BioVie Inc. (BIVI) Earnings Call Transcript & Summary

Hi, this is Craig with RedChip Company. Thank you for joining today's event with BioVie, which trades on the NASDAQ under the ticker BIVI. With us today, we have Cuong Do, President and CEO of BioVie. [Operator Instructions] Before we begin, please allow me to read the safe harbor statement. This call may contain forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. All statements pertaining to future financial and/or operating results, along with other statements about the future expectations, beliefs, goals, plans or prospects expressed by management constitute forward-looking statements. Any statements that are not historical facts should also be considered forward-looking statements. Of course, forward-looking statements involve risks and uncertainties. I now turn the webinar over to Cuong. Please go ahead.

Thank you, Craig. Thank you, everyone, for joining me today. I'm Cuong Do, I'm the President and CEO of BioVie. As you know, the company has 2 assets. Our lead asset is our drug candidate, bezisterim, formerly known as NE3107. In clinical trials, it is shown to reduce inflammation and the associated insulin resistance. Parkinson's patients have experienced improved motor control. Alzheimer's patients have experienced improved cognition and function, and everyone has seen lower levels of DNA methylation, which is essentially a modulation of the biological aging process. And we'll go into greater detail on all of that in the following minutes. Second drug is BIV201, which is being developed for ascites, which is an end-stage liver disease condition that is over 50% mortality rate within the next 12 months. And BIV201 has the potential to become the first therapeutic for that condition. As a company, our priorities are very clear. We want to launch our next Parkinson's trial, most likely in early 2025. Similarly, we will launch our trial in long COVID in early 2025. And we hope to launch our Alzheimer's Phase III in late 2025 as well. And we have a rich pipeline. We have a rich set of data readouts over the course of the next couple of years that will provide plenty of catalysts for the company and shareholders. As you may know, we are a company that believe that chronic low-grade inflammation as mediated by TNF alpha is a starting point for many things that start to go wrong in the body. So whenever you have TNF alpha, it drives something called [IKK and JNK], which leads to insulin resistance which has been implicated by diabetes, metabolic disorders in Parkinson's. When you have TNF alpha, it just drives a lot of inflammation through the release of various cytokines. TNF alpha also leads to the phosphorylation of tau in Alzheimer's, but also drives DNA methyltransferase 3A and B, which leads to the acceleration of our DNA methylation, which has been associated with a large number of age-related diseases. And of course, bezisterim acts on essentially reducing TNF alpha production. Bezisterim is a small molecule that patients takes twice a day. It freely crosses the blood-brain barrier, so it gets -- is able to get into the CNS. And as the team figured out the mechanism, it involves something called ERK or the Extracellular Regulated Kinase. It's been known for decades that ERK plays 2 very different roles in virtually every cell in our body. The first involves insulin signaling or insulin would bind to cell surface receptors, which activates a cascade that activates ERK for all of its cellular growth, repair and regeneration activities. This is known as homeostatic ERK. But ERK also plays a critical inflammatory role, where different extracellular signals would essentially activate MEK which then activate ERK into its active form, something called P-ERK or phosphorylated ERK. P-ERK would interact with nuclear factor kappa B to trigger the production of TNF alpha. And when you have TNF alpha, you create a forward-feeding pro-inflammatory cascade that just builds more and more inflammation. So it's obvious what you want to do. You want to block inflammatory ERK but not touch homeostatic ERK. But unfortunately, that is much, much easier said than done because dozens of teams over decades tried to do it, but no one was able to do so. All of those drug candidates ended up failing due to toxicity because no one was able to find a selective enough inhibitor of just inflammatory ERK. And frankly, that's where we got lucky. We did not set out to do this. We just got lucky and we were astute enough to recognize what we saw. It turns out that bezisterim blocks the activation of ERK and NF-kappa B, does not block ERK itself. So that's why it's very different than all of the other prior efforts because all the other prior efforts tries to block ERK. We are not blocking ERK. We're blocking the activation of ERK into its active form. And if you do not have activated ERK and you do not have activated NF-kappa B, you will not have the production of TNF alpha and everything that goes along with that. So this then has the ability to be applicable in a large number of areas. Our #1 priority right now is Parkinson's disease. Now it's been known for quite some time that 2 conditions must be present at the same time for a person to develop Parkinson's symptoms. The first is to have a low dopamine levels in the brain and then the second is to have inflammation and the associated insulin resistance. If you somehow are able to reverse insulin resistance in the brain, the body then is able to make use of the available dopamine. So people have tried lots of crazy things, frankly, to try to reverse insulin resistance, including what's shown in this chart, where this company tried to use inhaled insulin just to try to get some more insulin into the brain so that you could get more glucose available. And if you're able to do so, like shown here, you can get a little bit more insulin into the brain, it does lead to improvement and what's called the Part III score or the motor score on the Unified Parkinson's Disease Rating scale. But frankly, that is just not very practical. So to this day, clinicians have to resort to using a drug called levodopa to enhance the level of dopamine in the brain. Levodopa is a fabulous drug. It is able to restore muscle control, and that's why it remains the standard of care 5 decades after it was introduced. But levodopa has a number of challenges. 1 is that it has a short half-life, so it does not act for very long. And then the second is that its effect wanes over time. So the longer you take it, the activity wanes, so you end up having to take more and more higher doses of levodopa. But as you get into higher doses of levodopa, it causes something called levodopa-induced dyskinesia, which is the trembling that you see Parkinson's patients have. But when you have the dyskinesia, all you can do is reduce the dose of levodopa and wait for the dyskinesia to pass. But as you cut back on your levodopa, you lose muscle control. So you're just rigid, you can't move. So Parkinson's patients right now just really have a terrible challenging situation. And it's a situation that we believe bezisterim can address. Because in our preclinical work in rodents and nonhuman primates, we were able to show that bezisterim alone was equally effective at restoring muscle control as levodopa. Now that is a huge statement in and of itself because through the decades, no other drug has been able to show that it's equally effective as levodopa. And here, we have been able to show not only is it bezisterim equally effective as levodopa, but when you use the 2 in conjunction, you saw a synergistic effect. So this is disease score, so a lower number is better. So when you give bezisterim with levodopa, you saw that the monkeys here have the greatest muscle control. And at the end of the study -- at the end of the study, when we sacrificed the monkeys, we saw that those treated with bezisterim retained twice as many dopaminergic neurons compared to those that are untreated suggesting that bezisterim provides a neuro protective property, which to us is not at all surprising because we know bezisterim reverses insulin resistance, which means there's greater glucose availability in the brain. Secondly, we know that bezisterim increases blood flow in the brain, which means there's greater oxygen availability. So when you have more oxygen and glucose in the brain, it only bodes well for neuronal health. So based on this terrific preclinical data, we wanted to go into the clinic. So we conducted a small essentially safety study first. We enrolled 40 patients in a small trial that involve moderate to severe Parkinson's patients who are very difficult to treat. At its heart, it's a safety study, but we conducted it in a manner to see if we can get an efficacy signal. So we essentially replicated in humans what we did with nonhuman primates. So we treated patients with bezisterim and levodopa as shown in the blue and half the patients were given just levodopa alone with a placebo as shown in red. And after 28 days of treatment, you see that those treated with the combination saw roughly a 3-point difference advantage on the Part III score or the motor score of the unified Parkinson's disease rating scale. Now that's a clinically meaningful difference. But if you look at patients who are younger than 70 years old, that difference is over 4 points, which is a huge difference that you don't see very often. But what got us and our experts excited has to do with this what's called the time 0 muscle state shown in the shaded area here. I mentioned before that levodopa has a short half-life, which means that when Parkinson's patients take their evening medication and go to bed, the levodopa would wear off overnight. So that in the trial, as is in real life, none of the patients that were given just levodopa alone had control of their muscles in the morning. None. So that means that they were stuck, their muscles were rigid, they're stuck, they're stuck in bed. So their muscles are considered to be in the off state, first thing in the morning, whereas you can see that roughly 1/3 of the patients given bezisterim had control of their muscles in the morning. So their muscles were in the on state. So this gives us great encouragement and also gives us very clear human proof of concept that shows that bezisterim can be given in conjunction with levodopa to help moderate and severe Parkinson's patients improve their muscle control. And this has established the first of 2 legs of what we want to do in Parkinson's, namely combination therapy with levodopa. Our next trial will address the second leg, where we will give bezisterim alone to Parkinson's patients who need to go on to medication for the first time to address their symptoms. That trial will start in February, and we aim to have top line data readout by the end of 2025. And when both sets of trial, when is fully developed, we believe that bezisterim has the potential to become the first new therapy for Parkinson's since the advent of levodopa over 5 decades ago, and we believe this could easily create a $3 billion annual sales opportunity in the United States alone. So with that, let me -- in the interest of time, let me move on to Long COVID. Long COVID persists and remains a major problem in the United States today. Currently, 17 million Americans, adults are suffering from Long COVID and up to 4 million have such debilitation that they are unable to maintain their current job or career trajectory. And so while most of us believe that COVID is behind us, and it largely is behind us because of better medication and vaccines, Long COVID remains a real problem for about 5% of the world's population, and there are no approved drug treatments for it. And researchers over the course of the last couple of years have tied the symptoms of Long COVID to sustain inflammation that works through the exact same mechanisms where bezisterim works. And since bezisterim has the potential to modulate the activation of ERK NF-kappa B as it's mediated through these different mechanisms, it should have an impact on long COVID. And that's why the Department of Defense has given us a $13 million grant to fully fund an exploratory Phase II trial to see if this could work. Now this was a very, very competitive process, whereby we were, we believe, the only company that was only therapeutic that was given a grant to go and explore if could be done. And so this trial, we aim to start in February and with some luck in rapid enrollment, we hope to have data by the end of 2025 or early 2026 as well. So bezisterim in Long COVID. What -- a lot of people are most excited about is the application of bezisterim in Alzheimer's. We had -- if there's interest, we can come back and explain how it works and the mechanism and so forth. But most everybody wants to just jump to the data. So let me just start with the data. We unveiled our study at the end of 2023, and we saw some incredibly encouraging data. So on an endpoint called CDRs B, which is the same endpoint that was used by the FDA to approve 2 prior drugs, what we found is that patients treated with bezisterim for just 6 months experienced a 68% slowing of cognitive decline compared to those treated with placebo. And the #1 reported safety concern was a mild headache reported by fewer than 10% of patients. Now these are huge and incredible numbers. To give you context for what those numbers mean, the FDA has now approved 3 drugs, 3 monoclonal antibodies from Eisai, Biogen and Lilly. And those drugs on average has about a roughly 30% slowing of cognitive decline after 18 months of treatment. And all of those 3 drugs have significant concerns about safety involving brain swelling and brain bleeding. Now I give you these numbers not to make a head-to-head comparison. That's not the intent. You can only do that in the same trial. I give you these numbers to kind of put the context of what we see with bezisterim, 68% slowing of cognitive decline after 6 months of treatment with only 10% of patients reporting a mild headache is a very compelling efficacy and safety finding. And if you look around down the page here with all the other cognitive and functional measures, you see that the advantage that bezisterim has over placebo was equal to or much, much greater than what's been demonstrated for the comparative drugs. So very, very encouraging efficacy signals. But as we unblinded the trial, we learned that we had a problem. In that 15 out of our 39 clinical sites deviated from our protocol and enrolled patients they should not have. Now we have never seen anything like that before. No one conducting clinical trials in the U.S. has ever seen anything to this magnitude where 15 sites in 1 geographic area seemingly coordinated to ignore our protocol. So we have reported all 15 sites to the FDA for their investigation, and we know the FDA have investigated, are investigating and are handing out what I call 483 citations right now to some of these 15 sites that they visited. And in the meantime, we've also excluded all of the patients from those 15 sites from the data you see on this page. So despite the data, the efficacy signal being very encouraging, we missed on statistical significance, right, because we had to exclude so many patients. Now we have studied the data. We know the statistics behind this thing, and we've looked at scattering and all kinds of statistical measures. And we're absolutely convinced that if we had just gotten to 125 patients per arm as the study was designed to do, we would have seen statistical significance. And since we know this drug works, we're going to go and redo this trial. And our aim is to redo the trial at the end of 2025. And frankly, that's the reason why we have lost more than 95% of our market cap. We were worth well north of $500 million last year, and now we're down to somewhere between $20 million and $40 million of market cap now. So -- and that's -- and because it's been -- instead of talking to the FDA about accelerated approval, we're now having to find ourselves to go and redo the trial, which we will do because we're absolutely convinced that this drug works. Now lastly, let me just turn to the area of longevity, and then I'll turn it open for Q&A. To explain our work in longevity, I'd like to start with an analogy. So think of a DVD. When you first take a DVD out of its packaging for the first time, it is pristinely clean. So when you put it into the player, the laser has no difficulty reading and decoding the information that's contained on that disk. As a result, you get beautiful pictures and sound on playback. But as you use the disc over and over again over the years or decades, you may get scratches on it, you get fingerprints on it. And as a result, the laser would have difficulty cutting through all that gunk. And as a result, you get mis-decoding that leads to the stuttering and the skips that you may see. And it's all a problem of mis-decoding the information on that disk. And it turns out the exact same thing happens in our body. As you know, everything in our body is encoded for by our genes and our DNA. And as we age, there's a natural process called DNA methylation that takes place, whereby different methyl groups gets added to the surface of our DNA. And think of these methyl groups as the genetic equivalent to scratches and fingerprint smudges on that DVD. So as the DNA -- as the methylation accumulates, the molecules that are responsible for decoding it has trouble reading through. And so you get missed decoding of DNA. And that's why the hyper methylation of DNA has been associated with a large number of diseases, especially age-related diseases. And the extent of DNA methylation can be measured by various biological clocks. Now I give you all of that background to explain this data. So in the Alzheimer's trial, we took blood samples at the end of the study -- and we all sent them all off to be analyzed and we calculated something called age deceleration, which is the difference between your biological age as measured by these various biological clocks and your actual chronological age is the number of years we've been alive since birth. And what you see is that patients treated with bezisterim saw upwards of 5 years advantage over placebo on their biological age deceleration. Now before you get excited and think that this may be reversing aging or the fountain of youth, no, that's not what we're saying. We cannot slow down aging. We cannot reverse aging. But what we are saying is that we believe bezisterim may be able to play a role in modulating the accumulation of DNA methylation and therefore, hopefully keep -- play a role in keeping all of us healthier for a longer period of time by reducing the amount of accumulated DNA methylation. We have lots more that we can go into. I can answer any question you want. But let me just wrap it here by saying I believe that we have one of the most exciting portfolios around, including the fact that this is now the first drug candidate that has been able to demonstrate in a clinical trial and impact on DNA methylation in a manner that's tied to disease. I believe we represent a terrific buying opportunity for investors who have a 2-year investment horizon. We have lots of clinical readouts that will be coming up over the course of the next year. First, it would be our Parkinson's trial at the end of 2025. After that would be Long COVID, hopefully, by the end of 2025, early 2026 as well. And I believe that we represent a terrific opportunity not only because I'm the CEO of the company, I'm also one of the largest shareholders in the company as well, and I continue to put money into the company whenever there's an opportunity for me to do so. So with that, let me stop my screen share, and let's just -- I'd like to answer any questions you may have.

[Operator Instructions].

First of all, I apologize if the horizontal and blank boxes. There's something that's wrong with Zoom and the computer. I'm traveling that's something that's going on with this computer that nobody has ever been able to figure out. My apologies, but hopefully, you were able to see enough of it. The next question is, is [Taren Paiser] still the largest shareholder in the company? Yes, he is still the largest shareholder in the company. He currently owns roughly 15% of the company. Do we have any plans on executing any offerings in the next 2 quarters? We have no plans at this point for any additional follow-on offerings. But as you know, we are -- all biotech companies are always going to be always raising funds, right? So when an opportunity comes along that we just cannot refuse to take to pass, we may exercise our option to go and do some additional raise. But as of now, we have no plans for additional follow-on offerings. Next question. So what is the responsibility of BioVie in making sure that any trial that are run do not have the problems of the Alzheimer's trial? That's a great question. We believe what happened to us in that Alzheimer's trial, first of all, was not unique to us. But I think it was more a reflection of the reality of running clinical trials during COVID. We ran this trial. We recruited the patients during COVID during a time where, frankly, no one can go into the clinical sites. So we can only rely on the information that was put into the electronic systems, because our monitors and the CROs monitors could not go into the sites as we normally would. And large -- and thankfully, that is largely behind us. We now have greater access to the sites. So that's one. And we, as a company, chose to do something that's very different than other companies. Other companies who have swept it under the rug and just moved on. We chose not to. I chose not to because, 1, I think that is just wrong. And 2, those sites are -- some of those sites, many of those sites are still conducting clinical trials now for other companies as well. And we believe that if we made a big stink about it, we may be able to help other companies, other patients as well. And that's why the FDA is taking it for grant. It's taken it so seriously and are investigating those sites. After we made such a big think about it, we took such a public stance on it, we've been hearing from other companies that they face exactly the same problem as well. And we believe that is frankly, bad behavior that came about because of COVID. And hopefully, that is behind us. Next question, orphan liver disease drug, do you foresee raising as much capital as you just executed in the [indiscernible] clinical trials? Well, first of all, that program for BIV201 is the most de risk program I've seen in my 35-year career developing drugs. We know the drug works from decades of experience with the drug outside the U.S. but it was never approved in the U.S. because of a terrible safety profile. And with our novel formulation in BIV201, our clinical trials have already shown that it is safe. There's been no drug-related SAEs in the 2 trials that we have conducted with that drug. So we have high confidence that, that drug will work and will be approved. And we already have orphan and fast track designation for that drug. So you may be asking yourself, so why is Cuong so excited about the drug, but it's not our #1 priority, right? Parkinson's is our #1 priority because it is a relatively small trial. It's a relatively short trial and it's a relatively simple trial that we can conduct that will give us data by the end of 2025. BIV201 is a very -- it has a great risk reward trade-off. But unfortunately, it will also take us 2 years to conduct, and it will involve enrolling well over 100 patients into that trial, and it's going to cost us $25 million and $25 million that we, as a company, do not want to spend on the trial right now. So we are actively discussing with other companies whenever we can to find a partner. So that program is on hold until such time as we find a partner. The next question is, would we develop drugs simultaneously that are in different stages of clinical trials? Yes, the answer is yes, but it's all a function of capital availability. We are trying to be very capital efficient, right, at this point in time. And so our ability right now, given our current financial resources is to run the Parkinson's Phase II B in parallel with the Long COVID exploratory Phase II, because the Long COVID trial has been fully funded by the Department of Defense and the funding that we've been able to raise within the last couple of weeks allows us now to fully fund the Parkinson's trial. Progress with that ascites program. As you may know, we terminated a Phase II B trial in ascites midway through because we had, at that point in time, already had enough statistically significant data to show that those that completed treatment with BIV201 had dramatically lower levels of ascites fluid buildup. And since this is a condition that has 50-plus percent mortality within 12 months, we thought that the only responsible thing for us to do is to stop the trial early and to engage the FDA in a conversation of what it takes to move on to Phase III, that single Phase III that we need to conduct to get approval. As of now, we have received all the feedback that we need from the FDA to conduct the Phase III trial. So frankly, it is just awaiting funding for us to initiate the Phase III trial for ascites. The next question is, did we ever sue the labs that tainted to the last trial? Many, many people have asked me this question and have asked me why am I not turning the lawyers to sue the sites that tainted our trial. I have resisted doing that. Instead, we've taken the path of fully cooperating with the FDA and giving the FDA any and everything that they may need to investigate those 15 sites because they have far, far more investigative powers than we do. They have badges and they have guns as well. And they will do it in a manner that doesn't cost us anything, except time. The FDA does not move at a pace that we would like for them to move. They move at their own pace. But I think that in the long term, when the FDA rendered their findings, that's when we will turn the lawyers loose because we will have not only the law on our side, we will also have the FDA and their findings on our side as well. The next question is, can you explain why you did 3 [offerings] in 10 days? That's a very good question. SEC rules basically and NASDAQ rules currently have us in what's called baby shelf land. So the SEC has various rules on how much money you can raise based on your volume, your trading volume and your market cap. So for the first raise, because of those calculations, the maximum amount that we could have raised was a little north of $6.5 million. So that's what we raised. That's why we raised $6.5 million. And then the following day, the market volume continued to be very high. Our market cap went up. And so our bankers recalculated all of those numbers and said that we can raise another $6 million, right, to which we said, fine, we will go and raise another $6 million. So those were the 2 raises that we did most recently. And so it all really has to do with just what the rules are on how much money we can raise at any point in time. The next point is you have diluted us. How much more do you expect to do? I must tell you that no one ever likes to be diluted. And remember, I'm one of the largest shareholders in the company. So I'm one of the ones that are most diluted as well. But our judgment as a company and as a Board is that it's the size of the pie over the long term that ultimately matter. I've done this a long, long time now. And it's the size of the pie rather than your sliver of the pie. And it takes -- unfortunately, it just takes capital to conduct these various clinical trials. And if we're able to deliver on the clinical trials that allows us to go and launch a Parkinson's drug with a $3 billion annual sales opportunity or an Alzheimer's drug with a $30 billion annual sales opportunity, the market cap would not be what it is now. Our market cap, as I look today, was $40-something million. The idea is that we want the market cap to be multiple folds, tens of fold of this and it just takes capital to get there. So it's not fun any time that we have to go and do a raise. You do not see what goes on behind the scenes to try to do a raise. It's just not fun. We don't want to do it. We don't like to do it, but there are times when we just have to just to bring the capital into the company to conduct the trials that are needed. So let me move on to the next question. Why is it with such great test and results, why can't find a partner now? And right -- so the whole point is, if things are so great, why can't we find a partner? It's a great question. I get that question all the time as well. But let me give you some context. And the context is also -- my answer is also from the fact that I used to be on that side of the table as well. We've been in discussions with a good number of companies, several of whom we're very excited about the mechanism of action and we're eagerly awaiting the Alzheimer's clinical trial. And when we missed on statistical significance, they wished us well. They urged us to redo the trial. They said the trial was exactly what they needed to have seen for them to act. But since we missed on statistical significance, they're just going to wait. And the reason for that is no one, no one in a large pharma company has ever been fired for playing it safe. In fact, you only get fired for playing aggressively, you take a chance on something and if it doesn't work out. And the world out there is littered with promising Alzheimer's program that fails in Phase III. And so nobody wants to go and do a deal in Alzheimer's and then have it fail in Phase III. So that's the reason why a lot of companies are just waiting. The ones -- there are a few -- there's a handful of companies we're in discussions with that tends to be smaller or regional companies that are, frankly, willing to take more risk than big pharma. And so we have conversations about potentially licensing or partnering for geographic rights. And so I cannot give any answers as to when, what and so forth, if any, will materialize. But in our role, and our responsibility, we are exploring everything possible. Everything is on the table. Let me move on to the next question. Some parts of the genome are designed to be methylated to silence genes that may be helpful. And how does bezisterim get targeted to remove some but not all areas of our genome. That's a very astute question. DNA methylation is not a one-way street. DNA methylation sometimes activate a good gene. Other times, it silence a bad gene and so forth. And that's actually how bezisterim works. It doesn't completely just in one direction, turns things on or off. It actually is very gene specific. That's why I've been very meticulous in saying that it modulate and reduces DNA methylation at the right place. So we actually have studied the specific genes where bezisterim affects. Some of those, it turns on. It essentially -- these are regulator genes and versus suppressor ones. So the answer is a little more nuanced rather than turning everything off or reducing everything and so forth. But our scientists and our teams have been looking at it a CPG by CPG and a gene by gene level. Next question. What is the legal ramification with reference to your suit against your? So I guess that is a question about what is going on with the shareholder litigation that we have received? As you know, an unfortunate reality of business in the United States right now is any time that there is a significant drop in a share -- in a company's share price, ambulance chasing lawyers will essentially try to find 1 or 2 disgruntled investors and try to create a class action suit around that. So that's what we have faced. We have faced a class action shareholder litigation. You should know that 60% to 80% of these shareholder actions are dismissed at the motion to dismiss stage. And we believe our lawyers who are among the best in this industry are very confident that the suit will be dismissed. Our lawyers have an [80-plus percent] track record at getting these suits dismissed at the motion to dismiss stage. So where it stands right now is that we have filed our motion to dismiss. The plaintiffs have countered -- I mean, since they've provided their comments on it, we now have -- we need to provide our last comment and then the judge will rule on it. And the other is that even if we are not able to get it to dismiss, we are not too worried about it because we have insurance for this as well because, as you know, the real objective of the plaintiffs counsel -- at the plaintiffs bar in this is actually not to drive the company to bankruptcy or anything else like that. What they're really trying to do is to get the company to settle to the extent that it's covered by their insurance policy. And there are rough rules of thumbs behind this. And our economists have ran all the numbers and so forth, and they're highly confident in the worst case that we do not -- in the case that we do not get dismissed and we have to settle, the settlement amounts will be typical of what's seen and will be covered by our insurance. Let me move on. There's next question, where is nothing about ascites, you were waiting for the FDA and it's been over a year will Phase III trial will ever be initiated? As I mentioned before, we have received all the feedback that we need from the FDA at this point in time. And for us right now, this is purely a funding question. We need $25 million to conduct the ascites trial. And right now, that is $25 million, we do not have nor do we really want to spend at this point in time. So it is on hold, and that's why we're having partnering conversations around ascites to see if we can get that started. Why are you so motivated to back this drug for Alzheimer's and Long COVID? Let me take the easier answer first, Long COVID. Nothing has worked for Long COVID. It is a major significant need out there right now. It is a very debilitating condition. For those of us who do not suffer from Long COVID, it is easy to downplay the debilitation that those that are suffered by those who are. And I can tell you, by going to these long COVID sites and so forth, it is devastating what goes on to the 17 million Americans who have long COVID right now, 4 million of whom just can't even -- cannot focus the brain fog, fatigue just to keep their current jobs, right? So it's a huge need. And it's a -- and since Long COVID symptoms have been tied to the exact inflammatory pathways where bezisterim can affect. We believe that this is something that we should absolutely go and test, especially when the trial is fully funded by the Department of Defense. It's cost us nothing, right to conduct this trial because it's been fully funded by a grant. And so why are we so excited about Alzheimer's? I've been working in Alzheimer's since the late '80s. And I started out like everybody else working with the beta amyloid. And we all know that nothing works. And we believe we understand why every other drug has failed. And through that understanding, we have strong conviction that bezisterim could work very differently. It's all because we block inflammation at just the right place and time right before the production of TNF alpha. And that's -- and this, we believe, has the potential to become the first truly effective drug for Alzheimer's. And for the need of humanity, I think we owe it to ourselves and everybody else to go and try to figure it out. And if we can make it work, patients all around the world will benefit for it, and our shareholders will be very, very nicely rewarded for essentially having a drug for Alzheimer's. Next question, will you be able to collect biomarker data in Long COVID that may be relevant to Parkinson's and Alzheimer's? Yes, we will be collecting a battery of biomarker information, including NfL and GFAP. But those are the exact same biomarkers that we essentially want to look at for Alzheimer's and Parkinson. We're looking at a bunch of other biomarkers as well. I'm most excited about GFAP and NfL. Why did the share hit -- go crazy and hit $7? I must confess that sometimes you just cannot make this stuff up. As you may know, our shares typically trade around 200,000 shares a day. And on a Friday afternoon, 2 weeks ago, 3 weeks ago now, a day trader who's been following Alzheimer's and Parkinson's companies posted on X or formerly Twitter that he bought 4,000 shares in our company on speculation. And since he had a rather large following, that just we believe -- I've been told. So no one really knows. But the speculation or what we've been told is that then started a feeding frenzy. So in the course of the next 2 hours, 50 million shares traded. 50 million shares traded in 2 hours compared to 200,000 a day. So that happened on a Friday afternoon. So on a Monday, that went up to 100 million shares. So that's where things got up to $7 or so. And so that's when we just took the -- with all that liquidity, that's when we decided to essentially go and raise that first $6 million. Keep up the great work, proud of you and the team, much needed solution. Thank you. Well, thank you for the support. Thank you for everything that you guys do. Are there any revenue implications referenced in the Japanese patent approval? It's -- there's no direct revenue implications immediately that actually helps us with our partnering conversations that we're trying to have in Japan regarding that drug. So that's very -- that was terrific finding for us. Assuming all the trials go well, what would be the most optimistic time line for getting this drug to market? Let me give you -- you asked for the most optimistic time line. So let me give you the most optimistic time line. And that would be if we find a dramatic outcome in Long COVID, the most optimistic potential outcome is that by the end of next year or early 2026, we may go and have a conversation with the FDA about an emergency license, emergency use license, the same way that the vaccines were approved essentially under emergency use license because nothing works for Long COVID right now. And there is a major need. And if this drug works, that is the most optimistic outcome. The more realistic outcome is that we -- for Long COVID for Parkinson's, for Alzheimer's, we would need to conduct 2 Phase III trials for each one of those indications. And those 3 trials, assuming we have sufficient funding would mean that we would be in filing in the 2027 time frame. I'm being mindful of the time, so I'll take one last question. Well, here's the last question, was it an individual or your investment banker knowing he would get the stock cheap. I'm not sure what that really means. But our bankers don't trade on us. So it's -- the market is really there. We know that there's been a large amount of short interest in our stock. But when the stock had a run up there, I think that there may have been a short squeeze and so forth. So I think that stock is more balanced at this point in time. So -- but I am not a trader. I do not make opinions about that, but it is what it is. And frankly, I look and do the things I can control, which is focus on getting the trials conducted. So with that, let me just reiterate in that we have a terrific pipeline. In bezisterim, we have a novel drug that blocks inflammation at just the right place in time. And that's why in clinical trials it has shown that it can reduce inflammation and the associated insulin resistance. And because of that, Parkinson's patients have experienced greater muscle control. Alzheimer's patients have experienced a 68% slowing of cognitive decline after just 6 months of treatment with a mild headache being the #1 reported safety concern and everyone has seen modulation of their DNA methylation levels. In BIV201, we may have the first new -- the first treatment for ascites. We have an exciting 2 years ahead with multiple data readout. And I believe that's why we represent a terrific buying opportunities for investors over a 2-year investment horizon. Our shares are way undervalued right now. The value of our company is not the $40-something million that's represented in our market cap, and I believe the market cap will be different 2 years from now than it is now, and I say that as one of the largest shareholders in the company in addition to being the CEO. With that, I thank you, and let me turn it back to Craig for any last comments.

Yes. Thank you very much, Cuong. For more information about BioVie, reach us at 1-800 Red Chip or e-mail us at [email protected]. Please visit RedChip's Investor Information page for BioVie. It's biviinfo.com. There, you can view and download today's investor presentation as well as the fact sheet and sign up for news alerts on BioVie. Sign up for future webinars at redchip.com/events, where you can also see an archived version of today's BioVie webinar. Thank you to our many active participants today, and thank you very much, Cuong.

Thank you. Have a great day. Bye-bye.