Hello, this is Craig Alford with RedChip Companies. 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. We will begin with a brief presentation in a moment. Then we will answer your questions. Submit your question at any time by using the Q&A tool at the bottom of the Zoom window. 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 fact should also be considered forward-looking statements. Of course, forward-looking statements involve risks and uncertainties. Cuong, when you're ready, please go ahead. Thank you, everyone. Thank you, for joining today. My name is Cuong Do. I am the CEO of BioVie. At BioVie, we have two assets that are currently in development right now. Our lead asset is a drug candidate named Bezisterim, that's formerly known as NE3107. It's known as a modulator of inflammation, so it modulates the production of TNF-alpha. In various clinical trials, many patients treated with Bezisterim have experienced reduced inflammation and the associated insulin resistance. In our Parkinson's trial, Parkinson's patients have seen improved muscle control. In our Alzheimer's trial, Alzheimer's patients have been seeing improved cognition and function. All these patients have also experienced lowered levels of DNA methylation, which is essentially a modulation of the biological aging process. Our second drug candidate, where the heritage, the beginning of the company, is a drug called BIV201, which is a novel formulation of a drug called Terlipressin, which has the potential to become the first therapy for ascites, which is a horrible end-stage liver disease, condition that has greater than 50% mortality rate within a year. Before we go into the detail, let me give two near-term updates on expectations. We have two near-term catalysts. As you know, our Parkinson's trial has been fully enrolled since the end of 2025, those patients are continuing on through the trial. As such, the last patient is expected to come in for his or her last visit at the end of April. This basically puts us in line to have top-line data readout from this trial in the Q2 of 2026. That's coming up very quickly, right? I'm hoping that that will come by June, hopefully by May. The Q2 of 2026 is when we expect to have top-line readout from our Parkinson's trial. The other guidance, new guidance that we're giving is that our long COVID trial is expected to have top-line data readout towards the end of the summer of 2026. This trial has been enrolling very rapidly now that all of our large academic medical center partners are online. The large long COVID sites at Mayo Clinic, Yale, Stanford, UCSF, and Mount Sinai are all online. They are actively recruiting and enrolling some patients right now in that trial. As such, at the pace that we're going, we expect to have the last patient enrolled by the end of March, perhaps early April at the latest. That would mean that we will have top-line data readout, let's say, in the August timeframe of this year. Exciting few months coming up for the company with two top-line data readout of our Parkinson's and our long COVID trials. As you may recall, we are all about inflammation. Bezisterim blocks the production of TNF-alpha. TNF-alpha is considered to be the master regulator of inflammation. When you have TNF-alpha produced, it goes on to create more inflammation. It creates a forward-feeding pro-inflammatory cycle where it produces more chemokines, cytokines, and so forth that leads to more inflammation, all of which leads then to more TNF-alpha. Of course, this has been associated with a large number of diseases. TNF-alpha has also been known as a key driver of insulin resistance, right? Which of course leads to diabetes and various metabolic disorders. TNF-alpha has been implicated directly in the driving the serine kinase that phosphorylates tau to become phospho-tau in Alzheimer's disease. TNF-alpha is the key driver, a key driver of something called DNA methyltransferase 3A and 3B, which leads to the hypermethylation of our DNA, which has been associated with a large number of diseases, particularly age-related diseases. Bezisterim works to block the production of TNF-alpha, and it works through something called ERK with the Extracellular Signal-Regulated Kinase. Now, it's been known for decades that ERK plays two very different roles in virtually every cell in our body. The first having to do with insulin signaling, where insulin works through ERK for all of its cellular growth, repair, and regeneration activities. That's known as homeostatic ERK. ERK also plays an important role in inflammation, whereby various extracellular, cellular signals or agents such as cytokines and chemokines would enter the cell, activate m-ERK, which in turn activate NF-κB. NF-κB triggers the production of TNF-alpha. When you have TNF-alpha, it then just goes on to create, release more inflammatory factors and create this forward-feeding proinflammatory cycle. It's obvious what you want to do. What you want is to block inflammatory ERK, but not do anything with homeostatic ERK. Unfortunately, that's much easier said than done because dozens of teams over decades tried to do it, but no one was able to succeed. Everyone failed because they were not able to create a selective enough inhibitor of just inflammatory ERK. Frankly, that's where NE3107 comes in, or Bezisterim. Honestly, this is where we got lucky. We did not set out to do this. We just had our eyes open when we recognized what it does. It turns out that Bezisterim blocks the activation of ERK and NF-κB. As a result, when you do not have NF-κB activation, you are not going to get TNF-alpha. Right. When we saw this, it became very clear that Bezisterim has a critical role in a number of different disease conditions. Right now, we are focusing on Parkinson's. It has been known for some time, for decades, that two conditions need to be present at the same time for a person to develop Parkinson's symptoms. The first is you need low dopamine levels in the brain, and the second is you need inflammation and the associated insulin resistance. If you're able to reverse the insulin resistance in the brain, the body is then able to make use of whatever low level of dopamine that is currently there. Right? People have tried for a long time, including doing some really crazy things, far out things, like us-- in this case, using inhaled insulin, just trying to get more insulin in through the nose, get it up into the brain to see if you can reverse the insulin resistance. It does work. In this clinical trial, as you can see here, those that have received insulin, inhaled insulin were able to improve their muscle control significantly. Right. This is a disease score, so a lower score is better. Those that were treated with insulin saw an improvement of what's called their Unified Parkinson's Disease Rating Scale, part three or the muscle or the motor control. Right. Unfortunately, that is just not a very practical solution, right? You can't easily get inhaled insulin out to everybody and treat it, and it's just not as effective as you want it to be. It's not very practical. To this day, the only practical solution for Parkinson's patients is to use a drug called Levodopa that was introduced over five decades ago. Levodopa is a terrific drug. What it does is it enhances the dopamine level that's in the brain and therefore enhances muscle control. And it does a terrific job at that. It has several problems. One is that it has a short half-life, which means that patients have to take it multiple times a day, which is very inconvenient. The real problem comes in is overnight when people don't normally wake up in the middle of the night to take their evening, their overnight medication. That means that by the time they wake up in the morning, Levodopa has already worn off. It's gone out of the patient's system. That means they do not have muscle control. They're rigid. They can't get out of bed. This is part of the reason why Parkinson's patients don't like to schedule anything first thing in the morning, is because they can't get out of bed. They have to stay in bed, take their medication, wait an hour or so for the Levodopa to kick in before they can actually start to move and get out of bed. That's one significant problem with Levodopa. The second is that the effect of Levodopa wears off over time, so that the longer you're on the drug, you end up having to take higher and higher doses or amounts of the drug. As you get into the higher doses of Levodopa, it leads to something called Levodopa-induced dyskinesia, which is essentially the tremors, the trembling that you see many Parkinson's patients have. When you have the dyskinesia, all you can do is reduce the dose of Levodopa, right, and wait for the tremors to pass. As you cut back on the dose, you lose muscle control. These patients are in a terrible situation with a terrible trade-off that they have to make, right? We believe Bezisterim could be a solution for that. Because in our preclinical studies in both rodents and non-human primates, we saw that Bezisterim was equally effective as Levodopa in restoring muscle control. Now, that's a huge statement in and of itself because over the decades, no drug has been able to equal Levodopa, right? With the support from Michael J. Fox Foundation, the original study showed that Bezisterim alone was equally effective as Levodopa. We also found that when you give it in combination, when you give Bezisterim in combination with Levodopa, you saw a synergistic effect. You saw the greatest muscle control. You also saw a reduction in the dyskinesia. Most importantly, we saw that at the end of the study, when we sacrificed the monkeys and looked at their brains, those that were treated with Bezisterim retained twice as many neurons as those who were not treated with Bezisterim, suggesting that Bezisterim has a neuroprotective property to the drug, which to us is not at all surprising because we know that Bezisterim is, it reverses insulin resistance, which means there's greater glucose availability in the brain. We also know that Bezisterim enhances blood flow to the brain, which means that. When you have greater oxygen available in the brain because of greater blood flow and you have more glucose, that's only going to bode well for better neuronal health. Based upon that, we went into the clinic and enrolled 40 patients, whereby, frankly, we replicated in Parkinson's patients the study that we did with the non-human primates. We gave half the patients a placebo and Levodopa, as shown in red here, so essentially just Levodopa. Then we gave the other half Bezisterim and Levodopa, as shown in blue. After 28 days of treatment, you see that those that were treated with the combination saw about a 3-plus point advantage on the most, on the motor score, the part three score of the Unified Parkinson's Disease Rating Scale. That's a clinically meaningful improvement, and that is a huge deal because this is on top of what Levodopa alone is able to produce, right? I've said before, Levodopa is a great drug, and with the combination with Bezisterim, we make it even that much better. We also found is that those who are younger than 70 years old, presumably whose disease progression has not gone so far, that difference is over four points, and that you don't see that very often. This shows that you, in humans, that you can use Bezisterim in combination of Levodopa to help moderate and severe Parkinson's patients improve in their muscle control. We also found that it has a dramatic impact on the overnight effect, right? As I mentioned before, we saw in our trial, as seen every single day by hundreds of thousands of Parkinson's patients, none of the patients that were given a placebo and Levodopa, so just Levodopa alone, none of them had control of their muscles first thing in the morning, what's called the time zero muscle state. None had muscle control or could get out of bed, where roughly a third of Bezisterim patients had muscle control and could get out of bed. This establishes the first half of what we want to do in Parkinson's. Namely, we have shown that we have now human proof of concept that we can use Bezisterim in combination with Levodopa to help moderate and severe Parkinson's patients improve their muscle control. We completed this trial last year, and that's why we are now on to our second trial, right? That's the trial that's currently underway. In this second trial, we are enrolling 60 patients, right, who are earlier in their disease state. These are diagnosed Parkinson's patients who need to go onto therapy for the first time. We are giving half of them just a placebo, and then the other half we're giving Bezisterim. What we're trying to show here is that those that are treated with Bezisterim can see a delay of their disease progression. This trial alone would not show that, right? The next trial, the phase III trial that we will conduct, will be for a longer period of time. Explicitly, what we're trying to show in these combination of trials is that Bezisterim could become the first drug to modify the progression of the disease, to delay the progression of the disease. That's really the most important thing we're trying to demonstrate for Bezisterim in Parkinson's. This second trial establishes the second part of what we want to do in Parkinson's. This second trial is fully enrolled now, and we expect to have top-line data readout for this trial in the Q2, hopefully in the May or June timeframe of this year. In the interest of time, let me move on, and we'll come back and answer any questions you may have here. The second trial that we have underway right now is in long COVID. You may ask, why are we looking at long COVID, and what does this have to do with Parkinson's and Alzheimer's, where we have really focused for years? The short answer is we had no idea that long COVID was tied to Parkinson's and long COVID and Alzheimer's. First, to set the stage, long COVID symptoms are defined as persistent symptoms that last long after the COVID infection has been beaten, right? Many of us on this call may have been infected with COVID. After a couple of weeks or maybe longer, the body was able to mount an immune response to essentially get rid of the COVID infection. For the vast majority of us, our lives continue on, right? The infection is behind us. Unfortunately, right now, there are at least 17 million Americans who continue to suffer the lingering effect of the COVID infection, right? It shows itself in terms of brain fog, extreme fatigue, and malaise. Many of these patients cannot stay out of bed for more than a couple of hours at a time. That's why there's more than 3 million Americans who've had to quit their jobs or change their jobs simply because they cannot keep up with the physical demands of the job, right? There are no approved treatments for this. There are no treatments for long COVID symptoms. That's why there are these huge long COVID centers all around the country whereby these academic centers are just trying to provide palliative or symptomatic relief for these patients because nothing works. The situation is only getting worse. We estimate that there are tens of thousands of new patients that are getting diagnosed with long COVID each day. Right. How does Bezisterim comes in? It comes in because it's been shown over the last couple of years that long COVID symptoms result because there are fragments of the spike proteins and fragments of the envelope proteins continue to circulate around in a person's blood, right? While it is not infectious, the virus has been killed, so this is just a fragment of the virus, but it's that continues to circulate. The body believes that there's still an infection, so the body is constantly mounting an immune response to the circulating protein fragments. Because of that, it generates a lot of inflammation. Inflammation works through exactly the same mechanisms where Bezisterim affects, so namely ERK and NF-κB activation. Because Bezisterim blocks ERK and NF-κB activation, we believe it may become a mechanism to essentially break the cycle of inflammation creating more inflammation and more long COVID symptoms. Right. We have been granted a $13 million grant to fully fund the phase II trial that's currently underway. This grant allows us to enroll 200 patients, half of whom will be given a placebo, and then the other half will be given Bezisterim. We will follow these patients for roughly four months from beginning to the end. The last patient, last visit from our long COVID trial is expected in the back half of July, which means that this trial will be in a position to read out in the August timeframe of this year. Right. In the interest of time, let me just skip ahead. Well, let me skip ahead and just spend a few minutes on ascites. Our other drug candidate is BIV201, which essentially targets and treats ascites. Ascites is end-stage liver disease. When you get to this stage, the liver has been so scarred that it creates all kinds of portal hypertension. As a result, fluid cannot flow through the liver the way it normally does. The kidney is implicated. Therefore the kidney cannot get rid of fluid as well. All that fluid accumulates in your abdomen, right? You can see that this patient has a huge amount of fluid buildup, ascites fluid buildup. There is no approved treatment for ascites. The only thing that you can do right now is stick a large needle into the abdomen and physically remove 5 to 10 liters of that fluid, right, to get it to... through a procedure called paracentesis. Paracentesis does work. It does provide the patients with some initial relief, symptomatic relief. Since nothing has been done to address why the fluid accumulates to begin with, the fluid can reaccumulate, so these patients are back in the hospital every week or two to get another 5 to 10 liters of fluid removed. You can just imagine the stress and strain that this puts onto the body. Frankly, the only treatment objective at this point is to try to keep the patient alive long enough so that he or she may qualify for a liver transplant. Since there are not enough livers to go around, there is a greater than 50% mortality rate within a year, right? This has a huge medical need. Our solution is a novel formulation of a drug called Terlipressin, something that's been available in Europe, outside the U.S., for quite some time. It's a drug that acts as a very potent vasoconstrictor. Right? Everything in your body constricts. Because of that, it has a horrible side effect profile. Our solution essentially solves that problem. We take Terlipressin and we put it into a saline bag, and we connect it to a portable infusion pump that patients can wear on their belt, and we slowly drip the drug in over the course of 24 hours. In our first phase II trial, we showed that we were able to maintain a constant therapeutic dose of the drug by continuously dripping it in slowly over the course of a day. By doing so, we avoid the problem of creating these massive peaks that are associated with the bolus injections, which is this the way that Terlipressin is administered now, right? In this phase 2A, we saw no drug-related SAE, so significant severe adverse events, right? By avoiding the peaks, we avoided the safety concerns. We moved on to a phase 2B trial, where we were targeting enrolling 30 patients to try to measure how much ascites fluid buildup we can reduce. We decided to stop the trial early, halfway through, after 15 patients had been enrolled, because by then, we already had data showing that those that completed the treatment saw a 50+% reduction in their ascites fluid buildup, whereas those that were standard of care saw really no change. Right? Since this is a condition that has such high mortality, we concluded the best thing to do, the most ethical thing to do is to stop the trial early and engage the FDA into a conversation on what it would take for us to get to move the drug to phase three and registration. Since we already have fast track and orphan designation for this drug, all we need is one phase III trial to register the drug. The phase III trial is still about 200 patients large. As of now, we have received all the feedback we need from the FDA to initiate the trial. We're exploring some things to get the funding to initiate this trial. In interest of time, let me stop here by saying in BioVie, I believe we have a very, very exciting portfolio. We have two drug candidates in Bezisterim and BIV201. We have multiple shots on goal. Bezisterim is currently in the clinic for Parkinson's and long COVID. The Parkinson's trial is expected to have top-line data readout in Q2 of this year. The long COVID trial is expected to have top-line data readout by the end of the summer. Right. With that, let me stop here, and let's open up for questions. Thanks a lot, Cuong. Yes, if you wish to reach Cuong, please click on the Q&A button at the bottom of your Zoom window. A text box will appear, and then you will be able to type in your question. We already have some questions already submitted. Can't COVID live for a long time in the gut and then pass spike into the system? Frankly, we know that long COVID lasts for a long time. It does, it does circulate in the blood. From blood, it can go to a lot of different places. That's part of the reason why there's been no treatment. We believe that we may be able to provide symptomatic relief, but there's nothing that Bezisterim does that will get rid of the circulating the proteins fragments. That will have to come from a different solution. Hopefully, in the meantime, we'll provide a symptomatic relief, a solution for symptomatic relief for these patients, right? Just to give you a sense of how important that is, there is absolutely nothing available for these patients out there. If we get significant results at the end of the summer, our plan is to go to the FDA in the fall and have a conversation about what it would take to get accelerated approval or even perhaps emergency use authorization for the drug. Emergency use authorization is there for situations where there is a big unmet medical need, and there's nothing else that works, right? Depending on the data that we get, we will go and talk to the FDA about that. Just to kind of give you a magnitude here, we believe that Parkinson's, when fully developed, could be a $3 -$5 billion annual sales opportunity in the U.S. alone. Long COVID could be even bigger than that because of the numbers that are involved. There are one million Parkinson's patients in the U.S. There are 17 million long COVID patients in the U.S., one million of whom have it very severely, such that they've had to quit or change their jobs. This leads to a very, very large market. Thanks, Cuong. As a long-term investor, I have been hearing about liver ascites for quite some time. Previously, I was told BioVie was seeking a partner. What progress has been made, and when do you think you can bring this solution to the market? That's a great question. You share my frustration with the delay in developing BIV201. We have been looking for talking with partners. Unfortunately, the partners we've been talking to have the same problem that we have, which is they are also small cap companies who have had significant challenges raising $25 million that's needed to go and to conduct the trial and get this drug registered. We are continuing to do that. If you are a keen observer of BioVie, you may have noticed that we are also considering taking the ascites drug public through a separate company as well. We're working it through with our banks and advisors and so forth, and we believe market conditions over in the coming months may make it possible for us to put the ascites drug into a separate company and take that a portion of that company public to raise the funds that are needed to go and conduct that trial. We will hope to have this drug in the clinic this year. Thanks, Cuong. When the reverse split was initiated last year, the stock quickly fell to previous levels. Do you feel the reverse split was a good decision? The reverse split is a terrible thing to have to do, unfortunately it was the only solution that we have. We do not want to do a reverse split, nor would we ever voluntarily want to go through something like that. We faced a regulatory requirement, which was our shares need to be trading above $1 in order to be maintained on the NASDAQ. As it drifted below $1, the only way to get it above $1 is to do the reverse split. Our company, like many other biotech small cap companies also have seen the exact same problem over the course of the last 1 year, 2 years or so, which is frankly lack of interest. Our volume, our trading volume has also dried up as well. I am very frustrated with our volume, very frustrated with our share price. I do everything possible to try to get the word out about BioVie, frankly, the entire small cap biotech market is just severely depressed. I think that's the reason why our share price has been stagnant. Believe it or not, we are in a better state than some of the other companies that we track, right? Which is not great relief, right? What we are obviously hoping for and waiting for is positive results from our two clinical trials, hopefully that will get people to be more aware of what we're doing, more excited with what we're doing, and to come into our stock as well. Thanks, Cuong Do. Another question here about partnerships. How do you envision the structure for any potential partnerships? Again, have you been in any discussions with potential partners? Over the years, we've been in discussions with a good number of partners, right? Let me answer the question in two different parts. First is the question of structure. Structure, everything is on the table. Over the years, we've discussed things such as a potential partner licensing our product to anywhere to they potentially buying out the whole company, right? Everything is on the table regarding this potential, right? We will entertain anything that makes sense for the company. Of course, there's always a question of why hasn't a big pharma company done a deal with us and so forth. The short answer to that comes from the fact that in big pharma, no one has ever been fired for playing it safe. I get it. I've been on that side of the table as well. The world out there is littered with promising phase III assets in Alzheimer's that ultimately fail. Big pharma companies are just waiting for us to complete the trial to show with positive statistical significance, then they will swoop in, right? We know that there are big pharma companies that are monitoring us. We are continuing to have those conversations to keep the conversations warm. What they constantly tell us is go and do the trial and come back when the data, when you have positive clinical data that's statistically significant. They want a completely de-risked deal, right? Unfortunately, that just means it's the onus is on us to go and do the trials to show that this drug works. Thanks, Cuong. Why wouldn't a large drug or biotech company take a chance on investing in your company? Well, I think the answer is partly what I've just mentioned, which is, these big pharma companies are very risk-averse, right? No one wants to invest in a company in a field that has repeatedly failed, right? Alzheimer's and Parkinson's have had many failures in the past. People want to play it safe. They want now to wait for a drug that has completed phase III clinical trials before swooping in. Frankly, they know they will have to pay a premium and because by then, once we have a proven drug, we then can run an auction for the drug or run an auction for the company, and it goes to the highest bidder, right? Everyone knows that they will have to overpay for the drug in an auction, but they're willing to do that to avoid the downside risk of investing in something that fails later on. Cuong, anything happening with legal action against the testing centers in Florida whose malfeasance resulted in results which did not achieve statistical significance? That's a great question. It has been two years since we've had this problem, and over the course of those two years, we have been cooperating with the FDA and the Department of Justice. We've been working behind the scenes to urge them to move more quickly. What we know is that the FDA has inspectors out to, I believe, two handfuls of the 15 sites that we reported to them. They have sent inspectors out, and there have been a number of what are called Form 483 citations. I think that's the numbers, whereby, essentially saying that these sites did not adhere to the protocol, did not do things correctly. As well, there's been a few other kinds of reports and filings that the FDA has put in for many of the sites that they have visited. What we have been waiting for is for them to initiate a criminal prosecution. We believe a criminal investigation is underway. We will give it a little bit more time, right? If the FDA or the DOJ does not initiate the next set of litigation, we may initiate the litigation ourselves because part of the reason why we wanted to wait and cooperate with the FDA is that they have far more investigative power than we do, right? They what they do is frankly free to us. We do not have to pay money for various investigators and people to go out to the sites and so forth. More importantly, they have subpoena power, right? We know that the reports that the FDA have sent back to the sites, we get a copy of those through our contracts with the site. Basically, make it very clear that the sites that receive those reports did not follow what we, what they were supposed to, i.e., they were at fault. We will give it a little bit more time because if the FDA initiate litigation, it will make it easier for us just to jump under a coattail. If they do not do something within the coming months, we may choose to initiate the litigation ourselves. Hopefully, that explains the question. Thank you for the question. Cuong, this may be a good time to remind everyone that you have prior experience at Merck and Samsung. This person wants to know, given that prior experience, what lessons, including partnerships, would you be applying to BioVie's overall strategy? That's a very broad and big question, right? What I know in my three decades of developing drugs is that a company is valued based on its drug. If you have a drug, especially if you have a drug that's in phase III or a completed phase III, that's when the big value inflation comes in. It's important. It's lesson number one. Lesson number two is data from these trials becomes the catalyst whereby different companies get noticed, not only by investors but by potential licensors or acquirers. If we're able to get more than two, more than one, right? If we get two companies that are potentially interested in our asset or our company, you have a bidding situation. When you have a bidding situation for a drug where there are few alternatives, it very quickly leads to a bidding frenzy. I've seen that over and over and over again, obviously, that's what we are working to create here at BioVie, right? That we can get the drug into the hand of the best and most logical owner because they will have more resources. They can develop the drug and get it out for the patients. By doing so, going through that process would generate significant returns for our shareholders who've been backing us for all this time. This person writes, "Pardon my ignorance. Is the top-line data for Parkinson's and long COVID later this year phase II results? I believe the answer to that is yes. Both our Parkinson's and long COVID trials are phase II trials. Whereby we are trying to demonstrate the magnitude of the impact of the drug and to a certain extent safety, although we've already demonstrated safety. We've never seen a safety concern. While I do not make light of any safety observations, right. We believe that we have shown Bezisterim to be safe. What we need to do now is to show the magnitude of the therapeutic impact that Bezisterim has in Parkinson's and in long COVID. What that means is we want to measure how much improvement can Bezisterim-treated patients experience compared to those who were treated with placebo. By understanding that difference, we then can go and use a standard statistical model to estimate and to determine how many patients do we need to have in the phase III trial so that we can get the positive results and statistical significance that will be required for us to go and register the drug with the FDA. I hope that's clear. I certainly think so. Thank you very much, Cuong. We've got a few here to choose from. Let's get one about, Bezisterim here. As you said, you are, addressing with Bezisterim, Alzheimer's, Parkinson's, and long COVID, and longevity. What is the priority there? What's the hierarchy there looking like strategically? Number one priority is Parkinson's. Number two priority is long COVID with one proviso. If we get very strong results and the FDA is willing to have give us clear guidance on Accelerated Approval or emergency use for long COVID, that becomes the number one priority, right? Those two, the data will tell, and frankly, the FDA's reaction will tell. Long COVID is the big wild card because it's the first drug of its kind, and we just don't know how the FDA is going to react. Whereas Parkinson's is the first new drug in Parkinson's in over five decade. The registration path, the clinical trials, and so forth is fairly clear. Let me give some guidance. I believe there's a question about how long it will take, so let me give some timing guidance as well. When we get the positive phase II data from Parkinson's, it doesn't mean that we can turn right around and start the phase III trial right away. From phase II data until such time as we can start the trial, it could take at least six to nine months, time for us to plan the phase III trials, to get the clinical sites up and running, to raise the funding for the trial, and so forth. It could be six to nine months between Q2 of this year when we get results until such time as we can start the phase 3. Once we start the phase III, we expect that we can have the top-line data for the for the easy indication, which is symptomatic relief. We can have the top-line data within one year, right, for symptomatic relief. We will continue that trial probably for another year beyond that, so that we can demonstrate that we can help the patients, modify the progression of their disease, right? The ultimate trial will last longer, but that's when we get the final ultimate trial. That's where the true value comes in because if we're able to demonstrate for the first time that a drug can modify the progression of disease, that's the holy grail. I hope that answered your question. Okay. Well, we have reached, we're even beyond the 5 o'clock hour here, Eastern Time. Cuong, we'll wrap up here. We appreciate you taking the time to do today's webinar. For more information. Thank you so much. You got it. You got it. Please, Cuong Do, go ahead. Yeah. Thank you, Craig. Thank you, everyone, for joining today. Let me just reiterate and recap that at BioVie, we have two drug candidates in Bezisterim and BIV201. I believe we have a very exciting portfolio in these two drugs that are being developed for multiple different indications. Of course, Bezisterim is being developed for Parkinson's, long COVID, and Alzheimer's. Our Parkinson's trial is currently underway. Top-line data is expected, Q2 of this year. When fully developed, Parkinson's could become a $3 -$5 billion annual sales opportunity in the U.S. alone. The long COVID trial is expected to read out at the end of the summer. If it could become the first therapy for long COVID, when fully developed, that could dwarf the Parkinson's market size opportunity just given the need and the significant need that's there. In aside is our BIV201, we've received all the feedback that we need from the FDA to initiate or to move to the next stage of getting this thing into the phase III clinical trial. When developed, this could become the first therapy for ascites, which is a condition that has greater than 50% mortality rate within 12 months. This, we believe, could become a $2 billion annual sales drug in the U.S. alone. I thank you very much for your time. If you're interested in more information about us, please go to bioviepharma.com, and that's spelled B-I-O-V-I-E pharma.com for more information about the company and with clinical trials. Thank you so much for your time. You have a great day. Thank you, Cuong. Thank you. Just a bit more information. There's another page you can go to. Certainly, you can go to the page that Cuong just gave you. RedChip has a page too, bivinfo.com. That can also lead to the BioVie corporate page. When you're on bivinfo.com, you can also sign up for news alerts on BioVie. You can read the investor presentation, as of course you can also do on the corporate website. We also have a fact sheet that we create exclusively for BioVie on that webpage. You can download it very easily. You can also reach us if you want more information on BioVie at BIVI@redchip.com. Of course, you can always call us at 1-800 RedChip. Please watch Small Stocks, Big Money, RedChip's program featuring exciting small cap companies, including, of course, occasionally BioVie, every Saturday night at 7:00 PM. Eastern on Bloomberg U.S.A. Finally, please join our next webinar with Jackpot Digital. That'll be tomorrow at 4:15 PM U.S. Eastern, just like today. Register for all RedChip webinars at redchip.com/events. Thanks again to our many participants today. As always, thank you so much, Cuong. Thank you everyone. Have a great day.