Good day, and welcome to the MiNK Therapeutics Second Quarter 2022 Earnings Conference Call. Please note today's conference call is being recorded. All lines have been placed on mute to prevent any background noise. After the speaker's remarks, there will be a question-and-answer session. If you would like to ask a question during this time, simply press star followed by the number one on your telephone keypad. If you would like to withdraw your question, press star followed by the number one again. Thank you. At this time, I would like to turn the conference over to Kimberly Ha, Head of Investor Relations. Thank you, operator, and thank you all for joining us today. Today's call is being webcasted 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, Dr. Joy Zhou, Vice President of Manufacturing, Christine Klaskin, Principal Financial and Accounting Officer, and Melissa Orilall, Director, Global Financial Operations. Now, I'd like to turn the call over to Dr. Buell to highlight our progress and speak to our outlook for the remainder of the year. Thank you very much, Kimberly, and thank you all for joining us for our first quarterly earnings call. MiNK Therapeutics was launched as an IPO just about 10 months ago, and today we stand as the most advanced company pioneering allogeneic or off-the-shelf invariant natural killer T cells or iNKT cells in three active clinical programs. We have shown that we can isolate these cells from healthy donors. We can produce them at scale in our in-house GMP manufacturing suite. We've also demonstrated that our product retains full potency and tumor-killing potential after freezing. Thus, for all of our clinical trials, our cells are at the site when the patient needs them. Our focus is on isolating these high... The most highly conserved cells in immunity and delivering them to patients who need them most, patients whose immune system has failed to eliminate cancer or prevent serious complications from infection. Currently, we have three active clinical programs, and we expect to share data from these programs at a conference this year. As a pioneer in the field, we appreciate that MiNK must not only advance science at record-breaking paces, but also contribute to the growth of information in the application of iNKT's in immune-related diseases. By way of background, our immune system has two distinct arms to immunity, innate or natural immunity, that which we are born with and responds immediately when faced with a threat, and adaptive immunity, that which we acquire over time to adapt to new external threats like COVID-19. At MiNK, we are pursuing iNKT cells because of their unique properties to modulate both arms of immunity and leverage the strength of both T cells and NK cells. This makes them critical in every line of the body's natural defense. What happens without iNKT cells or when these cells are in limited quantity in vivo? What we've shown in preclinical models and in humans, when iNKT cells are not functional or are deficient, we observe the development of autoimmune diseases such as diabetes, heart disease, asthma, and cancer. A remarkable feature of these cells is their invariant T-cell receptor or TCR. This receptor is common in everyone, and this allows us to isolate cells from one individual, a healthy donor, and deliver them to another individual or a severely ill patient. Without engineering the cells and without rejection from the recipient, there is no graft versus host disease with these cells. In fact, we actually have evidence to suggest that iNKT cells could actually prevent rejection. They may help patients accept transplants and prevent graft versus host disease subsequently. This is why we're pursuing our iNKT cell therapies for cancer and other immune-related or immune-mediated diseases. We expect these cells to have a major impact with a significant effect specifically in solid tumor cancers. That's our focus. MiNK developed the platform to achieve this. For cell therapies to deliver transformative benefits across the majority of tumors, and I'm talking about solid tumor cancers, they need to be affordable, effective, and able to be manufactured at scale. Our recent progress, including the full internalization of our discovery platforms, our engineering capabilities, and now our internal GMP manufacturing, we're set up in the best position to deliver for these patients. Our newly appointed chief scientific officer is Dr. Mark van Dijk, an industry veteran who has built the platforms and technology that have given rise to dozens of clinical and commercial-stage novel antibodies, bispecifics, and TCRs, including those at Bristol Myers Squibb, Genmab, and Agenus. Additionally, we recently appointed Dr. Joy Zhou as head of manufacturing. Joy brings decades of cell therapy, cell and gene therapy manufacturing expertise from J&J, from Takeda, and more recently from Rubius. Now she's applying those internally here at MiNK. Our manufacturing platform and proprietary reagents are set up to deliver more than 10,000 doses annually. These programs and platforms are scalable to deliver nearly one billion doses with our own in-house capacity. Our proprietary reagents and process enable a product that is more than 99% pure iNKT cells from healthy donors, and these cells retain their tumor-killing potential after lengthy cryopreservation. Thus, they can be stored and delivered internationally. Our manufacturing team has delivered a process and infrastructure to facilitate a scalable and reproducible manufacturing process for allo iNKT that are available to the patient the moment they need them. They're currently distributed to our site for clinical trials internationally. We recently recognized our in-house GMP readiness with the completion of our GMP manufacturing runs internally at scale. This is a remarkable achievement and the first known industrialization of native iNKT cell manufacturing in the field. Importantly, this progress was completed with an already outfitted manufacturing facility and an experienced team. This was also completed without the capital-intensive requirements commonly necessary for cell therapy production. Today, our lead program, agenT-797, an allo cell therapy of native iNKT cells, is in three active clinical programs. Our phase I/II study of iNKTs alone and in combination with KEYTRUDA or OPDIVO in patients with solid tumor cancers launched in May of this year. Data readouts are expected at a major conference within the next few months. Our encouraging signals, including the reduction of metastatic liver disease in a patient with refractory rectal cancer, builds on data presentations from the Society for Immunotherapy of Cancer, otherwise known as SITC, last year. Our leading scientist, Dr. Mark Exley, presented that iNKT cells traffic to the liver, lungs, and bone marrow. They lyse tumors, and they persist. We believe that these features will contribute to these cells' ability to bring durable, protective benefit to patients with cancer. These data also support the potential benefit of iNKT cells over other cell types like gamma delta cells and natural killer cells. iNKTs are unique in that they can take advantage of their invariant TCR that recognizes the lipid ligand CD1d, which enables the initiation of T cell responses. Importantly, if you think about iNKTs with their invariant TCR, they're naturally engineered effectively to home to where they need to go. iNKTs also express activating NK cell receptors, making them able to initiate a potent NK cell-like cytotoxic response. Importantly, they don't express the inhibitory NK cell receptors, so they can retain and advance that response. Lastly, iNKT cells can modulate the tumor microenvironment and transactivate T cells and NK cells. We're also evaluating agenT-797 native allo iNKTs in relapsed refractory multiple myeloma. While progress has been made with BCMA CAR T therapies in myeloma, the treatments require cytotoxic lymphodepletion, and the durability is still somewhat underwhelming. Importantly, two-thirds of patients who progress following BCMA CAR T therapy still exhibit the BCMA antigen. The other feature of multiple myeloma is that it's rich in CD1d ligand, meaning that iNKTs will naturally home to this lipid antigen that's highly expressed in this cancer type. The cells will recruit T cells and NK cells and secrete tumor-killing cytokines without engineering. Importantly, we believe that agenT-797 can be administered without lymphodepletion, and we expect that these cells will also improve the durability of response in this tumor type. In our earliest patients treated, we reported lengthy disease stabilization beyond 10 months and suppression of tumor biomarkers in our first-treated patient. A 50-year-old male was treated with 100 million cells per dose and experienced a rapid reduction in M-spike protein, a greater than 50% reduction in tumor cells in the bone marrow, and disease stabilization exceeding 10 months. Enrollment's ongoing, and we plan to present more data later this year. These cells are also very active in controlling infection. iNKT cells are one of our earliest lines of defense and are particularly active in protecting lung epithelial tissue. This is critical in severe cases of acute respiratory distress, secondary to COVID or influenza, pneumonia, or other related diseases. As such, we've brought our therapy in to help during the heart of the pandemic. Our preclinical data had showed that these cells can extend survival in influenza, mitigate harmful consequences of pneumonia, and treat effectively SARS-CoV-1 and MERS in preclinical models. In our phase I trial of agenT- 797 in viral acute respiratory distress syndrome secondary to COVID-19, we previously reported a survival benefit exceeding 77% in our first release of 13 patients. These patients were predominantly elderly, all were on mechanical ventilation, and all had failed available therapies. We completed our phase I cohort evaluation, and we plan to present data before the end of this year, which will include expanded data of survival as well as other important secondary benefits of agenT- 797. These data have led to our iNKT cells identified as selectable for funding by the Defense Advanced Research Projects Agency, or DARPA, to investigate the cells against immune dysregulation in viral infections, including ARDS and influenza. Our next step with DARPA is to evaluate what our collaboration will look like, including contract negotiations, and we're thrilled with the possibility of supporting DARPA in mitigating current and future pandemic threats with agenT-797, a potential variant agnostic approach to disease mitigation. We expect to provide more details of our potential collaboration later in this year. In addition to the signals of clinical activity, we've also demonstrated that agenT-797 can be administered in patients with a host of immune diseases with a favorable safety profile at doses now up to a billion cells per dose. We've observed no neurotoxicity or cytokine release syndrome, and we've also been able to deliver these cells without lymphodepletion. MiNK's fully owned pipeline spans our next generation engineered iNKT programs, including CARs, TCRs, and bispecific iNKT cell engagers. Our BCMA CAR-iNKT and stromal-targeting CAR-iNKT are both in IND-enabling activities, and we plan to present data on these programs in an upcoming meeting this year. This includes the target selection and first data presentation on our stromal-targeting CAR-iNKT for solid tumors. Through our relationship with Agenus, we are uniquely positioned to launch novel combinations with our iNKT cells and potential best-in-class immune activating agents like Agenus' botensilimab. Our priority is to advance agenT-797 in its native form alone and in combination with checkpoint modulating antibodies with approaches that can lead to rapid registration, such as in combination with standard of care agents in cancers, including cancers of the liver, bladder, and lung. At MiNK, we remain focused on delivering our allogeneic off-the-shelf therapy to eliminate diseases of the immune system. I appreciate your time, and I will now turn the call over to Christine Klaskin to go over our financials. Christine? Thank you, Jen. We ended the second quarter of 2022 with a cash balance of $29.8 million as compared to $38.9 million at December 31, 2021. Cash used in operations for the six months ended and second quarter ended June 30, 2022, was $8.8 million and $4.6 million respectively, compared to $7.6 million and $3.4 million for the same periods in 2021. Net loss for the quarter ended June 2022 was $6.1 million or $0.18 per share, compared to a net loss for the same period of 2021 of $6.3 million or $0.26 per share. Net loss for the six months ended June 2022 was $13.9 million or $0.41 per share, compared to $10.2 million or $0.42 per share for the six months ended June 2021. I now turn the call back to Jen. Thank you very much, Christine. Operator, we will now open up the call for Q&A. At this time, I would like to remind everyone in order to ask a question, please press star, then the number one on your telephone keypad. We'll pause for just a moment to compile the Q&A roster. Your first question comes from the line of Kalpit Patel with B. Riley Securities. Yeah. Hey, good morning. Thanks for taking the questions. I guess first starting with the clinical update for agenT-797 in second half, can you provide details on expectations for this update? Maybe how many patients worth of data would be included, and should we see results from both, the monotherapy and combination-based arms? Thanks, Kalpit. Thanks for your question. We won't share, of course, the size of the cohort, but what I can remind you of is that we launched the program actually in May of this year. We announced our first in human dosing with dose escalation with the monotherapy cells as well as in combination with approved checkpoints KEYTRUDA and OPDIVO in patients with solid tumors. We have enrolled these cohorts actually at a quite fast pace, really somewhat of a record pace because of the interest in the program. I can share with you that the cohort will include, we believe, meaningful follow-up information on patients with advanced cancers enrolling in our phase I study with our monotherapy, as well as in combination with PD-1. Okay, got it. You mentioned early observations of disease modulating activity in a patient with rectal cancer and then maybe another patient with refractory multiple myeloma. Can you provide additional color on these data? You know, were they on monotherapy or combination-based therapy? And at what dose level of cells did they receive? Stay tuned, Kalpit. I don't wanna compromise some of the data that's specified in our abstract. We would- Okay. Look forward to getting this information out to you at the public presentation. Okay, fair enough. How are you know, based on the activity that you're seeing to date, how are you thinking about approaching multiple doses of agenT-797? Is there any data or learnings that you can point to that suggest multiple doses might be useful? I'll tell you. You know, what we have launched, when we launched the program, what our platform has been based on were really some very exciting findings of autologous iNKTs in solid tumor cancers, head and neck cancer, lung cancer, hepatocellular carcinoma. These data are publicly available. Some of the underlying hypotheses of the performance of the autologous cells would be that they can home and traffic to tissues. These are tissue-dominant iNKTs, and that's why they're in such low quantity in the periphery. Because of that trafficking, when they advance in through the lipid ligand CD1d, these cells will home to the disease site, and then they recruit T cells and NK cells, and they're actually one of the most highest interferon gamma secreting cells. The amount that they can produce really contributes to their ability to lyse. In the allo setting preclinically, we're seeing those same features. Now in the clinic, what we would expect to do is to recapitulate the data that has been observed with the autologous cells, but in a setting and with a platform that is scalable and accessible and of course, affordable to patients. The doses that were observed in the autologous setting, to go to your specific question, were really single administrations where we saw some pronounced benefit. Our dose plan today is a single administration. Of course, the patients are being dosed in combination with KEYTRUDA or OPDIVO, and we are now exploring persistence, how long the cells actually persist at the site of disease where we need them to be. Our preclinical data show that they persist beyond the measurement time of about 36 days. Some of our clinical data show that we can go far beyond that, in the clinic, and we will be exploring the best time to dose following the change in persistence of the cells. That's still under evaluation, something that we'll explore. The data that we have built our programs on has really been built on the autologous platforms that has shown that really sufficient tumor control. That tumor control is not only because of these cells' ability to modulate both arms of immunity, innate and adaptive, and recruit T and NK cells, but also to modulate the tumor microenvironment. We also will be sharing some data that may also inform that these cells can impact different markers of exhaustion, which is quite important in durability of responses. You know, it's. I think we'll be able to provide some additional color on next steps beyond the indications that we're going to be expanding in. We'll provide some additional information on dose and dose frequency. Okay, got it. One last question related to lymphodepletion. Is the plan to continue exploring agenT-797 without lymphodepletion in future studies, or do you think you might have sort of an exploratory cohort testing lymphodepletion before finalizing the next steps? Well, based on what we're seeing today, we would continue to proceed without lymphodepletion. We will consider exploratory programs, of course, in partnership with investigators, whether lymphodepletion could expand the benefit of our observations. However, lymphodepletion is really difficult for patients to endure. What we've seen, of course, from data that had come out with the J&J BCMA CAR is that these lymphodepletion may be attributed to some of the secondary cancers that have been observed with their product. To the extent that we can bring a more effective, durable, and more tolerable product to patients, that would be our goal. Our goal would be to administer the product without lymphodepletion, and we'll continue to explore all of the ways to optimize the experience for patients. So far, our plan is no lymphodepletion. Okay, great. Thanks very much for taking the question. Thank you. Your next question comes from the line of Jack Allen with Baird. Hi. Thank you so much. This is Jack Allen from Baird. I really appreciate you taking the questions, and congratulations on the progress. I guess the first one I had was a little bit outside of the solid tumor multiple myeloma setting, but as it relates to the negotiations with the public entities around the COVID opportunity, I'd love to hear some more color about any comparative contracts timing of that arm of the business moving forward. Okay. For the infectious disease program that we discussed today in our annual program. What we have identified, of course, in patients when we launched our IND, of course it was the very beginning of the pandemic, and the data that we had and others had generated show that these cells can modulate immune dysregulation, and they can dampen pro-inflammatory cytokines in lung, in particular, promote survival in influenza, great benefit in models of pneumonia and have quite a significant impact on SARS-CoV-1 and MERS. We went to the agency with that data in hand and we were cleared to start testing in COVID. We released data at SITC last year showing a 77% survival benefit in patients who were elderly and mechanically ventilated and who otherwise would have been predicted to have a 22% survival rate, so we were quite excited. We've continued to expand that cohort and now have really completed our dose-finding cohort and generated data that we plan to present this year at an upcoming conference. Those data were what supported the initial discussions. Now, as we have observed that just in the past, since 2013, we have had a number of pandemics. We were first dealing with Ebola and then, of course, MERS and SARS-CoV-2, monkeypox, et cetera. Our government is looking for variant-agnostic approaches in which they can really mitigate immune dysregulation, and these cells may actually present that opportunity. DARPA, of course, is. Their emphasis is on very high science, and that's something that we'll be partnering with them to elucidate mechanisms initially before expanding the cells in humans. We have a partnership that's under discussion right now that will help us better understand mechanisms of these cells in mitigating the harmful side effects of infections more broadly and viral ARDS. We would expand those findings, of course, to an expanded clinical program that would go beyond the COVID-19 pandemic and possibly be applied much more broadly. You will hear more this year about that partnership. Great. Thank you so much. Then, just one other question and I have one more follow-up. On the graft-versus-host disease program, I know you mentioned that the positive potential impact of the cells in graft versus host. I'd love to hear where things sit as it relates to advancing potentially agenT-797 in that indication as well. That's right. So, you know, for graft-versus-host disease, that's a beneficial profile, side effect really of these cells is it actually mitigates graft-versus-host. I think, Jack, we've shared with you and we could make public certainly some public presentations and publications of our team and our advisory team members' results of the mechanism as to why these cells may mitigate graft-versus-host. Now, there are two areas where these cells can be helpful. One is transplant uptake, the ability to actually have a successful hematopoietic stem cell transplantation, and then mitigate graft-versus-host as well. There are two points of intervention where we believe these cells can be helpful. Our focus, for the first half of this year has really been advancing our solid tumor program and finishing up the work that we had started in viral ARDS and multiple myeloma. We have now collected feedback from our scientific advisors and key opinion leaders in GVHD, and our program had been selected as a primary area of interest and for hematologists. We will be providing some more guidance of the launch of this trial, which we plan to launch this year, testing the cells and transplant acceptance as well as mitigation of GVHD, and we see an opportunity to do that, particularly in the earlier disease setting. Great. Thank you so much. Then my final question was, more recently, there have been a few comments made by reporters as it relates to peer reviewers and the potential acquisition of an iNKT program out in the domain. I was wondering if you had any comments as it relates to business development of your assets moving forward, and how are you thinking about advancing the various pipeline programs at MiNK into the clinic, maybe more the CAR programs? Sure. I think really importantly, Jack, you're bringing up an important point. The capabilities that we have at MiNK are really deep and broad. We were, of course, born out of a long-standing veteran in immuno-oncology, Agenus, and as such, we have the capabilities of delivering a platform that I think is unprecedented that I've seen so far in this field. We launched as a starting point the cells in their native form because of the features that they boast and what they can do for patients. We've also delivered now what I think is superior engineered programs that we will be disclosing at upcoming conferences. Our iNKT, our ability to launch our iNKT engager platform is something that I am not aware of any other companies have the capabilities to do. Our Chief Scientific Officer, of course, Marc van Dijk, is an expert across these platforms and has designed and developed these platforms for MiNK. We will pursue business development very strategically. Certainly non-dilutive partnerships such as government partnerships are really instrumental for our ability to expand and advance the technologies and capabilities that we have. Partners fall into that approach as well. We have a number of active discussions underway, and we'll certainly keep you informed on our progress. You know, I think to the extent that if you take a look at the productivity of partnerships that our parent company at Agenus has been able to deliver on, and that includes a number of programs that generated about nearly $1 billion in partnerships, transactions and milestones, you can see the scale that we were able to actually monetize our research productivity to finance and fund the business and bring our lead programs forward independently. MiNK shares that philosophy. The opportunity to actually have strategic collaborations that will allow us to take a full advantage of the depth and breadth of our research capability, that will be very important. Great. Sounds like a great plan. Thank you so much for the questions, and great congratulations on the progress. Appreciate it. Thanks so much, Jack. Again, if you wish to ask a question, please press star, then the number one on your telephone keypad. Your next question comes from the line of Matt Phipps with William Blair. Hey, Jen. Hope you're well. Couple questions for me. First, I think this is the first time I've seen the word armored used to describe the BCMA CAR T. Just wondering if you might be able to give us any hints at what that is ahead of seeing, maybe a post or something. I know others are looking at, maybe cytokine secretion or things when they talk about armored CAR T, so. Matt, you are so astute and I so enjoy working with you for that reason. We will be giving you some more clarity when we announce details around this program this year. We'll share with you how we've actually created a product that is differentiated not only by the CAR design itself, a CAR-iNKT, but also by how we engineered this to be differentiated and we think to be potentially superior to what's available today. Stay tuned on that. Okay, thanks. I guess just wondering if you can give us an idea if you're seeing any differences in the persistence and distribution of the cells in the ongoing solid tumor and myeloma indications compared to what you showed at SITC last year in the ARDS trial. Now that was that's really important. SITC last year, we presented data in the ARDS trial, but it was based on peripheral data only. The important point here is that these cells, upon administration, rapidly home to disease sites of interest. Rapidly. They are actually out of the periphery quite quickly, and the data we presented was exclusively the periphery, so it showed us sort of a low window of persistence. What's very important about data that we'll be presenting in an upcoming conference is we actually have insights into where these cells are homing and how long they persist in those locations that they are homing to. That includes biopsies from patients as well as important tissues of interest. I think that you will certainly see differences in the data that we present at upcoming conferences this year than what we presented as the peripheral distribution in patients with ARDS. Okay. Good. Thanks, Jen, looking forward to the updates. Really appreciate it, Matt. Thank you so much. At this time, there are no further questions. I'll turn the call back to management for any closing remarks. Thank you very much, operator, and thank you for your participation. We're really thrilled to have an opportunity to share an update on our progress, and we'll be looking forward to connecting at our upcoming data releases. Thank you again. Thank you for participating. You may disconnect at this time.