Ladies and gentlemen, thank you for standing by. Welcome to the Cullinan Therapeutics Corporate Update Conference Call. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question-and-answer session. To ask a question during the session, you would need to press star one one on your telephone. You would then hear an automated message advising your hand is raised. To withdraw your question, please press star one one again. Please be advised that today's conference is being recorded. I would like now to turn the conference over to Chad Messer, Vice President of Investor Relations. Please go ahead. Hello everyone, and thank you all for joining us on today's call to discuss our expanded focus in autoimmune diseases based on the exciting potential of CLN978, our CD19 by CD3 T-cell engager, along with our corporate name change to Cullinan Therapeutics. My name is Chad Messer, and I'm the Vice President of Investor Relations at Cullinan Therapeutics. Before we begin, I would like to remind you of the safe harbor provisions outlined on slide number two. During today's presentation, management will be making certain forward-looking statements which are based on current information, assumptions, and expectations that are subject to change and involve risks and uncertainties which may cause actual results to differ materially from those contained in such forward-looking statements. These risks are described more fully in the company's filings made with the Securities and Exchange Commission, including our annual report on Form 10-K. You are cautioned not to place any undue reliance on these forward-looking statements. In addition, this call contains time-sensitive information accurate only as of the date of the live broadcast, April 16th, 2024. Cullinan undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this call. As shown on slide three, we will begin today's call with opening remarks regarding our expanded focus on autoimmune diseases and our corporate name change from Nadim Ahmed, Cullinan's Chief Executive Officer. Following Nadim, Dr. Jeff Jones, our Chief Medical Officer, will talk through the clinical observations with CLN978 in B-cell Non-Hodgkin's Lymphoma, as well as our initial plans for development in autoimmune diseases. Nadim will then share an overview of the high unmet need and limited treatment options in autoimmune diseases. Lastly, Patrick Baeuerle, Cullinan's co-founder and Chief Scientific Advisor, will join us, and we will open the call for Q&A. I will now turn the call over to Cullinan CEO Nadim Ahmed. Nadim? Thank you, Chad, and thank you everyone for joining our call this morning. As you can see on slide four, today is a really exciting day for Cullinan Therapeutics, a new name for our company representing our strategic expansion into autoimmune diseases. This decision was primarily based on the promise of CLN978, our CD19 by CD3 T-cell engager, to address areas of unmet need across a broad range of autoimmune diseases. I will also point out that much of our discovery and development efforts to date have focused on the immuno-oncology space, and most of our molecules in our pipeline harness the immune system. At the same time, the biology of oncology and immunology has continued to converge. Therefore, expanding our presence into immunology is a very natural adjacency for us as a company and represents an excellent strategic fit. We've also made the decision to focus the development of CLN978 moving forward exclusively on autoimmune diseases, beginning with systemic lupus erythematosus, or SLE, as our first indication. We're also very pleased today to share, for the first time, the exciting new data from our lymphoma study, showing sustained B-cell depletion in patients, along with important clinical activity and favorable safety observations. In summary, we believe we have a unique opportunity with CLN978, which has the potential to be a first-in-class, off-the-shelf, disease-modifying treatment for a broad range of autoimmune diseases with a differentiated safety profile. We have also intentionally positioned ourselves with a robust cash runway, and now, with the private placement that we announced this morning, we have even more resources available to fully unlock the value of CLN978 with a cash runway now into 2028. Before I hand it over to our Chief Medical Officer, Dr. Jeff Jones, let me share a high-level overview of our CLN978 program and our pipeline overall. Turning now to slide five. CLN978 is a fully internally developed molecule and, importantly, is a wholly owned, non-partnered asset. Our approach to drug discovery and development has always been unique, what we refer to as modality-agnostic, target-driven research. Firstly, we identify high-impact targets, and in this case, we know that CD19 achieves broader coverage of the B-cell compartment compared to CD20 or BCMA. So clearly, CD19 is the optimal target. Then we pursue the best approach to prosecute the chosen target, and in this case, a T-cell engager likely provides the best therapeutic window and most patient-convenient modality to address the target CD19, with multiple advantages over CAR T-cell therapy. CLN978 is a very clear example of our unique approach in action, and the molecule was engineered for optimal biological activity. In terms of the CLN978 program, we plan to submit an IND in the third quarter of 2024, starting first with SLE but continuing planning for development in other autoimmune diseases. I would also like to point out that members of our existing team have deep immunology experience, which we're further augmenting by bringing in additional autoimmune disease expertise into the company through our recruitment efforts. While we've discontinued enrollment in our lymphoma study, we did gather important clinical observations from the patients enrolled in the trial. The data clearly demonstrate that CLN978 is a highly active molecule showing clinical activity at the first dose level with a favorable safety profile. Importantly, we also observed rapid, deep, and sustained B-cell depletion in patients. Jeff will cover these important new clinical data in further detail. On slide six, you can see our oncology pipeline remains on track. We have a highly differentiated pipeline across a range of cancer indications, giving us multiple near-term shots on goal. Our two highest-priority programs are CLN978 in immunology and CLN619, our MICA/MICB antibody in oncology, another potential first-in-class molecule addressing a novel pathway. We have a data-rich 2024 leading into the first half of 2025 with multiple data catalysts in the form of important clinical data readouts across our oncology programs. These include readouts this quarter of the updated CLN619 monotherapy data following the single-agent efficacy we presented at ASCO last year and, for the first time, presentation of the combination data with pembrolizumab. Later this year, we plan to share additional clinical updates from phase I clinical trials, the CLN049, our FLT3 x CD3 T-cell engager, which we're investigating in relapsed refractory AML and high-risk MDS, and CLN418, our B7-H4 x 4-1BB bispecific immune activator, being investigated across a range of solid tumors. We also expect to have our zipalertinib pivotal study in relapsed exon 20 non-small cell lung cancer fully enrolled by the end of this year. As you can see, our transition from a research-based organization to a development-stage company over the last two years has put us in a very strong position as we progress towards our goal of becoming a commercial-stage biotech company. And with that, I will now hand it over to Dr. Jeff Jones to further discuss the important observations from our phase I dose escalation study of CLN978 in lymphoma, as well as our development plans in autoimmune diseases. Jeff? Thank you, Nadim. Beginning now with slide eight, summarize your data from a recently published New England Journal of Medicine paper describing the remarkable clinical experience of 15 patients treated with CD19 CAR T therapy for the autoimmune diseases systemic lupus erythematosus, or SLE, idiopathic inflammatory myositis, and systemic sclerosis. All the patients with SLE or myositis experienced a complete resolution of their disease symptoms, while the systemic sclerosis patients demonstrated reduced severity of skin and lung disease. Importantly, all patients were able to stop taking chronic immunosuppressive medications without experiencing relapse or worsening of disease-related symptoms. These impressive results were achieved through an immune system reset characterized by rapid, deep depletion of B-cells, followed by sustained reduction in the autoantibodies characteristic of the respective diseases, despite recovery of normal B lymphocytes. Slide 9 highlights the safety profile of administering CD19 CAR T therapy to these autoimmune patients. The safety profile of CD19 CAR T therapy was generally favorable compared to what has been observed in oncology indications. However, infectious complications, in part caused by the lymphodepleting chemotherapy regimen, most likely, were frequently observed. 14 of 15 patients experienced urinary tract or respiratory tract infections, and two patients experienced herpes zoster virus reactivation. Important limitations of cell therapy for non-oncology indications are summarized on slide 10. Currently available CAR T therapies require lymphodepleting chemotherapy, which has been associated with increased risk for infection, infertility, and secondary malignancies. A further risk for secondary hematologic malignancies is related directly to the CAR T cells themselves, as reflected by a recent FDA mandate to include box warnings on all approved CAR T labels. Manufacturing lead times, reimbursement challenges, and the need to administer cell therapies in specialized treatment centers all limit patient access. This constellation of logistical and economic challenges may render retreatments upon relapse an unlikely option for most patients. We often get asked whether T-cell redirection by a T-cell engager can achieve deep eradication of tissue-resident B cells. In fact, B-cell non-Hodgkin's lymphoma typically occurs in extralymphatic tissues in many patients. Shown here on slide number 11 is the efficacy of three approved therapies for third-line-plus patients with follicular lymphoma, two of them CAR T therapies, and one of them the T-cell engager, Mosunetuzumab. As seen here, these three therapies have comparable efficacy as measured by either overall or complete response rate, evidencing similar activity in tissues beyond the peripheral blood. Now, moving to slide number 12, let me share a bit about CLN978, a CD19 by CD3 T-cell engager that Cullinan created to deliver the potency of a T-cell redirecting therapy but with off-the-shelf convenience. Designed to achieve high affinity binding to CD19, the molecule potently lyses CD19-expressing target cells, including those with very low levels of CD19 expression. The relative binding affinity of CD19 to CD3 was further optimized to maximize the therapeutic index. Finally, the overall structure of the molecule, while similar to a standard BiTE format, has been refined to include an albumin-binding moiety to extend serum half-life. The molecule was also designed for patient-friendly subcutaneous administration. Slide number 13 explains why we believe CD19 represents the optimal target to achieve the broad and deep B-cell depletion needed to affect an immune system reset. Unlike CD20 and other B-cell targets, CD19 achieves the broadest coverage of the B-cell compartment, extending from pro-B cells to plasmablasts and even some mature plasma cells, the cells primarily responsible for autoantibody production. Notably, and unlike BCMA, CD19 is not expressed on the long-lived plasma cells that play a crucial role in maintaining humoral memory and long-term immunity. On slide number 14, we depict a unique space we believe CLN978 occupies among therapies currently under investigation for autoimmune diseases. While there are many cellular therapies and antibodies targeting CD19, CLN978 has limited competition in the CD19 T-cell engager space. And while there are CD20 T-cell engagers in development for autoimmune indications, the CD20 target addresses a narrower portion of the B-cell lineage and also spares the autoantibody-producing plasma cells, as I just discussed. Let's now turn to some of the preclinical data that generated our initial enthusiasm for the potential of CLN978 in autoimmune diseases. On the left-hand side of slide number 15, note that a single dose of CLN978 induces rapid and deep depletion of B cells in non-human primates that was sustained for at least one month. The right-hand panels of this same slide further demonstrate that the induction of cytokine release observed when CLN978 is given intravenously can be attenuated by subcutaneous administration. This is an important feature of subcutaneous administration that we believe will greatly improve patient tolerability. While an important pharmacodynamic marker of B-cell depleting therapies, available data suggests that depletion of peripheral blood B cells is likely not sufficient to induce the immune system reset observed after T-cell redirecting therapies. The additional non-human primate data shown on slide number 16 demonstrate that CLN978 also produces deep B-cell depletion in the bone marrow, spleen, and various lymphoid tissues, including visceral lymphoid tissues in the gut lining. Clinical observations from our phase I dose escalation study of CLN978 in B-cell non-Hodgkin's lymphoma replicate these preclinical observations. Slide number 17 summarizes key data for the three patients treated at the initial starting dose of CLN978 in the lymphoma study, 30 micrograms administered subcutaneously once weekly. The slide is dense, so I will walk you through the data. Firstly, two of these three patients experienced objective clinical benefit, including one patient who experienced a complete response. We believe the observation of clinical benefit in patients with a tissue-resident disease like lymphoma bodes well for the prospect of achieving the type of immune system reset needed to benefit patients with autoimmune diseases. Equally as important, 30 micrograms of CLN978 administered subcutaneously once weekly had a favorable safety profile with maximum grade one cytokine release syndrome, or CRS, observed in two patients and no immune effector cell-associated neurotoxicity syndrome, also known as ICANS. CRS and ICANS are toxicities typically associated with both cellular therapies and T-cell engagers. For the two patients who experienced grade one CRS events, the events occurred only following the first infusion and did not reoccur with subsequent doses. In both cases, patients experienced a low-grade fever, which was treated with acetaminophen. The fevers resolved within four hours without the need for any additional intervention. Patient number three, who experienced a complete response to therapy, experienced transient grade one tremor concurrent with acute influenza infection. Within 48 hours after treatment with antiviral medication and corticosteroids, the flu symptoms and tremor resolved. Conservatively, the investigator elected to continue steroid medication with subsequent injections, but the steroid treatment was tolerated poorly. This patient subsequently experienced intermittent grade two restlessness and an episode of transient grade two confusion that resolved within 24 hours. Patient three also experienced a vascular access complication, a deep venous thrombosis associated with an indwelling catheter. This patient has a history of venous thromboembolic disease, and the investigator deemed the event unrelated to study drug. In terms of hematologic adverse events, all three patients experienced an expected transient lymphopenia following administration of the first dose of CLN978. This first dose effect is mechanistically based and a common observation at pharmacologically active doses of T-cell engagers attributable to T-cell margination and recruitment. More simply stated, this is only a transient redistribution effect. T-cell counts have returned to baseline within 96 hours following the first dose. So this transient lymphopenia is not expected to increase the risk for infection. Other adverse events observed on this study were low-grade. While one patient continues to receive study treatment as of the April 5th data cutoff, we have otherwise discontinued further enrollment to the lymphoma study to reprioritize development of CLN978 in autoimmune disease. But pictures, as they say, are worth 1,000 words. Baseline and post-treatment scans for subject number three, a patient with mantle cell lymphoma who had received three prior lines of treatment, including high-dose chemotherapy and autologous stem cell transplant, are shown on slide number 18. At baseline, a mass measuring 7.4 by 1.7 centimeters replaces the patient's left mandibular ramus and extends into the adjacent muscles. The treating physician reported that the mass was no longer appreciated on clinical exam 96 hours after administration of the first dose of CLN978. As these PET images obtained after seven doses show, the mass was markedly less metabolically active after treatment, consistent with a complete response to therapy. Moving now to slide number 19, you can see that CLN978 treatment achieved rapid, deep, and sustained B-cell depletion in both patients who had measurable levels of B cells in the peripheral blood at baseline. In subject one, who received nine doses of CLN978, B-cell depletion was maintained for several months following the last dose of study drug. Now, on slide number 20, we review key features of our planned study of CLN978 and SLE, which will be the first autoimmune disease indication we study. The study will begin with a limited dose escalation phase that incorporates step-up dosing and standard premedications to minimize the risk for CRS. Once we determine a dose for further testing, we will then further explore safety and preliminary efficacy in a larger number of SLE patients. During that expansion phase of the study, two or more dosing schedules may be explored. We are currently analyzing our data to determine the planned dose and dosing schedule as we prepare to submit the IND in the third quarter of this year. Now, I'll turn it back over to Nadim. Thank you, Jeff. On slide 21, you can see that SLE continues to affect a significant number of patients, and effective therapies remain limited. In the U.S. alone, we estimate that more than 120,000 patients could potentially benefit from novel therapies like CLN978. The issue with current standards of care is that they largely alleviate symptoms and do not address the underlying pathophysiology of the disease, which means most patients require lifelong immune suppression and are not able to experience treatment-free remissions. Far too many of these patients go on to develop lupus nephritis, which can lead to end-organ failure and sometimes death. Despite the fact that available treatments like Benlysta or Saphnelo largely alleviate symptoms rather than address the underlying disease, these two drugs still managed to achieve an estimated $1.5 billion in 2023 U.S. sales. However, by our own estimates based on the epidemiology data, the total addressable market in the U.S. for moderate to severe SLE patients is in excess of $11 billion, representing a compelling market opportunity for a potential disease-modifying therapy like CLN978. Where we see the opportunity of CLN978 is graphically represented on slide 22. On the left-hand side of the graph are the current standards of care, which have modest efficacy and generally require patients to remain on continuous immune suppression therapy. On the other hand, the early data we have seen so far for CD19-CAR-T appears at the other end of the scale, highly efficacious without the need for continuous immune suppression. However, for all of the reasons we discussed earlier, we believe CAR-T will likely be reserved for sicker, more refractory patients. As a result, this leaves a very large opportunity gap for CLN978 between the outcomes associated with current standards of care and up to those of CAR-T therapy. Through extensive discussions of rheumatology KOLs, one very important insight we have gained is that as long as CLN978 delivers outcomes that are significantly better than current standards of care in other words, to the right of current treatments in the graph, it has the potential for widespread adoption across multiple patient segments. While lupus will be the first autoimmune indication in which we develop CLN978, slide 23 lists many additional autoimmune diseases that have the potential to be addressed by a B-cell depleting T-cell redirecting therapy. We're giving careful consideration to many of these additional diseases as part of the overall development plan for CLN978. Finally, in conclusion on slide 24, the Cullinan Therapeutics team is committed to expeditiously exploring the full potential of CLN978 for patients living with autoimmune diseases. We firmly believe that T-cell redirecting therapies targeting CD19 are an incredibly promising way to achieve the powerful immune system reset that can potentially modify the course of not only SLE but many other autoimmune diseases. As a potential first-in-class opportunity, CLN978 is differentiated by off-the-shelf convenience and patient-friendly subcutaneous administration with the potential to deliver potent disease-modifying effects with a favorable safety profile. As demonstrated in patients with B-cell lymphoma, CLN978 can achieve rapid, deep, and prolonged B-cell depletion not only in the peripheral blood but also in tissue. We were also very pleased to see clinical activity, including remarkably a complete response at the initial starting dose of 30 micrograms. In terms of next steps, we intend to file an IND for SLE in Q3 of this year. For us, SLE is only the starting point of the story as we explore the full potential for CLN978 to favorably impact the lives of patients living with many other autoimmune diseases. Thank you for your attention. I will now turn the call over to the operator and ask Jeff and Patrick to join me to take your questions. Thank you. As a reminder to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster. The first question comes from Jeffrey Hung with Morgan Stanley. Your line is open. Hi. Good morning. This is Catherine on for Jeff. Congrats on the updates today, and thank you so much for taking our question. Can you talk about your expectations for the therapeutic dose range for SLE and how that compares to the starting dose that you studied for BNHL? Thanks, Catherine. For your question, this is Nadim. I'm going to object to that question. Again, thank you very much for the question. I think it's premature, as Nadim shared in the call, for us to provide specifics regarding the dose or range of doses we'll employ in the SLE. I would point to the fact that the 30 microgram starting dose employed in the B-cell non-Hodgkin's lymphoma study achieved rapid, deep, and sustained B-cell depletion with a favorable safety profile of no higher than grade one CRS. We also saw depletion of intra-tissue B cells in the case of the patient with complete response to therapy. So I think that gives a sense of the potential range over which the molecule is active. But again, specifics will be determined closer to the time of IND filing in Q3 of this year. Thanks for your question. Oh, that makes. Thank you. One moment for our next question. The next question comes from Andrew Berens with Leerink Partners. Your line is open. Hi. Good morning, guys. Congrats on the updates. Exciting times. I was wondering, are there any potential liabilities associated with the broader coverage seen with CD19 versus CD20? I think you showed that CD19 is expressed in plasma and pro-B cells, but the CD20 is not. And then do you think that using a CD19 TCE ahead of a CAR-T could limit the subsequent CAR-T activity? Any specific questions? I'll move to Jeff. Yeah. And these were his questions, and they're both two very interesting questions. So the first, in terms of the CD19 target itself, I think the observation from the CD19 CAR-T cell studies suggests that the breadth and depth of B-cell depletion is actually what's necessary to achieve the immune reset that led to the treatment-free remissions in patients with SLE and other autoimmune disorders. I think the important consideration there is twofold. One, that sustained B-cell depletion beyond several months in that case is probably not necessary for the effect. And there, you might leave patients at risk for infections if that degree of B-cell depletion was chronic. Number two, CD19 spares long-lived plasma cells that do express BCMA, for instance. So there, the observation from the CAR-T trials and what I would expect to hold true for TCEs is that long-lived humoral immune responses, including vaccine responses, would be preserved with the CD19 target. In terms of your second question, could you just repeat that one for me? Yeah. I'm just wondering if targeting CD19 with a TCE ahead of CAR-T therapy could limit subsequent CAR-T activity? Yeah. I don't think that's likely. I mean, certainly in the case of oncologic indications where there's selective pressure on malignant clones that might be lower in expression of CD19, you do see emergence of resistance to CD19-directed therapies. But in normal B cells in normal cells of B-cell lineage, I wouldn't expect any such phenomenon to hold. Okay. And so if I can maybe. Yeah. If I can maybe just make one more in. I know you showed us the study design, and it's early days. But is the goal to reset the immune system and then stop therapy, or is this something that you think would be a chronic administration maybe with yeah. Would it be chronically administered, or is it possible that it could be stopped and then retreated to PRN? Yeah. And it's a good question. I think that the observation, again, at least in SLE and the other diseases on which Jeff and colleagues have shared data, is that transient deep B-cell depletion can affect an immune system reset. In that case, you might consider dosing [7/8 or defined duration of period a defined duration of treatment that achieves a similar degree of B-cell depletion might be appropriate. I think one of the things about TCE versus CAR-T is that, one, it preserves a lot of opportunity for different dosing schemes. And number two, it does lend itself to the potential for retreatment at the reemergence of disease symptoms or other disease-related findings like perhaps autoantibodies production. Maybe in other disorders, the dosing paradigm might be different, but at least the TCE lends itself to that degree of dosing flexibility, unlike CAR-T. Thanks, Andy. Great. Congrats again. Appreciate it. One moment for our next question. Our next question comes from Marc Frahm with TD Cowen. Your line is open. Thanks for taking my question and congrats on all the updates today. Maybe just following up on Andy's last question, just what are those plans on kind of time-limited therapy in the initial trial? Is that kind of the initial design of your dosing scheme, or is that something you'll kind of only add in later trials trying to stop therapy if you're seeing the types of durable responses that we're seeing so far in the CAR-T cell space? Good morning, Mark, and thanks for your question. Jeff, is that okay? Sure. Again, I would just stress that the final doses and schedules that we include in the SLE trial will be finalized closer to IND filing in Q3. But I will state that I believe at the outset, we will be thinking more about the defined duration of therapy. That duration could be determined in part by ongoing analysis of our existing PKPD data as well as data that would be generated in the dose escalation phase of an SLE trial. But I don't anticipate in this first study that we would be dosing on a continuous schedule, unlike oncology. Thanks for the question, Mark. Okay. That's helpful. And then maybe if I just think through as we start to get data out of this, what do you need to see out of this trial in SLE to kind of start opening up some of those other opportunities that you showed on one of the last slides of all these other autoimmune diseases that are B-cell driven? Yeah. I think, Mark, it's not any specific first. I would say no specific finding from the SLE trial is gating for exploring those other indications. I think just as we make this important strategic pivot, this is where we're starting. But we would ultimately like to explore a number of different indications in parallel. That said, in terms of what we might expect to see in an SLE trial, I mean, I think it's the whole constellation of things, both symptom scores, patient's efficacy measures, autoantibody titers, and other serologic findings like complement levels as well as typical PKPD relationships, most importantly, the degree of peripheral blood B-cell depletion using a very sensitive asset. Yeah. Mark, I would add to what Jeff said. One of the key focus areas of the proceeds in the raise are going to be to optimize the full potential of CLN978. So what does that mean? Well, it allows us to expand our development plan across multiple indications, but it also allows us to conduct studies more in parallel rather than sequentially, to Jeff's point. So there aren't necessarily gating features of the lupus study before we would embark on other indications. So just wanted to make that clear also. Thanks for your question. Thank you. As a reminder to ask a question, please press star 11 on your telephone and wait for your name to be announced. One moment. Our next question comes from Kaveri Pohlman with BTIG. Your line is open. Yeah. Good morning, and t hanks for taking my questions, and congrats on the update. The clinical data so far is from lymphoma, which is clearly a high-burden disease. Can you tell us how you are going to utilize your learnings, especially in terms of building strategy to target SLE? Thanks for the question, Jeff. Yeah. It's a great question, and I think it just points you back to the key clinical observations. The first is that a single dose of CLN978 had achieved deep and rapid B-cell depletion, rapid meaning it was observable by peripheral blood flow 96 hours after a single dose. And so I think we understand as well that that dose was at the threshold of efficacy for non-Hodgkin's lymphoma, in which case it was sufficient to achieve a complete response in a patient with quite refractory mantle cell lymphoma. So if you think about that, it provides a very clear understanding that at a dose that has a favorable safety profile with no higher than grade 1 CRS, we are probably achieving the kinds of outcomes that would be necessary to achieve a therapeutic effect in an SLE where you are expecting rapid and deep B-cell depletion, including depletion of B cells in the tissue. And I think we've been able to show that quite surprisingly in a first-in-human study at the starting dose. We've been able to show that, as you say, in a place where it's probably more difficult to achieve than in autoimmune disease. Thanks for your question, Kaveri. Got it. Thank you. How big of a concern CRS is for autoimmune diseases, given that we don't really have to push doses hard to control a rapidly progressive disease like cancer? Yeah. I think that observation's correct. And if you look at the CAR-T data, you'll see that the safety profile for CAR-T appears to be more favorable than has been observed at similar doses in oncologic indications. And I think that's right. It's both a burden of disease, rapidly growing disease that lends itself to more severe cytokine release in oncologic applications of T-cell redirecting approaches. And I think something similar will hold for TCEs. And I think even with the grade one CRS we've seen, it would be our hope that we could demonstrate an even more favorable safety profile in autoimmune diseases. But of course, that's a clinical experiment that we will do as part of the SLE trial. Got it. And maybe a quick one. Can you tell us how many additional indications besides SLE you would plan to pursue for 978? Yeah. Let me take that one, Kaveri. Look, as you can imagine, it's a topic of intense discussion within the company at the moment. Right now, we're focused on submitting the SLE by third quarter indication by third quarter of this year. Then once we've identified additional indications that we plan to pursue, we'll make that known at the right time. Thanks for your question. Got it. Thank you. One moment for the next question. The next question comes from Soumit Roy with Jones Trading. Your line is open. Soumit, your line is open. Good morning, everyone, and congratulations on all the data. On the strategic front for the next two-three years, and especially with the change in name of the company to Therapeutics, do we expect the 978 asset to be kept in-house rather than being partnered out? And should we think opportunities beyond oncology could become the next focus? Thanks, Soumit, for your question. Yes. I would say with our strategic expansion into autoimmune diseases, we're now a company that is active in both oncology and immunology, which I do think is an excellent strategic fit given the fact that we're focused on discovery and development efforts today in oncology and immunology. We have some of that expertise, which we're further bolstering. For now, it's oncology and immunology. I would say that we're very fortunate, including with the new raise, that we have the human and financial resources to progress CLN978 on our own at this point in time. Understood. On the 619 front, potentially mid-year update, what can you tell us about expected cohort size, duration of follow-up? What is the maximum Keytruda combination arm dosage being administered already? Any color would be appreciated. Sure. Thanks for the question, Jeff, to repeat that one. Sure. So we expect to present the totality of data from the dose escalation phase of the trial, including both the first presentation of the combination arm of the trial as well as an update on our monotherapy experience that was first presented last year at ASCO 2023. We had a handful of patients above the 37 that we reported for monotherapy last year yet to accrue. That will be incremental in terms of patient totals for monotherapy and about half as many in the combination arm where we started several dose levels higher for the dose escalation. In both arms of the trial, we discontinued the dose escalation per plan at 10 milligrams per kilogram for CLN619. Thanks, Somit. Thank you. Thank you. Congratulations. You're welcome. Appreciate it. Thank you. At this time, I am showing no further questions. I would now like to turn the call back to Nadim Ahmed, Cullinan's Chief Executive Officer, for closing remarks. Thanks, Michelle. Well, I'll just repeat again. Today is a really exciting new chapter for our company as we add immunology as a new therapeutic area for us, which obviously has excellent strategic fit given our expertise in immuno-oncology. At the same time, we're really looking forward to developing CLN978, expeditiously, as an off-the-shelf potential disease modifying treatment across a range of autoimmune diseases. So thank you, everyone, for dialing in, and we'll be in touch. This concludes today's conference call. Thank you for your participation. You may now disconnect.