Good day everyone, and welcome to the MiNK Therapeutics fourth quarter 2023 financial results. Today's call is being recorded. All lines have been placed on mute to prevent any background noise, and after the speaker's remarks there will be a question-and-answer session. If you would like to ask a question during that time, simply press star one on your telephone keypad. If you would like to withdraw your question, it is star one again. I would now like to turn the conference over to Zack Armen, head of investor relations. Please go ahead. Thank you, Lisa, and thank you all for joining us today. Today's call is being webcast and will be available on our website for replay. I'd like to remind you that this call will include forward-looking statements, including statements regarding our clinical development, regulatory and commercial plans and timelines, as well as timelines for data release and partnership opportunities, among other updates. These statements are subject to risks and uncertainties, and we refer you to our SEC filings available on our website for more details on these risks. Joining me today are Dr. Jennifer Buell, President and Chief Executive Officer; Christine Klaskin, Principal Financial and Accounting Officer; and Dr. Marc van Dijk, Chief Scientific Officer. Dr. Joy Zhou, Head of CMC, is also here for any questions. Now I'd like to turn the call over to Dr. Buell. T o highlight our progress in 2023 and to speak to our outlook for 2024. Thank you very much, Zack. It's a pleasure to have you all with us this morning to hear about our accomplishments throughout the course of last year and what we plan to do in 2024. Throughout 2023 and into the beginning of this year already, we've achieved some significant milestones that I'm going to go through today, and these are all related to advancing our allogeneic iNKT, or invariant natural killer T cell programs. Notably, we initiated a Phase 2 trial in gastroesophageal cancer, a development I'll delve into very shortly. This pivotal program builds upon crucial data presented at four major medical conferences throughout the course of 2023, along with the publication of our findings in esteemed journals such as Nature Communications and Oncogene. Our comprehensive dataset and nearly 100 patients treated to date showcases the efficacy and activity of iNKTs in addressing solid tumor cancers and in other immune-related diseases such as acute respiratory distress syndrome, with promising outcomes observed. These achievements underscore our pivotal role in advancing state-of-the-art cell therapies on what we believe to be an optimal cell platform, positioning MiNK Therapeutics as a key contributor to the progress of living medicines. Today, MiNK stands as one of the most clinically advanced companies pioneering this novel cell type, iNKTs, and as a reminder, iNKTs are what we believe to be the most potent and highly conserved cell type in immunity. Through the progression of our clinical programs and robust R&D initiatives, we've made significant contributions to an expanding repository of clinical and preclinical data showcasing the distinct advantages of iNKTs in immune therapy for immune-related diseases. This year, our efforts have culminated in presentations at four major medical meetings and the publications of the two manuscripts that I just mentioned a moment ago. We've showcased our observations of activity in patients with cancer as well as patients with severe respiratory distress, both of which I'm going to go into in just a moment. But before going into our priorities for this year, let me just reiterate our fully integrated capabilities. These are unique to MiNK in this space, and these capabilities really underscore our efficiency and the progress we've been able to make to date. With our state-of-the-art discovery platforms, which Marc has shared with you and will go into some more detail today, our AI capabilities, our high-throughput genomic analyses and engineering capabilities, we possess the agility to swiftly identify targets and develop therapeutic approaches, whether through CAR-iNKTs, T cell engagers, TCRs, or native allogeneic iNKTs. These programs advance seamlessly through our fully internal GMP manufacturing capabilities, which have been optimized, further scaled, and received FDA clearance to produce material in-house for our clinical programs. We're advancing on multiple fronts with a focus on really revolutionizing treatment and access to these effective cell therapies in cancer, pulmonary diseases, and other immune-related disorders. Our flagship program is a native, naturally engineered, allogeneic donor-derived iNKT cell product. This is called agenT-797. It's now advancing in a Phase 2 trial in second-line gastric cancer. In addition, our collaboration with ImmunoScape, which we announced last year, it's spearheaded by Marc, empowers us to leverage the potential of our T cell receptor platform and programs, as well as our novel and proprietary targets. Furthermore, our T cell engager platform boasts unique development capabilities and also holds the promise that's really quite unique to MiNK of delivering engager T cells in combination with native iNKTs. This is innovative, it's strategic, and it's unique to what we can bring to clinical development. I'm going to speak a bit about our programs in oncology. As we look ahead to 2024, our focus really remains squarely on advancing our lead program, agenT-797. Our objectives are very clear. We must continue expanding our clinical dataset and exploring therapeutic areas with potential rapid development pathways. Our focus on 797 serves as a cornerstone of our vision, driving us forward to redefine treatment standards, positively impacting patients' lives with accessible living medicines designed to deliver benefit without the disabling side effects of standard chemotherapeutic approaches. This is particularly evident in patients with gastric cancer. In February, we announced a significant milestone with the launch of our Phase 2 study of 797. This trial focuses on combining 797 with botensilimab, which many of you are quite familiar with. Botensilimab is an Fc-engineered molecule. It's a multimodal T cell activator, which also binds to CTLA-4. This agent combines with balstilimab, an anti-PD-1 therapy. Both of those antibodies are through our collaboration with Agenus. This combination is also added on top of standard of care chemotherapy in second-line gastroesophageal cancers. This is a therapeutic area where there are currently no therapeutic or curative options for patients, and it's a critical need in oncology. The initiation of the trial follows a compelling clinical dataset presented at AACR and SITC last year, and most recently, the publication of a manuscript outlining 797's clinical activity in patients that are refractory to immune checkpoint inhibitors and prior chemotherapies, specifically in gastric cancer. This collective evidence showcases that 797's potential to overcome resistance to immune checkpoint inhibitors demonstrates durable disease stabilization and activity in refractory solid tumor cancers, including a confirmed response in chemotherapy and anti-PD-1 refractory gastric cancer. As a reminder, the patient who's published in Oncogene was a patient who failed prior chemotherapy, FOLFOX, as well as nivolumab and pembrolizumab. So this patient then was treated with cells in combination with nivo and had a partial response that was durable and remained so throughout the trial period. The trial is led by Dr. Yelena Janjigian. Yelena is the chief of gastrointestinal oncology at Memorial Sloan Kettering Cancer Center. The trial is supported by Stand Up To Cancer, and this Phase 2 study holds promise in really changing the treatment landscape for patients with this cancer. We launched the trial in February and have already accrued our initial cohort of patients and have had the pleasure of seeing some very initial preliminary positive signals, which we're quite excited about. These findings form the foundation of continued discussions with regulators to expand the benefit for patients with gastric cancer and a trial that we plan to provide an update for you before the end of this year. Now, beyond oncology, this is a growing area of therapeutic opportunity for cell therapies, and we are particularly well positioned in this space given our scalability and our efficiency in being able to generate allogeneic donor-derived iNKTs at scale that can be cryopreserved and retain their functional characteristics. This allows us to have the cells at the sites when the patients need them and able to be delivered at the point of administration without any delays from needle to needle time. So we've been working outside of oncology, and we made some important advancements with 797 outside of oncology. Our published data highlights the important role that iNKTs could play in immunity more broadly, and these include infections, inflammatory diseases, as well as autoimmunity. You're going to hear some data at an upcoming conference in the first half of this year about some important signals in the treatment paradigm with patients who have both autoimmunity and infections, which I think will make you as excited as it has made me. Last year, we presented data at the American Thoracic Society, and it showed a survival benefit of 75% in patients treated with agenT-797, and these data stand in stark contrast to 10% survival in the in-hospital case controls enrolled at the same time period of our trial. We'll present these data at a conference in the first half of this year, and we'll follow with an announcement about the next steps for this important program. I think, importantly, at the ATS conference, we also showed that patients on the most severe form of life support with ARDS, these patients are treated with ECMO, VV-ECMO, and those patients treated with VV-ECMO actually had a survival rate of over 80%, which is also really quite unexpected in this patient population. And again, you'll hear more data at an upcoming conference in the first half of this year. Now, these clinical trials have demonstrated promising results regarding the activity of iNKT cells in patients facing severe respiratory distress. Now, this is a condition affecting over 600,000 individuals annually in the U.S. alone. Compared to conventional therapies like corticosteroids, our trials have demonstrated these activities in critical endpoints such as respiratory function, oxygenation levels, as well as overall survival rates. And they present an important foundation for the development of 797 in patients with ARDS, potentially reshaping treatment paradigms for intensive and acute pulmonary care settings. In summary, our approach to rapidly advance iNKT cells in patients with respiratory distress underscores our commitment to addressing unmet medical needs and improving patient outcomes in oncology and beyond. And we're excited about the potential of these cells to make a meaningful difference in the lives of patients, and we look forward to providing an update in the months ahead. In order to support our growing 797 clinical programs, of course, we've maintained steadfast focus on delivering our in-house manufacturing of allogeneic iNKT cells. These cells—this is a critical capability led by Dr. Joy Zhou. A nd this removes any reliance that we currently have or had previously had on third-party CDMOs, and it ensures our end-to-end control over an efficient and reliable supply of our product. We are currently providing our in-house manufacturing product for our ongoing clinical studies and plan to do so for our in-house programs, as well as our collaborative programs that are under active discussion. Our CMC team has achieved a major milestone in developing and implementing an FDA-cleared end-to-end automatic, closed, and industrialized iNKT manufacturing process, which is fully in-house, demonstrating MiNK's internal manufacturing capacity in compliance with rigorous regulatory standards and its readiness for clinical production to support our trials. This process represents a top-notch industrialized allogeneic cell therapy manufacturing process and leverages our cutting-edge closed technology to streamline production from start to finish and minimize any manual intervention. This minimizes, of course, and in our hands, has eliminated contamination as far as we can tell at this point and maintains product integrity throughout the manufacturing process. I'm now going to turn the call over to Dr. Marc van Dijk to go over MiNK's technology platforms and another important component of our next-generation pipeline. Marc? Thank you, Jen. I'm going to talk a bit about our CAR-iNKT program, MiNK-215, and then about TCRs, recent activities there, and cell engagers. So on MiNK-215, given the potent tumor-infiltrating and immune-modulating activity of MiNK-215 that we've observed in preclinical studies, including lung cancer, we anticipate it actually may elicit clinical responses in difficult-to-treat solid tumors. So patients with microsatellite-stable or mismatch-repair-proficient colorectal cancer frequently have liver metastases, which is associated with very poor response to current pharmacological treatments, including immune checkpoint blockade. So the tumor microenvironment of colorectal cancer liver metastases is characterized by a highly immunosuppressive phenotype, which prevents the patient's T cells from infiltrating and attacking these metastases, even when these are reactivated and reinvigorated by immune checkpoint blockade using anti-PD-1 or anti-PD-L1 antibodies. This underscores the urgent need for innovative therapeutic approaches targeted specifically to patients with liver metastases. So to better model immune checkpoint blockade refractory human colorectal cancer liver metastases, we, together with our colleagues from Agenus, developed an ex vivo human organoid model that recapitulates the histological and immunological features of human disease. And our findings underscore that in treatment-refractory liver metastatic organoid models, MiNK-215 can potentially overcome the limitations of immune checkpoint therapy, effectively homes to sites of disease, reprograms the tumor microenvironment, recruits tumor-reactive T cells, and enhances tumor killing. This data will actually be presented at the upcoming American Association for Cancer Research annual meeting in April. Our additional unique research capabilities at MiNK include a proprietary library of phosphopeptide neoantigens derived from a wide range of solid tumors and hematological malignancies. We've assembled this target library over the last couple of years through internal efforts, expounding on the original acquisition of PhosImmune in 2015. We believe that these phosphopeptides represent broadly presented neoantigen tumor targets that can be utilized to discover potent T cell receptors that can then be used to attack solid tumors. To further our discovery and developments of new candidate T cell receptors, we entered into a research collaboration agreement with ImmunoScape. This collaboration is designed to accelerate the development of TCR-based therapies against novel targets in T cells, invariant NKT cells, and other modalities. In this collaborative effort, ImmunoScape will leverage its capabilities in multiplex antigen screening and in-depth T cell profiling to identify relevant TCRs targeting the library of phosphopeptide antigens. MiNK Therapeutics will further characterize these tumor-specific T cell receptors, leveraging its proprietary platform and capabilities to analyze and select TCR candidates for optimal tumor targeting when expressed in iNKT cells or as bispecific cell engagers. We believe that iNKT cells are perfect allogeneic host cells for expressing tumor-targeting T cell receptors and developing off-the-shelf TCR-based cell therapies. We look forward to working with ImmunoScape team to deliver new therapeutics that can potentially eliminate tumor cells and alleviate immune suppression for durable anti-cancer immunity, especially for solid tumors. Now, another development that we're actually very enthusiastic about is combining our off-the-shelf invariant NKT cells with cell engagers, both with existing third-party T cell engagers as well as with our own invariant NKT cell engagers. We've seen our off-the-shelf invariant NKT cells strongly enhance tumor killing and immune activation when combined with cell engagers in our model systems. We believe that co-administration of invariant NKT cells and T cell engagers has the potential to strongly increase clinical efficacy, especially in solid tumors where cell engagers have not yet shown great results. Invariant NKT cells have shown they can infiltrate solid tumors where conventional T cells struggle. We administer our iNKT cell product without lymphodepletion, which is crucial for maintaining the full immune potential of the patient. Co-administering invariant NKT cells with engagers could ensure that a wave of these very potent immune cells enter the tumor first. This not only helps ensure a focused attack, a focused direct attack on the tumor, but at least as important, combats local immune suppression and brings in the patient's own immune cells. We're actively exploring these combinations, and we look forward to updating you on our progress in the near future. I'll now turn the call back over to Jen. Jen? Marc, thank you very much. Excellent, excellent. So as we reflect, of course, on our advancements last year and throughout this year, I just wanted to touch upon our financial prudence that has supported our progress. We've remained really diligent leveraging our in-house manufacturing process, which is incredibly efficient, to significantly reduce our external dependencies as well as costs. Our Phase 2 trial in second-line gastric cancer is led by the world's expert in this tumor type and at a world-leading institution and externally funded by Stand Up To Cancer, which enables us to essentially access insights into a development pathway in an incredibly efficient way. We're excited about our ability to do that. Partnering remains core to our strategy, and as Marc has mentioned, the capability that we possess to be able to deliver our cells at such efficiency does allow us not only to develop the product independently but also to combine it well with therapeutics that may not be delivering the kind of clinical outcomes that are necessary for approval. That includes expanding the benefit of T cell engagers. This is an active dataset that we've generated in our own hands as well as in the hands of potential partners. We are quite excited about what the future holds, and we'll continue to be very prudent in the selection of our clinical programs to have high-impact trials and high-impact results as we continue to pursue ways of improving our financial health as well in parallel. I'm going to turn the call over to Christine to go over our financials. Thank you, Jen. We ended the year with a cash balance of $3.4 million. Since year-end, we received $5 million under our convertible note agreement that we executed last month with Agenus. Cash used in operations for the three and 12 months ended December 31, 2023, was $3 million and $15.8 million, respectively. This compares to $4.4 million and $18.9 million for the same periods in 2022. Our net loss for the year ended December 31, 2023, was $22.5 million or $0.65 per share, which compares to net loss for the same period in 2022 of $28 million or $0.83 per share. I will now turn the call back over to our operator for questions. Thank you. If you would like to ask a question on the phone lines today, it is star 1 on your telephone keypad. We'll pause for a moment. We'll take our first question from Emily Bodnar with H.C. Wainwright. Hi, good morning. Thanks for taking the questions. Excuse me. On your ClinicalTrials.gov listing for the Phase 2 gastric study, it looks like you're also combining with ramucirumab. So can you discuss what patients might be getting that in their treatment plan? Given that you're combining agenT-797 with several agents, how do you kind of think about the efficacy of components based on what we might expect with standard of care? Emily, this is an excellent question. So in something that we've thought quite a bit about, and I'll share with you, that we are developing the dataset to interrogate patients with iNKTs alone, with botensilimab plus with and without ramucirumab and paclitaxel. Now, RamTax, those are the standard of care agents used in second-line gastric cancer. They have very limited activity, as you know, probably just a little over 20%-25%, which gives us a big opportunity to really make a significant difference in the treatment landscape here. We will generate the dataset that will include how patients perform on the cells alone, how they perform with the cells on top of standard of care, as well as the cells in the multiple combination with botensilimab and the standard of care chemo. We already have some preliminary signals of each of these settings that we'll be sharing with you as we continue to develop the dataset in the second half of the year. It's really quite exciting, and it does give us an opportunity to present to the agency what we believe to be the most impactful would be and the speediest to develop would be dropping the therapies on top of standard of care ramucirumab. That allows us not to salvage patients post-ramucirumab. It allows us to take advantage of some of the neoantigen release from the tumor killing that does come along with chemotherapy. And we know that the cells can be dosed tolerably in that disease setting. We also know that they can combine tolerably with checkpoint modulating antibodies such as PD-1 and now with botensilimab. So I'm hoping that I answered your question. The dataset, in conclusion, will be cells alone, cells in combination with ramucirumab to get us on top of standard of care, and then the cells in the multi-combination that includes botensilimab. And I should say we did not include a ramucirumab arm alone because we have thousands of patients that have been treated with that combination and a robust dataset from real-world evidence to actually drive what the expectations are from the chemo alone. So we did not want to add that arm in the trial at this time. We would do so, provided there are positive signals. It would probably be a requirement to do so in a registrational study that would follow this sometime mid-year. Okay. That makes a lot of sense. Just a, I guess, confirmation question. Are you only evaluating patients who have failed one prior line, or is it a minimum of one prior line? Right now, we have it essentially as a minimum of one prior line, but really the focus is one prior line. These patients who have failed FOLFOX/nivo really have nothing to go to, barring their HER2 status. So they would essentially be treated with ramucirumab. So there isn't very much more for those patients to go on. Okay. Makes sense. And then last question. I know you talked about the $5 million convertible note from Agenus, but maybe just discuss strategies for bringing additional capital into the company. Thank you. Thank you very much, Emily. Absolutely. First, I should say that as you look at the prior year, 2023, you'll see that the financial consumption of about $15.8 million drove the execution and completion, really, of three clinical trials and our manufacturing optimization. So that really does speak to the efficiency that our team has been able to operate with. This year, of course, we're being even more financially prudent with the externalization of the financing for our clinical programs at this time. The cells are in high demand for trials such as the one that we're conducting with Dr. Yelena Janjigian. But we would like to, of course, conclude some financial transactions that would allow us to independently sponsor our own programs and accelerate the development. Now, this is going to come in three different ways, as far as we can tell right now. The first is, of course, through a strategic collaboration. As I have discussed previously, these are some very active discussions with individuals who first need to better understand iNKTs. We are the most advanced company bringing these forward. The science is lesser known, and that does require groups to get up to speed on what the science depicts. Our clinical data is very much helping that. It has required us to enable material transfer so that partners can work with the cells in their own hands. Much of that work has been done, and now discussions are starting to advance. A collaboration would not only help us to expand on the work that we're doing, it would also allow us to expand our discovery pipeline and could give us infrastructure outside of the U.S. where we currently do not have bandwidth or infrastructure. The other is, of course, a regional partner, which I also mentioned is something that we continue to be in active discussions for in R&D partnership, as well as access to the cells alone, essentially just supply arrangement for combinations in a pipeline. And of course, the third would be expanding our interactions with project-based financing and investors. And these, again, are active discussions that are underway. Great. Thanks for taking the questions. Of course. Our next question comes from Jack Allen with Baird. Great. Thanks for taking the questions and congratulations on the progress made over the quarter. I guess the first one on gastric. Could you provide some color on the cadence of enrollment? Are there any staggers early in the study with these multiple arms between the different patients? So I should share with you, Jack, that's a great question. And it is something that we in the industry have typically been plagued with, waiting 28 days per patient. I will say that given the experience and the visibility of Dr. Yelena Janjigian, she was able to navigate and negotiate this very aggressively with our regulatory partners. And we do not have any gaps. So there's no staggering in the trial, which is enormously helpful. In part, it speaks to the unmet need. It also speaks to her convincing argument about the unmet need and the urgency of delivering therapies for these patients. Got it. Great. I guess the cadence of enrollment, I should just say, it's moving really, really quite quickly. Got it. Could you speak to maybe the patient influx that they have with the new centers at Memorial Sloan Kettering and what the potential demand could be for this 40-person study? Well, I will just share with you without disclosing too much. I'll just share with you what Dr. Yelena Janjigian just presented to our team and board this week. She said, "I have patients lined up for this trial. The demand is very high." I hesitate to give any more further guidance, but I will say we will, I believe that we'll be on track to have concluded enrollment in the first half of this year. Got it. Great. And then just one more on the gastric study. What is the dialogue between MiNK and the investigator in the study? I guess how frequently are you getting updates as it relates to data, and how should we think about that dynamic? Dr. Yelena Janjigian has quite a bit of experience with Agenus's botensilimab-balstilimab combination, as well as now the cells. We have really quite frequent interactions with her. So we have a good sense of both the activity of the product as well as the safety profile of the product in real time. I should say, though, given her gravitas, it will benefit all of us to ensure that the data and her interpretations of the data will come really from Dr. Yelena Janjigian and her team. And we expect that to be at a major conference. So it would be coming from Dr. Yelena Janjigian's team. Got it. Got it. Great. And then shifting gears, I was hoping you could provide an update on some of the other non-oncology programs I know in the past you've looked at, potentially testing the cells in graft-versus-host disease. Where do things sit as it relates to those other opportunities beyond ARDS and oncology? So Jack, I am so grateful for your thinking on GVHD because, as we all know, the cells actually can naturally prevent GVHD, and we know that they can be dosed tolerably and quite impactfully. There are a few different settings that we have continued to pursue. We're working aggressively. We have the trial designed, and we're working aggressively to find the financial support to execute on this trial. It would be a very rapid trial in acute graft-versus-host disease and something that we could move forward very, very quickly. We do expect to announce this trial in 2024. Now, we had hoped to do so a little earlier this year. But as I've mentioned, we're being really rigorous about our financial prudence and garnering the kind of finances that we need to advance the program. This is something that with a small cohort of patients, we believe we can generate the data that would be necessary to support what a pivotal program could look like in this indication. And this would be really quite a large indication for us, and it's something that we're committed to moving forward very, very quickly. ARDS, though, should not be underestimated. And I can tell you, really, our observations of the demand is increasing in the post-pandemic era. We are seeing a much higher frequency of a couple of different pulmonary disorders that are presenting, including vulnerability and increased incidence of ICU in patients with bilateral pneumonia and patients with RSV, as well as secondary to influenza A. And this year really will profoundly contribute to the numbers that I mentioned earlier. The 600,000 patients annually was based on numbers that have been generated prior to 2022, and we expect those numbers to increase dramatically based on the observations today. Additionally, these cells can prevent secondary infections, fungemia, bacteremia, based on the observations that we've seen and published. That is a major contributor to ICU mortality in patients, even when they recover from respiratory distress. So those secondary components are really important. What we have observed in our clinical trials and published in Nature Communications is in patients on mechanical ventilation and on VV-ECMO, the administration of these cells do appear to be lifesaving in a number of patients. And so we're continuing to expand that trial, and we have the opportunity to do so in an incredibly efficient way through a Phase 2 trial, large national platform program that would allow us to interrogate the cells compared to standard-of-care corticosteroids, which we believe is going to we have a lot of confidence in what the cells can do compared to standard-of-care based on what our observations have been to date. So I don't want to underestimate the importance of what we can deliver for patients with respiratory distress and the urgent need to be able to do so. Got it. Thank you so much, Jack Allen. Congratulations again on the progress. Thank you, Jack. We'll take our next question from Mayank Mamtani with B. Riley Securities. Good morning. Thanks for taking our questions and appreciate the comprehensive update. Jen, could you talk to the status of your engineered iNKT cell efforts, including in autoimmune diseases, if there's any? And also, I was curious on the next steps on the ARDS program for 797. What sort of registration or data development do you have planned, understanding you may need a partner there? And then I have a follow-up for the gastric cancer study. Okay. So Mayank, thank you very much for the questions. I will say on the last part, and this is specific to the platform trial I just mentioned, there's an infrastructure and a capability in existence. And we have been invited to and we actually are in active contract negotiations to join a program that would be quite large, and we're going to be able to provide a very detailed update upon contract execution. Now, this is a trial that will be these operational costs will be covered. The platform and sites and centers are in existence. And the leadership of this platform are world experts and very high-profile individuals. So we were not only thrilled to have the opportunity to be invited to this platform program but also to the potential that it does offer to independently generate the data that may be supportive of a registrational program with 797. So I will provide very much more detail on this in the moment that we conclude the contract execution. With respect to autoimmunity, now, Jack, a moment ago, asked about our trial advancement in GVHD, an area that we've been very interested in advancing, and we're continuing to do so. Now, this would be something that we are pursuing aggressively, external funding. We have a few options that are coming to fruition now that will allow us to execute on a trial that's already been designed, including with investigators identified and contributing to the trial design and willing to execute. So that's one component of other immune-related diseases in addition to the ARDS. Now, as you know, these cells we have last, after SITC in 2022, we presented an R&D day, and we had a world leader in metabolic diseases and disorders and an expert in iNKT cell biology. And the potential of these cells to leverage their features and I could have Marc speak a bit to this in modulating immunity and addressing metabolic-related disorders is immense. It's something that we have the capability to produce material for, large populations of patients. And we also have been entertaining some discussions with partners on the development of these cells in this area. I'm going to have Marc just say two or three words about the potential in this particular space. And finally, I also should mention, and I have previously we are engaged and have been engaged with the government, given we're financing some of the programs that we have going forward because, as you know, respiratory distress is debilitating, and it is debilitating not only for individuals but also for our economy. And it falls into a category that's considered a national threat. So this is an area that we will continue to work with our government collaborators to support initiatives that are necessary to protect our national security. Marc, maybe just a moment on the metabolic opportunity. Yeah. And also more broadly, I think the autoimmune opportunity. And we've been looking at this. And Agenus is an antibody company. MiNK came out of an antibody company because there is an unmet need. You can only address so many parameters with an antibody, and a cell has intrinsically many more response mechanisms to its delivery arsenal. This is quite important in diseases such as cancer and autoimmunity and metabolic disorders because these are multifactorial. An antibody can do one thing, can do many things, a combination of antibodies, but cells have an infinitely more complex response mechanism and ability to influence. These invariant NKT cells are actually tissue-resident immune orchestrators. They actually are there to modulate and rebalance the immune system. A lot of these indications that we've now been pursuing, ARDS as well as graft-versus-host disease, have an intrinsic immune imbalance that you are aiming to restore with iNKT cells. These cells are able to do that. We've seen this in COVID patients and in some of our emergency use patients. It has a dramatic effect in restoring sort of immune normal function. And we also think that in metabolic disorders, we can actually achieve this. We've seen iNKT cells get into places where conventional T cells don't really like to be. And iNKT cells can go there and do change the environment to a much more stable and rebalanced situation. That's what we're looking for. And there are many immune disorders where we feel this will be of benefit. I think I'll leave it at that for now. Yeah. Look forward to learning more on that. Thank you. And then on the Phase 2 gastric cancer study, just early findings, I understand there. Could you talk specifically to your plan of understanding contribution between botensilimab and the cells, be it through clinical or translational data? I'm not sure if you've seen a ton of botensilimab data in this particular cold tumor. So if you could help us understand how you're thinking about that, Jen. Thanks again for taking our question. Mayank, thank you very much. So I had mentioned to Emily just a bit ago about the way that we will interrogate the activity of these cells. So for standard-of-care, thousands of patients' worth of data, we did not add in a standard-of-care arm into the randomized Phase 2. We don't need to at this point. So we will study the cells on top of standard-of-care, the cells on top of botensilimab with and without standard-of-care. Now, our ability to interrogate the addition of the additional benefit or the contribution of the cells to botensilimab is going to take shape in a few ways. It'll take shape in this study. But it also will take shape in a study that we will be announcing as well that will be externally funded in colorectal cancer in patients with metastatic disease to the liver. So as you know or for those of you who don't know, botensilimab has generated really remarkable activity in cold tumors. And more than 900 patients studied, 9 different tumor types that have been previously unresponsive to immune therapies are actually responding to botensilimab. And it opens up an enormous opportunity for patients with these diseases that have previously gone unable to be treated effectively. In metastatic colorectal cancer, MSS-CRC now, this is the largest population of colorectal cancers. It represents about 95% of the population of patients with colorectal cancer, and it's growing. It will represent the largest killer of men under 50 shortly. This has been widely published and available in both the scientific literature as well as in the lay literature. What we have observed with the activity in nearly 400 patients treated with MSS-CRC is that bot/bal standard-of-care therapies bring anywhere from 2%-3% tumor shrinkage. And we're seeing more than a tenfold improvement of tumor shrinkage in that indication when patients are treated with bot/bal. And while we have not yet achieved a median survival in the study, in the randomized Phase 2 study, we have observed a more than doubling beyond 2 years of survival, which is really, as far as we can tell, unprecedented in this indication. The one area where we believe we can improve upon the activity of botensilimab, we do see that botensilimab is active in generating a survival benefit in patients with metastatic disease to the liver, but it's not as active in shrinking tumors within the liver. Now, what we know about iNKTs is they actually home to the liver disease. And we have observed in our own hands that iNKTs can modulate disease in the liver. So we believe that in addition to the survival benefit that botensilimab can bring to patients with MSS-CRC with liver mets, we think that the addition of iNKTs may actually contribute to the reduction of disease burden in the liver and may actually expand survival benefit even further beyond what botensilimab could do alone. We will be testing that in an externally funded trial with a KOL that we will announce very shortly as soon as we launch that program, which is going to be happening in the first half of this year. Thank you, Jen. Looking forward to those updates. Thank you very much, Mayank. Thank you. That does conclude the question-and-answer session. I would like to turn the call back over to Dr. Jennifer Buell for closing remarks. Thank you very much, operator. Thank you all for your questions and your participation today. We really appreciate your continued support and look forward to speaking with you again soon. Thank you. Thank you, everyone. That does conclude today's presentation. Thank you for your participation today. You may now disconnect.