Welcome back, everyone. Next up is BioXyTran. They're an OTC QB 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. Their drug is a galectin inhibitor that not only neutralizes COVID-19 but also neutralizes influenza and RSV and prevents it from entering cells. They are currently 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, and its development is supported by an FDA-approved device that detects local tissue oxygenation. 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, nice to see you again. Before we get started with your presentation, I just want to let you know I've been following you and noticed you recently published another LinkedIn article on how to slow the aging process, hello, using the universal oxygen carrier. What I found interesting is you mentioned the universal oxygen carrier was equivalent to 18 hours of hyperbaric oxygen treatment. I know that's very popular right now at a lot of hospitals or med spas and smaller doctors.
Do you think your oxygen carrier could eventually replace the hyperbaric chambers?
Anna, this is a $3 billion a year business. Getting hyperbaric oxygen, it's really time intensive because for it to work best, you got to do it daily for at least an hour. That's a lot of time commitment when you're looking at these HBOT treatments. Whereas the alternative is our universal oxygen carrier, and that's just like a shot. You get it, and it's going to give you the equivalent of about 18 hours of HBOT therapy. If we get this universal oxygen carrier approved, this is going to be like a no-brainer for people because time is money. You can spend a lot more time doing fun things versus just kind of sitting there in a chamber, right?
It's for these reasons that I can foresee that almost all the hyperbaric oxygen patients are definitely going to much rather prefer the injection over the chamber.
Absolutely, they will. Thank you for clearing that up. It also looks like you revamped your investor presentation. When you are ready, the floor is yours.
OK, thank you. Let's start off with our title, Taking Inflammation Out of People's Lives. We want to be, we want to kind of rebrand ourselves as an inflammation company. The next slide here is a forward-looking statement. Now, let's look at the investing thesis for BioXyTran. BioXyTran has game-changing platform technologies. We've got three of them that we're going to go over today. We have clinical trial results that were, look, they're the best that are out there in the past decade. We've got 100% responders rate. We'll go through all that as well. We have good IP, proprietary science. Bottom line, we want to make the world a better space. This one bothers me. Our valuation is just ridiculous. It shouldn't be here, but we're trading at an $8 million valuation.
You know, I've been to a couple of conferences and tell people about what stage you're at at these conferences. These are professional investors. I don't think anyone's less than $200 million. Here we sit, trading at $8 million market cap. I think retail needs to step up, and I think we're at an ideal buying level. We also have a solid management team, and we have a solid strategy. We have a thin float shareholder base. You know there's a lot of potential upside here. I just need people to realize that. The final thing is we're in a lot of active licensing discussions. That's why I've been going to all these conferences. We're a carbohydrate company. We make complex carbohydrates. What do we do? We're going to treat viral infections. We're going to treat cancer.
We're going to and we have an oxygen transport molecule. We stabilize it with our copolymer. These carbohydrate drugs recognize galectin receptors. You know they'll also carry the oxygen atoms. Now that I mentioned the word galectins, what are these things? This is the definition, nice and big for you to all see. Galectins are protein receptors that recognize sugar molecules. They're specially designed proteins that recognize sugar molecules. Here's the punchline. They're responsible for chronic diseases. It's the key to chronic diseases. That's why galectins are important. Here, I explain it a little bit more in depth with a little graphic there. You'll see galectins, they're these structural things. You'll see the first one, they're kind of two Pac-Man behind each other. The other one's a rod. The other one looks like a snowflake.
Galectins stick to other galectins. Galectins also stick to those rods that are sticking up out of the cell surface. Those are called glycans. You will see like the middle one, it looks almost like an arresting wire. They are also responsible for signaling. Galectins are extracellular and intracellular. We are focused on the extracellular. Now, how big is the reach of these galectins? There is this article that says galectin- 3, one receptor for an alphabet of diseases. Just take a look at all these diseases. I mean, for every single letter of the alphabet, there is a disease. I just want you to see that. We are going to just gloss over it kind of quickly. There are a lot of chronic diseases here. That takes me to my investment highlights here. We have three platform technologies. The first one is a broad-spectrum antiviral.
The next one is cancer metastasis, as well as fibrosis. Then we have a blood substitute. We are going to start for those that haven't heard of us, we have an active FDA IND with our broad-spectrum. We finished a phase two study for antiviral. For the blood substitute, we are in preclinical trials and quickly moving toward getting an IND. Let's take a look at ProLectin-M. That's our first most advanced molecule, the antiviral asset. When I do this, what I'd like to do is we have a historic discovery in virology. You see, for the past 50 years, there's this idea that one drug, one antiviral. With our drug, ProLectin-M, we've basically debunked that theory. We have what we believe is the world's first broad-spectrum antiviral. The discovery was outlined in an article back in August of 2024.
It basically talks about viral adhesion has to happen first. The virus has to adhere to the cellular membrane first. It's the first step in the viral entry process. It comes in. You see, because what happens is you have these spike proteins. They're slippery. Why are they slippery? They're covered in sugar. The reason they're covered in sugar is to be invisible to the immune system. Otherwise, the immune system would see them, right? You've seen cells under the microscope. They're slippery. How do two slippery things stick to each other? They don't. They need help. The viruses basically hijack these galectins in their environment and use them as adhesion molecules. Let's finish this slide up. There's no broad-spectrum antivirals that currently exist right now. We're literally disrupting a $55.36 billion global antiviral market.
When I say our market valuation doesn't make sense, you just got to do the math. Here's an overview of our technology. When we say broad-spectrum, these are different families of viruses right there in the center. You'll see that there's three that are circled. No other antiviral has this sort of activity. That's really what we want to point out. We've done these three different families. We plan on doing more to prove out this platform approach. I'd also mention that I went over it fast, but we have a patent for 60 viruses, or patent pending, rather, for 60 viruses. We have clinical trial results. Let's go over them. We eliminate the virus and load within five days. We reduced infectivity, that's spreading it to one another, and we quieted the cytokine storm.
We have a robust antiviral response. We're going to breeze through this. This chart on the right is basically just one line of the graph on the left. What you really want to see is there's that red line there. All the green lines are the people that took the drug, right? You want to be above that line as quick as possible. You'll see that right at the three-day point, you know right where it breaks, that is where almost everyone in the green was above the line, except for a couple. 88% were PCR negative. At day seven, 100% were PCR negative. If you look here at the chart on the right, you'll see that 30% of the people were PCR negative, probably based on this curve, in about a day and a half.
Do we have viral rebounds? No. Paxlovid does. We do not. There is the chart. How about symptoms? Do we improve symptoms? Yes. You will see what happened is the top part of the chart is basically the baseline. The bottom is at day seven. When you look at the baseline, you know there is an even distribution between the blue, which is the group that took our drug, and the orange. You will see nothing but orange. I mean, just a teeny weeny bit of blue there, but pretty much nothing but orange. That denotes symptoms. It followed not only do we get reduced the virus, but the symptoms went away. What about a response? What about a long-lasting response? That is what this is, this idea of post-infection immunization. We built a robust response. This is what this graphic shows you.
Now, I am dying to get to this one because this one shows how we are, this is a comparison, but it's not a head-to-head comparison. Actually, it's unfair to us. We didn't do a trial with Paxlovid. We took their real-world data and compared it to our clinical data. What you'll see is there's this line of demarcation at the 30% level. How many people can get to the 30% PCR negative level? If you look, it takes us less than two days to cross that line versus Paxlovid, which is 20 days. I love to say, do you want to be sick two days or 20 days? It's almost a no-brainer. How does this drug work? We neutralize the spike protein. See, typically, what we're showing here is the antibody comes in.
You see where the purple meets the green on the top? It comes in there, binds to there. That prevents the virus from entering. That's the way you typically do it. Our molecule, it basically goes into that galectin fold. It's circled there in red on the left. It goes in there. It binds to that. It prevents the spike protein from entering. What you'll see is the sugar surrounds the spike protein. The spike protein on the left in light blue, it's naked. The way it exists in nature is with sugar on it. The sugar hides it from the immune system. You'll see the tip is never covered in sugar because if it was and it was hiding, it wouldn't be able to enter. Of course, the galectin fold.
We neutralize the antibodies, or we neutralize just like antibodies neutralize. How does it get rid of things? What we do is our molecule gathers up the virion. It latches onto them by the spike proteins. It travels through the body, eventually reaches the liver, and the liver purges it. We have other indications. Shingles was one indication there. You're going to see the before and after picture. This was a topical cream or paste that you put on, and you'll see how quickly it reduced it. It got rid of the pain. Conjunctivitis was another case study that we did. There are other indications. We could use this for long COVID. We have a special long COVID deck. All that, we're just hitting the high points.
The other thing, the next slide talks about bird flu. There's a very good case that this could work on bird flu. And we're actually pursuing some strategic relationships right now, you know working on signed NDA type stuff in bird flu. This is something this is Ebola. This came out of a BARDA slide deck. I just want to show you some of the things that we're working on. So, a couple of decks slides from our presentation decks made it in here. And we'll talk about cancer later on. The bottom line is this is an enormous market. There's no effective treatments out there for these viruses. And we believe we can make a difference. Now let's get to the next platform technology. We're talking about neutralizing cancer metastasis and fibrosis with ProLectin- I. Here's an overview of our platform technology.
We have an IV drug that can target cancer metastasis and fibrosis. It's designed to go after metastasis in late patients. We also have this other thing. The second bullet point is combination therapy to enhance existing checkpoint inhibitors. We're going to really talk about that and why that's important to us as a company. Combination therapy, galectins could be used in combination therapy with almost any treatment options out there. That is also in a cancer deck, specialized deck on cancer. Go to our website and take a look at it. ProLectin-3 is a target, strong potential in cancer since 2018. Let's look at some studies. Let's build a case. High galectin expression leads to bad outcomes. This chart takes a little bit of explaining.
The bottom line is the people with high galectin expression, that's bad. If you're a person who has high galectins, tumor staining on your tumor, that's not good. You'll see what happens is the people fail. I'm summarizing what's going on in this slide. The people fail, the people in red, they fail really fast, like 30, 60 days. They can't take Keytruda treatment. Look, 100% of the people that had low galectin expression had good outcomes. The question I pose is, what if galectins were blocked? Theoretically, Keytruda could be 90% effective in non-small lung cancer if you exclude people for high galectin- 3, according to this peer-reviewed study. Let's dive a little bit deeper. Why is that? A couple of things. Galectin effect, T cell anergy. Again, all this is covered in my cancer deck.
I'm going to kind of go over it fast. There's T cell anergy. Basically, the T cell goes into this wave of, we'll say, galectin, this galectin cloud before it gets to the T cell. It just gets all this plaque on it, on the actual T cell itself. What that does is it prevents these little grappling hooks, which are called lectins. They grab on and get good adhesion with the cell. They're mechanical. They're basically plastered in concrete. We go over that in the cancer deck. The other thing is T cell receptor downregulation. If you don't have as many probes out there on the T cell looking for these cells, you know you're not going to find as many. That also happens thanks to galectins. What else does galectin do?
Galectins are also reprogramming the tumor vasculature. What the heck does that mean? That has to do with the blood flow. You have a tumor here. You have a blood supply going to it. It grows. You know that's called angiogenesis. It grows inside the tumor and feeds it with oxygen and nutrients. Galectins are responsible for that. They are responsible for every part of the angiogenesis process. When you block lectins, you stop that, or you inhibit that. That is another key point. This also tells you this mechanism, again, go to the cancer deck. I am going to sum this up. It basically gets you into this non-inflammatory environment, this suppressive environment where it suppresses your immune response. That is what this chart talks about. What we did is we did an article.
This is the abstract of our paper. We did an article on immune checkpoint resistance. You see, why is this so important is because of the part on the right. Overexpression of galectins drives several key cancer progression mechanisms. You can see almost all the things to do with cancer involve galectins. If you block galectins, we're expecting good outcomes to happen. Galectins are essential for survival of the tumor. This is an article. It's a journal article. Again, let's not spend time on it. We figured out why all these immune checkpoint inhibitors don't work as well as they should. I mean, they cure some people. Why don't they cure the other people? This discusses this. The interesting one is in the upper left quadrant of those four charts there, it shows there's a blue line.
When you go to the cancer deck, look at it. There's a blue line there. And it basically galectins completely render Keytruda, I don't know, neutralize it, basically. That's what it is, neutralization of Keytruda. Keytruda is being given to a person. And it's just not going to work, according to this article. What happens? If you block galectins, here's the schematic. You rip these galectins off. Keytruda can now bind in its binding site. You see, what happens is galectins were occupying the binding site. Now Keytruda comes in. That could end the resistance. Here's another article that talks about it. When you add a galectin antagonist, you see over here on the left, when you have a suppressed immune system, and then you get Keytruda, and then it activates it a little bit.
When you get Keytruda plus the galectin antagonist, it's completely activated. That's what this chart is basically showing. Now, this is a great slide. Why? Because it shows you this is in pancreatic cancer. It's a Kaplan-Meier survival chart. Basically, you want that chart to be pegged right to the top. Like, you want it to be at 100%. It's not at 100%. There's a little bit because that would represent 100% survival rate of all the people. The way this works is there's 5% survival if you have pancreatic cancer versus I think it's 65% or 68% if you're galectin- 1 negative. If you don't have galectins, that's good. There's a 68% chance you're going to live, survive, rather. If you do have galectins in your positive form, it's about a 5% chance you're going to survive.
The whole idea is it just makes sense to block galectins. Then here's our clinical evidence. There are two clinical trials, reduction immune effects. All this stuff is on my cancer deck. It is just worth looking at this picture here. This is a before picture. The guy on the left, baseline, then completion of therapies. That was 90 days of treatment, 90 days of treatment. That is it. Then they stop. The guy got a complete response. When you compare that person, and he failed Keytruda a couple of times before, and all the tumors were resolved, this is incredible data. You know how old this data is? This data dates back to 2018. We think it is time that galectins are going to make it to the forefront. Here is another galectin antagonist. Both of these are not ours.
I want to be clear about that. They're not ours. But we have a common target, which is galectin- 3. And look, at the lowest dose, 40% achieved a partial response. And then they upped the dose a little bit. And then they went to 60. Well, that's combination therapy. How does that compare to the standard of care? It's 22%-38%. Let's just call it, let's high call it 30%. Look at the numbers. Even at the lowest dose, you're better in combination. And you're twice as good in combination at the higher dose. They didn't even do the next dose escalation. We don't even know how that would have worked. This is the checkpoint inhibitor landscape. Now, I want investors to just pay attention real hard here. This is our target market.
These are the 11 guys that I'm going to be talking to. I got a couple of them that I'm already in. I have phone numbers and stuff. I'm making my slide deck and my presentation is to talk to these guys. This is who we want to do a deal with because these guys need us. They need what we have to remain competitive. All right? I put it in blue. The pharmaceuticals with galectin- 3 blockers are going to dominate oncology. We are sitting in a power position. We have an $8 million market cap. ProLectin- I, that's for fibrosis. I just want to bring it, I want to bring it in. The same molecule will work on cancer and fibrosis. Again, it's this inflammatory cycle that's driven by galectins.
This inflammatory cycle, you're going to, when you go to the slide decks, take a look at this. What you see is you see this galectin. It's at the center there. It's the center of these feedback loops, these pro-inflammatory feedback loops. You even have TNF-α over here. Some people think TNF-α is the big thing in inflammation. It's not. It's actually galectins. Galectins have a bigger impact in these diseases. We're running out of time here. I'm going to go through my blood substitute as fast as I can. We also call it the universal oxygen carrier. It's our third platform technology. Look, we have proof of concept in animals. We have two of the four animal species tested. There is no change in side effects. Here's an interesting thing. Government discussions are being pursued.
We got one tomorrow, as a matter of fact. Let's show you how it works. The universal oxygen carrier works as a bridge. It's 1,000x smaller than a blood cell. You see this blockage here in this picture. The blue is going through, no problem. Obviously, no red blood cells are going through. The blue is carrying oxygen. That is the idea behind it. The way we make it is put in a little graphic there. You see, what we do is we extract these heme, these heme molecules. Then we stabilize it with our copolymer. That is how we make it. We have some incredible data here. We presented this to BARDA. This is some data. It is old data. It does not use our molecule, but it uses the same chemistry. We use the hemorrhagic model.
We took out 90% of the blood out of these dogs. What happened is you see something you just don't expect to see. The tissue oxygen tension, the tPO2, it actually went up. The model is supposed to have a 50% mortality in two to three hours. At these high settings, or at the high dosage levels, and that's in the center one, you'll see that it was statistically significant. We actually had a survival benefit in this study. Just miraculous stuff. This shows you what happens with mice. These mice, what they did is they clamped off an artery that was going to their vein. What happens is you see the white area there. That's what happens normally. Now, we add our molecule to it. It's a molecule with similar chemistry.
What happens is it goes right through the clot. You see the pink tissue on the hemispheres. See that? Right. I'm sorry.
We're going to wrap, huh?
Yeah, it's time. I mean, good ending with that mouse slide. But it is time to wrap it up. Really fascinating, as always. We've got so many questions for you. But we'll have to send them to you so you can answer on your own time. But thank you for this great update.
Wonderful.
All right. We'll see you again soon. Everyone, stay with us. We'll be right back.