne touch on this. One of the things that is very unique to FT596 as we've discussed that has three anti-tumor functionalities embedded into it. One of them is the IL-15 receptor fusion. I'll let Bob talk about some of the preclinical data we've seen with that IL-15 receptor fusion, which has led us certainly to the conclusion that we are looking at only giving one dose per cycle based on what we've seen pre-clinically and then I'll let Wayne talk about the conditioning regimen specifically that we're starting out for FT596, which I think you'll be very familiar with. It's a condition regimen that is used quite frankly by multiple groups in the CAR-T cell space that are conditioning and not depleting.

So Scott was mentioning that these modalities are tailor-made for NK cell expansion. And so for example, you take the IL-15 receptor fusion that brings in not just proliferation, but also survival and growth. So, these cells are autonomous. They can be cultured in the manufacturing process without the need for IL-2 and IL-15. That independence of cytokines support continues then to the in vivo models we have. And so we're very confident that the cells were persist. A second triggering mechanism that's going to give the sales persistence and antigen mediated expansion is the CAR that's been calibrated for NK biology has been highlighted by Scott in previous discussions. And so the combination of these two modalities really gives the cells a boost where one-time dose will be triggering enough of the activation, and expansion of the cells to have an effective clinical response.

And then as to the FT596 clinical trial specifically with respect to the lympho conditioning, it's essentially the same lympho conditioning regimen that's used for the CAR-T specifically three consecutive days of fludarabine and cyclophosphamide with the fludarabine dose of being 30 milligrams per meter square per dose and cyclophosphamide being 500 milligrams per meter square per dose. Importantly, with the FT596 Phase 1, it's currently written with a single administration of FT596, and then dose escalating based on that. But in line with all of the other products, our intention and goal is to get to a point where we can give multiple doses of multiple cycles of FT596. So even in the protocol, it's currently constructed as Scott mentioned, there is the opportunity to give an additional cycle of FT596 contingent on patients being clinically stable to receive a dose and that includes sufficient recovery from any treatment-emergent adverse events following cycle one and then any evidence of clinical improvement either clinically or radiographically. And then, as Scott mentioned, once that data packages reviewed with FDA then patients potentially could get another cycle of FT596. Ultimately, once we have sufficient data from at least several patients and had that discussion with FDA, the intention is that we would amend the FT596 Phase 1 study such that every patient coming on, would have the opportunity to receive multiple cycles of FT596 without having to going through a data review on an individual patient by patient basis with the FDA.

So just on the FDA patient review, how many patients would FDA need before they're comfortable in improving an amendment to the protocol? Have they disclosed what that number is?

We don't know what that number is. They've not disclosed that number to us. I do not believe it is a significant number of patients. I think the FDA was asking us to, as I have said before, I mean this is a first for cell therapy forget about iPSCs, this is a cell therapy that has three anti-tumor modalities engineered into it. And so, I think the FDA is appropriately asking us to demonstrate a little bit of safety before launching into a treatment paradigm, which is also novel giving multiple cycles of therapy.

That's fair. And I have a couple of follow-ups on the other programs. So on 500, Scott, you mentioned that you could potentially be enriching for tumors with partial or complete loss of MHC 1 expression as well as enriching for cancers with NK cell infiltration. so for both of these parameters, how well do they correlate in terms of, let's say lung or renal cancer?

So I think there is a high correlation with the lung. So I think about 40% of patients, 30% to 40% of patients that progress or fail on checkpoint inhibitor therapy. If you look at the tumor the actual tumors that the mechanism of resistance appears to be associated with significant down-regulation of MHC class I expression. Additionally, when you administer NK cells systemically, they absolutely traffic through the lung. So based on when you look at significant areas of resistance, areas of resistance that are associated with a loss of MHC class I and potential for NK cells to traffic and infiltrate lung as rises to the top of the list.

And then I guess on, you also mentioned that you may amend for a cytokine support. So are you thinking about administering IL-2 after dosing these cells?

Yes, yes. I mean historically what has been done with donor derived NK cell therapy and I believe it's also done with a particular cell therapy that is everyone has sort of people's attention right now. IL-2 is commonly given that doses. And so when we think about amending the protocol to now promote NK cell anti-tumor activity, yes, IL-2 would be an obvious thing to add with the dose.

And then, maybe if I could get a last question, and you talked about Jeff Miller presenting at SITC. What do you think is the biggest differentiator of your platform versus donor-derived NK cells? Is it non-cleavable CD16 component that you've talked about or is there some other component that you see differentiates?

The platform generally, just unclear…

Yes.

The platform generally, I think there is a multitude of factors that differentiate this platform. I mean we spoke a little while ago about just the nature of engineering. I fundamentally believe cell therapy will incorporate multiple engineering elements to best promote anti-tumor activity. And I believe that is going to be very hard to accomplish at scale in a predictable way and produce homogeneous product, if those edits are occurring batch by batch as part of the manufacturing process. I think that's going to be super challenging, not to mention super expensive. The engineering is one element because we've collapsed all the engineering into a one-time event at a master cell line. I do believe in the world of cancer immunotherapy just like oncology, there is very few agents that are given as a single administration and there is going to be plenty of data and there is plenty of data coming out with CAR-T cell therapy talking about the challenges of single dose administration, single antigen targeting that is leading to relapses and lack of durable responses. And so, to me, the idea of being able to give multiple doses over multiple cycles like monoclonal antibodies are given, but doing that with a cell therapy where you can now engineer in multiple mechanisms of action, I don't know any other way to do this other than use an iPS cell-based approach.

Our next question's coming from the line of Jim Birchenough with Wells Fargo. Your line is open.

Hi guys. Thanks for all the detail. Just one high-level question across FT500, 516 and 596 what's going to be the best opportunity to identify the efficacy of the cell therapy itself?

So I don't think it's a fair question, quite honestly. With respect to the product candidates. I mean FT596, I mean you're sitting here talking about three different functional modalities being embedded into it. So it's not a fair fight basic level between the three product candidates.

So, but given that I guess, I'm trying to understand with 596, it sounds like we're moving into Rituxan combo pretty quickly. Is there going to be a good opportunity to assess the monotherapy activity of the cells that at a reasonable dose and benchmark it against what we've seen from the CAR NK data from MD Anderson as an example?

There may be, but that's not our objective. Our objective is a belief that multi-antigen targeting as a best-in-class approach. I don't think we're alone in that belief and FT596 was designed to exploit it and that's where we're...

And then maybe just thinking about the Rituxan combinations, could you maybe speak to how many patients you need to treat or what level of response you need to see to rule out contribution from Rituxan and I get the point that you have maybe responses in some patients as low as 10% to 20%, but you need to treat quite a few patients to rule out that level of response at the lower bound of confidence intervals. Could you speak to that because I think it's at some point we're going to be trying to figure out the contribution of the cells and the antibody in this data going forward?

Well, to be clear, they will have failed Rituxan.

And the definition of Rituxan failure?

So the definition of rituximab failure is quite simply is a patient who received prior rituximab based therapy and either did not respond to that or progressed following an initial response. So that's just as a kind of a rough benchmark. If you look at what are these monoclonal antibody clinical experience in this patient population, there are basically two examples. One is single agent obinutuzumab and the other is the single-agent MOR208 that's the CD19 directed monoclonal antibody from MorphoSys. Both molecules have been tested at a single agent in a patient population of sales rituximab and it's been fairly consistent in diffuse large B-cell lymphoma, the complete response rates for both those ranges are approximately 10%. Best overall response is about 30%, 35%. Those numbers are a little bit higher in some of the more indolent lymphomas. So as we do our initial assessment of FT516 and FT596, those are the rough benchmarks that we used to see whether or not there is additional activity has confirmed by the cell product. But to your point, in order to rigorously rule that out, we would have to do it in an expansion cohort with the requisite number of patients to roll out that lower bound.

I would also just reiterate to be clear as Wayne discussed, the target product profile for FT596, we are looking for. I would say similar response rates that have been achieved with CAR-T cell therapy.

Our next question's coming from the line of Mara Goldstein with Mizuho. Your line is open.

So I have a couple questions, one on the FT500 program. What's the highest number of doses that an individual has received so far in a trial, or is that something that you're going to disclose at ASH? And then, I'm curious if you could characterize you know 516 program what mild cytokine support it means? And thirdly, just a question from a quasi, I guess regulatory question and that has to do with, in your interaction with the FDA's and sort of discussion in characterizing iPSC-derived cell products. Is the focus on sort of the phenotypically and functionality correctness versus safety and what does that access look like?

So I'll sort of go in reverse. There is a tremendous amount that goes into the regulatory discussions with respect to clearing an Investigational New Drug Application for clinical study. There are multiple elements that are important. I will tell you that characterizing the engineering events is absolute-characterizing the effective engineering, the integrity of engineering is absolutely important. Safety is absolutely important, and there's a whole host of factors that go into putting together the regulatory package and demonstrating to the FDA that we have a product that we believe is safe to justify clinical study and engineering certainly one of those elements. Looking at the engineered features, yes. And being able to characterize the product with respect to those features, I think is really important and I think it's one of the areas where we're aided by the fact that ultimately we can chase trace the final product back to a single clone, which ensures uniformity of those engineered features. I'll let Wayne talk about the clinical experiences with FT516, FT500 the clinical protocol with FT500 initially in its initial form was written to allow for up to six doses, so three doses in the first cycle, three doses in the second cycle. That is how it was originally written for the first part of dose escalation.

And then with respect to FT516, the dosing schedule of 516 similar in the sense that it's three weekly doses per treatment cycle given on day one, day eight, and day 15 of each treatment cycle and then patients would be eligible to receive up to two treatment cycles. So that would mean six total doses of FT516 and then your specific question around cytokine support, it would be IL-2 given out a dose of 6 million international units given subcutaneously with each dose of FT516. So there'll be a total of up to six doses of IL-2 support for the FT516 clinical trial.

Our next question's coming from the line of Daina Graybosch from SVB Leerink. Your line is open.

Good discussions thus far. One more question from me. Maybe taking it back to the very first question with more and more competitors coming in, I think as a testament to your approach and the value that you've been talking so much about, how do you think we should start comparing the data as it comes out from these competitors? What things in particular do you think are most interesting and helpful to compare pre-clinically both for the iPSCs as well as the CAR NK competitors that start to come?

So we're discussed -- just to be clear, discussing preclinical data, because I don't think we'll be discussing clinical data from a competitor for probably…

No, I agree. We're going to recycle pre-clinical data. So how should we judge that in your perspective and compare it to your programs pre-clinically?

Sure. I mean, I'll let Bob answer that question, because Bob has sort of the greatest purview view of what people are trying, I use the word trying, to do in the iPSC field. One thing I'll say before turning it over to Bob as much as people have talked about iPS cell technology. I mean we have spoken a lot about the value of selecting a single clone and we believe there is a lot of value to that. I still have not seen anyone talk about being able to select a single clone and make a master cell bank. I still have not seen that from one person. So when you see that let me know, but I'll let Bob go.

So that's a great question and Scott kind of started it and we've been talking about it the whole time. I mean, I think you could think about in four stages. The first stage is exactly what Scott said, when you make a master cell bank and that master cell bank has been generated from a single cell, what's the integrity of your master cell bank? How well have you characterized it? And do you have genomic stability after that massive expansion? So first, stage one, generation of the master cell bank that contains your moralities in a uniform manner that is well-characterized. The second stage is, lending specific differentiation. How well can you take that vial that you've created in the master cell bank and then guided through differentiation to make yourself the final cell product that fully mature tier NK cell that has the ability to do exactly what you told it or you engineered to do. So that's a second stage. Your manufacturing process to create homogeneous product every time that is of desired attributes. The third stage of that is now the distribution of that off-the-shelf product can you directly saw and infuse, can you make the bags, can you ship to the hospitals and can you go through that all that stability, all the things that the regulatory challenge of the manufacturing operations that clinical logistics. So that's the off the shelf stage. And then finally, it's the product itself. I think one of the things that we've been very proud of is not just manufacturing of iPSCs, but the intelligence that goes behind product development is still targeting approach is something that working with Michel Sadelain, Jeff Miller and collaborators, Dan Kaufman and [Kallie Mulberg] we've been able to put together and I think as the next year rolls out, you'll see more exciting products that are entry points of the solid tumor, for example. So the actual modalities you put in, it's also going to be acquired. So if you look at those four unique stages, I don't think anybody today can say we got it all covered. And the only reason we're here saying that we think we got all covered because we've been doing this for 12 years now.

A thing that I would add from just a more practical regulatory perspective, I mean one of the things I was asked about and I actually didn't touch on this. You have an iPS cell, right. That iPS cell has the potential to walk down arguably 200 different paths of life. The purity of your final product is going to be critical and we've discussed our purity levels. And then as Bob sort of touched on the potency post fall, if you have an truly have an off-the-shelf product is also going to be critical. So when people, we can talk about preclinical data in mice and all that kind of good stuff. But when you have a scalable manufacturing process that starts with a genomically stable master cell line that's clonal and when you have a final product candidate that is almost pure coming out of manufacturer with high potency post fall let me know, I'd be curious to look at that data.

And I'm not showing any further questions at this time. I would now like to turn the conference call back over to Mr. Scott Wolchko, for closing remarks.

Great, thank you everyone for participating in today's call. We look forward to seeing you in the next couple weeks, including at SITC and our ASH investor event. Thank you.

Ladies and gentlemen, this concludes today's conference call. Thank you for participating. You may now disconnect. Have a good day.