Biomea Fusion, Inc. (BMEA) Earnings Call Transcript & Summary

Good afternoon, and welcome to day 3 of the 40th Annual JPMorgan Healthcare Conference. My name is Gavin Scott, I'm a biotech analyst here at the firm. It's my pleasure today to introduce Biomea Fusion and CEO, Thomas Butler. Please note that we will be going straight to the Q&A session following the presentation. So please feel free to use the ask a question button on your screen or e-mail me directly. With that, I'll leave it to Mr. Butler.

Great. Thank you very much, Gavin, and thank you for having us. Despite a very challenging backdrop last year, it was really a breakout year for Biomea. We started the year with 7 employees, having just completed a Series A, raised about $50 million, really in the middle of our key toxicology studies to support an IND. Fast forward through the year, we went through the IPO process with Mike Connor, raised $150 million that really allowed us to build out the infrastructure of not only our R&D engine but to really fully explore 219, which we'll talk about later in the discussion. And really, going through and writing a 5,700-page IND, submitting it to the FDA, which was cleared rapidly, and then putting ourselves in position, on a CMC perspective, to generate all the material required for our first-in-human and get our first site activated to end the year at MD Anderson and, at the end of the day, all the while hiring 45 employees to get to 52. We also did a custom design and build of our research facility, our innovation center in San Carlos, so a really foundational year for the company. This year, at the end of the day, I'm on Slide 3, we have an experienced and very successful management team. We've worked together for a very long time, and we know the strengths and weaknesses of each other, and we're here to improve and sharpen everyone's skill set. We have a very efficient platform, which I'll cover later in the talk, and a very productive clinical asset, BMF-219, which we're really excited about, and then, of course, an expanding pipeline that will start and kick off in the first half of this year when we announce our second program. Our mission, which you see on the right-hand side, our tenet inside these walls is we aim to cure. We're doing what we do to not only improve but to extend lives for our patients. That's really what we're all about. And when you see the pathways that we select, the targets that we select to design our covalent reversible inhibitors, all of the work that we do to go into the IND and execute our clinical trials, it's really just with that in mind. I'm turning now to Slide 4. BMF-219 is a novel, irreversible, covalent inhibitor. We think of it as a pipeline in a pill, and it's because we believe that single-agent activity will have a dramatic impact in multiple indications. And it's really through strong pathway control, multiple shots on goal in indications, consistent on-target effect and a very wide safety margin. Turning to Slide 5. Our team, really 10-plus years of success together, made up of myself; my Co-Founder and partner, Ramses Erdtmann, President and COO of the company; Franco, CFO; Naomi, Heow, Steve Morris, with Alex really taking control of all of our clinical science work. Thorsten, I was lucky enough to have worked with him at Gilead on the Hepatitis C Cure program. And of course, Jim Palmer, our VP of Drug Discovery, and really the leader behind the creation and discovery of ibrutinib. Switching now to Slide 6. The tenet for what we do, we're extremely patient-focused and, of course, aiming to cure. Our vision is about really creating a novel suite of covalent inhibitors. And really, selecting the right biology, the right pathway to target with a covalent inhibitor is essential. There are certain attributes that you have to look at and validate when you pick your target. We do custom synthesis at a target basis. That leads to what we call, or what we believe, as really breakthrough chemistry for our covalent irreversibles. And what we do is we combine these all together, with menin as the centerpiece. We want to bring in and build proprietary combinations from our experience at Gilead, shutting down multiple pathways for viruses. Cancer is also typically led by multiple pathways. And we really want to change the paradigm of treating patients with one pathway at a time to multiple pathways at once and really give our best shot at these fast-growing tumors. And there's a lot of examples in history of successful covalent inhibitors, of course. And we typically remind folks that covalent inhibitors have been out there for a very long time. They've been very, very successful. And it's really through this notion of binding to your target permanently and shutting it down. This gives you the best chance for your pharmacodynamic effect. I'm on Slide 7. There's, of course, the medicine cabinet, pills of aspirin and penicillin that we're all very familiar with. We have some oncology examples, TAGRISSO and IMBRUVICA, of course, these oncology covalent inhibitors. And then most people don't realize that the antivirals Vyriad and SOVALDI are also covalent inhibitors, all showing significant improvement in the lives of patients. On Slide 8. There are several important attributes and really the driving force behind selecting covalent inhibitors. Why go after these? Why specifically focus on them? We think they give you the best chance for success and not only success in the clinical setting but also success in the commercial setting. The high selectivity really is imparted through a two-step process where you do the same understanding of the target, the same structural design of your molecule to that target, trying to leverage non-covalent engagement. But you add in a second step, which is to target a specific single amino acid within the pocket. And you can imagine you have to modify the angle of your molecule where the warhead is attached to and also vary the distance. And the combination of distance and angle gives you that efficient covalent binding and drives what we see in the middle as a deep target of activation. You've got to get that bond formation to happen. As soon as you do, you have significant control on that target. And then the greater therapeutic window comes in by balancing the two. You have to have the balance of the high specificity selectivity with the deep target and activation. And that combination, we think, is second to none. Flipping to Slide 9. This is a great profile or a great example of what a covalent inhibitor can do. This is a PK/PD curve of ibrutinib. And essentially, what we're showing you here is, look, if you understand the kinetics and the dynamic of your target and of your covalent inhibitor, you can shut down the protein even though you only have 4 hours of exposure. The control on that target lasts for a 24-hour period. And so that distance between the green line and the blue line is that benefit, right? Because you don't need to maintain exposure. You don't need to constantly expose tissues and plasma to your drug to shut down the site. And that just gives you more flexibility and tolerability and keep patients on your drug. Passing on to Slide 10, our technology platform. And really, at the end of the day, traditional small molecule drug design goes through target exploration, like we do when we go through our validation step, but the initial hit is through library screening. And library screening is you're screening not just thousands of molecules but usually tens of thousands and sometimes hundreds of thousands of molecules to see where you find the scaffold that fits or hits your target. You then have to go through painstakingly optimizing your molecule. And the problem tends to happen where you lead to selectivity specificity issues because that scaffold was actually designed for something else. It wasn't designed particularly for your target. That's very different than what we do. We do custom design. So we don't spend a lot of time having to tinker with specificity of the target. We really spend most of our time during lead optimization with the PK properties of the molecule. And that's why we're able to get from target to hit to now preclinical validation and IND selection within a 3-year period where typically it takes 4, 5, 6 years to get there. Turning to Page 11, our pipeline. For 219, we're pursuing up to 7 tumor types. We'll be enrolling up to 7 tumor types this year, in 2022. Because of all the work that we've done from a translational perspective and validation of menin with a covalent inhibitor has really afforded the capability of doing this. And then we're also announcing that we'll be taking BMF-219 into diabetes this year. And what's so exciting is, again, menin, as I've explained in earlier presentations, that menin is this toggle switch. And whether it's in the on position or the off position, 219 does a great job of resetting the toggle switch into the neutral position. For our second program, or target #2, again, this is a target that was selected based on our increasing understanding of menin. We select and understand the biology, and we want complementary pathways. This is what lends to this idea of proprietary combination. We want to shut down multiple pathways with menin as a centerpiece. Program 2 and 3 kind of will, of course, sit on their own two feet. And they will be able to go and have a dramatic impact with single-agent activity and they'll have single-agent success. And we just think that the future and long-term benefit will be with combination. We'll announce the second program in the first half of this year. And what you'll get with that announcement is, of course, the target. You'll get the molecule, the IND candidate, and all the preclinical data that supported the selection of the candidate. Program 3 is right behind program 2. So we made quite a productive effort in 2021 there. On Slide 12, what we're highlighting here is all the different tumor types that we're exploring with 219. We're exploring multiple tumor types again this year. And really, from an initial understanding of menin, when we first started this program, menin was very much focused in the acute leukemic area. There's a lot of literature out there that suggests otherwise, like prostate cancer, like endometrial cancer. And then, of course, if you go into other literature, there's support that I'll talk about later, but initially, the focus was really about the acute leukemias because of the understanding of MLL. And menin-MLL is a very important protein complex that drives these aggressive leukemias. We just learned with 219 that we'd disrupt not only that complex, we'd disrupt other protein complexes with menin as the centerpiece, and that lends to these other liquid and solid tumors. A strong pathway control, and this takes us to Slide 14. If you look at the complex with MLL, and this is an important piece just to highlight the mechanism of action and why we went after a covalent inhibitor is, MLL in the translocation, you look on Figure A on the top, the fusion mutation happens at the tail end of MLL, not the business end where it engages with menin. That site is completely conserved across all species. And what we thought was so novel is there's over 100 different fusion partners that have been elucidated. So technically, you can have a different binding affinity of menin to MLL depending on what fusion partner do you have, AF9 versus AF4 versus AF10. And you can certainly try to dose up to create an umbrella effect, but we decided to create a covalent inhibitor that actually goes after the target, menin. And its ability to disrupt menin is really independent of MLL. That really allowed us the flexibility of going into these other tumor types. BMF-219 then on Slide 15. When you look at these key oncogenes that are driving the acute leukemia, we looked, of course, at the target gene MEN1, which creates our protein menin. MEIS1, HOXA9 and DNMT3A are all very supportive gene signatures of this pathway. And what's great to see is just consistency. At the 24-hour time point, we do a great job in not only shutting down the key gene signatures but shutting down the target chain. On Slide 16, what we're highlighting here is some of the other genes that gave us a clue on what 219 is doing that's unique to 219, to this covalent inhibitors, and what potential there is outside of acute leukemia. And so if you look on the chart on the left, we highlight BCL2, we highlight MYC and HOXA9. Again, you look at HOXA9 and BCL2 reduction, it's actually equally matched with MYC, showing you greater than 90%. Conversely, reversibles tend to give you about 50% to 60% reduction. And we believe that, that nuance creates an opportunity to go into other tumor types like DLBCL and MM. And so as you flip now to Page 18, what you see on the left-hand side is menin complex. And as I mentioned before, menin is in multiple protein complexes. Menin-MLL is just one of them. We're showing you another, menin and MYC, with the chaperone protein NPM1. And the protein complex that menin is engaged with just dictates the particular tumor type. So on the right, if MLL and NPM1 are engaged, you get acute leukemias, ALL and AML with the MLL rearrangement as well as NPM1 mutant. With MYC, however, it's a completely different tumor setting. We had double-hit, triple-hit, double-expressor in DLBCL, you have various multiple myeloma genotypes as well as really RAS, RAF with KRAS-activated tumors like colorectal, lung and pancreatic. So on Slide 19, this is some of the initial research work that we did that gave us a clue on menin dependency. And much to our surprise, acute leukemia actually ranked #3, not #1, as initially proposed. DLBCL ranks #1 in terms of the proportion of tumors that are at or to the left of minus one, which represents a [ penny ] central or a critical menin dependency for that particular cancer. Multiple myeloma ranks 2; acute leukemia, #3; and then in the solid, that's where we get the KRAS-activated tumors. This served as kind of our initial kind of road map to explore these other tumor types. For Slide 20, I know this is a complex slide, but basically, what it says is, in a very unbiased manner, what we did was look at what 219 does from a transcription factor basis. And we can get into this a little bit in the Q&A. But what it's showing you is that we're really disrupting MYC. MYC is #2 on this list. And if you look down the list, you see the other bad actors like KMT2A, which is MLL, UC, JunD and others. It really gives you a highlight of this disruption that's quite broad for 219. And then on Slide 21, this notion of menin and MYC and KRAS-adducted tumors continues to unwind. And greater than 80% of these engagements is really derived with menin, engaged with MYC. And so MYC target genes are activated and driving significant aggressive growth in over 70% of human cancers. On Slide 23, what I wanted to look at was how does 219 exert cell killing because, at the end of the day, in order to drive a response, differentiation is great but it's got to be backed up with cell killing. That's what's going to give you your response and that's what's going to drive, hopefully, survival in these patients. And so what we looked at was, okay, for 219 again, the story is very consistent. Whether it's MV4-11, whether it's MOLM-13 or OCI-AML3 at 560 nanomolar or 0.5 micromolar, we see 90-plus percent cell killing capabilities. And that's just a different profile than what you observed with the clinical reversibles in terms of the ability to actually be effective and have cell killing, which is in the 12% to 15%. Transitioning to Slide 24, we're highlighting just again the consistency. That's really the important takeaway, whether it's MV4-11, which is a biphenotypic cell line; MOLM-13, which is the traditional MLL-rearranged cell line; or the FLT3-ITD, NPM1, OCI-AML3. At about 0.5 micromolar, you have near-complete control of tumor growth. And that's very different than what we observed with our own reversible inhibitors. Here, MI-503 is a nice example of that. On Slide 25, we now extended to outside of acute leukemia, exploring multiple myeloma and KRAS pancreatic cancer. This is MIA PaCa-2, same concentration and just displaying same consistency. We get nice pathway control. And particularly, in the KRAS world, we don't have a plateau effect. We don't have a problem getting to IC90, IC95 because we're not targeting KRAS. The KRAS-on, KRAS-off cycling doesn't really influence us. We're targeting menin here. And then on Slide 26, what we're highlighting now here is the patient samples that we got to really explore what are the concentration dependencies now if we took patient samples. And it's really important, from an ex vivo perspective, to look at is there variability. So we took a couple of samples that were treatment-naive NPM1 AML. We also took some MLL-rearranged AML samples that are also treatment-naive. And again, the key here is the percent of growth inhibition or control as well as the consistency you see across the board. At 1 micromolar, we do an incredible job of shutting down this growth inhibition. Conversely, with MI-503, you see that even though it's a nanomolar-potent molecule, you give less than 5% growth inhibition at 1 micromolar. And again, this inconsistency, you do see about 35% in the gray patient. On Slide 27, what we're highlighting here is now to double-hit a diffuse large B-cell cell lines, DB and Toledo. And again, the story is the same. Because of the control on MYC that we observe with BMF-219, we see nice potency in both cell lines. And conversely, for clinical reversibles, this is really predicated on what we think is based on the ability to disrupt MYC. And the green doesn't have great control on MYC. The red shows a somewhat moderate control on MYC. And you see it coming out in the cell line data in terms of the potency. On Slide 29, we did really a very thorough job to make sure that 219 was our key candidate. We start with glutathione reactivity. This is something that you do as a covalent drug developer. And what you're trying to test is, if you just take glutathione, which is basically a naked cysteine, how fast do you form adduct formation. And if you have a very reactive warhead, you form it very quickly. And what we did was take some of the commercial drugs out there and compare it to our covalent sister molecules 13 and 14 and compared it to 219. What's nice to see is out of the pack, that 219 performs just as well as ibrutinib and much better than neratinib from an adduct formation perspective. We also do a nice kinase paneling. We do SafetyScreen44 and really look at the specificity but also selectivity, on target, off-target effects. On Slide 30, now transitioning to in vivo works. One of the first models that we ran was using a disseminated model. This actually pushes the tumor into the bone marrow of the animal. It's the best way to replicate leukemia because leukemia is residing in your bone marrow, AML and ALL. And so what's important to note is, even just after 2 weeks of dosing, we get considerable antitumor effects without implicating the body weight. And really showing a durable response was our main goal here. And then if you transition to Slide 31, what we're telling you here is this profile for 219, not only do we get nanomolar potency in several tumor types that are menin-dependent, the hERG inhibition that we observed is 5% at 10 micromolar. And then we have consistent control across the key gene sets that we're looking for, which our HOXA9; MEN1, the target gene; as well as MYC. And throughout our toxicity studies, whether it was non-GLP or GLP, we had no histopath findings. 219 came out without delivering any of these typical signals that you would find for an oncology drug, which really was an impressive feat for 219. And then on the right-hand side, our target efficacious AUC is 2,000, just to speak to the nature of 219. On Slide 32, 219 should be considered a next-generation menin inhibitor. It's very different than the ones in the clinic. It has different properties in the way it disrupts menin. It has very different properties in the way it can target other tumor types. For us, and back to this aim to cure, we're after extending life, improving overall survival. I think that aligns well with everyone here watching this presentation. And in order to do that, the surrogate is typically PFS, progression-free survival. For AML, the response rate has been used as a surrogate. We all know from our experience that, that response rate does a terrible job of predicting overall survival. But the best thing you can do is look at complete response at 6 months, so you have a durable CR. And really, that's kind of the initial hurdle that one should look at when you're executing in the clinic against these disease types. We're very excited about 219's opportunity within the acute leukemias and beyond. Our trial design on Slide 33 highlights what we're doing in the Phase I for ALL and AML. That's split into 2 arms of non-SIP and SIP. That just allows us to go through the dose escalation much more efficient and understand the drug. And then once we get to our optimal biological dose, what we believe to be the optimal biological dose, we'll expand into the key patient populations. On Slide 34, we're highlighting here our plans to get into the other tumor types. So the trial is initiated and it's screening patients for acute leukemias, which is very exciting. We'll be enrolling DLBCL and multiple myeloma sometime in the first half. And then the solid tumor KRAS-activated tumors, lung, pancreatic and colorectal, we'll file the IND and get our trial up and running in the second half of this year. And then for the first time, we're announcing that we'll be developing 219 in diabetes. We'll be announcing preclinical data this year and then filing the IND and getting our site up and running in the second half of this year. And just to touch upon diabetes, and I know it even surprised us, we initially set out just to do pathway validation to see what menin could do and menin inhibition could do for these diabetes models. And to our surprise, our BMF-219 did a spectacular job. And we touched upon that a little bit in the press release. But at the end of the day, GLP-1 has been described as the gas for beta cells, and menin has been described as the brakes. And so really, when I explained that menin is a toggle switch, you can think of the tumor or the cancers leveraging menin in the on position and the beta ells leveraging menin in the off position. If we take menin out and we inhibit it with a molecule like BMF-219, what we're doing is allowing the beta cells to turn over. And our goal is to reestablish a healthy pool of beta cells. If you can do that successfully in animals and do that successfully in humans, what you're doing is resetting the clock for their disease. And so diabetes forms over many years over decades of hyperglycemia. So what we're after is creating a finite treatment and understanding how long we need to dose with a menin inhibitor and really reset the clock for these diabetes patients. This slide on 35 shows you in the STZ model where you physically destroy, either partially or fully, the pancreas. You form or you create a very hyperglycemic state, and that's the control on the right-hand side. The MEN1 excised never creates a hypoglycemic state because the brakes aren't on to stop preventing the beta cells from turning over. So the beta cells turn over, you repopulate the pool of beta cells in this animal quickly. And that's really what we're after here. Then on Slide 36, what we looked at was, at the end of the day, not only did 219 show a significant reduction of glucose levels in animals with hyperglycemia with type 2 diabetes, we saw a very durable effect, an effect without needing constant exposure. So that gets us very excited. We used 2 models: the Zucker diabetic fatty rat as well as the STZ model. These are the gold standards for exploring diabetes. And we used the STZ model in the type 2 setting. We'd love to also explore type 1 because, depending on the biology, if there is still a remaining pool of beta cells, we should be able to repopulate. And that's really what we're after. We want 219 to be an overall long-lasting treatment for diabetes. We're excited. We'll be engaging with the FDA this quarter to really hone in on the IND package and the clinical trial design, and we're looking forward to filing our IND and kicking this off this year. We'll be, of course, submitting the data for presentation and we're very excited to share this data with the rest of the community. So at Biomea Fusion, we have a technology platform that's been very, very efficient; very, very productive. We have a number of programs that are coming online, and we're very excited to announce program 2, and program 3 coming behind it. Lead molecule, we're after best-in-class with a safety profile that allows patients to stay on and have a durable impact on their disease. We initiated studies in up to 7 tumor types, both liquid and solid, this year and addressed a significant unmet need for patients at large. All the IND-enabling work is currently being done for diabetes, and we're well on track to get our site up and running this year. And from a capitalization perspective, we're well capitalized into 2024. On Slide 38, we highlight some of the key milestones. You should think about 219 in two ways: we'll continue to validate 219, get all the translational work and paperwork done to support all of these IND filings; and of course, enroll these patients, enrolling acute leukemia, enrolling DLBCL and MM in the near term and then looking to enroll the solid tumors in the second half of this year as well as getting our site up and running in the second half for diabetes; and then, of course, the second pipeline product announced in the first half of this year. So a big year for 2022. Thank you very much, and we'll open it up for Q&A.

Thanks, Thomas. [Operator Instructions] And I see a few popping up as we speak.

I'll bring in Ramses and Alex and Priyanka and Franco just to help address any questions.

Great. And there's definitely been a lot of progress since your IPO last year. I guess we can start with some of the more recent developments, particularly data presented at ASH, demonstrating broad utilization of menin inhibition. You mentioned some of that in your slides.

Yes, we did. Absolutely. So we can go to the slide, I believe, 20. Priyanka, do you want to talk about Slide 20, the impact of MYC and what we showed at ASH?

Yes. So I'd be happy to give more detail on this. So what this analysis has actually shown us is that the set of transcription factors that regulate these gene expression changes that we observe, that are caused by BMF-219, are more broad than what is restricted to just the menin-MLL interaction. And so this data set highlighted MYC and its binding partner, MAX, as top transcription factors that regulate these changes that we see in gene expression. And in addition to that, we also saw a known interactors of menin, such as JunD and CEBPA as well as KMT2A or MLL1, which is what we expect to see with a menin inhibition.

And one from the queue, I guess. Do you expect to see any resistance to develop to BMF-219?

Yes, that's a great question. So we're trying to force it. We're trying to force those through assay development. And at the end of the day, from our experience with BTK, obviously, you do get a cysteine-to-serine mutations in very low percentile. Those are some of the things that we'll be looking for with menin, do you get a cysteine-to-serine mutation. Based on all the work that we've done to date with our assay work, we haven't seen any resistance pop up. But typically, you have to incubate these cells over very long periods of time to try to force it. We're working on it.

And I guess a few on the safety side, also in the portal. But what are the theoretical safety concerns for irreversible inhibition and/or any on-target, off-tumor risks?

Yes, that's a great question. Typically, the initial concern comes in, and this is done through validation work when you select your molecule, what you want to understand is are there other proteins that 219 is binding to, right? And you do these kind of proteomic pull-down assays. And what's nice to see is when we did that work, the specificity for 219 is incredibly high. So from an adduct formation risk, we don't see it with 219. From an off-target perspective, keep in mind that, in order to get into diabetes, you have to execute a lot of the non-oncology toxicity studies. Most oncology molecules, I can tell you would not pass these studies. You have to do neurology. You have to do cardiovascular. You have to do respiratory as well as Ames and micronucleus. And the good news is 219 is passing these studies with fine colors. And I think it just speaks to the profile of 219. And if you think about it, this is a molecule that you can dose diabetes patients. Think about the flip side, what that means for cancer patients, what a molecule this could be.

And there's a few competitors in the space. They're clearly taking a different approach with reversible inhibition. I guess what are your overarching views on the competitive data that we've seen so far in the clinic?

Yes. I think at the end of the day, we don't have a ton of information other than which is just published. And clearly, Syndax has had success in their PK/PD effort. And the SIP inhibition has really done well for them in terms of getting to the right concentration and be able to deliver complete responses. What that does for us is really provide an incredible concept, right, that if you can get to the concentration needed for your molecule, which means that you're now able to have control on menin, you get these responses that you need for acute leukemia patients. For us, what's nice is that we believe that 219 is very efficient and you don't need as high of an exposure to drive these responses. And 219 does a great job of not only disrupting menin-MLL, which reversible inhibitors do, we hit menin and MYC quite hard. That's what gives us this broad therapeutic potential. It's really just because of the way it disrupts menin, it's quite different.

And now that you're in the clinic, presumably, we could maybe get clinical data later this year, not that you're guiding to that now. But just as that data mature, are there any things that you look to signal potential differentiation from those reversible inhibitors that do have clinical data, whether it's on the safety side or PK/PD data, et cetera?

Yes. What we look at, Gavin, right, is the exposure that's required to drive the response. And typically, if you're able to keep that below a certain threshold, that just gives you more flexibility at keeping patients on the right dose. And this isn't something that the reversible menin inhibitors have a challenge with. Really, any molecule has a challenge with that and it really has to do with what else your molecule is bumping into that's preventing you from dosing at the optimal dose. We think 219 affords you that flexibility and capability to get to an efficacious dose and stay on it. And this is a key attribute that we learned at Pharmacyclics. Ramses is sitting here next to me. And it seems quite obvious, but it only comes out when you really think about it, that patients can only benefit from your medicines if they're on it. So at the end of the day, we're trying to push forward a molecule that allows patients to stay on therapy.

And we have a few minutes here. I wanted to get to the opportunity in DLBCL and multiple myeloma. The question is, is menin enough of a driver to use as a monotherapy as it is in AML? Or will the drug have to be used in combination for those patients?

That's a fantastic question, and it has to do with the addiction to MYC. And if the tumor type, the subtype of DLBCL or MM is addicted to menin, we believe should lend to a single-agent activity. But again, we have to prove that biology out in patients. We should be able to see significant activity single agent. And where single agent is enough, then we'd be looking at what other combinations can be done to take care of what's missing.

Great. And with that, I think we're just out of time. So I want to thank you, Thomas, and the rest of the team for joining us today. I hope everyone has a great rest of the day.

Yes. Thank you guys very much.