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Operator: Good morning, and 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.

Zack Armen: 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 time lines 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.

Jennifer Buell: 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. And I’m really excited and proud to share that our dedication to advance the field of cell therapy has yielded a 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 and 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 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-1 KEYTRUDA or OPDIVO in clinical trials, and 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 iNKT 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 of Immunotherapy for 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-1.

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 development flexibility to deliver the benefit of these cells without toxicity observed with first-generation cell therapies. Furthermore, we concluded our Phase I study of 797, or allo-iNKTs in patients with viral ARDS. We reported 70% survival, which compares favorably in hospital control and CDC data of survival rates of 10% to 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 expected publication this year.

Now 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-iNKTs and indications outside of oncology is only made possible through the manufacturing productivity that our team has made. MiNK address the limitation 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 a 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 and 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. And 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.

And as we reported at SITC 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 in variant natural killer T cells can benefit patients in several ways. FAT is a protein that’s found in high levels on the stroma of many evasive solid tumor cancers, but is 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 inhibit the body’s immune response against cancer. So, by targeting FAP with CAR-iNKT is possible to overcome these barriers of resistance and activate a potent immune response against cancer. So, 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 the submission planned in 2024. Now 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 data sets and select solid tumor cancer indications where iNKTs can complement available and approved standard-of-care and we believe expands the benefit of available therapies to patients with specific tumor types and will 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 curation. I will now turn the call over to Christine to go over our financials.

Christine Klaskin: Thank you, Jenn. We ended the fourth quarter 2022 with a cash balance of $19.6 million as compared to $38.9 million at December 31, 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 period 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?

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Operator: Our first question comes from the line of Emily Bodnar from H.C. Wainright. Please proceed.

Emily Bodnar: Hi, good morning. Maybe for without like specifically talking about data, can you just comment on what may be for gastric cancer for an expansion cohort? And are gastric along the only indications you’re planning to evaluate? Or is just the first and then you kind of will look to see if there’s any others after that? And are they going to be combination cohorts or monotherapy cohorts? Thanks.

Jennifer Buell: Emily, thanks for your question. So, we are currently focused on expanding data sets and indications where we are quite enthusiastic about the result 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.

So those are the two that we’ve about and will 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.

Emily Bodnar: Okay. Makes sense. And maybe can you just reiterate the time lines for when you might have MiNK-413 enter the clinic?

Jennifer Buell: MiNK-413 are armored BCMA-CAR. We’ve brought that through the critical gating items for manufacturing for master cell bank. And this product could be ready for IND enablement in 2024.

Operator: Our next question comes from the line of Kalpit Patel from B. Riley. Please proceed.

Kalpit Patel: Good morning, and thanks for taking my question. 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? And then maybe what proportion of those patients would have lung cancer or gastric cancer?

Jennifer Buell: Thanks for your question, Kalpit. We’ll have to hold responding until you see the data set. But 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 preliminary expansion. So, it is a Phase II, the Phase I solid tumor study. It does have a mix of patients, predominantly those who are refractory to all prior therapy. So, 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. But our cohort, we completed accrual to it at the beginning of the year. So those will be presenting as much data as possible from that cohort by the time of the data presentation at AACR.

Kalpit Patel: Okay. And then in the planned expansion cohorts for lung cancer, are the patients going to be primarily checkpoint naive? Or are you going to include both checkpoint naive and checkpoint refractory patients in that study?

Jennifer Buell: Mostly checkpoint refractory for a few reasons. This — we have been able to demonstrate that we can dose monotherapy iNKT 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. and 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 trauma and do the past November, we presented data demonstrating that our iNKTs can actually reverse the CD8 exhaustion signature and also kill M2 suppressive immuno-suppressive macrophages. Both of those, we believe, set us up for bringing benefits 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-naive patients in — with non-small cell lung cancer are very far fewer of the population. So, we’re really focused on the refractory patients.

Kalpit Patel: Okay. Make sense. Thanks, very much for taking my question.

Operator: Our next question comes from the line of Jack Allen from Baird. Please proceed.

Jack Allen: 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 genesis proprietary CTLA-4 inhibitor, Botensilimab and any potential combination use there?

Jennifer Buell: Jack, I’m still glad you asked. We will be making some announcements at AACR about the combination, which we did not elucidate in our — about different combinations that we’ll be advancing both in our hands as well as in combination with some of the agents from Genesis portfolio. I think really importantly; Genesis most recent data presentation was at ASCO GI and Botensilimab. And for those who may be less aware, the product appears to be bringing extraordinary benefit to a host of solid tumor cancers that have failed prior therapies. So that includes MA SS, colorectal cancer as well as PD-1 refractory non-small cell lung cancer. At the 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.

And 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 both version and Botensilimab. So, in the model, it was the B15 OVA model with metastatic lung disease, and we saw that the combination of CTLA-4, PD-1 eliminated about 30% to 40% of the disease. The cells alone did about that same reduction and liver mess when you put the three or two together, so the cells in combination with Botensilimab or the cells in combination with Botensilimab and Beltsville and that we set saw near complete to our eradication. So, it sets us up for a few really important opportunities 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 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 it in a patient in our study with metastatic liver disease. We had the cells not only home delivery disease, but also modulate the disease and eliminate the disease in some settings in those liver mets. So, we do believe that there’s an enormous opportunity to expand the benefit of Botensilimab by adding the iNKT cells agenT-797 to this combination, and we’ll be talking more about that at AACR.

Jack Allen: Great. Thank you, so much. And 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 in graft versus host disease? And should we expect that that’s going to be a partnered indication at this point? And 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 iNKTs?

Jennifer Buell: Okay. Great questions, Jack. So, on the first, as I mentioned, of course, we’re in a really dynamic market where we need to be quite thoughtful. And 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 result in additional extent from our balance sheet right now, and that’s through strategic collaborations and investigators sponsored support as well. So, 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.

Our connectivity you’re referring to, that was a patient who had a fatality on the clinical trial. This is a patient with neuroblastoma. And that patient actually had metapneumovirus, which is commonly seen and it’s fatal in pediatric patients who are lymphodepleted. And as you can see from the trial with fast connect, 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 could administer the allo-iNKTs very tolerably, no neurotox, no CRS, no related serious toxicity, of upgrade three. So, 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 we’ll be sharing an update about site of the cells, even in that setting.

So, I think that the case with 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.

Operator: Our final question comes from the line of Matt Phipps from William Blair. Please proceed.

Matt Phipps: I was wondering on the FAP-CAR and the preclinical poster at SITC, some of the efficacy data was actually best combined with an NY-ESO one T cells. So how does that kind of preclinical data influence your thoughts around maybe combination development of this program? And then 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?

Jennifer Buell: Well, that’s a great set of questions, Matt. Thank you. So, for that program, we actually set it up using the NY-ESO-TCR and that model to exemplify what a chronic antigen stimulated environment would look like. So, what happens when immune cells are constantly perturbed. And then can these cells actually overcome that perturbation and also reinvigorate CD8+ T cells to curing potential. And at our poster at we actually demonstrated that we could do that. So that model was to help us better understand what these cells can mechanistic review to reverse exhaustion and then carry CD8+ T cells into the stroma and invoke killing. Now the design of that molecule with seeing gives us opportunities for a potential biomarker selected population.

We won’t restrict for that at the beginning, but we will measure for it upfront. So, we will look — if it will be another way to enhance clinical benefit by restricting the population to stop expressing tumors for it, we may have more broad activity independent of the biomarker selection. So, we’ll start broad, and then we will assess and then decide if we need to exclude or enrich for the tumors.

Matt Phipps: Got it. And then on the BCMA program, do you guys have evidence yet, I can’t — I don’t think this is a bit of kind of treating a multi-mile only cell line that relapsed or grew out of previous BCMA therapy, exposure was something maybe that’s kind of commercial or late stage? And I guess, why not go after different like GPRC5D or maybe a dual targeting construct, just given how entrenched BCMA therapies are becoming?

Jennifer Buell: Matt, BCMA therapy certainly are competitive. I hear that we’re seeing some remarkable progress with some of the more modern BCMA therapies, including very high response rate. But there is a continued problem and we have Marcellus Mouse on our Scientific Advisory Board. And 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 the patients despite the high response rates. And we also still see challenges and access for those patients, and both of which I think that the iNKT product can address. We we’ve been able to demonstrate really robust scalability with our manufacturing capabilities, and that would certainly to our ability to enable broader access to a BCMA We’ve also armored our BCMA with IL-15.

And we have conducted and we presented it 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 has — we have prioritized that program and we’ve announced that previously in order to be really selective with opportunities that we believe can bring significant value creation even sooner. Now the BCMA program is very exciting for us in a program that we’re committed to advancing because of the reasons 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 degeneration BCMA that is more accessible and sustainable compared to what’s available right now.

Operator: I would now like to turn the call over to Jenn Buell, CEO, for closing remarks.

Jennifer Buell: Thank you very much, operator. It was a pleasure to be with you all today and looking forward to speaking with you at AACR. Thank you again. Bye-bye.

Operator: Thank you, ladies and gentlemen. This does conclude today’s call. Thank you for your participation. You may now disconnect.