Earnings Call Transcript - INKT Q1 2026

Operator, Operator

There was an audio gap, and thank you for joining us today.

Jennifer Buell, Chief Executive Officer

Over the past several weeks, we've presented data at four major international scientific meetings beginning with findings in pulmonary fibrosis at a 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 natural killer T (iNKT) cells in cancer and severe lung injury. We're also very excited that next week, Dr. Terese Hammond, our Head of Pulmonary and Inflammatory Diseases, will present at the American Thoracic Society Conference in Orlando, Florida. She'll describe a combination of our invariant natural killer T cell technology, agent 797, in combination with an IL-15 superagonist named N-803 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 iNKT through cancer, severe lung injury, fibrosis and immune dysregulation 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. Unlike many conventional cell therapies, agent 797s are 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. What continues to distinguish this platform is its clinical activity and its practicality and scalability. 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 the feasibility of use in acute care settings. As a result, we are now able to evaluate our living medicines in clinical environments that were previously impractical for cell therapy due to operational complexity and cost. That same practicality is central to how we're expanding our platform through selected partnerships. In the first quarter of this year, we announced the collaboration with ImmunityBio to further advance our frame-targeted TCR-engineered iNKT cell therapy for pediatric cancers. This program is important, not only because it brings nondilutive 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. This ImmunityBio 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 recent core data presentations before turning it over to Dr. Hammond. At AACR in April, an investigator from Memorial Sloan Kettering presented data from our Phase II study in gastroesophageal cancer. This was an investigator-initiated trial led by the division chief, Dr. Elena, and her colleague, Dr. Sam. 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 the emergence of a meaningful tail of the survival curve. These were patients whose expected survival is typically measured in months. Yet here, median overall survival extended beyond 23 months in the primary cohort, and several patients remain alive years after dosing in refractory gastric cancer, which is highly unusual. What's become increasingly important to us over time is not simply whether transient responses occurred, 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 with increased follow-up on our Phase I trial, we observed durability of survival in multiple tumor types, including gastric cancer, 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-telling immune pathways, restoration of exhausted immune responses and remodeling of suppressive myeloid biology. Increasingly, these intrinsic immune-modulating properties appear to connect dramatically with the biology that we are now observing in inflammatory lung injury and ARDS. At the American Society for Gene and Cell Therapy conference, a member of our team presented translational analysis from phases of 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. This supports our belief that iNKT cells participate in modulating immune biology across profoundly different disease spaces. Again, the same donor-derived product, manufactured through our GMP 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 toward restoration-associated immune signaling. 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 on 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, but is prospectively confirmed to 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 medicines 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 accounts 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 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, in part because broad immunosuppressive or immunomodulatory approaches may be insufficient in patients who simultaneously require modulation of injurious inflammation together with preservation of pathogen-clearing immune function. We believe, based on our observations with iNKT cells and specifically agent 797, that we may represent a fundamentally different biologic approach. Unlike MSCs, iNKTs are active immunoregulatory 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 both from a regulatory perspective as well as a clinical perspective. Critically, this patient population is one where we believe we have already observed meaningful biologic and clinical signals both in clinical trials and through continued emergency use experience in critically ill patients who have few remaining therapeutic options. Our findings have emerged in real-world ICU environments, and specifically, Dr. Hammond is operating in those environments directly and she was the lead investigator on our trial. The data that we've now published and what we expect to see in the period ahead include evidence of local immune modulation within the lung, reductions in harmful inflammatory signaling and reduction in secondary infections. Dr. Hammond will speak more about this shortly. I want to highlight an important component of this effort as part of our partnership that we've developed with the First Lviv Territorial Medical Union in Ukraine. Our study has been approved by the Ukrainian Ministry of Health and now cleared by the U.S. FDA for dosing. Our team has had the opportunity to spend time on site evaluating the hospital, talking with the team, meeting with the critical care team and discussing their capabilities. We also reviewed the translational infrastructure and, most importantly, the patients. What we observed was remarkable: the clinical sophistication and quality of care being delivered under unimaginably difficult wartime conditions is credible. We believe this collaboration creates an opportunity to evaluate iNKT-based cell therapy in patients where the biology is particularly relevant and increasingly common in modern warfare-related critical care medicine. Modern conflict is increasingly producing survivors after devastating injury, but survival is complicated by downstream complications including multidrug pathogens, chronic inflammatory issues and downstream fibrosis. Programs such as BARDA-funded Breathes program have demonstrated that appropriately targeted anti-inflammatory intervention can improve survival in patients with severe pulmonary compromise. We believe the next evolution of therapy is capable of not only dampening harmful inflammation, as we've observed with agent 797, but also restoring immune coordination and pathogen control in patients with critical illness and immunosuppression, changing the trajectory of disease in these populations. This is becoming increasingly important not only to clinicians but also to government 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 is simply not feasible. The ability to deliver cryopreserved allogeneic therapy rapidly without lymphodepletion is operationally important. As I 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. We're grateful to contribute to this important effort at a time when it's urgently needed. Now as I prepare to turn the call over to Dr. Terese Hammond, I want to highlight next week's presentation at the American Thoracic Society meeting. Dr. Hammond will present data involving the combination of iNKT therapy with N-803, an IL-15 superagonist, and development plans in collaboration 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 a level of capital efficiency that's uncommon in the cell therapy sector, combining disciplined internal execution, scalable manufacturing infrastructure and nondilutive support from government and institutional partnerships. As I mentioned earlier, in the first quarter, our strategy was reflected in the ImmunityBio collaboration supporting the development of our prime-targeted TCR iNKT program in pediatric cancers, providing nondilutive support for IND-enabling activities together with potential downstream commercial participation. Our randomized Phase II trial that we mentioned yesterday has also been designed with a highly efficient operational infrastructure, leveraging substantial internal capabilities together with experienced local support in Ukraine, allowing us to execute a global randomized study while maintaining a very disciplined 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 mentioned this morning. I'll now turn the call over to Dr. Terese Hammond. Terese?

Terese Hammond, Chief Medical Officer / Head of Pulmonary & Inflammatory Diseases

Thank you, Jennifer, 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. These patients with severe hypoxic respiratory failure all require some form of respiratory support, be it supplemental oxygen, noninvasive ventilation, mechanical ventilation or the most intense form of lung support, extracorporeal membrane oxygenation (ECMO). They meet globally recognized criteria for acute respiratory distress syndrome and severe lung injury, including profound oxygen impairment, inflammatory lung damage and are all 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 to 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 matters because broadly suppressive anti-inflammatory therapies 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 of those scenarios. For the practicing pulmonary critical care physician, what stood out to me has always been that it's not a single improvement that we see from 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 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 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 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 an 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 to 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 case with persistent coccidioidomycosis infection treated with agent 797 and N-803. This case amplifies the observations we've seen: 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 cellular dysfunction 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, but because the biology appears increasingly capable of operating within this complexity. I'll stop there. Thank you for your time and attention. I'd like to turn the call over to Melissa Orilall to review our financials. Melissa?

Melissa Orilall, Chief Financial Officer

Thank you, Terese. Operationally and financially, the first quarter reflected continued disciplined 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 convertible notes during the first quarter of 2026. This further simplifies our balance sheet and facilitates advances into randomized clinical execution. Following this repayment, in the three months ended March 31, 2026, we raised approximately $3 million through our aftermarket 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 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 operations and plans, 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 trial. 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 programs 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 Jennifer for closing remarks.

Jennifer Buell, Chief Executive Officer

Thank you so much, Melissa, and Dr. Hammond. For us, 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 durable mechanistic validation, which is incredibly exciting. This is exactly where we want to be at a time when we can take our pharmacologic and clinical immunologic findings and apply them to a registration path that we believe will not only validate our earlier observations but also set a path for a more rapid route to bring solutions to patients who are critically ill. At AACR, we presented long survival in patients with refractory gastric cancer. We'll 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 ASGCT conference this week, we demonstrated that the same unmodified product produced distinct immune outputs 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 burn prospectively. Next week at ATS, we'll present important evidence supporting the potential role of immune restoration in persistent pulmonary infection, and we think this will have broad application. Additional data and plans will follow after that presentation. Most excitingly, yesterday we announced the initiation of our randomized Phase II trial, which is going to set us back for a clinical program from which we believe we will have a substantial amount of data in the second half of this year. We expect to present preliminary findings also in the second half of this year, which we're incredibly excited about. For us, the path is really clear: we've got to execute on a randomized study and be prepared to generate 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 impressive, and we couldn't be more excited to work with such a tremendous group of individuals. We'll now continue to evaluate our observations and the translation of those observations into meaningful clinical outcomes for patients who are critically ill. Thank you again for joining us this morning. I'll turn the call back over to the operator for questions.

Operator, Operator

Your first question comes from the line of Emily Bodnar from HC Wainwright.

Emily Bodnar, Analyst

Congrats on all the progress. I know you may 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 for that program?

Jennifer Buell, Chief Executive Officer

Thanks so much for your questions and your continued support. Regarding the randomized Phase II trial, we're designing the trial now and speaking with the agency in a matter of just a couple of weeks to expand from the randomized Phase II, which is a 1:1 randomization, into a seamless Phase III, which will be 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 III will be a consolidated group of patients, and we'll be back with the total number and updated details after our interactions with the agency. For the randomized Phase II, the plan is 90 patients split 1:1 randomization. These are ICU patients who will all be 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 can say today under embargo, 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 we had and what our plans are to develop the program further in a very difficult-to-treat indication. Fungal pneumonia is a substantial and growing problem. It's increasing in incidence and prevalence in the United States and is endemic in certain regions, particularly in certain climates. We're seeing a growing number of individuals affected by this very difficult-to-treat pathogen. There has also been public discussion around this particular biology as a potential threat in some contexts, and there are currently limited treatments for some forms of severe fungal pneumonia. The data we'll be presenting will help to elucidate mechanisms that we believe are important to mitigating such problems. While this is a case study and we will be conservative in interpreting the findings, the mechanisms are very clear. Based on what we've observed in respiratory distress overall as well as in this particular case, we think there's an important opportunity here to help patients with a critical and growing unmet need that is specific to these pathogens. We'll share more detail about the work underway with colleagues at ImmunityBio at the appropriate time. I'll turn to Dr. Hammond to speak briefly about fungal pneumonia as context without disclosing any embargoed data for ATS.

Terese Hammond, Chief Medical Officer / Head of Pulmonary & Inflammatory Diseases

Yes. Thank you, Jen, and Emily. Fungal pneumonia, specifically coccidioidomycosis, is an increasing threat. Coccidioides, sometimes called Valley fever, has really spread across the Western United States and is extending into some states in the Northwest, so it poses a formidable challenge. Other endemic and pathogenic fungi exist across the United States and worldwide. In wartime injured patients and other severely ill populations, fungal pneumonia and fungal infections are becoming increasingly prevalent. In terms of coccidioidomycosis, 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. Traditional antifungals don't work for everybody, and often you combine them with corticosteroids to try to improve outcomes, which isn't always helpful. The idea that we could actively modulate the immune system — shifting from a pro-inflammatory killing state to an anti-inflammatory healing state — is novel. We'll present more detailed data next week at ATS, but being able to demonstrate this clinically is a really important inflection point. In combination with an IL-15 superagonist like N-803, this could be potent not just for coccidioidomycosis but for pathologic fungal infections across the United States and worldwide.

Jennifer Buell, Chief Executive Officer

Thank you. I'll come back to your question about endpoints and readouts. More to come at ATS, and we're looking forward to providing more color about our activities in this setting. Importantly, our observations build on what we've previously published: you can deliver agent 797 in very difficult-to-treat critical illnesses. What we have observed is the potential to prevent secondary infections and clear pathogens, which will be important in the randomized Phase II that's actively underway as well as in future program discussions. To go back to the randomized Phase II, these are endpoints designed to meet regulatory rigor, which include endpoints commonly used in respiratory distress trials such as overall survival, ventilator-free days and number of days in the ICU. These endpoints occur relatively quickly in this setting, so based on our observations, we think we will have early readouts quite quickly, and we're set up to present these data in the second half of this year.

Operator, Operator

Your next question comes from the line of Mayank Mamtani from B. Riley Securities.

Mayank Mamtani, Analyst

Congrats on the operational progress you've been having. The H1/H2 context-dependent switching data was interesting. I want to understand a little bit about how the reprogramming is happening here. Is there a patient selection biomarker you can use prospectively to predict which patients will mount that desired immune phenotype? And then on the acute setting, you mentioned going from Phase II to Phase III seamlessly — are there requirements that are different in ARDS versus what you have previously discussed in oncology indications?

Jennifer Buell, Chief Executive Officer

Very thoughtful questions. I'll have Terese speak to some of the key findings, but on biomarkers: these questions are timely. There are emerging data to suggest biomarkers that differentiate inflammatory states in ARDS are predictive of response and may be predictive of response to our therapy. We're measuring those biomarkers, and we've designed the statistical plan to interrogate this prospectively and to stratify for inflammatory phenotype. We do believe there may be patients who respond more effectively if they have a specific biomarker profile. We'll be talking more about that as patients enroll and data evolve. Regarding the manufacturing and platform questions, there are a number of approaches to delivering iNKT cells. Some use iPSC-derived or cell line-derived approaches. At MiNK, we believe in a donor-derived approach that allows us to scale to billions of cells per donor using thymically educated iNKT cells. We've demonstrated that the same donor-derived product manufactured through a standardized process can be scaled and delivered across different disease settings. Delivering the same donor-derived cells in different disease settings and observing different immunologic and clinical activities is a profound advance in iNKT science, which we're very excited about. Seeing a tumor-killing Th1-skewed profile in oncology and a different, resolution-oriented profile in inflammatory disease from the same unmodified formulation is notable. Those findings not only help us elucidate biomarkers for the randomized Phase II but also give us confidence around development strategies in different disease applications. These data build on our previous findings in iNKT relevance for pulmonary fibrosis. I'll hand it to Terese to expand on the inflammatory cascade and clinical context and then come back.

Terese Hammond, Chief Medical Officer / Head of Pulmonary & Inflammatory Diseases

Thank you, Jen. During COVID, we had an important epiphany where we repurposed certain cancer medications for the robust inflammatory cascade that caused COVID respiratory failure. It opened our eyes to the overlap between cancer and critical illness: both can involve chronic inflammation. If acute inflammation doesn't resolve, it becomes chronic and substantially changes tissue biology, making patients susceptible to fibrosis, organ damage and other downstream consequences. Differentiating hyperinflammatory versus hypoinflammatory phenotypes in ARDS is critical. About one-third of patients with ARDS have a hyperinflammatory cytokine profile — very high interleukin-18, very high interleukin-6 — and for that subgroup, morbidity and mortality are substantially higher. If you can predict that and modulate it, outcomes can improve. That was part of the rationale for our Phase I/II trial and is central to our Phase II/III strategy, where biomarkers will help us separate and interrogate responder populations. This is not just important for understanding critical illness but also for enabling impactful therapies that can change the course of disease. Over the last decades, aside from low tidal volume ventilation, we haven't developed much that profoundly changes ARDS mortality. Improvements in biomarker measurement and immune understanding now allow us to move toward therapies with real impact. iNKT cells continue to captivate me because they are adaptable: they go to injured tissue, sense the environment and exert a response appropriate to the local inflammatory or tumor microenvironment that drives resolution or healing. More to come at ATS and as the year progresses we'll provide more detail on preliminary results. As a clinician who cares for these patients, I'm gratified that a potentially revolutionary cell therapy in critical illness is on the horizon.

Mayank Mamtani, Analyst

Very helpful and comprehensive. If I may just ask quickly on the commercial assessment work: given there hasn't been a disease-modifying drug in ARDS for decades, are there any analogues you've looked at as you think about the U.S. market and ex-U.S.? And relatedly, can you comment on what you're thinking about distribution and commercialization model? And is there anything nondilutive financing-wise that you'd want to take care of in the near term?

Jennifer Buell, Chief Executive Officer

Thank you, Mayank. As we've moved the program quickly, we've also launched our commercial assessment. From a distribution perspective, we've demonstrated that we can distribute these cells internationally and have developed proprietary shipping logistics and vessels necessary for distribution. We were able to ship cells to Ukraine under difficult conditions, which has given us confidence in the current process and product. We also have next-generation programs forthcoming that will further improve logistics. In the meantime, ARDS and respiratory distress affect over 200,000 individuals in the U.S. annually and more than 3 million patients globally, so it is a substantial problem. When we look at the cost of an ICU stay — often over $100,000 per patient, particularly when mechanically ventilated — reducing ventilator days and ICU length of stay would have enormous benefits for healthcare systems, especially during peak demand periods. There is substantial commercial opportunity. We plan to share a more detailed commercial plan in parallel with randomized Phase II data, which we expect by the second half of this year. At that time, we will present the data and more specifics on our commercialization and distribution plans. Thank you for your questions and continued support.

Operator, Operator

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.

Jennifer Buell, Chief Executive Officer

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.

Operator, Operator

This concludes today's call. A replay will be available in the Events and Presentations section of our investor website at investor.minktherapeutics.com/events-and-presentations. Thank you for participating. You may now disconnect.