This is Craig Brelsford 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, and 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. I now turn this webinar over to Cuong. Go ahead. Good afternoon, Craig. Thank you for joining. Good afternoon, everyone. Thank you for joining our update today. I'm very excited to share with you this afternoon some exciting progress at the company. As you know, we have several clinical trials underway right now, which makes it, I believe, we have one of the most exciting biotech companies around with an exciting portfolio. You may know that we have a Parkinson's clinical trial that is underway. It phase II trial, and now we can pick our enrollment has picked up relatively quickly within the last few weeks, and we can now project to be fully enrolled by the end of 2025. As a result of that, we would expect top-line data readout in the May-April timeframe of 2026. So this is a very exciting progress for us, and I'll describe more about this trial in a moment. You also may know that we have a Long COVID phase II trial that is underway as well. That trial is enrolling very well, and we expect to have further guidance on when that will be fully enrolled in about a month. The enrollment is going very well. We just really want to see how that is coming along in the next few weeks, and we will get full guidance at that point in time. We also like to announce that our ascites phase III clinical trial has been submitted, protocol has been submitted to the FDA, and we should hear back from the FDA any moment now. We submitted this three weeks ago, and we typically hear back within 30 days, and that 30 days should be coming up next week. And the exciting thing to announce is that we have significant cash runway. We have sufficient cash to go to the end of 2026, which is, of course, well beyond the timing of when the Parkinson's and the Long COVID trial are expected to read out. So just an overview. As you know, our lead asset is a drug candidate known as bezisterim that modulates the production of TNF-alpha, which is considered to be the master regulator of inflammation. In clinical trials, bezisterim has shown to be able to reduce inflammation and the associated insulin resistance. In our phase II trial, Parkinson's patients have seen improved muscle control. Alzheimer's patients have seen improved cognition and function, and all of these patients have seen lower levels of DNA methylation, which is essentially changing the biological aging process. Our second drug candidate is BIV201, which hopefully will become the first therapeutic for ascites, which is a terrible condition that has over 50% mortality rate within 12 months. As you know, we believe that chronic low-grade inflammation is the starting point for many things that go wrong in the body, and it all starts with TNF-alpha, which is considered to be the master regulator of inflammation. When you have TNF-alpha present, it just drives more inflammation. It creates a forward-feeding pro-inflammatory cycle that produces more TNF-alpha, more cytokines, chemokines, which of course has been associated with a large number of diseases. When you have inflammation, TNF-alpha drives insulin resistance that's been associated with Parkinson's and diabetes, and of course, TNF-alpha drives something called DNA methyltransferase 3A and 3B, which accelerates DNA methylation, which has been associated for a large number of diseases. Our drug candidate directly impacts the production of TNF-alpha. It's been, and it works through something called ERK and NF-kappa B. Now, it's been known for decades that ERK plays two very different roles in practically every cell in our body. The first involves insulin signaling, whereby insulin works through several pathways and essentially affects all, and ERK helps affect all the cellular growth, repair, and regeneration activity that goes in all of our cells. But it's also been known for all the time that ERK plays an important inflammatory role as well, whereby different extracellular signals, such as different cytokines, chemokines, would come into the cell. It would activate ERK, which then activates NF-kappa B to lead to the production of TNF-alpha. And as I mentioned earlier, TNF-alpha then drives a forward-feeding pro-inflammatory cycle that leads to more TNF-alpha. And so it's obvious what you want to do. You want to block what's called the inflammatory ERK without touching homeostatic ERK. But unfortunately, that's much easier said than done because dozens of teams over decades tried to do it, but no one was able to find a selective enough inhibitor of just inflammatory ERK. And that's where, frankly, we got lucky. We did not set out to do this. We just had our eyes open to recognize that our drug candidate, bezisterim, blocks the activation of ERK and NF-kappa B. So we are not blocking ERK itself, and that's why we do not suffer from the toxicity problems that have plagued all the prior ERK inhibitors. What we are doing, bezisterim, is blocking the activation of ERK into its active form, something called pERK. And without pERK, you're not going to have activated NF-kappa B. And as a result, you block the production of TNF-alpha, which is a huge deal because this is the starting point for many things that come after it in various disease cascades, one of which, of course, is Parkinson's. It's been known for quite some time now that two conditions need to be true at the same time for a patient 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 somehow able to just reverse the insulin resistance in the brain, the body is able to make use of the dopamine that's there to restore muscle function. Over the years, people have tried lots of crazy things, including using inhaled insulin, as shown here, to try to get a bit more insulin into the brain so that you can reverse the insulin resistance and free up that glucose. It does work. As you can see from this data, if you're able to get enough insulin into the brain, it reverses the muscle loss. The body's able to make use of the dopamine that's there. But that, unfortunately, is not a very practical solution. That's why to this day, the standard of care at Parkinson's remains the drug called levodopa, which was introduced over five decades ago. Now levodopa remains the standard of care for a reason. It is a very, very, very good drug in helping to restore muscle control. But it does have some deficiencies. The first is that it has a short half-life, which means Parkinson's patients have to take it every three to four hours or five hours because it wears off very quickly. It has a short half-life. The second is that its activity wanes over time, so that the longer you stay on the drug, the higher a dose you need to get that effect. So over time, as you get higher and higher doses, it causes something called levodopa-induced dyskinesia, which is a trembling effect. So when you have LID, all you can really do is cut back on the dose of levodopa and wait for the LID, for the dyskinesia to pass. But as you cut back on the dosage, you lose muscle control and therefore are not able to move, which is a terrible trade-off that Parkinson's patients have to go through. What we found in our preclinical studies in rodents and non-human primates is that bezisterim is equally effective as levodopa in restoring muscle control. Now, that is a huge statement in and of itself because no drug over the decades has been able to be equal or better than levodopa in restoring muscle control. But what we also found is that we give it in combination with levodopa, you saw a synergistic effect whereby you saw increased muscle control. Now, that is a huge deal. What we also found at the end of the trial, when we sacrificed the monkeys and looked at their brains, we found that those that were treated with bezisterim retained twice as many neurons as those that were treated with placebo, suggesting that there is a neuroprotective property to the drug. We're grateful to the Michael J. Fox Foundation. Fox Foundation for having funded this trial to help us understand that there is a potential neuroprotective property to the drug, which for us is actually not at all surprising because we know that bezisterim 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 there's greater oxygen available in the brain. So when you have greater glucose and oxygen availability in the brain, that only bodes well for better neuronal health. So based upon this preclinical data, we went into the clinic and enrolled 40 patients with moderate to severe Parkinson's. And we essentially replicated in these patients the study that we did in the non-human primates, whereby we treated the patients for 28 days. We gave half of them a placebo and levodopa, or essentially just levodopa alone, as shown here in red. We also gave half the patients bezisterim and levodopa, as shown in blue, and as you can see, those that were treated with levodopa experienced about a three-point improvement or a superiority on what's called the part three score or the motor control score of the Unified Parkinson's Disease Rating Scale. Now, that is a clinically meaningful difference, and what more is that that is on top of the tremendous improvement that levodopa produces by itself, so this is a huge deal. If you look at patients who are younger than 70 years old, presumably whose disease has not progressed quite as far, that difference is closer to four to five points, which is a huge deal that hasn't been seen very often, but the other thing that we observed has to do with what's called the time zero muscle state. As I mentioned to you earlier, I'm sorry, levodopa has a short half-life so the studies that the way the study is conducted, and this happens every single day for hundreds of thousands of Parkinson's patients, is that they would take their evening medication and go to bed and overnight, levodopa would wear off so that first thing in the morning, before they take their morning medications, none of the patients that were in our trial that were given a placebo and levodopa, essentially levodopa alone, had control of their muscle first thing in the morning so their muscles were in the off state so they were stuck and rigid and so forth and they had to wait, take their morning medication and wait until it kicks in before they had restoration of muscle control. In contrast, roughly a third of the patients that were given bezisterim had control of their muscles first thing in the morning. They can move. They can get out of bed. Now, that has just never been seen before. And that, of course, is all because bezisterim has a long half-life. It lasts for 12 hours, whereas levodopa lasts for maybe three, four, to five hours at most. So this trial gives us the first proof of concept in humans that shows that we can give levodopa alongside bezisterim and help moderate to severe Parkinson's patients improve their muscle control. And this establishes the first half of what we're trying to do in Parkinson's. And we are now conducting a second study to demonstrate the second part of what we're trying to do in Parkinson's, which is to show that bezisterim could be used as first-line therapy, as monotherapy in Parkinson's. So we are enrolling 60 patients in a clinical trial where we will give half the patients placebo, and then the other half, we will give them bezisterim alone. And the trial will go for three months. And what we're hoping to show at this trial is that over the course of three months, bezisterim can help slow the progression of the disease, slow the progression of muscle loss for patients who are treated, whereas those that are on placebo will continually have a worsening of their muscle control. This trial, as I say, is underway. This trial is expected to be fully enrolled by the end of the year. This trial is expected to have data readout in April or May of 2026. So this is a very exciting development for us. This trial was slow to enroll. The enrollment has picked up significantly in the past few weeks, months. And we're now expecting full enrollment at the end of the year. So now let me move on to Long COVID. The world really has moved on from Long COVID. Everybody assumed that it's behind us and so forth. But the reality is thousands of Americans are getting infection every single day. And 17 million Americans currently suffer from the debilitating symptoms of brain fog, fatigue, and malaise associated with Long COVID. And 3 million Americans have these conditions so severely that they have had to quit or change their job simply because they can no longer put up with the physical demands of their job. There are no treatments out there today. It is unbelievable to me. I did not know this, but there are huge, huge Long COVID centers and major academic centers around the country that are trying, such as Yale, Mayo Clinic, Stanford, UCSF, and so forth, that are trying to treat these patients using any combination that they could simply because there is really no treatment for Long COVID as it stands. Within the last couple of years, researchers have been able to tie the symptoms of Long COVID through inflammation. It's believed that Long COVID, essentially the spike proteins that remain in the body after the infection has been fought off, works through something called the TLR4, the Toll-like receptor 4. And the spike protein, the E protein, the envelope proteins also works through the Toll-like receptor 2, both of which worked to activate NF-kappa B and ERK in the cell. And since bezisterim has been shown to modulate the activation of ERK and NF-kappa B, there is good reason to believe that bezisterim may be able to modulate the inflammation that comes from the spike protein and the envelope proteins that continues to circulate around in the body. So that is the reason why we have been given a $13 million grant. In fact, we are the only company that has been given a grant to test a therapeutic to see if it can address the CNS symptoms of long COVID, the CNS symptoms, of course, being brain fog, malaise, fatigue that goes along with long COVID. We are currently enrolling 200 patients in a trial that is fully supported by our grant. We are randomizing the patients half to placebo and half to bezisterim. This trial essentially runs for three months. Then that trial, like I said, is currently underway. We hope to give full guidance on when the trial will be fully enrolled. We expect this to be on track for a data readout in the middle of next year. Again, a second data readout in 2026. With that, let me also move on to ascites. Ascites is the origin of the company. This is where the company started before we made the acquisition of bezisterim that brought us into the CNS realm. Ascites is a terrible, terrible end-stage liver disease. By the time you develop ascites, the liver has gotten so scarred that it's not able to process fluid the way it normally does. And it then also starts to affect the kidney. And as a result, fluid starts to build up in the abdomen. And there are no therapies approved for ascites. And so literally, the only thing that you can do is stick a large needle into the abdomen and physically remove the fluid that has accumulated there. But since nothing has been done to address why the fluid accumulates in the first place, these patients are back in the hospitals every one to two weeks to get another five to 10 L of the ascites fluid removed. Now, you can just imagine the strain that that puts up onto the body. And so frankly, the only treatment objective at this point in time is to keep the patient alive for as long as possible so that he or she hopefully may qualify for a liver transplant. And since there are not enough livers to go around, the life expectancy, the mortality rate, I should say, for this condition is over 50% over the course of 12 months. And our solution is a drug called terlipressin. We put our drug into a small saline bag. We hook it up to a portable infusion pump that patients wear on their belt. And we slowly infuse the drug over the course of the day. phase II-A trial that showed that the drug was safe. There were no severe adverse events that were drug-related. We then continued phase II-B trial to try to demonstrate efficacy of the drug. The plan was to enroll 30 patients in a trial. But halfway through the study, after 15 patients were enrolled, we had already received statistically significant data that showed that those that treated with our drug, BIV201, saw a 50% reduction in ascites volume, whereas those that are on the standard of care saw no change. And as I mentioned, this is a condition that has 50+% mortality rate within 12 months. So that's why we concluded that the only ethical thing to do was to stop the trial early and to engage the FDA in a conversation on what it would take for us to proceed to phase III trials for registration. And since we have already received fast track and orphan designation from the FDA, we only need one trial to register the drug. So as of now, we have had conversations with the FDA. We have received all the feedback we need from the FDA to design the trial, which we have done, and we have phase III protocol for the trial to the FDA. That was done three weeks ago, and the FDA has 30 days to respond to our protocol, and that 30 days is expected to be up next week, so by the end of next week, we expect to have comments back from the FDA on any changes, if any, and we don't expect any, which would then allow us to phase III. this trial is currently under way pending different fundraising mechanisms. We are in various discussions to see how we can raise $25 million to fully fund all of the work that would need to be done between now and registration for this drug. This for us is a big deal that will save a lot of lives. To kind of give you a sense of the magnitude that we're talking about here, there are about a million Parkinson's patients in the U.S. today. If we're just 10% penetration of that market, we believe that our bezisterim for Parkinson's could be at least a $3 billion-$5 billion drug annually in annual sales in the United States. With ascites, we believe this could become a $1.6 billion-$2 billion drug in annual sales in the U.S. alone. Any way that you want to risk adjust or discount these numbers, it will still lead you to a number that is substantially larger than our current market cap of $15 million. That's why I continually tell people that I believe we represent a great investment opportunity. We are the rare biotech companies that have significant cash runway well beyond catalysts. We will have two data readouts in the middle of next year, in the second quarter of, and maybe over the summer of next year. Our Parkinson's trial is expected to read out in April or May. And our ascites trial is certainly going to be reading out in the middle of next year. So we represent that company that has cash. We have a company that has multiple data readouts. So I believe we represent a terrific investment opportunity for investors who have a 12-18 months planning horizon, investment horizon, because we believe there is good reason to believe that these trials will be positive. With that, let me stop it here to see if we have any questions in the audience. Thank you very much, Cuong. To reach Cuong, there are two ways. You can press the raise hand button and raise your hand if you wish to speak to Cuong. Or if you wish to type in your question, you can push the Q&A button at the bottom of your screen and type in your question, as some persons already have done. Cuong, what is the size of the market for your ascites drug? What do you expect the FDA to do by the end of the month? For ascites, there is no drug available on the market right now, so we have taken a very conservative estimate to size the market, and that leads us to believe that our ascites drug, BIV201, could have annual sales of somewhere between $1.6 billion-$2 billion in the United States alone. There was a question about what do we expect from the FDA by the end of the month. Frankly, we expect them to not have any comments, which essentially means that we are then authorized to move on to phase III when we have the funding to do so. Okay. Lance. Well, we have someone who wants to speak to you, Cuong. Lance, please unmute your line, and Cuong is ready to speak to you. Yeah, I was wondering, with the ascites, do you have any information or any follow-up on the patients that were in the phase II trial, the ones that did so well? Is there any follow-up on that information? We have some anecdotal follow-up. We did not follow up. There was no post-study surveillance, if you will, that was put in place. But we do have anecdotal information that those patients continued to do well. In fact, we have one patient who actually never had to go back to have another paracentesis because the drug essentially helped address her ascites fluid buildup, which is exactly what we want to see. So that is very encouraging. And part of that gave us some of the information that we needed to go and design the phase III trial the way that we did. So hopefully that answered your question. It did. I have another one, quick one. With the ascites, you've been looking for a partner ever since that trial, which I don't remember was a year, a year and a half ago, or along those lines, and you haven't found anything. What makes you think that you'll be able to find somebody now? That's a very good question. As we look out there, the most logical partner for us is a company that was going through its own difficulty. They were bankrupt. They've been acquired by someone else. And for that company, this represents a small opportunity. That's why I think that just doesn't quite work out for them. There are two other companies that we were in discussions with, and they're highly interested in this. But frankly, they, like us, have had difficulty raising capital as well. And as you know, the biotech capital market has been brutal, absolutely brutal over the course of the last two years. So those companies like us have been keeping our eyes open for opportunities to fundraise. We believe that the capital markets are beginning to open up a little bit to give us some hope that over the course of the coming months, capital will become available for us to either individually and jointly fund the trial or essentially fund the trial through a different kind of partnership that we're exploring. Thank you very much, Lance. Cuong, what is the status of the once-daily bezisterim pill? Let me explain that. bezisterim is currently administered twice a day. Patients would take one capsule in the morning, one capsule at night. And obviously, when you're trying to address a population like Parkinson's or Alzheimer's, a once-a-day would be much, much better. We have initiated, and frankly, we have slow-walked the development effort for a once-a-day drug simply because we know it can be done. We know what needs to be done, but it will cost us about $1 million-$2 million to fully develop that once-a-day version. And so right now, what we want to do is to focus our resources on the Parkinson's trial and the Long COVID trial just to make sure both of those read out. And once that is behind us, we'll then pick up on a once-a-day version. And that is probably the version that we will take into the phase III trial for Alzheimer's and for Parkinson's as well. Thank you for the question. Cuong, you may be having bandwidth issues, and I'm suggesting that you cut your video and go only. Yeah. Thank you. Thank you. All right. Again, to reach Cuong, you can click on the raise hand button if you'd like to speak to Cuong, or click on the Q&A button if you'd like to type in your question. Cuong, we already have some questions here written in. Why do you only feel 10% of Parkinson's patients would take bezisterim? I would think, given the results so far, every patient would want it. I share that optimism. I think that the safe thing to do is to forecast a modest penetration and then let it grow over time. I would much, much rather under-promise and over-deliver rather than over-promise and under-deliver. It goes back also to the fact that bezisterim is a, I'm sorry, levodopa is a very, very good drug. And if you're already on levodopa, you then would need to take bezisterim on top of it, which at the time that we launched the drug, we will not have the indication for it. We expect to launch bezisterim as a monotherapy to go after newly diagnosed patients. So that is a population that needs it the most. The reason I say that is that the moment you are diagnosed with Parkinson's, you know you are on a one-way road of neurodegeneration, and your muscle control will only go down. So the faster that you can get onto a drug that can help slow that decline, the better for the progression of your disease. And so frankly, from a good of humanity standpoint, that's exactly what we want to do is to help those patients slow their progression. So that is our first indication. Our second indication is we will go back and phase II, which gives bezisterim in addition to levodopa to essentially get the market as a combination. But early on, we want to be safe, conservative, small forecast. Of course, there's going to be some off-label use where clinicians will give bezisterim to patients who are already taking levodopa. We're not going to forecast for that. We're going to wait until we actually phase IV trial that gives bezisterim with levodopa, show that it works, get the claims for it, then we will go and market for it. If that, of course, will take us into well beyond the 10% that we're conservatively forecasting now. Like I said, we would rather under-promise and over-deliver rather than the other way around. I hope that answered your question. Thanks, Cuong. Have you had any discussions with any major pharmaceutical companies for funding? Thank you for that question. Over the last couple of years, we have had a number of conversations with large pharmaceutical companies that are interested in Alzheimer's, Parkinson's, and CNS diseases. A number of them have actually shown interest, great interest in this mechanism of action because this is a very novel mechanism of action. Because as you know, in Alzheimer's, everybody has been talking about amyloid and to some extent tau for decades, and there's never been a drug that can essentially address amyloid and tau, which then also significantly alter the disease and slow cognitive decline, and we represent the first new mechanism at work in Alzheimer's and Parkinson's in decades. But in pharma, and I understand where they're coming from because I've been on that side of the table as well, the road is littered with promising drugs for Alzheimer's and Parkinson's that fail in phase III. And in big pharma, no one is ever fired for playing it safe. And so the reception that we have gotten from big pharma has been, "they wish us well." They really are wishing us well. They're monitoring us, and they basically tell us, "Come back when you have positive phase II or phase III data on these trials," and then we'll pick up the conversations there. So there's interest in our molecule. They're monitoring it, and they're just really waiting for phase III data in Alzheimer's and possibly phase II, more ideally phase III data from Parkinson's trial. And so I do not expect us to ever commercialize these molecules. My expectation is that when we demonstrate positive data, we will out-license the molecule to big pharma, or frankly, they will acquire our company. That's really the realistic outcome to expect for our company. I hope that answered your question. How long phase III trial last for ascites? This trial is unfortunately a trial that's going to take some time to enroll. We need to follow the patients for six months. So in theory, the trial is short, but the enrollment rate here will be relatively slow. And so we would expect to start the trial, to conduct the trial in both Europe and the US with some significant centers that work with these patients. But even that, this trial will take us at least 18 months, possibly 24 months from beginning to end. That's part of the reason why we did not prioritize this earlier is that it will take some time and $25 million to fully complete the study and to register the drug. Hopefully, that answered your question. What is the status of the class action? And is it a large drain on resources? To be honest, it is not a large drain on resources. Where it stands right now is we are in discovery stage. We had essentially, the way it works is that we put in our petition or motion to dismiss the trial at the very first stage. And frankly, the way that was not granted, and the way it was not granted is frankly, the judge bought our answers to virtually every argument. But the judge had a couple of other questions that were still unanswered in his mind, in her mind. And as a result, she asked us to go into discovery and essentially answered those questions. So we are now in the discovery mode whereby both the plaintiffs and us are essentially answering questions, putting up answers to various questions that are being asked. And once the discovery stage is over, we will then essentially put in place another set of questions for summary judgment. And as you should know, that unfortunately, many of these class action lawsuits are an insurance game. When any time there's significant movement in share prices, there's an entire group of ambulance-chasing lawyers out there that essentially goes out and tries to find one or two plaintiffs or shareholders who've lost some money to essentially try to get a class action suit started. Their objective is never to actually sue us or essentially win. Their entire objective is to get an insurance settlement and get essentially a payout by the insurance company, and as a result of that, over two-thirds of these suits are dismissed at the motion-to-dismiss stage or dismissed summarily without ever going to trial, and then a small minority of these, and then the remainder essentially are negotiated settlements, and the way it works is that we're now in the discovery phase, as I mentioned. We will eventually file our motion to dismiss. We believe that will be granted, and you should also note that our attorneys that are working on this have an 80% dismissal rate of these suits compared to the industry average of about two-thirds, and even if the suit is not dismissed, we believe we'll settle it, and we are still well within our insurance policy for the settlement of this suit. Frankly, it's not taking up that much time. It's really the lawyers going through the motions of it right now. Hopefully, that answered your question. Could you clarify phase III trial begins mid-2026 and lasts 18 to 24 months? That is our hope, is that if we get the funding for the trial, and it's such that we are able to initiate it whenever we initiate it, the trial, let's say, will be expected to run for about two years. That is phase III trial will work for ascites. We have time for a few more questions. Again, you can press the raise hand button or the Q&A button, depending on how you'd like to interact with Cuong. INmune Bio was another company focusing on TNF-alpha, and its recent clinical results were not as good as hoped. Did that trial provide any useful information about the method of action of bezisterim? Thank you for asking that question, and INmune Bio, of course, is one of a small handful of companies that work on inflammation as the mechanism to address disease, and that trial reboosted our conviction that bezisterim is the correct approach. INmune Bio's approach is not to block the production of TNF-alpha as bezisterim does, but to actually hope to try to mop up and block the activity of TNF-alpha after it has already been produced, which is downstream, and once you have all the TNF-alpha in the body, mopping it all up is very, very difficult, and you know that is, excuse me, the case from the entire class of antibodies now known as anti-TNFs, such as HUMIRA, STELARA, and so forth. These anti-TNF antibodies have been around for decades. That's why HUMIRA still remains a multi-billion-dollar drug that it is right now. And the experience with these antibodies, these anti-TNF drugs, shows that it's actually very difficult to mop up and block the activity of TNF-alpha once it's already there. And unfortunately, INmune Bio is doing exactly what those antibodies are trying to do in a small molecule. It just doesn't work quite as well. Although we know there is a signal and we know that blocking TNF-alpha can work. And the reason I say that is there have been large population studies out of the NHS and here in the U.S., Mayo Clinic and other places that looked at patients who are taking anti-TNF medication. And what they found is that for those that are taking anti-TNF medications, those patients have a 50% lower risk of developing Alzheimer's compared to those that are not taking anti-TNF medications. And of course, these HUMIRA and so forth do not cross into the blood-brain barrier. So it doesn't really help directly with getting into the brain, but the mere fact that you're reducing the TNF-alpha burden systemically for these patients also helps reduce some of the CNS burden of TNF-alpha. So it just shows that if you're able to reduce TNF-alpha, you reduce the potential risk of developing Alzheimer's. And that is part of the reason why we have even greater conviction now that bezisterim is the right way to go. And by blocking the production of TNF-alpha, we believe we block all the downstream negative consequences that come along with that, which then should help us not only with Alzheimer's, but with Parkinson's and Long COVID as well. Thank you very much, Cuong, and thank you everyone for all of your questions. For more information about BioVie, reach us at 1-800-REDCHIP or email us at bivi@redchip.com. Please visit RedChip's investor information page for BioVie. It's biviinfo.com. There you can view and download the investor presentation and fact sheet and sign up for news alerts on BioVie. Please be sure to watch Small Stocks, Big Money, RedChip's program featuring exciting small-cap companies every Saturday night at 7:00 P.M. Eastern on Bloomberg U.S.A. Join RedChip's next webinar with FatPipe on Wednesday, October 15th at 4:15 P.M. U.S. Eastern. Register for all RedChip webinars at redchip.com/events, where you can also view an archived version of today's webinar. Thank you to our many participants today, and thank you, Cuong. Thank you. Have a great day.