Welcome back, everyone. Next up is Bioxytran Inc. They're an OTCQB company trading under the ticker symbol BIXT. The company is a clinical stage biotech with three revolutionary platform technologies that were quickly developed using the power of AI. They have a broad-spectrum oral antiviral drug that recently completed clinical trials and achieved 100% viral reduction in seven days, a feat only accomplished by one other drug in the past decade. They recently published research on their historic discovery in virology, which debunked the 50-year-old notion that for every virus, you needed to develop a different antiviral. Their drug is a galectin inhibitor that not only neutralizes COVID-19, but also neutralizes influenza and RSV and prevents it from entering cells, and they're still recruiting patients for their dose optimization study, which will give them the ability to proceed with their registrational trial in India after they finish.
They have a second platform drug, an oxygenation molecule being developed to treat stroke, dementia, and sickle cell anemia. Due to the molecule's small size, it has the ability to carry oxygen into areas of poor circulation. The company has a third platform technology that's capable of treating cancer metastasis. Mike recently wrote a LinkedIn article on how galectins are the primary reason why we don't have 90% or more response rates in cancer immunology treatment. Mike, you recently reported you had a meeting with BARDA last week. How did that go for you?
You know, the meeting went really well. We had almost 70 people on the call from a number of organizations, including the NIH, the NIAID, the DTRA, and the DOD. And those are, you know, just to name a few. There was a lot of back-and-forth dialogue during the video conference. So the agency pretty much got a good feel for what we were about. And they appeared genuinely interested in helping us find basically these right programs to apply for funding. So I'd have to say the call went much better than I expected.
Fantastic. Good luck with that. I'm glad that happened. Talk a little bit about which one of your drugs were they most interested in?
You know, there are a lot of questions about influenza and our universal oxygen carrier. So, you know, one's the ProLectin-M and the other one's the BXT-25. So it's kind of a toss-up between the two. But, you know, what surprised me, though, was that, like, when one of these people seemed to perk up when we talked about Ebola and having a potential solution for it. So I thought that was interesting.
Absolutely. And what's your biggest takeaway from the meeting?
Well, I really liked the idea of getting non-dilutive sources of funding from the government. I mean, who wouldn't? But no, seriously, what we found out is that there are a tremendous amount of funding opportunities that are right for the taking. But it's going to take a lot of work to get to that point.
At least it's a good start to the year. That meeting with BARDA seemed very successful. Thank you for that update. I also understand you're going to give us a recap of your presentation for our conference today. Begin when you're ready.
All right. Well, thank you. I want to thank everyone, all the investors out there for attending this conference and coming on here. And let's just start off with our title here, "Breaking the One Virus, One Antiviral Paradigm." You know, that's how we start out with this presentation. So now we'll go to the next slide here. Here's what we're going to give a quick overview. And this is what I gave to BARDA, and we'll just, I'm just giving the whole presentation. Antiviral drugs targeting galectins. So that's one platform, blood substitute, universal oxygen carrier, and then immunomodulator for fibrosis and cancer metastasis. So with our first platform technology, we have two clinical trials with 100% responders rate in both of them, where symptomology basically went away within hours.
And we have an active FDA IND that's approved, ready to go for a blood substitute carrier or oxygen carrier. You know, the oxygen carrier will penetrate right through a blood clot. That's the theory behind it. So it goes right through the blood clot. But why couldn't we use this for extreme hemorrhaging? And that was the case that we were making to BARDA. And then finally, they are interested in antifibrotics. And these immune modulators should be able to halt fibrosis. Here's a nice overview of our product pipeline. What you'll see here is that ProLectin-M is oral. And it's our most advanced product. And we have ProLectin-I and ProLectin-F, but basically the same molecule. And you'll see the disease indications are COVID-19 and idiopathic pulmonary fibrosis.
You'll see where we're at on that stage is we're at the stage where we want to, you know, funding, you know, needed. But obviously, if we have the funding in place, we're ready to go with healthy human trials there. And then we're deep into the universal oxygen carrier in terms of the animal studies. And then I skipped over ProLectin-X, but ProLectin-X is just other viral indications, like, you know, Ebola, HIV, RSV, you know, influenza. Now, it's helpful to explain how Galectins work. Galectins are these proteins that recognize carbohydrates. And you can kind of see here in the graphic, there's little receptors on the cell surface sticking up there. And you see how they act as like little connecting points. And then they also connect each other. They're also adhesive molecules. And they bring cells together. And they also help viruses.
And this is the big news. The viruses stick to cells. That's also their function.
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This is the mechanism of action. Many understand that an antibody sticks to the tip of the spike protein. That's how the neutralization happens. Our immune system can see the antibody and engulf it, and there goes the virus. Now, what happens is what you see there on the left is a spike protein in its naked form. The immune system can see it, but it shields itself with the sugar that's coated around it. That's denoted in dark blue. You'll see there's two spots. One's the tip. You can't ever have the tip covered in sugar because that would kill the chance of the virus getting into the cell, because that's what it uses to unlock the cell with its receptor. The other part is how it achieves viral attachment. It's through that galectin fold there.
This is how we neutralize the spike protein. Our molecule comes in, binds the galectin fold, and it binds the region that would normally stick to the cell surface. This next slide talks about neutralizing bird flu, H5N1. H5N1 and H1N1, they're very similar in nature. There's this common receptor there. You can kind of see it. It's in between the two of the graphics. You know, it's the hemagglutinin spike, and it stops the viral entry. Over to the left, these are families of viruses. Now, what's so interesting about this is we operate within three families of these viruses. There's one missing there. It's the Coronaviridae. There's three of them. There's no other antivirals, again, no other antivirals that go across families. We're literally the first.
Now, this is a slide on our mechanism of action for the blood substitute or universal oxygen carrier. And what you'll see here is an artery with a clot in it. And you'll see the blood cells are kind of clotted up. However, the blue is still passing through. Now, the blue is just for graphical purposes. But the little blue molecule, it's like a pinprick compared to the blood in there for size. And we just can't denote it. So what's happening is the molecule is basically completely infused with oxygen and in the blood plasma. So it's like a fishnet. There's fish in the net, and the plasma goes right through that clot, if you would. Now, how do we make it? There's hemoglobin there. So that's basically start, you see in the lower right, start with the blood cell. And then we strain out the heme.
And then we stabilize the heme. Heme's basically iron. Iron carries oxygen, right? That's the heme. And it's identical in basically all mammals, the heme molecule. So it carries oxygen and the right type of oxygen. That's what we want. There's no reactive oxygen species. And then there's some numbers for you there, BARDA cares about. But for you, or for the investment public, let's focus in on the 100 hours half-life in animals. And then it's shelf stable, and we can store it at room temperature. The next mechanism that we had was idiopathic fibrosis. And you read up here, the ultimate fibrosis target spans multiple organs, multiple disease stages, and is relevant for all combination therapies. Well, what we have here, look, there's a liver, the kidney, the lungs, and the heart. They're all normal, healthy hearts.
But if you put chronic inflammation, which results in fibrosis, this is the disease that you end up with, nasty COVID, you know, the lung fibrosis, and then heart failure. And this mechanism here, you know, you just, you got to study it. I'm not going to, you know, for the BARDA guys, I really went through this. But for you guys, look here. Galectin-3 is at the center focus of it. And here are the bullet points on the right. Galectin-3 is implicated in all types of fibrosis. So it doesn't matter what organ it is. It acts on the same thing. It's universal. And then Galectin-3 is responsible for the scar and the chronic inflammation associated with fibrosis. And they also represent biomarkers for bad outcomes. So everyone sees, oh, Galectin-3 is elevated. Well, that's not good. It's a biomarker of bad outcomes.
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Went too far. This is our technology that we use to design new antivirals, so we use NMR spectroscopy. Long story short, we take a spike protein, so you give us. BARDA would give us a spike protein is the idea. We look at it, and we see if our molecule binds to it or other molecules bind to it, other carbohydrates bind to it. If it is, we got a match. It's really that simple of drug discovery. These are the areas of interest that we showed to BARDA. You'll see here uncontrolled hemorrhage, so our universal oxygen carrier, influenza antiviral. Obviously, we're talking about ProLectin-M. And then immune modulators, that's ProLectin-I and intravenous ProLectin-3 antagonists. And I just talked about FASTx, and they're actually discontinuing that program. But it might come back. You never know.
The next thing I talked about was recent developments in galectins, so a company called Galectin Therapeutics came out with their top line phase 2 data readout on the 20th of December, and cirrhosis is a disease there's no really approved drugs, and the only real solution, it's a liver transplant, and there's a lot of mortality associated with it, and this drug, Belapectin, is a Galectin-3 antagonist, and it showed statistically significant reduction in these esophageal varices at a certain dosage level. There was a 49% reduction in varices over the control at 18 months, but you know, what does that really mean? Why is it relevant to us? It's relevant to us, and you'll see it in the note there. This is not Bioxytran data, but a similar chemistry and supports our thesis.
But the thing is, FibroScan that indicated a 50% lower number of subjects with worsening stiffness. Now, FibroScan is a non-invasive way to measure fibrosis. And in clinical trials, it just hasn't succeeded anywhere. So this is really big news. And there's a strong indication that Galectin-3 antagonists are going to be able to reduce fibrosis. So we're excited about this. In terms of, you know, what we do is we distill things down into preclinical and/or in vitro, and then preclinical, and then clinical trial results. So this is the in vitro study. We did tox studies on both our molecules, PLM, PLI. You can see cell viability is over 100. There's no issues there. Next slide. We did in vitro studies on SARS-CoV-2. So now we're testing for efficacy. You see the slide there, efficacy.
I'm just going to tell you the results: reduction in viral load, reduction in viral presence. A lot of you haven't seen these slides before. This is some new data. In vitro evidence in influenza. On the left, you have Tamiflu versus ProLectin-M and ProLectin-I. You'll see 95% reduction. You'll see 65% reduction. You're saying, well, why isn't it going up to 100? You're going to see why in a couple of slides from now. It does. Again, here we are, influenza. We're highlighting the key to BARDA and to you guys, investors, broad spectrum antiviral activity. Next one is RSV. Again, look at it. You know, we're reducing the virus, broad spectrum antiviral activity. This slide, what it did, what I showed BARDA at least, is that we extrapolated out. You see for influenza, you can get to 100%.
So we want to make a compelling argument for them. So we showed them the data behind it. Now, this was the slide that I was mentioning to Anna at the beginning of this that had an impact on people. So here we have Ebola. And this is a crystalline diagram of Ebola. And you can kind of see what's circled. This is a glycan gap. Now I'm going to read you what the research shows us. Mucin-like structures partially cover the glycan gap, which is the site needed for proteolytic cleavage. Removal of mucins may be a prerequisite for binding. So what if we just stop this glycan gap up with what? A galectin blocker. See, galectin blockers are attracted to the glycoproteins. And then here's the other thing that we found.
A glycoprotein shedding of the Ebola spike protein into basically the blood triggers TLR4 and this pro-inflammatory cytokine response. So we're operating by blocking it and quieting the cytokine storm. That's the theory behind it. So we have strong potential to neutralize Ebola. Now we move on to the animal studies. Remember, we first talked about in vitro. Now let's talk about animal. No observed effects there. And there's a report. Next slide. No adverse clinical signals. And this is for our universal oxygen carrier. So safety, we're just sailing through because there's just no issues. But now this study will just, what I explained to BARDA is, look, we took out 10% of the blood and 20% of the blood in the universal oxygen carrier. So that's our blood replacement deal. And we expect to see changes in all these biomarkers there in red on the right.
We didn't see any. That in itself is an indication of efficacy. If you guys remember the press release, you know, we talked about that, but now here's a study that should really shed a little bit more light for you, and again, this is data, not Bioxytran data, but early chemistry developed by Dr. Platt, and again, it supports our theory, and what we did is we hemorrhaged out the dogs 90%, and this is what you see right in the middle. It says it's a hemorrhagic model, so in this model, 50% mortality is expected in two to three hours, right, so we hemorrhaged out the dogs 90%, with, and then we immediately resuscitated them with fluid, and what happens is something that you just don't see. Like you don't see tissue oxygen tension, that's tPO2. You don't see it go up.
It's supposed to go down, especially during a hemorrhagic situation, and so here on the right, you'll see the conclusions. We improved oxygen delivery and systemic hemodynamics. There were no side effects, and we got survival despite not being an endpoint of the study, and you can see the chart in the middle, and it was statistically significant over lactated Ringer solution, which is the other one, so again, it supports our theory, and then this is the next one that we had here. We did an animal study in rats, and you'll see we basically blocked, we pinched this artery off, and when you pinch the artery off, look at the top two pictures of the rat brains. If you look at the top two pictures, you see there's white. That's hypoxia, so we kept it pinched, the same amount of pinching.
And this time we infused the rats with our molecule or with the molecule, right? And then what happened is what you can see is you'll see oxygenation of the brain. Now we're going to transition to the clinical trial results. So we went through the in vitro. We went through the animal. Now we're looking at clinical trial results. In the virology, we eliminated the virus, reduced infectivity, required the cytokine storm. We have this thing called post-immunization infection. So we went over these clinical trial results. Here's our phase II data. We're looking for people to get PCR negative. So basically just get rid of the virus. And we started with people with CT values of 25. And then you'll see at day three, there's kind of a separation there between the green and the red groups. The green group is the group that got the treatment.
The red group is the control. And 88% were PCR negative at day three versus zero. And at day seven, 100% were PCR negative versus 6%. And then what we did here on the lower graph on the lower right, we just basically took all those points and basically plotted a best fit line on both of them. And the endpoint for Pfizer is 30% PCR negative for one of their studies. And you can kind of see how quickly we crossed through that. And the big disparity between our drug and the viral load and control. We don't have any viral rebounds with our molecule. And the symptoms improve. And basically you have symptoms in both groups, the blue and the orange. And you'll see the only left is orange. Well, orange is the control group. And the blue group is the treated group. So symptoms are gone.
We had post-immunization infection, and that's a new idea. The idea is we take the load off the adaptive immune system. Those are the first responders. So much so that you can build a strong, robust immune response. Then we compared Paxlovid versus Bioxytran. We explained to them, look, this isn't a fair comparison. It's unfair to Bioxytran because Paxlovid has people with underlying medical conditions. You kind of, I don't know if you can see that. It's not highlighted versus people on the left with Bioxytran were standard risk. You'll see we crossed the green line at a day and a half versus 20 days with Paxlovid. It really boils down to, hey, do you want to be sick a day and a half or two days? Or do you want to be sick 20? Here's a nice comparison.
And this is the value proposition that we really imparted with BARDA. And the mechanism of actions, we compared them, the broad spectrum. Look, we're broad spectrum. All the other ones are very focused on only one disease, COVID. And they're prone to mutations. Efficacy, efficacy is night and day. We talked about 100% patients are PCR negative. Granted, we're starting with people that aren't as sick. And they're just hoping to alleviate hospitalization. We didn't have any hospitalization. And safety profile was no observed issues at all. And the other ones, they have a couple of issues. Here's the FDA correspondent slide. We're running out of time. But here we had the IND. We had a hold. And then we removed the hold. So we just kind of let it all out there. Now, why do we get a clinical hold let out?
So I explained to them, that's the elephant in the room. Why? Well, because the FDA, the regulators, they didn't like the placebo. They said, you know, this placebo, the stuff in there exceeds the maximum daily allowance that we can have with the FDA. So we basically said, okay, fine. We'll get rid of the placebo. And then we're back to phase I. And then boom, they removed the clinical hold letter. But now the correspondence gave us invaluable insight in our path forward, which is we showed them two studies in India that showed the tolerability and the efficacy. And you know, obviously there are peer-reviewed articles. And we obviously had our IND. And they said, hey, so when you go forward, you need to find the optimized dose and the pharmacokinetics. And you're going to target standard risk patients. That's fine.
So as a result of that, we realized we didn't have to do any drug-drug interaction tests. That would complicate things. And but the last thing there, our CRO suggested, why are you guys just not going after testing upper respiratory tract infections rather than just a specific virus? And we're probably going to take their advice on that and go broad spectrum. And then finally, what do we have here? What do we need for phase I, phase II initiations? Well, it's going to be 40 people here with the FDA. And they said, saliva testing. Well, why are we doing saliva testing? Why are we talking about it? Because they want us to measure our carbohydrate, which is a neutral carbohydrate in the blood. And that's just not possible. So we needed to find an alternate method of measuring the drug in our blood.
That's what it was. We already proved that NMR. We proved that we're a galectin antagonist through NMR antagonism and NMR testing. Then finally, antiviral assessment inclusion. They basically said, hey, you know, when you enroll people, by the time you get the PCR test back to figure out if you're going to enroll them, it's changed. So look, just use the Abbott test kit. It measures PCR nucleic acids and the PCR. Do both. And this way you'll get people enrolled earlier. That was some really good impact. We just went through our clinical development plans here. You'll see that for PLM, PLI. I think I skipped over one here. Our universal oxygen carrier, along with how much money it's going to cost and that. We went over our manufacturing. We talked about our manufacturing facility.
We said, hey, we can do a tech transfer here in the U.S. Don't worry. So if BARDA, you ever, you want to give us some funding, we're going to do it here in the U.S. to make sure the supply lines are good. And then our intellectual property. The main thing there was convincing BARDA, hey, we have the freedom to operate unencumbered. We don't have any patents anywhere else overseas. We're not relying on anyone. So we're really good to go there. And there's also a list of our patents. And then finally, we ended up with, hey, here's our business strategy. You know, so we're going to, and you'll see there, or partner with smaller big pharma and the U.S. government. So we included them in there.
We showed them that we have a viable licensing type structure and that we will also hope to expand our glycovirology platform as well. And then finally, we had some BARDA questions. And they answered our questions and gave us very invaluable feedback. And that was pretty much the end of my presentation.
And right on time, Mike. Good job. And congratulations on all of this.
I practiced a lot for that presentation.
Truly. Three, two, one. You did it. Really good. Well, thank you so much. Really important work you're doing, helping people.