All right, everyone, I think we'll get started with our next Fireside discussion. Thanks, everyone, for joining. My name is Derek Archilla. I'm one of the senior biotech analysts here at Wells. For the next Fireside, we have Kymera Therapeutics. From the company, we have Nello Mainolfi, President and CEO, and then we also have Jared Gollob, Chief Medical Officer. Gentlemen, thanks so much for joining us.
Thanks for having us, Derek.
Thanks, Derek.
Awesome. Maybe just to start off, maybe, Nello, you can just help us in terms of just giving us high level of the company, what you guys are working on, and then we kind of dig into the more specific questions.
Yeah. So, you know, Kymera was founded about eight years ago with the mission of building an integrated commercial stage company using protein degradation to bring forth a new generation of medicines. And in doing so, going after targets that have not been drugged or drugged well before, where again, TPD will be the technology that will unlock the value of that particular biological pathway. We've been focusing in the past eight years, almost solely, at least what's publicly known, in oncology and immunology. We have taken four programs in the clinic in the past four years or so. We have our more advanced program is an IRAK4 degrader.
This is the first time that target has been addressed with a degradation approach that allows us to block both the kinase and the scaffolding functions. That program is now phase 2 with our partner, Sanofi, in both HS and AD. Then we have two programs in our immunology pipeline. They are about to enter the clinic. One is STAT6, which we'll, I'm sure we'll discuss. It's we'd like to call it Dupilumab in a pill. And then we have a TYK2 degrader, which we believe has the potential to maximize the pharmacology in that pathway. Then we have two oncology programs, STAT3 degrader, MDM2 degrader, both with data already publicly disclosed, with both PR and CRs in heme and solid tumors, across the two programs.
I would say that maybe high level, strategically, we started talking about much more early this year about our increased commitment in immunology. We believe, now is the time for oral drugs in immunology, and more importantly, it's the time for oral drugs with biologic-like activity. And that's what we believe a degrader can do in space. So we're excited to talk about that and any, obviously, other investments that we're making, we can discuss in the next few minutes.
Got it. Okay. Well, thanks for that. So maybe starting with the STAT6 program, obviously getting a lot of fanfare, as you say, potential Dupixent in a pill. I guess, you know, what gives you confidence that what we're seeing pre-clinically will translate in the clinic for humans? Is there anything specific that you would point to or kind of the data we've amassed so far?
Yes. Let me... I forgot to say something. I know Bruce is looking at me the wrong way. The other thing I wanted to add that is, you know, applicable to kind of an overview of the company, that, you know, we're also well capitalized with the recent financing, and we're, you know, above $900 million in cash. That allows us to get into the first half, actually, at this point, into the mid-2027, with the recent financing. More importantly, we're going to see lots of data for each of the individual program on both 474, STAT6, the two others. So in a great position to actually now focusing on execution. Now, going to STAT6. So the beauty about STAT6 is that is one of those extremely rare targets in the...
I would say, generally, in the history of our industry, where you have an upstream biologics that is probably to date, I actually checked the numbers the other day, it's the number one immunology drug. I think right now, sales about $2.7 a quarter, approaching $14 a year. That is one of the most compelling drugs in the industry. It's a drug that addresses Th2 inflammation, I like to say, and all the manifestation, the AD, the asthma, COPD, eosinophilic COPD, chronic sinusitis, EoE. So it's really an amazing drug that's well tolerated and helps almost a million patients worldwide now, has helped almost a million patients.
STAT6, which is the selective transcription factor for IL-4 and IL-13 signaling, is one of the few examples where you have a transcription factor that is selected for a receptor. And so once you have this one-to-one relationship between a receptor that has been drugged with a mega blockbuster drug and undrugged transcription factor, we believe that is a unique position to be as an innovative company with a technology that is built almost perfectly for addressing these difficult-to-drug targets. So STAT6 degrader comes, you know, from years of investment into this pathway. We've shown that if you block STAT6, you block IL-4 receptor signaling. If you block IL-4 receptor signaling, you actually block STAT6. So there is really a one-to-one relationship. We've shown that our catalytic degrader with picomolar concentrations is able to shut down the pathway completely.
We've shown that actually in human cell systems, we are more potent than the Dupilumab, the monoclonal antibody. I believe, at least to my knowledge, this is the first oral small molecule that is actually more potent than a monoclonal antibody. And then in vivo systems, which we've seen that really good doses of our degrader, KT-621, is able to completely remove STAT6 from blood, skin, and other tissues. And importantly, in one of the most translatable animal model, which is the house dust mite model, we are able to block not only downstream Th2 inflammation, but also, the manifestation of lung disease in these mice after thirty days of every day dosing, in a way that is similar, if not superior, than Dupilumab.
So this preclinical data is telling us that we have a unique opportunity to open a new paradigm in addressing that type of inflammation. More importantly, we do with a drug that has gone through preclinical safety study without showing any type of adverse event at any doses and any concentrations. So, you know, we're, as we said in August, we've completed our R&D enabling activities, and we're excited that soon enough, hopefully, we'll be able to initiate our phase I study.
Got it. So I just to confirm, just in terms of the models that you're using clinically, they're applicable. Like, again, if you see work there and you're working there, again, those are the same models, and you're replicating or at least getting better data than what you're seeing.
Yes, I think thank you for the question because I wanna be careful with this. So, what we're about to show, there are two important things. One is our ability to block IL-4, IL-13 signaling with targeting STAT6. And we've shown in a wide variety of systems, both in vitro and in vivo, that we can block downstream signaling of IL-4 receptor alpha, which, as you know, signals IL-4, IL-13 in the cell and in the nucleus. And STAT6 is the only transcription factor responsible to translate that signal. What we have also shown in these in vivo models, again, if I go back to the house dust mite model. This is a mouthful, and I've said it a hundred times, but still.
We've shown that in a model where you're actually replicating in this system an allergic response to actually house dust in mice. So you actually are having Th2 inflammation that is causing these mice. We're able to show that we block all these Th2 biomarkers at least as well as Dupixent. And then there is this downstream model of disease in the lungs. So I'm not saying that we've shown we're clinically superior to Dupilumab.
Right.
I just want to be clear. What we're saying is, in all these mechanistic models, preclinically, we are extremely competitive, if not even slightly superior to that drug.
Awesome. So I guess as you think about the phase I trial, I mean, obviously, we're gonna be looking at safety, very important. You know, what are some of the biomarkers that we should be paying attention to, to really understand, again, if you're getting that STAT6 degradation and kind of downstream impacts, you know, on, you know, Th2 biomarkers?
Yes. So maybe I'll answer some of it, and I'll let Jared answer part of it. I think the important goal of a phase I study with this technology, with the level of understanding that we have of this pathway, is our ability to show that we can safely degrade STAT6, at least to 90%. I think it's been shown by both our STAT6 degrader preclinically and actually upstream biologics, like IL-13 biologics or IL-4 receptor alpha biologics, that those biologics, when they block the receptor or the cytokine, they actually block phospho-STAT6 in 90% range. So we actually have established that correlation already.
So the most important data point would be that we can safely degrade STAT6 in blood and in skin, at levels that we've shown are clinically relevant based on our preclinical data. But maybe, Jared, is worth just talking about more broadly in our design-
Yeah, I can give you a quick snapshot of the design of the phase I study. So healthy volunteers, SAD, MAD study. The MAD will be 14 daily doses. And the trial, just as we did for the IRAK4, KT-474 phase I study, will have a number of different pharmacodynamic assays that will allow us to really quantitatively assess the impact on STAT6 degradation, both in blood and in the MAD, where we do multi-dosing also in the skin. So I think those assays will be key in showing that we can degrade, you know, greater than 90% in both those compartments, in blood and in skin, and can do so safely with PK that's predictable.
Also, even though these are healthy volunteers, we know that healthy volunteers have some Th2 tone at baseline, and there are two markers, Th2 biomarkers that are in the circulation. One is TARC, and one is IgE, and both of those can be followed in these healthy volunteers. We know Regeneron has published their data with Dupixent in healthy volunteers, showing about a 20+% reduction in IgE and about a 30%-40% reduction in TARC.
In healthy volunteers, so these assays can be a little bit noisy, because these are healthy volunteers, but you can see an impact on this Th2 tone, and we plan on including those analytes as well in our phase I study to be able to show where we're degrading STAT6 in healthy volunteers, that we can also have an impact, we think, on those biomarkers, IgE and TARC.
Would you expect a difference in the degradation in, I guess, you know, blood and skin of STAT6? You know, I guess, is it dependent on the tissues, or you think it'll be pretty consistent across?
Yeah, we think it'll be consistent. Our preclinical models, we have, you know, essentially floored, you know, STAT6, you know, degraded it to greater than 95%-98% across multiple different tissues. So for example, whether it's in dog or even in a non-human primate, we see a similar level of knockdown across different tissues: skin, blood, lymph nodes-
spleen, et cetera. So our expectation is that there should be a good correlation between knockdown in skin and blood for STAT6, and hopefully we'll be able to show that in the phase I study.
Got it. So let's obviously assume phase I looks good. We're seeing the activity, good degradation. I mean, do you just follow the Dupi playbook in terms of indications to develop, or, you know, what kind of. You're well capitalized, so there's a lot of different avenues you can take. But I guess, how do you think about the development strategy, you know, post phase I?
Yeah, I mean, I think high level, we have two important priorities. One is, path to registration and then breadth of, development, and those come hand in hand. I think we're in a world right now where, getting approved in the first indication and then initiating development on your second indication after that, is just not applicable anymore, given pricing pressures and other, mechanisms that are in place, for controlling that. So, I think what you'll see us trying to do is to try and parallel as much as possible, the large indication, and at the same time, trying to get to a phase III study ASAP. Those are the two priorities for our development plans, and we'll share more as we get through the different phases.
Gotcha. Understood, and then I was gonna ask in terms of, you know... Well, actually going back to the registration, would there be, you know, any indication that you would feel comfortable with going directly into, like, a registrational? Or do you wanna stop and, you know, do some dose ranging first? Like-
So, yeah.
How do you think you can, you know, accelerate the process?
Yeah, it's a great question. So, obviously, I, I'm not gonna comment on the specifics, but I would say that if you look at Dupixent, they have... Obviously, they had to actually work that out themselves, but you've seen that they were able to go into COPD directly in a phase III study, using data in asthma, to support the dose range finding. So one could see that as a potential approach, but I think it's too early for us to comment on the specifics. I think we just have to make sure that, we, we do what's required by the regulatory agencies and, creating the right databases for both efficacy and safety to get the drug approved.
Understood. And then just in terms of data, like, should we expect any additional preclinical data, you know, ahead of the phase I readout? And, you know, do you think? Like, what will that tell us, if anything? What-
Yeah, I mean, we have a presentation at the EADV in a couple of weeks. I think all that we will have before the phase I data will be incremental data that will continue to support the thesis that we put forth already. So I wouldn't expect there would be any, you know, paradigm shift-
Got it.
-in the interpretation of this program, going forward.
Got it. And then just shifting gears to IRAK4. So obviously, you provided an update, you know, positive from Sanofi, you know, kind of investing more in there and expanding the trials. Can you maybe just walk us through that? And I guess also just, you know, Sanofi's commitment to this program beyond just AD and Hidradenitis?
Yeah, I mean, so first it was, you know, a great piece of news to know that, you know, a partner that has already invested in two parallel phase II studies. Just reminding everybody, in the absence of a placebo-controlled, randomized proof of concept in any indication, we had an open label study in phase I, as you know well, that we all believed, including Sanofi, I hope I can say, we all believe was very encouraging and exciting, but it was very early data with small N.
So we were really excited and decided to parallel track these two indications, and I think we were even more excited when we were told that their intention was to accelerate the development by making this study that was, you know, naturally some kind of a proof of concept study into a proof of concept/dose-ranging study, so that the next would be a registrational study. So we're basically removing a study from the big development plan by expanding the existing one. And so just, you know, as we've said in the past, they elected to use an interim analysis of both the safety and the efficacy to make that decision.
All I can say is that the data that we both reviewed was supportive of this further investment, and so now all we're waiting for, in order to provide more specific guidance, is for the ClinicalTrials.gov page to be updated so that we can speak to, you know, what exactly is this expanded study. You know, we talked about at, you know, more doses, more patients, and different timelines-
Yeah.
- and we'll be able to update that once, you know, again, hopefully in the next month or so, a couple of months.
Will it be explicit on, like, you know, are you going higher with dosing or lowering? Like, again, what-
I think we'll be able to provide commentary on that.
Okay.
Yeah.
Gotcha, and then just in terms of Sanofi, you know, going beyond HS-
Ah, yes.
Is that something that you would have to wait for this proof of concept data to come out, and then they would like to expand to other indications-
Yeah.
-or how does that-
Forgot. Sorry, I forgot to answer.
Yeah, that's good. Yeah.
So yeah. The answer is, we've said is also that, you know, there's been a concerted effort across the two companies to prioritize next indications for this program. I think it's fair to say both companies believe that this mechanism is able to impact beyond HS and AD. I think we've been communicated by Sanofi that, you know, that there would. As I would totally agree, some level of further de-risking was required in order to start additional studies. Now, whether that was the IA that we've already seen or future data that we have, that hasn't been resolved as far as I know. So I'm sure once that has been resolved, we'll communicate, you know, as we can.
I mean, do you think that decision to expand the trials and obviously based on what you've seen, like, does it put to bed, you know, kind of making these comparisons between, like, IRAK inhibitors and IRAK degraders? And, you know, obviously-
Yeah
Everyone wants to be like: "Oh, if it doesn't work, then, you know, the degraders aren't gonna work. It's the target." But, you know, what do you think about that?
Yeah, and a great question. So maybe to remind everybody, IRAK4 is a mechanism that has been pursued for the past 12 to 15 years, I would say, by the industry, mostly initially with small molecule inhibitors. I would say with mixed, if not, most, you know, negative data. I think we had some interesting phase II data, proof of concept data in RA, and then negative data in HS from Pfizer, and then discontinuation in some studies from Gilead and some other studies from GSK. So, not GSK, what's the other company?
Bayer.
Bayer, yeah, sorry. And so the important aspect, though, is that we know we spent the past five years, or more, showing that both our preclinical data as well as our clinical data has demonstrated that the IRAK4 has a dual function that is both catalytic and scaffolding, and only by removing the protein, you are able to block the pathway fully. I believe our phase I data, although small n in the patient study, has shown really intriguing impact on signs and symptoms and scores of HS and AD. So I think we already have early differentiation data.
I believe that the continued investment from Sanofi into this program should tell us that there is more and more confidence that this is a mechanism that will prove to be pivotal and would prove to be a great asset for an oral drug with a good safety profile and a broad variety of diseases, but I would also say that in order for us that are science driven to complete this journey, that it's taken a while, you know, we'd love to have placebo-controlled, randomized, complete data set so that we can hold hands and agree that Kymera was right from the first place.
That's great. So maybe just shifting to another of the I&I targets. So you guys unveiled the TYK2 degrader also, which is also very interesting. So I guess, you know, just highlight for us, again, why that approach? Just kinda like what I asked about, you know, with IRAK4, relative to these inhibitors. There's obviously a few ones on the market, a couple have failed, there's a couple others out there, but why the degrader approach, you know, is probably the best approach for TYK2?
Yeah, so you know, I go back to the human genetics data. If you look at human genetics, loss of function of TYK2 has a very different profile than kinase dead TYK2, and so what we are saying is that in order to have the depth of pathway engagement, meaning the ability to block the pathways and suppress the pathway engagement, which means that we can block IL-23 , type I interferon, and IL-12 , you need a degrader, because TYK2 is another scaffolding protein, and this allosteric inhibitor only partially impacts the scaffolding function of TYK2.
And so our bar is that we believe that if we're able to replicate the TYK2 loss-of-function profile, which we believe we've shown already preclinically by removing the protein 95% plus, our activity will be measurable or comparable to a biologic like an IL-23 type biologics. And we love to be able to say that we're not just a superior TYK2 agent, but we are a TYK2 agent that is on par with pathway biologics. And very honestly, transparently, if we're not able to show that in early clinical development, and we're stuck into the quagmire of TYK2 inhibitors, then it's not worth further investment.
Got it. I mean, are you... And you've talked a little bit about maybe IBD or Crohn's as an area, and obviously, that's been a tough area for TYK2 inhibitors. So, like, is that kind of the proving ground to prove that out, or?
Maybe, Jared, you can comment on the-
I think for inflammatory bowel disease, I think one of the main sort of liabilities of TYK2, for example, is the fact that, you know, as a drug, it also hits the JAKs. It's blocking IL-10 signaling, and that clearly is a detriment when it comes to trying to treat inflammatory bowel disease. We know that, you know, children with IL-10 neutralizing antibodies actually develop inflammatory bowel disease. And so our ability to avoid hitting IL-10, we think, could be a major plus for us in inflammatory bowel disease. In addition to what Nello was referring to earlier, which is our ability to completely block IL-12, IL-23, type I interferon. That should be... give us success across an array of different indications, whether it be psoriasis or IBD or lupus. But I think the IL-10 angle in particular is probably important for success in IBD.
So can I just address-
Yeah, yeah
Part of your question?
Yeah.
Obviously, totally agree with Jared. The question is, what is the indication where you first can prove quickly that you have a differentiated asset? I'm not sure IBD will be the first one.
Right.
Given the complexity of that patient population and the fact that many patients would be on co-med. So probably there are other indications where you can quickly prove that you have a differentiated mechanism. You know, regardless of whether that will be the go-to-market indication. But let's maybe we'll address that next year, once we're closer.
Sounds good. I was gonna ask a question before we get on the oncology, but around the platform, and, you know, we've talked about, you know, STAT6, TYK2, IRAK4. I mean, I think when we talked about the platform, you know, many years ago, about, like, tissue-directed degraders, I mean, how much of that's built into the, if anything, or are you just doing more systemic, and that's something different for, you know, the other assets, so that it will be even more selective and more targeted?
Yeah. So, you know, our goal in the past few years has been, what are these pathways that have been validated? What are these nodes that you can degrade fully, safely? And I think IRAK4, TYK2, and STAT6 are perfect examples of those. I would say those are still using the concept of broad degradation-
Mm-hmm.
-where you're actually not required to have a selective or restricted degradation. The concept of using E3 ligase expression to direct degradation in particular tissues is one that we've invested heavily in. I would say it's extremely hard to do.
Mm-hmm.
but we still have efforts, and hopefully we'll be able to share more in the upcoming-
Someday.
meetings or events.
I mean, is it more applicable, like, in oncology versus I and I? Or like-
Uh, yes.
Is that-
I think that what's easier to do is to spare particular tissues.
Mm-hmm.
And so I think that is more of an oncology concept of, say, you know, I have a drug that has on-target toxicity in the bone marrow, on-target toxicity in the intestinal lining or in the heart, and so I'm gonna spare those tissues. I think that's probably where that type of concept is, in theory, you know, more directly applicable, but I would say I think it's applicable broadly. It just depends on what E3 ligase is spare, what tissues, and then what, which one of those are directly ligandable, which just means the challenge.
Got it. Okay. And then, yes, just shifting to oncology. So you've got the STAT3 and the MDM2. So maybe on the latter, on MDM2, just I think you're gonna have some data later this year. Maybe you can just kind of tee us up on that and, you know, I guess, kind of the development plan. I think you also are gonna present, I think it's preclinical data around, you know, kind of patient selection and maybe biomarker stuff. So it'd be really good to understand how that's gonna play a role in future studies.
Jared, do you wanna take that?
Yeah, I think, you know, so for both oncology programs, I think we've been encouraged by the fact that we've been able to dose escalate in both programs and been able to show on-target engagement in pharmacology at doses that are safe and fairly well tolerated, and we've been able to show antitumor activity in both liquid and solid tumors.
I think for MDM2, the last update we gave was in ASCO in June, and we showed, you know, not only favorable safety at the dose levels we had escalated to, where we're not seeing the typical myelotox that you see with small molecule inhibitors, nor were we seeing the same sort of GI tox at doses that were giving us good activation of the p53 pathway and actually very encouraging responses in AML, where we were seeing both complete and partial responses, as well as in a neuroendocrine tumor, Merkel cell carcinoma. So our aim really for the rest of this year is to continue dose escalating on across these two arms, solid tumor lymphoma arm and the liquid tumor, you know, AML arm.
It's possible that by later in the year, we may be finished with dose escalation, in which case, you know, we could be prepared to provide another update. But it's more likely, given the favorable safety, that dose escalation may continue across both arms, not just into the later part of the year, but maybe even into early next year. That would be a good thing, and that it sort of signifies that we're seeing favorable safety. So it might not be until the first part of next year that we provide the next update. 'Cause we'd like to be completed through dose escalation across both arms before we give the next clinical update for the phase I study.
In terms of the patient selection effort, you know, we are planning to present data this fall at the Triple Meeting to show for the first time the work we've been doing preclinically on finding sort of biomarkers that can predict for responsiveness to MDM2 degradation. This has been what we think is an important component for the solid tumor side of the program as well, that could help us further enrich for sensitive solid tumor types as we go from phase I into the next phase of development. So I think that'll be a good opportunity for us to share those preclinical data. So far, we have seen good translation from models preclinically, where we've seen activity like Merkel cell and AML and what we've seen in the clinic.
Our hope is that as we continue to flesh out this biomarker approach that we're developing from our preclinical data set, that that will also ultimately predict for where we can see the best responses in the clinic.
Got it. I guess for, you know, MDM2 and STAT3, we can hit STAT3 in more detail in a second, but just, you know, with the funds that you have and you're really looking to kind of, you know, continue to push in I and I, like, what happens to these programs? Do you wanna continue to develop them, you know, on your own, or do you want to partner them? Like, it's obviously you can fund them. It's just a matter of strategic focus.
Yeah. Well, I mean, I think we've said since the beginning of the year that our focus in the short to medium term is gonna be on immunology mostly. And I think it's not so much just a disease area commitment. I think it's a commitment to programs that we believe have potential large impact and large commercial opportunities. And if we have opportunities in oncology that will meet that bar, I think a company that wants to create value should continue to invest in that. I think if some of these programs are directed to smaller disease populations, maybe, you know, STAT3 is an example. You know, in the Hodgkin's lymphoma, it's actually a reasonable, sizable opportunity, but it's one that probably might best fit-...
a company that already has a clinical and commercial footprint in that area. And so you might see us thinking about partnership in programs where that is the scope of the development plan. Obviously, STAT3 is also an opportunity in solids with PD-1, so that opportunity-
Sure.
can be even more nuanced. But I would say that the strategy is that the programs that, you know, don't meet the bar of potential addressable population that we're seeing in the area of immunology, will be hard for us to invest on our own going forward.
Gotcha. Okay. And then just in terms of, like, going back to the I&I side for a second, just, you know, you've made that commitment, you've come out with some very interesting targets. So what's next there? Should we expect, you know, other kind of novel targets, you know, or, you know, kind of other validated targets that are on drug? I guess, where do you want to play.
Yeah. Yeah, as I said, I think, you know, our sense of urgency to continue to invest in our very productive research engine is also driven by the fact that I think we have an amazing competitive advantage over the rest of the industry in our ability to deploy our platform against these difficult to drug targets. I feel like the time is now to continue to test and to do things that others are not able to do. You know, STAT6, until we came out with the data, was thought to be an undruggable target. Now, everybody's working on STAT6 from what I hear on the street. And I think that's actually turned out to be true with IRAK4. We have lots of other IRAK4 programs behind us.
We have at least another three or four super exciting programs in immunology, going after first-in-class targets that have human genetics validation, where there are upstream biologics that are mega blockbuster drugs, and I think now is the time to, you know, continue to deliver on the promise of the technology. You know, if we're extremely successful, obviously, it's gonna be hard to fund all of our programs all over on our own, but I would welcome that problem.
Yeah. I mean, when you think about, you know, new targets, do you look at the end goal? Like, these are the big indications that we wanna, you know, look at and then work backwards, or you find the target and then look at it? Because, like, I guess it seems like for you guys, you're really focused on big pharma, large pharma type of indications, right?
Yeah, I mean, I think I would say our pipeline has grown organically. I think early on in the life of the company, I would say we didn't have the luxury to be designing our pipeline with a total commercial input on what our, you know, synergies between, you know, programs would be. But I think now we are in the position to say, you know, we believe we're, we're probably best positioned as a company right now to address Th2 inflammation. We believe we can best positioned to address IL-23 inflammation with our TYK2 degrader. We believe we're best positioned with an IRAK4 degrader in the IL-1 pathways. Now, there are two or three other areas that are complementary to these, that will allow us to kind of own the other big areas of immunology.
And then, you know, the conquering the world scenario will be that you wholly own lots of these assets, and you start thinking about what are the rational combination that will allow you to own even bigger areas of the space. So that's how we're thinking about building the rest of our pipeline.
Got it. And then maybe last question, the last minute here. So, you know, not many years ago, a couple of years ago, I mean, obviously, degraders started to come more to the forefront, and everyone was like, "You know, our technology's better, our platform's better." I guess, where are we now? I mean, are we kind of just like, degraders or degrader? Is there really the secret sauce of the platform? Is it more just, you know, the medicinal chemistry, you know, that's not necessarily the degrader, but, yeah, what... Like, where are we on that now? Again-
Yeah.
And do you feel like there is really a differentiated degrader platform?
This is a half an hour answer in the twenty seconds I have left. But I would say that what we focused on is target selection. I think you could tell that we're highly differentiated. I think capabilities to fulfill the target selection strategy, all the targets that many of the targets we're going after are first-time liganded targets, and our ability to translate these programs in the clinic with almost perfection. And I think when you put all of that together, you can call that platform, or you can call that building a real drug development and eventually commercialization companies. I'm gonna guess that not everybody has built that, but you know, I think it's hard for me to say where, you know, who's better, who's worse.
I think the products that we can produce are highly differentiated, and I think every platform company should be judged on the product that they produce and not the platform they have.
Excellent. Well, we'll leave it there. Nello, Jared, thank you so much.
Thank you.