Good day, ladies and gentlemen, and welcome to the Altimmune, Inc. Q3 Earnings Conference Call. At this time, all participants are in a listen-only mode. Later, we will conduct a question-and-answer session and instructions will follow at that time. [Operator Instructions] As a reminder, this call may be recorded. I would now like to introduce your host for today's conference call, Will Brown, Chief Financial Officer of Altimmune. Will, you may begin.

Thank you, operator, and good morning, everyone. Thank you for participating in Altimmune's third quarter 2021 earnings conference call. Members of the Altimmune team joining me on the call today are Vipin Garg, our Chief Executive Officer; Scot Roberts, our Chief Scientific Officer; and Scott Harris, our Chief Medical Officer. Following the prepared remarks, we will hold a question-and-answer session. A press release with our third quarter, 2021 financial results was issued last night and can be found on the IR section of the Company's website. Before we begin, I would like to remind everyone the remarks about future expectations, plans, and prospects constitute forward-looking statements for purposes of Safe Harbor provisions under the Private Securities Litigation Reform Act of 1995. Altimmune cautions that these forward-looking statements are subject to risks and uncertainties that could cause actual results to differ materially from those indicated, including those related to COVID-19 and its impact on our business operations, clinical trials, and results of operations. For a discussion of some of the risks and factors that could affect the Company's future results, please see the risk factors and other cautionary statements contained in the Company's filings with the SEC. I would also direct you to read the forward-looking statement disclaimer in our earnings press release issued yesterday and now available on our website. Any statements made on this conference call speak only as of today's date, Wednesday, November 10th, 2021, and the Company does not undertake any obligation to update any of these forward-looking statements to reflect events or circumstances that occur on or after today's date. As a reminder, this conference call is being recorded and will be available for audio replay on Altimmune's website. With that, I will now turn the call over to Dr. Vipin Garg, Chief Executive Officer of Altimmune.

Thank you, Will, and good morning, everyone. We appreciate you joining us today for a discussion of our third quarter 2021 financial results and business update. The third quarter has been a very productive time for the Company as we reach several key milestones in the development of Pemvidutide. First, we delivered on the 12-week Phase 1 study results in our trial in overweight and obese subjects. The data we generated exceeded our expectations as we demonstrated double-digit weight loss in the 1.8 milligram arm with favorable effects observed on blood pressure, serum lipids, and other measures. We believe we achieved a high watermark in weight loss given that dose titration was not used and there were no modifications to diet or physical activity. Most other programs in this class of drugs must use dose titration that is gradually increased dose to maintain tolerability. Dose titration presents considerable challenges for patient satisfaction and compliance, and logistical challenges for time-constrained primary care physicians charged with prescribing these therapies. So, it's highly encouraging that with straight dosing, we saw primarily mild GI side effects with no study discontinuations due to adverse events. The next key milestone we met was the acceptance of our U.S. NASH IND for Pemvidutide and the initiation of a 12-week Phase 1B NAFLD clinical trial to explore Pemvidutide's effect on liver fat in this -- in the NAFLD population. They're highly encouraged at the prospects of this trial, as we announced this morning, the results from an exploratory analysis that all of the patients with hepatic steatosis or fatty liver in the Phase 1 trial that received 1.8 milligram or 2.4 milligram of Pemvidutide experienced reduction in liver fat to undetectable levels after only six weeks of treatment. These findings speak to the potency of Pemvidutide both to…

Thank you, Vipin, and good morning, everyone. First, let me quickly recap our 12-week Phase 1 placebo-controlled single and multiple ascending dose study of Pemvidutide. The study was conducted on Australia under a clinical trial application and enrolled otherwise healthy, overweight and obese volunteers. The SAD portion of the study enrolled 36 subjects and the MAD portion enrolled three cohorts at doses of 1.2, 1.8 and 2.4 milligrams randomized 4-to-1 to drug or placebo weekly for 12 weeks. The study did not employ dose titration. Subjects receiving the 1.8 milligram weekly dose achieved an absolute mean weight loss of 10.3% at 12 weeks of treatment with Pemvidutide, with a similar degree of weight loss of 9.0% at the 2.4 milligram dose and 4.9% at the 1.2 milligram dose. Pemvidutide was well tolerated even in the absence of dose titration with no adverse events leading to discontinuations and predominantly mild adverse events. Favorable trends were observed in secondary measures, including a 28% decrease in total and LDL cholesterol, and a 38% decrease in triglycerides at the 1.8 milligram dose. Remarkably, these changes occurred in only 12 weeks. Glucose homeostasis as assessed by plasma glucose and hemoglobin A1C was maintained, and there was an improvement of insulin sensitivity as assessed by the HOMA-IR. Systolic and diastolic blood pressures also decreased in the absence of significant increases of heart rate. We've also had the opportunity to perform an exploratory analysis of the MRI-PDFF data on liver fat content in the subset of subjects through the initial six weeks of treatment. While the study enrollment criteria did not pre-specify a minimum liver fat content, it did enroll a number of subjects with hepatic steatosis or fatty liver, defined as a liver fat content of greater than or equal to 5% to enable an early…

Thank you, Scott. I will now provide a brief update on Altimmune's third quarter 2021 financial results. More comprehensive information can be found in our Form-10-Q filed with the SEC last night. Altimmune ended the third quarter of '21 with approximately $200 million of cash, cash equivalents, and short-term investments, representing a cash burn of approximately $18 million during the quarter. We continue to have sufficient cash to operate through 2023. Turning to the income statement revenue in the third quarter was a $158,000 compared to $2.9 million last year. The change in revenue during the periods was primarily due to a decrease in revenue attributable to the T-COVID program. During the comparable period in 2020, we were performing a lot of activities in the Phase 1-2 trial of T-COVID, which was completed earlier this year. We are currently collecting the related accounts receivable as the contract was completed during October. Research and development expenses were $29.2 million in the third quarter, compared to $17 million in 2020. The increase in R&D expense was primarily the result of AdCOVID related development costs, including the expensing of payments made to Lonza for the construction of a manufacturing suite. We continue to evaluate our strategic options with the respect to that space. The increases were offset by a decrease in the value of contingent consideration related to changes in the fair value of contingent consideration liability connected with the acquisition and development of Pemvidutide. As a reminder, we will -- Oh one last development milestone upon the dosing of the first patient in a Phase 2 trial of Pemvidutide This milestone is payable in shares of our stock and we estimate about 850,000 shares when we meet that milestone. General and administrative expenses remain consistent between the periods at $4.2 million in both of the third quarter of 2021 and 2020. Net loss for the 3 months ended September 30th, 2021 was $33.5 million or $0.81 of Net loss per share, compared to $17.8 million or $0.54 Net loss per share during 2020. The difference in the Net loss is primarily attributable to the higher research and development expenses and a lower contract revenue. I will now turn it back over to Vipin for his closing remarks. Vipin?

Operator, that concludes our formal remarks, and we would like to open the lines to take questions. Could you please instruct the audience on the Q&A procedure?

[Operator Instructions]. Your first question comes from the line of Seamus Fernandez with Guggenheim.

Hey, thanks for the question. So, guys, the first question really is, what additional color can you provide us on these five patients, the ALTs directional changes there? Anything with regard to the liver fat comparisons as we actually have looked at other drugs in NASH space, the FGF21 class appears to have rapid liver defatting as well, which I think only the absolute best number matches up to what you guys are showing in these five patients. How confident are you that this is going to expand to the broader array of patients? So then separately, a lot of investor concerns around ALTs, but you guys only had one patient that had an elevated ALT, efruxifermin had a similar type patient and its own clinical study. Maybe we can talk a little bit about the potential non-drug-related mechanisms that could be at play here like rapid liver defatting, I guess, which is drug-related, but is obviously may not be a direct effect of the drug, but it maybe defatting of the liver itself. And then separately, rapid weight loss, which some of our thought leaders also comment can have associated liver enzyme elevations that result in absolutely no liver damage whatsoever. And then those ALTs decline over time. So love to just kind of get a sense of your thoughts as you continue to compile the data and the data evolve? Thanks.

Yeah. Thanks, Seamus. Thanks for the question. There are lots of questions there, we’ll try to answer them all. Let me just start out by saying that we're very, very encouraged with this data, both the weight loss data and now the liver fat reduction data. Yes, these are small numbers and this is early data, but it's very consistent. Every single subject that had baseline liver fat content of 5% and higher reached below the limit of detection on 1.8 milligram and 2.4 milligram dose, so the two most effective doses. So, we'll talk more about it. B0ut as you know, we are doing a much larger study in NAFLD and really to us, this is a window into what we might see in that study. So, the potential of this drug, both in obesity and weight loss and now in liver fat reduction seems really, really good and that's what we're excited about. We think we will have a drug here, both for obesity -- not only for obesity, but also for NASH. With that, I'll turn it over to Scott Harris to talk -- to provide you more color on these five subjects, as well as talk about the ALT.

Sure. Good morning, Seamus. So regarding the ALT elevations, none of these five subjects had any changes in the ALTs. And as we've said in the past, ALT elevations are often sporadic and unexplained in studies, particularly in first-in-human studies. And in fact, as you've noted, they frequently been reported with other drugs. We did report on the prior patient with ALT abnormalities, I would finish that conversation to say that we have many patients in trial with more dramatic changes in MRI-PDFF, and also to your question about weight. Changes in weight as well who did not experience ALT abnormalities, including a subject who dropped his liver fat content from 19.5% to below the limit of detection without an ALT elevation. So, we don't think that the data currently supports that hypothesis, but obviously more information is needed. Regarding the comparison to other drugs, it has to be emphasized that the reduction of the MRI-PDFF to below the limit of detection is unchartered territory. Companies have not reported this in the past. We've achieved a degree of liver fat reduction that has not been realized by other drug development programs, where the goal is merely to normalize the liver fat content to 5% of less, the head of the imaging laboratory that performed the MRI-PDFF analysis who has very extensive experience and these assessments, advises that the observed reduction in liver fat was among the largest he had seen so far, if not the largest. So, I would emphasize that while the study was small and exploratory, the pattern that we've seen, its level of reduction in liver fat that's not been observed with previous compounds.

Great, and also quite rapid as well. And maybe just to provide a little bit more color on the NAFLD study. Can you just help us, what is -- are there -- what are the thresholds for enrollments as it relates to liver fat content? And I assume for simplicity reasons, biopsies are likely not going to be included in this Phase 1 study. But just wanted to get a little bit more color on the enrollment criteria for that study in the pace of enrollment that you anticipate as a result of the more, maybe restrictive criteria. Thanks.

Thanks for the question, Seamus. Well, if anything, the enrollment criteria are less restrictive than they were in the Phase 1 study, and we'll include a wider variety of patients. Now, the threshold for liver fat in that study is 10%. That's the cutoff that's been used by most sponsors. And as you mentioned, there will not be a biopsy in this study. This is a non-invasive study based on liver fat content. But I would emphasize that this population will now include older subjects, as well as subjects with diabetes, and we actually expect the pace of enrollment to be very rapid.

Great. Well, I'll jump back in the queue and congrats on some really intriguing data. Looking forward to the next dataset from your Phase 1b.

Thank you.

Your next question comes from the line of Yasmeen Rahimi with Piper Sandler.

Hi, team. Thank you so much for taking my question, and congrats on the great new data that you shared with us. I have a number of very short, tailored questions for you. I'm going to go just one-by-one. The first question directed to you is, what was the average weight loss that was observed in these five patients that really got great live fat reduction? So, let's start there.

Right. The average weight loss that I have for you is at week six. I would imagine that the numbers that we totaled would be approximately double that, although, I don't have that number in front of me. And the average weight loss in these subjects was -- with a range of weight loss was between 3.1% and 4.7%. So, the average weight loss was approximately 4%.

Thank you.

Again, Yasmeen, that was at week 6.

Okay.

So, it doubled in week 12.

Thank you. Second question directed to you is, was there any other MRI PDFF analyses done at an earlier point? I'm trying to understand, I mean, we're already at the plateau of 90%, but sort of what the curve looks like in terms of the flow. If you could just comment on that, and then I have 2 more short questions.

Thanks, Yasmeen. So, the way the study was conducted, there was a baseline MRI PDFF in week 6 and then week 12. We don't have the week 12 data yet, so we don't have a slope other than to be able to tell you what happened at baseline and at week 6.

Thank you. The next question I think for us and a lot of our clients are asking us to just really understand the translation of weight loss between overweight population versus the NAFLD population that you will be enrolling in your 1B. So, when we look at the data from other [Indiscernible] [Indiscernible] what we notice is that the presence of being an [Indiscernible] patient does not impact the degree of weight loss. But what does impact it is the presence of diabetes. So, I would like you to maybe explain to us, should we be expecting weight loss rates that we saw in obese population to be similar to the NAFLD populations? Specifically, the NAFLD non-diabetic? And then the second thing is, what do we know about GI tolerability based on historical data when we go from an old obese population to NAFLD?

Thank you for the question Yasmeen. So, you're correct that studies with drugs in other mechanisms have shown approximately a 30% lower weight loss with diabetics. So, our prospective plan in this study is to readout in weight loss in both the non-diabetics in the population and the diabetics and stratify enrollment in that manner because it is an important covariant in the amount of weight loss that will be achieved, although not in the amount of liver fat reduction. so that's to your first point. Regarding the adverse events, we do not feel that there will be any difference in the adverse event profile going forward because of the inclusion of other patients. It's been said by experts in the field, that diabetics actually realized lower adverse events than non-diabetics. Also, I recognize that as we go from Phase 1 to Phase 2, in general because of the change of the way the studies are conducted, adverse events drop between Phase 1 where we have intensive monitoring, often in-patient in Phase 2. So, I would say that as we move from the Phase 1 study to the Phase 1b NAFLD study that we'll actually see no worse than the adverse events that we have, if not an improvement.

Thank your team for clarity, I'll jump back in the queue.

Our next question comes from the line of Liisa Bayko with Evercore ISI.

Hi, thanks. Most of my questions have been answered, but I guess I'll just kind of rip off the last series of questions. Can you just comment on the effect of age? I know these patients were slightly younger than perhaps future studies will be. And just wanting to understand what you know about the effect of age on weight loss and also loss of fat in the liver. And if that would have any impact. And if you could just comment a little bit on what the age of these patients -- these 5 patients where you [Indiscernible] at liver fat. Thank you.

Right. So, it's been showing in other studies, as well as our studies. We did an analysis of that which we presented, but it's also been discussed in the [Indiscernible] programs. There is no effect of age and weight loss and if there is any effect, there's a higher level of weight loss as you get to older age. So, translating from a younger population, in this Phase 1 study to the next study or studies that we'll be doing, if anything, based on that information, we will be seeing more weight loss. There's also been no effect of age on the degree of fatty liver reduction that's reported in other programs. The average age of this cohort was similar to these 5 patients with similar to the general cohort that we reported on earlier.

Thanks.

Your next question comes from the line of Jon Wolleben with JMP Securities.

Hey, good morning and thanks for taking the questions. [Indiscernible] can you just remind us what doses you're studying in the NAFLD study, how many patients are in that one, as well as how many patients are in the? [Indiscernible]

Thank you, Jon. So, we're going to be taking 3 doses into NAFLD study, 1.2, 1.8, and 2.4 milligrams. There will be 72 subjects in that study. That means 18 per each of the [Indiscernible] So then it also includes a placebo [Indiscernible] and the DDI study will be 36 subjects.

Got it. And with deliver meeting coming up this weekend, I'm not sure if you had a chance to take a look at this yet, but I saw an interesting analysis for semaglutide, where they found that 69% of the histologic improvement was due to weight loss. So, I'm wondering kind of your thoughts on that analysis and then also what you might expect with a direct acting [Indiscernible] effect with kind of game types.

Right. Well, we would agree with the interpretation, but recognize that with semaglutide, it has no direct effects from the liver, so we didn't [Indiscernible] entirely on weight loss. In the similar analysis on hemoglobin A1C at 1 year that they performed in their step program, the majority of the hemoglobin A1C drop that they had was not due to the incretin effect, that is the stimulatory effect of GLP-1 and insulin secretion, which did give better acute diabetic control in the first few weeks. If 52-weeks, the majority of the drop-in hemoglobin A1C was due to the weight loss. So that paralyze what you've just said about the effects of weight loss on histologic improvement. Now, as you aforementioned, is a direct effect of glucagon here on the liver, which is different from semaglutide and which differentiates a Pemvidutide from GLP-1 mechanisms semaglutide. So, we believe that there is an opportunity for even greater weight -- fat reduction, as well as greater weight loss with the additive glucagon agonism. So, we agree with your assessment.

Interesting color. Thanks again for taking the questions.

You're welcome.

Your next question comes from the line of Mayank Mamtani with B. Riley Securities.

Good morning, team. Congrats on the progress and thanks for taking our question. So -- maybe if I can just quickly ask a follow-up on the NAFLD study and just comparing the baseline characteristics of the Phase 1 obese study that we talked about. What is the expectation -- sort of differences that you may have on the baseline ALT levels that the NAFLD study would have? I think you had about somewhere between 20 to 30 in the obese healthy volunteers’ study. And just trying to understand what might be the difference in [Indiscernible] that you may observe on ALT given now that we have a good idea on what you have on PDFF and weight loss as we think about the NAFLD study.

Mayank, I'm going to try to answer the question. I'm not sure if I fully understand that. So please [Indiscernible] in if I don't answer your question completely. In the Phase 1 study that was recently completed we allowed up to two-fold elevation. And we'll have a very similar cut off in the upcoming study. I'm not really sure I understand your question about the kinetics. Could you please elaborate on it --?

Sure.

-- so, I can answer it?

Yes. We -- just based on your ALT data from the Phase 1 study, we are not seeing -- It's like except for that one anomaly, we are not seeing a significant lowering for example, but generally in NAFLD studies, you would want to see that ALT dropped along with liver fat, and weight loss. So, should we should we be expecting that as you go into the NAFLD diabetic and non-diabetic study? Just curious.

I understand now. Yeah, we should expect that. Recognize that in the study that we recruited because these patients, in general, we're not a NAFLD population. We're not going to see or have the opportunity to look at ALT dropping [Indiscernible] I was in the Phase 1 study. But specifically recruiting people where we're going to be having a pharmacologic effect on liver fat, which is driving the ALT. We should see that reduction in the upcoming NAFLD study.

I understood. And then on the lower dose, 1.2 milligrams dose level. Scott, did we have any patients there with elevated liver fat? Just curious what would the findings, if any, on the MRI PDFF says for that dose level.

Right? We had two patients at the 1.2 milligram dose, who had elevated liver fat. One with 19% and one with 11%, approximately, the drops there were 27% and 70% for a mean of about 48%. So, the effects were they're very comparable on other drugs, but not as robust as the reductions at 1.8% and 2.4%. Where in each of those arms, the reductions were greater than 90% into below the limit of detection.

Wow, that's amazing. And then, on the IND package for obesity, just remind us how this is different than NASH IND? Just what goes into it? Just curious.

So, the heavy lifting Mayank was done by the NASH IND because that's where the major parts of the IND were presented. Things like the manufacturing, the toxicology, and also some of the early clinical data. Now, the emphasis of the obesity IND will mainly be clinical. And we will provide the first study to be conducted under the IND, that's a requirement of the IND. And we'll update with any additional data from the Phase 1 study and from our chronic tox. So -- which it will be completed before that study. So really it's a smaller IND oriented mainly towards the clinical development program with some additional [Indiscernible] dates. But the heavy lifting was done with the NASH IND submission in August. And as you know, it cleared in September.

Great. And the final question on HepT and [Indiscernible] I understand we are a little away from the data, second half of next year. I'm just curious how you might be thinking of this being deployed as a combination. I think you commented on this being used with [Indiscernible], but it's becoming clear that at least in [Indiscernible] and [Indiscernible] gets out of what you need and the importance of an immunostimulant is becoming increasingly clear. So, you might be in a sweet spot there. Have you thought of thinking about this more strategically? As you look to be part of a protent combination for developing functional gear for [Indiscernible]

Mayank. I'm going to ask A - Scot Roberts on the line. I'm going to ask Scott to answer that question, Scott.

Hi, Mike and thanks for that question. You've hit the nail on the head that's exactly how we see this. The thinking is to create a window with even lower levels of surface antigen than are currently encountered with new treated patients alone. And that would provide a better field for the immunotherapy to stimulate the T-cell response. So, as you know, the [Indiscernible] approaches mean to do that, it's not really clear if they're doing that well, and we're [Indiscernible] not doing it for a long term, but they can create that window of opportunity for a HepTcell to work better. So that's how we're thinking about that and we think that there's a lot of potential in the approach.

Thanks for taking our questions.

Your next question comes from the line of Patrick Trucchio with HC Wainwright.

Thanks. Good morning. I just have a couple of follow-up questions. The first one's on NASH. I'm just curious based on your discussions with regulators in Europe and North America. How likely or unlikely do you think a change in the regulatory endpoints as they currently exist for potential approval of NASH compounds? How likely or unlikely is that to change or is it more likely just stay how it is for foreseeable future?

Thanks for the question, Patrick. It's extremely important. I'm not aware of any public announcements that FDA or EMA will be revising their guidance’s for NASH approval. I think that there is a great deal of talk that they should change and perhaps have to change to veer towards non-invasive assessments and steer away from the liver biopsy. But I can't give you any further guidance myself. It’s the likelihood of either those regulatory bodies making a change and when it would occur.

Got it. And then just on HepTcell on the Phase 2 program. Can you remind us if this study [Indiscernible] to demonstrate a certain reduction in surface antigen? Or what would you need to see in [Indiscernible] to give you confidence that it can act as pulling immunostimulatory to combine with another -- with a direct acting antiviral?

Right. So, the study has 2 key endpoints. The primary endpoint is a 1 log reduction in surface antigen. In the study, it is powered to show [Indiscernible]. Another key endpoint is the clearance of the surface antigen. We think that that should be achievable as well, but we don't have our power oriented towards that. The approval endpoint will be the clearance of the antigen, probably. Although that discussion with the agency has not taken place. clearly to get reductions is extremely meaningful as we move forward, especially in combination therapies with partners.

Got it. Just 1 last 1, just in terms of potential collaboration on Pemvidutide. How are you thinking about that? Is there a point in development in which you would look for collaboration partner, how far long do you bring this program on your own?

Yes Patrick, thank you for the question. I mean, as we have said previously, we are well positioned to take the program through the next phases of trials here without funded to do that, our goal is to really increase the value of this asset with each study. So that's why we are planning multiple different studies to really -- to gather a very compelling package. Ultimately, we think this is an asset that we will have a partner. At what stage, I can't tell you exactly right now, but we are marching towards that goal and making good progress.

Perfect. Thank you very much.

And a reminder to ask a question, [Operator Instructions]. Please stand by while we compile the Q&A roster. Our next question is a follow-up question from the line of Liisa Bayko with Evercore ISI.

Hi, this is relating to what we talked about earlier with baseline fat level, but I know future trials are going to be looking at patients with at least 10% liver fat as a cutoff. Can you maybe talk that higher threshold, it impacts outcome to patients with higher baseline levels of liver fat? Would you expect to see the same more or less? Like how much more difficult is it to reduce liver fat from a higher baseline? Thank you.

I would phrase the question as a positive. The higher the liver fat, the greater the opportunity for the percent reduction. As we saw in the program, the data that we presented, Liisa, we had a patient with -- with patients with up to 19.5% liver fat, who not only dropped their liver fat content by substantial amounts. Not only do we normalize liver fat to 5%, we actually dropped that 19% in just 6 weeks to below the limit of detection. These are -- this is unchartered territory. Drugs have not done this before, so we think that the opportunity to expand the change and see an even greater change is even higher. So, in moving to a 10% population, I think the opportunity to duplicate these changes are great and see really unprecedented changes in liver fat.

Okay. Thank you. And that's really helpful. And then just you may have addressed this already, but were any of those 5 patients, the 1 of the 5 patients, with elevated ALT?

No. The patient with the elevated ALT, Liisa, had a liver fat content of baseline with 3.7% and that patient drop below the limit of detection. So that patient was not included in this -- the analysis that we just provided. But I would also emphasize the patients that we've reported on with much greater reductions in liver fat content as I just mentioned, from 19.5% to below quantitation and another one, 17% below quantitation. I could go through the series here, did not, repeat, did not have ALT drops.

Elevation.

Excuse me, elevations. So consequently, although that might have been the framework for initial conjecturing [Indiscernible] hypothesis generating, the data that we have that we're reporting now, does not confirm a relationship between the drop-in liver fat and the ALT elevation.

Understood. Thank you. And then just one more question. Moving forward [Indiscernible] include diabetic s in your studies and maybe you can describe the impact of diabetes on weight loss for us. Thank you.

Yeah. So, as we talked about earlier, traditionally in drug development programs, diabetics have lost less weight over the course of a trial; the 9 diabetics typically about 30% less. So, based on that, in our NAFLD study, we will be stratifying subjects. That's the 12-week NAFLD study that we've recently launched, Liisa, restratifying subjects, but the presence or absence of diabetes at baseline and analyzing the weight loss separately. in the Phase 2 study that we'll be conducting in launching next year, we are enrolling non-diabetics. So that will be a pure look at that population and the weight loss in that population. And as I mentioned before, should we conduct the 12-week extension to the NAFLD study, we'll have 24-week data on weight loss in both non-diabetics and diabetics. And probably around the middle of next year.

Okay and then just -- is there a certain proportion of diabetics that you want to have in the study? [Indiscernible] understanding you're stratifying them but do you expect it to be like a third or are you cut off at 50%? Is there some number?

Right.

Overall.

I mean, I think that [Indiscernible] 30% to 50% is probably an initial good estimate.

Okay. Thank you.

Welcome.

At this time, there are no further questions.

Thank you, everyone, for participating today. We appreciate the opportunity to share our results and outlook with you, and thank you for your continued interest. Have a nice day.

Ladies and gentlemen, this concludes today's conference call. Thank you. You may now disconnect.