MiNK Therapeutics, Inc. (NASDAQ:INKT) Q1 2024 Earnings Call Transcript

MiNK Therapeutics, Inc. (NASDAQ:INKT) Q1 2024 Earnings Call Transcript May 14, 2024

MiNK Therapeutics, Inc. misses on earnings expectations. Reported EPS is $-110.07431 EPS, expectations were $-0.16.

Operator: Good morning, and welcome to the MiNK Therapeutics’ First Quarter 2024 Conference Call and Webcast. [Operator Instructions]. Please note this event is being recorded. If anyone has any objections you may disconnect at this time. I would now like to turn the conference over to Zack Armen, MiNK’s Investor Relations. Zack 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 include forward-looking statements, including statements regarding our clinical development, regulatory and commercial plans, and timelines, as well as timelines for data release and partnership opportunities among other updates. These statements are subject to risks and uncertainties, and we refer you to our SEC filings available on our website for more details on these risks. Joining me today are Dr. Jennifer Buell, President and Chief Executive Officer; Dr. Marc Van Dijk, Chief Scientific 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 for this quarter.

Jennifer Buell: Thank you very much, Zack. It’s a privilege to connect with all of you this morning to discuss our achievements in the first quarter and the milestones that advance our long-term strategic goals. Today, I will highlight our latest clinical advancements notably in our leading programs, AgenT-797 and MiNK-215. I will also discuss our strength and financial foundation and outline our plans for sustained innovation and growth. Let’s start by our progress in streamlining operations and our financials. This quarter, we focus on advancing our pipeline, improving our operational efficiency and fortifying our financial health. Since this time last year, we have successfully reduced our operating expenses by over 45% through improved manufacturing efficiency, strategic infrastructure alignment and most critically, the external nondilutive financing to support our ongoing Phase II trial in second line gastric cancer.

This financial prudence has enabled us to allocate resources more effectively towards accelerating our key clinical programs. Importantly, yesterday, we announced an investment of $5.8 million at a 25% premium from a new investor committed to our vision. This funding will be dedicated to support the rapid advancement of MiNK-215, our innovative CAR iNKT Cell Therapy targeting fibroblast activation protein or FAP solid tumors. MiNK-215 is our lead program from our Discovery pipeline that we are particularly excited about and this investment underscores unique potential of the program. We previously presented data at the American Society of Cell and Gene Therapy showing exciting preclinical activity of MiNK-215 and FAP expressing non-small cell lung cancer tumors.

More recently, as a matter of fact, just this past month at the American Association of Cancer Research or AACR Annual Meeting, our scientists presented compelling data demonstrating 215’s ability to eradicate tumors in human organoid models of colorectal cancer with liver metastases. These recent advancements build on our prior findings and position 215 as an important component in addressing the urgent need for effective treatments in colorectal cancer. This is now the leading cause of death in men under 50 and the second in women in that same age category. Our findings show that administration of MiNK-215 not only improves immune mediated tumor destruction, but also targets and depletes immune suppressive FAP expressing stellate cells, thereby enabling increased immune infiltration or CD8 T cell infiltration into the tumor.

More simply, this mechanism enhances the body’s ability to mount a robust T cell response against liver metastases, which can be further amplified by the combination with immune checkpoint inhibitors. While Marc is going to go through this in more detail, our scientists demonstrated this benefit with the combination of MiNK-215 and Agenus’s late-stage antibodies, botensilimab, a multifunctional T cell activator and balstilimab, a PD-1 antagonist which are advancing in late-stage clinical trials. These were the data that were presented at AACR and Marc will highlight these in just a few moments. Now I will turn to our lead program 797 and as a reminder, this is our allogeneic unmodified iNKT Cell Therapy advancing in Phase II clinical trials.

In February, we achieved a significant milestone for this program with the launch of the Phase II investigator sponsored study and externally funded program in second line gastric cancer. This pivotal trial is evaluating the combination of 797 with boat botensilimab and balstilimab and this combination is on top of standard of care chemotherapy. The study is led by Dr. Yelena Janjigian. She’s the Chief of Gastrointestinal Oncology at Memorial Sloan Kettering Cancer Center and the program is supported and funded by Stand Up to Cancer, an organization dedicated to funding and developing the most innovative and promising cancer research. Enrollment in the trial is actively underway. We eagerly anticipate initial data from the trial, which we expect later this year.

Beyond cancer, we’ve also continued to advance 797 in pulmonary diseases specifically in severe respiratory distress. This is a condition affecting over 600,000 individuals annually in the U.S. alone. Most recently, the full data set from our Phase I clinical trial was published in Nature’s Communications just a couple of months ago. These data highlighted the clinical activity and important role that iNKT cells play in this disease. There are currently no effective or active or approved therapies for patients with severe respiratory distress. We are excited to share additional updates from 797 at the upcoming American Thoracic Society 2024 Annual Meeting or the ATS meeting in San Diego, California on May 21st. Dr. Terese Hammond, a critical care and pulmonology expert, will present the data from the continued dosing of patients with severe respiratory distress through our compassionate and expanded access mechanisms.

Her latest case is a patient following renal transplant who was diagnosed with severe acute respiratory distress and treated with 797 under emergency use. While the data have not yet been disclosed and will be disclosed at the conference, this presentation further supports our previously published data and underscores a significant unmet need in severe respiratory distress. We’re excited about the potential of iNKT cells to make a meaningful difference in the lives of these patients and we expect further updates on this program in the months ahead. Overall, the progress we’ve made this quarter position us to accelerate the development of our iNKT cell platform and programs, and these include programs that are actively advancing in the clinic as well as our lead Discovery programs.

We’ll also expand and continue our inhouse manufacturing of iNKT cells, setting the stage for an exciting year in 2024 with 797 in pulmonary respiratory distress and the advancement of our Phase II trial in gastric cancer. We continue to be unwavering in our commitment to improving patient outcomes and we deeply appreciate your continued support. I’m now going to turn the call over to Dr. Marc Van Dijk to provide deeper insights into the MiNK-215 program. Marc?

Marc Van Dijk: Thank you, Jen. Good morning, everyone. I’m Marc Van Dijk and I will provide some further insight into the unique properties and promising potential of iNKT cell-based cancer therapies which are uniquely designed to maximize efficacy of solid tumors to 2 key differentiators — actually 3. Targeted tissue homing, relief of immunesuppression and the avoidance of lymphodepletion and the latter is very, very important for the overall outcome of cancer treatment in our opinion. Our clinical data covering 80 patients across cancer and severe pulmonary disease indicates that our lead iNKT T cell therapy AgenT-797 rapidly translocates from the bloodstream to essential tissues such as the liver and the lungs. Importantly, these cells remain active and detectable for up to six months post infusion.

This prolonged presence is elemental as it significantly amplifies the body’s own immune response enhancing the potential for durable therapeutic effects in cancer and other immune related diseases. Turning to our latest advancements, I would like to focus on MiNK-215 the subject of our news this week and differentiated first class armored CAR iNKT therapy targeting fibroblast activated protein or FAP for short. This therapy is specifically engineered to counteract the challenging immunosuppressive environment found in epithelial origin tumors including colorectal and non-small cell lung cancer. In preclinical models, we have previously reported that MiNK-215 showed robust efficacy in small cell lung cancer models resulting in substantial tumor elimination in the lung and improved survival compared to T cells in the lung.

These findings were commensurate with restoring the killing capacity of partially exhausted T cells and increasing T cell infiltration which is consistent with the natural properties of native iNKT cells. We further reported that MiNK-215 specifically targeted and eliminated FAP expressing cancer associated fibroblasts thereby disrupting the tumor promoting stromal network and reducing immune suppression in the local tumor microenvironment. We’ve recently expanded upon this data at the recent AACR meeting as January alluded to in April of this year where we showcased MiNK-215’s effectiveness in an advanced preclinical organoid model for colorectal cancer liver metastases. Liver metastases are notorious for limiting the success of traditional immunotherapies in patients with microsatellite stable colorectal cancer.

These tumor metastases typically create an immune exclusive environment characterized by a lack of T cells and an abundance of immune suppressive cells which conventional treatment struggle to overcome. MiNK-215 an IL-15 armored CAR iNKT cell therapy targeting FAB is designed to overcome these challenges. It not only remolds the tumor stroma to facilitate deeper T cell infiltration but also enhances the immune system’s ability overall to fight cancer more effectively. Our preclinical results have shown that MiNK-215 can trigger significant tumor reduction and even eradication and in this treatment resistant model of liver metastases and as Jen already alluded, it showed that it can deplete have sort of FAP expressing stellate cells which is a key immunosuppressive component of these liver metastases and this provides new hope for patients who currently have very limited options.

Our team is committed to advancing this innovative therapy to the clinical stage and with the recently announced financial backing and the relentless efforts of our research and development teams, we’re on track to accelerate IND filing to early 2025 and aim to produce clinical grade material as early as this year. This underscores our commitment to not just involve in science but also to bring potentially lifesaving treatments to patients as quickly as possible. I will now turn the call over to Christine to go over our financials. Christine?

Christine Klaskin: (Technical Difficulty) Cash balance of $5.8 million. This is prior to the receipt of the funds Jen mentioned earlier. Cash used in operations for the three months ended March 31, 2024, was $2.5 million compared to $4.4 million for the same period in 2023. Net loss for the first quarter of 2024 was $3.8 million or $0.11 per share compared to a net loss of $5.7 million or $0.17 per share for the first quarter of 2023. I will now turn the call back over to the operator for questions.

Q&A Session

Operator: Thank you. [Operator Instructions] Your first question comes from the line of Emily Bodnar with H.C. Wainwright. Please go ahead.

Emily Bodnar: Hi, good morning. Thanks for taking the questions. A few for me, I guess. So first one, if you can maybe comment on how the enrollment in the Phase II gastric study has been going so far since you enrolled the first patient in February and then could you maybe clarify how many patients are expected to be treated with each of the three treatment arms in that study? And then last question is a bit of a financial question, but given your operating expenses have decreased quite a bit this quarter, could you maybe just comment on what your current priorities are pipeline wise and which indications, you’re kind of focusing on and which ones are kind of taking more of a back burner at the moment? Thank you.

Jennifer Buell: Emily, thank you very much for your question. We’ll start with your first question, which is about enrollment into the Phase II gastric cancer trial. So maybe just as a reminder, this trial did not require us to do — to wait to do essentially a 28-day wait between patients. So we were able to enroll patients very quickly into the trial and continue to do so and that allows us to get exposure to patients that will get the cells alone, the cells plus BOT/BAL and RAM tax standard of care in second-line gastric cancer. We have been able to dose — we have not specified publicly yet the number of patients in each cohort, but suffice it to say, we will have a requisite number of patients that will not only allow us to demonstrate safety of each of these products alone and in combination, but also activity so that we could decouple where we see the most pronounced benefit for patients and, essentially in about a 40-patient study, we will be able to tease out contribution of components to some extent as we start to expand the cohorts and deepen signals in the areas that we see the most profound benefit.

We do believe that mechanistically that the combination of BOT/BAL iNKT with standard of care may not only be beneficial to patients but also quite tolerable and we’ve been able to demonstrate that so far in the first patient to have been enrolled. We do have patients that have been exposed to all five agents and those patients are tolerating the combinations quite well and we’re pretty excited to share an update on those, which we expect will be the second half of this year. Given the pace of enrollment in the first quarter of this year, we started enrolling in February. We’ve been able to bring in patients as I mentioned really quite quickly. So we’ll have some mature data to present at a late year conference, I’ll say second half of this year.

And additional information will be elucidated during those presentations. So I think that addressed your enrollment in the Phase II and the number of patients while we haven’t been discreet about the total number of patients in each one of the arms, we will have exposure of a proportion of patients on each of the arms with the largest proportion of patients on the multi combo, which is iNK T cells, agent 797 plus botensilimab and balstilimab. So that’s the multifunctional immune activator that also binds to CTLA-4 from Agenus. Balstilimab is Agenus’s PD-1 and then of course standard of care RAM tax in this patient population. Financially, I’m going to conclude your questions with your financial question which will be allocation of funds. So our operational efficiency really was in-large part to the reduction that we saw this year in particular, at least in the first quarter is largely driven by the external funding of the Phase II gastric cancer trial.

So MiNK had been executing on a number of trials, sponsor driven trials, Phase I trial in ARDS, also our phase I trial in solid tumor cancers and we can, had also AgenT-797 in the multiple myeloma study. What we have been able to now continue to pursue is expand on the cohorts that we’re really most excited about. The phase II trial in gastric cancer is funded, through Stand Up to Cancer’s Torrey Coast Foundation, which is essentially the designated, foundation that is focused on accelerating effective therapies for patients with gastric cancer. Dr. Yelena Janjigian, the Chief at Memorial Sloan Kettering, is the leader of that dream team, it’s called and this is the trial where she’s been focusing her efforts to expand therapeutic options for patients with second-line gastric cancer.

That has resulted in the most significant reduction in our operating expenses to expand that trial and to have it off the cost offset through nondilutive external parties. Additionally, our ARDS programs are an area of great interest to us as I mentioned earlier and we have not only concluded and published our Phase I study, we’re continuing to treat patients under a compassionate access while we are preparing to launch a randomized Phase II trial which we will be conducting with nondilutive financing support as well as some support from our own team. So it will be a joint program largely externally financed, and it will be conducted through a large platform trial and that will allow us to also continue to control our operating expenses. So our focus will be on really delivering the Phase II gastric cancer study, ascertaining the data this year and developing a pathway to advance that program as quickly as possible.

We also, in parallel, will be expanding our signal in acute respiratory distress severe and a large randomized clinical trial that will be largely externally financed, high priority for the company. The signals that we observed that we published in Nature Communications showed the true pronounced benefit that we believe these cells can bring to patients that showed rapid excavation, clearance of virus, prevention of secondary infections and we saw survival rates that exceeded 75% in a population of patients that historically saw a mortality rate that exceeded about 65%. So this is a dramatic improvement over what’s been available to patients, which is currently corticosteroids and that’s where we’re focusing our effort at this point in the clinic.

Additionally, as I mentioned earlier, our Discovery programs and our pipeline continue to mature and during our last call, which was our 2023 annual summary, Marc Van Dijk presented how we’re advancing our TCR portfolio through a partnership with ImmunoScape. We will be, as I just announced, today and yesterday morning, we’ll be advancing our MiNK-215 program through our new investment, which will allow us to accelerate the development of this very promising armored FAP CAR iNKT and we’re looking to generate clinical grade material as early as this year and get it into the clinic as quickly as possible with an imperative to try to do so by early 2025. I hope that answers your question.

Emily Bodnar: Yes, very helpful. Thank you.

Operator: Your next question comes from the line of Jack Allen with Baird Jack. Please go ahead.

Jack Allen: Great. Thank you so much. I guess the first question I had was on the 215 program. As you look to advance that asset into the clinic, what sorts of solid tumors do you expect to study that in? How do you think about the clinical development there? And then I have a few follow ups on both the ARDS program and then also, a question about where things sit in graft-versus-host disease as well.

Jennifer Buell: Excellent. Well, Jack, we’ll start with the first, which is 215. Now, as we approach the clinic, we’ve been able to interrogate a lot of preclinical functionality of the molecule and determine where we believe this could be best fit and most impactful in the clinic. Obviously, FAP expressing tumors would be our area of great interest. We will explore the asset more broadly, but with an emphasis in FAP expressing colorectal cancers. This is an area of high unmet need. We know that the disease is really growing in prevalence and incidence in a younger population and there’s an urgent need to move therapies forward as quickly as possible and the preclinical data we presented at AACR really demonstrates the potential of this molecule in FAP expressing colorectal cancer.

Similarly, we shared some very exciting data in a FAP expressing non-small cell lung cancer preclinical models. Those are some very obvious unmet areas of need where we believe there’s not only a development opportunity, but we have a molecule that can actually biologically address the gap that we’re currently observing in patients with FAP expressing tumors in lung as well as in colorectal. So that’s where we’re starting. Of course, we will interrogate the molecule and a couple of other disease indications expressing FAP sarcoma represents another one, but this is an opportunity for us to pursue and even optimize and accelerate development by the identification of patients with FAP expressing tumors with a large emphasis in non-small cell lung cancer and colorectal cancer.

Jack Allen: Got it. That’s great color and then as it relates to ARDS, where do things sit as it relates to securing that external funding? What are the potential aspects that need to be buttoned up there before you have that funding? And then on graft-versus-host disease, I believe there was also a previous discussion of an external program there. I’d love to hear any updates as it relates to that getting off the ground as well.

Jennifer Buell: Absolutely. So on the external funding, we have the platform trial identified and the team that essentially is responsible for the operational execution of that platform trial is, has already designed the protocol and started activating centers. We have agreed to the terms of the contract and we’re just making some final modifications with respect to the budget allocation over time, which we expect we should wrap up sometime even as early as by the end of this week. That’s our goal to do so, and then we would be announcing it shortly thereafter. On graft-versus-host disease, we are pursuing, an investigator sponsored trial. This is an area, of course, of unmet need and Jack, you did a brilliant job in summarizing not only the potential of the cells in this indication, we’ve also deepened our own scientific insights into how these molecules and these cells may actually have a profound effect in not only mitigating but then preventing graft-versus-host disease in patients who are undergoing hematopoietic stem cell transplantation.

We have not yet announced the launch of that program. So we have designed the program, but we have not yet accumulated the financing that would be necessary to launch it. So during this time, we are being really quite prudent about our focused efforts in the clinical programs that we’re advancing, but we will continue to find ways to get graft-versus-host advancing and this is a this is a priority for us to be able to do so, but it’s not an area that at this very moment we can allocate capital to doing at this at this time.

Jack Allen: Got it. That makes a lot of sense. Contributions again on the progress and thanks for taking the question.

Operator: Your next question comes from the line of Matthew Phipps with William Blair. Please go ahead.

Matthew Phipps: On the FAP CAR, I know in a lot of the preclinical work you’ve done, you’ve combined it with other therapies, including other kind of, like, TCR directed T cells and just curious how you think of a monotherapy activity of this or if it is something that has to be combined, whether it’s the IL-15 addition is something that can drive enough activity or again really should think about this being combined with other things?

Jennifer Buell: Matt, this is an excellent question and we have invited a couple of special guests onto the call today who are leading up this effort that includes the interrogation of 215 as a monotherapy and the kind of efficacy that we’re observing with the molecule in that capacity, which would be really important milestone for us to demonstrate monotherapy activity and in the case that we may need to expand that and address other tumor escape mechanisms, we are in parallel exploring where those optimal combinations may take. So there are three people on the line, and you’ll be familiar with them and this is Dr. Dhan Chand, he’s the Head of Discovery at Agenus, the one of the inventors on botensilimab and leading up our Discovery and combination, efforts, at Agenus.

Dr. Nils Rudqvist with whom you may not have met before. Nils is an accomplished scientist who joined us from MD Anderson Cancer Center. He was associate professor there and prior to that, he was at Weill Cornell, working in the Radiation Oncology Department and his and his emphasis is really on optimizing immune biology and determinants of how to modulate the tumor microenvironment and enhance efficacy. Eleni is also our Head of Discovery in our Cambridge, U.K. site for MiNK Therapeutics and this team together has been working to address exactly this question. I’m gonna turn it to Dhan just to lead in and give you a quick review of how we’re thinking about this and from my perspective, our goal would be to launch, interrogate monotherapy activity, particularly in FAP suppressing tumors, which would give us the most rapid development path forward and identify areas where we may want to expand efficacy with combinations And I’ll turn it over to Dhan to give you some deeper insights and he could work with Eleni and Nils and give you some more, a deeper response to your question.

A –Dr.Dhan Chand: Thank you for the question. So to the first part, we do expect monotherapy activity with MiNK -215 and for several reasons based on the preclinical data. First, in preclinical models, we observed direct tumor killing of FAP expressing cells, including expressing cancer cell fibroblast and tumor cells. In turn, we’ve observed that post there was a massive infiltration of T cells within the tumor microenvironment, which is particularly evident in cold tumors like liver metastases or other tumor models that we’ve tested. So we do expect monotherapy activity given the ability to promote T cell infiltration and remodel the tumor microenvironment to enhance T cell responsiveness, we expect this to be an ideal combination partner with BOT/BAL, particularly in areas where we have seen non responsiveness to PD-1 CTLA-4.

The data which includes both the liver metastases model as well as pancreatic models in situations where the tumors are refractory to BOT/BAL adding iNKTs including MiNK-215 can open up a response to checkpoint therapy and indeed promote monotherapy activity as well.

Jennifer Buell: Thank you, Dhan. Matt, did you have any other questions?

Matthew Phipps: No, that’s it for me.

Operator: Okay. And with that, that concludes our Q&A session. I will now turn the conference back over to Jennifer Buell for closing remarks.

Jennifer Buell: Thank you very much, and thank you all for joining us today. We look forward to continuing to keep you updated on our progress and advancements with a real focus on advancing our clinical stage programs, continuing to strengthen our financial foundation and deliver innovative medicines to patients with cancer and other immune mediated diseases. I appreciate your time today.

Operator: This concludes today’s conference call. [Operator Closing Remarks].