管理層發言
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 Stefanie Perna-Nacar from MiNK Therapeutics, MiNK Investor Relations. Stefanie, 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 SEC 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. Terese Hammond, Head of Development, 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?
Thank you, Stefanie. 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 two 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 infection. There remains 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 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, it does not require patient-specific manufacturing, HLA matching, or lymphodepletion. And that last point is biology rather than logistics. iNKT cells recognize lipid antigens presented by 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, and critically ill mechanically ventilated patients in that setting place 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. Terese Hammond presented the initial observations from the first patients treated with agenT-797. The MHSRS symposium is the Department of Defense'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. Importantly in war, and specifically in Ukraine, a high proportion 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 infection. The serum and bronchoalveolar 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—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 and the randomized portion is actively activated, 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 named-patient access program. This program launched in Brazil 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. MiNK 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-1300-02 will be directed to the study. This program 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 pathogen suppression, lung immune restoration, and activation of tissue repair pathways following treatment with agenT-797 and the IL-15 superagonist N-803 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 different and context-dependent immune responses depending on the disease environment. We observed immune activation in cancer and inflammation-regulating activity in patients with ARDS without genetic engineering. 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.
In cancer, our phase 2 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 botensilimab and balstilimab with an induction strategy associated with long-term 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. 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 $0.62 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 $7.0 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. This modest increase was specific and deliberate, reflecting the cost of operationalizing our randomized phase two study, activated and initiated in the Lviv site. We completed the regulatory work supporting Ministry of Health authorization, dosed the first patients, and laid 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 two 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-dilutive funding; both the graft-versus-host disease trial at University of Wisconsin and the pediatric PRAME program are externally funded. 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 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 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 and an off-the-shelf product that can reach critically ill patients without patient-specific manufacturing, and a paid named-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-1300-02, activate our U.S. sites, expand the comparative clinical and biologic data set, and execute our named-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.
分析師問答
Thank you. And our first question comes from the line of Emily Bodnar with H.C. 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 could walk 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. I guess, how confident are you that the day 28 survival that you've observed is due to agenT-797? Thank you.
Hi, Emily. Thanks so much for the question. 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 hypoxia and pneumonia, and they meet the global definition of acute respiratory distress syndrome. So this is all-cause pneumonia; these patients could have a virus or trauma or other complications that lead to hypoxemic pneumonia. In this study, we have a run-in scheduled for about 10 patients where all patients received the cell therapy, and then we launched the randomized portion of the study. We presented data on those patients that did receive the cell therapy, and these were the first two patients treated in the study. The first was a 41-year-old female with poorly controlled diabetes and pneumococcal sepsis. I can have Dr. Hammond, if you're available, share the case details and speak both to the profile of the patients and to your expectations on how they might have done without the cells.
Yes, of course, Jen, and thank you for the question, Emily. As Jen said, these are adults. We're trying to decrease the amount of exclusion criteria, so these are folks with moderate to severe hypoxemic pneumonia, and they can also have coexisting trauma. 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 multidrug-resistant pneumonia from the very moment that they were intubated, so before they were even treated. In the most simplistic terms, patients with moderate to severe ARDS, especially when they have complex infections, have somewhere between a 30% and 50% chance of mortality during the course of their first 28 days in an ICU. To be able to survive 28 days, especially in the setting of very severe pan-resistant organisms, I think is provocative.
As Jen said, these are unrandomized patients and we're reporting the results in a preliminary manner. But I think we feel confident that, going into the randomized portion of this trial, agenT-797 added to the very best standard of care has already suggested that modification of the immune system, restoration of barrier protection, and reinvigoration of an immune response in a critically ill patient may have distinct benefits over and above what we do every day to try to get these patients through their critical illness.
Our next question comes from the line of Mayank Mamtani with B. Riley Securities. Your line is open.
Yes, good morning. Thanks for taking my questions and I appreciate the level of detail on pipeline progress. On the same ARDS lung injury trial, could you comment on how many patients have been dosed and randomized in the randomized portion to date? I believe you have a 90-patient target and maybe you can comment on the enrollment rate as you see it in both Ukraine and as FDA sites come on board, and your expectation for U.S. enrollment? Also, are there any phenotype or inflammation pattern differences you expect in ex-U.S. versus U.S. patients?
Thank you for the question. 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. We're expecting to continue enrollment at a rate consistent with the sites selected for this study. Particularly with seasonality, we do see upticks in enrollment, so we would expect to have between four to eight patients per site per month when all sites are actively enrolling. We have our center in Ukraine that's actively enrolling and our centers in the U.S. will start enrollment in September. We are intending to seek a meeting with the FDA in order to move the trial from our randomized phase II into a seamless phase III study. That will allow us to generate data from the randomized phase II and then move directly into the confirmatory phase III in a very rapid fashion.
We have not had the meeting yet, but we are preparing to do so in the impending weeks. Regarding differences in the patient population: as Terese mentioned, the patients treated in Ukraine have multidrug-resistant pathogens, which are quite severe and a major problem in areas of conflict. Recent publications show high prevalence of multidrug-resistant pathogens in those injured in that setting. It's an opportunity for us and our colleagues within the military to evaluate what these cells can do in that context. Will the profile be the same in the United States? I believe the profile may be a little different. I'll ask Dr. Hammond to weigh in on her perspective—she's treated patients with agenT-797 in her ICU and can speak to the profile she expects to see in the U.S.
Yes, absolutely. What struck me at the MHSRS meeting was that these very virulent, multidrug-resistant organisms are traveling from the point of injury across evacuation paths for both combatants and non-combatants in conflict zones and now spreading across Europe. I think it's only a matter of time, especially as conflicts escalate, before we start to see emergence of more of these virulent organisms. Gram-negative organisms—Klebsiella, which can be pan-resistant to all antibiotics, Acinetobacter, and Pseudomonas—are the big three affecting conflict zones in Ukraine and beyond, and they are infiltrating tertiary hospitals in Europe. This is a really big problem. I treat patients in Central California. We do see antibiotic resistance in patients who have been in the hospital for long periods or in nursing homes; I may see one or two cases of pan-resistant infections a year. I'm not used to having young people come in from the community and acquire these very virulent infections before they've been in the hospital 24 or 48 hours.
By the time they've been hospitalized or intubated for 24 to 48 hours, it's a very different pattern that we're seeing in Ukraine. I think this is an opportunity to look deeply at the host immunology when exposed to these virulent antibiotic-resistant organisms. I hope we don't see them to the same extent in the U.S. as we open sites, but I think this is on the horizon and something we must take very seriously. The more science we can put behind the management of these pan-resistant infections, the better off we will be as a medical society, whether here in the U.S. or abroad.
Would you expect the phase III population focus to be comparable to the pan-resistant population you described? And I was also wondering about the acute endpoints used here: at some point would making the trial placebo-controlled be unethical, so is there a possibility of changing the randomization ratio in phase III versus phase II? Lastly, could you comment on any process for data-sharing practices with DoD or BARDA? I know you mentioned the FDA, but I'm curious how DOD is involved here.
Thanks, Mayank. I'll start. The population we would expect to be comparable to our Phase II population, and the results in Phase II will give us an opportunity to conduct a sample size re-estimation. We're looking at a primary endpoint that includes 28-day mortality, which is an FDA-driven endpoint. We are also looking at secondary endpoints such as ventilator-free days, pathogen control, and immune reconstitution. It's premature to speak to some of our government interactions in detail, but we do have a newly appointed board member, Dr. John Holcomb, who is a trauma surgeon and very actively involved in improving medical care specific to conflict zones, military personnel, and civilian care—his work has led to approvals for important resuscitation products. He's an incredible scientist and strategic leader and partner for us. Because of the increase in conflict zones internationally and patient movement, we're seeing the spread of multidrug-resistant pathogens, including patients traversing from Ukraine into hospitals in Europe and beyond. Improving outcomes for these patients will help to strengthen public health and national security, which is of interest to many stakeholders.
Got it. And if I may just ask about the Brazil paid program: maybe you could explain the rationale for choosing that geography and, to the extent possible, comment on pricing, how you're seeing demand locally, and whether other regions are interested?
Thanks, Mayank. The 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 see increased demand. We won't speak to pricing yet, but the program is active and we have patients in; some patients were brought in just after the close of the quarter, and we'll be reporting those patients in our Q3 update. We're enabling access; our efficient manufacturing process allows us to have inventory that supports clinical development and responsible access. Requests have come from patients with cancer as well as those with other serious conditions. As the program expands, we'll provide more detail and announce expansions as we complete regulatory processes in new territories.
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 on upcoming developments in the program. Thank you.
This concludes today's call. Our replay will be available in the Events and Presentations section of our investor website at https://investor.minktherapeutics.com/events-and-presentations. Thank you for participating. You may now disconnect.