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 speakers' remarks there will be a question-and-answer session. 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 Orla, 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. And we've also demonstrated that our product retains both 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 the most highly regarded 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 and the application of iNKTs in immune-related diseases. By way of background, our immune system has two distinct arms to immunity: innate or natural immunity that we are born with and responds immediately when faced with a threat, and adaptive immunity that 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. So 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 is that when iNKT cells are not functional or are deficient, we observed 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, allowing us to isolate cells from one individual, a healthy donor, and deliver them to another individual, 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 have evidence to suggest that iNKT cells could 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, specifically in solid tumor cancers, that is our focus, and MiNK has 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, has set us up in the best position to deliver for these patients. Our newly appointed Chief Scientific Officer is Dr. Marc 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, Takeda, and more recently from Rubius, and 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 1 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-iNKTs that are available to patients the moment they need them. They're currently distributed to our sites 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 1/2 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. Boussios, presented and showed that iNKT cells travel to the liver, lungs, and bone marrow. They prefer tumors, and they persist. We believe these features will contribute to the cell's ability to provide 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. So importantly, if you think about iNKTs with their invariant TCR, they are 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. And 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 relapse/refractory multiple myelomas. 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 it's rich in CD1d ligand, meaning that iNKTs will naturally home to this lipid antigen that is highly expressed in this cancer type. The cells will recruit T cells and NK cells and secrete tumor-killing cytokines without engineering. And importantly, we believe that AgenT-797 can be administered without lymphodepletion, and we expect 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 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 is 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 brought our therapy to help during the heart of the pandemic. Our preclinical data has shown 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 1 trial of Agent-797 in viral acute respiratory distressed 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 1 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 being identified for funding by the Defense Advanced Research Projects Agency, or DARPA, to investigate the cells against immune dysregulations and 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 this year. In addition to the signals of clinical activity, we've also demonstrated that 797 can be administered in patients with a host of immune diseases with a favorable safety profile at doses now up to 1 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 wholly 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 iNKTs 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' balstilimab. 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.

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 period 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'll now turn the call back to Jen.

Thank you very much, Christine. And operator, we will now open up the call for Q&A.

Your first question comes from the line of Kalpit Patel with B. Riley Securities.

Yes. Hey, good morning. Thanks for taking the questions. I guess, first, starting with the clinical update for AgenT-797 in the 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 will share, of course, the size of the cohort. But what I can remind you of is that we launched the program 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 checkpoint KEYTRUDA and OPDIVO in patients with solid tumors. We have enrolled these cohorts at quite a fast pace, really somewhat of a record pace because of the interest in the program. So 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 1 study with our monotherapy as well as in combination with PD-1.

Okay, I understand. You mentioned early observations of disease-modulating activity in a patient with rectal cancer and possibly another patient with refractory multiple myeloma. Can you provide more details on this data? Were these patients on monotherapy or a combination therapy? Also, at what dose level of cells did they receive?

Stay tuned, Kalpit. I don't want to compromise some of the data that's specified in our abstract. We look forward to sharing this information with you at the public presentation.

Okay, fair enough. Based on the activity you’re seeing so far, how are you considering the approach for multiple doses of AgenT-797? Is there any data or insights you can share that indicate multiple doses might be beneficial?

We have launched a program focused on exciting findings regarding autologous iNKTs in solid tumor cancers, including neck cancer, lung cancer, and hepatocellular carcinoma. This data is publicly available. One key hypothesis about the performance of these autologous cells is their ability to migrate to tissue, which is why they exist in low quantities in the periphery. Through trafficking and the interaction with lipid ligand CD1d, B cells can target the disease site, recruiting T cells and NK cells, which are highly effective at producing gamma. This production is vital for their survival. In preclinical studies, we observe these same capabilities, and in clinical settings, we aim to replicate the successful results seen with the autologous cells in a manner that is scalable, accessible, and affordable for patients. The dosing in the autologous setting, which is relevant to your question, involved single administrations that demonstrated significant benefits. Our current plan is also for a single administration, with patients being treated alongside KEYTRUDA or OPDIVO. We are investigating how long these cells last at the disease site — our preclinical data indicates persistence beyond 36 days, while some clinical results suggest it may extend even further. We are determining the optimal timing for dosing in relation to cell persistence, which remains under evaluation. The foundation of our programs is built on autologous platforms that have demonstrated effective tumor control. This control stems not just from the cells’ abilities to adjust T and NK cell responses but also from their influence on the tumor microenvironment. We will share additional data that highlights how these cells can affect various markers of exhaustion, which is crucial for durable responses. I believe we will be able to provide further insights into our next steps, including details on expanding indications, as well as information on dosing and frequency.

Is there a plan to continue exploring AgenT-797 without lymphodepletion in future studies, or might there be an exploratory cohort testing lymphodepletion before deciding on 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. And what we've seen, of course, from data that has come out with the J&J, BCMA-CAR is that these lymphodepletions 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. So 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. But so far, our plan is no lymphodepletion.

Okay, great. Thanks very much for taking the questions.

Thank you.

Your next question comes from the line of Jack Allen with Baird.

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 in 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. I think about the timing of that arm of the business moving forward?

Okay. So for the infectious disease program that we've discussed today in our annual program, what I will share is that we identified patients when we launched our IND; of course, it was the very beginning of the pandemic. The data that we had and others have generated show that these cells can modulate immune dysregulation, and they can dampen proinflammatory cytokines in the lung, in particular, promote survival in influenza, and show great benefit in models of pneumonia and have quite a significant impact in SARS-CoV-1 and MERS. Now, as we have observed since 2013, we have had a number of pandemics. So we were first dealing with Ebola, and then, of course, MERS and SARS-CoV-2, monkeypox, etc. Our government is looking for variant-agnostic approaches in which they can really mitigate immune dysregulation. These cells may actually present that opportunity. DARPA, of course, 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. So we have a partnership that's under discussion right now that will help us better understand the mechanisms of these cells in mitigating the harmful side effects of infections more broadly and viral ARDS. Then we would expand those findings to an expanded clinical program beyond the COVID-19 pandemic and possibly apply it much more broadly. You will hear more this year about that partnership.

Great, thank you so much. And then just one other question and then I have one more follow-up. But on the graft versus host disease program, I know you mentioned the positive central impact of the cells in graft versus host. I'd love to hear where things fit as it relates to advancing potentially AgenT-797 in that indication as well?

That's right. Graft versus host disease is a beneficial side effect of these cells as it actually reduces graft versus host. We've shared some public presentations and publications from our team and our advisors explaining the mechanism by which these cells may help. There are two areas where these cells can be beneficial: one is in transplant uptake, enabling a successful hematopoietic stem cell transplantation while also mitigating graft versus host. We believe these cells can serve in both of these areas. Our focus during the first half of this year has been on advancing our solid tumor program and completing our work in viral-ARDS and multiple myeloma. We have received valuable feedback from our scientific advisors and prominent figures in GVHD. Our program has been identified as a primary interest for hematologists. We will provide more details on the launch of this trial, which we plan to initiate this year, testing the cells for transplant acceptance and mitigation of GVHD, particularly in earlier disease stages.

Great, thank you so much. And then my final question was, more recently, there have been a few comments made by reporters as it relates to a peer of yours and the potential acquisition of an iNKT program out in the domain. I was wondering if you had any comments as it relates to the business development of your assets moving forward? And how are you thinking about advancing the various pipeline programs that will make it into the clinic, maybe more of the CAR programs?

Sure. So 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’re, of course, born out of a long-standing veteran in immuno-oncology, Agenus. 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 cells in their native form because of the features they boast and what they can do for patients. We've also delivered now what I think is a superior engineered program that we will be disclosing at upcoming conferences. Our iNKT engager platform is something that I am not aware of any other companies having the capabilities to do, and we have our Chief Scientific Officer, of course, Marc van Dijk, an expert across these platforms, who has designed and developed these platforms for MiNK. We will pursue business development very strategically. It includes certainly non-dilutive partnerships such as government partnerships that 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 will keep you informed on our progress. I think if you look at the productivity of partnerships that our parent company, Agenus, has been able to deliver on, that includes a number of programs that generated about nearly $1 billion in partnership transactions and milestones. You can see the scale that we can monetize our research productivity to finance and fund the business and bring our lead programs forward independently. MiNK shares that philosophy. The opportunity to have strategic collaborations that will allow us to take full advantage of the depth and breadth of our research capability will be very important.

Great, sounds good, good plan. Thank you so much for the questions and congratulations on the progress.

I appreciate it. Thanks so much, Jack.

Your next question comes from the line of Matt Phipps with William Blair.

Hey Jen. A couple of questions from me. So 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 hint of what that is ahead of seeing maybe closer to something I know others are looking at, maybe cytokine secretion or things when they talk about armored CAR T cells?

Matt, you are so astute, and I enjoy working with you for that reason. We will be giving you more clarity when we announce details around this program this year. We'll share how we've created a product that is differentiated not only by the CAR design itself, a CAR-iNKT, but also how we engineered this to be differentiated, and we think it could potentially be superior to what's available today. So stay tuned on that.

Okay, thanks. And then 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 saw last year in the ARDS trial.

Yes, that's really important. Last year, we shared data from the ARDS trial, but it was solely based on peripheral data. The key point is that these cells quickly migrate to their areas of interest after administration, leaving the periphery quite swiftly. The data we presented focused only on the periphery and displayed a low level of persistence. However, the data we will share at an upcoming conference will provide insights into where these cells are migrating and how long they remain in those locations, including biopsies from patients and important tissues of interest. Therefore, you will notice differences in the data we present at upcoming conferences this year compared to what we previously showed regarding peripheral distribution in patients with ARDS.

Thanks, Jen. I look forward to the data.

I 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 the 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.