Gonna start the next session of Citi's biopharma back to school summit. I'm Gal Nachimovitz, biotech analyst here at Citi. There are microphones in the room for those listening live, and also welcome to those on the on the webcast. So it's my pleasure to have with me senior management from Cariboo, Rachel Horowitz, CEO and founder of the company. So welcome, Rachel. Thank you so much. Thanks very much. Glad to be here. Thanks very much. Glad to be here. So, yes, welcome. Maybe we can just start with a a quick overview of the the company, the technology platform, you know, and and just the key the key studies that you're running today. Absolutely. Cariboo is a a CRISPR genome editing company, and at the heart of our organization is what we call the Chardonnay technology. So this is a next generation CRISPR technology we invented here at Cariboo that drives much more specific genome editing than first generation CRISPR Cas nine. Today, we are using the Chardonnay technology to advance two wholly owned CRISPR edited off the shelf CAR T cell therapies, one each for lymphoma and multiple myeloma. Each of these are being evaluated in ongoing phase one clinical studies, and we've committed to pretty significant data readouts for each program, before the end of this year. So it's certainly, I think, a a busy time and an important time for our company, and we'd be happy to dig into expectations for each of those data readouts and and the state of each of those programs today. Okay. Yeah. Let's do that. So let let's start with lymphoma, which is the c v ten. So so what yeah. Tell us what about what studies are gonna be reading out later in the year, and what what's that gonna teach teach you about the next steps for a pivotal study? Yes. So c b 10 is our off the shelf CAR T cell therapy targeting c d 19. What really sets it apart in terms of construct design is using the Chardonnay technology to knock out PD one. Obviously, the role of PD one in T cell biology well well precedes CB 10, and we're leveraging that understanding through this edit to to try to prevent premature CAR T cell exhaustion. Right? Our our goal for CB10 is to develop an alloCAR T that can be on par with the auto CAR Ts. And yet we know right off the bat, there's an important difference between a patient's own T cells and leveraging donor T cells. And, of course, that difference is that donor T cells are foreign to the patient's immune system and will be fairly rapidly rejected by the patient's immune system post dosing. And so by using the p d one knockout, our goal is to not change that time frame. It's still a fairly rapid rejection. The cells are gone about 30 post dosing. Instead, our approach is to try to keep those CAR T cells as active as possible for as long as possible by getting rid of PD one, and therefore trying to prevent premature exhaustion through the PD one, PD L one axis. We have been evaluating CB ten in the clinic for a little more than four years at this point. And and quite remarkably, the very first patient ever dosed with c b ten, remains in complete response today. And so I think he is a wonderful example of how durable outcomes can be with CB10, for this lymphoma patient population. Now in the intervening time, we've done quite a lot of work, so I'll quickly paint a picture of that to help set expectations for the the key data that we'll be reading out, in the back half of this year. We began all of our work, of course, with traditional dose escalation. We ultimately expanded multiple doses and selected 80,000,000 CAR T cells as our r p two d. In that body of work, and that was about almost 50 patients worth of data, we also learned something we think is foundational, not only for CB ten, but but for the field of allogeneic CAR T cell therapies. And that is that relatively modest partial HLA matching between patients and their T cell donors seems to drive better outcomes relatively for patients. So we shared this observation at ASCO twenty twenty four, where at that point in time, the data suggested that if at least four of the 12 HLA alleles are matched, patients were experiencing outcomes with CB ten that looked a lot like the auto CAR Ts, both in terms of overall response rate, CR rate, and durability of of response. At the time, we said this was a really important observation, and we need to prospectively evaluate this. Right? All of that thus far had been a retrospective analysis. And so at the time, we created a new 20 patient cohort in the phase one study, specifically intended to ensure that each of those 20 patients gets a dose of CB ten where the patient and the donor share at least four HLA alleles. And and our goal, quite frankly, is to see more of the same. Right? Our goal is to see outcomes that look to be on par with the auto CAR Ts. We've now fully enrolled that cohort. And what we've committed to is that we will share data from that cohort. And we know that that duration of response is super important. And so we've committed that we'll share data, once a majority of those 20 patients are at or beyond the six month mark. And just based on the cadence of how things go, actually, you know, a meaningful number of them will be at or beyond nine nine or twelve months, by the time we're able to share these data. We shared, you know, as as recently as as the press release with our q two financials that as the study continues to progress, we are continuing to see evidence that CB10 drives responses that have the potential to be on par with auto CAR Ts. Now in addition, of course, to all the data that we plan to share in the back half of this year, we also aim to share plans for next steps. And we are actively discussing with the FDA right now what the pivotal path could be for c b 10. So the intention is to provide one update with both the data and the pivotal strategy together. Okay. So you you covered a a lot of territory there, so that was good. Of course. So what so when you say on par with the AutoCAR T's, I mean, you're not doing obviously, this is not a, you know, head to head situation. That'll be later potentially if that's what you do. But, so what what how are you gonna make make that assessment? Is it just gonna be know, because what you did before was sort of an overlay, which was good just graphically. Is it that kind of thing where you're gonna show, you know, median PFS, the curves kinda look the same? Is there more to it than that, or that's kind of the exercise? Yeah. I I think that's a really great visual tool, and I expect we'll use something like it again. What for those of you who aren't familiar with it, what you guys referencing is, historically, we've taken data, for example, from the Zuma seven study, which was the study that led to the approval of Yescarta in the second line setting and and kind of do the the cardinal no no of overlaying data from multiple trials by populating that with some of the data from the ongoing antler study. And and I think PFS is a great way to capture actually many of these data points together, right, because it's it's not just about response. It's also about the durability of those responses. And, of course, safety is really critical too, and having a a generally well tolerated safety profile is is important. You know, what we've shared historically is a is a generally well tolerated safety profile. And and, in fact, one where the the rates of grade three ICANS are much lower than what you see with Yescarta in the commercial marketplace. So something we've we've been very encouraged by. And I guess, technically speaking, you do I mean, people say you will capture safety in in PFS, obviously, because you True. The True. The the the the the quick, you know, stopping the drug if it's not tolerated. So so with the HLA matches, so the idea there is is it is it the idea to also another avenue for preventing exhaustion, or is it different? I think it's really about PK. So when we look at the PK data for all patients and then bifurcate the datasets to look at patients who have relatively low matching and then kind of, I don't know, two two to three, four plus HLA matching, the PK looks completely different. So with with the little to no matching, the peak is about an order of magnitude lower than the other patients, and the cells are cleared much more rapidly, which makes sense. Right? Some some modest level of HLA matching appears to facilitate better expansion and proliferation and longer duration of what we hope are active CAR T cells proliferating in the blood. So it's it's about being more self like, and that's what's keeping the PK better, or there's something else going on? Yeah. I that's a nice way of thinking about it. I I think that's right. Right? It ultimately, the patient's immune system wises up and figures out this is not me and rejects it. But I I it appears there's sufficient similarity early on Okay. That the the the timeline, if you will, is is much slower. Okay. I mean, of course, when you embarked on this program at the beginning many years ago before you even did did the end of the trial, I mean, you you and your scientists knew about HLA and matching. But I guess at that point, it just it it wasn't apparent enough that that should be elevated to kind of a an inclusion exclusion criteria even though you you obviously knew this. Yeah. This was an important biological question that our team had, you're right, from day minus one. Yeah. We actually wrote the protocol to collect HLA typing on all of the patients, which is not something you would otherwise do with these lymphoma patients. So we wanted to be able to build that database to ask this question. Intriguingly, for reasons that I I don't know the reason the answer to, the FDA, proactively offered a suggestion that we not do HLA matching at the beginning of the study. I don't know what they knew that we didn't at that point in time. Perhaps they simply wanted to make sure we didn't overcomplicate the process in the beginning. I'm I'm not sure. But this this collection of data over time allowed us to then, I think, very nicely with a robust dataset look backwards and see this really intriguing and encouraging signal. Okay. And so four, for whatever reason, I guess, was sort of the threshold number above which it didn't really matter anymore and below which it did matter a lot? Yeah. Great. Great observation. And that was, of course, based on the data that we had, all of which was matching or lack of matching by chance. So there weren't a lot of patients who had more than, say, four or five alleles matched by chance. Mhmm. So in the more recent cohort, in in this 20 patient cohort that we've enrolled, we've set the floor at four. Enrich And so for the higher one. Correct. Correct. And so there, you know, there are some patients who have as many as, I don't know, eight or nine matches, something like that. So we'll we'll be able to tease the data even further. Okay. So that's coming and the timing for that is what? Is it you have you said is is it gonna be a medical meeting, or is it gonna be something else? Yeah. We we've committed to a corporate event, and not not a medical meeting Okay. And by the end of this year. Alright. And then at that point, you'll be able to take that data to the FDA, or will you have already spoken to the FDA at the point where you tell us the data? We will have already spoken to the FDA by the time we put the data out. We are we are having those discussions and engagements now. And so we expect that we would be able to share not only all the data that I've just described, but also the pan the plan, I should say, for a pivotal trial. Okay. And so so you're I mean, essentially, you're you're following this data as as in real time, essentially. So you're aware of it. You just have to keep it under wraps for now. What what are the different, you know, possibilities for the for the phase three trial? What do you wanted to see? What do you think FDA wants to see? Where will the meaning of the minds be? Yeah. It's a great question. I I probably can't give a lot of detail, but I can paint a picture of how we think about the ultimate opportunity for c b ten, and that there are, I think, multiple different trial designs, multiple of which we continue to discuss with the agency that that could satisfy, really achieving some of those outcomes. If we think about why allo is so important in the lymphoma setting, it's driven by the fact that actually so few patients are accessing the autocar Ts today. So today, in The US, something like only about twenty percent of lymphoma patients are accessing auto CAR T's. Said another way, eighty percent of lymphoma patients are not benefiting from the tremendous outcomes that can be driven by cell therapies. There are two primary reasons for that. One is the disease itself. I've seen academic papers that say something like forty percent of lymphoma patients have disease that is too severe, progressing too rapidly to wait for an auto CAR T. They just simply cannot wait for that process of scheduling an apheresis and manufacturing and and ultimately getting their drug. They need something now. Well, c b ten's in the freezer now. Right? That's a really attractive component of an allo CAR T like c b ten. And in fact, in the antler study, on average, patients conclude eligibility and start lymphodepletion in two days. Right? They're just off to the races, and and that's a complete game changer compared to the timelines for auto CARs. The other key driver for why those eighty percent of patients aren't getting auto CARs is geography. The majority of lymphoma patients are treated in the community setting, and yet the auto CAR Ts are almost exclusively available at top tier academic institutions. And so there's there's just a fundamental physical gap between where the therapy is and where the patients are. And I think it's a lot more obvious to think about how you can bring an AlloCAR T into the community compared to what it would take to really deliver an AutoCAR T at scale in the community. So we we've a few different trial designs that we're looking at that I I think would achieve our objectives of of bringing AlloCAR T to, that patient population. Okay. So so you I guess you you don't wanna get into the super weeds on that. Sorry. You go. Okay. Stay tuned. But you but but we're gonna learn what the design is by the by the end of the year? Yes. Yes. Okay. And and, I mean, I guess I mean, the advantage of going up against the the the AutoCAR T would be if you achieve equal equivalents with with a much faster delivery turnaround time for patients, then that's a win. On the other hand, it's a higher bar. And then the I don't have to answer this. On the on the other hand, if you did the chemo immunotherapy, then I guess lower bar, but maybe you can claim a little less. So I guess it depends how you do it. Okay. Alright. And so that will be at an investor you said an investor event in the in the in the fourth in the fourth quarter fourth quarter, or you didn't say that? I didn't say fourth quarter. I said before the end of the year. Before the end of the year. Okay. Got it. Alright. And then any other oh, I I wanted to ask about you know, you asked talked about accessibility and and having it in two days, and then it's in the freezer. So and I remember you were saying it's it's 12 it's 12 different lines that covers, like, 90% of the population. So that so if someone needs it, they just find the one that has at least the four for that person. And you're gonna you did the math on that, and you cover everybody. Yeah. When when we first shared these data, that's exactly the math that we did, that if if you wanted to supply kind of all US lymphoma patients with a four plus match dose of c b ten, thirteen different donors, 13 different batches would cover ninety plus percent of of the lymphoma population, which is a very achievable lift with with the manufacturing capabilities we have access to today. And how would it work? Would you you know, if you have it if it's in all the different community hospitals, then you have to kinda airlift it to the you leave you leave certain supply at each place. How does it work? We we have no ask of the sites to store this. I think that's one of our wins is we don't need them to have sophisticated cryostorage capabilities. We maintain centralized warehouses, or I should say a third party on our behalf maintains centralized warehousing of frozen lots of c b ten. And so from a a patient's perspective or or even the physician's perspective, this is all inside the black box. You know, one of the simple tests they undergo early on in screening is an HLA typing test. Our supply team gets that information, goes into the database, and says, you know, that that's the batch. That's the dose that's gonna be best for this patient, and it is drop shipped in its own bespoke little CryoDoer that can be stored on-site. So we try to make it as user friendly as possible for any site, but certainly for community sites who may not have kind of the the rich infrastructure that some of the academic sites have for cell therapies. Okay. And how how much more scale up is I mean, how much more scale up is needed to to get to supply the the market? Are you there yet? Or No additional scale up in our process is necessary. Our process today is ready to go. One manufacturing run gives us enough cells for 200 to 300 doses. So we're really excited about where we sit today from a scale perspective. And where do you where where is this all happening in in in SF area? Where is your facility? We we don't own our own facility. We we work with CMO partners. Okay. I don't think we've ever said specifically where it is other than it's in The United States. Okay. Well, that's kinda what I was trying to get at for obvious reasons. Okay. So so that's kind of the the the update on on Antler. Any anything else you wanted to comment there with regard to the to that? So that that just to clarify, that's so you'd it's it's it's prospective in the sense that you're picking the greater than four, and then sort of implicitly, you're comparing to what was done without picking. I mean, because you're not doing the prospective less than four. Correct. Exactly. That's exactly correct. Yes. We we can look at our historic data for any compare contrast. But of of course, at at least in my mind, the true compare contrast, it's the AutoCAR T's. Right? Are are we able to dial in the appropriate strategy to use c b 10 to drive outcomes that are on par with auto CAR Ts? That is that is what we are aiming to do. And, you know, look. As as I mentioned, as recently as our our q two press release, we said we continue to see evidence that c b 10 is driving outcomes that can be on par with auto CAR Ts. Okay. And so the so the so the data coming up will be it'll be very clear, essentially, what what the situation is. And then, I mean, more of, like, a nerdy scientific question is, you know, if you for you mentioned there's some that even have up to eight. Like, would they be be be would they be performing even better? I mean, that's something to look at, I suppose, method. It is a really interesting question. Right? And and I think one of the key questions is is there some plateau beyond which incremental matching is no longer sort of incrementally beneficial? These are all things that our team is continuing to look at. You know, it's a 20 patient dataset. I wanna be clear about, you know, the the statistics we can and cannot run on that. But I I think there's a tremendous amount we are learning with just the totality of patients we've dosed about many attributes that make for a good batch of c b ten of of which, you know, HLA matching is a piece of the puzzle. Okay. Alright. Well, let's talk about the myeloma program as well. So that's one where, correct me if I'm wrong, but I don't think you've you've quite qualitatively made some comments, but you've never said anything very concrete numerically about data yet. Very correct. Right? So so when when is that's also happening this this half. Also happening this half. Exactly. Okay. Tell us a little bit more about what to expect. Correct. So this will be the first time we're sharing data from this program. So c b eleven is our off the shelf CAR T cell therapy targeting BCMA. And here, we use the Chardonnay technology for a slightly different editing armoring strategy. Here, we've really focused on what we call immune cloaking, Basically, trying to ensure that the CAR T cells sufficiently persist, functionally persist long enough to drive the outcomes we're looking for. And so the approach that we took here was to knock out all endogenous HLA class one expression, which, by the way, thinking about what we've learned from CB 10, means CB 11 kinda starts straight out of the gate mimicking a six out of 12 match. So that that's nice. And then further engineering the cells that they overexpress HLAE, which is one of the minor class one antigens intended to help prevent the patient's natural killer cells from too rapidly rejecting the therapy as well. Now bar to beat here, what what has our focus been? Our focus has really been squarely on the bispecifics. When we talk to myeloma physicians and ask them where would an AlloCAR T fit in the treatment landscape, you know, what what are the attributes it needs to be relevant for your patients, what we uniformly hear is the comparator is the bispecifics, and that's because that's the only other asset class that is readily and broadly available off the shelf. You know, I told you only about twenty percent of American lymphoma patients access auto CAR Ts. It's even worse than myeloma. It's like ten percent of myeloma patients are accessing the auto CAR Ts. So as remarkable as some of those products are, they're irrelevant for the vast majority of myeloma patients. And so as we as we think about what our our go no go criteria look like, you know, we are looking at at least being on par with the bispecifics in terms of efficacy. So that's, let's call it, sixty to seventy percent overall response rate. And then I think importantly, physicians always remind us of just the the the cost to the patient experience for the continued repeat dosing that is necessary for bispecifics. Right? You typically remain on them until you can't tolerate them any longer or you relapse or both. And so these patients are getting sicker and sicker and sicker as they're getting beaten up by that contrasted with the potential benefit of of a one and done therapy, right, that that could long to lead to, you know, a period of time that is treatment free. That would be really encouraging for these patients. So bartabeat is, you know, in the same ballpark at least with the bispecifics, and we've done quite a lot of work. So this this will be, I think, a a meaningful first data update. We've evaluated, two different lymphodepletion protocols, both of which are actually in the range of what you'll see ahead of commercial auto CAR Ts. So it's been the same fludarabine dose in both regimens. We started with, three hundred side dose, went to a five hundred psi dose. And that shift from three hundred to 500 really unlocked encouraging efficacy. And so what we're committing to in terms of this update is at least 25 patients, with with that five hundred psi lymphodepletion protocol, where all twenty five of those patients will at least be at the three month post dosing mark. Some will be significantly beyond that. And our plan here is to not just share the data, but also to share plans, for next steps for dose expansion. Okay. So sorry. Which this is at which dose for the twenty five? So the twenty five patients would come from the five hundred psi lymphodepletion protocol, and then it'll be multiple different cell doses that have been evaluated with thyroid. Asking. Yeah. So how many which ones is it? Because it was quite a latter. Right? Yes. So let's see. We evaluated ultimately four different dose levels, with that approach, a 150, 350, 450, and 800,000,000 CAR T cells. And so out of that update, will it be will it be a clear conclusion as to which of those would make the most sense with the with the 500 side to take forward? Right. The plan is to not only kind of update where we are with our understanding based on on all those patients and the data, but also the plans for dose expansion. Okay. And and and, obviously, having the the this, you know, what is what is the sixty six percent increase in the in the this siderapine dose. This gives you better lymphodepletion. Now you you saw a step change there. Correct. Okay. Okay. And then the comment about the, you know, on par with bispecifics, which that, of course, makes sense and, know, you wanna be on par for all sorts of reasons for clinically as well as, you know, how investors think about the story. But but also, you mean, you made the point that the treatment burden with the bispecifics. So I imagine there must be some KOLs out there with let's say, well, look. I mean, if you're not to say it's gonna be this, but if you were, like, 55 or 60% and you're still one and done and versus a 65 and it's, you know, keep going every however often bispecifics are. I don't know what's the regimen. Every two weeks? I don't know what it is. It depends on like that. But frequently an argument that there's there's some tolerance. There's some wiggle room there. Right? Don't know how how how the KOLs think about that. I think that's right. And, you know, we've we've even heard similar things in the lymphoma setting, right, where we've set our our bar to be on par with auto cars. Often physicians will say, well, that that's nice. But Mhmm. You know, the the value of off the shelf, the value of readily available is really important, and influences how they would choose. So it's not just efficacy. It's it's all the pieces of the puzzle. Yeah. But Okay. But certainly, as as we think about the bar, it's it's the bispecifics and and at least being on par with them. Okay. But you didn't mention specifically FDA discussions on myeloma, or is that also happening this this this cap? No. Our our protocol already gives us, clear direction on dose expansion, so we don't need their input at this stage. Certainly, term, it'll be important to interact with them as as we think about future development for the program. But, you know, sometimes in these FDA meetings, you say you're talking about one thing. But since it's the platform, sometimes other, you can kinda get advice on some of the other programs too. Right? I mean, does that is that a is that conceivable or not not really? You have a very you're very mission focused on on the Antler stuff. That's a that's a great question. I mean, I think probably most drug development teams are gonna approach these discussions in a pretty mission focused way. Yeah. However, I will say, you know, there's a lot about what we do that is a platform. Even our manufacturing strategy, I would call a manufacturing platform approach, where there's so much that we've done and leveraged for CB ten that c b eleven now benefits from as well. So there's there's a tremendous amount of learning and benefit that happens across the two programs. Okay. So those are the two the two clinical programs. You had some other programs. Was it ROAR one? What what was it called? CLL one with your AML target. So so that one you put on the side for now. Is that something that would could come back with more capital, or you're just gonna leave it for now? I doubt it. I'd I'd say of of the two things we hit pause on, which was a CLL one targeted CAR T for AML and the other was, lupus for c b ten. If I had to choose, I I'd probably prioritize the autoimmune opportunity for c b ten largely because we now have this wealth of experience with c b ten in oncology that has taught us a lot about the way c b ten behaves, about its safety profile, and importantly, its efficacy profile. And we see really deep and durable B cell aplasia with c b ten, and that's obviously exactly what you want to try to drive in the autoimmune setting. So maybe someday we'll have the opportunity to revisit that either alone or or with a partner. Okay. Now both of these indications are sort of in, you know, relapsed refractory disease. You know, you gotta get to that goal first, obviously, and get the approval. But is there could these types of allo approaches go into earlier lines of therapy? I think so. You know, I I think there's a lot that we can learn from and borrow from as we look at the auto CAR Ts, obviously, each of which started in, you know, third line and later for lymphoma, fourth line and later for myeloma, and multiple of those programs have now sort of incrementally moved earlier and earlier sometimes for very targeted patient populations. I see no reason why an allo like CB ten couldn't follow in that path through future clinical development. So if you get these two, you know, into late stage studies and approved, you know, I I remember I asked you once why you didn't do the p l one and the HLAE at the beginning. But if you get validation of those independently and then you also said about the the the the HLE is, like, having six missing, so it's like you're kind of, by default, matching six, then you could that could be the next thing. I mean, you probably have the the cells in the lab somewhere. Yeah. It's it's such an interesting scientific question. You know, if if we could rewrite time or or work at a parallel universe, what what would we do differently? And I I think more than anything, we have learned so much. Right? As we think about the total number of patients across both antler and camouflage, we have, I think, one of the largest AlloCAR T datasets. We've learned a tremendous amount about what are the the key elements that matter, which are the ones that we can control, how our genome editing technology can alter or influence some of those in really important ways. I would love us to be able to leverage some of those in future programs, whether they might go after the some the same targets or maybe different targets in different diseases. So speaking about, you know, pivotal trials and and other things that's gonna cost cost money. What's the you know, you you you you did some spend rationalization, couple very recently extended the runway. So do you have the funds at the moment to, you know, sometimes people say, well, you shouldn't start as phase three. It's not ethical to start unless you know you have the money because you can't stop in the middle. So how do you stand from that perspective? Yeah. Great question. So as of the '2, we have about a 184,000,000 in the bank, and that funds our current set of plans into the 2027. That does not cover the pivotal trial that you just articulated. So we know we'll need to access additional capital in order to do that work. Okay. And you also had I know you had a strategic investment from Pfizer, but that was a myeloma specific, if I recall. Do they have interest in further, you know, allocations? Yeah. Great question. So they, about two years ago, made a $25,000,000 equity investment in Cariboo at a pretty healthy premium at the time with a specific strategic interest in c b eleven in multiple myeloma. What that bought them was for three years, so we're two years into that three year clock, three years is seated at the table. They get access to confidential data updates approximately quarterly, sometimes even more frequently. We get their feedback, which is super helpful. And they also have a thirty day right of first negotiation. And that would be triggered if if another third party gave us a term sheet, then we would turn to them, and and they'd have their thirty days to decide what to do. Okay. Well, in the last few minutes, let's think about even further into the future. So you do the studies. You raise the money. You do the studies, the studies work, and now you have to commercialize. So you've already talked about some of the operational aspects of that with the cryopreservate and then the the shipping. What else are you doing to do market research or to get everybody lined up that when it when the product's available that you can, you know, you hit the ground running? Yeah. These these are great and important questions, and and they're fun to think about. And I'd say especially with with c b ten since, of course, we're we're discussing pivotal strategies right now, there's there's a big vision. Right? I think there's a big opportunity and a big vision that c b ten could really grow the pie in terms of the number of lymphoma patients who can access cell therapies. I certainly think there's an opportunity to compete with the auto CAR Ts. Right? Our goal is to have an allo that is on par with the autos. And if that's true, we could compete compete commercially for some of the patients who are going to auto CAR T. But I think perhaps even more excitingly, the opportunity to increase that, right? And whether that's through providing benefit of cell therapy to the patients who simply can't wait, and otherwise we're going on salvage chemo or who knows what, as well as patients in the community. And so I think we have a really important opportunity to look at how to leverage expertise that is a resident in some of these community sites to best position c b 10 in the community in addition to the academic sites where we've done most of our clinical work today. I mean, another, obviously, big picture question, and there's plenty to do in The United States, but, you know, people get, sadly, blood cancers all over the world. So, you know, are you thinking about is there work being done with do you have sort of a field office in Europe, or I just think you're not at that point yet? We've we've actually broadened the antler study already to multiple other countries. So we've got it open in both Israel and Australia. Oh, you do? We do. We've and and we've enrolled, patients ex US in large part because it's given us access to different kinds of patient populations. So for example, in The US, you know, academic sites, they have ready access to auto CAR Ts. And so by and large, the patients who come on a study, they're they're going to be sicker. Right? They're going to be that fraction of patients who cannot wait for an AutoCAR T. It's not a geography access problem they're already at. You know, name your favorite academic It's that they cannot wait. And so that sort of filters for one group of patient characteristics. Whereas, for example, Australia had no commercial auto CAR T in the second line for most of the work that we've done in Antler. So it gave us access to a different group of patients, some of whom are some of the patients in the confirmatory cohort we'll be talking about later this year. Okay. Well, very good. Thank you so much. We look forward to, to the, the update. Thanks, Yigal. Really appreciate it. Okay. Welcome.