Viking Therapeutics, Inc. (VKTX) Earnings Call Transcript & Summary

Welcome to the Viking Therapeutics Phase II VENTURE-Oral Dosing Study Top line Data Conference Call. [Operator Instructions] As a reminder, this conference call is being recorded today, August 19, 2025. I would now like to turn the conference 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; Karen Modesto, the company's Executive Director, Clinical Development; and Greg Zante, Viking's Chief Financial Officer. Before we begin, I'd like to caution that comments made during this conference call 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, time lines and milestones. Forward-looking statements are subject to risks and uncertainties that could cause actual results to differ materially and adversely, and 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 today. Earlier this morning, we issued a press release describing the top line results from Viking's Phase II VENTURE-oral dosing trial evaluating VK2735, our dual agonist of the glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide receptors in adults with obesity. We are pleased to share with you on this call an overview of the initial primary and secondary endpoint data as well as key takeaways from the study at this point. Before we discuss the results, I'd like to remind everyone that we have only recently received these data. While we believe we have enough information to report on the study's success on the primary and secondary endpoints, we have not yet had time to rigorously evaluate every line item in the data, nor have we received all of the results that we ultimately expect the study to generate. As these are top line results, there may be differences in certain elements of the data that arise upon receipt of the final results later this year. We would not anticipate these potential changes to have a significant impact on the 13-week results we are reporting today. As additional data become available, we'll provide further updates. We also plan to present the results at future medical meetings, so we may wish to preserve certain details until those presentations. As a reminder, VK2735 is a dual agonist of the GLP-1 and GIP receptors in development for the potential treatment of obesity. Co-activation of these receptors has been shown to decrease glucose, reduce appetite, lower body weight and improve insulin sensitivity in patients with obesity, type 2 diabetes or both. Due to these 2 mechanisms having complementary activities, this approach has shown generally improved therapeutic benefits compared with GLP-1 monoagonism. During the first quarter of 2024, Viking announced positive results from a Phase II study, which we call the VENTURE study that was designed to evaluate the efficacy, safety and tolerability of VK2735 dosed weekly by subcutaneous injection for 13 weeks. This trial successfully achieved its primary and secondary endpoints. Subjects receiving VK2735 demonstrated statistically significant reductions in body weight from baseline ranging up to 14.7%. The results also showed that treatment with VK2735 was safe and well tolerated through 13 weeks of weekly subcutaneous dosing with the majority of reported adverse events characterized as mild or moderate. Based on the VENTURE Phase II study results and following receipt of feedback from a Type C meeting and the subsequent end of Phase II meeting with the FDA, the company advanced the subcutaneous formulation of VK2735 into Phase III development for obesity. In June, we announced the initiation of the VANQUISH Phase III registration program. The VANQUISH studies consist of 2 trials evaluating VK2735, one in adults with obesity and one in obese or overweight adults with type 2 diabetes. Enrollment in both of these studies is continuing. In parallel with the development of the subcutaneous formulation of VK2735, Viking has also been developing an oral tablet formulation of this compound. The company believes a tablet formulation could represent an attractive treatment option for those who may prefer to initiate treatment with an oral therapy or for those seeking to maintain the weight loss they have already achieved. An important differentiator of our obesity program is that it includes both a tablet formulation and a subcutaneous formulation that utilize the same molecule. We believe this may mitigate potential safety or tolerability challenges that can occur when transitioning patients from one treatment to another. In a prior Phase I study, the oral formulation successfully achieved its objectives with cohorts receiving VK2735 demonstrating dose-dependent reductions in mean body weight from baseline ranging up to 8.2% after 28 days of daily dosing. The oral formulation of VK2735 also demonstrated encouraging safety and tolerability through 28 days of once-daily dosing at doses up to and including 100 milligrams. The majority of observed treatment-emergent adverse events were mild or moderate with most reported as mild. These results were presented at the 2024 Obesity Week Conference last November. Based on these Phase I results, earlier this year, the company announced the initiation of a Phase II study of oral VK2735 in subjects with obesity. This study called the VENTURE-oral dosing study was a randomized, double-blind, placebo-controlled multicenter study designed to evaluate the safety, tolerability, pharmacokinetics and weight loss efficacy of VK2735 dosed as an oral tablet once daily for 13 weeks. The primary endpoint of the study was the percent change in body weight from baseline after 13 weeks of treatment. Secondary and exploratory endpoints evaluated a range of additional safety and efficacy measures. In March, the company announced that enrollment in the VENTURE-oral dosing study had been completed. The trial enrolled 280 adults who were obese or who were overweight with at least one weight-related comorbid condition. Participants were evenly randomized to 1 of 6 dosing arms or placebo. Earlier today, we issued a press release announcing the top line results of the VENTURE oral dosing study. We are pleased to report that this trial successfully achieved its primary and secondary endpoints with subjects receiving oral VK2735 demonstrating statistically significant reductions in body weight compared with placebo. Additionally, the results showed that treatment with oral VK2735 was safe and well tolerated through 13 weeks of daily dosing with the majority of the reported adverse events being categorized as mild or moderate. On the primary endpoint, subjects receiving oral VK2735 demonstrated statistically significant reductions in mean body weight from baseline ranging up to 12.2% as well as statistically significant reductions in mean body weight relative to placebo ranging up to 10.9%. Weight loss in all treated cohorts appeared to be progressive through 13 weeks and did not show evidence of plateauing. Statistically significant differences compared to placebo were observed for all doses above 15 milligrams starting at week 1 and were maintained throughout the 13-week treatment period. We believe the results suggest that further weight loss could be achieved through extended dosing beyond the 13-week treatment period of this study. In support of this, available data from participants being evaluated for pharmacokinetic measures demonstrate continued weight loss through the week 16 assessment visit. Key secondary endpoints in this study included an evaluation of the proportion of subjects achieving at least 5% and 10% weight loss after 13 weeks of treatment. All cohorts receiving VK2735 oral at doses above 15 milligrams demonstrated statistically significantly higher proportions of subjects achieving 5% and 10% weight loss relative to placebo. Up to 97% of subjects in the VK2735 treatment groups achieved at least 5% weight loss compared with 10% for placebo and up to 80% of subjects in VK2735 treatment groups achieved at least 10% weight loss compared with 5% for placebo. The VENTURE oral study also included an exploratory dosing arm designed to evaluate the transition from a high daily dose to a low maintenance dose. This arm was intended to help us understand the potential to transition subjects to low doses following induction of weight loss with either the injectable or high-dose oral formulations. Participants in this arm were rapidly titrated to 90 milligrams daily doses and maintained at 90-milligram daily for 4 weeks. These subjects were then titrated back down to 30-milligram daily doses and maintained at 30-milligram daily for the remaining 7 weeks of the study. At the time of dose reduction, mean weight loss observed in this cohort was 8.1%. Following the 7-week maintenance period at 30 milligrams, mean weight loss had improved further to 9.2%. These results suggest that low-dose maintenance therapy may represent an effective means of retaining and potentially further extending weight loss that has already been achieved. In addition, these data, along with the gradual weight loss observed in the 15-milligram daily cohort suggests that doses below 30 milligrams daily may also provide effective weight maintenance. Turning to safety and tolerability. Oral VK2735 demonstrated encouraging safety and tolerability with the majority of observed adverse events being reported as mild or moderate. Treatment and study discontinuation rates among VK2735-treated cohorts were generally dose-dependent with higher dose cohorts demonstrating slightly higher rates than placebo. Approximately 11% of VK2735-treated subjects discontinued the study early compared with approximately 5% for placebo. Treatment-emergent adverse event rates in the study were marginally higher in the VK2735-treated cohorts relative to placebo, driven primarily by expected differences in gastrointestinal-related events. With respect to severity, 99% of observed GI adverse events in the study were reported as mild or moderate. Nausea was reported among subjects receiving both VK2735 and placebo. Among subjects receiving VK2735, 99% of reported nausea was characterized as mild or moderate. Vomiting was reported in 26% of VK2735 treated subjects compared with 10% among subjects receiving placebo. Consistent with what was reported in the prior Phase II study of injectable VK2735, GI-related adverse events were most prevalent in the first week of the study with observed rates generally declining through the course of the study. Across the combined study arms, weekly rates of nausea or vomiting did not exceed 5% at any point after the third week of treatment. We believe GI-related adverse event rates might be further reduced through lower starting doses and/or slower dose escalation. In summary, we are excited to share the top line results from this study, and we believe they provide support for the continued development of oral VK2735 for the treatment of obesity. The promising early efficacy profile observed in this study, combined with the encouraging tolerability and safety profile to date suggest oral VK2735 could provide an important future treatment option for patients with obesity. In addition, the results of the exploratory maintenance dosing cohort provide an encouraging proof of concept that transitioning patients to low-dose maintenance therapy could represent an effective approach to long-term weight control. We look forward to evaluating this further in an upcoming study expected to begin later this quarter. In closing, I'd like to thank the investigators and patients who participated in the VENTURE-oral dosing trial, and I'd like to thank the clinical, CMC and all supporting staff here at Viking for their outstanding work in successfully executing this study. Thanks for joining us today, and I'll stop here and open the line for questions.

[Operator Instructions] The first question is from Steve Seedhouse of Cantor.

First, I just wanted to ask, Brian, what you attribute the higher adverse event rates in this trial versus the Phase I oral study to? And I have a follow-up.

Steve, thanks. Yes, I think it's important to note the placebo rates were also higher than we saw in the earlier study. And when you look at the delta between the treated arms, it's not very big. The 90 might be the largest there. But overall, it's reasonably flat across doses there relative to placebo. And I don't know why the placebo was higher and the baseline rates were higher here. It could be -- and this is speculation, but it could be that there is such an expectation with this mechanism for GI-related adverse events that it maybe makes people a little bit more sensitive or expecting them and could raise the reporting rates. I think that another contributor could be the relatively rapid titration rates we had here. The Phase I suggested we could titrate quickly. We did titrate quickly. I think moving forward, we would probably slow down that titration rate. And I think it's important to note when you look at other recent studies, the placebo rates for both nausea and vomiting seem to be a little elevated versus the historical rates reported in obesity studies. And that might reflect the earlier comment I made about sort of the heightened expectations of GI adverse events.

I just -- I wanted to follow up the -- I think most people have already assumed that anything maybe at 60 milligrams or higher wouldn't, let's say, be optimal from a cost standpoint. But obviously, it's good to see the bioavailability is still higher at those doses. But I just wanted to confirm, is 30 milligrams, in fact, commercially viable from your perspective, from a cost and margin standpoint, using today's API costs? And then is it fair to say given that and given the totality of the clinical data here, the 30 milligrams is sort of the sweet spot for dosing the oral formulation going forward?

Yes, Thanks. I think the 30 is absolutely commercially viable, and I think higher doses are also commercially viable. I think a really important finding from this study was the maintenance arm, where there was this temporary high dose applied followed by a low maintenance dose, and we saw a pretty robust reduction in body weight and then a further reduction in body weight following transition to the lower dose. And when you look at the 15-milligram arm overall versus baseline, that's also trending down throughout the course of the study. So it might suggest that for real maintenance, a dose below 30 might be even as effective as the 30.

The next question is from Joon Lee of Truist Securities.

For the maintenance cohort, how are you able to deconvolute the variable that patients on 30-milligram cohort are still losing weight at week 13. And also, can you elaborate a little bit on the study that's due to start later in the quarter to show improvement in GI tolerability using maybe optimized titration regimen?

Thanks, Joon. Yes, on the maintenance cohort, people were transitioned from 90 milligrams to 30 for 7 weeks, and it was its own cohort. So I'm not sure. I mean, there wasn't any deconvoluting. They were assessed like the other cohorts and at all time points after week 1 showed a statistically significant difference versus placebo. Sorry, I forgot the second part of the question.

So you're planning to start a trial later in the quarter and that trial hopefully incorporates some titration regimen to ameliorate some of the GI tolerabilities? And also, are you able to break out discontinuations due to GI AEs? I think Lilly reported it that way instead of just the overall discontinuations that you're reporting.

Yes. Yes. Thanks, Joon. Yes, the maintenance study starting later this quarter, we'll look at a variety of both subcu monthly doses as well as oral doses. And the results of this study are going to inform the optimal doses to use in the maintenance setting. So we don't have all the data yet, but we'll use the data set here to help us plan that study. Yes. And for the discontinuations due to GI adverse events, there was one in the placebo and one in the 30-milligram dosing arm. So what we observed and what we mentioned in the press release, I think, is GI adverse events tended to happen early and then pretty rapidly resolved. And so we've always felt that this is a signal that is tunable and we've seen this in other studies. If you can titrate more slowly that should reduce the incidence of GI adverse events. But even when they occur, they seem to resolve fairly rapidly with continued dosing.

And sorry, Brian, just a clarification. So are you saying that a lot of the discontinuations were actually not related to GI AEs? And if so, what drove discontinuations that is not GI related?

Yes. There were -- I'd say the majority of the discontinuations of treatment. What I mentioned was discontinuation of the study, people who just discontinued the study completely. Discontinuation of treatment was primarily driven by GI adverse events, and that was primarily driven by nausea rates across all arms. Those are in the table there in the press release.

The next question comes from Jay Olson with Oppenheimer.

We're curious about the 120-milligram dose, which seems to have slightly better efficacy than the 90 milligrams, but 120 milligrams may have significantly higher discontinuation compared to the 90 milligrams. So -- are you planning to continue studying the 120-milligram dose? Or do you think 90 milligrams is the top dose for future studies? And then we have one follow-up if we could.

Yes. Thanks, Jay. It's -- I think it's premature to identify the go-forward doses until we have the full complement of data and the sort of the PK curves that tell us exposure response data. But for that -- for all of these arms, I think a slower titration rate would likely reduce the -- any sort of a tolerability signal.

Okay. And then I guess if we did assume that maybe we could exclude the 120-milligram dose from these study results, how would you compare the discontinuation rates from VENTURE-oral to the discontinuation rates of orforglipron in Phase II, considering the fact that was a longer study. I think it was 36 weeks. And maybe having seen what the trajectory of discontinuation was, did it slow down significantly at the end of the 13 weeks? Or I guess, just how would you compare those 2 studies in terms of discontinuation?

Yes. I don't have the trajectory of discontinuation rates for either study in front of me. We have mapped out the incidence of adverse events, but I don't know those data, especially for the orforglipron Phase II trial.

The next question comes from Mayank Mamtani with B. Riley Securities.

The 90 mg to 30 mg maintenance dose transition cohort weight loss data obviously looks quite interesting, Brian. Are you able to speak to what the GI AE profile was for that cohort? And was it consistent with, for example, the 90 mg cohort that you reported in the table earlier? And wonder if 60 to 30 seems like a sweet spot versus maybe 90 to 30 as you think about what that sweet spot would be for you?

Yes. Thanks, Mayank. The 90 to 30 was titrated a little more rapidly than the flat 90, but the adverse event profile was pretty similar. I think with all of these more steady, like a 4-week block would probably be ideal as far as the titration rate. But overall, the 90/30 was pretty similar to the flat 90.

And when will we see the time course kinetic profile of the GI AE that you're kind of qualitatively are talking about, but we'll get to compare that to the VENTURE data that you reported earlier? Is that planned for obesity week or something?

Yes. We'll probably have some data, not on obesity week, but updating our corporate deck. And the time course does look I would say, very, very similar to the graphs that were in the poster for the subcu formulation back at Obesity Week in November.

The next question comes from Mike Ulz of Morgan Stanley.

Maybe just a follow-up just for the upcoming maintenance study, Brian, you mentioned maybe a slower titration would help reduce GI effects. I'm just curious if there's other like key learnings from the data you shared today that will help inform that study realizing it's still early here, but any thoughts there?

Yes. So the goal of that study will be the transition from weekly to monthly or weekly to oral. It won't be sort of an exploration of tolerability. I think we have an idea on what the tolerability profile looks like. So the learnings from this study really as they relate to the planned study are on the maintenance cohort and then ultimately, what the exposure response data show once we get the PK data.

The next question comes from Annabel Samimy with Stifel.

So clearly, you have some very competitive efficacy definitely at the higher end and even at the mid dose, and it seems that you have a lot of room to balance that with the tolerability given where others are coming out. So with this information, how do you think about the dose range going into the next trial? Do you think you need to test as a wide range, I guess, a wide range would give you plenty of flexibility compared to some others that seem to be capped at a certain level. But how are you thinking about the range of dosing going into the next trial? And then just as a quick follow-up, like the injectable Phase II venture, do you think you have enough information to move into Phase III with the oral at this point?

Yes. Thanks, Annabel. With respect to the second question, I think premature to speculate in the absence of the dose response -- exposure response data that we hope to get later, maybe towards the end of this quarter. With the dose range for a subsequent study, whether that's a IIb or III, it would probably tighten a little bit from here, but it will be multi-dose study, but what would the top and bottom doses be, I don't know at this point. It's just hard to speculate without the full complement of data.

The next question comes from Biren Amin of Piper Sandler.

Maybe if I could just ask around the high discontinuation rate, specifically across all doses, including the placebo group. Was that due to the -- was there like a carrier or an excipient that was included in the placebo group that may have caused the higher rates of nausea and vomiting that have been seen in this study compared to other obesity trials? And I have a follow-up.

Biren, yes, thanks. No, I don't think it's anything related to other components of the tablet. We noted in earlier comments, the placebo rates have escalated a little bit. We saw in, for example, a study at ADA this summer, a placebo arm that had up to 60% vomiting and up to 60% nausea with nothing particularly unique in that formulation. So it seems to be -- and again, this is speculation, it seems to be -- we're in a little bit of a different world now from when we initiated that subcu study and the first oral study. Everybody knows somebody who's on a GLP-1 therapy and everybody knows the GI adverse events that are sort of expected from this mechanism. And that likely contributed to maybe a little bit of a sensitivity to people looking for it and it gets reported a little bit higher. I don't know, but there's nothing in the formulation that would have led to an elevated adverse event profile.

Got it. And then what's the difference between discontinuation treatment early versus discontinued study early? I would assume that if one discontinues treatment early, would they also not discontinue from the study?

No. And it's an important point. Discontinuation from the study is people drop out of the study completely and don't return to their clinical sites for any follow-up visits. And the way we kind of look at that is it's a little bit of a proxy for someone who has a really bad experience, whether it's an AE or something else. They are just done with the study and they don't return. Discontinuing treatment means you've stopped taking the therapy but continue to return to the site for your scheduled clinic visits, but you're not taking the treatment anymore.

The next question comes from Ryan Deschner of Raymond James.

Just curious what you now see as the ideal titration rate for subsequent studies based on this? And regarding details on discontinuations not associated with adverse events, what did that break down for reasons look like?

Yes. Thanks, Ryan. For that, I would say withdrawal of consent, I don't have the table in front of me withdrawal of consent is probably the highest reason for discontinuation. And as far as the cadence for future studies, probably a 4-week block would be preferred if we were to start a little bit lower in dose and spread the steps out a little bit. I would anticipate different time course of AEs and a different overall AE profile. It is important to note, though, even with this accelerated titration rate that the incidence of nausea, vomiting, constipation, diarrhea dropped off precipitously after the third week and really from week 1 to week 2 precipitously, a little bit of a bump up in week 3 as that was the first titration step. But then subsequent weeks, even with an up-titration did not show an increase in any GI adverse events. So it really is quite similar to the subcu profile.

The next question is from Andy Hsieh with William Blair.

Just 2 quick ones for us. One is about the maintenance dose. Brian, you mentioned about potential exploration for the lower 15-milligram dose. And I'm just curious if that's informed just purely by the weight loss kinetics or also by the PK? And if so, if you could comment on that. The second has to do with the upcoming kind of maintenance master protocol trial that you're planning. You mentioned about the weekly oral option. And I'm curious if any sort of data that you presented to date informs how should we think about the oral dosing regime?

Yes. Thanks, Andy. As far as the 15-milligram for maintenance, we did see in this study, a steady weight loss in that lowest dose, and it was significant -- statistically significant versus baseline at week 13. And when we look at that and then the continued weight loss following the transition from the 90 to the 30, it suggests that something lower than 30 could probably be an effective maintenance regimen. We don't have all the PK data from the -- we don't have any PK data from the study. So that will be very helpful in helping us kind of think about the doses there. And same high weekly dose, it would be nice to have the PK data to understand where that 120 went with exposures and how that might help us plan what that weekly dose would be. As you titrate up with the subcu and then you step from subcu to oral, you're going from a pretty high weekly exposure to almost certainly lower exposure when you go to the weekly oral. So we would expect pretty good tolerability on that step. I think reasonable likelihood that you would have exposures that would [Technical Difficulty].

The next question comes from Thomas Smith of Leerink Partners.

Can you just remind us how 2735 was formulated here with the tablets and what the pill burden was in this study? And then how are patients being dosed with respect to the fasting requirements in the study here?

Yes. Thanks, Tom. They were -- these patients were dosed after an overnight fast. We have not done a food effect study, so we don't know if fast will be required. I would assume so, given that it's a peptide and those are difficult to absorb anyway. So any other GI contents may interfere with that exposure. So I would expect that without food is going to be an optimal dosing regimen. As far as pill counts, these were 30-milligram tablets, and so people took 4 30s at the top dose. We wouldn't expect the subsequent studies to require that level of pill burden at this point.

Got it. That's super helpful. And then can you just comment -- I know you talked about the GI-related adverse event rate in that 90 mg to 30 mg maintenance dose cohort. I was wondering if you could just comment on the overall discontinuation rate that you saw there and how that compares to the 90-milligram cohort.

Yes, it was similar. I don't have that right in front of me. It was similar. They titrated about twice as fast -- actually, exactly twice as fast. But as far as discontinuations, they were similar between the 2 arms.

The next question is from Joe Pantginis with H. C. Wainwright.

Very nice data. I apologize, I'm going to take a completely different avenue of questioning or just one question, if you don't mind. So Wegovy was just approved for MASH. So this is the second drug approved. So I was just curious about your unchanged or potentially different views about the positioning of 2809. Again, sorry for the left turn there.

No problem. Thanks, Joe. No, we had an end of Phase II meeting last year with the FDA for the MASH indication, and we were given the impression that biopsy would likely be required -- well, not likely, would be required for patients to be randomized. And that -- given the high failure rate of biopsies, it just seems like a challenging path forward given the high screen failure rates and the other drugs approved that don't require a biopsy. If the FDA's position on that would change, we would certainly be interested in proceeding there. But that's not the -- it's not our understanding based on direct feedback and it's not our near-term plan.

I appreciate that. And looking forward to updated data once you get it on the 2735 titration study. A lot of great information is going to come from that.

The next question comes from I-Eh Jen of Laidlaw & Co.

We have one here which is that based on the data at this point, would you consider subcu to oral maintenance will potentially be better than just the high oral to lower oral maintenance or there's more to consider?

Yes. Thanks, Jen. Yes, we've always thought that the maintenance market was probably the most attractive market for the oral. And it's a substantial market. It represents an expansion from the existing market. So if you can develop an effective maintenance therapy for people to transition on to once they've reached the target weight range, we think there's a tremendous opportunity there. And what we see in these data is, I think, compelling evidence that low oral doses are effective at providing that weight maintenance effect.

Would that reflect on the next study? Or you were still doing a little bit broader reach before you're making a final decision?

Well, yes. Thanks, Jen. Well, we will be doing this upcoming maintenance study where we have people on a weekly injectable dose and then we transition them to either a monthly injection or a low-dose oral. As far as the subsequent study with the oral by itself, we need to evaluate the full complement [Technical Difficulty] before we really map those plans out.

The next question is from Hardik Parikh of JPMorgan.

Just 3 for me. First is this high level. Based on today's call or today's data, how has your view evolved on the role that oral 2735 can play in the market? And then the second one is just wondering did the AE rates have any variability when you look at it based on regions or any kind of patient characteristics? And then finally, how did the AE kind of evolve once in that step-down cohort once patients step down from the 30 to 90 to 30? Was it similarly high rates? Or did they go down?

Yes. Thanks, Hardik. On the last one, we do not have the cohort by cohort AE time course. We have the whole study time course. So we will receive that later this quarter. I would anticipate that there would be no increase in AEs going from 90 to 30 though. As far as the positioning, I think we see at 12 weeks here with robust and progressive weight loss, I think, a pretty competitive efficacy profile. We know that adverse events and others have shown it with these mechanisms are modulated by titration rates. So were they higher here? Yes, they were a little bit higher. They were higher across the board in placebo really notably. And when you look at the delta between placebo and treated, there isn't a very large delta. So we think that maybe starting at a lower dose, maybe expanding the titration steps will likely impact the adverse event profile and the progressive weight loss that we observed suggests that we have a very, very competitive efficacy profile that even if you slow down the titration steps, the long-term effect of the drug should be really highly competitive.

The next question comes from Roger Song with Jefferies.

Two from us. One is, Brian, can you comment on the kinetics on the discontinuation time point. Given most of the AE or GI AE is coming within 2 weeks or 3 weeks. And then the other one is related to the patient retention strategy. Just curious, given the very high discontinuation on the placebo element well, just curious about your strategy, any difference or similar to other obesity trial. Any optimization you think from your perspective, maybe from an industry perspective can be implemented given the increasing competition on the obesity trial out there?

Yes. Thanks, Roger. With respect to retention, I think one attractive feature to many trial participants is an opportunity to participate in an extension study. And so we might consider that in subsequent studies. It's an opportunity for people to roll into a longer-term extension guaranteed for the placebo participants to receive a treatment. As far as the time course of discontinuations, we do not have that breakout available at this point. We just have the overall rates. And -- so it's hard to speculate. I would anticipate that they would track the adverse event profile, but I don't know that.

As we are nearing the conclusion of today's call, our final question will come from Justin Zelin with BTIG.

Two for me, Brian. So first on the slower titration schedule makes a lot of sense. I was just wondering, given VK2735's longer half-life, whether you consider dosing the oral formulation less frequency than once daily, for example, every other day to smooth tolerability while maintaining efficacy. And just secondly, were antiemetic or GI supportive medications allowed in the study to manage GI adverse events in the study? And if you've noticed if that helped at all keeping patients on study.

Yes. Thanks, Justin. I don't have the use of antiemetics. They were not used prophylactically. So I assume that when someone had GI adverse events that merited use of Zofran type -- any sort of an antiemetic that those were prescribed, but they were not used prophylactically. As far as the different dosing regimens, yes, it is something we've considered and that's one of the reasons we've considered this weekly potential oral regimen is that the half-life and hopefully, the exposures would provide effective weight maintenance on a less frequent time frame. As far as the normal induction therapy using every other day, yes, I think that could be effective. It requires a little bit different packaging when you go to every other day, it's more of a blister pack than a bottle. But I think it's feasible. And I think, I mean, it's a good suggestion, and we have thought about it, but haven't made any decisions on that.

This concludes our question-and-answer session. I would like to turn the conference back over to Ms. Diaz for any closing remarks.

Thank you, everyone, for joining us today. Thank you for your continued support of Viking Therapeutics. With that, we'll end the call today. Thank you, and have a good day.

The conference has now concluded. Thank you for attending today's presentation. You may now disconnect.