MiNK Therapeutics, Inc. (INKT) Q3 2026 Earnings Call Transcript

Operator: Good morning, and welcome to MiNK Therapeutics Third Quarter 2026 Conference Call and Webcast. [Operator Instructions] Please note that this event is being recorded. I would now like to turn the conference over to Stefanie Perna-Nacar from MiNK Investor Relations. Stefanie, please go ahead.

Stefanie Perna-Nacar: 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, time lines 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. Terese Hammond, Head of Inflammatory and Pulmonary Diseases; and Melissa Orilall, Principal Financial Officer. I'd like to turn the call over to Dr. Buell to highlight our progress from this quarter. Dr. Buell?

Jennifer Buell: Thank you, Stefanie. 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 3 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 for Cancer Research in April, investigators from Memorial Sloan Kettering reported a 77% disease control rate in patients treated with agenT-797 in combination with botensilimab and balstilimab 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 antitumor 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 for Immunotherapy in Cancer, 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 named 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-797 is investigational, thus every paid named patient request originates with a treating physician and is authorized on a case-by-case basis by regulators. This program shows 3 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 products 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 to execute the rest of our strategy. Turning to acute lung injury and ARDS, our randomized Phase II program. Acute respiratory distress syndrome, or ARDS, is one of the largest unsolved problems in critical care. We estimate that approximately 93,000 U.S. 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 you for the second half of 2026. We observed no major serious adverse events attributed to 797, and we 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 IIb/III study, a seamless Phase III 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 III. 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 agenT-797 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. Terese Hammond. She leads our inflammatory and pulmonary programs and actively practices critical care medicine. Dr. Hammond?

Terese 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 I/II trial during the COVID pandemic, and that is why I joined this effort. Roughly 40% to 50% 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 rigth 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 are very sick patients with multidrug-resistant infections, yet their fevers resolved, their oxygenation rapidly 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 endpoint survival without ECMO at day 14, then mortality at day 28 maps to the decisions we actually make at the bedside, 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 can be given in any ICU, it can 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 ILDs 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.

Jennifer Buell: Thank you so much, Terese. In September, 797 was selected as a therapeutic cell system for the ARPA-H BioStabilization Systems or BoSS program, where ARPA-H is committing up to $87 million over a 4-year period to move living medicines from cryogenic storage toward room temperature. Cold chain is 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 Immunotherapy 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 II study at Scripps led by Dr. Darren Sigal is combining BOT/BAL 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. Jesús Gil at Imperial College London, we showed that agenT-797 and MiNK-215, 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. MiNK-215 also reaches the FAP-positive stroma that shields tumors and drive 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, randomized 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 GvHD prevention funded by the NIAID STTR award and further funded by the Mary Gooze 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 nondilutive. These are fully funded externally. I will now turn the call over to Melissa to discuss our financials.

Melissa Orilall: Thank you, Jen. We ended the quarter with $7.5 million in cash and cash equivalents compared to $8.8 million at June 30. 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 physician requests and case-by-case regulatory authorizations. Our net loss for the quarter was $2.6 million or $0.50 per share compared with $2.9 million or $0.65 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 10-Q, 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 cell therapy provider for the ARPA-H BoSS program, as Jen mentioned. And we continue to strengthen our balance sheet through partnerships and licensing, nondilutive funding and equity or debt financing with the priority of funding the randomized study through its readout. I will now turn the call back to Jen for closing remarks.

Jennifer Buell: Thank you, Melissa. Now stepping back and looking over the last 5 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 G&A costs have come down. And we've added a fourth source of nondilutive funding support alongside the STTR award, and that includes the clinical Mary Gooze 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 expense. Our priorities into 2027 are specific: activate the U.S. ICU sites and sustain enrollment in the 1300-02 study, seek FDA alignment on the adaptive Phase IIb/III 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 named 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.

Operator: [Operator Instructions] Your first question comes from the line of Mayank Mamtani with B. Riley Securities.

Mayank Mamtani: I appreciate the level of detail remarkable progress on so many fronts. 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 VV-ECMO utilization rates, recognizing there could be differences in care across different geographies. I don't know how you're accounting for that. And then there was a recent Phase III program related regional licensing deal I don't know if you want to maybe put your program in context of how maybe the peer landscape for this disease state is kind of evolving? And maybe 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.

Jennifer Buell: Mayank, thank you so much for the questions. I also have Dr. Terese 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 are -- what we can tell you is that the observations that we continue to see are validating our observations from the already published Phase I/II 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, 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% and sometimes higher than that. We continue to see patients from our previously published data of over 70% to 75% survival rates in our early observations that we're continuing to validate through our Phase II 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. Terese?

Terese Hammond: Yes, Jen. And thank you, Mayank, for the question. So we've been rigorous about selecting centers. The selection process is active in 4 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. They're being prone when oxygen ratios reach a threshold that's 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.S. centers that not only have very high ICU censuses 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 II, hopefully seamless Phase III trial, one of the important considerations will be early modification, early improvement in oxygenation so that we can forego or prevent escalation to ECMO.

Mayank Mamtani: It's very helpful.

Jennifer Buell: Thank you very much, I'm sorry, go ahead. I was going to answer your second question. But please go ahead.

Mayank Mamtani: No, no, please go ahead, Jen, on the partnership, if you want to comment on that.

Jennifer Buell: Yes. And so I assume that you're referring to the Edesa 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 nondilutive 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 Edesa 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 multidrug-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 multifactors, 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 molecule -- 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 our published Phase I, Phase II 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 can make a meaningful impact for patients and the market is recognizing that as well.

Terese Hammond: I was just going to emphasize one point that you made. So here we are sort of 5, almost 6 years post COVID. And we're recognizing sort of this hyperinflammatory phenotype in about 1/3 of patients, not just with COVID, but all cause ARDS, have very high mortality rates. And now 5 years post-COVID also have 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.

Mayank Mamtani: Actually, my follow-up was going to be 2-parter on exactly the things you just talked about. On that hyperinflammatory learning you're having about the cells, are there any clear biomarkers that cut across a severe disease state like ARDS or there could be other larger chronic inflammation conditions also that could be relevant? And then my specific question was on the FDA meeting before year-end. If you could maybe just talk about what the different discussion topics that are on the table in context of maybe the specific endpoint, the ECMO free days versus mortality and then maybe also how the Phase II patients count towards the registration cohort and maybe any designation you're pursuing? Sorry, that was a multiparter, thanks for taking question.

Jennifer Buell: Mayank, thank you so much. I 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 have been -- 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 to 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 VV-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 precedents 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 just -- we want to ensure that the patients from the randomized Phase II can contribute to the Phase III 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 II trial that those patients will then contribute to the ongoing expanded randomized Phase III, 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 have -- 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 Immunotherapy for Cancer essentially demonstrate 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 senescent cells actually are pro-inflammatory. So these -- by clearing senescent cells, you're actually reducing some of the inflammation cascade that we observe in patients following acute -- acute critical illness like ARDS. Therefore, if these cells can not only reconstitute immunity, clear inflammation, essentially serve as an anti-inflammatory 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 those -- the elimination of senescent cells and the elimination of 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 sequelae 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. Terese?

Terese Hammond: Yes, Jen. I mean, sort of points to some of the work that we're doing with Anne Sperling at the University of Virginia that we've reported on previously, showing that really, it's a spectrum. So acute inflammation that becomes chronic eventually will propagate fibrosis. And 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 fibrosis is 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 explanted lungs, looked at the lymph nodes within those lungs. So these are patients that are pending transplant for idiopathic pulmonary fibrosis and other types of fibrosing lung disease. And what she found was astonishing. She found active immune capabilities within 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 invariant natural killer T cells. So I think all along the spectrum of acute inflammation, chronic inflammation, fibrosis and ultimately, terminal fibrosis 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.

Mayank Mamtani: Yes, that explains some of the survival work you intend to do in the future.

Operator: Your next question comes from the line of Matthew Keller with H.C. Wainwright.

Matthew Keller: 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?

Jennifer Buell: So nice to have you on the call, Matthew. Thank you. Dr. Darren Sigal'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 botensilimab and balstilimab in patients with MSS colorectal cancer who have metastatic disease to their liver.

Operator: [Operator Instructions] This concludes the Q&A session. I will now turn the call back over to Dr. Jennifer Buell for closing remarks.

Jennifer Buell: 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.

Operator: This concludes today's call. A replay will be available in the Events and Presentations section of our Investor website at minktherapeutics.com. Thank you for participating. You may now disconnect. Goodbye.