Good day, and thank you for standing by. Welcome to the First Tracks Biotherapeutics conference call to discuss ANB033 top line phase Ib cohort one results in celiac disease. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question and answer session. To ask a question during the session, you will need to press star one one on your telephone. You will then hear an automated message advising that your hand is raised. Please note that today's conference is being recorded. I would now like to hand the conference over to your speaker, Mr. Dan Faga, President and CEO. Please go ahead, sir.
Thank you for joining us this morning. 2026 has been a very exciting initial year out of the gate for First Tracks. Our top-line data for ANB033 from cohort one in celiac disease exceeded our expectations. After my introductory remarks, Dr. Paul Lizzul, our CMO, will review the study results in detail. I will then discuss next steps before we open the call to Q&A. This presentation contains forward-looking statements. First Tracks is focused on developing differentiated therapies that fundamentally change how autoimmune inflammatory diseases are treated for patients in need. Today, we are focused on ANB033, a potent and subcutaneously delivered CD122 antagonist that was discovered by our research team. This program has true pipeline and product potential across GI, derm, and broader autoimmune diseases. Our first indication development is to treat celiac disease. Celiac is the largest autoimmune disease without an improved therapy.
It is a serious chronic immune-mediated disease affecting more than 2 million adults in the U.S. Currently, our phase Ib trial is underway across two separate cohorts in celiac disease, as well as another GI-related disorder called Eosinophilic Esophagitis, or EoE. Today, we are focused on reading out top-line results for the first cohort from celiac, which was a gluten challenge. The basic goal of any placebo-controlled gluten challenge is to show the active drug arm prevents histological damage and the emergence of symptoms relative to placebo. However, the most positive outcome would be for patients in the drug arm to also see a protective effect on both measures. This means both any incremental histological damage would remain below the threshold considered clinically meaningful, as well as prevent an increase in symptoms. At a high level, ANB033 achieved every single one of these aims.
As far as we are aware, ANB033 is the first therapeutic to show statistically significant and clinically meaningful protective effects on both gluten-induced intestinal damage and symptoms in a gluten challenge. Importantly, ANB033 had a clean safety profile and was well-tolerated. We believe this data set is compelling, differentiated, and reinforces the potential advantage of blocking both IL-15 and IL-2 signaling. With that, I will turn it over to Paul to review the results in more detail.
Thanks, Dan. Let me begin with a brief review of how ANB033 works. CD122 is the beta subunit of a receptor complex required for signaling of both IL-15 and IL-2 cytokines. Dysregulated signaling by these cytokines through CD122 is integral to the survival and proliferation of pathogenic CD8 + T cells, CD4 + T cells, and NK cells, which are central to the initiation and maintenance of inflammation in celiac and many other immune-mediated diseases. ANB033 is an investigational high-affinity CD122 antagonist that blocks signaling of both cytokines through the receptor complex. As a result, it aims to inhibit the pro-inflammatory activities of the downstream signaling pathways, thereby reducing inflammation and its downstream effects. ANB033's dual mechanism of action to simultaneously reduce both IL-15-driven inflammation and IL-2-mediated T cell proliferation in adaptive immune responses differentiates it from therapies that only target IL-15.
ANB033's dual pathway inhibition is particularly relevant in celiac, a disease marked by excessive production of both IL-2 and IL-15. As this illustration shows, gluten is presented to gluten-responsive CD4 T cells, triggering a cascade of immune activation beginning with Th1 cells. As shown in the gold box, ANB033's ability to block IL-2 signaling in the lamina propria of the gut reduces the upstream CD4 T cell response, T cell proliferation, and importantly, interferon amplification of IL-15 expression. Apart from the impact on inflammation, IL-2 is also correlated with the GI symptoms associated with gluten ingestion, supporting the potential for ANB033 to show differentiated improvement in symptoms compared to IL-15 inhibitors. The olive box highlights the downstream role of IL-15, which plays a direct role in inducing IEL proliferation, leading to epithelial barrier destruction.
CD122 positive IELs are highly sensitive to IL-15, and ANB033 blocks these cells from causing downstream tissue damage in the lamina propria. As a result, ANB033's dual inhibition of these cytokines addresses both the upstream immune response to gluten and the downstream inflammatory response that collectively cause intestinal damage and symptoms. Let's turn to the clinical foundation for ANB033 in celiac. In our 80-participant phase 1a study in healthy volunteers, ANB033 was well-tolerated with no safety signals observed across all doses. Following subcutaneous administration, ANB033 has a half-life of up to three weeks, which allowed us to initiate our phase 1b trial with a convenient treatment profile, and in the future, explore extended dosing regimens. The dose shown here in green was the lowest subcutaneous dose tested.
After a single administration, we saw deep target engagement with CD122 + CD8 T-cells decreasing by 74% and CD122 positive NK cells decreasing by 98%, versus essentially no change with placebo. A dose response was observed on relevant PD biomarkers, and we modeled the phase 1b dose in our celiac trial to achieve greater than IC90 on CD8 T-cell subsets in the target GI tissue. Now, let's turn to the phase 1b trial in celiac disease. The study has two separate cohorts. Cohort one enrolled patients with a baseline endoscopy Vh:Cd ratio of greater than 2, which is indicative of more modest mucosal damage. After a dose loading period, these patients then underwent an intense gluten challenge to demonstrate prevention of further mucosal damage on ANB033. A second endoscopy was performed at the week six primary analysis.
The second cohort is enrolling patients with a broad range of baseline histologic damage and symptom severity, and we will evaluate them over 12 weeks. These patients with more severe damage at baseline did not receive a gluten challenge. This cohort is assessing the ability to demonstrate a benefit in mucosal healing with ANB033. As a reminder, this global placebo-controlled study enrolled participants across the U.S., U.K., Western Europe, Australia, and New Zealand. Let's look at cohort one in more detail. We evaluated 32 patients who were randomized approximately one to one, with 17 on ANB033 and 15 on placebo, who completed dosing and the gluten challenge. Participants received three subcutaneous loading doses of ANB033 or placebo at week zero, two, and four. They then completed a 14-day gluten challenge, consuming a total of 6 grams of gluten per day. This was equivalent to approximately two slices of bread.
The primary analysis was conducted at week six, and the study assessed safety and tolerability and evaluated key histologic measures, including change from baseline in the Vh:Cd ratio, the change in IEL density, and the VCIEL composite scale. We also captured the daily frequency and severity of symptoms. We enrolled patients whose baseline characteristics were well-balanced between the ANB033 and placebo arms. The baseline Vh:Cd ratio across both arms was 2.75, a typical population enrolled in gluten challenge studies. With that, let's turn to the results. The Vh:Cd ratio is an objective and clinically important histological measure of intestinal structure and damage. Biopsies were taken from the duodenum in the worst affected endoscopic area and evaluated by a centralized expert pathologist. At the week six primary analysis, ANB033 demonstrated a statistically significant Vh:Cd histological benefit versus placebo. The mean change from baseline was -0.17 for ANB033 versus -0.66 for placebo.
The magnitude of the mucosal injury, as captured by the decline in the Vh:Cd in the placebo arm, was robust and indicative of the expected outcome from an effective 14-day gluten challenge. The remarkable 75% reduction in Vh:Cd decline relative to placebo for ANB033 resulted in a clinically meaningful placebo-adjusted delta of 0.49 that was statistically significant with a p- value of 0.009. Importantly, in the ANB033 arm, the mucosal histology was preserved. The 0.17 change in Vh:Cd remained below the approximate 0.25 threshold considered clinically meaningful. Let's look at IEL density on the left, which exceeded expectations. ANB033 not only prevented an increase but reduced intraepithelial lymphocytes, or IEL density, despite an intense gluten challenge. As a reminder, abnormally high IELs are a hallmark of celiac and cause tissue damage.
At week six, the mean change from baseline in IELs was a decrease of 1.2 with ANB033, whereas it was increased by 18.8 with placebo for an overall placebo-adjusted delta of 20. This result was statistically significant with a p- value of less than 0.001. The VCIEL composite combines the Vh:Cd and IEL into a single unified scale. On VCIEL, the ANB033 achieved a statistically significant placebo-adjusted delta of 3.33. This collectively represents preservation of villous architecture and a reduction in immune cell response that drives tissue injury. The histologic findings are only part of the story. Just as important are how patients feel and function. Participants completed the Celiac Disease Symptom Diary, or the CDSD, which is a validated patient-reported outcome measure that assesses the frequency and severity of five key celiac disease symptoms, which are abdominal pain, bloating, nausea, diarrhea, and tiredness.
The placebo patients experienced a marked increase in their symptoms that is consistent with what you would expect during an intense gluten challenge. Treatment with ANB033 prevented an increase in those same symptoms throughout the entire challenge. Stepping back in a very practical way, it is also recognized that when celiac patients have exposures to gluten, they will often resort to taking medications to try to help manage their symptom burden. This is exactly what we saw in the placebo group, with 47% of patients reporting they took permitted medications to manage their GI symptoms, whereas only 6% of ANB033 patients took a concomitant medication while on treatment. It was remarkable that despite so many placebo patients taking these types of medications, the change in symptom scores on ANB033 versus placebo were not only meaningful but also statistically significant from the first through the seventh day.
Finally, the benefit extended to moderate to severe symptoms, which were significantly lower with ANB033 than with placebo from the first through the 12th day. Now turning to safety. As you can see, there were no treatment-related serious adverse events and no adverse events leading to treatment discontinuation in ANB033-treated patients. There were numerically fewer moderate-severity events in ANB033 relative to placebo. However, it is also notable what happened to placebo patients during the study. We saw a remarkable increased incidence of GI adverse events reported in the placebo patients. This was correlated with the gluten challenge and further corroborates the patient's self-reported symptom data, as well as their increased utilization of concomitant medications. In totality, the favorable safety and tolerability profile observed for ANB033 to date is particularly encouraging for a therapy under development for chronic use in immune-mediated diseases. Dan, I will pass it back to you now.
Thanks, Paul. ANB033 demonstrates statistically significant and clinically meaningful results versus placebo on both key outcomes, gluten-induced intestinal damage and symptoms. Equally impressive is ANB033's protection of the intestinal mucosa across every histological measure evaluated during an intense gluten challenge. In addition, the impact to patients was tangible. Those who received ANB033 experienced fewer GI adverse events and were substantially less likely to require medications to manage their symptoms. Given the modest size of this trial, the statistical significance achieved is even more notable. In particular, seeing consistency across symptom scores and all histological measurements provides increased confidence in our data. To put these results into context, we have shown them alongside other CD122 antagonist IL-15 targeting programs. It is important to recognize that cross-trial comparisons are limited, and there have not been any head-to-head studies conducted.
What we do have with ANB033 is a potent CD122 antagonist with extended PD that is administered subcutaneously. The data from our trial speaks for itself. We believe there is value in the consistency of the results across histology and symptoms, reinforcing the potential advantage of ANB033 blocking both IL-15 and IL-2 signaling. As I said earlier, celiac is the largest autoimmune disease without an approved therapeutic option available for patients. Biopsy-confirmed prevalence rates suggest nearly 1%, or more than 2 million adults in the U.S., have celiac, and as many as twice that number of patients are positive for serological markers. With diagnosis rates known to increase upon approval of the first therapy for a disease, we expect to see the rate in celiac disease increase to more than 50%, exceeding 1 million adults in the U.S. alone over the coming years.
25%-40% of patients are considered to have non-responsive celiac disease, or NRCD, meaning they continue to experience symptoms and frequent significant mucosal damage despite adherence to a gluten-free diet. Market research suggests that a safe and effective celiac drug can command specialty pricing, and payers are likely to reimburse with limited utilization management. Taken together, if all U.S. adult NRCD patients were treated, it implies a market opportunity greater than $20 billion. This excludes the potential to treat a broader set of patients who, even with symptom control, have moderate to severe mucosal injury, which may lead to downstream clinical complications. Our unique experience with patients in both cohort one and cohort two may inform multiple registrational paths forward. As mentioned at the top of the call, ANB033 has true pipeline and product potential.
Today's top-line readout is planned to be presented at ICDS in Melbourne in mid-November. Cohort two of ANB033's phase Ib trial in celiac, designed to assess mucosal healing through 12 weeks in patients with a broad range of preexisting histological and symptom severity, is on track to complete enrollment imminently, with top-line data anticipated in the first quarter of 2027. As a reminder, FDA has already granted ANB033 with Fast Track designation. We plan to continue to engage with the FDA and other regulatory agencies to align on the next phase of development for ANB033 in celiac. We anticipate starting a late-stage trial in 2027. In addition to celiac, our phase Ib cohort for ANB033 in EoE is enrolling, with top-line data anticipated in the third quarter of 2027.
Today, we also announced one of our two additional planned phase II trials that we will initiate in the first half of 2027 will be in vitiligo. Additional details on this trial design will be disclosed upon study initiation. Overall, we are incredibly excited about ANB033's broad potential across multiple immune-mediated diseases and the progress we are making to realize it. We will now turn the call over to the operator for your questions.
Thank you. Ladies and gentlemen, to ask a question at this time, you will need to press star one one on your telephone and wait for your name to be announced. To withdraw your question, simply press star one one again. As a reminder, in order to accommodate all participants in the queue, please limit yourself to only one question per person. Please stand by for our first question in queue. Our first question coming from the line of Anupam Rama with JPMorgan. Your line is now open.
Hey, guys. Thanks so much for taking the question, and congrats on the data. It looks great. I just had a quick regulatory question. With these cohort one data in hand, what are the gating factors to starting that pivotal study in the next year? Do you have to wait for the cohort two data to speak with regulators? Thanks so much.
Hey, thanks, Anupam. It's Paul. To answer your second question, no, we don't have to wait for cohort two, and obviously we're really excited about these data, and going to the FDA will be an important step. Obviously we're going to have to have conversations with them about the path forward. But certainly cohort two is not a gating factor to the development path here.
Yeah, I'll just add on to that. We believe there may be multiple paths to registration, and we've often talked about prevention and healing slightly differently. I think to Paul's point, these are exactly the discussions we'll take with regulators. We shared a lot of information today. We have a lot more information internally, and there's more information to come. I think it's an exciting time for patients. I think with this information, we'll be able to work with the FDA to discuss what the right primary or co-primary endpoints are going to be with either or both of those paths moving forward.
Thank you. Our next question in queue coming from the line of Yasmin Rahimi with Piper Sandler. Your line is now open.
Good morning, team. Congrats with really the outstanding data and really remarkable to see also a statistical separation in symptoms, which raises my question. If you could help us understand what your expectations are for cohort two. I know before this data, you had communicated just any trend would be important, but now with the strong data on hand, makes us think about how we should be thinking about the cohort two data upcoming in 1Q. Congrats again.
Yeah. Thanks, Yas. It's Paul. I don't think we're changing how we're approaching cohort two here. As we've always stated, coming into this, that trial, we're looking for a signal and trend there, and we'll continue to do that. Certainly, we're encouraged by the data today that exceeded our expectations. But if you recall, that cohort two, that's not a gluten challenge study, and we're giving a similar loading dosing regimen and then looking for healing out at 12 weeks. I think at this point in time, certainly cohort one data are encouraging, but we'll continue to look for that signal or trend in that study.
Thank you. Our next question coming from the line of Michael Yee with UBS. Your line is now open.
Hey, guys, thanks. Good morning, and congrats on the data. A two-part question, but one topic. The mechanism of action, of course, we find unique and of course is differentiated from a couple of others in the space. Is there any information here that you think leads you to believe that there's added benefit? Perhaps it's just the delta of efficacy or that you would perhaps be able to see the healing more clear based on the mechanism in cohort two, given the longer duration. The first question is just sort of a mechanistic question, and what do you think would be needed to show that that's differentiated? To that point, on cohort two, as a follow-up to the last question, do you believe that you can control placebo well?
Because if you go look back at historical studies, placebo can actually go up on Vh:Cd because people are more vigilant in these studies. So maybe just make a comment about how you are thinking about controlling those patients. Thank you.
Yeah, thanks. It is Paul. On the first question, certainly as we have discussed and showed in our mechanism of action slides, we certainly believe that there is an added benefit to being able to inhibit or impact IL-2 signaling, both from a perspective on the histology, but also importantly on the symptoms as well. I think that is what we are likely seeing here reflecting in the data with the very strong signal we are seeing here on symptoms in the study. Showing both of those at the same time is really unique, as we have said before. The second question was on placebo. Yeah. So in cohort two, certainly you are correct. In studies, there is a potential for patients to be a little bit more diligent about how they are behaving and doing in a gluten trial.
But as we said in that trial, we are certainly looking for a delta there and a signal between the active and the placebo arm. So even if there is some relative improvement in the placebos, if they are behaving better on their gluten diet, we would anticipate to see much more activity and protective effect in the active arm.
Thank you. Our next question in queue coming from the line of Dave Risinger with Leerink Partners. Your line is now open.
Yes, thanks very much. Just wanted to add my congratulations to you, Dan, and team on the exceptional results. I think slide 16 is quite helpful in terms of framing the performance of ANB033. Could you just add a little bit more color to contextualize the intensity of the gluten challenge relative to other trials, and also discuss the statistical significance that you noted being different from the first day? Thanks very much.
Yes, I'll address the comment on the intensity of the challenge. I think as we've been describing for many months, there are multiple ways to run a gluten challenge across a number of days, how much gluten you're given in any single day, the way the gluten is administered. What we're emphasizing here is that even in a relatively short course trial over 14 days, what you could observe on the placebo arm, in terms of the degradation of Vh:Cd, what we're seeing here in the 0.6 - 0.7 range, and this was a very significant outcome or impact on the patients that were randomized to that placebo arm. The intensity was there, and I think the other attribute that, again, quite frankly, I think exceeded expectations only because no other drug has seen this before in this space.
The patients on placebo, half of them were taking medicines along the way to control the symptomatic impact. That really says a lot, and that really bridges into, we saw statistical significance on the drug arm on a relative basis on histology on Vh:Cd, but we also showed that protective effect. We know it was a hard-hitting challenge given how big of an impact Vh:Cd had on placebo. Then on symptoms, and Paul, you can add onto this. On the symptoms, what was quite amazing here is right out of the gate. That's why we're emphasizing the statistical significance as early as that first day. There was a very meaningful prevention of symptoms or increase in symptoms on the active drug arm.
It was immediate, and there was a question earlier on what could be potential reason that we're seeing this since the protective effects of, I think maybe the power of really blocking both IL-2 and IL-15 signaling. We're emphasizing as well that the patients on the active arm did not see any increase in symptoms throughout the entire study. I think that's what's truly notable here. We know we have a hard-hitting challenge in only 14 days. We gave a very significant two slices of bread a day challenge on a daily basis. I think the results, as we've been mentioning, speak for themselves on a relative basis, not just active versus placebo, but then across looking at the results from other trials with very different gluten challenges. You want to add anything, Paul?
I think you covered it, Dan. Good job.
Thank you. Our next question coming from the line of Yatin Suneja with Guggenheim Securities. Your line is now open.
Hey, guys. Let me add my congratulations as well. Very good results. Maybe just continuing on the previous topic that, Dan, you talk about differentiation. When we look at the data and we compare it across the board, obviously, you have shown the highest delta, but I'm particularly interested in understanding how do you see the CD122 differentiating from IL-15, because it seems like IL-15 are reducing this Vh:Cd ratio to below the clinical meaningful. However, the data across CD122 seems to suggest that you do provide a better protection. Can you maybe comment, is there a thesis beginning to emerge where at least CD122 seem to be superior, at least in celiac, or it's too early to say?
Look, I think this is a small study, and some of the impact is in the p- value itself in a small study and seeing how just highly significant these results are. I am glad you are hitting on this, Yatin. It is not just the spread versus placebo. We need to show the drug has a real clinical effect in trials in a placebo-controlled way. From a patient perspective, the most important thing here is the, again, it is on both types of outcomes here. It is the prevention of deterioration in the, in this case, very significant exposure to gluten, in a way that is not clinically meaningful. That was an incredibly important outcome while still showing that placebo-adjusted delta was statistically significant. Again, it is hard. It is still early days here for the broader field.
With a CD122 antagonist, we are able to show a very tangible symptomatic outcome here that was statistically significant, but again, also clinically meaningful. The thing that pairs with the delta versus placebo on symptoms is the fact that patients did not see an increase in symptoms when they were exposed to gluten in this trial throughout the entire study. We are running the second cohort on healing. We are not going to be giving them this intense gluten hit. So it is going to be a very different type of trial running in cohort two. I think we have the potential there. Although, we have to see, right? Because it has not been done before. But we have the potential there to see pretty significant healing or increase in Vh:Cd in a very different type of trial design.
That is why we were saying earlier there could be multiple paths forward here in registration. I think the reason we are able to say that with confidence is we have a mechanism of action, a potent drug, not just a CD122 antagonist, but it is a potent molecule that could give us viability across multiple ways to treat a really large patient population here that have various issues on presentation. Whether that is damage and they do not know they have the damage because they do not have acute symptoms every single day, or on the flip side, they are very prone to or sensitive to exposures to gluten. They might feel an impact out of the gate, but otherwise, they had a healthy Vh:Cd that just deteriorates over time. There is multiple ways to look at this.
We are really excited about the results today, and we think this opens up at least one of those two paths forward.
Thank you. Our next question in queue coming from the line of Derek Archila with Wells Fargo. Your line is now open.
Hey, good morning, and congrats on the data. Just a quick question. Did you capture the serum IL-2 kinetics in the hours after the gluten exposure by each of the arms? I guess, would this data be presented at ICDS? Thanks.
We did a large number of assessments and evaluations in a very thorough, comprehensive translational package. These are top-line data. We don't have all that information. At this point in time for ICDS, we're committing to what we're presenting today, and that likely will be it. We'll make determinations in the future as to what additional data will be presented.
Derek, I appreciate that question a lot. We don't have that information yet, although given the quality of the clinical results, I'm quite excited to ultimately have the access to that information internally. I think we are ultimately going to have a lot of judgment call here given the competitive intensity of what we share translationally. We do think a lot of the devil is in the details on how you're going to design a very successful and de-risked registrational trial. Some of what I think we've already learned by seeing the symptom data, which is why we kept. We actually described today, I think, a little more than we thought we were going to coming into these results from a public perspective. There's a lot of amazing information we now have internally, and the translational information's going to stack on top of it.
But the thing that we're focused on most here is ensuring that not only we move quickly, but that we maintain a competitive intensity on a relative basis over, I think, the next critical 12, 18 months as we're all moving forward into late-stage or registrational trials.
Thank you. Our next question in queue coming from the line of Andy Chen with Wolfe Research. Your line is now open.
Hi, this is Riley on for Andy. Comparing your Vh:Cd data versus Teva side by side, if we disregard the delta completely, your absolute is 0.17, but Teva's is 0.43. Is that difference meaningful at all to clinicians, or does that difference have any meaning when it comes to whether it might be a good leading indicator for a cohort two? Thanks.
Yeah. So I'm not going to comment on this relative to the competitor. But what I think is a major takeaway from this call and the data we're presenting with the 0.17 on active is it is clearly below a range that is considered clinically meaningful in terms of deterioration, i.e., we did not see a meaningful deterioration on active in this study. And that is really important here in terms of the, we think, the commercial viability of these types of approaches moving forward in the field of treating celiac disease.
Thank you. Our next question coming from the line of Gavin Clark-Gartner with Evercore ISI. Your line is now open.
Hey, guys. Congrats on the data. Obviously, super interesting to see the symptom benefit emerge here, given that other therapies using similar trial designs haven't really shown a symptom benefit in this setting. I'm just curious, moving forward, if this changes how you view the potential use of gluten challenge in other prevention-based studies, maybe as we keep looking increasingly at the symptom side?
Yeah, Gavin, unfortunately, I think it's a little bit of a repeat what we've been saying here is we have learned a lot in this study and really the intention of running a phase Ib. We gave a very hard-hitting amount of gluten very quickly over a 14-day period. We did not have dropouts in this trial, but we did observe placebo patients needing the equivalent of what was rescue medicine or concomitant medicine to control symptoms. This is exactly what we were hoping to see. I know yourself and others are going to be very focused on what do registrational trials look like. Like I keep saying, we have a lot of ideas for one or more paths moving forward.
We're going to take a very, I think, impressive data set forward to the FDA and have the right discussions to work with them on how do we think about the right endpoints on both histology and a PRO to progress forward. Like I said, there could be one or more paths to doing this that we could pursue in parallel.
Thank you. Our next question in queue coming from the line of Martin Fan with Wedbush Securities. Your line is now open.
Hey, guys. Thanks for taking the question, and congratulations on the data. Again, another question on the late-stage trial, but since we haven't yet disclosed the doses, do we see room to go potentially higher on dosing as we think about late-stage trials? And then also the extended dosing intervals and thoughts about potentially exploring those during that trial.
Yeah. That's correct. We haven't disclosed the dose. Again, I think similarly, for competitive reasons, we're going to keep that undercover for right now. But I'll emphasize, we do think the dose that we are using in this trial, which in this case we really think of as a loading dose, was already, one, subcutaneously administered, and two, as we've been forecasting, I think we could lean into this further. I don't think we're going to be testing higher doses. I do think we're going to have the opportunity to test lower doses with extended dosing intervals in future trials.
Thank you. Our next question coming from the line of Etzer Darout with Barclays. Your line is now open.
Great. Thanks for taking the question. Congrats on the data today. Just to touch on your comments, Dan, this is what I was going to ask. If you could talk a little bit about exposure levels that you reached in the study, whether or not you're getting close to what you believe is the top of your efficacy range and ultimately what it means for cohort two data as well as studies like eosinophilic esophagitis, which you'll be presenting next year. Just commentary around exposures. Thank you.
Yeah. We'll have more to say or think about this over time as we have access and have reviewed the translational data, I think is the honest answer. From the clinical results, again, this wasn't the largest study, but the p- value that we observed in a study like this and the protective effect of the drug, it really is almost impossible to have better results than this. When you look at it was protective on histology on every outcome measure, and we saw no impact or increase of symptoms for patients that actually received the drug. You just can't do better than that. I think I'll leave it at that. It's a great way to end today's discussion.
Thank you. There are no further questions in the queue at this time. Ladies and gentlemen, this concludes today's conference call. Thank you for your participation, and you may now disconnect.