Good morning. Welcome to MiNK Therapeutics' fourth quarter and full year 2022 conference call and webcast. All participants will be in a listen-only mode until the question and answer session. Please note, this event is being recorded. If anyone has any objections, you may disconnect at this time. I will now turn the call over to Zack Armen, Head of Investor Relations at MiNK. Thank you, 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 contain forward-looking statements, including statements regarding our clinical development, regulatory, and commercial plans, as well as timelines for data release and partnership opportunities. These statements are subject to risks and uncertainties, and we refer you to our SEC filings for more details on these risks. Joining me today on the call 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 in 2022 and plans for the year ahead. Thank you so much, Zack. Good morning, everyone. Thanks for joining our fourth quarter and full year 2022 earnings call. It's a great pleasure to be with you today and to share an update on the progress of our company. I'm really excited and proud to share that our dedication to advance the field of cell therapy has yielded quite exciting and differentiated results in 2022 and set us up for a very active 2023. We've made important strides in advancing iNKT cells, our platform, in generating critical data in research as well as in the clinic, some of which we've already presented publicly and more of which will be coming your way this year. Recall that agenT-797, our lead pro-product advancing in the clinic, is an allogeneic, unmodified or naked iNKT cell. These cells have shown promise as a monotherapy as well as in combination with approved anti-PD-1s, KEYTRUDA or OPDIVO, in clinical trials. These are trials in patients that are heavily pretreated with solid tumor cancers. We're excited to present an update on this progress at the upcoming AACR meetings next month, and we'll also be announcing our plans for developing iNKTs in solid tumor cancers such as non-small cell lung cancer and relapsed refractory gastric cancer in collaboration with world leaders in these diseases. These data build upon our earlier presentation at the Society for Immunotherapy of Cancer, or SITC Conference in Boston last November. We also detailed our findings in our inaugural R&D day last November, where we reported on our lead program, and we showed that it can be demonstrated tolerably alone and in combination with commercially approved anti-PD-1s. We demonstrated that we could dose patients tolerably up to 1 billion cells per dose without lymphodepletion and with no observations of cytokine release syndrome, CRS, or neurotoxicity. These data enable the development flexibility to deliver the benefit of these cells without toxicity observed with first-generation cell therapies. We concluded our phase I study of 797, our allo iNKT, in patients with viral ARDS. We reported 70% survival, which compares favorably to in-hospital control and CDC data of survival rates of 10%-22%. Even more compelling were the observations of a reduction in secondary infections that are oftentimes fatal in patients in the ICU. We've submitted these data to a top-tier journal and expect a publication this year. These results in patients with viral ARDS have generated great interest from government and public financing and private financing opportunities. We're currently in discussions to externally finance the development of iNKT cells in acute infections and associated fatal consequences like respiratory distress, an indication for which there are no approved therapies. We'll be providing more updates on the advancement of these discussions this year. The development of allo- iNKT is an indication outside of oncology is only made possible through the manufacturing productivity that our team has made. MiNK has addressed the limitations of the use of cell therapy products beyond oncology and in infections in many ways. First, we focused on the development of iNKT cells, which have shown promise in treating viral infections and respiratory illnesses. By using iNKT cells, we can avoid some of the limitations associated with traditional cell therapies, such as the need for matching donors and recipients, the use of lymphodepletion, and the limitations of cost and scalability. We've addressed this. We've invested in high-throughput manufacturing technology which allows for the rapid production of large quantities of iNKT cells, generating billions of cells from a single donor and thousands of doses per donor. Our process is now FDA-cleared for implementation into our clinical trials without external dependency. Our manufacturing approach is designed to make iNKT cell therapy more accessible to patients and to improve the scalability of cell therapies overall. As we continue to make progress in our clinical programs, we're also making important advancements in deepening our understanding of the novel mechanisms of action of iNKT cells and their unique advantages over available cell therapies. At the end of last year, we presented data elucidating the long-hypothesized mechanism of iNKT cells that underscore their potential as a highly effective living medicine for patients with cancer. Specifically, our scientists demonstrated that iNKTs have the killing power of NK cells and the memory of T cells. They activate dendritic cells. These are signalers that help the immune system recognize tumors. We've shown that iNKTs also kill M2 macrophages. M2 macrophages are immunosuppressive cells that constrain the body's ability to fight tumors. We also reported that iNKTs can restore the tumor killing capacity of exhausted T cells. This is a very important mechanism in which CD8 T cells become exhausted and lose their tumor-fighting capability. As we reported since the last year, iNKTs can overcome this mechanism and reinvigorate exhausted CD8 T cells, restoring their killing capacity. These mechanisms help to explain some of the early signals of benefit that we've observed in solid tumor cancers. Additionally, our research team has made important progress on our pipeline, including the development and advancement of MiNK-215. MiNK-215 is an armored IL-15 FAP-CAR-iNKT designed to target the tumor stroma and modulate the tumor microenvironment to increase tumor killing capability. Targeting FAP, which is fibroblast activation protein, with CAR iNKTs, these are chimeric antigen receptor invariant natural killer T cells, can benefit patients in several ways. FAP is a protein that's found in high levels in the stroma of many evasive solid tumor cancers, but it's absent in most normal tissues. By targeting FAP-CAR-iNKT, we could specifically seek out and destroy cancer cells that express FAP while leaving healthy cells intact. Moreover, FAP is known to play a key role in promoting tumor growth and metastatic disease, and FAP inhibits the body's immune response against cancer. By targeting FAP with CAR iNKT, it's possible to overcome these barriers of resistance and activate a potent immune response against cancer. In summary, targeting FAP with CAR iNKTs can provide a highly specific and effective approach to fighting cancer while minimizing damage to any healthy tissues and boosting the body's natural immune defense. The molecule is an IND-enabling studies for an IND submission planned in 2024. We are in dynamic markets and a unique time where fiscal responsibility and prudence will be critical to delivering the value of our science and the potential of our technology for patients with cancer. Partnering remains core to our strategy to fully leverage the potential of our platforms and products quickly, and these include public and private collaborations. At MiNK, we'll focus our internal efforts on deepening our datasets in select solid tumor cancer indications where iNKTs can complement available and approved standard of care and we believe expand the benefit of available therapies to patients with specific tumor types. We'll further elucidate our development plans with the data release at the upcoming AACR conference. We will continue to leverage our research productivity and exciting findings outside of oncology through strategic collaborations. I will now turn the call over to Christine to go over our financials. Thank you, Jen. We ended the fourth quarter 2022 with a cash balance of $19.6 million as compared to $38.9 million at December 31st, 2021. Cash used in operations for the year and fourth quarter ended December 31, 2022, was $18.9 million and $4.4 million, respectively. This compares to $12.8 million and $1.7 million for the same periods in 2021. This increased funding was related to the internalization of our cGMP manufacturing of agenT-797 for clinical trial supply, which has increased our production and results in decreased supply cost prospectively. Net loss for the quarter ended December 31, 2022, was $7.8 million, or $0.23 per share, compared to a net loss for the same period of 2021 of $5.8 million or $0.18 per share. Net loss for the year was $28.0 million or $0.83 per share, compared to $30.2 million and $1.16 per share for the year ended December 31, 2021. Thank you. We'll now turn the call over for questions. Operator? The floor is now open for your questions. To ask a question at this time, please press star one on your telephone keypad. At any point you'd like to withdraw from the queue, please press star one again. You'll be provided the opportunity to ask one question and one further follow-up question. We'll now take a moment to render our roster. Our first question comes from the line of Emily Bodnar from H.C. Wainwright. Please proceed. Hi, good morning. Maybe without, like, specifically talking about data, can you just comment on what made you select gastric cancer for an expansion cohort? Are gastric and lung the only indications you're planning to evaluate or are these just the first and then you kind of will look to see if there's any others after that? Are these going to be combination cohorts or monotherapy cohorts? Thanks. Emily, thanks for your question. We are currently focused on expanding data sets and indications where we are quite enthusiastic about the results. Gastric and lung are opportunistic for two reasons. One, when patients are refractory to anti-PD-1 therapy, there are very limited treatment options for them, and that includes in patients that are PD-1 refractory with lung cancer, the patients are treated with docetaxel, 9% response rates, and there's an enormous opportunity to expand benefit. We also see quite a bit of complementarity by adding ourselves into this setting, either alone or in combination with approved PD-1s. These indications enable a path forward where we may be able to develop the product quite rapidly as a monotherapy on top of available standard of care. Those are the two that we've spoken about, and we'll deepen the discussion following our data presentation at AACR on some other areas where we'll be continuing to explore the benefits of iNKTs in different solid tumor cancers. Okay. Makes sense. Maybe can you just reiterate the timelines for when you might have MiNK-413 enter the clinic? Thanks. MiNK-413 are armored BCMA CAR. We've brought that through the critical gating items for manufacturing for master cell bank. This product could be ready for IND enablement in 2024. Our next question comes from the line of Kalpit Patel from B. Riley. Please proceed. Yeah. Hey, good morning, and thanks for taking the questions. Maybe starting with expectations for the AACR update, can you give us a sense of how many patients worth of data we should expect there? Maybe what proportion of those patients would have lung cancer or gastric cancer? Thanks for your question, Kalpit. We'll have to hold responding until you see the data set. Just a reminder, what we have spoken about is we launched the trial in March and had completed accrual for the phase I dose escalation and dose escalation and preliminary expansion. It is a phase I solid tumor study. It does have a mix of patients, predominantly those who are refractory to all prior therapy. These are late-line patients. They are a standard phase I cohort with some operational enrichment for certain tumor types, which you may see some enhanced representation of specific tumor types in the cohort. Most of which is a measure of the limited therapeutic options for patients at this stage, in development. Our cohort, we completed accrual to it, at the beginning of the year. Those, we'll be presenting as much data as possible from that cohort by the time of the data presentation at AACR. Okay. In, in the planned expansion cohorts for lung cancer, are the patients gonna be primarily you know, checkpoint naive, or are you gonna include, you know, both checkpoint naive and checkpoint refractory patients into that study? Mostly checkpoint re-refractory for a few reasons. This, we have been able to demonstrate that we can dose monotherapy iNKTs in patients who have failed prior IO therapy, and we have been able to dose in combination. We could do so tolerably to 1 billion cells. We'll be sharing the data from those signals. I think importantly, one thing that is commonly observed in patients who are PD-1 refractory is the exhausted CD8 T cells for those cells that actually cannot enter the stroma. At SITC this past November, we presented data demonstrating that our iNKTs can actually reverse the CD8 exhaustion signature and also kill M2 suppressive immune suppressive macrophages. Both of those, we believe, set us up for bringing benefit in patients who have actually failed anti-PD-1 therapy because of the translational data that we've been able to generate and present. IO ref IO naive patients in with non-small cell lung cancer are very far fewer of the population. We're really focused on these refractory patients. Okay. Makes sense. Thanks very much for taking the question. Mm-hmm. Our next question comes from the line of Jack Allen from Baird. Please proceed. Great. Thank you so much, and congratulations on the progress. I guess my first question was around the decision to move forward with the PD-1 inhibitors. I was wondering if you had any comments about the thoughts that you had previously had around Agenus' proprietary CTLA-4 inhibitor, botensilimab, and any potential combination use there? Jack, I'm so glad you asked. We will be making some announcements at AACR about the combination which we did not elucidate about different combinations that we'll be advancing both in our hands, as well as in combination with some of the agents from Regeneron portfolio. I think, really importantly, Regeneron most recent data presentation was at ASCO GI on botensilimab. For those who may be less aware, the product appears to be bringing extraordinary benefits to a host of solid tumor cancers that have failed prior therapies. That includes MSS colorectal cancer as well as PD-1 refractory non-small cell lung cancer. In their most recent earnings call, they shared the response rates that are really exceeding, I think, 50% in that cohort of patients with non-small cell lung cancer. What we had previously collaborated on were preclinical studies that actually demonstrated the synergy and complementarity of agenT-797 or iNKT cells in combination with botensilimab, the uronide version, and balstilimab. In the model, it was a B16-OVA model with metastatic lung disease, and we saw that the combination of CTLA-4 PD-1 eliminated about 30%-40% of the disease. The cells alone did about that same reduction in liver mets. When you put the three or two together, so the cells in combination with botensilimab or the cells in combination with botensilimab and balstilimab, we saw near complete tumor eradication. It sets us up for a few really important opportunities that could that could be expanding the benefit of what we see with botensilimab because of the complementarity of the mechanisms that I mentioned before. We have some additional preclinical data that we will also be releasing in other indications where the combination may be quite productive. One of the areas that we believe the cells can expand the benefit of botensilimab is in patients with metastatic liver disease. What we see, and we've shared a bit about, is that in a patient in our study with metastatic liver disease, we saw that the cells not only home to liver disease, but also modulate the disease and eliminate the disease in some settings in those liver mets. We do believe that there's an enormous opportunity to expand the benefit of botensilimab by adding the iNKT cell agenT-797 to this combination, and we'll be talking more about that at AACR. Great. Then I just have two quick follow-ups. I guess, on the first one, outside of oncology, how are you thinking about the timetable as it relates to development of engraft versus host disease? Should we expect that that's going to be a partnered indication at this point? Then outside of the broader MiNK portfolio, I was wondering if you had any comments on a recent clinical hold from one of your competitors on an autologous iNKT program and how we're thinking about the safety of allogeneic versus autologous iNKT. Okay. Great, great questions, Jack. On the first, as I mentioned, of course, we're in a really dynamic market where we need to be quite thoughtful. For GVHD, we see an enormous potential there, and we have some supportive data to indicate a quick path forward to bring benefit to patients, both not only for GVHD, but also for engraftment success. This is an area where we have, we are looking at ways of advancing this into the clinic in ways that would not not result in additional expense from our balance sheet right now, and that's through strategic collaborations and investigator-sponsored support as well. We'll be talking more about that soon. We've designed the program, and it is designed in a way that we believe can bring the cells forward to a potential very rapid approval, and we'll be making some announcements about that program in the upcoming weeks. The, the athenex data that you're referring to, that was a patient who had had a fatality on a clinical trial. This was a patient with neuroblastoma. That patient actually had a metapneumovirus, which is commonly seen, and it's fatal in pediatric patients who are lymphodepleted. As you can see from the trial with AstraZeneca, they actually lymphodepleted their patients, which is not something that we believe we need to do. We have not lymphodepleted. We've demonstrated that we can administer the allo iNKTs very tolerably, no neurotox, no CRS, no related serious toxicities above grade III. We're in a position where I do believe that the cells can be administered and dosed really quite tolerably without lymphodepletion. And we also are seeing and will be sharing an update about the persistence of the cells even in that setting. I think that the case with AstraZeneca is related to lymphodepletion and subsequent viral infection secondary to the lymphodepletion that led to a very unfortunate circumstance for this patient. I don't think that it reads through to the safety or tolerability of iNKT cells. Great. Thanks so much. Thank you. Our final question comes from the line of Matt Phipps from William Blair. Please proceed. Morning, Jen. You know, I was wondering on the FAP-CAR. In the preclinical post you had at SITC, some of the efficacy data was actually best combined with, you know, NY-ESO-1 T cells. How does that kind of preclinical data influence your thoughts around maybe combination development of this program? Do you plan on trying to look at any biomarker for enrollment or, like, an immune-excluded phenotype or just how do you pick patient populations for that program? Well, that's a great set of questions, Matt. Thank you. For that program, we actually set it up using the NY-ESO-1 TCR and that model to exemplify what a chronic antigen-stimulated environment would look like. What happens when immune cells are sort of constantly perturbed and then can these cells actually overcome that perturbation and also reinvigorate CD8 T cells to killing potential? At our poster at SITC, we actually demonstrated that we could do that. That model was to help us better understand what these cells can mechanistically do to reverse exhaustion and then carry the CD8 T cells into the stroma and invoke killing. Now, the design of that molecule with FAP targeting gives us opportunities for a potential biomarker-selected population. We won't restrict for that at the beginning, but we will measure for it, you know, upfront. We will look if it will be necessary to enhance clinical benefit by restricting the population to FAP-expressing tumors or if we may have more broad activity independent of the biomarker selection. We'll start broad, and then we will assess and then decide if we need to exclude or enrich for the FAP-expressing tumors. Got it. Thanks. On the BCMA program, you know, Do you guys have evidence yet, I can't remember. I don't think this was at SITC, but of kinda treating a multiple myeloma cell line that relapsed or grew out of previous BCMA therapy exposure with something maybe that's kind of commercial or late stage. I guess why not go absolutely in different like GPRC5D or maybe a dual targeting construct just given how entrenched BCMA therapies are becoming? You know, Matt, BCMA therapies certainly are competitive. I hear that we're seeing some remarkable progress with some of the more modern BCMA therapies, including very high response rates. There is a continued problem. We have Marcella Maus on our scientific advisory board. What we see is that patients continuously progress on BCMA, and 2/3 of them still express the BCMA antigen. So there does appear to be a challenge with respect to durability of response in those patients despite the high response rates. We also still see challenges in access for those patients, both of which I think that the iNKT product can address. We've been able to demonstrate really robust scalability with our manufacturing capabilities. That would read through certainly to our ability to enable broader access to a BCMA. We've also armored our BCMA with IL-15. We presented at SITC, and I'll share that poster with you. We did present data that actually demonstrated superior antitumor immunity using our IL-15 BCMA CAR iNKT compared to what's commercially available right now. That program, due to its competitive nature, we have prioritized that program, and we've announced that previously, in order to be, you know, really selective with opportunities that we believe can bring significant value creation even sooner. The BCMA program is very exciting for us and a program that we're committed to advancing because of the reasons that I mentioned previously. It is a program that we would contemplate strategic collaborations for as well, and we've been embarked in discussions, predominantly with groups who actually need a next-generation BCMA that is more accessible and sustainable compared to what's available right now. Great. Okay. Thanks, Jen. Thank you, Matt. I would now like to turn the call over to Jen Buell, CEO, for closing remarks. Thank you very much, operator. It was a pleasure to be with you all today. Looking forward to speaking with you at AACR. Thank you again. Bye-bye. Thank you, ladies and gentlemen. This does conclude today's call. 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