Kymera Therapeutics, Inc. (KYMR) Earnings Call Transcript & Summary

Good afternoon, everyone. My name is [indiscernible]. I'm a member of the health care team at JPMorgan. And it's my pleasure today to introduce Nello Mainolfi, the founder, President and Chief Executive Officer of Kymera Therapeutics. As a quick reminder, if you'd like to ask a question, please do so using the Q&A tool at the bottom of your screens. And with that, I'll pass over to you, Nello.

Thanks, [indiscernible]. Thanks, everyone. Thanks for the opportunity to come here today virtually and present to you, tell you about Kymera. So I'd like to start with maybe Slide 3. And in the course of the presentation, we'll go through a couple of slides with questions. And those questions are questions that have defined the path at Kymera for the past 4, 4.5 years. So the first question around which we really founded the company in 2016 was, what if you could remove disease-causing protein with a small molecule-based technology? And what is, by doing so, you're able to expand the druggable protein? Thanks to the power and the targeted approach of targeted protein degradation. So that's what really was the initial thrust that allowed us to get Kymera off the ground. And happy to tell you more about how that's evolved over the past 4 years. So just to give you a quick snapshot, we were -- we founded Kymera with Atlas Venture here in Cambridge in 2016. We're close to 80 employees today. We closed the year 2020 with a cash balance of about $460 million, which we believe will take us into 2025. We'll cover some of this later in the corporate section. We invested heavily in the past 4 years or so in both our pipeline and platform, which we believe has propelled Kymera to be really unique company in protein degradation. We believe in partnership in a way -- as a mean to organically grow the company and to find those win-win opportunities. So we've closed 3 strategic partnerships in the past 4 years, 1 with GSK, which is more technology-based, I would call it pretty competitive to find lesions for -- small molecule lesions and targets in E3 ligases as we'll see in the next few slides. A more typical discovery partnership with Vertex to work outside of oncology and immunology in a wide variety of disease areas that we'll talk about later, briefly. And then more recently, we were able to partner with Sanofi, our IRAK4 immunology degraded program. And this was with the goal of accessing as many patients as possible, as soon as possible and competing with immunology powerhouses with our program and go into as many diseases as possible as soon as next year. So our internal pipeline is focused in oncology and immunology, as I just mentioned. 2021 would be obviously a transformative year for us. We will be going from a preclinical company into a clinical-stage company with 3 programs in the clinic. And in fact, it will be a first in many times. They will be the first protein degrader. They would be dosed in healthy volunteer. It will also be the first bifunctional degrader to be dosed to patients with autoimmune and autoinflammatory inflammatory diseases as well as, obviously, will dose cancer patients also later in the year. And so we plan to dose up to if not more than 100 individuals in 2021, which we believe will be able to deliver, I would say, probably the richest data package in protein degradation with regards to safety, pharmacology and proof of biology. So going into just a high-level vision of the company, we're trying to build a fully integrated biotech that can discover, develop and commercialize degraded therapies. We think we have unique opportunities expand the druggable proteome, thanks to technology, evolve the technology beyond what's known today. Staying true to our ability to go into target selection, thinking about highly clinically validated pathways where [indiscernible] have not been dragged or drugged well with any other modalities where protein degradation can provide that unlocking solution. We believe, obviously, data-driven decision making, more importantly, in a culture of scientific innovation. So to just give you a brief overview of our pipeline, as I mentioned, the 3 programs already, briefly. We have our KT-474, which is a selective IRAK4 degrader for autoimmune and autoinflammatory diseases. That will enter SAD portion of our Phase I study in the next few weeks, as we mentioned a couple of days ago. We also have -- and again, as I mentioned, first time further integrator into healthy volunteer, at least a targeted integrator. This will be followed by our IRAKIMiD program, which sees as -- as we'll see it in a minutes, degradation of IRAK4, Ikaros and Aiolos of both IRAK4 as well as the even substrate for delivering potentially the first targeted therapy in lymphoma. So this will enter the clinic -- the program is in IND-enabling activities entering the clinic in the second half of 2021, followed by -- in the last quarter of the year, the statutory program in liquid and solid tumors. We have several early programs that we haven't disclosed, yet. We plan to disclose, hopefully, the first new program in a R&D Day that will have later in the year. And then we have also, as I mentioned -- collaboration programs, we have another project with Sanofi, that is in the discovery stage. And then we have a, as I mentioned, broad collaboration with Vertex across 5 instant disease areas outside of oncology and immunology, and really makes Kymera, I would say, a disease-agnostic protein degradation company. So before going into the specifics, so this is on Slide 6. Before going on to the specifics of our programs, on Slide 8, just to orient everyone around the technology. So what is targeted protein degradation. So targeted protein degradation is a small-molecule-based technology that is based on well-characterized pharmacology that happens in our cell every single moment, every single day, which is protein homeostasis. Protein homeostasis is controlled by series or proteins called Ubiquitin Proteasome System that regulates protein levels. And the most important class of those proteins together with the proteasome are the E3 ligase. So on your Slide 8, in blue, you can see depicted and E3 ligase that is responsible in the absence of the molecule, you're not seeing the animation. So you're seeing the full slide. So in the absence of the heterobifunctional molecule, let's just talk about the basic concept, recognizes a green protein, which is the protein substrate upon special proximity on the species 2. There is an ubiquitination event. So there is a transfer of the protein in brown -- in dark orange from the E3, E2 ligase complex onto the protein of interest. And then that protein -- that target protein is recognized by those protein proteasome and degrader. So with this targeted protein degradation do introduce a heterobifunctional molecule on your slide in that basically brings a disease-causing protein ideally in green to the UPS system to the E3 ligase in blue, generate this new ternary complex and drives the degradation of that disease-causing proven. So highly efficient, catalytic and with potential prolonged income. And what problem is trying to solve is on the next slide. So we've -- I'm sure you've seen through this conference, many technologies that have advanced our ability to execute on the sequencing of the genome and understanding of the role of protein diseases. But regardless of all these advantages, we're still dragging about 15% to 20% of the proteome, mostly limited by either technology or delivery, and what the real potential of targeting protein degradation is today is the opportunity to expand that druggable proteome and go ask a protein that have been undrugged to date. And the reason for it is because we are matching the power of genetic-like knockdown, which is degradation, with the flexibility of a small molecule therapeutics. So with that and with the into, what is Kymera doing or what Kymera has done in the past 4 years? And what will it be doing in the next 5 and 10 to understand and evolve the space of protein degradation. So going to Slide 10. Maybe just highlight 3 key buckets of investments that we believe makes Kymera unique in drug development. The first one, which covers the first 2 key bullets there is expanding the toolbox of E3 ligases. So just to repeat, E3 ligases are protein that are responsible for recognizing and degrading protein. There are 2 or 3 that are well-characterized and used in the public domain insufficient to drag all targets. So how do we go about expanding that toolbox? So we'll tell you that in the next minute. We're also a transitional medicine company. So we're thinking about how do we translate preclinical PK/PD and efficacy relationships into the clinic. So spent a lot of time understanding those relationships as well as, obviously, this is a chemistry-based technology. So understanding how to identify define lesions and how to make this heterobifunctional molecule into pharmaceutical active, well-behaving molecules is another area of big investment. For today, I'd like to tie only one of these three. And again, go back to the questions, what if we could remove this disease-causing proteins only where it's pathological relevant. This is the foundation, I would say, of the next phase of growth for Kymera. And just to give you a better sense for that, going from Slide 11 to 12, really thinking about, again, taking a translational medicine approach to how one can evolve the E3 ligase toolbox. And what we've been able to do, and this is still a work that is continuing to be in progress and will probably be for years to come. What we've been able to do is identify, thanks to a collaboration with an external academic organization, identify the expression profile of all these detectable E3 ligases at the protein levels in all cells marks and tissues in the human body. At the cell level and also into healthy versus disease level. And with that, we really have the blueprint of expression, localization and eventually function of these E3 ligases. So when we think about matching a target protein biology with an E3 ligase like is localization and expression is really trying to elicit the best and more selective pharmacology. So if you look at this slide, again, Slide 12, in the middle panel here on the right, you see that we've been able to identify E3 ligase that have restricted expression, expressed in some issues but not in others. And also, as E3 ligase 10, E3 ligases that are expressed only in one particular cell path. So imagine that you can have targets that you want to [ share ] The pharmacology in tissues that you know will not tolerate that pharmacology. Or imagine that you can have targets where you know the biology is very relevant in 1 tissue, but it's probably not tolerated in all others. So those are the translation hypothesis that we're advancing at Kymera, and the new generation of programs that we'll be talking about in the next few years. So just to spend a minute on, Slide 13, how do we think about target selection? So we believe strongly, just if you follow the slide on the left that there is the intersection of these 4 principles that will give us, in our mind, the best target for protein degradation. And as we know, every platform has -- the choice of targets is really the definition of success. So we believe that it's important, obviously, to work in unmet medical need areas as most companies presenting here in the past 4 days. We believe, though, that we want to work in pathways where there is high degree of validation, but where a key node a key central node biology has not been dragged or drugged well by any other modality, where protein degradation will provide the unlocking solution. And then especially in oncology, being able to identify that population that will be best served by that program. So to give you 2 examples of the pathways that we will discuss today, the IL-1/TLR pathway, highly validated many antibodies to cytokines that signal through IL-1 receptor. But we haven't been able to drive that pathway in the cell with a single or small molecule to the fullest possibility. And this is what we believe an IRAK4 degrader can do. It can behead the biological superiority of all the IL-1 family cytokine antibody blockers because we can block all of them in a single molecule and also the convenience of the oral small molecule. For the pathway below the JAK/STAT pathway, again, well-characterized, validated human genetics, human pharmacology, commercial valuation just like above, but all upstream. No one has been able to drive or drug well the key oncogenic constriction factor that is responsible for both oncogenesis in some cases, but also for immune regulation. And we believe that here, we have a really unique program by targeting the statutory key central node that, again, protein degradation can do other technologies haven't been able to do to the same extent. So I was thinking, I'll use the next 15 minutes or so to -- or less, to give you highlights of these 3 programs that we just talked about. So going on Slide 15. So just to repeat, highly validated pathway, why IRAK4 degradation. So we talked about the IL-1/TLR receptor downstream, there is MYD88, IRAK4 and other members of this so-called myddosome complex. We've been close to dragging this pathway well, and actually, Pfizer is a Phase II active molecule that blocks the catalytic kinase activity of IRAK4. In our case, we have an ability to not only block the kinase function but actually, removing the protein, blocking the scaffolding function, which basically allows the myddosome complex to function. So we have a superior pharmacology to what -- either an antibody to the receptor or to the cytokines or an inhibitor can have And just very briefly, obviously, I'm skipping a few slides here. If you look at our presentation on our website, but you can see that functionally, what happens if you degrade IRAK4 in an immune context. So here, these are immune cells on Slide 16 that they're activated with either LPS or R848, which is our activators of this pathway. And then we look at what happens at inhibiting IL-6, which is a downstream cytokine, in the presence of a degrader in orange or a very selective IRAK4 kinase inhibitor either in green or in blue. So you can see that we have superiority in blocking, not only in IC50 but actually in depth of blockade of the pathway, which shows you the biological superiority of the approach. The slide that I like most actually of this program is Slide 17. This is going into a nonrodent model and dosing once-a-day orally our IRAK4 degrader. And then in day 15, looking at IRAK4 levels in blood, in skin, in spleen, in kidney, or liver and lymph nodes and basically demonstrating that we're able to downregulate, degrade the target almost fully with every -- in every single tissue with almost every dose in a way that was really well tolerated by the [ audience ]. And this is what gave us really that confidence to develop this compound further. Another really important data set now is looking at HS patients as with see HS is one of the diseases that we're investing into in terms of development with Sanofi. Here, we're taking blood for from HS patients and then looking at the [indiscernible] across different cell paths. And you see that regardless of the starting concentration of IRAK4, in blue. We're able to degrade IRAK4 to the same level. So this is in green. Again, regardless of that, in a way that is quite similar to basically in IRAK4 no background, which is the color in orange. And this is the type of data that we will present in more from a noninterventional study in HS and AD later in the year. So where are the opportunities. On Slide 19, on the left. Obviously, we believe this is a broadly active antiinflammatory lesion, obviously, we have to show that clinically but the opportunities are broad going from Hidradenitis Suppurativa to Atopic Dermatitis to arrays. So the millions of patients that we could impact with this therapy. So looking forward to get through the Phase I and then begin our randomized Phase II studies in collaboration with Sanofi. So what's coming ahead? We will complete and dispose the rest of the data for our noninterventional study in the first half of the year, we will begin our SAD study soon and then transition into an MAD study after we and the FDA reduced the SAD study in both healthy volunteer and eventually in patients with HS and AD. So this will be, again, as I mentioned, highly rich data set where we will establish the proof of mechanism through monitoring IRAK4 level in blood and skin and also downstream disease-relevant cytokines. So going into the next program, picking up the pace a bit, IRAKIMiD. So here is now a dual degrader concept. We are staying in the same pathway. We're now instead of looking at activation of, this is Slide 21, of IL-1 or TLR, we're looking at MYD88 as the oncogenic driver of diffuse large B cell lymphoma, at least of a subset of that population. And so degrading IRAK4 has the ability to block that activating mutation from firing downstream. What we've also found that if you actually also target a contiguous pathway the interference signaling by degrading the IMiD substrates. You're actually able now to intersect the 2 pathway at the key downstream effector, which is the NF-kB pathway and provide profound antitumor effect. That are superior to any single agent that we've seen preclinically so far. And so this is basically a combo mechanism in a single molecule. Going to Slide 22, very quickly, just to give you a better sense of what the molecule looks like just on the top left. So it has an IMiD binder that binds cereblon linked to an IRAK4 binder. So cereblon is used to both degrade IRAK4 and also degrade the typical established IMiD substrates, namely Ikaros and Aiolos to elicit this synergistic pharmacology. The beauty on Slide 23 of this dual mechanism is that while it targets 2 pathways, it's still selected for MYD88. In fact, on the table that you see on Slide 23. You see that we are degrading not only IRAK4, Ikaros and Aiolos but we're impacting cell viability, very importantly in MYD88 mutant and not in wild type. And more importantly, we're doing so irrespective of co-mutations that are present in those cells, as you see in the middle of that table. So showing that this has the potential to be targeted therapy that will be -- will have the flexibility to be active in the presence of other co-mutations. On Slide 24, just to show you that we understand really well, not only the efficacy on the [indiscernible], we have a single-agent activity by dosing every week or every other week, or every 2 weeks actually in these models, but we also understand what is the type of degradation needed in the middle pane, you can see after 2 doses, day 1 and day 2, we're able to see sustained Ikaros and IRAK4 degradation for several days. Allowing us to have infrequent dosing as our plan dosing in the cleaning. So we plan to dose day 1, day 2 or even day 1 only once either every week, every other week or even less. And you can see on the right side of the slide, we actually never disclose these data, but in nonhuman primate, we're able to maintain, for example, the IRAK4 levels down for up to you can see up to 15 days upon this dosing paradigm that I mentioned. So going to the opportunities here. So we started this program with the goal of developing a targeted therapy in the diffuse large B cell lymphoma selected by MYD88 mutation, which represents about 7,000 patients a year, 25% of total. But we're also, obviously, looking beyond diffuse large B cell lymphoma, either MYD88 mutation diseases, for example, Waldenström or other diseases that might be or are impacted by this biology that many of which are actually characterized in the literature. So we plan to completely the IND-enabling studies, and enter our Phase I in the second half of the year and going into -- enroll relapsing refractory B cell lymphoma patients including, obviously, MYD88 and establishing, again, that proof of mechanism first and then proof-of-concept next year as well. And obviously, we can talk about in the Q&A, if there are more questions on the design path forward. So the last program, very briefly here, STAT3. This is the typical undrugged transcription factor on Slide 27, that has up to 30,000 papers pointing to a role in many disease states. As we mentioned, highly validated upstream effector kinases, but no one has been able to drug well STAT3. So we had really a unique opportunity here. Again, the goal is to enter the clinic in the fourth quarter. So lots of work for us to both confirm, validate the biology in this states preclinically. But also lots of work to prioritize. And so we have -- we've prioritize cancer for now over immunology and fibrosis, which is slightly behind in our drug development process. And within cancer, prioritized opportunities where there is a clear dependency on STAT3 activation as the driver of oncogenesis as well as then in solid tumors, as we've also discussed in presentations in other medical meetings. Just to give you just a brief snapshot of the data. If you have the tumor type, like this ALCL, that is dependent on the level of [indiscernible] STAT3, and obviously, STAT3. All you need is really to knock it down substantially for a few days. You can see here we dose once a week for 3 weeks, on Slide 29, and after we stop dosing on week 3, we can see co-remissions of these tumors that are durable also after we stop dosing our degrader. So this is one of the profiles that, obviously, we would love to see in patients when we look at data towards the end of the year or next year. So again, our Phase I study will be a multicenter dose-escalation study to look at safety tolerability, proof of mechanism, proof of biology and initial activity. And we're looking at Phase Ib expansion cohorts in both liquid and solid tumor, prioritizing where STAT3 a key driver and then looking at solid tumor, both alone and in combination with both targeted therapy and/or immune checkpoints. So I thought I'd spend 2 more minutes on Slide 32, just to remind you, I've already given you the qualitative overview of our partnership. Again, these are win-win opportunities to grow the company in an organic way, the financial aspect around the slide, I'd like to focus more on the strategic aspect of these collaborations. Again, building the company, becoming a disease-agnostic protein degradation company, powering up development retaining 50% of U.S. right in terms of development and promotion and commercialization. And using, if I may use this word, these collaborations to allow Kymera to grow organically and build those functions in an organic way. On Slide 33, just a quick snapshot. I don't plan to go through these numbers actually. Just to say, we raised about $600 million to date, $220 million were just from upfront-s in partnerships, so let's call it nondilutive. And we just raised our -- only last year, we raised about $450 million together with the IPO that we closed in August. And as I mentioned earlier, we are going -- we started 2021 with about $458 million if I want to be precise, in cash. As we said, this would take us based on our plan and excluding milestones into 2025. Obviously, we are very aware that we have opportunities to accelerate our growth of our platform of our pipeline as well as our clinical opportunities. So we will always -- we save the option to accelerate any of that -- any of those. Slide 34, just to close the presentation. These are really the near-term milestones. I mentioned most of them already. Just draw your attention to the rest of the noninterventional study that will -- we will disclose in HS and AD patients later in the first half, beginning of dosing of healthy volunteer for our Phase I KT-474. And importantly, this really reached proof of mechanism, proof of biology data in the fourth quarter, which again, will be up to probably 100 individuals, including patients. So it will be probably the richest data set that we see so far in the space. And then clinical entries for the other 2 programs as well as expansion opportunities in other indications for those 2 programs. So I want to thank you for the attention, and happy to take any questions.

So I was told that I'm going to read the question. that have been submitted into the chat line. I want to introduce Jared Gollob, Chief Medical Officer; Bruce Jacobs, our CFO, that will assist in the Q&A. So reading the first one, so there was -- I mentioned about the partial clinical hold. So as we mentioned in our conversation, we have the phone call with the FDA on this program. Verbally, we were given the okay to begin our Phase I in the SAD portion as we're planning. And the desire from the FDA was to look at the Phase I data in terms of safety, PK and PD at the point that we will look at it the interim data when making a decision about what to take into the MAD portion. So it's enabling an active participation of the FDA as we're taking a degrader for the first time in healthy volunteers. So the other question -- Jared, anything to add to this?

No, no. I think you covered it.

Excellent. The IRAK -- will the IRAKIMiD be administered IV? So just to clarify, so as we've shown in this presentation data, both PO and IV. And actually, we have the same level of efficacy with the same dosing paradigm, meaning dosing frequency, whether with we dose IV or PO. Our strategy is to enter the clinic with an IV formulation to establish proof-of-concept and understanding what is the dosing paradigm and dosing frequency that is best suited for efficacy and safety, and we believe we can do it quicker with IV. We believe that with the line of therapies that we're going, this is well-accepted by physicians. At the same time, once we understand that, we will have the option as we're advancing the PO formulation to also follow that up, whether to follow the IV or to think about taking in prior line of therapies or maintenance therapies as the program advances. How frequently and how will this be competitive versus other DLBCL therapies? Jared, do you want to take this one? I assume you see the questions on the slide.

Yes. Actually, can you just repeat...

I repeat it once more. How frequently and how will this be competitive versus other DLBCL therapies like Q3W plus bispecifics.

I see. Okay. Yes, I think right now, I mean, we know that we can get very substantial antitumor activity in our xenograft models with intermittent dosing. And we've been able to dose as intermittently, as every 2 weeks and see complete tumor responses in MYD88-mutant DLBCL. We plan on interrogating multiple different schedules in the clinic, including weekly, every other week and even less frequently than every other week if the PK and PD support that. I think from a competitive standpoint, I think the sort of robust activity that we've been seeing in this genetically defined subset, MYD88-mutant DLBCL tells us that we should be very competitive. We would really essentially be the first drug in relapsed DLBCL that is really indicated for a genetically defined subpopulation that has a worse prognosis compared to MYD88 wild type. So we think that if we achieve the sorts of complete responses and have robust response duration in our clinical trials, we should be able to achieve accelerated approval in relapsed/refractory patients.

Great. Thanks, Jared. What is your view on the published Janssen paper? So that's a great question. Thanks for asking. So let me take this. So where they concluded IRAK4 is relevant as a targeting reform. So what Janssen showed is actually not dissimilar from what we have seen. We've seen that if we use a selective IRAK -- maybe they do have the best or the most potent molecules. But what we have seen is if you use an IRAK4 degrader only in MYD88-mutant lymphoma, you're not able to drive the level of antitumor effect that one would expect from a single agent. And that is actually the scientific reason for us to build this dual-degrader molecule, that degrades also Ikaros and Aiolos. And in fact, we hypothesized together with actually others at NIH that published them this years ago,4 that actually the interferon pathway through IRAK4 and Ikaros and Aiolos. Is one of the escape mechanism that allows NF-kB to continue to signal even when you downregulated with an IRAK4 inhibitor or better with a degrader. So in MYD88-mutant lymphoma, we believe that IRAK4 alone is insufficient to drive the level of activity that we, as a company, we want to spend time and money developing. In other areas, there are possibilities for IRAK4 degrader only in those areas we're actually exploring as well besides the IRAKIMiD concept. Next question is, what should we look to as the first proof-of-concept for Kymera's TPD platform? So assuming that by proof-of-concept this meant clinical proof-of-concept, we believe that our Phase I -- again, this is healthy volunteer and patients with HS and AD looking at broad biomarker of both degradation and disease as well as scheme, will be probably the richest data set to demonstrate proof-of-concept of, let's call it, degradation and disease-relevant degradation in the clinic. And again, we expect to present that, assuming success in the fourth quarter of this year, hopefully, in the early part of that, and followed by all the other programs that will follow in the months after that. Okay. So for the STAT3, are you selecting patients or are these all comers? Jared, do you want to take that one?

Yes. In the Phase I study that Nello described, initially, it will be all comers. So in the Phase Ia dose escalation, that includes both liquid and solid tumors. I think once we have established a maximum tolerated dose and essentially a recommended Phase II dose, we then plan to have expansion cohorts in Phase Ib that would now start to focus on certain subsets. And in particular, the STAT3 dependent hematologic malignancies like peripheral T cell lymphoma, cutaneous T-cell lymphoma, LGL leukemia. Those would be the patients that we would start to select for to show initial clinical proof-of-concept and where we think there would be accelerated approval paths in the relapsed/refractory setting.

Thanks, Jared. So 2 remaining questions. We've got 3 minutes to go. I want to say some time for my favorite question, which is the last one. But before we get there, what is the point of differentiation between your STAT3 degrader and other [ prelegal ] compounds? I mean all I can say is that it's really difficult to develop a selective STAT3 agent. What's even more difficult is to develop a selective STAT3 degrader. We know we have it. We've demonstrated specificity and proof-of-concept there are a lot of pathway inhibitors. There might be also selective inhibitors out there. I just can't comment on that. I just focus on what we've been able to achieve, which is, to be honest, really difficult. And glad that we're able to solve for it. The last question, there are several TPD companies out there, what makes Kymera so special? So hopefully, in this presentation, I was able to explain a little bit why, but maybe I'll just try and focus on it. I think what we're trying to do here is to build a company that will be developing and registering degrader medicines for many years. And that requires a level of commitment to understanding the platform to evolving that platform to really understanding what are the best targets to go after and how you select it and how you develop it. And you're not probably going to get everything right. But the commitment to do it and building a pipeline with breadth and with depth, that we believe has franchise potential across many businesses and really allows protein degradation to unlock the power of the technology that it has. I think that's what we're trying to do. And I think if you look at both our target selection and the targets and companies that we're going after. If you're looking at the questions that I had in the slides, like restricted or selected degradation. I think if we're able to accomplish that. We're not going to just be a unique protein degradation company. We're going to be a unique drug development company because we'll do something that no other technology can do, which is doing selective pharmacology. So I know I have to wrap up. So I want to thank everyone for the attention. Great questions, engaging questions. Sorry, I couldn't see who was asking the questions, but hopefully, the answers were satisfactory. And hopefully, we'll be back next year.