Greetings, welcome to the results from Elicio Therapeutics phase II AMPLIFY-7P Study and Sharpened phase III Development Strategy for ELI-002 7P in Adjuvant Pancreatic Cancer conference call. At this time, all participants are in a listen-only mode. A question and answer session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star zero on your telephone keypad. As a reminder, this conference is being recorded. I'd now like to turn the call over to your host, Brian Ritchie, with LifeSci Advisors. Please go ahead, sir. Thank you, operator. Good morning, everyone, welcome to Elicio Therapeutics conference call to discuss results from the phase II AMPLIFY-7P study and the path forward for ELI-002 7P in adjuvant mutant KRAS-driven pancreatic cancer. Earlier this morning, Elicio issued a press release reporting top-line results from the study. In addition, following the call, the company will post a presentation on the investor relations section of its website that we will reference during today's call. The complete data set and supporting analyses are included in the file presentation. While today's discussion will focus on the key findings, clinical implications, and development strategy moving forward. Before we begin, I would like to remind everyone that comments made during this call will include forward-looking statements within the meaning of the federal securities laws. These statements are based on current expectations and assumptions and involve risks and uncertainties that may cause actual results to differ materially from those described. Please refer to the company's SEC filings and today's press release for a discussion of these risks and uncertainties. Elicio undertakes no obligation to update any forward-looking statements except as required by law. Joining me on today's call are Robert Connelly, President and Chief Executive Officer of Elicio Therapeutics, Dr. Christopher Haqq, Executive Vice President, Head of Research and Development and Chief Medical Officer, and Dr. Shubham Pant, Professor of Gastrointestinal Medical Oncology at The University of Texas MD Anderson Cancer Center and a principal investigator in the AMPLIFY-7P trial, and an internationally recognized expert in pancreatic cancer. Dr. Pant will provide his perspective on the clinical implications of these findings and the ongoing unmet need in this disease. With that, I will turn the call over to Robert Connelly, President and Chief Executive Officer of Elicio Therapeutics. Robert? Thank you, Brian, and good morning, everyone, and thank you for joining us today. While we are disappointed that the AMPLIFY-7P study did not meet its primary endpoint, we believe the data set generated important clinical and biological insights that have informed a clear development strategy moving forward. The study helped identify the patients most likely to benefit from ELI-002 7P, demonstrated biological activity through the association of KRAS-specific immune responses with clinical outcomes, established a favorable safety profile, and informed a precision medicine phase III strategy focused on patient selection and extended treatment duration. These results strengthen our conviction for the potential of ELI-002 7P as an off-the-shelf mutant KRAS-targeted immunotherapy, and we believe the clinical and biological findings from this study have broader implications for the development of amphiphile-enabled immunotherapies across mutant KRAS-driven cancers. Today, Chris will review the study results in detail and discuss how these findings have informed our proposed precision medicine phase III strategy. With that, I will turn the call over to Chris. Chris? Thank you, Bob. Good morning, everyone. As Bob mentioned, although AMPLIFY-7P did not meet its primary endpoint, we believe the study identified a robust signal in completely resected patients that informs future development and provides a clear path forward for ELI-002 7P. Turning to slide three, this slide summarizes what we believe are the key conclusions from the AMPLIFY-7P study. First, the trial did not achieve its primary disease-free survival, or DFS, endpoint, in the intent-to-treat population. However, we believe that the overall data set generated important clinical and biological insights that inform a clear path forward for ELI-002. Second, we observed early separation of the DFS curves during active ELI-002 treatment, suggesting antitumor activity in the adjuvant setting. Third, post hoc analyses demonstrated a stronger treatment effect in completely resected R0 patients, who were the majority of patients enrolling in the study, supporting our phase III development strategy, which will now be focused on in this group. Fourth, we observed a significant association between mutant KRAS-specific T-cell responses and improved disease-free survival, supporting that the immune responses generated by ELI-002 may translate into meaningful clinical benefit. Finally, ELI-002 7P maintained a favorable safety and tolerability profile, supporting future extended treatment duration and combination strategies. Taken together, we believe these findings identify a clear precision medicine path forward for phase III development focused on R0 patient selection and extended treatment duration. With that overview, let's move to slide four and review the study design. This slide summarizes the design of the AMPLIFY-7P study. As you can see, it is a randomized phase II study evaluating ELI-002 in patients with mutant KRAS driven pancreatic ductal adenocarcinoma or PDAC following completion of standard local regional treatment. The study enrolled 144 patients across 24 U.S. sites and randomized patients 2:1 to receive either ELI-002 or standard of care observation. Eligible patients had stages one through three mutant KRAS positive pancreatic cancer, underwent either R0 or R1 surgical resection, were radiographically free of disease at enrollment, and had completed standard local regional therapy, including surgery and perioperative or adjuvant chemotherapy. Before reviewing the results, it's important to understand the distinction between R0 and R1 resection status. Patients with an R0 resection have no microscopic tumor remaining at the surgical margin. While an R1 resection indicates microscopic residual disease remains following surgery or within 1 millimeter of the margin. This distinction is clinically important because R0 patients generally have a lower residual disease burden and slower recurrence kinetics, whereas R1 patients face substantially higher risk of recurrence. I'll come back to discuss this later in the deck. Patients assigned to ELI-002 received an initial immunization series followed by a booster phase, while patients assigned to the control arm underwent standard observation. The primary endpoint of the study was disease- free survival. Secondary and exploratory endpoints included tumor biomarker response, overall survival, safety, and immunogenicity. The primary objective of the study was to determine whether ELI-002 could improve DFS following completion of standard local regional therapy in a population at high risk for recurrence and for whom no approved treatment options currently exist after the completion of standard therapy. With that background, let's move to slide five and review the primary DFS results. In the intent- to- treat population, the study did not meet its primary endpoint of improving disease- free survival, with a hazard ratio of 0.85 and a P value of 0.533. While the primary endpoint was not achieved, we observed several encouraging observations. First, if you look at the Kaplan-Meier curves, you can see that separation between the treatment arms emerged early during the five- month active ELI-002 treatment period. To better understand this observation, we conducted post hoc landmark analyses at three and six months. Approximately 14% absolute DFS benefit was seen consistently during active treatment at both three and six months, suggesting early clinical activity within treatment arms and the separation persisting through nine months. While these analyses are exploratory and should be interpreted accordingly, we believe they provide evidence of antitumor activity during active treatment and suggest that ELI-002 was influencing disease recurrence dynamics while patients were receiving therapy. Importantly, these findings raise an important question for future development, whether extending treatment duration beyond the initial immunization and booster regimen may help sustain antitumor benefit. This observation is one of the key elements informing our proposed phase III strategy, which I will discuss later in the presentation. Before that, I'd like to review analyses that helped us better understand which patients appear most likely to benefit from treatment. Turning to slide six, we evaluated disease- free survival in patient populations with differing levels of recurrence risk. As shown on this slide, we observed a stronger treatment effect in patients who underwent complete surgical resection, which is called R0. In the intent-to-treat population, which included all 144 randomized patients, the unstratified hazard ratio was 0.79 with a P value of 0.25. When we evaluated the R0 resected population, representing 121 of the 144 patients enrolled in the study, the hazard ratio improved to 0.65 with a P value of 0.048. Importantly, the R0 population represents approximately 84% of patients enrolled on the AMPLIFY-7P trial. Potentially representing a large patient population with high relapse risk, with no current treatment options. We believe these findings are important because a patient population with lower residual disease burden may be well suited to immunotherapy like ELI-002. These findings helped inform our thinking around future study design and prompted us to examine whether baseline prognostic factors could help explain a stronger treatment effect observed in the R0 population. Now let's turn to slide seven. We examined baseline prognostic factors across the two treatment arms. Importantly, the study was randomized based on metastasis to lymph nodes as a stratification factor, and nodal status was balanced between treatment arms. We then performed multivariable analyses to evaluate factors associated with recurrence in AMPLIFY-7P. These analyses identified R1 resection status as a significant adverse prognostic factor with a hazard ratio of 1.56. When we reviewed the distribution of R1 patients across treatment arms, we observed that a higher proportion of patients randomized to ELI-002 had undergone R1 resection compared with patients in the observation arm. Specifically, 19% of patients in the ELI-002 arm had an R1 resection status compared with 10% in the observation arm. Because R1 resection is associated with a substantially higher risk of recurrence, this implies that the imbalance meaningfully and negatively impacted the ELI-002 arm. To correct for the R1 imbalance, we further evaluated outcomes in the R0 resected population. Importantly, these findings do not change the primary intent-to-treat result. However, they help explain why a stronger treatment effect was observed in the lower residual disease R0 population. The results of those analyses are shown on the next slide. This slide summarizes the treatment effect observed in the two populations we have discussed. As shown here, the unstratified DFS hazard ratio in the intent-to-treat population was 0.79. However, in the completely R0 resected population, representing 121 patients, the hazard ratio improved to 0.65 with a small P value of 0.048. Importantly, the Kaplan-Meier curves in the R0 population separated immediately and remained separated throughout the observation period, with an observed advantage for ELI-002 patients in delaying the time to relapse, 23.8 versus 12.8 months. We also saw a decrease in the proportion with relapse, a 9.5% absolute advantage at 18 months. The analyses shown here support the potential for improving treatment effect in the lower residual disease R0 population and help this R0 analysis define the patient population we believe is most appropriate for future phase III evaluation. Importantly, these clinical observations were also supported by strong mechanism of action immunologic signals, which I will discuss on the next slide. Now turning to slide nine. This slide addresses what we believe is one of the most important findings from the study, the relationship between immune response and disease-free survival. ELI-002 was designed to generate robust mutant KRAS-specific T cell responses. We evaluated whether the magnitude of the immune response generated by treatment was associated with clinical outcome. Using the threshold previously defined in our phase I studies and subsequently published by Wainberg, Pant, and O'Reilly in Nature Medicine, patients who achieved greater than a 9.17-fold increase in mutant KRAS-specific T cells experienced substantially better outcomes than those below the threshold. Among the 90 evaluable patients treated with ELI-002, the hazard ratio was 0.22, with a P value of less than 0.0001. We believe this analysis demonstrates a strong and highly significant relationship between the magnitude of mKRAS-specific T cell response and disease-free survival, with patients generating the strongest immune responses experiencing the most favorable outcomes. While correlation does not establish causation, these data provide important biological validation of ELI-002 7P activity and support the potential relationship between immune response and clinical outcome. We believe this finding strongly supports the proposed mechanism of action and reinforces the rationale for continued development of ELI-002 in patients most likely to benefit from treatment. Next, I'll review the safety profile observed in the study. Turning to slide 10. ELI-002 demonstrated a favorable safety and tolerability profile throughout the study. Importantly, there were no treatment-related discontinuations and no treatment-related deaths. Only 5% of patients had a dose delay, and no patients discontinued ELI-002 due to toxicity. When comparing overall adverse events between treatment arms, we observed proportionally fewer adverse events, fewer Grade 3 or higher adverse events, and fewer serious adverse events in the ELI-002 treatment arm compared with the observation arm. We believe these findings demonstrate that ELI-002 was well-tolerated and support evaluation of extended treatment duration while also providing flexibility for future combination strategies. Taken together, the efficacy, immune response, and safety findings from AMPLIFY-7P inform a refined development strategy focused on R0 patient selection and extended treatment duration. Turning to slide 11. This slide summarizes how the key findings from AMPLIFY-7P inform our proposed precision medicine roadmap to a phase III study. First, we observed a stronger treatment effect in the completely resected R0 patients, representing 121 of the 144 patients enrolled in the study and the majority of patients treated, generally in the adjuvant setting. Consistent with the biology of lower residual disease burden and slower recurrence kinetics, we believe R0 patients represent the population most appropriate for future evaluation of ELI-002. Second, the early separation of the disease-free survival curves observed during active treatment, a separation maintained through approximately nine months, supports evaluation of extended ELI-002 dosing to sustain and potentially enhance antitumor benefit. Taken together, we believe these findings support a phase III strategy focused on completely resected R0 patients and extended ELI-002 7P dosing. We believe this strategy directly reflects the clinical and biological findings from AMPLIFY-7P and provides a clear and actionable blueprint for future phase III development. Before concluding, I'd like to spend a few minutes discussing the clinical rationale underlying the proposed phase III strategy and why patient selection and disease biology are important considerations in the adjuvant setting. Turning to slide 12. Despite advances in surgery and systemic therapy, recurrence remains one of the great challenges in pancreatic cancer. Today, there are no approved therapies following the completion of standard locoregional treatment, leaving most patients in a period of observation despite substantial recurrence risk. We believe the adjuvant setting remains particularly attractive for immunotherapy because tumor burden is at its lowest and the immune system has the greatest opportunity to establish durable tumor control before clinical recurrence occurs. These considerations informed our efforts to better understand which patients may derive the greatest benefit from ELI-002 and ultimately help shape our proposed phase III strategy. On slide 13, one of the key findings from AMPLIFY-7P is the importance of residual disease burden and recurrence risk in shaping treatment outcomes. Patients who undergo complete R0 resection generally have a lower residual disease burden and slower recurrence kinetics than patients with R1 resection. Importantly, R0 patients represent the majority of patients treated in the adjuvant setting. From both a biological and clinical perspective, lower disease burden settings have historically been where immune-based therapies may have the greatest opportunity to provide benefit. Turning to slide 14. A related point is that R1 resection status is often more than simply a surgical margin finding. It also indicates a different disease biology is present. Numerous studies have demonstrated that R1 resection is associated with more aggressive disease biology and a higher risk of recurrence. With that overview, I'd like to invite Dr. Pant to share his perspective as a pancreatic cancer specialist who has participated in the phase I study of ELI-002, published in "Nature Medicine." Dr. Pant, from a clinical perspective, what do you think about the differences between R0 and R1 resected pancreatic cancer patients in your practice and in these findings? Chris, thank you so much for summarizing all the results really well. You're exactly right, Chris. As you said, R1 is a very different disease. It's a small percentage of our resected patients, but they truly represent a different disease, again, because the microscopic margins are positive, so they have a higher rate of recurrence. You have kind of that tumor still around, and that's one of the reasons why the recurrence rate is higher with an R1 versus an R0 resection. Like you just presented, that's why we do a phase II study, to really figure out which patient population will benefit from a bigger phase III study, potentially. I think this tells us kind of a path, like you said, of this patient population, which is still a substantial number of patients with resected pancreatic cancer. Remember, Chris, in pancreatic cancer, even after resection, there's a 50%-70% chance of recurrence. That's a high percentage of patients in which the cancer can come back. You kind of have this right patient population, which is a majority of our patients with resected pancreatic cancer, R0 resection, to potentially look at this phase III trial. As an investigator being part of the phase I and the phase II, I'm looking forward to participating in the phase III trial of this patient-selected population. I think, Chris, you summarized everything really well. That's all I had to add. Thank you. Great. One final question. Based on your experience in pancreatic cancer drug development, is there anything you'd like to add about key considerations for late-phase studies? Yeah. I think the main thing is, again, that we really need to know the patient population we are going after. I think traditionally, this is the path that we should be taking as investigators. If we talk about phase I, you do the phase I trial, you kind of see the safety, you do the phase II, you look at where the efficacy lies then do the larger phase III following that to truly potentially give the benefit to the patients who might benefit from the therapy. Thank you so much, Dr. Pant, for those perspectives. Turning to slide 15. Based on the clinical and biological insights generated from AMPLIFY-7P, we believe we have identified a clear path forward for ELI-002 7P. Our first priority is to engage with the FDA in an end-of-phase II meeting to discuss the AMPLIFY-7P results and align on the design of a potential phase III study. AMPLIFY-7P was not designed as a pivotal study, and the purpose of phase II development is to learn from the data and identify the patients and treatment approaches most likely to succeed in a registrational trial. The proposed phase III incorporates the key learnings from this trial, including enrollment of completely resected R0 patients and extended ELI-002 dosing to sustain the antitumor immunity over a longer period of time. More broadly, we believe these findings provide an important support for mutant KRAS-directed immunotherapy and continued evaluations of ELI-002 across KRAS-driven cancers. While today's discussion has focused on adjuvant pancreatic cancer, we believe the biological principles demonstrated in AMPLIFY-7P may have general implications across multiple KRAS-driven malignancies and support the broader application of AMP-enabled immunotherapies across multiple oncogenic drivers. I want to thank patients, families, and site staff who participated in AMPLIFY-7P. With that, I'll turn the call back to Bob for closing remarks. Bob? Sure. Thank you, Chris, and thank you, Dr. Pant, for joining us today and sharing your perspective. We believe the findings discussed today provide a clear path forward as we engage with regulators, advance our phase III planning, and continue working to bring new treatment options to patients with KRAS-driven cancers. Subject to financing, our goal would be to initiate a registrational phase III study in adjuvant mutant KRAS-driven pancreatic cancer following regulatory alignment. Our cash runway extends into the fourth quarter of 2026, and we are actively evaluating strategic financing and partnership opportunities to support the advancement of our planned phase III program and broader AMP platform development efforts. We remain focused on advancing ELI-002 7P through regulatory discussions, refining our phase III strategy, and unlocking the broader potential of our AMP-enabled immunotherapy platform for patients with KRAS-driven cancers. With that operator, we are ready to begin the question and answer session. Thank you. If you'd like to ask a question, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star two if you'd like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. Our first question comes from the line of Michael King with Rodman & Renshaw. Please proceed with your question. Hi. Good morning, guys. Thanks for taking the questions. I know you've stated a couple of times that the study didn't achieve its primary endpoint, and while that may be true, I think your remarks about hypothesis validation are certainly spot on. I just had a couple of quick questions. On the R0s versus the R1s. It may be hard to tell, but are surgical techniques important here? In other words, is this operator-dependent? I guess you can account for that in a randomized phase III trial with entry criteria. Maybe Dr. Pant can comment on this as well, but is there some kind of operator dependency on who can get an R0 versus an R1, and did that perhaps play into the outcome? Yes, thank you. Yeah, this is Dr. Pant. In some parts, yes. Honestly, it's more about the tumor, when it's kind of how the tumor looks. In the beginning when they're taking it out, it's a little bit bulkier and everything, it leads to more R1 resection. Though, yes, operator-dependent to some part, honestly, the big volume centers, a lot of which were part of the ELI trial, I think those surgeons are doing enough to kind of get those resections. Sometimes, again, it's the tumor. Again, like we've talked about, it's the tumor biology and the extent of the tumor when they're taking it out, you can get R1. Earlier on, it used to be a factor. Now it's less of a factor. They still could represent a factor, I would think it's less of a factor, more to do with tumor biology. Okay, thank you for that. Just maybe two quick follow-ups for the company. Chris, was post-surgical therapy permitted or conducted in the control arm at all, and could that have influenced the DFS in the control arm of the study? Yes. Thanks, Mike, for the question. The patients assigned to the control arm were purely observed, they did not have any other anti-tumor therapy applied during the trial. After achieving or after observing a disease-free survival event, a confirmed relapse crossover was permitted. The crossover period does not affect the primary endpoint of disease-free survival because all those outcomes were observed before the crossover period. Okay. Thank you for clarifying that. Also, was there any KRAS TKI use prior to any of these surgeries, or was it too early for that? The AMPLIFY-7P study began enrollment in January of 2024 and was completed by December of 2024. In general, there was little to no use of small molecule therapy targeting KRAS in this population. Okay. I swear this is my final question. In terms of trial design going forward, I just wonder how you think about adjuvant studies like the RASolute protocols for daraxonrasib and how that might affect your inclusion/exclusion criteria and your ability to enroll. Thank you. Thanks. The advent of small molecule therapy in the metastatic setting has led to encouraging observations. There isn't any adjuvant data yet that we are aware of. We will anticipate that the ELI-002 program would be complementary rather than competitive with such approaches. We think that immunotherapy is well-suited to the adjuvant setting because of the favorable safety profile. In comparison, small molecule therapies will generally lose efficacy over time as tumor changes occur that lead to resistance. We think that ELI-002 is particularly suited to the adjuvant population, which is the setting of the study of AMPLIFY-7P. Thank you. Thank you. Our next question comes from the line of Mayank Mamtani with B. Riley Securities. Please proceed with your question. Yes. Good morning, team. Thanks for taking our questions and very interesting learnings here on the go-forward phase III path. Just on the R0 arm, if I may, the DFS of 13 months below the ITT, which was 21 months, despite the ITT including the high-risk R1 patients. Was just trying to understand any differences in how maybe the original consolidated therapy patterns exist for R0 versus R1 and what other reasons that we didn't know about earlier could have driven the higher control arm performance here, which looks like roughly five patients that drove that DFS really higher than what you had thought. If you could maybe just double-click on that would be great. I know it's early, but any control arm DFS assumptions that you're thinking of phase III, is it going to be in this 20-month range, as you think about the phase III, or is it going to be lower than that? I have a couple of follow-ups. Thanks again for the question. The DFS observations in AMPLIFY-7P are sensitive because the median observation is represented by the survival curve, which straddles the 50% line for many months during the observation period. Because of that, the study is more sensitive to variations in the patient population that can shift the median, in some cases, as you note, substantially. Instead of the median estimate, which is sensitive to small numbers of patients, we think it's best to focus on the hazard ratio and the P value because the hazard ratio and the P value are driven by the entirety of the disease-free survival curves. In the imbalance that we observed, 23 patients with R1, only five were included in the standard of care arm versus the 18 patients or 19% in the active arm. We think those small numbers and the influence of one or two patients doing better or worse here or there could shift the median. The more important facet is to look at the overall impact, which is read out by the hazard ratios and P values. The control arm DFS that you're thinking for phase III, are you able to, or is it too premature? Sure. We'll look at modeling that. We think that with the adjustment for the R1, the 12.8 months observed in AMPLIFY-7P is likely a good guide for what we would plan in the phase III pivotal trial. Okay. In terms of the next tranche of data coming, Chris, I think you have one forest plot here, but you may have many more planned. If you could maybe just give us some color and, specifically, I was interested in any T-cell kinetics data for what main form, what extended dosing regimen could give you, and if there's any data from this study or prior study that tells you that there's a waning of response that you might be able to control in the next study, where obviously the tail for some of these studies is the exciting part, and you could draw that further out from an efficacy standpoint. Yes. We will be assessing the optimal regimen to continue the additional dosing of ELI-002. As you note, the period from 9-12 months is one of great risk for patients participating in the adjuvant pancreatic cancer setting, and the total duration, et cetera, we will finalize as we take a look at those data in conjunction with the rich translational data generated from the T-cell analyses that you've seen. It is very early in the analysis of AMPLIFY-7P, as we've just received these unblinded results, and we will continue to conduct additional analyses that we expect will best inform the phase III strategy and which we'll discuss with the FDA and global regulators. Once those discussions are leading to the final design, we'll share those with the community. Okay, great. My final question on maybe just the survival trend or data, how that is trending, if you could comment on that. Just on the end of phase II FDA meeting, has that timing been firmed up? Would that require any survival trend also to be part of that discussion? Thanks again for taking our questions. Thank you. Overall survival at this time shows a trend in favor of ELI-002. However, it's too early to be conclusive with only approximately 20% information fraction. We plan to continue the observation for overall survival as resources permit. We expect that these data, both disease-free and overall survival, as well as the safety profile and translational data, will be important components of our upcoming discussions with the agency. We anticipate the discussions to happen this year, and we'll communicate when we have confirmation on the timing expected for the interactions. Great. Thank you. Thank you. Ladies and gentlemen, as a reminder, if you'd like to join the question queue, please press star one on your telephone keypad. Our next question comes from the line of Boris Peaker with JonesTrading. Please proceed with your question. Hi, this is Dania for Boris. Thank you for taking our questions. First, when will the data be presented or published in a scientific meeting? Sometime this year? Also, if you can add color for how large would a new phase III have to be and how long it would take. Any added color for that would be appreciated. Thank you. Thank you. The results from AMPLIFY-7P will be presented at a major academic and clinical meeting upcoming. We will communicate when we hear back from the program committee about the presentation details. That is expected this year. In addition, you asked about the sample size. What I can say is that, given the sample size of 121 for our analysis of R0 patients already demonstrating a nominally significant P value of 0.048, we expect the trial size to be in the few hundreds range and not a large trial that would be over 1,000, for example. As we finalize the protocol design and have that vetted by our interactions with regulators, we'll communicate additional details there. Thank you. A last question. Are you thinking of having an exploratory arm of the combination, as you mentioned that ELI-002 is a good combination candidate? What would you combine with, for example? Thank you. Yeah. Thank you. We do think the safety profile observed for ELI-002 opens it up to many combination possibilities. Particularly, we are thinking of the R1 patient group, which we plan would be excluded from the pivotal phase III, but could be included, as resources allow, in a second standalone study that would evaluate a combination. Combinations of interest include checkpoint inhibition, include KRAS small molecules. There's a number of promising agents like that. We'll be speaking with the clinical investigators and regulators, and we'll update as soon as those plans are finalized. Thank you very much. Thank you. One moment, please. Our next question is a follow-up from the line of Michael King with Rodman & Renshaw. Please proceed with your question. Thanks for taking the follow-up, guys. Chris, can you talk about your intentions to present the biomarker data by KRAS mutation type and what evidence you may have of antigen spreading of the non-traditional KRAS mutation responses? Thank you. Thank you. The allele present for the mutation in KRAS is an important aspect of our study. Our study enrolled primarily patients with G12D, G12V, and G12R. Only small numbers of patients with other mutations present in the exon 2, 12th, and 13th position were enrolled in our trial. We do look forward at the future academic presentation to sharing the results of ELISpot analysis examining each of the different KRAS alleles. In addition, you point out the antigen spreading data, which is very intriguing, where in prior studies and in the active arm of the current AMPLIFY-7P, we observed that bystander T-cells recognizing different antigens, not specific to KRAS, but instead other oncogenic drivers or passenger mutations that are in a particular patient's genome, were also joining in the immune response. It will be fascinating to correlate whether those observations are associated with the disease-free survival and overall survival outcomes here. As those analyses are conducted, we'll plan to report those at major scientific and clinical meetings as well. Thank you. Ladies and gentlemen, that concludes our question-and-answer session. I'll turn the floor back to Mr. Connelly for any final comments. Thank you. Thanks everybody for joining. Great questions. We're very encouraged by this data, by the phase II, and we look forward to the next stage, and we'll be talking to you about that soon. Once again, thank you for your time today. Thank you. This concludes today's conference call. You may disconnect your lines at this time. Thank you for your participation.