MiNK Therapeutics, Inc.

Good morning and welcome to NK 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 Perdenacar from NK Therapeutics, NK 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 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, Stephanie. Good morning, and thank you for joining us. The second quarter was an important period of execution for MNIC. 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. 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 C1300-02. This is our randomized phase two 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 dose 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. Terese 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 multi-drug 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. They're 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. NNK 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 C13002 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 and 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 super agonist 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 two 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 botanosilumab and balsilumab 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.