MiNK Therapeutics, Inc. (INKT) Earnings Call Transcript

Good morning and welcome to MiNK Therapeutics' first quarter 2026 conference call and webcast. [Operator Instructions] Please note this event is being recorded, and I would now like to turn the conference over to Stefanie Perna-Nacar from 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 of MiNK Therapeutics, 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.

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 of Gene and Cell Therapy, showing the context-dependent immune activity of invariant natural killer T cells in cancer and severe lung injury. We're also very excited that next week, Dr. Terese Hammond, our head of pulmonary inflammatory diseases, will present at the American Thoracic Society 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 superagonist named Anktiva, 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 iNKTs, severe lung injury, fibrosis, and immune dysfunction overall. For those newer to MiNK, our focus is on the development of off-the-shelf iNKT cell therapies designed to repair dysregulated immune biology in diseases characterized by immune failure and stress, inflammatory injury, and impaired pathogen control. And unlike conventional cell therapy, agenT-797 is administered without lymphodepletion or HLA matching. From 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 costs. 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 the collaboration with C-Further to advance our PRAME-targeted, TCR-engineered iNKT cell therapy for pediatric cancers. This program is important not only because it brings non-diluted support and potential meaningful commercial economics, but also because it applies our off-the-shelf iNKT 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. The C-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. E. Elena Janjigian, and her colleague, Dr. Sam Patan. 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 immunotherapy 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 I 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 Society of Gene and Cell Therapy Conference this week in Boston, Dr. Young Soon from our team presented translational analyses from patients with cancer and ARDS treated with the same donor-derived agenT-797 product. It's 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 GMP process produces 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 agenT-797 in combination with standard of care versus placebo plus 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 II-III 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 plans. 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 U.S., 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. Prior 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 paracrine 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 agenT-797, may represent a fundamentally different biologic approach. Unlike MSCs, iNKTs are active immune effector 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 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. Hammond 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 cleared by the U.S. FDA for dosing. And our team has had the opportunity to spend time on site evaluating the hospital, talking with the critical care team, discussing their capabilities. We also reviewed the translation 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 is incredible. And we believe this collaboration creates an opportunity to evaluate iNKT-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 the 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 agenT-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, environments where complex individualized manufacturing are simply not feasible. The ability to deliver cryopreserved allogeneic therapy rapidly without lymphodepletion or HLA matching is operationally important. And as I've mentioned, the trial is now cleared 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 N-803, or Anktiva, an IL-15 superagonist in development and commercial development with our colleagues at ImmunityBio. 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 with 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 quarter, the strategy was reflected in our C-Further collaboration supported the development of our PRAME-targeted TCR-iNKT program for 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 cash burn profile. As a result, we've looked at the results, 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. Terese Hammond.

Thank you, Jen, and good morning, everyone. I want to begin by discussing the actual patients we're enrolling in our Phase II-III study, because I believe understanding the intended target population is critically important to understanding both the scientific rationale and the potential regulatory trajectory of this program. Patients with severe hypoxic respiratory failure all require some form of respiratory support, be it high-flow oxygen, noninvasive ventilation, mechanical ventilation, or the most intense form of lung support, extracorporeal membrane oxygenation, or ECMO. They meet globally recognized criteria for acute respiratory distress syndrome and severe lung injury, including profound oxygen impairment, inflammatory lung damage, and all are at substantial risk for prolonged respiratory failure and mortality. Importantly, these patients represent a real-world, critically ill population. Some present with highly hyperinflammatory disease, elevated cytokine signaling, diffuse alveolar injury, endothelial dysfunction, and rapidly progressive respiratory collapse. Others evolve into profoundly hypoinflammatory or immunologically exhausted states characterized by impaired pathogen clearance, secondary infection, prolonged ventilator dependence, fibrosis, and multi-organ dysfunction. From a clinical and regulatory perspective, distinguishing these distinct populations of patients matters, because therapies that broadly suppress inflammation may behave very differently depending on whether a patient is in an active hyperinflammatory phase versus an immunologically exhausted phase of disease. One of the reasons our earlier observations captured our attention is because agenT-797 appeared to function in both scenarios. As a practicing pulmonary critical care physician, what stood out to me, what has always struck me, has been that it's not simply inflammatory improvement that we see through using these cells, but a combination of inflammatory modulation together with evidence of immune recovery and pathogen control. Many patients with severe respiratory distress don't die solely from early inflammatory injury; they die later from persistent respiratory failure, healthcare-acquired multidrug-resistant infections, opportunistic fungal infections, immune exhaustion, and progressive organ dysfunction. When we see profound depletion or exhaustion of critical immune populations in severe disease states, the path forward becomes increasingly logical. We just need to restore what's missing. That's particularly relevant in modern critical care environments, including wartime medicine. In Ukraine, clinicians are managing highly complex patients with trauma-associated respiratory failure, prolonged ICU stays, resistant bacterial and fungal infections, and severe inflammatory injury, and these conditions are occurring simultaneously. These are highly relevant populations for understanding how immune restoration therapies may function and benefit patients. The translational findings we presented at ASGCT this week provided important biologic basis for these observations. In ARDS patients, the same donor-derived agenT-797 product is associated with restoration-oriented anti-inflammatory cytokine signaling, including interleukin-4 and interleukin-13. Contrast that to oncology patients, where the cytokine profile was distinctly different with pro-inflammatory TH1-associated interferon-gamma activation and cytotoxic immune engagement. Importantly, these divergent responses of agenT-797 emerged without disease-specific engineering or modification. These data suggest the cells may retain the ability to respond dynamically to the immune environment they encounter. At ATS next week, I'll present a patient with persistent Coccidioides immitis infection treated with agenT-797 and N-803, or Anktiva. This case amplifies the observations we've seen with a case of immune dysfunction and persistent inflammatory injury where conventional antifungal therapy and corticosteroids have not been sufficient. Following treatment, we observed evidence of both inflammatory stabilization and progressive fungal pathogen clearance. This is important because it reinforces a broader clinical question emerging across pulmonary and critical care medicine: in some forms of severe respiratory disease or critical illness, does immune failure itself become the dominant biology? That question is increasingly relevant, not only for ARDS, but potentially for trauma-associated lung injury, severe infection with multi-organ failure, fibrosis, and broader disorders of immune dysregulation. The reason many of us are excited about invariant natural killer T cell biology is not because it simplifies these complex diseases; it's because the biology appears increasingly capable of operating within this complexity. So I'll stop there. Thank you for your time and attention. And I'd like to turn the call over to Melissa Orilall to review our financials. Melissa?

Thank you, Therese. Operationally and financially, the first quarter reflected continued disciplined execution as we advanced multiple clinical and translational programs simultaneously. We ended 2025 with approximately $13.4 million in cash and cash equivalents, and subsequently completed the repayment of approximately $5.2 million associated with the Agenus convertible note during the first quarter of 2026. This further simplifies our balance sheet as MiNK advances into randomized clinical execution. Following this repayment, in the three months ended March 31, 2026, we raised approximately $3 million through our at-the-market sales agreement, resulting in a quarter-end cash balance of approximately $9.5 million. Importantly, while continuing to advance a randomized ARDS development program, translational oncology initiatives, and next-generation iNKT platform programs, we continue to operate with a level of capital efficiency that is truly uncommon within the cell therapy sector. As Jen highlighted earlier, our randomized ARDS program benefits from substantial internal execution capabilities combined with experienced local CRO support and established clinical infrastructure in Ukraine. This enables us to execute a global randomized study with a highly disciplined and efficient cost structure. As such, based on our current operating plan, we believe our cash position provides a runway for at least the next 12 months, including the initiation and continued execution of our randomized clinical trials. The net loss for the first quarter of 2026 was approximately $2.7 million, or $0.57 per share, compared to approximately $2.8 million, or $0.70 per share, for the same period in 2025. Overall, these results reflect our focused investment strategy in advancing the agenT-797 clinical program while maintaining disciplined control over operating expenses and prioritizing programs with clear translational, clinical, and regulatory pathways. With that, I'll turn the call back to Jen for closing remarks.

Thank you so much, Melissa and Dr. Hammond. For us at MiNK, this is an incredibly exciting time. With some announcements that have just recently come out over the past few weeks, we have now moved from early signal generation towards really durable mechanistic validation, which is incredibly exciting. This is exactly where we want to be at a time when we can now take our pharmacologic findings, our clinical and immunologic findings, and apply them to a registration path that we believe will not only validate our earlier observations, but also set us up for a more rapid path to bring solutions to patients who are critically ill. Now just quickly, at AACR we presented prolonged survival in patients with refractory gastric cancer. We'll continue to follow those patients and we'll be providing an update on next steps for our gastric cancer program in the future. At the Cell and Gene Therapy Conference just this week, we demonstrated that the same unmodified product produced distinct immune output across cancer and ARDS. This secures not only our manufacturing process, but also amplifies the scalability and the opportunity. Our team has already generated the material needed for the majority of our clinical program, which means we do not expect to have substantial manufacturing burns prospectively. Next week at ATS, very important evidence supporting the potential role of immune restoration and persistent pulmonary infection, which we think will have broad application and additional data and plans will follow after that presentation. And of course, most excitingly, yesterday, the announcement of the initiation of our randomized Phase II trial is going to set us up for a clinical program, which we believe will have a substantial amount of data during the second half of this year, so before the end of this year. And we will expect to present preliminary findings also in the second half of this year, which we're incredibly excited about. So for us, the path is really clear. We've got to execute on our randomized study. Most importantly, prepare to generate, produce, and present some data from that program by the end of this year. We'll continue to interrogate biology rigorously and contribute to science as we have continued to do. Our scientific team is just so humbling and impressive, and I couldn't be more excited to work with such a tremendous group of individuals. And we'll now continue to evaluate our observations and the translation of those observations to meaningful clinical outcomes for patients who are critically ill. So thank you again for joining us this morning.

[Operator Instructions] Your first question comes from the line of Mayank Mamtani from HC Wainwright. Please go ahead.

Hi, good morning. Thanks for taking the questions and congrats on all the progress. Maybe start with the ARDS trial. Can you disclose how many patients you're enrolling in each of the arms you discussed? And then, given your guidance for initial data in the second half of this year, maybe just touch on what endpoints you expect to have by that time point. And then separately on the ImmunityBio collaboration that you discussed, can you talk about kind of the basis in terms of the collaboration and also what trials you're currently evaluating with their Anktiva?

Hi, Emily. Thanks so much for your questions and your continued support. Regarding the trial, the randomized phase two trial, so we're designing the trial right now and speaking with the agency in a matter of just a couple of weeks to expand from the phase two, which is about 90 patients, randomized phase two, and it's a one-to-one randomization going into a seamless phase three, which will be only based on the effect estimates that we have observed and that we expect to observe in the randomized part of the trial. We believe that the extension into the randomized phase three will be a very consolidated group of patients. So we'll be back with the total number and the updated data on ClinTrials at that time after the interactions, but for the randomized phase two, 90 patients split at a one-to-one randomization. These are patients that are in the ICU and patients that will be all treated with standard of care. And we'll have agenT-797 on top of standard of care versus placebo on top of standard of care. Regarding the data presented next week at ATS, of course, there are some limitations to what we could say today, so we're looking forward to providing a deep dive into the data, as well as a broader look at how we came to this combination with our colleagues at ImmunityBio, the observations that we had and what our plans are to develop the program further in a very difficult to treat—and I'm going to ask Dr. Hammond to speak a little bit about this. Fungal pneumonia is a substantial problem and it's a growing problem. It's increasing in incidence and prevalence in the United States. It's endemic in certain regions and territories in the U.S., particularly those arid climates. We're seeing a growing number of individuals affected by this very difficult to treat fungus. And there has also been some news around this particular technology as the possible biologic threat, which there are currently no treatments for fungal pneumonia. The data that we will be presenting will help to elucidate mechanisms that we believe are going to be really important in mitigating any problem with respect to this type of exposure. While this is a case study that will be very conservative about how we interpret the findings, the mechanisms are very clear, and based on what we've observed in respiratory distress overall, as well as now this particular study data to be presented, we think that there's an important opportunity here to help patients with a critical and growing unmet need that's really specific to this particular pathogen. And this is where we will share some more detail about the work that we have underway with ImmunityBio. And I'll turn it to Therese to speak just a moment about fungal pneumonia just as a setup but without disclosing any of the data under embargo for ATS.

Yes, thank you, Jen, and—and Emily, thank you, as Jen said, for your continued support. Fungal pneumonia, specifically Coccidioides immitis, is an increasing threat. So cocci, or it's sometimes called valley fever, has really spread across the western United States. It's extending actually into some of the states in the northwest. So a very formidable challenge in fungal pneumonia and frankly, cocci is in the western United States, but other endemic and pathologic fungi are across the United States. And even in—we've actually had conversations with our colleagues at First Union in Lviv. In war-injured patients, fungal pneumonia and fungal infections are becoming increasingly prevalent. So, in terms of cocci though, the real problem is that you have to eliminate the pathogen before you can heal the patient. And these pathogens are incredibly difficult to eliminate. Antifungals, traditional medications that have been used for these medications don't work for everybody. And oftentimes you combine them with corticosteroids to increase the chances of controlling the infection itself, which isn't always helpful in all patients. The idea that we could modulate, actively modulate the immune system, go from a sort of pro-inflammatory killing state to an anti-inflammatory healing state, it's really novel. And we'll present more detailed data next week at ATS. But being able to demonstrate that clinically is a really important inflection point for us and—and certainly, you know, in combination with something like the Anktiva IL-15 superagonist could be really potent in not just the cocci infections, but pathologic fungal infections across the United States and—and frankly worldwide.