Good morning, everyone, welcome to the Viking Therapeutics phase 2b VOYAGE Study Top Line Data Conference Call. At this time, all participants are in a listen-only mode. Following management's prepared remarks, we will hold a Q&A session. To ask a question at that time, please press star key followed by one on your touchtone telephones. If anyone has difficulty hearing the conference, please press star and zero for operator assistance. As a reminder, this conference call is being recorded today, May 16th, 2023. I would now like to turn the floor over to Viking's Manager of Investor Relations, Stephanie Diaz. Please go ahead, Stephanie. Hello, and thank you all for participating in today's call. Joining me today is Brian Lian, Viking's President and CEO, Marianne Mancini, the company's Chief Operating Officer, and Greg Zand, Viking's Chief Financial Officer. Before we begin, I'd like to caution that comments made during this conference call today, May 16, 2023, will contain forward-looking statements under the Safe Harbor provisions of the U.S. Private Securities Litigation Reform Act of 1995, including statements about Viking's expectations regarding its development activities, timelines and milestones. Forward-looking statements are subject to risks and uncertainties that could cause actual results to differ materially and adversely. Reported results should not be considered as an indication of future performance. These forward-looking statements speak only as of today's date, and the company undertakes no obligation to revise or update any statement made today. I encourage you to review all of the company's filings with the Securities and Exchange Commission concerning these and other matters. I'll now turn the call over to Brian Lian for his initial comments. Thanks, Stephanie, and good morning to everyone joining us on the call. Earlier this morning, we issued a press release describing the results for the primary endpoint from Viking's Phase 2b VOYAGE trial evaluating VK2809, our novel liver selective thyroid hormone receptor beta agonist in patients with biopsy-confirmed non-alcoholic steatohepatitis or NASH. We are pleased to share with you on this call an overview of the initial data and key takeaways from the study at this point. Following my prepared comments, we'll open the line for questions. Before we discuss the results, I'd like to remind everyone that we've only recently received these data. While we believe that we have enough information to report on the study's success on the primary endpoint, we have not yet had time to rigorously evaluate every lab value, biomarker, and line item in the data. As you might imagine, these datasets are large. We are still in the process of receiving and reviewing what are sure to be additional tables, figures, and sub-analyses. We'll provide additional updates moving forward as warranted. We also plan to present the results at a future medical meeting, so we may wish to preserve certain details until those presentations. As a reminder, VK2809 is an orally available tissue and receptor subtype selective agonist of the thyroid hormone receptor that possesses selectivity for liver tissue as well as the beta receptor subtype, suggesting promising therapeutic potential in a range of metabolic disorders. In a prior phase IIA trial in patients with non-alcoholic fatty liver disease, VK2809 successfully achieved both its primary and secondary endpoints, demonstrating significant reductions in liver fat and plasma lipids. In that study, cohorts treated with VK2809 experienced up to 60% median relative reductions in liver fat content, and the majority of patients receiving VK2809 experienced at least a 30% relative reduction in liver fat content. Another important benefit observed in the phase 2a study was VK2809's ability to reduce plasma lipids, including LDL cholesterol, triglycerides, and atherogenic proteins, all of which have been correlated with increased cardiovascular risk. The phase IIa trial also demonstrated VK2809's promising safety and tolerability profile. No serious adverse events were reported, and the rates of gastrointestinal disturbances, such as nausea and diarrhea, were lower among VK2809-treated patients when compared to patients treated with placebo. Based in part on these impressive data, the company believed that VK2809 represented a potentially best-in-class therapeutic for the treatment of NASH. The potential market for this indication is significant. In the U.S., NASH is a leading cause of cirrhosis and liver failure and is estimated to affect over 10 million Americans. Based on our prior clinical data and the high unmet medical need in NASH, we designed a phase IIb trial called VOYAGE to evaluate VK2809 in this setting. The VOYAGE trial is a randomized, double-blind, placebo-controlled, multicenter international phase IIb trial designed to assess the efficacy, safety, and tolerability of VK2809 in patients with biopsy-confirmed NASH and fibrosis. The target population includes patients with at least 8% liver fat content as measured by magnetic resonance imaging-proton density fat fraction, as well as F2 and F3 fibrosis. Up to 25% of patients may have F1 fibrosis, provided that they also possess at least one additional risk factor. The primary endpoint of the VOYAGE study, which we are reporting today, evaluated the change in liver fat content from baseline to week 12 in patients treated with VK2809 as compared to patients receiving placebo. Secondary objectives include an evaluation of histologic changes as assessed by hepatic biopsy after 52 weeks of treatment. The study randomized patients into five arms: placebo, 1 milligram every day, 2.5 milligrams every day, 5 milligrams every other day, and 10 milligrams every other day. As a reminder, the lowest dose of 1 milligram daily was intended to identify a minimally effective dose level and was therefore designed to enroll only half as many patients as the other arms. In order to accelerate completion of enrollment in the study, we elected last year to suspend enrollment of patients in both the 1 milligram daily dosing cohort as well as a middle dose cohort, which was enrolling patients into the 5 milligram every other day dosing arm. As a result, these two cohorts are enrolled at approximately half of their originally targeted levels of 37 for the 1 milligram cohort and 75 for the 5 milligram cohort. The remaining three cohorts enrolling placebo, 2.5 milligrams daily, and 10 milligrams every other day, proceeded toward their original enrollment targets of up to 75 patients per arm. Based on enrollment levels achieved last year and our powering assumptions for histology, we closed enrollment late last year at approximately 250 patients. This study size and structure allows us to remain well powered on histology endpoints in our two most important treatment arms, while also proceeding to the desired endpoint evaluation in a timely manner. Today, we are pleased to report that the study successfully achieved its primary endpoint, with patients receiving VK2809 experiencing clinically and statistically significant reductions in liver fat content from baseline to week 12 as compared with placebo. VK2809 treated patients demonstrated statistically significant reductions in LDL cholesterol, triglycerides, and atherogenic proteins compared with placebo. Specifically, the results demonstrated that patients receiving VK2809 dosed at 10 milligrams every other day, experienced a mean reduction in liver fat of 52% from baseline. Patients receiving 5 milligrams every other day experienced a mean reduction of 37% from baseline. Patients receiving 2.5 milligrams every day experienced a mean reduction of 45% from baseline. Patients receiving 1 milligram daily doses experienced a mean reduction of 17% from baseline. By comparison, patients receiving placebo experienced a 4% mean reduction from baseline. We also performed a responder analysis at week 12. As a reminder, in this setting, a responder is defined as a patient who experiences at least a 30% relative reduction in liver fat. Prior studies have shown that patients achieving this degree of liver fat reduction have a higher probability of demonstrating histologic benefit in NASH. In the VOYAGE study, after 12 weeks of treatment, patients receiving VK2809 experienced significantly higher response rates compared to patients receiving placebo. Among patients treated with VK2809 dosed at 10 milligrams every other day, 85% demonstrated at least a 30% relative reduction in liver fat. At 5 milligrams every other day, the response rate was 67%. At 2.5 milligrams daily, the response rate was 78%. At 1 milligram daily, the response rate was 53%. By comparison, the response rate among patients receiving placebo was 14%. Each of the response rates for VK2809 cohorts was statistically significant compared to placebo. It's interesting to note that when adjusted for placebo, the mean reductions in liver fat observed in this study are essentially the same as those observed in our prior 12-week NAFLD study. The similar efficacy observed in the current study is impressive, as the VOYAGE trial is much larger and enrolled a more advanced disease population of biopsy-confirmed NASH patients with fibrosis in the F2 to F3 range. In addition, the doses in the VOYAGE study are generally lower than those used in the prior 12-week study. We believe these data provide further evidence of VK2809's highly targeted delivery into liver tissue, which is an important differentiating characteristic of the molecule and a competitive advantage compared to other agents in development for NASH. It also speaks to the consistency of effect from thyroid receptor beta activation on liver fat across a range of disease stages. The VOYAGE trial also included an analysis of the effect of VK2809 on plasma lipids. These lipids, including LDL cholesterol, triglycerides, and atherogenic proteins, have been correlated with increased cardiovascular risk and a number of studies evaluating other NASH development programs have demonstrated elevations in these lipids following treatment. In the VOYAGE study, patients receiving VK2809 demonstrated statistically significant reductions in LDL cholesterol from baseline, ranging from 15% at the 1 milligram dose to 21% in the 10 milligram every other day cohort. By comparison, patients receiving placebo demonstrated LDL cholesterol reductions of 1% from baseline. The robust reductions in these lipids are consistent with those observed in our prior phase IIa study and provide further evidence that VK2809 may offer a cardioprotective benefit. Turning to safety. Consistent with the prior 12-week phase IIa study, VK2809 was shown to be safe and well-tolerated in this study. As of the early March cutoff for safety data, adverse event rates were similar among patients randomized to VK2809 compared with placebo. Discontinuations due to adverse events were also low and well-balanced among VK2809 treated patients and placebo patients. Turning to tolerability, as in all prior studies, VK2809 continues to demonstrate an excellent tolerability profile. In particular, there were no clinically or numerically meaningful differences in gastrointestinal-related side effects such as nausea, diarrhea, or stool frequency among VK2809-treated patients compared with placebo. Liver function tests, including ALT, AST, bilirubin, direct bilirubin, and alkaline phosphatase were similar among VK2809-treated patients and patients receiving placebo. There were no numerically or clinically meaningful differences in thyroid hormone markers among treated versus placebo patients. On vital signs, VK2809-treated subjects demonstrated no changes to blood pressure, heart rate, or body weight relative to placebo. The VOYAGE study also includes an exploratory assessment of biomarkers that may be relevant for predicting histologic changes in NASH. While 12 weeks is likely too early to definitively assess histologic benefit, modest but statistically significant reductions from baseline were observed in certain measures, including the ELF Test, NIS4, and TIMP-1. We'll continue to assess these through the course of the 1-year treatment window. Overall, we believe the impressive efficacy signals observed in this study, combined with the benign safety and excellent tolerability profile, provide meaningful differentiation for VK2809 relative to other development programs for NASH. In summary, I'd like to say that we are happy to report positive results from this study with mean placebo-adjusted liver fat reductions in excess of 40 across relevant treatment arms and response rates ranging up to 85%. We believe these data bode well for potential histologic benefit for these patients. Finally, as just described, we are encouraged by the consistent safety and tolerability profile as reaffirmed in this study. We look forward to sharing the histology data from this study in the first half of 2024. In closing, I'd like to thank the investigators and patients who have participated and continue to participate in the VOYAGE trial. I'd like to thank our employees here at Viking for their outstanding work in successfully executing this study. I'll stop here and open the line for questions. Ladies and gentlemen, at this time, we'll begin the question-and-answer session. To ask a question, you may press star and then two using a touch-tone telephone. To withdraw your questions, you may press star and two. If you are using a speakerphone, we do ask you please pick up the handset prior to pressing the keys to ensure the best sound quality. With these instructions in mind, once again, if you would like to press star and one to join the question queue. We'll pause momentarily to assemble the roster. Our first question today comes from Joon Lee from Truist Securities. Please go ahead with your question. Hey, guys. Congrats on the positive data. Thanks for taking our questions. Impressive efficacy and tolerability. Just, you know, one SAE on the drug arm. Can you elaborate a little bit more on what the symptoms were that this patient exhibited and in which dose arm this happened? Thank you. Yeah. Hey, Joon. This was a patient with a past history of attempted suicide and suicidal ideation and depression who experienced an episode of suicidal ideation and depression. That was in, I think it was a 10 mig QOD arm, but I'm not positive on that one. Got it. you know, as a go-forward strategy, 2.5 milligrams QD and 10 milligrams QOD they both look pretty viable. do you have a preference at this point as to what could be a Phase III dose? Thank you. Great question, Joon. We don't yet. I think the best thing to do here is wait for the histology data, which we'll receive next year, and then we'll have a much better view of what's the better arm. I think we have two great choices at this point. Okay, one last one. Will this be presented at EASL or has that passed the submission for abstract? We're probably gonna present this at AASLD and not EASL. Thank you. Thanks, Joon. Our next question comes from Naz Rahman from Maxim Group. Please go ahead with your question. Hi, guys. Congrats on the data. Thanks for taking my question. Just I wanna talk with the GIAE and tolerability a little bit. Did you find that the GI GIAE were transitory, or did they generally occur early in the trial? Uh, actually- Sorry. I'm sorry. Go ahead. Yeah. Did they, like, occur early in the trial, or were they just, like, consistent throughout the course of the trial? Honestly, they were so low that we didn't do a time course analysis. I mean, they're no different from placebo. I didn't think that exercise was worthwhile. Did any of the patients have to take any medications to manage any of the GI AEs? They were no different from placebo, so we didn't, I don't know if anybody received medication for them. They were pretty much zero across the board. Gotcha. Just one more question. Just on the liver fat reduction, did you see a similar magnitude of liver fat reduction in the F2 and the F3 patients, or did you see different, I guess, rates of efficacy between the two groups? We don't have that stratum, that level of detail on the data just yet. Got it. Thanks for taking my questions. Thanks, Don. Our next question comes from Jay Olson from Oppenheimer. Please go ahead with your question. Oh, hey, congrats on these results, and thank you for the update. Based on this level of MRI-PDFF reduction, can you talk about any thoughts you have about how the biopsy data may turn out and also the timing of that? I had one follow-up, if I could please. Yeah. Thanks, Jay. You know, there have been multiple prior studies that do indicate a correlation between increased liver fat reductions and histologic benefits, including NASH resolution and fibrosis regression. These are the largest liver fat reductions that we're aware of from an oral agent at this stage of development. To the extent that is a good predictor, we feel good about the probability of success on the histology endpoints. We expect to have those data in the first half of next year, and it's a little too early to narrow that further at this time. Okay. Great. Thank you. Sorry, go ahead. Oh. No, I just said thanks. Since you have two successful and very significant opportunities in front of you now, can you just talk about how you'll prioritize those and especially with regards to capital allocation and any additions you may need to make to your organization? Yeah. It's a great question. Fortunately, we're very well capitalized now, so it's pedal to the metal on both programs. We will be adding staff in key areas, for clinical support, and regulatory affairs. We won't grow too aggressively. We'll just add as needed. I think we've done a lot with an extraordinarily lean organization, and we've demonstrated really consistent high productivity. I don't, I don't think we're planning to grow immensely, but we'll add where we need to add moving forward. Okay. Great. Congrats again on these results. Thanks for taking the question. Thanks, Jay. Our next question comes from Annabel Samimy from Stifel. Please go ahead with your question. Hi. Thanks for taking my question. Congratulations on some pretty strong results. You know, it looks like I know that you're just still doing some analyses on the doses and waiting for the histological data, but it looks like you have a pretty good range of doses there. Just backtracking a little bit, how did you choose which doses to stop at 50% enrollment, and why? Is it possible that you might go with all three doses just to give patients different options going forward in terms of dosing? Yeah. We'll probably choose 1 or 2 doses to move forward with. We felt that the 1 milligram, since that was always intended to be simply an exploration of the minimally effective dose, that that could be trimmed without any meaningful impact on the study. Then we felt that having a daily and an every other day cohort complete the study would be useful for comparison. We chose the higher dose on the 10 mg QOD and then the 2.5 mg on the daily. Okay. Got it. In terms of the side effect profile, I understand that you barely had any tolerability issues in AE. Was there any, kind of dose response related to, the side effect profiles, or was it pretty clean across the board? It was very clean. Actually, it's interesting. The 1 milligram you know, smallest cohort, but that seemed to have more AEs, and I think that's just a function of small numbers, but nothing dose related at all. Okay. Got it. Just on the, in the histological endpoints, I guess I just wanted to clarify, you said you saw both, clinically and statistically significant differences on those histological endpoints, or it's still too early to sort of draw any conclusions from that? On the, on the markers. No. On the biomarkers. I apologize. Yeah. They're very modest differences. I think it's a little early to pound the table on those at this point, but they are statistically significant. pretty modest at this point. It'll be interesting to see how those mature. Okay, great. Thank you so much. That was helpful. Thanks, Annabel. Our next question comes from Joseph Pantginis from H.C. Wainwright & Co. Please go ahead with your question. Hey, guys. Good morning. Congratulations on the data. Brian, I wanted to start with a little historical perspective on two fronts. First, I wanna offer my congratulations 'cause having covered you from essentially the beginning, you know, and I don't wanna jinx this, but you're essentially four for four now with your clinical programs, including two from VK2809. That, being part done, congratulations on that. Secondly, with regard to the AE profiles now and what you're seeing from these two robust data sets, there had been a very long-term bear case, however you wanna call it, regarding cardiovascular events and the potential for cardiovascular events for VK2809. Do you feel you've put this to bed at this point? Well, thanks, Joe, for the kind words at the beginning of your comments. Really appreciate it. With cardiovascular safety, there's never really been any issue with cardiovascular safety. That's always been sort of the boogeyman out there, but never been any signal of cardiovascular imbalances or signals in any study. This is the ninth study that VK2809 is in. In the current study that holds true as well. There's absolutely zero imbalance in cardiovascular AEs among treatment arms. Yes, I really appreciate that. I'll take today's data and obviously waiting for additional updates, but I'll take the leap forward now and say, do you wanna take any, at least broad strokes with regard to regulatory next steps? Yes. We would hope to complete the study, you know, in the first half of next year, at least have the data in the first half of next year. Talk to the FDA in an end-of-Phase 2 meeting, probably, you know, toward the end of next year. Great. Thanks a lot, and congrats again. Thanks, Joe. Our next question comes from Steven Seedhouse from Raymond James. Please go ahead with your question. Hey, good morning. Thanks for hosting the call and taking the question. Wanted to ask about, it's interesting that at 12 weeks in both your study and also for the resmetirom phase II study, there's no improvement in ALT at week 12, although with resmetirom, it seems like it manifested at week 52 in their phase III based on what they've reported. I'm curious why you think that is given, you know, the liver size change being profound. You talk about signals being apparent already on some of the non-invasive fibrosis markers. I mean, do you expect basically a statistically significant improvement in liver function test to manifest over time? Thanks, Steve. We do see, you know, a modest, I'd say small numerical improvement in the treatment arms versus placebo at this point, but it's not statistically significant. I don't know that it's clinically meaningful. I think the baselines for patients on ALT in these studies is always very noisy. I mean, it's not uncommon to see a 50% change in ALT between a screening visit and a randomization visit. It's not a great marker in our view. We do think that this mechanism is a little slower to manifest those ALT changes. Over a longer period of time, we would expect to see that come into play. Overall, it's a pretty noisy marker. Got it. Just one last point of detail at least on this psychiatric essay. I'm curious why it was even being treatment-related. Is it just a general association between hypothyroidism, I guess, and food disorders, or did this patient specifically have some excursions on like TSH or anything in the thyroid hormone axis that caused the investigator to draw a link there? Then if you wanted to just widen the lens and comment in general, is thyroxine use or sort of exclusion thyroid hormone axis something that was prevalent in this study at 70 degrees? Thanks. On thyroxine use, there were some individuals who were on baseline thyroxine. You could enter the study if you had well-controlled hypothyroidism with meaning a stable dose of thyroxine. there were some people in the study who were on, you know, stable doses of thyroxine. With the person with the suicidal ideation had a history of suicide attempts, bipolar disorder, schizophrenia, just a very long list of psychiatric issues, probably should not have been enrolled in the study, but was not forthcoming about those historical issues on enrollment. there was an episode of suicidal ideation and depression. we have no... I mean, there's no correlation between the thyroid hormone and depression or anything like that. As a matter of fact, our understanding is that there's another company, exploring a thyroid hormone agonist for the treatment of, major depressive disorder. I'd say the converse would be what might be expected. All right. Thanks so much. Bye-bye. Thanks, Steve. Our next question comes from Thomas Smith from B. Riley Securities. Please go ahead with your question. Hey, guys. Good morning. Thanks for taking the questions. Let me add my congrats on the data. I guess first, can you, just remind us of the biopsy read methodology you used to enroll these patients and, how you're planning to evaluate the histology endpoints at week 52? I know you could enroll up to 25% F1 patients, but do you have a sense of the, kind of the split between F2, F3 versus F1 in these cohorts at this point? Yeah. Thanks, Tom. we don't have that breakout just yet, but the last update that I received, which was a few months ago, was that it was working out to be about 25% F1 and about 75% F2 and F3. we were tracking on in line with what the study was designed to allow. With the pathology read, we use a single reader who when anybody is on the borderline of, you know, F2 and F3 or anybody with a baseline NAS of four, they automatically go to a second reader. the first and second readers must reach consensus for the person to be characterized properly and enrolled in the study. At the end of the study, the same approach will be used. Okay. Got it. That's helpful. Just on safety, I was wondering if you could just elaborate on some of the reasons for treatment discontinuation related to adverse events. Was there any pattern there related to any specific AE or organ system? No, no. They were pretty low across the board. I don't have that list in front of me, but there was nothing, that you could say was clustered or anything like that. It was just low across the board. Okay, great. Got it. Thanks for taking the questions, guys. Appreciate it. Thanks, Tom. Our next question comes from Scott Henry from ROTH Capital Partners. Please go ahead with your question. Thank you. Good morning. Congratulations, Brian. Just a couple questions. First, I wanted to ask about the rationale. For the differences in liver fat reductions between the 2.5 milligram once a day and the 5 milligram every other day dose, do you think that's, you know, due to the baseline stats? It looks like a little lower liver fat in the every other day dose, just curious your take on the differences there. Yeah. That's a good question, Scott. I don't know the differences or why they arise. It seems like when you go to the pulsatile approach, you might wanna use a slightly higher dose, though. And we saw that, I think, in the prior study as well. The 5 mg daily was at least as good on many metrics as the 10 mg every other day in the prior study. Here you're seeing the 2.5 mg daily as good or better than the 5 mg every other day. When you go to that intermittent dosing, higher doses might be useful for better efficacy. I think that's all we can say at this point. Do you think that the baseline impacts the efficacy as well? I mean, typically it's easier to show a bigger difference in a sicker patient. Yeah, it could. What we've seen, at least in the prior study, is that it didn't have that big an effect. I think it could have some modest impact if you have a higher baseline to have a larger% reduction. It just wasn't that clear in the prior study that was indeed the case. Okay, thank you for the color. Just on the adverse event profile, the 10 milligram every other day dose had slightly higher adverse events. Just curious your take as to the clinical relevance of those differences. Do you view those as material, or do you view that more as noise? Just your overall take on the way the adverse event profile changed over doses. We don't think it's material. You know, there was 1 SAE in the entire study. I think that's important. When you look at the rates of treatment-emergent adverse events that lead to discontinuation, that's another important metric. Really, you know, no difference from placebo there. I don't think there's any meaningful read on a modest change in AEs as you go across doses here. All doses were really, really well tolerated. Okay. great. Thank you for taking the questions. Thanks, Scott. Our next question comes from Andy Tsai from William Blair. Please go ahead with your question. Great. Thanks for taking my question, and congratulations to the Viking team. I have one followed by some housekeeping questions. Brian, obviously after 12 weeks of treatment, this is just a snapshot. I'm just wondering if you can comment either on MRI-PDFF or the lipid panel. What trend lines are you thinking? Are they all still trending down and therefore with longer follow-up you should have a more profound, you know, efficacy results, as we kind of look into 36 weeks or longer? You know, in terms of the PK/PD profile, kind of following the previous question, do we know if the 2.5 every other day and 5 every... Sorry, 2.5 every day and 2.5 every other day are, you know, there are really significant differences in terms of PK/PD or half-life? Yeah. The exposures between those two arms are pretty similar. It may be that when you dose just more regularly, you see the slightly greater effect. I don't think if you ran a statistical significance between those two arms, and we haven't done that, I doubt they're statistically significantly different. With respect to the time course of changes, you know, what we have seen in prior reports of thyroid agonists is that efficacy does tend to trend a little higher with prolonged use. We'll see how that pans out in this study, I think we're starting from a great week 12 magnitude. If it grows from here, we'd be thrilled. If it stays the same from here, I think it's still the greatest effect so far from an oral agent. We're satisfied there. On plasma lipids, you generally don't see an improvement beyond 12 weeks on LDL and trigs. Having them improve at all is a great characteristic of this mechanism. Great. Maybe one last one. Do we have a sense of what percentage of patients enrolled in the trial have Type 2 diabetes? Oh, that's a great question. We do know that. I don't have it off the top of my head. I just don't have that handy. We do know those data. There are Type 2- Okay Right. Right, right. For sure. Absolutely, given the overlap. Okay, sounds good. Congratulations again, thanks for taking our questions. Thanks, Andy. Our next question comes from Justin Zelin from BTIG. Please go ahead with your question. Hi, Brian. Thanks for taking the question. Congrats on these very impressive results. Maybe just a quick question on the adverse event profiles. They were noted drug-related treatment adverse events that were not GI related. I was wondering if any were accumulated and if, you know, there are any of interest that you could speak to. Well, the those adverse event tables are many, many, many pages long, so, you know, you have headache and, you know, dizziness, those sorts of things that show up. We had examples of COVID. That wasn't drug-related, but just another example of an AE that shows up in these tables. There was no, you know, obvious trend or pattern to adverse events that would differ among treated and placebo patients, though. I think that's the key. That's, again, you know, kind of confirmed when you look at the overall drug-related treatment emergent adverse events. Actually, the rate was slightly lower in the treated arms versus placebo and in the treatment emergent adverse events leading to discontinuation, also, lower rate versus placebo. All of the arrows there, sort of point in the same direction, and it speaks to the excellent tolerability profile of the drug. As a reminder, you know, before we started this study, there were 8 completed studies, and there was never an SAE observed in a treatment arm. Just confirmed in this data set how well-tolerated the drug is. Got it. That makes sense to me. Just to follow up on the last question, I don't know if you have this data yet, but did you notice any trends for patients who were diabetic in the trial, whether they performed differently than those who did not have diabetes? We haven't looked yet. We haven't received the efficacy sort of stratified like that yet on, you know, fibrosis, diabetes presence or absence. We will be looking at that. We just haven't received that yet. Got it. Maybe for my last question, are you able to comment on the usage of GLP-1 medications or tirzepatide in the study and whether it was balanced between the arms? Yes. There was an exclusion criterion. If you were on a GLP-1 agonist, you had to be on a stable dose for at least 3 months prior to entry. If you initiated treatment with a GLP-1 agonist during the study, you had to be discontinued because it was a contraindicated medication. There were a couple like that were discontinued, despite our or the investigators urgences to have people not go on a GLP-1 agonist. Some people did anyway, and they were discontinued, but those numbers were relatively small. Got it. Great. Thanks so much for taking my questions and congrats once again. Thanks a lot, Justin. Ladies and gentlemen, with that, we'll be concluding today's question and answer session. I'd like to turn the floor back over to Stephanie Diaz for any closing remarks. Thank you, everyone, for joining us today. Thank you for your continued support of Viking Therapeutics. With that, we will end the call. Have a great day. Ladies and gentlemen, with that, we'll conclude today's conference call and presentation. We thank you for joining. You may now disconnect your lines.