Viking Therapeutics Inc (VKTX) 2023 Q2 法說會逐字稿

Welcome to the Viking Therapeutics Second Quarter 2023 Financial Results Conference Call. (Operator Instructions)

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; and Greg Zante, Viking's CFO.

Before we begin, I'd like to caution that comments made during this conference call today, July 26, 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, 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 afternoon to everyone dialed in by phone or listening on the webcast. Today, we'll review our financial results for the second quarter and first 6 months of 2023 and provide an update on recent progress with our clinical programs and operations.

The first half of 2023 has been exceptional for Viking, with the company announcing positive clinical data from 2 programs and completing a successful financing to support the continued development of our pipeline. During the second quarter, we announced positive results from the Phase 2b VOYAGE study of VK2809 in patients with biopsy-confirmed nonalcoholic steatohepatitis or NASH. The study successfully achieved its primary endpoint, confirming VK2809's best-in-class therapeutic profile for the treatment of NASH.

In the first half of the year, we also announced data from our first clinical study of VK2735, a dual GLP-1 and GIP receptor agonist for the potential treatment of obesity. This Phase 1 single ascending dose and multiple ascending dose study demonstrated encouraging safety and tolerability and positive signs of clinical activity following 28 days of treatment. I will review these clinical results later in today's call. Along with the Phase 1 results for VK2735, we also announced the initiation of a new clinical study to evaluate a novel oral formulation of this compound.

Finally, during the second quarter of the year, we announced the closing of a successful public offering of common stock, raising gross proceeds of approximately $288 million that we plan to use for the continued advancement of each of our programs through key clinical milestones. I'll provide further details on our operations and development activities after we review our financial results for the second quarter and first 6 months of 2023.

With that, I'll turn the call over to Greg Zante, Viking's Chief Financial Officer.

Thanks, Brian. In conjunction with my comments, I'd like to recommend that participants refer to Viking's Form 10-Q filing with the Securities and Exchange Commission, which we expect to file today.

I'll now go over our results for the second quarter and 6 months ended June 30, 2023, beginning with results for the quarter. Our research and development expenses for the 3 months ended June 30, 2023, were $13.9 million compared to $13.5 million for the same period in 2022. The increase was primarily due to increased expenses related to preclinical studies, manufacturing for our drug candidates, stock-based compensation, salaries and benefits and third-party consultants, partially offset by decreased expenses related to clinical studies.

Our general and administrative expenses for the 3 months ended June 30, 2023, were $9.8 million compared to $4.1 million for the same period in 2022. The increase was primarily due to increased expenses related to legal and patent services, stock-based compensation and salaries and benefits.

For the 3 months ended June 30, 2023, Viking reported a net loss of $19.2 million, or $0.19 per share compared to a net loss of $17.4 million, or $0.23 per share in the corresponding period in 2022. The increase in net loss for the 3 months ended June 30, 2023, was primarily due to the increase in general and administrative expenses, noted previously, partially offset by increased interest income compared to the same period in 2022.

I'll now go over the results for the 6 months ended June 30, 2023. Our research and development expenses for the 6 months ended June 30, 2023, were $24.9 million compared to $26.1 million for the same period in 2022. The decrease was primarily due to decreased expenses related to clinical studies, partially offset by increased expenses related to manufacturing for our drug candidates, stock-based compensation, salaries and benefits and regulatory services.

Our general and administrative expenses for the 6 months ended June 30, 2023, were $19.4 million compared to $7.8 million for the same period in 2022. The increase was primarily due to increased expenses related to legal and patent services, stock-based compensation and salaries and benefits.

For the 6 months ended June 30, 2023, Viking reported a net loss of $38.8 million, or $0.44 per share, compared to a net loss of $33.5 million, or $0.43 per share in the corresponding period in 2022. The increase in net loss for the 6 months ended June 30, 2023, was primarily due to the increase in general and administrative expenses, noted previously, partially offset by increased interest income compared to the same period in 2022.

Turning to the balance sheet. At June 30, 2023, Viking held cash, cash equivalents and short-term investments of $392.9 million, compared to $155.5 million as of December 31, 2022.

This concludes my financial review, and I'll now turn the call back over to Brian.

Thanks, Greg. I'll begin my comments with an update on our lead program, VK2809. VK2809 is an orally available, small molecule agonist of the thyroid hormone receptor that is selected for liver tissue as well as the beta isoform of the receptor. During the second quarter, the company announced positive top-line results from the Phase 2b VOYAGE study evaluating VK2809 in patients with biopsy-confirmed NASH and fibrosis. We were very pleased to report that this study achieved its primary endpoint with patients receiving VK2809 experiencing statistically significant reductions in liver fat content from baseline to week 12 as compared with placebo.

The median relative change from baseline in liver fat as assessed by magnetic resonance imaging, proton density fat fraction, ranged from 38% to 55% among patients receiving VK2809. Importantly, up to 85% of patients receiving VK2809 experienced at least a 30% relative reduction in liver fat content. This level of efficacy is associated with the greater likelihood of histologic benefit in NASH.

Additionally, VK2809-treated patients demonstrated statistically significant reductions in low-density lipoprotein cholesterol, triglycerides and atherogenic lipoproteins, all of which have been correlated with cardiovascular risk. It is important to highlight that a number of studies evaluating other NASH development programs have demonstrated elevations in these lipids following treatment. In contrast, the Phase 2b VOYAGE data indicates that VK2809 may be unique in its potential to offer a cardioprotective benefit.

Also important, VK2809 demonstrated encouraging safety and tolerability in this study. 94% of treatment-related adverse events among patients receiving VK2809 were reported as mild or moderate. Discontinuations due to adverse events were low and balanced among placebo and treatment arms. As in prior studies, VK2809 demonstrated excellent gastrointestinal tolerability in this study. Rates of nausea, diarrhea, stool frequency and vomiting were similar among VK2809-treated patients compared to placebo. These findings are consistent with a prior 12-week Phase 2a trial evaluating VK2809 in patients with hypercholesterolemia and nonalcoholic fatty liver disease.

The Phase 2a study also successfully achieved both its primary and secondary endpoints, demonstrating significant reductions in liver fat and plasma lipids. Importantly, the reductions in liver fat were durable with the majority of patients remaining responders, 4 weeks after completion of dosing. The 12-week study also demonstrated the promising safety and tolerability of VK2809 with no serious adverse events reported. In our view, the top-line results of the VOYAGE trial, combined with the 8 previously completed studies of this compound, support our belief that VK2809's broad lipid-lowering properties along with its safety, excellent tolerability, significant liver fat reduction and oral route of administration, establish it as a best-in-class therapeutic for the treatment of NASH. We look forward to reporting data from the secondary and exploratory objectives from the VOYAGE study, including the evaluation of histologic changes assessed by hepatic biopsy after 52 weeks of treatment in the first half of 2024.

Transitioning to our newest program, I'll now highlight recent progress with our lead obesity candidate, VK2735. VK2735 is a dual agonist of the glucagon-like peptide 1, or GLP-1 receptor and the glucose-dependent insulinotropic polypeptide, or GIP receptor that is being evaluated for the treatment of obesity. Initial in vivo data from this program demonstrated improvements in weight loss, glucose control and insulin sensitivity among diet-induced obese mice following treatment as compared to a GLP-1 mono-agonist when administered at the same dose for the same period of time.

In addition, the observed reductions in liver fat content were generally larger among animals treated with our compounds relative to those observed among animals treated with the GLP-1 mono-agonist. Based on these and other preclinical findings, Viking conducted a Phase 1 single ascending dose and multiple ascending dose study of VK2735 to evaluate its preliminary safety, tolerability and pharmacokinetic profile as well as its potential impact on exploratory measures. Earlier this year, we announced positive results from this trial with VK2735 demonstrated promising safety and tolerability, a predictable PK profile and encouraging signs of clinical benefit.

The single ascending dose portion of this study enrolled healthy men and women and evaluated escalating doses of VK2735. The results of this portion of the study demonstrated that single doses of VK2735 were safe and well tolerated and that the compounds PK profile demonstrated favorable characteristics in humans. Following single subcutaneous doses, VK2735 demonstrated a half-life of approximately 170 to 250 hours, a Tmax ranging from approximately 75 to 90 hours, and excellent therapeutic exposures.

The multiple ascending dose portion of this study enrolled healthy men and women with a minimum body mass index of 30 kilograms per meter square. These subjects received VK2735 once weekly for 28 days. In this portion of the study, VK2735 demonstrated encouraging safety and tolerability and positive signs of clinical activity. All cohorts receiving VK2735 demonstrated reductions in mean body weight from baseline, ranging up to 7.8%. Cohorts receiving VK2735 also demonstrated reductions in mean body weight relative to placebo, ranging up to 6%. Statistically significant differences in body weight compared to placebo were also maintained or improved at the Day 43 follow-up time point, 21 days after the last dose of VK2735 was administered.

In addition, all cohorts treated with VK2735 demonstrated improvements in plasma glucose levels relative to placebo, though not all cohorts achieved statistical significance. VK2735 also demonstrated encouraging safety and tolerability following single and repeat dosing. The vast majority, 98% of observed adverse events were reported as mild or moderate and 99% of gastrointestinal-related adverse events were also reported as mild or moderate.

Given VK2735's promising tolerability, we believe that higher doses may be achieved with longer titration windows, and we plan to evaluate further dose escalation in future studies. Based on these Phase 1 results, the company plans to initiate a Phase 2 trial of VK-2735 in patients with obesity later this quarter. In addition to the formulation of VK2735 that is administered subcutaneously, we are also pursuing an oral formulation of this compound. Earlier this year, we announced the initiation of a Phase 1 clinical study to evaluate a novel tablet formulation of VK2735. This study is an extension of the Phase 1 single ascending dose and multiple ascending dose study concluded earlier in the year.

The oral portion of the study is a randomized, double-blind, placebo-controlled study in healthy volunteers who have a minimum body mass index of 30 kilograms per meter squared. Subjects will receive daily oral doses for 28 days. The primary objective of the study is to evaluate the safety, tolerability and pharmacokinetics of VK2735 following 28 days of oral dosing. Exploratory endpoints include changes in body weight and plasma glucose. We believe the potential availability of both subcutaneous and oral formulations of VK2735 could provide patients with flexible dosing options and expand the compound's potential market opportunity. We expect to report the initial results from this study in the fourth quarter of this year.

I'll now provide an update on our third clinical candidate, VK0214. Like VK2809, VK0214 is an orally available small molecule thyroid hormone receptor beta agonist. VK0214 is currently being evaluated in a Phase 1b clinical trial in patients with X-linked adrenoleukodystrophy, or X-ALD. X-ALD is a rare and debilitating metabolic disorder. Patients with X-ALD have genetic mutations that disable the function of a peroxisomal transporter of very long chain fatty acids. As a result, patients are unable to efficiently metabolize very long chain fatty acids, and the accumulation of these compounds is believed to contribute to the onset and progression of X-ALD.

Viking is currently enrolling a Phase 1b study evaluating VK0214 in patients with the adrenomyeloneuropathy or AMN form of X-ALD. AMN is the most common form of X-ALD affecting approximately 50% of patients. The decision to advance this program is based on positive results from a prior Phase 1 study in more than 100 healthy volunteers. In that study, VK0214 demonstrated dose-dependent exposures, no evidence of accumulation and the half-life consistent with anticipated once daily dosing.

Subject to receive VK0214 experienced reductions in LDL-cholesterol, triglycerides, apolipoprotein B and lipoprotein (a). VK0214 also demonstrated an encouraging safety and tolerability profile with no serious adverse events reported and no treatment or dose-related signals observed for GI side effects, vital signs or cardiovascular measures.

The ongoing Phase 1 trial is randomized, double-blind, placebo-controlled, multicenter study in adult male patients with AMN. The primary objectives of the study are to evaluate the safety, tolerability and pharmacokinetics of VK0214 administered once daily for 28 days. But it also includes an exploratory assessment of changes in plasma levels of very long chain fatty acids. This study continues to enroll and we expect to complete enrollment later this year.

Beyond the clinical achievements announced in the first half of the year, Viking also completed a successful public offering of common stock, raising gross proceeds of approximately $288 million. These funds position us well as we continue to invest in both the expansion and advancement of our pipeline.

In conclusion, the first half of 2023 has been an exciting period for Viking. With respect to our lead program, VK2809, top-line data from our Phase 2b VOYAGE study affirmed our belief that VK2809 is a safe and effective therapeutic with best-in-class features, demonstrating significant reductions in liver fat, while providing cardioprotective benefits through robust lipid reductions. To date, VK2809 continues to deliver the largest reductions in liver fat reported for any oral agent at this stage of development.

With respect to VK2735, our dual GLP-1 GIP receptor agonist, the company's recently completed Phase 1 study demonstrated promising safety and tolerability and significant reductions in body weight following 28 days of dosing. Given these positive results, we plan to initiate a Phase 2 study of VK2735 in obesity later this quarter. In addition, we are pursuing a novel tablet formulation of this molecule that we believe will offer patients important dosing options and significantly expand the compound's potential market opportunity.

Finally, the Phase 1b study evaluating VK0214 in patients with adrenomyeloneuropathy continues to enroll, and we anticipate completing enrollment later this year. As we look ahead to each of our currently anticipated clinical milestones as well as others in the future, we are well positioned with a strong balance sheet with approximately $400 million in cash to support the aggressive development of our pipeline.

This concludes our prepared comments for today. Thanks again for joining us, and we'll now open the call for questions. Operator?

(Operator Instructions) And our first question here will come from Steve Seedhouse with Raymond James.

I wanted to ask first about the oral GLP, GIP tablet formulation. So you're going to have the Phase 2 study -- obesity study underway in the third quarter and you'll get the oral data later this year. I'm just curious what then becomes sort of the next step strategically for that molecule, if you can add it to that Phase 2 -- parallel Phase 2? And also specifically, are there any preclinical data necessary for the tablet formulation that you need to clear like with FDA for a separate IND for instance?

So the path forward would parallel the plan for the subcu formulation. So if the oral formulation looks promising, then we would seek to move that into a Phase 2 study that would likely be similar in design to the subcu Phase 2 study.

With respect to the FDA requirements, it will likely be under a separate IND and probably have some more CMC-related information included in it. But we don't think anything will be, I think, gating to moving forward.

Okay. And also, there was a lot of data, of course, at ADA and emerging now for the oral formulations of some of the GLP-1 mono-agonists. And you guys have presented animal data comparing the subcutaneous version of this to semaglutide or tirzepatide preclinically. Is it possible or easy to do those comparisons with sort of oral control molecules preclinically as well? Do you have a sense of how your tablet formulation stacks up preclinically against what's out there and through Phase 2 now?

Yes. It's a good question. So we don't expect the oral efficacy to be on the same level as the subcu efficacy. And that's just -- we just don't know that we'll be able to achieve the same level of exposure as the subcu it's -- I doubted. But that doesn't mean there's not a terrific opportunity for it. When we looked at the oral formulation in some of the earlier animal models, it was effective at weight loss and it does show efficacy, probably, I don't know, 50%, 60% as good as the subcu.

We didn't pursue any specific dose-ranging comparisons. But in the 14- and 21-day models, they were -- it was very effective, but probably about 60%. I'm not remembering that percentage perfectly, so don't quote me on that, but it's probably [60-or-so-percent] as effective as the subcu.

And I mean, are you able to get your hands on or synthesize the control molecules for some of these other clinical-stage emerging oral GLP-1 candidates? Do you have a sense of how it's backed up laterally as opposed to just versus your own subcutaneous formulation? Preclinically, of course.

We've done a little bit of that. I don't want to get into the compounds we have tested against, but we have done a little bit of that. And I think from what we've seen, it looks very encouraging, but these are animal models with a lot of pretty large air bars. But I think we're comfortable with what we've seen in animals as far as exposures and weight loss thus far.

Our next question will come from Jay Olson with Oppenheimer.

For the oral 2735 data expected later this year, can you just talk about what kind of data we should be looking for and how you plan to disclose that?

Did you say the clinical data or preclinical data, sorry?

Clinical.

Oh, clinical. It would probably be roughly similar to what we announced with the subcu. So we'd look at PK and safety and tolerability and preliminary effects on body weight changes. We aren't doing the MRI-PDFF with the oral, but everything else, I think, is very parallel to the subcu.

Okay. And is that going to be QD dosing and are there any dietary restrictions around dosing?

It is QD dosing. We haven't disclosed dosing details on whether or not there are restrictions, but we don't think anything would be particularly problematic.

And then given the ongoing supply shortages for some of the competing weight loss compounds, can you just talk about the cadence of enrollment for your 2735 studies?

Yes. It's a little lumpy with 2735. This is a single site in Australia, and it comes in fits and starts, but we think we can have data from the study by the end of the year. But you have a little burst of enrollment than a little dry spell and then a burst of enrollment. So it's similar to the subcu enrollment pattern.

And maybe one last question. Beyond GLP-1 and GIP, are there any other mechanisms for obesity that you're interested in?

Yes. We have, I'd say, a fairly robust effort in the metabolic disorders and obesity in particular. I think not everything is ready for prime time right now, but we hope to talk more about those in the coming quarters. But I think we've got some exciting projects in-house here.

Our next question will come from Joon Lee with Truist.

Just a follow-up on -- from Steve's prior question. Did you say you saw around 50% to 60% of the weight loss effect for your oral formulation versus the key formulation? And so in other words, 3% weight loss placebo-adjusted in the Phase 1 MAD study. Is that the bar or are there other considerations like different dosing regimen that makes that extrapolation difficult? And I have a follow-up.

Yes, I think that extrapolation is very difficult because the animal studies are sort of sledgehammer studies, you're dosing at levels that aren't really relevant to people just to understand whether or not an effect exists. So I wouldn't use that as a benchmark for expectations in people. We just don't know yet what the effect in people would be.

And can you just remind us how many arms you're testing in the oral formulation?

Yes, the ore formulation would be 5 arms. It will be placebo and then for escalating dose arms. We do have flexibility to add arms in that study if we like -- just like in the subcu study at cohorts, I mean.

Looking forward to data. And in terms of VK2809 for NASH, assuming good biopsy results in the first half of next year, what are you looking for in a potential partner who can take it forward? And how quickly do you think you can find such a partner?

Yes. Well, I think great question. I think it depends on the -- on what the data look like. We're excited to see how the biopsies turn out and that I think will drive the interest. And the speed in which we would move forward, we would hope to upon completion of the study schedule and in a Phase 2 meeting with the FDA as soon as possible to discuss the design and outline of the Phase 3 program.

Our next question will come from Annabel Samimy with Stifel.

This is Stacy calling in for Annabel. I guess 2 on our end. How are you thinking about the landscape following ADA and the strength of some of the new programs in the orals emerging? Do you feel that in your clinical trials, you might find populations that might be more suited to have dual agonist than single or triple? And how do you start identifying those patients? And I guess you're seeing potential encroachment from triple G for NASH or at least that's -- how it's been interpreted. Can you talk about the feedback from your side on how [tirzepatide] might affect your opportunity?

Yes, a lot of talk about some of the data from ADA and how obesity uptake, the uptake of new obesity drugs is projected and how it looks right now, it looks very exciting. And I just -- as a reminder, we have an obesity drug. So to the extent those drugs are used widely, that's great, because we think we've got a phenomenal molecule in the VK2735. At this point, we haven't really seen from the obesity drugs compelling antifibrotic signal. So I think in that sense, some of the liver targeting agents and different mechanisms may have an edge on just an obesity type drug.

I think when you look at the ADA updated guidelines that were announced at the conference, the ADA conference, the suggestion to screen earlier for NAFLD and NASH, we think that's a great update to the guidance. We think that, that will raise awareness. And I think really serve to funnel more patients into the GI specialist setting where they're probably more likely to receive a targeted agent versus just an obesity agent. And so we think that increase in awareness is, I think, favorable to the -- more of the pure NASH drugs.

But at the end of the day, these are large markets. NASH is a pretty substantial market. There will be room for multiple modalities to coexist. If someone has morbid obesity and NASH, maybe something like retatrutide would be suitable for some period of time. But there are plenty of people who don't fit that description and very large populations that people aren't necessarily obese and they have NASH. If you look at Asians, they typically get a skinny NASH. So we don't necessarily see obesity drugs just taking over the NASH world. I think that's an overstatement.

And our next question will come from Andy Hsieh with William Blair.

So I have one for 2735. You mentioned about the flexibility to add another arm. I'm just curious about what considerations you'll be put in, in making that determination, especially in the context that some of -- when you dose escalate, especially in such short time intervals, sometimes, the magnitude of weight loss don't really separate. Instead, the difference is really where they plateau. So I'm curious about kind of the thinking into adding that additional arm.

And then in terms of oral dosing versus subcu, just curious if you have disclosed that and it will be helpful to kind of get an understanding of kind of the ratio between the subcu dosing normalize to weekly versus the oral dosing?

So with the oral dosing, we just have the flexibility in the protocol to add cohorts. It's not -- we have to make that decision based on the data and the data would be exposure, PK, tolerability data. Those would be kind of the primary drivers to understanding whether or not we want to add another cohort. With respect to the doses that are planned, I think we said previously, we're looking at 2.5 mgs per day of 5 milligrams per day, 10 milligrams per day and then 20 milligrams per day. And so those would be the planned doses. And then if we make any changes, we'll -- we have some flexibility there in the protocol.

And our next question will come from Yale Jen with Laidlaw & Company.

I've got 2 here. The first one is from the meeting -- the recent meeting that the triple G product, at least on the efficacy side of things seems to be very promising. My question to you is that with adding a glucagon agonist, is there something for you guys to consider? Or you feel this is probably not necessarily the best strategy forward? And I have another follow-up.

We have looked at the triple agonists here. And in our hands, we couldn't get them to outperform the dual agonist that target GLP-1 and GIP. What we do see from some of the data on the triple agonist compounds is that, the incremental benefit on weight loss is -- it's there. It's relatively modest, given the -- I think, significant change in the adverse event profile. So with elevated hypersensitivity and potentially concerns on cardiac safety, we'll see how those pan out long term, but those would be potential challenges that may or may not be worth it in every patient. So right now, we're looking at the GLP-1 GIP dual agonist. There may be other mechanisms outside of glucagon that could be layered on to those 2 and provide a very nice enhancement of the signal.

And maybe just one more question here, which is for the Phase 2 subcu study you were going to start. Any color in terms of what level of longer duration or other aspects in the trial design you can reveal?

So we're going up to 15 milligrams -- we plan to go up to 15 milligrams in this study. It's a 13-week study. And we would plan to titrate in 3-week blocks to move up to the 15-milligram dose level. So I believe at the end of the study, if you are randomized to the 15-milligram arm, you would be on that arm for about 4 weeks.

And our next question will come from Thomas Smith with Leerink Partners.

Just a couple on the obesity program. I think you've alluded to obesity week historically is a reasonable venue for presenting the detailed Phase I data. Can you just comment on whether that's still your expectation? And I guess, what additional data sets we should be looking forward to with the detailed presentation beyond the top line?

Yes, we did submit an abstract as a late breaker. And I don't know when those notifications will be sent out. We haven't notified yet. And we would hope to have -- we did collect a lot of different -- and we looked at plasma lipids -- I'm sorry (inaudible) and plasma glucose is what I meant to say. And we also looked at liver fat. So maybe some more color around some of those things as well as a little bit more on the PK side, we haven't talked a lot about PK, but probably expect to have a little bit more PK data.

And just wondering if you could just elaborate a little bit on the regulatory progress with 2735 in the U.S. And I guess, specifically, if you could comment on whether you filed the IND and if you have it, I guess, what the gating factors to filing the IND would be?

Yes, we have recently filed the IND and we hope to be able to start the study in the third quarter, but we have not -- we're still in that window right now. So there aren't any gating factors that we're aware of today that would preclude that, but we haven't heard back yet.

And just one last question, if I could, on the VOYAGE trial. And I know you've commented previously about using one pathologist to screen patients for entry. And I guess that they're on the board of F2, F3 or if they have an as equal to 4, they get referred on to a second pathology review. Maybe if you could just comment or give us your latest thoughts on how you're thinking about the biopsy evaluation for the 52-week biopsies? Are you considering adding additional pathologists or maybe changing to a consensus review methodology? Or just what are your latest thoughts on the histology efficacy evaluation?

Yes, it's obviously, a lot has evolved since we initiated the study. We think we're best served now to sort of keep the 2 reader approach where you have a primary reader that sends things to a secondary reader when they are on the cusp of different radiations F2 versus F3 or anybody with an [NAS of 4] would still go to the second read. And they -- those 2 pathologists must reach consensus. And I'm not aware of any time thus far that they haven't reached consensus. So I think that it's working for us now in a Phase 3 trial, we would probably move to maybe a 3 reader approach. But right now, we're going to stick with what's currently in the protocol.

(Operator Instructions) Our next question here will come from Justin Zelin with BTIG.

So Brian, we recently saw an acquisition in the obesity space. Could you give us the latest thinking on the BD strategy at Viking either bringing things into the company or likewise out?

Oh, yes. Thanks, Justin. Our plan today is to develop things really as far as we can. We don't see ourselves launching either a NASH or obesity product, but we will continue as aggressively as possible with the clinical development of our programs and be open-minded to opportunities as they arise, things that make sense for the company and our shareholders. But that's we're focused on is our own internal programs. Right now, I'd say bringing new things into the company, probably a lower priority given that we have our hands full.

And our next question will come from Dylan Dupuis with ROTH MKM.

Just one quick question on the Phase 2 obesity study that you guys are planning to start. Just around the dosing cohorts and at what point do you think you'll need to start implementing those situation strategies in the dosing curve? Thank you.

Yes, we do plan to titrate the lowest dose in the Phase 2 study would be a 2.5 mg fixed dose but subsequent doses would be higher and will titrate into those doses in 3-week blocks. So for example, second cohort is a 5 milligram cohort. We plan to do 3 weeks at 2.5 mgs and then the remainder of the trial at the 5-milligram dose. So that's how we anticipate the titration scheme working.

And this concludes our question-and-answer session. I'd like to turn the conference back over to Stephanie Diaz for any closing remarks.

Thank you all for your participation and continued support of Viking Therapeutics. We look forward to updating you again in the coming months. Thank you.

The conference is now concluded. Thank you very much for attending today's presentation. You may now disconnect your lines.