IBIO | iBio, Inc. | earnings call 2026-09-04
Verbatim transcript (source: faster-whisper-small.en)

Great, thank you so much. So good afternoon everyone. Thank you so much for joining us at the Wells Wells Fargo Healthcare Conference. It is my true pleasure to introduce iBio, specifically introduce Martin Brenner, CEO and CSO of iBio. For anyone that does not follow the name closely, iBio is a San Diego headquartered biotechnology company. As of this year, a clinical stage company which is major, major progress. And they, the company is really focusing on building on building long acting antibodies for obesity, but building on what comes after GLP1s, focusing on cardiometabolic and cardiopulmonary disease. When we talk about what comes after GLP1, we really focus on the quality of the weight loss and the durability of that weight loss. And we'll definitely get into those points today. The company has quite diverse pipeline and deep pipeline, right, covering a significant breadth of opportunities, fat selective weight loss, muscle preservation, pulmonary hypertension and heart failure and amylin. Please welcome Martin Brenner and we will dive right in. So maybe Martin, we can start out with where we're sitting from today in the next five years. Can we talk a little bit about how you see obesity landscape, how you see obesity regimen? And what does that look like? And where will the market effectively settle on? Yeah, I think we have a couple of other complex chronic diseases we can take as a playbook for obesity, right? We have seen this before in type two diabetes in hypertension. We're likely looking at a hyper segmentation of the market. We're really not interested in treating obesity like a cosmetic disease. We're really interested in actually treating the underlying pathologies that lead to cardiovascular disease to metabolic disease that are shortening health spans of people. To achieve that, I think it's fair to say that combination therapies will actually be the predominant way of doing this, as we've seen before in other diseases. I think the the GLP ones, I should broaden this group, the weight loss drugs like the emilins, the GLP ones, the dual and triple Gs, they really solve the question of lowering the body weight. But we have not solved the question yet how we actually keep the body weight low. We also don't know about the durability of the beneficial effects on the cardiovascular side. If you're looking at the bariatric surgery field, that was the first time we could lower body weight. Again, very invasive with a scalpel. But even after bariatric surgery, where you cut out part of your stomach, you still actually after years and years, you see the body weight regaining. So we really have not solved this long term strategy. And I think there's a huge unmet medical need to do this. Obviously, what you're going to see as well is the improvement in the adverse effect profile. We know that a lot of patients on GLP1 are going to have adverse effects, gastrointestinal adverse effects mainly. And I think the early emilin data that Eli Lilly and others have shown is there might actually be beneficial effects of an emilin over a GLP1. But I think this is going to evolve over the next years just to kind of keep patients on drug longer without having actually these adverse effects. And then you mentioned the quality of the weight loss. I think this is something we're at the moment underestimating. It actually is not muscle or bone density that makes us sick. It's actually inflamed visceral fat, the fat around our inner organs that actually makes us sick. And I feel like this is one of the areas where I think we're going to evolve in the obesity space very rapidly. And can we actually prove which the proof is outstanding, can we prove that a reduction in visceral fat is actually conveying all of these cardiovascular and metabolic beneficial effects? Or is it really overall weight loss that is doing this? Obviously, we strongly believe it is driven by a loss in inflamed adipose tissue. But this quality of weight loss might it be preserving muscle to have a healthier aging population that can still actually walk up some stairs and the reduction of visceral fat to kind of protect against cardiovascular and metabolic disease. I think that's going to be an important piece of the future. Yeah, that's very helpful. When we think about sort of the current standard of care, as well as Amilen coming on as potentially a secondary pillar or a foundation, right? And then we think about your asset, right? 610. Where does that come in? So how are you thinking about your lead asset in your pipeline? Where does it fit in on top of ingredients, on top of amylens, you have amilen of your own? Can you take us a little bit through that and how you're thinking about the pillars here? So, active in E or inhib in E is a really interesting target because it has a very strong genetic validation. And the last one that we saw with equally strong validation was PCSK9. And not only the gene that makes active in E is correlated, if you suppress this, that you have protection against cardiovascular disease and metabolic disease. Also, its receptor, which is called Alx7, shows the same beneficial effects. So, this whole pathway really is related to metabolic and cardiometabolic disease protection. That's what makes this target so interesting. When we got into this space two and a half years ago, we were quite surprised that nobody had made an antibody. And Naive, as we were, stumbled into this space and said, well, just going to make one. And we actually succeeded, but it was really tough. We utilized a lot of novel technology on our platform, a lot of novel screening technologies for antibodies to actually make that active in E antibody. And to this day, we're still the only ones with an antibody. There's other companies that approach this with SIRNA, but we believe that antibodies is a way more developed and, you know, validated modality right now. Not that the SIRNA's are not fantastic drugs and not catching up, but at the moment, there's just way more approved antibodies and doctors know how to use antibodies in treatment and SIRNA is just a little bit new. Maybe we can double click on that, right? And sort of talk a little bit about the difference in the modalities specifically for active in E and why potentially the antibody will be a solution to some of the shortcomings, perhaps that we have seen currently with the RNA. Yeah. I think the most intriguing aspect of an antibody is that you can block the active in E molecule completely. It's a molecule that is made in the liver, secreted into the blood. And this is the compartment in the body that is perfect for antibodies. It's also at a relatively low level in blood so that you don't have to inject so much antibody to neutralize it. As IRNA's, at least to this day, seem to have a limit of about if you average it out of about 85% inhibition. So if you think about it, it's a faucet that drips out of the liver. You cannot switch it off completely. There's always a little coming out and active in E is a very, very potent molecule, even small amounts cause an effect. And what we and others have seen in animal models is that the more you block the pathway, the better the efficacy. And so because you can only go to 85% with SIRNA on average, and we have just shown in our non-human primate study that we can block with a single injection all of the active in E molecules in blood for at least eight weeks, we believe that could actually lead to better efficacy down the road. Now, this has to be proven in humans to be very clear, but it gives us an advantage there. And of course, this is a long acting antibody. So we're offsetting a little bit the advantage of an SIRNA that can be actually administered very infrequently. But the half-life in our monkeys is more than 30 days. And there's a significant extension to regular antibodies which have maximally half-life of about 14 days. So our estimated human half-life is somewhere in the 50 to maybe even 100 days range. So that gives us confidence that we can dose this maybe every three months, upside scenario would be every six months. Right. And that's very helpful. I think maybe we can talk a little bit about the importance of long acting, right? And I think typically we see a lot, well, in the, you know, sort of in the last say past 12, 18 months, long acting amyloid, right? And what does that mean and what will that sort of contribute to the treatment landscape? I think maybe a two-fold question. One, your own amyloid and how does that sort of, how is that a part of your thesis in in-combo with active in-end or not? The two long acting ones. How are you thinking about combination of a two-long acting or a single long acting amyloid or combo amyloid and hebe? So amyloid is a really interesting molecule, right? Because when the first amyloids came out, we thought it will be a niche product for the three to 5% of people that don't tolerate GLP ones. And I think the whole field was turned upside down by data that we saw from Eli Lilly on Ellora Lindtide, Eli Lilly's amyloid. And that, you know, caused a significant amount of weight loss comparable with the GLP one and might, you know, ultimately show a little bit of a mob benign adverse effect profile. So what people tend to forget is GLP ones don't universally lower body weight in everybody. There's a huge spread between 3% and 30%. And so it's not really uniform. And there's patients that will definitely benefit from another mechanism. What has proven, amyloid is a very old molecule. We've done this many, many decades ago. And the first amyloids had to be dosed three times a day, peptide with a short half life. There was no weight loss. And then the ones daily and the ones weekly came in the longer the half life got, the better the efficacy on weight loss became. So obviously, an antibody compared with a peptide has a much longer half life. And we believe that can contribute to even better efficacy. If these molecules and, you know, have that extended half life in humans as well. The second really interesting aspect of amyloid is we still don't understand to this day, if there's certain receptors, subtypes of amyloid, there's multiple amyloid receptors, which one is it actually that conveys efficacy? And is there one that actually produces side effects that we don't want to see? We don't know. So the solution for that is obviously making selective antibodies against the individual receptor subtypes and testing this. And to our knowledge, we're the only company that actually has four molecules on amyloid. One is a so-called dacra molecule, a dual Calcitonin amyloid receptor agonist that hits not only the amyloid receptors, but also Calcitonin. We have a so-called Sera profile that hits amyloid receptor 1 and 3. And then we have individual molecules that hit only receptor 1 and only receptor 3. Now, this is not a simple program that we're doing, but with these molecules in tow, we can actually go in, say, non-human primate studies and figure out what is the best profile that basically causes the best effect size and at the same time, the lowest amount of adverse effects. And that is the whole interesting story about our MLM program. Once we understand which of these profiles is the best to move forward, we will then obviously move only one into the clinical development, not four at the same time. Right. Right. No, absolutely. And I think a couple of times already, you noted the adverse effects, right? And the importance for you management of those, right? Maybe we could spend just a little bit of time with that sort of in this next generation of obesity treatment. And as the landscape continues to evolve, that management of adverse effects, and we often come back to that 3 to 30%, right? And there's a 30% clinical trial sort of results. That's not the real world example, right? Or what we see in the real world. But again, those adverse effects, how are you looking at that? And how important is the management of adverse effects in your mind? I think our patients tell us everything about this. Because if you look at the GILP1 space, and I'm generalizing this on purpose. I don't want to highlight one over the other molecule. They're in similar fashion doing this. But patients never tolerate the highest dose. They always back off one or two doses because they are the tolerable ones for them. And what this does is that it causes an overall roughly weight loss of about 10% in real world data, real world effect size. And that tells you something, right? We don't reach the clinical trial efficacy of 25%, 35%. And this is because those higher doses cause these significant adverse effects. And imagine now you have a combination where you have a lower dose of a GILP1 and combine this with, say, an active knee antibody that causes further reduction in fat and body weight. You could actually get away with a lower effect, a adverse effect profile, but at the same time restore the full efficacy of a high dose of GILP1. This is how we're envisioning combinations going forward. Can we actually combine things in a way that we distribute the burden on multiple pathways so that we don't have to max out on the pathway where we're running into adverse effect territory? Yeah, that's very interesting. I want to just maybe go back a little bit to another comment you made earlier about there was nobody before you who created an antibody for active knee, right? And not just an antibody who created an antigen. And that's a proprietary platform. That's very like a proprietary to iBio. Can you just make me put that into context? What does that mean for what's next? What I mean, you talked a little bit about the sort of variations on a team for Amel and right and sort of fine tuning the receptors and what you're combining with. You know, sort of what is the potential here, really? What else could we think about as we think about the potential of the capabilities of this platform? So we're usually not touting that we're an AI company because that puts you in a group of companies we do not want to belong to. For us, AI is a tool. If you think about the process of making a medicine, that's at least 10,000 steps. We enable three to four with generative AI. Now, these are really important steps because they enable us to do molecules we couldn't imagine before, right? But we're definitely toning this a little bit down. We don't talk about AI drugs and everything. For us, what is really important is that at the end of all the technology we apply is a molecule that actually looks like a medicine. And that sets us apart from a lot of the typical AI companies that create molecules that are interesting but don't really look like drugs and likely are not going to be used in humans any time soon. And to do this, we have actually developed our technology on both ends of this equation of antibody discovery. The first equation is really our antigen, so the drug targets. How can we represent complex drug targets in a much simpler form that we can actually screen on them, that we can use them for structural information? This is something we've been working on for the last eight years. And that's technology that originated from a company which we bought the assets of, was called Rubrik Therapeutics, a pioneer in antibody discovery. AI enabled antibody discovery. And in the meantime, what we've done then utilizing the technology, we also worked on the other end of the equation, which is the antibody. Because when there's a drug target with a so-called epitope where the antibody binds that has a biological function, there has to be also a binding region on the antibody. And you have to evolve both at the same time. And not a lot of companies do actually both sides of that equation. And that allowed us to not only solve the structural issues others had with activity, it also allowed us then to design libraries of antibodies where we ultimately found our molecule. The interesting part is that molecule is very, very unique. We're going to publish about this. It's going to take a while. This is going to be a high-level journal we're trying to get into. But that antibody has very unique characteristics that we have never seen in an antibody before. But interestingly enough, it comes from a naive library. So it is in a library that we sampled from hundreds of humans of beings. So it's not something we created in the lab. It's just something our technology enabled us to find. And just to give you an idea of the scale, we screened a billion, one billion molecules. And we found only one that neutralized activity. So I'm fairly sure this molecule sits in other libraries of competitors. It's just about finding it. And that's what set us apart in this case. Finding that needle in a haystack, right? Exactly. It's amazing. And it sounds like the use of AI capabilities for the right, you asked the right question, and you got the answer, right? But it's the matter of asking the right question. Correct. And it needs to translate into something. It needs to translate into a drug-like molecule. If it's just a hypothesis or if it's a molecule that cannot be developed as a medicine, there is no use in it. And sometimes old-fashioned technologies actually do the same thing. And then why would you actually build large models around this? We only use AI in places where we really cannot solve problems. And it has been highly successful to use that way. Very helpful. I noted at the beginning that you're a clinical stage company now, right? Which was a major, major event and major catalyst. And congratulations on all the success. Maybe we can spend just a little bit of time on iBio600, right? So the molecule is in the clinic. You publicly disclosed that the vast, vast majority, right? Only about one participant has been dosed across all four SAD cohorts. And you've also significantly enhanced your leadership, right? By bringing in Molly Clark. Correct. Can we talk a little bit about sort of the build out of the clinical program, the build on a clinical developmental plan, and what is Molly doing in the company now? How do you see the sort of the next key steps in the 600 program? And what should you be, we'll be looking out for and what should we expect? It was very interesting because we've built a very broad pipeline around obesity. We're one of the few small companies that really have an integrated obesity cardiometabolic pipeline. So we can create these molecules really rapidly. Our myostatin program took two years and a few days to go from paper exercise, drawing the molecule on paper, what it should do to actually dosing the first patient. So we've gotten really good at this early discovery stage to produce molecules that would go in the clinic. Now what we're building as the next step is we're now building a very efficient team that allows us to go to the end of phase two. That's the next step, right? For a small company doing a phase three trial in obesity is a very, very tall order. We're talking 300 million to 800 million dollars for a phase three. Obviously where we are right now, given the valuation of the company, given where we are in the stage that is an unreachable goal at the moment, but that doesn't mean we cannot grow there. And growing to that point is creating clinical assets that are valuable that we can either partner or that allows us to increase the valuation of the company and raise more money to kind of conduct these trials. And that's what Molly is building right now. So we have survived so far, I should say. I think surviving is the best word with consultants. Yes. But we wanted an expert in the company and we had a lot of demands on that role. So Molly Carr is our chief medical officer. She joined the company five weeks ago and we made it really hard on us because we wanted somebody who has experience across the entire development stage. She has done surgeon evaluation. She has done early or late stage preclinical assets, moved them in the clinic and she's gone all the way now to approving insulin, lung acting insulin for Eli Lilly. And so she's seen the entire process. We're also a biotech company. So we all wear multiple hats and we pride ourselves in being a very lean company. You can get quickly lost in the woods if you keep hiring and hiring. So we have a very detailed and very carefully crafted hiring plan that allows us to strategically hire the right people at the right time. And Molly is building this plan out right now and is executing on that plan. So obviously we're looking for clinical operations. We're looking for regulatory. We're looking for medical affairs and all of the team we're putting together right now to successfully and rapidly develop the molecules we have in preclinical development now to get them to the end of phase two, which is kind of a huge milestone and inflection point for a small company. Absolutely. Can we talk a little bit about what we should be looking for in the sad, mad outcomes that you're in right now, that you are running in right now? What, you know, sort of given the unique nature and the novelty of your antibodies, right? The ones that are not out there, you're not creating B2s, right? These are truly innovative antibodies that you're creating. How should we think about the PK profile, right? How should we think about that sort of next gen level where we are looking for the quality of the weight loss? What does success look like here? So first of all, obesity seems to be a highly addictive space for investors. And we often have the question, do you see weight loss in a single ascending dose study? The answer is no. Single ascending dose studies are for safety and PK. We want to make really, really sure that we have safe molecules. And I understand the wish to see signs of efficacy, but whenever we talk about real weight loss, a single dose is likely not going to be good enough unless you have something like an amylin molecule or a GLP1. So we want to be very, very careful in our messaging around these safety studies. What we're really trying to understand in phase 1A and phase 1B is how is the molecule characterized? Can we actually find out what is the right dose and the right dosing frequency to go into phase 2? That makes phase 2 development where we go in real patients much, much easier. But obviously, there's always this wish, can we early on see signs of efficacy? And we're not the only ones. We're enrolling patients that are not necessarily lean. They're slightly overweight, sometimes a little bit on the obese side. But we also have to balance this all the time because obese patients often have comorbidities which exclude them from these early safety studies. So yes, we want to do imaging. We want to do DEXA scans and MRIs on patients early on just to see can we actually see target engagement and can we see early signs of efficacy? But that's also very dangerous because it goes down a path where people ask more and more and more efficacy data in these early trials. And you can very easily get lost in trying to prove efficacy early on, not power your study correctly, and then end up with a molecule that's not well characterized and also has not actually convincingly shown efficacy. So that's what we're not struggling with, but where we want to separate ourselves from maybe others that have gone too far down a path of saying, we want to give you everything in a phase one. That's not what we're planning to do. But if you think about quality weight loss, it's very relatively straightforward to look at biomarkers. This is usually imaging. We can go to MRI, we can very carefully characterize visceral fat around the inner organs. We can very carefully characterize skeletal muscle mass. We can even look at bone density. All of these measures we can look at very early on and can see are there signs of improvement. And based on studies in non-human primates with all myostatin molecule, we have seen that visceral fat or fat generally is reduced after a single injection. So there's a really decent likelihood that we can see where this leads. Now, is this conclusive evidence and it's going to work? No, it's not. But what it helps us to do is it helps us to compare to other mechanisms that have been in there for molecules that are far further down in the development path. And we can look at early signs of efficacy. Are we comparable? Are we better? Are we worse? And at least it gives us a little bit of a longer input or longer view on where we need to be on the phase two development. And that's a benefit of not being always the first in the disease area, not being the first on a mechanism, even if your modality is the first. And so, yeah, we're definitely benefiting from the experiences others had in that space before. But yeah, imaging is a really important step for us early on in differentiating. I don't want to go as far as say body composition. Body composition is not an approvable endpoint, but we know that visceral fat drives outcomes. So visceral fat could be a very good biomarker for us going forward. Just as an example, you can look at the fat around the heart and you can image this with an MRI and you can see reductions relatively quickly. And a cardiac MRI can also show the function of the heart, acute function. And so you could get early glimpses of is the heart function improved if you do that? Again, not an out endpoint that is approvable, but an early sign that this might have actually beneficial effects down the road. And we have to then do outcome struts to actually prove that. Right. In the longer term, right, you have to show demonstrate that durability, right? This is not an overnight effect, right? Exactly. Which contributes to that $800 million expense right around those phase threes. I think what's also interesting about the Asset600 is that in a way it's a pipeline in a program, right? It has the applications beyond the obesity, right? In sarcopenia and other muscle loss settings. So, you know, how do you think about that? And how do you think about sort of the lead indication and then building on and that indication expansion that tends to be quite attractive for not just the investor, but the strategic as well. We have seen on the myostatin side a little bit of an up and down in the last two years. So, two and a half years ago, there was a lot of excitement and multiple clinical trials were started. And then when the readout was coming, you know, the interest ebbed away a little bit. And what we've seen in the last few months was kind of people are getting really excited about this. And it has to do with, you know, what we're seeing in outcomes right now in trial readouts. So, Regeneron is going to read out their Turvogromap study at EASD in Milan, the European Diabetes Meeting. And then we're hoping to see BioHaven's result on their myostatin molecule at obesity week. So, I think there's some more excitement coming around those assets. What was particularly intriguing for us was some of the Regeneron data that we have seen abstracts, not the data yet, but just abstracts. And it seems to be working better in people that already lost muscle mass. And that is exciting because we always felt like a myostatin drug to preserve muscle is probably better geared towards an aging population and not maybe as a younger population. And this now is actually confirmed very intriguingly in monkey studies. Regeneron did also extensive monkey studies, but they used younger monkeys. And we used very old, we used geriatric monkeys for our study. And we saw better improvement in muscle mass. And we felt first, maybe this is the molecule, but maybe this is really also the age of the animal. Interesting. And so, there's some intriguing novel developments. We truly believe preserving muscle mass is important. We know from other studies that looked at weight loss, not with GLP1, just by dieting, that if you weight cycle, so yo-yo dieting and stuff like that, that you're actually long-term losing muscle mass. You lose a lot of muscle while you lose weight and you don't regain a lot of muscle when you regain. And you do this multiple times. Your muscle mass gets lower and lower and lower. And that leads, your muscle pulls on your bone, that leads to more frail bones and instability, your fall, break a bone. And all of the cardiovascular benefits might be there, but you might actually end up in a nursing home early. And that's what we want to prevent. We want to keep people basically on their own feet, keep the muscle strength there, and then not to forget between the age 60 and 90, you lose about 25% of muscle mass. And this goes at the same time with a reduction in basal metabolic rates. So the amount of energy you turn over every day. So that means a 90-year-old should cut food intake by 25%. I don't see this happening any time soon. So retaining muscle actually helps to stay for the softest world because muscle obviously burns more energy than adipose does. So there's more of a holistic approach to kind of that quality of weight loss. But these endpoints, we need to actually define these endpoints. They need to be approval by endpoints with approval outcomes before we actually can take that step. We're not the only ones who are driving this field forward. We're a very small part of that space. Right. No, that's very helpful. Maybe we have approaching the end. I just want to open up to the room if there are any questions. Maybe I'll ask. We talked about at the top of the hour, you know, sort of one of your strategic priorities and the focus has been on that weight maintenance. To date, right, we have not seen labels with the weight maintenance. It's clearly defined or is a major note of part of the label. And there is really no approved path. Very much linking back to your just now comments, what are those approval endpoints? So I guess maybe given that that is one of your strategic priorities, how do you see the past opening up? Could you suggest any of those approval endpoints for the inclusion of maintenance in the label? I think it all starts with basically defining an unmet medical need, right? So we speak, obviously, with a lot of doctors who prescribe GLP ones. And many of them are telling us the weight loss problem is solved. We now can lose enough weight. What is not solved is keeping the weight down. And I think this unmet medical need will drive ultimately that the approval process will change. It has to change. It is an unsolved problem. And if you regain that weight, and then you have to go back on the drug, we know that the outcomes will be detrimental. So your point of what will be the endpoints is really important should we declare just an artificial endpoint by saying we prevent weight regain by 50% within one year. What does this mean for overall health? Right? And so I think what what is missing right now is really kind of tying the body weight loss to cardiovascular outcomes. And the GLP ones will help us do that. These studies are happening. There's multiple studies that you know, the large obesity companies are conducting right now to look at other things than just weight loss with with GLP ones might this be cardiovascular health might this be even breast cancer is being studied. So we will know a lot more over the next few years, how actually that reduced weight and maintaining this reduced weight is actually, you know, helping overall health. And that will allow us to tie this to kind of fixed endpoints. Ultimately, I think it's the easiest to kind of name a level of weight regain prevention, just to have kind of a comparable outcome with that. But I think there have to be outcomes attached to that percentage point. Might it be cardiovascular outcomes? Or might it be outcomes on metabolic disease? And so on and so on. But I think those endpoints are fairly well established. We know this from the type two diabetes space, when SGLT2 inhibitors came on the scene, and suddenly, you know, reduced cardiovascular risk by 40%. We know exactly what to look so it's not like we don't know these these endpoints. I think it's just tying them to a certain weight, or prevention of weight regain. That's that's all it takes. Very helpful, very helpful. In the last minute and a half. What are the key milestone or the key catalyst events that we should be looking out for over the next six to 12 to 18 months? That's a lot. So our myostatin program, iBio600, we have now dosed the SAT completely. So every person in the single ascending dose has been dosed. Because this is such a long acting molecule, we don't know the half life yet, we have to wait several months before we can determine it reliably. So expect us to read out safety and PK data first quarter next year. We obviously image these patients again, we're not going to see weight loss, but we might see, you know, trends towards improving, you know, fat mass and improving muscle mass in a DEXA scan. It's a very crude way of looking at this, but it helps us understand are we hitting the target. So that's next quarter, next first quarter, or first quarter 27. Our lead program, active in E, antibody iBio610, we are on track of filing in Australia clinical trial notification end of this year. And that puts us to first patient dosed beginning of next year. Again, this is a SAT study, again, with a half life extended antibody, expect six months down the road, then interim data from that SAT study. And then our bi-specific molecule for pH half path, we have declared development candidate in June this year. We're planning a filing late in the second quarter 27, early third quarter 27. And that puts us as first patient dosed also third quarter 27. So that's going to happen next year. And then on the MLN side, we don't know yet because we still have to kind of drive what which of the molecules will actually make it forward. And what we're also doing at the same time, as an antibody company, we really want to own the space around active in E. So we're working obviously on other molecules like an Alx7, it's a receptor of active in E antibody, and also on a second generation active in E that attaches an incretin, which we have not decided yet which one to the antibody, which takes the regulatory risk of the weight loss off the table. So those are all molecules that are relatively early in development, but they're all kind of marching along. And hopefully we'll have some preclinical data on those assets as well. It's amazing. Thank you so much. Thank you so much for your time today. And very impressive. Congratulations on all the success. Thank you. Thank you. Thank you all. Thank you.