MiNK Therapeutics Inc. Q1 2023 Earnings Call
Speaker 1: Ladies and gentlemen, thank you for standing by and welcome to the Make Therapeutics First Quarter 2023 Financial Results Call.
Speaker 1: I would now like to turn the call over to Zach Arman, Head of Investor Relations. Please go ahead.
Speaker 2: 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.
Speaker 2: 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.
Speaker 2: These statements are subject to risks and uncertainties, and we refer you to our SEC filings for more details on these risks.
Speaker 2: Joining me today on the call are Dr. Jennifer Buell, President and Chief Executive Officer, Dr. Mark Van Dyck, Chief Scientific Officer, Dr. Joie Zhu, Head of Manufacturing, and Christine Plaskin, Principal Financial and Accounting Officer.
Speaker 2: Now I'd like to turn the call over to Dr. Buell to highlight our progress from the quarter.
Speaker 3: Thank you very much, Zach. Good morning, and thank you for joining our first Clutter 2023 earnings call.
Speaker 3: We're very happy to be here with you and to present an exciting first quarter which actually culminated in a significant presentation at the American Association of Cancer Research Conference or the AACR conference just a couple of weeks ago.
Speaker 3: Dr. Benny Carneiro, a medical oncologist and associate professor at Brown University Oncology, presented data on our phase one study. He reported first of its kind clinical benefit of an allogeneic or off-the-shelf INKT therapy.
Speaker 3: Inpatient with solid tumor cancers. Dr. Cardieri specifically highlighted clinical responses and biomarker responses in patients who have failed all available therapies including anti-PD1 therapy.
Speaker 3: We observe these responses in patients with metastatic gastric cancer, not a 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 self-derivating development.
Speaker 3: Make remains with the forefront of this technology advancing INKT in the clinic. And we're advancing with not only the clinic, as well as in our manufacturing suite, but also we're advancing a very robust pipeline of novel therapies that Dr. Mark Fondai will share with you shortly.
Speaker 3: So first I'm going to highlight the clinical data in a bit more detail.
Speaker 3: At AACR we reported that our lead product, this is Agent 797, an allogeneic off-the-shelf product of native non-engineers in variant natural killer T-cells.
Speaker 3: HM-797 delivered benefits to patients with heavily free treated cell-at-you-more cancers.
Speaker 3: Thirty-four 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 lymphodepletin agents, and we administered 797 alone or in combination with timrelizumab or nivolumab.
Speaker 3: We reported the agent 797 was well tolerated after a billion cells, dose, and promoted clinical acid in a range of heavily-creted cell-atumor cancers. And in particular, we saw an encouraging activity in a patient with metastatic gastrocancer who had no prior response to an anti-PD1 therapy.
Speaker 3: And that includes a single treatment with anti-pubulism at the patient with C4 psychoso. And after failure on pubulism at the patient with C2V, in combination with standard care chemotherapy, again with no response.
Speaker 3: After being treated with a single dose of agent 797, in combination with Novolumab, the patient achieved a partial response with a 42% reduction in tumor burden. And this continues now beyond nine months. Sorry, that was our reporting period. This response is continuing at nine months.
Speaker 3: We also saw benefit in other solid tumor cancers including durable disease stabilization and biomarker responses in patients with non-small cell lung cancer who had failed prior anti-PD-1, vesicular cancer, appendiceal cancers, and other solid tumors. The safety profile of 797 was found to be tolerable to a million cells, no evidence of neurotoxicity. The World War 2
Speaker 3: No dose limiting toxicity for a surge, and no severe cytokine release syndrome, greater than great-three reported in the trial.
Speaker 3: And really importantly, we gained insights into the persistence and the homing and the immune modulating activity of INKT cells in patients. We found that while INKT cells rapidly leave 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.
Speaker 3: This is really quite important because this demonstration shows that these cells actually can be viable and persistent without having to liporeduplete patients.
Speaker 3: We also reported important translational findings that highlight I&KT's ability to generate and drive immune cells into the tumor for destruction of cancer cells, and Mark's going to tell you a bit more about these data in just a moment.
Speaker 3: Overall, our findings showcase the potential of analysis of off-the-shelf IKV self-derivate in combination with anti-PD1 and TANFU's resistance to current treatment, including immunotherapy.
Speaker 3: They support the expansion of our solid tumor program into PD-1 refractory non-spolusome cancer as well as gastric cancer.
Speaker 3: And our trial and cancer cancer is being led by a world leader, Dr. Elena Jenjigian.
Speaker 3: She's a chief of Deutschland stone caugie and memorials on Kettering Campus Center.
Speaker 3: 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 who will be treated with a cell therapy in combination with standard of care chemotherapy as well as in combination with alternative therapy.
Speaker 3: With the various fighting multi-functional anti-speciliate for antibody, which is advancing in late-based trials.
Speaker 3: Botanilumab is a lead program from our parent company, Agenet. Now as a refresher, we have previously published preclinical models and data which demonstrates a potent synergy between I.N.K.P.s.
Speaker 3: and Silamab is a lead program from our parent company, Agenis. Now as a refresher, we have previously published preclinical models and data which demonstrates the potent synergy between INKPs and type PD-1.
Speaker 3: now and FOTEN-CILAMAP. We published those data and presented them previously at AACR.
Speaker 3: These data reveals that in-modeled, pre-clinical models of metacetic lung disease, the combination of INKT cells, PD1, and Bowton cell maps resulted in near-complete tumor elimination in this model, E-16 model.
Speaker 3: These data and the safety and clinical benefits that we've observed with 797 in solid tumors support our next phase of development with this program.
Speaker 3: We expect to provide additional data updates as well as more detail on our clinical programs in the second half of this year.
Speaker 3: I will now turn the call over to Dr. Mark Bundite, our chief scientific officer, who will provide an update on an next generation pipeline, which includes the IND enabling activities of our novel, that car INKT cell therapy.
Speaker 3: As well as more detail about the functional attributes of 797 that we believe underscore the observations of clinical benefits in fellow tumor cancers. Mark.
Speaker 4: Thank you, Jen. We're quite excited about the observations at the AACR of clinical benefit in patients with heavily pretreated metastatic cancers.
Speaker 4: These patients are the ones who inspire our work as we leverage our INKT platform to expand the clinical benefit observed with approved therapies and develop innovations to address areas where current therapies actually fall short.
Speaker 4: So our technologies, which you'll hear more about at our annual shareholder meeting, includes the ability to generate armored car anchor teams.
Speaker 4: develop INKT engagement, cell engagement, and advance novel PCR therapies.
Speaker 4: In addition to our native clinical stage, Agent 797 program, our most advanced preclinical programs include scorching snowflakes, armored allogeneicbolt, February 9, 2019, and winterS
Speaker 4: and the next generation armoured BCMA INKT. So our LEG program, Agent 797, is designed to expand clinical benefit observed with approved therapies.
Speaker 4: And our data at ASCR is the first glimpse of the possibility of these cells to deliver all 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.
Speaker 4: So we've previously shown that Agent 7 and 7 can improve the antitumor activity of immune cell that are present in the tumor microenvironment.
Speaker 4: Specifically, we've shown that IK T cells can activate dendritic cells, preferentially kill N2 macrophages, and restore killing capacity of exhausted T cells.
Speaker 4: So in data, a certain from our clinical trial of Agent 797, we showed that Agent 797 induced pro-inflammatory cytokine responses, including significant increases in interferongamol, a homework of IKT activation, and potentially indicative of tumor IKT activation, which is paramount to tumor control and tumor destruction.
Speaker 4: Importantly, fine KT cells are naturally tissue homing.
Speaker 4: So in preclinical data previously presented, we've demonstrated that INKT's could be administered without lymphoid depletion.
Speaker 4: They are rapidly traffic out of the circulation, but in days of administration and inter-tissues, including bone marrow, liver and lung, where they remain as some cases exceeding 35 days.
Speaker 4: So in our clinical trials, we reported the similar pattern of rapid translocation out of the circulation, while they remain at detectable limits and persist for approximately eight weeks.
Speaker 4: In our patient with durable response beyond nine months, we also showed that ITPs drive clonal T cell expansion in cancers with a high neo-antigen burden. Immunogenicity really triggering the expansion of these cancer-fighting T cells.
Speaker 4: While we plan to report more detailed information of INK teams in the tumor microenvironment at a later update this year.
Speaker 4: Currently, our data demonstrate a mechanism of INK T cells to enable T cells and NK cells trafficking to tumors, reinvigorate partially exhausted T cells, and improve effective functions within the tumor microenvironment, which is exemplified in these patients with clinical or biomarker response after a single dose of agent 797.
Speaker 4: As we continue to expand the potential of IKT in solar cancer, we have advanced our next generation IKT programs, including our Nobel I-15 armored Fat Car IKT Mink 215.
Speaker 4: 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 tissues such as the lung. In preclinical models, we reported very exciting data showing the potential of MINK215, 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 Boy, one of our lead scientists at MINK...
Speaker 4: We'll 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 Jim for closing comments.
Speaker 3: Thank you, Mark. Well, I get more and more enthusiastic about these, the data that we're advancing, the technology, the science behind these very powerful cells. And in conclusion,
Speaker 3: I'm really happy to share with you the progress that we've made in advancing this platform, and as Mark just mentioned, it's not only addressing and expanding the benefits of available therapies for patients today, but what they will need tomorrow.
Speaker 3: This process, of course, is made possible by the incredible advancements.
Speaker 3: of Dr. Joy Dao and her team in our CMC group.
Speaker 3: Our 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 therapies.
Speaker 3: entities. Enjoy us with us today's and 30 questions. We'll also be showcasing a deep dive into our manufacturing process, technology, and advancements at our annual meeting this year.
Speaker 3: 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.
Speaker 3: 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.
Speaker 3: and specific set of solid tumor cancers sets us up very well. And we're doing this with a team of under 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 you.
Speaker 3: of being able to financially support the initiatives that I shared with you throughout the course of the year and into Wellington next year. Christine. Thank you, Jen.
Speaker 5: 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.
Speaker 5: with $5.7 million, or 17 cents per share, compared to the net loss for the first quarter of 2022 of $7.8 million, or 23 cents per share. Thank you, and we'll now turn the call back to the operator for questions. The floor is now open for your questions. To ask a question, please press the Q and A button.
Speaker 1: Our first question comes from the line of Emily Bodnar from HC Wainwright. Your line is open.
Speaker 6: Hi, good morning and thanks for taking the question. Is there anything you can share about?
Speaker 6: details for the non-small-for-long cancer expansion study. And then also I believe you previously said that you were going to also do an expansion in testicular cancer, so that also still the plan. And then at this point, do you think you're just focusing on combination approaches? Or do you still think there's a role for monotherapy in your...
Speaker 3: and non-small cell lung cancer, we are advancing our phase one into a phase 1b, and we're able to enrich a little bit more clearly in lung cancer, the more prevalent tumor in non-small cell lung cancer in patients who are refractory. There's really nothing for those patients and very low response rates, we believe.
Speaker 3: that when patients fail anti-PD-1 therapy, they have a profile where INTPs may benefit, as Mark mentioned just a bit ago. And adding on to what's available, standard of care is actually, allows us to take a monotherapy approach to development. Just taking standard of care, taking to our own standard of care.
Speaker 3: when it's not active for those patients, adding on to that gives us an opportunity for rapid development. So while we do see a path for INKTs alone, and we've seen benefit, as you can see with the data presented at AICR, we do see benefit with INKT 797 specifically.
Speaker 3: without other therapies, both long-term disease stabilization and biomarker responses. We see more robust activity and a very clear task to rapid task to registration when we can add on to available therapy and expand the benefits or reinvigorate a patient's immune system and reactivate it to respond to what's currently.
Speaker 3: six or eight that will take advantage of the pharmacology that we're seeing as well as make the treatment burden as light as possible for our patients.
Speaker 3: With respect to the particular cancer, that is also a study that will also continue to insert deep signals with that indication. It's a bit rarer and so we are just currently enrolling some more patients to deepen our understanding of the biology of patients you fail prior therapy for the particular cancer. But that's an area that we do see better, better than one of the two.
Speaker 7: Just taking the questions and congratulations to the team on the progress made throughout the quarter. I wanted to ask on the updates around in COVID, I think in the press release you outlined that there will be some data presented in late May here. I'd love to hear what we should expect ahead of that data set. And any comments you have around, I think there were some ongoing negotiations with DARPA around potential funding for some of these viral.
Speaker 7: disease, I guess response programs above you here any update there. Thank you so much.
Speaker 3: Thank you so much for your question. I am incredibly excited about a data and that coming data presentation at the the pulmonary conference. It's an international conference of infectious disease and pulmonary science. The largest of it's time to go 30,000 participants.
Speaker 3: It's in Washington, D.C. this year, and our presentation is slated to be presented by Dr. Tharay Tamman, who was a lead investigator in our phase one trial, a pioneer in delivering cell therapy to patients with infectious disease, and the presentation is on Sunday, the 21st. And we'll share a bit more about that data at the release of it. What we see is the opportunity here now, and very importantly, to be able to do that.
Speaker 3: feasible, they could be cryopreserved, they could be administered in the hands of non-oncology experts, these are ICU experts and an emergency room critical care physicians.
Speaker 3: who don't have as much experience with cell therapy products. And we were able to deliver benefits just on patients that we reported pronounced benefits in our cohort that showed survival rates in patients who were elderly, mechanically ventilated, and we saw survival benefits of over 70% alive after.
Speaker 3: that had a survival rate of less than 22% and the CDC data, which was really comparable with the in-hospital controls at the time of our enrollment. We've also demonstrated that we can administer these cells not only tolerably, we saw no cytokine release in the population.
Speaker 3: exmo procedure. This is a procedure that requires heavy intervention. It's very difficult. It's recirculating the patient's blood supply and we were able to administer themselves in that setting and see benefits as well.
Speaker 3: where we've administered the cells and saw some remarkable benefit in patients who have cleared COVID but had secondary infections and that were resistant to all available antibiotic therapy and the cells actually promoted some really exciting data in that setting. So you'll hear
Speaker 3: all about the data sets there. In advancing this program, we do believe that the data work serving is really far too good to turn away from, yet our focus and our prioritization has really been advancing the cell and cell-acumur cancers. Well, our negotiations are with non-deludent government sponsored sources and...
those discussions are very actively underway and we will certainly be making some public announcements about the collaborations in the upcoming year term.
Great. Thank you so much for that comprehensive answer. And then just one brief follow up on the car I am KT's and very much looking forward to that presentation as well. I thought coming is she's team eating. I'd love to hear a little bit more about your development strategy as it relates to the car I am KT's.
Are these assets that you booked to bring forward on your own? Would you look to partner these assets as well to hear how you're thinking about that? Thank you so much.
Jack, thank you. I want to make one last comment I didn't make about the cells in ACS, and I'm going to come to the FACAR and KT. We also will report some very important translational data that shows what these cells can do biologically in cancer. We saw that these cells can help to tumors and generate a pro-inflammatory phenotype, which is what we really...
need in that setting. What we see in infections, particularly in acute ARDS, is that the cells actually induce an anti-inflammatory phenotype, which is really powerful and showcases how these cells can modulate immunity based on the disease setting that they're in, which makes them a really remarkable candidate and also underscores...
the next steps in our platform. I'm the Fat Car INKT in partnering. Partnering is absolutely core to our strategy. As you know, we've been an incredibly aggressive team. Mark and I have worked together with the Agenis group, and we allowed the access to our...
remarkably fast and innovative discovery research in finance to business in parallel. So through nearly a billion dollars in partnerships, we were able to continue to finance our innovative pipeline at Agenet and Mink. Mark and his research team have continued that pace of discovery and innovation. And for our ability to get the science into as many hands and out.
yet have the infrastructure work or bandwidth. You will be hearing more about that and also in the near term and our strategy and access to advancing.car IMPT very quickly. So if I could just say those today, we are well positioned to advance that car IMPT through the IMPT enabling and into the clinic.
and that's a very high priority for our company. Great, thank you so much.
Thank you. Our next question comes from the line of Matthew Fitz from William Blair. Your line is open. Thanks for taking my question. Jen, I'm wondering if you guys think, what could be special about that gastric pancreas patient that had such a strong response? They had an MSI.
high tumor, but I've been respond to two prior rounds of checkpoint inhibitors. Do you think MSI patients in general might be more prone to INKP selectivity, but they have more CD1D expression or anything like that?
That's a great question and I'm going to turn it over to Mark just after a couple of words. There are a few points that I'd like to have Mark also expand on that we observed, which included the tumor microenvironment modulation that I'll have Mark sort of further expand on.
period of time and then no longer. And in this case we saw absolutely no response not on Pembromana, not a NEBO combo, and not until we added the cells. And there are a couple of features that we presented and Mark will go into that may help us better understand the disease modifying benefits in this particular data set to the extent.
that it is translatable across MSI tumors, we will explore and are actively doing so. Our clinical trial with Dr. Zunjian will allow us to answer this question as well. Mark, I'll open it to you to say a few words. Yeah, thanks, Jen. It's an interesting question and we've been...
directed therapy. This isn't enough to actually either get into the tumors pervasively and actually start doing something. And what happened after IKT infusion is that somehow that got unlocked and these T cells started to do what they were actually generated for is attack the tumor cells.
So what we see in pre-tinical models is that, you know, IKT cells are more resistant to quite a few of the immune-suppressive mechanisms that tumors employ to keep T cell down. And what we see, for instance, are fat car model, but also in some of our 797 pre-tinical models, is that...
these tumor suppressive, these new suppressive mechanisms actually get neutralized or countered by INK T cells. If you could think about the local TGF beta or actually the cells that secrete TGF beta, CXCO12 that keeps the T cells out, all of those actually, and specifically the myeloid component all of those get translated, transformed into...
pro-inflammatory, non-immune suppressive environment and that actually brings the T cells in and also reinvigorates the T cells. We've also seen that for instance supernatant that we get from activated INK T cells is able to rescue partially exhausted T cells. So all of those mechanisms I think contribute as a whole as a package it's not a one-trick pony.
to activating the T-cell that are there in the guest to conservation, but obviously you're not able to do anything. And I think that very well fits what we see in our pixel-in-the-com models as well. And is one of the key features that we think is going to build the platform for IKT cells in solar tumors.
Great, thanks, Mark.
Our next question comes from a line of CalPIT Patel from B Rylei Securities. Your line is open.
Good morning. This is Andy on for CalPIT. Thank you for taking our questions. Starting off, what should we anticipate next from agent 797 and solid tumors? Is there any dose escalation work still remaining?
Thank you. We will continue to interrogate dose frequency and optimization. Though I should say to you that I feel based on the pharmacology data that we've generated and the signals of activity that we've identified and the colorability profiles.
We feel very close and confident with our dose, but it will be important just to strengthen our data packet for future regulatory interactions to continue to deepen our scientific exploration of dose and dose frequency. The next phase for us will be multiple doses and that will be happening near immediately.
Great, and then maybe one additional follow-up. With your upcoming presentation on Mink 215, is it fair to say that you're prioritizing this program ahead of 413 and maybe give us a sense of the timelines of when we should anticipate these programs to address clinic?
Sure, sure. So I'll answer the second question which is on 413. I personally believe and in our key opinion leaders have continued to emphasize this point that there is a critical need for an accessible, affordable product that targets BCMA.
that expands the duration, the durability, and really eliminates the continued antigenic profile, the BCMA target. What we do see today with autologous products is that they work well, high response rates. They're not as durable as they need to be, and when patients progress, about two-thirds of them are still revealing the antigen BCMA.
So I do think that there's a major opportunity to advance an allogeneic, off-the-shelf, armored VCMA that shows superior qualities as a next generation therapy for patients. For Mink to do so, given the competitive landscape, we would be an intensive effort and one that we are unwilling to pass down.
deep prioritizing to FAP, which is novel, engineered, and within our solid tumor strategy. So our BCMA program has continued to advance. We've continued to deliver the manufacturability and scalability, and we're interrogating it and getting it ready for a Phase 1 clinical trial, and it's really quite closed.
Yes, this would be something that we have advanced some discussion to really expand our book points in leverage additional, external, non-delutive capabilities to advance this program in this competitive setting. That far, NDP is really we think.
in outstanding products. Our preclinical data continues to get stronger. The profile of the molecule is very compelling. The need is great. And there are a host of cell tumors that are expressing cancers that actually, we believe we can bring benefit to. And for all of those reasons, we've accelerated this novel and differentiated product.
into the forefront of our trial, and we will be filing an IND in 2024. That will bring us into the clinic very, very quickly. We have a very fast path from IND filing to first in human, and so those would be tied together really quite quickly towards the middle to second half of 2024.
Thank you, ladies and gentlemen. This does conclude today's call. Thank you for your participation. You may now disconnect.