MiNK Therapeutics Q3 2023 Earnings Call Transcript

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Provided by Quartr
November 9, 2023

There are 9 speakers on the call.

Operator

Good morning, and welcome to MINQ Therapeutics Third Quarter 2023 Conference Call and Webcast. Please note, this event is being recorded. I will now turn the call over to Zach Armand, Head of

Speaker 1

Thank you, operator, and thank you all for joining us today. Today's call is being webcasted and will be available on our website for replay. I'd like to remind you that this call will contain forward looking statements, including statements regarding our clinical development, We refer you to our SEC filings for more details on these risks. Joining me today on the call are Doctor. Jennifer Buell, participants are in the line with our Chief Scientific Officer, Doctor.

Speaker 1

Mark Van Dijk, Chief Scientific Officer and Christine Klaskin, Now, I'd like to turn the call over to Doctor. Buell to highlight our progress in 2023 and plans for the year ahead.

Speaker 2

Thank you, Zach. It's a pleasure to have you all with us for May's Q3 earnings call 2023. I'm excited to report on the excellent headway we've made this quarter, particularly with our proprietary INKT A pinnacle of this progress was presenting compelling new data Our flagship product, HS-seven ninety seven, at the recent Society For Immune Therapy of Cancer or SITC Annual Meeting that took place To reiterate, 797 is an allogeneic INK T cell therapy. It's distinguished by its scalability, robust immune modulatory properties and its administration without the need for toxic preconditioning regimens, A testament to the versatility and promise of these cells. The findings we reported at Sify Mark is going to tell you a bit more about that shortly.

Speaker 2

So last Friday, we reported an update On the durable clinical benefits from AGM-seven ninety seven across a diverse set of tumor types In patients who have exhausted all other treatment options. Notably, in late stage metastatic cancer, We observed long term durable disease stabilization and biomarker responses in more than 30% of the patients treated and these are patients with non small cell lung cancer refractory to prior therapies, testicular cancer and appendiceal cancers Additionally, the durable responses in a patient observed with second line metastatic gastric cancer continued. This patient was unresponsive to prior chemotherapy These data provide continued evidence of the potential that AGEN-seven ninety seven holds in patients with solid tumor cancers. Our data presentations also underscore the benefit of INKP cells beyond cancer, including in infections, have a question and answer session. The American Thoracic Society meeting, the International Lung Meeting, and we showed an improved survival More than 75% when patients were treated with HN-seven ninety seven compared to in hospital controls It ranges anywhere from 10% to 30% in survival rates, and these include patients who are on the most severe form Of life support, patients on VV ECMO where their blood was being oxygenated externally, that's a step past mechanical ventilation.

Speaker 2

And we had Reported earlier in patients with viral ARDS and mechanical ventilation also showed a survival exceeding 75% Compared to in hospital controls of 10% to 22% at that same time point. We continue plan to expand this program through externally financed These data along with the others presented earlier this year at AACR continue to demonstrate that ATN-seven ninety seven is well tolerated up to a 1,000,000,000 cells alone as well as in combination with some of the most widely used immune therapies. And these cells also promote clinical benefit in a range of solid tumor cancers. Another important finding from these data are the new translational insights that we've generated into INKT cells, their immune modulating mechanisms Our data demonstrated that 797's ability to persist, I'm going to turn the call over to Doctor. Marc Bendyke, our Chief Scientific Officer of Maine to discuss more about these discoveries.

Speaker 3

Thank you, Jen. As we continue to deepen our understanding of the IK T cells' unique mechanisms in the clinic, We're more and more encouraged by the potential of what they can do for patients with cancer, use alone or in combination with other agents. The durable responses in cancer patients require an active and vigilant immune system to prevent the tumor from escaping and going back again. A key finding in our cancer trial is that we have observed clear signatures of activation of the patient's immune system upon infusion The clearest signals of this are the systemic immune activation are changes in cytokine levels. We see these changes both systemically in the blood as well as locally within the tumors in the patients we treated in this trial.

Speaker 3

One such signal is interferon gamma. This is a key immune activating cytokine and a hallmark of INKT activation Interferon gamma spikes in the blood of all patients 24 hours post infusion of AGN-seven ninety seven, potentially indicative of tumor INKT activation. The spike in serum interferon gamma correlates with dose and interestingly patients treated in combination with anti PD-one Potentially indicating elevated immune system activity when combining anti PD-one with AGEN-seven ninety seven. Now to retain control of the tumor, the patient's immune system needs to remain vigilant. In that respect, it's important that the anticancer activation state of the patient's immune And our data showed 1st of a kind persistence of an allogeneic Pine K T cell therapy in cancer.

Speaker 3

Here we used a very specific independent method based on high sensitivity donor specific SNP analysis By Duplex Sequencing of peripheral blood mononuclear cells, we found that AGEN-seven ninety seven persists for at least 6 months. And in addition to showing such long persistence, we also saw that HN7977 levels in blood of patients appears to correlate with response. They appear higher in patients with partial response and stable disease. So for a telogenetic cell product to stay around for 6 months is remarkable, Even more so when it is administered without lymphodepletion, which is a toxic pretreatment use for the majority of cell therapies in clinical use today. Even more remarkable Our finding that AGEN-seven ninety seven persistence was apparently independent of HLA matching.

Speaker 3

Traditional knowledge have it that the higher degree of HLA matching is between donor tissue and the patient, the longer the donor tissue will be tolerated and stay functional. Our finding that allogeneic IgT cells persist in our responding gastric cancer patient for at least 6 months, even when there is only 1 out of 12 HLA match, provides further support for the unique nature of invariant natural killer T cells and underpins the great potential for therapies used in cancer Over to you, Jen.

Speaker 2

Mark, thank you. This is really profound work and unique set of findings that are quite different than what we observed with the other available And witnessing observing the theoretical advantages of INKT cells actually come to fruition in clinical practice As well as in translational data observations is a true testament to your team's our team's dedication and innovation. Appreciate your overview, Mark. As we reflect on our scientific advancements, it's also really important to acknowledge our attention and financial prudence that has truly underpins our journey. Our discipline is demonstrated by our contained cash flow with our clinical progress in which we launched 3 clinical programs.

Speaker 2

We studied INKT cells, allogeneic off the shelf cells in patients with virally induced acute respiratory distress and presented those data at 4 different conferences. We launched a trial of INK T cells alone and in combination with commercially approved Here at AACR and also last year as well, the most pronounced observations were the findings Long term durable clinical benefit co correlating with the translational insights that Mark just presented. And we've done this with a contained cash outflow and it's been carefully managed to support the completion of these programs Looking ahead, we anticipate a meaningful reduction in our quarterly cash Manufacturing has included our ability to have an FDA cleared process that is now automated, closed and fully internalized, Now importantly, advancing our clinical programs has been critical for us and we're continuing to do so in a few different ways. First, our Phase 2 clinical trial in second line gastric cancer Led by Doctor. Elena Jinjigyun, Chief of Gastrointestinal Oncology at Memorial Sloan Kettering Cancer Center is on track to launch this quarter.

Speaker 2

This trial will include the combination of the cells on top of standard of care chemotherapy As well as the combination of cells on top of standard of care chemotherapy and combination with botanistilumab and balsilumab, This is an optimized multifunctional T cell engaging technology that also binds anti CTLA-four from our collaborators at Agenus And falciliomab, an anti PD-one therapy from Agenus as well. Next, Specifically, GVHD, these externally funded trials will be designed to build on the exciting survival data have reported in patients with virally induced respiratory distress. This is an unmet need where there are currently no approved therapies. And finally, acute GVHD remains a severe and often fatal complication in more than half of the patients undergoing Hematopoietic stem cell transplantation. INK teams have demonstrated the natural capability to not only improve engraftment success in these patients, but also Given our robust tolerability data, we are advancing external and externally funded trial to address this important unmet need.

Speaker 2

We believe that small and effective trial can generate data to support this opportunistic indication where rapid and development pathways are available. You will hear more on all 3 of these programs later this year. And parallel to our clinical endeavors, our team is advancing our GMP manufacturing capabilities and continuing to scale our ANKP cell production, as I mentioned We're continuing to ensure that we can meet the therapeutic needs of patients battling cancer and other immune related diseases. Our progress has advanced with effective financial prudence. We've judiciously allocated resources, emphasized data generation, scalability Our manufacturing process, which underscores our commitment to cost effectiveness and operational efficiency.

Speaker 2

Additionally, to strengthen our balance sheet, we're in discussions with strategic partners on regional partnerships, research and development collaborations and manufacturing services, All of which are focused on accelerating our development speed, advancing our innovation more rapidly and leveraging our I will now turn the call over to Christine to go over our financials.

Speaker 4

Thank you, Jen. We ended the 3rd quarter with a cash balance of $6,400,000 As compared to $10,600,000 at June 30, 2023 $19,600,000 at December 31, Cash used in operations for the 3 9 months ended September 30, 2023 was $4,200,000 and $12,700,000 respectively. This is a decrease when compared to $5,600,000 and $14,400,000 for the same period in 2022, reflecting our financial prudence that Jen just described. Net loss for the 9 months ended September 30, 2023 was $17,000,000 or $0.50 per share, Compared to net loss for the same period in 2022 of $20,200,000 or $0.60 per share. I will now turn the call back to the operator for questions.

Operator

The floor is now open for your questions.

Speaker 2

Your first question comes from Emily Bodnar from H. C. Wainwright.

Speaker 5

Hi, good morning and thanks for taking the questions. Maybe firstly, if you can put into context Some of the data that you presented at SITC, I know you talked about the 6 month persistence, maybe you can discuss What the typical persistence is, cell therapies in the autologous setting? And, you also had a median PFS of 6 months in combination. So maybe just discuss what you would expect the PFS to be with

Speaker 2

Emily, thank you so much for the question. And I have Mark with me. I'm going to have him give you an overview of the translational data presented at SITC. And I would say with respect This is a patient population who have failed all prior lines of in their disease setting and they were really quite sick. It's a heterogeneous Phase 1 population.

Speaker 2

We observed that In some cases, we've had patients, of course, with refractory cervical cancer, non small cell lung cancer who had failed prior chemo, We had patients with testicular cancer who had failed 4 prior lines of therapy. The median Prior lines of therapy exceeded 4 for this population. Their typical PFS, as you can imagine in this particular setting On the currently available therapy would have been far less than that, closer to about 1.8 to 2 months, Depending on the tumor type. So that's just for framing, we are seeing and we're continuing to follow patients Now for progression free disease free survival as well as overall survival. The translational data, I'll turn it over to Mark to give you a sense of the reference What we would expect, what we have seen as we've gone through the data over time, what we've seen in comparative cell types And what we believe that this may mean for the development of the product, Mark?

Speaker 2

We may have a little technical glitch from Mark. Can you hear him, Emily?

Speaker 5

No, I just hear you.

Speaker 2

Okay. Okay. I think Mark is now unmuted. Thank you.

Speaker 6

Is this better?

Speaker 2

Yes. Perfect. You're on.

Speaker 3

Okay, good. Yes, I was just already well on my way to answering the question. So, the fact that this we see 6 months persistence in an allogeneic non HLA matched therapy without any preconditioning is I haven't seen that anywhere yet. In autologous CAR T cell trials, patients are heavily pretreated with lymphodepletion to make room for the new T cells coming in and those T cells are from the patients self, which is a full HLA match. And they are they spike and then they go away.

Speaker 3

And in some cases, like pediatric cases, The autologous T cells have been detected for decades, but that's in a full HLA matched setting or by the patient's own T cells. In any other allogeneic setting that I've seen reported on, I haven't seen any persistence reported on longer than a month. And that's also with patients that have received quite toxic heavy preconditioning lymphodepation to Tone down the immune system of the patient and extend the persistence that way. We don't do that. So we have no pretreatment and we have no HLA match and we still see 6 months persistence.

Speaker 3

And I haven't seen that reported anywhere else or any other cell type in the settings. That's what we think fairly unique and we think a special property of these INK T cells.

Speaker 5

And then maybe if you could just provide an update on your

Speaker 2

Great question. This is we absolutely are. We've got our Sacchar INKT and our BCMA CAR INKT Best in class activity with this pre clinically and we've completed effectively the IND enabling packet. I have mentioned that as we have Contemplated advancing our programs forward, BCMA is something that we have been in deep are participating in the next generation therapy for companies who are actively are developing this program with a broader footprint than MINK. So that is something that continues to be advancing.

Speaker 2

The BAP CAR INKT We are planning our IND. We're still on track for our 2024 submission.

Speaker 3

Yes. Just on the data, I mean, we're actually quite are excited about this whole our FabCAR INKT program because it has even more impact on the tumor microenvironment that we've seen with the native INKT cells. And Specifically for highly resistant solid tumors, we think that that is a benefit. We see that it really potentiates the immune system to go in and changed the tumor market environment from cold to hot, and we think that that's going to really help extend the reach of native INK T cells in cancer. Is one of the fundamental mechanisms to tackle tumor suppression is by attacking the sort of immune suppressive stroma and that's what Fabcon and KTs have shown to do very, very well, both in vivo systems that we've actually reported on a couple in a couple of conferences this year as well as all in vitro data that we hope to actually Probably pretty soon.

Speaker 3

So full speed ahead for this program for us.

Speaker 5

Awesome. Thanks so much.

Speaker 2

Thank you. Your next question comes from Jack Allen from Baird.

Speaker 7

Great. Thanks so much for taking the questions and congratulations on the progress made throughout the quarter. Maybe my first one on the translational data. Mark, you spoke a bit about the persistence, but could you elaborate a little bit more on the expansion of these cells and what you're seeing in the acute dosing as it relates to translational data from the data from the 797 program?

Speaker 3

Yes. So that's a good question. So what we see is typically when you the moment we infuse these cells, are quite rare in the normal blood, but we infuse 1,000,000,000 cells at the time of dosing, which at the time of infusion is about 15% to 20 are in the range of 2% of your total white blood cell count, which is a bolus. And that we think is one of the reasons why you get a systemic effect of immune participation on the whole immune system. Beyond that, what we see is that these cells continue to be detected in blood for over 6 months.

Speaker 3

Now we don't have definite evidence that which part of the tissues they go from clinical data. Pre clinically, they go to lung, liver, bone marrow. So we expect that in patients themselves this would also be the case and we expect them to go to tumors and some evidence of that we do see. We can't currently say how much of that is driven by expansion and active division of IK T cells. The detection level in blood over the 6 months remains relatively stable, Although in responding patients, we see a sort of cycling and the cycling may mean 2 things.

Speaker 3

1, they're actually actively dividing 2, they're actually trafficking between the departments in the body, and we can't currently distinguish between those 2, but they do stay around for much longer than we had thought they would be able to stay around Got it.

Speaker 7

Got it. Great. And then, you made some comments on the call as it relates to partnership discussions. Can you elaborate a little bit more about what kind of partnerships you're contemplating? Would these be indication specific or product specific?

Speaker 7

How are you thinking about that path

Speaker 2

Thanks, Alex. This is such an important part of our strategy. And maybe just As a reminder, Mark and I have both together shared leadership roles that our parent company Agenus, where we were incredibly successful and prolific at establishing partnerships that not only expand our discovery engine and capability, but also Speed the development of agents. So our discovery capability is incredibly prolific here at Menck with Mark and his team producing discovery targets and particularly in engineering them all in house. And I'm going to have Mark speak a little bit are participating in the Q1 of 2019.

Speaker 2

We are in active discussions at this time, We are in active discussions at this time with companies who need innovation And who are very interested with quite a large appetite to be able to take on some of our discovery items. So Could we help a partner in that regard? And those are one of the types of discussions we're talking to partners about would be Supporting the discovery engine through a research and development collaboration. In addition, the opportunity for us To take 797, the clinical data that has been generated to date and fully exploit its benefit and that is an optimal combinations and are participating in the clinic and we've seen in our own hands that these cells can be incredibly powerful in the clinic in combination of course with widely used chemotherapies as well as most commonly used immunotherapies like anti PD-one, KEYTRUDA, Opdivo. In addition to that, we've demonstrated preclinically that these cells can expand the benefit of what we observe with engagers in the clinic as well as some other more novel technologies.

Speaker 2

So we are also contemplating the strategic collaborations that would enable us to provide access to 797 to expand the benefit income and optimal combinations for patients with cancer and those are both Global discussions as well as regional partnership discussions that are actively underway. There are some parts of the world where mink does not have a footprint and being able to leverage participants regionally will also help us to expand our footprint and chasing our development speed in these in different parts of the world. So Certainly, the research and development capabilities leveraging those capabilities and supporting the acceleration of bringing some of these acknowledges to the clinic more rapidly as well as leveraging the clinical data from 797 to support expanded benefit For patients with cancer through really optimal combinations and the soonest to start of course would be our combination in the clinic with second line gastric cancer. The INKT cells will be in a randomized study, the cells on top of standard of care chemotherapy And then the cells on top of definitive care chemotherapy plus, the really exciting products, botanilumab and balsilumab From Agenus, and that trial, as I've mentioned earlier during the call, will be run through, Yelena Jigian And externally financed, trials like that are being actively pursued in our discussions through collaborators at this time.

Speaker 7

Got it. Great. And if I may, just a couple more. On the autoimmune diseases, it's good to see that on the slide here as it relates to the As I read the slide, it mentions that 2023 IND potentially in a Phase 1 study initiation. Should we expect that in the coming months here?

Speaker 7

And then just briefly, as it relates to innovative programs, I see that you've added a PRAME program to your early discovery aspect of your pipeline, I'd love to hear any thoughts you have around the PRAME target and its potential across multiple solid tumors.

Speaker 2

Excellent. On the first question, which is with respect to advancing a clinical program with INK in patients with acute graft versus host disease, that is something that we plan to launch this year with Into the clinic effectively amending the IND with our new study program that's very close to getting into the clinic at this are at this time. So we believe we'll be announcing that this year. We're on track to do so. We're certainly planning to do so.

Speaker 2

With respect to the PRAME TCR, I'll have Mark say a few words about that.

Speaker 3

Yes. That's a pretty exciting program for us Because we've actually been working on TCRs for quite a long time now. We have several of them generated, including what we believe is a very, very good TCR for PRAME. And PRAME, as you know, has actually already started to show some really good benefit in solid tumors With a T cell approach to this and given the sort of properties of INK T cells and actually getting into difficult places in the tumor, even suppress tumor microenvironments and then enhancing them with a PRAME TCR, we believe will probably extend or has the potential to extend clinical benefit Beyond what T cells could do with PRAME, and that's what we're hoping to exemplify. And currently, it's in preclinical stage, and this will be one of the programs that we will progress Following the FabCAR program that we are currently speeding to an IND, but we're quite excited about that.

Speaker 3

And also the specific thing of this is these INK T cells now express are 2 TCRs, the pain TCR as well as the invariant TCR from IK T cells and they're both useful and they're both active in the tumor market environment. So that's I think the unique aspect of combining TCR expression with INK T cells and then specifically the frame program as a front runner, I think it's a very valuable program for us.

Speaker 7

Great. Thanks so much for taking all the questions and congratulations again on the progress.

Speaker 2

Thanks so much, Jack. Thanks. Your next question comes from Mayank Mamtani from B. Riley.

Speaker 8

Hi, this is Brian Kani on from Mayank. Thanks for taking our questions. Just I guess first regarding the landscape in gastric cancer, we saw Doctor. Jin Ji Bien give a presentation on Tuesday And I think there was another presentation on or that was on TIGIT and I think there was another presentation on ADC I was just wondering how you think the cells fit in the emerging landscape Given the digit in the ADC's?

Speaker 2

Absolutely. So I'm I'm familiar with that presentation and we agree we actually have discussed this with Yelena. And right now as you can see, There's a very significant and relatively urgent need for patients in the second line setting after REMTAPS failure. And being able to expand the benefit of what's currently being available to patients in a rapid way is quite opportunistic. And in addition to that, We believe that based on the observations we've seen in GI cancers overall with botecilumab and balsilumab and this is in patients now over are 741 patients treated in which the products are quite active both In the disease setting in CRC, but also more broadly outside of CRC in lung cancer, ovarian, endometrial.

Speaker 2

And we see have a very strong visibility, not only at the disease sites, but also at metastatic sites that have largely escaped attack by other available therapies like Metastatic lesions to the bone, the peritoneum and liver. Given the preponderance of evidence that we've seen here and the data observations, We do believe that the cells in combination not only will expand benefit with what's currently available, which is quite a rapid have for us with the cells on top of chemo, but also the cells on top of chemo with expanded benefit from bot valve combination, We believe could be immensely beneficial to patients and quite potentially a potential best in class approach for patients with gastric In addition to that, we've also had some preclinical observations and observations from others That the cells combine really quite effectively and tolerably with other agents and those including gators as well as ADC technology. So I think that when we look at these cells and I'll have Mark say a few words specifically immunologically about what's happening When we administer these cells, so not only we're administering without HLA matching, without lymphodepletion, no toxic preconditioning, The cells are tolerable to over 1,000,000,000 cells now per dose.

Speaker 2

And we see that these cells appear With technologies approved therapies today as well as some of the developing technologies that are not yet approved. And therefore, I see a place in which these cells, just like I mentioned earlier with the expansion of benefit from our observations with We also see expansion of benefit with some of these other more novel technologies. And Mark, to give you a little bit of Additional insights expanding on the observations we presented at SITC today in that regard.

Speaker 3

Yes. And I think I mean, So a lot of the IO failures that we see today, we think are due to, at least in large part, resistance within the tumor microenvironment. And a big part of that, for instance, is myeloid cells, macrophages and myeloid macrophages and myeloid derived suppressor cells. And one of the unique features of NK T cells is that through their invariant TCR, they target CD1D, which is universally expressed on all myeloid cells. And we've also seen that they can actually modulate M2 macrophages So that's an additive effect beyond what is possible with checkpoints.

Speaker 3

And we think that together with checkpoints, They can start really changing the microenvironment in a way that can shape a much better immune response to the tumor. So that's why we think INK T cells on top of in the gastric cancer or chemo or standard of care that changes the way the tumor sort of operates Really helps augment the overall clinical response that we think is possible because it starts to address non overlapping immune suppressive mechanisms in the tumor itself. So that's what we and also of course the fact that we now add these cells to patients without lymphodepletion, we don't attack their immune system. If you lymphodeplete patients you actually diminish their immune system quite significantly. We don't do that.

Speaker 3

We don't do that because we don't need it, but we also don't do that because we think it diminishes the overall effect of the infusion of INK T cells on conjunction with, for instance, what checkpoints can be can achieve in a given clinical setting. So that's the key reason why we think INK T cells are a great additive to pretty much all the ILO therapies out there at the moment. Did I answer your question?

Speaker 8

Yes, yes. No, that's helpful. And I guess maybe just to follow-up on the trend that you mentioned between Responses and peripheral levels of 797. I'm just wondering if you think there's an update there right now to give you confidence in that trend and what we would

Speaker 3

You mean on the persistence? Yes, we continue to follow that quite actively because to be honest, it surprises us. And also in light of our thinking about how to redose, if should redose and when to redose. This is key data for us to help us decide when it makes sense to redose and why we would do this or in what patients, for instance. So we'll be collecting a lot more data on this phenomenon of persistence and also how it relates to responses in patients because we have some early indications that The levels of INK T cells we detect are higher in patients that have either stable disease or partial response and we try to understand why that is and what's happening.

Speaker 8

Got it. Got it. And then lastly, I guess, I wanted to ask on the testicular patient that dropped out. I'm just If you could give us any details on the reasoning behind that and if there's any update on the other testicular cancer patient that And also I think that the SITC poster mentioned an expansion cohort for testicular. Can you give us any details on that?

Speaker 2

Absolutely. So what we're looking at here is in patients who actually have Refractory testicular cancer, there's currently nothing available for them. And the observations that we've Cerebral disease stabilization in the patient who is continuing in the trial and we're continuing to follow those patients. And we also continue to follow everyone for survival, Even if they've made choices to come off the trial, just in order to Spend more time with family and not necessarily in the clinic. And part of that choice, given that we are administering the cells With a single administration, right now in this current trial, it's we get enough information from the patients Now biologically from the paired biopsy samples as well as peripheral samples that we collect.

Speaker 2

So that patient who Did discontinue just the follow-up period of the study is still accessible to us and available to us. The other patient is a continued durable disease stabilization and it's really quite intriguing. So we will expand the trial in our own hands. Our Phase 1 trial going into a Phase 1b adding a dose, an additional dose to patients and specifying some Deepening our understanding in some specific disease areas where we have seen some very provocative signals of activity In patients who are not responsive to other therapies and that includes gastric, it includes non small cell lung cancer and it includes relapsedrefractory testicular cancer. And so those data will continue to develop over time and we'll be sharing updates At upcoming meetings, of course.

Speaker 8

Great. Thanks for taking our questions.

Speaker 2

Thank you. Your next question comes from Matt Phipps from William Blair.

Speaker 6

Hey, Ted, thanks for taking my question and the update. Given the just outsized effect in that gastric cancer patient, do you think there's any reason to specifically look at MSI high cancers?

Speaker 2

Well, that's a very intriguing question. More broadly, there is first, I'll have maybe Mark for the broader group just highlight a couple of the observations that we've seen with respect to microsatellite MSI High as well as MSS. Some of our patients are stable, our microsatellite stable. But there is there may be a biologic rationale to your point, Matt, about expanding our observations more broadly In a tumor in a pathologic agnostic way, but using MSI high, particularly in some of the combinations given the observations we're seeing as well as some germline tumors where we have seen some continued evidence of activity. Maybe Mark?

Speaker 3

Yes. So MSI high is an interesting tumor type because you could expect there's more new epitopes there. So there's more intrinsic T cell priming in the patients. And it's one of the indications where pembrolizumab is approved, which sort of capitalizes on that existing T cell response. So those tumors are not entirely cold.

Speaker 3

But this particular patient was progressing on nivo was progressing on pembro. So clearly, that was not enough. There was still some resistance in the tumor microenvironment that Prior to his treatment with INK T cells, so he was progressing even in that state. When we added INK T cells, it appears that some of the blockage So that's what I alluded to earlier that we think there is overlapping and additional benefit of IK T cells by reducing suppression that is not tackled by standard I O therapies. And the gastric cancer patient is clearly the best example we have of that particular mechanism there.

Speaker 3

Do we see this also in other tumors? I think it helps if you have an existing T cell response and of course having been pretreated with PD-one and then progressing probably has led to a well in gastric cancer patient indicates that that potentially is possible. So we hope to see more of that.

Speaker 6

It's fair if I missed it, but given how have you said how frequently you're going to test redosing or multi dosing given the persistence you've seen?

Speaker 2

That's again, Mark, I could ask you to give some insight. This I'll tell you what we're Currently our clinical team is thinking at this time is the most important component for us right now is as we continue to separate out The administration and the trafficking and the persistence based on where the cells are localizing peripherally, locally at the site of the tumor does give us a sense that we could dose probably we don't need to dose Any less than 6 weeks, so it gives us an opportunity to dose at around the 6 week mark, which enables us to combine really well and favorably with widely used standard of care therapies at this time, particularly in some of the tumor types that we're seeing our most pronounced benefit. And in doing that, we may and this will be something that we're going to explore more deeply in our expansion cohorts. Can we push that persistence out, which we're still monitoring in the patients who are on the trial? Does it change the dynamics within the tumor environment based on the localization, and should we explore delaying that to possibly 12 weeks?

Speaker 2

And we don't know the answer to that at this time. But based on the fact that we have seen very transient allo antibodies, which we presented at their 2 years ago, we've already established that we believe we could dose safely without any rejection And 6 weeks appears to be the time point that is in the sweet spot where we may optimize the benefit and optimize the convenience That was your final question. I now turn it over to Doctor. Buell for closing remarks. Thank you very much, operator, and thank you all for your time and attention and continued support to Mink.

Speaker 2

I appreciate your time.

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Key Takeaways

  • Data showed durable clinical benefit (over 30% disease stabilization) in heavily pretreated solid tumors—including NSCLC, testicular, and appendiceal cancers—with ongoing responses in metastatic gastric cancer.
  • In patients with viral ARDS on mechanical ventilation or VV-ECMO, AGN-7977 treatment achieved over 75% survival versus 10–30% in historical in-hospital controls.
  • AGN-7977, an allogeneic iNKT cell therapy, was well tolerated without lymphodepletion or HLA matching and demonstrated first-of-kind persistence for at least six months, correlating with patient responses.
  • A Phase 2 trial in second-line gastric cancer is set to launch this quarter, testing AGN-7977 with chemotherapy and Agenus’s anti-CTLA-4/anti-PD-1 antibodies, alongside externally funded viral ARDS and acute GVHD programs.
  • Cash reserves declined to $6.4 million at quarter end—despite reduced quarterly cash burn—underscoring the need for additional financing or strategic partnerships.
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Earnings Conference Call
MiNK Therapeutics Q3 2023
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