Okay, great. Hopefully, everyone can hear me. I'm Yigal Nochomovitz, one of the biotech analysts at Citi. This is Citi's Virtual Oncology Summit for 2026. We've been doing this for a number of years. We have companies across the cap spectrum participating for firesides as well as for one-on-ones. We even had a KOL yesterday on breast cancer. Today is day two, and the session today is with the leadership of Caribou. It's my pleasure to introduce the President and CEO, Rachel Haurwitz, as well as Sri Ryali, the CFO. By the way, if anyone listening has questions for either Rachel or Sri, just email me, and I will do my best to see those and relay over to the management. So welcome, Rachel and Sri. Thank you again. It was great to see you recently at JPMorgan not so long ago. But, of course, the pace is fast, and I'm sure there's a lot - a lot is happening. But maybe just to start, if you could, you know, for those a little bit less familiar with the company, start with the premise of what the tech - the core technology is, what your goals are, you know, what disease areas you're focused on. And then we can get going from there into, you know, the problems you're trying to solve as far as moving away from auto CAR-Ts. So, Rachel - Great. Thank you. Yeah, Yigal, thank you so much for the opportunity to join you for this conversation today. At the heart of Caribou is our next-generation CRISPR technology, the chRDNA technology platform, and its true advantage is enhanced specificity. It results in genome editing that is orders of magnitude more specific than first-generation CRISPR-Cas9. For several years now, Caribou has been laser-focused on leveraging this technology to develop allogeneic CAR-T cell therapies. Today, we are advancing two off-the-shelf CAR-T cell therapy programs for hematologic malignancies. Vispa-cel has been developed in the large B cell lymphoma setting, second-line. We've recently concluded our phase I study, and this is now a pivotal-ready program. I know there's a lot to dive into there. We're very excited about vispa-cel. It is demonstrating in phase I that it can drive outcomes that are on par with the autologous CAR-T cell therapies, which is incredibly exciting to see, and with its off-the-shelf nature, really unlocks the opportunity to deliver the power of cell therapy to a much broader patient population. CB-011 is the company's second program. It's an off-the-shelf CAR-T cell therapy for multiple myeloma, targeting BCMA. At the end of last year, we shared our first-ever clinical update on that program. We had enrolled 48 patients in the dose escalation portion of the phase I study, called CaMMouflage. Again, very exciting data there, where in the recommended dose for expansion cohort, we are seeing response rates that far exceed the benchmark of the bispecific antibodies. We are actively enrolling patients in the dose expansion portion of that phase I trial right now, and we've publicly guided to reading out on dose expansion data, as well as much longer follow-up on dose escalation data this year. So yes, to your point, Yigal, a busy and exciting moment for Caribou right now. Okay. Well, you know, I guess before we get into tons of details on data and responses and everything, maybe, you know, you had a very interesting ASH event with some experts, which I attended, as you know. And, you know, they talked a lot about the premise of allo and how that could be transformative for patients that just, you know, can't for whatever reason or another, the auto CAR-Ts aren't gonna work. Mainly, or one reason being logistics, big reason being logistics. But maybe you could sort of expand on that and kind of just talk about the learnings from that session, 'cause I think those are very important in terms of, you know, helping people understand what you're doing. People talk about allo, and they say it's interesting, but they may not fully appreciate, you know, the impact. Yeah, perfect setup, and it was a great conversation where we had four different physicians: two representing large academic centers that do a lot of auto CAR-T cell therapy, and two representing large community hospitals that have no access to cell therapy, who are very excited about vispa-cel and CB-011, and who would very much like to be part of the pivotal study for vispa-cel. So I'll back up for the, the why, right? The why starts with the incredible anticancer activity that auto CAR-T cells drive. They are extraordinary therapies across both lymphoma and multiple myeloma. And yet, the fraction of patients who benefit from the auto CAR-T cell therapies has remained incredibly low. In second-line large B cell lymphoma, only about 25% of patients are able to get an auto CAR-T cell therapy dose. In myeloma, it's far worse. It's about 10% of myeloma patients who get an auto CAR-T cell dose. This is largely for two reasons: speed or urgency of the need of therapy, and geography. So in terms of the speed piece, many patients simply cannot wait the four, six, eight, 12 weeks it takes to go from the idea of getting a dose to actually receiving a dose. Their disease is already too far progressed or is progressing too rapidly to wait for that kind of therapy, and they urgently need to move on to some sort of other anticancer agent. The other key element is simply where the patients are and where the therapies are, and it's not the same place. The majority of lymphoma and myeloma patients are treated in the community setting. and yet the auto CAR-Ts, by and large, are only available at top-tier academic institutes. Many patients are simply unable to pick up and move with a caretaker, by the way, it's not just themselves, but take a caretaker with them to one of these academic centers for, let's call it, at least six weeks, to receive their care and monitoring. So it's set up that the haves and the have-nots in terms of benefiting from cell therapy. This is obviously the tremendous promise of allogeneic CAR-T cell therapies like vispa-cel and CB-011. With vispa-cel in particular, we are very excited to be exploring a pivotal trial design that would leverage not just academic sites, but also community hospital sites for the pivotal study itself, which, of course, would very nicely set the foundation for a potential future commercial launch that would have a footprint both in the community and in the academic setting. And so the conversation, Yigal, that you and I were able to listen to on the sidelines of ASH at the end of last year, really centered on that need. What was driving that need, both from a clinical medical perspective and a system access perspective? And then the enthusiasm that we heard from all four of those physicians, both from community hospitals and academic institutes, for why they would be so excited to deploy vispa-cel or CB-011 for their patients. We heard, for example, from the community physicians, they have patients who they would love to give a cell therapy to. The patients are unable or unwilling to go to another site to do that, and so they end up with something else. And the something else does not have curative intent the way cell therapies do. So the opportunity to have a cell therapy in the community hospital setting could be transformative. Now, excitingly, we also heard from the two academic physicians, who by the way, have ready access to the commercial products, how impactful it would be to have an off-the-shelf CAR-T cell therapy, both for the patients who can't wait, but also for the patients who can. But why not give them a therapy faster if you can, right? If you have an off-the-shelf CAR-T that's readily available, why would you ask a patient to wait six, eight, 12 weeks to receive a dose? So it was a really, I think, encouraging conversation to hear from these very different stakeholders and very different care environments, why vispa-cel or CB-011 could be an excellent solution for their patients' needs. As you pointed out, I mean, this really is the majority of the market, potentially. You said up to 10% of myeloma, I think you said 25% of, LBCL. So, you know, 75%-90% of the patients out there are open for, for a therapy like, like yours, potentially. Correct. Yes, and as I mentioned, the cell therapies, CAR-T or historically transplant, are the only approaches that I think physicians would label as having curative potential or curative intent. You know, other regimens, be it, say, bispecific antibodies or chemoimmunotherapy regimens, they do not yet have any established data to suggest that they have curative potential. So the opportunity to leverage an off-the-shelf CAR-T cell therapy for those patients is remarkable. Okay, so let's talk then in a little bit more detail about, you know, what you've shown as far as the lead program for LBCL. You know, what have been the key conclusions thus far? You said you know, you've demonstrated results. The headline, I guess, is that it's on par with what you've seen with the auto CAR-Ts, but, you know, expand upon that. I mean, that's been shown in, obviously in, in a cross-trial setting. But explain a little bit more about how you're gonna, you know, flex out that thesis with your plans for the pivotal. Yeah, great, great question. So we've enrolled 84 patients in a ANTLER phase I study evaluating vispa-cel, as of a data cutoff date towards the end of last year. Through that work, we initially started in, you know, fairly late line, broad set of B cell non-Hodgkin lymphoma histologies, enrolled 16 patients in dose escalation, and those data were incredibly exciting. We were, in those late line patients, seeing auto CAR-T-like outcomes. We actually took those data to the FDA, and proposed that we leapfrog further development into the second-line large B cell lymphoma setting. This was several years ago at this point. FDA green-lit that, and that has given us the opportunity to really focus on what we think is the most relevant patient population in terms of unmet need and the commercial opportunity, which is second-line large B cell lymphoma. So during this work, we've learned a tremendous amount, right? Between ANTLER and CaMMouflage and other clinical work we've done, we've dosed more than 140 patients with our allogeneic CAR-T cell therapies. So we're now sitting on one of the largest clinical translational datasets from allo CAR-T cell therapies, and we've learned so, so much about what correlates with successful outcomes for patients. So maybe long story short is the go-forward strategy for vispa-cel and CB-011 leverages these critical learnings. So for vispa-cel, there have been really two major translational learnings. One is the importance of the age of the T cell donor. It turns out T cell donors between the ages of 18 and 29 drive far more durable outcomes than T cell donors 30 and older. Personally, I find that a bit offensive. I thought my T cells were pretty decent, but I guess I learned something in this process. And so we've just applied that across the board for our manufacturing platform for both programs. The other piece of the puzzle that we've learned is about the role of very modest HLA matching between patient and donor. This was a biological question we had early on before we ever started this study. You have to look no farther than the entire field of transplant biology to appreciate that HLA matching typically plays a critical role. And so we wanted to understand in the context of vispa-cel, whether HLA matching matters. What we've learned from our data is, yes, it does, and the relative level of matching necessary to drive auto CAR-T-like outcomes is incredibly modest. There are a total of 12 HLA class I and class II alleles. You only need to match two of them to support auto CAR-T-like outcomes. So we have a 35-patient cohort from our phase I data set that represents this go-forward strategy. We often refer to it as the optimized profile, so that's young donor starting material and two or more HLA alleles matched. That data set has a median follow-up of almost a year, and we see overall response rate and complete response rate that are bang on with the auto CAR-Ts, and I think perhaps most excitingly, 12-month progression-free survival, north of 50%, again, bang on with the auto CAR-Ts. So I think it has finally answered one of the big questions in the field: Can an allo ever drive the kinds of durable responses that have been achieved with auto CAR-Ts? And for vispa-cel, the answer is yes. If you look at the progression-free survival curve, there's that really nice plateau, where a little more than 50% of these patients are maintaining these very durable responses. We have some patients out more than three years in that cohort, who only received a single dose of vispa-cel and have maintained that complete response ever since. Okay, so just so people understand it, that you've solved for this being younger, 18-29, and the two... the at least two matches. But it sounds like it has to be both, or can it be, are there cases where it can just be one of them, or that doesn't... Or you just decided that that's the Venn diagram that you're gonna go for? Yeah, it's a great question. Neither of these is magic, neither of these is binary. We have patients who've been dosed with older donor T cell material with fewer than two matches, who've had very durable outcomes. So, there's nothing perfectly prognostic about either of these, but both together correlate with better outcomes for patients. And so to your point, yes, it's the overlap of the Venn diagram that is most compelling, and it's pretty easy to execute on. You know, for quite some time now, the only leukopaks that we've brought in for manufacturing new batches of vispa-cel or CB-011 have been from younger donors. Easy, check mark. And in terms of driving the matching strategy, we simply handle this on the supply side. So we have modeled the lymphoma patient population that we anticipate participating in our pivotal study, and we only need 10 lots of vispa-cel in the freezer to have sufficient diversity to give 99% of patients a dose of vispa-cel with at least two alleles matched. By the way, we expect that to be an average of seven alleles matched. So by 10, so 10, essentially 10 donors, is that what you mean when you say lots? 10 donors. 10- Exactly. 10 individuals, and that, that covers it with high- Correct. 99%. Okay, so then just remind everyone about where you are with all of what you've just said and the structure of the, the pivotal study. I mean, how much can you... I, I'm assuming that's those ingredients, those specs for the are gonna be there, but what else, what else can you tell us as far as where, what your plans are with the, with the design of that trial right now? Yeah, great question. So yes, that is, that is the go-forward supply strategy for vispa-cel. You know, young donor and sufficient supply to deliver 2+ to 99% of patients. And the trial itself is intended to be reflective of feedback we have received from the FDA, encouraging us to focus on an incredibly high unmet need population of patients in the second-line large B cell lymphoma setting. They have encouraged us to focus on patients who are not eligible for auto CAR-T and not eligible for auto stem cell transplant. Now, before anyone thinks this is a tiny niche patient population, I'll highlight, this actually reflects a majority of the second-line setting. We asked Headland Strategy to help us kind of understand this patient population, and they estimate that about 60% of the entire second-line patient population is dual ineligible, and that's driven by a myriad set of factors. And I'll say, as a non-physician, they largely boil down to, "Can't wait." Their disease is such that they cannot wait for 8-12 weeks for a dose of an auto CAR-T, and they need therapy more urgently. So we're excited to serve that patient population in particular as we think about the unmet need and the impact. And it also sets up a trial design where we believe we have an incredibly high likelihood of technical success. So the control arm, this would be a randomized controlled trial, approximately 250 patients. The control arm will be treated with one of likely multiple choices that the investigator could choose of standard of care immunochemotherapy regimens. I'll note, we are continuing our engagement with the agency. One of the ongoing discussions is nailing down the final list of regimens that would be appropriate for physicians to choose from for this study. One example of what we've discussed with them is Pola-BR. If you look at the historical published data for Pola-BR in the second-line setting, and you look at the progression-free survival curve, it just coasts back down to baseline, right? This is not a curative regimen. That is true also, for example, for R-GDP or R-GemOx, or some of the other regimens that are routinely used in the second-line setting. If you look even at, say, median PFS for those regimens, they range—call it the high water mark, is somewhere around probably nine months of median PFS. Some of them are two, three, four months of median PFS. So we think that's a really compelling setup for very high likelihood of technical success. I should note, in terms of the endpoint, we've discussed progression-free survival with the agency, and that is—it's not a landmark analysis, it's an event-driven analysis, which, again, supports our expectation of very high likelihood of technical success for this study. What would be your base case assumption for the therapy for you? I mean, what was your latest median PFS that you would be comparing the two to three to nine range, which is a big range, but what would be your base case there for the power- Yeah, we- In the system? That's a great question. With a median follow-up of almost a year on our phase I dataset, that 35-patient cohort, we have not yet reached median PFS, and the 12-month progression-free survival is north of 50%. Obviously, that aligns. So we think it's a setup that has very high likelihood of success. And I should step back for a moment, Yigal. I just walked you through how all of our data compare line for line, exactly the same with the autologous CAR-T cell therapies, based on their published data from the pivotal studies that led to their approvals in the second-line setting. And yet, the patients we have enrolled don't look like the patients who were enrolled in the pivotal studies for, say, axi-cel or liso-cel. We have enrolled our phase I study at sites that have ready access to the commercial autologous CAR-T cell therapies. So the patients who came on ANTLER fit this definition of can't wait or who have other reasons why they were unable to benefit from autologous CAR-T cell therapy. And so- And, uh- ... in spite of that higher-risk, sicker patient population, we still saw data that is on par with the autologous CAR-Ts. Okay. So based on the numbers you've cited, it's conceivable if you get to a median, it would be longer than 12, I would think, potentially. Correct. Okay. And then just in terms of the market, as you were walking through the numbers... I mean, I know, I know doing these market analyses, it can get a little fuzzy, and, you know, you can never get super, super precise. But, you know, you sort of said 60% would be in this category of ineligible for auto CAR-T or stem cell transplant, so that would be where you're targeting. And then, on the other side of the spectrum, there's the, I think, 25% that would be, you know, in position to do auto CAR-T because they could wait, or they're in an urban center. But then there's, like, you know, a little bit in between there, who... Is there another group of patients, or is that just, like, fuzzy math, and we don't really know? Yeah. It's a great question. There probably is another group of patients, that there's probably some selection in between who really should be getting auto CAR-T, but for whatever reason, are not. As we look at the pivotal study, you know, that population, the dual-ineligible population, and we're working with the agency on defining the most appropriate eligibility criterion for that study, that population will be the bullseye for the pivotal. That's the approach. Okay. As we think about the commercial opportunity, though, what we've heard from both physicians and payers is that there's an expectation that there would be quite a lot of physician discretion to look at a patient in their clinic and say: "Yes, I think this, this patient needs therapy urgently. Vispa-cel is the right choice." And so we do expect, commercially, that there would be patients who could benefit from vispa-cel, who may not have perfectly fit the criteria for the pivotal study. Okay. Of course, it's also always important to talk to calendars and timelines. So you're- sounds like, you know, you've had a, made a lot of headway with the FDA. It seems like you're pretty, pretty strong sense as to where this is gonna shake out as far as the final design. Maybe, maybe it's already locked and loaded. But tell, tell us what, what exactly is the... You know, when is the study gonna start? Does it depend on additional capital or not? Maybe Sri can comment on that. And just timelines, like, what- when is this all gonna... You know, are you gonna launch this, this trial? Yeah. So our gating items to start the study, as Rachel noted, are the ongoing engagement with the FDA. We've had constructive dialogue with them to date, and those discussions are continuing. They're iterative. Rachel noted one of the elements, finalizing the regimens in the control arm. There are some other elements as well that we're looking to nail down before we can initiate the study. And to your point, Yigal, we will need additional capital to be able to fund the study through data readout. Assuming those things come together in the first half of this year, that would put us in a position to initiate the pivotal trial shortly thereafter and get us on track for data readout, a PFS endpoint, sometime in 2028. Okay. That's very good. That's pretty clear. Okay, and then what other, you know, once you start that study, will there be other incremental looks at longer follow-up from ANTLER or other, you know, analyses of the ANTLER patients to look for extended durability or other features of those patients that are worth exploring, you know, on longer timelines? Yeah, we definitely will plan for additional looks at the ANTLER data, including this year, for follow-up, to see how those patients are progressing. And we've committed to share that data at a medical meeting later this year. But you, you're correct, that also opens up the possibility for additional data cuts beyond 2026. And then we have milestones for our other program that we haven't talked in detail about, CB-011, for multiple myeloma, that we'll plan to share at medical meetings this year and beyond. Okay. All right, let's switch over to CaMMouflage then. So Rachel, maybe you can just summarize very quickly what the, you know, what you've learned so far as far as what lymphodepletion and what dose and, you know, how you see the efficacy. You mentioned, of course, that it's a, you know, beating or doing better than the bispecifics. So tell us a little bit more detail about that, and then the plans to get that study into a larger registrational study. Yeah, absolutely. Maybe I'll just start with the benchmark for success. You know, when we talk to KOLs, and this has been true for years, and ask them how an allo CAR-T would fit in the treatment landscape for multiple myeloma, they uniformly point us to the bispecific antibodies as the benchmark for success. That's, of course, because the bispecifics are really the only approach that is broadly and readily available off the shelf for these patients. And what they tell us is they'd love to see an allo CAR-T that has responses at least on par with the bispecifics, because then they would see this tremendous benefit of just the one-and-done nature of cell therapy over the repeat treatment burden of the bispecifics. And of course, in particular, they highlight the repeat infection challenges that those patients face. So that's been kind of our setup and our goalpost for how we would judge success for CB-011. As I mentioned a few minutes ago, we did quite a lot of work in dose escalation. We enrolled 48 patients. It allowed us to evaluate two different lymphodepletion regimens and multiple cell therapy doses. The two LD regimens are within what I'll call the standard range. If you look at the commercial heme auto CAR-Ts, there's kind of a small range of Cytoxan that different cell therapies follow, and we kinda painted the edges of that. So on the low end, 300 mg/m² of cyclophosphamide, on the higher end, 500 mg/m². So we started on the lower end, 300 mg/m² of Cy, with a standard dose of fludarabine. We enrolled 13 patients across three different dose levels. Only one of those patients experienced CB-011 CAR-T cell expansion and persistence, and that patient, as of our data cutoff date, was in a stringent, complete response, MRD negative, 21 months later. And so that initial data set told us if you can create the right environment for CB-011 to expand, it has the potential to drive profound outcomes. And so that's why we decided to modestly deepen the lymphodepletion from the 300 to the 500, and that really unlocked quite encouraging activity. We evaluated four different cell therapy dose levels, using that, now selected regimen for lymphodepletion, and based on the efficacy, selected a single dose of 450 million CAR-T cells as the recommended dose for expansion. As of the time of our data cut that we shared towards the end of last year, we already had 12 BCMA-naïve patients who had been treated at that 450 million CAR-T cell dose with the selected LD. We were just so excited to see response rates that are far north of the bispecific antibodies, an ORR of 92%, a CR/sCR rate of 75%, and perhaps most impactfully, an MRD negativity rate of 91%. MRD negativity is obviously a really important prognostic indicator in the field of multiple myeloma, indicating depth of response, and being suggestive of the duration of response. Already, as of that data cutoff, many of the patients were out six months or more, in VGPR or CR/sCR. So really encouraging initial data, motivating our further investment and dose expansion. So our protocol allows us to enroll up to 30 patients in any given cohort. So I just told you we had about 12 patients already in that cohort. So we will, we will fill that up with an additional, you know, 18 or so patients to get to that 30 maximum, to build, to build a, a bigger data set to better understand CB-011's potential. We've committed to two things in terms of data readouts for CB-011 this year. One is, of course, that first look at the dose expansion data, and the other is a, a much longer follow-up on dose escalation. Okay, so just so we're clear, the 12 you had, that was at 450 million cells at the 500 Cy, right? Exactly. Correct. That's where you got the very high 90% and what you just cited. Okay, but then there were a bunch of other patients where you had tested lower doses and different lymphodepletion, but those, that was all just part of the exploration. But what you're angling for for the pivotal trial would be what- that 450 and the 500, that's the plan? Correct. That, that is our regimen to go forward with. And I, I realize I didn't answer the last piece of your question, which is about what a pivotal study could look like for CB-011. As we look at the myeloma space, there are probably a variety of paths forward for continued development for CB-011. I'd characterize it as everything from the kind of go big or go home, where you aim for the largest patient population possible to really try to address that very significant gap of the 90% of patients who are not accessing auto CAR-Ts today, all the way through to maybe far more focused and potentially more capital-efficient strategies, where we could laser our focus on specific patient populations, such as those with extramedullary disease or who have relapsed following a prior BCMA-targeted therapy. So we're continuing to build our datasets to better inform the appropriate next steps. I will say, in that RDE cohort, in those 12 BCMA-naïve patients that we shared towards the end of last year, a few of them had extramedullary disease. It's been really encouraging to see what a profound positive impact CB-011 has had on those patients. So we think that's a really encouraging initial signal. Okay. And then you'd shown some data, I think, last year at one of the meetings, ASTCT, I believe. Looking at the immune cell biomarkers, CD8-positive T cells. Was that correlated with the high responses? Like, what did you see there? Yeah, great question. So we were able to share supportive translational data at the recent ASTCT/CIBMTR Tandem Meeting, an oral presentation on CB-011, a poster presentation on vispa-cel. And with CB-011, part of what we did was kind of a deep dive into understanding the phenotype of the CB-011 CAR-T cells. Right, we all think of T cells as being kind of this monolith. They're one thing, they're obviously not. There are many different flavors of T cells. So we were really intrigued to see that at peak, there's a high proportion of central memory T cells. So why does this matter? In sort of broader T cell biology context, central memory T cells have high proliferative capacity, they have self-renewing capacity, and they have the ability to rapidly differentiate into effector T cells upon target re-engagement. So it's kind of all the things you hope a CAR-T cell could do. Specifically in the world of CAR-T cells, several datasets that have been published historically have shown that central memory phenotype tends to correlate with better in vivo expansion, persistence, and perhaps most importantly, anti-cancer outcomes. And then specifically in the world of multiple myeloma, if you actually look at some of the translational data that's been published for CARVYKTI, the CB-011 phenotypic profile is incredibly similar to CARVYKTI's. Right. And then getting back to the pivotal for myeloma, I mean, what would you go for there? You could... I guess you could try to go head-to-head with bispecifics, or you... And you could do that with either superiority, or you could just do, like, a non-inferiority and basically argue, you know, on the tolerability side and the one-and-done side, that there are many strategies there. How are you thinking about all that? Yeah, it's a great question, and I'd say probably the best answer I can give you is stay tuned. We are planning our first discussions with the FDA later this year to talk about the art of the possible with them. But yes, I think you've shined a light on sort of a key element here, which is there are many potential paths forward. And certainly as we think about the right patient population to target, whether that's defined by which therapies they have failed, or how many prior lines of therapy, or a combination of the two, it could set up some of these different asset classes as being appropriate control arms. Maybe bispecifics are part of that, maybe they're not, depending on these different trial designs. Okay. And then just in terms of, you know, the target market here and the, well, just geographically or the community centers, are— You know, one question we get a lot, which I'm sure you're well equipped to answer, is just how to do or how they manage the lymphodepletion regimens that you're going forward with, you know, relative to what they may be more used to or more comfortable with. Just walk us through, like, that aspect of it and so that everyone is ready to do it the way that's needed to get the best leverage out of the allo therapy. Yeah, this has turned out to be actually a very funny question. We get it all the time from investors, right? Investors are looking from the perspective of: "Okay, I understand the LD in front of auto CAR-Ts. vispa-cel follows a deeper LD. Is that harder? Is that more complicated?" And then you layer on the, "Oh, and they're going into the community. How will the community physicians react to this?" So we started just taking that question to a lot of these community physicians who are very excited to be part of this study, and they actually didn't understand the question. It didn't make sense to them, and it's because these community physicians, they're not just treating lymphoma patients. And by the way, they're not treating any of them with CAR-T cell therapies, so they have no reference point for what normal LD is. They're, if not pan-heme, pan a whole bunch of tumors, including often solid tumor patients as well, and they are used to giving just giant wallops of chemotherapy to these patients. So our lymphodepletion protocol in front of vispa-cel is actually quite modest compared to many of the chemotherapy regimens they routinely use for their patients. So that has not at all been an issue in the conversations that we've had with community physicians. And I'd say at the academic centers, our data speak for themselves at this point, both in terms of not only the efficacy, but also the safety data. I realize we haven't talked about that, but the safety profile that we've seen with vispa-cel across the phase I experience is a well-tolerated safety profile that is on par with liso-cel, which is the favorable of the two of the commercial auto CAR-Ts with respect to safety. And we know that's why, since liso-cel is routinely given outpatient, we believe it's quite appropriate to deliver vispa-cel outpatient, either at academic sites or in the community setting. In terms of the community, we've probably been more focused on: How do we pick the right community partners? There's a lot of enthusiasm. We wanna make sure we're choosing the right sites, and one of our kind of easy ways to filter for that is to focus on sites that have already built a bispecifics practice. It means they've had to put in place the 24/7 care model to track AEs like CRS and ICANS. And so we believe they'd be well-positioned to deliver vispa-cel in their setting as well. Well, well, I'm just wondering if you can talk specifics there, like what fraction of the community centers have built that, you know, bispecific care facility? Like, is there a number that you can cite to give us a sense as to how well that's, you know, penetrated the United States market? I think it's fair to say more than we need for our pivotal study, that- Okay. ... that will not be the limiting number. And growing. We looked at this a year ago, and as we continue to look at it, we see more community practices bringing on bispecifics. Okay. And then just final question, assuming, you know, you move to commercialization for both, for both, lymphoma and myeloma, this is something that would be done, you know, by Caribou or is there a thought you would need to have external support from a larger company or not? Just any quick thoughts on that? Yeah, look, we are gearing up to run the vispa-cel pivotal study ourselves, and I'd say our big aspiration is to be the company who commercially launches vispa-cel here in the United States. Now, I was careful to point out geography. You know, we do expect that for a broader global reach, partnership would be mission-critical, and certainly never say never. There could be a lot of potential to partner here in the U.S. to accelerate or broaden the commercial reach of vispa-cel as well. Okay, very good. Thank you. A lot to look forward to and, hopefully get to see the start of the, the phase III and, second-line LBCL very soon. So thanks again, both of you. Thanks, Yigal. We appreciate it. Sure.