Good morning everybody, and welcome. I'm Chris Shibutani, a member of the Equity Research team, and we're very glad that you could join. Once again, welcome Caribou to present and discuss. We have a terrific team here, obviously. Rachel Haurwitz is joining me on stage to engage once again in a discussion, a very busy year, and also from the company at our event this year, we welcome Jason O'Byrne Chief Financial Officer, and Amy Figueroa, who always does a great job with our investor relations effort. Rachel i t's great to see you. Likewise t hanks so much for having us. Lots to overview. I do want to use this time to make sure that we sort of level set and get an outline in terms of, Caribou as a company, a lot of progress that you've made, and in particular, we're really going to zero in on some of the highlights. It's a very positive and active ASCO that you had. But big picture, who is Caribou? Oh, great place to start. Thank you. Caribou is a CRISPR genome editing company, and we are using our proprietary next generation CRISPR technology platform to advance a pipeline of wholly owned, off-the-shelf CAR-T cell therapies. Today, we have three allo CAR-Ts, being developed in four phase one trials across both oncology and autoimmune diseases. I think it's been such an exciting journey from the standpoint of thinking about different innovative modalities, and I think Caribou, in particular, embraces so many of the very important aspects, certainly CAR-T and cell therapies. You know, a tremendous arc, both from investors, but especially for patients, really just delving into delivering the kind of clinical benefits that I think wouldn't have been imagined a decade ago. But clearly, with every innovation, there's the identification of some challenges. Caribou's been very much a part of that whole directional effort going into allogeneic efforts. Maybe just highlight a little bit about what's proprietary from a historical standpoint, coupled with the fact that you always have some cool acronym-driven names. Absolutely. So I'll start with the flavor of CRISPR that we use, which we call the chRDNA technology. Mm-hmm. This is actually a next gen CRISPR technology that a few of my colleagues invented here at Caribou. Really, their, their thought process, the challenge they were solving for, is the specificity of genome editing, meaning when you modify the genome, you actually edit the one site you intend to and avoid off-target consequences elsewhere. Very easy for us to sit here and say, but actually quite challenging to accomplish in the lab. And so what a couple of our colleagues did is identify that they could create new guides. So rather than using the all-RNA molecules that Mother Nature gave us, they made these hybrid guides that are part DNA, part RNA, and it turns out the inclusion of DNA in the guide dramatically improves the specificity of genome editing. This is important for a couple of reasons, right? Probably the most obvious one is you avoid accidentally changing other parts of the genome that could have negative consequences in terms of the activity or the safety of the cell therapy. The other piece is, I think, incredibly important and maybe slightly less obvious, and it's about the ability to multiplex and to do so while maintaining genomic integrity. Because to your point, we have focused really exclusively on an allogeneic strategy for CAR-T cell therapies, and we immediately recognized there are things we're going to have to alter in the T cell genome to really empower appropriate antitumor activity for these applications. So you need to be able to do multiplex genome editing at high efficiency while maintaining genomic integrity, and this platform allows us to do that. I think what's so fascinating about Caribou, and about you in particular, and how this company has continued to emerge and develop, is I always think about innovation from the standpoint of science and the ability to translate into business and markets, and then the appeal for investors, and I think very much the progression of how that has all played out. For those who don't know, you're very much one of the most high-profile protégés of Jennifer Doudna, who obviously, who has, been just a sentinel figure in terms of progress this century from a scientific standpoint. Recognizing the opportunity here to bring that science into the business context, juxtaposing across the original first generation, you know, sort of autologous approaches to CD19, but your emphasis on the allogeneic approach, which recognizes... When we think about business models and, and thinking about prospective market opportunities, that is one of the very important gating factors there. And then from an investor perspective, so much progress that has been made, and you use words like, such as efficiency, which I think is, at the end of the day, where the rubber meets the road, the patient experience, these patients with very advanced diseases, thinking about what their needs are and how sensitive they are to things such as waiting and time. So I think what was fascinating was that the ASCO meeting brought to bear some of the progress that has been made, which I think really takes you to a different level. Let's talk about that lead asset. Is it CD19? CB-010, that's right. CD19 CAR-T. Just tell us a little bit what this is, and then we'll delve into sort of where we've been at and where we're going. Absolutely. This program is the one that's being dually developed both in oncology and autoimmune, and our ASCO update really- Yes, everybody's flexing cell therapy into autoimmune. Got to be there, and you guys are right up front. Indeed, and the ASCO update really centered on the oncology work that we've done. Yes. This program, as you, as you noted, is an off-the-shelf CAR-T targeting CD19, and as far as I know, it is the first allo CAR-T in the clinic with a PD-1 knockout. Mm-hmm. That is the, what we call, armoring strategy- Mm-hmm ... that we've used for this program. Really, the thought process there is to try to take the brakes off the CAR-T cells themselves. The idea being that while they're present, prior to immune-mediated rejection, we want them to retain as high an antitumor activity as possible. Certainly, our preclinical work allowed us to hypothesize that that PD-1 knockout could result in a better therapeutic index compared to other CD19 CAR-Ts... and I believe that's what we've seen bear out in the clinic. For example, we've selected 80 million CAR-T cells as the recommended phase II dose. Mm-hmm. Certainly compared to many other assets, that's, that's quite a low dose. Right. I think that, that process, I think CAR-T, boldly speaking, a bunch of years ago, we thought about almost throwing hand grenades, which were, you know, very capable of accomplishing a great deal, but without sort of the specificity and, you know, and the discipline perhaps. And I think a lot of your approaches have been very specific at curating that. I know that there's been a lot of progress and work that's been done about dosing. You mentioned the 80 million. Talk a little bit more, contextualize that in terms of the, the work that you've done to pressure test and to come to that decision level. Certainly. So what we were able to share at ASCO was an update that included actually a total of 46 patients, 16 from dose escalation, who we had initially updated on about a year ago. Right. And then the first 30 from dose expansion. Now, I'll highlight, these were actually two slightly different patient populations. So when we started this study with a 3 + 3 dose escalation design, typical first in human trial, relapsed or refractory non-Hodgkin lymphoma, there were many different aggressive subtypes that were eligible. Mm. These were largely third line and later, sometimes much later, patients, as you would expect. We were very encouraged by the data from those 16 patients. We initially disclosed the six month readout on them about a year ago, and the headline was, "CB-010 can drive the kinds of durable responses achieved by an auto CAR-T." So actually, we took those encouraging data to the FDA and asked for permission to leapfrog into the second-line setting, recognizing that's really both where the unmet medical need and the ultimate commercial opportunity were converging. The FDA greenlit that, so all of our dose expansion work has been exclusively done in second-line large B cell lymphoma patients. Because of that shift in patient population, we actually decided to take all three doses we had evaluated in dose escalation, 40, 80, and 120 million CAR-T cells, into dose expansion as well- Mm ... to really do robust dose finding work. Ultimately, there were no meaningful differences across the three dose levels in PK, PD, or safety, and so we were really able to tease out differences in efficacy across the three, and that's where 80 stood out amongst the other two, and why we chose it for our go-forward strategy. Yeah. It takes me back to thinking about some of the early nascent gen one versions, where people thought very much about quantity of cells, quality of cells, sort of what you did in preparation while, you know, you were ex vivo, et cetera. Is there anything in particular that you, you in particular, I imagine in the war room, you, when you signed off on the 80 million cell dose, that gave you conviction? Honestly, it was entirely data driven, right? Being able to look at a large enough body of evidence from the number of patients we had dosed, and to see a statistically significant signal that made us convinced that 80 was the right go-forward strategy. Now, there are other aspects about thinking about this tool and its potential, and being able to have maybe sharper insight into navigating where we're gonna have a higher probability of success, right? I think the potential scope of clinical benefit is so significant, but with all of these therapies, you want to be able to still mirror your efforts in identifying patients. And in that regard, I think there's some very proprietary insights that have become revelatory from the HLA typing that you've done. Explain a little bit better the backdrop for that, and what you believe that you have in terms of defining that patient cohort. Yeah, you've, you've hit the nail on the head. So before we ever even brought CB-010 into the clinic, which of course is our first clinical stage asset, one of the questions our research team had is whether HLA matches between the patient and the donor of their T cell product would impact outcomes. Now, scientifically, it's a pretty obvious question to ask. Mm-hmm ... if you think about the world of transplant, right? Mm-hmm. In bone marrow transplant- Yeah ... or even solid organ transplant, either high- very high levels of HLA matching between the patient and donor are mission critical for success of the transplant itself. And so to answer that question, we actually designed the trial to intentionally collect HLA typing information on all of the lymphoma patients and all of the T cell donors who contributed T cells that we used to make batches of CB-010. So we've been collecting this data set over time, and finally felt like we had a large enough, robust enough data set to really dig in and try to answer that question. Turns out the answer to the question is yes. What we've identified is that patients who, by chance, in this case, because we were not purposefully matching anyone, patients who by chance received a dose of CB-010, where the patients and the donors shared at least four of 12 HLA alleles. Mm-hmm ... those patients are having far better outcomes. Part of what we shared at ASCO was actually mapping progression-free survival by different levels of matching. And I think the data are actually quite profound. With a four-plus match- Mm ... we're seeing patients have progression-free survival with a median of 14.4 months, and that's in contrast to a little less than three months for the other patients. That 14.4 months is a really important number- Mm ... as we think about our ultimate objective, which is to develop an allo CAR-T that can meaningfully rival the auto CAR-Ts, and those data put us on track to do that. Mm-hmm. This brings to bear so many thoughts that are that go back and forth between just sort of the advancement of science, but then commercial context, right? The word precision highly valued, intellectually important, but sometimes has a bit of a countervailing influence to maybe a skeptical investor who thinks about TAM, right? To a certain extent, it's, it's nicer to think about all comers, right? But the reality of truly making meaningful advances, which is an opportunity and a mindset that I can always tell that you, in particular, embrace, and just from the strategic decision-making that the Caribou team has made, is very important. So it's like a biomarker-based approach, broadly speaking. How did you decide upon that four out of 12? Because there are cut points, and I have this discussion with precision oncology companies. It's just like, okay, you have this biomarker, and you have this measurement, you know, and arbitrarily chose five out of ten scale. Where did the four come from? And again, you know, there must have been some consideration and debate about being a little bit more liberal with that versus just sort of saying, "What is optimal?" How did four get there? Yeah, really important question. Entirely data-driven. So keep in mind- There's a consistency to this. Indeed. Wow! God, scientific integrity. Continue. Keep in mind, this is all by chance, right? Mm. We were not intentionally providing partially matched product to any of these patients. Yeah. By chance, I think about the best match we've seen was 6 out of 12, so that gives you- Okay ... a sense for the range. Yeah. It allowed us to really dive in and look at these various different levels, almost allele by allele, if you think about these numbers. Mm-hmm. Really, our backstop is wanting to be in a position to meaningfully rival the auto CAR-Ts. Right. And so that's the target, and then you look at the data to ask, "Do any of these thresholds support the ability to hit that objective? Mm-hmm. And in this data set, four was the magic number for achieving that objective. I also want to pick up on something else that you mentioned, which is the vision of delivering cell therapy to an all-comer patient population. That is 100% our vision- Mm ... and our expectation for this therapy. Mm-hmm. To actually achieve that, we've done some modeling to say, "Okay, if you want to be able to deliver this style of partially matched product to the vast majority of patients- Mm-hmm ... how many, you know, batches do you need in the freezer to accomplish that? Right. It's actually a pretty modest number. We only need about 13 batches to serve approximately 90% of patients who would be eligible for our phase III trial. So we expect that future pivotal trial that we plan to initiate in the second half of next year to be all-comer with respect to HLA type. To provide clarity, the total denominator, the patient group that we're talking about, is the LBCL? Correct. Second-line LBCL. Right. Yeah. No, and I think that's, that's a very important distinction, and yet it's strategic because while you have your end game in mind, like all worthy, complex scientific endeavors, it's chess, right? And so I think you can achieve some degree of success and go further along, which will then enhance and nourish through clinical experience and incidental additional learnings that can come along the way, which I think is just, you know, just foundational to having scientific open-mindedness and making the kind of observations that you did, which go all the way back to the discovery of penicillin. So I think there's a common core mindset thread that I think is very valuable from a strategic standpoint. So, but then you also do bring up something that's always been at, you know, as part of the core equation, making the donuts, having the capacity, et cetera. Talk to some of the logistical aspects of production, and in particular, you talk about sourcing from, you know, the cells, et cetera. Yeah absolutely. I think the allo CAR-T field is lucky to follow on the heels of the auto CAR-T field- Mm ... because it's created really a robust marketplace of CMOs who have broad capability across all of the components of cell therapy manufacturing. So we have found it most strategically and financially efficient for us today- Mm ... to actually outsource our clinical production. So inside our four walls at Caribou- Mm-hmm ... we have very strong process development and analytical development capabilities. So our team really owns creating the recipe, if you will- Mm ... scaling it up, optimizing it, and then tech transferring it to third-party providers who have both clinical and demonstrated commercial expertise and capability, and we believe that we are well suited to continue using this network of partners, to supply us for what we would need, and that number is 13, right? We expect to have at least 13 batches on hand to initiate the pivotal trial next year. Okay, great. I think that's gonna be a topic that will be continuing to be closely monitored by investors. It's just simply the world that we're at, whether it's putting needles and syringes upon obesity drugs or recognizing the supply of vectors. It's... We're making soufflés here. We're not punching out cookies and crackers here, so we're. This is a complex process, very sophisticated, so that's important to bear in mind. So every time we have this discussion going forward, I'm gonna make sure to bring that up. Investors love to do inappropriate side-by-side comparisons, caveat, caveat, caveat, but it's what we have. So let's talk about how you would sort of frame how we should think about comparing data, yours versus the autologous backdrop, both from an efficacy standpoint and safety. Yeah, absolutely, and I'll bring it back to what is our objective for CB-010. Yeah. I actually think it makes this comparison pretty fair as a result. Our objective is to develop an allo CAR-T that can meaningfully rival the auto CAR-Ts, and that's with respect to both safety and efficacy. Even we are guilty of trying to make some of these cross-trial comparisons as well. It's what we have, and so- Exactly. Yeah. Yeah. Even part of our ASCO presentation was taking our in-progress data- Yeah ... from our partially HLA-matched patients and comparing that against ZUMA-7, which is the trial that led to the approval of Yescarta in the second-line setting, and looking at the PFS metrics for those two. And honestly, it's that comparison that continues to give us great enthusiasm for CB-010 and its potential, and our belief that it does have the potential to meaningfully rival the auto CAR-Ts. We did something similar with safety as well, and really laser-focused on some of the key AEs, and I'll highlight a few of them for you. Obviously, unique to the allo setting is the risk of GVHD. We've never seen GVHD in our study to date. Obviously, you hear a lot about both CRS and ICANS, and we really focused on the grade three or higher events. Actually, zero grade three or higher events of CRS, which is very encouraging and certainly favorable to the auto CAR-Ts. And I think importantly, a much lower rate of grade three ICANS compared- Mm. -to Yescarta as well. Prolonged cytopenias are about the same ballpark as Yescarta, perhaps a bit lower. So I think overall, a compelling safety profile as well. Mm-hmm. And then just to make sure that we're acknowledging some of the nuance with these comparisons, clinical development preconditioning regimens, have we've learned, in the clinical landscape and clinical development, what would be fair to point out in terms of how your patients are coming up to the starting line versus maybe the phase III trials that were done a few years back? Yeah, great question. I'll highlight both how are they, how are they being lymphodepleted, but also, who are they? Who, who are these patients? Mm. -who are enrolling in our study? Maybe starting with who the patients are first. Actually, the majority of physicians who put a patient on the dose expansion portion of our trial told us they picked ANTLER, picked our study, because they had a patient who could not wait for auto CAR-T. Mm. So it inherently tells you there is something more challenging about these patients, the aggressiveness, the speed of their disease. In fact, to your, your earlier point, their need for therapy now- Right ... not their need for therapy four, six, eight weeks later. Certainly, as you dig into the patient characteristics, we can see a very high fraction of them, I think it was 70%, had an IPI score of 2 or higher, so quite poor prognostic indicator, high levels of LDH at baseline. A lot of signals that these are actually quite significantly sicker patients- Mm-hmm ... than who would routinely receive auto CAR-T. And yet, I already told you, we shared data that demonstrated that CB-010 can drive responses that meaningfully rival the auto CAR-Ts, and I think given that that's been done in a more challenging patient population, that's incredibly encouraging. You're right, there are also differences in terms of the lymphodepletion approach. Because CB-010 is allo, and we recognize it will be immune-rejected faster than your average auto CAR-T, we've actually used a deeper lymphodepletion. The same two drugs, cyclophosphamide and fludarabine. Mm-hmm ... but simply more of each. And so I think it makes it that much more important that the safety profile we're seeing is either on par or favorable to the auto CARs, even in spite of using a deeper upfront lymphodepletion. I think that's totally aligned. It's your whole mindset in terms of how you're approaching this, is to extend boundaries, and the reality of what's happening in your clinical development is to acknowledge where that white space is and that challenge. So let's talk about what's going forward. We're about to enroll about 20 additional patients, right? And tell us a little bit about that, how you expect that to continue to go, and when we'll learn the next card to turn, I suspect. Yes. Yes, so we're- Some meetings next spring. Indeed. We're very encouraged by this observation that the partial HLA matching can really drive better outcomes, and as I mentioned, thus far, this has been a retrospective analysis of patients who received these doses by chance. So our objective now is to prospectively confirm this observation. So you're right, we're creating a new 20-patient cohort- Mm-hmm ... open to enrollment this month. We will ensure that each of those 20 patients receives a dose of CB-010 Mm-hmm ... where they, and the patient and the donor share at least four HLA alleles. So these data are, I think, incredibly important for confirming the signal that we have seen, and then ultimately initiating the pivotal phase III that we plan to start in the second half of next year. As we think about these 20 patients, it's obviously not just the initial response, it's some measure of duration of response- Absolutely ... that is critical as well. Right. we have guided to reading out this 20-patient cohort in the first half of next year with a goal of having a mix of 3-6 months of follow-up at least- Mm-hmm ... on every patient- Mm-hmm ... to really be able to speak to duration. Yeah. No, three months is investors being impatient and science being curious. Six months is a little bit more the Rubicon that I think that a broader audience, and particularly regulators, pay attention to. But I bring up regulators in particular because if I understand the genesis of this 20-patient cohort, it's not necessarily at the command of the FDA, but it's more reflective of your own ethos in terms of thinking, this is something that would be the right thing to do from a development strategy standpoint. 100%. We felt it was quite prudent to confirm this ahead of initiating a- Mm-hmm ... pivotal trial, and let the FDA know that's what our plans are. When you're climbing Everest, make sure you have the equipment. Absolutely. So, I think we've talked anything else further about this CB-010 for this aspect? Is there anything you'd like to highlight or additional things? Maybe just the last thought I'll share is, what does success look like? Mm-hmm ... in the commercial setting? Sure. If we're lucky enough to get there. Absolutely, yeah. I, as I've shared probably too many times at this point, our goal is to meaningfully rival the auto CAR-Ts. Right. What does that mean in terms of long-term potential?... we see really two bites at the apple here. One is the potential to compete for the patients who are receiving auto CAR-T therapy treatment today. Mm-hmm. The other is to really grow the pie. Yeah. If you look at the commercial numbers today, and if you listen to some of the things that the Gilead team has shared, it's only about 15%-20% of second-line LBCL patients in the U.S. who are receiving auto CAR-T therapy today, and that's in spite of extraordinary data out of the- Mm-hmm ... ZUMA-7 and TRANSFORM trials. So it tells you it's not restricted by data. There's something else happening there. Mm-hmm. And certainly what their teams have shared is that it's a question of where the patients are and where the therapy is- Yeah ... and those are two different locations. Yep. By that, I specifically mean the majority of second-line patients are cared for in the community- Yeah ... and yet it's really the MD Andersons of the world who are- Right ... set up to deliver the infrastructure required for an auto CAR. Obviously, the holy grail for an allo CAR- Mm-hmm ... is to much more deeply penetrate the community setting. Mm-hmm. And so our first step on that journey is we now have the green light from the FDA to deliver CB-010 outpatient, and so we're excited to work with some of our current sites to do exactly that. Right, and then to contextualize for investors, that ambition that you have is very realistic, I think. You know, we have had conversations during the course of this conference this week, Adam Lenkowsky, who heads up the commercial effort for Bristol, with the legacy Juno platform with Breyanzi. They talk about that appetite and that hunger for CAR-T-based therapies, the acknowledgment from the clinical community that this is something that's ready for prime time in an outpatient setting, and that certainly, you know, brings payers to the table as well. And this is going back to the original precept of just being able to take patients with really difficult prognoses and doing some really transformational things and arguably using words such as cure as some of the objectives here. So I think very important work here and, the opportunity to coexist. Investors should not be thinking of a zero-sum game in my mind, but really, as you say, expanding the pie and penetrating that, and so I think that there's a real opportunity set that's here. Let's talk about expanding the TAM and being the adventure of going into immune-mediated disease. Feels very twenty twenty-four, right? I think it was actually one of the more... You know, if I was riding that airplane back from San Francisco, some of the buzz was like, "Wow, cell therapy into immune-mediated disease. Mm-hmm. I would argue that others have been beginning to talk about this. Again, yesterday, I was on the stage with Chris Boerner, and he wanted to highlight sort of the lupus data that they're gonna have for CD19 here. You guys are very much well-equipped, positioned scientifically, strategically, with your team to move into this level. Tell us what we should know about your approach. Yeah, absolutely. Maybe I'll start by we're very actively working on initiating our phase one trial for lupus. We got the, Mm-hmm ... IND clearance in April of this year. Yep ... and plan to initiate that lupus trial by the end of this year, but maybe I'll go to why. Absolutely. Obviously, there's some very encouraging small end data sets out of academia demonstrating that a single dose of an auto CAR-T can have this profound impact on these very sick lupus patients. That's obviously very exciting to see that this modality has such tremendous potential for them. Now, as we think about everything we just talked about, CB-010 in oncology- Mm-hmm ... and the encouraging safety and efficacy profile we've seen there, well, we think that meaningfully de-risks the likelihood that CB-010 could be quite beneficial for these lupus patients as well because fundamentally, it's the same mechanism of action. And in fact, there's a PD piece of data that we can really laser in on from the oncology work to give us quite a bit of confidence on the lupus side. Hmm. If you look at, for example, the most recent New England Journal of Medicine paper from Dr. Schett and his colleagues- Hmm ... they showed that on average, their autoimmune patients experience about 110 days of B cell aplasia- Mm-hmm ... meaning no detectable B cells for 110 days. Well, that's exactly what we see in our ANTLER trial- Mm-hmm ... as well. I think their numbers were- One day difference or something? One twelve- Right ... versus 114 in ANTLER. Yeah. Let's call it equal. Exactly. And so we look at that and say, "You know, all the stars are aligning in terms of what we've learned from oncology- Mm-hmm ... to give us great confidence that CB-010 could be quite impactful for these patients," and so we're very excited to be doing the work right now to get that trial up and running. I will highlight there's obviously a flurry of activity for cell therapies for these patients- Yep ... but actually very few off-the-shelf approaches. And something we've spent a lot of time with rheumatologists trying to understand is: What is the relative value of an auto versus an allo for this patient population? In oncology, I think it's obvious, you want treatment as fast as possible. Right. Days matter, weeks matter, months matter. I'm not sure that days matter in the context of lupus. Mm-hmm. Yet what we've heard is this tremendous enthusiasm for an allo approach for actually very different reasons, and it has to do with how an auto CAR-T is made. What we've learned is that for a lupus patient to undergo apheresis, to undergo collection of their T cells to make an auto CAR-T, they have to go meaningfully down or off most of their maintenance meds- Mm ... for three weeks. I've heard as much as two months- Mm-hmm ... in some cases. Mm-hmm. That's a huge ask of this patient population. Mm-hmm. We don't have to ask them to do that, right? They're not undergoing apheresis to receive an allo CAR-T. We've heard quite a lot of enthusiasm from the KOL community. Right. I think that often gets referred to as bridging therapy, and in many of those patients, that's bridged too far- Right ... to consider from the context, 'cause you do wanna have an overall outcome here. Any particular rate-limiting steps to think about progressing? Everyone's trying to get underway here, but any unique considerations? I'd say many of the boxes have been ticked, right? We've got the cleared IND. Mm-hmm. We have product in the freezer. Mm-hmm. At this point, it is working with sites to get them up and running and ready to enroll patients. Mm-hmm. I will note that this is different from getting a cell therapy up and running for oncology, right? In the oncology setting, a sponsor needs to find an oncologist who is- Mm-hmm the champion for the trial. They have access to all the resources at their site, meaning a clinical research staff who knows how to treat patients with cell therapies. Mm-hmm -and the physical infrastructure, the, in-person beds, et cetera- Mm-hmm to actually do that. Mm-hmm. Well, rheumatologists don't have any of those things, right? Mm-hmm. And so to deliver cell therapies to autoimmune patients- Right ... you really need the site to build a bridge between rheumatology and oncology- Mm-hmm to access all of those shared capabilities, knowledge, and resources. So I think our team at Caribou has a bit of a leg up as we think about the field. Most people are bringing cell therapies that have failed in oncology, have no ongoing clinical development in oncology- Mm-hmm into autoimmune. So they're starting with a blank sheet of paper. Mm-hmm -to find sites to get excited, and they need two teams, rheumatologists and oncologists, to get on board. We have about 30 open sites for our oncology trial. I'm not saying all of them will be part of the lupus study- Mm-hmm But many of them are a great first place because we already have half the equation solved. Right. It's about building that bridge into rheumatology. Yep, that makes sense. And then I think you've also come up with a thematically cool name for this trial. Is it GALLOP? That's right. Okay, we can always count on a sense of fun and joy. In GALLOP, is there some underlying G stands for this? Hold off for a- It can't all just necessarily be, you know, attractive from the standpoint of figuring with the Caribou theme, but I'm gonna insist upon an underlying definition. In the moments that we have left, I don't wanna disregard the fact that there has been a pipeline behind as well, multiple myeloma, CB-011. Let's give a little bit of airtime there. Yes. Tell us about that. How are we doing? It is our off-the-shelf approach, targeting BCMA. We use what we call an immune cloaking strategy, so this is actually manipulating the- Right presentation of HLA class I on the surface. As far as I know, it's the first allo CART in the clinic to have this kind of armoring strategy. Mm-hmm. We are in the midst of dose escalation. So we've cleared dose levels one and two, no DLTs, actively enrolling patients at dose level three. Mm-hmm. We've committed to our first data readout on this program by the end of this year. phase 1, by the end of this year. BCMA, obviously an outstanding target, therefore, crowded, got bispecifics and stuff. What do you think you need to see? We think the bar to beat here is the bispecifics, and that's really strong feedback from the. Mm-hmm. We ask them where they would position an allo CAR-T population, and they uniformly tell us bispecifics are the comparable. It's the only other approach that is readily and broadly available off the shelf, if you will. Their expectation is efficacy on par, so let's call that 60%-70% overall response rate, with a baked-in expectation that the infections challenge would be mitigated with an allo CAR-T relative to what they see with the bispecifics. Okay. No, outstanding. So let's just encapsulate for investors here. We sit at midyear. So many investors in the sort of the innovation biotech space, more small midcap focus. There is a blend of investors, many who are foundational and longer term thinking. That is really probably very important and foundational to your investment bases, and I know historically has been the case. Perhaps for the folks who are a little bit more catalyst driven in terms of where their benchmarks are, remind us between now to the end of the year, it seems we have a couple things in terms of confirmation of progress points, as well as the potential for some data. So 6-12 months, just remind us, cap off what those key events are. Absolutely. By the end of this year, 2 commitments. Yep. We will share initial clinical data on CB-011, the myeloma asset. Mm-hmm. We will initiate the GALLOP trial in lupus patients. In the first half of next year, we plan to disclose data on those 20 new patients in the ANTLER trial- Mm-hmm who are receiving partially matched product to really cement in the second half of next year. I'll also mention. We've also opened that trial now for the first time ever to patients who've had a prior CD19-targeted therapy. Mm. We'll enroll a 10-patient cohort and read that out in the first half of next year as well. That is an essential sleeve when you think about the next decade ahead, which, you know, knock on wood, the opportunity for the autologous to permeate that you're gonna have that cohort of patients who've already gotten past that threshold of acknowledging that they are gonna be amongst the pioneers engaging in the adoption and having their life experience be guided by cell therapies, take it to that next level. So that seems the inevitable questions that need to be asked. So and then also reassure folks, Jason is guardian, what kind of a balance sheet to help support things? Importantly, we ended... cash on hand, strong balance sheet, ability to execute on all the programs we've discussed, plus our clinical asset for AML, which we didn't have time to discuss today, and that gives us a runway into Q1 of 2026. That's true. CB-012, CB-012. We'll get that on the transcript. I apologize. We'll get that into there a little bit more in the next opportunity to talk. Always wonderful to engage, always very thoughtful, such robust science, great integrity to the approach that you have. Wishing you all the best with all the progress points. Looking forward to hearing about it. Thank you. Thank you, Rachel. Really appreciate it.