All right. Good afternoon, everyone. Welcome. Thank you for coming. Our CEO, Bob Connelly, was meant to be here, but because of a personal matter, he wasn't able to join us. Brief intro, I'm Pete DeMuth. I'm the CSO at Elicio, and I'll be walking you through our slides for today. We are a publicly traded company, so I'll just pause here for forward-looking statements and disclaimers. All right. To start off with some brief highlights, Elicio is a lymph node targeted immunotherapy company developing a suite of lymph node targeted immunotherapies for a variety of cancer indications. These are intended to be off-the-shelf products. To give you a bit of background, the technology is based on a platform that was built out of MIT called the Amphiphile or AMP platform. This is a technology which is meant to improve the targeting of immunotherapies precisely to the lymph nodes to target the immune cells, which we envision as a key mediator of anti-tumor activity. This is meant to be very broad in applicability for a variety of cancer immunotherapy indications. I'll talk you through some detail, but mostly a summary of our phase 1 trials, and then briefly describe some of our Phase II results, as well as give you a view to where we're going with that lead program in Phase II. Our lead program is ELI-002, which is a lymph node targeted immunotherapy targeting mutated KRAS. It's an off-the-shelf immunotherapy product we've been developing to date in GI indications, including pancreas cancer and colorectal cancers. We published recently in the last two years some updates on this program in Nature Medicine in 2004 and 2005, and I'll give you some highlights of the data set from those two publications as we get into the update. We have a number of value-creating catalysts that I'll speak about, most notably our Phase II trial, which is currently ongoing. We're expecting final analysis of the primary endpoint in the first half of this year. We have a number of other catalysts which I'll note as we get into the later slides in the presentation. Briefly just mention our pipeline. As you can see, ELI-002, which is our lead program, is being developed in a number of indications. Our lead program, as I said, is in pancreas cancer. You can see it's in Phase II. we also have a number of indications that we're looking to expand into with future opportunities, as well as pipeline assets that are earlier stage, ELI-007 and eight, which are targeting BRAF and p53 mutated cancers. Just to speak briefly about the key differentiation for this technology and this program, as I mentioned, we are using the AMP platform to target immunotherapy specifically to the lymph nodes. With this mechanism of action we've seen in our clinical trials to date, robust T-cell responses expanded as much as 44 times over the baseline levels present in patients when they enter trials. This is designed to overcome some of the historic challenges that have been evident for peptide immunotherapies. With those robust immune responses, we've seen correlation to clinical benefit in our phase 1 trials. I'll speak more about that as we get into the slides later. As far as, cost of goods, we envision this as an off-the-shelf strategy with low cost, very simple manufacturing, and rapid commercial scalability. Can also be practically utilized in a diverse, patient background, variety of HLAs, which I'll speak about in a slide later on. We also see effects of personalized immunotherapy. Essentially T-cells, which are targeting not only the KRAS driver mutations, which are targeted specifically by the therapy, but antigen spreading to other mutations present in individualized cancers. Because of the platform utility that we, that I described, we envision a number of assets that could be moved forward with the similar platform mechanism of action to address other indications and unmet need. I'll spend a few slides just talking you through the background on the platform. As I mentioned, this is called the Amphiphile or AMP platform, originally developed at MIT and now in development at Elicio, is a platform designed to target immunotherapy directly to lymph nodes, which has been a long-standing challenge for the field. You can see from this slide, it's in essence a bioconjugation methodology where we can chemically modify a variety of constituent immunotherapy payloads. These can be taken from a number of different types of classes of molecules, including small molecules, peptides, or nucleic acids, as well as small proteins, where the unifying feature of all of these conventionally is that they're designed to target the immune system, but because of their size, they're not typically able to enter the lymph nodes or other secondary organs which direct the immune response against cancer. To overcome this and to reprogram their biodistribution in the body, we've designed the chemistry that you can see on the left side of this slide. It includes two structural domains. The one on the far left in green is a fatty acid that is designed to mediate interactions with endogenous albumin in the body. Albumin being a fatty acid transporting protein by nature, this can achieve lymph node targeting because albumin, given its larger molecular size, is preferentially taken up into lymphatic vessels and then directed into lymph nodes. This is a way to essentially shuttle these immunotherapeutic payloads, which otherwise would not get to lymph nodes directly to immune cells in those tissues. The intervening domain in orange is a polymeric linker that we've designed to promote pharmaceutical properties like solubility, as well as to improve the timing and location of release of the payload to serve the particular biological interests that we have. Just to build you through the mechanism of action, starting here from the left, we can do subcutaneous administration of Amphiphile molecules. Once in the tissue space, Amphiphiles can readily interact with a large concentration of endogenous albumin present within the tissues. They do this through the chemical structure that I just described. This does two important things. One, it prevents those molecules from going back into the blood. And then being shuttled to relevant sites for the immune response. Secondly, it preferentially redirects them through lymphatic uptake, through lymphatic vessels directly into lymph nodes, where those agents can be absorbed onto immune cells taken up, and this kicks off the process of immune activation towards the tumor. Typically, we think of this as it relates to antigen-presenting cells, and those cells are then able to convey the information to the adaptive immune response T cells in this case, which can then become tumor specific and execute the anti-tumor functionality that we're looking for in our therapeutic indications. To bring this to a summary, the approach here, as I've described, makes use of albumin to concentrate these immunotherapeutics directly in the lymph nodes where they can be taken up and then used to redirect the tumor-specific immune response in the lymph nodes. This turns out in preclinical studies and now in some of our clinical studies, to be very important for determining the magnitude of the T cell response that is generated against the tumor, as well as many of its functional characteristics. Just to give you one example of what this looks like, preclinically, in this case, targeting a tumor-associated antigen that's very well known, called gp100, a conventional form of this type of peptide immunotherapy gives T cell responses that are about 2% of all the T cells present in the animal's circulation. Whereas the same vaccine or immunotherapy given in the Amphiphile format expands that population to more than 50% of the total CD8 population. Just to say a few more words broadly about the differentiation of this approach, we've certainly been excited to follow the progress of small molecules in this case, targeting mutated KRAS. As I mentioned, this is the indication for our lead program, ELI-002. It's promising and encouraging to see the progress that single variant inhibitors have had with the G12C programs. Overall, I think there's improvement to be made in terms of the duration of clinical benefit that we can expect from these programs. In parallel, we've seen personalized cancer immunotherapies showing significant promise in several clinical studies. Some drawbacks of these approaches include manufacturing that can be long and costly, as well as primarily the targeting of non-essential tumor mutations. We're trying to build on this at Elicio with a differentiated approach to target immune responses in the lymph nodes, raise T cells to target essential driver mutations, do that in an off-the-shelf manner. Of course, targeting KRAS gives us the opportunity to potentially treat patients that represent about 25% of all human solid cancers. A huge potential opportunity for this type of therapy going forward. Let me expand on this a little bit more deeply in a description of our ELI-002 lead indication. Firstly, just to say a few words about the KRAS market opportunity. KRAS, as you probably know, is a ubiquitous, and very frequently mutated driver mutation in a variety of human solid cancers. Approximately 25% of human solid cancers have a mutated KRAS gene, and specific indications of interest are shown here, with about 90% of pancreas cancer having a mutation in the KRAS pathway, as well as about one-third and 25% of colorectal and non-small cell lung tumors, respectively. There are a number of other key indications of high interest for potential future expansion as the program moves forward. Next, I'll just describe to you the ELI-002 drug product. To walk you through, there are two types of constituent active pharmaceutical ingredients in ELI-002, the first being antigenic peptides. These are shown on the top of this slide, where you can see in red a sequence of amino acids representing the mutated KRAS sequence. These, of course, are modified with the amphiphile chemistry that you can see on the left in green and orange to promote lymph node targeting. The peptide itself has been designed to include a variety of different sequences that could be presented to T cells and stimulate both arms of the T cell immune response, including CD4s and CD8s. I'll be speaking about two different programs here, the first being the 2-peptide program, which includes G12D and G12R amphiphile peptides in our first clinical trial for Phase I, and now our commercial formulation, which is called 7P, which includes an additional 5 mutated residues here representing the G12 and G13 mutant alleles. In addition to the antigenic peptides that we include in the therapy, we have on the bottom, shown here, our immunomodulator, which is called Amphiphile-CpG. It's made up of a single-strand DNA sequence with a TLR9 agonistic motif, and that is modified with our lymph node targeting moiety in green. The idea is that in concert, these are administered and then redirected through the lymphatics by albumin binding to immune cells in the lymph node. All right, to say a few words now about our first clinical studies. You can see here this is a monotherapy study design. We're not doing any combination with checkpoint inhibition or chemotherapy. We have focused in this first clinical study on GI indications, including pancreas and colorectal cancer. This is what we call the extended adjuvant setting. Patients come into the trial after completing what is the complete local regional curative intent therapy, in this case, including surgery as well as chemotherapy, in some cases, radiation. At that point, they're screened onto our study. We confirm that they have a KRAS mutation aligned to the product. They, at this point, have no evidence of radiographic disease based on medical imaging, but are nonetheless at high risk for relapse because they have an MRD positive status, and we adjudicate that through ctDNA measurements or tumor, serum biomarkers like CA19-9. At that point, these patients come onto our study. They're given a series of therapy doses throughout a prime and boost series, we follow them for the primary endpoint, in this case, safety. We also have the opportunity to look at immunological responses, T cells targeting KRAS, as well as more classical clinical endpoints like disease-free and overall survival. I'll just note in this study, we had 20 patients that enrolled with pancreas cancer and five patients with colorectal cancer. These data, as well as others, throughout the slides here, are included in two publications in Nature Medicine over the last two years. If you're interested in following up on additional details, those are available there. Just to say this in more of a patient journey, paradigm, what you can see is that patients with either pancreas or colorectal cancer come on to prior therapy, which includes surgery, chemotherapy with or without radiation. At that point, there's no more available therapy for them, but we take them into our screening period. Again, confirm KRAS, no evidence of overt disease by radiography, but minimal residual disease positive. We know from past historical studies that the standard of care of observation for these studies leads to median relapse-free survival of between five months and 12 months, depending on whether it's the pancreas or the colorectal subtype. A very poor prognosis overall for these patients. The idea is as they come onto our study, they're receiving therapy, and we're looking for an elongation of the time that they are free from disease progression and longer survival times. There's a lot of detail, again, in the article that you can reference if you're looking to learn more. Just to summarize what we've seen in the last two updates that we've made on this clinical trial, the first in 2024 and the final analysis done in 2025, you can see that the median relapse-free survival in these two analysis was 16.33 months, that's about threefold longer than what I indicated was the historical precedent for MRD positive pancreas cancer in the adjuvant setting. That's certainly encouraging. The median OS, you can see here, went from 16.33 to 28.94 months in the final analysis, about 12 months longer than what's expected for this patient group in the MRD positive pancreas indication. The other thing that we've seen is a consistent correlation between the strength of the T cell responses that the therapy induces toward KRAS and the clinical benefit that those patients have in the primary or in the endpoints looking at relapse-free and overall survival. In the first study, we used a median. In the second, we used a statistically defined, Receiver Operating Characteristic curve threshold of either 12 or 9-fold respectively over baseline. You can see the correlations down here in this portion of the slide where the risk for relapse was decreased by 88%, relative to those that have below threshold T cell responses. The risk for survival was decreased, or the risk for death, I should say, is decreased by 77% compared to those patients that did not have T cells above the threshold for this study. It's great to see this correlation between the mechanism of action, T cell responses, and the clinical endpoints that we're following to assess antitumor activity. After this first Phase I, we went on to do a second Phase I, which was the lead into the Phase II that we're currently conducting. These studies explored the 7-peptide version of the product, and this is a summary slide meant to capture the main findings from the 39 patients treated in the 2 Phase I trials for ELI-002 2P and ELI-002 7P. You can see patients treated again primarily were PDAC, but also some CRC patients. These included dose-ranging efforts for both the peptide components as well as the adjuvant components of ELI-002. We were able to select the optimal doses for Phase II of both the constituent parts. We've shown throughout the follow-up for both of these studies that ELI-002 was both well-tolerated and safe with no DLTs or SAEs observed. We established the recommended Phase II dose, which was selected throughout the course of the studies based on the T cell responses and the antitumor biomarker responses. We also were able to assess T cell responses, as I mentioned, and their correlation to the relapse-free and overall survival endpoints. The strength of that correlation is certainly encouraging going forth into the Phase II. In addition to seeing T cells targeting the driver mutation KRAS, we saw a phenomenon known as antigen spreading, in which the initial immune response can trigger immune responses targeting other antigens present within the tumor. This is more of a personalized immune response. It's certainly been interesting to follow and something that we'll continue to study going forward into the next phase of development. As I mentioned, you can follow these QR codes if you want additional detail on the two articles that were published on the initial Phase I study. I'll talk a little bit now about where we stand. We've, as I mentioned, completed the Phase I portion of the 7P study, which we just reviewed. This is an overview of the Phase II portion of the study, in which we focused on pancreas cancer exclusively. Again, this is a monotherapy design. Patients are enrolled based on the presence of a KRAS mutation that is represented within the therapeutic product, so one of the seven mutations that are within the antigen complement of the therapy. Patients, again, very similar to Phase I, complete upfront therapy, surgery, chemotherapy, and radiation are confirmed to have no evidence of disease. The one difference here that is important to point out is that at this point, patients with either MRD positive or negative status were allowed into the study. The idea being that overall prognosis for both of those populations is unfavorable and both could therefore benefit from an effective therapy. The study is 2 to 1 randomized. So two -the arm that gets twice as many patients is the active arm, the ELI-002 arm, and that's compared to observation, which is the standard of care for this patient population. It's 144 patients that were enrolled over the course of about 11 months back in 2024. I'll note the primary endpoint here is disease-free survival. At the point where patients in the observation arm complete that primary endpoint, they have the opportunity then to cross over to active treatment. We will have the opportunity to get some data on more radiographically evident disease. The other endpoints that we'll assess will be tumor biomarker response in the MRD positive subset, as well as looking at overall survival, safety, and the iRECIST response rate for the crossover patients. Throughout, we have been looking at the immunogenicity responses. We will continue that to see whether that mechanism of action correlates to the clinical effects that we observe. We've at the moment completed our IDMC-led interim analysis last summer. The outcome of that was a confirmation of the prior safety profile and tolerability profile that was seen in the earlier phase studies, as well as an indication of preliminary efficacy based on the recommendation of IDMC to continue the study unmodified to the final analysis. The final analysis is now set for we are projecting it for the first half of 2026. It is an event-driven analysis, so we're following that closely. In the meantime, we've also had productive interactions with FDA to establish some guidelines for the prospective Phase III trial that we would conduct. Major outcomes from the meetings that we had with them was alignment on the basic design of the study, including a randomized blinded trial that will use the investigator-assessed DFS as the primary endpoint, and that will be using a modified RECIST criteria, again, which is quite similar to what we've used in the prior studies to adjudicate for relapse. All right. While we're at the moment blinded to the clinical primary endpoints for this study, we are able to study the translational aspects of the treatment arm of the study. In this case, that means the T cell responses, and we've been interested to compare the T cell responses observed in these Phase II patients, 90 of which were able to be evaluated in comparison to the prior Phase I data that we obtained. What you can see here is a side-by-side assessment of the T cell response rate. In phase 1, we observed a 100% response rate. That's very similar to what we observed in the 90 patients for Phase II with a 99% response rate. In fact, 89 of the 90 patients having KRAS specific T cell response to induced while on therapy. The median fold change you can see in Phase II exceeds what we observed in Phase I, with patients having a median of 44-fold increase in their T cell responses relative to baseline. While we don't yet know what threshold of T cell response might correlate to the clinical activity observed in this Phase II portion of the trial, we do know that 80% of the patients in this treatment arm have a response that exceeds the 9.5-fold threshold that was important for separating clinical benefit from non-benefit in our Phase I study. We've also been able to look at HLA association. Just to remind you, our studies to date have not required a particular HLA for patients to enroll. With this larger patient group, 90 patients in our Phase II, we were able to do an assessment of the potential correlation between the presence or absence of any particular HLA and the T cell responses that were observed. We did not see a positive or negative association there that rose to the level of significance, suggesting that a broad diversity of patients could potentially be treated and benefit from this therapy. Finally, as I introduced earlier, we've been looking at antigen spreading as a mechanism that could broaden the immune response beyond the driver mutation KRAS to other tumor-associated but personalized antigens. Our findings here in the Phase II were very similar to what we observed in the prior Phase Is, with 13 to 15 evaluable patients having an antigen spreading T cell response beyond their mutated KRAS specific T cells. I'll just speak briefly here at the end about some growth catalysts and where we're going as a company. Obviously, the biggest catalyst to keep in mind is the readout of the Phase II final analysis. As I've said, that's an event-driven analysis, but it is projected for the first half of 2026, after which we will interact with the FDA to lead us towards the Phase III that would follow. There are a number of other growth catalysts to keep in mind, including additional investigator-sponsored trials, one of which includes a combination with checkpoint inhibition in the neoadjuvant PDAC space, as well as the potential to expand the pipeline opportunities to BRAF and p53 with further resourcing. Our financial overview as of September 30th, 2025. With that, I will pause and take some questions if there are any. Thank you.