Good afternoon and welcome to the Elicio Therapeutics KOL event. At this time, all attendees are in a listen-only mode. A live question and answer session will follow the formal presentations. To our covering analysts, please use the raise hand feature to be added to the queue. As a reminder, this call is being recorded and a replay will be available on the Elicio website following the conclusion of the event. I will now turn the call over to Christopher Haqq, Executive Vice President, Head of Research and Development, and Chief Medical Officer of Elicio Therapeutics. Please go ahead, Chris. Great. Thank you very much. Let's go ahead to the next slide, please. Today, the company will be making forw ard-looking statements, so I'll just pause here for a moment to allow time for you to read this. There's additional information on our website, if needed. Okay. Let's go ahead, please. Great. My name is Chris Haqq. I'm the Chief Medical Officer for Elicio Therapeutics, and it's my pleasure to welcome you to today's call, where I will discuss promising observations that suggest the potential for ELI-002 to help patients with metastatic KRAS-mutated pancreatic cancer. I'm joined today by two expert oncologists, Dr. Peter Hosein, Professor of Clinical Medicine from the University of Miami Sylvester Comprehensive Cancer Center, and Dr. Zev Wainberg, Professor of Medicine from UCLA and Co-director of the UCLA Health Gastrointestinal Oncology Program. In today's agenda, Dr. Wainberg will cover the expectations for complete response based on prior studies. Dr. Hosein will present his clinical observations when patients that previously received ELI-002 went on to receive subsequent therapy containing a checkpoint inhibitor. I'll then cover the translational data and our Elicio plans to build on these observations with a prospective study. Let's move to the next slide, please. Let's go one more forward, please. Today, the key messages we'll communicate are about three patients who were previously treated with ELI-002 7P, who later achieved complete responses following nivolumab-based therapy. The responses included radiographic, metabolic, and biomarker normalization, and all patients had microsatellite stable disease, which has previously been considered refrac tory to immunotherapy. The observations are hypothesis-generating and do not establish causality. However, these findings motivated deeper clinical and translational analyses and set the stage for a prospective study of concurrent ELI-002 and checkpoint inhibition added to standard therapies in metastatic PDAC. To understand why these observations are notable, Dr. Zev Wainberg will first review historical experience with different therapeutic modalities, and when checkpoint inhibitor therapy was added to standard regimens in past trials for patients with metastatic pancreatic cancer. Zev? Thanks, Chris, happy to be here to go over some of this. Next slide, please. I think we know that metastatic pancreatic cancer remains a huge challenge. We've struggled compared to other cancers at achieving what we would define as complete and durable responses. You could see here how rare and infrequent it is, regardless of the regimen used, regardless of the combination used, to have true complete responders in pancreatic cancer. Anecdotally, most oncologists who treat a lot of this will tell you they've only seen one or two in their career, and they can't explain why. Next slide. When we think about immunotherapy in pancreatic cancer, by and large, we've struggled, at least with the classical immunotherapies, checkpoint inhibitors. No matter the context, whether it's given with chemotherapy or with radiation for disease that may be more localized, we've still been unable to shrink tumors down. That's why essentially no immunotherapy drugs have ever been approved for pancreatic cancer. Next slide. I'll hand over to Peter, who will go over some interesting observations that he's observed in the context of ongoing clinical trials with the Elicio products. Thank you very much, Zev and Chris, and thanks for having me this afternoon. Next slide, please. What I would like to present are data related to patients who enrolled on the AMPLIFY-7P study, receiving ELI-002 and exp erienced relapse after a period of time following the ELI-002 therapy. Those patients were treated in a uniform fashion at our institution. What we observed in these three patients who had recurrences after the ELI-002, after treatment for recurrent disease with chemotherapy plus an immune checkpoint inhibitor, in this case, we used nivolumab as immune checkpoint inhibitor combined with radiotherapy. We found all three of them achieved complete radiographic response using objective criteria both by the RECIST criteria, which uses CT imaging, as well as the PERCIST criteria, which uses PET imaging. We'll show you the data on the biomarker, tumor marker responses as well. All three of these patients had KRAS-mutated pancreas cancer. All of the patients' tumors were mismatch repair proficient, microsatellite stable. We observed persistence of mutated KRAS-specific T cells post-chemotherapy in the salvage setting after the recurrence. The T cell responses were both CD4 positive and CD8 positive. Chris will show you the data also regarding antigen spreading after the recurrences. At least two of these three responses have been maintai ned now over a sustained period of time, and I'll show you those data on the next slide. Let's move to the first case, please. All right. This is a table summarizing the data. All three patients had codon 12 mutations. Two of them were G12D, one were G12V. These are the most common KRAS mutations. The column that starts with nivolumab start to PR/CR denotes the time of recurrence, which is coinciding with the time of the start of the chemotherapy plus immunotherapy, to the time when it took to achieve a partial response or a complete response. The next column over gives you the duration of response. The duration of response was varied from 2.2 months-11.6 months. The responses were achieved between 1.5-6 months, and patients who achieved a complete response, the range was 2.5-6 months. The first patient shown did have disease progression soon after achieving a response, whereas the other two patients had more sustained responses. We'll show you that if you can move to the next slide. This first patient, this is a patient who had upfront surgery for pancreas cancer, underwent adjuvant chemotherapy and was enrolled in the AMPLIFY-7P study following that. There was a five-month period where they received ELI-002 7P, which is denoted in the fig ure on the left with a light blue line with the triangles showing that the time points. 0 time point means the start of the ELI-002 going on to five months of therapy. During this time, the CA 19-9 levels started rising. The graph is showing the CA 19-9 trend. At the time of the first dotted line, the vertical dotted line is week 18 when recurrence was confirmed by PET and by biopsy in regional lymph nodes. The PET scan on the right side is showing you where the white arrows are, showing you lymph node recurrences. One of the two upper areas are paraesophageal, in other words, next to the esophagus, and then another one lower down in the mesentery. The bottom panel is showing you a cross-sectional axial view of the same thing. At that point when the recurrence was diagnosed, radiotherapy was given, which is denoted by this orange arrow, and then nivolumab as well as gemcitabine paclitaxel was given. Gemcitabine paclitaxel would be a standard therapy in this situation, and the nivolumab and the radiotherapy were added to that. You can see the CA 19-9 level coming all the way down and maintaining almost close to the normal range for a few months. That was accompanied by resolution of the PET uptake on the right panel on the scan. This patient achieved a complete radiographic response by RECIST and a complete metabolic response by PERCIST. That response lasted for a short time, only 2.2 months. Next slide. The second patient we had, this was a slightly different sequence of events. Prior to getting ELI-002, this patient actually had upfront chemotherapy for localized pancreas cancer, followed by surgery. After surgery, the patient was enrolled on the AMPLIFY-7P study, received the 10 doses of the ELI-002, as shown on the left. Then again, similar to the previous patient, the CA 19-9 level was rising and a PET-CT scan showed a positive lymph node next to the stomach in an area called the gastrohepatic ligament. That was biopsied, proven to be recurrent disease, and this patient again was treated in a similar fashion with gemcitabine paclitaxel alongside nivolumab. After achieving a response with decreasing CA 19-9 and rad iographic improvement on imaging, this response was consolidated with radiotherapy. The nivolumab was continued for an additional four months. The nivolumab was stopped at that time because of some toxicities due to the PD-1 inhibitor. There was a complete response documented both by PET and CT scan after that therapy was given. The second vertical dotted line at week 69 shows you the follow-up PET scan where the uptake is no longer visible. It sustained for another few months. The patient had a separate location of disease progression where the same treatment was restarted. Again, that patient achieved a response and is pending start of radiotherapy in the near future. This one was a longer duration of response. It was 11 months with a time since the recurrence of 13 months. Again, both radiographic response by CT and PET criteria. Next slide. This is the final patient. This patient also had chemotherapy first for localized pancreas cancer, had surgery. Then was enrolled in the AMPLIFY-7P study, received 10 doses of ELI-002 over the first five months. Again, similar patterns, CA 19-9 rising. This patient had what we call a local recurrence. A local recurrence is a recurrence that occurs in the same location as a primary tumor where it was resected, as shown by the arrow and the PET scan in the middle. That was biop sy-proven as recurrent pancreas cancer and was started on therapy, similar treatment as the previous two patients with gemcitabine paclitaxel with nivolumab. Again, had a biomarker response, radiographic response, both by PET and CT, consolidated by radiation therapy. That response has now been sustained for 9.2 months. More recently, the CA 19-9 levels started rising, but there were some other issues with this patient with an infection, so as of the last scan, has not had any evidence of disease progression or recurrence. This was the last patient, all three of them showing objective responses, both by imaging and biomarkers. Next. The summary is that we had three consecutive patients who had recurrences on the AMPLIFY-7P study who were all treated in a similar fashion. All of them had microsatellite stable pancreatic cancer, which would not be expected to normally respond to immune checkpoint inhibitor. These patients had unexpectedly long benefit from this subsequent therapy, and one of them has an ongoing response. Again, as we noted, this is notable relative to the historical experience with what normally happens with patients who have recurrent pancreas cancer. Next. Great. Thanks, Peter, very much for presenting the notable clinical observations. The hypothesis that follows from this is that ELI-002 may induce durable KRAS-specific T cells that are important for respo nse to subsequent therapy. If this hypothesis is correct, it follows that translational data should show that KRAS-specific T cells, number one, they should persist beyond the initial ELI-002 treatment. Number two, they should modulate the tumor environment. Number three, bystanding T cells that recognize the tumor through additional mutated proteins that are not KRAS should allow for a broadening of the immune attack. Subsequent therapy with a checkpoint inhibitor could take the brakes off the immune responses in this setting and might contribute to the deeper antitumor activity observed. Because of the translational samples that were available in the AMPLIFY-7P trial, as well as the biopsies that Dr. Hosein mentioned, there were translational findings in the three patients that we could look at to examine the biological plausibility of this model. Let's go to the next slide, please. Here, you can see that increased T cell infiltration was observed following ELI-002 in patient one and in patient two when comparing their primary tumor specimens on the left to biopsies taken at the time of rela pse on the right and before the subsequent checkpoint inhibitor-based treatment began. Appropriate samples were not available to carry out this analysis for patient three. In the immunofluorescent panels on the lower images, the orange color identifies the pancreatic cancer through the cytokeratin marker. The blue color identifies the T cells with their CD3 marker, and the green are the specific subtype of T cells, killer T cells, identified by the CD8 marker. The red color also shows the expression of PD-L1, which is a possible resistance mechanism for ELI-002 that is engaged by checkpoint inhibition. The data in this slide suggests that ELI-002 may create the more inflamed hot tumor microenvironment needed for immune therapy to be potentially able to help and support the hypothesis that immunoactivation could be involved in the clinical responses that were observed. We next asked in the next slide, whether ELI-002 immune responses remain detectable over time. As you can see here, the mKRAS specific T-cell responses persisted after chemotherapy and checkpoint inhibition in all three patients. The responses observed included both CD4 and CD8 T cell populations and the mutant KRAS-specific T cells were polyfunctional, which means they knew how to make key mediators and cytotoxic molecules. The observations also support the hypothesis that ELI-002 induced T cells might be important to subsequent therapy. Importantly, in the next slide, we'll examine whether the immune responses can broaden beyond KRAS. Here we're looking at what's called antigen spreading data for the three patients. Each box in the graphs represents a unique non-KRAS tum or mutation. We observed immune responses extended beyond KRAS in each. The antigen-spreading events began during the period of ELI-002 monotherapy in two of the three individuals and further increased when the checkpoint inhibitor-based therapy was subsequently added to address the metastatic relapses. The majority or 82% of personalized tumor antigens evaluated were immunogenic, and this suggests that anti-tumor immunity not only persists when ELI-002 has been given but may broaden also when checkpoint inhibition is added. Together, the clinical and translational findings are consistent with the hypothesis that ELI-002 may improve treatment for metastatic disease and inform our clinical development strategy. Let's move to the next slide, please. Motivated by these observations, Elicio is building a staged data-driven metastatic clinical development plan. The initial focus is on recurrent metastatic pancreatic cancer with no more than three lesions to keep the patients very similar to the ones that Dr. Hosein has treated. With confirmation of the signal and subject to funding, we plan to expand into treatment-naive, broader combinations, and bulkier tumors. The trial is planned for small cohorts designed for rapid learning, with clinical biomarker and immune data altogether to guide the next steps. The first study within the strategy is outlined on the next slide. The AMPLIFY Metastatic trial that's planned is designed to prospectively test the hypothesis generated by the observations you've seen today. The initial combination will put together ELI-002 7P, chemotherapy, and PD-1 inhibition. Patients with recurrent and treatment-naive metastatic disease will be evaluated for clinical and biological activity. We believe this study could provide a platform for expansion to additional cohorts to evaluate combinations with ELI-002 over time and subject to funding. The study is intentionally designed to generate informative data quickly. Let's move to the next slide, please. The key takeaways here are that complete responses are rare in metastatic PDAC. We're working with investigators to finalize the study design, initiate study start-up activities, and advance our metastatic PDAC program, subject to funding. The trial aims to generate prospective evidence for the hypothesis presented today and will provide key data to inform future development, not only in the metastatic setting, but the combination also could be relevant to phase III development strategy in adjuvant as well. Let's go to the next slide, please. In summary, complete responses observed following prior ELI-002 treatment are notable relative to the historical experience. They're supported by a biologically plausible translational dataset and warrant a prospective evaluation. I want to thank the patients, families, and site staff that have taken part in the AMPLIFY clinical trials of ELI-002, and we look forward to advancing this work and discussing your questions. Thank you, Chris, and to our KOLs. At this time, we'll be conducting a live Q&A session. To our covering analysts, please use the raise hand feature to be added to the queue. Kindly hold for a brief moment while we poll for questions. Our first question comes from Michael King with Rodman & Renshaw. Please go ahead, Michael. Thanks for taking the question. Good afternoon, guys. Good afternoon to the physician guests as well. Couple of questions. Obviously, Chris, these are small numbers of patients. Do you feel like you've got enough sort of material? I know these are rare events and maybe the physicians can chime in as well from their experience. Have they ever seen responses like this? Do you have enough quantity of data to suggest that a study of the design you spoke about is ready to go? Do you need more data to come in? Maybe conjoined with that, can I just ask you what was the rationale for using nivo in the first place? Because typically these are super cold tumors, not responsive to PD-1. Why was the decision made to follow up the therapy with PD-1 therapy? Thank you. I'll start. Thanks for the question. I'll start, then I'll invite Dr. Hosein and Dr. Wainberg to comment as well. One noteworthy feature that we've seen in phase I with the ELI-002 program is the modulation of the tumor environment. In the Nature Medicine publication in 2024, by Pant et al., we had a couple patients that had biopsies performed at the time of their progression. Like the biopsies presented today, an infiltration of the tumor with T cells was observed. Even from phase I development, we've had consistent data now across all the patients who've undergone biopsy, where we've seen that the ELI-002 appears to allow for T-cell infiltration to occur. Now because those biopsies are obtained at a time of relapse, we also know that that suggests a mechanism of resistance for ELI-002, because while the T cells are present and have changed the tumor environment, the primary tumors have not seen a kind of T cell infiltration. It's not sufficient to allow for complete tumor eradication. It's suggestive that there could be a checkpoint active that's preventing those T cells that are now present in the tumor environment, converting it from cold to hot, to be able to do the job, to be able to eliminate tumor cells. Dr. Hosein, would you like to comment as well? Yes. Thanks, Chris. It's exactly what you said is, we were familiar with the data from the phase I study, especially the patients who had biopsies done. One of those was one of my patients. Typically, we don't see T cells in the pancreas tumor microenvironment, CD8 positive T cells, that is. That was a proof of concept to me, and that was enough to roll the dice and try to get a PD-1 inhibitor. As a clinician in the setting of recurrent pancreas cancer, you are looking at a patient who has a very poor prognosis. Doing something innovative in that setting, I think, is warranted and patients were very willing to accept off-label therapies, rather than chemotherapy only. We know also that there were very high levels of induction of T cell responses demonstrated by some of the figures that we showed you before during the ELI-002 treatment period. Our thinking was that since there was such high levels of educated T cells circulating and the cancer was still recurring, there had to be some disconnect or some barrier that was preventing these T cells from doing the job. That was the rationale for including the PD-1 inhibitor. Regarding the first part of the question about the number of patients, it is true that we're only talking about three patients here. However, if we had one out of three responses, we probably would not be having this call today. Since we had three consecutive responses, we didn't cherry-pick these patients. These were all patients who recurred on the trial at our site. Three consecutive patients had a very similar pattern of benefit with the subsequent therapy. We think that there's a signal there. Of course, we're still talking about small numbers, but I think it's, in my opinion, justified to plan a study. It's not going to be a 500-patient study. It'd be maybe a few dozen patients to further investigate this hypothesis. Thanks very much. Dr. Wainberg, did you want to comment as well? No, I don't have much to add. I think anytime you see this kind of observation, it's unique and so the obligation is to pursue it. I think that's what we ought to do. Great. Thank you. Thank you for your questions, Michael. Our next question comes from Robert Burns with H.C. Wainwright. Please go ahead, Robert. Hi, gentlemen. Just a few from me, if I may. When we think about the data that you presented last week, obviously the R1 resected population didn't perform as well compared to R0. When we think about the metastatic setting, obviously the tumor burden is going to be a lot higher. Long-term, if we're assuming phase III development eventually down the road, comparing it to the RASalute-303 trial versus RASalute-304, the sample size you'll have to actually run it in is a lot higher. Do you think that it might be more prudent to evaluate the combination with a CPI in the adjuvant setting? Sort of like the paper by Huff and colleagues, in Nature Communications that was published earlier this year did. Then I've got a few more after that. Sure. I'll address the first part of the question. We're very excited by the potential that the planned study will allow us to know the safety of the combination in prospective fashion, and provide evidence that could be applicable not only to development in the metastatic setting, where we do think the combination will be necessary, but also potentially to the adjuvant setting. In the AMPLIFY trial that we reported last week, we could see that the duration of benefit was very long for the R1 patients. I will turn it over to Dr. Hosein to comment because we do know the R0 versus R1 status for the three patients that were reported today. Yeah. All these patients had margin negative resections, all were R0. Yeah. Thanks so much. I think you had an additional question? Yeah. Given the data that you've seen with AMPLIFY-7P, wouldn't it be more prudent to run a phase I in combination with the CPI in the adjuvant setting versus the metastatic? Oh, well, we think that these observations are quite remarkable. The metastatic setting has some advantages in that the readouts can be rapid through the assessment using the RECIST radiographic responses as well. As mentioned, it's potentially applicable across the different clinical settings, including adjuvant as well, and that's something that we plan to explore. The study is designed in a modular fashion that additional cohorts could be added with the necessary resources to be able to broaden the development. That's exactly right. We're in a window of opportunity time now. As you know, it takes some time to meet with FDA to conduct all the steps that are a precursor to the launch of a larger phase III study. That window of opportunity allows us to gather data rapidly in the study that you've seen outlined today, that we would be able to exactly know if a cohort should be added into the phase III trial that would evaluate the combination. That's exactly why this study is so important. I completely agree with you. These findings are pretty remarkable, although in small sample sizes. One more, if I may. When you think about the phase I trial in the metastatic setting in combination with the CPI, how are you thinking about the sequencing of the vaccine versus the checkpoint inhibitor? Do you think that you'll also do, towards the end of the dosing, just a vaccine, no ICI phase, sort of like what Huff and colleagues did? We're meeting with the investigators who participated in our AMPLIFY studies, to finalize the design of the treatment. Based on the preclinical observations in the field, we think it's very clear that it is needed to start the ELI-002 first. The priming event to prime T cells is ideal to be on board before the first dose of checkpoint inhibition. Then a period of maintenance also is ideal, where the immune surveillance can continue, even if patients have experience of toxicity from the chemotherapy component that might necessitate cessation of the cytotoxic components. That's what's planned at a high level, and we'll be able to communicate more after we finalize the design with our investigators and submit the protocol to FDA. Awesome. Thank you. I'll jump back in the queue. Thank you for your questions, Robert. Our next question comes from Mayank Mamtani with B. Riley. Please go ahead, Mayank. Yes. Thanks for taking our questions, really appreciate all the detail provided here. I was just curious in terms of the total number of patients who received subsequent therapy in this fashion, chemo and nivo. Is there like a denominator on these three CRs we are able to put in? Was just curious if the immune phenotype, that pattern you saw, is that there's a way to also look at beyond these three CRs and how broadly you did see the antigen spreading phenomena? I am not completely sure if I understand, other sites were also administering nivo therapy post-progression in the metastatic setting. If maybe some color on site variability could be provided on how they were managed on nivo at other sites beyond Dr. Hosein's sites, that would also be helpful. Sure. We'll be able to look at that in the future. This was a rare event. It's not standard for subsequent treatment to include nivolumab. The three patients from the University of Miami were the first to undergo this therapy. We have now made the other investigators on AMPLIFY aware of these findings, so that it's possible in the future the patients and their physicians could elect to include a checkpoint inhibitor when additional patients may have a relapse after ELI-002 treatment. We'll track that over time, but there's no additional patients for whom we have enough treatment yet that they have reached the scan time when we could know a result. There will be anticipated to be more data in the future, but the denominator is three at the present time. Other sites, are there other sites that you would also get data from, or is this the only site that you have data and you'll continue to follow up? We do think that additional sites are now poised to follow the observations that Dr. Hosein made. We do think that there will be additional numbers in the future. Many patients, as you know from the AMPLIFY-7P randomized trial are still free from disease progression. The results from that trial have shown quite durable outcomes, long progression-free times relative to all the prior studies. It may take some time before there are additional data here until we are able to open our prospective study, which we believe is the right way to move forward with the observations we've seen. Okay. Maybe just on that prospective planned phase I triplet. My understanding is that does not include radiation or will it include radiation? How much you're able to tease out the contribution of components. As you know, there is obviously the question around the RASalute program, both in the adjuvant and the metastatic setting. It's not clear where pan-RAS plus chemo or pan-RAS alone would be the comparator. Maybe just talk a little bit about what you're looking to show there. I don't see any numbers, like number of patients that was on that slide. If you can fine-tune what kind of updates you would have once that gets going and how many patients you would feel comfortable going into the next stage of development where you're also contextualizing the pan-RAS inhibitor also coming into that setting. Thanks again for taking our questions. Sure. The studies that are planned use cohorts using a Simon two-stage design, where we would look at a number of patients, approximately 20, that are initially treated, then we would take a look at the response rate as well as the complete response rate relative to historical observations. As you know, since those are so rare, these trials could rapidly meet a proof of concept. It might not even be necessary to complete the planned enrollment in o rder to know that there was a strong signal present. In addition, the investigators and the company are talking about the different therapies that could be applied in this context. We think it may be feasible to apply the period with the chemoimmunotherapy and ELI-002 and utilize the radiation if needed, only after the scans establish the response pattern. That may be something to address the contribution of component, which will be relevant and interesting to the development program. I don't know, Dr. Hosein, if you want to comment as well. Yeah. There are data out there from the EXTEND trial, which shows that adding radiation to an oligometastatic setting in pancreas cancer could be beneficial. As Chris said, we are planning to meet with all the investigators to try to agree on a design moving forward. Whether that would include radiation has not been determined yet. Okay. Thank you for taking our questions. Thank you for your questions, Mayank. Our next question comes from Boris Peaker with JonesTrading. Please go ahead, Boris. Awesome. Thanks. Take my questions. I guess the first one, I just want to get a sense of the CA 19-9 and what that observation means. On treatment on ELI-002, we saw a consistent increase in CA 19-9, I think, for all the patients. Maybe I can comment here that, of course, the three patients who were reported today were a subset, of course, of patients who did experience a relapse. The response pattern as we observed in phase I, as well as the more current studies, have shown that patients who remain free from relapse are typically both biomarker responders with decreases in CA 19-9, as well as having higher levels of T cell response. It's even interesting that these patients reported today, who had robust T cell responses, but not the highest, could then undergo subsequent therapy and despite that, achieve a response in the metastatic setting. I think that's an interesting observation. Even if the response pattern with the CA 19-9 marker indicates that the monotherapy wasn't enough in some patients, when the checkpoint was added, that appears to address the mechanism of resistance and result in these notable sort of depth of response observations. Got it. Maybe for the future planned study, how do you optimize, I guess, not just for response rate, but for duration of response as well? Is there an ideal time gap from ELI-002 treatment to chemo and immunotherapy? How would you try to put that into the protocol? Sure. In the adjuvant setting, the combination would then aim to prevent the need for that by preventing relapse. Ideally, that would not be needed. In the setting where patients have recurrence, Dr. Hosein's observation suggests that the combination altogether As soon as possible has led to these unexpectedly good outcomes. That's w hat the protocol that is planned prospectively will aim to recapitulate. Great. Thanks for taking my questions. Thank you for your questions, Boris. Our next question comes from Kevin DeGeeter with Ladenburg. Please go ahead, Kevin. Hey. Yeah. Thanks for this call, really informative. Maybe just following up on the last question. For the planned study in the first-line, I guess with triple regimen. Can you comment on PFS or other metrics for duration of response that would be really clinically interesting? I appreciate the complete responses on their own are important and really are informative, but on durability, yeah, any kind of benchmarks that you can offer would be helpful. Sure. Actually, I think Dr. Wainberg and Dr. Hosein are the best to answer that question. Maybe let me start with Dr. Wainberg. Would you like to comment on that? You mean on the value of PFS or? Yes. I think obviously that PFS is one of these metrics that you look at usually in randomized studies, obviously in the context of pancreatic cancer, we're usually still looking at OS as the primary endpoint for regulatory findings. In small studies, I think we look at PFS as valuable, insofar as sort of giving us some clues. I think that it's certainly not as valuable as overall survival and predicting in that regard. Yeah. Maybe, Dr. Hosein, do you want to comment as well? Yeah. If I understood the questions, benchmarking the planned phase I study with multiple cohorts. The truth is, I think your question implies this, that this is a moving target right now in the era of RAS inhibition. If RAS inhibition makes it into the frontline with chemotherapy or as monotherapy, then the PFS is yet to be defined. In that setting, in a small study, which is what is planned, objective responses would give you a clearer efficacy signal than progression-free survival. If you have an uncontrolled study without an untreated control arm or standard of care control arm, then you have to use objective response rate. Because let's say you take highly selected patients who are fit, those patients in general would have a longer PFS than historical controls. In the study, which is planned, it's likely that objective response will be used as a metric for efficacy. Of course, when you go to a registrational study, we would be looking at PFS and OS. In a context like this, we showed objective responses in these three patients that we just presented. I think it's likely that the next planned study in metastatic patients will use objective response as a readout to measure effic acy there. Thanks very much. Yeah. I'll just maybe add that, in the planned study, we would of course look at duration of response. Just as a reminder, some of the initial approvals of RAS inhibitors for lung cancer relied on response rates and duration of response in an uncontrolled setting. We'll be able to look at that in the initial phase Is. Of course, with positive data, we would discuss with FDA about how to take that forward into a pivotal design that could support an approval. All these outcomes could, because they're reliant on radiographic assessment, they could be observed quickly relative to the time required for the adjuvant study to reach its data and support a BLA in that fashion. A follow-up, if I may. Currently, in many institutions, some patients do get a FOLFIRINOX-based regimen up front. Just any thoughts on kind of viability or interest in a FOLFIRINOX checkpoint ELI-002 combo? Is that worth exploring? Or do you think the relative toxicity of that in the context of a triple regimen, you're more interested in staying primarily with a GEMOX-based regimen? Sure. I think it's important when moving from findings like you've seen today to keep the treatment as close as possible to what Dr. Hosein observed, and that's the motivation for the initial evaluation of the gemcitabine and nivolumab-based therapy. However, of course, we're interested in broadening, as I mentioned, to additional agents and platforms. In that regard, we actually already have one that's getting underway at Memorial Sloan Kettering. There is an investigator-sponsored trial in the neoadjuvant setting that is evaluating the combination of ELI-002 together with FOLFIRINOX and with checkpoint inhibitor as well in that study. That will provide very interesting data over time and, in the neoadjuvant setting, has the very nice feature that the same sorts of assessments of the tumor microenvironment will be readily possible since the patients are going to proceed to surgery. We'll learn also for the FOLFIRINOX regimen, which is very important in pancreatic cancer from that study, as well as the one that's planned here for the metastatic patients. Great. Thank you for taking our questions. Thank you for your questions, Kevin, and to all of our analysts. I'll now turn it back over to Chris to close out the call. Great. Thanks very much, everyone, for attending today. We thank again the patients, families and site staff that participated in these studies and look forward to advancing the development of ELI-002. Thanks again.