Perfect. Thank you everyone for joining us. I'm pleased to be joined by Scott Wolchko, President and CEO of Fate Therapeutics. Thank you so much.
Thank you for having me.
Yeah, of course. 2023.
Yeah.
A lot of changes for Fate. Maybe we can start there. Just talk us through what happened here, how much change has really come about for Fate on the back of this Janssen termination?
Sure. obviously, the termination was sudden, with respect to its developments. It really caused us to obviously, you know, take a hard look at the strategic direction of the company, our assets. We continued to favor the development and the unique value of our iPSC-derived cell therapy platform, both the development of NK cells as well as T- cells, including for hematological malignancies and solid tumors. Coming out of that collaboration, we really focused the company and favored our platform and its unique value in developing differentiated products for hematological malignancies and solid tumors.
Maybe dig, just to dig a little bit more into that, I guess maybe what has changed specifically from what you were doing prior to maybe the more focused approach you're taking now?
Yeah, I mean, actually, the termination came about in an interesting time. I mean, in advancing our iPS-derived cell therapy platform, our initial programs were less sophisticated with respect to their engineering. One of the unique values of an iPS-derived cell therapy approach is you can actually embed multiple pieces of functionality into a cell therapy. The real true differentiator of the platform, if you will, is that you can create these multiplexed engineered cells by engineering iPSCs. You go back, you know, iPS-derived cell therapy did not exist several years ago, we started building our platform in a really systematic way, where we engineered in one edit or two edits and then got to three edits.
really, with this, sort of, with the termination and the refocus of the company, we have focused for the most part on cell therapies that we don't think could really be created in any other way. really, the multiplexed engineered cell therapies, the product candidates, both, for instance, on the NK cell side, where we have 4 and 5 edits, as well as on the T-cell side, where I think one of the most exciting products we're focused on is a solid tumor product candidate under the collaboration with Ono, where we have 7 edits.
Mm-hmm. Is there an optimal number of edits? I guess maybe thinking in the context of some of your competitors who are not doing any edits.
Absolutely.
- maybe help us understand that.
Yeah, I mean, I think it really depends on the setting. I think we've seen in the field of cell therapy, where certainly in lymphoma and even in myeloma, you can do a single edit and have quite remarkable results. I think in that same context, when autologous CAR T-cell therapy has been studied, for instance, in solid tumors, we've seen less than stellar results. I think you really have to think about what mechanisms you want to build into the cell and why, and what you're trying to achieve. One of the interesting areas for opportunity that I think that exists in development, including in lymphoma and myeloma, is, for instance, post-CAR T-cell therapy. Obviously, the first-generation autologous products have remarkable results and are reaching many patients.
They're not yet curative for the vast majority of patients, and most patients progress or relapse, and that creates opportunity to treat patients that are continuing to be in need of product. When you think about that, and you think about patients that have progressed and are more advanced in their disease, you do want to think about developing or building in multiple different mechanisms of action to aid the patients.
In terms of NK cell therapy, there are now an emerging field of other players in this space.
Mm-hmm.
What differentiates you from these others? Is it the additional editing that you're doing in the engineering, or is there another component? How important is the specific cell source that you're using for these iPSCs?
I don't, I don't think cell source is that important. I think, especially in the context of when you're engineering in functionality. We're introducing synthetic biology to a cell. I think the goal is that synthetic biology is essentially carrying the day with respect to safety and efficacy, as opposed to simply the cell itself. I think also, when we think about the NK cell therapy space, I think historically with NK cells, we've seen in the field exquisite safety with respect to unengineered NK cells. I think relative to T-cells, we've seen very modest efficacy with respect to unengineered NK cells. I think at the end of the day, with respect to leveraging NK cells and some of the unique advantages, you do want to build in multiple pieces of synthetic biology.
One of the areas I think is exciting for NK cells, and I think, you know, the field has seen this, is NK cells have the unique ability to synergize with monoclonal antibody therapy and developing pieces of functionality that you can engineer into an NK cell, so they maximally synergize with a monoclonal antibody. For instance, we have a high-affinity, non-cleavable CD16 receptor. We have uniquely taken that approach and engineered that into our NK cells. We think that maximizes the ability of those cells to synergize with monoclonal antibody. We've also engineered in CARs because we also believe in the ability to attack a tumor from more than one angle or direction.
The idea of multi-antigen targeting, leveraging a CD16 receptor in combination with a monoclonal antibody, as well as having a CAR on board to hit a second antigen, we think that's a way to uniquely attack, for instance, tumors, including tumors that have different levels of expression of different targets.
... you're still following some of the patients that had been treated prior.
Yes.
Maybe help us understand the duration that you'll be following them, what you're looking to understand, particularly in the context of what you mentioned, that many of those were at lower doses or had fewer engineering functionalities in there.
Yeah, I think it's really important. Like I said, we build out the company in a really systematic way, trying to understand the functionality of first and then second generation, and then ultimately continuing to build off of that and exploiting our platform. I think understanding the baseline of those first-generation products is really important. As you sort of alluded to, you know, while we have continued to favor development of now more advanced and more sophisticated product candidates, we do want to understand the baseline of activity of those first-generation products.
With respect to FT516 and FT596, our first-generation product candidates in the space of lymphoma, we're going to continue to follow patients for up to a year to understand, for instance, their durability of response, including comparing both FT516, which has just the CD16 receptor, versus FT596, which added a CAR to achieve multi-antigen targeting.
Mm-hmm.
We can begin to understand the baseline value of FT516, as well as the addition of a CAR to achieve multi-antigen targeting, at least in the context of these earlier generation products.
Perfect. Any expectations there on how to think about durability, and will this maybe be a data set that you reveal to the broader investment community?
Yeah, I think our goal is to work with investigators to share the data sets. Obviously, we are developing more sophisticated product candidates, but I think understanding the baseline is important, and I think especially in patients where we're interested in further developing, understanding what, for instance, the baseline responses have been. For instance, many of the patients we had treated are post-CAR T-cell therapy. I continue to think that that's a really interesting space for development, and, you know, again, being able to assess our next-generation products against that is important.
Perfect. Maybe we can dig into some of your programs that you have ongoing. 576.
Yes.
You shared some initial data at ASH last year. Maybe we
Same dose data for an NK cell, yeah.
Maybe walk us through.
Yeah.
What you presented there.
I think one of the things that we have learned in treating patients with NK cells, certainly different than what we've seen with the autologous T-cell product candidates, is that NK cells are not T- cells. They're very different biology. I think for to maximize the therapeutic response with an NK cell, you will be required to give multiple doses. An NK cell does not expand like a T- cell does.
Mm-hmm.
If you give, you know, a dose of an NK cell, you're going to have a essentially that same sort of therapeutic effect, whereas with a T- cell, you definitely get expansion. NK cells have a relatively short half-life. They don't last as long as a T- cell. It, to achieve a sort of similar equivalent potency, I think with NK cells, you're going to have to give multiple doses. With FT576, we started out as a 1 dose. We're getting ready and transitioning now to a 3-dose schedule with FT576 in myeloma. In that study, we're looking at, for instance, a monotherapy arm, where we're looking at 3 doses at 1 billion cells per dose just to test the CAR targeted against BCMA. As I alluded to, we think these cells can synergize with monoclonal antibody therapy.
We have a second arm where we're actually now assessing the combination with, for instance, monoclonal antibody, to look at that dual antigen-targeting impact. We look to treat, you know, 10-15 patients over the next 6-9 months, and I think, you know, in the early, let's call it the first half of next year, I think we'll have a good sense of with respect to the directionality of that program. I continue to think that obviously in myeloma, there are a tremendous amount of patients. We've seen a great therapeutic impact from CAR T-cell therapy.
Mm-hmm.
Despite that, the vast majority of patients require additional therapy, and I believe allogeneic cell therapy will be a very exciting therapy for patients.
Maybe describe to us your confidence that the 3 doses at 1 billion cells per dose is at a level that should, you know, produce an active anti-tumor?
T. activity.
Yeah.
Yeah, yeah. No, absolutely. I mean, some of it's based on preclinical models, some of it is based on observations in lymphoma. We know what the autologous CAR T-cell dose is in lymphoma.
Mm-hmm.
We know what dose we started to see activity at with respect to NK cells in lymphoma. Obviously, a higher dose, and obviously, we were, you know, looked at for single, 2, and 3-dose schedules. If we at least extrapolate that lymphoma data set to myeloma, as well as looking at our preclinical data, we're fairly confident that the 3-dose schedule with an NK cell is certainly going to be necessary, and 1 billion cells should be a dose that is certainly within the range, based on what we've seen preclinically, as well as what we've seen from the T- cell dose that's required in myeloma.
If you needed to dose escalate, is the option to go to a fourth dose, fifth dose, or is it better to do the three-dose regimen at a higher dose concentration?
It's a good question. It's a totally fair question. I think our belief, generally speaking, with respect to cellular therapy, whether it be autologous or allogeneic cell therapy, I think this is... I think we have confidence in this, even based on having conversations with investigators, the responses happen quickly. I think you can generally tell within the first two to three weeks whether a patient is responding and responding profoundly to therapy. From that perspective, we think it's important to sort of drive that maximal impact, as quickly as possible. We favor dosing patients on a multi-dose schedule within the first two weeks. Could you continue to dose? Yeah, you could potentially continue to dose.
Mm-hmm.
We do think the vast majority of the therapeutic activity, if you will, happens in that first two weeks of period. We think really optimizing the dose schedule during that period of time is critical. Yeah, I think that's really important with respect to really front-loading dose, because I think we know from the autologous CAR T-cell therapy world that responses happen quickly.
That's a good segue to the competitive landscape here. Autologous CAR Ts, you've alluded to Abecma. Well,
Yeah.
Abecma, CARVYKTI. Clearly, they've set high bars here.
Yeah.
What would the profile of FT576 need to look like to move this forward?
I don't think of the first development pathway for FT576 as a displacement strategy or directly competing against those cell therapies. I think those cell therapies will absolutely Right now, patients are treated in 4, 5, 6 lines of therapy with respect to multiple myeloma. I think autologous CAR T-cell therapy is absolutely going to be a line of therapy. I tend not to think that patients will receive multiple lines of an autologous CAR T-cell therapy, as opposed to, yeah, most patients are going to get an autologous CAR T-cell therapy. They will require additional cell therapy. I tend to think of the profile of FT576 and its initial development strategy as following those therapies and not necessarily having to compete against those therapies. Engagers are also being utilized post-CAR T-cell therapy.
I tend to think of, you know, for instance, that space, you have to evaluate your therapeutic profile based on what's available to patients. I tend to think of the therapeutic profile, at least initially, post-CAR T-cell therapy, more similar to an engager profile, which generally I think we could agree, probably has 50%-60% response rates, 20%-30% CR rates.
Perfect. One of the things coming out of ASH, there was a lot of talk about in multiple myeloma, maybe going beyond just targeting BCMA.
Mm-hmm.
As you think about maybe the next steps, either for five, probably not FT576, but another asset to be developed in-
Sure
... myeloma.
Absolutely.
What are your initial thoughts there?
Yeah, no, absolutely. I think, it's one of the things that we are excited about and, you know, we think is really exciting about our platform, whether we continue to build off of actually the FT576 master cell bank or, you know, start from scratch and build a new asset, which could be a T- cell, as an example. Yeah, I think that's, I think one of the unique values of being able to engineer in multiple pieces of functionality into a cell therapy is this ability to achieve multi-antigen targeting. For instance, you know, multiple lines of therapy that target BCMA. There are other targets that are really interesting. CD38 is a durable, seems, appears to be a durable target in myeloma.
576 is actually designed to engage CD38 with a monoclonal antibody. GPRC5D is actually a really interesting target that's also emerging as well as others. I think we do have a platform that can uniquely incorporate these pieces of additional functionality and targeting.
Perfect. 522.
Yeah.
maybe we can speak a little bit about that. You've had some very, very early data.
Mm-hmm
remind us what you've seen here, from a preclinical standpoint.
Yeah. I mean, there's a perspective in the world of allogeneic cell therapy, where in order to, let's call it, say, have similar types of results to autologous CAR T-cell therapy, a more intense conditioning has been delivered to patients, and that's obviously not patient-friendly. It's obviously not necessarily the best therapeutic approach. One of the things that we think about cell- therapy, including to like max, really maximize the value of an off-the-shelf cell therapy and reach patients, including earlier in care, is how do you begin to move away or reduce the dependency on Cy/Flu conditioning? It's a huge challenge in the field.
Mm-hmm.
Autologous CAR T-cell therapy involves obviously Cy/Flu conditioning. T-cell engagers do not, keep that in mind from a competitive landscape. If you really want to sort of maximize the full benefit of an off-the-shelf cell therapy, thinking about and considering how do you begin to move away from Cy/Flu conditioning or significantly reduce it, is important. FT522 was designed in that context. How do we develop a cell therapy that potentially can thrive and show sort of activity in the background of a patient's functional immune system? With FT522, we're actually going to test that. The IND is clear. We have a first arm that tests FT522 in what I would consider for sort of a traditional cell therapy paradigm. Cy/Flu, rituximab, 3 doses of the cells.
A second arm of that study, though, removes Cy/Flu, where we're simply dosing rituximab and the cells. That will obviously give us a really good test of the functionality of FT522 and show its sort of safety and efficacy profile without Cy/Flu.
You've been alluding to this ADR technology.
Yes
... but have not yet described it, maybe just for people in the audience.
Sure. Yeah, I think this is, this is the unique feature of FT522. Can't take full credit for the technology. It was originally developed at Baylor College of Medicine, which we identified a couple of years ago and in-licensed. It's, it's a, it's a really unique piece of technology, especially for an NK cell. As I sort of talked about, NK cells, I think in order to sort of rival T- cells, you need to increase the potency of an NK cell and you need to continuously further activate the NK cells. This piece of technology is actually a second CAR. It targets 4-1BB. 4-1BB is highly expressed on a patient's immune system, whether it be NK cells or T- cells. This piece of technology, which is embedded in FT522, actually serves two purposes.
If you give that cell in the background of a functional immune system, these cells will essentially become activated off of the host immune system. We think these cells can actually thrive and increase their potency in the background of an immune system. I think this is important, too. Not only does it help the cell, but to the extent you have avoided fully ablating a patient's immune system, that immune system is now potentially on board to help drive response, which is really interesting, I think, in the context of five two two, because obviously five two two is an NK cell. You're delivering a sort of innate immunity to the patient, synergizing with a monoclonal antibody. Since you're not, in at least in the second arm, you're not ablating the patient's immune system.
The patient's T- cell compartment is available to help drive response, and so this may be an opportunity to get sort of synergy between innate and adaptive immunity.
Have you mentioned yet when we can expect to see this data, particularly in that second arm? To really understand the significance of ADR, particularly.
Yeah, I think it'll take some time. I think we'll have a good sense, at least internally at Fate. I think by the middle of next year, we'll have a good sense of at least the initial observations between the two arms, the Cy/Flu experience.
Mm-hmm.
Versus the non-Cy/Flu experience.
If you find that the ADR technology is doing what you're hoping for.
Yes.
It negates the need for Flu, Cy/Flu.
Cyflu.
How transferable is this technology to other assets that you're developing?
Very. I mean, that's the benefit of the platform, right? At some basic level, we're building master cell lines, and those master cell lines are built one time, and what's unique about those master cell lines is you can continue to build off of those. For instance, FT576, as an example, does not include ADR technology. FT576, though, exists today as a master cell bank. We're able to take that master cell bank and continue to add functionality to it. We have T- cell master cell banks.
Mm-hmm.
We can introduce this technology into those T-cell Master Cell Banks.
Perfect.
That's one of the great things about the platform, is it does provide for rapid innovation and additional added functionality to already existing product candidates.
Okay.
you know, it's a little bit of a curse-
Okay.
because you want to continue to innovate, but it's exciting.
Perfect. The first indication here we've talked about is for B-cell lymphoma.
Mm-hmm.
-for FT522, you've also now disclosed this idea of moving beyond B-cell lymphoma.
Mm-hmm.
Maybe talk us through that.
Yeah. I think, you know, whether it be with CD19 or FT522, I mean, I think if you go back 6-9 months, there's been some now remarkable results with autologous CAR T-cell therapy in the setting of autoimmunity. It's the whole idea that the CD19 targeting can deplete a B cell population and lead to a functional reset, that's very exciting. Autoimmunity has, is sort of full of opportunity with patients in need. I think cell therapy in the world of autoimmunity is just beginning. I mean, we're at the very beginning steps of cell therapy. What's exciting and differentiating, for instance, about FT522 and thinking about FT522 in autoimmunity, again, if you can move away from Cy/Flu.
Mm-hmm.
-significant advantage. Off-the-shelf cell therapy, where you're not necessarily relying, unfortunately, on, for instance, the patient's immune compartment, which in autoimmunity is often sort of hampered and damaged, and patients are on immunosuppressive therapy, so you can't necessarily harness the patient's immune system, an effective way to make an autologous CAR T. There's some really unique advantages for an off-the-shelf product candidate. FT522, I think is super interesting. It may allow you to lighten up on Cy/Flu conditioning, which is a huge benefit for patients. It's CD19 targeting, which could allow for B-cell reset. Plasma cells are often implicated in autoimmune disease. FT522 is designed to, for instance, synergize with a CD38 targeted mAb, which could attack plasma cells. The ADR technology that we talked about is a CAR that targets 4-1BB.
Mm-hmm.
In autoimmunity, you often have times with respect to, let's call it autoreactive T- cells, that are contributing to the pathology of the autoimmune disease. If FT522, if that CAR, that ADR construct could be leveraged to actually attack autoreactive T- cells, there's multiple different mechanisms within FT522 that I think are exciting and potentially relevant for autoimmunity. We're doing a bunch of work now in trying to understand which might be the sort of the first therapeutic step-
Mm-hmm.
that might sort of uniquely exploit the advantages of FT522.
What is the time frame that we might start to see you move into an indication? I mean, maybe identify an indication and move towards that?
Probably by, I think by the end of this year, I think, we'll start to get initial data with FT522.
Okay.
We'll begin to understand its therapeutic profile, and I think that'll help inform the first steps we're, you know, may take in autoimmunity with FT522.
I guess maybe when you refer to the data that's coming later this year, it'll be in B-cell lymphoma.
We have the data internally.
Oh, okay.
Internal data.
Got it.
Internal data.
Okay. Is there anything you would look for from the B-cell lymphoma data to inform translation to autoimmunity, or?
Yeah, I think we can certainly look at the B-cell compartment and looking at with respect to the depth of B-cell depletion with FT522.
Mm-hmm.
As an example, to help inform the potential of FT522 in autoimmunity.
Got it. With the FDA-
I think, we can actually, for instance, back to sort of is the ADR construct allowing us to lighten up on Cy/Flu, really important...
Mm-hmm.
Interesting for autoimmunity. By the way, how are the patient's T- cells reacting to that ADR construct to understand what kind of impact we're having on targeting the patient's T- cells, which again, in the context of autoimmunity, you may have an autoreactive.
Mm-hmm
... T- cell component to it. I think there's multiple different pieces of translational data with respect to FT522 early on, that could absolutely inform our directionality in autoimmunity.
With the IND, you would be able to amend your existing IND, or would you need to file a completely separate one as you move?
I think it would be a separate IND, although we are, because it's a platform, we're likely cross-referencing-.
Got it.
The oncology IND.
Perfect.
Clinical protocol is certainly different.
Sure.
It's probably a separate IND.
Got it. 819.
Yeah.
This is really the first that we had seen of an iPS cell, iPSC-derived T- cell.
I think it's the first iPS-derived-
Yeah
... CAR T-cell in the world.
Yes.
Yes.
Walk us through what you presented at ASH last year.
Yes.
What makes me so excited?
first, iPS-derived CAR T-cell, a lot to learn.
Mm-hmm.
Right? With respect to this. The first patients that we presented at ASH, I, you know, I think we presented maybe 10 patients at ASH. Most of the patients actually were previously treated with CAR T-cell therapy, and so very, very difficult patient population. We were excited that at relatively low doses of an iPSC-derived CAR T-cell in a patient population that had already been treated with CD19 targeted therapy, we certainly saw activity with these cells, both PR, CR, including in patients with aggressive lymphomas that had gone through multiple lines of therapy. Right now, we're dosing patients at about 500 million cells. I think the dose is 540 million cells. Single dose, so a very different.
Mm-hmm.
Paradigm than NK cell. Single dose of a T- cell, 540 million cells, like very similar to FT576. We're gonna treat, you know, the next 10-15 patients. Continue to be very interested, at least in patients that are post-CAR T-cell therapy, to the extent they're CD19 expression.
Yeah.
We need to confirm that and look at the profile there. That patient population, in particular in lymphoma, aggressive lymphoma, post-CAR T-cell therapy, significant unmet need. Response rates of what's considered standard of care today are very low, and progression-free survival is only a couple of months.
Mm-hmm.
Definitely significant unmet need.
remind us, are you still looking at fractionated dosing?
We looked at fractionated dosing early. We've looked at the PK profile of one versus three doses and felt very comfortable proceeding with a single dose.
Got it. I think we're seeing many other companies maybe also look at this post auto CAR T-...
Yeah
... setting. How would you say FT819 is differentiated from these other assets?
I think, yeah, I think it depends. I mean, I think FT819 being off-the-shelf is a significant advantage. I think, you know, if you're coming in with an autologous CAR T-cell therapy, post autologous CAR T-cell therapy, even if you're going after a different target, I think that's a challenging approach. I think as patients progress, their immune compartment becomes more challenged...
Mm-hmm
... and dysfunctional. I think post-CAR T-cell therapy, there is a significant need for a component of the therapy that provides cellular replacement. I think that's a unique feature. I think, you know, it is still a CD19 targeted therapy. We have absolutely not taken full advantage of our platform with the FT819.
Sure.
Like I said earlier on, we've built out the company in a very systematic way. 819 was the very first iPS-derived CAR T-cell. It was our first step.
What other functionality would you like to engineer into FT819 as you think about other targets or antigens to target there?
I mean, certainly we have, at least preclinically, we're confident that, and we'll test it with FT522, that we can create cellular therapies that have multiple, let's call them CAR-targeted mechanisms within them. Feel confident that within a T- cell, you can add a second CAR, as an example. Feel confident within a T- cell that you could actually have a CAR as well as a TCR. I think one of the things that has surprised us, and this is something that came out under our collaboration with Ono in developing our, you know, our 7-point edited cell therapy for solid tumors. The CD16 biology that I referred to on the NK cell side, that allows NK cells to synergize with monoclonal antibody, we didn't necessarily think that T- cells had that same potential.
When we've preclinically added our CD16 receptor to T cells, we're clearly seeing somewhat surprisingly, synergy between T- cells and monoclonal antibodies. That's another aspect as we, when we think about continuing to evolve the platform, at least in hematologic malignancies, additional functionality that we could add. Solid tumors, like we've done with Ono, is a whole different game because there are a whole host of mechanisms that we think are relevant to successfully attack solid tumors, whether that's homing of the cells to actually the site of the tumor, whether that's overcoming the tumor microenvironment, whether it's preventing exhaustion of cells, it's a very different ballgame...
Yeah.
-than hematological malignancies.
Well, maybe let's. That's a good segue to eight two five.
Yeah.
maybe describe that, and to your point, what functionality has been engineered into that specific?
FT825 has been a super interesting journey. I mean, we entered into a collaboration with Ono four years ago for the development of FT825, and I give Ono all the credit in the world. We sat down four years ago on a whiteboard and designed a cell therapy that literally did not exist and had some sort of a, you know, canyons to cross in order to figure out how to develop this cell therapy. Some of the challenges that I sort of allude to in the area of solid tumors, you know, you have to figure out how to effectively, you know, traffic the cell to the site of the solid tumor. When you get to the solid tumor, it's a pretty hostile environment. There's a lot of immunosuppressive signals that will, you know, fight against that cell.
You have to figure out how to cause that cell to infiltrate and engage a target. We set out with Ono and basically said, "Look, here are the key challenges that exist in solid tumors," at least as we saw them, you know, 3 or 4 years ago. We've now embedded 4 or 5 pieces of functionality into this cell therapy to combat what I think has emerged as some of the top challenges in treating solid tumors, namely homing, tumor suppressive microenvironment, fighting to infiltrate tumors, and thinking about novel ways to safely target tumor versus healthy tissue.
You had some early solid tumor data, albeit from other assets.
From NK cells. With NK cells.
Right.
Yes.
Any lessons that you could take from that can be applied here? It's a very different.
I think it's very different. I mean, you know, at some level, I think we had seen with the early versions of our product candidates in solid tumors, which were NK cells.
Mm-hmm.
Again, I think we saw that you can synergize with a monoclonal antibody, and I think that can aid in driving efficacy, but I think it also served to highlight, quite honestly, the multiple mechanisms of resistance-
Mm-hmm
-that need to be addressed in figuring out how you can successfully attack cell solid tumors with cell therapies.
Maybe, just how are you thinking or maybe what is your appetite for business development or partnerships now? Ono stands as a success, Janssen.
Yep
...a little bit of a setback, but how are you thinking about that?
I don't know. It was a setback. look, I think Fate Therapeutics is a platform company. I think platform companies should be built with partners. Yes, we've had a partnership that's been, four years in the making, quite successful, and we've now built a very novel cell therapy that I think at some level is unrivaled with respect to seven edits and potential to address solid tumors. you know, the Janssen collaboration, I wish would have worked out a little bit differently than it did, obviously. I continue to be very pro on collaboration. I think we're a platform company.
I think we have some of the keys to the solution of attacking cancer, but I don't think we have all the keys within Fate Therapeutics, and that's like, you know, it's gonna take a little bit of a team and a village.
I guess maybe in the context of the Ono and the Janssen partnerships, is there a characteristic of a potential partner that you would be looking for as you?
Yeah. I mean, I fully appreciate that. For instance, when you look at Ono and you look at Janssen, I mean, both have incredibly strong cancer franchises, right? While I think we're a platform company, we don't have all the answers in cancer. Bringing additional, like, really smart people to the table that know potentially more about cancer biology than we do, check. I think that's wonderful. We also aren't the company that is going to develop, for instance, or identify the latest and greatest target to go after in oncology. One of the things that we prioritize in our collaborations and thinking about partners is partners that can also contribute those, that type of targeting technology. We have a terrific platform. We have a wonderful sort of cellular chassis.
Mm-hmm.
We look to partners that can contribute sort of, you know, targeting technology that we can build into that chassis and that we can, you know, partner with for development.
Perfect. Maybe just as we come up on time, the next 12 months, could you just walk us through the catalyst path here, and where should investors be?
It's gonna be quiet, from a data perspective. I think, you know, with respect to FT576 in myeloma and FT819, on the T- cell side in lymphoma, I think by the middle of next year, we'll have data packages internally, where we'll be able to understand the development pathways of those programs. FT522, I think internally, we'll start to get a good sense of where we stand in the next six to nine months. TBD on when we're ready to disclose that data set. I mean, I think today we really want to have an understanding before we make the disclosure of the differences between the Cy/Flu versus the non-Cy/Flu arm.
The Ono program, our goal is to treat the first patient, with shared goal with Ono, joint development team, by the end of this year, and so, you know, potentially data late next year, potentially.
Perfect. Well, with that, Scott, thank you so much-
Thank you very much.
-for joining us. Thank you, everyone.
Thanks.