MiNK Therapeutics, Inc.

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 Zach Arman from Mink's Investor Relations. Zach, please go ahead.

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 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, Zach, and thank you all for joining us today. At Mink, we continue to be the most clinically advanced company industrializing off-the-shelf and variant 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 in 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 and late-stage strategic partnership discussions continue. With increased market capitalization following the Oncogene publication, signaling growing investor confidence in INKT therapies. This visibility has led us to refine the structure in 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 demonstrates how INKT therapies can address some very challenging and refractory cancers. And 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 antitiget-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, Doctors Benjamin Garmese and Tony Greco. And earlier, in the same Nature 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 two trial in collaboration with Memorial Sloan Kettering Cancer Center, Dr. Yelena Janjigian and Dr. Sam Saturn. These data were presented at ASCOGI and at AACRIO, showing that 797's ability not only to rapidly traffic the tumor, turning immunologically cold tumors hot, even in PD1 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 of 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 I trial of 797 will specifically evaluate the prophylaxis of acute GVHD in adults more than 18 years of age undergoing allohematopoietic stem cell transplantation from any donor type, matched sibling, or one allele unmatched or haploidentical following essentially standard treatment, which is myeloblative reduced intensity or non-myeloblative conditioning with post-transplant cyclophosphamide. Eligible patients will have a KPS greater than 70 and meet standard allo indications. The commercial opportunity is substantial. In US and Europe alone, we see an estimated more than 20,000 patients eligible in this setting. The preliminary data published by Dr. Jenny Gumpers, one of our leading scientific advisors, have demonstrated early in preclinical settings the mechanism of action that we believe underlie the ability of these cells to not only prevent GVHD but also to enable 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 antipathogen immunity, have already shown very encouraging survival signals and 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 GBHC 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 University of Wisconsin Cancer Center grant to Dr. Jenny Gumpers and Dr. Hongtao Li, our HSCT trial is expected to begin enrollment this year. Dr. Gumpers and Li'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 programs. 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, MINT215, was featured most recently in Frontiers in Immunology. And what our lead Scientific Advisory Board Chair, Dr. Mark Exley called, one of the world's foremost experts in INKT biology, has called and 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 limitation seen with conventional T and engineered NK therapies. So looking ahead, we anticipate several important catalysts. We expect top line data from our phase two gastric cancer trial by the end of 2025. the initiation of our GVHD phase 1 trial in the same time period, and further advancements 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 to advance multiple programs in parallel while preserving shareholder value. I'll turn the call over to Christine Klaskian to review the financials.