Good morning, and welcome to the Jefferies Global Healthcare Conference. My name is Tim Odutola, a member of the Jefferies Healthcare Investment Banking team. Today it's my pleasure to introduce Martin Brenner and Felipe Duran of iBio. Thank you. Thank you, Tim. Thank you. Before we begin, just want to let you know we might be making some forward-looking statements. Obviously, our legal team would appreciate us showing this up on the screen. When we started this process, we knew that GLP-1s were life-changing. We also knew that it came with some constraints. What are those constraints? Some gastric issues, some durability of weight loss, muscle mass, bone density issues. How could we address those? Additionally, we know that there's a rebound effect. Once you come off GLP-1s, most patients gain a majority of their weight, but that weight is actually mostly fat. You're basically regaining your body mass to where you started. How did we approach this? We wanted to design a portfolio approach of products that basically prevented muscle mass loss. It reduced side effects. It also sustained weight loss for a longer period of time and decreased dosing frequency. Our complete portfolio approach has been created on validated targets, focusing on fat-specific weight loss, targeting caloric and energy with less side effects, last but not least, making sure that we are increasing muscle mass. The overall effect of this was basically created with our platform. All of these molecules were complex to create, specifically our activin E program, which is the only antibody right now, with an antibody approach. Over the next 18 months, iBio has numerous inflection points that we are extremely excited to be sharing with you. We recently just dosed our first patient in IBIO-600, which is our long-acting myostatin program. That readout or interim readout will be completed by the end of this year, which puts us at additional studies, hopefully in the early part of next year. Our lead asset, which is our IBIO-610, our long-acting activin E molecule, is completing CMC work and will be filing in Australia by the end of this year. That puts us at first patient dosed first quarter of next year, and interim readouts by third quarter, fourth quarter of next year. Lastly, we have a bispecific program. That's our myostatin activin A program. We are rapidly advancing that program into developmental candidate and hope to have first patient dosed by second half of next year, again, in Australia. That's a very unique molecule, as we are both targeting obesity and PH-HFpEF. As many of you know, 35Pharma was just acquired by GSK, which also has this target. Other players in the space, such as Merck, sotatercept, has also been proven that this is a very important molecule for patients. I want to lastly, before I hand it over to Martin, state that we have cash into second quarter 2028, which helps drive all of these inflection points through the clinic. Martin. Thank you, Felipe. I'll start with the pipeline. I wanted to really kind of pause here for a second and explain what this really means. Obviously, our first molecule has just entered the clinic, which we have released this week. What I think is really important is this is one of the few portfolios in obesity that is focused to post GLP-1s. As Felipe mentioned, our goal is not to drive cosmetic changes in humans. Our goal is to really attack the underlying pathologies that actually make people sick. People do not die of obesity. People die of associated cardiovascular disease and metabolic disease complications. That is important. We have approached this, if you will, from a 360-degree angle. Our first program being IBIO-600 in the clinic being a myostatin molecule. We usually call this a myostatin with a twist. It has a GDF11 component that helps with fat reduction, it also is a long-acting molecule, which actually is pharmacologically better geared to show better efficacy. Here we're really trying to protect muscle as a really important organ for specifically elderly. We all, as humans, lose muscle mass over time, preventing that muscle loss is important for bone density, fracture risk reduction, and so on. We're also looking at fat-specific weight loss because, again, really highly inflamed visceral fat around our inner organs is the tissue that makes us sick in obesity. Activin E has been shown not only to reduce visceral fat but also reduce inflammatory responses in fat tissue. It's a very important drug for us going forward, not just because it has an advantage to shape body composition. You do not want to lose healthy tissue like muscle and bone. You want to lose actually the tissue that makes you sick. It also is emerging, if you will, as a player in weight maintenance. If you look at the latest data for GLP-1, and I should broaden this to other incretin drugs like GIP/GLP/glucagon, we can consider now that we have solved weight loss. There's enough drugs out there with significant weight loss capacity. What we have not yet is something that keeps the body weight off. I think it is pretty clear now, after years of use of GLP-1s and other molecules, that patients do not stay forever on these drugs. Weight maintenance will move pretty clearly in the focus going down the path, and activin E is in a very good spot to potentially be the first weight maintenance drug. We have molecules that are a little bit further away from the clinic. I want to highlight really briefly our bispecific molecule, as Felipe indicated. We have been very pleased with the success that sotatercept has provided for patients with PH-HFpEF. That is a very severe disease, and these patients have a life-changing quality of life, if you will, through sotatercept. Obviously, ligand traps are a little bit limited with hitting different TGF-beta family members that cause bleeding risk. There is always kind of a more limited space to prescribe these drugs, a limited patient population. We believe by not going down the path of a ligand trap, but constructing an antibody logically with the components in mind that actually drive disease pathology, we might have a better chance to have a better risk-benefit ratio for this molecule. What this means ultimately is that this might be a drug that could be prescribed a little bit sooner so that patients don't actually become Group 2 PH-HFpEF patients, but we can actually prevent that progression to that disease state. We have not declared development candidate, but this will come later this year. Last but not least, want to highlight our amylin program. As you've probably seen since last year, Lilly's eloralintide data, amylin has really moved out of a niche compartment that would replace a small amount of, or would be used for some patients that are not tolerating GLP-1s or have no effect on GLP-1, to probably a molecule that is now capturing a much larger market share. Obviously, we believe that the selectivity for amylin receptors is playing a role, but also the bias of the molecule in a signaling capacity and the half-life are playing crucial roles. We, to our knowledge, are the only company that does have an antibody approach against amylin receptor, which conveys exquisite selectivity, but also can provide this extended half-life that is relevant for efficacy. Sorry. Thanks, Felipe. I want to jump real briefly into activin E. We're not going to go down deep into data, but what is really kind of intriguing about activin E is that it's a highly genetically validated target, not just activin E itself, but also its receptor ALK7. This is one of the most highly validated targets that are currently out there and known. Obviously, we have some clinical validation from multiple siRNA companies like Wave, Arrowhead, and now Base Cure, that are paving the way and also helping us then to decide what is the fastest path to a phase II proof of concept. The intriguing part about activin E is it is a truly fat-specific weight loss agent. It is also playing a role in inflammation, which is obviously a comorbidity that has been on the radar for multiple pathologies like neurodegeneration, like cardiovascular disease, like kidney disease. Overall, this is a very promising novel mechanism. I do not want to give you the impression that we know a lot about the biology. We know the genetics of this target, but the biology needs to be explored in clinical development, and that is what we are planning to do over the next few years together with our competitors that are slightly ahead of us. I want to briefly highlight why we believe an antibody might be a very competitive and better approach to targeting the pathway. First and foremost, you might have seen this from now multiple siRNA companies. While in rodent models, the knockdown efficiency in the liver is nearly 100%, the higher the species, starting with non-human primates and obviously humans, your knockdown efficiency goes down to about 70%-85%. If you compare this with rodent data where we see more inhibition of the pathway actually creates better efficacy, we believe the last 15% that are on the table are quite meaningful to block. Obviously, an antibody against a plasma protein that is around 500 picograms per milliliter in concentration is almost an ideal target for antibody inhibition. The next is that I think the one downside of an antibody against this RNA is dosing frequency. If you take a regular antibody that's dosed every 2 to 4 weeks versus once every 6 months, maybe once a 1 year dosing, that is a downside. I think by extending the half-life of this antibody, we can compensate quite nicely for that. Our base case is truly every 3-month treatment, and it could be extended to potentially twice a year. I think we leveled the playing field to a nice degree on that. Last but not least, what we have gotten as feedback is also, and the question is: Can this actually be co-formulated with an incretin, for example, in the same syringe? Obviously, there's precedent, and we can actually show in formulation studies that it can be co-formulated. Of course, the formulation technologies for siRNA makes this a lot more complex to do. Last but not least, antibodies do have the advantage of being a fully established modality in the space. Doctors trust antibody treatments. They have been using antibodies for a long time. We have a nonlinear scaling model for antibodies, so we can actually produce antibodies anywhere from a 200-liter batch to a 20,000-liter batch. There's kind of an exponential scalability of that. Whereas with synthetic drugs like peptides or siRNA, what you have is kind of a more linear scaling. You want to double the output, you have to double the amount of synthesizers you're using. We believe in a complex and large indication like obesity, there might be a benefit, at least initially, for an antibody. That doesn't mean that we do not believe that siRNA doesn't have a place. We truly believe there is space for multiple players. We truly believe some patients will benefit from an siRNA and others will benefit from an antibody as well. We're going to jump over this, yeah. What I wanted to show you is the three use cases that we foresee for this molecule going forward. We're fully aware that the regulatory path to an obesity drug right now is 5% weight loss within a year. Based on the clinical data we've seen, this might arise to a challenge. At least in mouse models, we have seen that we can use activin E as a monotherapy and reach appreciable weight loss. Why we might not have seen this in humans yet is because these are very early phase I studies and maybe 2A studies. If you don't have enough fat tissue volume-wise to lose, you will not see this on the scale as pounds lost. We believe to really show the weight loss capacity of an activin E, we need to go in radio obese patients. That's definitely going to not happen in a phase I. This is going to be a phase II study, and we believe an antibody has a slightly better chance to reach the 5%. What you're seeing here is, yes, it's the approval path, monotherapy weight loss, but it's unlikely that the molecule will be used as a monotherapy because we have drugs that are causing a lot more weight loss. What we do believe is the first and most important use case initially is the co-treatment in combination with incretins or with amylin. What you can see here, at least in rodent studies, there is clearly an additive effect on the weight loss. What is really interesting is these are complementary actions, so activin E does not reduce food intake. Obviously, GLP-1s and amylins do. So there might be a very good complementary role for both molecules used in combination. Long term, what we believe is the most important use case and could emerge as the most important use case is the weight maintenance. This is really where we have absolutely nothing from a pharmacologic perspective to keep patients' weight off. What you see here is not just our data, this is data in rodents that we have also seen from Wave Life Sciences. What we can do is we can drop the body weight in mice. That's this yellow square that you're seeing. When we stop the GLP-1 treatment and keep treating these animals or treat them with activin A antibody, we can actually prevent that weight regain. That was kind of one of the most important findings that has been confirmed by Wave as well. We are now seeing clinical development in weight maintenance, which is going to be very exciting. Last but not least, when we started a pretty complex non-human primate study, there was no human data available. Now, it's a little anticlimactic what we're presenting because we're confirming what we see in humans. It speaks to the translatability of the non-human primate model to humans versus the limited translatability of mouse models. What you see here is that our half-life extended antibody has a 33.2-day half-life in non-human primates. If you use different ways of allometric scaling and see what that half-life in humans could be, you're getting to a range of somewhere 50-100 days. The 47 days is underestimating because this is based on the formula that assumes a two-week half-life of antibodies in non-human primates, whereas on the top left, you're seeing nine half-life extended antibodies that have real-life measurements for half-life in humans and also in non-human primates. If we use that correlation, we're getting to about 100 days. I think a fair assessment is somewhere between 75 and 100 days where we're likely going to end. That actually gets us in good company. There's antibodies with 38-plus days half-life in humans that can actually be dosed twice a year. We believe that still leaves the chance open for twice-a-year dosing. What was really important initially was that we actually used monkeys that are aged, that are obese, and so reflect a lot better our population and the patient population we're trying to treat. What we found here is, at least on our MRI and DEXA scans, that we can see a visceral fat reduction. It's very much in line of what you probably have seen clinically from Wave and Arrowhead, and obviously also a reduction in total fat loss. What puzzled us a lot initially when Wave and Arrowhead reported their data was the increase in lean mass. There's actually no mechanistic link to increase in lean mass by activin E. When Wave first reported it, we felt like this could be a blip, early study, small patient population. Arrow had reported it again. If you find it twice in two studies, it's probably not a coincidence anymore. Now we actually could confirm this even in non-human primates. We still don't know if this is just increasing body water or if this is actually increasing bone density or muscle. TBD, and we need longer studies to actually really in-depth explore that. Just from a perspective of data release, that monkey study was pretty complex, and we're going to release more data at ADA in a few days. That is kind of body composition in more detail. At EASD in Milan in September, we're going to release inhibition data in blood after antibody dosing. At ObesityWeek end of the year, we're going to release the entire data set for the monkey study. We wanted to go really briefly back because we had a major milestone this week. The first molecule ever from iBio in our platform actually entered clinical development. We've dosed the first patient. That's our myostatin program. Myostatin has been really kind of a very interesting target two years ago. Multiple companies went into the clinic to use it as a weight loss agent in combination with GLP-1, mainly Scholar Rock and Regeneron. Lilly entered the space with bimagrumab. What these molecules show you are the bookends of efficacy that you can achieve, right? The true and only myostatin inhibitors like trevogrumab and apitegromab have now been demonstrated, or it has been demonstrated in clinical development that they will not drive weight loss. These were intensive studies. These were big studies in phase II. They were a year long. Highly unlikely that they will be used in that aspect. bimagrumab, on the other hand, showed fabulous efficacy, but at the same time has been shown to have increased diarrhea in clinical trials. There has been an increase in LDL, and of course, the patient population we're targeting is at risk anyway for dyslipidemia, for cardiovascular disease. An LDL increase is really not a signal you want to see in a drug and might limit the breadth to how many people that can be prescribed. What we feel is what we've done with our molecule that has two different angles. One is the long half-life of the molecule. The second is the addition of GDF11 inhibition. We feel with adding GDF11 and the long half-life, we thread the needle very nicely between those bookends. What we anticipate is a safety profile that is likely much, much closer to the pure myostatin inhibitors, a very benign safety profile. At the same time, we're expecting efficacy to be much, much closer to bimagrumab. That is important because, obviously, this is a molecule that generally is meant to prevent muscle loss, not just in a niche population, but in a broader obesity population. We're very excited to have started that phase I clinical trial. We're expecting to read out interim data end of the year. This will be mostly safety and PK data. We're really interested. This is an even longer-acting molecule. We're expecting half-life somewhere between 100 and 150 days, which will be important because pill burden and adherence to treatment protocols in complex and chronic diseases is low. Having a twice-a-year or even a quarterly injection definitely will help with driving efficacy because patients remain on protocol. Just briefly, showing the monkey half-life. Again, these are aged and obese monkeys to be as close as possible to our patient population. We have measured the 52.4-day half-life, which then will translate somewhere to between 100 and 150 days roughly. That is one of the first key measures that we want to do. Why we believe this is important, and you can go to the next slide. Next slide. Sorry. Next one. Why we believe this is important is because we're cutting out trough values in exposure. myostatin antibodies have to diffuse from blood into muscle, and if you lose exposure in blood, fewer antibodies will actually arrive at muscle, and that eats into efficacy. Cutting out these trough values before you start dosing the next dose is going to be highly important. It also shows that we can model this out and co-formulate this molecule. If you have a weekly GLP-1, for example, you can co-formulate this with a very low amount in the syringe, and at the same time, it would just accumulate over time. If you have a monthly incretin molecule, it can also be co-formulated. We have quite a bit of flexibility for the dosing interval and kind of tie this into another treatment paradigm with an incretin. Very good. One key highlight that I want to put out here today is that this is monkey data that we've done. This is a single dose of five milligrams per kilogram in aged and obese monkeys. What we've seen is a pretty now typical picture on muscle growth. Muscle growth goes up between four and eight weeks and then remains roughly the same at 12. We've seen actually muscle growth leveling out after a certain amount of time. What is more intriguing and likely attributable to the GDF inhibition is that you see a continuous reduction in fat in these monkeys. Now, I want to highlight this is a focused DEXA scan on a region of interest. That means upper body and thigh region. It's not total body composition, but what is intriguing is that the fat mass seems to be going down. For weight loss, specifically if you have increased muscle mass, which drives weight up, you have to actually show that you're continuously further reducing fat. This is what made us so excited about this molecule. Very good. Really in a few more minutes, the early programs that we're pursuing, we have not yet declared development candidate for our bispecific program, activin A and myostatin for PAH, HFpEF. We are at the moment down to the last four candidates that we're moving, which one will actually enter IND enabling. This summer, we will have a development candidate ready. We're currently ramping up to do in vivo studies, if you want to go to the next one. Just to prove that the different mechanisms are important. What sotatercept has shown us in PAH HFpEF is that it's a multi-organ disease that is driven by tissue remodeling, and TGF-beta family members actually prevent that, or blockade of TGF-beta family members. By reviewing the literature, by looking very carefully which components actually contribute to disease progression, we landed on three molecules, activin A, GDF11, and myostatin. We have proven for all three that they drive fibrosis in human cardiac fibroblasts, and preventing their action seems to be contributing to a large degree to the efficacy. Next slide, please. What you see here is on the left side, this is just a surrogate assay. We use primary human muscle cells, and we added all three molecules, myostatin, activin A, and GDF11, and blocked those. The combined blockade of all three gives you a much more significant growth in muscle. When we actually blocked all three mechanisms, not with a single molecule, but with two different molecules that hit all three pathways in a mouse model of HFpEF. I want to caution you, the mouse models are not very translatable, but it's the only thing we have right now to at least compare molecules. We actually have an increased Fulton index. Fulton index really measures the weight of the right heart versus the weight of the left heart and the septum, and causes a reduction in the Fulton index. Kind of shows that you have a reduced pressure coming from the lungs so the right heart doesn't have to grow that much. That was very positive as a proof of concept, and the studies that we will do with the final molecule that will be a declared development candidate are ongoing and others will start within the next few weeks. Last but not least, I want to highlight the complexity of finding the right amylin molecule. We know from early days, when the company Amylin still existed, that half-life is a real big driver in providing efficacy. We now know from the modern amylins, lorcaserin and others, that the bias towards G protein signaling is very important. We've also come to the conclusion that hitting the amylin receptors, either as a biased effect, so lower or less hitting of the calcitonin receptor, more of the amylin receptors, is beneficial. To our knowledge, we're the only company that has three molecules available. We have a purely selective amylin 3 antibody. We have a purely selective amylin receptor 1 antibody. We have a so-called SARA profile, a molecule that hits both amylin receptor 1 and three. We have also a DACRA molecule, which you're used to from former molecules. These are fusion proteins, so we have a part of the amylin protein peptide fused to this antibody. The antibody provides you the selectivity to the receptor, and at the same time, it replaces the C-terminus of amylin and pushes basically the amylin into the binding pocket. This way, we can truly interrogate this pathway. We can answer the question if it's amylin receptor 1 or amylin receptor 3, or if both actually contributing to efficacy, and we can also see what role the calcitonin receptor plays. Is it just a sink for the peptide because it binds there, or is it actually contributing to weight loss? We're excited for these molecules. It's early. Because of the exquisite selectivity, we believe we can really help understanding how amylin actually works in humans. With that, I would like to open it for questions. Thank you, Martin. Thank you, Felipe. Jefferies has a few questions to kick us off here, and then we'll pass it out to the group. First question being, why is iBio uniquely positioned as the only antibody company targeting activin A, and how did the company develop this capability? That's a very good question. When this target was published by both Regeneron and Eli Lilly in a very high-level journal, we felt like we're going to be behind. It turned out to be very complicated. The first hurdle we had to overcome is making recombinant activin A that is falling into the same shape as endogenous. That proved to be very complicated. We believe that a lot of companies that started early had actually antibodies, but against the misfolded protein, and that's why they were not neutralizing. The second issue we found is it's not that you don't have activin A antagonists in libraries that are existing. The problem is finding the very, very few molecules among the billions of molecules. The selection strategy was something we had to rejig multiple times, and the way we solved this was by deeply integrating the AI models we're using for antigen design. We modeled basically the binding or the proposed binding regions of activin A to the receptor and selected antibodies that purely only bind to those. Our platform helped us actually get there, but ultimately, rejigging our screening strategy multiple times and optimizing this ultimately provided that success. We do believe that multiple libraries might have that same antibody. The question is will you find it in your library. Okay. Thank you. Quick follow-up question here as well. How does iBio's antibody-based approach differ from siRNA therapies, and why does the company believe its approach is superior? Yeah. I think we believe that further inhibition of the pathway is going to be beneficial on efficacy. The reason why we believe this is that we don't see efficacy starting at 10% pathway inhibition. We see efficacy starting 50%, 60%, 70% pathway inhibition. If you believe that all of the action on efficacy happens between 70% and 100% inhibition, 85% gets you halfway in this window. We don't feel there's a logical explanation why efficacy just should stop halfway there. We're really intrigued about that possibility. Again, this has to be proven in humans. We're not able to show this in rodents as a comparison because actually the siRNA in rodents is causing a near complete knockdown of the target. We're really excited to hopefully start this clinical trial early 2027 to see how far we can actually inhibit the pathway and if there is additive and additional efficacy that we can get out of it. We believe it is possible, but obviously we have to do these clinical trials to show that. Okay. Thank you so much. I now open up to the group. Does anyone have any follow-up questions here? We can pass the mic around. All right then. Well, thank you so much