Marker Therapeutics, Inc. (MRKR) Earnings Call Transcript & Summary

Good morning, ladies and gentlemen, and welcome to Marker Therapeutics Conference Call. [Operator Instructions] As a reminder, this conference is being recorded. I would now like to turn the call over to Mr. Tony Kim, Chief Financial Officer at Marker. Please go ahead.

Thanks, and welcome, everyone. The press release containing the interim study results with our MultiTAA-specific T cell therapy in pancreatic cancer, as reported during the ASCO annual meeting late last week, are available in the News section of the Marker Therapeutics website. Joining me for the call today are Peter Hoang, our Chief Executive Officer; Dr. Mythili Koneru, our Chief Medical Officer; and Dr. Brandon Smaglo, Lead Investigator for the TACTOPS trial. Dr. Smaglo is currently Associate Professor in the Department of Gastrointestinal Medical Oncology in the Division of Cancer Medicine at the University of Texas MD Anderson Cancer Center in Houston, Texas, and was formerly at the Baylor College of Medicine where he led the TACTOPS pancreatic cancer trial. As a reminder, we will be making forward-looking statements during today's call. These statements are subject to risks and uncertainties that may cause actual results to materially differ from those forecasted. A description of these risks can be found in our most recent Form 10-Q on file with the SEC. I would now like to turn the call over to Peter.

Thanks, Tony. Hello, everyone. Good morning, and thank you for joining us today. As you know, this past Friday, we were delighted to report encouraging interim data from the ongoing TACTOPS Phase I clinical study being conducted by the Baylor College of Medicine with our MultiTAA-specific T cell therapy in patients with advanced or metastatic pancreatic cancer. The data were selected for presentation during the ASCO 2020 Annual General Meeting, which is being held virtually this year and reviewed by our lead investigator, Dr. Brandon Smaglo, who joins us here today and will be available to take your questions towards the end of the call. The several ongoing investigator-sponsored studies at Baylor with our MultiTAA therapy, including TACTOPS, have demonstrated the potential of this multi-antigen approach across various cancer types, including liquid and solid tumors. In addition to broad antitumor activity and epitope-spreading, which have led to durable clinical responses, our therapy was well tolerated with no incidence of cytokine release syndrome or neurotoxicity. As you know, based on these results, we are advancing acute myeloid leukemia as the lead indication for our first Marker-sponsored study for which we are currently preparing to launch. Heading into our own trial, we are particularly excited to discuss the TACTOPS findings in pancreatic cancer with you as these data support the growing body of evidence that our novel MultiTAA-specific T cell therapy has the potential for potent and durable antitumor effects. These results are particularly challenging to achieve in solid tumor cancers, such as pancreatic adenocarcinoma. So the applicability of our therapy may be really quite broad. At this point, I would like to hand over the call to Dr. Mythili Koneru, our Chief Medical Officer, for some top line observations from the TACTOPS trial. Mythili?

Thanks, Peter. To give you a clearer picture of the treatment challenges faced by physicians today and why we are so encouraged by this data, I'd like to briefly review some important details about this devastating disease. Unfortunately, pancreatic cancer holds one of the lowest survival rates among other malignancies. The American Cancer Society estimates that close to 60,000 people in the U.S. alone will be newly diagnosed with pancreatic cancer this year. About 47,000 total will succumb to this disease. There are many factors that contribute to these low survival high mortality rates. For one, disease is often detected past the point at which surgical resection is feasible due to the lack of early detection markers. Additionally, the location of the tumor, the challenging tumor microenvironment, the advanced age of the patients and the systemic effects of the disease, all limit the options for local therapy. The standard of care treatments for pancreatic cancer today are chemotherapies. While they do provide some benefit, they also carry a long list of serious side effects. It is evident that the need for new therapies in pancreatic cancer is dire. To this end, we believe that our novel MultiTAA-specific T cell therapy could potentially offer clinical benefit for these patients without the toxicities of standard of care treatment. While there are several patient cohorts in the study, the focus of the ASCO presentation as well as today's discussion are patients in Arm A. These patients presented with an advanced disease state and received at least 3 months of standard of care chemotherapy, gemcitabine, nab-paclitaxel or FOLFIRINOX before receiving up to 6 administrations of our MultiTAA-specific T cells in conjunction with our chemotherapy regimen. The pretreatment period is significant because those 3 months represent the period in which a chemo-driven response would typically occur. As Dr. Smaglo would detail in just a moment, we saw that a number of patients in the TACTOPS trial experienced responses after this period had ended, suggesting MultiTAA's potential to produce added benefit in this patient population. We also observed that in addition to multiple targeted antigens, our therapy recognized nontargeted antigens. As the tumor microenvironment varies from patient to patient, the ability to address these differences may offer a significant benefit to patients. This epitope spreading was seen in all the responders and suggest that MultiTAA therapy may contribute to a potent, broad and durable treatment effect. We recognize that historical studies such as ACCORD, which compared FOLFIRINOX to gemcitabine, and IMPACT, which compared nab-paclitaxel/gemcitabine to gemcitabine alone represent patient populations that are slightly different compared to the Baylor Phase I TACTOPS study. The TACTOPS study was open to only those patients that did not progress in the first 3 months. In order to get a better sense of the expected PFS values compared to the historical PFS, we commissioned an outside biostatistician to exclude those patients who progressed in the first 3 months. Based on her analysis, the biostatistician calculated that the modified PFS for patients who receive FOLFIRINOX was 8 months, while the modified PFS for patients who received nab-paclitaxel/gemcitabine was 6.8 months. We expect these results to provide more of an apples-to-apples comparison to those enrolled in the Baylor TACTOPS study. Based upon these results for 9 of the 13 patients, the cancer was controlled for a period longer than historical controls relative to the type of chemotherapy used. While the patient numbers in this trial are actually relatively low, we are extremely encouraged by these results, which are consistent with what we reported during AACR back in July 2019. We are looking forward to continuing to follow these patients and reporting additional data that may support MultiTAA's further development in this challenging disease area. And now to provide the interim results from the TACTOPS trial in more detail, I'd like to hand off the call to the lead investigator, Dr. Brandon Smaglo.

Good morning, everyone. It's a pleasure to be with you this morning. I appreciate the introduction and the opportunity to talk about our work from Baylor in a little bit more detail with you following our presentation this past weekend. I think the stage has certainly been set to summarize what a challenging disease pancreas cancer is to treat. One thing that I do just want to emphasize is that progress in pancreas cancer when compared to tumor types that you might consider to be sort of a cousin, certainly, gastric cancer, colorectal cancer, has not been as robust as what we've seen in those other diseases. In fact, if you were to look back at the progress made in advanced pancreas cancer over the past many decades, unfortunately, the outcomes of pancreas cancer, if anything, have gotten worse, but certainly have not seen any type of an improvement that we've seen with other cancer types. I think a big part of the reason for this, and certainly, there's multiple factors, but the big reason has to do with what we can do with systemic or medical therapy. As has already been alluded to, our options for systemic therapy are largely limited to chemotherapy, and frankly, chemotherapy regimens that bring with them a fair amount of toxicity and so would not be something that every patient at the outset of the treatment would even be eligible for. Certainly our go-to, if possible, would be FOLFIRINOX. But with the toxicity this regimen brings, a fair number of patients will just never be candidates for this treatment. This may have nothing to do with your cancer, but have a lot to do with, for example, the comorbidities that they bring to the table, their performance status at baseline, certainly age will factor into that and so on. Even for those patients who can receive FOLFIRINOX, this is not a chemotherapy that can be continued indefinitely even if it is effective in treating that patient's cancer. Because of the accumulation of toxicity that patients will experience, there will eventually be a need to deescalate or even stop that therapy for those reasons. For those patients who are not candidates for FOLFIRINOX, a good plan B, as you heard, would be gemcitabine and nab-paclitaxel, also called Abraxane. But again, while perhaps less toxic, at least conventionally than FOLFIRINOX, this is not without its side effects as well. So an important challenge in moving the needle forward in pancreas cancer is that when we are trying to expand beyond our standard of care options, we're already limited by the fact that we have very little margin for additional toxicity if, for example, we were to add a therapy on top of our standard of cares. And so for that reason, a trial like this one, where we can use a T cell or other immune therapy is very attractive because we're able to roll it into our conventional therapy and not really have to add upon what the patients may already be experiencing with toxicity. So for the study, our patients, as you heard, underwent a 3-month induction with chemotherapy. And it was during that time that their T cell therapy product would be generated. This is a fairly straightforward process for the patients. They had to undergo a peripheral blood draw. It was a single blood draw, albeit a fairly large draw was done. It's close to a unit of blood. But nevertheless, this was done peripherally. There was no need for apheresis, and there was no lymphodepletion that was involved in it. They could then go on with their initial chemotherapy, while our scientists in the labs would use from that blood draw, the patient cells to expand and generate the cell product that we would ultimately give back to them as a therapy. Now an important challenge in designing this or any therapy when it comes to the targets that we're going to select. And certainly, a challenge here would be the possibility for immune escape. This would be true for an individual patient whose tumor cells may not uniformly express a single antigen target. This would also be true across different patients where if different levels of expression of different targets are seen, what therapy might be good for one patient may not be quite as effective for another. And so therefore, the challenge is that if we're limiting what a subset of the patient's tumor we're targeting with an antigen, that may give an opportunity within tumor heterogeneity for there to be an immune escape. And so in our approach to overcome that, we are simultaneously targeting a number of different tumor-associated antigens, 5 specifically. And this process is done by targeting multiple epitopes within each antigen for some level of redundancy. And again, this process is done in a native or non-engineered process, which we intended would limit some potential for side effect and toxicity. The antigens that we targeted were Survivin, SSX, MAGE-A4, PRAME and NY-ESO-1. Rationale for this group, number one, these are antigens that are fairly consistently expressed by different pancreatic adenocarcinomas. Additionally, these are antigens that are not expressed on native tissue. The exception is Survivin, but it has been very well described that targeting Survivin doesn't have any clinical effect on the patient's own cells. And finally, there is some history for targeting these antigens in other cancer types with the cell and gene group at Baylor. And so there already was some proof-of-concept making these attractive sites to target. In generating the T cell product, we had used the patient's dendritic cells as the antigen presenting cells, and we're using whole antigen in the process for expanding the product. The value of this would be, for example, to overcome the restriction that could be imposed by the use of, for example, a transgenic T cell receptor for a single peptide. Additionally, this allows us to simultaneously develop cells that can target multiple antigens, getting back to that concept of trying to overcome potential tumor immunization. We have -- and I'll reference the deck that is available online, but we have graphically represented the breakdown of the CD4 to CD8 cells if you're interested. And in that information, you also see some safety data, and I'm referring specifically to Slide 20 that indicates that none of the lines that have been developed have reacted against nonmalignant autologous cells. So this does seem to be a very safe product. Now as you heard, the idea here would be for each patient to go on to the study after 3 months of an initial standard of care chemotherapy with the caveat being that, that chemotherapy be effective for controlling that individual's cancer. Over the course of the next 6 months, they would continue that same chemotherapy while once per month receiving a reinfusion of the dose of the T cells. The cells were given at a fixed dose. No additional lymphodepletion was given. If once enrolled in the trial, we are looking essentially for endpoints of safety and feasibility, also exploring efficacy. With an intention to generate 6 doses of T cells for each patient, I can tell you that of the 13 patients we enrolled on the trial, we developed enough product to give 12 of those 13, all 6 doses. The final patient had enough product generated to give 2 doses in total. In your slide deck, there are a number of standout examples for how patients had done, and I'm going to just highlight a few of these. Among them, I think our best outcome was patient -- so-called patient number 7. And the reason I highlight this patient, this individual radiographically went on to develop a complete response to therapy. We have examples of this individual's CT scans at a baseline prior to going on to the study. So that is to say, at the completion of that 3-month induction with chemotherapy and then at the end of the 6 months of T cell, so 9 months on total therapy. And fortunately, that individual had a radiographic complete resolution of her disease. For this patient, we have also illustrated our ability to detect the targeted antigens of interest as compared to a baseline as well as nontargeted antigen. And this story is repeated for essentially all of our patients, where we are able to determine which antigens were more detected with the therapy. But also in seeing the nontargeted antigen expression and detection, that indicates to us that not only do we have evidence of epitope spreading, but activation of the endogenous immune system as well. And we've illustrated this in the slides for a number of different patients, but that's just a slice of what we have seen across the spectrum of our patients. Several additional good radiographic outcomes are illustrated in the slides as well. Going through Slides 24, 25, 26 and 27, you can see similar responses for -- in addition to patient 7, patients 1, 3 and 12, all of whom went on to have a radiographic partial response as per RECIST criteria from the time that they were enrolled in the trial and started to receive T cells. A few details of these patients that I think are worth noting, these do, first of all, give a breakdown of patients with both chemotherapy types, so some who received the gemcitabine and Abraxane regimen, such as patient number one. You also note that while the increased detection of targeted and nontargeted antigens is seen across all of these patients, it's a different subset of the antigens. And I think the highlight there is that for a situation where different patients' tumors are going to have different targets of interest, it's very convenient to be able to simultaneously target multiple antigens not knowing what are going to matter for that individual in their tumor treatment and still be able to have a good and meaningful effect without having to add to their toxicity, add to the therapy that they need and so on. Moving on a little bit. I will reference you to Slide 28 and some of the changes in tumor measurements. Now Slide 28 will give you sort of a slice of everything that happened with the patients here, and then we'll break these down a little bit more into detail. But first of all, what I'll highlight for you is that for patient number 7, and again, this was the individual who went on to have a complete response radiographically. What's exciting to note here is that for this individual that CR was not demonstrated until the completion of 9 months of therapy, that is to say until completion of all 6 doses of the T cells. And additionally, the intensity of that patient's tumor response seemed to have picked up some momentum towards the end of treatment. Now conventionally, what we would expect with chemotherapy alone is that by the 3-, let's say, 6-month mark, we would see a plateau in that patient's tumor response. We would typically at best expect that response to maintain its velocity, if you will. And so the fact that for this patient between months 6 and 9, so that is to say, in the last 3 months that the patient was getting her T cells, the velocity of response seemed to pick up steam, would seem to indicate that there has been some additional benefit to her tumor response as compared to what we would expect to see with chemotherapy alone. And if you'll reference Slide 31, you'll note that this has been a very durable response that is still ongoing. Obviously, that's just one example. But fortunately, other patients did have a similar change in terms of the intensity of their tumor response when the T cells were introduced. I will reference Slide 32, and highlighting here patients 1, 3 and 12. These 3 individuals all had a radiographic partial response as per RECIST criteria from the time that they went on to the T cell therapy. And again, in conventional expectation, we would think that by the 3- to 6-month mark with chemotherapy alone, we would see a plateau in terms of their tumor response. At best, we would expect the rate of their tumor response to more or less be the same and that, in fact, for these patients, there was an increase in the response when the T cells were introduced after month 3 is very encouraging for what additional effect that therapy was having beyond what the chemotherapy alone would be able to achieve. I think one further example...

[ I'd like to add ]…

Peter, go ahead.

I'm sorry, Dr. Smaglo. I just wanted to interject with a couple of questions. So in light of the 4 late objective responses that you saw amongst these patients, is it also correct to say that for all of the patients who qualified for receipt of cells that their clinical status at the end of the chemotherapy-only period was all stable disease, that there were no objective responses during the chemotherapy-only period?

Yes, that is a fair statement. So there -- I think to put it succinctly that for those patients on the trial who did demonstrate a response of their disease, that response was observed from the time that they went on to trial with the T cells as opposed to being able to, for example, roll in or account their standard of care chemotherapy-only period. Yes, that's correct, Peter.

Thank you.

No problem. And so just continuing along that thought line for induction responses with the T cells, I think one very clear example of this, as illustrated in Slide 33, we had a couple of patients who, per RECIST criteria, had tumor that was stable. But in point of that effect and actual measurement, there was some slight amount of growth in their tumor. These are patients 8 and 10. Again, if we had these patients continuing on their same standard of care chemotherapy alone, our expectation might be that they would continue to have a slow but steady degree of tumor progression. However, in these 2 patients, the opposite was seen when the T cells were added on top of that therapy, their tumor started to respond again. And again, this would seem to suggest that the T cells were able to accomplish something above and beyond what their chemotherapy treatment was doing. We have, on Slides 34 and 35, a summary of all of our patients who have treated in the best responses that they've had. These are broken down by the type of chemotherapy that was used. So 4 of the patients received chemotherapy with gemcitabine and nab-paclitaxel. And these patients are summarized on Slide 34. 3 of the 4 patients had an ongoing therapy beyond what we would historically consider to be a progression for your overall survival cutoff, which is very exciting to see. Tabled on Slide 34 as well is the best response that these patients' tumors had while on the trial with T cells. And so again, one patient had a partial response and 2 had a stable disease, which is very encouraging. The same type of information is presented for the remaining 9 patients who received FOLFIRINOX, and this is in Slide 35. And again, you will note that a number of the patients, 6 of the 9 were still on their first-line therapy when they crossed the historical median overall survival threshold. And patient 12 exceeded the modified median progression-free survival as well for a total of 7 having a good outcome there. Again tabled on the right are the best responses that these patients' tumors had while on therapy. One that I would highlight just as sort of a little bit of an explanation is that patient number 2, who had a fair amount of metastatic disease, had a mixed response to first assessment where there were some tumors that were responding to therapy, actually, but others that were progressing. Obviously, this would mean that we would need to seek out other therapy for this individual. And then unfortunately, she went on to pass away suddenly from a pulmonary embolism. And so we don't really have the ability, of course, to say what could have been if she had gone on to a different type of therapy after this. Otherwise, again, summarizing this group are a number of different responses. The majority of patients having stable disease, but there were some partial responses with the therapy as well, and we've sort of summarized these in earlier slides. There is a summary on Slide 36 of CA 19-9 trends because this is, I think, something that can, in certain instances, provide us additional information for how well our patients are responding to therapy. This is broken down just based on the order of magnitude for the CA 19-9 for the different patients, just so they would be a little bit clearer. Unfortunately, I don't think there's a lot of additional information that we learned from this for a couple of reasons. First of all, because there was that long 3-month period of chemotherapy induction before patients went on to the trial. As is sort of seen geographically, a lot of the CA 19-9 response that could have happened already happened within that first 3-month period. The other thing, though, is that there does seem to be a fair amount of sort of -- we saw 2 things as opposed to a consistent trend while the patients are getting the T cells. And this may be an artifact from the T cell therapy itself. When we did see these sort of up-and-down levels of the CA 19-9, we didn't have any correlation that patients were doing better or worse, either clinically or radiographically. And so this may be an artifact of this type of a treatment. Point being that, unfortunately, I don't think for this trial anyways, we have a lot of additional information to garner from the CA 19-9 values and trends over time. I'm going to make a few summary points now, and then I'll turn it back over to the team into questions. One thing you will notice as we've gone through this deck is we haven't really talked about the side effect, and that's because there really hasn't been any to discuss. And that's very encouraging. Again, for a type of cancer, where our best standard of care ends up being toxic, to be able to add therapy and it seems meaningful therapy to these patients treatments and have no additional side effect for them to have to shoulder is very exciting. I think we're very excited to see how durable the cancer control has been for these patients. Again, a number of the patients, 9 of the 13 exceeded their overall survival historical control. And that is certainly, I think, meaningful for an early study like this with small numbers. Additionally, seeing tumor responses in the patients where we did is very encouraging. It certainly proved feasible to generate product for these patients fairly consistently. And so the issue of being able to actually deliver on a therapy that is fairly complex, I think, is very exciting. It definitely had a study -- definitely a study that had a good tolerance, good cancer treatment results. And the background data that we were able to generate as well, suggesting the epitope and antigen spreading and activation of the endogenous immune system is very exciting. I think looking forward, it will be exciting to be able to potentially explore a therapy like this further with chemotherapy, perhaps rolling these cells into treatment earlier than 3 months. And we do have the ability, fortunately, to refine which antigens we target a very simple pivot, if need be, which makes us a very dynamic therapy as it may be required. I'm going to pause there. I'll turn it back over to the rest of the group, and I'm happy to be a part of questions that you all may have. And thank you very much for joining me and hearing a little bit more about the work I've been doing. I appreciate it.

Thank you, Dr. Smaglo. I think we'll turn it over to any questions that we may have from participants on the call.

[Operator Instructions] Our first question today is from Matt Biegler of Oppenheimer.

I wanted to ask about the translational data showing MultiTAA expansion in patients that achieved responses. And I was wondering whether there was a correlation between peak expansion and clinical responses. So maybe asked a different way, did you also see expansion in patients with no clinical benefit?

The short answer is, yes, we did. So there was expansion regardless of whether it was a deep response or whether it was just stable disease. It is, I think, a little bit muddled there is when we're talking about peak response. It tends to be the best response that we've seen across that patient's entire collection. We're looking at the antigens at a number of different times, and it didn't necessarily seem to be that the peak response correlated to the time point when the patient was having their best response. So there was definitely antigen spread and epitope spreading across the board for these patients, but it didn't necessarily mean that, that was when they were having their best response.

Okay. That makes sense. And then maybe a question for Mythili. I just want to make sure that I understand the historical control analysis that you did. Does that exclude the 4 patients who were unable to receive MultiTAA due to the rapid disease progression? I think there was either 3 or 4 patients that fell into that category. And then if you include those 3 or 4 patients and kind of like a whole intent-to-treat analysis, how does that compare to historical controls?

The -- are you referring to the modified PFS that was calculated?

That's right.

So yes, the modified PFS calculation was based on the ACCORD and IMPACT papers. And basically taking that data and excluding those patients that progressed the first 3 months, you can calculate what the median PFS would have been for patients that had stable disease or better after 3 months, and that's where that number comes from. And I think this more accurately represents the patients in the TACTOPS study because of the fact that, as Brandon has mentioned -- Dr. Smaglo has mentioned that the patients that progressed did not go on to receive the MultiTAA T cells. The number of patients in gemcitabine/nab-paclitaxel that exceeded the modified median PFS values were 3 of the 4 patients. And then if we look at the FOLFIRINOX group, only 2 of the patients did not meet the modified median PFS expectation compared to the rest in the group. So I think we're very encouraged by this data. And -- but we do not have an equivalent calculation for the median OS values. That calculation is a little bit more complicated because we need to get more of the primary data to really understand how to adjust for the patients that progressed in the first 3 months and then later died. So we were not able to perform similar calculations to determine what a modified median OS survival would be for these 2 historical papers, but we're in the process of trying to get the primary data to do similar calculations for that -- those values. Did that address your questions, Matt?

Yes, yes. No, that makes sense. And then finally, Peter, maybe one more, if I may. So I guess kind of what are the next steps for the program? It seems like the FOLFIRINOX arm seemed to perform a little better. I guess are you considering taking these learnings into a company-sponsored trial?

Yes, Matt, that's a great question. Let me actually go back to your prior question. So I think that to fully answer the question that you gave us there, I think that the approach here was sort of the inverse of what you suggested, which is that rather than looking at the 4 patients who fell off study because of progression, what we did was we really tried to adjust the historical data to exclude those patients who would be equivalent to the 4 patients who fell off our study. And typically in those studies, either with FOLFIRINOX or gem-abraxane, you typically see between, call it, 10% to 20% of patients progress within the first 3 months. And so those were patients that we sought to exclude in our modified study, which is what increased the median overall progression-free survival from 6.4 months to 8 months in the FOLFIRINOX group and from 5.5 months up to 6.8 months in the gem-abraxane group. Now your question about how our 4 patients compares to historical, 4 out of 17 patients would be -- would sort of represent somewhere between the typical falloff rate to a rate that is somewhat higher than the historical rate of falloff, which might imply that these patients were in generally less well condition than the historical groups. But that would be the comparison, which is that typically in the historical control groups between 10% to 20% of patients were lost to progression within the first 3 months versus the 4 out of 17 that you saw in the TACTOPS group. With respect to these studies, I think that the results are interesting. I mean from our perspective, both the late responders and the data that we now see with respect to extended progression-free survival in the patients is certainly interesting to us. I will defer to my -- to speak more about how we look at that from an overall clinical development perspective. But what I'd say is that between the data that we're seeing here, with respect to a reasonably large number of unexpected late responders, with respect to performance against historical progression-free survival and overall the low numbers of mortality events that we've seen so far, it certainly seems very promising, particularly when we stack it on top of many of the anecdotal observations that can be made about some of these patients, such as patient 7, the complete responder who generated a complete response between month 6 and month 9 of therapy, which is, as you know, quite late, but also managed to get that complete response in the face of a reduction in that patient's chemotherapy. That patient was seeing a significant amount of neuropathy at month 6. And so at month 6, that was actually having one of the 3 major elements of the FOLFIRINOX cocktail, the oxaliplatin, removed from the chemotherapy regime, and despite the reduction in the chemotherapy regime, generated the complete response at month 9 after that reduction. I think that all of these things for us, point to some very interesting findings. And My, I think I'll kick it over to you to talk about how we consider that in the context of the company's overall clinical development plan.

Thanks, Peter. As Peter has mentioned, we are very encouraged by this data, and we're trying to think of ways to appropriately craft a potential study moving forward. And as we mentioned in today's call earlier, we are looking forward to also following these patients further to really determine how they'll continue with further time, both just in overall survival and how they go on to other therapies as well. So but I think we will continue to report on those findings.

Okay. Great. Congrats on the data, guys.

Thanks, Matt.

[Operator Instructions] There appears to be no further questions at this time. I would like to turn the call back to Peter Hoang for closing remarks.

Thank you very much. And I'd like to thank everyone again today for joining our call. As you've heard, the growing body of data in this trial continue to be very encouraging and demonstrate evidence of our therapy's potential in pancreatic adenocarcinoma, which is a highly challenging hard-to-treat cancer. We will be following these patients closely and enrolling new patients to further evaluate durability of our therapy. We look forward to providing you with additional updates from the trial as they occur. Have a great day, everyone, and please reach out to us if you have any additional questions.

This concludes today's conference. You may disconnect your lines at this time. Thank you for your participation.