Good morning and welcome to MiNK Therapeutics' Second Quarter 2025 Conference Call and Webcast. All participants will be in a listen-only mode until the question -and -answer session. Please note that this event is being recorded. If anyone has any objections, you may disconnect at this time. I would now like to turn the conference over to Zack Armen from MiNK's Investor Relations. Zack, please go ahead. Thank you, operators, and thank you all for joining us today. Today's call is being webcast and will be available on our website for replay. I'd like to remind you that this call will include forward-looking statements, including those related to our clinical development, regulatory and commercial plans, timelines for data release, 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, and Christine Klaskin, Principal Financial and Accounting Officer. Now, I'd like to turn the call over to Dr. Buell to highlight our progress from this quarter. Thank you, Zack, and thank you all for joining us today. At MiNK, we continue to be the most clinically advanced company, industrializing off-the-shelf invariant natural killer T cells. Based on our observations and experience with these cells, we continue to believe that these are the most important cells for immune reconstitution and disease elimination. We'll talk about a little bit of that today. We're pioneering the science, and as you can see from all our financials, we have some of the most disciplined operations and efficient use of capital in this space. In the first half of this year, we've made meaningful clinical progress scientifically and operationally, with important financial actions that now extend our runway beyond mid-2026. This position is the result of deliberate burn rate reduction, streamlined operations, and the strategic integration of high-impact funding. In this quarter, we achieved significant milestones. We published important observations from our clinical trials, including a complete clinical response in a 49-year-old man with metastatic testicular cancer. This patient had failed all standard therapies and multiple investigational therapies, as we reported in Nature’s Oncogene just last month. I'll go into more of the details shortly. This durable response underscores the potential of our iNKT platform, particularly allo-iNKTs, agenT-797, to address unmet needs in cancer and other immune-related diseases. Additionally, we also reduced our Q2 operating cash burn by over 30% year -over -year, reflecting our operational efficiencies. Momentum in late-stage strategic partnership discussions continues, with increased market capitalization following the Oncogene publication, signaling growing investor confidence in iNKT therapies. This visibility has led us to refine the structure and terms of the potential partnerships that were under discussion to maximize value for science, operations, and our shareholders. We remain in active dialogue with multiple parties and continue to see strong interest in our science and our platform, with the goal of securing partnerships that can expand our capabilities, extend our runway, and accelerate our program execution. To summarize the landmark clinical cases that I just highlighted a moment ago, the data that we published in 2025 demonstrate how iNKT therapies can address some very challenging and refractory cancers. In July, Nature’s Oncogene publication, our report of a durable complete remission in a 49-year-old man with metastatic testicular cancer, unresponsive to platinum-based chemotherapy, high-dose chemotherapy with stem cell rescue, checkpoint inhibitors, and anti-TIGIT-based therapies, shows the potential. A single dose of 797 infusion, without lymphodepletion and without HLA matching, achieved a sustained remission for now more than two years, with no cytokine release syndrome or GvHD. These findings were led by oncology experts, Dr. Benjamin Garmezy and Tony Greco. Earlier, in the same Nature’s Oncogene journal, we presented a refractory gastric cancer case, also resistant to chemotherapy, immune therapy, and checkpoint inhibition. This patient, after a single administration of agenT -797, experienced greater than 40% tumor shrinkage that was durable beyond the 10 months in the monitoring period. These data spurred our currently ongoing phase 2 trial in collaboration with Memorial Sloan Kettering Cancer Center, Dr. Yelena Janjigian, and Dr. Sam Sutheran. These data were presented at ASCO GI and at AACR IO, showing that 797's ability not only to rapidly traffic the tumor, turning immunologically cold tumors hot, even in PD-1 resistant cancers. Our iNKT cells are a rare immune subset with intrinsic tumor homing capability. The capacity to infiltrate disease tissue and with the unique immune regulatory function that can both activate anti-tumor immunity and temper harmful inflammation is unusual and very unique to this cell type. Unlike conventional T or NK cells, iNKTs recognize glycolipid antigens presented by CD1B molecules, enabling them to engage targets that are not accessible to most other immune effector cells. This dual capacity to kill directly and to orchestrate other immune components positions iNKTs as an important element on the therapeutic armamentarium in both oncology and immune-mediated diseases. Now, our exciting frontier beyond oncology, we are applying iNKTs to immune complications or hematopoietic stem cell transplantation and to severe inflammatory syndromes such as Acute Respiratory Distress Syndrome. The opportunity here is substantial. In stem cell transplantations each year, thousands of patients with advanced hematologic malignancies, including AML, CML, MDS, and ALL, undergo allogeneic transplantation. These patients, more than half of them, face risks of graft-versus-host disease, failed engraftment, and disease relapse. Our upcoming phase 1 trial with 797 will specifically evaluate the prophylaxis of acute GvHD in adults more than 18 years of age undergoing allogeneic hematopoietic stem cell transplantation from any donor type, matched sibling, matched or one allele, unmatched or haploidentical, following essentially standard treatment, which is myeloablative, reduced intensity, or non-myeloablative conditioning with post-transplant cyclophosphamide. Eligible patients will have a KPS greater than 70 and meet standard allo-indication. The commercial opportunity is substantial in the U.S. and Europe alone. We see an estimated more than 20,000 patients eligible in this setting. The preliminary data published by Dr. Jenny Gumperz, one of our leading scientific advisors, has demonstrated early in preclinical settings the mechanism of action that we believe underlies the ability of these cells to not only prevent GvHD, but also to enable successful, more successful engraftment. Success is substantial. If agenT -797 is effective in this indication, this could represent alone a first-in-class high-value opportunity to transform transplant outcomes while meaningfully expanding our commercial reach. In respiratory distress, 797's immune-modulating properties, reducing hyperinflammation while preserving anti-pathogen immunity, have already shown very encouraging survival signals in clinical experience, including virally associated ARDS. The global respiratory distress incidence is over 3 million cases per year with no approved modifying therapies. Even a targeted subset, such as mechanically ventilated patients with moderate to severe ARDS, could represent a substantial market opportunity. We expect to announce relatively soon the advancement of a randomized phase 2/3 study with external funding to advance iNKT cells in patients with respiratory distress, building on our published data in Nature’s Communication. Now, these programs, the GvHD program and the ARDS program, are going to be advanced through some substantial support externally. With DoD funding for the STTR grant and supportive funding from the University of Wisconsin Cancer Center grant to Dr. Jenny Gumperz and Dr. Hung Tao Lee, our HSCT trial is expected to begin enrollment this year. Dr. Gumperz's and Lee's early work suggests that iNKTs can enhance donor stem cell engraftment, limit GvHD, and potentially obviate the need for cytotoxic lymphodepletion ultimately. This would be a paradigm shift. This program will use a dose escalation design with two different doses to evaluate safety, GvHD incidence, time to engraftment, relapse rates, early immune reconstitution, and prevention of infections. Importantly, this trial and associated translational research are funded to proceed with minimal capital impact. Finally, our engineered iNKT program. While our lead focus remains on our native allo-iNKT program, we're also developing engineered approaches that appear to be best in class based on our preclinical observations. Our CAR -iNKT program, MiNK-215, was featured most recently in Frontiers in Immunology, and what our lead Scientific Advisory Board Chair, Dr. Mark Exley, calls one of the world's foremost experts in iNKT biology, has called an iNKT manifesto. These data were published just three weeks ago, and this work outlines a framework for applying engineered iNKTs to solid tumors, potentially overcoming some of the trafficking and persistent limitations seen with conventional T and engineered NK therapies. Looking ahead, we anticipate several important catalysts. We expect top-line data from our phase 2 gastric cancer trial by the end of 2025, the initiation of our GvHD phase 1 trial in the same time period, and further advancement of our MiNK-215 program, including the potential addition of a strategic partner or more than one strategic partner. With a lean cost structure, a strong balance sheet, and multiple value-creating milestones ahead, MiNK is well-positioned d to advance multiple programs in parallel while preserving shareholder value. I'll turn the call over to Christine Klaskin to review the financials. Thank you, Jen. We ended the quarter with a cash balance of $1.7 million, and since quarter end, we've strengthened our financial position by raising an additional $13 million through equity sales. This reinforces our resources and extends our cash runway through the middle of next year, providing a solid foundation to advance our programs and execute on the upcoming milestones Jen just highlighted. Our net loss year to date reflects the continued investment in the progression of our agenT -797 program and increased non-cash expenses compared to the prior year. Net loss for the second quarter 2025 was $4.2 million or $1.06 per share, compared to $2.7 million or $0.73 per share for the second quarter of 2024. For the six months ended June 2025, our net loss was $7 million or $1.76 per share, compared to $6.5 million or $1.82 per share for the same period in 2024. I'll now turn the call back to the operator for questions. Thank you. To ask a question, press star then one. To withdraw, press star then one again. Our first question comes from the line of Mayank Mamtani with B. Riley Securities. Your line is open. Yes, good morning, Team. Thanks for taking our questions and congrats on a strong quarter. Could you talk a bit more about this preventative GvHD trial design, you know, number of patients, endpoints you're looking at? It looks like you're looking at two dose levels. It would also be helpful to put this in context with what we have as approved different mechanisms, I believe, post-transplant in the late-line GvHD setting. I have a couple of follow-ups. Thank you, Mayank. Great to hear from you. This trial is going to be, it's designed currently as a phase 1. We'll do a couple of patients as a run-in for safety with a lower dose, just a handful of patients. Then we'll move to a higher dose, which has been our target dose, which is a billion cells per patient, which we believe is going to be the target dose here as well. That will expand for signal seeking in about 20- 25 patients for the first part of the trial. We have an opportunity to expand this, and we believe, based on the preclinical evidence, and when you look head-to-head with some of the commercially available agents right now in preclinical models, the iNKTs not only appear to be more tolerable, but also more effective. There are a couple of areas where these cells can be more effective because they don't just mitigate GvHD, they can enable engraftment success, which will also mitigate GvHD. Getting these cells in early, enhancing engraftment success, and then preventing infections, which we've seen both in virally induced lung conditions, as well as in some of our oncology programs, is going to be an important part of this. GvHD, mitigating GvHD, of course, is additional to that. A more tolerable regimen that could be more effective, not only in engraftment success, infection reduction, and GvHD mitigation. Thank you. On the 797 gastric cancer study, it looks like you are going to have some updates before year end. Could you maybe give a little bit more color on what that could be and if any medical conferences you're targeting? Lastly, I didn't see in the press release about the FAP-CAR -iNKT program that you have with the cash balance that you have now. Is there plans to maybe fast-track that, or are you trying to be more focused on the autoimmune side of things? Thanks for taking your question. Thank you very much. There are a couple of questions. I think I'll start with your first. Gastric cancer, we started enrolling now over 18 months ago, and therefore we have some mature clinical follow-up. We presented data at AACR IO, and it was a plenary session and a poster presentation by Dr. Sutheran. What we have been able to show is that in a disease setting that is essentially an immune desert, when we administer 797, we essentially see CD8 T cell infiltration across the stroma into the tumor and then disease elimination. The biomarker data are publicly available on our website. They'll also be published in a formal peer-reviewed journal. What we did not present at AACR IO was the clinical follow-up on these patients. We look forward to getting the survival follow-up and seeing some of the immune-modulating properties of these cells deliver something that we believe is not only clinically valuable, but presents a substantial survival benefit for patients with this very difficult-to-treat disease. With respect to the FAP -CAR -iNKT, our focus right now is to advance these cells in some of these immune-mediated diseases. We see this has been on our hot list for a substantial amount of time. We're thrilled to be able to advance this in partnership with the University of Wisconsin Cancer Center, as well as the Do D, to get these cells into this very important disease setting. We think that there's a way to interrogate the biology in the disease setting that we'll launch in, that we're going to test in first, and ultimately changing the paradigm of how patients are currently undergoing stem cell transplantation, which is an incredibly difficult regimen. It's also difficult for the patient. They spend many, many weeks alone in a hospital. I think that these cells can make a substantial change here. That said, our FAP-CAR -iNKT, you've seen the data that we've presented at AACR and at SITC and at the cell therapy meeting. The differentiation of this product is very impressive. We have essentially developed the viral vectors in a GMP environment, and we've conducted a substantial amount of the IND preclinical activity. We've done quite a bit of work, and we've been able to do so very efficiently. Now in our own hands, we have the capability to start to do small-scale manufacture of that at very limited cost. Therefore, we do believe that we can advance this program to an IND with limited expense. We also have quite a bit of partnering interest on this program, and there may be a collaborator that will work with us to advance this that will further accelerate our ability to do so and also minimize the financial impact on the company in doing so. It is our highest priority, and our capital will be focused on getting the immune-related disease settings underway very aggressively. Our FAP-CAR -iNKT will move in parallel, but with less financial impact. Understood. I'll hop back in the queue. Thank you, Jen. Our next question comes from the line of Matt Phipps with William Blair. Your line is open. Hi, thanks for taking the question. This is Eric on for Matt Phipps. Just one question. I know you guys have previously mentioned maybe running two potential studies in graft-versus-host disease, maybe one more focused on the prophylactic setting and another more focused on acute steroid or graft-free patients. I was just wondering if you're finding updated thoughts on this development plan. This program that's now funded and advancing is essentially in the prophylactic setting. Patients will be engrafted. I'll share with you in follow-up, Eric, some of the details that I outlined on the call earlier. Effectively, patients will receive their engraftment, their treatment, their engraftment, and they'll be dosed with the cells to interrogate engraftment success, minimizing infections, graft-related infections, transplant-related infections, and mitigating GvHD. The trial will incorporate our ability to do so. We will not be administering it right now in patients who are actively experiencing GvHD. We'll be preventing it. Got it. Thanks. Our next question comes from the line of Emily Bodnar with H.C. Wainwright. Your line is open. Hi, good morning. Thanks for taking the question. I'm curious if you can give us more info on how much these two grants are. I guess what percent of the clinical trial costs for the GvHD program would you expect us to fund? I'm curious if you could give more color on the phase 2/3 trial you mentioned in ARDS and what the registrational path could look like there. Thanks, Emily. For the first, these are fully funded. MiNK does retain the ability with the partnership that we have with the university as well as the PIs to provide support if there are specific questions that we want to ask, biomarker questions, translational data, things that are not currently drafted into the program that are ancillary and may strengthen some of the scientific literature with this. It is at our discretion. The trials are going to be going without our capital infusion, but infusion at our discretion. It gives us quite a bit of flexibility to interrogate more biomarkers and expand the trial or support acceleration of the program in some capacity. Respiratory distress, this is near and dear to us. We have some announcements that we are planning to come out relatively soon. Our observations, just as a quick reminder, are that we saw patients who were elderly, intubated, mechanically ventilated, and some on VV-ECMO. We not only saw substantial improvements over what's best available care for patients right now in the ICU, with survival exceeding 80% in patients on VV-ECMO and 75% on those mechanically ventilated, which particularly at the time that we studied, and this was when patients, this was in the early time during the pandemic, when patients were dying at very rapid rates. The comparable control from a control group in the same centers that we were testing the cells, the survival was between 10% and 22%. These data have excited us quite a bit. Importantly, we've also had the opportunity to interrogate some of the cytokines, the local immune modulation of these cells, and we've published the anti-inflammatory signal. Secondly, we also observed a reduction in secondary infections, including no bacteremia, fungemia, etc. We also had a couple of emergency use cases, some of which we just dosed the cells, and others we had the opportunity to dose the cells plus commercially available cytokines. What we've observed is that these cells are the most critically important component of the regimen for these patients. You'll be seeing some data coming out relatively soon showing that upon administering these cells within 24- 40 hours, we could see complete elimination of a fungemia, particularly cocci, which is a problem, and it's causing atypical pneumonia, which is growing in prevalence in our country and worldwide. That is really quite concerning. We believe that this trial will address a few things. One, that the FDA has clear guidance on the outcomes of respiratory distress. Despite the fact that there are currently no approved trials, no approved products to treat respiratory distress in patients right now, this therapy appears to be, in the words of Dr. Terese Hammond, our lead investigator, the most broadly acting therapy that she has had her hands on in the ICU. We will look at 28-day mortality. That's the FDA's convention and what they've suggested to us. We will also look at prevention of secondary infections. We will look at ventilator-free days, getting patients off of a ventilator to also help prevent some comorbidities associated with the ventilator use. We will look at oxygenation as well. That's an important part of this. In our clinical trial, we observed that we very quickly enhanced pulmonary function and also oxygenation in the lungs upon administration of the cells. This trial will be designed to give us the full scope of what these cells can do with primary endpoints designed for FDA registration. That is something that we will certainly do in partnership with the FDA. Great. Thank you. If you would like to ask a question, press star then the number one on your telephone keypad. There are no further questions at this time, and this concludes the Q&A session. I now turn the call back to Dr. Jennifer Buell for closing remarks. Thanks, operator. Thank you all for joining us and for being with us today. We're eager to share further updates on our clinical and strategic progress, which will be forthcoming. Thanks again. This concludes today's call. Our replay will be available in the Events and Presentations section of our investor website at https://investor.minktherapeutics.com/events-and-presentations. Thank you for participating. You may now disconnect.