Answer your questions. Welcome to 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 and 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.
Good morning, everyone. Thank you for joining today. My name is Cuong Do. I am the President and CEO of the company. Give me one minute to get my screen share up and running again. Our company has two assets. Bezisterim is a novel modulator of inflammation, and BIV201, which potentially has the potential to become the first drug to treat ascites, which is a terrible end-stage liver condition. We have had a very exciting August and September. About 45 days ago, we reported out on our Parkinson's phase II trial, and just within the last week or two, we have reported out on our Long COVID trial. We will spend today mostly on these two clinical trial results. As we look forward to the remainder of this year, we have a lot more data to analyze from the trial, so we will provide additional clinical updates.
Excitingly, we plan to meet with the FDA in an end-of-phase II meeting for Parkinson's, and we expect to get formal feedback from the FDA on our Parkinson's phase III design, by the end of the year, perhaps even by Thanksgiving time. We believe that inflammation is a starting point for a lot of things that go wrong in the body, particularly starting with TNF-alpha. When you have the production of TNF-alpha, which is considered to be the master regulator of inflammation, it leads to a lot of the bad things that you see on this page. That is where our drug candidate bezisterim comes in. Bezisterim is a small molecule that is orally bioavailable, so patients take two capsules a day, one in the morning and one at night.
It freely crosses the blood-brain barrier, so it gets into the CNS, and it is believed to block the activation of ERK and NF-kappa B. By blocking ERK and NF-kappa B, you block the production of TNF-alpha. Essentially, when you have TNF-alpha, it leads to a forward-feeding pro-inflammatory cycle, so it just creates more inflammation. When you have TNF-alpha, it activates something called IKK and JNK. IKK and JNK binds to the insulin receptor substrate one and two, and blocks insulin's ability to bind to that same IRS1/2, thereby causing insulin resistance. So by blocking ERK and NF-kappa B, we block the production of TNF-alpha, we reduce inflammation, and we have reversed insulin resistance. That is how bezisterim is believed to work. You can see the impact of that first in Long COVID. This is a trial that we reported out on just the last couple of weeks.
Long COVID affects a large population. There are up to 20 million adults in the U.S. that are affected with Long COVID. Nearly 4 million have it so badly that they are considered to be disabled. They can no longer keep up the physical demands of the jobs because they are suffering from brain fog, fatigue, and post-exertional malaise. Research has tied these conditions to inflammation that works through exactly the same mechanisms where bezisterim affects. That is the reason why we believe bezisterim has the potential to become the first therapy for Long COVID, because there is absolutely nothing that is available now. All the trials on Long COVID have failed. First, it is important to recognize that Long COVID is not the same as COVID. COVID is the infection caused by the virus. Many of us have had it.
Many of us have been able to ward it off, and life just resumes. Life goes on. Unfortunately, for the 20 million Americans who have Long COVID, they continue to suffer from these different conditions, and it lingers for years after the initial infection. We believe that bezisterim may have an impact on those conditions. So we conducted the ADDRESS-LC phase II trial. It is a signal finding trial that is designed to essentially identify which endpoint could show that bezisterim could work, to measure how big of an impact bezisterim could afford patients that are on drug, and to identify the patients that can benefit from this drug. All of this is needed so that we can design the phase III trial.
The phase III trial is really the critical trial where you have to have a single endpoint or a few endpoints, and all you are looking for is statistical significance. Does it work or does it not work with statistical significance? That is a phase III trial that we now will plan. This phase II trial gives us the information to do so, the planning. In this phase II trial, we evaluated 22 different clinical outcomes. We collect blood samples, and we did all of this with the support with a $13 million grant from the Department of Defense, now the Department of War. We have always known that Long COVID is a very complicated heterogeneous situation, condition. At baseline, we had 203 patients enrolling in our trial.
We have always known that patients that have high inflammation or high symptom burden are the ones that are most likely to respond most quickly and most profoundly. So we always pre-specify certain subgroup populations with the FDA before we unblind the study. We did exactly that here. One of those ways of specifying subgroups is based upon disease severity, right? Which disease symptoms. Here what you find is in the trial, we had 112 patients with high fatigue, we have 98 with brain fog, and 70 with post-exertional malaise. We always talk of Long COVID essentially involving those three symptoms. Interestingly, you see that only 15% of the patients have all three symptoms with high severity, right? Yet, another 35% have some combination of two symptoms, and another 35% have some combination of just one symptom.
The important thing to recognize here is that if you do not have a symptom, it is not possible for you to improve on it. Here you see 112 patients with high fatigue. That means all of these patients that are red and in green do not have fatigue, and therefore they have no room to improve. That is a critical thing to keep in mind as we go through the data. Because here, as you look at what happens on the results for all 203, you see that on 21 out of the 22 endpoints treatment, you see a favorable treatment effect. It is to the right. The Cohen's d is positive, meaning that the treatment effect favors bezisterim. But interestingly, none of these endpoints reach statistical significance of p equal 0.05 or less. That has to do, we believe, with what we talked about here.
Only if you have fatigue, if you look at this fatigue, only this 112 patients can really improve on it, which means that the improvement for all these patients, the red and the green, is zero. While you see some impact, some effect favoring bezisterim treatment, you do not get statistical significance you have because so many of those patients, those that do not have high fatigue, do not show improvement. That is the reason why we pre-specify in our submissions to the FDA that we will look at different subgroups based upon the symptoms they have and severity. By doing so, you see a remarkable outcome. If you look at patients who have high fatigue, the impact doubles. The Cohen's d doubles. You see that patients have statistically significant improvements on fatigue and other measures.
You see the p values here are less than 0.5 for five measures, and you get trending improvements on another three. You need to have fatigue to be able to improve on fatigue with statistical significance. Similarly, if you look at patients who have high post-exertional malaise at the start of the trial, those patients improve on post-exertional malaise, the DSQ-PEM, with statistical significance. But these patients also improve on their cognitive impairment, on their brain fog. This actually is very easy to imagine and to see. Sometimes when I, and I am sure many of us on this call, if we wake up early in the morning, if it is too early or whatever it is, we could be groggy and so forth. We are just not thinking clearly. Fatigue directly affect our ability to think clearly.
For these patients who suffer from high post-exertional malaise, those patients are suffering from it all the time. Here, by bezisterim's ability to help patients improve under fatigue, not surprisingly, they are improving on brain fog as well. Similarly, if you have high brain fog, you improve on brain fog. This shows that bezisterim has the ability to help patients improve on all three of these symptoms, of fatigue, malaise, and brain fog, but you need to have the symptom to begin with in order to improve. This is the reason why our experts and all of the experts in the field are so excited about this. Because there has been dozens of trials that have all failed to demonstrate impact on any endpoint.
Whereas here, bezisterim, this is the first trial that has been able to show to have an impact, not on one, but on all three of the neural symptoms of Long COVID. This is the reason why all 12 of our PIs and our advisors, all 12 out of 12 that we have spoken to so far and polled strongly recommend that we move quickly to phase III because this is the first thing that has worked for these patients in the community. Remarkably, consistent, bezisterim continues to show that it's a very safe drug. There was zero serious events and so forth. The safety profile is incredible because in this population, virtually everybody is taking one or more other kinds of medications.
The last thing you want is to add to this mix a drug that potentially could have drug-drug interaction or lead to other problems, and we just did not see any of that in this trial. This gives us great excitement that bezisterim could become the first therapy for Long COVID, and we're still waiting for some additional biomarker data to come back from the labs in the next 45 days or so. We will analyze that and give additional readouts at that time. Based upon we have the totality of the data, we will then ask for a meeting with the FDA and end the phase II meeting with the FDA later on this year to go and discuss our plans for phase III for Long COVID. With that, let me— Excuse me one second. With that, I'd like to move on to Parkinson's.
Parkinson's is known as a progressive neurodegenerative disorder that leads to problems with both motor and non-motor symptoms. There are no disease-modifying therapy out there. There's great unmet need for a new medication that can address motor and non-motor symptoms and hopefully modify the progression of the disease. When we talk about non-motor symptoms, I'm going to ask you to focus on the green part at the bottom of this chart that we found in a great article. We just shamelessly copied and pasted it here. When we talk about non-motor symptoms, we're talking about sleep disorders, there's depression, cognitive impairment, lots of GI problems, and constipation. These symptoms often show up for years before a patient is actually diagnosed with the motor symptoms.
When you have the motor symptoms diagnosed, sooner or later you will go onto a drug called levodopa or similar drug to help address the motor symptoms, to help you improve your muscle control, but those drugs eventually lead to other complications. As you can see over time, the progression of the disease only heads in one direction. It only heads up. What we believe is there is the need and the potential to change that. To conceptually display what we mean is if you look at the dashed line, this is directly what happens to a patient's symptoms if it goes untreated. It just continues to get worse over time. But as you go onto levodopa to address the motor symptoms, you're addressing the motor symptoms, so you're shifting that curve down.
But since nothing has been done to address the underlying progression of the disease, it continues to progress at the same pace, but at just a lower level. What we believe is needed is for a therapy that bends that curve, that changes the slope of that curve, and we believe that bezisterim has the potential to do so. That is why we conducted the SUNRISE-PD trial, where we looked at four different things. We looked at inflammation, biomarkers of inflammation, because that is how we are convinced bezisterim works. We conducted a proteomic study looking at different plasma proteins of inflammation and CNS disease. We looked a lot at neuronal injury, and we looked a lot at clinical outcomes. In our entire trial of 57 patients, what we see is that patients treated with bezisterim do not worsen as quickly as patients that are treated with placebo.
The way to read this chart is that a bigger positive number is greater progression. You see that those that are treated with bezisterim, shown in blue, do not worsen as quickly as those that are treated with placebo. But we do not see statistical significance at this gross level of 57 patients in the whole population. But again, we know that patients who have inflammation or have higher disease burdens are the ones that will respond most quickly and most profoundly. That is why we pre-specified with the FDA before we unblinded the data that we unblinded the data.
What we found is that patients that have high inflammation, as shown by high baseline levels of platelets, you see that those treated with bezisterim not only slowed the progression, we saw a reversal, an improvement of something called the Unified Parkinson's Disease Rating Scale that comes in three parts. Part one is the non-motor, part two is the activities of daily living skills, and part three is motor symptoms. Part three is the endpoint that the FDA has used historically to approve Parkinson's drugs. They have also used the total score. Here, either part three or total, you see that we win statistically. So we have statistical significance showing that bezisterim-treated patients improve on treatment. But you also see that we win on part one, which is the non-motor endpoint, as well as the activities of daily living.
This is the reason why we believe that bezisterim has the potential to become the first drug to address both the motor and the non-motor symptoms of the disease. Of course, you may know that the non-motor symptoms are considered to be the biggest unmet medical need in the Parkinson's population at this point. We also created something called the EPNIC-15, which puts together motor, non-motor, and all of those endpoints into a single measure, EPNIC-15. Let me focus your attention to the left chart. Here on the EPNIC-15, an improvement is a smaller number, a negative number. Here you see, if you focus on the left side of this chart, you see that the majority of the patients that improved are those that are treated with bezisterim, as shown in blue.
Those that are stable, that did not change, are those majority are treated with bezisterim. The fact that you did not improve or did not worsen is a win in our part, in our mind, because we believe that we prevented these patients from worsening. Conversely, if you look on the right-hand side, most of the patients that are worsened were on placebo. You see very, very big statistical significance here when you look at this metric. Another way of looking at the data is you see that 25% of the patients treated with bezisterim meaningfully improved compared to just 4% of those that were treated with placebo. Now, conversely, only 14% of those treated with bezisterim meaningfully worsened compared to 46%.
When we look at the totality of this data, we conclude that bezisterim treatment help patients meaningfully and statistically significantly improved on both their motor and non-motor symptoms, thereby positioning bezisterim to potentially become the first drug to address both motor and non-motor symptoms in Parkinson's. Let me move on to look at biomarkers. We looked at 380 different biomarkers in what's called a proteomic study. In that battery, there were seven Parkinson's-specific biomarkers, and all seven moved in a beneficial manner. That's statistically significant. There were 36 biomarkers of neuronal injury. Over 90% of those biomarkers moved in a beneficial direction. So highly statistically significant. There were over 150 different biomarkers of inflammation. Over 75% of those moved in a beneficial manner. So highly statistically significant. We also dived more deeply in neurodegeneration.
I'm particularly interested in looking at something called neurofilament light, or NfL, and the other is GFAP. NfL and GFAP are well-recognized biomarkers of neuronal degeneration. The longer that you have the neurodegenerative disease, the more that these biomarkers continue to increase. They get released into your blood, higher and higher levels the longer you have a neurodegenerative disease. But in this trial, you can see that those patients that were treated with bezisterim saw a significant decline of their biomarkers, particularly NfL. The reason I'm interested in NfL is that this is the biomarker that's been used as the primary endpoint to get two drugs approved, one for ALS and the other is for MS. You see a statistically significant reduction with bezisterim treatment.
In dark blue here, dark, thick blue, we give the composite of all of these different biomarkers, and we re-plot it on the right-hand side. On the right-hand side, we also give the placebo composite, and you see that they just move in a completely different direction. So highly statistically significant. We look at this, and we can conclude that bezisterim has the potential, when looked in a much longer study, as we plan to do in a phase III study, bezisterim has the potential to become the first drug to slow the progression of the disease. If you're slowing the progression, and here's the signs of it, you're slowing the increase of these neurodegenerative biomarkers. We have asked for a meeting with the FDA, an end of phase II meeting with the FDA, to discuss our phase III trial design.
We have good ideas of what needs to be done. We've worked on this with our advisors. We don't believe that we will have any trouble with the FDA on this trial design. We expect to get formal feedback from the FDA by the end of the year. If so, with funding, we believe we can start the phase III trial by the middle of next year or so. I see that in the interest of time, let me stop it there, and let's open it up for questions.
Thank you very much, Cuong. To submit your question, we invite you first to join us on Zoom. Use the link provided. Once in Zoom, click the Q and A button at the bottom of your window and type your question into the text box. Because of the great number of participants today, we can take your written questions only, and we have many of them already. With so much good news on the results, why is the stock getting crushed? When do you expect to put in for the stage three trials? Well, let's work with that. The first one, please. Thank you.
I wish I can give you a great answer, right? Unfortunately, what we are experiencing is what other biotech companies are experiencing as well, where people sell on the news. Unfortunately, the shorts really had it in for us, right? Some short sellers made a lot of money by essentially driving our shares down. They were able to do that because everybody was expecting us to go and raise some capital on the back of the good news. So basically, they sell. Some of this, we believe, were just naked shorts and so forth, which is highly illegal, but there's nothing we can do about it. Just to kind of give you some context, we have about 8 million shares outstanding in the total float. On the day that we announced our Parkinson's result, which are really good results, over 120 million shares were traded that day.
Right? So it was just like every single share was traded 15 times over, which was absolutely crazy, and that ultimately drove our share price down. Because of that, we decided not to do the raise, right? When we decided not to do the raise, our shares spiked up because of the short coverage. There was a classic short squeeze because people had to cover their short positions, right? It's been lingering in the $2-ish position for some time, $2 per share for some time. I believe that it woefully undervalues our company, right? I think over time, as people truly understand the results, and perhaps as we get formal feedback from the FDA, I believe our shares will rally, right?
I say that not only because I am the CEO of the company, I am also one of the largest shareholders in the company that is buying shares in the company. For the first time in a very long time, the lawyers cleared me to buy shares because I no longer have material non-public information. So when that became possible, I and other members of our management team bought more shares.
Thank you, Cuong. Where does BioVie stand on their liver drug at the present time? It was announced in January that ThinkEquity was going to bring it public under the symbol OPTN.
Right now, the liver drug, that is the BIV201, is on hold. We have agreement with the FDA on what is needed to proceed to phase III to get the drug registered, but we need to raise about $25 million in funding for it. That is why we were planning to put all of the ascites assets into a new company called Option Therapeutics and go and raise funding for Option through an IPO. Market condition just has not allowed us to do that, right? So we are just waiting for market conditions to improve, and at the first opportunity, we will proceed down that path.
Given BioVie's current cash position and the recently established ATM, does management believe it has sufficient liquidity to reach the next major regulatory or clinical value inflection points without issuing a substantial amount of equity at approximately today's valuation? Is management's objective to use the ATM primarily as a bridge rather than as the principal source of financing for the next stage of development?
That's a great question. Thank you for that. I've refused to do a raise given our current depressed share price. That would be too dilutive to existing shareholders, and I just don't think that is the appropriate way to go. I'm not going to use the ATM as the primary mechanism to raise additional funding, partly because we're a baby shelf lab, so we're somewhat limited on how much we can raise with the ATM anyway. The ATM is there, just good corporate practice. Whenever there's an opportunity to opportunistically raise some cash, we will do so. But we are not doing it in a manner to drive that will lead to our share price being depressed. We will have to raise capital at some point in time in the future to fund the trials.
I've received the feedback from some potential investor to say they would feel much more confident in the shares of the company when they get formal feedback from the FDA about the phase III design. That's why we are so focused on the end of phase II meeting with the FDA to get formal feedback on the phase III design. We believe that will create a catalyst for our shares to rally. When the shares rally, under the right conditions, we would consider raising the capital then.
With these great results, how close are we to partnering with a large drug company?
We are just now preparing to restart those particular conversations. Pharma companies always want to have the data. Frankly, they want somebody else to go and pay to do the next trial rather than do it themselves. Creating the right competitive environment so that a company is forced into taking action is ultimately how you get partnering conversations to really work in our favor. We're taking our time to do it the right way. That takes months, not weeks. We're initiating the process to have the right conversations with the companies that we've had conversations in the past.
With regard to SUNRISE-PD, are you asking the FDA to consider that one successful, adequate, and well-controlled phase III trial, together with SUNRISE-PD phase II data, and the mechanistic biomarker clinical evidence already accumulated, provides sufficient efficacy evidence for an NDA?
We do not believe that one phase III trial would suffice. It would be nice to have that, and of course, that was always going to be part of our conversation with the FDA. We are planning on conducting two phase III trials, right? And we have good ideas of what that phase III trial would be. There will be 160 patients each. We would conduct one in the U.S., another one ex-U.S., so that we can get global registration for bezisterim in Parkinson's.
In presenting ADDRESS-LC data initially, you mentioned the possibility of breakthrough therapy, fast-tracked, or other expedited designations within the FDA. Is this still the case?
We are preparing the application for breakthrough right now, and we will be submitting that within weeks in due course. We are still waiting for biomarker data to come back from the Long COVID trial. We collected a lot of blood samples, and what we would like to do is to batch them all together at the very end of the study and go and have all of them analyzed at the same time, so that we minimize what is called batch to batch variation. Right? One would think that when you run a test today, tomorrow, the day after, on the same sample, you will get the exact same results. You do not. Right? There is variability. Right? So what we would like to do is to put everything together and run it all in one batch.
The labs usually take about a couple of months to run all the samples to get it back to us. We're just waiting for the biomarker data to come back, so that we can tie together the outcomes, the clinical outcomes data with the biomarker data to try to explain what's going on and build a much stronger case. Here in Long COVID, we are cautiously optimistic that we would only need one additional phase III trial because we believe the trial that we have just completed was not only well-controlled, but it was large enough to demonstrate the effect. We are cautiously optimistic that we may only need to conduct one trial. Furthermore, we are in the process of applying for some grants that potentially could pay for the phase III trial as well.
More to come in the coming months as we learn more on that.
When will additional ADDRESS-LC biomarker data be shared?
As I just mentioned, we're still waiting for the data to come back. I would guess that before the end of the year, we will share additional data on the biomarkers. Frankly, we need to kind of move on that because there are some scientific conferences that we would like to present the data at early part of the year.
Thank you, Cuong. Please discuss the comment made that said the Long COVID trial misses statistical significance in full population.
I do not consider that we missed statistical significance in the full population. We have to think about different trials as having different objectives, and therefore, have to be judged differently. In a phase III confirmatory registrational trial, the objective is to demonstrate statistical significance on the primary endpoint. You have a primary endpoint, and the only objective of the trial is did you get P value of 0.05 or less? That's the only objective of a phase III trial, to show that it works and that if you have statistical significance. A phase II trial is different. A phase II trial is exploratory, and very few phase II trial has statistical significance at the entire population. Phase II trials are exploratory to help you identify which endpoint show that the drug works with which population.
You hope to get statistical significance on the endpoint and in that population. That's where we believe we have demonstrated in spades that the drug works, because in patients with fatigue, we had statistical significance on five different endpoints, three of which were fatigue endpoints. With patients with malaise, we had statistical significance on the one metric that's malaise, so DSQ-PEM, but we had statistical significance on another half a dozen endpoints having to do with brain fog or cognitive impairments. For patients who have brain fog, they improved on all four cognitive impairment endpoints with statistical significance. We believe we absolutely hit on statistical significance with the relevant endpoints and the relevant population. We consider this phase II trial to be a major win. With that information, we now know how to design the phase III trial.
Our team has done this in the past, and we don't believe that we'll have any difficulties with the FDA around the way that we're thinking about the phase III trial. We look forward to discussing with them in due course.
When do you expect BioVie to pursue further Alzheimer's disease trials?
That program is proceeding far, far too slowly. Unfortunately, that is all funding related. Our priorities right now, unfortunately, has to be Long COVID and Parkinson's, because these trials are relatively small and short. The Long COVID is only a three-month long trial for phase III. The trial, we believe, is only going to be about 230 patients large. It's 250 patients large or so. So these are relatively short and inexpensive trials to conduct, especially if we can get a grant to cover some of that cost. In contrast, the Alzheimer's trial is going to be long. It's at least six months long, extendable for another 6- 12 months. It's going to be large. It's going to be like 400 patients large.
So we just have to prioritize, and we will start that when the capital markets allow us to have the ability to raise the capital, or when a partner materializes that wants to work with us on that.
Can you explain in simple terms what this drug, bezisterim, actually does in the body?
Sure. Let me take us back to a bit of high school biology. We all know that every cell in our body needs energy, and energy comes in the form of ATP. In high school biology, we all learned that glucose goes through the Krebs cycle to produce ATP as the energy for the cell. Cells need to absorb glucose from the outside of the cell. When it comes to glucose regulation, insulin is the key. Think of insulin as the key that has to fit into a lock on the surface of every cell in our body. When everything is working well, insulin fits in the lock, opens up the door, glucose can be absorbed, everything goes fine. But when you have inflammation, when you have TNF-alpha present, it activates IKK and JNK, as I mentioned earlier.
Think of inflammation as rust that builds up on the lock. When you have a rusty lock, insulin, the key, cannot fit in, cannot open the door, so the cells cannot get the glucose that it needs. So those cells start to malfunction, and over time they die. Of course, our neurons are the most energy-starved cells in the body, and that is the basis for neuronal degeneration. That's why the term Type 3 diabetes has been coined to describe the metabolic underpinnings of the neurologic diseases. How bezisterim works, we believe, is that it blocks the production of TNF-alpha. So think of it as it's getting rid of the rust that's on the lock. By blocking TNF-alpha, reversing insulin resistance, you're now allowing insulin to do its work.
You're allowing cells to be healthy again, and you're keeping those cells alive, versus if without the drug, cells would have gone on to die. So hopefully that explains it in a very simplistic manner and a bit long-winded. But the drug reverses insulin resistance, thereby it restores cells' ability to absorb glucose and function.
Thank you, Cuong. Someone said, "Nice presentation." So thank you for that. Thank you for your attendance as well to that person and to everyone here. Next question, Cuong. How do you plan to leverage or prove the great potential disease modifying rather than just disease treatment potential of bezisterim, particularly with respect to Parkinson's disease, given the biomarker data? Will this require additional or lengthier studies?
Yes. Well, the study that we have designed, we are trying to kill two birds with one stone. We are contemplating conducting a phase III trial with 160 patients, but that has multiple endpoints. The primary endpoint will come after six months of treatment to get at symptomatic relief. That is where we hope to show that we help patients improve on both their motor and non-motor symptoms after six months of trial. And that is enough data for us to go and file to get registration approval. But as that six months come to an end, we will extend it for another six, potentially 12 months, so that we continue to monitor these patients to see if their progression of the disease has changed from what is expected. And all patients that were originally on placebo, at that point in time, will move onto drug as well.
If we see if there is progression that it is a very complicated design to explain, but it is done all the time in clinical trials by essentially what is called a study extension. You monitor patients less intensively for a longer period of time to see what happens to them over time. And if you can show that their disease progression has changed, that is how you can get a disease modification claim.
We will give everyone a moment to consider any more questions they may have for Cuong Do, the President and CEO of BioVie.
Okay. Seeing no other questions, let me bring us to a close by summarizing that in bezisterim, we have a remarkable molecule that works to reverse insulin resistance and reduce inflammation. In our clinical trials that we have discussed today, bezisterim has been able to help Long COVID symptoms of patients who have the relevant symptoms at baseline, improve on their fatigue, malaise, and cognitive impairment, also known as brain fog. The key to understand this drug is to recognize that you need to have the symptom to begin with to improve on that symptom. That bezisterim has shown that it is the first drug that we know of that has been shown in a clinical trial that it can help patients address not just one, but all three of these symptoms, with the critical proviso that you need to have the symptom to be able to improve upon it.
We are very excited about this, and all of the key opinion leaders in the field, all the clinical trialists in the field that we have worked with and interacted with are excited about the results, and they are urging us to move it to phase III as quickly as we can. Also, bezisterim has demonstrated it can help patients improve their Parkinson's symptoms, both their motor and their non-motor symptoms, and it has shown early signs that can slow neuronal degeneration by essentially reversing the biomarkers of neural degenerative diseases, particularly NfL and GFAP. We are very excited about this drug. We do not believe that our shares adequately represent and factor in the true value of the drug. We are doing everything we can to get the word out to help people understand the true value of the drug.
We believe that the meeting with the FDA and the clear guidance from the FDA on our Parkinson's phase III design will provide the next catalyst for our shares to rally. I believe we are highly undervalued at this point, and I say that as one of the largest shareholders in the company, and I say that as a member of management who has been buying shares when allowed. I thank you for your time, and please find out more about our company by going to bioviepharma.com. We are also traded on the Nasdaq under the ticker symbol BIVI. Thank you very much for your time today. Have a great day.