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.

And thank you all for joining us today. Today's call is being webcast and will be available on on our website for replying. 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 Buell, President and Chief Executor Officer of New Fair Treatment, Dr. Therese Hammond, Head of Development, and Melissa Orleal, Principal Financial Officer. I'd like to turn the call over to Dr. Buell 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 and 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 dependence, immune activity of invariant natural killer 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 ANTIVA, 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, from cancer, 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, 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 the collaboration with C-Further to advance our frame-targeted, PCR-engineered, INKT cell therapy for pediatric cancers. This program is important not only because it brings non-dilutive 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. The See Further collaboration allows us to extend Mink's platform into a validated tumor or 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 2 study in gastroesophageal cancer. This trial is an investigator-sponsored trial led by the Division Chief, Dr. Yelena Gengigian and her colleague, Dr. Sam Zatarn. The population was heavily pre-treated, 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 modulations 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 observe 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. Jan Soon 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 observe distinct immune outputs depending on the disease environment. Now, this supports our belief that IDKT 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-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 1-2 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 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 United States, and 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 periclinic 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. T's, I-NKT's, 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 adoptions. 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. Dr. Hamill 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 in unbroken Ukraine. Our study has been approved by the Ukrainian Ministry of Health and now clears the US 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 BREEZE program have demonstrated that appropriately targeted anti-inflammatory interventions 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 the 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 allergenic therapy rapidly without lymphodepletion or ACLA 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 supereigonists 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 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 quadrant, the strategy was reflected, and our C-further collaboration supported the development of our PREM-targeted PCR-INCT program pediatric cancers, providing non-diluted 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 and internal capabilities, together with some experienced local support on the ground, allowing us to execute a global randomized study while maintaining a very disciplined burn 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.

Thank you, Jen, and good morning, everyone. I want to begin by discussing the actual patients we're enrolling in our Phase 2-3 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. These 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 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. It's 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, health care acquired multi-drug resistant infections, opportunistic fungal infections, immune exhaustion, and progressive organ dysfunction. When we see profound depletion or exhaustion of critical immune populations and severe disease state, 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 immune responses or Agent 797 responses 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 imidus infection treated with Agent 797 and N803 or ANGTIVA. This case amplifies the observations we've seen. It was a case of immune dysfunction and persistent inflammatory injury where conventional antifungal therapy and corticosteroids had 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 Oriel to review our financials. Melissa?

Thank you, Therese. Operationally and financially, the first quarter reflected continued discipline execution as we advance 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 agenda's convertible note during the first quarter of 2026. This further simplifies our balance sheet and makes 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 our randomized ARDS development program, translational oncology initiatives, and next-generation IEKT 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. Operate and 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 57 cents per share, compared to approximately $2.8 million, or 70 cents per share for the same period in 2025. These results reflect our focused investment strategy in advancing the HN797 Clinical Program, while maintaining disciplined control over operation expenses and prioritizing programs with clear translational, clinical, and regulatory pathways. With that, I'll turn to call back to Jen for closing remarks. Thank you so much, Melissa and Dr. Hammond. For us, it makes this an incredibly exciting time with some announcements that have just has 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 now 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, and patients with refractory gastric cancer will continue to follow those patients, and we'll be providing an update on the 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, and 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 FACE-2 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 and 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 into meaningful clinical outcomes for patients who are critically ill. So thank you again for joining us this morning. I'll turn the call back over to the operator for questions.

Thank you. To ask a question, please press star then the number one on your telephone keypad. To withdraw your question, please press star and number one again. We will pause for just a moment to compile the Q&A roster. Your first question comes from the line of Emily Bodnar from H.C. Wainwright. Please go ahead.

Hi, good morning. Thanks for taking the questions and congrats on all the progress. I want you to 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 immunity bio 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 ANTIVA?

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 CLIN trials at that time after the interactions, but for the randomized phase two, 90 patients split at 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 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 Immunity Bio, 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 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 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 colleagues at Immunity Bio. 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 Emily. Thank you, as Jen said, for your continued support. Fungal pneumonia, specifically coccidioides imidus, is an increasing threat. So coccidioides, or is sometimes called valley fever, has really spread across the western United States. This is extending actually into some of the states in the northwest. So a very formidable challenge. in fungal pneumonia and and frankly coxie is in the western united states but other endemic and pathologic fungi are across the united states and and even in uh uh we've actually had conversations with our colleagues at first union in blaviv uh in war injured patients fungal pneumonia and fungal infections are becoming increasingly prevalent. So in terms of COXI, 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. That 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 certainly, you know, in combination with something like the Anctiva IL-15 super agonist could be really potent. in not just the COXI infections, but pathologic fungal infections across the United States and, frankly, worldwide.

Dr. Hammond, thank you very much. And I'm going to come back, Emily, to the last two questions that you had about the So more to come at ATS, and we're looking forward to providing a bit more color about our activities in this particular setting. And importantly, our observations build on what we have previously published and that you could deliver agent 797 and very difficult to treat critical illnesses and what we have observed now is the potential to prevent secondary infections in clare pathogens which will be important in the randomized phase two that's actively underway as well as in some future interactions that we'll be talking about next week following uh to go back to the randomized Phase 2, though, we talked about the sample estimates, but the endpoints, these are essentially endpoints. We've designed the trial to meet the regulatory rigor and scrutiny, which include endpoints in respiratory distress, such as overall survival, ventilator-free days, and number of ventilator days, and number of days in the ICU as well. So these are the endpoints that the trial are built around. The endpoints happen very quickly in this particular setting, so based on our observations, we think we will have early readouts quite quickly, and we're setting up already to be publicly presenting these data in the second half of this year.

Perfect. Thanks for the call. Your next question comes from the line of Mayank Mamthani from B. Riley Securities. Please go ahead.

Yes, good morning, team. Thanks for taking our questions, and congrats on a ton of operational progress you've been having. At the ASGCT, the TH1, TH2 context dependent switching data was, you know, interesting. Obviously, want to understand a little bit like your understanding of how the reprogramming is kind of happening here and is there a patient selection biomarker you can use prospectively, you know, to predict which patients will mount that, you know, desired immune phenotype. And then on the CMC, you know, for acute setting, I was just curious, you know, you want to have the similar phase two to phase three. So are there requirements that are different in, say, ARDS versus maybe what you have previously discussed

in oncology indications, for example? Mayank, thank you. Always see your very thoughtful questions. And I'm going to have Therese speak to something very important, findings. Your question on biomarkers are so timely, and there are data to suggest that biomarkers that are emerging that differentiate the inflammatory state for patients with ARDS are predictive of response and may be predictive of response with our therapy, which we believe they may be. This could help accelerate development timelines for us. We're measuring that. We've designed our statistical plan to actually interrogate this prospectively and stratify for the inflammatory state of patients. We do believe that there may be patients who may respond more effectively to the therapy if they have a specific biomarker present. We'll be talking more about that as the patients enroll and the data evolve. But it's such an important question. What was remarkable about the data that we presented yesterday, now there are a number of approaches to interrogating INKT cells and delivering them. And there are technologies that may take, that seek to take an off-the-shelf approach that are IPSC-derived or cell-line-derived donor-derived cells. Now, we believe at Mink that actually developing a process that allows us to scale to billions of cells per donor using donor-derived cells, And these are thymic-educated INKT cells, which have now demonstrated substantial activity and very specific activity, which the data at the Cell and Gene Therapy Conference we presented yesterday, that immune modulation, independent of the disease. So taking the same donor, the same manufacturing process, standardizing it, generating billions of cells through that manufacturing process so the scale is there, delivering it to patients, the same donor-derived cells, in different disease settings and seeing very different immunologic, biologic, and clinical activity is a profound advancement to the science of INKT development, which we are just immensely excited about. So taking those signals and observations of applying this particular formulation in patients with cancer and seeing essentially tumor-killing profile, activation, TH1 skewed, and a very different profile from the same formulation in patients with an inflammatory disease, essentially a pulmonary problem, And having those same cells effectively dampen that inflammatory problem is just groundbreaking, frankly. And we'll be looking forward to publishing these data very soon after the presentation. Those findings helped us to not only elucidate biomarkers for our upcoming randomized phase 2, but also have really impressive confidence around development strategies in different disease applications. And these data, of course, build from the previous findings that we presented in February of the INKT cell importance in pulmonary fibrosis. And I'll have Therese just speak to a couple of things. One, this inflammatory cascade that happens, we see it in critical illness, we see it in cancer. Patients essentially become vulnerable to a disease setting. Sometimes it's an infection. It could be cancer. you see this cascade that happens, an inflammatory cascade that results in fibrosis, fibrotic lesions in some cases and in other cases in cancer and in some cases both. And what we are observing now and presenting in sequence are the observations that by reconstituting the immune system at such an important time with a therapy that can modulate both innate and adaptive immunity, we may be able to get into a mechanistic approach where we can start to mitigate these problems. Going into ARDS and patients with and without trauma allow us to explore this in a setting that we have seen those inflammatory assaults, whether it's from an infection, from a trauma, do result in downstream fibrotic lesions, and we may be able to prevent that and prevent the sequelae that comes from these complications. And I'll turn that to Therese to say a little

bit more about that. Yes, thank you, Jen. You know, during COVID, we sort of had this important epiphany where we repurposed cancer medications for this robust inflammatory cascade that caused COVID respiratory failure and was responsible in the beginning for such profound devastation and death. I think it opened our eyes to the fact that cancer and critical illness are not that different. The basis is all chronic inflammation. And if you can't take acute inflammation, resolve it, it becomes chronic. And as it becomes chronic, it substantially changes the biology of our bodies and makes us susceptible to different pathways that both have bad consequences, either neoplasm or cancers or fibrosis and end-stage tissue damage. So I think that this concept of sort of hyper-inflammation, resolution of inflammation is incredibly important. And that's where our understanding, especially I can speak mainly to ARDS, has been really enlightening and it's been driven over the last few years by a couple of visionaries who've understood that developing biomarkers and understanding the course for ARDS is important and differentiating and recovering from the disease. About a third of patients with ARDS are going to have the so-called hyperinflammatory cytokine profile. Things like interleukin 18 will be very, very high. Interleukin 6 will be very, very high. And for that third of patients with hyperinflammation, their morbidity and mortality is substantially higher. And if you can predict that and if you can modulate that, I think that that was part of the rationale in our phase 1-2 trial. Certainly going into our Phase 2-3 trial, we're heavily depending on biomarkers to help us separate and help us interrogate the data that we collect from Agent 797-INKT therapy. It's just an important component of not just understanding critical illness, but finally having impactful therapies that can change the course of critical illness. The fact that in the last 26 years, we really haven't developed anything else in ARDS other than low tidal volume ventilation to really profoundly change mortality. Well, that just has told us that we're well behind the curve. And as we've had an improvement in our ability to measure biomarkers, an improvement in our understanding about what the immune system does, We've been able to, I think, move along this path to where in the very near future, we'll be able to significantly impact therapeutic and treatment decisions. These cells, INKT cells, Agent 797, from the very beginning have captivated me for multiple reasons. But I have to say the one thing that continues to impress me and I think was really on display at the American Society of Cell and Gene Therapy presentation poster is the fact that these cells are adaptable. They go to tissue that's injured, they taste the environment, they read the room, and they exert a response. They elicit a response through the local inflammatory or tumor microenvironment that drives either resolution or healing. So, you know, more to come. I'm excited to present at ATS next week, excited to be able, as the year progresses, have more detail about our preliminary results. And I'm just gratified as a clinician, as somebody who takes care of patients every day, that a truly revolutionary and important new therapy, cell therapy, in critical illness is on the horizon.

very helpful and comprehensive. And if I may just ask quickly on the, you know, any commercial assessment work, Jen, that has occurred, you know, to Teresa's earlier point, there hasn't been a lot in, you know, for decades, launching an acute care inflammatory disease modifying drug. In this setting, are there any other analogs you've looked at as you think about, about, you know, sort of the U.S. market, but also ex-U.S. And I think relatedly, if you can maybe comment on, you know, what you may be thinking from a distribution commercialization model standpoint and if there's anything non-dilutive financing-wise that, you know, you'd want to take care of in the near term. Thanks for taking our questions.

Thank you so much, Mayank. So, yes, as we have been moving the program so quickly, we have, of course, in parallel launched our commercial assessments. From a distribution perspective, we've been able to demonstrate that we could take these cells and distribute them internationally, and we've really mastered the process to be able to do so. So from a distribution perspective, we've landed the process, the proprietary shipping logistics and vessels that'll be necessary so that the logistics are really quite easy. As a matter of fact, we're able to ship these cells to Ukraine, even under really difficult conditions, wartime conditions. That has given us quite a bit of confidence in the current process in the product, and we haven't yet spoken about our Next Generation programs, which will be forthcoming that will make the logistics even more exciting for the field. However, in the meantime, ARDS is a substantial problem. Respiratory distress impacts over 200,000 individuals in the U.S. annually and more than 3 million patients globally worldwide. So this is a substantial problem. There are some analogs that have demonstrated to be really quite active and broadly active in this particular setting. When we look at the expense of a patient in the ICU, it's over $100,000 essentially and many times a day, particularly if the patient's on VV ECMO. These are substantial healthcare costs, and it also, when the longer patients are in the ICU, the fewer patients, and we saw this during the pandemic, fewer patients can be treated. So moving patients through the ICU very quickly and getting them extubated and out of the ICU quickly will have an enormous benefit to the healthcare system overall, particularly when we're succumbing to heavier demands seasonally, as well as, you know, different exposures and threats that enter the system. So there's a substantial commercial opportunity at this point. I'd like to lay that out for public consumption in parallel with data from the randomized phase two, which we expect to be no later than the second half of this year. And we've already designated some locations where we will be presenting our findings. So at that time, I think it will be more appropriate to share the data as well as the commercial preparation and plans to support patients in this critically ill population. So thank you. Thank you very much for your questions and

continued support. Thank you, Jen. Again, if you would like to ask a question, please press or a number one on your telephone keypad. There are no further questions at this time. This concludes the Q&A session. I now turn the call back to Dr. Jennifer Buell for closing remarks.

Please go ahead. Thank you, operator. And thank you all for joining us today. I appreciate your support and we look forward to providing additional updates very soon. Thanks again.

This concludes today's call. A replay will be available in the events and presentation section of our investor website at investor.mingtherapeutics.com slash events dash end dash presentations. Thank you for your participating. You may now disconnect.