Thanks for that introduction. Good morning, everyone. Thanks for being here. I will be giving you an overview, a corporate update on Elicio Therapeutics. Elicio is a publicly traded company, so briefly, these are my disclaimers. Just to get started here with a few words of introduction, Elicio, as was mentioned, is a clinical stage immunotherapeutics company. We are developing a range of immunotherapeutics using our amphiphile or AMP platform technology. This is an approach which has been developed to improve the lymphatic targeting of immunotherapies with the goal of improving the immunological response against those cancers. We have a belief that this could be broadly applicable across a variety of cancer indications.
We're developing this currently in our lead program, ELI-002, in which we have conducted two phase I trials in the midst now of a randomized phase II trial. The initial data has been published twice in the last years in Nature Medicine. We have, as I said, our lead indication, ELI-002, which is an off-the-shelf immunotherapeutic, targeting mutated KRAS, which is present in 25% of human solid cancers. It has a number of opportunities in different cancer indications, including pancreatic cancer and colorectal cancer. We have, as I mentioned, an upcoming catalyst here in the next few months, mid-year, where we expect to read out the randomized data from our phase II indication in metastatic, or excuse me, adjuvant pancreatic cancer indication. Excuse me. Briefly just touch on our pipeline.
As you can see, ELI-002 is our lead indication with phase I data in pancreatic cancer. This is progressing now into our phase II. We also have promising data from a completed phase I in colorectal cancer, as well as a number of indications or opportunities to expand into other indications with mutated KRAS expression and earlier stage programs targeting other mutant drivers in cancers, including BRAF and P53. I'll just briefly mention a few of the key areas of differentiation for your ELI-002 and our AMP platform assets. As I mentioned, this makes use of a technology that is developed to improve the lymphatic targeting of immunotherapies. This is intended to overcome the historic challenges of these immunotherapeutics and their limited ability to generate antitumor immune responses.
We have in our first phase I studies demonstrated robust immune responses, and the T cell mechanism of action in those studies was strongly correlated to clinical benefit. We're looking to build upon that, of course, going forward using an off-the-shelf approach. This can improve the cost, delivery, availability of these products going forward. We've also released data recently showing that these types of approaches can be useful in patients with a very diverse background of HLA, enabling benefit in a wide variety of patients. In addition to the KRAS-specific immunogenicity that is generated, we have observed the development of what we refer to as personalized tumor immunity. This is the targeting by the immune response of other antigens present in the tumor but not explicitly present in the therapy itself.
As you saw on our pipeline slide, we have multiple assets that we're looking to bring forward, both in KRAS and other indications, including high-frequency mutations such as P53 and BRAF. I'll just speak for a few minutes about our lead asset, ELI-002, our phase I data, and build towards an introduction of our phase II program and what you can expect in the coming months. Firstly, just to introduce the KRAS space, this is an area of significant opportunity in oncology. KRAS is a very frequently mutated driver oncogene in a number of cancers across a number of indications. It is present in approximately 25% of all human solid tumors with large indications in pancreas cancer, colorectal cancer, non-small cell lung, as well as several others.
To introduce you to ELI-002, this is the schematic for the program. I've not had time today to go through the platform technology and the mechanism of action, but I'll introduce that to you briefly here in this slide. ELI-002 has 2 types of components shown here in the slide. On the top are a collection of mutated KRAS synthetic long peptide antigens. These are shown in red. These can be of 2 different formulations, one which includes 2 peptides covering the G12D and G12R mutations. We've since moved to a 7-peptide formulation, which covers those 2 mutations, as well as 5 other mutations, which are common in KRAS mutated cancers. These are modified chemically with the green and orange chemical structure that you see in the slide. This is the amphiphile chemistry.
It's intended to mediate binding to endogenous albumin present in the tissues at the injection site. This is responsible for chaperoning these agents effectively through the lymphatic vessels to deliver them to immune cells in the lymph nodes. These synthetic long peptide antigens are combined with an immunoactivator, which is the bottom component shown in the slide. This is called amphiphile CpG. It's based on a CpG DNA TLR9 agonist, the role of this component is to activate the immune responses in concert with delivery of the KRAS mutated peptide antigens. Together, these can deliver the signals that immune cells need to recognize mutated cancer and then to eradicate it throughout the body. Let me just give you an overview of the phase I study.
This is ELI-002, a study focused on monotherapy, so we have not done any combinations in this study with checkpoint or chemotherapy. You can see the enrollment here consisted of 20 pancreatic cancer patients as well as 5 colorectal cancer patients. Importantly, this is for the study which enrolled patients in the adjuvant setting. They've had all of the known curative intent therapy, which is standard for this indication, which in this case includes chemotherapy, surgical resection, as well as radiation in some cases. Those patients, unfortunately have a very poor prognosis. They go on to almost universally relapse in a relatively short period of time. In our study, we've enrolled them based upon confirmation of KRAS expression.
They also enter the study at a point where they have no evidence of radiographic disease, but they are confirmed to be what we call minimal residual disease positive or MRD positive. This means that they have a tumor biomarker in their blood, and this indicates that they are at a very large risk for recurrence relatively quickly. The advanced stage of these patients are shown here, relatively, late stage 3 and 4, as well as 100% pretreatment, as I mentioned, with that curative intent standard of care.
The endpoints primarily are safety, but we also were able to look at initial indications of tumor biomarker reductions and clearance as a prognostic leading indicator for clinical benefit, the development of KRAS-specific immunological responses, which is a mechanism of action for the drug, and then, the more classical clinical benefit endpoints of relapse-free and overall survival. As I said, the results for these, this study have been published in the last 2 years in Nature Medicine. You can follow the QR codes here to look at that data in more depth if you are interested. Just for the sake of time, I'll briefly summarize some of the key highlights from those datasets, which are summarized here in this table. In the initial dataset, we were able to see that the relapse-free and overall survival was 16 and 29 months respectively.
You can see that this compares quite favorably with the historical precedent, roughly 3 times longer than patients typically go without recurrence and an additional year of overall survival compared to that MRD positive pancreas cancer precedent. In addition, we observed 100% of patients generating mutant KRAS-specific T-cells, and we correlated the strength of those T-cell responses to the relapse-free and overall survival with an 88% reduction in the risk of progression for patients that exceeded a particular threshold in their T-cell response and a 77% reduction in the risk for death in patients that exceeded that same T-cell threshold. In this case, we've observed a very consistent and a statistically significant correlation between the mechanism of action, mutant KRAS-specific T-cells and the clinical benefit that patients appear to be experiencing.
We have, as I mentioned, expanded our development program to include what we call the 7 peptide formulation. This includes 7 additional mutant KRAS peptides that are present in the vast majority of KRAS-driven cancers. Here I'm just showing you side by side the results from the 2 phase I, the one studying the 2P formulation and the 7P formulation. Again, as you go down the rows, you can see a collection of pancreas and colorectal cancer patients were enrolled. We progressively optimized the dose of the 2 components that I introduced earlier. First, the peptides and then the adjuvant CpG. We've seen very consistent safety and tolerability throughout this clinical program. Very good profile of adverse events. Nothing greater than grade 2. No dose-limiting toxicities or dose modifications observed. It's a very well-tolerated agent to date.
We also saw a strong frequency of T-cell responders throughout both studies here. 100% of patients generating the mutant KRAS-specific T-cells that we know have correlated with clinical benefit in those studies. A very consistent threshold of response, which separates patients that do exceedingly well versus those which reflect more of the historical standard. In addition to the KRAS-specific T-cells that we've observed, as I mentioned, we observed these personalized tumor-specific immune responses generated through what we call antigen spreading. The vast majority of patients here, 70%, are generating these responses that go beyond the KRAS driver mutant oncogene. Let me just speak for a few minutes about the phase II study. This is an ongoing study which has built on the phase I experience that I just described. Again, this is being done in monotherapy.
Here we focused on pancreas cancer, for patients that have expressed one of the seven mutants present in the product. These are again upfront respectable pancreas cancer stages 1 through 3. Patients are deemed to be no evidence of disease following standard of care therapy. In this case, we've allowed patients that are MRD positive or negative to be enrolled for treatment. You can see the randomization of the design there in the middle with patients being 2 to 1 randomized between treatment and the standard of care, which in this case is observation. We have enrolled those patients over the course of the last 18 months. The endpoints here, the primary is disease-free survival, and we're expecting the final analysis for that endpoint around mid-year of this year.
This is built upon an interim analysis that was conducted by a data monitoring committee, late last year, which suggested the safety profile was consistent with what we had observed in phase I and early signs of preliminary activity that they were hoping to build upon in the final analysis. I mentioned, some of the key milestones that we've hit recently, the positive interim analysis by the IDMC and the final event-driven disease-free survival analysis that is anticipated mid-year of 2026. We have also aligned with the FDA on the basics of the phase III design that would follow this study, specifically a randomized blinded trial with primary endpoint of disease-free survival that will be investigator assessed and also assessed using a modified RECIST criteria in which lesions are confirmed by further imaging and/or biopsy.
While we wait for the blinded clinical data final analysis, we have been able to conduct analysis of the secondary and exploratory endpoints, including the KRAS-specific immunological responses. We reported these over the last six months, and here I'm showing them in comparison to what we observed in phase I. Firstly, we've seen 99% of patients generate a KRAS-specific T-cell response. This compares favorably to what we had seen in phase I, very consistent. We did see that the magnitude of those responses was slightly increased 44-fold over baseline relative to the 18-fold we observed in the phase I component.
While we don't know what threshold of T-cell responses will correlate with clinical benefit in the blinded final analysis, we can say that 80% of patients in the treatment arm have achieved an immunological response that exceeds the 9.5 threshold that correlated with clinical benefit previously. We've also confirmed that the responses in this case do not appear to be restricted to particular HLA haplotypes, that enables us to potentially treat a large proportion of the patient population. This antigen spreading phenomena that I had introduced earlier was also very consistent here with 87% of the patients exhibiting immunological responses against personalized tumor mutations found. We have a number of catalysts and milestones to mention.
I think the most important one to close on is the upcoming final analysis of the randomized phase II, which is projected to be at the midpoint of 2026. We will, of course, look for that to enable financing and to provide resources for further growth, including the phase III conduct as well as other clinical development opportunities. I'll finally close with a financial overview, importantly noting that our operating capital will provide support throughout the time where we will be expecting to read out the randomized phase II into the fourth quarter of this year. Thank you for your attention. I don't know if we have time for questions, but if not, please find me afterwards if you have any questions. Thank you.
Hi, everyone. My name is Matthew Guggenbiller. I'm an associate on Alec Stranahan's biotech team. Thanks for coming to the Vegas conference, day 3. Appreciate you guys coming out, and I'm pleased to be joined by Aclaris Therapeutics, who are gonna be running through some slides. Over to you.
Yeah. Hi, good morning. I'm Hugh Davis. I'm the President and COO for Aclaris Therapeutics. Thanks to Bank of America for having us at their healthcare conference. The normal disclaimer and cautionary notes regarding forward-looking statements. Aclaris Therapeutics is an innovator in immunological assets for important unaddressable disease. Addressing validated targets is key to success while we are really understanding how to take innovative approaches to our portfolio. Two examples would be bispecifics and ITK oral inhibitors that'll be best in class. We have a research lab in St. Louis that is state-of-the-art scientific platform in kinase biology and world-class scientific acumen across the company. In 2026, we have a quite a catalyst calendar that I'll speak to later.
As I mentioned, addressable inflammatory diseases of dermatologic, immunologic in terms of respiratory and IBD disease is important, with, you know, an impact in millions of patients just in the U.S. alone. In Aclaris, we are going after these respiratory and dermatologic conditions with first-in-class types of molecules. It's unusual for a mid-cap to have such a strength in large and small molecule development and therapeutics. Yet we have both ITK franchise that has JAK-like efficacy. That we're looking to expand on with broad ITK selectivity, as well as in biologics, where we have potential first-line therapies. Really what we're looking to achieve is very was a higher efficacy ceiling in these patients with derm and respiratory disease.
We also have the opportunity for extended dosing intervals with our biologics portfolio, leveraging our biology and our drug design. We have a phase II bosakitug anti-TSLP mAb that's currently gonna read out by the end of this year. It's a 100 subject placebo-controlled study in AD with moderate to severe. Following is ATI-2138, which is our ITK/JAK3 inhibitor. This completed a phase IIa study in atopic derm as a POC. Now we're pursuing lichen planus as our phase IIb indication that'll initiate by the end of this year. ATI-052 is the bispecific that targets both TSLP and IL-4R. We've completed the healthy volunteer portion of that, I'll go over that momentarily. We have 2 phase Ibs ongoing in severe atopic derm and moderate to severe asthma.
Our 9494 molecule is gonna be moving toward an IND submission by the end of this year. In terms of bosakitug, our TSLP antibody, TSLP is extremely important because it has a pleiotropic, broad set of activities, where we hit dendritic cells, mast cells, fibroblasts, and even ILC2s, innate side of the immunity, it's the master regulator of TH2 pathway indications. When we consider going after TSLP and inhibiting it's really with this pleiotropic activity in mind. We have a best-in-class molecule in our mind with over 400 hours of residence time on TSLP.
We bind, and it dissociates very slowly, with 400 hours of residence time relative to other clinical development candidates that we've tested, and it's about 25-30 times longer residence time than tezepelumab, the only approved anti-TSLP antibody to date. When we compare to tezepelumab, the structural crystal structure work that Amgen put out years ago and published, you can see that we have 3 CDRs on the heavy chain that's binding to the C terminus of TSLP. It's an affinity-based interaction. Whereas bosakitug has all 6 CDRs in both the heavy chain and light chain that are contacting the TSLP molecule all the way from the C terminus to the N terminus. It's binding, and it's not letting go.
This molecule has already completed a POC study in atopic derm, where the data showed over 90% of subjects had an EASI 75 response, and an IGA 0/1 88% response, IGA 0/1. We've taken this forward into a phase IIb, or a phase II, sorry, in atopic derm, and as I mentioned, that'll complete by the end of the year, and that's in moderate to severe patients. The same anti-TSLP antibody is a component of our bispecific, and this time we have the TSLP and also scFvs that bind IL-4R. What we've been able to show is that this molecule is about 4 times more potent than the combination of dupilumab and tezepelumab in inhibiting chemokine secretion from PBMCs that have been activated with TSLP and IL-4.
In the healthy volunteer portion of the phase I, we've shown extended PK duration out to 20 weeks after the last dose, at week 4, so 16 weeks of coverage at the 480 and 240 milligram dose. This pharmacokinetic profile also matches up with the pharmacodynamic profile in target engagement, where we've shown that TSLP-activated whole blood from these subjects in the healthy volunteer portion of the study have 100% inhibition of the TSLP-stimulated TARC and up to week 20 after the last dose at week 4. The IL-4 stimulated is inhibited for at least 12 weeks at 100% inhibition by the 480 milligram cohort.
The PK/PD effect that we're seeing here actually gives us the potential to dose this drug up to every 3 months. The AE profile was very quite favorable, and we saw no SAEs and no TRAEs and no conjunctivitis. This molecule will be moving into an asthma study. We're initiating that effort now and initiating the study by end of year, and ultimately, we would take this into both respiratory and dermatologic conditions listed here. On the other side of the therapeutic wall in small molecules, as I mentioned, Aclaris is quite adept at ITK therapeutic development. We have a number of best-in-class oral inhibitors in this space.
Initially an ITK inhibitor would cross over TH2 and TH17. As well as innate lymphoid cell biology, with the TXK bispecific, it would also cross over into TH1. You're getting broad applicability with an ITK inhibitor. Our first molecule that was in the clinic that is an ITK/JAK3 inhibitor, this has a unique bispecific-like mechanism, where we're inhibiting both the T cell receptor activation upstream and the effector cytokines downstream. We're able to hit where CD8. We're inhibiting the cytotoxic destruction of targets by the CD8 T cells, we're inhibiting the T cell proliferation activation and survival by inhibiting cytokines. ATI-2138 was also in a proof of concept study in atopic derm.
It was a 12-week study, what it showed was that our itch profile was particularly good. We saw a greater than 4-point improvement in PP-NRS in 63% of subjects. This is, as you can see, on the slide, against other biologics and other kinase inhibitors, this is best in class. Also, on the skin clearance, EASI scores and BSA, we saw 77% drop in EASI score. This drug has shown in a POC study to have a significant itch relief, an improvement in disease severity, and extent of disease. In addition to the clinical output, we saw in this in the pharmacodynamic analysis, we saw that we had marketed and sustained target occupancy and functional ITK inhibition across the dosing interval.
This is a BID drug at 10 milligrams, and so it's a very potent molecule. Ultimately, we're showing that we're seeing strong downregulation of these ITK-dependent pathways across TH2, TH17, and TH1. The safety profile was also quite good, and so we also have the potential then to increase the exposure of this drug in future studies. The next study that we're looking to initiate by the end of the year is a study in lichen planus. Lichen planus is a dermatologic condition, where we see impact in both the oral and cutaneous portions of the body, as well as a lichen planopilaris, which is a scarring alopecia in the scalp with hair loss and scarring.
You can imagine that this disease affects quality of life in these individuals. We're taking this on. The prevalence is between 0.1 and 1% of the population. Interestingly, as we've seen in other diseases like HS, where the indication is usually the prevalence is usually very low initially until drugs come on board that can treat it, and then you see that you grow that population over time, as there's relevant medications for it. We know that in this case, lichen planus does not have an approved therapy, it's an unsatisfied market, and an opportunity for biologic-like pricing and even accelerated regulatory pathway is being pursued as it's an orphan indication.
With ATI-2138, we're taking that into lichen planus, and it's a basket study with mucosal and cutaneous, as well as lichen planopilaris, and that'll initiate by the end of the year. We have other dermatologic and respiratory indications that could potentially follow. The other molecules, ATI-9494, are moving, as I mentioned, into an IND by the end of this year, and then we also have a third-generation ITK selective inhibitor that would show up in 2027. As we're looking forward, the momentum in 2026 is really taking us with multiple clinical catalysts by the end of the year. With ATI-052, the bispecific, we currently have the 2 phase I-B studies ongoing, 1 in severe atopic derm and 1 in asthma.
Both of those we're gonna read out in the second half of this year, with an initiation of the phase II-B program in asthma by the end of the year. bosakitug, the monovalent TSLP antibody is in phase II, as I mentioned, and we're expecting top-line results also by the end of this year. ATI-2138 is going to be initiated in a new phase II-B trial by the end of this year in lichen planus, as I mentioned, oral mucosal and lichen planopilaris. Our next gen ITK inhibitor is going to be filing an IND by the end of this year. We're able to do this with our cash runway out through 2028, covering all of the catalysts and efforts that I just enumerated.
We currently have about $190 million on the balance sheet as of the end of March. Thank you for your time, and I appreciate, again, the opportunity to present at Bank of America Healthcare Conference.