Please be advised that today's conference is being recorded. I would now like to hand the conference over to your speaker today, Martin Brenner. Please go ahead, sir. Good morning and thank you for joining us today. Before we begin, I would like to remind you that during this call, the company will be making forward-looking statements regarding our current expectations and projections about future events that are subject to risks and uncertainties. References to these risks and uncertainties are disclosed in detail in the company's periodic and current filings with the U.S. Securities and Exchange Commission. No forward-looking statements can be guaranteed, and actual results may differ materially from those discussed today. The information on this conference call is provided only as of today, and we undertake no obligation to update these statements except as required by law. Joining me on the call today is Cory Schwartz, Director and Head of Research and Early Development at iBio. Recently, we have been receiving a great deal of questions about our myostatin activin A bispecific antibody program as a potential next-generation therapy in heart failure. Today we want to take the time to walk you through the full rationale, what we are targeting, why we believe the biology points us there, and how a differentiated precision approach could offer something genuinely new in an area where the broader pharmaceutical industry is clearly converging on with urgency. Before we get into the science, I want to note this is a space that has seen dramatic validation in the last few weeks, with GSK entering into an agreement to acquire 35Pharma Inc., a next-generation activin pathway company, for $950 million. We view this transaction as strong support for our approach and rationale. We will come back to that. To understand why our bispecific antibody program makes strategic sense for iBio in heart failure, and especially in pulmonary hypertension resulting from heart failure with preserved ejection fraction, it helps to first revisit who we are and what we have been building. At iBio, we have been focused on next-generation obesity therapeutics, but our thesis has always gone deeper than simply lowering body weight. Obesity becomes dangerous not just because of excess weight. It becomes dangerous when it impairs physical function, drives cardiometabolic disease, accelerates organ fibrosis, and ultimately leads to heart failure. Mortality risk in obesity correlates far more closely with loss of function and organ damage than with BMI alone. People don't die simply from being overweight. Morbidity occurs because of the downstream diseases driven by excess adiposity. From the beginning, our goal has been to target the biology underlying those outcomes, not just the number on the scale. Our pipeline reflects such philosophy. IBIO-600 targets myostatin and GDF11 and is designed to preserve or restore skeletal muscle during weight loss, addressing the well-documented problem of lean mass loss that can undermine the functional and metabolic benefits of weight reduction using currently approved therapies. IBIO-610 targets activin E and is designed to selectively reduce adiposity, especially the metabolically harmful visceral fat depot that drives systemic inflammation and cardiometabolic risk and which responds poorly to caloric restriction alone. Together, these programs aim to improve the quality of weight loss, not just the quantity. As we advanced these programs and deepened our understanding of the TGF-β superfamily, a key insight emerged. The same biology driving functional decline in obesity also appears to be a central driver of pulmonary hypertension resulting from heart failure with preserved ejection fraction, specifically the condition known as PH-HFpEF. The convergence of these pathways across disease states is not coincidental. It reflects a shared underlying biology involving the same ligands, activin A, myostatin, GDF11, and the same tissue targets, the pulmonary vasculature, the myocardium, and skeletal muscle. That is what led us to conclude this is not an adjacency for iBio, it is a direct extension of the biology we have already been developing drugs against. With that context established, I'll turn it over to Cory to walk through the biology. Cory, please. Thank you, Martin. Let me start by taking a step back and defining the disease landscape we are entering. Heart failure with preserved ejection fraction, called HFpEF, is an umbrella term for a heterogeneous group of patients in whom the heart pumps normally in terms of ejection fraction but does not relax properly between beats. The heart becomes stiffer, filling pressures rise, and patients experience the classic symptoms of heart failure, breathlessness, fatigue, exercise intolerance, despite what appears to be normal pump function on conventional testing. HFpEF now accounts for approximately half of all heart failure cases and is strongly associated with obesity, diabetes, hypertension, and aging. HFpEF is not a single disease. It is a syndrome with multiple phenotypes, and that distinction is clinically and strategically important. Our initial focus is on a specific and severe subset, pulmonary hypertension resulting from HFpEF, or PH-HFpEF. In this population, the elevated left-sided filling pressures characteristic of HFpEF push blood backward into the pulmonary vasculature, causing what is termed combined post and pre-capillary pulmonary hypertension, also called CPCPH. This is a condition in which both the left heart disease and progressive remodeling of the pulmonary vessels must be addressed. Pulmonary hypertension occurs in a significant fraction of all HFpEF patients, with some studies reporting 50% or higher. Pulmonary hypertension is also associated with significantly worse outcomes, including mortality. Why start here for iBio? Because this is where the activin pathway biology is most directly clinically validated, where the unmet need is clearest, and where our mechanism has the clearest line of sight to meaningful endpoints. beyond PH HFpEF, we see the broader cardiometabolic HFpEF population, that is, patients driven primarily by obesity, metabolic syndrome, and systemic inflammation rather than pulmonary vascular remodeling as a compelling potential expansion of this program. The biology overlaps significantly, and iBio's existing work in obesity and metabolic dysfunction positions us especially well to pursue that broader population over time. We are actively working through the science and development strategy to determine the optimal path forward, and we will share more as the program matures. Looking at the existing treatment landscape for both PH HFpEF and broader HFpEF makes the unmet need concrete. Diuretics remain the backbone of symptom management but do nothing to modify the underlying disease. RAS inhibitors, beta blockers, and aldosterone antagonists have all shown limited efficacy in large HFpEF clinical trials. SGLT2 inhibitors represent the most significant advance in HFpEF pharmacology over the last several years and are able to reduce hospitalizations and cardiovascular death but leave significant room for further improvements in patient outcomes. GLP-1 receptor agonists offer metabolic and weight reduction benefits in obese HFpEF patients, but whether they produce durable structural cardiac reversal remains to be established. In the PH-HFpEF subset specifically, where pulmonary vascular remodeling has become an independent pathological process, none of the existing HFpEF therapies have demonstrated meaningful effect on reversing the structural remodeling of blood vessels. The common thread across almost all of the current approaches is that they manage downstream consequences rather than targeting the underlying pathology of vascular remodeling. That gap is precisely what we believe the activin pathway, targeted with appropriate selectivity, could address. The TGF-β superfamily is a large family of secreted signaling proteins that includes activins, growth differentiation factors like myostatin, and bone morphogenetic proteins. These ligands signal through a variety of different type one and type two receptors. ACTR2A and ACTR2B are two of note and regulate a broad range of physiological processes, including muscle differentiation, fat metabolism, vascular tone, and tissue repair. In healthy individuals, these pathways are tightly balanced. In disease states like PH-HFpEF, that balance breaks down and certain members of this family transition from physiological regulators to pathogenic drivers. Three members of this family of particular interest are activin A, myostatin, and GDF11. These ligands signal through overlapping receptor complexes and should be viewed as part of a shared pathogenic axis rather than as separate biological stories. Across the heart, pulmonary vasculature, and skeletal muscle, this signaling network is linked to fibrosis, vascular remodeling, impaired metabolism, and functional decline. Core features of PH-HFpEF. In that sense, these ligands are more than biomarkers of severe disease. They appear to participate directly in disease progression, making the pathway an especially compelling therapeutic target. The proof of concept demonstrating that this biology can be therapeutically harnessed has come from ligand traps. That is, soluble receptor-based fusion proteins that broadly sequester multiple TGF-beta superfamily ligands. Sotatercept, now approved as Winrevair for pulmonary arterial hypertension, is the defining example. In the phase III STELLAR trial in PAH, Sotatercept produced a 40.8-meter improvement in six-minute walk distance compared to placebo in patients already on stable background therapy. A significant clinically meaningful result that translated into improvements across multiple important secondary endpoints. It has since become a commercial success, generating over $1 billion in sales in its first full year on the market. More recently, and more directly relevant to our own program, in November 2025, Merck reported top-line results from the phase II CADENCE trial, which was specifically designed to evaluate sotatercept in CPCPH due to HFpEF. CADENCE met its primary endpoint, demonstrating a statistically significant and clinically meaningful reduction in pulmonary vascular resistance at 24 weeks compared to placebo in this patient population. Due to the lack of currently approved treatment options in PH-HFpEF, Merck has indicated that it intends to proceed to phase III development. This is an important result. It directly validates that activin signaling is a driver of pulmonary vascular disease in the PH-HFpEF population, and importantly, that targeting this pathway can move key clinical endpoints. The broader pharmaceutical industry has responded with conviction. Just in the last few weeks, GSK announced it had entered into an agreement to acquire 35Pharma Inc., a clinical-stage TGF-β superfamily company, for $950 million in cash. The most advanced asset at the center of this deal is HS235, a next-generation activin signaling inhibitor that has completed phase I testing in healthy volunteers with patient studies in PAH and PH-HFpEF population set to begin soon. Critically, HS235 is specifically designed with enhanced selectivity, reduced binding to BMP9 and BMP10, the ligands associated with the bleeding and vascular adverse events observed with broader ligand-blocking approaches. In acquiring 35Pharma Inc., GSK's Chief Scientific Officer, Tony Wood, stated explicitly that they view HS235 as a potential best-in-class medicine with a differentiated safety profile and metabolic benefits, and that they see the activin pathway opening broader opportunities across the metabolic, inflammatory, vascular, and fibrotic drivers of multiple chronic diseases. GSK also noted that the pulmonary hypertension market is forecasted to grow to $18 billion by 2032, with activin signaling inhibitors expected to represent roughly half of that. We view both the results of the CADENCE trial from Merck and the GSK transaction as powerful proof of principle for the pathway we are targeting. They also illustrate the central problem our program is designed to solve. Broad ligand traps, while clinically meaningful, introduce safety trade-offs, including bleeding risks and other findings that are mechanistically linked to inhibition of BMP9 and BMP10. These are not trivial concerns for therapies that patients will take chronically. The next generation of this class needs to be more selective, and that is precisely what iBio's product candidate has been engineered to accomplish. We designed our bispecific program from first principles, asking not, how do we make a better version of a ligand trap, but rather, which specific ligands are actually driving disease, and can we target only those while preserving the beneficial signaling of other ligands? The answer, based on our analysis of the biology and the available evidence, pointed to three ligands in particular, GDF8, which is also known as myostatin, GDF11, and activin A. These are the drivers of pulmonary vascular remodeling, skeletal muscle atrophy, cardiac fibrosis, and metabolic dysfunction in these patient populations. Critically, the ligands we have specifically chosen not to block, BMP9, BMP10, and activin B, we believe serve important homeostatic functions we want to preserve. Specifically, BMP9 and BMP10 regulate vascular tone and endothelial homeostasis. Their inhibition is mechanistically linked to the bleeding events and hemodynamic side effects that have been observed with broader ligand traps. This is the very safety profile that GSK's acquisition of 35Pharma acknowledges as a key limitation of existing approaches as well that they're trying to address. Activin B is distinct from activin A in its metabolic role. It is reported to induce FGF21 expression and contribute to improved glucose handling and insulin sensitivity. Blocking activin B could potentially undermine the metabolic improvements that are a core part of the benefit we're trying to deliver, particularly in the obese, metabolically compromised PAH population. Our design deliberately spares both. This is what we mean by intentional selectivity. It is not a compromise or a limitation of an antibody-based approach. It is a design choice grounded in mechanistic understanding. By targeting the right three ligands with precision, we believe we can deliver similar efficacy to ligand trap-based approaches with a potentially improved safety profile that is appropriate for chronic long-term administration. When you translate that biology into what patients actually experience, the rationale becomes concrete. Patients with PH-HFpEF can be severely functionally limited, breathless at rest or with minimal exertion, unable to participate in rehabilitation or normal daily activities. The pulmonary vascular remodeling, driven in part by activin A, contributes directly to the hemodynamic obstruction at the heart of their disease. The skeletal muscle dysfunction driven by the myostatin and GDF11 axis compounds their functional disability and metabolic impairment. By targeting all three axes simultaneously, pulmonary vasculature, myocardial, and skeletal muscle, without the potential safety risk of broad pathway inhibition with a single selective agent. We believe we will address the disease at multiple fundamental levels in a way that is novel and differentiated. Looking further ahead, the same mechanistic rationale applies with modifications to the broader cardiometabolic HFpEF population, where obesity-driven systemic inflammation, visceral adipose dysfunction, and TGF-β superfamily dysregulation converge to produce ventricular stiffness and exercise intolerance through partially overlapping but distinct mechanisms. We are actively evaluating how our bispecific program could be developed in that larger patient population, including whether the initial PH-HFpEF data could help inform and de-risk that expansion. This is an area of active strategic planning, and we look forward to potentially providing more clarity as the program matures. Our internal preclinical data supports the mechanistic hypothesis and gives us confidence while we advance towards a development candidate. We have engineered a series of bispecific antibodies with the selectivity profile I previously described. High-affinity blockade of GDF8, GDF11, and activin A with demonstrated sparing of BMP9, BMP10, and activin B at physiologically relevant concentrations. We have characterized binding kinetics and functional blocking activity against each target in cell-based assays. In human cardiac fibroblast experiments, which we view as a key translational model, we have demonstrated that activin A, GDF8, and GDF11 are all direct drivers of pro-fibrotic signaling, including collagen synthesis and myofibroblast activation through SMAD2 and SMAD3 phosphorylation. In our internal rodent HFpEF model, designed to replicate the obesity-related cardiometabolic phenotype through high-fat diet and hypertensive stress, selective blockade of GDF8, GDF11 and activin A produced results consistent with disease-modifying activity at the level of cardiac remodeling. Specifically, in our obese HFpEF mice, the selective blockade reduced the Fulton index. The Fulton index is a standard measurement used to quantify heart enlargement by calculating the weight ratio of the right ventricle relative to the rest of the heart. In our research, it serves as a key metric to prove that a therapy is physically reducing the structural strain and thickening of the heart muscle caused by disease. We're cautiously optimistic in how we interpret these results. Rodent models are imperfect surrogates for human disease, which is itself heterogeneous. The directionality of the data is consistent with our mechanistic hypothesis at every level, from cell-based signaling assays to tissue-level gene expression to functional cardiac endpoints. Importantly, what enables iBio to execute on this program is the combination of deep TGF-beta superfamily expertise and our mammalian display and AI-enabled antibody engineering platform. Engineering a bispecific that blocks three specific ligands with the required potency and selectivity while maintaining the developability, stability, and manufacturability profile appropriate for chronic subcutaneous use is a genuinely demanding antibody engineering problem. GDF8, GDF11, and activin A share significant structural homology with the very ligands we're trying to spare, so achieving clean discrimination requires precision that a conventional antibody discovery approach might struggle to deliver. Our platform was built for exactly this kind of challenge. Our next forecasted public milestone for this program is the declaration of a development candidate, which we are targeting to announce by the third quarter of this year. Now, I'll turn the conversation back to Martin for some closing remarks. Thank you, Cory. To close, I want to put the opportunity in perspective. Pulmonary hypertension associated with HFpEF, PH HFpEF, is a severe progressive condition with no approved disease-modifying therapies. It affects a patient population that is meaningfully sized, more likely underdiagnosed, and carries high morbidity and mortality. The recent CADENCE trial data confirms the activin pathway is biologically active and therapeutically relevant in this exact population. The pending acquisition of 35Pharma by GSK, announced in the past weeks, confirms next-generation, more selective activin pathway inhibitors as a high-value priority for both pulmonary arterial hypertension and for PH HFpEF. Beyond PH HFpEF, the broader cardiometabolic HFpEF population represents a substantially larger opportunity, tens of millions of patients worldwide, driven by the global epidemics of obesity, diabetes, and aging. We believe our biology and our platform uniquely position us to pursue that larger horizon as well, and we are working actively to define the best development path forward. The convergence of clinical validation, strategic industry activity, and iBio's own mechanistic differentiation makes this a compelling moment for this program. We built iBio to target the biology driving the worst outcomes in obesity-related disease. PH-HFpEF and ultimately cardiometabolic HFpEF is where that biology leads. We believe our intentionally selective bispecific has the potential to be a meaningful part of the next generation of treatments in this space. Thank you for joining us today. We look forward to your questions. Thank you. As a reminder to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. One moment while we compile our Q&A roster. Our first question will come from the line of Roanna Ruiz with Leerink Partners. Your line is open. Please go ahead. Hi, this is Michael on for Roanna Ruiz at Leerink Partners, and we have two questions. First, what is the mechanism behind the bispecific antibody being able to target three ligands? Is the antibody targeting, like, a shared epitope between the two ligands? And my second question is, how confident are you that the bispecific antibody will not have any tolerability issues that were shown in previous activin A antibodies, for example, Regeneron's garetosmab? Thank you. Hi, Michael. Thank you for the question. I will hand the first part of the question over to Cory on talking about how we can actually blocking three different ligands with a pure bispecific molecule. Cory. Yeah, thank you for the question. The bispecific antibody has two arms, as a bispecific antibody typically does. One of the arms is specific for activin A, and the other arm is dual targeting, blocking both GDF8 and GDF11. Those two ligands have significant homology, and we were able to target both with a single binding domain. Michael, your question about the safety profile. Obviously, we are designing these molecules with a PK profile that is meant to be a sub-Q dosing and also reducing kind of the peak trough values that we're seeing in exposure. So, if you think back to garetosmab, it's an IV dose, it's a relatively high dose, so you can expect very high Cmax, which likely contributes to the effects that you're seeing in the combination with myostatin that is currently ongoing in Regeneron's COURAGE trial. Great. Thank you. Thank you. One moment for our next question. Our next question will come from the line of Jay Olson with Oppenheimer. Your line is open. Please go ahead. Oh, hey. Thanks for providing this update and taking the questions. We had a few questions. Maybe just to start off at a high level. What's the role of GDF11 in PH-HFpEF? And can you just talk about the binding affinity of your bispecific to GDF11 and the relative contribution of efficacy from GDF11 versus myostatin? Hi, Jay. This is Cory. That's a great question. GDF11 has been observed to be elevated in some patient populations. Our antibody binds very potently to both GDF8 and GDF11, reaching the limits of detection in our assays, so we can't exactly quantify how high the affinity is. As far as the contribution of GDF8 versus GDF11 versus activin A in the biology and in the pathology, I think that's hard to describe, and it likely varies between different patients. Okay. Understood. If I could ask a couple follow-ups, please. We definitely appreciate the selectivity for the three key ligands driving cardiac and skeletal muscle while sparing others. You spoke about the bleeding risk associated with BMP9 and BMP10. Are there any safety risks for molecules that also target activin B? There have been recent publications that suggest that Activin B could play a role in driving FGF 21 expression, which has positive metabolic consequences. Due to that, we made the choice to spare Activin B, especially due to many HFpEF patients and PH-HFpEF patients suffering from metabolic dysfunction as well. Okay. Understood. Maybe one last question from us. Can you just talk about the target patient population for PH-HFpEF? Are you planning to enroll obese patients with PH-HFpEF? Jay, this is Martin. A little bit too early to say before we actually go in first, of course, the safety study. I think what we can learn from the journey of sotatercept is what we're definitely gonna apply to our thoughts and to our strategies. At this point, it's really too early to be precise about the population, but by the time we will get closer to the clinic, I think we'll have a lot more clinical data coming from Merck that will help us to inform how we're gonna design the phase II. This is a very, very sick population. As you know, this is not a population that you know suffers from mild metabolic derangements. We wanna be very, very careful how we enroll and what the characteristics are that we're gonna enroll. At this point, I'm sorry, I can't tell you exactly what the population's gonna look like. Okay, fair enough. We'll stay tuned. Congrats on all the progress, and thanks again for taking our questions. Thanks, Jay. Thank you. One moment for our next question. Our next question comes from the line of Patrick Dolezal with LifeSci Capital. Your line is open. Please go ahead. Hi. Thanks for taking the questions. First one, just curious how a bispecific targeting activin A, you know, myostatin and GDF11 could be potentially differentiated from a co-formulation or a combination of two monoclonals or, you know, three hitting each of those respective targets. The second question is just how you guys have been thinking about partnering versus going it alone for this asset, if there's any sort of further thoughts at this time, given the progress and, you know, the strategic interest that we've seen in this space. Thank you. Very good. Thank you, Patrick. This is Martin. I'll tackle question one and hand it over to Cory for question two. Obviously, antibodies usually have a relatively decent way to co-formulate. What we believe we can create is kind of a, if you will, a fixed-dose combination that satisfies, you know, the same flexibility, because our experience so far with myostatin and also with activin E is that these pathways can be blocked significantly strongly, and for extended duration. We're not too worried about affinities or the pathway in 100%. Yes, it is possible to Could you repeat the second question for me? Sorry, Patrick. No problem. Yeah, just curious how you're thinking about partnering versus going it alone for this program as sort of, you know, things are progressing and strategic interest has become apparent in this pathway. Yeah. That's a great question. We're at an early stage in the program right now, and we're really excited about how we're demonstrating the biology and showing how the molecule works. I think we're a little early to have a concrete strategy on how far we take this ourselves or look for a partner and what the right thing strategically is for the company. Certainly, we're evaluating all the different options there. Got it. Thank you. Thank you. One moment for our next question. Our next question will come from the line of Keay Nakae with Chardan Capital Markets. Your line is open. Please go ahead. Great. Thanks. Martin, how should we be thinking about what your objective is in terms of the balance of the saturation of the three targets? Is activin A where you want to have more of that occurring, or how should we think about that? No, I think what we wanna see is kind of a balanced inactivation of the pathway. As you know, they're converging and they are in part replacing each other. It's gonna be important that we actually block all three pathways in a similar fashion. Now, obviously, we have done some modeling upfront, as Cory mentioned earlier, with binding affinities, but I think ultimately, it'll really come down to individual patients and how much these individual ligands are increased. That's also an ongoing quest of ours to kind of see, is there a way to, you know, narrow down the population that has certain parameters increased and others not that would fit at least for an initial phase II study the bill a lot better than, you know, just going in very broadly. Yeah. A similar type of question, which of the three, if any of the three, is most important with respect to the remodeling of the left pulmonary artery? I'll let Cory answer that question. That's also an interesting question. You know, we don't have conclusive data to say which is the most relevant for that remodeling. Some literature might suggest that activin A plays a more significant role there. I don't know that we quite have conclusive data to say that is 100% the case in every patient. Okay. I guess maybe the third question is, do you feel like the goal would be simply to arrest that process, or is there any possibility of reverse remodeling? I think we're a little early to say. Certainly, we would aspire to see reversal of remodeling, but we're early in the program where we, you know, don't have clarity whether this is a blocking or prevention of further remodeling or reversal of the remodeling. Okay. Let me just ask one last question then. What do you still need to optimize before you nominate a candidate? Yeah. We have several very promising candidates that we're trying to discriminate between to pick a single molecule to move forward. The biological activity of all of the candidates is quite robust, and now we're trying to select a candidate that's the best fit from a manufacturability and developability perspective. Our target is to have a subcutaneously administered molecule, which for a bispecific, we wanna make sure we take our time and pick the right development candidate. Okay, great. Thank you. Thank you. One moment for our next question. Our next question will come from the line of Catherine Novack with JonesTrading. Your line is open. Please go ahead. Hi, afternoon. Thanks for taking my question. I guess, you know, thinking about seeing potential data from development candidates down the line, what's the best way to think about possibly comparing your bispecific to sotatercept or other ligand traps pre-clinically? You know, are we looking at downstream signaling, relevant animal models of disease? You know, what's the best way to frame that given the different mechanisms of action? Yeah. This is a, I think, a two-part answer here. First, head-to-head comparison in animal models of HFpEF, I think are reasonable to perform. That will certainly be something we explore as we advance the development program. The second thing that we keep in mind as we run these studies is that when we run, for example, a mouse model of heart failure, these mice are only surviving for a month, right? Then the study ends. A molecule that's very efficacious over the course of a month but has long-term safety risks might look very good in a mouse, but maybe not be something that you want a human patient to be taking for years in a chronic setting. We view the de-risking of the sparing of the BMP9, the BMP10, and the Activin B as benefits that might be harder to demonstrate in preclinical models but give a lot of upside and safety promise for the molecule as we advance towards human testing. Okay. Is there a, you know, a relevant NHP model for this? You know, other than just looking at PK in NHPs, is there, you know, is there another situation where we could see efficacy in an NHP prior to clinical trial initiation? We're currently weighing what the optimal development path is there. There are potentially monkey models. There's also potentially pig models. Given the validation level of the biology in humans and the models that are available, we haven't quite settled on what the right first large mammal to be tested is. Okay. Great. Thanks for taking my questions. Thank you. One moment for our next question. Our next question will be from the line of Ben Burnett with Wells Fargo. Your line is open. Please go ahead. Hey, thank you very much, and congrats on this exciting program. I wanna just kinda double-click on kind of the maybe points of differentiation that are expected relative to Sotatercept. I guess, really, what level of activin A inhibition do you need to sort of improve on Sotatercept? Is it may be understood if Sotatercept is maybe insufficiently inhibiting activin A and GDF11 and some of these other targets? Yeah. We don't wanna disparage sotatercept, right? This is a drug that has been life-changing for many patients. When we think about the differentiation, you're right. By sparing some of the other ligands and potentially getting a deeper level of pathway inhibition because of that selectivity, you know, we think it's possible that that could lead to better outcomes, but we're still exploring what the impact of that is. This degree of inhibition is a very challenging thing to measure in preclinical models. Unfortunately, we really will not be able to say conclusively until, you know, we're in clinical development. Okay. Thank you. Thank you. One moment for our next question. Our next question will come from the line of Mayank Motwani with B. Riley Securities. Your line is open. Please go ahead. Yes. Good afternoon, team. This is Mayank Motwani. Thanks for taking our questions. In terms of the target product profile, you mentioned subQ is a part of it. Is there a frequency of administration you're you know trying to also figure out as you get through candidate selections and do you know some of the NHP work? Then on the animal work that we've seen out there, you know, there's also the CMI drug class. I was just curious how you think of some of the contractility and fibrotic mechanisms, you know, contrasting with the obvious finding on GDF data. If you would have plans to not just be restricted to PH and may also consider HFpEF broadly. Yeah. Thank you for the question. For the dosing frequency, if you're aware of our pipeline, we have experience with half-life extended antibodies, and that's certainly something we're considering. At the same time, given the acute nature of this, shorter periods of administration might be more favorable. We haven't guided yet towards a targeted dosing frequency. It's something that will be guided by our preclinical studies, by our safety studies, and then by our early clinical work. With respect to disease areas beyond PH-HFpEF and different disease models, these are areas we're actively exploring. I think the clearest line of sight for us to clinical success is with PH-HFpEF. We are, you know, I think, putting the hardest push there. But as we advance the molecule, we certainly will be looking to expand beyond that and try it in different disease-relevant models. In your IND filing, you know, you will may have to submit a phase I protocol, like what initial SAD/MAD work, you know, here would be relevant to, you know, watch out for even the GLP toxicology work that you do to kind of rule out some of the safety, you know, mechanistic differences that you know, we are talking about versus TGF data. Fortunately, here, you know, there is data in the literature that can guide us towards safety signals to be on the lookout for. I think as we design our pivotal GLP safety studies, those will factor in. I think it's a little early for us to guide towards dose levels or phase I design protocols. Those are things we're still developing at this time. Understood. Thank you for taking the question. Thank you. This concludes today's question and answer session. Ladies and gentlemen, this also concludes today's conference call. Thank you for participating, and you may now disconnect. Everyone, have a great day.