Viking Therapeutics, Inc. (NASDAQ:VKTX) Q1 2019 Earnings Conference Call May 2, 2019 4:30 PM ET
Stephanie Diaz - Investor Relations
Brian Lian - President & Chief Executive Officer
Michael Morneau - Vice President of Finance & Administration
Conference Call Participants
Fang-Ke Huang - SunTrust Robinson Humphrey
Timur Ivannikov - Raymond James
David Bautz - Zacks Investment Research
Andy Hsieh - William Blair
Yale Jen - Laidlaw & Company
Mayank Mamtani - B. Riley FBR
Good day, and welcome to the Viking Therapeutics First Quarter 2019 Earnings Conference Call and Webcast. All participants will be in a listen-only mode. [Operator Instructions] After today's presentation, there will be an opportunity to ask questions. [Operator Instructions] Please note this event is being recorded.
I would like to now turn the conference over to Stephanie Diaz, Investor Relations. Please go ahead.
Hello, and thank you all for participating in today's call. Joining me today is Brian Lian, Viking's President and CEO; and Michael Morneau, Vice President of Finance and Administration.
Before we begin, I'd like to caution that comments made during this conference call, today, May 2, 2019 will contain forward-looking statements within the meaning of the Securities Act of 1933 concerning the current beliefs of the company, which involve a number of assumptions, risks, and uncertainties.
Actual results could differ from these statements 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 the initial comments. Brian?
Thanks, Stephanie, and thanks to everyone listening on the webcast or by phone. Today we'll provide an overview of our first quarter financial results, as well as an update on recent progress and developments related to our pipeline programs and operations.
During 2018, Viking reported best-in-class data from two clinical programs VK2809 for hypercholesterolemia and fatty liver disease, and VK5211 for the stimulation of muscle and bone following hip fracture. The success and momentum of 2018 have continued in 2019, as we reported new data from our Phase 2 trial of VK2809, which further validated the molecules promising potency and safety.
Specifically, recently presented data evaluating VK2809 doses of 5 milligrams per day, showed that this lower exposure results in efficacy that is similar to that observed at the higher 10 milligram dosing arms reported previously. We presented these latest results last month in a late breaking poster at the EASL conference in Vienna. We are currently preparing for our next study with VK2809, which will be a Phase 2b clinical trial in patients with biopsy-confirmed NASH. I'll provide further detail in a few minutes. But first, we'd like to review our first quarter financial results.
I'll now turn the call over to Mike Morneau, Viking's Vice President of Finance and Administration to discuss our financial results. Mike?
Thanks, Brian. In conjunction with my comments, I'd like to recommend that participants refer to Viking's 10-Q filing with the Securities and Exchange Commission, which we expect to file later today for additional details. I'll now go over the financial results for the first quarter ended March 31, 2019.
Our research and development expenses for the three months ended March 31, 2019, were $4.5 million compared to $3 million for the same period in 2018. The increase was primarily due to increased manufacturing expenses related to our drug candidates, pre-clinical study efforts, use of third-party consultants, stock-based compensation and salaries and benefits, partially offset by a decrease in clinical study expenses.
Our general and administrative expenses for the three months ended March 31, 2019 were $2.3 million compared to $1.8 million for the same period in 2018. The increase was primarily due to increased expenses related to stock-based compensation, salaries and benefits, and use of third-party consultants.
For the three months ended March 31, 2019, Viking reported a net loss of $4.9 million and a basic net loss per share of $0.07, compared to a net loss of $3.6 million and a basic net loss per share of $0.08 in the corresponding period in 2018. The increase in net loss for the three months ended March 31, 2019 was primarily due to the increase in research and development and general and administrative expenses noted previously, offset by an increase in interest income and the elimination of the change in the fair value of debt conversion feature liability, as well as the amortization of debt discount due to the company's repayment of debt in May 2018.
The decrease in net loss per share for the three months ended March 31, 2019 is primarily due to the additional shares outstanding at March 31, 2019 versus those outstanding at March 31, 2018, given the additional shares issued by the company in June and September 2018, through public equity offerings.
Our balance sheet at March 31, 2019 showed cash, cash equivalents and investments totaling $298.7 million. As of April 30th, 2019, Viking had 72,047,657 shares of common stock outstanding.
This concludes my financial review, and I'll now turn the call back over to Brian.
Thanks Mike. In the first quarter, we continued to build upon the momentum gained in 2018, which was the result of positive Phase 2 data from our two clinical stage programs, VK2809 for liver disease and VK5211 for muscle growth. As a reminder, VK2809 is an orally available small molecule 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 lipid disorders, including non-alcoholic steatohepatitis or NASH.
In September of last year, we announced positive results from a Phase 2 trial of VK2809 and patients with hypercholesterolemia and fatty liver disease. The trial achieved both its primary and secondary endpoints, demonstrating potent reductions in liver fat content and improvements in plasma lipid measures. These results were presented in November during the oral late-breaker at the AASLD conference.
Additional updated results were presented last month in a late-breaking poster at the annual meeting of the European Association for the Study of the Liver or EASL. This Phase 2 trial randomize patients to receive VK2809 doses of 5 milligrams daily, 10 milligrams daily, 10 milligrams every other day or placebo for 12 weeks. The trial's primary endpoint evaluated the effect of VK2809 on LDL cholesterol after 12 weeks of dosing compared to placebo. The secondary endpoint evaluated change in liver fat as assessed by MRI proton density fat fraction or MRI-PDFF.
As we reported at both the AASLD and EASL conferences, with respect to the trial's primary endpoint, VK2809 treated patients achieve statistically significant reductions in LDL compared with placebo treated patients. In addition, VK2809 treated patients experienced statistically significant improvements in other lipids, including triglycerides and the atherogenic proteins, apolipoprotein B and lipoprotein A.
With respect to the key secondary endpoint, VK2809 treated patients experienced significant reductions of liver fat as assessed by MRI-PDFF. The magnitude of this response remains unprecedented among oral agents and development today. Specifically, patients receiving VK2809 dosed at 5 milligrams daily for 12 weeks experienced a median relative reduction in liver fat content of approximately 54% from baseline. Patients receiving VK2809 doses of 10 milligrams every other day experienced a median relative reduction in liver fat content of approximately 57% from baseline, and patients receiving VK2809 doses of 10 milligrams daily experienced a median relative liver fat reduction of approximately 60% from baseline.
Across all VK2809 cohorts, the median relative reduction in liver fat was approximately 57%. By comparison, patients receiving placebo, experienced a median relative reduction in liver fat of approximately 9%. The trial also included a responder analysis, which was intended to assess whether the observed reduction in liver fat may predict broader clinical benefit.
Patients were characterized as responders, if they experienced at least a 30% reduction in liver fat content. This threshold is of interest as multiple studies have demonstrated that when liver fat is reduced by 30% or more, a corresponding increase in the odds of improved overall histology is also observed.
In this study, all patients treated with VK2809 dosed at 5 milligrams daily, experienced at least a 30% reduction in liver fat content. Approximately 77% of patients receiving VK2809 dose at 10 milligrams every other day demonstrated at least a 30% reduction in liver fat content.
And, among patients treated with VK2809 dose at 10 milligrams per day, approximately 91% experienced at least a 30% reduction in liver fat content. The responder rate across all VK2809 cohorts in this study was approximately 88%. By comparison, approximately 17% of patients receiving placebo demonstrated the response.
VK2809 also demonstrated an encouraging safety and tolerability profile in this study. No serious adverse events were reported among patients receiving VK2809 or placebo, and the overall numbers of adverse events were relatively evenly distributed across treatment arms.
Mean ALT and AST levels among patients receiving VK2809 were also reduced relative to those of patients receiving placebo, and there were no clinically or numerically meaningful differences in other liver function test between patients treated with VK2809 or placebo.
VK2809 also demonstrated encouraging cardiovascular safety in this study. No changes to vital signs or cardiovascular toxicity markers such as troponin, CK-MB or NT-proBNP were observed among VK2809 treated patients compared with placebo and CV related AEs were similar between treated and placebo cohorts. Finally, VK2809 was shown to be well tolerated in the study, and there were no differences in gastrointestinal related adverse events compared with placebo.
Overall, we're very pleased with the profile VK2809 demonstrated in this study, and in particular, we're excited that such robust efficacy was maintained at the 5 milligram daily dose, which was the lowest dose study. Perhaps one of the most distinguishing characteristics of VK2809 is its potential to improve overall liver health while providing global cardiovascular benefits through reductions of systemic lipids such as LDL and atherogenic proteins.
Given these encouraging results, we are currently preparing to initiate a Phase IIb study at VK2809 in patients with biopsy-confirmed NASH. In the first quarter, we requested a pre-IND meeting with the FDA, and were granted a meeting date in the midsummer timeframe. Following this meeting, we plan to file an IND to initiate the study.
While details regarding study design have not been finalized, we anticipate the trial will target patients with F2 and F3 fibrosis as well as a limited number with F1 fibrosis. We expect the study to evaluate more than one dose of VK2809 for up to 12 months of dosing. We will provide further information about the study as we move closer to initiation.
I'll now provide an update on our VK0214 program. VK0214 is a small molecule thyroid receptor agonists that we are evaluating as a potential treatment for X-linked adrenoleukodystrophy or X-ALD. X-ALD is a devastating disease caused by a defect in a peroxisomal transporter called ABCD1.
As a result of this defect, patients experience sustained elevations, a very long chain fatty acids in plasma and tissue, which are believed to contribute to the severe cerebral and motor neuron toxicities that are hallmarks of the disease.
Like VK2809, VK0214 is an early orally available small molecule thyroid receptor agonist that possesses selectivity for the beta receptor subtype. Early data have demonstrated that activation of the thyroid beta receptor may stimulate the metabolism a very long chain fatty acids, potentially leading to a therapeutic benefit in the setting.
In late 2017, we and our collaborators at the Kennedy Krieger Institute, completed a 25-week study evaluating VK0214 in an animal model of X-ALD. The results of this study show promising effects on markers of disease, notably an improvement in very long-chain fatty acid levels in both plasma and tissue.
We are currently conducting IND enabling work for this program and plan to file an IND later this year to initiate a proof-of-concept study in humans. We are very excited to be advancing this program into the clinic as data-to-date have demonstrated that VK0214 may offer the first pharmacological treatment for this debilitating disease. We look forward to filing our IND later this year.
Finally, on the corporate side as Mike described earlier, we have been fortune to maintain a robust balance sheet which coupled with our judicious use of capital, provides sufficient runway to see us through multiple clinical inflection points. We are grateful for the support from our investors and look forward to keeping you updated as our pipeline progresses.
In conclusion, we are pleased that our success and momentum from 2018 has continued into the first quarter of 2019. New data from our Phase 2 trial of VK2809, which will reported at EASL last month, demonstrated that the exceptional potency and safety profile previously observed in both 10 milligram doses were essentially maintained when cutting the dose in half to 5 milligrams.
This finding supports our belief that VK2809's unique liver targeting mechanism provides robust, tissue-specific effects with the potentially improved benefit-to-risk profile relative to historical programs targeting this receptor.
Importantly, VK2809 treated patients also experienced statistically significant reductions in LDL cholesterol, triglycerides, and the atherogenic proteins, apolipoprotein-b and lipoprotein-a, which indicates potential long-term cardiovascular benefit.
We remain on track to file an IND for VK2809 and initiate a Phase 2b study in biopsy-confirmed NASH later this year. We also continue to make progress with the pre-IND work required to move our VK0214 program into the clinic for the treatment of X-ALD. We plan to file an IND for this program in the second half of 2019.
This concludes our prepared comments for today. Thanks again for joining us and I'd now like to open the call for questions. Operator?
Thank you. We will now begin the question-and-answer session. [Operator Instructions] The first question today comes from Edward Nash with SunTrust Robinson Humphrey. Please go ahead.
Thank you so much for taking our question. This is Fang-Ke on for Edward Nash. The first question is -- so in the 2809 Phase 1/2 trial, a mental trial, we see that is continuing which is kind of ancient rate with the placebo arm is relatively high and I just want to understand what's the reason for this combination and how you can control that for the Phase 2b? And I have a follow-up.
Yeah, thanks Fang-Ke for the question. Yeah, the trial -- the Phase IIa study was, I would say, a fairly burdensome study for patients. They had to come in for multiple Holter monitors as well as extended stays at clinic visits for 6 hour telemetry for just to measure for cardiovascular safety. So that resulted in some people just sort of getting fatigued with the schedule events and the time commitment that was required. We do not expect those burdens to be imposed on the upcoming study.
So we would hope that the discontinuation rate is lower in the upcoming study. I think the more important component of discontinuations is to consider that the highest rate of discontinuations was actually I think in the placebo relative to the treatment arms. And so, I think that should help address any misperceptions about safety and tolerability associated with receiving VK2809.
Great. That's very helpful. And the second one is on 214. So in your April corporate presentation, you mentioned different long chain fatty acid influence C20 to C22. Just want to understand, is there any differences in terms of toxicity between these different long chain fatty acid. And which one is more important than the other? And then secondly, when we are trying to understand what's the potential benefit, do you have like impatience what goes out of toxin of these different long chain fatty acid are going to be therapeutic important. Do we have any update on that?
Yeah, yeah, thanks. These are key questions. So the most toxic of the very long chain fatty acids or the most important when it comes to toxicity is the C26 long chain fatty acid. The C28 and C30 are also toxic, but they're not produced in as great an amount as the C26. The reason that the shorter chains are of interest and it's important to note that we have a very robust effect on the shorter chain fatty acids is that the chains are elongated through a two carbon elongation process. So C20 is compared to C22 is compared to C24 is compared to C26.
So over time, when you deplete that pool of the shorter chain long chain fatty acids, presumably you reduce the overall production and systemic exposure of the C26 long chain fatty acid, as well as the C28 and C30. It is not known how great a reduction is required to provide clinical benefit. That's one of the key questions I think everybody is interested in for this disease. We've heard various estimates anywhere from 5% to 25% and it's also not known how important plasma versus tissue reductions are. Fortunately, we show effects in plasma and tissue and in a CNS. So -- but again, we won't be able to determine real clinical benefit until we get a little further along, but thanks for the questions.
Great. Thank you so much.
Our next question comes from Steve Seedhouse with Raymond James. Please go ahead.
Yes, hi. This is Timur Ivannikov on for Steve Seedhouse today. And our first question today is about the doses being tested in the ongoing GLP-toxicity studies. What coverage does the top rodent in HP dose give you over, let's say, five milligram or 2.5 milligrams once daily for VK2809 in human?
Yeah, so we haven't disclosed the details on dosing in the GLP talks studies. I would say the exposure margins should be sufficient, but we haven't disclosed those details.
Okay, okay. Thanks. And maybe another question regarding the Phase IIa study and this question is about the initial bump in ALT, and maybe -- could you talk about the magnitude of that bump in the five milligram versus the 10 milligram arms, and does that magnitude of the bump correlate with the dose?
Yeah, I think -- so the bump doesn't occur in everybody. It tends to -- when it does happen, it tends to be early and it tends to resolve without any interruption of dosing. It is a dose related, so that when you look at means as you increase the dose, the mean tends to be a little bit higher. Interestingly, when you look at the 12-week data though, the largest reduction relative to placebo is actually observed in the highest dose. And so that's consistent with this benefit that you see from a robust reduction in lipid content.
Okay, got it. And then, I guess, our final question not sure if you can answer, but I don't know if you could talk about the selection of -- dose selection in the next study. Maybe what is the current thinking on the five milligram dose since that data is pretty new. Not sure whether you've come to a decision of whether to include this five milligram dose in the Phase IIb study?
Yeah, it's a good question. We're not going to disclose the details of the study design until we get a little bit closer, but I would say there will be a representation from the Phase IIa study in the upcoming study as well as some additional doses. And I think what we've seen pretty clearly from the data is that, you can likely reduce the dose and still achieve meaningful clinical benefit. And so, I think we've got a great flexibility here in choosing doses for the next study.
Okay. Thank you very much. Appreciate the details.
Our next question today comes from David Bautz with Zacks Investment Research. Please go ahead.
Hey, good afternoon Brian.
The first question I have is, are you seeing any partnership interest in 2809, and if so, what are those potential partners think of the TR beta class in general. Basically wondering, I mean, there's been a lot of disinformation out there about 2809, and I'm wondering if that's having any potential impact on partnerships?
Yeah. So I don't want to give too much color on any discussions we may or may not be having, but I would say, people recognize the potency and safety profile and really there aren’t many questions about the safety profile from any interested third parties. I think there's a fair amount of comfort there.
Okay. And as far as the upcoming trial, how concerned are you about patient enrollment with so many other NASH trials going on right now?
Yeah, it's a key question. We're very concerned. I think all of those other studies, sponsors would say something similar. But knowing that there is a lot of competition for patients out there, you plan accordingly. And I think everybody will be making every effort to try to mitigate any competitive issues that might limit enrollment. But it's just a factor of this space. It's a very high interest in the industry and a lot of studies under way. We don't think it will be -- certainly, wouldn't be worse than the Phase 2a study. We think it would be quite a bit easier to enroll that's -- the upcoming study than the prior study though.
I appreciate you taking the questions.
The next question comes from Andy Hsieh with William Blair. Please go ahead.
Hi. Thanks for taking my questions and congrats on the progress. So I have a question about the eDISH analysis that you have done on the EASL posters. So it's like non -- none of the patients were considered matching the Hy's Law, there are some patients -- including some placebo patients in the quadrant, Temple's Corollary quadrant So just curious how your interpretation of this, I guess, FDA design eDISH analysis?
Yeah, it's a really interesting analysis. And I think that the pure eDISH is a plot that looks set to total bilirubin and -- I'm sorry maximum total bilirubin and maximum ALT in any given exposure window. We did two plots. We looked at the maximum bili and ALT, as well as the end of study bilirubin and ALT. And the reason for that was to demonstrate further that even when you see a transient pop in ALT, it tends to regress with continued exposure and that's very clearly what the eDISH shows.
Interestingly, you don't see over time more greater population in what's called the Temple's Corollary quadrant, which indicates a greater risk of moving into Hy's Law. We didn't see -- not only did we not see anybody coming close to Hy's Law quadrant, but over time, you see a regression from Temple's Corollary into the more normal quadrant, which is the lower left quadrant in that draft. And at the end of the studies, and this is a combination plot, you're looking at Phase 1 and Phase 2 since there has been so much historical interest in that Phase I study.
At the end of that analysis, there are actually a higher percentage of placebo patients in the Temple's Corollary quadrant relative to treated patients, which is just -- it's not consistent with something that would be harmful to liver and it's totally consistent with something that would be improving liver health.
Great. Yes. Thanks for that detailed explanation. Also curious about just any updated [Technical Difficulty]
I'm sorry you cut out there, Andy.
Sorry, about that. Can you hear me now?
Yes, I can hear you now. I didn't hear the last part of the question.
Oh, sorry. Okay. So during the last quarterly call, you talked about the single-payer systems potentially are very interested in VK5211. I was curious if there's any update on that and any potential path forward?
I don't recall discussing the single payer system with respect to VK5211. I'm looking around in the room here, I don’t -- maybe, I'm misremembering the question.
Or maybe you talked about Japan, maybe not specifically on single payer system, maybe a payer that you'd like see in Japan or maybe in Europe.
Yes, yes. Sorry. Yes. So, in Japan, what we learned through numerous interactions since the study reported was that the patients tend to stay in the hospital for a longer time period relative to western markets. And as a result, since the Japanese insurance structure is to bundle hospital payments there was little room for pricing flexibility there. And so, that was surprising to us. And actually, not only was it surprising to us but it was surprising the parties that conducted that – those market research exercises.
We don't think that's necessarily the case in the Western markets. Most of the time hip fracture patients are discharged much more rapidly in the West relative to Japan. So we don't think that would feed into any decisions in Western markets. I think more problematically for hip fracture, is the registration endpoints.
What we've learned from discussions with FDA is that the anticipated registration path would involve a Phase 3 trial that combines function and quality of life. And those are each individually difficult end points, but when you combine them, it makes it exceptionally difficult to complete successfully without a large -- very long study and it's something that we're not going to pursue alone.
Okay, great. Thank you for answering all my questions.
The next question comes from Yale Jen with Laidlaw and Company. Please go ahead.
Good afternoon and thanks for taking the questions. You mentioned earlier in the script presentation that for the Phase 2b study you were focus on F2 and F3 fibrosis and with a more level of F1 patients. Would you mind elaborate a little bit more and then maybe the rationale behind it?
Yeah, thanks Yale. So the F2, F3 population, it's around a-third of the overall NASH market. We anticipate that that will be the most likely reimbursed segment of the market, at least initially. Those are the patients who have the greatest risk of progressing to further complications with their liver cirrhosis and the compensated cirrhosis liver failure.
And so, that's why we'll be looking at that end of the spectrum. We will include F1's though, just to understand any differences in those two patient groups and understand what the drug's relative efficacy is across those. And so to stratify in the statistical analysis plan for efficacy in these various populations.
Okay, great. That's very helpful. And maybe just a housekeeping question that just -- we just realized that -- we just learned that for the quarter, first quarter of this year, you guys, on the cash front used probably less than maybe $2 million in cash. I know the cash flow statement probably will be reported in the Qs, but just curious what make you guys have such a tighter expenses for the quarter?
Yeah. So the budget -- I appreciate the question, because I'm always surprised that the cash balance as well. It feels like we spend more money than we do and some of this so is -- the spending is offset a little bit by interest income. So we do realize over a $0.5 million a month in interest income, and so that provides an offset. If you look at the overall OpEx, it's -- I think it's about 50% higher this year than last year if I'm not mistaken.
And maybe the last final question here is that, in terms of the study of the first Phase I study you will have probably pretty next year in 0214. Could you give a little bit overview or overall projection of how this study will be designed. And I know you probably give more details later on when you complete IND filing, but any colors on that for time being? Thanks.
Yeah, thanks Yale. So we haven't given a lot of detail here, but I think you could think of this study would be a fairly unique design. We would have a single ascending dose component that rolls into a multiple ascending dose component that rolls into a two or three dose 28 days study in patients with X-ALD. And most likely patients with the AMN form of disease and we would evaluate and that component of the study a very long chain fatty acid level changes after 28 days.
Okay, great. Thanks a lot and congrats on the progress.
[Operator Instructions] Our next question comes from Mayank Mamtani with B. Riley FBR. Please go ahead.
Thanks for taking my question and congrats on the progress. I have a couple on 2809, and then one on 214. On 2809, I mean, you have a very high-quality problem of having improved responses at lower doses. So just taking a step back, how do you think about like finding that lowest effective does now obviously that you've done that study like how low you could go. It's a bit opposite to traditional drug development. So if you can just comment on the framework, how you're thinking about that?
And then the patient population like you said, you haven't offered, you didn't have biopsies, so you don't know the F fibrosis status of what patients you had in Phase I, but now that you go into F1, F2, F3, how do you think about the effect size on MRI-PDFF. I think that would be just helpful to understand how you're thinking about that. Again, I know you're not going into the specifics, but just on fat reduction, on ALT reduction, some of those things that you'd be looking to measure before you have the histology data in a few -- in a couple of years. It would just be helpful. How you're thinking about that? And then I have a very brief question on 214?
Yeah, thanks Mayank. And so as far as exploration of that minimal effective dose, we will include some lower dose cohorts in the upcoming study at least one anyway. And when you look at the 14 day data, it looks like around 1 milligram is where you start to see some activity.
And so, I think going below that may not be a wise exercise. But at 1 milligram based on a 14 day data, you might see something and since the drug is delivered -- targeted over a longer period, you might see a really nice effect down there.
The FDA always wants to understand where the minimally effective doses are, so I think coming down from 5x, makes sense given that we see identical F, so essentially a 5x and 10x.
With respect to the efficacy across severity, so there's -- I think often misconstrued that we didn't have NASH patients in this study. Absolutely, there were NASH patients in this study. We cannot prove that, because we were not allowed to biopsy.
But I think it's incorrect to assume there was not a significant representation of NASH in the study. When we look at other programs that have targeted liver fat, and metabolic parameters, it seems to show -- the data seem to show similar efficacy across different baseline severities.
And so, we think that this mechanism should demonstrate benefits as you increase in severity, but we'll certainly find that out, but that seems to what the data show at this point. And we know it shows that certainly on other measures of efficacy if you look at plasma lipids and if you look at liver fat, baseline does not seem to have a major impact.
So, it's hard to see why -- if there's an effect on fibrosis, it's hard to see why it would be there with F1 and not necessarily F2. So, I hope that makes sense, but good question.
Q – Mayank Mamtani
That does and maybe if I can ask a follow-up on NASH itself. So obviously on the Phase II stage, we're seeing more companies, especially the bigger ones, getting into partnering and pursuing combinations.
Like, do you intend to do that maybe at some point while you do -- while you go through your Phase II or do you intend to do that maybe at a future time point once, you have data from the histology?
A – Brian Lian
Yeah, it's a good question. There's a lot of interest in combinations. I think we want to be opened minded and flexible and certainly we're receptive to conversations that would allow us to move forward and explore combinations.
They would have to be arrangements that would make sense for Viking as well as the other party. And so, as those arise, we will evaluate them individually. But certainly, we don't need to complete the next study to begin thinking about combinations.
Q – Mayank Mamtani
Sounds great, and then very briefly on 214, is there any natural history study that is already published or is work in progress at maybe the institute you're partnering with. That shows this correlation of long fatty chain assets with some functional outcome that maybe is being looked at as a reference point. Again, I understand not a lot of work has happened with this disease population?
A – Brian Lian
Yeah, yeah, so there are natural history studies in the ALD population and of the AMN population. The correlations with very long chain fatty assets have not been part of those studies. We do know that when you reduce very long chain fatty acids, it seems to reduce inflammatory signaling.
And in animals, it seems to delay the onset of the phenotype. But it's just one of the challenges with orphan diseases. It's often hard to really get a good handle on the translate ability to humans until you actually get into the human studies. So that's not really a great answer, but just it's a reflection of the lack of data there.
Q – Mayank Mamtani
Okay, sounds great. Thank you for taking my questions.
A – Brian Lian
This concludes our question-and-answer session. I would like to turn the conference back over to Stephanie Diaz for any closing remarks.
Thank you again for your participation and continued support of Viking Therapeutics. We look forward to updating you again in the coming months. Have a great afternoon. You can all disconnect now. Thanks.
The conference is now concluded. Thank you for attending today's presentation.