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, Joseph Palumbo, Chief Medical Officer of BioVie, and Mark Stacy, a key opinion leader and the William E. Murray Professor of Neurology, Movement Disorders Division at the Medical University of South Carolina. 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 facts should also be considered forward-looking statements. Of course, forward-looking statements involve risks and uncertainties. Team BioVie, please go ahead. Thank you, Craig, and thank you everyone for joining today. Before I start, I would like to thank everyone who has worked so hard for so many years to get us to where we are today. Our team has worked countless hours, sometimes pulling all-nighters and so forth, weekends, to get us here. It is on their behalf that I am speaking to you today regarding this. I would also like to acknowledge two people in particular. It is Clarence Ahlem and Chris Reading, who are senior members of our team, who literally have spent decades of their lives working on this to get us to where we are today. We affectionately call them the fathers of bezisterim. Craig has, I will let you read this by your leisure. But let us start with bezisterim. What is bezisterim? Bezisterim is a small molecule that is orally bioavailable. Patients take it twice a day, a capsule in the morning and a capsule at night. It freely crosses the blood-brain barrier, and it is believed to block the activation of something called ERK and NF-κB. When you block NF-κB and ERK, you block the production of TNF-α. Therefore, what you are doing is you are breaking the continuous forward-feeding pro-inflammatory cycle that essentially is going on. By blocking NF-κB and TNF-α production, it is also believed that it is blocking the activation of something called IKK and JNK, which is essentially implicated in insulin resistance. IKK and JNK, when they are activated, bind to something called the insulin receptor substrate 1 and 2, and when they bind to IRS 1 and 2, they prevent insulin from binding there. That is the direct linkage between inflammation and insulin resistance, and that is the key to how bezisterim works. We conducted the SUNRISE-PD phase II trial to figure out what to do to get the data that is needed to design the phase III trial. The SUNRISE-PD was designed as a short, three-month-long study. It is a classical signal-finding study to essentially identify which endpoint we can get an efficacy signal. Which endpoints have the most favorable treatment benefits? It is to measure the magnitude of this difference and to identify the populations where the drug works best for, and all of that allows us to design and size the phase III trial. That is the critical trial. That is the trial where you basically say, "What is the primary endpoint, and did you meet your statistical significance or not?" That is the thing that really matters. It is in the phase III trial. The phase II trial is a signal finding. It is trying to get us the information so that we can do that in phase III. In this phase II trial, we evaluated a series of motor and non-motor endpoints. We created something called the Early Parkinson's Neuro-Inflammation Composite 15, which is the EPNIC-15. We will go much more detail about that as we go over the course of this presentation. We looked at the classical metrics of Parkinson's, something called the Movement Disorder Society's Unified Parkinson's Disease Rating Scale. It has three parts. Part I deals with non-motor symptoms, Part II deals with activities of daily living, Part III is motor, and then you add them up to get the total score. We also looked at something called the Parkinson's Disease Sleep Scale 2. At sleep. We looked specifically at sleep because in our prior trial we saw a signal on sleep. We also looked at quality of life using something called PDQ-39. In addition, we evaluated a series of biomarkers, and we conducted what is called a proteomic study that evaluated 380 different proteins in our blood plasma. As part of that battery, we looked at biomarkers of neurodegeneration. We will come back much more to this, but I especially love NfL, which is neurofilament light and GFAP. We looked at neuroinflammation, and we also looked at peripheral inflammation. That is what we tried to do. That is what this study was designed to do. This is what we found. We found that patients treated with bezisterim appeared to have experienced a statistically significant treatment advantage compared to those on placebo. We looked at the clinical outcomes, where we saw significant impact on the EPNIC-15. We saw that 283 out of the 380 proteins we looked at moved in a direction that is beneficial and that has been shown by others to slow the progression of disease. We looked at different metrics of neurodegeneration, and those moved in a very beneficial manner. Of course, we looked at various measures of inflammation. We also saw that while bezisterim appeared to have an effect across the trial population, we also found that our hypothesis that patients who have higher inflammation at the start of the study would be the ones that benefit the most and would respond the fastest, and that is exactly what we found. Those with higher inflammation at baseline experienced statistically significant advantages over placebo across all clinical measures that we looked at, including UPDRS Parts I, II, and III and the total score, as well as EPNIC-15. I will share more of that as we go along. The biomarker results also suggest that bezisterim may be slowing neurodegeneration over time. This is a big deal if we can show this, and certainly this is something, a hypothesis that we would be testing as we move into phase III registrational trial. Lastly, but not least, bezisterim continues to demonstrate a very safe profile. It was well-tolerated. The safety profile was very similar to placebo. Before I go into deeper, let me set the context for why these data are so important. First of all, we know that Parkinson's is a progressive neurodegenerative disease. Once you have it, the brain's cells will continue to die, and neurodegeneration will continue to happen. Right now, the community largely views Parkinson's as a motor disease, characterized by low dopamine levels in the brain, which then leads to muscle disorders and slowing of motor symptoms. Unfortunately, it misses all the non-motor symptoms right now. Since that is such an important part of this, I am going to dive deeper into non-motor, and we will spend a lot of time on non-motor discussions. We found this chart in a great journal article. So frankly, we just liberally borrowed it. We copied and pasted it here. The green at the bottom discusses non-motor symptoms. Non-motor symptoms include things such as sleep disorders, depression, cognitive slowing, GI symptoms, and a lot of constipation. The important thing to note here is that many of these non-motor symptoms exist for years, many, many years before the actual diagnosis of the motor symptoms. These non-motor symptoms continue to worsen, and some patients would say it is the non-motor symptoms that could be worse than the actual motor symptoms themselves. Once it is diagnosed, somewhere along the way, patients will get put onto therapy, and the current standard of care for Parkinson's treatment is levodopa, which is a great drug that has been around for over five decades. But treatment with levodopa and similar drugs also creates their own treatment complications as well. The thing to note about this chart is that it all heads upwards. The disease continued to progress. Things always get worse. It never changes. It never gets better. That is where we believe is the big unmet need. What we are trying to do with bezisterim and the unmet need that we are trying to address is conceptually depicted on this chart. The dashed line at the top—think of it as the top line on this chart. The disease, if untreated, will continue to progress. Then as you get put onto levodopa, what you are doing is that you are shifting that curve down because you are addressing the motor symptoms of the disease. Right? So, you are shifting this curve down. But since nothing has been done to address the underlying reason for the disease progression, the disease continues to progress. What we are trying to do is, and we believe the big unmet need in the community is, something that changes that trajectory, something that can slow the progression and essentially bend that curve. Right? As I move on, let me ask that my others are in the panel. Mark and Taryn, I am not sure why you are on the panel. If you can just take yourself off camera, right, and mute yourself as well. Thank you. Joe as well. Okay. So we know that bezisterim works on inflammation. The neuroinflammation hypothesis essentially goes something like this: It is peripheral inflammation that is activated by TNF-α and NF-κB, as I showed before, that essentially leads to neural inflammation and oxidative stress, ER stress, and so forth in the CNS, which then leads to neuronal loss, which then leads to clinical progression. That is the hypothesis for what is really going on, right? This hypothesis is partly associated with a term called Type 3 diabetes. That was coined by Dr. Suzanne de la Monte from Brown, who is also one of our scientific advisors. She believes, and we totally believe, and many other people believe in her thesis, that neural degeneration has an underpinning metabolic reason that essentially starts with insulin resistance, and insulin resistance is caused by inflammation. What we did in this trial is, again, a signal finding study that is very short and very small, all aimed at getting us the data to design the phase III trial. In this trial, we looked at four different things. The first is inflammation. This is really our primary endpoint: inflammation. Does bezisterim have an impact on inflammation? We also looked at what is happening with biomarkers associated with the disease. The third thing is we spent a lot of time looking at neuronal injury, things such as neurofilament light and GFAP. NfL and GFAP are known biomarkers of neurodegeneration, so they naturally increase in our blood samples as neurodegeneration progresses. And we are asking the question, can bezisterim have an impact on the progression of, and the release of, NfL and GFAP? And of course, we look a lot at clinical scales. Before we dive into the numbers, let us spend a minute to understand what the numbers mean. We look at the numbers, and we look for two things. One is just how big of a treatment effect there is. So how big of a difference is there between the treatment group and the placebo group? And statistics has a tool to allow us to do that, to understand that, and that is called Cohen's d, which measures the size of the difference, the size of the effect. A Cohen's d of 0.5 is really good, it is a moderate-sized impact difference. A 0.8 is a large impact. Anything beyond 0.8 is just absolutely massive and huge. The way that all the numbers are arranged is that a negative value means that is a treatment benefit, right? As you will see, most of bezisterim's treatment effects are in the large range. So the first thing, treatment effect—how large is it? The second is what is the likelihood that that could be a fluke or coincidence? That is why we looked at the P value. The smaller the P, the better, right? Statistical significance is defined as having a P value equal or less than 0.05. So that is when we say something is statistically significant. It means that it had an impact, and it has a P value equal or less than 0.05. Let me start by just showing the baseline characteristics. We had 57 patients enrolled in this trial. Roughly half were in each of the arms. The bezisterim arm had 28 patients. The placebo arm had 29. And I will let you read through this at your leisure. This is available at our website. But as you can see here, the treatment and the placebo arms appear to be balanced at baseline. They were very similar. While our primary endpoint was inflammatory biomarkers, everybody wants to talk about the clinical outcomes because this is Parkinson's. So let's start there. In the entire treatment population of 57 patients, we looked at the EPNIC-15 and the MDS-UPDRS scores. Across the population, what you see is that patients treated with bezisterim, as shown in blue, have a smaller change from baseline. Right here, a positive number means people are getting worse. So what this shows is that patients treated with bezisterim are getting worse at a slower pace than patients that are treated with placebo. Okay. In the entire population, if you look at the P values, we did not get statistical significance of these different P values. But this is not uncommon. This happens in the majority of phase II trials. Remember, the second I mentioned before, the purpose of the phase II trial is to find the endpoints where the drug could work and with which populations that it could work. As I mentioned before, we have long had the hypothesis that patients with higher inflammation levels at baseline will be the ones that will respond the fastest and the ones that will respond with the greatest impact. That's exactly what we found. The hypothesis turned out to be true. What we found is that patients with higher baseline inflammation as measured by platelet levels that are greater than 230 at baseline. 230, frankly, we chose that because it's the median. The median platelet count for the population was 233. So 230 was a convenient number. Half of the population in the study had higher platelets. What you will see in this chart is actually quite startling. You see that patients who have higher inflammation not only did not have a slowing of worsening, they improved. Patients treated with bezisterim improved over the course of three months of treatment. On the Part I score, that's looking at non-motor symptoms, Part II score, that's looking at activities of daily living, and Part III score, which is the motor score. Historically, this is the metric that the FDA uses to approve a Parkinson's drug. Of course, when you add it all together, they improved on the total score as well. If you look here, the statistical numbers are very high. Of course, when you look at the EPNIC-15, and we'll come back to the EPNIC-15 later, the P value here is highly, highly statistically significant. Before you may start thinking or concluding, "Well, maybe bezisterim doesn't work for patients who have low platelets or low inflammation," that is not the case at all. You can see that on the next page. This page shows the entire population of 57 patients, arranged by their platelet counts at baseline. What you see on EPNIC-15, on Part I score, Part II score, that slope is very flat. The vast majority of the patients have the numbers below zero. We took the bezisterim results, subtracted out the placebo results, and if it's below zero, it means it favors bezisterim. What you can see is about 80% of the patients, regardless of their inflammation level, benefit from bezisterim treatment. On Part II, that is for Part I. Part II is even higher than that. It is only when you get to Part III that you see a slight slope. Here you see that about half of the patients benefit from bezisterim treatment. What does all of this mean? It means that we now have what we call an enrichment strategy for designing the phase III trial. We want to go into the phase III and be assured that we can win statistically on Part III score, because that is most likely what the FDA will want us to demonstrate at a minimum. At a minimum, what that means is that when we go into designing the phase III trial, we will enroll just more patients with higher inflammation, and perhaps we will stay with platelets, or perhaps we will go with another metric of inflammation. We know that higher inflammation patients are the one that respond the most and the fastest. We will enrich the population, the sample, for the phase III trial. That means we will over-enroll patients with higher inflammation so that at the worst case, at a minimum, we will win statistically on Part III. Of course, we will have the conversation with the FDA about including Parts I, Parts II, and perhaps even the EPNIC-15 as part of our endpoint. Given this data that you see on this page, we are highly, highly confident that we have a drug that we can go and discuss with the FDA with a trial design that would allow us to get approval at a minimum on motor symptoms by improving motor symptoms. The data here would suggest that we would be able to have a win on non-motor symptoms as well. What that means, when you step back from all of the numbers, is that we believe that bezisterim could become the first drug that could have an impact on both motor and non-motor symptoms of the disease, and that will be a drug that will uniquely meet the currently unmet need in the community. Takeaway number one, potentially the first drug to address both motor and non-motor symptoms of the disease. We did not stop there. We have said that all prior drugs have been approved largely on motor symptoms. The Movement Disorder Society, the name itself says it all. When you look at the last 10 drugs that were approved, six of them were based primarily on daily off time, which looks at what portion of the day and how long the time during the day is your muscle in the off mode, so you cannot move. They are stiff. Two of the last 10 approvals were based on Part III score. All motor endpoints. We know that bezisterim affects muscle function. We know that from our prior clinical trial, our first clinical trial in Parkinson's. We also know it from this trial. But if you use only motor endpoints, you are not getting at what we know is to be a much broader clinical impact that bezisterim could have, and you would undervalue what could be the first therapy for both motor and non-motor. And this is where we learned along the way. We started this trial in April of 2025, and it was earlier this year that we learned about something that Biohaven did. Biohaven is a great company. It has a great, terrific management team that I personally have a great amount of respect for. And they are known to be working on Parkinson's right now. They started this fairly recently, and they are also known to be looking at the mechanism having to do something with inflammation. So Biohaven worked with BroadStreet and Pentara. Pentara is perhaps the leading biostatistician in the industry. We have been working with Pentara for many, many years. So they worked together to create and publish on something that they called the Parkinson's Composite Scale, or PARCOMS. Which is their effort, I believe, to see if in one metric they can get a measure of both the impact on motor and non-motor. So frankly, we just borrowed a page in their playbook. We frankly just copied what they did. We worked with Pentara to create the EPNIC-15 to include these 15 different domains of Parkinson's. These were pre-specified. We hypothesized that these are the ones that bezisterim can most impact based upon our understanding of how the drug works. Therefore, that is where the EPNIC-15 comes from. We did it because we wanted a measure, a single measure, that can assess both motor and non-motor impact of the drug. And what we found was startling. Let me first focus your attention on the left-hand side of this chart. This chart plots what happens to each individual patient. So each patient is a bar. It plots the change from baseline to see if the patient improved, as shown by a negative number; if they stay stable, stay the same, as shown by a zero; or if they worsened, as shown by a positive number. Now, let me call your attention to the left half of this chart. What you immediately see is that the majority of the patients that improved or remained stable are the ones that are on drug treatment. They are on our blue lines. And remember, this is a neurodegenerative disease. So if we can help the patient slow the progression, prevent them from worsening, and allow them to be stable with a zero score, that is a win in our book. Conversely, if you look at the right-hand side of this chart, you see that most patients that worsened are the ones that were on placebo. So as a result, patients that are on bezisterim, collectively as a group, led to an EPNIC score of a negative 0.04. The placebo group had a positive 0.18. And look at Cohen's d, which looks at the treatment effect. It is huge. And as a result, the statistics here are highly, highly statistically significant. Showing that patients treated with bezisterim had an advantage. Another way of looking at this data is to look at the right-hand side. Here, you see that 25% of the patients treated with bezisterim meaningfully improved over the course of three months, compared to only 6% of patients on placebo having meaningfully improved. Conversely, if you look at the other end, you see that only 14% of the bezisterim treatment group worsened meaningfully over the course of three months, whereas 46% of those on placebo meaningfully worsened. When we look at this data, we interpret it to mean that patients treated with bezisterim experienced a statistically significant and clinically relevant improvement or advantage over those on placebo on both motor and non-motor outcomes. Let me now move on to the biomarkers. We conducted a study that looked at 380 different proteins found in our blood plasma. Out of that battery, there were seven that were specific to Parkinson's disease. We found that all seven of them move in a beneficial manner that helps to contribute to the slowing of the disease. statistically significant. We looked at 36 different biomarkers having to do with neuronal injury, and over 90% of those biomarkers moved in a beneficial manner. Highly statistically significant. There were over 150 different biomarkers of inflammation, and over 75% moved in a beneficial manner. Also, highly statistically significant. We named some of those on the right-hand side here. Let me call your attention to the last two rows. Here, we did not get 0.05 statistical significance, but we did get what's in statistics known as trending, which is also very good. We saw advantages on amyloid beta, amyloid beta 42, and p-tau217, which are known biomarkers of Alzheimer's. Some of you may know that we had conducted an earlier Alzheimer's study that was longer in duration, it was six months long and saw a signal that bezisterim was having an impact on amyloid beta and p-tau there as well. We are very excited to pick up that same signal here after just three months of treatment. We, of course, wanted to dive deeper into neurodegeneration. What we found is that in the group treated with the bezisterim-treated group, we look at particularly NfL. I especially like NfL because this is a known biomarker that the FDA has used as the primary endpoint to approve two drugs already. One for ALS and one for MS. The other is GFAP. What we found in this trial is that initially these biomarkers do go up. Frankly, we don't know how to explain that yet. No one really knows how to explain that yet. This is consistent with what has been reported by other studies that test these kinds of drugs. They go up, and in other studies, they slow, they increase, they may be stable. What we see in our trial, especially with NfL, is we see a very rapid, statistically significant decline. Suggesting that we are slowing the release of NfL, namely, we are slowing neurodegeneration. You also see the same trend for amyloid beta and p-tau, where we're slowing the increase. When you put it all together, you see this composite line in blue. We replot that composite line for the bezisterim treatment on the right-hand side, and we add to it a composite for all the placebo patients, and you see a very stark difference. The bezisterim-treated patients saw a decline from baseline on these neurodegenerative biomarkers, whilst the placebo patients saw an increase. The effect size is good, a statistically significant finding. We also found the information that basically shows us mechanistically how the drug could be working. In the interest of time, let me move on. I'll just close with the safety information. What we found was the drug continues to be very safe. There were no serious adverse events in the trial, no severe events, and certainly zero death. There were only two treatment-related AEs, one in the treatment arm and one in the placebo arm. In the treatment arm, that AE was very mild, and the patient continued on to do study. Let's put it all together and see what this really means. First of all, the drug has an excellent safety profile. In this trial, it's consistent with everything we've found to date. Bezisterim demonstrated clear target engagement, has an impact on inflammation, has an impact on the proteomic study, the 380 panel that we saw, and has an impact on neurodegenerative biomarkers. There is an apparent clinical impact on both motor and non-motor symptoms. It has a favorable biomarker for disease modification. It gives us clear rationale for the design of the phase III. The way that we're thinking it right now is that we would have two phases to the phase III. The first phase would be a six-month-long study that gets at symptomatic relief. We would use, most likely, Part III score as the primary endpoint, and if we use the enrichment strategy that I talked about before, that's how we ensure ourselves a win, a win on statistical significance. We will also put in there the non-motor symptoms as well. Six months to the primary endpoint of symptomatic relief. With the data at that six-month point, we can go to the FDA and seek approval for registration. At the same time, with that same patient, we would extend for another 12 months to see if we can get an impact on disease progression. Can we show that we're modifying the progression of the disease? Lastly, we are not all about Parkinson's. We are very excited at Parkinson's. Of course, the results here are phenomenal. It is beyond what typically would be expected to get from a phase II trial. We also have another trial underway that's finishing. That's our long COVID trial. If everything goes according to plan, we should be able to report out the data of that in the next 30 to 60 days. We now need to start planning for an end-of-phase II trial with the FDA, whereby we will discuss with them the phase III trial designs. We need to plan, work with our experts to plan the phase III, start planning for the trials, and so forth. Right now, we've looked maybe at the tip of the iceberg in how much data that we have. We need to continue analyzing the data, prepare for presentations and conferences, and start to submit these to various scientific journals. We will provide additional feedback and readouts over the course of the coming weeks and months as we learn more. Of course, everybody wants to know what's happening with partnering conversations. We will reactivate those in due course now that we have data, which is what the larger pharma companies have been waiting for. In summary, let me just recap that today we have discussed the top-line results for Parkinson's, and we believe bezisterim could become the first treatment in Parkinson's that could address both the motor and non-motor symptoms of the disease. We believe bezisterim could become the first treatment to slow the progression of the disease, and it may become the first new approach to treating Parkinson's since levodopa was introduced over five decades ago. If we are able to demonstrate that in phase III, we believe this will be easily a $3 billion-$5 billion annual sales product in the U.S. alone. We did not talk long COVID, but long COVID is coming to an end. We believe bezisterim may become the first treatment for long COVID, and given that it affects so many more people, that could become a $10 billion annual sales product in the U.S. alone. With that, I would like to stop my screen share. I would like to ask Dr. Mark Stacy to come on screen, as well as Joe Palumbo to come on screen. Mark, let me turn it over to you. Based upon what you have heard me describe here, what is your takeaway? What are your thoughts about what you have heard? Well, thanks, Cuong. It is always exciting to think about these data, and the more chance I get to look at them, the more excited I get. From a more historical perspective, I remember starting my fellowship with Dr. Joseph Jankovic, a very famous movement disorders person, and he had just published a paper looking at tremor-dominant versus postural instability and gait disturbance in Parkinson's disease. The scientific world had erupted with disagreement. There cannot be two kinds of Parkinson's disease. Now we fast-forward for another 40 years, and we are talking about Parkinson's disease as synucleinopathies, as alpha-synuclein degenerative disease. There are statements that occur that we will find hundreds of different causes of Parkinson's disease. This study underscores that. You have looked at more than 400 biological markers, and in theory, all of them could play a role in a particular type of Parkinson's disease. What you have really found is this platelet marker as a way to identify and enrich this population. Those data are striking. They are striking from a potential neuroprotective standpoint and from a potential motor control standpoint. I am all in on this. I think this is a very interesting molecule that is going to generate hundreds of new thoughts about how we treat Parkinson's disease. You are ahead of the curve. Well, thank you, Mark, for those comments. Now with that, Craig, let me turn it over to you, and let's start the Q&A. I am sure there must be a lot of questions from the audience. Yes, there sure are, Cuong, and thank you for that excellent presentation. Yes, to reach the BioVie team, please click the Q&A button at the bottom of your Zoom window. Once there, you can type your question into the text box and send your question from that text box. Because of the great number of participants today, we can take your written questions only today. We have many of those, Cuong. Here's the first one. You mentioned that the results allow you to have an enrichment strategy. What does that mean when designing clinical trials? Thanks for that question. That, of course, is a key part of what we will be focusing on now as we design the phase III trial. Enrichment simply means we over-enroll a population that we think the drug will work for. Let me give you an example, and I am just going to use round numbers. This is purely hypothetical, so please do not take it for anything more than it is. If we were to enroll 100 patients in a trial, the data that we saw here would suggest that about half of them would be higher inflammation, and about half of them would be lower inflammation. Since we know that bezisterim works faster and with a bigger impact for those that are in higher inflammation, and since we want to have an insurance policy to make sure that we win on Part III scores on the statistics, we would just over-enroll. We would just, let's say, enroll another 25 patients with higher inflammation. That's all it really means. We will over-enroll the patients that meet the characteristics that we have here in this particular case, inflammation. I hope that answered the question. Thanks, Cuong. What does the phase III trial design look like, and will the FDA agree to that? Sure. I somewhat alluded to that before. Joe, let me start, and then you can chime in to see and build it out. We are thinking that the regulatory agencies, of course, are very conservative. They like to do the things that they have done before, right? All Parkinson's drugs have been approved based upon motor symptoms, right? That essentially comes down to Part III scores, sometimes Part II and III, but majority of the time, it's Part III scores. We don't want to stress or put anything at risk. So chances are, we will have our primary endpoint as Part III score. But the FDA also knows that there is a huge unmet need around non-motor symptoms, right? That's been well known. In fact, the Parkinson's Foundation conducts an annual survey of their community, and every single year, non-motor symptoms comes up to be the number one or the number two unmet need in Parkinson's. So of course, we will go and make the argument that Part I score, Part II score, the Parkinson's Disease Sleep Scale 2, and perhaps even EPNIC-15 should be part of our endpoints as well, right? Those are our early symptomatic endpoints for the first six months of the study. Notice, we are extending the study from what we just did here from three months to six months. Again, that is an insurance policy to make sure that we're able to see bigger separation between those that are on placebo and those that are on drug. Remember, it's neurodegenerative, so the longer you're on placebo, the more worse things you're going to experience. The longer you're on drugs, chances are the more benefit you're going to get. So even widening benefit between the groups. That's the six-month symptomatic endpoint that we can use to go to get approval, to seek approval. As we end the study at six months, that doesn't mean we stop. We will extend with those very same patients for another year, perhaps. Right? We can design it so that we can stop whenever we get the results that we want. The results there, of course, is to show that we're having an impact on slowing the progression of the disease. There are a number of different ways that that could be shown, and we'll work with our experts on that. So clinical trial, the primary endpoint is around symptoms at six months, extend that for another 12 months to get disease modification. We just do not believe there would be any reasons why the FDA would disagree with that, because that is a very classical design. Give them what they seek at a minimum, Part III score, give them beyond that, and they would love that. They are there to help the patient community as well. Hopefully that answered that question. Joe, anything to add? I think you have covered it. The wonderful thing here is you have two activities. You have what we have seen to be improvement in symptoms, and we also have the ability to slow the disease. At least we hope so, right? That is what the biomarkers suggest, that is what this data suggests, and this is what we would have to prove in the next study. Thank you, gentlemen. The neurodegeneration data look really interesting. What needs to be done in phase III to get a disease modification claim? Yeah. I think I touched on that a little bit. We would need to extend the study for 12 months or so beyond the first symptomatic relief endpoint. The longer we extend it out, we believe that there will be even greater and greater separation. We will be able to show that patients that are on treatment, one, hopefully, will see a benefit on the biomarkers of neurodegeneration of GFL, NfL, and GFAP, right? The FDA loves biomarkers, right? So we will absolutely track those. Then the other, of course, is what is happening to them on UPDRS Parts I, II, and III, EPNIC, and anything else that we can show. If there is a tight correlation between biomarkers and disease progression, that is a home run. If we could just show a change in disease modification, the trajectory over time, that is a big deal as well. Mark, Joe, anything to add on that? I think in the second phase of the study, the most important thing is to see the change of slope in the active study group. In that slide you showed, where you were just treating a patient like levodopa did, you didn't see a change in slope. Patients continued to progress, but they had an improvement in symptoms. With bezisterim, you should see a change in the slope to identify disease modification. Yeah. Terrific. Thank you, Mark. Let's go to the next question, Craig. Craig, can you give us the next question? Excuse me, I was muted. How can one contact a doctor doing a physician-initiated study of bezisterim? Great question. Thank you for that. Let me first explain what an IIT, a first investigator- initiative trial. The FDA has many different kinds of clinical trials that they would consider and approve. This is what we just saw today: your classical what is called a sponsored trial, where a company would conduct a trial. There are trials where a researcher can initiate it himself or herself. So if Mark wanted to go and do a clinical trial, he can go and initiate a trial himself. We believe that bezisterim has a much broader impact than what we as a small company can study by ourselves. We have put in place a program where we would support investigator-initiated trials, where if an investigator comes to us with a plausible hypothesis for how this patient could benefit from our drug, or if a patient has a condition that we are studying but does not qualify for a clinical trial, we could support that investigator, and they would need to submit a protocol to the FDA and get authorization from the FDA. They would need to get approval by what is called an IRB, that looks after safety of patients in trials, and they have to do a number of further things. But if they cross all of those hurdles, we would support the trial by giving them drug, free access to drug to see if the drugs work for patients. And we have done this for a number of different indications. Frankly, the first study that we did in Alzheimer's was an IIT. We have supported a trial in traumatic brain injury. From the early data that we have in long COVID come from IIT. With that said, there is not a simple place that you can go and look, oh, these are the clinicians that are doing IITs, so that just does not happen. At this point in time, I can just tell you that there are IITs underway or being considered in the New York metropolitan area, and then there is one in the San Francisco metropolitan area. And I believe there is one in Miami area as well. If you are in that area, in those areas, and if you have something perhaps in Parkinson's and so forth, reach out to us, and then we will endeavor to. We will ask those clinicians if they are open to having a conversation, and if they are, we will endeavor to connect you. But that is the only way to do it. Or if you have a clinician that is interested in initiating a trial, we would entertain and have that conversation as well. If I can add something, one of the great byproducts of this phase II trial is the company learned how to recruit patients. You work closely with websites, you work closely with the Davis Phinney Foundation and the Parkinson's Foundation, and you figured out how to recruit patients rapidly and in the right phase. You also figured out and demonstrated that patients could be seen in their homes versus traveling to long distances to be seen in an office. That is one of the more exciting pieces of data that we will look at, because I think you will prove that it is cheaper to see patients in their home, and we already figured out to collect data. If the questioner is worried about Parkinson's disease enrollment, you have figured that out, and it will be easy for patients to seek enrollment. Yep. Next question. I was in the trial 2B study. What is ahead for me? Oh, Joe, that is a hard question. I will let Joe answer that one. Number one, talk to the clinician, the trialist, with whom you were treated. I cannot know your name. That is all. Blinded to me. Our hope is that we will be able to provide drugs to people who have been in this study. That requires a discussion with FDA. But it starts with you talking to the individuals who treated you and making yourself known to them, and then they would let us know. Yeah, that is what we would have to do. Thank you for that. Yes. Is it reasonable to assume that you may have an answer for long COVID before Parkinson's? That is a very hard question. The short answer is a maybe. The reason I say that is the following. That trial hopefully will read out in the next 30 - 60 days. We will go into the FDA for an end-of-phase II meeting in the fall or later on this year. If the result is phenomenal, I don't know what that means, but if it's phenomenal, it could be the first therapy for long COVID, which is a condition that affects 17 - 20 million U.S. adults, 4 million of whom have it so badly that they've had to quit or change their jobs simply because they cannot keep up with the physical demands of the job, that they're essentially on disability. So huge unmet need. If we get phenomenal results, knowing the big unmet need, we may go and ask the FDA to consider an accelerated approval and perhaps an emergency use authorization. The chances of an emergency use authorization are very small. Let me be very clear. That is a small chance, but we have to ask. If we get any of that, the beauty about long COVID is that we know how to recruit that very, very rapidly, and it's likely to be a short trial. It's three months to the primary endpoint instead of six months for Parkinson's. Since we are the only company that's testing a new drug in long COVID, we've benefited from the support of many of the leading academic medical centers out there. So places, academic medical centers that have long COVID sites. Places like Yale, Mount Sinai, Northwestern, Mayo Clinic, Stanford, and UCSF all worked very closely with us, and we were able to very rapidly enroll 200 patients in that phase II trial. I think we could be counting on their support again when we move to phase III. When you take all of that together, there is a possibility that long COVID could get to registration before Parkinson's, but time will tell. That's purely speculation on my part, the answer I just gave. Next question. Given that bezisterim targets many of the same neuroinflammatory pathways involved in traumatic brain injury, do you envision bezisterim being tested for the treatment or prevention of the destructive neurochemical sequelae of TBI? That one's yours, Joe. Yeah, we're impressed by it as well. Yeah, that is a good observation and good science. We'd like to get there. There are a number of other targets we'd like to get to. As a very small company right now, we have to stay focused on what we're focused on. But that's something we've already looked at briefly in an investigator-initiated study. The answer is yes. You're spot on. The person who had been in the trial has followed up. "Thank you. How do I get in touch with the clinician to continue? I can't emphasize how important this is to me. I have a feeling I got the drug and want to continue with its progress. Okay. Very quickly, I'm assuming then that you were seen at home, because that would be how you were managed. The best way is to contact the organization that had done the study with you, so that would likely be the people who came to your home, and have them follow up. If it was from a clinical trial site, you would need to contact them. If all else fails, talk to your neurologist and have them contact us on your behalf. We're not trying to pass the buck. No, not at all. I'm just not allowed. You are just not allowed. We are just not allowed to know who the people are, right? That is why it always has to work through your clinician or the organization that helped with the clinical trial. We care very much. We really do. But your identity cannot be known to me. That is the only reason why. On slide 14, the MDS-UPDRS Part III panel shows bezisterim roughly 4 points worse than placebo below about 250 platelets. Will low platelet patients be excluded from phase III, and how are you treating that as a safety consideration? Short answer is low platelet patients will not be excluded. We will enroll everybody, the entire spectrum, because we believe over a six-month study, we will win on that. We do not believe that there is a safety concern looking at platelets. I think we will take everybody, but we will enrich the phase III sample by enrolling more higher inflammation patients in the group as well. And we have time for a final question here at the one-hour mark. My understanding is that bezisterim statistically reduced biological markers of neuroinflammation across all groups and platelet counts in this study so that even subjects who did not show improvement on observable physical measures nevertheless showed reduced statistically significant neuroinflammation. Is this correct? If so, can bezisterim potentially slow down the progression of disease even in these patients, as would be demonstrated by a longer study? Joe? That is exactly the right question to ask. Your observations are our observations. We have biological engagement in processes that mean a lot. We also showed improvement in certain patients, more maybe on the Part II and the Part I at lower platelet counts. But putting that aside, the findings with NfL, with neurofilament light, are extremely encouraging. Your question is our question. We think probably so, but that is what we would have to test. That is exactly what we would have to test. All right, so with that, since we are out of time, let me just bring the call to a close. Let me thank everyone for joining today, and let me just recap by saying that we are extraordinarily excited about the results that came out of this trial. The results suggest that bezisterim is having a statistically significant impact on both motor and non-motor symptoms of Parkinson's. It is showing an impact on neurodegeneration. Thereby, we have a hope of being able to show that we can slow the progression of the disease, and it is having an impact on all these different inflammation biomarkers. We have gotten far more out of this phase II trial than one would expect to be able to get from a small and short trial. We certainly have data that we need now to go and design the phase III trial. Our next step is to design that phase III trial and request an end of phase II meeting with the FDA sometime very soon, and we will go in and have that conversation. We will give further updates over the course of the coming months on any additional insights that we find from analyzing the data, furthermore, and of course, any feedback from the FDA on the phase III trial design, which we will make available when the time comes. Thank you very much, everyone. Have a great day. Thank you very much, Cuong. 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 is biviinfo.com. There, you can view and download the investor presentation and fact sheet and sign up for news alerts. Finally, join RedChip's next webinar with Comprehensive Healthcare Systems on Tuesday, August 18th, at 11:00 A.M., U.S. Eastern. Register for all RedChip webinars at redchip.com/events. Thanks again to the many participants today, and thank you, Cuong, Joe, and Mark.