The Life Sciences Investor Forum. On behalf of OTC Markets and our co-host, Zacks Small-Cap Research, we are very pleased you've joined us. The next presentation is from Lakewood-Amedex Biotherapeutics. Please note you may submit questions for the presenter at any time. You can also view a company's availability for one-on-one meetings by clicking "book a meeting." At this point, I am very pleased to welcome Kelvin Cooper, Chief Executive Officer and Director of Lakewood-Amedex Biotherapeutics, which trades on Nasdaq under the symbol LABT. Welcome, Kelvin. Thank you very much. It's great. Good morning, everyone. I'd like to thank the organizers of the Life Sciences Investor Forum for giving me this opportunity to talk to you all today. I'm here to tell you about the exciting story of how we're advancing a novel class of antimicrobials, the Bisphosphocin class, for the treatment of infectious diseases. Here are the typical required forward-looking statements that I'm sure you're all familiar with. What I'll do now is, before I get into what the company's doing, is describe the background to the challenge of antimicrobial resistance. Antimicrobial resistance is the ability of microbes to evade treatment by our current medicine chest of antimicrobials. An example pathogen that many people have heard of and maybe even encountered is MRSA, or short for methicillin-resistant Staphylococcus aureus. Antimicrobial resistance, or AMR as it's commonly abbreviated to, is a global problem. Has been identified as a major healthcare priority by the World Health Organization. On a worldwide basis, AMR is directly responsible for over 1 million deaths a year and contributes to almost 5 million deaths a year. Interestingly, that exceeds the annual death rate of HIV/AIDS or even malaria. Financial burden is also large. AMR is projected to cost about $3.8 trillion in lost GDP by 2050 if it's not successfully tackled. In the U.S. alone, AMR was estimated to cost $4.6 billion in 2021. Unfortunately, there is a dearth of new antimicrobial discovery efforts, the majority of the few new developments being incremental improvements on existing drug classes, which makes them susceptible to future resistance development. As a consequence, the main reason that many of the newly launched drugs are held in reserve is to avoid resistance development to those new drugs. What's different about this Bisphosphocin class? Well, we believe the Bisphosphocin class has the potential to mitigate the impact of global AMR crisis because they are broad-spectrum antimicrobials with activity against all the susceptible and clinically relevant resistant pathogens. They are rapidly cidal, and that includes activity against biofilm, which is a source of persistent infection. They also possess a favorable resistance profile with, we believe, a very low risk for resistance development, whether that resistance is induced, intrinsic, or acquired, and we have laboratory data to support those beliefs. Class can be delivered locally and therefore can achieve high concentrations at the site of the infection. Consequently, also with low systemic exposure, this also reduces the likelihood of systemic side effects such as GI side effects, microbiome changes, and the consequence of that, immunological changes. That's our class of agents. How do they work? We believe the mechanism of action is proposed to be through disruption of the lipid bilayer membrane of microbes. We have evidence supported by in vitro mechanistic studies, including, for example, SYTOX Green dye studies, which I could describe if there are questions, and also electron microscopy studies. The action is extremely rapid, leading to microbial cell rupture and then death in minutes at the concentrations that are easily achieved and even surpassed in what we are targeting to take into the clinic. Importantly, of course, the class is selective for microbial cells over mammalian cells, and that's thought to be based on charge differences of the different membranes of mammalian cells and microbial cells. However, we need more experimental work, and we have that plan now to further elucidate the mechanism to get really into the fine detail of that mechanism. Our lead program was selected pretty much based on selecting an indication with high unmet medical need and to take advantage of those differentiating characteristics that I just described. Skin and soft tissue infections would constitute an excellent target for treatment, especially as in many cases, those infections are amenable to local or topical application directly on the wound, directly on the cut, the ulcer or whatever. From the very many of skin and soft tissue infection indication possibilities, we have to choose one to allow us to get through regulatory approval. We chose to target infections in diabetic foot ulcers because there's a large population and the high unmet medical need in those patients. As we all know, diabetes is a disease that affects many, many people around the world. In fact, of the 830 million people in the world with diabetes, about one-third of them will develop a foot ulcer in their lifetime. About a half of those will then become infected at some point in their lifetime, with many patients facing recurrent events. At this moment, there are about 19 million people with a diabetic foot ulcer worldwide, and about 1.6 million of those are in the U.S. Infections are a critical risk factor for amputation, alongside the presence of peripheral artery disease, which is a direct consequence of diabetes. Approximately 15%-20% of diabetic foot ulcer infections involve resistant pathogens, primarily MRSA, as I described earlier on. The high unmet medical need for this indication comes from the poor outcomes of current standard of care, where there's high recurrence in amputation rates. In fact, 80% of amputations in diabetics are directly linked to an infection which started out as a mild infection and then with poor treatment, led to a serious infection, which eventually led to the amputation. Now, the standard of care for an infected diabetic foot ulcer does include an oral antibiotic, but interestingly, there is a lack of clinical data to show that they actually provide any benefit in the first stages of infection. You can explain this. It can be explained by the underlying poor perfusion of the wound in a diabetic. Their peripheral circulation is lower because of the diabetes. That then, by taking an oral antibiotic, would lead to very low concentrations of the antibiotic at the site of infection, and not enough to reach their MIC, or their minimum inhibitory concentration, which can kill the bacteria or stop them from growing. In contrast, a topical agent would get directly to the infection, and you can go in at a fairly high concentration. We've selected one member of the Bisphosphocin class to advance into the clinic. It's called Nu-3. In line with the rest of the class, it has the following characteristics at broad-spectrum in vitro activity, includes all the resistance strains and biofilm activity. It has robust efficacy in skin infection models in animals, and I'll describe some of that in a few minutes. We have formulations which is designed specifically for local administration. The initial work, in fact, was done with just a solution formulation, but we've now progressed to a gel formulation. Again, I'll provide a rationale for why we did that in a few slides. Compound has an excellent safety profile in all the preclinical toxicology program, which required before you can take a compound into human studies. It also includes an FDA-required study to evaluate the effect of the drug Nu-3 on normal wound healing. I'm happy to say that study showed that there is absolutely no effect at doses that are multiples of the expected clinical doses. Nu-3 does not stop wound healing. The wounds heal normally. We have an open IND; investigational new drug application is open and active. I just wanted to spend just a few minutes describing some of the supporting preclinical data, just to show you exactly what we have. Here shows a graph of the preclinical in vitro data, and I thought it'd be useful to show a time kill. This slide shows time kill against E. coli. coli, but we've got similar data against MRSA, Pseudomonas, and other bacteria which are likely to be found in diabetic foot ulcer infections. The way to look at this slide is along the left-hand side are the log counts of bacteria. So, six being a million bacteria and zero obviously being none. The light blue line here is the control, that is no drug was added. As you can see, the infection stays the same throughout the 20 minutes of this study. The next three curves, the dark blue, the orange, and the green, show varying concentrations, increasing concentrations of Nu-3 from 25 up to 100 mg/mL. This matches almost identically what we expect to do in the clinic with the top dose being 100 mg/mL or 10%. Again, we can see here then that the bacteria, E. coli in this case, are killed in less than five minutes. The entire 100,000 count of bacteria are eliminated. In the next slide, I get to show you some in vivo data. This is a single-dose application, and it compares the gel formulation with the solution formulation. Again, on the left-hand side in this slide here is the percent inhibition of the bacterial growth. On the bottom is the time course of the experiment. You can see in the blue is the solution at 10% application to the wound that's created in an abraded skin on the back of a mouse. Within an hour, it's gone to pretty much 99% inhibition, and two hours later, the same. At four hours, it's starting to tail off, and by eight hours, that inhibition is gone. The gel's formulation is persistent and shows the same level of inhibition of bacterial growth throughout the course of this experiment. Of course, we don't do just single doses in the clinic, what I have on the next slide is a five-day multiple dose infection. What we have here then is, again, the same inhibition on the left-hand panel, a comparison of 5% gel and 10% gel, where you see that at the end of five days, they're fairly comparable. The dark blue is twice a day; the light blue is once a day treatment. You can see that 5% and 10% gel is very comparable. In the middle set of bars here is the 5% gel, where we've given an extra five days of the recovery. Again, we've seen fairly good inhibition. Just to summarize what we have then with Nu-3, we believe is that it's the right drug based on broad-spectrum activity, hits the resistant organisms and hits biofilm. It's the right application because it's local, so we get directly to the site of the infection. It's the right mechanism because it's rapid, and we believe has a very low potential for resistance. That's the preclinical data, the rationale for why we would want to go to the clinic. What I want to do now is describe a couple of early experiments that we have done in the clinic in human studies to support the further development of Nu-3. The first study was a safety study in normal volunteers; the phase I PATCH study. This is required by the FDA prior to treating patients, where you treat normal volunteers with the, in this case, a low concentration of the solution to see if there's going to be any irritation in the skin. Fortunately, there was no irritation, we were able to then move on to the next experiment and clinical study, which was an exploratory phase IIA study in patients with infections in their diabetic foot ulcer. The study was a duration of eight days. It's double-blinded, randomized, so no one knew exactly what they were getting. We used doses of 0.1%, 1% and 2% solution. We used 30 patients who were analyzed in the group. Of course, in an early phase II trial, your primary endpoint is safety. I'm happy to say that there were no drug-related side effects in this small trial. As a secondary endpoint, we look at pathogen reduction and ulcer surface area measurements. Our primary goal, of course, is to reduce pathogens and clear the infection. It was interesting to also look at ulcer surface areas because that's ultimately what you want to do, is to actually have the wound close as well. Wounds don't close unless they're clear of the pathogens. The trends for this showed the positive effect on pathogen reduction, and interestingly, a positive effect on ulcer surface area. That encouraged us to move forward. What we now plan to do, oh, by the way, we did switch from that solution formulation. I should've mentioned that we switched to a gel formulation because we believe that a gel formulation is going to have much better adherence to the ulcer, especially as many ulcers are actually on the plantar side or the bottom of the foot. The other advantage of switching to this gel formulation is it allows us to increase the applied dose, and that means we can cover all of that time kill data that I showed earlier on, all the in vitro MIC data and the in vivo doses. We're fairly confident in the doses that we selected. It's important to note as well that infectious disease animal studies are far more predictive of outcomes in human trials than most other therapeutic areas, which have very challenging animal modeling. Here are the current clinical studies that we are planning. The first one we plan to do is a phase IIA study. This will be a single-blinded, randomized study, and it's escalating doses that are run in parallel, 2%, 5% and 10%, which we expect to provide some kind of dose response, hopefully a positive dose response. The treatment is for 14 days, twice a day, followed by 14 days of follow-up with no treatment. Again, the safety evaluation is critical here. That will be the primary endpoint. We're also going to look at the infections, and we have a quantitative evaluation of infections, bacterial counts, and identification of the bacteria or the pathogens that are in there. We'll also monitor the signs of infection and wound size changes during the course of the study. This study is in preparation, and as we have announced, we engaged Perry as our CRO for the clinical trial. Today, we announced that the world-renowned expert in diabetic foot care, Professor David G. Armstrong, will be the chair of the phase II study, and he'll also serve as our scientific advisor for the DFU program. The expectation of an August 1st patient visit is what we're looking to do, and we're targeting the end of the year for completion of this study and readout. Pending, of course, a successful outcome, we plan to move to a larger phase II study, which will be a double-blind, placebo-controlled study using two doses in parallel. We'll plan a 14-day treatment again, compare once a day versus twice a day, and again by a 14-day follow-up. The exact protocol with doses and once a day versus twice a day and how to load those arms will depend largely on the outcome of the single-blinded study earlier on. All the elements of the phase IIb study have already been fully reviewed and aligned with FDA. We are fairly confident that we can move ahead. Once we get, of course, beyond phase II, and of course, assuming successful outcome of the phase II program, we would expect to conduct an end of phase II discussion with the FDA. We'll plan for at least two phase III trials, one in Europe and one in the U.S. To prepare for that, we would need to conduct additional clinical studies on skin sensitization at the chosen dose and assess the full pharmacokinetic profile of the topical Nu-3. We're also expected to do additional toxicology studies, such as carcinogenicity, reproductive toxicology. We'll need to consult the FDA exactly on what those studies would entail. We also have some additional CMC manufacturing work, which we require to completely define the commercial dosage form and any other manufacturing requirements that are needed to go into a phase III study. Those three latter elements we would conduct in parallel with the phase IIb, such that we are phase III ready. As also I discussed earlier on, we believe the commercial opportunity for this indication is large. There are a lot of diabetics, a lot of people with diabetic foot ulcers, and a large occurrence, incidence of foot ulcer infections. However, we'd like to do some additional work on that to refine the commercial opportunity for IDFU, as well as looking at other skin and soft tissue infection opportunities that could be targeted with the therapy, assuming we have the appropriate clinical evidence. This would include discussions with patient groups, physicians, payers, and regulators. We believe that the Bisphosphocin class can be considered as a platform technology with a potential to treat a number of other diseases. Because the class is amenable to a range of formulation opportunities for local application, including topical gels, solutions, and aerosols, we've looked at other indications. Aside from studying Nu-3 and its development in IDFU, we've conducted preclinical evaluations of several other members of this class, including Nu-8, Nu-10, and Nu-11. In clinical indications that are of interest, such as complicated urinary tract infections, specifically catheter-associated urinary tract infections, where we have shown in vivo efficacy in preclinical animal models with intravesical solution formulations. Also of interest are pulmonary infections, such as hospital, community, or ventilator-acquired bronchial pneumonia, and infections in cystic fibrosis, where again, we have shown in vivo activity in preclinical animal models of Pseudomonas, Aspergillus, and Acinetobacter infections with an aerosolized formulation of these drugs. We have a very strong IP position. We have a very robust portfolio, and we've actually just recently announced patent issuances for both formulation patents and composition of matter patents. In total, we have 71 issued patents, of which 27 are for formulation, 37 for composition of matter, and we have another 30 pending patents, which will take us, with some of their recent applications, extend through 2044, the earlier ones being through to 2038. We include the major geographies, U.S., Europe, Japan, China, India, and many others. Of course, the extension or the exclusivity does not include patent extensions that could be applicable with a good coverage of these compounds. We have a very experienced management team. Myself, 45 years in pharmaceutical. Peter Ceccacci, who's our CFO. Also, he actually has 25 years of experience in financing and accounting. Thomas Balzer, who is our Chief Medical Officer, also 30 years in the pharmaceutical industry. We also have a very experienced board with both Doug Manion and Joseph Tucker, who we recently announced as a new board member with direct experience in the pharmaceutical industry, and Joseph Tucker, who is in fact a CEO of a small biotech. Then Lenny DeRoma, who is a businessman and provides a lot of interest, useful background, and advice on how we do our financing and manage our company. In conclusion, we've discovered a novel, highly effective class of antimicrobials with Bisphosphocins. A broad-spectrum, rapidly cidal, with low potential for resistance. Local treatment gives us a great potential with low systemic side effects. We're advancing Nu-3 for infections in diabetic foot ulcers. We have a robust patent portfolio, and we have near-term milestones, which include the phase II trial as our proof of concept with a readout towards the end of this year. I appreciate all of your time today. To recap what's just happened to Lakewood-Amedex over the last two months since we became a public company. We've appointed a new board member. We've announced positive resistance data for our lead candidate. We've announced Perry as our CRO, announced additional data on the lead candidate in diabetic foot ulcers, IP for the formulation, IP for composition of matter, and again, just today, the renowned expert, David Armstrong, the study chair for the phase IIA trial. If you want to stay informed when we issue additional news, please sign up for our email alerts. Just go onto our Lakewood-Amedex Biotherapeutics website, the investor part of that, and sign up there and you'll get the news. I will stop there and take any questions. Okay, I have one question which I can read out. "From an investor's perspective, how should we think about the broader pipeline potential of the Bisphosphocin class beyond Nu-3? Are there follow-on candidates or adjacent infection settings already mapped out?" I would say to that, as I said earlier on, we do have indications for catheter-associated urinary tract infection mapped out. We have a whole discovery and development plan mapped out with financing that we need funding for, that would take us through to an IND, which would allow us to then go into human clinical trials in catheter-associated urinary tract infection. Similarly, we've got mapped out a plan for pulmonary infections, where we can take one of those compounds, Nu-10, Nu-11, or Nu-8, or another compound in our large set of molecules as an aerosol formulation into the treatment of pulmonary diseases. Yes. Then in terms of adjacent infection settings, we can imagine that if the proof of concept is positive, we could look at other infections in wounds, whether that be surgical wounds, burn wounds, even combat wounds. We have ideas about how we could advance all of those into different indications. Hopefully that will answer that question. Let me see if there are others. I have another one here. "As the company reported positive antimicrobial and wound healing signals in earlier Nu-3 work, what gives you the most confidence that those trends will translate into a clear phase II readout?" I would say that in moving from a solution formulation to a gel formulation, we're much more confident about the adherence of our drug into the wound. I would say also that we now have being able to go to up to a 10% gel formulation, that we have more than adequate coverage of the MICs and the time kill and the in vivo data. Again, that would give us more confidence that those trends could translate into that phase II readout. Another one actually is a very important question here we have. "This Bisphosphocin platform and the near zero resistance data we've highlighted seems pretty unique. How big an opportunity do you see in entering microbial resistance beyond the initial DFU indication?" As I said, I think that going into where you can treat locally, I believe we can invent or develop a formulation that can be applied. I see it has broad applicability to all sorts of infections. Some of the data that we've done, for example, to show this zero resistance was we tested against lots of different bacteria with very different mechanisms of action for resistance, whether that be cell wall modification or cell wall biochemistry modification, cell wall biogenesis modification, whether that be protein synthesis modification, also efflux mechanisms and membrane mechanisms. We have shown our compounds show equal activity against all of those mechanisms. We've also tried to induce resistance by doing a 21-day passage experiment at sub-MIC levels. Typically, that will lead to resistance emergence, and we showed that with a control experiment with ciprofloxacin, where it had a 2,000-fold increase in MICs being much more resistant. Whereas our compound showed very little resistance development, had the same MICs at the beginning of the study and at the end of the study. Interestingly also, we tried that ciprofloxacin-resistant organism against our compound, Nu-3, and it was very effective, just the same as for all other bacteria. I understand I've got pretty much to the end of my time; I will hand it back to the moderators. Once again, I thank everyone for your attention today, and please do go to our website and sign up if you want to get more news