Greetings, welcome to the Mineralys fourth quarter and full year 2022 earnings call. At this time, all participants are in a listen-only mode. A brief question-and-answer session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star zero on your telephone keypad. As a reminder, this conference is being recorded. It is now my pleasure to introduce your host, Dan Ferry of LifeSci Advisors. Please go ahead, sir. Thank you, operator. Good afternoon, everyone. Welcome to our fourth quarter and full- year 2022 conference call. Today, after the market closed, we issued a press release providing our fourth quarter and full- year 2022 financial results and business updates. A replay of today's call will be available on the investors section of our website approximately one hour after its completion. After our prepared remarks, we will open the call for Q&A. Before we begin, I would like to remind everyone that this conference call and webcast will contain forward-looking statements about the company. Actual results could differ materially from those stated or implied by these forward-looking statements due to risks and uncertainties associated with the company's business. These forward-looking statements are qualified by the cautionary statements contained in today's press release and our SEC filings, including our annual report on Form 10-K and subsequent filings. Please note that these forward-looking statements reflect our opinions only as of today, March 15th. Except as required by law, we specifically disclaim any obligation to update or revise these forward-looking statements in light of new information or future events. I would now like to turn the call over to Jon Congleton, Chief Executive Officer of Mineralys Therapeutics. Jon? Thank you, Dan. Good afternoon, everyone. Welcome to our first corporate update and financial results conference call. I'm joined today by Adam Levy, our Chief Financial Officer and Chief Business Officer, and Dr. David Rodman, our Chief Medical Officer. I'll begin with a brief overview of the business and recent milestones, followed by David, who will discuss our clinical programs. Then Adam will review our fourth quarter and full year financial results before we open up the call for your questions. The past few months have been a truly transformative period for Mineralys as we announced positive phase II proof of concept data for our product candidate, lorundrostat, our proprietary orally administered, highly selective aldosterone synthase inhibitor that we are initially developing for the treatment of patients with uncontrolled hypertension or resistant hypertension. As we will discuss in detail later on, these phase II data support the planned initiation of our pivotal program in 2023. Before we get to the updates on our program, I want to offer a few key points about our target indication, the therapies currently available in the market, and the unmet need among patients failing to achieve their BP goals with current therapies, which should allow you to see why we're so excited about this opportunity and our clinical data to date. To start, over 115 million patients in the U.S. have sustained elevated blood pressure or hypertension, and over 30 million hypertensive patients in the United States are unable to achieve their BP goal despite treatment. Within this population, over 10 million patients suffer from resistant hypertension, defined as failing to achieve goal on three or more medications. Furthermore, obesity, particularly when associated with visceral adiposity, is a major cause of hypertension, accounting for 65%-75% of the risk. Uncontrolled hypertension is a serious medical condition, as patients with hypertension that persists despite taking two or more medications have a significantly elevated risk of developing heart disease, stroke, and kidney disease. For example, it is estimated that uncontrolled hypertension patients have a 1.8 x greater mortality risk due to cardiovascular disease and a 2.5 x greater mortality risk due to stroke. Despite numerous options available to treat hypertension, including thiazide diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and mineralocorticoid receptor antagonists, the majority of hypertension patients require multiple therapies to achieve their target blood pressure. Also worth noting is that many of these therapies designed to address hypertension were introduced several decades ago, when the incidence of obesity was below 20% and abnormal aldosterone production affected less than 10% of the U.S. population. As a result, these therapies failed to adequately address the shifting biology of hypertension, particularly in the obese population with a body mass index equal to or greater than 30. Current guidelines, while well thought out, emphasize an empirical approach. In other words, mainly trial and error. While first and second-line treatment, often an ACE inhibitor or angiotensin receptor blocker plus thiazide diuretic, have general efficacy, they are often unable to normalize blood pressure. Third-line agents tend to produce only a 6 mm-7 mm mercury improvement. However, this incremental reduction does not always adequately enable patients to reach their blood pressure goal. Many patients require three, four, or more antihypertensive agents in an attempt to achieve their target blood pressure. In addition, while hypertension is an asymptomatic disease, many of the currently available treatments have side effects and tolerability issues which may limit their use. For example, patients taking ACE inhibitors often develop a chronic cough, and men taking spironolactone often develop gynecomastia, otherwise known as breast enlargement. Notwithstanding this significant and growing unmet need, there's been a lack of U.S. FDA-approved novel therapies targeting hypertension, with no new class of antihypertensive treatment approved within the last 15 years. There's also a heavy cost beyond that of the health of the individual patient, as estimates show that hypertension and related health issues resulted in an average economic burden of about $130 billion each year in the United States. This brings me to our late-stage clinical candidate, lorundrostat, a proprietary, orally administered, highly selective aldosterone synthase inhibitor designed to reduce aldosterone levels by inhibiting the enzyme CYP11B2, which is responsible for producing the hormone. We are targeting aldosterone because abnormally elevated aldosterone levels are a key factor in driving hypertension in approximately 25% of hypertensive patients. Our goal is to emphasize a precision medicine approach in the development of lorundrostat and identify predictors of enhanced response, a toolkit to inform when and how to use lorundrostat in order to help patients achieve their goal blood pressure. We began this journey of bringing targeted treatments to hypertension with our phase II proof-of-concept study, TARGET-HTN, which was completed last year. Top-line data from this study, announced in November 2022, show that we demonstrated the clinically meaningful reduction in systolic blood pressure with 50 mg and 100 mg once-daily dosing. We pre-specified certain variables to determine if they predicted an enhanced response in subjects. In this pre-specified analysis, we demonstrated that concomitant use of a diuretic yielded a 12.9 mm mercury placebo-adjusted reduction in systolic blood pressure with 50 mg once daily of lorundrostat. We also demonstrated that a body mass index greater than or equal to 30 predicted an even greater response with 50 mg once daily, yielding a 16.7 mm mercury placebo-adjusted reduction in systolic blood pressure. Given the rising epidemic of obesity, its correlation to abnormal aldosterone levels, and the risk of uncontrolled hypertension, we believe our phase II data offer a critical finding that we will further investigate in our pivotal program. In summary, hypertension remains an area of significant unmet need with significant implications to long-term patient health. The clinically meaningful reduction demonstrated in TARGET-HTN with lorundrostat represents a substantial benefit to the millions of patients struggling to achieve their blood pressure goal. At Mineralys, our goal is to develop lorundrostat in a novel, targeted manner with a toolkit to inform enhanced clinical response. Let me now turn the call over to Dr. David Rodman, Chief Medical Officer of Mineralys Therapeutics, who will offer a review of our clinical data and ongoing clinical program for lorundrostat. Dave? Thank you, Jon, and good afternoon, everyone. Today, I will provide an overview of trial results for lorundrostat, then provide an overview of the pivotal program that we're preparing to initiate in the first half of this year. As Jon touched on earlier, TARGET-HTN was a 200-subject, two-part, phase II randomized, double-blind, placebo-controlled, dose-ranging, multicenter trial designed to evaluate the safety, efficacy, and tolerability of orally administered lorundrostat for the treatment of uncontrolled and treatment-resistant hypertension. The study population was balanced for gender, age, body mass index, use of two versus three or more background antihypertensive medications, and baseline blood pressure, which averaged approximately 142 mm of mercury systolic. There was good representation by the African American individuals. Part one of the trial explored the dose and exposure response characteristics of lorundrostat. Part two was designed to study the effect of lorundrostat in individuals with normal to high renin levels. We were pleased to announce in November 2022 that TARGET-HTN successfully met its primary objective, reduction in systolic blood pressure assessed by automated oscillometric blood pressure measurement in subjects dosed with lorundrostat versus placebo for eight weeks. Placebo-adjusted reduction of 9.6 mm of mercury and 7.8 mm of mercury in the 50 mg and 100 mg once-daily cohorts with P values of 0.01 and 0.04, respectively, were observed. There was no advantage to splitting the 50 mg dose to 25 mg twice daily. This supported our hypothesis that the observed 10-12 hour half-life of lorundrostat was sufficient to achieve blood pressure reduction without a longer half-life that may have a greater risk of sustained potassium elevation. Secondary endpoints, such as diastolic blood pressure and 24-hour average nighttime and central blood pressure, were also reduced and supportive of the primary findings. Importantly, no observed effect on morning and stimulated cortisol levels was found, which is consistent with the 374-fold selectivity of lorundrostat for aldosterone versus cortisol production. Lorundrostat was well-tolerated with uncommon treatment-emergent adverse events, most frequently related to mild hyperkalemia. There was one treatment-related adverse event of hyponatremia in the top dose cohort, which did not require special intervention and spontaneously resolved after discontinuation of lorundrostat. In a planned analysis of factors associated with increased response to lorundrostat in part one of the trial, hypertensive subjects with obesity, defined as body mass index greater than 30 kg per meter squared, demonstrated significant reduction in placebo-adjusted systolic blood pressure of 16.7 mm of mercury in the 50 mg once daily cohort and 12.3 mm of mercury in the 100 mg once daily cohort. The obesity findings supported our hypothesis that dysregulated systems biology associated with crosstalk between visceral adipocytes and the adrenal cortex links obesity to aldosterone-mediated, uncontrolled, and treatment-resistant hypertension. In contrast, there were no consistent differences in clinical response to lorundrostat based on gender, race, age, or the number of baseline antihypertensive medicines. Although use of a thiazide diuretic in either a two or three-drug regimen was associated with greater blood pressure reduction, with a reduction in placebo-adjusted systolic blood pressure of 12.9 mm of mercury in the 50 mg once daily cohort and 10 mm of mercury in the 100 mg once daily cohort. In November 2022, we held an end- of- phase II meeting with the Food and Drug Administration's Cardiorenal Division to review our program, including the results of the TARGET-HTN trial, and discuss our planned pivotal program for lorundrostat in hypertension. We have designed our pivotal program and overall drug development program based on FDA feedback at this meeting. As a result, we intend to initiate the pivotal program for lorundrostat in the first half of 2023, starting with the ADVANCE-HTN trial. This is a randomized, double-blind, placebo-controlled pivotal trial in up to approximately 300 adult subjects to further define the safety and efficacy of lorundrostat. Prior to randomization, subjects will be transitioned to a standardized background treatment regimen consisting of an angiotensin receptor blocker, a thiazide-like diuretic, and if needed, a calcium channel blocker. If hypertension persists on the standardized regimen, subjects will be randomized to 1/3 cohorts and treated for 12 weeks. 1/3 of subjects will be randomized to placebo, 1/3 to lorundrostat 50 mg once daily, and 1/3 to lorundrostat 50 mg once daily, and then increased at week four to 100 mg once daily if blood pressure goal has not yet been achieved. The primary endpoint of the trial will be change in systolic blood pressure as measured by 24-hour ambulatory monitoring at week 12 in the two active arms versus placebo. We anticipate having top-line data from this trial in the first half of 2024. We also plan to initiate a randomized, double-blind, placebo-controlled, three-arm, phase III pivotal trial in the second half of 2023. The proposed trial is expected to have a similar design as the ADVANCE-HTN trial, except subjects will remain on their previously prescribed background regimen of either two or more antihypertensives, including a diuretic, maintained at the maximum efficacious or maximum tolerated dose level. Approximately 1,000 hypertensive adults will be randomized one to one to one to the same three regimens as in the Advance trial. Change in average 24-hour ambulatory systolic blood pressure will be the primary outcome measure. The top-line data from this trial is expected in mid-2025. Subjects from both pivotal trials will be offered the opportunity to roll over into an open-label extension. In addition to those trials, we plan on initiating a randomized, double-blind, placebo-controlled phase II trial in mid-2023 to evaluate the safety and efficacy of lorundrostat in subjects with chronic kidney disease, with top-line data expected in the first half of 2024. In summary, with the transition of lorundrostat to pivotal trials, we have the opportunity to develop the first built-for-purpose precision therapy for hypertension. Following the science, we designed the TARGET-HTN trial to not only establish the benefit, risk, and dose response of lorundrostat, but also to test if inappropriate production of aldosterone was a significant driver of hypertension in obese individuals. We found that inhibiting the production of aldosterone in the study population as a whole, and particularly in the subset of individuals with obesity, led to what we feel is a substantial clinical benefit. Going forward, our intent is to confirm the observations from TARGET-HTN and leverage the evolving science to allow us to implement a precision approach to the treatment of uncontrolled and resistant hypertension. I will now turn the call over to Adam, who will provide a financial review for the fourth quarter and the full year ending 2022. Adam? Thank you, Dave. Good afternoon, everyone. Today, I will discuss select portions of our fourth quarter and full- year 2022 financial results. Additional details can be found in our Form 10-K, which will be filed with the SEC later today. R&D expenses for the three months ended December 31st, 2022, were $7.8 million, compared with $6.6 million for the same period last year. R&D expenses were $26.3 million for the full year ended December 31st, 2022, compared with $16.3 million for the same period last year. The increase in full year R&D expenses was primarily due to increases of $7.4 million in preclinical and clinical costs related to the research and development of lorundrostat, $1.7 million for the clinical supply, manufacturing, and regulatory costs, and $0.9 million in personnel expenses for additional employees to support the research and development. G&A expenses were $2.2 million for the three months ended December 31, 2022, compared with $0.5 million for the same period last year. G&A expenses were $5.2 million for the full year ended December 31, 2022, compared with $2.4 million for the same period last year. The increase in full- year G&A expenses was primarily due to higher professional fees of $1.7 million related to accounting, legal, and other support and personnel expenses of $1.1 million associated with additional employees. Net loss was $29.8 million for the full year ended December 31, 2022, compared with $19.4 million for the same period last year. The increase was primarily attributable to the factors described earlier. Cash, cash equivalents, and marketable securities were $110.1 million as of December 31, 2022. In February 2023, we completed an IPO of our common stock for net proceeds of approximately $202 million after deducting underwriting discounts, commissions, and estimated offering-related expenses. With that, I'll ask the operator to open the call for questions. Operator? Thank you. We will now be conducting a question- and- answer session. If you would like to ask a question, please press star 1 on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star 2 if you'd like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. Please hold while we poll for questions. Our first question comes from Greg Harrison with Bank of America. Hey, thanks for taking the question, and congratulations on the IPO and all the progress. Maybe first off, just what are your thoughts on lorundrostat's future positioning in the market, and how are you thinking about differentiation versus MRAs that could put lorundrostat ahead of them as a treatment option? Yeah, Greg, thanks for the kind words. Nice to connect. As we think about the positioning for lorundrostat, it matches to a large degree the clinical development strategy. We're looking to identify basically a toolkit that could help predict enhanced response to lorundrostat and ideally in a third-line position. We've tested with both payers and physicians that combination of utilization at third line with predictors of response, which, you know, based on the phase II data that David just walked you through, could be a BMI over 30 that's gonna give you an even more enhanced response than we saw at the top-line data. It's why it's important to bear in mind what meta-analysis would indicate as far as what a third agent can provide in blood pressure reduction of 6 mm to 7 mm of mercury. If we can provide that double-digit reduction as a third-line agent, we think that becomes very compelling based on the work we've done with payers and that we've done with physicians in testing that target product profile. Why we also think the MRAs will not be competitive in that space is frankly, spironolactone, which is the predominant MRA used, has been around for 60 years. I think the market, as it relates to hypertension, has largely voted against the utilization. We know that in national market share data, it's about 2.6% of the hypertension prescriptions are for spironolactone, and it's largely for the off-target effects that have been an issue, such as gynecomastia, fertility issues with women, glucocorticoid steroid issues, and then lastly, hyperkalemia at increased doses to get the kind of efficacy that may be matched with lorundrostat. We believe that with the data that we're generating, the approach that we're taking, bringing a targeted approach, really enables us to bring a safe and highly efficacious drug into third-line treatment, where we think can really resonate and meet a lot of the unmet need as far as helping patients get to goal. Great. That's super helpful. Maybe just one more. What steps are you taking to maximize your chances of repeating the impressive data you've shown to date when you run your pivotal programs? Yeah. Greg, really good question. I wanna hand it over to Dave, but I first wanna give him kudos, both he and his clin ops team, because I think TARGET-HTN gave us a lot of information not only about lorundrostat but how to mitigate and manage the risk going forward into the pivotal program. Dave, do you wanna add a few additional thoughts as far as the learnings that are gonna be applied? Yeah. Sure thing. Thanks, Greg. First of all, we were quite gratified that the effort we put into the TARGET-HTN trial resulted in very precise measurements. We had a placebo effect of 4 mm of mercury with the automated oscillometric blood pressure and close to zero with 24-hour ambulatory blood pressure. For the next trials, we're gonna use 24-hour ambulatory blood pressure as the primary outcome measure. That's been a trend in other trials, and it was discussed with the FDA at our end- of- phase II meeting, and we got agreement that that was the proper endpoint. I will say one other thing that we're implementing is to have very good data on adherence, so compliance with both the background regimen and the experimental therapy. We're using some technology advances that are fairly recent that are gonna allow us to know in quite good detail on a real-time basis if the subjects take their pills and what time of day, so that we can immediately intervene. I think those two things, compliance and a more precise way to measure it, lead to an even more precise point estimate of blood pressure response. I'm confident that the trial will deliver very appropriate and accurate results in the first half of 2024. Great. Thanks again. Thanks, Greg. Thank you. Our next question comes from Umer Raffat with Evercore ISI. Hi, guys. Thanks for taking my question. I have two very quick ones here, if I may. First, I saw you guys posted a new trial today. I don't know why I thought the primary endpoint would be SBP, and I know that's ABPM, which is obviously a more robust endpoint. I was curious if, A, how you thought about that, and B, should we expect ABPM to be the primary endpoint you guys run with in future trials, including pivotal ones as well? Thank you very much. Well, why don't I take that question too? A good question. We had discussions with our the principal investigators at the Cleveland Clinic, our clinical advisory board, and then took that to the FDA to get a consensus on this. It was clear that the consensus was that while either AOBP, so office systolic blood pressure or ABPM can be used to register drugs that, the preferred one in 2023 is to use 24-hour average ambulatory blood pressure. For that reason, we chose it for this study as well as future studies that we've got plans to initiate later in the year. Yeah. Umer, just to clarify, the study that went up on ClinicalTrials.gov today is the first of the two pivotal. As you noted, it has 24-hour ABPM as the primary. The phase III that's intended to get underway in the second half of this year will have the same primary endpoint. Thank you very much. Thank you. Our next question comes from Annabel Samimy with Stifel. Hi, guys. Thanks for taking my question. Just to follow up on a couple of things that you mentioned. First, when you talk about the toolkit that you're gonna be using to be able to identify the right patients to put this in, is this strictly gonna be, I guess, a clinical assessment based on weight or resistance level, or are they actually gonna be testing for aldosterone? What are the types of things you might put in this toolkit? I guess that's the first question. Just to follow up on the ABPM, I know you mentioned it, but can you just remind us the difference between the in-office measurements that you conducted and the ABPM that you conducted? What's the magnitude of difference that you saw between those two measurements, just for us to sort of have a frame of reference? Yeah. Annabel, good to hear from you. I'll go first, and I'll actually take the second question, then I'll have Dave speak to the first one. We really saw pretty concordant data, Annabel, between the AOBP, which was at the in-office measurement, and the 24-hour average reduction. Both were in the double-digit neighborhood. You know, with the 50 mg in the AOBP, we saw about a 9.6 mm mercury placebo-adjusted reduction, and we saw about a 10 mm mercury placebo-adjusted reduction in the 24-hour average. That was replicated in the central BP as well as the nighttime benefit. That's why we were, you know, I was really thrilled that the team had the forethought to do both measurements, was very supportive, very concordant, and it gives us a good sense of what to expect going into the pivotal program, having done it in the phase II proof-of-concept. Let me turn it over to Dave to give you some thoughts on the toolkit and what we know so far, and what we're looking to continue to gather. Yeah. Great question. In terms of a hierarchy, because we had such a strong signal when we used obesity as a categorical variable, in other words, we just said, "If you're obese with a BMI over 30, what's your response? If you're non-obese, what's your response?" We saw fairly dichotomous results. There was a very high response rate with a robust reduction in blood pressure in the obese patients. In the non-obese patients, there were some individuals who responded, but most had a modest response or no response. Your question is very interesting. First of all, as a clinician, knowing that obese patients are hard to treat, having just a predictor like obesity, and we'll expand it to waist-to-hip ratio, which is more directly a measure of visceral adipocytes. That by itself will be an extremely useful precision tool. It sounds low- tech, but in fact, it's gonna deliver great benefit with a highly enriched responder population. We aren't gonna stop there, and your question about aldosterone is an interesting one. We looked at spot measurements of aldosterone, and like everyone else, we found that they were extremely variable and somewhat difficult to use. We're gonna be implementing 24-hour urine measurements of aldosterone going forward in the next trials, and we'll explore that question you asked. One important issue to remember though, is that there are interindividual and ethnic differences in the response, the sensitivity to aldosterone, so it's not just the aldosterone level. I think we'll see something there, but I don't know that it will be predictive enough. We are also gonna explore other biomarkers related to the abnormal positive feedback loop that's generated between visceral adipocytes and the adrenal gland. One of the important ones is leptin, which we, which has been shown to increase aldosterone production, and we anticipate that increased leptin will be associated with an increased response to therapy. We'll be looking at many other potential, find, you know, additional measures that could be useful, particularly in the subjects who aren't obese but might benefit from the drug. Got it. If I could just squeeze in one more, as you're thinking about, the trial in the CKD population, this is a CKD population that has uncontrolled hypertension. Is this meant to be a proof of concept to move into other cardiorenal indications, or is it just to specifically look at this CKD population? I think it's- Hypertensive population. Yeah not the CKD. Annabel, we wanted to get a, you know, a sense from a profiling standpoint, what lorundrostat would do in a population with a more compromised renal function. We'll be looking at, you know, the eGFR 30-45. The two pivotal studies will be going down to an eGFR of 45. We anticipate that study getting started mid-year, we'll be able to provide updates on that study in more detail, probably at the May earnings call. Great. Thank you. Yeah. Thank you. Our next question comes from Rich Law with Credit Suisse. Please go ahead. Hey, guys. Congrats on the IPO from me as well. A couple of questions for you. Can you give more information about that CKD profiling study? What's the study size, and what is the power to show? Is this study pivotal? If so, like, what does it add to your potential indication or label that you wouldn't be able to otherwise? I have a couple more follow-up questions. Yeah, Rich, thanks. Thanks for the kind words. As I noted to Annabel's final question, we'll have more details in May. The predominant goal of that study is to get characterized response in a special population, and that's with reduced kidney function, again, in that 30 ml- 45 ml per minute per 1.753 meter squared measurement. You know, we'll talk about size in May as we finalize that. You ask, is it pivotal? I think it's probably part of the package to be able to provide additional data, again, in a patient with more compromised renal function. Again, we'll provide more data, more details in May. Okay, great. The other question is, given the mixed results that we saw in the non-obesity patients, and I think David mentioned it a little earlier as well, why not just use obesity as an enrollment criterion instead of a pre-specified analysis? If not, like, will you expect the non-obesity patients to perform better than your phase II study showed? Yeah, that's a great question about design. Because those studies were small, we really want to replicate and confirm the results. Excluding obese patients from the trial would, first of all, preclude us from doing that. Quite honestly, the FDA just wouldn't allow that kind of a design. Instead, what we can do is in a larger trial, like a phase III trial, we can get really into the granularity. For instance, when we say that non-obese patients don't respond, that's not true. It's a continuous variable. If you have a BMI of 29.5 or you have a BMI of 30.5, those two people are going to have a similar response. It's going to be less than somebody with a BMI of 40 and more than somebody with a BMI of 20. By going into a much larger group, we can look at that as a continuous variable as well, as well as look at our toolkit, which includes potential biomarkers, to get to a point maybe where what we could tell a clinician, and this is just hypothetical, is, yes, if you have an obese patient who's failed two drugs, then you should probably think about using this drug because it's likely to have a very good response. On the other hand, we can also say, if you have a patient with a BMI less than 30 who's also having difficulty with blood pressure control, then you can try the drug, and we'd like to have it be better than empiric. In other words, just give them and see if it works. We're going to continue to explore other biomarkers, largely, as I mentioned, with an idea towards pulling out those people who have super responses but they're not clinically obese. They are just physiologically obese. Got it. That makes a lot of sense. If you may, I'm just going to squeeze in one more question. Can you, for the pivotal study, will you include any cardiac imaging or structural-related endpoints? Thank you. Yeah. Great question. Right now, we don't have plans to do that. We're open to the idea of a sub-study to look at that. We'll be talking with external experts on whether there is a proper plan to do it that way or to do it simply as a small, standalone trial. There's no plans to do that at this point. Operator, are there any other calls? Our next question comes from Mohit Bansal with Wells Fargo. Oh, great. Thank you for taking my question. My congratulations as well on the IPO. I have one question because, I mean, you have been mentioning the drug really works better among obese patients. The way we think about it's possible that this drug may have some usage in earlier lines of therapy as well if it can be shown that there's a subset of patients who benefit more than others. In that context, what would it take for physicians to use this drug among obese patients more, and maybe in earlier lines? Do you have to run additional trial or subgroup data enough? I mean, how do you convince the doctors that this is a subset where you need to use this drug earlier than anyone else? Anything else? Yeah. Mohit, this is Jon. I appreciate your question. I think our view is, based on the market need, based on just the dynamics of a highly genericized space and the multifactorial nature of hypertension, that a launch profile for lorundrostat, as third line with an informed toolkit of where to really predict enhanced response, is the way to enter the market. That doesn't mean that there may not be an opportunity for second-line use or maybe even first-line use. I think that's going to be part of the stage development for lorundrostat. I think we've got a clear signal coming out of TARGET-HTN that there is a segment of patients that can have a very clinically substantial response to lorundrostat on the backbone of, say, an ARB, and we clearly saw an interaction with a diuretic. We're looking to move into the pivotal program informed by that proof of concept study, giving us a sense of de-risking moving into a replicate population in the phase II pivotal with a standardized background of an ARB and a diuretic, and in some cases, a calcium channel blocker, and with their existing background into phase III. That's, that's our view of entering the market. It doesn't mean this drug will not work earlier. We just think that's going to be part of the life cycle development of this program as we advance it. Got it. If I can squeeze one more in. In your trials, you are combining the uncontrolled and resistant hypertension patient population. Is there any difference in terms of the physiology of these patients, where, you know, a drug like yours could work better among uncontrolled, it is easier to show benefit among uncontrolled versus resistant or vice versa? That's a really interesting question. Now, looking at the TARGET-HTN study, we certainly didn't see any major difference between whether the subject was on two drugs or three drugs. Obesity and use of thiazides were much bigger predictors. We'll be diving into that, though, in much more detail. We had a 50/50 split in those kinds of subjects, two versus three or more in TARGET-HTN, which gave us great visibility into your question. We're gonna be looking at that in more detail in these larger studies. I think what we'll find is that it doesn't matter, but that it's probably quite reasonable to say that after you've failed to be controlled on an ACE ARB and a thiazide, if you put, you know, all of the generics in a row and our drug, it's much more likely, based on our data, you'll respond to our drug. It's a matter of saying that right now, the guidelines tell you it's totally empiric. Essentially, what we call an N-of-1 office experiment in each individual, which is a very poor way to do it because blood pressure is quite variable. We think that by giving them a toolkit, we will be able to get through that hurdle of the sort of randomness of empiric treatment and the really transformational potential for precision medicine. I think I'd just add. Sorry. I'd add one point to that, Mohit, is as we've had dialogues with the FDA, they don't really view the world as uncontrolled or resistant. It's for the treatment of hypertension. From our standpoint, you know, we wanna make sure we respect the medical community that wants to know what drugs do in resistant hypertension. That's why those groups are in our intended populations. We're really interested in the biology and trying to understand where aldosterone is in a dysregulated state and can exquisitely respond to a highly selective aldosterone synthase inhibitor like lorundrostat, regardless of whether they're failing to get to goal on two or three or more background meds. Got it. This is super helpful. Thank you very much. Appreciate it. Sure. Thank you. There are no further questions at this time. I would now like to turn the floor back over to Jon Congleton for closing comments. Thank you, operator, and thank you to everyone for joining us today. We're very excited about the progress we've made over the last year, and we're enthusiastic about the upcoming milestones for 2023. We look forward to updating you as our pivotal program for lorundrostat continues to advance. With that, we'll close the call. Thank you. That does conclude today's teleconference. You may disconnect your lines at this time. Thank you for your participation.