Hello, this is the BioVie webinar. We'll be getting started in one minute. Hello, 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 is Cuong Do, President and CEO of BioVie. We will begin with a brief presentation in a moment, and then we will answer your questions. Welcome to everyone joining us today on X, YouTube, LinkedIn, and other social media platforms. To submit your question, we invite you to join us on Zoom. Use the link provided. Once in Zoom, click the Q&A button at the bottom of your window and type your question into the text box. 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, please go right ahead. Thank you, Craig, and thank you everyone for joining this afternoon. My name is Cuong Do. I'm the President and CEO of BioVie. At BioVie, we have two assets. Our lead asset is a drug called bezisterim, which modulates the production of TNF-alpha. In clinical trials, bezisterim has shown that it can reduce inflammation and reverse the associated insulin resistance. Parkinson's patients have seen improved muscle control. Alzheimer's patients have seen a 68% slowing of cognitive decline after just six months of treatment. Everyone has seen lower levels of DNA methylation, which essentially is a modulation of the biological aging process. Our second asset is a drug candidate named BIV201, which has the potential to be the first therapy for ascites, which is a terrible end-stage liver disease condition that has greater than 50% mortality within 12 months. We have two very near-term catalysts. The top-line readout for our Parkinson's trial is now expected in the summer of this year, so in the next month or two. Our Long COVID trial is expected to have top-line readout in late summer and perhaps early fall. Our company, we are all about inflammation and insulin resistance. How that starts is really in Parkinson's. We believe that the current perspective on Parkinson's is too limited. The medical community currently view Parkinson's as a disease that's characterized by loss of muscle control and driven by insufficient levels of dopamine in the brain. That is required, of course, we believe that is too narrowly defined and misses on two critical dimensions. The first is that it ignores the non-motor symptoms that Parkinson's patients have. For years before the actual diagnosis of Parkinson's, these patients start to experience non-motor symptoms that has to do with sleep disorders, anxiety, depression, and cognitive slowing, such that by the time the motor diagnosis is made, over 90% of patients already have experienced these non-motor symptoms for years. Unfortunately, these non-motor symptoms are currently just ignored because very few people can pay attention to it or believe nothing could be done. Of course, the current Parkinson's therapies are not able to address these non-motor symptoms. The second reason it's too narrowly considered is that it disregards the underlying metabolic drivers for the disease that essentially starts with inflammation and insulin resistance. We believe that future treatments should address both motor and non-motor symptoms, and we believe it also needs to address the underlying metabolic drivers. The metabolic driver starts with insulin resistance. Because it's been known for decades now that two conditions need to be present at the same time for someone to develop Parkinson's symptoms. The first, of course, is low dopamine levels, but the second is insulin resistance. If you're able somehow to reverse the insulin resistance, the body adjusts and is then able to make use of the dopamine that's there. Unfortunately, over the decades, nothing has been done to be able to reverse the neuroinflammation and the associated insulin resistance in the brain. As such, all treatment approaches up until now has been to increase the level of dopamine so that you can restore muscle control through the use of a drug called levodopa. Now, levodopa is a terrific drug, and that's why it remains the standard of care five decades after it was first introduced. It's a terrific drug in helping Parkinson's patients restore muscle control. It does have limitations, one of which is that it has a very short half-life. That means patients end up having to take it two, three, five times a day, and that could become problematic overnight as you sleep. As you sleep, the drug wears off, and when you get to the morning, Parkinson's patients can't move. They can't get out of bed. That's the reason why Parkinson's patients do not like to schedule anything first thing in the morning, is because when they wake up, they take their morning medication, wait an hour in bed for the medication to kick in before they can actually start to move and get out of bed. That's one very significant limitation. Perhaps the most dire limitation is that Parkinson's fundamentally is a neurodegenerative disease. That means the longer you have the disease, more and more of your neurons essentially have died away. The way to address that is you actually have to end up taking higher and higher doses of levodopa. As you get into higher doses, it leads to something called levodopa-induced dyskinesia, which is the uncontrollable jerky motion that you see Parkinson's patients have. When you have the dyskinesia, all you can do is reduce your levodopa dose. As you cut back on the dose, you lose muscle control. It's a terrible situation that Parkinson's patients have, but it's a situation that we believe bezisterim can help address, because in preclinical studies in rodents and in non-human primates, in monkeys, we found that bezisterim alone was equally effective as levodopa in restoring muscle control. Now, that's a huge statement in and of itself because no other agent's been able to match levodopa in its ability to restore muscle control over the decades. What we also found is when you use bezisterim in combination with levodopa, you get a synergistic effect. We saw maximum muscle control. This as being a Z-score, a lower score is better. This is better muscle control. What got us and our experts most excited is that at the end of the study, when we sacrificed the monkeys and looked at their brains, we found that those that were treated with bezisterim and levodopa retained twice as many neurons as those that were treated with levodopa alone, suggesting that there is a neuroprotective property to the drug. That, to us, is not at all surprising because we know bezisterim reverses insulin resistance. That means there's greater glucose available in the brain for neurons. We also know that bezisterim enhances blood flow to the brain, and that means there's greater oxygen available in the brain. When you have greater oxygen and glucose availability, that only bodes well for better neuronal health. Based on this information, we went into the clinic and enrolled 40 moderate to severe Parkinson's patients and essentially replicated in humans the study that we did with the monkeys. We enrolled half the patients in an arm that gave them a placebo and levodopa, so essentially levodopa alone, as shown in red. The other half were given the combination of bezisterim and levodopa, as shown in blue. What we found, essentially, was the same as what we saw in the monkeys. Essentially, those that were given the combination had significantly greater muscle control than those that were treated with just bezisterim alone. In addition, we found that roughly a third of those that were given the combination had their muscle in what's called the on state first thing in the morning, meaning that they had control of their muscles. They could get out of bed first thing in the morning before they take their morning medication, whereas none of those that were given just the levodopa alone had the ability to move first thing in the morning. The other thing that we found that was interesting is that we started to see a signal that bezisterim has some effect for non-motor symptoms. Namely, these 40 patients, a number of them told us that they actually had better sleep, they had actually better anxiety and depression scores, and so forth. Here, with this study, we have established human proof of concept that you can use bezisterim in combination with levodopa to help moderate to severe Parkinson's patients improve their muscle control. This establishes the first half of what we want to do in Parkinson's. We are now concluding a study to establish the second half of what we want to do, which is to use bezisterim alone with Parkinson's patients at a much earlier stage in their disease. We enrolled 60 patients who are needing to go onto therapy for the first time to address their symptoms. Half of those patients were given a placebo, and the other half were given bezisterim. The trial aims to show that bezisterim can help these patients address both their motor and non-motor symptoms. This trial has completed the patient-facing portion. The last patient has already come in for his or her last visit, and we are now in the process of essentially cleaning the data, waiting for biomarker results to come back from the labs, which is frankly the thing that's taking the longest time. Once we have all the data, we'll lock the database and start the analysis of the data. If everything goes according to plan, we hope to announce the results of this data within the next month or two, probably. Let's plan, let's call it sometime in late July, early August, is when we hope to have results from this Parkinson's trial. When fully developed, we believe that bezisterim can become the first new therapy in Parkinson's in over five decades. It has the potential to be the first therapy to address both motor and non-motor symptoms of the disease. It has the potential to be the first therapy to potentially modify the progression of disease, namely slow the progression of the disease. When fully developed, this, we believe, could become the $3 billion-$5 billion annual sales opportunity in the U.S. alone. Let me now move on to Long COVID. You may be asking yourself, why are we talking about Long COVID, and what does this have to do with Alzheimer's and Parkinson's? The honest truth is, we had no idea ourselves when we started on this journey. It was our experts who helped us understand the situation. I've had COVID now three times. I count myself among the lucky majority of people who have COVID. Namely, when we had the infection, our immune system kicked in, got rid of the virus, the body returned to normal, life goes on as usual. That's why the whole world essentially thinks that COVID is long behind us. Despite the fact that there are 30,000 people who are still getting COVID each day right now. There are 17 million Americans who do not have it so lucky. These 17 million continue to suffer the lingering after effects of the infection that shows up as brain fog, fatigue, and severe post-exertional malaise. 3 million have it so badly that they've had to quit or change their jobs simply because they can no longer keep up with the physical demands of their jobs. Many of them essentially are on disabilities. Within the last couple of years, researchers have tied these Long COVID symptoms to inflammation that works through something called the TLR4, the Toll-like receptor 4, which leads to the production of TNF-alpha, which, of course, is exactly where our drug candidate, bezisterim, affects. What's really going on with these patients, what's believed to be going on with these patients, is that after their immune system got rid of the virus, they still have fragments of the spike protein and the envelope protein continuing to circulate in their bodies. While there's no active infection, their immune systems still believe that there is one, so the immune system is constantly mounting a response. As it goes through that immune response, it's producing a lot of TNF-alpha, which is the inflammation which then is then associated with these Long COVID symptoms. That's what our experts helped us to understand. These experts also told us about a grant program that we applied to, where we received a $13 million grant. We're the only organization, company, nonprofit organization of any kind, that received a grant to test a therapeutic to see if it can address these CNS symptoms of Long COVID, of brain fog, malaise, fatigue. Using that grant, we have enrolled 200 patients in a trial with the help of some of the best leading Long COVID centers out there. Places like Yale, Mount Sinai, Mayo Clinic, UCSF, Stanford, and so forth, have helped us enroll 200 patients in a trial that randomized half to placebo and the other half to bezisterim. We are exploring a number of endpoints having to do with cognition, malaise, fatigue, and a number of biomarkers as well. This is an exploratory study that's looking at about 20 of these different endpoints. This trial is now fully enrolled. Yale enrolled the last patient a couple of weeks ago, which would put it on track to have the last patient come in for the last visit sometime in early August, early to mid-August. We should be in a position to have top-line data readout at the end of August to early September as well. The data really looks promising. If we get the promising results upon unblinding that we hope to see, this would allow us to go to the FDA in the fall to have a conversation about an accelerated approval or an Emergency Use Authorization. We believe we can get a Breakthrough designation for this as well. That, we believe, would make us a strong takeover target or partnering target for big pharma companies out there. We believe Long COVID could represent a $10 billion-plus annual sales opportunity in the U.S. alone. Just recognizing the time here, let me stop it here and let me recap on where we stand. We believe that BioVie represents a terrific opportunity for investors. We have two imminent data readout in the coming months. We have sufficient cash to last towards the tail end of the year. Despite that, we are still lumped in with the other biotech microcaps. Whereby our current market cap is $10 million, which is a fraction of our current cash balance. That's the reason why I believe we represent a terrific investment opportunities for investors who have a 12-month planning horizon. I say that not only because I'm the CEO of the company, I also am one of the largest shareholders of the company as well. I have significant amounts tied up in the company over the years. With that, let me stop it here and open it up for any questions you may have. Thank you. Thank you very much, Cuong. To submit your question, we invite you to join us on Zoom. Use the link provided. Once in Zoom, click the Q&A button at the bottom of your window and type your question into the text box. Cuong, we've already received several great questions here. Here's the first one. BioVie has two clinical top-line data readouts expected in the coming months. Can you give us any more details about those? Well, I cannot really give much more because right now our team is going through the process of conducting the trial. What I can tell you is that we look at the data on a regular basis as they come in on a daily basis, primarily to monitor for safety, just to make sure that the drug is safe. Right? As of now, bezisterim continues down to essentially replicate what we know from historical trial, namely that it's been very safe. There are no drug-related severe adverse events, very few adverse events at all. We also see from the blinded data a promising pattern of separation, whereby some people get better, some people get worse, and some people stay the same. Right? If the ones who got better are the ones that are on drug, upon unblinding, these studies would represent a terrific steps forward for the patient community. All we can really tell right now is on Parkinson's, we are cleaning the data and getting ready for database lock as we wait for the biomarker data to come back from the vendors. On Long COVID, the patients are going through the trial, the monitoring process. They're taking their drugs. They're coming in for visits periodically, and we should have the last patient, last visit in the early to mid-August timeframe. Hopefully, that answered your question. Thank you, Cuong. As you made clear in your presentation, you are different from most of the world that thinks that Parkinson's disease is caused by low dopamine levels leading to loss of motor control. You point to inflammation. Can you tell us more, please? Yes. Well, let me answer that by starting with a very basic biology review. Every cell in our body needs energy to function, and that energy comes in the form of glucose. You may remember from your high school biology how glucose, remember the Krebs cycle and how that produces ATP and so forth. It all starts with glucose. When it comes to glucose regulation, insulin is the key actor. Think of insulin as a key that has to fit into a lock, a receptor on the surface of every cell in the body. That receptor is called the insulin receptor substrate 1 and 2. Insulin is the key that has to fit into the lock so that it could open the cell, the cell could then absorb and take in glucose. When you have inflammation, that's TNF-alpha. TNF-alpha also triggers and drives something called JNK and IKK that also binds to the IRS-1 and 2. Think of inflammation as rust. It's the rust that builds upon your lock, and when you have a rusty lock, the insulin key cannot fit in, and therefore it cannot open the door for glucose to come in. As a result, the cell starts to malfunction, and over time, cells die. Recall that neurons are among the most power-hungry, glucose-hungry cells in your body. Okay? When you have inflammation that leads to insulin resistance, it affects the entire brain. If you have a problem that starts from the substantia nigra, that leads to Parkinson's, because those cells that use and make dopamine starts to die. If the problem comes in other parts of the brain, you then could have problems with Alzheimer's, ALS, and so forth. Right? Inherently, it starts with inflammation leading to insulin resistance that provides the metabolic driver of many of these neurodegenerative diseases, starting with Parkinson's, going on to Alzheimer's, and many others. I hope that answered your question. Yes, it does. Thank you very much, Cuong. Thank you, everyone, for all your great questions. We've got many coming in here. Cuong, is there a pronounced placebo effect for Parkinson's brain-wise? The emotion of hope causes the release of dopamine, which may influence results, and how do you control for that effect? That is a great question. Thank you so much for that. You are absolutely right in saying that there is a potential for a high placebo effect in conducting Parkinson's trial. Just the fact that you're thinking about it or doing something about it could lead to higher release of dopamine. We have done several things that are quite innovative in this trial. First, to avoid any placebo effect that people may have just by the mere fact that they're leaving their house and coming into our clinical site, we actually sent nurses out to their homes to conduct the assessments, to reduce the variability of what's going on. We basically try to keep people in their same environments, just not to trigger any anxiety or anything that could create a placebo effect. Nurses would go to the patient's home. All the activities there are recorded by video, and all the videos across all of the patient's home, across all of the clinical sites, are then scored by a central rater, so that you, again, do not have variability. You have a single person reviewing all the videos from all of the patients, so that you then have consistency across all of that. That helps reduce the placebo effect by having patients in their home. It helps reduce variability by having a single rater. The second thing that we did to try to avoid the placebo effect is in our protocol, we designed in what's called a placebo run-in, which is patients would come in, or the nurses would go out for the first visit, call it Visit 1, and we would assess their activities and so forth on the various scales that we use. We wait 30 days, we repeat that again. If there's been a change in the various assessments, well, that's most likely a placebo effect because nothing has been done in that 30 days. No drug has been given or anything like that. If there was a significant change, that patient then became ineligible to participate. Only if those two metrics, those two visits, were roughly dissimilar, were you then randomized into a placebo arm or the drug arm. Those are the things that we did to try to minimize and avoid the placebo effect that is common in many Parkinson's trials. Thank you so much for that very perceptive question. Thanks, Cuong. How do you compare your Alzheimer's disease solution to LEQEMBI and Kisunla? Yes. Well, we are very, very different from the two approved drugs. Perhaps the easiest way to answer that is for me to bring up a chart. Give me one minute to share my screen. When I first started working in Alzheimer's in the late 1980s, everyone, myself included, we focused on the amyloid plaques and the amyloid buildup. Here on this chart, everything that's in blue is a part of the amyloid pathway. Everything in red is a drug that is trying to modify the pathway in some manner. Over the years, we started looking at tau and tau tangles as well. The reality is over those five decades, those four, five decades that I've been working at it in Alzheimer's, there's never been a drug that can reduce plaques and tangles and arrest or reverse the cognitive decline in Alzheimer's. Within the last decade or so, more and more researchers are coming around to the point of view that plaques and tangles themselves are not the toxic agent that's causing neurodegeneration, but they're inflammatory in nature. They cause inflammation that works through the TLR4, the Toll-like receptor 4, receptor here that we talked about in Long COVID, or RAGE and other receptors. As you can see, many other things cause inflammation as well. All of these things share one thing in common. They all activate ERK and NF-κB to produce TNF-alpha. Of course, when you have TNF-alpha, you have more cytokines and more APP. APP leads to more amyloid buildup. TNF-alpha actually drives this kinase that turns tau into phospho-tau. We are very different than all the other drugs in that we block the production of TNF-alpha, which is considered to be the master regulator of inflammation. The drugs that were mentioned, LEQEMBI and lecanemab and donanemab, they actually try to reverse the production of amyloid and block the production of the plaques. The reason I believe that those drugs have only had a limited impact on the disease progression is that the only thing that they're doing is they're reducing the inflammation that's created and driven by the plaques. It hasn't done anything about the inflammation that's driven by the other factors. That's why they've only seen a very modest impact on cognitive decline. Whereas we believe we will have significantly greater impact because we block everything. As you may know, we had a phase III trial in Alzheimer's. Using the same endpoint that was used here for LEQEMBI, for example, CDR-SB, we had a 68% slowing of cognitive decline versus placebo after just six months of treatment. To put that into context, the anti-amyloid drugs had, as a class, roughly a 30% slowing of cognitive decline versus placebo after 18 months of treatment. Right? We have had a very mild side effect profile. The number one reported side effect was a mild headache reported by about 8% of patients. Whereas, as you know, the other drugs have had significant concerns about brain swelling, brain bleeding, such that they need to be followed by, monitored by PET. Right? We look forward to the day when we can essentially proceed further and go to the next phase III trial to show statistical significance of the results that we're seeing here in this trial that has fewer patients. I hope that answered your question. Thanks, Cuong. Status of the ascites drug, is there a spinoff anticipated? A great question on that as well. We have, as of now, received all the feedback that we need from the FDA to proceed to the next step. Okay. To essentially conduct the one registrational trial that's required, because as you know, we already have orphan and Fast Track designation. We have filed an S1 to take a company called Option Therapeutics public. Our intention is, when market conditions are right, we will put the ascites drug into Option Therapeutics. We would endeavor to raise $25 million, $30 million or so for that company, and that would allow it to conduct a trial that's needed. Right. We believe that trial would probably take about two and a half years to conduct and to get it registered. Right. Right now, we're waiting for market conditions to be right for us to be able to go out and try to raise about $25 million for the ascites program by floating, by taking Option Therapeutics public. Thank you, Cuong. Can you show the potential revenue chart for Parkinson's, Alzheimer's, Long COVID, and ascites? Thanks, Cuong. Great job. You know, I wish I had the most updated chart on that to show in one place the numbers. I do not, but let me give you the numbers. Right. We believe that ascites could be a $1.5 billion-$2 billion annual sales drug in the U.S. alone. We believe that Parkinson's could be a $3 billion-$5 billion annual sales drug in the U.S. alone. Long COVID could represent a $10 billion annual sales in the U.S., and of course, Alzheimer's is going to be the blockbuster. That could be a $30 billion-plus annual sales product in the U.S. alone. Right? Thank you for asking that question. That just reminds me that I have to go and put that chart into the next version of the deck. Thank you very much, Cuong. Let's give everyone a moment to consider any more questions they may have for Cuong Do, the President and CEO of BioVie. Click the Q&A button at the bottom of your Zoom window. A text box will appear, and you can type in and submit your question. This person wants to know more about collaborations. Could you go into more depth with those collaborations that you mentioned with large pharma for the co-development or out licensing of bezisterim in specific regions or indications? We've had a number of conversations with larger pharma companies, and the feedback from them has been pretty consistent. Which is, they are very intrigued with this mechanism of action and the drug, and they want us to essentially come back to them when we have the clinical results. I get it. I've been on their side of the table as well. Right? What I've learned in big pharma is that no one ever gets fired in big pharma by playing it safe. Right? As you know, the world out there is littered with promising Alzheimer's and Parkinson's drug that has failed in phase III, phase II, and that's why big pharma companies now are quite shy and quite reticent of doing collaborations and deals before you actually get data that actually is much further along. Those conversations have been had. They're on hold. Right? I think we will reengage when we have additional data. Right? I think COVID could also be a very interesting conversation for us to have in the very near future as well. Thank you, Cuong. How much would an Alzheimer's trial cost total, start to finish? That's a very tough question to answer, but let me give you a ballpark. Based upon what we know now and what we have modeled out, we believe an Alzheimer's trial could take $25 million-$30 million to conduct. That's one trial, and we would need to conduct two of them. Right? The total cost to bring bezisterim to market for Alzheimer's would be $50 million-$60 million. Right? That's part of the reason why the program is currently on hold until such time as market conditions would allow us to go and raise the funds, right? That's why we have focused everything so far on Parkinson's and Long COVID, because those trials tend to be smaller, easier to do, and shorter to conduct. Cuong, will there be any analysis of blinded data on Parkinson's as you did with Alzheimer's? We are conducting those analyses right now, well, we have been conducting for Parkinson's as we go along. We purposefully have chosen not to re-share or release any of them for the reason that was alluded to in an earlier question, which is we want to avoid doing anything that could lead to a placebo effect. If we announce, for example, that, oh, we're seeing great separation with patients, that could lead those patients into clinical trials or even the clinicians in the clinical trials to actually start to see things that may not be there. That's the reason why we have chosen not to say anything or announce anything about the blinded data, as we've gone along. Thanks a lot, Cuong. Can you recommend where to go to learn more about the mechanism of action and other pharmacological details of bezisterim? All of the information is currently available at our website. Please go to our website, which is www.bioviepharma.com. There's a section there that talks about our science, where you could go deeper into the science. Under the Investor section as well, you can see links to the KOL events that we have held within the last few years on these indications, right? Just a few weeks back, we had a KOL event on Parkinson's, and about a year ago, we had a KOL event on Long COVID, right? We are considering doing another KOL event on Long COVID in the next couple of months just to kind of reacquaint everyone in the market to what we're doing on Long COVID, the causes of Long COVID, and why we're optimistic bezisterim could help address Long COVID. Doing all of this to essentially build awareness in advance of our data unveiling, late summer, early fall. It seems that so much of what BioVie is doing is based on its approach to inflammation and aging. Tell us again how your approach to inflammation and aging differs from your biopharma peers. Frankly, you can count on one, possibly two hands, the number of companies that are working in inflammation and CNS diseases out there. The whole world has really focused on, in Alzheimer's, for example, on amyloid and tau. We believe that is just a dead end, right? We have tried for years to basically sound the alarm and say that is a dead end. We're a tiny company, and so as a result, we don't get a lot of attention, and we actually just have to go out there and demonstrate it. We count ourselves among the two handful of companies that are working with inflammation as the key driver of disease pathology. What also makes us very different is also our approach on insulin resistance. Because bezisterim blocks TNF-alpha right before it activates JNK and IKK, it actually reverses insulin resistance. Please remember that bezisterim was originally brought into the clinic as a diabetes drug, and in that first trial, it showed exactly what you would want to see in a diabetes drug. It reversed insulin resistance, and it brought all these different biological systems back into normal ranges, so glucose, HbA1c, cardiovascular, and so forth. That was before the team truly understood the mechanism of action and how it blocks TNF-alpha. Once we understood that, we recognized that bezisterim's role is potentially much bigger in the world and in addressing the biggest unmet medical needs right now, essentially Alzheimer's, Parkinson's, and a number of other CNS diseases. I believe that's what makes us very, very unique in the biopharma world out there. We, I believe, have the most unique molecule and leads us to have the most interesting portfolio in the biotech world. Thanks, Cuong. We probably have time for a few more questions. We've been getting so many great questions. Thank you so much to all of our participants. This is medical related here. If someone has type 2 diabetes and inflammation and insulin inefficiency, are they more likely to get Alzheimer's? The answer to that is unfortunately yes, absolutely. If you have type 2 diabetes and insulin resistance, statistics shows that you are at a significantly greater risk of developing Alzheimer's, Parkinson's, and other CNS diseases. Let me give the statistics the other way around. Right. If you look at Alzheimer's patients, the Mayo Clinic and NHS out of the U.K. have shown that about 80% of Alzheimer's patients have or are developing insulin resistance. The comparable statistics with Parkinson's is about 50% of Parkinson's patients have or are developing insulin resistance, right? That's the part of the reason why we so strongly believe that many of these diseases have a metabolic underlying underpinning driver to it. It's not just about just low dopamine or amyloid and so forth. It really starts with TNF-alpha, which is the master regulator of inflammation. When you have TNF-alpha, you're going to create insulin resistance, and insulin resistance starts to kill off cells. That's why neurodegeneration is a real problem. That's the link between inflammation, insulin resistance, and neurodegeneration in our belief. All right. We are just at the top of the hour. We'll wrap up here, and if you do have any questions for Cuong Do, no matter whether they were answered today or not, you can write us at bivi@redchip.com and we will make sure that Cuong sees your question. For more information about BioVie, again, you can write us at bivi@redchip.com or you can call us at 1-800-RED-CHIP. 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 watch Small Stocks, Big Money, RedChip's program featuring exciting small cap companies every Saturday night at 7:00 P.M. Eastern on Bloomberg USA. Finally, please join our next webinar with Foremost Clean Energy tomorrow at 4:15 P.M. U.S. Eastern. Register for all RedChip webinars at redchip.com/events. Thanks again to our many participants today, and as always, thank you, Cuong. Thank you everyone for joining. Have a great day.