Good afternoon, and welcome to the WindTree Therapeutics Investor Presentation. At this time, all attendees are in a listen-only mode. A question and answer session will follow the formal presentations. If you'd like to submit a question, you may do so by using the Q&A text box at the bottom of the webcast player. As a reminder, this call is being recorded, and a replay will be made available on the WindTree website following the conclusion of the event. I'd now like to turn the call over to Craig Fraser, President and Chief Executive Officer of WindTree Therapeutics. Please go ahead, Craig. Hi, thank you. Good afternoon, everybody. Let me start up by saying I'm gonna be making some forward-looking statements today. I encourage everybody to read our SEC filings for full information. So, I'm gonna take the time to introduce you a little bit to WindTree, tell you what we have going on, what's our objectives. I'll certainly conclude by looking at the next several weeks and several months, and what are the next milestones. Of course, today, the star of the show really is our exciting new data that our Chief Medical Officer, Dr. Steve Simonson, is gonna be bringing you through. Also joining us is Eric Curtis, our Chief Operating Officer. Eric's gonna talk a little bit about the market and the opportunity, particularly in our lead indication area of cardiogenic shock. But just to orient you to WindTree, WindTree is a Nasdaq company. We trade on Nasdaq under the stock symbol of WINT. And we're a company that's focused on, frankly, people at their moments of crisis, when they're in the hospital, in the ICU, intensive care unit, with a failing heart. So acute decompensated heart failure, with and without cardiogenic shock. Cardiogenic shock's a severe manifestation of heart failure that we'll tell you about, that we're focusing on with our lead program. Istaroxime, we brought it in through a merger and acquisition a number of years ago, but we put it in front of top key opinion leaders in the area of heart failure in the U.S. and Europe, and they really got us excited about the profile, how unique that we're seeing as very attractive and very innovative profile. We're seeing this consistently through four phase II studies now, two in heart failure, and more recently, two studies, the SEISMIC study, if you will, in cardiogenic shock that we're gonna focus on today. It's a profile that's been very consistent across a wide range of severity in all regions of the world, and across many, many, many measures. In fact, in today's data, you're gonna see, in this last study, we're just swimming in data that happens to be very positive. But we know a lot about the drug now, and we're excited with how we're gonna bring this forward. Cardiogenic shock has proven to be a really unique opportunity, one that has an attractive regulatory pathway that I'll tell you about, and it's a sizable market that has a lot of need. We also, as a company, already have a couple licenses in place, so possible potential deal revenue as we move forward. We, in fact, did a cardiovascular asset-related license, a regional license, earlier this year. That was about a $139 million license with double-digit royalty potential. There is some deal revenue potential for us and our shareholders as we move forward. We also recently acquired and continue to build out our oral platform, not just next-generation istaroxime-like products that have oral bioavailability, which are really exciting because they can be chronic therapies. We also have this very novel oncology platform that we just recently brought in, in a stock deal, that's very innovative, that we'll be talking more about later on today. Of course, we're gonna focus on istaroxime. It's a company that's run by a really experienced team. All of us have many decades of experience in both large and small companies, and I'm really proud of the team's ability to do what we say we're gonna do and deliver, especially being lean and throwing the funds that we have into R&D. So our portfolio is led by istaroxime, this novel dual mechanism agent that the lead program is cardiogenic shock. We also have an active acute heart failure program. We have the next-generation oral SERCA2a activators. That's the unique mechanism that istaroxime has. So istaroxime's an IV product for hospitalized patient, but we have the chronic therapies that can be fast follow-ons as well, that are quite exciting. And I mentioned a moment ago this unique profile. Just to set this up, how we got into cardiogenic shock. What we had done. Well, we had executed two acute decompensated heart failure studies, 120 patients each, so about 240 patients studied, with istaroxime in patients hospitalized due to their heart failure, which is the big market. In fact, heart failure is the number one reason for hospitalizations in the U.S. and Europe of the elderly, and we saw in those studies this unique profile, in that not only was istaroxime improving the function of the heart, getting the heart tuned up, more output, more flow to the body, but doing so, unlike other agents, where you're accomplishing that by trading off blood pressure, which is a nice-to-have to get blood pressure up. It's a nice-to-have in heart failure. It's a critical thing, as you'll hear, in cardiogenic shock. But we were getting blood pressure up, getting the pump going better, getting organ perfusion. Kidneys like pressure, and in fact, we were increasing renal function, GFR, if you will, which is a big deal in these patients that are overloaded with fluid. You have to be able to have the kidneys pee it off. And at the same time, doing that without trading off, kicking up heart rate, which kicks up myocardial oxygen demand. Also, arrhythmias can often come with that, and instead, we were keeping heart rate down and keeping arrhythmias at bay. Again, very unique and desirable. When we talked to the FDA with this heart failure, that picked up a fast track designation. But coming out of that meeting, our medical reviewer mentioned to our CMO, Steve, "Hey, have you guys thought about cardiogenic shock?" And we had been hearing that from our advisors, and they pointed to the fact that an agent could get approved for cardiogenic shock, with the pivotal endpoint being in classic shock, a correction of blood pressure, because in these patients, blood pressure, or lack thereof, is a killer. In this industry, in biotech or in cardiovascular, to have something that's such a straightforward drug effect as a primary measure instantly takes your mind to a favorable pathway, as long as mortality and safety, of course, the totality of the evidence is there. But that efficacy measure is just a faster, less expensive pathway if you can work there. So the real question was, do we have the therapeutic horsepower to work in these more severe patients? And the answer is a resounding yes. With that, Eric, why don't you tell us a little bit about shock? Absolutely. Thank you, Craig, and hello, everybody. So cardiogenic shock, let's talk about a high-level review of this. But let's start with heart failure and make sure that we're all on the same page. As simply defined, heart failure is the inability of the heart to adequately pump blood throughout the body so the body can operate the way that it needs to. But cardiogenic shock is a severe presentation of heart failure, and it's characterized by low blood pressure and inadequate blood flow to vital organs of the body. And so when a patient begins to get into this state, it requires very urgent treatment. And the blood pressure, the systolic blood pressure's normal is 120. In these patients, they're below 90, sometimes 80, 70, or even 60. As a result, when these organs begin to become compromised, mortality is very, very high, 20%-30%, you can see here on the slide. To give you a little perspective on that, if you have a heart attack, myocardial infarction, mortality rate's around 7%. This is a really very, very devastating disease we're talking about here in cardiogenic shock. Now, in the market values, we did an assessment with a worldwide assessment around market value. We got US hospital claims data and epi data outside the US, applied some patient numbers with regional pricing assumptions, and we have a $1.25 billion market globally. Of that $1.25, the US and Europe is $1.0 billion market potential. So a nice-sized market for a smaller company like ours. And the potential, as Craig was mentioning, for a relatively faster and less expensive developmental and regulatory pathway. When you look at the time, cost, and the risk of around classic valuations, this is something that is, very, very attractive for us to be entering into. We wanted to contemplate the question, what would the ideal treatment for cardiogenic shock due to heart failure look like? We began to list these items. First one here, the ideal treatment would improve systolic and diastolic cardiac function. That's the root cause of cardiogenic shock. The ideal treatment would also improve blood pressure and organ perfusion, and it would not harm the kidneys. Why is that important? Because if the kidneys don't operate well, then the excess fluid can't be eliminated through urination properly, and this can be a complicating factor. It's very important not to harm the kidneys when you're entering treatment. The ideal treatment would also not increase heart rate, because this increases myocardial oxygen demand and the energy requirements of the heart. Generally speaking, if you're increasing the heart rate, you're not headed in a good direction for the patient. The ideal treatment would also not increase the risk for cardiac arrhythmias or abnormal beating of the heart. These can be very serious and sometimes deadly, and so we wanna make sure we avoid this area. The ideal treatment would also contribute to effective diuresis or removal of that excess fluid, and have a rapid onset of action with a predictable effect that can be titrated to patient needs. Now, here's the problem. Problem is that there are no good treatments. There are no treatments that accomplish all those things that are currently available on the market. We really heard this a lot from our scientific advisory team. We knew it from the literature. So the fact is that these currently available treatments have unwanted side effects a lot of times, like arrhythmias or decreasing blood pressure, renal dysfunction, and sometimes even increases in mortality that limit their use. They're really regarded as more rescue medicines that will be used when there's nothing no other choice to be made, and physicians feel, you know, very wary about a lot of times utilizing medicines that they know have bad side effects. We'll hear from Dr. Mebazaa later on about his perspective on this topic. But we wanted to substantiate more of what we were hearing and seeing by some market research. And so we went to 100 U.S. clinical cardiologists who treat cardiogenic shock as part of their job responsibilities, and we asked them the question: How much drug innovation is needed in treating cardiogenic shock? 99 out of 100 of those clinicians said, "Drug innovation is highly needed." Now, I've been doing market research for a long, long time. I rarely ever see 99 out of 100 clinicians agree on anything, and certainly, this was a very impressive result to begin to see that. We showed these same clinicians a blinded profile of istaroxime, and we asked them the question: How likely would you be to use istaroxime to treat your early cardiogenic shock patients? 84% of those cardiologists responded they'd be likely to extremely likely to use istaroxime to treat their early cardiogenic shock patients. Then last, we asked them, "When would you use istaroxime to treat your cardiogenic shock patients?" The majority of those 100 clinicians said it would be the first thing they'd use before existing therapies today. So to wrap this totally together for you, there are four clear reasons why we've really prioritized cardiogenic shock. The first reason is there are just no good therapies available today in the current market to be able to treat cardiogenic shock effectively. Number two is that there's no other drugs in development other than istaroxime for cardiogenic shock. Number three, it's a $1.25 billion market. Number four, Craig mentioned the favorable regulatory pathway. This is something that you don't often see in cardiovascular disease state, and so it's very, very attractive. Steve? Thanks. Thanks, Eric, and hello, everyone. Let me start by reviewing how istaroxime works, because istaroxime is a very interesting and unique molecule. It's given to hospitalized patients by IV infusion, and it has two mechanisms of action. The first mechanism is to inhibit the sodium-potassium ATPase, and this results in an increase in calcium inside the cell and produces a stronger force of contraction. The second mechanism, and perhaps the most unique part of istaroxime, is that it activates a pump called SERCA2a, and SERCA2a acts to decrease intracellular calcium after the contraction takes place. It pumps that calcium into the sarcoplasmic reticulum inside the cell, where it's stored until the next contraction. This allows for the myocardium or the heart muscle to relax more efficiently. The first mechanism results in a better squeeze, more blood's pumped out per contraction, and the second mechanism relaxes the heart muscle to allow it to fill more effectively for the next heartbeat. SEISMIC was executed in two parts, A and B, with a similar design to each. We prospectively planned to combine parts A and B for analysis of the primary endpoint. This design allowed us to evaluate several dosing regimens as we prepared for late-stage clinical trials. Part A dosed istaroxime for 24 hours. In Part B, we dosed 30 patients with istaroxime or placebo for up to 60 hours. We enrolled patients with SCAI S tage B cardiogenic shock due to acute heart failure. These patients had persistent hypotension or low blood pressure, and their systolic blood pressure was in the range of 70 to 100 millimeters of mercury. The primary endpoint was systolic blood pressure over the first six hours of study drug infusion for the istaroxime-treated patients in parts A and B, compared to the placebo group. This analysis included 90 patients. Secondary endpoints included systolic blood pressure profile over six hours in Part B alone and several other physiologic assessments. In Part B, all patients were required to have a pulmonary artery catheter in place for some of the measurements we were taking. This slide shows the primary endpoint, the systolic blood pressure profile over six hours for parts A and B on the left, and for Part B alone on the right. In both analyses, there was a substantial and statistically significant increase in systolic blood pressure over this time period, a very positive result for SEISMIC. The other thing I'll point out in these graphs is that the istaroxime and placebo curves start to separate at the first time point assessed. A rapidly acting agent is important in treating an acute condition like this. Here we see the blood pressure profile over twenty-four hours, and you can see again that there are persistent, substantial, and significant increases in systolic blood pressure. On the next slide, we see that the blood pressure profiles through the end of the infusion show the same thing. Istaroxime continues to produce increases in systolic blood pressure that are statistically significantly increased compared to placebo. Again, a very positive outcome throughout the infusion period for istaroxime. This graph shows pulmonary capillary wedge pressure over sixty hours of study drug infusion. Pulmonary capillary wedge pressure is an assessment of filling pressures of the heart. This pressure is elevated in acute heart failure and reflects back pressure into the pulmonary system that can lead to pulmonary edema. Istaroxime produces a marked statistically significant reduction in pulmonary capillary wedge pressure within six hours of starting the infusion, and this effect persists throughout the dosing period. This slide shows pulmonary capillary wedge pressure and cardiac output over 48 hours. As we saw in the previous slide, pulmonary capillary wedge pressure is decreased, and on the right panel here, cardiac output, which is the amount of blood pumped out by the heart per minute, is substantially increased. The filling pressures are decreased, and forward flow or cardiac output is substantially increased. Poor cardiac output is the fundamental problem in heart failure and cardiogenic shock, and istaroxime improves the pump, reduces congestion and fluid overload, reduces the back pressures as reflected by the pulmonary capillary wedge pressure, as well as improving blood pressure. Istaroxime produces these changes without increasing heart rate. This means that the improvement is coming by improving the stroke volume or the amount of blood that is ejected per beat. Heart rate is a determinant of myocardial oxygen demand, as you heard from Eric, and we are improving the cardiac function in an efficient way that does not increase those myocardial oxygen requirements. Another assessment of cardiac contractility can be seen in the pulse pressure. This is the difference between systolic and diastolic blood pressure. Since the diastolic blood pressure is relatively constant, this reflects the force of contraction of the heart, and it is increased persistently and significantly by istaroxime. Mixed venous oxygen saturation, or SvO2, is an assessment of organ perfusion and the adequacy of oxygen delivery to the tissues. In heart failure and shock, this value goes down because the cardiac output is low and the tissues extract more oxygen out of the blood. As cardiac output improves and blood flow to the tissues increases, less oxygen is extracted from the blood, and mixed venous oxygen saturation, when the blood returns to the heart, gets higher. We see here that istaroxime substantially improves SvO2 as soon as 12 hours after starting the infusion, and this is maintained over the 60 hours after starting dosing. This is another sign of overall patient improvement. As you heard, maintaining renal function is important, particularly in heart failure, where we need to use the kidneys to get rid of the fluid overload that these patients have. Many of the drugs used to treat patients in this setting have detrimental effects on the kidneys. You can see here that istaroxime increases renal function compared to placebo, and we've seen this pattern of effect in all of our two B studies of istaroxime. Improving cardiac output and renal perfusion contributes to effectively diuresing patients and maximizing the effect of diuretics to get rid of the fluid overload. You can see that both treatment groups had a decrease in weight, reflecting diuresis. The difference was numerically greater in the istaroxime group, but did not reach statistical significance in this sample of 30 patients. Nevertheless, it suggests that istaroxime patients are being more effectively diuresed and dried out. The stability throughout day thirty is notable here. This slide shows the New York Heart Association classification over ninety-six hours. Istaroxime significantly improved heart failure severity over this period. As patients are effectively treated and recovering from their decompensated heart failure and shock state, they need to be started on medications to manage their chronic heart failure condition and prepare for discharge. Recently, a four-drug goal-directed medical therapy regimen has become the standard of care for these patients. In this graph, you can see the proportion of istaroxime-treated patients in the blue bars, compared to the proportion of placebo-treated patients in orange, who were put on each of the four classes of goal-directed medical therapy. More istaroxime patients were put on each class of goal-directed medical therapy compared to placebo. This may help these patients prepare for discharge sooner, and successful initiation of goal-directed medical therapy may contribute to keeping them out of the hospital longer, avoiding readmissions, and keeping them alive. Istaroxime is facilitating this by getting these patients out of their decompensated state with an improved blood pressure and in a position to get on these drugs, all of which have a tendency to lower blood pressure. Looking at safety and tolerability from this trial, you can see that there were more adverse events reported by the istaroxime group, but this difference was driven primarily by GI upset and infusion site discomfort that have been seen in previous trials with istaroxime. Here are the serious adverse events from the trial. Serious adverse events were not common and reported less frequently in the istaroxime group. Although the numbers are small in part B, worsening heart failure was reported by 18% of placebo patients, compared to 5% of istaroxime-treated patients. Overall, a very favorable evolving safety and tolerability profile. We have also looked at a composite endpoint of heart failure reported as an adverse event, heart failure readmissions, or death through day 30. Clinical outcomes like this will take on more meaning as our program expands and gets larger. But you can see in the combined evaluation of the 1.0 dose from part A, along with part B of SEISMIC, we see approximately a 50% reduction in this assessment. This endpoint was met by 20% of the placebo patients, compared to 10% of istaroxime-treated patients. If this holds up as our program grows, it will become a very meaningful and important assessment for regulatory and health economic reasons. So that was a rapid run-through of a lot of positive data from SEISMIC, and I'll try to summarize it here. Istaroxime produced a rapid and meaningful increase in systolic blood pressure that was maintained throughout the period of observation. Assessments of cardiac function, like cardiac output and pulmonary capillary wedge pressure, were significantly improved. Improved organ perfusion was supported by the findings of increased mixed venous oxygen saturation. Renal function was significantly increased and maintained compared to placebo. And New York Heart Association heart failure classification was significantly reduced by istaroxime, and more patients were successfully transitioned to goal-directed medical therapy for long-term management of their condition. All of this was achieved with a safety and tolerability profile that was favorable and consistent with what has been reported for istaroxime in our previous studies. SAEs and worsening heart failure were less frequent in the istaroxime group, and although I didn't show the data on this, importantly, istaroxime did not increase clinically significant arrhythmias compared to the placebo group. So I will turn things back to Craig, and … Steve, do you want to cover down on where we go from here? Sure. I will. After we completed SEISMIC, we embarked on the SEISMIC part B study that we've just reviewed, and in parallel with that, we have initiated a study in more severe patients, what are called SCAI St age C cardiogenic shock patients. These patients not only have low blood pressure, but they have established hypoperfusion of the organs, so their organs are starting to see the effects of inadequate oxygen delivery, and this is an important population for us to have experience in as we prepare for our phase 3 study. The study is open and is enrolling, and we look forward to reporting the results of this study in due course here. Thanks, Steve, so to close out cardiogenic shock, I think as you heard from Eric, the opportunity is quite pronounced. These patients are really sick, 20%-30% mortality in classic shock, very long hospital length of stays, a lot longer outside the U.S., and these are ICU stays. Intensive care units, cardiac intensive care units, and the costs are really high, and when we look at real-life data, it's about $175,000. So to make a difference here with what we're seeing with istaroxime, particularly this really unique profile of istaroxime, we can generate the type of evidence and outcomes and pharmacologic outcomes that I get quite excited, particularly as we grow a program. When you think about what we're hitting on with statistical significance at these size studies, as we go to do our phase three, we should bring a lot of those things that are positive trends across the line, at least that's our hope and plan. Currently available agents, of course, have these undesirable side effects. You can get blood pressure corrected by giving a common agent, norepinephrine or epinephrine, adrenaline. It'll race the heart, it'll kick up heart rate, and therefore get some output, cardiac output, which is an equation in it, but you wear the heart out, you kick up arrhythmias that can be fatal as well. So not to have the efficacy without trading that off is something that's been more than desired for many, many years, and there's nothing else in development. All the activity in shock over the last decade or so has been on the mechanical side for the really super severe bottom 15% of shock that heads off to a cath lab to be mechanically supported. And then, the valuation, particularly as a lead indication, I'd love to show up at the U.S. hospitals and in Europe with, with this type of product, with this type of valuation as a, as a first entrance. So as we look forward, I wanna look back, actually. Eric talked about what is a target product profile, what is our objective, what's an ideal treatment? I think as you see in our program to date, and with the information that Steve has just presented, that we really have a compelling program here with this opportunity to make a big difference in low blood pressure, heart failure, and in cardiogenic shock, that when I look across the ideal state, if you will, we're hitting across the board with that. You know, and I'll give one perspective that's a bit of a personal perspective or that of our scientific advisor and executive committee or Steve. I think many of the folks on the phone right now, we've done this for many decades to be able to collect so much data that we did in this study by having the PA cath, Holter monitors. I think you see a lot of data that we've collected. Despite the size of the study, to have statistical significance and so much going our way like this, it is really remarkable, and it gives us more confidence in the signals and the therapeutic effect that we're seeing and the safety profile to push this agent and continue on with the program. Like I said, we're quite excited with what we have here. Before we hear from Dr. Mebazaa, who's calling in from Japan right now, I wanted to cover down on the other program with istaroxime, and this is being led by our partner. Acute decompensated heart failure is the top of the funnel. This is the market that is the number one reason for hospitalizations in the U.S. and Europe, and people over the age of sixty-five. We probably have all had relatives with chronic heart failure, and where the heart is bigger, baggy, just inefficient. And there'll be these episodes where the patient goes into fluid overload, pulmonary edema, and it just becomes a downward spiral of how the body, the kidneys, start retaining fluid in reaction to that drop in pressure. And they end up in the hospital, and they're put on a powerful IV diuretic, begin the week-long journey of getting dried out and trying to figure out how to tune up their heart. There's about 1.5 million admissions per year, so it's the big mega market, the number one highest cost of a Medicare diagnosis. And there really has been a lack of advancements on the acute heart failure side. We're seeing a lot of great things, especially with these new classes of agents for chronic heart failure and reduction, but not so much in these critical inpatients, so what we're doing there is, after having the positive 2A and 2B study in heart failure and working with bigger revenue-producing pharmaceutical partners, is advance acute decompensated heart failure program by our partners, and as I mentioned, we have a partner that's a regional partner for Asia Pacific. We've already had a positive phase 2B in that part of the world, and they're preparing to start the phase 3 study. We've been working with them on the protocol. We work hand-in-hand with them, of course. I look forward to giving all of you an update on first patient and enrollments in the phase 3 heart failure program, and this is being paid for, frankly, on their dime, right, and with their resources. Through partnership, we will also be advancing acute heart failure while we keep the lead indication being cardiogenic shock. I also want to remind everybody that we do have also in our portfolio, the next-generation SERCA2a activators. These are unique because they also can be IV and oral. They have oral bioavailability. We have a dual mechanism, SERCA2a, and sodium-potassium ATPase. So basically, the son of istaroxime that has oral bioavailability that could follow, fast follow-on, all fresh IP, and we have a pathway blazed by istaroxime and how you do these in the fast follow-ons. Then we have a pure SERCA2a with just that mechanism. As Steve told you, that mechanism's responsible for causing greater cardiac relaxation. There is a type of heart failure, about 45% of heart failure. It's called heart failure with preserved ejection fraction. These tend to be female and older patients that have these stiff hearts that don't fully relax, and that's their source of heart failure, because they're not getting enough fluid volume to be pumping. And so pure SERCA2as are a really attractive target, and SERCA2a has been a much sought-after target in the world of heart failure. Big pharma companies had programs on it, but it's been elusive. Our scientists were the first ones to figure out how to really get to SERCA2a activation in a very novel way. So the platform consists of istaroxime with two lead indications, and then these fast follow-ons that also have oral bioavailability. So we have a kind of a multi-asset platform as we go out and do business development type of activities. So as we look to the second half of this year, in the next several weeks and the next several months, while it's been a busy year for us with the activities we've done earlier in the year, with getting a study up and running, executed, and now bringing positive data across the line, doing regional licenses, expanding our early portfolio. Now with the results of this study, we have activity in SCAI Stage C. That data is planned for pulling some data off in late Q1, so about six months from now. We also have the start-up of phase 3 for acute heart failure, which I'll be doing updates on. We also are quite active on the business development front for non-dilutive support and funding with partnerships globally, and we'll give further information on our preclinical activities and platforms here in the months to come, and as always, continuing to drive capital efficiency and non-dilutive funding and partnerships along the way with it, so with this, I'll point out now, these figures are from our last Q. We did do a PIPE financing since the month of June. At the last time we reported, our shares outstanding up one point six. We also, again, as a reminder, have a couple deals in place, cardiovascular deal, and our legacy acute pulmonary care platform, called Aerosurf, that we also have in a global partnership, so there's potential deal revenue as well. So with that, I know we're still waiting on Dr. Mebazaa. I think many of you saw his quote in the press release. He is in Japan, and he may be having a hard time dialing in right now. So while we're waiting for Dr. Mebazaa, and I know, Eric, you pinged him, do we have any questions that we would like to cover? Yes, we do, Craig. So let me read a couple of these. First one is: Why is WindTree prioritizing cardiogenic shock over acute heart failure? Yeah, that's a great question. Because I think as you look at shock, we do see that the time, risk, cost, and return valuation of how do you spend your money, what you can get for it, where the need is in the market, what you can charge against that big backdrop, from a pricing standpoint, with really strong reimbursement, that is found in a hospital. When you do a full assessment like that, and again, considering the attractive regulatory pathway and what you have to do, it is just so attractive to make it our lead indication, 'cause it could come to the market quicker and, at the same time, cost us less along the way, and as a small-cap or a micro-cap company, obviously, that's really important. Acute heart failure is a big area, but it's also big, big programs with a lot of cost. It is the thing to do in conjunction with partnership. So we think we have the right strategy with this. We certainly want to be doing both. We are doing both, but we can run with cardiogenic shock as we're doing. And with what we're seeing with these results, it puts a lot of wind in our sails. Thanks, Craig. And, the next question is: Could WindTree commercialize cardiogenic shock in the United States on its own, or would it seek partnership for that? Yeah, we absolutely could, and the way we think about business development and just in general, and let me back up and say, one of the things about creating a company in acute care, when I say acute, I mean hospitals, something that's directed towards the hospital marketplace. I think acute care, institutional-based things, as well as rare disease, for the most part, most rare disease, are great areas to do a start-up on. Because those are two areas in particular that you can pivot from a dev stage company into direct commercialization. Now, let me talk about hospitals. I've done this a couple times in my career, Eric as well. We've done it together in two companies, all the way back many decades ago, where you're development stage. To go into the US hospitals, whether on your own or as part of a co-promotion, if you did a deal with a bigger company, is very doable. It's something that requires about seventy representatives, some MSLs, and a type of a structure that you can get at it. You can target a couple thousand hospitals. Now, to try to go out into the community and sell in general to cardiologists in community practice, no, that's a thing for bigger companies. So as we think about our business development, certainly we want to do either additional regional deals off of this information in pre-phase III, regional being Europe, Middle East, North Africa, and Latin America, and we've done development just like this study in Europe, US, Latin America, so we've been doing development globally. Get some partnerships there, and if we do a global partnership that includes the U.S., we would like to have co-promotion rights. Even if it's a bigger partner taking it, we'd like to have that optionality to pivot our company into a revenue-producing company as well here in the next couple years. The last question we have, Craig, is: Given the promising phase II results, what partnerships or financing strategies is WindTree pursuing to support the next stages of development and commercialization? Yep. For partnership, did you say, Eric? Yes, partnership or financing strategies. Yeah. So I think I talked a little bit about partnership. Really, we're starting to see some really nice cardiovascular deals in the last year or two. I think there was a time, and, you know, I came out of the oncology world, where it seemed like every deal was an oncology deal. But in the last couple years, and certainly very recently, the industry is making a swing back to cardiovascular. It dawned on everybody that, hey, the number one killer is still cardiovascular disease. And I also think that we're seeing some of these new agents, like the GLPs and so forth, that have really started to impact chronic cardiovascular, and some exciting therapies that have a focus back on cardiometabolic. And as such, people are back shopping that space, if you will, or shopping for assets. With data like this that we have, and that SERCA2a mechanism, and that multi-asset platform, really, we see kind of the ideal time is when you're wrapping up phase 2, getting ready for your end-of-phase 2 meeting with the agency and with the EMA. And that's really I know from being on the other side of the table, places like J&J and Pfizer, that's when the ideal time is to do deals for both parties' part. So we're looking, and we're quite active in discussions right now. We're really looking for this coming year, next several months, to be the time that's gonna be like a sweet spot for partnerships, at least in our plans. That helps with funding. When you start even when you do regional deals, you start dividing up the cost. Here, as we think about phase three for shock, it's not gonna be driven by what we need for our efficacy measures. You see small trials now in statistical significance, however we do it. It's gonna be, what's an adequate safety database to put a new molecular entity on the market? So it's gonna be a couple hundred patients, but even then, that's fairly fast, and you talk about if it is that, a clinical cost under $20 million, again, for phase three and to run through to a filing. But putting partnership into that and starting to divide up those costs by regions makes things quite doable. From a funding standpoint, we've been able to bring in funding this year, at two different points. We do have an equity line of credit in place. We're not always using that, but WindTree tends to have decent liquidity. So as we continue to drive up news and deliverables and liquidity, and I think a company that has a lot going on and is constantly putting out news, that can lend itself to be one of the factors at helping with funding along the way. And then, we have supportive top shareholders that we continually work with to make sure that we have what's necessary resource-wise. For instance, bring that SCAI Stage C data at the end of Q1 across the line, and then keep going from there. So, beyond that, we run as a very lean, very efficient organization, particularly for a public company, that takes our dollars and puts them into the value-generating type of activity, like clinical development. So- Those are the questions we have, Craig. Okay. And Steve, I'll kind of mention to you. I know you talked with Alex, talked about the quote. He's been on the executive committee, and I apologize to everybody. Alex is literally in Japan and come off of a plane, and this is unlike him to have these technical difficulties to get on board. We will make sure that we capture his messages, add it to this recording and this deliverable, so that you can catch it after the fact. I know just from talking with him last evening, what he was gonna say, and we really wanted you guys to hear about how he thinks about this product in terms of how revolutionary it is, versus what they have to work with today. These guys are super, super excited, and I apologize to you all who were expecting to hear from Alex on this call. But we will get his messages put into here if he's having, you know, the technical difficulties, such is life as he was coming into this from Japan rather than Europe as well. Steve, I don't know if you'd add anything else, but... No, it's unfortunate he couldn't get the connection, but, I think, as you say, we will get his comments, and, I think it will be particularly interesting to hear his perspective on the currently available therapies, and, the limitations that we have there, and what an opportunity there is for istaroxime to fill in and do something that currently available drugs cannot do for cardiogenic shock patients. Again, thank you, everybody. Thanks for following the company. We're gonna keep you updated. We have a lot of activity, a lot of news flow coming in the weeks and months to come, and like I said, hopefully, you can see why we're so incredibly excited about these results that truth be known, even exceeded kind of our upside as we looked at this study. We can't be more pleased with what we're seeing, and we're really happy to share it with you today.