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Operator: Ladies and gentlemen, thank you for standing by. Welcome to the MiNK Therapeutics’ First Quarter 2023 Financial Results Call. I would now like to turn the call over to Zack Armen, Head of Investor Relations. Please go ahead.

Zack Armen: Thank you, operator, 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; Dr. Marc Van Dijk, Chief Scientific Officer; Dr. Joy Zhou, Head of Manufacturing; and Christine Klaskin, Principal Financial and Accounting Officer. Now I’d like to turn the call over to Dr. Buell to highlight our progress from the quarter.

Jennifer Buell: Thank you very much, Zack. Good morning, and thank you for joining our first quarter 2023 earnings call. We’re very happy to be here with you and to present on an exciting first quarter, which actually culminates in a significant presentation at the American Association of Cancer Research Conference or the AACR conference just a couple of weeks ago. Dr. Benny Carneiro, a medical oncologist and associate professor at Brown University Oncology presented data on our Phase I study. He reported first pivot kind clinical benefit of an allogeneic or off-the-shelf iNKT therapy in patients with solid tumor cancers. Dr. Carneiro specifically highlighted clinical responses and biomarker responses in patients who have failed all available therapies, including anti-PD-1 therapy.

We observed these responses in patients with metastatic gastric cancer, non-small cell lung cancer, testicular cancer and long-term disease stabilization in a number of other solid tumor cancers. These data underscore what we believe to be the most flexible and impactful cell therapy in development. MiNK remains at the forefront of this technology advancing iNKTs in the clinic as we’re advancing this not only in the clinic as well as in our manufacturing suites, but also we’re advancing a very robust pipeline of novel therapies that Dr. Marc Van Dijk will share with you shortly. So first, I’m going to highlight the clinical data in a bit more detail. At AACR, we reported that our lead product, which is agenT-797, an allogeneic off-the-shelf product of native non-engineered invariant natural killer T cells.

AgenT-797 really benefits the patients with heavily pretreated solid tumor cancers. 34 patients with metastatic cancer, who have exhausted all available treatments, including prior anti-PD-1 treatment were treated with a single dose of agenT-797 without administration of toxic lymphodepleting agents, and we administered 797 alone or in combination with pembrolizumab or nivolumab. We reported that agenT-797 was well tolerated up to 1 billion cells dosed and promoted clinical benefit in a range of heavily pretreated solid tumor cancers. And in particular, we saw encouraging activity in a patient with metastatic gastric cancer who had no prior response to anti-PD-1 therapy, and that includes a singular treatment with anti-PD-1 pembrolizumab that patient received four cycles.

And after failure on pembrolizumab the patient received nivolumab in combination with standard of care chemotherapy, again with no response. After being treated with a single dose of agenT-797 in combination with nivolumab, the patient achieved a partial response with a 42% reduction in tumor burden and this continues now beyond nine months, that was our reporting period. This response is continuing at nine months. We also saw benefit in another solid tumor cancers including durable disease stabilization and biomarker responses in patients with non-small cell lung cancer who have failed prior anti-PD-1, testicular cancer, appendiceal cancer and other solid tumors. The safety profile of 797 was found to be tolerable to 1 million cells, no evidence of neurotoxicity.

No dose-limiting toxicities were observed and no severe cytokine release syndrome greater than Grade 3 reported in the trial. And really importantly, we gained insights into the persistence in the homing and the immune-modulating activity of iNKT cells in patients. We found that while iNKT cells rapidly leads the periphery and enter in home to tissues, we see that they’re also still persistent and detectable in the periphery for about eight weeks. This is really quite important because this demonstration shows that these cells actually can be viable and persistent without having lymphodepletion. We also reported important translational findings that highlight iNKT’s ability to generate and drive immune cells into the tumor for destruction of cancer cells.

And Marc is going to tell you a bit more about these data in just a moment. Overall, I will refine and showcase the potential of an allogeneic off-the-shelf iNKT cell therapy in combination with anti-PD-1 in cancers resistant in current treatment including immune therapies. They support the expansion of our solid tumor program into PD-1 refractory non-small cell lung cancer as well as gastric cancer. And our trial on gastric cancer is being led by a world leader, Dr. Yelena Janjigian. She’s the Chief of Gastrointestinal Oncology at Memorial Sloan Kettering Cancer Center. The trial will advance through non-dilutive grant funded programs targeted to start in just a few weeks and is planned to enroll about 40 patients over nine centers who will be treated under Memorial Sloan Kettering’s umbrella and they will be treated with the cell therapy in combination with standard of care chemotherapy as well as in combination with a very exciting multifunctional anti-CTLA-4 antibody, which is advancing in late-phase trials.

Botensilimab is a lead program from our parent company, Agenus. Now as a refresher, we have previously published preclinical models and data, which demonstrate the potent synergy between iNKT, anti-PD-1 and now Agenus’ botensilimab. We published those data and presented them previously at AACR. These data reveals that in models – preclinical models of metastatic lung disease, the combination of iNKT cells, PD-1 and botensilimab resulted in near complete tumor elimination in this model, B16 model. These data and the safety and clinical benefit that we’ve observed with 797 in solid tumors support our next phase of development with this program. We expect to provide additional data updates as well as more detail on our clinical programs in the second half of this year.

I will now turn the call over to Dr. Marc Van Dijk, our Chief Scientific Officer, who will provide an update on our next-generation pipeline, which includes the IND enabling activities of our novel FAP-CAR-iNKT cell therapies as well as more detail about the functional attributes of 797 that we believe underscore the observations of clinical benefit in solid tumor cancers. Marc?

Marc Van Dijk: Thank you, Jen. We’re quite excited about the observations at the AACR of clinical benefit in patients with heavily pretreated metastatic cancers. These patients are the ones who inspire our work as we leverage our iNKT platform to expand the clinical benefit observed with the two therapies and develop innovations to address areas where current therapies actually fall short. So our technologies which you will hear more about at our annual shareholder meeting includes the ability to generate armored-CAR-iNKTs, develop iNKT engagers, cell engagers and advance novel TCR therapies. In addition to our native clinical-stage agenT-797 program, our most advanced preclinical programs includes armored-allogeneic FAP-CAR-iNKT and a next-generation armored-BCMA-iNKT.

So our lead program, agenT-797 is designed to expand clinical benefit observed with approved therapies. And our data at AACR is the first glimpse of the possibility of these cells to deliver on these benefits. It’s a well-known phenomenon that anti-PD-1 therapies are effective at countering tumor immune suppression. However, chronic use of these therapies leads to immune exhaustion. So we’ve previously shown that agenT-797 can improve the anti-tumor activity of immune cells that are present in the tumor microenvironment. Specifically, we’ve shown that iNKT cells can activate dendritic cells, preferentially kill M2 macrophages and restore killing capacity of exhausted T cells. So in data, ascertain from our clinical trial of agenT-797 we showed that agenT-797 induced pro-inflammatory cytokine responses including significant increases in interferon gamma, a hallmark of iNKT activation and potentially indicative of tumor iNKT activation, which is paramount to tumor – control tumor destruction.

Importantly, iNKT cells are naturally tissue homing, so in preclinical data previously presented, we’ve demonstrated that iNKT’s could be administered without lymphodepletion. They have rapidly traffic out of the circulation, but in days of administration and into tissues, including bone marrow, the liver and lung, where they remain in some cases exceeding 35 days. So in our clinical trials we reported the similar pattern of rapid translocation out of the circulation, while they remain at detectable limits and persists for approximately eight weeks. In our patients with durable response beyond nine months, we also showed that iNKTs drive clonal T-cell expansion in cancers with a high neoantigen burden, immunogenicity really triggering the expansion of these cancer-fighting T cells.

While we plan to report more detailed information of iNKTs in the tumor microenvironment at a later update this year. Currently, our data demonstrate the mechanism of iNKT cells to enable T cells and NK cells traffic in two tumors, reinvigorate partially exhausted CD8 T cells and improve factor functions within the tumor microenvironment, which is exemplified in these patients with clinical or biomarker response after a single dose of agenT-797. As we continue to expand the potential of iNKTs in solid cancer, we have advanced our next-generation iNKT programs, including our novel IL-15-armored FAP-CAR-iNKT MiNK-215. Cancer-associated fibroblasts, which are targeted with this therapy are key tumor supportive components of the immune suppressive tumor microenvironment in several cancers, including non-small cell lung cancer.

This adverse tumor microenvironment can be addressed by our fibroblast targeting or FAP-CAR-iNKT therapy, which naturally homes to tissue such as the law. In preclinical models, we reported very exciting data showing the potential of MiNK-215, which demonstrated robust efficacy in non-small cell lung cancer preclinical models, eliminating tumor burden in the lungs and enhancing tumor-specific CD8 T cell infiltration through stromal remodeling. This is a program we’re actually very excited about, and Dr. Shannon Boi one of our lead scientists at MiNK, will be presenting new data at the American Society of Gene and Cell Therapy Annual Meeting on May 19th. I will now turn the call over to Jen for closing comments.

Jennifer Buell: Thank you, Marc. Well, I get more and more enthusiastic about the data that we’re advancing the technology and the science behind these very powerful cells. And in conclusion, I’m really happy to share with you the progress that we’ve made in advancing this platform. And as Marc just mentioned, not only addressing and expanding the benefit from available therapies for patients today about what they will need tomorrow. This process, of course, is made possible by the incredible advancements of Dr. Joy Zhou and her team in our CMC group. Her current process, our manufacturing process is designed to generate over 5,000 doses per year, and we are building currently and expect to have a fully donor independent process over the course of this next year.

And this development will come without some kind of capital intensive efforts associated with most cell therapy entities. And Joy is with us today to answer any questions, we’ll also be showcasing a deep dive into our manufacturing process technologies and advancements at our annual meeting this year. Very importantly, and what has been contributing to our high efficiency is our team is small, and we’ve kept it that way. And we’ve made tremendous progress launching the company as an IPO in October of 2021, advancing three clinical programs, highly efficiently and now identifying tumor types that may allow us to develop agenT-797 on a rapid path to development to expand benefit to patients and a specific set of solid tumor cancer sets us up very well.

And we’re doing this with a team of only 35 people. And as Christine will share with you, we’ve been able to manage our team and our expenses very efficiently, and we’re looking forward to being able to financially support the initiatives that I shared with you throughout the course of the year and into – well into next year. Christine?

Christine Klaskin: Thank you, Jen. We ended the first quarter of 2023 with a cash balance of $14.9 million as compared to $19.6 million at December 31, 2022. Our cash used in operations for the first quarter was $4.4 million, which compares to $4.2 million for the same period in 2022. Net loss for the quarter ended March 31 was $5.7 million or $0.17 per share compared to a net loss for the first quarter of 2022 of $7.8 million or $0.23 per share. Thank you. And we’ll now turn the call back to the operator for questions.

Operator: The floor is now open for your questions. [Operator Instructions] Our first question comes from the line of Emily Bodnar from H.C. Wainwright. Your line is open.

Operator: Our next question comes from the line of Jack Allen from Baird. Your line is open.

Operator: Our next question comes from the line of Matthew Phipps from William Blair. Your line is open.

Operator: Our next question comes from the line of Kalpit Patel from B. Riley Securities. Your line is open.

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