BioVie Inc. (BIVI) Earnings Call Transcript & Summary

Hello. This is Craig with RedChip Companies. Thank you for joining today's event with BioVie, which trades on the NASDAQ under the ticker BIVI. With us today, we have Cuong Do, President and CEO of BioVie. We will begin with a brief presentation in a moment and then we will answer your questions. You may submit your question at any time by using the Q&A tool at the bottom of the Zoom window. Before we begin, please allow me to read the safe harbor statement. This call may contain forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. All statements pertaining to future financial and/or operating results, along with other statements about the future expectations, beliefs, goals, plans or prospects expressed by management constitute forward-looking statements. Any statements that are not historical facts should also be considered forward-looking statements. Of course, forward-looking statements involve risks and uncertainties. I now turn the webinar over to Cuong. Please go ahead.

Thank you, Craig, and thank you, everyone, for joining us today. I look forward to, I'm sure, telling you the story about BioVie. I understand a number of people on the call are new to our story and what we're trying to do. So I will take it from the beginning and kind of walk us through and then we'll leave plenty of time at the end for any questions you may have. BioVie has 2 assets in the clinic right now. The first is a drug called bezisterim, which, in the clinic, has shown that it can reduce inflammation and the associated insulin resistance. And Parkinson's patients have experienced improved motor control, Alzheimer's patients have seen dramatic slowing of cognitive decline and everyone has seen a lower levels of DNA methylation, which essentially is affecting our biological aging process. In addition, BIV201 is a drug for ascites, which is late-stage liver disease, and that may become the first therapy for a condition that has over 50% mortality rate over the course of 12 months. So I look forward to telling you more about these drugs over the course of the time today. We believe that chronic low-grade inflammation is the starting point for many things starting to go wrong in the body, and it all starts with TNF-alpha, which is the master regulator of inflammation. When you have TNF-alpha, it leads to insulin resistance, it drives more inflammation and it drives something called DNA methylation, which is essentially accelerated aging. Right? And that's where our drug comes in. Our drug is bezisterim. This is a small molecule. So patients take 2 capsules a day, 1 in the morning and 1 at night. This drug was originally brought into the clinic as a diabetes drug. And as such, it showed the profile of exactly what you would like to see. It reversed insulin resistance, and it brought glucose, HbA1c, and a bunch of other biological systems back into norms. Right? But that was before the mechanism of action was really understood. And as the team figured out how the drug works, it involves something called ERK, or the extracellular regulated kinase in how that activate something called NF-kappaB to produce TNF-alpha. And remember, I just said TNF-alpha is the master regulator of inflammation. And we honestly got lucky. We did not set out to do this, but it turns out that bezisterim selectively blocks ERK and NF-kappaB activation and as a result, it blocks the production of TNF-alpha. And once we understood this mechanism, it became much, much more clear that bezisterim plays a much larger role in the world beyond diabetes. And 2 of those worlds that we wanted to explore are Parkinson's and Alzheimer's. So let me first turn to Parkinson's. Now it's been known for a long time that 2 things need to be true at the same time in order for a person to develop Parkinson's symptoms. The first is you need to have a low dopamine level in the brain and the second is you need to have inflammation and the associated insulin resistance. If you do not have insulin resistance, the body is able to make use of whatever level of dopamine that's available in the brain, right? So everyone's been trying to figure out how to address the insulin resistance component of it, and no one has ever figured out a practical solution on doing so. As a result, the only thing that clinicians can do nowadays is to replace the low dopamine environment by using a drug called levodopa that was first introduced over 5 decades ago and remains the standard of care. And what got us very excited is that in our preclinical work using rodents and nonhuman primates, essentially monkeys. Our researchers showed that bezisterim alone was equally effective as levodopa. Now that is a profound statement because no other drug over these decades have been able to show that it's equally effective as levodopa in restoring motor control. Right? But we also saw something that's very exciting, which is when you give it in conjunction with levodopa, you saw the most motor control. So this is a measure of the Z score, right? So a lower score is better. So when levodopa is given in conjunction with bezisterim, code name, NE3107, you saw the most motor control. And at the end of the study, when we sacrifice the animals and look at their brains, the monkeys treated with bezisterim retain twice as many neurons compared to those that were untreated, right? And you can see it in these pictures where there's greater density of neuron surviving compared to those monkeys that are uncontrolled. This suggests that there is a neuroprotective property. And to us, this makes all the sense in the world because bezisterim reverses insulin resistance, which means there is greater glucose that's available to neurons in the brain. We also note that bezisterim enhances blood flow to the brain from various imaging studies that we have done. That means there's greater oxygen availability in the brain. All of that bodes well for greater neuronal health. So based upon this exciting preclinical data, we wanted to bring it into the clinic and see what we can find in humans. So we enrolled 40 moderate-to-severe Parkinson's patients who, frankly, were very, very difficult to treat. This, at its heart, is a safety study that was requested by the FDA. But we structured the study in such a manner so that we can actually essentially replicate what we did with the nonhuman primates in human subjects. And this is what we found. Patients that were treated with bezisterim and levodopa are shown in the blue line. And we compare that to patients who are treated with just levodopa shown in the red line. So here, patients treated for 28 days with bezisterim experienced a 3-point advantage on something called the Part III score or the motor score on the unified Parkinson's disease rating scale. Now that is a clinically meaningful difference, right, which is a big deal, not too many drugs can show a clinically meaningful difference compared -- when you compare to levodopa, which fundamentally is a terrific drug. But what got us excited is when you look at patients who are younger than 70 years old, presumably whose disease is less advanced and who have more surviving remaining dopamine in their brain, that difference was around 5 points. Now that is a huge difference that you do not see very often. And on top of that, what got our experts and ourselves very excited has to do with what's called the time 0 motor state. One of levodopa's big problems is that it has a short half-life such that when Parkinson's patients take their evening medications and go to bed, the levodopa would have worn off overnight such that in the morning, none, none of the placebo-treated patients have retained their motor control, right? And as a result, they could not move, cannot get out of bed and so forth, whereas roughly 1/3 of patients treated with bezisterim still had control of their muscles in the morning, right? So their muscles were in what's called the on-state. Now that is a statistically significant difference that we did not expect to see, but we're very excited to see it. And it bodes very well and it speaks volumes about the level of intrinsic promotoric activity that bezisterim has. Now our plans for developing bezisterim for Parkinson's involves 2 parts. The first is what I just described to you here, which is to give bezisterim in combination with levodopa, right, for patients who are more advanced in their disease. But the second part is to give bezisterim alone to newly diagnosed Parkinson's patients who need to go into medication for the first time to control their Parkinson's symptoms. And that is our #1 priority as a company going forward. We are all focused on starting that trial later on this fall. And that trial aims to enroll somewhere between 50 and 100 patients, and we expect to have data from that trial by the fall of 2025, right? So when fully developed, the 2 sets of clinical trials, one for combo with levodopa and the other as monotherapy, we believe this could become the first newly -- new treatment for Parkinson's since levodopa was introduced over 5 decades ago. And as such, we believe that, in Parkinson's alone, bezisterim represents an over $3 billion in annual sales in the United States alone. So this is a very significant indication for us. But more importantly, it's a huge advance for the 1 million or so Parkinson's patients that -- in the U.S. and 150 million -- thousand, excuse me, 150,000 or so patients that are being diagnosed each year with Parkinson's. We believe this could represent a tremendous advancement for these patients. So now let me turn to our work in Alzheimer's. There's much more detail here, and we can come back if there's questions about this. In Alzheimer's, when I first started working in Alzheimer's back in the late '80s, everyone was focused on the amyloid pathway. And along the way, we started focusing on taus and tangles as well. And -- but unfortunately, over these decades, there's never been a drug candidate that can reverse the extent that plaques and tangles in the brain and arrest or reverse the cognitive decline in Alzheimer's. Such that over the course of the last decade or so, more and more clinicians are becoming convinced of 2 things. One is that plaques and tangles themselves are not the toxic agents that is causing neural degeneration, right? In fact, what they are doing is they're causing neuroinflammation, right? But many, many other things cause neuroinflammation as well. But all of these factors share one thing in common, they all activate ERK and NF-kappaB to trigger the production of TNF-alpha, which then leads to insulin resistance, which, of course, as I explained before, that's where bezisterim comes in. Bezisterim blocks the production of TNF-alpha at where we believe is considered to be the central node of inflammation. And that's why we believe bezisterim will be very different than the other drugs that have come before it. You may have been tracking, following, heard about a drag called LEQEMBI from Eisai that was approved by the FDA last year to treat Alzheimer's. That drug does a terrific job at reducing the level of plaques in the patients' brains, right? But patients have experienced only a 27% slowing of cognitive decline after 18 months of treatment, right, which many people have considered to be a very modest level of impact. As we look at the totality of the data, we believe what's really going on is that LEQEMBI has reduced the level of inflammation that's driven by the plaques, but it hasn't done anything about the inflammation that's driven by all these other factors out there, right? And that's where we believe bezisterim would distinguish itself because we -- bezisterim doesn't really care with inflammatory stimuli came from. It blocks it all and what we believe is the central node of inflammation, right? So that's, like I said, is the first of 2 difference that clinicians have begun to recognize in recent years. The second is that the Mayo Clinic, the NHS and so forth have shown that 80% or so of their Alzheimer's patients have or are developing insulin resistance. And it's gotten to such a point where more and more clinicians are referring to Alzheimer's as Type 3 diabetes because of the insulin resistance. And again, this is where bezisterim comes in because it blocks TNF-alpha, it reverses insulin resistance. Right? And based upon this understanding of how bezisterim works, we took it into the clinic where we saw some very promising results. First, we look at something called CDR-SB, which is the same measure of cognition or cognitive ability that was used by Eisai and Biogen for their clinical trials that got their drugs approved by the FDA. What we found is that patients treated with bezisterim for 6 months experienced a 68% slowing of cognitive decline compared to those treated with placebo. And the #1 reported safety of concern was a mild transient headache reported by about 8% of patients in this trial. And it's been consistent with the safety profile that we've seen from all of the prior clinical trials in bezisterim. And to give you some contrast, the closest thing to this has been what's reported by LEQEMBI, which showed a 27% slowing of cognitive decline after 18 months of treatment. But these patients also experienced significant safety concerns as well involving brain swelling, brain bleeding such that these patients have to be monitored consistently by PET scans. Right? And if you look up and down this page, what you will see is that the advantage that bezisterim has over placebo is equal to or greater than what has been shown in clinical trials for the other comparable drugs here. So what we have shown in this trial is very, very promising data that shows a terrific magnitude of impact that bezisterim has on cognition and function. But unfortunately, as we unblinded the trial, we ran into a problem we experienced. What we found is that 15 out of our 39 clinical sites deviated from our clinical protocol and good clinical practice, which is something that we have never seen before. No one conducting clinical trials in the United States has ever seen 15 sites in the same geographic area, essentially what seems to be coordinating to deviate from clinical protocol. As a result of that, we have referred all 15 of these sites to the FDA for their investigation. And we know that the FDA is investigating right now and are now beginning to hand out what are called 483 citations. Right? And in the meantime, we excluded all the patients from these 15 sites from the data that you see on this page, right? So the data at this stage come from only the sites that we have confidence in. And because we excluded all these patients, we missed on statistical significance despite having strong efficacy directional information, which is a real shame. We know this drug works. We know the statistics here, and we have stared at this and studied it at length. And that's why we are highly confident that we have -- if we had gotten to just 125 patients in each arm as the study was originally designed, we would have shown the efficacy as well as statistical significance. But as I mentioned before, we are highly confident that this drug works, and that's why we are not giving up. We are going to redo this clinical trial. And our plan is to restart this clinical trial, probably third quarter of 2025, which gives us time to finish the development of a once-a-day version of bezisterim that should be available early next year, or spring of next year. Bezisterim, I failed to mention, is a drug that you take twice a day, once in the morning and once at night, right, which is, of course, not as ideal as a once-a-day drug for a patient population that is already forgetful to begin with. And that's why we will do the next trial with a once-a-day version of bezisterim, which will be better for patient, but it also will give us an extra 7 to 10 years of patent protection as well. So let me move on. We have much more data on Alzheimer's here if you want to go back to this in the Q&A. But let me now move on to our work in longevity and aging. And I'd like to start with an analogy. And the analogy is that of a DVD. When you take a new DVD out of its packaging, it is pristinely clean, you put it into the player, the laser would have no trouble decoding the information that's on that disk. And as a result, you'll get pristine pictures and beautiful sound. But as you play back this over and over again over the years, you'll get scratches on it, you make fingerprint smudges on it. And as a result, the laser would have difficulty cutting through the gunk and decode -- to decode the information. And that's why you get the stuttering, the skipping on the playback. It turns out that our body works in exactly the same way. As you know, everything in our body is encoded by our genes and our DNA. Right? And as we age, a natural process called DNA methylation takes place, whereby these different small methyl groups gets added to the surface of our DNA. So think of this as the same thing as the fingerprint and the scratches on the DVD. And as you get more and more of this methyl groups on the surface, the molecules that are responsible for decoding our DNA would have trouble cutting through to decode and read our DNA. And that's why you'll get miss coding -- miss decoding. And as you get more and more methyl groups, so if you get hypermethylation of DNA, it's been associated for a large number of diseases out there, especially age-related diseases, which makes sense because that's the older we get, the more accumulation of DNA methyl groups that you will have on our DNA and the more accumulation, the more missed decoding you get, and that's been associated with a large number of diseases. We also know that the extent of DNA methylation can be measured by various clocks. And one of the most widely used clocks was created by Steven Horvath out of UCLA. Now I give you all this background just to explain the results we show on the next page. Because in the Alzheimer's trial, we took blood samples at the end of the study, and we set all of those samples to Horvath and his team, who analyze the blood samples and gave us back data on something called age deceleration. Age deceleration is simply the difference between a person's biological age as measured by the clock and your actual chronological age, which is the number of years we've been alive since birth. And what we found is that patients that were treated on 6 months of bezisterim experienced roughly a 4 years age deceleration advantage compared to those on placebo. Now before you get too excited and start to think that this is the [indiscernible] for reversing aging or something like that, please stop, that is not what we are saying. We will all age. We will all get older. And I do not know of anything that we can do to reverse or stop or change that. But what we are saying is that bezisterim may be able to reverse, slow or alter the degree of DNA methylation that takes place in our body. And as such, we hope to alter the linkage between DNA methylation and age-related diseases. And by doing so, we hope to be able to keep all of us healthier for a longer period of time as we all age. And to be completely transparent and honest, we still do not know what is the best way to go and develop this drug in longevity, right, because aging is not a disease. The FDA is not going to give us a claim for a drug that changes the aging process. So that's why we're currently working with our collaborators to try to figure out how best to conduct different clinical trials to show that bezisterim may be altering the pace or the progression of different age-related diseases. And if we can show that alteration of progression with enough diseases, we may be able to claim that bezisterim as a molecule is having an impact on changing the progression of age-related diseases. But more to come. Like I said, we do not know exactly how to develop this, but we know the science behind this molecule. We can tell you that it's affecting DNA methylation. We can also tell you what specific genes are being affected by changing this DNA methylation, right? So we can go much more into all of this in the Q&A, if you like. But with that, I'd like to spend just a few minutes on ascites or drug, BIV201.Ascites essentially is late-stage liver disease. When you get to this point, the liver has been so scarred that it's not able to process fluid the way that it normally does, right? So as such, that fluid accumulates in the abdomen, right? So it becomes real -- any of these patients become extraordinarily distended and clinicians try to use herculean drugs off labels, to various other things. But fundamentally, when it comes down to it, the last thing that you can do, the only thing that you can do is put a large bore needle right into the abdomen and drain the fluid that is accumulated there. Right? But since nothing has been done to address why the fluid accumulates in the first place, these patients are coming back to the hospital every week or 2 to get another 5 to 10 liters of fluid removed. Now you can just imagine the stress that puts onto the body, right? And frankly, the only treatment objective at this point in time is to try to keep these patients alive long enough in hopes that they can qualify for a liver transplant. And we all know that there's not enough livers to go around, and that's why there's -- the life expectancy or the mortality rate for ascites patients at this point is over 50% within a year. And our drug, the solution here is a drug called terlipressin. So we put the drug into a small saline bag, we hook it up into a continuous infusion pump, a portable continuous infusion pump that patients would wear on their belt. We had conducted a Phase IIa trial, which showed that this patient -- that the drug is safe. We've then conducted a Phase IIb trial to demonstrate efficacy to try to figure out the magnitude of impact that the drug would have. We originally planned to enroll 30 patients, but we stopped the trial midway after we only enrolled 15 patients because we already had statistically significant data showing that those patients that completed the treatment saw a 50-plus percent reduction in their ascites fluid buildup, and we saw a significant lengthening of time between when they have to come back into the hospital for more removal of the ascites fluid through a procedure called paracentesis. In fact, we actually had a patient who actually didn't have to come back at all for any additional paracentesis, right? And that's in contrast to the standard of care where there's nothing happened, right? And that was this very statistically significant difference. Right? And since the mortality and the medical need is so high, we concluded that the only responsible thing to do was to stop the trial early and engage the FDA in a conversation on how to move this on to Phase III. And since we already have Fast Track and orphan designation for this drug, we only need to conduct one Phase III trial to register the drug. And as of now, we have received the feedback that we need from the FDA to conduct this trial, and we believe we need to only enroll roughly 200 patients in this trial to collect the data that we need to register the drug. But despite that, we have put this trial on hold because we want to find a partner that is willing to fully fund or co-fund this trial with us, right? We're in discussions with a couple of parties right now, and we're hoping to have progress on those conversations over the course of this year. So this -- and frankly, in my 30-something years of developing drugs, this is the most derisked program I've ever seen because we know that it is safe and it's efficacious. We just now need to go and enroll 200 patients to conduct this trial. Right? And you may ask the question, why isn't this our #1 priority instead of Parkinson's? Parkinson's is our #1 priority because it is an even smaller trial. We only need to enroll 50 to 100 patients. It is a short study, right? It's only 3 months to primary endpoint such that we can have results by third quarter or so of next year. And in contrast, the BIV201 trial here, it will take us 2 years to get to the results. While despite the fact we love this drug, the practical prioritization would make this third priority in our mind, right? So let me just recap before I turn it -- open it for Q&A. We have 2 molecules that have the potential to fundamentally change the way the diseases that they focus on are treated. NE3107 or bezisterim is -- has been shown to reduce inflammation and reverse insulin resistance. As such, Parkinson's patients have seen improved motor control, Alzheimer's patients have seen dramatic slowing of cognitive decline and all of these patients have seen a significant impact on their DNA methylation or the biological aging process. And in BIV201, we have a drug that potentially could become the first treatment for ascites, right, which is a condition that has terrible mortality and no approved therapy right now. And each and every one of these conditions represent significant market opportunities. The ascites drug alone, this is an orphan condition, but this has the potential for $1.5 billion in annual revenues in the United States alone. In Parkinson's, that is a $3 billion in annual sales in the U.S. alone, and we believe that Alzheimer's could represent a $30 billion in annual sales in the U.S. alone. And as such, any way that you want to discount, risk adjust these revenues opportunities, it will still lead you to a valuation number that is significantly larger than our current $30 million in market cap. And that's why I believe we represent a terrific buying opportunity for anyone who has a longer-term investment horizon. And I say that not because I'm the CEO of the company. I say it principally because I'm one of the largest shareholders in the company. I am still the fifth or sixth largest investor in the company now. I participated in the raise that we did earlier this year. I put my money where my mouth is and I continue to buy in the open market when the lawyers clear me to do so when I do not have material nonpublic information, right? And so with that said, let me stop here. Let me stop the screen share and let's go to the Q&A, right? So [ Dave ], if we can turn it open to the Q&A.

Yes. Thank you very much, Cuong. Yes, we are now taking your questions. Because we have so many people on this call today, we're only going to take your written-in questions. Please push the Q&A button and type in your question. Many people already have done so, Cuong. What is your cash position now? And how long will that cash last with all the trials?

That's a great question. We reported about $30 million in cash at our last Q. And our fiscal year is about to end in about 3, 4 days -- 4, 5 days, right? And so within the next 45 days or so, we would be issuing our annual report, right, to give you an update on our cash position. But our guidance is that we have sufficient cash to start the Parkinson's trial and last through perhaps early part of next year. And I think that's part of the reason why our shares have been beaten down. I think the market expects that we need to go out and do a small raise. And I think that's part of the reason why our shares have been beaten down to where it is right now. Hopefully, that answers that question.

Could you go into more depth about partners for ascites? What's it going to take to get someone interested in partnering ascites?

Yes. Ascites has been a very interesting situation. There is one company that we somewhat compete with, coexist with, and that's a company called Mallinckrodt, who also has been trying to bring -- has been working with the drug, terlipressin. And they have gotten approval for terlipressin to treat a very small complication from ascites called HRS, or hepatorenal syndrome, only in hospital settings and only as a bolus infusion, right, which is a very, very small indication and because of the safety concerns that are associated with that drug and it has been associated with that drug for decades now all around the world, it has a black box warning. We, because of our approach of using continuous infusion, do not have the safety concern, right? And we are upstream from that. We are working at ascites or even earlier than ascites as well. So we have addressed a much larger market. So one would have imagined that Mallinckrodt would be a natural partner for us. But I must confess, I just don't -- I do not know this company. I do not know how they think and so forth. So our various conversations with them has not led to anything because they have just higher priorities. And I understand that companies have their own priorities, right? And this is for them a tiny, tiny little drug and that's why no one at Mallinckrodt pays attention to it. And we have been in discussion with 3 other companies, small companies that love this drug, right? But they, like us, have had difficulty raising the funds to fully fund the clinical trial that's needed here. And the clinical trial here would be a $25 million program to develop ascites. And so we are keeping the conversations warm with those companies and the ones that are able to raise the funds the first and come back to us are the ones that we will take to the next step of conversation. It's not like there's no interest. We have companies that are interested in the molecules. But given the current capital markets and how treacherous it is, they are having difficulty raising funding and that's why we have not been able to do a deal here. But we hope that will change over the course of the next 6 to 12 months.

Thank you very much, Cuong. Regarding COVID, what -- I'm sorry. Sorry, I want to get to the Phase III trial. This person asks what information has been uncovered surrounding the sabotaged Phase III trial for NE3107? And why is it taking so long to rebuild that trial?

Well, first of all, I don't want us to have any conspiracy theories or anything about sabotage and so forth. That is not at all what we said. All that we have said is that we've found 15 sites that engage in what we believe as misconduct. These sites deviated from our clinical protocol. So they did not follow the protocol to the letter, which, frankly, when you conduct a clinical trial, you have to follow the protocol. That's why it's there. And these 15 sites did not adhere to GCP, which is good clinical practice, which are the regulations that the FDA has set out for what needs to be done when you are conducting a clinical trial. And what made it so disconcerting is that all 15 of these sites were in the same geographic area. And that's why we took a very public and hard stance on this. Some larger pharmaceutical companies -- let me put it this way. You will always find a site here or there that, through accident by happenstance or even my sheer will, will do things that are crazy, right, or then don't do -- don't follow instructions, don't follow GCP. But we have never seen nor has anyone conducting clinical trials in the United States ever seen 15 sites in the same geographic area, having the same pattern of this disregard for GCP and our protocol. And that's why we referred all 15 sites on to the FDA. I can tell you that as of now, the FDA has investigated some number of these sites. I don't want to give the exact number because I want to give the FDA complete freedom in what they are doing. And as of now, the FDA has started handing out what are called 483 citations to some of the sites. And in other sites, they have carted off large numbers of documents or scans of documents for further evaluation. I do not presume to make any judgment or inference from what the FDA is or is not doing. All I can report is that the FDA has taken our reference to them very seriously, and they are finding problems at some number of these sites. Excuse me. And we know that they are continuing to investigate. And of course, the natural question that follows on to this, right, I get from investors and friends and others all the time, which is why are you not going after these sites, suing them and so forth, right? Everybody wants me to unleash the lawyers and sue everybody at this point in time. And I'm not going to do that. We are resisting doing that because the reality is the FDA has far more investigative power than we do, right? They have the ability to show up at sites anytime they want to investigate. And frankly, they have badges and guns as well, right, in criminal situations. So what we're going to do is we are letting the FDA pursue their course of investigation, and the FDA will work at their own pace, doing whatever they like to do, and we will wait for their findings. And once their findings have been fully revealed, we then will then figure out what's the proper recourse that we'll be taking with these 15 sites. I hope that answered your question.

Thank you, Cuong. Would partnerships include possibly looking for a buyer of the whole company, this person asks, especially with the stock now at $0.45 a share?

Everything is on the table, right? And those were -- and I made that very clear over the course of my conversations with the various pharma companies that we engage in conversation before we reveal the data. But let me be very, very blunt and clear, I have been on their side of the table before, right? Remember my time in big pharma. And please remember, no one in big pharma has ever gotten fired for playing it safe, right, or being conservative, right? And if you look back at the history of Alzheimer's research, the field is littered with promising Alzheimer's drug that failed in Phase III clinical trials, which then lead pharma companies to be even more conservative, right? So the conversations that we had, these pharma companies told us that the trial that we conducted was exactly the trial that they were hoping to see. But when we revealed the data that missed on statistical significance, they basically said they wish this well and they want us to go and redo the trial and they will still be there when we have the new data, right? Because as you look around, all of the other companies that are now getting back and getting more interested in Alzheimer's are really still focused on the traditional beta amyloid and tau pathway. There's literally one handful of companies that is focused on inflammation or non-Abeta and tau company. And we're one of the ones that are furthest along or one, I believe, 3 companies that are in Phase III clinical trials at this point in time, right? And so it is not that because we're cheap with a low market cap of $30 million that's going to lead big pharma to come and swoop in and buy us. It is a matter of time now where we need to go and redo this trial for Alzheimer's and show the trial for Parkinson's that lead to statistically significant data that will generate the interest, right? And that's why I say we represent a significant buying opportunity for investors who have a long-term investment horizon because over the course of the next 2 or 3 years, as we complete these trials, we believe that the results will be very promising, and that will create the catalyst for dramatic improvement of our share price.

Thank you. Now that COVID question. What part of the long COVID population, symptoms, diagnosis, does BioVie plan on targeting for the DoD study? And would vaccine status play a role in determining participation?

Let me be very clear. No one out there fully, fully understand what causes long COVID. No one. But the leading experts in the field are coming to the -- an emerging point of view that long COVID symptoms are highly driven by chronic low-grade inflammation, particularly through something called a toll-like receptor 4, right, TLR4, and a few other receptors. And it happens to be that's exactly how bezisterim works as well, right? Different molecules right now would go through these very same receptors to trigger the production of TNF-alpha in cells that eventually needs to the symptoms of Alzheimer's, Parkinson's that we've talked about all along. The DoD, and these experts that we've been working with, believes that by bezisterim's ability to block inflammation after it's been triggered by the same receptors, gives it an opportunity to perhaps have an impact in long COVID, right? So that's why they have given us a $13 million grant. We have received $500 million so far to pay for the planning of the clinical trial. And as soon as we give the office called the OHRO, the protocol, and they clear it that it's actually safe for human clinical trials. So of course, it's going to be safe for human clinical trial because we have to have our own IRB, right? So at the moment that they clear it for clinical trial -- for human clinical trials, we'll then get the remaining part of that grant. Let me be very clear, this grant has already been fully, fully funded by appropriations back in 2021 or 2022 by Congress and the DoD. So the money has already been there. We have been granted the full $13 million. We just actually need to show that the protocol or the trial that we want to conduct is safe for humans. And then they will -- we will get the remaining funds to initiate the trial, right? And we expect to get the funding for -- to initiate the trial probably in the late August, early September time frame of this year. Hopefully, that answers the question.

Thank you very much, Cuong. We are right at the top of the hour. We do have a few questions. We're going to send those to Cuong so that he can see them, and we will now wrap up with some ways to reach BioVie and to get more information about the company. You can call us, of course, at 1-800- RedChip, that is 1-800-733-2447 or e-mail us at [email protected]. Please also visit RedChip's investor information page for BioVie, it's biviinfo.com. There, you can view and download the investor presentation used today and the fact sheet and sign up for news alerts on BioVie. Please be sure to watch Small Stocks, Big Money, RedChip's program featuring exciting small-cap companies, including last Saturday, BioVie, every Saturday night at 7:00 p.m. Eastern on Bloomberg USA. Join RedChip's forthcoming webinars, Genetic Technologies tomorrow, Thursday, June 27, Lobo EV on Wednesday, July 24, and Nutriband on Thursday, July 25, all 3 of those webinars will start at 4:15 p.m. U.S. Eastern. Register for those events and for all RedChip webinars at redchip.com/events, where, in a few moments, you can also view an archived version of today's webinar with BioVie. Thanks again to our many participants today. And thank you very much, Cuong.

Thank you, Craig, and thank you, everyone, for joining. Have a great day.