Thank you, operator, and thank you all for joining us today. Today's call is being webcast and will be available on our website for replay.

I'd like to remind you that this call will include forward-looking statements, including those related to our clinical developments, regulatory and commercial plans, timelines for data releases, and partnership opportunities. These statements are subject to risks and uncertainties.

Please refer to our SEC filings available on our website for a detailed description of these risks. Joining me today are Dr.

Jennifer Buell, President and Chief Executive Officer; Dr. Therese Hammond, Head of Development; and Melissa Orilall, Principal Financial and Accounting Officer.

I'd like to turn the call over to Dr. Buell to highlight our progress from this quarter.

Dr. Buell?

Thank you, Stefanie. Good morning, everyone.

For those new to MiNK Therapeutics, we are advancing a clinically validated, allogeneic, invariant natural killer T cell platform, one that is fundamentally differentiated in its ability to restore and coordinate immune function across diseases or even in immune failure. Unlike conventional cell therapies, our MiNK iNKT cells are off the shelf.

They are administered without lymphodepletion, without HLA matching. We've demonstrated clinical activity with a very favorable safety profile.

MiNK cells are now in phase 2 clinical trials in patients with solid tumor cancers and autoimmune inflammatory conditions like GvHD and severe lung disease. Clinically, in cancer, MiNK cells have demonstrated durable survival beyond 23 months with complete remissions extending beyond 2 years in heavily pretreated refractory cancers, with an expected survival of about 6 months.

Outside of cancer, we're also seeing clinical activity in patients with hypoxemic pneumonia or otherwise called severe acute respiratory distress, reinforcing the broader applicability of our immune restoration cell product. We're excited to discuss with you today our upcoming trials.

We have secured external funding to advance MiNK cells into graft-versus-host disease with the trial in the activation phase at University of Wisconsin. We have also externally funded a trial in phase 2 in patients with gastric cancer with results presented last year at AACR and expected to be presented at a major conference in the first half of this year.

Finally, our soon-to-be-enrolling, MiNK-sponsored, randomized phase 2 trial in patients with severe hypoxemic pneumonia or ARDS, a condition that affects approximately 200 to 300,000 patients per year. We'll talk more about that in just a few moments.

Most importantly, we're doing this with a level of capital efficiency that's really uncommon in cell therapy. We're combining disciplined internal execution with non-dilutive funding through government and institutional partnerships.

We're manufacturing at a scale that appears to be the most efficient in cell therapy at this time. At the same time, we continue to build scientific validation through multiple data presentations and peer-reviewed publications, many of which will be out in the first half of this year.

Now, history tells an important story here on execution, and looking back at 2025, it was a year that we moved really from promise to proof, establishing durability, validating our mechanism, demonstrating that this platform can be advanced with both rigor and efficiency. In 2022, we demonstrated that our results were really quite durable clinically and biologically.

At the Society for Immunotherapy of Cancer annual meeting in late 2025, just a couple of months ago, we presented updated clinical data in heavily pretreated checkpoint-refractory solid tumor cancers. This is a substantial and growing population of patients.

These were patients who had exhausted standard options. What we observed was meaningful: median overall survival exceeding 23 months in combination with commercially available PD-1 therapies, complete remissions extending beyond 2 years, long-term survival across multiple solid tumor cancers including gastric, thymoma, renal, adenoid cystic cancers, and lung cancer.

These outcomes matter, particularly in this patient population, and importantly because they have persisted over time. At the same time, we've deepened our understanding of how this is working.

We saw activation and expansion of important immune cell populations, dendritic cells supporting antigen presentation, repolarization of macrophages towards pro-inflammatory anti-tumor states, and reinvigorated or exhausted T cells with restored function. We also observed controlled increases in cytokines such as interferon gamma, IL-2, TNF alpha, consistent with a productive immune response without systemic toxicity.

The takeaway for us is very straightforward. The durability we're seeing clinically is supported by a coordinated immune activation state.

This is not a single pathway effect, and it's what defines MiNK iNKT cells as our platform. In scientific validation beyond oncology, we asked how this biology goes beyond cancer.

This year at the Keystone Symposia, Dr. Therese Hammond, our Head of Pulmonary Critical Care Medicine, presented human data showing significant depletion of iNKT cells in patients with end-stage idiopathic pulmonary fibrosis.

This is important evidence of immune deficiency in patients with immune dysfunction. When you see that forward, the path becomes really clear: restore what's missing.

This is how we're approaching expansion: follow the biology, validate in humans, and then move into clinical execution. We've taken this approach in patients with hypoxemic pneumonia or ARDS.

This is a very serious condition. It's growing in prevalence and incidence, and it's affecting currently approximately 200 to 300,000 patients annually with a mortality rate of 30% to 40% and no approved disease-modifying therapies.

In our phase 1/2 trial in this particular population, we dosed critically ill patients with respiratory distress. These patients were on mechanical ventilation and/or VV ECMO.

These patients are consuming substantial resources in our ICUs, and our results showed that we can get the cells into patients in community hospitals. We can dose to a billion cells without deleterious tox.

As a matter of fact, the cells were tolerated quite well. We not only did not see cytokine release, we, in fact, dampened pro-inflammatory signals or harmful inflammation.

We observed prolonged survival, 70% of patients alive compared to 10% of patients within hospital controls. We observed that these cells could locally modulate immune function in the lung, and they can restore function of lung tissue, specifically endothelial function and improved oxygenation in these patients.

We saw rapid extubation. We saw patients coming off of the most severe life support, VV ECMO.

We saw that these cells also not only cleared infectious pathogens, but also we saw a reduction in the onset of secondary infections. This is important because secondary infections are often the cause of death for patients in the ICU.

As a result of these findings, we are now well on our way to announcing the first dosing of patients in our randomized phase 2 study that's designed to expand to a phase 2/3 study. This is a global program.

It's designed very efficiently, and it's planned to launch with our colleagues at top centers in Ukraine and in the US. These are real-world environments that we are able to reach because of the practicality of our approach.

We have an off-the-shelf therapy with a favorable safety profile and no requirement for complex infrastructure. We're working very closely with the Ministry of Health in Ukraine and the US FDA to advance this program.

With dosing starting eminently, we expect initial clinical data in the second half of this year. These are very rapid trials.

This will be our first randomized, controlled study in pulmonary diseases designed for clinically meaningful and regulatory-aligned endpoints. We believe this will enable MiNK to pursue rapid development pathways.

Now, in other disease settings, we've spoken to you about our graft-versus-host disease program already. We've shared more detail foundation of this program and the study design.

In fact, our intent is to help patients undergoing hematopoietic stem cell transplantation, where more than half of the patients have graft failure and GvHD. We plan to not only improve engraftment success, but prevent acute GvHD.

This study is important. It's garnered the support of two distinct sources of non-dilutive funding.

The NIH NIAID STTR award supports the development of preclinical and translational work, while the Mary Goo's Clinical Trial Award directly funds the clinical trial execution at the University of Wisconsin, including patient enrollment and trial operations. The clinical trial is in final review at the university with clinical initiation targeted for the first half of this year.

We believe we'll be dosing very soon. This structure allows us to advance into immune-mediated diseases and immune tolerance settings without incremental capital burden.

It's disciplined expansion. It's funded, targeted, and aligned with our platform.

Non-dilutive funding is part of how we operate. In 2025, we secured multiple sources of non-dilutive capital funding, including NIH funding, philanthropic support, and consortium funding through See Further most recently, which includes approximately—it's over a million dollars to get into our IND-enabling studies and meaningful double-digit downstream economics.

The See Further collaboration is particularly important not just for the non-dilutive funding to support IND-enabling development of a really important target, a PRAME-targeting iNKT TCR, but for what it represents strategically. This program was selected as one of the first within the See Further consortium, an international pediatric oncology initiative supported by Cancer Research Horizons, LifeArc, and Great Ormond Street Hospital, reflecting external validation of both the maturity of our platform and its potential in high-need settings such as pediatric cancer.

The collaboration advances our PRAME-targeted, TCR-engineered iNKT program combining a well-characterized tumor antigen with our iNKT platform, which is designed to bridge innate and adaptive immunity and coordinate broader immune responses within the tumor microenvironment. Importantly, the program is structured to generate rigorous, comparative preclinical data across multiple pediatric tumor models to support data-driven candidate selection and advance to first-in-human studies.

From a strategic standpoint, the model allows us to advance a next-gen program in a high-need indication with non-dilutive capital. It also allows us to leverage leading academic and translational experts without building that infrastructure or expanding it internally.

MiNK gets to retain meaningful double-digit downstream commercial participation, and we preserve the platform flexibility through a non-exclusive structure. This is simply not a funding mechanism.

It's really a way to expand the platform, de-risk early innovation, and create long-term value while maintaining capital discipline. Taken together, these sources of capital have enabled us to advance clinical programs and expand the pipeline and generate translational data while preserving shareholder equity.

It's deliberate, and it's a repeatable part of how we're building MiNK. On the financial discipline front, we're doing more with less.

We strengthened our financial position over the year with our cash increasing to about $13.4 million from $4.6, and our operating costs decreasing nearly 40% over the course of the year. The key takeaway is that we've increased cash while reducing burn and continuing to execute on important programs.

With the scale and complexity of the work we're now undertaking, including randomized clinical trial execution, multi-program advancement, and increasing external engagement, we've strengthened our financial leadership. We recently appointed Melissa Orilall as Principal Financial Officer.

Melissa brings deep experience in financial operations, planning, and disciplined execution, including her work at the Whitehead Institute and in corporate banking. Her focus is on ensuring that our capital allocation, reporting, and operational execution is tightly aligned as we advance through this next phase.

Now, on our expanded pipeline, as I've mentioned, we continue to advance our PRAME TCR-iNKT program by non-dilutive funding. Further, our MiNK-215, which is our CAR-iNKT program targeting stromal resistance, is very important.

We've continued to build our translational dataset on this asset as we responsibly bring it into IND-enablement. These currently do not have a specific near-term catalyst, but we would expect to be announcing some within the next 3 to 5 months on our 215 program.

As our dataset has strengthened, we have seen increased external interest in 797 and iNKT biology. Some of you have actually reached out to me specifically about third parties who have announced the combination of 797 in their clinical trials.

As I've mentioned now publicly, MiNK has not formally announced any of our strategic collaborations yet. Strategic partnering does remain core to our strategy, and we plan to continue to keep you apprised as these developments ensue.

What to watch for in 2026: this year, we are focused on some substantial and measurable milestones, which are really quite exciting. In the first half of 2026, as I've mentioned, we expect to initiate our randomized phase 2, phase 2/3 ARDS hypoxemic pneumonia study and the activation and dosing in our GvHD trial.

In the second half of the year, we do expect to have initial clinical data from both of those programs, not only representing our first randomized dataset in pulmonary diseases, but also early immune and translational readouts in GvHD as well as in lung disorders. In parallel, during the first half of '26, we'll continue to build scientific validation through multiple data presentations and peer-reviewed publications extending the datasets presented at SITC and Keystone.

Taken together, these milestones are designed to generate clear, interpretable data that informs our next steps both in development and in potential regulatory and strategic pathways. Now, I'd like to turn the call over to Melissa to review our financials.

Melissa?

Thank you, Jen. During 2025, we executed an at-the-market facility in a disciplined manner, ending the year with a cash balance of $13.4 million.

Since year-end, we have raised an additional $3 million through this program, extending our runway through 2026 and supporting key clinical milestones. Our net loss for the fourth quarter of 2025 was $2.6 million, or 56 cents per share, compared to $2.5 million, or 62 cents per share, for the fourth quarter of 2024.

For the full year, net loss was $12.5 million, or $2.93 per share, compared to $10.8 million, or $2.86 per share, in 2024. These results reflect continued, focused investment in advancing our agenT-797 clinical programs while maintaining disciplined control over our operational spend.

I will now turn the call back to Jen for closing remarks.

Thank you so much, Melissa. Thank you all for being here.

I think just in closing, I'll just reiterate that for us, if you just step back, the story is pretty simple. In 2025, we demonstrated durability, we showed mechanistic validation of our technology, as well as human disease relevance.

Those data have now set the stage for what we're doing going forward. In 2026, we're executing on an important randomized, controlled clinical trial as well as signal detection and clinical advancement in very important disease settings, including GvHD.

We'll be generating clinical data and publicizing that very quickly and advancing towards potential paths for regulatory approval. We have multiple readouts planned in the first half of this year with data from our upcoming trials and preliminary readouts in the second half of this year.

We're excited, and I look forward to your questions. I'll now turn the call back over to the operator.

Hi, good morning. Thanks for taking the questions.

A couple from me, maybe starting with the phase 2 pneumonia and ARDS study. Could you kind of talk through how many patients approximately that trial is going to be and what the appropriate control arm is here?

Then, you also talked about development in IPF, what sounds like would need to be a separate trial, maybe just talk about how you're thinking of these different indications. Thank you.

Hi, Emily. Thanks so much for your question.

Absolutely. We have not publicly posted the program in hypoxemic pneumonia.

What I'm going to share with you is that currently, in the disease population that we're pursuing, there are no approved therapies. Patients are treated with standard of care.

This is the same state that we were in when we conducted our phase 1/2 trial establishing the dose of these cells in this population of patients. What we've demonstrated is that patients are predominantly treated with steroid therapy, and of course, anti-infectives, antifungals, etc., but really physician's choice in this disease setting.

We have two things that are really important. One, we've already observed and presented that these cells appear to be quite active in restoring immune functionality and clearing pathogens independent of steroids being on board, which is unique.

Many times, there's a concern about immune suppression with steroid use, standard-of-care steroid use, and we're not observing that. These cells appear to be sort of steroid-resistant, their ability to modulate immune function, clear pathogens in the presence.

We will be looking at physician's choice, effectively standard of care, the cells will be added on top of standard of care versus the cells alone. A critical piece of this is Dr.

Therese Hammond is leading up our pulmonary disease programs. She's also clinically still seeing patients in the ICU.

Therese is boarded in pulmonary critical care, neurocritical care medicine, and has been treating patients with this disease profile for now decades of her life. For us to be able to have such a thoughtful leader on this program and such an informed clinician, it gives us a real opportunity to position these cells and to bring them forward into patients who we believe they will be most effective in.

Taking the cells plus or minus standard of care gives us not only the differentiation of the cells, the added potential of the cells, but also maybe paradigm-changing for these patients in the ICU.

Great, thank you. Maybe—

Sure.

Oh, sorry. Can I just ask one more?

On the second-line gastric cancer trial, could you just remind us the status of that and when we may be able to see efficacy data from that study?

You will be seeing some efficacy data in the first half of this year at a major conference, which we'll be announcing relatively soon. We're excited about that.

I did not answer your question about IPF. Pulmonary fibrosis, end-stage in particular, is another disease setting.

It's effectively an immune-related condition. We've demonstrated that with our human data, and it's a substantial opportunity for us to develop the cells in IPF.

We have some important preclinical observations as well as some now human data demonstrating that this is a pathway where we believe the cells can bring benefit. You're going to be hearing more about the design of that trial and the development path as we advance over the next couple of months.

We will very likely host a special meeting in this disease setting. We have selected a scientific advisory boards of informed clinicians in this space and have developed a program to advance.

We'll be very responsible though about how we're going to be funding that program, you'll hear more about that relatively soon.

All right. Thank you.

Yes, good morning. Thanks for taking our questions, and appreciate the comprehensive update.

Just on the last point on IPF and even GvHD, what target patient population, Jen, you have in consideration and wonder what differentiating aspects to some of the recently approved antifibrotic, anti-inflammatory approaches you aspire to have the cell therapy be positioned against? Then, I have to ask on some of the IL-15 iNKT cell combination trial launching on ct.gov, could you help us understand how and what this 30-subject kind of total exposure would inform what you are looking to independently do with looks like the randomized, controlled trial in the ARDS setting?

I was not sure if the populations that you are exploring are overlapping across those combination and randomized trial settings. If you could clarify that, that would be great.

Mayank, thank you for your questions. I want to make sure that I have them correct, because you did cut out for just a moment.

I think on the randomized ARDS trial, the patient populations will be identified as hypoxemic pneumonia. There's a very specific global ARDS definition system that allows us to be very specific and selective about this patient population.

They will be selected and identified based on their oxygenation, very quantifiable way of interrogating this, as well as important organ function state. We will put the detailed eligibility criterion on clinical trials.

This is another program where we're going to be announcing very soon upon the announcement of the launch of the randomized phase 2, as well as the dosing in GvHD, we'll be hosting a very special R&D meeting that will allow you to talk with our experts, our clinical development experts, as well as review a deep dive of the programs and the eligibility of these patients. In ARDS, there are currently no approved therapies, this becomes standard of care, becomes really a physician's choice in this disease setting.

There are no functional cell therapies in this setting. What we've been able to observe in our early-stage development is that our cells really persist, and that they are not vulnerable to steroids.

That allows the cells to continue to modulate immunity in this setting, and we observe that. We see we can administer the cells, a billion cells tolerably.

We observe that the cells are in the peripheral system for some time, a number of days, before they then home very specifically to lung tissue. We've been able to use a special technique that allows us, particularly in ventilated patients, to take samples from within the lung tissues called the bronchial lavage is the assessment that we can test in order to interrogate the immune cell, the local immune modulating capability of the cells.

It gives us two opportunities: in addition to just radiologically looking at what's happening clinically within a patient's lungs, we can start to see clearance of pathology, clearance of some inflammatory markers. You can see this radiologically.

Then also, when we really dig into lung tissue, we're able to see what is actually happening. In these patients, we see the substantial pro-inflammatory signatures, and what we've publicly disclosed and will be publishing even more this year in the first half will be some of the anti-inflammatory signals that we see here in this population of patients.

We're really dampening pro-inflammatory signals, we're eliminating fungal infections, we're eliminating some gram-negative bacteria, which is a major problem. This becomes an even more substantial problem in some austere regions like war zones or places where we will be studying these cells, where multidrug-resistant organisms are a substantial problem.

Given that we've already been able to demonstrate not only with our clinical trial that we published on, but also through emergency use that we've continued to help patients with, we've demonstrated that we can impactful clinical activity and modulate some of these multidrug-resistant organisms, clearing them from patients with some of the most severe critical illnesses. This is such an important part of the work that we're doing right now.

You'll hear more about the eligibility of these patients, and I'm going to invite you specifically to talk with some of the experts in this disease setting. I think that was a longer way of answering the simple question on standard of care

and

what will be adequate controls, which would be really just physician's choice in this population.

I appreciate it. Thank you, Jen.

I don't know if I missed that or my question got out, if you could address the combination approach with the IL-15 agonist, that trial that launched on clinicaltrials.gov, what the rationale was and how is that different than the study that you just referenced? Thank you.

Mayank, thank you. Thank you very much.

The study that I've referenced is the MiNK-sponsored randomized phase 2 trial that we have not yet posted on clinical trials. We will be doing so; it's currently in review.

The study that you're referring to, and I'm grateful that you brought it up, I've received a host of inbound inquiries about this from investors as well as from regulators, and I want to be very clear that MiNK has not formally announced any collaboration or any clinical trials with the IL-15 superagonist. I think that's an important thing to understand.

If we are to advance with these types of strategic collaborations, we will be very public about doing so. At this time, strategic collaborations are really important to MiNK, and we have a number of discussions that are actively underway, not only for clinical trial combinations—there's a lot of excitement about 797—but also for broader strategic collaborations, as well as minority financial investments in the company, none of which have we publicly disclosed at this time.

We will do so during the appropriate time.

Thanks, Jen.

Thank you, operator, and thank you all so much for your participation today.