Now, thank you so much for joining us today at this presentation. I'm Alice Nettleton, one of the associates from Tim Anderson's U.S. Large Cap Biopharma team here at Bank of America. We're excited to host Mineralys today for a 15-minute presentation, specifically Jon Congleton, CEO. They recently presented their first quarter results on Monday. Looking forward to hearing about some of the exciting updates from your data recently, as well as your first quarter updates. Over to you, Jon. Very good. Thank you. Very good. Thank Very good. Thank you, Alice. I appreciate the invite. I appreciate being part of the Bank of America conference. My name is Jon Congleton. I'm the CEO of Mineralys, where we're focused exquisitely on targeting aldosterone and cardiorenal metabolic conditions. I'll be making forward-looking statements. There we go. When I say targeting aldosterone, why does that matter? It matters because about 25%-30% of all hypertension patients have dysregulated aldosterone that, based on research and literature, I would say is linked to visceral adiposity. It's a shift from 40 years ago when I was a young sales rep with less gray hair is by about 5%-10%. There is some really interesting underlying biology that's driving this condition. The reason it's needed to be targeted is because there are not a lot of viable and highly utilized therapeutics right now addressing aldosterone. We're really pleased with, in the first quarter, the two pivotal studies that read out with really positive data that I think not only supports the thesis that aldosterone needs to be targeted, but that lorundrostat as an ASI and aldosterone synthase inhibitor is an ideal way to do that. We saw a 19 mm absolute reduction in our LAUNCH- HTN in the real-world study that I'll get into in more detail in a moment, and a 15-millimeter mercury reduction in the ADVANCE- HTN study, which is probably the most rigorous hypertension study ever done. We also have two proof of concept studies. We know that hypertension has significant overlap with a great many cardiorenal metabolic comorbidities. CKD is one that data will be reading out later this quarter. Our OSA study we initiated in the first quarter of 2025. Cardiorenal metabolic syndrome is and has been evolving as a thesis over the last 5 to 10 years. I think historically it was viewed as you treat hypertension, you treat diabetes, you treat CKD, you treat heart failure almost as independent entities. It is just as likely to go to a cardiology meeting and hear a talk about the kidney as you'll go to a nephrology meeting and hear a talk about the heart. There is so much interplay between these systems. Hypertension and diabetes are really the genesis and nexus points that link all of these cardiorenal metabolic syndromes together. Aldosterone, we have known for decades, is in a dysregulated state a driver of pathology. What I think has grown in appreciation over the last several years is the right side of this slide. The left side is the mineralocorticoid receptor interaction with aldosterone. That drives your sodium-potassium electrolyte balance. It basically controls water volume in the system and blood volume. The right side really drives fibrosis, oxidative stress, and inflammation. The issue is the only therapeutic you have available right now to affect aldosterone is a mineralocorticoid receptor. It blocks that left-hand mechanism, but in a compensatory response, drives aldosterone higher and perturbs the right side. The aldosterone synthase inhibitor class, one of which we think we're best in class, but there are three that are in clinical stage development, affect both sides because you're reducing the actual ligand that can drive those pathways. ASIs, aldosterone synthase inhibitors, have been a target of interest for big pharma for about 15 years. Merck, Novartis, Lilly had what I would call first-generation ASIs. They struggled with one really key point, and that's selectivity. The selectivity relates to being able to inhibit aldosterone versus not inhibiting cortisol. There's about 93% homology between these two synthetic pathways. You have to be very selective just for aldosterone and not affect or inhibit cortisol. Lorundrostat's data has best-in-class selectivity for that. We think it has an ideal half-life as well, 10-12 hours. What that translates to is within an hour of taking the drug, you pretty much reduce aldosterone below the lower limit of detection. That lasts from a PD standpoint for about 14-16 hours. The remainder of time, it actually comes back to about 30% of baseline, which we think helps mechanistically to clear potassium. You see reasonable selectivity from baxdrostat and vicadrostat. I think the half-lives are going to be what's going to be really informative as these programs read out clinical data. How does a longer half-life or a shorter half-life translate into efficacy and safety? I can tell you, based on our clinical program, such as LAUNCH, that 10-12 hour half-life and that selectivity has translated into a really, really nice and transformative clinical profile. LAUNCH- HTN is the largest hypertension study completed with an aldosterone synthase inhibitor. We tested two doses, 50 mg through a 12-week course and 50 mg with the option to titrate up. The titration point is important here because I'll be sharing some subset analysis where we can pool both arms because everybody's on 50 and haven't had an option to titrate up. This is looking at lorundrostat's benefit on existing background treatment. This study was really built for the primary care physician. This is the kind of practice they have. They may not be optimizing background meds, but this is how lorundrostat would be used broadly within primary care. About 40% of these patients in the trial were uncontrolled on two meds. About 60% were resistant to hypertension, had a good representation of African American, about 30%. About two-thirds were obese within this study. About 90% were either overweight or obese. The absolute change was significant, great statistical significance, but really clinically meaningful. At six weeks, you're seeing about a 17 mm mercury reduction absolute, which is what physicians fundamentally look at. Scientifically, you want to look at the placebo adjusted, which was nine, great statistical significance. A physician basically could take an existing patient who's not at goal, put them on this drug, and within six weeks see about a 17 mm mercury reduction. That is meaningful. It validates the need to target aldosterone, but certainly shows the value of lorundrostat. The nice thing is the effect's not only durable, but potentially improving over time. If you link it back to mechanistically, that may be that dual mechanism. The early reduction is likely related to diuresis. This continued durable effect may be some level of vascular remodeling. That's something we're going to continue to look at over time. We'll be reporting data at the European Society of Hypertension a week from this coming Saturday with more detail. We have looked at multiple different subsets: race, gender, age, eGFR level. That'll be reported on the 24th of May. We have previously shared that whether someone's on two meds, so uncontrolled, or on three or more meds resistant, you see a similar response. Very robust. This is at week six. Again, 16 mm and 17 mm mercury absolute reduction. There is also significant favoring as far as an odds ratio of getting to goal within six weeks. 44% of the patients versus 24% on placebo were able to achieve goal. That is getting to below 130 mm of mercury in office measurement. A significant benefit for patients that prior to this had not been at goal. Probably the biggest on-target safety profile you want to look at or safety marker, really there are four. Potassium is probably one of the key ones. We know these drugs are going to increase potassium. ACE inhibitors do, ARBs do, MRAs do, ASIs do. If you affect the RAS system and create diuresis to lower BP, you are going to shift that sodium-potassium profile. You want to be really mindful of what is the mean change. It was about 0.3 mmol per liter in this study, but also what are the incidental incursions above 5.5 and above 6. We see here two tables. One is the observed and then the other is confirmed. It is really important to confirm potassium measures because you have what is called factitious hyperkalemia. It is just an error in the draw. If you break red blood cells, you release potassium and you get a false read. The confirmed number is where you really want to focus. You are seeing an incidence of 0.6% or 3 out of 538 subjects had a confirmed reading above 6. In that case, you would just want to either dose-reduce lorundrostat or the background meds, but a really, really mild potassium profile. As anticipated, we saw this in the proof of concept. This has been seen with ACEs and ARBs. You lower blood pressure, you relieve the pressure on the kidney, that water hammer as it's called, and you see the eGFR come down. That is a good thing because absent reducing that blood pressure, kidney function is just going to progressively go down. When you relieve pressure, it goes down slightly and then it stabilizes over time. That is what confers a benefit to the kidney. From a safety standpoint, really clean profile, very well tolerated, 2.4% incidence of serious adverse events, 2.6% discontinuation rate. Really pleased with what LAUNCH- HTN speaks to the primary care provider. ADVANCE is part of this comprehensive program that we wanted to build out a dataset that enables lorundrostat to be part of the hypertension guidelines, but also speaks to the cardiologist. What we do here is we take patients off their background med and we absolutely optimize to HA hypertension guidelines, take high-dose medications, use smartphone technology to confirm compliance, and use 24-hour ambulatory to measure. At this point, we did the titration at week four. When I show you the pooled data, that will be at week four. You'll see the mix of baseline characteristics here. Very proud of how the team really efforted to ensure that we had proper representation of Black or African American. That is a very high-risk population for uncontrolled blood pressure. Again, a couple of things I'll point you to. We saw a very rapid pronounced reduction in BP. In this case, it's 24-hour ambulatory, 15 mm of mercury, sorry, 11 mm of mercury at week four, 15 by week 12. Again, you're seeing that rapid reduction, but then a pronounced durability and potential improvement over time. Similar to what we saw with LAUNCH, you're seeing an odds ratio above 3 of getting to goal. Again, this is within 4 weeks. And these are patients that are literally maxed out on what is currently available. So when the question is, well, do you really need another drug? You have all these generics, you've got a lot of different modes of action. When you max out the best of what is available and you still can't get patients to goal, this drug is helping those patients get there. And we know if you get to goal, you're significantly reducing your cardiovascular risk long term. The potassium profile here again, really modest change. We're seeing about 2% incidence above a potassium of 6. Again, it's an on-signal effect that you want to see to show that the drug is working, but you want to make sure that you're not having excursions that are too high above 6. Again, a very mild profile as it relates to that. As seen with LAUNCH, again, we're seeing a change in eGFR. Again, this confers a benefit to kidney function. Safety profile, very compelling. I'll point out one thing here, the discontinuation rate of 12%. We had an interesting finding early on in this study. This study started before LAUNCH did. We know that there's an interaction and made one with lorundrostat where there's an inhibition of that pathway. Creatinine shares that pathway. So there's this competitive transport. Creatinine gets falsely elevated. eGFR typically gets measured with creatinine. This interaction basically had some subjects with a more pronounced reduction in eGFR, and we had sites stopping patients because they were concerned. We went out and communicated to sites, this is a bit of a false read because of the competitive interaction with the transporter with creatinine. Said use cystatin C, and you see a quick course correction. Of those 12 subjects that stopped, 6 were due to the eGFR that we just had to convey the interaction with creatinine. I would take you back, I will not do it due to time, but if you look at the same number for LAUNCH, it was about 2.6%. It was just a matter of education. We do have, because of these overlapping comorbidities, we do have two proof-of-concept studies underway. The Explore- CKD is going to be reading out later this quarter. This is a 60-subject study, exceptionally well-powered because it's crossover design. Primary endpoint we're going to be looking at is change in BP. It is powered to show a clinically meaningful reduction. We will be looking at other markers of kidney function, most specifically change in eGFR, which at this point is very well characterized. We would anticipate a slight reduction in eGFR as we've seen previously. We're going to see how that translates into albuminuria and proteinuria. We'll look at 24-hour UA as well as UACR, and we'll also be looking at safety signals like potassium and sodium. Really interesting study. We initiated this in Q1. We're still accruing enrollment in this trial, so we're not guiding to top-line data just at this point. There's a huge overlap between overweight, obese, resistant hypertension, and OSA. This population probably has the highest cardiovascular risk profile of anyone. There's a lot of interesting data linking aldosterone to AHI, but more specifically that during those apnea-hypopnea events, you see massive spikes in blood pressure. We're actually going to be doing beat-to-beat blood pressure measurements and correlating those to those apnea-hypopnea events. This study, I think, will be really informative for not only the hypertension profile, but potentially for other indications like AHI as well as some cardiovascular benefits. Here is the pipeline that we have right now. We've now checked two boxes very positively with ADVANCE and with LAUNCH. The Explorer studies are forthcoming. The open label extension is really the final big piece that will enable the pre-NDA meeting that we announced during our earnings call Monday that will occur sometime in the fourth quarter. Stepping back, this is a highly genericized market. I started my career in this when it was a branded space. 60 million treated patients, 30 million still cannot get to goal. Some of that is due to compliance. Some of that is due to, are you on the right drug? Some of that is due to, are you on the right dose? Fundamentally, our two studies have shown when you weed out some of those yeah buts, there's about 20 million patients that probably are at risk of stroke, heart disease, or kidney disease. Those three are in the top eight of global burden of disease. We have not solved these problems. That's why I'm excited to be here driving this forward. Just very quickly, we put the profile of lorundrostat in front of cardiologists and primary care, 95% intent to prescribe. It speaks to the interest in this space, the need in this space, and the response to the profile of lorundrostat. Lastly, thrilled to be working with the team that we have. We did announce Monday, Eric Warren has joined us as CCO to help us really crystallize the commercial opportunity here as well as help with strategic partnering discussions. Lastly, cash balance, $343 million as of our Q1 reporting. I think I went over time a little bit. Hopefully not too bad. Happy to address any questions. Otherwise, I'll let you go to the pool.