Good morning and welcome to Mink Therapeutics' second quarter 2026 conference call and webcast. All participants will be in a listen-only mode until the question and answer session. Please note this event is being recorded. I would now like to turn the conference over to Stephanie Pernanakar from Mink Therapeutics, Mink 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 commercial plans, timelines for data releases, and partnership opportunities. These statements are subject to risks and uncertainties. Please refer to our FCC filings available on our website for a detailed description of these risks. Joining me today are Dr. Jennifer Buell, President and Chief Executive Officer, Dr. Therese Hammond, Head of Development, and Melissa Orilal, 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. The second quarter was an important period of execution for MINK. We moved Agent 797 into a randomized Phase II study in patients with acute lung injury and ARDS. We presented initial Day 28 observations from treated patients and established our first international paid named patient access program. Together, these reflect the model we are building, rigorous clinical development, rapid delivery of an off-the-shelf cell therapy, and responsible access for patients with urgent unmet needs. Critical illness is still treated largely by supporting failing organs while clinicians wait for the underlying injury to resolve. Ventilators support the lungs. Vasopressors support the circulation. Antibiotics address breast infection. There remained no approved pharmacologic therapy shown to reduce mortality in patients with ARDS or to restore coordinated immune function after severe lung injury. More than half of the patients with ARDS succumb to their disease and die. Our thesis is that this is fundamentally a problem of immune regulation. Patients with severe hypoxemic respiratory failure, die because the host response to the insult destroys the lungs, the epithelium, the endothelium, the barrier. What has been tried in this indication has largely either suppressed immunity globally, such as corticosteroids do, or stimulated it, but neither restores regulation. Invariant natural killer T-cells are a regulatory T cell population. They sit at the interface of innate and adaptive immunity, and they read the tissue environment that they are placed into, and they direct the responses accordingly. Agent 797 is an allogeneic off-the-shelf invariant natural killer T cell product. It's designed to address several linked features of critical illness, uncontrolled infection, dysregulated inflammation and impaired tissue repair. Just as important, it is available from inventory in real time. It does not require apheresis, does not require patient-specific manufacturing, HLA matching, or lymphodepletion. And that last point is biology rather than logistics. INKT cells are restricted by an important TCR that's common in all of us. This TCR is named CD1D, which is essentially non-polymorphic. So these cells can be given from a healthy donor to any patient without matching and without the graft-versus-host risk that constrains conventional allogeneic T-cell development. That combination, biologic activity, and practical deployability is central to our strategy. During this quarter, we initiated dosing into study C-1300-02. This is our randomized phase 2 study of Agent 797-plus standard of care versus placebo-plus standard of care in adult patients with acute lung injury and moderate to severe hypoxemic respiratory failure, meeting the global ARDS definition. The study opened at First Lviv Territorial Medical Union in collaboration with Unbroken Ukraine. We dosed the first patient within days of Ministry of Health authorization during an active conflict in critically ill, mechanically ventilated patients. That setting places extraordinary demands on patients, clinicians, and the health system. It also demonstrates why the logistics of a therapy matter. A cell therapy cannot change critical care if it cannot reach the patients in time. Last week at the Military Health System Research Symposium, Dr. Therese Hammond presented the initial data from our observations from the first patients treated with Agent 797. MHSRS, the Symposium, is the Department of War's principal medical research meeting focused on bringing effective therapies to areas of war and to patients who are in need, both civilian populations injured as well as those heroes fighting. They address very important questions on access to medicines that can help patients with immune restoration. Agent 797 acts on the host response rather than on the specific organism. It's pathogen agnostic, which is directly relevant, where multidrug-resistant infections are common and antibiotics fail. And importantly, in war, and specifically in the Ukraine, more than 100% of those injured are infected with multidrug-resistant pathogens. And those patients are treated both locally as well as in other hospitals in Europe, which is accelerating the spread of these pathogens. In our trial, we reported that our patients were alive and without fever at day 28. Importantly, they showed improved oxygenation, resolution of ARDS with return to spontaneous breathing, and liberation from vasopressor support. The microbiologic findings indicated control of baseline infections. The serum and bronchial lavages showed lower inflammatory markers and biologic changes associated with immune recovery, epithelial repair, and pulmonary vascular recovery. No major serious adverse events were attributed to Agent 797 in these initial patients. Now, these are early patients, and these patients are part of the run-in. their non-comparative observations from a small number of patients, and we should not over-interpret these results beyond what they show. The purpose of the randomized study is actually to generate the comparative evidence needed to determine whether 797 improves outcomes in these patients on top of standard of care. And we believe that as this trial continues to enroll in the randomized portion is actively activated, then we expect to be able to demonstrate this activity in this program. What we have shown is an early view of the clinical and biologic patterns we designed the study to evaluate. And notably, the clinical course and the mechanistic readouts moved in the same direction over the same interval, which is the pattern you would predict if the mechanism is host-directed immune regulation. Enrollment continues in Lviv, Ukraine, and activation of U.S. centers is actively underway. We expect to report additional data in early 2027. Our second advance to report this quarter was the establishment of Mink's First International Name Patient Access Program. This program launched in Brazil and in collaboration with our colleagues at Orphan Drug Consultants, a local team on the ground in Brazil and South America. This program is important for three reasons. First, it establishes a treating physician. It enables a treating physician to request 797 for an individually identified patient with serious unmet needs subject to case-by-case regulatory authorization. Second, this is a paid program. MNC receives payment for products supplied on a per-patient basis. While this is not a commercial launch, it is an important step in demonstrating that our existing inventory can support both clinical development and responsible physician-directed access. Third, the program establishes the operational infrastructure required to deliver an off-the-shelf cell therapy across borders. That includes local regulatory submissions, importation, logistics, and pharmacovigilance. Moving a cell therapy product reliably from inventory to an individual patient is where cell therapy programs typically fail, and it is not a capability that can be acquired at the point of approval. Our capabilities established now globally in Ukraine, in Brazil, and expanding in the U.S. can inform responsible access in other markets over time. To be clear, Agent 797 remains investigational. This program is not a marketing authorization, and it is not a substitute for participation in a clinical trial. Patients eligible for C-13002 will be directed to the study. MINK does not identify or solicit patients. Requests must originate with the treating physician and receive the required per-patient authorization. Now, our work in critical illness is supported by a growing body of translational and clinical evidence. Earlier this year at the American Thoracic Society International Conference, with concurrent publication in clinical immunology communications, We reported evidence of a pathogen suppression, lung immune restoration, and activation of tissue repair pathways following treatment of AGEN-797 and the IL-15 superagonist N803 in a patient with severe fungal infection. In Boston, earlier this year, at the American Society of Gene and Cell Therapy, we presented evidence that the same off-the-shelf INKT product, manufactured from the same donor batch, produces a different and context-dependent immune response, depending on the disease environment. We observed immune activation in cancer and inflammation-regulating activity in patients with ARDS without genetic engineering. And at the Keystone Symposium earlier this year, human lung tissue analyses identified INKT depletion as a mechanistic feature of advanced pulmonary fibrosis, extending the same immune restoration logic from acute injury into chronic fibrotic disease. And in cancer, our Phase II data in patients with PD-1 refractory gastroesophageal cancer showed a 77% disease control rate and durable survival in a subset of patients treated with Agent 797 in combination with botanfilimab and valfilimab with an induction strategy associated with longer progression-free and overall survival. Across these programs, the consistent scientific question is whether INKT cells can restore coordinated immune function when the immune system can no longer adequately control infection, regulate inflammation, repair tissue, or mount an effective anti-tumor response. And our trials and ongoing programs are designed to answer these questions. I will now turn the call over to Melissa to discuss our financials.

Thank you, Jen. We ended the second quarter with $8.8 million in cash and cash equivalents, compared with $9.5 million at March 31, 2026, and $3.4 million at year-end 2025. Our net loss for the quarter narrowed to $3.1 million, or 62 cents per share. compared with $4.2 million or $1.06 per share for the second quarter of 2025. For the first six months of 2026, net loss was $5.9 million or $1.20 per share, compared with $7 million or $1.76 per share for the same period last year. Our cash used in operations was $2.1 million for the quarter, compared with $1.6 million a year ago. Now, this modest increase was specific and deliberate, reflecting the cost of operationalizing our randomized Phase 2 study, activating and initiating the Levive site, completing the regulatory work support and Ministry of Health authorization, doping the first patients, and laying the groundwork for the U.S. sites which are now coming online. This investment directly supports the randomized evidence needed to evaluate the potential of this program. I will now turn the call back to Jen for closing remarks.

Thank you, Melissa. As Melissa noted, the modest increase in operating cash use reflects the launch and execution of a randomized Phase II study. Outside of that targeted investment, our financial discipline remains unchanged. We have not added fixed infrastructure, our footprint and headcount remain deliberately lean, and our manufacturing model is inventory-based rather than patient-by-patient. We also continue to prioritize non-diluted funding, both the graft-versus-host disease trial at University of Wisconsin and the pediatric PREM program are externally funded. And importantly, our paid named patient access program allows us to continue enabling responsible access to Agent 797 for patients with cancer and others with critical illness when requested by their treating physician and authorized by local regulators. At the same time, this program establishes the international infrastructure needed to deliver our off-the-shelf cell therapy across borders. And it also provides some resource support for our ongoing clinical trials. An important part of our advancement is based on the clinical experience and scientific understanding established through our oncology programs, which created the foundation for evaluating Agent 797 in critical illness. We are now advancing this important initiative in acute lung injury and ARDS while preserving a responsible pathway for patients to access the therapy outside of our ongoing clinical trials. This quarter, we advanced the essential elements of that strategy, a randomized Phase II study designed to generate rigorous evidence, an off-the-shelf product that can reach critically ill patients without patient-specific manufacturing, and a paid name patient program that broadens responsible access and begins to establish an international delivery pathway. Our ambition is to change the role of cell therapy from a complex intervention confined largely to specialized cancer centers to a readily available therapy that can be delivered when and where patients need it. The broader opportunity is significant. In cancer and critical illness, the underlying challenge is a loss of coordinated immune function. In critical illness, the initial infection, injury, or other insult may begin the crisis, but the subsequent loss of immune regulation can determine whether the patient recovers or progresses to prolonged organ failure and untimely death. If the earlier clinical and biologic patterns we are observing are confirmed through randomized evidence, this approach could have relevance beyond severe pneumonia and ARDS, including trauma, transplantation, cancer, and fibrotic diseases. Our priorities are clear. Continue enrollment in Study C-13002, activate our U.S. sites, expand the comparative clinical and biologic data set, and execute our name patient program responsibly. We are encouraged by our progress, disciplined about what remains to be proven, and focused on generating the evidence required to determine whether Agent 797 can meaningfully change outcomes for patients with critical illness, while continuing to enable access for patients as our broader clinical programs advance. Thank you for joining us today. Operator, we will now open the call for questions.

Thank you. To ask a question, press star, then 1.

To withdraw, press star, then 1 again.

And our first question comes from the line of Emily Bodnar with HC Wainwright. Your line is open.

Hi, good morning. Thanks for taking the questions and congrats on the progress. I guess maybe to start with the hypoxia, pneumonia, and ARDS data that you mentioned, can you confirm how many patients were included in this run-in that you discussed? And then along with that, it'd be great if you kind of walked through the baseline characteristics of these patients that they presented with and how you would expect these patients to have performed on standard of care had they been on that instead. and I guess your confidence that the day 28 survival that you've observed is due to Agent 797.

Hi, Emily. Thanks so much for the question. And I'll share with you the data that we've presented publicly, and those slides will be available on our website as well. These are patients with hypoxemic pneumonia, and they meet effectively. And I'll have Dr. Hammond go through some of the profile elements of these specific patients that we presented. but they meet the global definition of acute respiratory distress syndrome. So this is all-cause pneumonia. These patients could have a virus or a trauma or any other complications that may succumb them to having hypoxemic pneumonia. And in this study, we have a run-in scheduled for about 10 patients where all patients receive the cell therapy. and then we launched the randomized portion of the study we presented data in those patients that did receive the cell therapy and these were patients and we presented data on our first two patients treated in the study and the first was a 41 year old female and she had poorly controlled diabetes and pneumococcal sepsis and so at its submission actually I could have Dr. Hammond if you're available to share the case and you could speak both to the profile of the patients but then also to your expectations on what they would have succumbed to without the cells.

Yeah no of course Jen and thank you for the question Emily. So as Jen said these are adults they're we're trying to decrease the amount of exclusion criteria so they're folks with moderate to severe hypoxemic pneumonia, and they can also have coexisting trauma, so we're not excluding trauma patients from enrollment. Essentially, the first two patients that we treated in Lviv were somewhat different than the patients that I treat in the U.S. in the sense that both of these patients had multi-drug resistant pneumonia, multi-drug resistant organisms from the very moment that they were intubated, so before they were even treated. In sort of the most simplistic terms, patients with moderate to severe ARDS, especially when they have complex infections, have somewhere between a 30 and 50 percent chance of mortality during the course of their 28 their first 28 days in an icu um to have to be able to survive 28 days especially in the setting of very severe um pan-resistant organisms i think um is provocative as jen said these are just unrandomized patients we're reporting the results of this just as a preliminary in a preliminary manner but I think that we feel confident that going into the randomized portion of this clinical trial agent 797 added the very best standard of care has certainly established already a suggestion that the modification of the immune system, the restoration of barrier protection, the reinvigoration of an immune response in a patient who's critically ill may have some really distinct benefits over and above what we do every day to try to get these patients through their critical illness.

Thank you for the details.

Our next question comes from the line of Mayank, Momtani, with B. Riley Securities. Your line is open.

Yes, good morning. thanks for taking your questions and you know appreciate the level of detail on pipeline progress so on the same ARDS lung injury trial if you could maybe comment on how many patients have been dosed and randomized in this randomized portion to date I believe you have a 90 patient target and maybe if you can comment on the enrollment rate as you see in both Ukraine but also as FDA sites come on board, you know, your expectation for U.S. enrollment. And are there any phenotype inflammation pattern differences you expect in ex-U.S. versus U.S. patients? If you could comment on that.

Mark, thank you for the question. So the study is currently underway in Ukraine and expanding into the United States. We haven't spoken to specific numbers of patients enrolled at this time. Enrollment is continuing. We expect to have our preliminary readouts from the randomized phase two portion of the study in the first half of 2027. So we're expecting to continue enrollment at a rate that is consistent with the sites that are selected for this study. and particularly with seasonality, we do see upticks in enrollment as well for obvious reasons in this program. So we would expect to have between four to eight patients per site per month when all of the sites are actively enrolling. We have our center in Ukraine that's actively enrolling in our centers in the U.S. that will start enrollment in September. I think you had asked, so I should also mention, for this program, we are intending and seeking a meeting with the FDA in order to move the trial from our randomized phase two into a seamless phase three study. So we'll be able to share an update on that in subsequent calls. We have not had the meeting yet, but we are preparing to do so within the impending weeks. And that will allow us to generate data from the phase one, I'm sorry, from the randomized phase two, and then move directly into the confirmatory phase three in a very rapid fashion. And from the immune, I think you had asked about the differences in the patient population. What Therese had mentioned is the patients who have been treated in Ukraine have multidrug-resistant pathogens, and these are pretty severe and it's a major problem in areas of war. As patients traverse from one destination to the next, they generally succumb to multidrug-resistant organisms. And in Ukraine, there are some recent publications showing that about 100% of these individuals are succumbing to multidrug-resistant pathogens. So it is an opportunity for us and our colleagues that have quite a bit of interest from the military to evaluate what these cells can do in that setting as well. So essentially respiratory distress coming from multidrug-resistant pathogens in addition to some other complications, as Dr. Hammond mentioned. Will that be the same in the United States? I believe that the profile may be a little bit different, and I'll ask Dr. Hammond to weigh in on her perspective. She's treated a number of patients with Agent 797 in her ICU, so she could speak to the profile of patients that she's expecting to see in the United States.

Yeah, no, absolutely, and thank you for the question. I think that what struck me at the NHSRS meeting that we were in, that we recently attended, was just the fact that these very virulent, multi-drug-resistant organisms are traveling from sort of point of injury across the evacuation path for both combatants and non-combatants in conflict zones, and now spreading across Europe. And I think all of us feel like it's only a matter of time, especially as conflicts escalate, before we start to see emergence of more of these really, really virulent organisms. And their grand negative, Klebsiella, which is pan-resistant to all antibiotics, Acinetobacter, Pseudomonas, those are the big three that are really affecting conflict zones in Ukraine and beyond. and also infiltrating tertiary hospitals in Europe. So this is a really big problem. I treat patients in Central California. We do see resistances to antibiotics in patients that have been in the hospital for long periods of time that are coming to us from nursing homes. I may see one or two cases of hand-resistant Klebsiella, for example, a year. In these patients that have been ill for a long time, usually on chronic ventilator therapy, I am not used to having young people come in from the community and acquiring these very virulent infections, even by the time they've been in the hospital for 24 or 48 hours or been intubated for 24 or 48 hours. So it's a very different pattern that we're seeing in Ukraine. As Jen said, I think this is an opportunity for us to look deeply at the immunology of the host when they're exposed to these virulent antibiotic or antibiotic-resistant organisms. I hope that we don't see them to the same extent that we're seeing in the Ukraine as we open up the U.S. sites, but I think that this is on the horizon for all of us and something that we have to take very seriously, the more science we can put behind the management of these pan-resistant infections, the better off we are as a medical society, whether it's here in the U.S. or abroad.

Thank you for all that, Peller. And would you expect phase three population focus to be very comparable to span-resistant that you're talking about? And I was also wondering the acute endpoints used here, you know, at some point would make placebo control unethical so is there like a randomization ratio you could look differently in phase three than phase two uh and and lastly if you could comment on any you know process-wise data sharing practices with dod bada i know you mentioned fda but was just curious how how you know dod is involved here thanks i'll start here um so the population we would expect to be to be comparable um to our phase two population.

So the results in the phase two will also give us an opportunity to conduct a sample size re-estimation. So with the, we're looking at a primary endpoints that include 28-day mortality, and that's an FDA-driven endpoint. We're also, of course, looking at other secondary endpoints, ventilator-free days, pathogen control, immune reconstitution, and et cetera. I won't speak too much to some, at this point, it would be premature to speak about some of our government interactions, but I could share with you that our appointed, we have a newly appointed board member, Dr. John Holcomb, who's a trauma surgeon and also essentially very actively involved in driving improvements in medical care specific to conflict zones, military personnel, and, of course, the Bridge to Civilians. His work has recently led to the approval of plasma as a product for resuscitation in patients. who's an incredible scientist and very thoughtful strategic leader and partner for us. And the work that we're doing, as Therese mentioned, because of the increase in the number of conflict zones that we have internationally and then also the exposure as we move patients from different regions, we're seeing a spread of these multi-drug resistant pathogens. and that includes patients traversing from Ukraine into hospitals in Europe and beyond. So improving outcomes for these patients will help to strengthen our national security overall, and that's a major interest for all of us.

Got it. And if I may just ask about the Brazil PAID program, maybe just the rationale for choosing that geography, And if you could, to the extent possible, comment on, you know, pricing, how you're seeing demand, both locally, and I'm sure other regions are also interested in this. Any thoughts on that, Jen?

Thanks, Mayank. Absolutely. So this program launched in Brazil due to a number of physician inquiries and the speed with which the regulators moved there. We're expanding the program as we do see increasing demand during this time. So we won't yet speak to pricing, but I'll share with you that we have launched the program. It's active, and we have patients in, and we will be reporting that those patients were brought in just after the close of the quarter. So we'll be announcing some of the financials in our Q3 update. In the meantime, I would say we're enabling access. We have an incredibly efficient manufacturing process, and it does allow us to convey some of those efficiencies to patients that have a broad – our requests are pretty broad for patients who are coming in. Some patients are requesting those patients with cancer as well as patients with other indications. So as the program expands, we'll speak more to the detail of it. the regions will be expanding and will announce those expansions as we get through the regulatory processes in different territories.

Thank you so much. Looking forward to the talk. Of course.

Thanks, Ryan.

And again, if you would like to ask a question, press star, then one. To withdraw, press star, then one again. There are no further questions at this time. This concludes the Q&A session. I will now turn the call back to Dr. Jennifer Buell for closing remarks.

Thank you, operator. Thank you all for participating. I appreciate your support. We look forward to keeping you in the loop and with upcoming developments on the program. Thank you.

This concludes today's call. Our replay will be available in the events and presentation section of our investor website at https colon double slash investor dot mink therapeutics dot com slash events and presentation. Thank you for participating. You may now disconnect.