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DATE

Friday, May 15, 2026 at 8:30 a.m. ET

CALL PARTICIPANTS

• Chief Executive Officer — Jennifer Buell
• Chief Medical Officer — Terese Hammond
• Chief Financial Officer — Melissa Oriolall

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TAKEAWAYS

• Cash Balance -- $9.5 million as of March 31, 2026, reflecting repayment of $5.2 million in convertible notes and $3 million in funds raised through an aftermarket sales agreement during the quarter.
• Operational Runway -- Management projects the company’s liquidity to support operations for at least the next 12 months, including the initiation and execution of its global randomized clinical trial.
• Net Loss -- $2.7 million ($0.57 per share), compared to $2.8 million ($0.70 per share) for the same period in 2025.
• Randomized Phase II Trial Design -- The ARDS trial will enroll 90 patients in a 1:1 randomization, comparing agent 797 plus standard of care versus placebo plus standard of care, with endpoints including overall survival, ventilator-free days, and ICU length of stay.
• Clinical Data Update Timing -- Preliminary results from the randomized Phase II ARDS trial are expected to be presented publicly in the second half of 2026.
• Mechanistic Findings -- Results presented at recent scientific meetings highlight that agent 797 produced “distinct immune output across cancer and ARDS,” suggesting disease-context dependent biological activity from the same unmodified, donor-derived product.
• Manufacturing Status -- The company stated, “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.”
• Pediatric Oncology Collaboration -- In the first quarter, a collaboration agreement was announced to support development of a TCR-engineered iNKT program for pediatric cancers, providing nondilutive funding for IND-enabling activities and potential future commercial economics.
• International Trial Approvals -- The ARDS trial received regulatory clearance for initiation from both the Ukrainian Ministry of Health and the U.S. FDA.
• Upcoming Data Presentation -- Data highlighting the combination of agent 797 with an IL-15 superagonist in severe pulmonary fungal infection will be presented at the American Thoracic Society Conference.

SUMMARY

MiNK Therapeutics (INKT +1.71%) advanced its randomized Phase II ARDS trial with regulatory approvals and detailed its design, targeting 90 ICU patients and primary endpoints related to survival and respiratory outcomes. Management confirmed sufficient cash to provide operational runway for at least the next 12 months, including initiation and execution of the randomized clinical trial, and repaid all convertible notes to simplify the balance sheet. Company updates pointed to expanding scientific validation for the iNKT cell platform’s context-dependent effects across both oncology and pulmonary indications, supporting scalability and future path toward rapid registrational development.

• “preliminary findings” from the ARDS trial are anticipated in the second half of the year, with management emphasizing a “seamless Phase II/III pathway” aiming for uninterrupted registrational progress.
• The company reiterated operational execution using disciplined investment, scalable manufacturing, and nondilutive external partnerships to maintain capital efficiency.
• Management identified significant commercial potential for ARDS treatment, with U.S. annual incidence cited at over 200,000 and global incidence above 3 million.
• Manufacturing infrastructure enables international logistics, as evidenced by product delivery to Ukraine under challenging conditions.
• Biomarker-driven patient stratification for ARDS is part of the study design, supporting accelerated development and potential for tailored patient response analysis.

INDUSTRY GLOSSARY

• iNKT cells: Invariant natural killer T cells, a unique immune cell subset with roles in modulating cancer and inflammatory disease responses.
• ARDS: Acute Respiratory Distress Syndrome, a severe lung condition often requiring ICU admission and mechanical ventilation.
• IL-15 superagonist: Engineered cytokine designed to enhance immune cell activation, often used to boost cell therapy efficacy.
• TCR: T-cell receptor, a molecule on immune cells guiding specific recognition and targeting of disease-associated antigens.
• IND-enabling activities: Preclinical and regulatory steps required before submitting an Investigational New Drug application to the FDA.

Full Conference Call Transcript

Operator: [Audio Gap] and thank you for joining us today. Over the past several weeks, we've presented data at 4 major international scientific meetings beginning with findings in pulmonary fibrosis is 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 week, we presented mechanistic findings at the American Society for Gene and Cell Therapy, showing the context dependence immune activity of invariant [indiscernible] T cells in cancer and severe lung injury. We're also very excited that next week, Dr.

Tara Cement, our Head of Pulmonary inflamatory 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 superagonist names ANTA 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 IMTT through cancer, severe lung injury, fibrosis and immune discussion overall. For those newer to link, our focus is on the development of off-the-shelf IMTT cell therapies designed to repair disregulated immune biology and disease is characterized by immune failure inflammatory injury and impaired pathogen and control.

And unlike conventional cell therapy, 797s administered without pumper depletion 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 [indiscernible], 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, the full ability in acute care settings. As a result, we are now able to evaluate our living medicines in diseases in clinical environment 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 selected partnerships. In the first quarter of this year, we announced the collaboration with [indiscernible] further to 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 we can 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 and be especially challenging. These 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 recent core data presentation before turning it over to Dr. Hammond, [indiscernible] CR in April, investigator Memorial Sun Cetera presented data from our Phase II study in gastroesophatheal cancer. This trial is an investigator [indiscernible] trial led by the division Chief, Dr. Elena [indiscernible], and her colleague, Dr. Sam Satan. The population was heavily pretreated checkpoint refractory with historically poor expected outcomes and limited therapeutic options at his failure on prior first-line therapy. We observed prolonged survival in patients who received induction immune therapy prior to chemotherapy, including emergence of a meaningful tail of the survival curve. Now these were patients whose expected survival is measured typically in months.

Yet here, median overall survival extended beyond 23 months in the [indiscernible] primary cohort, and several patients remain alive years after dosing and refractory gastric cancer that 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 continues to mature and the increased follow-up on our Phase I trial, we observed durability of survival in multiple tumor types, and that includes gastric cancer, cinema, 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. And 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 cell gene and cell therapy conferences we've been based Dr. [indiscernible], from our team presented translational analysis from phases of cancer and ARDS treated with the same donor-derived 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 space. Again, the same donor-derived product manufactured through our GMV process, reduce 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. [indiscernible] will go into this in more detail. Importantly, these observations emerge 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 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 endpoint and operational infrastructure that we believe will not only validate the observations in our earlier Phase I/II study, and is 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 pace 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 luxury and ARDS remain among the most serious unresolved commissions in critical care. [indiscernible] effect 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 hydrogenating and the complexity of prolonged illness.

Fire approaches, including mezzanine stromal cell or MSC therapies, demonstrated feasibility and a favorable safety profile that fails to consistently improve survival and randomized studies. And in part, because broad immunosuppressive or [indiscernible] approaches may be insufficient in patients who simultaneously acquire modulation of an injurious inflammation together with preservation of pathogen clearing immune function. And we believe, based on our observations with ITC cells and specifically agenT-797 may represent the fundamentally different biologic approach. Unlike MSCs, iNKTs are active immunofactor cells capable of localized modulation of inflammatory signaling together with coordinated activation of innate and adaptive immune pathways, including the ability to bear systemic pathogens.

Our intended target population are patients who can be identified clearly characterized biologically and stratify thoughtfully using globally recognized clinical and physiologic criteria. That matters from both a regulatory perspective as well as a clinical perspective. Critically, this patient population is a population where we believe we have already observed meaningful biologic and clinical signals both at clinical trials and through continued emergency use experience and critically ill patients who have few remaining therapeutic options. And our findings have emerging real-world ICU environment, and specifically, Dr. Hammond is operating in those environments bigly and she was the lead investigator on our trial.

And [indiscernible] was the data that we've now published and what we expect to see in the period 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. [indiscernible] 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 first Levis territorial Medical Union and unbroken Ukraine. Our study has been approved by the Ukrainian Ministry of Health and now cleared the U.S. FDA for dosing.

And our team has had the opportunity to spend on site, time on site, evaluating the hospital, talking with the team, meeting with the critical care team discussing their capabilities. We also reviewed the translational infrastructure and most importantly, the patients. And what we observed was remarkable. The clinical sophistication and quality of care being delivered under unimaginably difficult work time conditions to be credible. And we believe this collaboration creates an opportunity to evaluate IMTT based cell therapy in patients where the biology is particularly relevant and increasingly common and modern warfare in critical care medicine.

Modern complex is increasingly producing survivors after devastating injury, but survival as a company by complications, including multidrug pathogens, chronic inflammatory issues and downstream fibrosis. Programs such as BARDA funded Breathe program have demonstrated that appropriately targeted anti-inflammatory intervention can improve survival in patients with severe pressure compromise. But we believe the next evolution are therapy is capable of not only a dampening harmful inflammation as we've observed the 797, but also restoring immune coordination and pathogen control in patients with critical illness and immunogen. Changing the trajectory of disease in these populations is becoming increasingly important, not only to clinicians but also the government 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 cryopreserve allogeneic therapy rapidly without some depletion for alienating is operationally important. And as I mentioned, the trial is now clear to proceed by the Minis 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 is time when it's originally needed. Now as I prepare to turn the call over to Dr. [indiscernible], I want to highlight next week's presentation at the International American Thoracic Society meeting.

[indiscernible] will present in June involving the combination of IMTT therapy with NAI or [indiscernible], and IL-15 superagonist and development of commercial development with our colleagues at us buyout. Importantly, these findings further expand the potential applicability of ITT biology in disease settings characterized by persistent infection, immune regulation 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 to government and institutional partnerships.

As I mentioned earlier, in the first quarter, the strategy was reflected and I see further collaboration supported the development of our prime targeted CCR IT program pediatric cancers, providing nondilutive support for IND-enabling activities together with potential downstream commercial participation. Our randomized Phase II trial that we've mentioned and announced it yesterday has also been designed with a highly efficient operational infrastructure, leveraging substantial internal capabilities together with some experienced local support on the 1 allowing us to execute a global randomized study while maintaining a very disciplined burn of 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. Tere Hammond. Tere?

Terese Hammond: Thank you, Jim, 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 [indiscernible] slot oxygen, noninvasive ventilation mechanical ventilation or the most intense form of lung support, extracorporal membrane oxygenation or [indiscernible]. They need globally recognized criteria for acute respiratory distressed 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 collate. Others evolving to profoundly hypo inflammatory 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 of broadly suppressed inflammation may behave very differently depending on whether a patient is 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 those scenarios.

For the practicing pulmonary critical care physician what stood out to me, what has always struck me has been that it's not a [indiscernible] 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, the dilator 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 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 more time 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 the patient with persistent oxide is modus infection treated with agenT-79 and 803 [indiscernible]. This case amplifies the observations we've seen was a case of immune dysfunction and resistent 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 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 disregulation. 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 Oriol to review our financials. Melissa?

Melissa Orilall: Thank you, Therese. 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 [indiscernible] convertible notes during the first quarter of 2026. This further simplifies our balance sheet and make advances into randomized clinical execution. Following this repayment, in the 3 months ended March 31, 2026, we raised approximately $3 million through our aftermarket sales agreement resulted 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 ARES program benefits from substantial internal execution capabilities, combined with an 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 [indiscernible], 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 Jim for closing remarks. Thank you so much, Melissa, and Dr. Hammond.

For us, it -- 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 or clinical immunologic findings and they will apply them to a registration path that we believe will not only validate our earlier observations but also set a staff for a more rapid path to bring solutions to patients who are critically ill. Now just quickly at AACR, we presented for 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 cancel program in the future. At the 7 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 amplify 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, 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 back for a clinical programming, which we believe will have a substantial amount of data before the -- 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 a randomized study, most importantly, prepared 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 humbly and impressive, and we 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.

Operator: [Operator Instructions] Your first question comes from the line of Emily Bodnar from HC Wainwright.

Emily Bodnar: Congrats on all the progress. I know you 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 what their [indiscernible]?

Jennifer Buell: Thanks so much for your questions and your continued support regarding the trial, the randomized Phase II 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 II, which is about patients randomized Phase II, and it's a 1:1 randomization. Going into seamless Phase III, 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 III will be a very consolidated group of patients.

So we'll be back with the total number and the updated data on clinical trials at that time after the interactions. But for the randomized Phase II, 90 patients split at 1:1 randomization. These are patients that are in the ICU in 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 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 climates. We're seeing a growing number of individuals affected by this very difficult to treat fungus.

And we -- 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'll 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 ImmunityBio. And I'll turn it to There to speak just a moment about fungal pneumonia just as a setup, but without disclosing any of the data under embargo for ATS.

Terese Hammond: Yes. Thank you, Jen. And Emily, thank you, as Jen said, for your continued support. Fungal pneumonia, specifically [indiscernible] imidaz is an increasing threat. So [indiscernible] or sometimes called Bally fever has really spread across the Western United States is it extending actually into some of the states in the Northwest, so a very formidable challenge in fungal pneumonia and frankly, Cox is in the Western United States, but other endemic and pathologic fungi or across the United States. And even in -- we've actually had conversations with our colleagues at First Union and Viveve in war injured patients, fungal pneumonia and fungal infections are becoming increasingly prevalent.

So in terms of Coxy, 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 module it actively modulate the immune system, both 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, in combination with something like the NTIVA-IL-15 super agonist could be really potent in not just the Cox infections, but pathologic fungal infections across the United States and frankly, worldwide.

Jennifer Buell: Thank you, -- and I'm going to come back all to the last 2 questions. you had about the endpoint. 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 and clear pathogens, which will be important in the randomized Phase II that's actively underway as well as in some future interactions that we'll be talking about next week.

Following -- to go back to the randomized Phase II though, we talked about the sample estimates, but the end point. These are essentially -- 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 I see a number of ventilator days a number of days in the ICU as well. So these are the endpoints that the trial are built around -- the end points 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.

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

Mayank Mamtani: Congrats on the operational progress you've been having at the ASGCT, the H1 H2 context-dependent switching data was interesting. Obviously, I 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 to predict which patients will mount that desired immune phenotype. And then on the for acute setting, I was just curious, you want to have the senior Phase II to Phase III. So are there requirements that are different in, say, ARDS versus maybe what you have previously discussed in oncology indications, for example.

Jennifer Buell: [indiscernible] Very thoughtful questions. And I'm going to have Theres 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 made predictive of response with our therapy, which we believe they may be. This could help accelerate development time lines for us. We're measuring that. We're also -- we've designed our statistical plan to actually interrogate this prospectively and stratify for the inflammatory patients. This, 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 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 II, 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 to raise to speak to a couple of things. One, this inflammatory cascade that happens, we see it in critical illness, we see it in cancer. Patients are 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 in an adaptive immunity, we may be able to get into a mechanistic approach where we can start to mitigate these problems. Going into ARDS and with -- 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 sequel that comes from these complications.

And I'll turn that to Therese to say a little bit more about that.

Terese Hammond: Yes. Thank you, Jen. 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. They're all -- 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 cancer cancers or fibrosis and end-stage tissue damage.

So I think that this concept of sort of hyperinflammation, 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 understood that developing biomarkers and understanding the course for ARDS is important and differentiating and recovering from the disease. About 1/3 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 1/3 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 I/II trial. Certainly going into our Phase II/III 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. Is this 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 title 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 and 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 we'll be able to significantly impact therapeutic and treatment decisions. T 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 to the local inflammatory or tumor micro environment. that drives either resolution or healing. So 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 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.

Mayank Mamtani: Very helpful and comprehensive. And if I may just ask quickly on the any commercial assessment work Jen that has occurred as an earlier point, there hasn't been a lot for decades launching an actor in amor disease-modifying drug in this setting? Are there any other analogues you've looked at as you think about sort of the U.S. market but also ex U.S.? And I think relatedly, if you can maybe comment on what you may be thinking from a distribution commercialization model standpoint? And if there's anything nondilutive financing wise that you'd want to take care of in the near term.

Jennifer Buell: 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 assessment. 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 will 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, or time 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. And 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 in many times a day, particularly if the patients on me. These are substantial health care costs. And 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 extabated. And out of the ICU quickly will have an enormous benefit to the health care system overall, particularly succumbing to heavier demands seasonally as well as different exposures and threats that enter the system. So there is a substantial commercial opportunity.

At this point, I'd like to lay that out for public consumption, in parallel with the data from the randomized Phase II, 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'll be more appropriate to share the data as well as the commercial preparation and plans to support patients in this and critically ill population. So thank you. Thank you very much for your questions and continued support.

Operator: [Operator Instructions] 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: 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: 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 your participating. You may now disconnect.