Good afternoon, welcome to the Jefferies Global Healthcare Conference. My name is Nick Pecora with the Jefferies Investment Banking team, and it's my pleasure to introduce Eric Easom, CEO of AN2 Therapeutics. Thank you very much. Glad to be here today. Get started. Forward-looking statements, I'll be talking about things that have forward-looking statements, please take that into account. All right. Just to introduce AN2 Therapeutics, we are a boron chemistry company. We do R&D internally and develop our own pipeline. We have a broad pipeline. We have three clinical stage assets now that are in phase II proof of concept study. Two of those do not have any FDA-approved drugs for the indications. I'm going to go through those. The immediate projects we're working on are polycythemia vera or PV, we're going to go into depth a lot about each one of these. PV is our latest addition to the pipeline, there's a lot of excitement and potential around that program. Mycobacterium abscessus is a nontuberculous mycobacterium, kind of [teria] family of diseases. There are no FDA-approved drugs for that. We have an oral project that I'll also be speaking about. Then the third one is for Chagas disease. This is a parasitic infection where parasites go into your muscle tissue, most particularly the heart, and cause quite a bit of cardiac issues in patients. We'll talk about that as well. We put out a press release this morning about our phase I data and also efficacy data in non-human primates, which is quite exciting and moving forward into phase II. Near term, we're going to have data on all three of these programs, and we'll be sharing that as soon as the fourth quarter of this year and throughout next year on all these programs. We have a number of research programs that are driven, again, by our boron chemistry internal capabilities, and we have two oncology programs, one in PI3 kinase, and then one in ENPP1. I'm going to go through all of these here today. In terms of milestones that are coming forward, so with PV, we're in the process of getting a phase II study off the ground, and we'll be initiating that in the third quarter of this year. We'll have data later this year and primarily into next year, where we'll really have a lot of proof of concept in an open-label, multi-part study. This is a big market opportunity. It's already a well-validated market with other competitive drugs, and so we'll talk about how we position into that in a bit. For Mycobacterium abscessus, this is an infection, a bacterial infection, chronically in the lungs. We have initiated a phase II IIT study with a number of prominent key opinion leaders in the U.S. We expect data next year. This is fairly large. It's orphan, but in terms of large market potential opportunity here, there's 15,000 patients in the U.S., 50 kind of in major markets. We'll go through some of the detail, but we've got lots of readouts here on that. Chagas disease, we just this morning put out a press release with our phase I data showing good PK and safety profile that supports phase II studies. Importantly, we also put out non-human primate data, which get naturally infected. This is about as close to proof of concept as you could get. We're excited about that. We'll be starting a phase II later this year. We'll have top-line data around third quarter of next year. There's 10 million Chagas patients in the world with parasites in their heart muscles. You can imagine this is a really bad disease. There's no FDA-approved treatment for this. In the U.S., there's about 300,000 estimated patients, potentially much higher. We don't really measure it and don't know. These are projections of the vector that transmits here in the United States. I'll go through a lot more details, but it's much more common than you think. We have the two cancer projects, which I'll spend a little less time and focus more on the clinical for today. All right. For PV, we are studying our drug oral epetraborole. This is in the process of starting a phase II, which we intend to get going in the third quarter. It's an oral treatment. It's targeting red blood cells only, so it's very specific to red blood cells, and we have a lot of clinical and pre-clinical data that enable this, and I'll go through that in a bit. That really shows that we've got lots of data that has potential. We're going to run this study to show that in PV patients, we believe we'll get the same effect. The goal of treatment. With PV, there's two primary goals. These patients have essentially excess red blood cells, and your blood coagulates and thickens and causes the potential for thrombotic events. There's two kind of known clinical measures that physicians try to control in patients. One of those is hematocrit. Being able to control the amount of red blood cells that a patient has is one of the critical parameters that increases the risk, or decreases in the case if you control it, potential thrombotic events, which is the real risk to patients. They have other symptoms. They have enlarged spleens and other fatigue associated with the treatments, because oftentimes the treatments are frontline therapy as phlebotomies and other agents that cause off-target cytoreductive agents, that cause off-target activities. You want to alleviate symptoms and ultimately to reduce the risk of some kind of a thrombotic event, stroke, et cetera. This is the high risk for patients. Patients have mutations in JAK kinase, which basically signal to progenitor cells to produce a lot more red blood cells than are necessary. That's the fundamental cause of this. By having a red cell-targeted therapy, it's not a broad cytoreductive agent that reduces red cells, white cells, much like an oncology- type of agent. You can treat the disease potentially without having all the side effects and have a much better quality of life for patients. Currently, they use phlebotomy or bloodletting frequently in patients. Patients that we'll be studying in our trial have at least three phlebotomies every 24 weeks. It's pretty common. You're taking multiple phlebotomies, and then they use low-dose aspirin to control platelet production, which is the other high risk besides hematocrit. Those are the two clinical therapies that are used. Then cytoreductive agents, as I've said, they use hydroxyurea and other agents to try to control the red blood cells. The issues oftentimes are you hit other cells besides just the red cells. All right. As I mentioned, we have lots of enabling data. These data are from epetraborole. We studied it in nontuberculous mycobacteria patients. You can see that hematocrit, the EBO is the blue or dark line, 500 mg once a day. The red line is basically background therapy or placebo. You can see a nice reduction in hematocrit over the first four weeks. Then it kind of plateaus. Over the course of six months and even longer in these patients, there was over 100 patients, you get a 10%-12% reduction in hematocrit or 4 percentage points. As soon as you take therapy off, it returns to baseline. This shows the very specific nature. It's stepwise. This is what you want to see in this type of patient. Patients who have high hematocrits, the idea would be you'd phlebotomize them or reduce them to lower than 45%, which is in the normal range, and then be able to maintain them rather than having to continuously do phlebotomies and reduce, and they're very fatigued. Then they eventually eat their way back up to high hematocrits, and then you have to phlebotomize them again over and over for the rest of their life, essentially, is how it's treated. If you had a medication that could do this in a very controlled, red cell- targeted way. These are the enabling data from non-PV patients. The goal of our phase II study is to show that in PV patients, we see a similar effect and that we can control hematocrit. We also have replicated these results in many other trials. On the left-hand side, you're seeing a one-month phase I study at multiple doses of epetraborole. You get this is just kind of zeroing in on the first month, but you can see a nice, not really rapid drop like you might see with cytoreductive agents, but a good, fairly rapid rate to get it under control. Then as soon as you take off the drug, you get a return back to baseline. On the right-hand side, these are long-term chronic tox studies in NHPs that were done. These doses are in doses for NHP. For effect, one of the questions we always had was at high doses, so at 450 mg per kilogram, that's equivalent of 4,500 mg once a day oral. It has the same shape. There's not this bottomless drive hematocrit down too low. Here you're seeing maximum of a 6 percentage point, which is a pretty big drop in hematocrit, and then returning to baseline. That was the NOAEL dose on this study. We've seen it repeated. Whoops. In terms of specificity, white blood cells, a lot of these agents will also have effects on other cell lines. You ideally wouldn't have that. You'd have a red cell- specific, like epetraborole. We see nothing in this same group of 105 patients in white blood cells compared to placebo. You see a slight mild increase in platelets, nothing of concern here at all. This is again, the kind of profile you'd want to see. As I mentioned, there's two primary clinical pillars that physicians want to try to achieve to reduce the thrombotic event. One of those is hematocrit control below 45%, the other is platelet reduction. You can see with current therapies, this was done in a large study that less than 57% of patients after three months were not controlled with current therapies. Given that it's the biggest treatment goal and that you have 57% of patients are not well-controlled, there's still a significant unmet need to try to control hematocrit in these patients. That's why we need additional therapies to do this, like epetraborole, and having an oral red cell- selective agent would be ideal that has minimal titration. Other drugs in this space have kind of onerous titration schedules, they're slow acting, and they have ultimately tolerability and other issues. There's a big need, I think, for more tools to help patients reduce the thrombotic risk, and that's where epetraborole would fit in. Okay. In terms of the study, we're doing the phase II. We'll have essentially three parts. The sentinel group will start in the third quarter of this year. This is open label, both the sentinel and then this part one are open label. The sentinel will look at 10 patients at a very low dose. We've never dosed a PV patient, so we want to go in, we're dosing at 250 mg every other day just to look at safety, PK, make sure everything lines up. Then we'll enter into this dose titration where they would start at 250 mg once a day and then individually titrate patients to the control that they need. If you need a little more, you could go to 500 mg once a day or 750 mg once a day, and we'll analyze all that data. Ultimately, we'll randomize patients in part two to a placebo-controlled trial where we can incorporate more subjective measures like PROs that measure fatigue and other elements that come into play in addition to lowering phlebotomy needs for these phlebotomy-dependent patients. I should have mentioned, these are going to be phlebotomy-dependent patients that have three or more phlebotomies over the previous 24 weeks, and they can also be on a cytoreductive agent, and you would add epetraborole on top of that to show that we can control hematocrit. We'll have data throughout later this year, potentially on the sentinel group. We may not see a lot of efficacy given the low dose, just as kind of a starting. Really in the dose titration throughout the early part of 2027 into mid-year, we'll have a lot of data coming out of that part one open label that we'll be able to share. Okay. I just covered the data readouts there. All right. Going to our next program. Mycobacterium abscessus is part of the nontuberculous mycobacterium lung disease. This is a chronic infection that essentially affects the bacteria that affects the lungs. It is a related bacteria to tuberculosis, which is transmitted human to human. Abscessus is a environmental pathogen that you pick up in soil. It's in hot water heaters, hot tubs. That's where the exposure comes from, and ultimately, you have a much higher five-year mortality. It basically deteriorates the lung function. They become very fibrotic in cavities and ultimately is detrimental to lung function. It's chronic. It's very serious in patients. There's about 15,000 of NTM patients in the U.S. It's mainly older, mainly post-menopausal women, but also men can have it. They often have comorbidities with COPD and other lung diseases, and there are no approved therapies from the FDA. The real catch here, I think, is that patients who have this, they end up having a lot of coughing, breathing difficulties. They're very fatigued, and it's just a race to the bottom over time. Basically, old antibiotics are used, and in abscesses, the drugs that work are IV antibiotics. You have to take IV infusions every day, multiple- drug cocktail. Think of oncology type of a treatment. The idea of having an oral therapy as kind of backbone to this regimen, and ultimately an all-oral regimen, would be a huge advancement to patients and their quality of life, and hopefully you can kill the bacteria and get them back to normal. epetraborole has shown great promise in this area, and particularly for Abscessus. We have its differentiated profile I've mentioned. It's a novel mechanism, so there's no pre-existing resistance. Many of these drugs have been used for decades, and patients have developed resistance. These patients are often, as I mentioned, treated for months and years on end, like multiple years. There's a real potential to develop multi-drug resistance, which is why they're dosed in these cocktail combinations. We think we have a good safety profile. Oral would be great for patients. The trial we're running is a 84-patient trial. It's being run by, the PI is Kevin Winthrop, one of the primary authors and world experts in this space out of Oregon Health Sciences, and a number of other prominent physicians who also treat many patients in the U.S. We have microbiological and PRO endpoints, We've done extensive PK/PD dose selection for this study. Oops. I'm stuck on this slide here. Hang on. There we go. Okay. Another important part is we've tested a number of clinical isolates that came from patients' lungs, We look for how potent our epetraborole is against these Mycobacterium abscessus pathogens. You can see here we are really potent against over 100 isolates. It's got a really tight range. For those of you who've been following our story, we also did a MAC trial in really severe, advanced, late stage refractory MAC patients. The MIC90s in those cases were 16 μg/ml and 32 μg/ml. Here we're over 250 times more potent against the bacteria, which is important in PK/PD. The patients we're studying are naive, so they're going to have minimal cavities. We're doing all this in early-stage patients to really show the antibacterial effect, and then we would go into further studies. I may need some help on advancing the slide here too. Oh, here we go. Here I've got on the next two slides, a number of animal studies. We've done these with a researcher at Johns Hopkins. We compare ourselves to imipenem, which is one of the IV-only antibiotics that is considered to be the gold standard. Here you can see our oral drug compared to a control, which is shown in the green, is we show efficacy that's similar or almost as good as the best drug that we have for this, which is this imipenem IV antibiotic at two doses. This was super exciting to the researcher at Johns Hopkins because they've never really seen an oral drug to be as effective as their best drug they have for this disease in animal models. On the next slide, there's one other oral drug that's in development now, called omadacycline. Here you can see this drug has performed a phase II, shown very positive data, and is starting to be used more and more in abscesses patients. It's a drug by Paratek. You can see our drug in the same animal models is cidal versus a more static profile in terms of bacterial killing. We've got a very effective against a drug that's been shown to have very good phase II activity. It gives us more confidence that our phase II data will be on track. We're doing two dose groups in the phase II study, so you can see here, and it's already started. We've started dosing. We made an announcement in the first quarter, and we'll have data late next year for this study. That's what I just mentioned there. Okay. The next one that I really want to highlight is Chagas disease. Chagas disease is a parasitic disease of muscle, but the muscle that gets you in trouble is the heart. These parasites, you get bitten by a so-called kissing bug, is the common name. The kissing bug transmits parasites. They go into your muscle, and they live silently. This is really a silent killer of patients. They live in the heart for years and years, and they cause inflammation and fibrosis in the heart, and then you ultimately end up with heart failure in about 30% of the patients, or patients dropped out of an aortic aneurysm, is the endgame, and about 30% of patients have serious outcomes. It also affects the GI and other parts. Our drug, AN2-502998, is a drug we discovered. It's an oral therapy that's used. There's 10 million Chagas patients. There's not a drug approved by the FDA for chronic Chagas, and there's 300,000+ patients, as I mentioned. This is a real unmet need. Many people don't know this, or they think of it as more of a global health issue, it's really an entire Latin America, or the Americas, including North America, and I'll show you some distribution. This just shows a patient heat map, if you will, or a map of where you see concentration of Chagas disease all over the United States. This is where patients, the estimates have come from. They're in the most populous states and also where there's a lot of Latinos, including California, Texas, Florida, the South. The kissing bug vector, the other thing I want to mention is there's infected kissing bugs that exist pretty much from Indiana across the U.S. and South. The vector is right here in the United States. It's in Central America and South America. It's a real serious problem. We have no idea really about transmission. It's not measured. We don't know that much about it, but we do estimate there's 300,000 in the U.S., a couple hundred thousand in Europe, in Spain, Portugal, places like this. Our drug, there's two drugs that are approved for more of an acute pediatric form of the disease. When you first get bitten, you get a mild flu-like disease. It's rarely, if ever, noticed and missed, and 99% of the patients have chronic form of disease that causes the serious heart. These drugs can be used, but they're not very effective, and they have a lot of safety and tolerability issues in older patients. Our drug hits a novel mechanism of action, CPSF3. It's involved in mRNA processing, and so this is completely enabled by our boron chemistry. We have a sister drug that we're part of the discovery for another trypanosome disease called African sleeping sickness that just showed phase III data of 96% cure in patients with that disease and has been recommended recently by EMA for approval. We know this mechanism works in t rypanosome diseases and so forth. Importantly, and what we mentioned this morning is we've run a third monkey study. The one I'm showing here is two months of dosing. This was the first one we did. This was done at a prominent cancer facility in Texas. They have primate colonies that they use for medical research. Here you can see the blue line is we were able to cure parasite cure or sterile cure, which is critical because if you don't kill all the parasites, they will recrudesce and come back for out to a year, and we even tracked these with our researcher, Rick Tarleton, at the University of Georgia for multiple years. We know we cure these monkeys of parasite. The middle line there is benznidazole. That's the one that's approved for acute disease. It doesn't work very well in this model, and it's similar results in human. Then you have pretty severe toxicity issues that make it almost impossible to treat patients. Then the bottom line is just there to show, Eisai Pharmaceuticals and also Merck had a compound similar to this, both failed in clinical trials, and you can readily see it in this monkey model. This monkey model is not really a model. It's a natural infection by the kissing bug with genetically diverse parasites, and so we're able to cure. We have high technical confidence, and the data we announced today was 28 days, so we plan to dose in the human study for that. Basically, this just goes into more detail about the monkey model. All this is available in our corporate presentation, so I'm going to, for speed, skip forward a few slides here. The other point that we try to make is that Chagas disease is the closest example we can give is like hepatitis C. Hepatitis C in the United States was a major problem. About 30% of patients develop liver disease, liver transplants, liver failure, liver cancer they end up with. Chagas is about the same, except it's the heart, not the liver. It's smaller. It's about 1/10 of the size, 300,000 versus 3 million. As you may recall, the hepatitis C market was a $200 billion-$300 billion market. We think we have a real opportunity here not only to help the 10 million patients with a drug that can actually cure the parasites and help the disease, but in the U.S. and in other major markets, there's a significant market opportunity that we're working on that is not really out there. We've got the phase I data in NHP we just announced today. We'll initiate a phase II later this year, and then we'll have top line around third quarter of next year on this phase II study. Here, just to summarize, we've got three phase II programs that are going to read out data starting later this year and throughout next year. We have a lot of value creation, a lot of risk mitigation, a lot of potential to help patients with really serious diseases. Because we're a boron platform and we follow a lot of biology, we've also got a couple oncology programs I'll just quickly highlight. One's a PI3K. We have our compounds that we are going to bring forward into development that we think are pan mutant specific, more in the [cinovation] mode, if you think about it, versus a Relay compound that's kinase-centric. Then we have an ENPP1 program for oncology. I think I'm out of time, but I'll leave it there, but lots of good work going on, and we're excited about all of this. Thank you.