Hello? Yes. Great. Thank you so much. So good afternoon, everyone. Thank you so much for joining us at the 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 a major progress. The company's really focusing on building long-acting antibodies for obesity, but building on what comes after GLP-1s, focusing on cardiometabolic and cardiopulmonary disease. When we talk about what comes after GLP-1, 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.
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. We have seen this before in type 2 diabetes, in hypertension. We're likely looking at a hypersegmentation of the market. We're really not interested 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 GLP-1s are, I should broaden this group. The weight loss drugs, like the amylins, the GLP-1s, the dual and triple Gs, they really solve the question of lowering the body weight.
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. 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 GLP-1 are going to have adverse effects, gastrointestinal adverse effects mainly.
I think the early amylin data that Eli Lilly and others have shown is there might actually be beneficial effects of an amylin over a GLP-1, 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. Then you mentioned the quality of the weight loss, right? I think this is something we're, at the moment, underestimating. It actually is not muscle or bone density that makes us sick. It is actually inflamed visceral fat, the fat around our inner organs, that actually makes us sick.
I feel like this is one of the areas where I think we're going to evolve in the obesity space very rapidly in 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. No, that's very helpful. When we think about the sort of the current standard of care, as well as amylin coming on as potentially a secondary pillar or a foundation, right? Then we think about your asset, right?
IBIO-610. Where does that come in? How are you thinking about your lead asset in your pipeline? Where does it fit in on top of incretins, on top of amylins? You have amylin of your own.
Yeah.
Can you take us a little bit through that and how you're thinking about the pillars here?
Activin E is a really interesting target because it has a very strong genetic validation.
The last one that we saw with equally strong validation was PCSK9.
Not only the gene that makes Activin E is correlated if you suppress this, that you have protection against cardiovascular disease and metabolic disease. Also, its receptor, which is called ALK7, shows the same beneficial effects. This whole pathway really is related to metabolic and cardiometabolic disease protection. That is 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.
Naive as we were, stumbled into that space and said, "We are just going to make one.
Sure.
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 Activin E antibody.
Yeah.
To this day, we are still the only ones with an antibody. There are other companies that approaches with siRNA.
Trying different modalities
but we believe that antibodies, they're a way more developed and validated modality right now. Not that the siRNAs are not fantastic drugs and not catching up, but at the moment, there's just way more approved antibodies.
Yeah
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 talk a little bit about the difference in the modalities.
specifically for Activin E and why potentially the antibody will be a solution to some of the shortcomings
perhaps that we have seen currently with the siRNA.
Yeah. I think the most intriguing aspect of an antibody is that you can block the Activin E molecule completely. It is 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.
Right.
It is also at a relatively low level in blood, so that you do not have to inject so much antibody to neutralize it.
Yeah.
siRNAs, at least to this day, seem to have a limit, if you average it out, of about 85% inhibition.
Yeah
It is a faucet that-
Yeah
drips out of the liver. You cannot switch it off completely. There is always a little coming out. Activin E is a very, very potent molecule.
Even small amounts cause an effect. What we and others have seen in animal models is that the more you block the pathway, the better the efficacy. 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 Activin E molecules in blood for at least eight weeks. We believe that could actually lead to better efficacy down the road. This has to be proven
Right
in humans, to be very clear, but it gives us an advantage there. This is a long-acting antibody, so we're offsetting a little bit the advantage of an
Yes
siRNA that can be actually administered very infrequently. The half-life in our monkeys is more than 30 days.
Yes.
That's a significant extension to regular antibodies, which have maximally a half-life of about 14 days. Our estimated human half-life is somewhere in the 50 to maybe even 100 days range.
Wow.
That gives us confidence that we can dose this maybe every three months. Upside scenario would be every six months.
Right. That's very helpful. I think maybe we can talk a little bit about the importance of long-acting, right? I think typically we see a large, well in the, let's say past 12, 18 months
Yeah
long-acting amylin, right?
Yeah.
What does that mean, and what will that contribute to the treatment landscape? I think maybe a twofold question. One, your own amylin and-
how is that a part of your thesis and in combo with Activin E or not, the two long-acting ones? How are you thinking about combination of a two long-acting or a single long-acting amylin or
Yeah
combo amylin HEB?
Amylin is a really interesting molecule, right? Because when the first amylins came out, we thought it will be a niche product for the 3%-5% of people that don't tolerate GLP-1s. I think the whole field was turned upside down by data that we saw from Eli Lilly on eloralintide, Eli Lilly's amylin. That caused a significant amount of weight loss comparable with the GLP-1.
It might ultimately show a little bit of a more benign adverse effect profile. What people tend to forget is GLP-1s don't universally lower body weight in everybody.
There's a huge spread between 3% and 30%.
Right.
It is not really uniform, and there are patients that will definitely benefit from another mechanism. Amylin is a very old molecule. We have done this many, many decades ago, and the first amylins had to be dosed three times a day. Peptide with a short half-life.
There was no weight loss. Then the once-daily and the once-weekly came, and the longer the half-life got, the better the efficacy on weight loss became.
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 then have that extended half-life in humans as well. The second really interesting aspect of amylin is we still do not understand to this day if there are certain receptor subtypes of amylin. There are multiple amylin receptors. Which one is it actually that conveys efficacy, and is there one that actually produces side effects that we do not want to see? We do not know. The solution for that is obviously making selective antibodies against the individual receptor subtypes and testing this.
Yes.
To our knowledge, we are the only company that actually has four molecules on amylin. One is a so-called DACRA molecule, a dual calcitonin amylin receptor agonist that hits not only the amylin receptors, but also calcitonin. We have a so-called SARA profile that hits amylin receptor 1 and 3, and then we have individual molecules that hit only receptor 1 and only receptor 3. This is not a simple program that we are 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.
Right.
That is the whole interesting story about our amylin 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. No, absolutely. I think a couple of times already you noted the adverse effects, right?
The importance for you, management of dose, right?
Yeah.
Maybe we could spend just a little bit of time with that in this next generation of obesity treatment. As the landscape continues to evolve, that management of adverse effects, we often come back to that 3%-30%, right?
Yeah.
There is a 30% clinical trial sort of results.
Yeah.
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-
Yeah
in your mind?
I think our patients tell us everything about this, because if you look at the GLP-1 space, I'm generalizing this on purpose, 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. What this does is that it causes an overall roughly weight loss of about 10% in real-world data, real-world effect size. That tells you something, right? We don't reach the clinical trial efficacies of 25%, 35%.
Yeah.
This is because those higher doses cause these significant adverse effects. Imagine now you have a combination where you have a lower dose of a GLP-1 and combine this with, say, an Activin E antibody that causes further reduction in fat and body weight. You could actually get away with a lower adverse effect profile, but at the same time, restore the full efficacy of a high dose of GLP-1. 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 a 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 Activin A, right? Not just an antibody, you created an antigen. That's a proprietary platform.
That's very proprietary to iBio. Can you just maybe put that into context? What does that mean for what's next? You talked a little bit about the sort of variations on a team for amylin, right?
Sort of fine-tuning the receptors and what you're combining with. What is the potential here, really?
Yeah.
What else could we think about as we think about the potential of the, and the capabilities of this platform?
Yeah. 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. 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 anytime soon. To do this, we have actually developed our technology on both ends of this equation of antibody discovery. The first equation is really our antigens, 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.
Yes.
That's technology that originated from a company, which we bought the assets of, was called RubrYc Therapeutics, a pioneer in antibody discovery, AI-enabled antibody discovery. In the meantime, what we've done then, utilizing that 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.
You have to evolve both at the same time, and not a lot of companies do actually both sides.
Right
of that equation. That allowed us to not only solve the structural issues others had with Activin A, 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 are going to publish about this. It is going to take a while. This is going to be a high-level journal we are trying to get into.
Right.
That antibody has very unique characteristics that we have never seen in an antibody before. Interestingly enough, it comes from a naive library. It is in a library that we sampled from hundreds of humans, of beings.
It is not something we created in the lab, it is just something our technology enabled us to find.
Okay.
Just to give you an idea of the scale, we screened 1 billion molecules, and we found only one that neutralized Activin A.
I am fairly sure this molecule sits in other libraries of competitors.
Right.
That is what set us apart in this space.
Right. Finding that needle in a haystack, right?
Exactly.
That is amazing. It sounds like the use of AI capabilities for the right. You asked the right question, and you got the answer. But it is the matter of asking the right question and-
Correct
what you're trying to build.
Correct. It needs to translate into something. It needs to translate into a drug-like molecule.
Right.
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, right?
Right.
Sometimes old-fashioned technologies actually do the same thing, 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 it that way.
Very helpful. I noted at the beginning that you are a clinical stage company now.
Yes
Which was a major event and major catalyst, and congratulations on all the success. Maybe we can spend just a little bit of time on IBIO-600. The molecule is in the clinic. You publicly disclosed that the vast majority, only about one participant, has been dosed across all four SAD cohorts. You have also significantly enhanced your leadership by bringing in Molly Carr.
Correct.
Can we talk a little bit about there is the build-out of the clinical program, the build-out of clinical developmental plan. What is Molly doing in the company now? How do you see the next key steps in the IBIO-600 program?
Yeah.
What should we be looking out for, and what should we expect?
It was very interesting because we have built a very broad pipeline around obesity. We are one of the few small companies that really have an integrated obesity cardiometabolic pipeline.
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.
Wow.
We have gotten really good at this early discovery stage to produce molecules that would go in the clinic. Now what we are building as the next step is we are now building a very efficient team that allows us to go to the end of phase II. That is the next step, right? For a small company, doing a phase III trial in obesity is a very, very tall order. We are talking $300 million-$800 million for a phase III.
Right.
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 does not 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 conduct these trials, and that's what Molly is building right now.
Right.
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. 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 insulins, long-acting insulins for Eli Lilly and Company. 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.
Yeah.
We have a very detailed and very carefully crafted hiring plan that allows us to strategically hire the right people at the right time. Molly is building this plan out right now and is executing on that plan. Obviously we're looking for clinical operations, we're looking for regulatory, we're looking for medical affairs, and all of that 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 II, which is 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, right, that you are in right now?
Yeah
that you are running in right now. Given the unique nature and the novelty of your antibodies, right?
Yeah.
The ones that are not out there. You are not creating me-tos, 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?
Yeah.
What does success look like here?
Yeah. First of all, obesity seems to be a highly addictive space for investors.
Yeah.
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. 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 GLP-1. We want to be very, very careful in our messaging around these safety studies. What we're really trying to understand in phase Ia and phase Ib 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 II? That makes phase II 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? 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.
Right
which exclude them from these early safety studies. 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. That is also very dangerous because it goes down a path where people ask 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 is not well characterized and also has not actually convincingly shown efficacy. That is what we are, not struggling with, but where we want to separate ourselves from maybe others
Yes
that have gone too far down a path of saying, "We want to give you everything in a phase I." That is not what we are planning to do. But if you think about quality weight loss, it is 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 our myostatin molecule, we have seen that visceral fat or fat generally is reduced after a single injection. So there is a really decent likelihood that we can see where this leads. Now is this conclusive evidence that it is going to work? No, it is not.
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?
Understand.
At least it gives us a little bit of a longer input, or longer view on where we need to be on the phase II development. That's a benefit of not being always the first-
Right
in a disease area, not being the first on a mechanism, even if your modality is a first. So yeah, we're definitely benefiting from 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.
Right.
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. So you could get early glimpses of, is the heart function improved if you do that? Again, not an 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 trials to actually prove that.
Right, in the longer term, right?
Exactly.
You have to show, demonstrate that durability, right?
Yeah.
This is not an overnight effect, right?
Exactly.
Which contributes to that $800 million expense right around those phase III's.
Yeah.
I think what is also interesting about the asset 600 is that in a way it is a pipeline in a program, right? It has the applications beyond the obesity.
Yeah.
Right? In sarcopenia, in other muscle loss settings. 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 strategics as well, right?
Yeah. We have seen on the myostatin side a little bit of an up and down in the last two years. 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, the interest ebbed away a little bit. What we have seen in the last few months was kind of people are getting re-excited about this, and it has to do with what we are seeing in outcomes right now in trial readouts. Regeneron is going to read out their trevogrumab study at EASD in Milan-
the European Diabetes Meeting. We are hoping to see Biohaven's result on their myostatin molecule-
Right
at ObesityWeek. I think there is 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.
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.
Interesting.
This now is actually confirmed very intriguingly in monkey studies. Regeneron did also extensive monkey studies, but they used younger monkeys. We used very old, we used geriatric monkeys for our study, and we saw better improvement in muscle mass.
We felt first maybe this is the molecule, but maybe this is really also the age of the animal.
Interesting.
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 GLP-1, just by dieting, that if you weight cycle, so yo-yo dieting and stuff like that you are 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. You do this multiple times, your muscle mass gets lower and lower and lower, and your muscle pulls on your bone, that leads to more frail bones and instability. You'll 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.
Right.
We want to keep people basically on their own feet, keep the muscle strength there. 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 rate, so the amount of energy you turn over every day. That means a 90-year-old should cut food intake by 25%. I don't see this happening anytime soon.
Right.
Retaining muscle actually helps to stave this off as well because muscle obviously burns more energy than adipose does.
Yeah. Interesting.
There's more of a holistic approach to kind of the quality of weight loss. But these endpoints, we need to actually define these endpoints. They need to be approvable endpoints with approvable outcomes before we actually can take that step.
Yeah.
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. Okay, no. Maybe I'll ask. We talked about at the top of the hour sort of one of your strategic priorities and the focuses has been on that weight maintenance, right? To date, we have not seen labels with the weight maintenance
Yeah
is clearly defined or is sort of major note or part of the label, and there is really no approved path. Very much linking back to your just now comments, what are those approvable endpoints? I guess maybe given that that is one of your strategic priorities, how do you see the path opening up and could you suggest any of these approvable endpoints for the inclusion of maintenance in the label?
Yeah. I think it all starts with basically defining an unmet medical need. We speak obviously with a lot of doctors who prescribe GLP-1s, 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 a drug, we know that the outcomes will be detrimental.
Yeah.
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? I think what is missing right now is really kind of tying the body weight loss to cardiovascular outcomes.
The GLP-1s will help us do that.
Right.
These studies are happening. There's multiple studies that the large obesity companies are conducting right now to look at other things than just weight loss with GLP-1s. Might this be cardiovascular health? Might this be, even breast cancer is being studied.
Right.
We will know a lot more over the next few years how actually that reduced weight and maintaining this reduced weight is actually helping overall health, and that will allow us to tie these two kind of fixed endpoints.
Yeah.
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.
Yeah.
I think there have to be outcomes attached to that percentage point.
Yeah.
Might it be cardiovascular outcomes? Or might it be outcomes on metabolic disease? And so on and so on. I think those endpoints are fairly well established. We know this from the type 2 diabetes space, when SGLT2 inhibitors came on the scene
Right
and suddenly reduced cardiovascular risk by 40%. We know exactly where to look. It's not like we don't know these endpoints.
No.
I think it's just tying them to a certain weight or prevention of weight regain. That's all it takes from here.
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?
There's a lot. Our myostatin program, IBIO-600, we have now dosed the set 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 trends towards improving 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?
That is next first quarter or first quarter 2027. Our lead program, Activin E antibody, IBIO-610, 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 SAD study, again, with a half-life extended antibody. Expect six months down the road, then interim data from that SAD study. Our bispecific molecule for PH-HFpEF, we have declared development candidate in June this year. We are planning a filing late in the second quarter 2027, early third quarter 2027, and that puts us as first patient dosed also third quarter 2027. That is going to happen next year. On the amylin side, we do not know yet because we still have to kind of drive which-
Right
of the molecules will actually make it forward.
Right.
What we are also doing at the same time, as an antibody company, we really want to own the space around Activin E, so we are working obviously on other molecules like ALK7, that is the receptor of Activin E antibody, and also on a second-generation Activin E that attaches an incretin, which we have not decided yet which one-
Yeah
to the antibody, which takes the regulatory risk of the weight loss off the table.
Those are all molecules that are relatively early in development, but they are all kind of marching along and hopefully we will have some preclinical data on those assets as well.
That is amazing. Thank you so much. Thank you so much for your time today.
Thank you.
And very impressive. Congratulations on all the success. Thank you.
Thank you so much.
Thank you all.
Thank you.