MiNK Therapeutics Third Quarter 2026 Financial Results - MINK THERAPEUTICS INC

Good morning, and welcome to Mink Therapeutics' third quarter 2026 conference call and webcast. All participants are in listening mode until the Q&A session. Please note that this event is being recorded. I would now like to turn the conference over to Stephanie Hernanacar from Mink's Investor Relations. Stephanie, please go ahead. Thank you, Operator, 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 those related to our clinical development, regulatory and access plans, timelines for data releases, our named patient program, our cash resources, and our partnership opportunities. These statements are subject to risks and uncertainties. Please refer to our SEC filings, including the Form 10-Q we filed this week, available on our website for a detailed description of all these risks. Joining me today are Dr. Jennifer Buell, President and Chief Executive Officer, Dr. Therese Hammond, Head of Inflammatory and Pulmonary Diseases, and Melissa Orlall, Principal Financial Officer. I'd like to turn the call over to Dr. Buell to highlight our progress from this quarter. Dr. Buell? Thank you, Stephanie. Good morning, and thank you for joining us. A year ago on this call, we said that by this time, we expected to have a randomized trial running in critical illness, multiple clinical programs enrolling, and a path toward pivotal development. All three are now in motion. This quarter brought that closer. Patients are being treated, data are accumulating, and physician demand has produced patient access outside of clinical trials and marks our first revenue with Agent 797. Over the course of this year, we have had a substantial amount of visibility. At AACR, the American Association of Cancer Research, in April, investigators from Memorial Sloan-Kettering reported a 77% disease control rate in patients treated with agent 797 in combination with botansilumab and balacilumabe in PD-1 refractory gastroesophageal cancer. And following that, at the American Cell and Gene Conference here in Boston in May, we showed that the same off-the-shelf cells derived from the same donor can drive an anti-tumor response in cancer and a restorative anti-inflammatory and pathogen clearance response in patients with respiratory distress. These cells read the disease and respond to it. These data were exemplified in the same year at the American Thoracic Society, the Military Health Science and Research Symposium, and the Society of Immune Therapy in Cancer, where where we added lung, clinical, and senolytic data that I will cover shortly. Our strategy is deliberately focused. We're using randomized evidence in severe hypoxemic respiratory failure to establish a rapid development pathway for agent 797. And with the validation of this technology, the case for deployable immune restoration in critical illness. We extend this platform into fibrosis, cancer, and engineered INKT medicines where the biology is differentiated. Our capital deployment is focused on our randomized readout, the biomarker work that explains it, the regulatory execution, and the reliable supply. And I'll take you through each piece in turn. First, our global name patient access program. In the third quarter of this year, we recognized pre-commercial product revenue, our first, from Agent 797 supplied on a paid per patient basis under our named patient import pathway in collaboration with Orphan Drug Consulting and BAP, now open in multiple countries outside of the United States. Agent 7 97 is investigational, thus every paid named patient request originates with treating physician and is authorized on a case-by-case basis by regulators. This program shows three things. One, the product we manufacture and hold in inventory here in Lexington, Massachusetts can support a clinical program and physician-directed access at the same time. We can reliably move a cryopreserved cell product across borders, and physicians are requesting it for patients with serious, unmet medical needs outside of our clinical trials. This infrastructure is a template we intend to apply in additional markets. In August, our program was a plan, and today it's active in treating patients. This is the pace at which we intend execute the rest of our strategy. Turning to acute lung injury and ARDS, our randomized phase two program. Acute respiratory distress syndrome, or ARDS is one of the largest unsolved problems in critical care. We estimate that approximately 93,000 US patients a year fall within our initial target population of ventilated, pneumonia associated, moderate to severe ARDS. Based on our current modeling, that represents a substantial annual market opportunity with potential to expand into other causes of severe lung injury. Our randomized placebo-controlled Phase II study of 797 plus standard of care in adults with acute lung injury and moderate to severe hypoxemic respiratory failure continued enrolling in Lviv, Ukraine, during this quarter. U.S. activation is in its final stages, and we expect to begin dosing in the U. S. before year end. In August, Dr. Hammond presented initial day 28 observations from the first treated patients at the MHSRS conference, the first look we guided to for the second half of 2026. We observed no major serious adverse events attributed to 797, and can now extend that picture to additional treated patients. The comparative readout is expected in 2027, reflecting the planned pace of our enrollment. We plan to refine the study as an adaptive Phase 2B 3 study, a seamless Phase 3 study. The initial randomized stage will enroll about 124 patients with the ability to expand to as many as 300 patients. The proposed endpoint is hierarchical, survival without VV ECMO at day 14, followed by all-cause mortality through day 28. We plan to meet with the FDA before year-end to discuss the design, including whether the randomized stage can contribute directly to a registration-enabling phase 3. Alignment on this design would make the path to registration materially more efficient. Acute lung injury is fundamentally a failure of immune regulation, uncontrolled infection, dysregulated inflammation, and impaired immune repair at once. INKT cells read the tissue environment and direct the response. And HN797 appears to deliver from inventory without apheresis, HLA matching, or lymphodepletion. To put this into clinical context, I'm going to turn the call over to Dr. Therese Hammond. She leads our inflammatory and pulmonary programs and actively practices critical care medicine. Dr. Hammond? Thank you, Jen. I actively treat patients in the ICU, as Jen mentioned, and ARDS is one of the conditions I see most often and can do the least about. My first experience with Agent 797 was during the Phase 1-2 trial during the COVID pandemic, and that is why I joined this effort. Roughly 40 to 50 percent of these patients die, and after decades of trials, there's still no approved drug shown to reduce that mortality. What we offer today is support, the ventilator, proning, and when all else fails, veno-venous ECMO. We keep patients alive and wait for the immune system to right itself, but in a large percentage of cases, that doesn't happen. What struck me about the first patients treated in Lviv was this pattern. They're very sick patients with multidrug-resistant infections, yet their fever's resolved, their oxygenation rapidly improved, improved. They came off the ventilator and vasopressors, and immune markers in both blood and bronchoalveolar lavage, lung fluid, tracked their recovery. That's the coordinated response we hoped for with INKT cells. We have seen them deliver. Granted, these are small numbers of patients without a comparator, and this is exactly the reason we're advancing into the randomized trial. The end point, survival without ECMO at day 14, then mortality at day 28, maps to the decisions we actually make at the bedside. And because Agent 797 comes from inventory with no matching or conditioning, it can be given in the window the very first few days when it really matters. It can be thawed. It kan be given. In any ICU, it kan be infused simply. There's a second reason this matters to me, many ARDS survivors leave the ICU with lungs that keep scarring, driven by the same inflammation, senescent cells, and activated fibroblasts behind the interstitial lung diseases that I see beyond the ICU in the clinic. Many of these IODs have no treatment options beyond transplant or palliative care. If these cells can also clear the senescent cells that sustain fibrosis, modify or modulate chronic inflammation, as the preclinical work Jen just described suggests, the same therapy that we're using in studying for acute lung injury could reach well beyond the ICU and into the clinic and into other interstitial lung diseases. With that, I'd like to turn it back to you, Jen. Thank you so much, Therese. In September, 797 was selected as the therapeutic cell system for the ARPA-H Biostabilization Systems or BOSS program, where ARPA H is committing up to $87 million over a four-year period to move living medicines from cryogenic storage toward room temperature. change the single largest barrier to taking an allogeneic cell therapy beyond specialized centers. We've already delivered 797 to ventilated patients within days of Ministry of Health authorization in a conflict zone. Removing the freezer would let a living immune therapy be stockpiled like a conventional drug in community hospitals and in austere settings. INKT cells are also a demanding stabilization benchmark, so success here would matter for the whole field. Mink participates on a fixed fee basis, which means as we advance and perform, we continue to accumulate and be eligible for reimbursement for our efforts. Finally, our scientific progress. Last week at the Society of Mink Therapy for Cancer, we presented data in a human organoid model of microsatellite-stable colorectal cancer with liver mets, a setting with no approved immune therapy, and where BOT and BAL alone produced no significant tumor cell killing. Adding Agent 797 shifted suppressive macrophages towards an antigen-presenting phenotype and unlocked tumor killing. The rationale for the ongoing Phase 2 study at Scripps, led by Dr. Darren Siegel, is combining BOT, VAL, plus INKT cells in patients with MSS colorectal cancer with metastatic disease to their liver. We are excited to present data in the beginning of next year on this program, the clinical program. Also, in collaboration with Dr. Jesus Gill at Imperial College London, we show that agent 797 and MINK215, our FAP-targeted IL-15 armored CAR-INKT candidate, act as living senolytics – this is very exciting – clearing the senescent zombie cells that chemotherapy and radiation leave behind. MINK215 also reaches the fat-positive stroma that shields tumors and drives scarring. These cells fuel treatment resistance in cancer and progression in fibrotic lung disease, giving us one thread from oncology to the lung and ultimately to aging. We will continue to develop this data set in sequence, randomize evidence first from our ongoing trial, and then into deeper data sets with senescence and fibrosis in the clinic. And finally, our Phase I study in prevention of GVHD is activating at University of Wisconsin. The investigator-sponsored Phase I Study of 797 for GVHC Prevention, funded by the NIAID STTR Award and further funded by The Mary Guth Clinical Trial Award, is moving towards first dosing. Our colleagues at UW have informed us that it expects the first patients to be scheduled to dose by December. The start, while it has moved from our first half guidance, is now moved to the second half, but we certainly expect to activate and enroll patients this year. This study, as well as the Scripps Institute study, remain non-dilutive. These are fully funded externally. I will now turn the call over to Melissa to discuss our financials. Thank you, Jen. We ended the quarter with $7.5 million in cash and cash equivalent, compared to $8.8 million at June 30th. Importantly, this quarter, we recognized our very first pre-commercial product revenue from Agent 797 supplied through our Named Patient Program. This program just launched this quarter and we expect demand to vary from quarter to quarter based on position requests and case-by-case regulatory authorizations. Our net loss for the quarter was $2.6 million, or $0.50 per share, compared with $2,900,000, or $.65 per share a year ago. The cash used in operation was approximately $1.3 million in the quarter, down from approximately $2.1 million in the second quarter, our lowest quarter of the year. We are focusing our spend on the randomized study and reducing costs elsewhere. Our G&A expenses decreased 44% to $1 million, primarily from lower professional fees and stock compensation expense. Our R&D expenses increased to $1.8 million from $1,1 million, primarily reflecting the timing of our clinical trial activities, including our randomized Phase II study and preliminary translational analysis presented at major conferences in this quarter. As disclosed in our 10Q, we will strengthen our balance sheet with additional funding and currently meet the requirements as a going concern. As we announced earlier this quarter, MINK was selected as a self-therapy provider for the ARPA-H BOSS program, as Jen mentioned. And we continue to strengthen our balance sheet through partnerships and licenses, non-dilutive funding, and equity or debt finances, with the priority of funding the randomized studies through its readout. I will now turn to call back to Jen for closing remarks. Thank you, Melissa. Now, stepping back and looking over the last five quarters, we took biology from refractory cancer into critical illness, started a randomized Phase IIb trial, began treating patients through paid access, earned federal validation for deployability, and connected our oncology work to our fibrotic lung disease platform, and over the same period, our net loss per share and GNA costs have come down, and we've added a fourth source of non-dilutive funding support alongside the STTR award, and that includes the clinical Mary Guse award, as well as our C-FURTHER partnership in advancing our PRAME-TCR in pediatric patients with blood cancers. We are spending where the randomized trial requires it, and our externally funded programs are advancing alongside and not at its expense. Our priorities into 2027 are specific. Activate the USICU sites and sustain enrollment in the 1302 study. Seek FDA alignment on the adaptive phase 2B3 design and pursue supportive designations that will help to accelerate development. report comparative data in 2027, support first dosing in our GVHD program, extend our name patient access program into additional markets where regulations allow, and, of course, advance our collaboration with ARPA-H and deployable cell therapy work. Across cancer and critical illness, the underlying problems we are addressing is a loss of coordinated immune function. If the early clinical and biologic patterns we are observing hold up under randomized evidence, an off-the-shelf therapy that restores that coordination and that can be stocked and delivered like a conventional drug would change what cell therapy can do and where it can be given. The clinical value proposition is intact, and our job really is to advance and protect the readouts that can really validate the platform that we're moving forward. I appreciate your continued support. Thank you for joining us today. Operator, we will now turn the call over for questions. Thank you. To ask a question, please press star and then 1. To withdraw, press star, and then one again. Your first question comes from the line of Mayank Mamthani of B. Reilly Securities. Your line is now open. Yes, good morning, team. Thanks for taking our questions, and I appreciate the level of detail, remarkable progress, and so many friends. So on the Phase IIb ARDS randomized trial, are you able to share the treatment effect you're assuming on both the absolute mortality rate and then maybe also on the VVAC more utilization rates, recognizing there could be differences in care across different geographies. I don't know how you're accounting for that. And then, you know, there was a recent phase three program-related regional licensing deal. So I don' know if you want to maybe put, you know, your program in context of how maybe the peer landscape for this disease state is kind of evolving. And I don't know if you have any thoughts on that Japan-specific license for that antibody that was done recently. And then I have a couple of follow-ups. Mayank, thank you so much for the questions. I also have Dr. Therese Hammond here to speak a bit about standard of care. So, with respect to the data observations to date, we do plan to present and have been invited to do so at some major conferences next year, first half of next year. So, we will be releasing more formal data analyses at that time. However, currently, what we can tell you is that the observations that we continue to see are validating our observations from the already published Phase 1-2 study. So our 28-day mortality is still very consistent with what our observations were earlier, which give us quite a bit of optimism and enthusiasm for the program. And we'll continue to keep you apprised as the data evolve. We plan to be dosing in the United States before the end of this year. Our trial is continuing to enroll in Lviv, Ukraine, and will then certainly be active, you know, as I mentioned, in the U.S. as well. What I will say is that our program has been designed and protocoled to really standardize for U. S. like treatment, which means hospital ventilator settings, as well as standard of care therapies, available therapies for patients. So that's an important part of the program so that all patients contributing to the enrollment will be treated in accordance with U.S. treatment guidelines for standard of care. Despite what's available to patients, though, I just want to remind you mortality remains in patients not treated with the cells of about 40 percent and sometimes higher than that. We continue to see patients from our previously published data of over 70 to 75 percent survival rates in our early observations that we're continuing to validate through our phase two trial. With that, I'll invite Dr. Hammond to say a few words about the standard of care and the treatment paradigm that we've essentially ensured meets U.S.-like treatment paradigms in Lviv, Ukraine, as well as then, of course, our approach to invite surgical ICUs as well as medical ICUs to programs that are launching in the United States and dosing patients before the end of this year. Therese? Yes, Jen, and thank you, Mayank, for the question. So we've been rigorous about selecting centers. The selection process is active for U.S. centers, but rigorous about making sure that standard of care is adhered to. We also visited Lviv, Ukraine prior to deciding on enrolling that site to really validate in person that the same standards we use in the United States when patients are admitted with ARDS are adhered to in the Lviv ICUs. That means patients are getting lung protective therapy. They're getting early antibiotics. They'RE getting steroids where appropriate. TheyRE being proned when oxygen ratios reach a threshold that universally felt to be appropriate. And more importantly, as we move into the U.S. and as we start to enroll patients by year end, we are selecting U.F. centers that not only have very high ICU sentences of these ARDS patients, both medical and surgical ICUs, but also ones that can rapidly escalate to ECMO based on very conventional standards, really put out by ELSO, the Extracorporeal Life Support Organization. So these groups have already demonstrated, oftentimes with platinum or gold ELSO designation, that they manage their ECMO patients appropriately. That way, we can try to ensure uniform decision-making in terms of when to escalate to ECMO, and as Jen said, for the phase two, hopefully seamless phase three trial, one of the important considerations will be early modification, early improvement in oxygenation so that we can forego or prevent escalation to ECMA. Thank you very much, Jason. And Mayank, I'm sorry, go ahead. I was going to answer your second question, but please go ahead No, no, please go ahead, Jen, on the partnership if you want to comment on that And so I assume that you're referring to the ADESA-QR agreement, and that's an encouraging example of strategic interest in ARDS overall We have, as you know our pursuit to continue to strengthen the balance sheet is really based on non-dilutive funding as well as strategic collaborations, which are all very actively advancing. With respect to ARDS, there is a growing interest in this space and there are, I believe, a couple of reasons for that. The first is that the FDA has now been far more specific about the intended target population definitions around that population and the urgency to bring new therapies forward. Currently, there are no effective approved therapies for patients with ARDS. The ADESA product is essentially a TLR4 agonist and has demonstrated some activity in earlier phase trials. What we see with our product, though, is not only can we address some of the immune inflammatory components of ARDS, so we very rapidly see that upon administration, we see an anti-inflammatory signature, which is incredibly important in this ICU setting, particularly in patients undergoing critical care with critical illnesses. That anti-inflammatory signal enables essentially the lungs to start healing. And in addition to the anti-inflammatory, we see pathogen clearance, including in patients in Ukraine who have more than 100% of them have one or more multi-drug resistant pathogens. And we have been able to make a meaningful difference for those patients, and in particular, clearing some of those pathogens, gram-negative pathogens as well, both important to enable lung healing. And in addition to those multi-factors, we also see cytokines that are related to epithelial tissue repair. So in addition to the factors that we're helping to ameliorate to enable lung healing, we also see that the cells are directly impacting molecules, essentially modulators of lung healing of specific tissue health healing. We've presented a lot of that publicly and we're quite excited about what this presents. So taken together with the trial actively underway and with the multimodal characteristics that these cells appear to bring very rapidly within about 48 to 72 hours in patients in a critical setting. We hope to not only take patients at risk for going on the most severe form of life support, that's called VV ECMO as Dr. Hammond mentioned, and prevent them from going on this very invasive, difficult procedure, and then of course promote 28-day survival and beyond, consistent with our observations from published phase one, phase two trial. So with that, I think I appreciate your thinking. And I think that there are a number of reasons as to why you're seeing a growing strategic interest in this space. There are now therapies that actually could make a meaningful impact for patients and the markets recognizing that as well. Jim, can I just add one? Well, I was just going to emphasize one point that you made. So here we are sort of five, almost six years post COVID. And we're recognizing sort of this hyper-inflammatory phenotype in about a third of patients, not just with COVID, but all-cause ARDS, have very high mortality rates. And now five years post-COVID also have very, very high rates of persistent pulmonary disability. So continued fibrosis, continued decrease in lung function, continued issues with return to work, and with quality of life. So I think that that's also the sort of the aftermath of COVID also has pointed us to the concept that we need to mitigate acute inflammation early, completely, avoid the progression to chronic inflammation, and do something in addition to sort of modulating inflammation to improve recoveries, and I think some of the restorative functions that we've seen in patients treated with cells are very compelling, very provocative. Actually, my follow-up was going to be two-parter on exactly the things you just talked about. On that hyper-inflammatory, you know, learning you're having about the cells, Are there any, you know, clear biomarkers that cut across, you know, a severe disease state like ARDS or, you know, there could be other, you know, larger chronic information conditions also that, you know, could be relevant. And then my specific question was on the FDA meeting before year end, if you could maybe just talk about what, you know, the different discussion topics that are on the table, in context of maybe the specific endpoint, the ECMO-free tier versus mortality, and then maybe also how the phase two patients count towards the registration cohort and maybe any designations you're pursuing. Sorry, that was a multi-parter, but thanks for taking the question. Mayank, thank you so much. I so appreciate your rigor. With respect to the biomarkers, We have not yet published the biomarker data set that we've been continuing to accumulate and develop, and there's published literature on a developing set of biomarkers that may help not only to identify patients and differentiate them between their inflammatory state, hyper and hypo, but there also may be similar sets of biomARKers that can help predict response to therapy and identify patients who are more likely to respond to certain types of therapeutic intervention. And we've got our own developing data set in which we do have what we believe to be an important predictive set of biomarkers that can help us identify patients more quickly who would be more likely zu respond. Currently, we're enrolling all patients into the study. We're stratifying them by their biomarker status, and we're continuing to evaluate and validate those markers prospectively in our study. That will be part of a discussion with the agency to help us understand how to identify patients who may be able to benefit more quickly from different therapeutics. Regarding the FDA interactions, we really are seeking their feedback on a couple of things. One is a win ratio evaluation for hierarchical endpoint prevention of IV ECMO, which is a very invasive procedure and also requires one-on-one dedicated ICU nursing staff and respiratory therapy, really essentially by the bedside with great frequency for these patients, incredibly intensive for the patient and also incredibly difficult and intensive for hospitals. And that is an important endpoint for us to be able to restore patients' breathing quickly, prevent ECMO within the first couple of weeks of treatment, and then also restore lung function, increase ventilator-free days, and enable the patient to have lung healing quickly is a very important outcome for us. So we want to ensure that we're aligned with the FDA, and we have seen some precedence with this type of a design that has led to approved therapeutics. And our design is really quite consistent with the established precedents so far. So we'll certainly seek their feedback and gain their alignment and partnership, which we have done since the beginning of the program. And in addition to that, we want to ensure that the patients from the randomized phase two can contribute to the phase three in a seamless way. Therefore, when we have a data readout, which we are anticipating to be around the third quarter of next year for the initial randomized phase two trial, that those patients will then contribute tothe ongoing expanded randomized phase three, which we believe will move really quite quickly for enrollment, so that all patients participating can contribute in a protocol that we hope can support registration of the program ultimately. So we will not proceed with aggressivity without great support and partnership with the agency, and that's something that we're continuing to engage them on. And similarly, the biomarkers may help us to speed development and enhance our pathway in a few different ways. And to the last part of your question, those same biomarkERS, which we've just presented at the Society of Immune Therapy for Cancer, essentially demonstrates invariant natural killer T cells as effectively something called living senolytics. What we've seen is that these cells not only can restore immunologic activity and function, but also these cells can eliminate senescent cells. And these same senescence cells actually are pro-inflammatory. So by clearing senescent cells, you're actually reducing some of the inflammation cascade that we observe in patients following acute critical illness like ARDS. Therefore, if these cells can not only reconstitute immunity, clear inflammation essentially serve as an anti-inflammory capability within the lung tissue. Clear some of the problematic pathogens that are actually resulting in the inflammatory cascade in the lungs and promote lung healing, it could be an extraordinary opportunity for us to bring a meaningful difference to patients in critical care. And the elimination of senescent cells and the eliminationof some of these elements that I just mentioned to you and the biomarkers that we're observing, we believe will also prevent progression to some of the long-term fibrotic conditions that impact patients with acute pulmonary disease. Dr. Hammond mentioned this during her talking points earlier today in the script, and I'll have her reiterate her perspective. But our goal would be not only to get patients out of the ICU breathing independently and alive, surviving beyond what's currently available to them, but also to prevent the sequela from that episode, which would be long-term fibrotic lesions in their lungs, which sometimes could lead to idiopathic pulmonary fibrosis and other chronic conditions. We want to eliminate that. Therese? Yeah, Jen, and it sort of points to some of the work that we're doing with Anne Sperling at the University of Virginia that we've, that was reported on previously, showing that really it's a spectrum. So acute inflammation that becomes chronic eventually will propagate fibrosis and the, in the end, the very most severe form of interstitial lung disease, idiopathic pulmonary fibrosis can then occur. What's really interesting is as a pulmonologist until very recently, I thought that idiopathic pulmonary fibrosus was really the end of the line. You either transplanted the patient or you place the patient on palliative care because it's a progressive disease with just a tremendous amount of disability. Dr. Sperling in her lab has looked at a variety of of explanted lungs looked at the lymph nodes within those lungs so these are patients that are that are pending transplant for idiopathic pulmonary fibrosis and other types of fibrosing lung disease and what she found was astonishing she found active and immune active immune capabilities within these these lymph nodes so these lymph nodes were still active immune sites. They were producing germinal centers. And most importantly, when we joined her in a reanalysis, they were depleted of very natural killer T-cells. So I think all along the spectrum of acute inflammation, chronic inflammation, fibrosis, and ultimately terminal fibrosus or even cancer, the reconstitution of the immune response, the modulation of inflammation, and especially the resolution of acute inflammation so it doesn't become chronic is a really key perspective here, a really key element here of recovery and certainly plays an enormous role in long-term quality of life and functioning post-injury. So the survivors also have sequelae that can be quite debilitating. Yeah, that explains some of the survival work you intend to do in the future. I appreciate all the color. I'll hop back in the queue. Thank you. Your next question comes from the line of Matthew Keller of H.P. Wainwright. Hey, good morning. Thanks for taking our questions. So switching gears slightly with some just brief questions, I was wondering where does enrollment stand in the colorectal study? And then maybe can you comment on the type of data that we could expect from a future readout from that program? So nice to have you on the call, Matthew. Thank you. Dr. Darren Siegel's investigator-sponsored program is actively enrolling. He's enrolled past the first couple of safety cohorts, and the data are accumulating. We expect to have a readout very early in 2027 and have already established the pathway, we believe, to be able to present at probably one of the earliest GI conferences on the cohort. It is not for me to share an update specifically on the patients enrolled, but suffice it to say there's a meaningful cohort, enough so for us to get an impression of the data observations in patients with liver MET, MSS, colorectal cancer. And again, just for those who are not aware, this is a combination program. The INKT cells, agent 797, is administered in combination with botanstilumab and valstilamab in patients with MSS colorectal cancer who have metastatic disease to their liver. Perfect. Appreciate the caller. And again, happy to be here. Thanks again. Again, if you'd like to ask a question, please press star followed by one on your telephone keypad. that star followed by one on your telephone keypad. We will pause for a brief moment to wait for the questions to come in. This concludes the Q&A session. I will now turn the call back over to Dr. Jennifer Buell for closing remarks. Thank you, Operator, and thank you all for your continued support. We're incredibly excited about what's to come in the impending weeks to months, so thank you again for joining. this concludes today's call a replay will be available in the events and presentation section of our investor website at minktherapeutics.com thank you for participating you may now disconnect goodbye