of the day. We've got Lakewood-Amedex with Kelvin here, and I'll pass it off to him. Briefly, just want to introduce myself as well, Dan Milinkovic with Winning Media. We are one of the sponsors of the show. We have a massive 700,000+ investor audience, and we've worked for 20+ years to help micro and small-cap companies get exposure in the market, help with liquidity, volume, et cetera. Without further ado, I'll let him speak to Lakewood-Amedex.
I'm actually on a lapel mic.
Oh
I should be good, thanks. Thanks for showing up this afternoon, and I'd like to thank John and ThinkEquity for letting me give this talk to everyone. I'm going to be talking today about a new class of antimicrobial agents which we discovered. They're our own compounds, in-house developed. To do this, I first of all wanted to introduce the problem that we're trying to solve. These are the usual forward-looking statements which I'm required to put in. The big issue we're trying to deal with is antimicrobial resistance. If you don't know what that means, it means that the current medicine chest of antibiotics really is severely compromised, and most of them have some kind of resistance mechanism which makes them completely ineffective. The scope of this problem is enormous. Worldwide, there are 4.7 million people die because of an antimicrobial resistant problem.
It's actually more than the combined deaths of HIV, malaria, and AIDS combined. It's a massive issue. I worked at Pfizer for 30 years, and I was in infectious disease during that time. At the time, it was a scare that people said, "Oh, it's going to be a terrible problem. Antimicrobial resistance is coming." Well, now it's here, and if you've ever heard of something called methicillin-resistant Staphylococcus aureus, MRSA as they abbreviate it's an extremely serious infection, which if not treated with a narrowing number of drugs that can work, it can be fatal. The reason is because the systemic antibiotics are used. If your child gets sick, you go to the doctor, you want them to prescribe something, even if it's not really a bacterial disease. You'll get an antibiotic, and that leads to additional resistance being developed.
Just being treated once in the last 10 years with an antibiotic leads to a form of resistance being developed in your microbiome. It is a very serious problem. Antibiotics are used regularly in agriculture, so they are used not as antibiotics but as growth promotants. They stop animals from getting sick, and they get bigger and more muscular. This is a big issue. The big problem we have is that systemic antibiotics, typical oral or IV antibiotics right now, are extremely vulnerable to resistance. What has happened is there are lots of companies developing additional antimicrobials, but the problem is they have from the same classes, same resistance profiles. What happens is these medicines are put on the shelf.
They are not used because there is a scare that resistance will emerge against them, and so these are last resort medicines, which makes it quite difficult to develop this kind of drugs because it is difficult to get people interested. Why are we interested in this then? What we have got is a new class of agents which work completely differently from the current antibiotics. They kill bacteria rapidly, and because of that, we do not believe that resistance is going to be emerging against these bacteria. We have tried in the lab to generate resistance to the bacteria and have failed. The way you do that is you treat bacteria at a low concentration of drug for three weeks, and at the end of it, you see if there is now resistance to the drug you are using.
We couldn't develop resistance, whereas a ciprofloxacin, which is a common antibiotic, we had it as a control in that experiment. It got 2,000-fold resistance to the bugs that we were using. We used MRSA as one of our example bacteria, which is very difficult as I said earlier on. They are also broad spectrum. They hit gram-positives, gram-negatives, and all the multi-drug resistant organisms. They are what we call cidal against biofilm. Biofilm is a big issue in repetitive infections, so you may know someone who gets repetitive UTIs or repetitive lung infections. What happens is the bacteria go quiet. They hang around, they are not reproducing anymore, they are not growing anymore, and they wait until the environment is right, then they reemerge, and that has been a big issue. Our drugs kill biofilm organisms as well. We have already covered the resistance thing. What we do is deliver locally as well.
Instead of going systemic, where you are likely to cause some kind of side effects, your typical side effects, antibiotic GI side effects, but it also, as I mentioned earlier, induces resistance and impacts your immune system. So we go local, and that means if skin, soft tissue infections directly on the wound, whether it be a surgical wound, a burn wound, or anything, a wound like that. If it is a lung infection, it goes directly into the lung. A urinary tract infection directly into the bladder, and they will not get systemic exposure. It will not affect the microbiome, and you do not get the side effects. So that is what we claim. We have evidence obviously, and I will show you some of that evidence. How do they work?
What we think they do is that this is a picture of a membrane that goes around a bacteria. These compounds invade the membrane and just basically blow it apart, which kills the bacteria rapidly. As I said, we hit all the resistant strains, whether it's methicillin-resistant, vancomycin-resistant. In fact, we work against the biodefense pathogens. It's kind of interesting. The recent Russian lab Yersinia pestis potential infection, our drug works against Yersinia pestis. If that ever becomes a problem as an inhaled drug, we've got something ready. What we're focusing on is a skin and soft tissue infection. We've targeted diabetic foot ulcers, and the reason for targeting diabetic foot ulcers is because there's a huge medical need here that's unmet.
830 million people have diabetes around the world, and about a third of those are going to develop a diabetic foot ulcer at some point in their life. Of those, half become infected. If you don't treat that infection properly, that will lead eventually to an amputation. In fact, one out of five diabetics that have a foot ulcer will have an amputation. one in five, which is an amazing number of people. If you have an amputation, your life expectancy for five years is less than 30%. Anyone with a diabetic foot ulcer has a life expectancy reduced by 30% for five years. So it's a very serious disease. The current treatment doesn't really work that well. It's basically just wound care.
People do give oral antibiotics because that's the standard of care, but it's well documented these don't actually have any clinical evidence that they work. It makes sense. There's low peripheral circulation at a foot ulcer, and that's part of the reason why you get a foot ulcer is the blood supply is very low. Actually, your innervation, your nerves, are also poorly supplied with blood, and they start to die. So you can't actually feel your foot. If you're walking around bare feet and scuff it, because of the low blood supply, the skin is thin, it'll break, and you'll get an ulcer. Trying to give an antibiotic with low blood supply means the drugs just don't get there in a high enough concentration to work. We go directly on to the wound, directly where the infection is, and kill the bacteria.
We have selected one compound, a compound we call Nu-3. It's got broad spectrum, just like the rest of the class. In vitro shows all activity against all the resistant strains and biofilm, which in diabetic foot ulcers is also a big issue. If you're treating, the bacteria just go quiet on the wound, and then in the right conditions, they'll just grow back again. We kill biofilm. We've got skin infection models, robust activity, and I'll show you a little bit of data on that. We've got a formulation that's designed for local administration. We did some early trials with a solution, but if you can imagine putting a solution on the bottom of your foot, it's going to come off pretty quickly. We now developed a gel formulation. We've done all the correct toxicology program.
The FDA required us to show that the drug does not impact wound healing at all. We have done that study. FDA is quite happy with what we have done, and we did it at very high topical doses. We have also given the drug IV, and it is, again, no systemic side effects. This is a very safe drug. We have an open IND. It is an Investigational New Drug application with the FDA, and it is open, and we are active. I am going to give you a little bit of a biology lesson. This is the in vitro profile. What we are looking at here is the time to kill about 300,000 bacteria. The top line is no drug, and then these lines are the various concentrations that we put in the solution. Along the bottom is the minutes.
This shows you that within 10 minutes, at 100 mgs per ml, the bacteria are completely dead. You can imagine then we are putting a gel on somebody's foot in an infection. Within 10 minutes, according to this, we should kill all the bacteria. That is something that we are moving forward in the clinic now. This is now an animal model of a skin infection. We induce a skin infection in an animal model, then apply our formulations. We have done both solution, as I mentioned earlier on, and the gel. You can see that this is no treatment, 100% infection. Both the solution and the gel very quickly bring it down within two hours to almost nothing, but the gel keeps it there. Solution, you show regrowth. Again, this reinforces that the gel formulation is the way to go to get into the clinic.
Then we have also done multiple doses over five days, and we have tried once a day, QD, and twice a day, BID. As you can see at the 5% gel, the BID is more effective. It sustains the activity even past the end of the treatment. We have five days treatment, wait for five days and look again, and the BID has kept it off, and drug is not being applied those past five days. That was enough in vitro and in vivo data for us to move ahead into the clinic. We believe we have got the right drug because of its profile. We are applying it locally, which is the right way to do it, and the mechanism of action is so rapid that we do not believe resistance is going to emerge. We do have some clinical evidence already that this drug works.
We had done, and we were required to do this, the FDA requires a safety study in normal volunteers where you get them to volunteer to have the drug applied to their back, both on their normal skin, untreated skin, and on the abraded skin. We actually strip skin off someone's back and add this drug there to see if it irritates the skin, causes sensitivity or some kind of reaction. It did not. We were quite happy with that. Then we did a very small exploratory study in patients with infections in diabetic foot ulcer. Concentrations were low, 0.1%, 1% and 2% versus a placebo, double blind. No one knew what they were getting. At low concentrations, there was no safety findings. But we found that the 2% only showed a trend for pathogen reduction, that is eliminating the bacteria.
And interestingly enough, we didn't expect this, a reduction in the surface area of the wound. The wound is starting to close. And really, that's the gold standard of treating a foot ulcer, is you would like it to see it closed. But typically, it will not close until the infection is cleared. It can't clear. Our conclusions back then were that this is well-tolerated, safe, but we don't believe this is a high enough dose. 2% showed some activity, but it's not enough. We then did some additional toxicology studies to go to higher concentrations, and we changed the formulation, as I mentioned earlier, from a solution to a gel. These are the trials then that we have set up with the FDA. We've been through the discussions with the FDA on both of these trials. This is the one that's currently underway.
It's a single-blinded study, which means that we don't know which drug the patients are getting. The patients don't know what drug they're getting. But the people who are treating them do know what's going on. What we do is we take a biopsy out of the wound the day they enter the trial. We take another biopsy at day seven, and then a third biopsy at day 14 after two weeks of treatment. That gets sent off to a central lab to count the bacteria and look for the pathogens. The idea would be, what we'd like to see is that we reduce the number of pathogens in the wound over that two-week treatment period. And we're going with two concentrations, the 2% that we found had some activity earlier on, but we're also going to 5% and 10%. And these are in parallel.
We're not doing this in a sequence, we're doing it in parallel. That is ongoing. We announced the first patient first visit a few weeks ago. That trial is ongoing. What we expect to do is have that trial complete, and the data readout in the first quarter of next year. Assuming it's positive, we'll then move on to the phase IIb study, which is double-blinded versus placebo, both once a day and twice a day. This study has already been discussed fully with the FDA, and they're perfectly happy with us to move ahead on this profile. Once we see the outcome of this, we'll manage this a little, probably make some changes to the protocol, but we're in really good place. Beyond that, right now we're in phase II in the U.S. Beyond that, you need to go international. We'll need to go into Europe.
The phase III studies would need to be conducted internationally. What we need to do to get there is that phase IIb study, but there's also a couple of other pharmacokinetic study, skin sensitization study. Look for some partners, because once you go to phase III, that's a massive undertaking. Hundreds of millions of dollars potentially. And then we also need to do some manufacturing work to get ready to start the phase III with the commercial dosage form. We do have other assets. In fact, we announced last week that we have preclinical activity against pulmonary infections and urinary tract infections. With a positive proof of concept, we could go ahead with multiple indications with the compounds that we have in development. Upcoming milestones. Completed the manufacturing. The site enrollment was done in the second quarter.
We completed the manufacturing, completed the site, and started the clinical trial. What we'd like to do by the end of the year is complete that trial with the last patient last visit, and then have top-line results in the first quarter of next year. We've got a robust intellectual property profile, over 101 patents. 72 have been issued. They're global patents all around the world, both for composition of matter, which means we protect the actual compound, and for formulation. We protect the formulation and the use. We've covered everything that we can think of for that. We believe that the competition is not that strong in this area, so we're well-placed. There's only one direct and comparable competitor. A compound called RECCE 327 from a company called Recce. It's an Australian company. Their compound's in late-stage development, but it's in Australia and Indonesia.
They do not have an open IND, so they're a long way from even moving into the U.S. As I had mentioned earlier on, the standard of care is oral antibiotics, but they don't work. Guidelines are based on general infection stewardship. You're committed to give some kind of antibiotic even though you know it's not really going to work that well. Over the counter, there's nothing approved for topical treatment. This is the team. Myself. Pete Ceccacci is our Chief Financial Officer. Thomas Balzer has spent 30 years in the pharmaceutical industry. Then we have a board. Doug Manion is a pharmaceutical CEO, has been a CEO. Lenny is our businessman, and Joe Tucker is also a CEO of a biotech company. I'll round up and finish up there with we've got a phase II-ready product.
It's in phase II now being run to treat infections in diabetic foot ulcers. We've got preclinical and early clinical data to show that this works. It's potential for first-in-class infection therapy, and because of the fact that we don't believe resistance will be a problem, this could become a first-use drug as well instead of being put on the shelf. That's really what we're hoping is going to be the thing that we'll be able to sell this on. Our nearer-term milestones, as I said, we've got that. The phase IIA is underway, and we've got a very robust IP estate. I think that was it. So happy to take any questions from you.
John.
John.
Something that would be great to share, because you really opened my eyes with this, is what you've learned in your 30 years in Pfizer. I think most of us just sort of think, wow, anything from animal to approval sort of all has the same odds.
Right.
And you really enlightened me with why you are an infectious disease.
Yeah, sure.
Kind of give that. I think that is just a great learning element for everyone.
Yeah, thank you. So during Pfizer, I led discovery efforts in cancer, respiratory, allergy, inflammation, immunology, and infectious diseases. And what we did a lot of research on this, the drugs that get discovered in infectious diseases have a much better pathway through to being approved versus a cancer drug or an immunological drug or a depression drug or any of those. And the reason is very, it seems obvious when you think about it, because if you induce an infection in an animal, it is the same bacteria that you are using that is going to be in the human. And as long as your drug can get to where that infection is and kill it in the animal, then you are just doing almost exactly the same thing in the human. As long as the drug can get to that same bacteria or bug in the human, it should kill the bacteria.
That is why the success rate is so much higher. Going from discovery through to an NDA and approval is one in 10 for an anti-infectious disease program. For cancer, it is one in 50. For Alzheimer's, it is one in 75. So that gives you a view of the odds, and that is why the people at Lakewood-Amedex believe that this has really got the legs to move forward because we have that animal data which shows topically you apply it to an infection, it stops the infection, kills the infection right away. So thanks, John, for that.
I am going to give you one more. This company went public through a direct listing, and it was $140 million.
Yes.
I think initially at $8 per share. That is the good news. The bad news was they took a very interesting, how Nasdaq approved it, but a convertible preferred that pretty much had a moving floor. So today, as they have now reached an agreement to buy out, knock on wood, hopefully the balance of it, the market cap is currently around $4 million or $5 million. So while they have progressed and everything is leading towards near-term results, this thing is as cheap as we have ever seen.
Yeah.
Just in case people look at the drop, it is not correlated to people thinking this is not going to work. It was this particular instrument that the trigger has come out of.
Yeah. The reason we took the instrument, because that was a last resort to keep the company moving forward. We were private before that. It was very challenging to raise funds as a private company. We knew that once we went public, there would be a greater opportunity, but we also realized it was going to be a tough road ahead of us. We're in that tough road right now. Yeah.
What are some of the endpoints that you need to measure, and how long is the measurement period?
Thanks for that question. The endpoints for the phase II-A trial are going to be bacterial counts, signs of infection, and wound size. Wound size is a secondary measure. It's not really expecting to see much about that.
We'll be, as I said earlier on, taking bacteria out of the wound and sending off to a central lab to count them. The expectation is to look at a dose response. We have a 2%, 5%, and 10%. We would expect there to be increasing response as we go up that dose number. Also might work faster as well. We have a two-week treatment period. We would like to see by one week, maybe the 10% works much better than the 5%, better than the 2% at one week. Then at two weeks, maybe the 10% and 5% look the same, but 2% still is not up there. Those are the kind of endpoints we're looking at, as well as looking at signs of infection, which are, does it smell bad? Is there exudate from the wound? Is there pain, inflammation?
Those are the things you look for. Yep. Great.
All right.
All right. Yep. Thanks very much. Thank you.