Good morning, everyone, and thank you for joining us today. Before we begin, I would encourage everyone to follow along on the slides provided. 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. Reference 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 from the results discussed in the forward-looking statements. The information on this conference call is provided only as of today, and we undertake no obligation to update any forward-looking statements made on the call on account of new information, future events, or otherwise except as required by law. On the call today representing the company are myself, Felipe Duran, the Chief Financial Officer, and Dr. Martin Brenner, iBio's Chief Executive Officer and Chief Scientific Officer. At iBio, we are building the next generation of antibody medicines to tackle one of the world's most significant public health challenges: obesity and its cardiometabolic complications. During the call, we will share why the medical community is looking for new treatment options for obesity, how iBio's platform gives us an edge on developing those options, and what our preclinical data show about the three programs we have advanced in just over a year to potentially aid the medical community, but most importantly, underserved patients. One of the most important advances in modern obesity treatment has been the emergence of GLP-1 receptor agonists and other incretin-based therapies. These drugs have transformed the field by enabling weight loss that, in some cases, rivals the effects of invasive bariatric surgery. As physicians and patients gain real-world experience, it's becoming increasingly clear that first-generation therapies, while groundbreaking, leave important gaps, and that's where next-generation treatments like ours come in. Let me turn the call over to our CEO, Martin, to discuss why we're developing next-generation obesity drugs. Thank you, Felipe. First, many patients remain on GLP-1 therapy for only a short time. Much of this is due to gastrointestinal side effects like nausea and vomiting, which can lead to dose reductions and, in some cases, discontinuation, ultimately limiting the drug's effectiveness. Second, once GLP-1 therapy is stopped, weight often comes back, and quickly. Studies show that patients may regain up to 80% of the lost weight within a year, and fat tends to return faster than muscle, further worsening the composition of weight regained. Third, not all the weight lost on GLP-1s is fat. In fact, 30%-40% of the weight loss is from lean mass, including muscle, bone, and water. This has potentially serious long-term implications, especially for older adults, where muscle loss can lead to reduced mobility and increased frailty. One recent clinical trial even linked this type of lean mass loss to measurable declines in muscle function. Dr. David Kessler, former Commissioner of the U.S. FDA, captured his experience in a guest essay published in The New York Times on May 7th. He shared his personal journey with GLP-1 therapy: the initial weight loss, the weight regain after stopping, and ultimately his decision to come off the medicine. It's a powerful reminder that for many patients, the story doesn't end with GLP-1s. While incretins have opened the door, there's now a clear call for next-generation therapies: treatments preserving and even possibly building muscle, targeting fat selectively, and delivering durable long-term results with a tolerability profile suitable for long-term use across a wide range of patients. iBio's response to the evolving needs in obesity treatment is built on a fully integrated antibody discovery platform, designed from the ground up for precision, speed, and developability. At the core of our platform is an AI-enabled epitope steering engine, enabling us to precisely direct antibodies to functional hotspots on even the most challenging targets, often considered undruggable. When combined with our antibody optimization platform, which deeply integrates generative AI tools with mammalian display technology, we can progress from concept to development-ready antibody in as little as seven months. It does not stop at rapid discovery. We have also hardwired developability and manufacturability into our optimization process. We do not just improve affinity. We build in high expression, enhanced stability, and other key properties from the start. This ensures the antibodies we create are not just potent, but truly ready to become medicines. In short, we do not just discover antibodies. We design precision biologics engineered to serve large, underserved patient populations with the efficiency and quality needed to succeed. That design philosophy isn't just baked into our platform. It drives our entire R&D, which is anchored in three pillars. First, we focus on therapies complementing or following GLP-1 treatment, or that offer well-tolerated monotherapy alternatives for patients who can't or won't stay on GLP-1s. Second, we pursue targets with strong human validation, either genetic or pharmacologic. This reduces development risk and increases the likelihood of generating first or best-in-class molecules. Third, we've created a competitive edge by tying together our platform, our team, and our pipeline. This keeps our programs moving fast and keeps us moving ahead with strategic clarity. This strategy allowed us to build and rapidly advance a pipeline with several differentiated antibody programs. Our most advanced program is iBio 600, a long-acting anti-myostatin inhibitor now in IND-enabling studies. We're about to begin GLP toxicology, and we remain on track to dose our first patient in the second quarter of 2026. Next, iBio 610, our first-class Activin E antibody, has delivered compelling results in mouse models. We've recently selected our development candidate, and it's currently being tested in non-human primates. We expect data from that study at the end of Q3 this year. If the data confirm what we've seen in rodents, we'll move swiftly into IND-enabling CMC and safety studies. Just this morning, we unveiled the latest program in our partnership with Astral Bio, targeting the amylin receptor. Interest in this mechanism has been steadily rising, especially as clinical data emerged from both DACRA molecules, which target both the amylin and calcitonin receptor, and newer agents targeting amylin receptors alone. Our platform has allowed us to generate both DACRA-like antibodies and, more importantly, highly selective amylin receptor antibodies. Even more impressively, we've been able to target specific receptor subtypes, avoiding the off-target involvement of the calcitonin receptor, which could offer meaningful clinical advantages. We're incredibly excited about this program, and you'll hear more from us on its progress in the months to come. Now, let me walk you through iBio 600, our lead program and key value driver for the company. iBio 600 is a long-acting anti-myostatin antibody, and we are preparing to initiate GLP toxicology studies shortly. We're on track to file an IND or equivalent in the first quarter of 2026, with the goal of dosing our first patient in the second quarter. The target, myostatin, is one of the most well-validated in muscle biology. It's a key negative regulator of muscle mass, and we know from human genetics that individuals with myostatin loss-of-function mutations are unusually muscular, strong, and lean, with no known adverse effects on health. Importantly, iBio 600 goes beyond traditional myostatin inhibition by also targeting GDF-11, a closely related molecule that suppresses muscle growth and contributes to fat accumulation. This gives the antibody a dual mechanism of action that we believe will translate into broader efficacy. We've designed iBio 600 for extended durability. In non-human primates, we observed a half-life of 52 days. When scaled to human physiology, we project a half-life of between 74 and 130 days. That extended pharmacokinetic profile opens the door to potentially dosing patients just twice per year, an important convenience and compliance advantage. In terms of data, we've tested iBio 600 in aged, obese, non-human primates, a model that closely mimics humans aged 65 to 75 with a BMI over 30. Following a single five milligram per kilogram injection, we observed an approximately 8% increase in muscle mass at both eight and 12 weeks, along with a reduction in fat mass of 12%-15% over the same period. These are highly encouraging results, particularly given the single-dose design and the age and obesity of the model. In addition to strong pharmacology, iBio 600 has been engineered for scalability and accessibility. Our early CMC data show excellent developability with expression levels around 10 grams per liter and formulation concentrations of 150 milligrams per milliliter. This positions us to efficiently produce the antibody at the scale needed to serve a broad obesity population. To our knowledge, no other myostatin inhibitor in development has demonstrated this combination of extended half-life, dual targeting of myostatin and GDF-11, and simultaneous increase in muscle mass and reductions in fat after a single dose, while also showing strong manufacturability characteristics. Looking ahead, we believe iBio 600 can play multiple roles in obesity care. As a monotherapy, we believe it has the potential to achieve the 5% weight loss thresholds required for regulatory approval. As a combination therapy, it can enhance GLP-1 or amylin-based treatments by helping preserve muscle mass during weight loss. As a maintenance therapy, it can help patients maintain weight loss and muscle mass after transitioning off incretin therapies, addressing a critical unmet need in long-term weight management. In short, iBio 600 is a highly differentiated dual-action biologic with strong preclinical evidence, a highly convenient dosing schedule, and the scalability to serve a broad patient population. We're excited about its potential as we are preparing to enter the clinic in 2026. Now turning to iBio 610, our second program and another example of how we're using our integrated AI and antibody discovery capabilities to pursue differentiated first-in-class biologics. iBio 610 is an antibody targeting Activin E, and it has just reached the development candidate stage. We've successfully produced a non-GMP batch, and this material is now being used in an ongoing non-human primate study, which we expect to read out in late Q3 of this year. If successful, we plan to enter IND-enabling studies in the fourth quarter this year with an IND or equivalent filing anticipated toward the end of 2026. Activin E is a liver-derived protein, and its relevance in human disease is supported by strong human genetic evidence. Individuals with loss-of-function mutations in INHBE, the gene that encodes Activin E, have been shown to be protected from obesity, cardiovascular disease, and type two diabetes. What makes Activin E especially attractive is its mechanism of action. It promotes fat-specific weight loss without affecting other tissues like muscle. Despite this promise, Activin E has historically been considered a target nearly undruggable with antibodies. To our knowledge, iBio 610 is the first and only Activin E antibody in development. That is not a coincidence. Activin E has proven extremely difficult to drug, but thanks to our discovery platform, which integrates generative AI with powerful screening and optimization methods, including our mammalian display platform, we were able to generate this first-in-class antibody that binds Activin E with sub-nanomolar affinity and potently blocks signaling in both engineered cells and, critically, in primary human adipocytes, which is considered a highly translational model for human fat biology. iBio 610 has also been engineered for extended half-life, and the current non-human primate study will give us our first real-world look at the durability and potential dosing intervals. Encouragingly, the manufacturing process has been smooth so far. We produced 16 grams of material for the non-human primate study easily and early, an early and promising sign for future scalability. From a pharmacology standpoint, iBio 610 is an approximately 150 picomolar antibody, and it inhibits Activin E signaling in engineered cells with sub-nanomolar potency. In obese rodents, iBio 610 led to approximately a 9% reduction in total body weight, but importantly, that reduction was entirely fat-specific with a 26% reduction in fat mass and no loss of lean tissue. When combined with the GLP-1 receptor agonists, the effects were synergistic, producing a body weight loss of slightly over 35% and a reduction in visceral fat of approximately 69%. That is particularly relevant because visceral fat is strongly linked to cardiovascular and metabolic risk. In an obese mouse study, we tested iBio 610 in the weight maintenance setting, dosing it after an initial GLP-1-driven weight loss. iBio 610 completely prevented weight regain, maintaining fat mass reduction throughout the duration of the study. That kind of durable fat loss after cessation of incretin therapy is a critical unmet need and one that iBio 610 may uniquely address. To our knowledge, iBio 610 remains the only Activin E antibody in development, which speaks to the technical difficulty of the target, but also to our platform's unique ability to overcome those hurdles. The fat-specific mechanism, the synergy with appetite-regulating drugs, the weight maintenance potential, and the early signs of strong developability combine to make iBio 610 a highly differentiated therapeutic opportunity. We believe iBio 610 is best studied as a monotherapy first and as a compelling combination partner. Most importantly, we see iBio 610 playing a critical role in maintaining weight loss after patients transition off these therapies, helping to sustain fat mass reduction and support long-term health outcomes. I'm excited to introduce the newest program in our partnership with Astral Bio, which we unveiled this morning. This program targets the amylin receptor, and it has already advanced from early to late discovery, a stage that enables us to begin in vivo testing of multiple candidate molecules with diverse pharmacological profiles. The amylin receptor, or AMYR, is a heterodimeric GPCR composed of the calcitonin receptor and various receptor activity-modifying proteins, so-called RAMPs. It is activated by amylin hormone co-secreted with insulin from pancreatic beta cells. When stimulated, amylin receptors play a crucial role in promoting satiety and slowing gastric emptying, enhancing the feeling of fullness after a meal. Because of this, they represent a very promising target for the treatment of obesity and other cardiometabolic diseases. Now, what differentiates our approach is the application of iBio's AI-driven antibody discovery platform, which has enabled us to generate a diverse portfolio of antibody and antibody peptide fusion molecules that can agonize either specific amylin receptor subtypes or act more broadly across multiple subtypes with a DACRA-like profile. This level of precision and versatility in GPCR agonism is extremely difficult to achieve and positions us to identify a best-in-class therapeutic candidate with an optimal balance of weight loss efficacy, gastrointestinal tolerability, and preservation of lean mass. To support these claims, we recently tested one of the novel engineered amylin receptor agonist antibodies in an obese rodent model. The molecule reduced acute food intake by 60%, which is comparable to the effect of a clinically advanced DACRA peptide. What's important here is that our first-generation molecule demonstrated both amylin and calcitonin receptor activation, but through our AI-guided optimization workflows, we've already been able to generate next-generation molecules that are selective for amylin receptor subtypes and avoid calcitonin receptor activation entirely. From a technical perspective, peptide-based amylin agonists have faced challenges with achieving receptor specificity and extended half-life. Antibodies offer a natural advantage in terms of pharmacokinetics, but historically, it's been very difficult to generate antibody-based agonists that activate complex GPCRs like the amylin receptor. Using our platform, we have now solved both challenges, producing molecules with long half-lives and achieving either broad DACRA-like activity or precise subtype selectivity. To put this in context, amylin analogs currently in clinical development have shown up to 22.7% body weight loss in combination with semaglutide and nearly 12% weight loss as monotherapy. Our program aims to build on and extend these results by targeting complementary signaling pathways, which could lead to enhanced efficacy when combined with GLP-1 receptor agonists or serve as standalone treatment for patients who are intolerant or unresponsive to GLP-1-based therapies. In short, this program exemplifies how our AI-enabled platform is solving long-standing challenges in antibody-based drug discovery, allowing us to go after complex, high-value GPCR targets like the amylin receptor with speed, precision, and therapeutic ambition. These new next-generation molecules will enter rodent efficacy studies early in the fourth quarter of this year, and we look forward to sharing the results when available. In closing, we believe we're entering a new chapter in obesity treatment, one that builds on the breakthroughs of first-generation incretin therapies, but also responds to the clear and growing call from patients and physicians for more. Patients are asking for therapies that address the adverse effects of current treatments, that offer better tolerability, and most importantly, that deliver durable long-term weight loss. At iBio, we're answering that call. Our pipeline is built on genetically validated targets and designed to complement or extend existing therapies by preserving muscle, selectively reducing fat, and sustaining weight loss after treatment ends. Our AI-enabled discovery engine, combined with DeepBiologics' expertise and a uniquely agile team, allows us to move from concept to development-ready molecules in record time while building in developability and manufacturability from day one. Together, this creates a competitive advantage centered around our pipeline, where platforms, people, and product strategy reinforce each other. We're confident that this model positions iBio to deliver the next wave of differentiated antibody therapeutics, and to do so with speed, precision, and quality. Thank you, and now we'll turn the call to the operator for Q&A. Thank you. If you'd like to ask a question, please press star 11. If your question has been answered and you'd like to remove yourself from the queue, please press star 11 again. One moment while we compile the Q&A roster. Our first questions come from Kay at Chardon. Your line is open. Yes, hi. It's Kay at Chardon. Maybe my first question related to iBio 600. Last week, we did see data from Scholar Rock's and Lilly's study for their apitegromab combined with tirzepatide, and it did show, I think, some positive results reducing the ratio of muscle loss to fat. Maybe comment on your thoughts of that study outcome as reported and how your drug is differentiated. Very good. Thank you, Kay, and good morning. Yeah, I think this is a really relevant question. I think the last few weeks have shown three key studies reading out in the muscle-sparing and muscle-protecting space. Number one was Regeneron reporting the Courage trial, and then obviously Scholar Rock reading out the apitegromab data, but also Eli Lilly with bimagrumab that has just released data yesterday at the ADA conference. We're highly encouraged by the data we've seen from Scholar Rock and from Regeneron. I think it really has proven that, number one, there is a significant muscle loss on GLP-1 therapy so that there is truly a need to preserve that muscle. And number two is that we have seen also that it is possible to preserve that muscle mass to a pretty large degree. Now, given that most molecules in Trevogrumab from Regeneron and also Apitegromab from Scholar Rock only target myostatin, and our molecule targets GDF-11 as well, we believe that gives us a little bit of an edge or could give us an edge on efficacy, and that together with a long half-life kind of cuts out these exposure troughs of shorter-acting antibodies where you probably sink below a certain inhibition of myostatin, which eats into your efficacy as well. It is highly encouraging to us, especially combining this with a study that a small company, Viro, has recently published that have linked actually the preservation of muscle mass to a preservation of muscle function as well. There was a stair climb test, and basically, these adults were still able to climb the same amount of stairs after the muscle mass has been protected. Highly encouraging, and we're really looking forward to kind of move our molecule in phase one. Because of the long-acting nature, we expect the interim readouts, at least very early on, signs of efficacy somewhere halfway through our phase one. Okay, great. For the amylin agonist you're talking about today, what's the next step and timeline for that candidate program? That's a very good question. We have been attending the American Diabetes Association meeting last week, and what has become very clear is there is an extremely high interest in amylin molecules. Might this be small molecules? Might this be injectable peptides? What is currently really missing is that nobody knows exactly what profile you have to create. Is calcitonin receptor necessary and relevant, or is it actually adding to your adverse effect profile? The adverse effect profile of several of these molecules has not been as promising, so we believe by creating the tools that we create right now with subtype-specific antibodies that can very, very selectively activate these receptors, we're able to discover which biology and which contribution of which receptor will be beneficial for efficacy and might even be able to reduce the adverse effects that some are seeing. Okay, great. Thank you. Our next question comes from William Wood with B-Rally Securities. Your line is open. Hi, thanks for taking our questions and very nice data, or at least announcement this morning on the new program and amylin antibody agonist. I was curious if you could just provide, maybe touch on a couple more, a little bit more detail on what specific properties of this asset stood out in your decision process, maybe how you feel that targeting or using an antibody approach versus amylin may be differentiated based on peptides or small molecules. Also, maybe if you could provide if this will be targeting sort of one amylin or multiple, and if that strategy is set in stone or there's still some sort of wiggle room in exactly the defining characteristics of the molecule you'll be bringing forward? That is a very good question. Thank you for that. You're absolutely right. I think antibodies have two advantages, right? Number one is the long half-life. As you remember, amylin receptors have been pursued for a long, long time. The initial molecules that actually were moved into the clinic were short-acting, and so were lacking efficacy. It looks like this is a mechanism that really benefits from long-term activation. Peptides can be engineered to act longer, and I think we see the first ones coming out, even potentially being monthly treatments. Obviously, an antibody with a natural half-life, even non-half-life extended of 16-23 days, has a huge advantage. Our engineered antibodies, especially if you look back at our anti-myostatin antibody, we can create extremely long half-lives compared with this. We believe that is a really differentiating factor for us. As to the selectivity, you are absolutely right. We are not set in stone yet. What we are creating right now is we're creating molecules against the amylin receptor one, the amylin receptor three, and then an antibody that has DACRA-like properties, so hitting all three amylin receptors and also calcitonin. This will allow us then to kind of compare these molecules and tease out what is really contributing to efficacy, which part is really contributing to adverse effects. That'll allow us then to move the molecule forward that we deem is the most suited. Now, you could argue this is kind of a long time, and you have to optimize these molecules. I really want to highlight our mammalian display platform here because we can literally take one of these molecules and within three weeks optimize this to a level where we can actually move this forward into IND-enabling studies. We have the speed, we have the efficiency to really test this principle and really come out with a best-in-class molecule that then can rapidly be advanced. Awesome. I appreciate that. Just thinking maybe a little bit broader in terms of how this fits into your current programs, just you've developed or have been thinking about developing biospecifics. Do you see this fitting in potentially as a biospecific or even tri-specific later on, sort of once you further on in development? Yeah. As you know, we've developed our pipeline really with the mindset of how can we actually get to a best combination, right? We obviously do not own a GLP-1 receptor agonist, but obviously, amylin can be slotted in the same area with appetite-reducing drugs. That can be very, very easily combined with, say, an activin E antibody. Of course, we need to think very carefully about this because if you're targeting a receptor, that antibody binds to a certain cell-type receptor, whereas if you go after a soluble protein that occurs in plasma, you need basically more antibody in plasma. Sometimes there's technical difficulties, but that doesn't mean you cannot co-formulate, right? We do have in mind that some things can be combined. For example, a myostatin and activin E might be very, very amenable for development of biospecific. We obviously have an activin A myostatin biospecific already in development. We are thinking very carefully about how can we actually combine these therapies with basically minimizing the burden on the patient when it comes to adverse effects, but still maximizing the outcomes. Obviously, an amylin plus something that is weight maintenance, like a myostatin or an activin E, might be very good combinations, either as multi-specifics or as co-formulation therapies. Got it. Very helpful and understood. Congrats again. I'll hop back in queue. Thank you. Thank you. Our next question comes from Dev Prasad with Lucid Capital Markets. Your line is open. Hi. Thank you for taking our question and congrats on the update. I have a question on activin E molecule. Can you add more color on the molecule, although it's first-in-class, how it's distinct versus others in terms of molecule and also being first-in-class, how this molecule can be positioned for next-generation obesity treatments? Very good. I think you have to go back to the activin E protein itself to explain how difficult this is. Activin E has really been plagued with a lot of researchers and scientists trying to make this protein outside of the body, so-called recombinant protein. This is a very complex protein that has multiple internal structures that stabilize the protein itself. This protein has been made outside of the body, but it did not fold correctly. What this does is it is actually creating surfaces that are artificial and that are highly attracting antibodies very highly. Those antibodies, although detecting the falsely folded protein, did not detect the endogenously folded protein. That is why the whole field came to a halt. What our platform was able to do is we picked certain areas of activin E and made small representations, small proteins that represented several areas of that, and we used that for our screening purposes. That allowed us then to find an Activin E antibody that truly targets the endogenous Activin E. We believe there's some significant hurdle if you don't have access to a platform like ours to create antibodies. Again, as evidenced by this, the target has been linked to obesity, cardiometabolic disease, and type 2 diabetes three years ago in very elegant back-to-back articles in Nature Communications, I believe, by Regeneron and Alnylam. That is why you're also seeing the knockdown efforts. We have two competitors that use siRNA approaches. As I mentioned, it's a liver-targeting, it's a liver-derived protein, and the knockdown efficiency in liver has in rodents already shown efficacy. These programs are slightly ahead of us. They have entered clinical trials earlier this year. We see this as a very strong validation. Not only have two molecules already gone through GLP toxicology, they have also entered clinical trials, and we're expecting, based on the long-acting nature of siRNA, that we're seeing very likely the first results by the end of the year. It is very supportive of what we're doing. Now, as you know, knockdown strategies, and this is based on patents and literature that we have combed through, achieve about a 60% reduction of circulating Activin E with knockdown strategies, while an antibody, of course, can potentially block Activin E by 100%. It depends on the dose, really. We see that we have an advantage, A, from an efficacy perspective here, but we also see an advantage because antibodies can actually be combined, can be made in multi-specifics, and obviously, siRNA is a single drug that is hard to kind of put in the same syringe with another drug. Great. You said IND filing will be in the second half of 2026. Correct. What are the next steps that you are looking from now to that second half? Yeah. Very good question. We are currently running a non-human primate study, again, in aged obese monkeys to reflect better the human population we want to treat. That study is ongoing. We expect data from this study to read out sometime to the end of the third quarter this year. That is a study that actually combines not only monotherapy, but also is being used on top of a GLP-1. We expect to see fat loss. We expect to see body weight loss in that study. If the study shows what we have seen in rodents, we are rapidly advancing this molecule into IND-enabling studies. That means we start the CMC work and start the safety work. Based on the expression that we've seen and that the molecule behaves really well in manufacturing so far in a non-GMP fashion, we believe we can really quickly move through that CMC process. As you know, antibodies require a quite long development process. It's probably going to take somewhere between 10 and 12 months to get through the manufacturing process. Okay. Great. Thank you. Our next question comes from Kemp Doliver with Brookline Capital Markets. Your line is open. Hi. Thank you. And good morning. With regard to 600 and phase one, do you expect that you will explore the three dosing regimens that you highlighted? Also, have you determined if the means of administration will be IV or subq, or is that something you're going to also explore in phase one? Thank you. No, thank you, Kemp, for that question. First of all, iBio 600 will be exclusively subcutaneously. We do not believe that an IV drug is useful in a very broad and diverse obese population. It has to be, we have to be able to self-administer this. It has to be able to fit into an autoinjector. Number two, because of the extended half-life of iBio 600, we want to make sure that in our phase one A, we are looking very, very carefully at the safety profile, at the pharmacokinetics, because the pharmacokinetics will be dramatically important for us when it comes to the dosing intervals. As I mentioned before, we have modeled this out from the non-human primate PK, have assumed some very conservative human half-life and absorption rates, and we have still gotten to twice-a-year dosing with that modeling. Obviously, that data, the PK data, will be critical. Now, because of the long-acting nature of the molecule, we believe that at one point in some dose cohort, eight weeks in, we will see, very similar to the non-human primates, an increase in muscle mass and a reduction in fat mass. This is why, at least for now, we're planning to enroll overweight patients. We believe we see early signs of efficacy at one point in that phase one A. Now, beyond phase one A, obviously, this is going to be, as you mentioned, we have to think very carefully about the applications, clinical applications for this molecule. Very obviously, what stands out is the co-treatment with GLP-1 drugs, but also how quickly can we then actually move into the weight maintenance regimen that I mentioned earlier. That is still ongoing debates. Our goal is to get to the end of phase two, so, if you will, human proof of concept as fast as we can, but considering that there's multiple options. That phase two study will definitely be a more complex study than a typical monotherapy. Got it. Just to be clear, with regard to the dosing regimen, they'll really be investigated in phase two, correct? Yes, that is correct, right? I think most of the modeling that relies on non-human primates just has to be refined. We need to really understand what the half-life is going to look like. Is there obviously a correlation between dose and exposure levels? So far, all of that has worked very well with the antibody in non-human primates, but obviously, we need that human data to be sure about that. We've modeled actually not only that we can dose twice a year. As you can imagine, this is a molecule that could potentially be put in the same syringe as a GLP-1 receptor agonist or an amylin. We have also modeled out what kind of the dosing regimen and the volumes might look like and amounts if we go to a once-weekly dosing. It is being co-formulated with one of the incretin drugs. We have also modeled that, as you can imagine, because of the long half-life, the amounts we would have to add to a GLP-1 drug are tiny, which obviously improves our chances of successfully co-formulating this with existing GLP-1 drugs. Great. Thank you. Thank you. Our next question comes from Mazi Alio Mohammed with Leerink. Your line is open. Thanks, Martin, for the thorough update. Just two from me. First, do you anticipate any different pharmacodynamic properties or desensitization kinetics relative to endogenous ligand binding for the newly announced amylin molecule? Another one for me is actually, have you profiled hypothalamic or brainstem neuronal activation post-administration for the new asset that you announced? Really, really good question. We have not gotten that far. This is very sophisticated mechanistic studies. You're absolutely right. We definitely want to see, to our knowledge, the amylin receptors reside mostly outside of the blood-brain barrier, which should be very easily amenable with antibodies. Our feeding study in mice has already shown this. We're not concerned at this moment. What you said before is really relevant, right? If you think about GPCR receptor biology, and I think if I go back to the very early receptor agonists, small molecule agonists, they have often been optimized for being highly, highly potent and have high affinity, which led to receptor internalization, right? If you have receptor internalization, you shut down the pathway. Now, I think one great example that we're seeing out there how antibodies can actually prevent this is you can actually have an antibody bind to the receptor, hook that up with a peptide, and while the peptide agonizes the receptor, the antibody retains the receptor on the cell surface. Now, we can measure this, right? This is a characteristic we can very easily dial in. I just want to give you an example from the oncology world, right? If you're having an ADC antibody, you want this antibody to internalize rapidly to deliver the payload. Whereas if you have a bispecific antibody that needs to attract T cells, you want that antibody to retain and remain on the cell surface as long as possible to give it the best chance to attracting a T cell. This is a very similar principle that we're applying here. We truly believe that antibodies can actually lock this molecule at the cell surface. And if you're taking a small look over to Amgen with maritide, I think that is at least speculated what happens with maritide and why it is so powerful because actually that molecule retains at the, that receptor retains or remains at the cell surface. Thank you very much. Thorough response. Thank you. Thank you. Our next question comes from Justin Zelin with BTIG. Your line is open. Thanks for taking our questions and congrats on the progress here. I wanted to also ask about the amylin agonist here. You made some comments that calcitonin may not be, let's say, part of the strategy or a selective amylin might offer a better profile here. I was just wondering if you could speak to some evidence of that that either yourself or others have generated here and just a follow-up. 100%. I think this is a really good question. I am sorry, I cannot give you a direct answer what is the best. I think nobody can at this point. If you're looking at Novo Nordisk's novel molecules that claim to be very selective for amylin receptor, that I think is one way to look at this. You can also look at Eli Lilly's molecule where there seems to be a balanced activation of both. I think we will very soon see if kind of a balancing away from the calcitonin receptor actually provides better adverse effects. There are voices that clearly say maybe calcitonin receptor, at least a small involvement, might be important. As you can imagine, because we can tune the selectivity of our antibodies so very, very carefully, whatever we learn from future clinical developments and whatever we learn from our very selective molecules from an adverse effect profile, from an efficacy profile, we can obviously use this to our advantage and then create a molecule that has the right balance. At the moment, I do not think anybody has the answer of what the right balance is. At least we have the tools now to interrogate this question. Understood. Just on the amylin itself, do you see this as being able to provide a good profile as a monotherapy, or do you envision that it will be combined with another agent such as an incretin or another asset in your portfolio? Yeah. You have to think of combining this with a GLP-1. Both affect food intake, right? I think having zero food intake is not combinable with life. I would argue that this would be a very good combination for something that is preventing muscle loss. I think that could be a very good combination. I think there is a very, very good chance this will become a monotherapy. Remember, there is still a population. It is a small population right now, which is given 100 million obese patients that can be treated, still a big population. Some people do not respond to GLP-1. Some people even gain body weight on GLP-1s. We have not fully understood why that is. We have also patients that have obviously very severe adverse effects even after a single administration of a GLP-1 receptor agonist. I think there will be a growing population that is unable to take GLP-1s that need an alternative. So far, amylin seems to give us the most pronounced weight loss of all the other therapies that are out there. I do believe there is a monotherapy, a very big monotherapy potential. Like with GLP-1 receptor agonists, I think we do need to protect muscle mass. Having this in combination with a myostatin antibody might be a very, very smart way moving forward. Right. That makes sense to me. Maybe my last question just on amylin is I assume that this would be directed towards an obese population. Any issues with patients that might be comorbid with type 2 diabetes with an amylin-based approach? Do you see any kind of potential issues there? Huh. You're pointing something out that's very, very important. We're really in the early stages, right? At the moment, I think we're considering obese people as a single population. I can tell you that's not the case, right? You mentioned type 2 diabetes. That's a clear comorbidity. We can highlight cardiovascular disease. We can also highlight kidney disease as comorbidities. I think as we move on and understand better the differences in this large population, I think you will also see better tailored therapies. At the moment, I wouldn't want to make a distinction because I think the data is missing. I would clearly say you will see that differentiation not only based on adverse effect profile. You will see that differentiation and use cases of these drugs in the future based on what we're learning from clinical readouts from these subpopulations. Great. Thanks for taking my questions. Congrats again. Thank you. I'm showing no further questions at this time. I'd like to turn the call back over to Martin Brenner for closing remarks. Thank you for joining us this morning. We are excited to keep you appraised of iBio's progress and these next-generation cardiometabolic assets. Thank you for your participation. This does conclude the program. You may now disconnect. Everyone, have a great day.