Good morning, and welcome to the Structure Therapeutics conference call. At this time, all participants are in listen-only mode. Later, we will conduct a question -and- answer session. Please be advised that this conference call is being recorded. I would now like to turn the call over to Corey Davis of LifeSci Advisors. Thank you, Dan, and good morning, everyone. Earlier today, we issued a press release providing top-line results from the ACCESS II clinical program for aleniglipron, our oral small molecule GLP-1 receptor agonist. A copy of this release and the presentation accompanying this call are available on the investor relations section of the Structure Therapeutics website. I'd like to remind everyone that some of the statements we'll make on this call and information presented in the slide deck may include forward-looking statements, which you see here. These forward-looking statements involve a number of risks and uncertainties that could cause actual results to differ materially. Please refer to this slide, as well as our SEC filings, for a more detailed description of the risk factors that may affect our results. Please also note that these forward-looking statements reflect our opinions only as of the date of this call, Monday, March 16th, and we undertake no obligation to update such statements to reflect events that occur after such date, except as required by law. Now I'll turn the call over to Ray Stevens, the Chief Executive Officer of Structure Therapeutics, to start the presentation. Go ahead, Raymond. Thank you, Corey. Good morning, everyone, and on behalf of everyone at Structure Therapeutics, thank you for joining us today to discuss our positive top-line data from three different studies of our oral GLP-1 pill, aleniglipron. This morning, we will present the results from the now completed ACCESS II program and the results from two additional pre-specified interim analyses, which were conducted after median follow-up of 20 weeks on our ACCESS open label extension study and our body composition study. These data follow from the successful results reported back in December of 2025 and is the first of several additional data releases that we anticipate over the course of 2026. After my introduction and summary, Dr. Blai Coll, our Chief Medical Officer, will review the data in more detail. At the end, we'll turn the call back over to the moderator to manage Q&A. The new data we are sharing today continues to demonstrate that aleniglipron has a compelling and differentiated profile with potential best-in-class oral GLP-1 efficacy that is very consistent across all the studies we have reported to date. Let's begin by summarizing the data we shared in December, starting with the Phase IIb ACCESS study. At 36 weeks, aleniglipron showed a placebo-adjusted mean weight loss of 11.3% at 120 mg with no signs of plateauing. We observed an overall 10.4 AE-related treatment discontinuation rate in the study. Moving to the ACCESS II study. At 36 weeks, aleniglipron showed a placebo-adjusted mean weight loss of 15.3% at the two highest dosages of 180 and 240 mg, and again, no evidence of weight loss plateauing. Following the re-randomization period at week 28, we observed zero AE-related treatment discontinuations at doses up to 240 mg. For the ACCESS open label extension and body composition studies, after a median follow-up of 10 weeks, we saw a more favorable tolerability profile by using the lower 2.5 mg starting dose compared to 5 mg starting dose. There was zero AE-related treatment discontinuations. Finally, aleniglipron showed an excellent safety profile in over 500 participants across all studies up to 44 weeks. There were no events of drug-induced liver injury, no off-target safety signals across all dose levels, and no events of QTc prolongation. Moving to the right-hand side of the slide, today we're very excited to be sharing the full data readout for the ACCESS II and pre-specified interim analysis from ACCESS open label extension and body composition studies. The data highlights best-in-class potential for efficacy within the oral GLP-1 pill class in approaching the efficacy observed with the injectable GLP-1 class. Starting with the ACCESS open label extension for patients continuing at 120 mg and after a median follow-up of 20 weeks or 56 weeks total on aleniglipron, the study observed a body weight loss of up to 16.2% with no signs of plateauing. We observed an AE-related treatment discontinuation rate of 2%. For the now completed ACCESS II study, at 44 weeks, we saw a placebo-adjusted mean weight loss of up to 16.3% at 180 mg and 16% at 240 mg. There were no signs of plateauing. For those participants who achieved re-randomization, only one patient discontinued due to AEs up to 240 mg dose. Moving to the ACCESS open label extension and body composition studies where patients started at 2.5 mg. After a median follow-up of 20 weeks, the data suggests an improvement in tolerability by starting low at 2.5 mg and titrating more slowly compared to the ACCESS studies. We are pleased with the GI tolerability results associated with a very low AE-related treatment discontinuation rate that remains below 4%. Finally, for the greater than 625 participants treated across all studies up to 56 weeks at 120 mg and 44 weeks at 240 mg, we saw no events of drug-induced liver injury, no off-target safety signals across all dose levels, and no events of QTc prolongation. I will now turn the call over to Dr. Blai Coll, our Chief Medical Officer, to walk through the details of the top-line data, what we believe to be the potentially best-in-class oral GLP-1 pill that can scale to meet the global demand for patients who are waiting. Thanks, Raymond. We want to share with you exciting data today from the aleniglipron program, as Ray alluded to, and review with you key questions to continue the patient journey of aleniglipron towards a chronic weight management indication. First, what is the top dose to move forward the program? Number two, does weight loss continue beyond week 36? Third, while tolerability is optimized by starting low and going slow, are there initial signs of weight loss? Number four, related to that, does the tolerability improvement associated with a 2.5 mg start and titrate slowly persist over time? Finally, very important, does aleniglipron maintain an absence of off-target effects? To address those questions, we will focus on ACCESS to completion up to 44 weeks and top dose of 240 mg, and we will provide additional pre-specified interim analysis from the ACCESS OLE and the body composition studies. Let us start with the first set of questions around top dose and efficacy beyond 36 weeks, reviewing the top-line data from the ACCESS II study. As a reminder, you can see next slide the design of the ACCESS II study, where 73 participants living with obesity or overweight and at least one comorbidity were randomized to aleniglipron or placebo. Participants started at 5 mg of aleniglipron in 4-week titration steps to reach 120 and got re-randomized on week 28 to 120, 180 mg or went to 180 for four weeks before reaching target top dose of 240 mg today. We've reported 36-week data in December, and today we will be focusing on the efficacy up to 44 weeks and the tolerability profile after re-randomization. A reminder of the baseline characteristics with age between 50 and 52 years old, predominantly female participants, 62% and 67%, with a baseline BMI of 39.9 for the group randomized to aleniglipron. Per eligibility criteria, both HbA1c and blood pressure were within normal limits. Next slide summarizes the primary efficacy endpoint based on the primary efficacy estimate, showing a very clear separation of curves early in the trial that continues all the way till week 44, showing a 13.6% weight loss for the 120 mg group, 15.3% for the 180, and 15% for 240 mg. There is additional body weight reduction between week 36, reported in December, and week 44 as the final data point in the study. In the bar graph on the right, we show the placebo-adjusted estimates with a 14.7% reduction for 120, 16.3% for 180, and 16% for 240, representing an absolute weight loss ranging from 33-39 lbs. Overall, a clinically and statistically highly significant body weight reduction at 44 weeks with greater efficacy at doses higher than 120. The categorical analysis of body weight reduction based on 5%, 10%, or at least 15% weight loss also yielded clinically relevant results, with 93% of participants on 180 achieving at least 10% and 61% reaching a 15% or greater weight loss. Additionally, and as part of an exploratory analysis, 32% of participants receiving 180 achieved a 20% body weight loss or greater at the end of the 44 weeks. With the compelling level of efficacy, let's transition over to the tolerability analysis after re-randomization. As you can see in the top panels, we're describing the occurrence of vomiting for 120 and 180 mg of aleniglipron, where one participant in each group had an event of vomiting. For the 240 -mg arm in the bottom left, four participants experienced events of vomiting starting at week 37. Interestingly, just one participant assigned to the 180 -mg arm discontinued due to an adverse event after re-randomization. Overall, the tolerability profile after re-randomization showed no serious adverse events and a 3.7% discontinuation due to an adverse event. Importantly, the majority of participants on aleniglipron, 70%-100%, completed the last 12 weeks in the study at target dose, defined as having a compliance rate during that period of time at least of an 80% compared to just a 60% in the placebo arm. The gastrointestinal profile showed no substantial differences between 120 mg and 180 mg arms and a higher occurrence of nausea and vomiting in the 240-mg arm. To summarize ACCESS II, potential best-in-class efficacy with a 16.3% body weight reduction, placebo-adjusted for the 180-mg arm. Importantly, the tolerability profile for higher doses shows a low number of AEs leading to discontinuation, with the incidence of gastrointestinal events at 180 comparable to the 120-mg dose. An important consideration to the patient journey is centered around the continuation of body weight reduction and the tolerability by starting aleniglipron at 2.5 mg and titrating more slowly. To address those two questions, we will review the pre-specified interim analysis from the open label extension study of ACCESS. The design of the study is shown in this slide, where 151 participants from ACCESS completed the first 36 weeks of the study and signed up to continue for the open label extension portion. Patients at 45 with an N of 28 during the double-blind treatment got uptitrated every four weeks to reach 120 mg. Similarly, 42 participants assigned to 90 mg in the randomized period were uptitrated to 120 for the open label portion, and the participants on 120 in the double-blind period continued on 120 for the remaining period of the open label extension. The participants initially assigned to placebo in the bottom row started on 2.5 mg of aleniglipron at week 36 and titrated every four weeks and will eventually reach 120 mg. We will focus today on the analysis after a median follow-up of 20 weeks. We will start off with the description of body weight changes. Graph showing the body weight reduction in percentage in the Y-axis for the participants in the four arms of the study. Let us start with the gray line depicting the placebo crossover participants with a reduction of around 1% at the end of the randomized period. At week 36, they started on aleniglipron 2.5 mg, indicated by the blue circles, and titrated up on a four-week scheme to reach a 6.4% weight loss after a median exposure of 20 weeks. The participants assigned to 45 mg in the randomized period, shown in triangles, were uptitrated every four weeks to reach 120 and showed additional body weight reduction from week 36, achieving a 13.3% weight loss at week 56. Participants assigned to 90 and 120 during the double-blind treatment, the two bottom lines in the graph, were dosed at 120 mg and experienced additional weight loss ranging from 15.3% to 16.2% after a median follow-up of 20 weeks. From a tolerability perspective, we describe in the slide nausea on the left and vomiting on the right from those 38 placebo crossover participants starting at 2.5 mg. We observed very low occurrence of nausea and without a specific temporal pattern up to week 56, where doses of aleniglipron were approximately of 30 mg, and no events of vomiting reported up to week 56. Overall, this slide shows the tolerability profile during the open label period starting at week 36 and after a median follow-up of 20 weeks. The number of treatment-emergent adverse events is higher in the placebo crossover group since this represents the first time those participants started exposure to aleniglipron. Additionally, the study shows a low number of AEs leading to discontinuations, three at 2%, and ranges of nausea from 11.6%-39.9% and vomiting ranging from 7.1%-16.3%, with diarrhea and constipation less commonly reported. In summary, from the open label extension, the study showed clinically relevant and additional body weight reduction beyond week 36, up to 16.2% weight loss at 120 mg. Tolerability is characterized by very low numbers of AEs leading to discontinuations, 2%, and the additional data reinforces the tolerability improvement by starting at 2.5 mg and titrating more slowly with no vomiting events and no discontinuations in that group after a median of 20 weeks in the study. Let's now transition over to the body composition study to address the questions around the level of efficacy by starting at 2.5 and titrate slowly and key tolerability markers. A reminder of the study design, 71 participants living with obesity were enrolled in 11 sites across the U.S. 59 participants randomized to aleniglipron with the same titration scheme as described in the ACCESS OLE, starting at 2.5 and titration on a four-week basis to eventually reach the 120 mg target dose. We will share results of their median follow-up of 20 weeks corresponding to the 30 -mg titration step. A reminder of the baseline characteristics with average age ranging from 49-55, predominantly female participants, 64%-67%, and BMI of 38 across the first groups. In this slide, you can see the description of body weight changes in the study with the placebo participants shown with a gray line, with body weight reduction fluctuating at around 2% at week 20. Importantly, the participants receiving aleniglipron showed a consistent and differentiated body weight reduction, achieving a 6.8% weight loss after a median follow-up of 20 weeks, coinciding with the 30-mg titration step. In tolerability, you can see the panels on the left describing events of nausea on top and vomiting at the bottom for the aleniglipron-treated patients, and on the right, the occurrence in placebo participants. We observed fluctuating events of nausea coinciding with the titration steps, but overall showing a tapering down over time with very low prevalence of vomiting events, as shown in the lower left panel. This data suggests a different pattern compared to ACCESS and ACCESS II, where starting at 5 mg was associated with a higher peak of both events during the first four weeks in the study. This profile is associated with a low number of AEs leading to the study drug discontinuations with just two participants, 3.4%, happening at weeks nine and 11, both due to gastrointestinal symptomatology. Overall, in the body composition study, we see very low AEs leading to study drug discontinuations, with 50.8% of participants reporting at least one event of nausea and 23.7% reporting vomiting. It is important to highlight here that the placebo event rate of some of the gastrointestinal events is high in the study, showing 33.3% of placebo participants reporting nausea, 8.3% vomiting, and 50% of participants reporting diarrhea, data points that should be considered in interpreting the overall profile. The increased awareness of the gastrointestinal events in the class of GLP-1 receptor agonists by clinical sites and participants, along with data capture involving eDiaries, may artificially inflate the rate of subjective events such as nausea. In summary, for the body composition study, participants starting at 2.5 mg of aleniglipron and titrating slowly show preliminary signs of body weight reduction, achieving a 6.8% after 20 weeks of median follow-up. Importantly, from a tolerability perspective, the data supports the start low, go slow strategy with very low number of study drug discontinuations due to adverse events at 3.4%. To summarize the tolerability, you can see in the slide a comparison of the two titration strategies taking patients to 30 mg of aleniglipron. In ACCESS and ACCESS II, patients started at 5 mg and titrated every four weeks to reach 30 mg in 12 weeks, indicated with the dark blue bar graphs. In the body composition and in ACCESS OLE patients, we followed a start low and go slow strategy of starting at 2.5 mg, titrating every four weeks to reach 30 mg in 20 weeks, shown in orange. It is important to highlight the duration of the two sets of data are not the same, with longer capture of events for the start low and go slow titration in body composition and ACCESS OLE 20 weeks compared to 12 weeks in ACCESS. Additionally, as stated in a previous slide, the reporting of nausea may be subjective and should be interpreted with caution. Comparing those two sets of studies at the same dose, the data suggests an improvement in the three parameters, nausea, vomiting, and especially AEs leading to study drug discontinuations. This further supports the strategy starting low and going slow by starting at 2.5, keeping four-week titration steps, and escalating the dose not more than 2.5-fold. We are very pleased with those results that will better inform the design for the upcoming studies. Lastly, and very importantly, let's review the off-target safety profile. As reported back in December from ACCESS, the new data from ACCESS II, an interim analysis of the open-label extension and body composition studies confirms the lack of drug-induced liver injury events. There are no cases of liver enzyme increases above 10x, and importantly, all cases of fluctuations in both ALT, AST resolved while continuing study drugs. With that, we wanted to summarize the key findings from today's data readout. First, we have characterized the profile of aleniglipron, demonstrating best-in-class efficacy, reaching 16.3% body weight reduction at 44 weeks for the 180 mg group, and the tolerability markers between that arm and 120 mg are comparable. Number two, data suggests there is no plateauing effect in efficacy up to 44 weeks in ACCESS II and up to 56 weeks in the ACCESS open label extension at 120. Three, by starting low at 2.5 and titrate slowly, there are initial signs of body weight reduction to achieve a 6.4%-6.8% weight loss after a median follow-up of 20 weeks. Four, the additional data from starting slow at 2.5 and titrating more slowly reinforces the continuous optimization in key tolerability markers. Lastly, yes, we continue maintaining no events of drug-induced liver injury or other unexpected off-target effects. With that, let me turn it over back to Raymond for the concluding remarks. Thank you, Blai. As we wrap up, we believe that the totality and consistency of the data presented today, together with all the data that we have presented to date on aleniglipron, provides a compelling evidence that aleniglipron, our oral GLP-1 pill designed and manufactured to meet the global needs, has a differentiated clinical profile. To address the global obesity pandemic. 2026 will be a transformational year at Structure Therapeutics as we continue to share more data from four additional studies for aleniglipron throughout 2026, including the completion of the ACCESS open label extension and data readouts for the type two diabetes obesity, switch, and body composition studies to further solidify a best-in-class profile. We have an end of phase II meeting scheduled with the FDA in Q2 and remain on track to initiate phase three in the second half. As you'll see from this pipeline, aleniglipron is only one piece of the portfolio as we build the broadest oral small molecule metabolic obesity portfolio at Structure Therapeutics. Next up is the amylin program, where we have two amylin molecules, ACCG-2671 and ACCG-3535, in development. ACCG-2671 started a phase I clinical trial in December as the first and most advanced oral small molecule amylin receptor agonist to enter the clinic, and we anticipate data from phase I in the second half of 2026. Given the importance of the amylin target in our first-in-class approach, we named a second development candidate at the end of last year. ACCG-3535 is our second generation DACRA with a different chemical scaffold and will enter the clinic by end of this year. We view aleniglipron in our amylin molecules as foundational backbones that can be used both as monotherapies and in combination with other mechanisms to address the different obesity patient segments and the various cardiometabolic indications beyond obesity. We have a preclinical programs underway combining our GLP-1 and amylin backbones that we have shared previously at international medical conferences, and the chemistry team continues to work on our GIP and glucagon molecules to be used in combination with our backbone molecules. At Structure, we believe that only oral small molecules can scale to meet the needs of the global obesity patient population. The currently available injectable peptides serve only a very small fraction of the more than 100 million people in the United States who are living with obesity or are overweight. By 2030, it's estimated that more than 1 billion people globally will be living with obesity and 3 billion will be living with either overweight or obesity. Patients need more options. The world needs more options. We believe that developing oral small molecules gives us a competitive advantage in being able to scale and make medicines more accessible to people living with obesity. I especially wanna highlight how proud I am of the work done by our chemists and manufacturing teams in preparing for aleniglipron production at the scale needed to meet this global demand. With today's update, the positive ACCESS II data at higher doses and progress in our ACCESS open label extension and body composition studies continue to demonstrate best-in-class potential with our once-a-day oral aleniglipron pill. A medicine designed to be accessible, scalable, combinable, and represents an important solution in addressing a global healthcare challenge. I will now open the call for Q&A. To ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. In the interest of time, we ask that you please limit yourself to one question. Please stand by while we compile the Q&A roster. Our first question comes from Yasmeen Rahimi with Piper Sandler. Your line is open. Good morning, team. Thank you for the excellent presentation. Could you maybe comment on clearly, the strategy of starting low and going slow seems to be working really well and that you're not reaching a plateau. Could you think about helping us understand if you can do any modeling to figure out if aleniglipron's differentiated weight plateauing effect? In other words, can you model and see is it at a year and a half that you reach plateau? Is it two years? Is there any evidence? Then also, is there any mechanistic rationale for the lack of plateauing effect? Then I'll jump back in the queue. Yes, this is Blai. Thank you. I missed the first part of your question. I got the second part. Hopefully, I can cover everything. You're asking about the plateauing effect, and the lack of- If you could model it. Yeah, that's right. If you could model and predict when. Yeah. Plateauing could achieve and what is the reason for a differentiated plateauing effect? Yeah. Thanks for your question. Absolutely, that's what we're doing right now. It's using that 44-week ACCESS II and all the way to 56 in the ACCESS OLE to inform the model that will help us predict the level of efficacy. We don't see a plateauing effect as of yet to week 44 and 56. This is a differentiated element, and we're very pleased with the results. Potential mechanisms of action there behind that clinical observation is that, as you know, we have seen proportional exposure all the way to 240 mg of aleniglipron, and that can be behind that additional body weight reduction that we're seeing beyond 36 weeks. Thanks for the question. Hopefully, I covered everything that you were asking. Thank you. Our next question comes from Evan Seigerman with BMO Capital Markets. Your line is open. Hi, guys. Thank you so much for taking my question. Really congrats on the data. I wanted to touch on the difference between the 180 mg and 240 mg doses. Clearly, both performing the same. Do you have a hypothesis as to what's happening here? Are we getting pharmacological saturation? Is there something else nuanced in the data? Just helping parse through this, you know, very good data, but I wanna know kind of the differences between these two, dosing arms. Thank you so much. Thanks, Evan, for the question. This is Blai again. I'll take the question. Yeah, as you well pointed out, we don't see differences in efficacy between 180 and 240. The results in efficacy and body weight reduction are comparable at the end of the 44 weeks. Interestingly, though, what we're seeing is that the pattern of efficacy, it's very similar between 180 and 240. Then in tolerability-wise, which is, you know, always the things that we need to couple with the efficacy, the 180 mg behaves very, very similar to what we've seen for 120. At the end of the day, I think the most important conclusion of ACCESS II is that we're getting valuable, highly valuable data to inform the design of the phase III, to design the modeling, and that ultimately will result in the identification for the top dose for phase III. Thank you. Our next question comes from Seamus Fernandez with Guggenheim Securities. Your line is open. Oh, great. Thanks for the question. Congrats on the data and the consistency, and thanks for the robust presentation overall. Actually, Raymond, I wanted to talk a little bit about the scalability of the product. I know this is something that we've talked about before, not really finding a lot to critique in the data. Wanted to maybe provide a better understanding of how you've approached the scalability to reach, you know, 100 million patients or more. You know, I know that comes down to the design of the molecule, but there's a lot that goes into this, so I was just hoping you might help investors think about, you know, what it takes to get to 100 million patients in this market. Thank you, Seamus, for the question. We were in the fortunate position. GLP-1, you know, receptor is very well characterized. The peptides, you know, we stand on the shoulders of giants, as they say, with all the characterization of the peptides over the years. We were in the fortunate position to be able to really focus on design early on at the very beginning as we're thinking about design principles. Not just efficacy, not just safety, not just tolerability, but also at the very beginning, we thought about manufacturing. So as an example, we felt it was important for manufacturing not to have any chiral centers that require chiral separation, just as one representative example. This is an important step in the manufacturing. We were able to remove, you know, any of those chiral centers that would require chiral separation. That's one example. Again, as I highlighted in my closing remarks, you know, the chemist and our manufacturing team, they've just done a phenomenal job at, you know, the synthetic route, at optimizing based on the molecule itself, the entire process, to really allow us to be able to scale this to the global needs that are required. Thank you. Our next question comes from David Risinger with Leerink Partners. Your line is open. Thanks very much. Congrats on all of the disclosures today. Could you please provide some color on how you're thinking about the go-forward start low and go slow strategy for phase III? Specifically, what period of time do you envision titrating patients from 2.5, you know, at day zero to 180 mg in phase II? Thanks very much. Thanks, Dave, for your question. Blai Coll, you can start. Yeah. Good question. Thanks, Dave. The plans based on the data that we've released today and back in December as we've communicated, starting at 2.5 mg is the most optimized starting dose for aleniglipron. We plan to keep the four-week titration steps. As released today, we're not planning to escalate the dose every time we titrate more than 2.5-fold. This is the combination of starting at a low dose at 2.5 and going slowly to reach the target doses. The final doses for phase III are still to be determined. It is currently ongoing work at Structure Therapeutics with the data we just released, plus the modeling that we're actively pursuing. Two additional comments there is that it's important to see not only that we're optimizing the tolerability, we're reducing significantly the number of these leading to discontinuation with these current titration steps, but we're also seeing early signs of body weight reduction. This is the two factors that we're laser focused on. We know from contacting with clinical investigators and data from the market research that it's, of course, very, very important to optimize tolerability while you are also seeing effects in terms of body weight reduction. This is what the data is pointing out right now. Dave, you know, you and I have had this conversation before about, you know, the titration schedule and how long a titration schedule should be. Based on our research, what we found is what's most important is that patients will get bored if they do not see weight loss after four weeks or eight weeks. So that's something that's really important to consider. What I really like about the data that we're showing today, and back to the December data, is that we are seeing weight loss at the starting dose of 2.5 mg. Even better, you know, what I like is we're seeing this very nice, smooth linear weight loss from the very beginning, starting at 2.5 all the way out to 30 mg to date. We see similar curves with the longer studies to 44 weeks and 56 weeks. We think that's really important. It's better than these exponential weight losses that we see where people lose half of their, you know, half of their weight is due to water loss, and it's very rapid. We really like the profile that we have, and we believe that the data that we've shown, patients will lose weight at the very beginning, starting at 2.5, and that will keep them very engaged, as they progress through, going on aleniglipron. Thank you. Our next question comes from Terence Flynn with Morgan Stanley. Your line is open. Hi, thanks for taking the questions. I guess just any thoughts on where you might present the full ACCESS data. Is it likely at ADA, or is there another venue that you guys are considering? I would love your latest thoughts, Ray, on potential partnership discussions and what that might look like. Thank you. Blai, you wanna take the first one and I'll take the second? Sure. Thanks, Terence. Yes, I think, you know, medical conferences later in the year and you're mentioning ADA, there's also EASD and Obesity Week in the fall. We have a lot of exciting data and we'll be informing as appropriately. Yeah, that's a reasonable assumption. Terence, on your second question, in regards to strategics, we continue to interact with strategics. The data that we demonstrated today and back in December shows very strong best-in-class efficacy for aleniglipron. We'll continue those dialogues. We also have the amylin program that'll start having data readouts in the second half of this year. We'll keep you updated as that progresses. Thank you. Our next question comes from Prakhar Agrawal with Cantor Fitzgerald. Your line is open. Hi, thank you for taking my questions, and congratulations on this update today. Maybe one on oral amylin. Seems like the second half update will be just that. Maybe if you could talk about what will be disclosed at this update and how are you thinking about the MAD readout timing and where are you with the chronic tox studies with the oral amylin. Maybe just a clarification on the liver enzyme. There were like ALT, AST elevations of 5 x upper limit of normal, few cases, but if you can clarify whether these were transient and whether patients are discontinuing the drug. Thank you. Blai, you wanna take these? Sure. Thanks, Prakhar. In regards to the oral amylin, yes, we're guiding to second half results from the single ascending dose. Currently, you know, designing multiple ascending dose. The multiple ascending dose design will largely depend on the findings on the single ascending dose. More to come on that end. Highly scrutinized program, of course, very excited, and we're very excited about the progress of this program so far. More to come on that end. In terms of the ALT, AST elevations, we're not seeing a different pattern compared to what we released in December. All the fluctuations that participants continue on study drug and the ALT, AST come back to normality. Very, very pleased to see that there's no events of DILI that the participants that experience any of those fluctuations despite not stopping study drug or discontinuing drug or reducing the dose, the ALT, AST levels got back to normality. Prakhar, just as a reminder, back at the beginning of the year, we did update our corporate deck on the amylin program, and we did share the schema of the titration scheme. That continues to be work in progress. We are right on schedule. As they say with phase Is, no news is good news in that study. Thank you. Our next question comes from Samantha Semenkow with Citi. Your line is open. Hi, good morning. Thanks for taking the question, and let me add my congratulations on the data as well. Another one for me for the oral amylin asset. I'm just wondering if you take a look forward, how are you thinking about what a competitive profile would look like from, like, an efficacy and tolerability profile for oral amylin? If you could give some thoughts around both a monotherapy and potential combination view for that asset. Thanks very much. Yeah, let me give Blai a little bit of a break here. And then Blai, you can add on to anything that I miss. First of all, Sam and Prakhar, thank you guys for asking about amylin. Even though this call is for aleniglipron, we know there's a lot of interest in amylin these days. You know, the way that we're sort of looking at this is we still believe very much in the amylin mechanism for a number of different reasons. One, the safety profile tolerability is very strong from the data that we've seen to date. And so that, we think is really important. Second, there is a subset of the population that do not respond to GLP-1s. You know, we feel for those individuals, we think amylin is a potential option for them. Lastly, we have presented previously at international medical conferences, the combination of our oral GLP-1 together with our oral amylin, and we see this very synergistic effect between the two, so for additional weight loss, if one wants to go to that level. I think in terms of tolerability advantages, we continue to be intrigued by the selective weight loss, which we think is also an important area. There's a number of reasons why we remain excited about amylin and in the combinations. Blai, anything else you wanna add to that? No, just one comment, Samantha. I think good question on how we're developing the amylin. We'll develop as monotherapy for now, but also with the intent to combine. As we've said in the opening remarks, we have the ability to have that combination of different mechanisms of action that, as Ray alluded to, can potentially be synergistic. That's the plan that we have for the amylin program. Thank you. Our next question comes from Jonathan Wolleben with Citizens JMP. Your line is open. Hey, thanks for the update and taking the question. Wondering if you could talk a little bit about the differential properties between aleniglipron and orforglipron and the results you're seeing here with the clinical profiles, just to better understand what's going on mechanistically here? Yeah. I'll start. At sort of a very high level, we see four different reasons for differentiation. Clearly, efficacy stands out. This is the most efficacious oral GLP-1 out there from the data that we've shown now. Second, in terms of off-target safety, very pleased with the profile. We think that in terms of tolerability, similar in regards to tolerability. Third, manufacturing, something that was asked earlier on. Really proud and pleased with the manufacturing that we've been able to accomplish for aleniglipron. That is a distinct advantage, the lower cost of goods and scalability is quite significant. Fourth, combinability. You know, the differentiation with combinability. We n ot only did we design this molecule to be efficacious, safe, manufacturing at scale that's needed, lower cost of goods, but we also designed it so it was very combinable with other molecules, whether it's other incretins in weight loss or non-incretin molecules as we look forward, in lifecycle management. Those are the four different reasons why we believe it's highly differentiated. Thank you. Our next question comes from Roger Song with Jefferies. Your line is open. Great. Congrats for the data. Really like the consistency, as you said, Ray Stevens. Real quick to you from us. The first one is. Now, we already see this, the 2.5 starting dose all the way to 20 weeks for the tolerability. Just curious about the expectation about longer follow-up. Do we, you know, expect to see some late incidence of the GI AE, particularly from those new patients versus the existing patient will change the profile? And then very quickly on the phase 3 design, knowing you will have a diabetes and then potentially the switch maintenance data coming out the second half. Understand it's not gating factor for the phase III start, but how those data will inform the phase 3 and how much you will change the phase 3 with those data. Thank you so much. Thanks, Roger. I'll take the question. Starting at 2.5 and up to 20 weeks, yes, we will see more incidence events. What we're seeing right now, this is also consistent with what orforglipron saw. It's more of a random effect over time. There's no temporal trend anymore when you find the right starting dose and the right titration steps as we've been showing with starting at 2.5 and going all the way to the 30 mg with those 20 weeks. Yes, we will be seeing most likely an increased incidence there. But the most important thing is that we are keeping the number of AEs leading to discontinuations very, very low. This is the hardest endpoint or the most robust endpoint, and we're very pleased with that data. Number two, on the phase III design, there's nothing gating. We're collecting information on the switch, but we don't see that as a key factor for informing the phase III. The type two diabetes phase II, we need to get that data and having the exposure at higher doses than 90 mg for type two diabetes, but it's not gating. We're already. We have all the data ready to have the interactions with the regulatory agencies. Thank you. Our next question comes from Andy Hsieh with William Blair. Your line is open. Great. Thanks for taking my question. Just a quick one on slide 16. For the 90 -mg open label study, you see kind of a precipitous drop from week 52 to week 56. I'm just curious about what's happening here. Also at the bottom you said no statistical model applied. If you can just kinda clarify for us what that means in terms of plotting out the chart. Thank you so much. Yeah, thanks, Andy. This is Lyle. I'll take the question. So the 90 mg in OLE, you see that drop between weeks 52 and 56. Take into account that at these two different time points we see different patients. This is probably the reason why we're seeing such a dramatic difference. This is an open label. It's interim and not all the patients have completed week 56, so that's one of the reasons why we see some differences that most likely will stabilize over time. At this point, though, with after 20 weeks of median follow-up in the open label extension, we will see potential differences in the final numbers, but directionally are. I think we're very strong in the levels of efficacy. The second question, in regards to the nature of this data. This is descriptive, it's not modeled. There is no LSM or MMRM statistical approach here, for multiple reasons. One, it's because it's an interim and it's an observational study and that's why we don't have any modeling applied yet. Andy, one follow-up on that. The 90 mg is going to 120 mg, so those two curves, the 120 mg, they should converge at some point. I think we're starting to see that in addition to it is a median 20 weeks. We're getting a range of participants at different levels. Thank you. Our next question comes from Corinne Johnson with Goldman Sachs. Your line is open. Corinne, your line is open. Please check your mute button. Hello? Hello? Yes, we can hear you. We can hear you, Corinne. I was not muted. I have no idea why that was a problem. Okay, so I was just saying I know it's a work in progress, and you guys are still going through it all, but could you speak to how you're thinking about determining a go-forward top dose given the weight loss you see at all three top doses really, depending on the time point, is reaching about 16% weight loss? And then also what are the implications for the duration of the phase III, depending on which top dose you kind of go forward with, given that start low dose slow titration strategy? Thanks. Thanks, Corinne. Yeah, as we've indicated, we're very pleased with the characterization in the dose range finding studies from 45 mg to 240 mg. We're currently work is ongoing on the definition of what will be the top dose, but I think, you know, the data is very consistent and very compelling in both terms of efficacy and the tolerability management for that 120 or higher doses. That's for the top dose. Implications on that top dose in terms of the duration, I think it's very clear that, based on the FDA guidance, we'll need to do a 52-week maintenance once we achieve the target dose and then, you know, starting at a low dose and titrating slowly to optimize that tolerability. It will not significantly alter the overall duration of those studies. Thanks. Thank you. Our next question comes from Annabel Samimy with Stifel. Your line is open. Hi, this is Jayed on for Annabel Samimy. Congrats on the great data. Just one question from us. On the body composition trial, I know the interim analysis, but were you able to get any early insights into lean muscle loss versus fat loss in these patients? Thanks, Jayed. Unfortunately we don't have the data yet 'cause the collection of the DEXAs are still blinded and we look forward to report the results at the end of the study, but we don't have that data as of yet available. Thank you. Our next question comes from Hardik Parikh with JP Morgan. Your line is open. Hey, thank you for taking the question. Just had one high level one. You know, with this update I'm just wondering internally what aspects of aleniglipron's tolerability profile do you still have more confidence now, and what are still kind of the major unanswered questions for you guys? Like I know the 2.5 starting dose, you know, we saw some encouraging signs on discontinuation rates and vomiting, while we saw some higher rates for other GI events, including the placebo arm, as you mentioned. Just how do you think the aleniglipron's tolerability profile can still change going forward in phase III versus what you saw in the OLE and the body comp studies? Thank you. Thanks, Hardik. I'll take that and Ray, please feel free to chime in. We're very pleased with the results of the tolerability that we're seeing starting at 2.5, maintaining the four weeks and not escalating more than 2.5-fold. We're seeing decreases in nausea, seeing decreases in vomiting. As we've said in the call, most importantly, we're seeing a dramatic reduction in the number of AEs leading to study drug discontinuations. That, at the end of the day, I think it's the key pillar for a successful phase III program. Of course, there are learnings from the open label extension. There are learnings from the body composition that we're including in or we're planning to include in the protocols for phase III that we'll continue optimizing those results. We're very pleased with where we are right now, at the completion of the dose range finding studies. Ray, anything else to add? Yeah, you know, this gives me the opportunity to really praise Blai and the clinical team. Overall, they've shown tremendous innovation and creativity in the design of these studies. For example, including the open label extension when we released the data back in December, really taught us the power of participants and knowing that they can continue on a study and seeing that really high continuation rate of people wanting to continue on aleniglipron. I think that was really powerful. We learned that lesson. It was kind of what I describe as an experiment within an experiment. Here we have the same situation between the body composition study and the open label extension starting at 2.5 mg. Blai and the team have continued to evaluate different variables. At the end of the day, all. What all this data is really for is for us to design the best possible phase III. I think we have probably one of the most comprehensive phase II datasets where we've explored a number of different things to give us that very successful probability of completing phase III with the TPP of exactly what we want. Thank you. Our next question comes from David Risinger with Leerink Partners. Your line is open. Yes. I just had a question on slide 18, please. In the right column, the placebo crossover data was a little peculiar. Do you have any color on the conflicting figures which show nausea at 40% and vomiting at 0%? Thanks very much. Yes, Dave, this is Blai Coll. Thanks for the question. This is the overall incidence that we've seen on those participants that started on aleniglipron at week 36. As we've indicated, the 40% of nausea, it can be highly subjective. We're not seeing any events of vomiting there. Now, whether this is the protocols are very, very similar. This is the same protocol that we use for ACCESS. It's very similar to the body composition study. Those participants may be influenced by being in the study for the 9 previous months, receiving placebo, so highly motivated. And we're also seeing some preliminary signs of site not being very aggressive in terms of the up titrations if there's any symptomatology of nausea, and those down titrations persist longer compared to the body composition. These are learnings that we can incorporate into the phase III. This is the most important thing. In addition to the low number, very low number of AEs leading to discontinuation. As you see here, we don't see anybody discontinuing up to 20 weeks of follow-up, which is again, as we've said, it's the most important factor. Thank you. This concludes the question and answer session. I would now like to turn it back to Ray Stevens for closing remarks. Thank you all for joining us today for our ACCESS II top line data readout and ACCESS open label extension and body composition updates. We look forward to keeping you updated with multiple data readouts throughout 2026 as we advance aleniglipron forward and continue to progress our amylin in combination oral pill programs to make this class of medicines more accessible to all. This concludes today's conference call. Thank you for participating. You may now disconnect.