MiNK Therapeutics, Inc.

off-the-shelf product of native, non-engineered, invariant natural killer T cells. Agent 797 delivered benefits to patients with heavily pretreated solid tumor cancers. Thirty-four patients with metastatic cancer who have exhausted all available treatments, including prior anti-PD-1 treatment, were treated with a single dose of Agent 797 without administration of toxic lymphodepleting agents. and we administered 797 alone or in combination with pembrolizumab or nivolumab. We reported that agent 797 was well tolerated up to a billion cells dose and promoted clinical benefit in a range of heavily pretreated solid tumor cancers. And in particular, we saw encouraging activity in a patient with metastatic gastric cancer who had no prior response to anti-PD-1 therapy, and that includes a single treatment with anti-P1 pembrolizumab, the patient received four cycles of, and after failure on pembrolizumab, the patient received nivolumab in combination with standard of care chemotherapy, again with no response. After being treated with a single dose of agent 797 in combination with nivolumab, the patient achieved a partial response with a 42% reduction and tumor burden, and this continues now beyond nine months. Sorry, that was our reporting period. This response is continuing at nine months. We also saw benefit in other solid tumor cancers, including durable disease stabilization and biomarker responses in patients with non-small cell lung cancer who had failed prior anti-PD-1, testicular cancer, appendiceal cancers, and other solid tumors. The safety profile 797 was found to be tolerable up to a million cells, no evidence of neurotoxicity. No dose-limiting toxicities were observed, and no severe cytokine release syndrome greater than grade three reported in the trial. And really importantly, we gained insights into the persistence and the homing and the immune-modulating activity of INKT cells in patients. We found that while INKT cells rapidly leave the periphery and enter in home-fit tissues, We see that they're also still persistent and detectable in the periphery for about eight weeks. This is really quite important because this demonstration shows that these cells actually can be viable and persistent without having to look with a patient. We also reported important translational findings that highlight IMKT's ability to generate and drive immune cells into the tumor for destruction of cancer cells. And Mark's going to tell you a bit more about these data in just a moment. Overall, our findings showcase the potential of an allogeneic, off-the-shelf INKT cell therapy in combination with anti-PD-1 in cancers resistant to current treatments, including immunotherapy. They support the expansion of our solid tumor program into PD-1 refractory non-spal cell lung cancer, as well as gastric cancer. And our trial in gastric cancer is being led by a world leader, Dr. Yelena Jinjigian. She's the Chief of Gastrointestinal Oncology at Memorial Sloan Kettering Cancer Center. The trial will advance through non-dilutive, grant-funded program targeted to start in just a few weeks and is planned to enroll about 40 patients over nine centers who will be treated under Memorial Sloan Kettering's umbrella and who will be treated with a cell therapy in combination with standard of care chemotherapy, as well as in combination with a very exciting multifunctional anti-CTLA-4 antibody, which is advancing in late-phase trials. Botansilumab is a lead program from our parent company, Agenis. Now, as a refresher, we have previously published preclinical models and data which demonstrate the potent synergy between INKTs, Anti-PD-1, and Botansilumab. We've published those data and presented them previously at AACR. These data reveal that in preclinical models of metastatic lung disease, the combination of INKT cells, PD-1, and botanosilumab resulted in near complete tumor elimination in this model, B16 model. These data and the safety and clinical benefits that we've observed with 797 in solid tumors support our next phase of development with this program. We expect to provide additional data updates, as well as more detail on our clinical programs in the second half of this year. I will now turn the call over to Dr. Mark Van Dijk, our Chief Scientific Officer, who will provide an update on our Next Generation Pipeline, which includes the IND-enabling activities of our novel FAPCAR-INKT cell therapies, as well as more detail about the functional attributes of 797 that we believe underscore the observations of clinical benefits in solid tumor cancers.

Mark. Thank you, Jen. We're quite excited about the observations of AHDR of clinical benefit in patients with heavily pretreated metastatic cancers. These patients are the ones who inspire our work as we leverage the INKT platform to expand the clinical benefit observed with approved therapies and develop innovations to address areas where current therapies actually fall short. So our technologies, which you'll hear more about at our annual shareholder meeting, includes the ability to generate armored CAR INKTs, develop INKT engagers, cell engagers, and advance novel PCR therapies. In addition to our native clinical stage agent 797 program, our most advanced preclinical programs include armored allogeneic FAPCAR INKT, and the Next Generation Armored BCMA INKT. So our lead program, Agent 797, is designed to expand clinical benefit observed with approved therapies. And our data at AACR is the first glimpse of the possibility of these cells to deliver on these benefits. It's a well-known phenomenon that anti-PD-1 therapies are effective at countering tumor immune suppression. However, chronic use of these therapies leads to immune exhaustion. So we've previously shown that Agent 797 can improve the anti-tumor activity of immune cells that are present in the tumor microenvironment. Specifically, we've shown that IKT cells can activate dendritic cells, preferentially kill M2 macrophages, and restore killing capacity of exhausted T cells. So in data ascertained from our clinical trial of Agent 797, We showed that agent 797 induced pro-inflammatory cytokine responses, including significant increases in interferon gamma, a hallmark of INKT activation and potentially indicative of tumor INKT activation, which is paramount to tumor control and tumor destruction. Importantly, INKT cells are naturally tissue homing. So in preclinical data previously presented, we've demonstrated that INKTs could be administered without lymphodepletion. They rapidly traffic out of the circulation within days of administration and into tissues, including bone marrow, liver, and lung, where they remain in some cases exceeding 35 days. So in our clinical trials, we reported a similar pattern of rapid translocation out of the circulation, while they remain at detectable limits and persist for approximately eight weeks. In our patient with durable response beyond nine months, we also showed that INKTs drive clonal T cell expansion in cancers with a high neoantigen burden. Immunogenicity really triggering the expansion of these cancer-fighting T cells. While we plan to report more detailed information of INKTs in the tumor microenvironment at a later update this year, currently our data demonstrate a mechanism of INKT cells to enable T cells and NK cells trafficking two tumors, reinvigorate partially-exhausted CD8 T cells, and improve effector functions within the tumor microenvironment, which is exemplified in these patients with clinical or biomarker response after a single dose of agent 797. As we continue to expand the potential of INKTs in solid cancer, we have advanced our next-generation INKT programs, including our novel IL-15 armored FATCAR INKT, MINK215. Cancer-associated fibroblasts, which are targeted with this therapy, are key tumor-supportive components of the immune-suppressive tumor microenvironment in several cancers, including non-small cell lung cancer. This adverse tumor microenvironment can be addressed by our fibroblast-targeting, or FAP, CAR-INKT therapy, which naturally homes to tissue such as the lung. In preclinical models, we reported very exciting data showing the potential of MINK215 which demonstrated robust efficacy in non-small cell lung cancer preclinical models, eliminating tumor burden in the lungs and enhancing tumor-specific CD8 T-cell infiltration through stromal remodeling. This is a program we're actually very excited about, and Dr. Shannon Boy, one of our lead scientists at MINK, will be presenting new data at the American Society of Gene and Cell Therapy annual meeting on May 19th. I will now turn the call over to Jen for closing comments.

Thank you, Mark. Well, I get more and more enthusiastic about the data that we're advancing and the technology and the science behind these very powerful cells. And in conclusion, I'm really happy to share with you the progress that we've made in advancing this platform. And as Mark just mentioned, not only addressing and expanding the benefits from available therapies for patients today, but what they will need tomorrow. This process, of course, is made possible by the incredible advancement of Dr. Joy Zhao and her team in our CMC group. Our current process, our manufacturing process, is designed to generate for 5,000 doses per year, and we are building currently and expect to have a fully donor-independent process over the course of this next year. And this development will come without the kind of capital-intensive efforts associated with most cell therapy Enjoy it with us today to answer any questions. We'll also be showcasing a deep dive into our manufacturing process, technologies, and advancements at our annual meeting this year. Very importantly, and what has been contributing to our high efficiency is our team is small, and we've kept it that way, and we've made tremendous progress. Launching the company as an IPO in October of 2021, advancing three clinical programs highly efficiently and now identifying tumor types that may allow us to develop Agent 797 on a rapid path to development to expand benefit to patients. And a specific set of solid tumor cancer sets us up very well. And we're doing this with a team of under 35 people. And as Christine will share with you, we've been able to manage our team and our expenses very efficiently, and we're looking forward to being able to financially support the initiatives that I shared with you throughout the course of the year and well into next year. Christine?