Duran, who is the CFO of the company. Maybe the best way to get kicked off is to talk about the history of the company, and the platform, and how the story has evolved in recent years. Cool. Very cool. Sure. I'll talk a little bit about the history and then hand it over to Martin to talk about the platform. The company was founded back in 2008, 2009. It was a consortium of three entities to basically bring vaccines for the U.S. Army on a plant-based approach. From then to about 2015, they operated under that platform. In 2015, they pivoted into a CDMO. In 2018, 2019, the previous management was brought on to basically enhance that CDMO. They raised capital under, you know, to basically bring a COVID vaccine to the market. That's when Martin and I were brought on to the company. Fast forward to 2022, we pivoted. We bought the assets of a company called Rubrik Therapeutics that brought to us the platform that we currently use to discover our hard-to-drug antibodies. Martin and I took the reins in January of 2023 as CEO and CFO, respectively. We basically pushed the platform for that year, and we had three validating points. The first validating point was a research agreement with Eli Lilly that allowed us to basically work with them on a hard-to-drug molecule that they had spent seven to eight years trying to develop binders on. In eight months, we did more than they did in eight years. Those conversations are ongoing. We continue to be good partners and help them with that molecule. The second, we sold a PD-1 agonist that was acquired when we acquired the platform, to Otsuka. We got $1 million upfront and then $52.5 million of commercial milestones. And then lastly, what got us into obesity, we signed the collaboration agreement with a company called AstroBio. That discovery collaboration allowed us to basically work on four obesity targets, which we then had the rights to in-license three of those four. We've already in-licensed myostatin, and Activin E, and obviously Amylin, and the fourth molecule that's not named yet would be the other molecule that we could in-license. The most interesting thing there is that we've done 100% of the work, right? You know, that collaboration came with it some investors and a pipe and has allowed us to move forward. That's where we're at. We have a very interesting platform, and we've continued to, you know, tailor our obesity strategy, based on the market. Very cool. Understood. I think investors are very familiar with obesity treatments that are currently on the market, GLP-1, but obviously there is a lot, a lot of dynamics in the pipeline. You mentioned a few assets: Activin E, myostatin, Amylin. Maybe at a high level, how are you thinking about the next wave of opportunities in obesity and why did you decide to focus on those targets specifically? If you think about it, the GLP-1 receptor agonists in general have actually ushered in a revolution in how we treat obesity, right? Before that, the only way we could treat obesity in a significant way was bariatric surgery, which was highly invasive, irreversible. With the GLP-1 receptor agonists, for the first time, we have a pharmacologic intervention. We do not need a scalpel anymore. As efficacious as these drugs are and as powerful as these drugs are, and they have been in more than 10% Americans now, when we got into the obesity space one and a half years ago, we realized that, A, it is going to be very competitive in that space of GLP-1s. B, there are still unmet medical needs for patients that these molecules do not cover. We have immediately focused on those areas. You can call this next generation drugs. You can call this, you know, on top of GLP-1, but that's what we focused on initially. Treating on top of GLP-1 after patients come off of GLP-1, we've seen, you know, the dropout rates are really, really high. Also, can we find alternatives to GLP-1? That's how we've built the strategy. We also in this case have not just built a pipeline of individual programs. We've literally built a portfolio, if you will, of programs where we can attack obesity from multiple angles. We have a food intake reduction molecule with Amylin. We have a fat-specific weight loss target with Activin E. We have also muscle-sparing agents with our bispecific myostatin Activin A and our myostatin molecule. If you will, it de-risks not only kind of the pipeline from a perspective of different mechanisms, it also de-risks it because we're still debating, you know, how much will payers actually take these drugs, and pay for these drugs versus the patient has to pay for them themselves. Having these multiple aspects is definitely de-risking the pipeline. Understood. And, you mentioned a few assets, a few different approaches, different treating different aspects of the disease. Maybe you could talk about the stage of each of those assets, and kind of what are the next value inflection points and the steps that you need to take to get there? Absolutely. First, it was obviously very important that we create a barrier for entry, because, as I mentioned, it's a hyper-competitive space. I think we have already two molecules in that portfolio that actually have not yet been copied where we are the only ones actually having assets that way. Our most, or highest priority molecule right now is an Activin E antibody. This target has been linked to cardiovascular and disease obesity, metabolic disease about three and a half years ago, by some top level companies. Nobody so far has been able to create an antibody. We're having competition from the siRNA side so that gene can be knocked down in the liver. That program is currently in IND enabling. We are just finishing a monkey study that should read out, beginning of next year. We already have the PK data for that study, which is very promising, points towards the twice a year dosing. The next step here would be to create a cell line. We're in the middle of creating a cell line in CMC and then completing the tox study. The goal currently is to file for an IND equivalent in Australia at the end of 2026. That would put us, for the first patient dose, somewhere in the first half of 2027. Mm-hmm. And so this molecule, the idea is to use it in combination with GLP-1. You mentioned after the patient comes off of GLP-1, what use case or use cases have you envisioned? It's a very good question. First of all, I think there's a very clear approval path for a molecule like this as a monotherapy. This is the most defined regulatory path to do that. Based on the preclinical data we've seen, this is absolutely feasible, but it's likely not gonna be the biggest use case. The biggest use case is very likely as a co-treatment on top of GLP-1, a combination that will allow you to back off of the GLP-1 dose. Again, in real world data, GLP-1s, you know, lower the body weight by about 10%, not clinical trial like, you know, 20%-25%. This is because patients back off of that highest dose and adding an Activin E might actually get you to the same efficacy as a high dose of GLP-1 without the adverse effects. The last and most interesting use case is actually if patients come off of GLP-1, or an Amylin, and Activin E is gonna be used as a weight maintenance drug. So far, we have no other mechanism that would actually keep the body weight down. We all can lose body weight, either through diet or GLP-1 receptor agonists, Amylin, but to keep the body weight off, that's at the moment the biggest unmet medical need. I see. Okay. And then maybe to take a step back. So these molecules that your platform, that are coming out of your platform, are they just regular monoclonal antibodies? There's no, nothing like difficult about manufacturing them, or is it, is there more to it than, like that? We have built that platform and, as you've seen, we're avoiding the term AI company very much. For us, AI is a tool that helps us to make medicines. AI enables a few steps in the 10,000 steps to make a medicine, right? We're very cautious about this, but these are critical steps. What we use is, as the last step of antibody optimization, a mammalian display system that is coupled with a generative AI tool, which allows us to create highly developable antibodies. It's not like we're designing something in silico that we later on have to test if it can become a drug. What comes off of our platform are highly developable molecules. Our first antibody that went through CMC is a myostatin antibody. We've produced the first GMP batch for phase I at 8 grams per liter. The second molecule, the Activin E antibody, we've done just transient transfection to produce some material for formulation studies at 2.5 grams per liter. These are usually levels where you start manufacturing a regular antibody. There's nothing special in the sense of, we have created some novel structures, or novel modalities. It's, these are antibodies, but of course optimized, on our platform for developability. Mm-hmm. I think you already touched on it, but for iBio 610, what would be the next data point that we can get excited about, which I guess would still be preclinical, right? Yeah, correct. So, beginning of next year, the monkey study readouts. So we do have the PK. We have a very long half-life in monkeys that we just read out last week at Obesity Week, which projects a human half-life of up to 100 days, which puts us straight into the area where we can dose twice a year. The efficacy part of that study, it's a complicated mouse, monkey study where we test actually all paradigms, monotherapy, combination, and then also rebound. Can we actually protect these monkeys from regaining weight after they've been on GLP-1? There's a lot of imaging that we do. The life phase will end towards the end of this year, but the analysis of all of the imaging data and blood chemistry will take a while. What are you hoping to see there? What should we be hoping to see? Just Just maybe a couple of goal posts or a couple of data points. It's really, really hard to judge because it's the first time somebody is really doing an extensive non-human primate study. What will likely happen is that some of our competitors will have actually clinical data by that time. Of course, clinical data will be phase I A, so this is more towards half-life and safety. There might be a sliver of efficacy in these data points. We might actually see more mechanistically how Activin E is actually behaving in higher species. Understood. So maybe we can talk about iBio 600, as well, and where we are with those, with that program and kind of what's coming up. Very good. iBio 600 is a long-acting anti-myostatin molecule. This was the first molecule we designed, and as a testament to the platform, we actually, from a paper exercise to development candidate, went in seven months. We are almost done with CMC now. This molecule should be going through tox from now until the first quarter of next year. We are filing in Australia, probably in the second quarter next year. That is kind of the next milestone for that program. It is a unique molecule because if you look at the market, you have the pure myostatin inhibitors, or inhibitor from Regeneron, Trevogrumab, that only blocks myostatin. Then you have on the other side of the spectrum, Eli Lilly's Bimagrumab, which is an antibody against the receptors of multiple TGF beta molecules. Whereas the Regeneron molecule is likely gonna be a little bit limited in efficacy, but it's clean from a safety perspective. You see with bimagrumab, better efficacy, but you also see, for example, increases in LDL, which of course in an obese and diabetic population is not a desired outcome. We believe with our molecule, we have two advantages that slots us closer to the efficacy of bimagrumab, but probably on a safety perspective, closer to trevogrumab. We added inhibition of GDF11 that was a little bit controversial five years ago. There were companies out there that actually did recombinant GDF11. Most of the biology got debunked. At the moment, we know that GDF11 has a pretty significant effect on fat tissue, which myostatin does not. The combination of both in a single molecule actually allows us to reduce fat quite significantly and increase muscle at the same time. Again, we believe we're closer to effect size of a bimagrumab, but we're staying away from LDL increases, which is likely coming from other TGF-beta members. Assuming the development of that molecule is successful and it's in the market, what role do you think it would fill? Would it be almost like a next generation, better alternative to GLP-1 or, This would be clearly an add-on to GLP-1, right? Because, there's, for a long time, we have known that if you actually weight cycle, if you lose weight and regain weight through diet, you actually have an increased risk for frailty fractures. Just at ObesityWeek last week, somebody has now put a poster out that, even with GLP-1 use, years later after using GLP-1s, your fracture risk actually goes up. This is very likely driven by the muscle loss that you see, bone density loss. If we can actually prevent this, if we can, if we can prevent falls by retaining muscle mass, that's definitely gonna be an added benefit to a GLP-1 treatment. Understood. And, can we talk about Amylin and your, your view on, on that space and how your molecule positions there? We're in a really good position with Amylin because we can actually watch how Lilly and Novo are kind of fighting this out clinically right now. I think the question is, do you need calcitonin receptor involvement or is a pure Amylin receptor, a so-called SERA, selective Amylin receptor agonist, is that necessary? Now, so far, we only have genetic evidence from a mouse that we need receptor one and receptor three from Amylin. But again, it's mouse physiology and it's knockout data. All of the molecules, all of the peptides out there, even if people claim they're selective, they're biased, right? At therapeutic doses, you hit both receptors and you also hit the calcitonin receptor to a degree. What we have been able with our platform was to create antibodies that are selective against receptor subtypes. We have a whole toolbox. We have a receptor three, Amylin receptor three specific agonist. We have an Amylin receptor one specific agonist. We have one that actually activates both. We also have one that activates the two plus calcitonin. Last but not least, we have a calcitonin only molecule. We can actually interrogate the biology for the first time pharmacologically and not just with genetics. We can go now in a higher species like non-human primates and figure out what is the right profile. Once we know what the right profile is, we then have an antibody fusion, which is a really interesting molecule because it allows us to do two things. It allows us to extend the half-life significantly. The dosing frequency will go down. If you look back at the history of Amylin, we started with three times daily dosing with barely any efficacy. Now we're having with extended half-life, we see better and better efficacy. We truly believe that longer half-life will be beneficial. The second part is, as you know, Amylin has some challenges in manufacturing. What we did is we actually replaced this challenging piece to manufacture, the C-terminus, with an antibody construct. The antibody provides the position to go to the receptor subtype we want. That fragment of Amylin is actually ramped into the binding pocket of the receptor and activates the receptor. On the one hand, it is longer half-life, it removes some manufacturing issues, and it should provide much better stability because the fragment of Amylin we're using is very short. It's basically protected by this huge bulk of the antibody against degradation. Mm-hmm. What is next for that program and then the timeline? We're entering rodent studies as we speak. We'll likely go until the end of the year until we figure out what the right profile is. Then we're gonna have a relatively, you know, expensive and expansive non-human primate study to move these constructs forward. If we see early signs of efficacy in this monkey study next year, we're gonna jump straight into CMC with that molecule. Mm-hmm. Maybe to take a step back and just try to sum up iBio as a company. Obviously very large addressable markets that you're going after. You have a few assets that are differentiated. How are you seeing, maybe to look into the future, how are you seeing this market evolving and iBio sort of breaking through or differentiating in that market? I think what we're seeing now very, very slowly happening is that we are starting to understand that obesity is not one market, right? There are subpopulations like we've seen before with cardiovascular disease, with type two diabetes. There are just multiple comorbidities that we have to take care of, right? We also know that complex diseases cannot be treated with a single molecule. Never worked in the past, will not work for obesity. What we're seeing is very carefully, some of the more advanced companies, strategically advanced companies in this space are thinking about combinations, how we can actually address certain unmet medical needs, how we can smartly combine mechanisms, right? It does not help if you stack food intake. If you reduce food intake to zero, we will be malnutritioned and dead. You need to find orthogonal mechanism like an Activin E on top of a GLP-1. I think the market will mature in that direction that we will have kind of a maintenance level, that can and should be dosed very infrequently. We're shooting for twice a year. Then on top of this, there will be, you know, the significant weight loss effects, that will likely be combined. Mm-hmm. And, in terms of corporate strategy, it's, it's obviously the early days still, but, I guess how far are you looking to take these programs on your own? Are, are you talking to potential partners, maybe potential future partners and kind of what, what that feedback has been like with those conversations? I'll hand this over to Felipe. Great. So in terms of partnerships, obviously we've been very selective. We were able to raise capital in August to advance our Activin E as well as our bispecific, and continue the development of our early stage assets. We want to make sure that we're finding the right steward. Right now we are looking to see if we partner out our myostatin program. 'Cause as Martin mentioned, we know that that molecule would be best with someone that has a GLP-1 franchise. So, you know, we're actively looking for the right steward for that program. Other than that, we are being very selective in terms of, you know, who we speak to and when we speak to them. Great. And you mentioned the, the recent financing. Can you talk about your current cash position, cash runway, and maybe downstream financial plans? Sure. In August, we raised $50 million upfront with a potential for another $50 million in a very unique structure. It was all pre-funded warrants stapled to a Series G warrant for an additional $25 million. That Series G would be triggered on the acceptance of any of our INDs. As Martin mentioned, the first potential IND would be our myostatin program sometime in the second half of 2026. Post that, there is another $25 million on a Series H, which would only be triggered after the inducement of the Series G warrants. It is a three-tiered stapled with pre-funded, Series G, and Series H. If you consider the Series G all in, exercised, we would have cash through 2027. Right now, with just the $50 million, we have through first quarter 2027 calendar year. Okay, great. Maybe just before we wrap up, to recap the upcoming catalysts, which I know you just mentioned some of them, but you kind of ran through them quickly, so maybe that would be helpful. Sure. So Activin E, we will have non-human primate data sometime in the first half, hopefully first quarter of next year. We would then take that straight into, well, completing CMC and tox, to have a filing in Australia by the end of 2026, first human dose sometime in the early 2027 timeframe. Our bi-specific is around three to six months behind that program. So that would bring us into IND filing in the first half of 2027 with first patient dosed in Australia sometime in, in late 2027. Our myostatin program, we will complete all the tox studies, either by the end of this year, first quarter next year, have filing in Australia in first half, first patient dosed, some, sometime, right after that in Australia. Our Amylin, we're completing developmental candidates now. we would get into non-human primate, non-human primates in the first quarter, first half, and hopefully, speed into CMC and tox with that program. Okay, great. I appreciate the time and the opportunity to dive into the story. It sounds like an exciting couple of years ahead of you. Definitely. Thank you very much. Thank you. Thank you. Thank you. Thank you so much.