MiNK Therapeutics, Inc.

Good morning and welcome to Mink Therapeutics' first quarter 2026 conference call and webcast. All participants will be in a listen-only mode until their question and answer session. Please note this event is being recorded, and I would now like to turn the conference over to Stephanie Perinanakar from 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 SEC filings, also available on our website, for a detailed description of these risks. Joining me today are Dr. Jennifer Buhl, President and Chief Executive Officer of NECARE Tutics, Dr. Teres Hammond, Head of Development, and Melissa Orleal, Principal Financial Officer. I'd like to turn the call over to Dr. Buhl to highlight our progress from this quarter. Jennifer? Thank you, Stephanie. Good morning, everyone, and thank you for joining us today. Over the past several weeks, we've presented data at four major international scientific meetings, beginning with findings in pulmonary fibrosis at the Keystone Symposium in February, followed by a presentation of our Phase II clinical data in refractory gastric cancer at AACR in April. And most recently, in fact, just earlier this week, we presented mechanistic findings at the American Society for Gene and Cell Therapy showing the context-dependent immune activity of invariant metastatic T cells in cancer and severe lung injury. We're also very excited that next week, Dr. Therese Hammond, our head of pulmonary inflammatory diseases, will present at the American Thoracic Society Conference, the international conference in Orlando, Florida, and she'll describe a combination of our invariant natural killer T cell technology, agent 797, in combination with an IL-15 super agonist named Anceva, and the modulation of dysregulated inflammation and pathogen clearing responses in severe pulmonary fungal infection. Taken together, These presentations describe an increasingly coherent biologic and clinical story around IMKTs in cancer, severe lung injury, fibrosis, and immune dysfunction overall. For those newer to MINK, our focus is on the development of off-the-shelf IMKT cell therapies designed to repair dysregulated immune biology in diseases characterized by immune failure, inflammatory injury, and impaired pathogen control. And unlike conventional cell therapy, 797 is administered without lymphodepletion or HLA matching. In the approximately 100 treated patients to date, we've observed a favorable safety profile together with increasingly reproducible biologic and clinical observations. And what continues to distinguish this platform is its clinical activity and its practicality. At Mink, we believe we've addressed many of the barriers that have historically limited the broader application of cell therapy. These include manufacturing complexity, scalability, timing, and deployability in acute care settings. As a result, we are now able to evaluate our living medicines and diseases in clinical environments that were previously impractical for cell therapy due to operational complexity and cost. Now that same practicality is central to how we're expanding our platform through selective partnerships. In the first quarter of this year, we announced that collaboration would see further to advance our frame-targeted PCR-engineered IMKT cell therapy for pediatric cancers. This program's important, not only because it brings non-diluted support and potential meaningful commercial economics, but also because it applies our off-the-shelf INKP platform to a setting where speed, tolerability, and access matter profoundly. For children with aggressive cancers, delays from individualized manufacturing and intensive pretreatment can be especially challenging. To see further collaboration allows us to extend MINK's platform into a validated tumor antigen strategy while preserving our focus and capital discipline. Now, I'll summarize our recent core data presentation before turning it over to Dr. Hammond. At AACR in April, investigators from Memorial Sloan Kettering presented data from our Phase II study in gastroesophageal cancer. This trial is an investigator-sponsored trial led by the Division Chief, Dr. Yelena Janjigian, and her colleague, Dr. Sam Sattar. The population was heavily pretreated, checkpoint refractory, with historically poor expected outcomes and limited therapeutic options after failure on prior first-line therapy. We observed prolonged survival in patients who received induction immune therapy prior to chemotherapy, including emergence of a meaningful tail of the survival curve. Now, these were patients whose expected survival is measured typically in months, yet here, median overall survival extended beyond 23 months in the immune-primed cohort. And several patients remain alive years after dosing. In refractory gastric cancer, that is highly unusual. What's become increasingly important to us over time is not simply whether transient responses occur, but whether coordinated modulation of dysfunctional immune biology can actually fundamentally alter long-term disease trajectory and survival in patients with otherwise limited therapeutic options. As follow-up continues to mature, and this includes follow-up from our Phase 1 trial, we observed durability of survival in multiple tumor types, and that includes gastric cancer, thymoma, renal cell carcinoma, and germ cell cancers. Importantly, These observations were accompanied by translational findings that show coordinated modulation of the tumor microenvironment, including activation of important tumor-killing immune pathways, restoration of exhausted immune responses, and remodeling of suppressive myeloid biology. And increasingly, these intrinsic immune-modulating properties appear to connect directly with the biology that we are now observing in inflammatory lung injury and ARDS. At the American Cell Gene and Cell Therapy Conference this week in Boston, Dr. Yan Sun from our team presented translational analogies from patients with cancer and ARDS treated with the same donor-derived 797 product. This is very important. We observed distinct immune outputs depending on the disease environment. Now, this supports our belief that INKT cells participate in modulating immune biology across profoundly different disease states. Again, the same donor-derived product manufactured through our GMV process produced profoundly different immune biology in very different disease settings. In cancer, the biology showed a Th1-oriented tumor-killing cytotoxic immune activation. While in severe lung injury, the profile shifted towards restoration associated immune signaling, and Dr. Hammond will go into this in more detail. Importantly, these observations emerged, again, from the same unmodified allogeneic product. Yesterday, we announced the initiation of our randomized Phase II clinical trial. evaluating 797 in combination with standard of care versus placebo standard of care in patients with severe acute lung injury and respiratory distress identified using globally recognized ARDS criteria. This study has been carefully designed with endpoints and operational infrastructure that we believe will not only validate the observations in our earlier Phase I-II study, and if prospectively confirmed, support rapid development through a seamless Phase 2-3 pathway integrated already into the protocol framework. This structure allows us to move very efficiently from validation of our earlier observations into a potential registrational development strategy without interruption between phases of development. We expect to speak with the FDA in the impending weeks on our trial design and development plan. The need for new medications is significant. Acute lung injury and ARDS remain among the most serious unresolved conditions in critical care. ARDS affects an estimated 3 million people globally and approximately 200,000 people annually in the United States, accounting for about 25% of mechanically ventilated ICU patients. Mortality remains very high. Approximately 40 to 50% of patients die from their disease. Despite decades of research, development of medicines for patients with this critical pulmonary problem, or ARDS, has been challenged by biologic heterogeneity and the complexity of prolonged illness. Higher approaches, including mesenchymal stromal cell, or MSC therapies, demonstrated feasibility and a favorable safety profile, but failed to consistently improve survival in randomized studies. and in part because broad immunosuppressive or paroxysmal approaches may be insufficient in patients who simultaneously require modulation of an injurious inflammation together with preservation of pathogen-clearing immune function. And we believe, based on our observations, that INKT cells, and specifically HS797, may represent a fundamentally different biologic approach. Unlike MSCs, INKTs are active, immune-affected cells capable of localized modulation of inflammatory signaling together with coordinated activation of innate and adaptive immune pathways, including the ability to clear systemic pathogens. Our intended target population are patients who can be identified clearly, characterized biologically, and stratified thoughtfully using globally recognized clinical and physiologic criteria. That matters from both a regulatory perspective as well as a clinical perspective. Critically, the patient population is the population where we believe we have already observed meaningful biologic and clinical signals, both in our clinical trials and through continued emergency use experience in critically ill patients who have few remaining therapeutic options. And our findings have emerged in real-world ICU environments, and specifically Dr. Hammond is operating in those environments daily, and she was the lead investigator on our trial. And through the data that we've now published and what we expect to see in the future is that we've observed evidence of local immune modulation within the lung, together with reductions in harmful inflammatory signaling and reduction in secondary infections. And Dr. Hamm will speak more about this shortly. I want to highlight an important component of this effort. It's part of a partnership that we've developed with First Lviv Territorial Medical Union and Unbroken Ukraine. Our study has been approved by the Ukrainian Ministry of Health and now clears the U.S. FDA for dosing. And our team has had the opportunity to spend on-site, time on-site, evaluating the hospital, talking with the team, meeting with the critical care team, discussing their capabilities. We also reviewed the translational infrastructure and, most importantly, the patients. And what we observed was remarkable. The clinical sophistication and quality of care being delivered under unimaginably difficult wartime conditions was incredible. And we believe this collaboration creates an opportunity to evaluate INTP-based cell therapies in patients where the biology is particularly relevant and increasingly common in modern warfare and critical care medicine. Modern conflict is increasingly producing survivors after devastating injury. But survival is accompanied by complications including multidrug-resistant pathogens, chronic inflammatory issues, and downstream fibrosis. Programs such as BARDA-funded BREATHE program have demonstrated that appropriately targeted anti-inflammatory intervention can improve survival in patients with severe respiratory compromise. But we believe the next evolution are therapies capable not only of dampening harmful inflammation, as we've observed with 797, but also restoring immune coordination and pathogen control in patients with critical illness and immune exhaustion. Changing the trajectory of disease in these populations is becoming increasingly important, not only to clinicians, but also to governments and global health systems. Our program also demonstrates the practicality of an off-the-shelf approach in a real-world critical care setting. These environments where complex individualized manufacturing are simply not feasible. The ability to deliver cryopreserved allogeneic therapy rapidly without lymph depletion or easily matching is operationally important. And as I've mentioned, the trial is now clear to proceed by the Ministry of Health in Ukraine as well as by the U.S. FDA. And we're proud to support this initiative alongside physicians and humanitarian leaders, and we're grateful to contribute to this important effort at a time when it's so urgently needed. Now, as I prepare to turn the call over to Dr. Hammond, I want to highlight next week's presentation at the International American Thoracic Society meeting where Dr. Hammond will present findings involving the combination of INKT therapy with N803 or INTIVA and IL-15 superegonus in development and commercial development with our colleagues at Immunity Bio. Importantly, these findings further expand the potential applicability of INKT biology in disease settings characterized by persistent infection, immune dysregulation, and severe inflammatory injury. Operationally, we're continuing to advance our programs at the level of capital efficiency that's uncommon in cell therapy, combining disciplined internal execution, scalable manufacturing infrastructure, and non-dilutive support through government and institutional partnerships. As I mentioned earlier in the first quadrant, the strategy was reflected, and I see further collaboration support in the development of our frame-targeted PCR INTT program pediatric cancers, providing non-dilutive support for IND-enabling activities together with potential downstream commercial participation. Our randomized Phase II trials that we've mentioned and announced just yesterday has also been designed with a highly efficient operational infrastructure, leveraging substantial internal capabilities together with some experienced local support on the ground, allowing us to execute a global randomized study while maintaining a very disciplined capital essentially cash burn profile. As a result, we believe our current cash position provides operational runway for at least the next 12 months, inclusive of the launch and continued execution of the randomized trial that we've mentioned this morning. I'll now turn the call over to Dr. Therese Hammond. Therese?