Good morning, everybody. Welcome. I'm Eric Joseph, Senior Biotech Analyst with JPMorgan. And our next presenting company is Kymera Therapeutics. Presenting on behalf of the company is Founder and CEO Nello Mainolfi. After his presentation, there'll be a Q&A session. So if you want to ask a question, we'll bring a mic around to you. And for folks tuning in via the webcast, feel free to submit questions via the portal. All right? Nello, thank you.
All right. Thanks, Eric, for the invitation. And I think we're in the same room last year, too. Thanks, everybody, for joining us today. First, probably Happy New Year, everybody. So it's exciting for me today to focus on a couple of important points. One, I want to share with you all an update on where we are with Kymera, where we are with our strategy, our focus, our vision, and then spend some time on what we're planning to do in 2025. As hopefully many of you have seen our press release this morning, it's a very busy 2025. So it's an opportunity to provide a bit more color, a bit more context, and then answer, I'm sure, great questions that Eric is thinking about right now. So Kymera is a science-first clinical stage company with what I believe it to be really a best-in-industry oral immunology pipeline.
How are we doing this? We believe that combining this rapid potential of targeted protein degradation with the right target, we can deliver oral therapies with biologics-like profile that we believe will disrupt health care. Given that right now we're focused in immunology, we believe we have an opportunity to completely disrupt immunology treatment paradigms. How do we do this? I think we stand on key pillars that I'll touch upon the next slide, but some key areas that Kymera, I believe, is really unique on. Obviously, we're a leader in the protein degradation space. We have built, as you've seen a few slides, some really excellent capabilities to identify small molecule ligands to difficult-to-drug targets. With that, a really unique target selection strategy. Many of you know our targets. We'll disclose some new targets as well.
I think we continue to be at the forefront of that space. So as I mentioned, I believe Kymera stands on three key pillars. One is, I would say, a clear vision, strong execution, and continued impact. On our vision, if you've known us for a while or for a little, hopefully, it's clear that the whole company, and this is not just me or a few executives in this room, the whole company is energized by the desire and the ambition to change lives of patients around the world with our innovative medicines. And as we do that, continue to build, eventually, a global commercial stage company. Right now, we're focused on building a lot of development capabilities on the existing ones to prosecute some of the phase II and phase III studies that we've started to discuss that are actually coming up as early as this year.
We've been always well capitalized, so fortunate to have investors that have continued to believe in our vision. We've raised $1.7 billion to date. Luckily, we still have about $850 as of December 31st, which will allow us to get through the middle of 2027, but more importantly, through actually several phase II data readouts across our pipeline. So lots of value inflection points in 2025, in 2026, in 2027. Execution, this is something I'm extremely proud of. We have delivered five new molecules into the clinic in the past four years since 2020. And we are on path to deliver a total of 10 by 2026. I think this is the level of execution that I expect it to be really up there. Impact, we've dosed more than. I think much more than 300 between healthy volunteer and patients.
Something I'm proud of, we've helped patients with many diseases from HS to AD to lymphomas and other oncology indications over the years. More importantly, for each one of our programs, we've been able to show, demonstrate the desired profile. We always show that we can saturate target degradation more than 90% with the desired safety and efficacy profile, and that is, I think, quite a compelling statement when you think this is still a relatively new modality and we are a relatively early company, so I'm going to do a crash course on targeted protein degradation in one slide. I know many of you know. I'm sure Eric can actually walk people through this slide, so the key opportunity with TPD is the ability to actually complement many of the technologies that have been developed over the years and provide a really differentiated product.
Hope to deliver on the promise of the so-called genomic revolution. All the technologies that we've been developing in the past 10, 15, 20 years have advanced our ability to deliver innovative medicines at scale. But the reality is that the undrugged or poorly drugged proteome is still there, and it still needs solutions for. Actually, the main reason is, even with highly impactful technologies like oligo-based therapeutics, you actually have a huge limitation with delivery, especially, and being tissue-agnostic. The potential of TPD is that you can use a small molecule and then a small molecule binding event to a disease protein, and then you can deliver a genetic-like knockdown with the flexibility and convenience of an oral small molecule. That's really the value proposition. As with any technology out there, you're only as good as the targets that you choose.
We have taken the approach of target selection being front and center. On the previous slide, I talked a lot about our mission to change immunology with oral small molecules that would have biologics-like efficacy. Why immunology? Immunology, as everybody knows, at least everybody in health care, is a very large market. I think what probably can be missed is that it's a largely underserved market. Our team put together numbers for the top 10 indications in immunology. They're written very lightly in the bottom, but the ones that you would expect: AD, asthma, COPD, HS, psoriasis, all the common or relatively common immune inflammatory diseases. If you look at all diagnosed patients in the major seven markets, these are 160 million patients. The patients that access advanced systemic therapy are about five million.
It's about 3% of total patient number access highly effective advanced systemic therapy. That is a $100 billion market. Two-thirds of those therapies are injectable biologics. While, obviously, I think everybody is trying to fight over the 3%, I think the biggest opportunity here is to develop drugs that will increase dramatically access to systemic advanced therapy. We believe that the best way to do it is to advance degraders, oral degraders that have biologics-like efficacy. I apologize if something off. I lose my computer with slides, but at least they look good on that screen. No apologies needed. I guess to myself. Again, the bottom line is, if you have an oral drug that can really replicate the profile of a biologic, you should be able to provide advanced systemic therapies to many more patients.
And so not only can you displace or fight or compete with biologics in the 3%, but it's really to expand access to also the 97% that are receiving either suboptimal therapies or no therapies. And just to be clear, these are both mild, moderate, and severe patients. So the number that we put there is just a question mark, $500 billion market. I'm 100% sure the number is wrong, but it gives you an idea of really a huge untapped market. So let's go more into the technical parts of this. Why do we believe that when you look at the overall profile, an oral degrader can be superior to both established injectable biologics and traditional small molecules? So injectable biologics have transformed immunology. Actually, they have transformed many other disease areas. They validate the targets, and they've helped patients.
If you think about psoriasis, 15 years ago, it was treated with almost chemotherapy, right? Now it's treated with highly effective therapies. That's thanks to a lot of the work that has been done in that space. But there's obvious drawbacks. Expensive, challenging to prescribe and reimburse in many areas of the U.S. and the rest of the world. They have, obviously, issues with immunogenicity. They have challenges with storage. And importantly, patient quality of life is critical, right? So inconvenient and painful route of administration for many patients, especially children. So surveys have been done in this space. I don't want to keep repeating the same things, but a survey that actually some of our colleagues in J&J did a couple of years ago, you ask hundreds of patients on biologics, would you switch to an oral with the same profile? 75% of them said yes.
So clearly, there is a huge unmet need in that space. Why small molecules have failed to deliver? There are lots of small molecules in pathways that have been validated by biologics that have come short on efficacy. That's a fact. There is a picture on our slide that really speaks loudly to, if you look at PASI 90, psoriasis, and you look at TYK2 versus IL-23, there is a big delta. I think part of the reason is some targets do not have the biological power. But I think a lot of the reasons come down to the fact that small molecule occupancy-based pharmacology relies on PK/ PD relationship.
When you have a peak-to-trough difference in a small molecule inhibitor, you're not going to be able to completely saturate that pathway. A degrader, we've shown extensively, can reach full degradation and steady state and completely block the pathway. That's where the technical opportunity is to have degraders that have the ability, through pathway inhibition, through a catalytic mechanism, to decouple PK/ PD and have complete pathway blockade and reach biologics-like saturation of pathway, again, with an oral profile.
Okay. Thank you. So we're on slide seven for people on the webcast. I was asked to reference slides, by the way. Going to slide eight. So I'm going to spend the next two slides to talk about key areas that we believe Kymera is really unique in. And I think when I say unique, I'm not referring to just the protein degradation space, but I'm talking to biopharma in general. I think we have a very unique target selection strategy. Soon, we'll disclose another program that will fit nicely in this slide. So our key philosophy is really undrugged or poorly drugged targets in pathways that have strong genetic validation. Ideally, the target of human genetics data with pathway to impact millions of patients.
So if you look at IRAK4, TYK2, these are two targets that have been drugged with small molecules, we believe, not fully, where a degrader can provide a biological, and we believe, a clinical superiority. STAT6 is an undrugged transcription factor that has not been drugged. And our company, Kymera, is the first company to go after this target with an oral degrader. I think one other thing that we're very proud of at Kymera, although we might have some mixed feelings, is the fact that our target selection has also inspired many companies to follow our footsteps. So you see targets that we put on the map first, and now we have several companies pursuing. So it shows you the leadership in the space as well. Another point that I actually don't make enough is the capabilities that we've built at Kymera.
If I had put this slide up five years ago, I wouldn't be able to stand behind it with the same level of credibility. This is something that we've grown over the years. And I believe, having been in small and large companies in my career, we really have industry-leading capabilities. And I would probably point to three key without, hopefully, upsetting the rest of the team that is working on many other things. But one is our ability to identify small molecule ligands to targets that have not been drugged before. Now we've shown it over and over and over again with all these transcription factors and undrugged proteins that we're going after. And this has led to more than eight development candidates in the past few years, more than four targeting undrugged transcription factors. You've seen some of them. You haven't seen all of them yet.
I think capabilities to understand ternary complex through cryo-EM. This is actually a very expensive capability that allows us to have exceptional understanding of how these molecules interact in 3D and how to optimize and refine their properties. And then we have a world-class team, of which I'm an honorary member being a chemist by training, that has been able to deliver molecules with picomolar potency, good bioavailability, even distribution across all relevant tissues. And this has translated in really amazing translation in all the programs so far in terms of PK/PD safety and efficacy. Again, in the first few slides, really to tell you a bit more about Kymera, our strategy, our vision, our capabilities. Now we're going to talk about our pipeline and programs.
Starting from our pipeline, so we've divided in the wholly-owned programs versus the partner programs. So starting from top, so obviously, STAT6, as I said last year, that this was going to be one of the most exciting programs in industry. And I think everything that has happened in the past 12 months continues to substantiate that statement. We are, as you know, in phase I. We'll talk all about where that program is going. The real opportunity there is a dupilumab-like profile in an oral pill. TYK2 is a program, KT-295. This is on slide 10. 295, we will start phase I in the second quarter of the year. And this is really, for the first time, replicating the loss of function profile of TYK2. And we believe that will lead to biologics-like efficacy.
We're very excited about a new program that we're going to be disclosing in a company-sponsored event in the first half of 2025. This is yet another undrugged transcription factor that is genetically validated, for which we believe we have the first oral drug that is moving into the clinic. We're around 12 months, within a year, away from being in the clinic. And then just to remind you, with IRAK4, this is a program, again, that we started at Kymera. We took it through phase I. Our partner, Sanofi, is doing a great job advancing the program in two parallel phase IIb studies in HS and in AD. Again, great opportunity to do better than the upstream biologics that have already shown exciting data in many indications. So this speaks to each individual pathway a bit about the point that I made before.
I'm not going to go necessarily through this slide 11, each individual market opportunities. But I think oral degraders in immunology have the opportunity to disrupt commercially that market. We can use STAT6 again as an example. If you look at TH2 diseases in the seven major markets, we're talking about more than 100 million patients. Right now, only 1% have access to systemic advanced therapy. Again, mostly biologics. That's a more than $10 billion market. Again, if you think about mild, moderate to severe, split 50/50, there are tens, if not hundreds of billions of dollars of potential commercial value for a program that can expand access dramatically. TYK2 is a much more mature market if you look at indications on the slide. Psoriasis, SLE, UC, et cetera. Still, it's 11% penetration if you, again, think about diagnosed patients in the seven major markets.
IRAK4, we have an ambitious plan here. This is just to showcase. I'm not saying that Sanofi is going to develop in all these indications that are on the slide, but these are indications that mechanistically could be accessed by an IRAK4 degrader. Again, you can see that 3% is worth $55 billion. Again, the point is the same as I made in the first slide. This is just with more accuracy for each program. The opportunities are huge if you're able to have a drug that will expand dramatically the number of patients that can be treated. The next few slides, I'm going to give some slide 12 vignettes on TYK2 vignette on IRAK4, and then we'll spend a bit more time on STAT6, and then we'll wrap up. I think I'm doing great on time, I think. TYK2, just a bit of history.
This is one of the most well-validated targets in terms of human genetics. There is obviously validation of TYK2 small molecule inhibitors and upstream biologics. This is a scaffolding kinase that has not been drugged fully. If you look on the top right of that slide, you see that the loss of function profile is very different than what can be achieved, for example, with the kinase inhibitor profile. So clearly, the opportunity to disrupt IL-23, type 1 interferon, IL-12 while sparing IL-10 is, we believe, highly differentiated, and how we're going to do this? By having a highly specific degrader, KT-295, that you see in the bottom of the slide, that is able to completely degrade TYK2 if needed. We believe this is going to be highly differentiated. So it's in IND enabling studies with phase I start in the second quarter of 2025 and data towards year-end.
IRAK4, obviously, is a much more mature target, so it doesn't need a huge amount of introduction. But again, also here, pathway validated. We have exciting data, actually, on this pathway with the IL-1 alpha/beta in HS in phase III now, IL-33 in COPD and asthma, IL-1 and IL-36 in more indications. And think about if you have an asset that is intracellular, an oral drug that should be able to block all of those cytokines with a single agent, you expect to see some really, really exciting efficacy. So we've shown that inhibitors have now been demonstrated to be insufficient. The degrader really is the only modality to block the pathway fully. We've shown in phase I that you can degrade the target more than 95% in healthy volunteers.
This results in patients in some early but really exciting impact in both HS and AD as measured by either HiSCR or EASI scores, as we've disclosed in the past. This trial, again, as I've mentioned earlier, is in a phase II study, phase IIb studies in HS, hidradenitis suppurativa, and in AD, atopic dermatitis with Sanofi being in charge of those studies with data in 2026. Let's move on to STAT6. Again, as I mentioned earlier, this is, for us, clearly one of the most exciting programs in the industry. We have the first agent that has moved into phase I in October of 2024. We'll do a really relatively quick recap of what we've generated so far for this program and then talk about the future.
This is one of the really rare examples of a transcription factor that has a one-to-one relationship with an upstream receptor, meaning that everything that's signaled through the receptor has to signal through STAT6. And in fact, what happens once you activate IL-4 receptor, STAT6 is recruited to the receptor, is phosphorylated, and then translocated into the nucleus. It's an opportunity to target an intracellular target with an oral drug and replicate, we believe, what has been accomplished with, for example, an IL-4 receptor alpha biologics. Besides the pharmacology that, obviously, we've built preclinically, we are obviously benefiting from extremely strong human genetics data. We have humans that have gain of function of STAT6. This leads to severe allergic diseases, as you'd expect.
We also have human loss-of-function that have been identified relatively recently that are healthy and have also mechanistically fall in line with TH2 disease protection. Obviously, historically, this is a difficult-to-drug target. We've done plenty of work on this target. We've demonstrated at some point we published the data that if you want to replicate dupilumab-like pathway saturation with a once-a-day oral drug, you need a degrader. That is the only way to mimic dupi-like effect. No other modalities, including traditional small molecules, can reach the level of saturation that we can with a degrader with a single daily oral drug. So a few highlights of the data. 621 is one of the most selective and potent compounds we've made in the history of the company. As you see on slide 16, we are highly selective for STAT6. We do not degrade any other target.
I would say that we only bind to STAT6. We do not bind to any other target, so we have extreme specificity. This is a potent oral degrader. We degrade all relevant cell lines and cell types, human cell types, extensively, T cells, monocytes, B cells, keratinocytes, all the ones that are relevant to TH2 inflammation. Importantly, when you look at IL-4/13 signaling, we can block the pathway in human cells equally, if not more potently. In this slide, we're showing a couple of examples where we're even more potent than a monoclonal antibody. This actually translates well preclinically in models. This is a house dust mite asthma model. This is highly relevant to TH2 inflammation. With those, we actually expose mice to house dust mites. They actually generate TH2 inflammatory response, and with those, they reach about 90%+ degradation.
We're able to impact a plethora of TH2 biomarkers. In this slide, we're only showing target, but if you go on our website, you'll see probably 10 or 12 different biomarkers, as well as impact on actually a disease score like goblet cell metaplasia. Importantly, this drug, KT-621, is able to degrade the target in a dose response fully and in all the relevant tissues in non-human primates and other species preclinically, and importantly, in all the campaigns that we run in IND enabling studies, we did not see any adverse events, which give us the confidence and the excitement to go into humans with an excellent safety and efficacy profile, so I don't want to rediscuss on slide 20 the commercial opportunity, but I want to actually frame our strategy for the program.
Again, for a disease that has 100 million plus patients around the world, again, as you can see from the slide, really almost evenly split between mild and moderate to severe, our overarching strategy is to develop a drug that will be able to serve all of these patients. Again, not only, let's say, compete with the existing biologics in the moderate to severe market. Actually, the most important thing there is to expand penetration into those moderate to severe patients. Actually, the opportunity is also to do it in mild patients. We're prepared and ready to even use multiple molecules if needed to take over this market and, more importantly, to continue to be the leader in STAT6 biology and drug development.
Just to give you an example of what we mean when we say disrupt treatment paradigms in TH2 diseases, for example. What we did on this slide is really show with these arrows what is the series of medicines that patients with, for example, atopic dermatitis and asthma have to go through. In many cases, these are children. Children and adults need to take and asthma is probably the best case to use. They need to be exposed to a series of medicines that do not address the underlying inflammation. In many cases, corticosteroids that have severe adverse effects. They have to go through all of that to then be eligible to have advanced systemic therapy that actually treats the underlying disease, which in these cases are mostly biologics.
So I think ethically, one would expect that if you have a drug that is as active and addresses the systemic underlying inflammation, that drug not only, obviously, should be able to treat the very severe patients, but should be able to actually be accessed by patients much earlier in their treatment paradigm, especially in a disease like TH2 where you have an atopic march that is underlying the disease, meaning your disease will get worse with time unless you treat it. So that's what we're talking about. And I think when we talk about children, especially, this is the responsibility that we feel at Kymera to do. So cooling down. So let's talk about slide 22, where we are with the program. So as we disclosed in October of last year or early November, we started our phase I study on October 22nd.
This is, let's call it a typical SAD and MAD study. We're looking at multiple single ascending doses and then multiple ascending doses of 14 daily doses. What we're looking in this study is, importantly, obviously, PK, safety, and degradation. Based on the robust pharmacology that we built at Kymera and that is understood in the industry, if we're able to demonstrate that we can robustly degrade STAT6 and we can do it safely, we believe this is going to be a paramount dataset that should come out of this phase I study. As many of you know, some TH2 biomarkers that are still within the limit of normal have been modulated, not robustly, but modulated by other agents, including dupilumab, even in healthy volunteer, by 10%, 20%, 30%. So we'll measure those too. But I want to and we expect to modulate them too.
But I want to stress that clearly the key deliverable here is to show that a novel target, STAT6, can be safely degraded because we believe from there we will have huge opportunity to change, as I said, life of patients around the world. Just a quick update, as was in the press release. So recruitment is still ongoing. We've completed several SAD and MAD cohorts to date. So on the next slide, before going to the last slide, I wanted to tell you a little bit about our overall development plan. So we believe so first of all, I should say there are eight indications in which Dupixent has either been approved or is as positive phase III data. Actually, seven have been approved and one, I believe, not yet. And just as a general statement, we're committed to develop 621 in all of those indications.
How we're planning to do it is we've divided these indications into two main buckets: dermatology and GI in one, respiratory in another one. We believe that by running parallel phase IIb studies in individual AD and asthma that represent the rest of the term, GI, and respiratory indication, we'll be able to identify a dose that can be used not only to run phase III studies in AD and asthma, but also in all the remaining indications. So we believe that will allow us to do accelerated, late, parallel development across all the indications.
So we believe that thanks to the work that's been done with other agents in this pathway, not only we've learned, but I think we hopefully have built an even more efficient way to develop this drug that will allow us to do parallel development in as many indications, to be honest, as we can afford. The other important points that we're making today. So we're starting phase IIb studies, AD in four quarters of the year, and asthma early next. Between the healthy volunteer and the IIB, we're running a phase Ib in AD patients. Maybe it's best that I'll describe the sequence and the reasons for that in the next, which is the final slide. So this slide is really speaking to slide 24. I apologize that here and there I forgot to call out slides. Slide 24, last slide. So I'm done with that.
So, just going through the next inflection points in the next, I would say, 18 months, right, through middle of 2026. So, starting with STAT6. So, as I mentioned, healthy volunteer data 2Q 2025, so very soon. And the key data will be really safety, STAT6 degradation in blood and skin. I mentioned about biomarker. We'll measure it. That's really not the best place to measure it. That's one of the reasons why we built this phase Ib AD study. In a relatively short, small study, 28-day study, we'll be able to show, hopefully, that we can have a really robust biomarker signature in both blood and skin that we'll be able to compare to dupilumab. The dupilumab profile, even in 28 days, is very well established. So, in 2025, we'll be able to have healthy volunteer safety degradation.
Then we'll read biomarkers in blood and skin in AD patients, including 20-day efficacy. So we'll be able to also look at some EASI score then. And then at the end of the year, start two phase IIb studies in AD and asthma. So that's really what we're planning to do. So lots of work for the team and lots of exciting both data as well as big studies that are going to be initiated. I believe this is the busiest kind of program that we've built in the history of the company. For TYK2, as I mentioned, starting phase I second quarter, and data towards the end of the year where, again, there'll be safety TYK2 degradation in blood and skin. Also there, we'll likely look at some ex vivo biomarkers.
But really demonstrating that we're able to deplete the target well is going to be critical. Then we'll disclose a new program this year that will be in the clinic in early 2026. And then to remind you for IRAK4 data in 2026. So I'll end here. I'm sure I took probably more time than I should have, but happy to take any questions. If you have time for a couple of questions also.
Just on the how we should think about the translatability of the healthy volunteer data with KT621 in second quarter and how that sort of will you expect that to de-risk or relate to the patient setting, both in AD and in asthma, and specifically there, I guess, how should we be thinking about the relative level of STAT6 expression from healthy to disease context?
Okay. I think two questions may be in there. One, I think what we've shown preclinically and actually human genetics corroborate that if you decrease the level of STAT6, you see IL-4/13 signaling that is impacted and reduced or blocked. We believe if we are able to show that you degrade STAT6 90%+ , the translatability of that concept into patients should be equal to what has been seen with upstream biologics. Why we believe the healthy volunteer data is so critical is because if we're able to show that we can get to 90%+ and that's safe, I think that's telling us we have a drug in our hands. With regards to translatability of degradation in patients, across our experience with many programs, we've seen that degradation in healthy and degradation in patients is usually parallel.
We've shown that with IRAK4 too. Obviously, we'll have an opportunity to further demonstrate that in the phase Ib in AD, but all our understanding of 621 and how it behaves and how potent and catalytic the mechanism is, we don't expect that to see anything different in terms of profile between healthy and patients.
And it seems like there's an increasing number of STAT6 competitors or compounds entering the field, kind of probably riding in your way. Looking across the space there, I guess, how do you what other than being first in position, having a leading position, how do you think about other ways of engaging the I guess, what is very important by way of engaging the target that will contribute to activity here? I guess other approaches that are non-degraders, do you see them being effective also?
So yeah, so there's two questions there too. So I want to, or at least I interpreted, two questions. So one, the competitive intensity of the target. I like to quote our program lead of STAT6, Chad, that hopefully is listening. I think this is a race in the finish line. What we're showing is we have years ahead. We are years ahead of our existing, let's say, competitors or admirers. And I think our goal is to expand further the gap. And I think what you're seeing in terms of development plans are, I think, aggressive is probably an understatement. So that's one. On, I really actually hate to be discussing other companies' programs because I cannot speak to their programs. What I can speak to is our own effort. So we have had extensive effort with small molecule inhibitors of STAT6. Nobody knows about it.
We haven't disclosed it. We have not published it, but we will one day, and we know that if you want to have dupilumab-like pathway blockade, 621 pathway blockade with a single daily oral drug that is actually matching that blockade and the efficacy in these high bar models, not some in vitro system, you cannot use an oral small molecule inhibitor. You need to use a catalytic degrader. That's where we stand, and we're not standing on it because we're a degrader company, but because we have extensive experience in that space. And that will be disclosed at some point.
We can try.
Ole Vestmark, Copenhagen, Denmark, thank you for your talk. So you mentioned EOE within the IBD space. Do you have any plans of going into either Crohn's or UC at some point?
With STAT6 or?
In your programs.
Oh, yeah. I mean, we have multiple programs. So, immediate plans with STAT6 to go into UC, into IBD in general, there is no immediate plan. It's not a highly TH2-driven disease, unless we learn other things. Obviously, with TYK2, we believe that target needs to work in IBD based on human genetics. And the fact that it hasn't worked in other cases with small molecules, I think it speaks to the inadequacy of the small molecule, not of the target. So we're definitely keen on that. I think there is an opportunity with 474 and IRAK4 too, but obviously, that is a decision that also scientifically we'll have to make.
Okay. We'll have to leave it there for time. Thanks very much, Nello.
Thank you.
Thanks, everybody, for joining in.