Good morning, and welcome to the Kymera Therapeutics Fourth Quarter 2023 Results Call. All participant lines will be in the listen-only mode. After today’s presentation, there will be an opportunity to ask questions. Please note, this event is being recorded. I’ll now turn the conference over to Justine Koenigsberg. Thank you. Please go ahead.

Good morning, and welcome to Kymera’s investor update. Joining me this morning are Nello Mainolfi, President and CEO; Jared Gollob, our Chief Medical Officer; and Bruce Jacobs, our Chief Financial Officer. Following our prepared remarks, we will open the call to questions. We ask that you limit your questions to one and a relevant follow-up to allow enough time to address everyone’s questions. Before we begin, today’s discussion will include forward-looking statements about our future expectations, plans, and prospects. These statements are subject to risks and uncertainties that may cause actual results to differ materially from those projected. A description of these risks can be found in our most recent 10-Q filed with the SEC. Any forward-looking statements speak only as of today’s date, and we assume no obligation to update any forward-looking statements made on today’s call. With that, I will now turn the call over to Nello.

Thank you, Justine. As always, we appreciate everyone joining us for our quarterly call today. This is a particularly exciting call for us, as we’re reporting from our new corporate headquarters in Watertown, Massachusetts, just down the road from our previous office. Our new building provides added space for our growing team, enabling us to maintain a strong on-site presence as we enhance and scale critical capabilities for our R&D organization, especially in areas like CMC, as well as other development functions. We look forward to the opportunity to welcome those of you who would like to visit us at our offices in the future. As many of you know, we’re on-site five days a week. During our prepared remarks, we’ll cover three main topics today. First, I’ll provide an update on our strategy to build the best-in-industry oral immunology pipeline. Next, Jared will provide an update on our clinical and newly disclosed immunology programs, as well as our two clinical oncology programs. Before we open the call for questions, Bruce will review our financial results. At our Immunology R&D Day in early January, you heard us discuss our strategy for building a best-in-industry oral immunology pipeline of first-in-class highly valuable programs. We believe we’re uniquely positioned to change existing treatment paradigms for immune-mediated diseases with our innovative and differentiated oral degrader medicines. As we reported this morning, with $745 million in cash and a runway into the first half of 2027, we’re well capitalized to continue to support these very ambitious goals. I thought I’d start with a few comments reflecting on what has led Kymera to our current strategic positioning with an innovative immunology pipeline of oral degraders with biologic-like activity potential. As those of you that have been following us for a long time know, we have been driven by our unique target selection strategy. We’re focused on first or best-in-class opportunities, particularly on undrugged or poorly drugged targets for which protein degradation is either the best or the only solution. We’re dedicated to pathways that have strong clinical and genetic validation where there is a clear path to early clinical differentiation. Our focus is on those indications that represent large clinical and commercial opportunities that create significant value for patients and shareholders. As you all know, we pioneered the first protein degrader program in immunology with our IRAK4 program, which, in addition to STAT3, were the initial targets at Kymera when it was founded in 2016. It was the early clinical results with the IRAK4 program with KT-474, the deep and well-tolerated degradation and the early signs of clinical efficacy that inspired us to increase our focus in immunology. Additionally, we believe the activity and fidelity of translation of our TPD platform in the KT-474 Phase 1 trial serves as an important read-through and informs the probability of success of our new STAT6 and TYK2 oral immunology programs. One aspect of the current landscape in immunology that is particularly notable and creates a significant opportunity for Kymera is the dominance in the market of injectable biologics. These antibody-based therapies have transformed and revolutionized the treatment of immune-inflammatory diseases with what, in many cases, have been great clinical outcomes for patients. At the same time, monoclonal antibodies, as you know, are injected, costly to manufacture, and can be inconvenient for patients. To put this in context, in a recent industry survey, 75% of patients taking biologics said that they would switch to orals with an equivalent profile. We believe this creates significant opportunities for effective and well-tolerated oral medicines, particularly for protein degraders. While traditional small molecules offer convenience benefits, they frequently cannot match the powerful pharmacology of biologics, as they don’t have the ability to block these pathways at the same level. We believe—and have shown with preclinical and early clinical data—that protein degraders have the potential to provide a unique solution with biologics-like specificity and activity, but with the flexibility of oral small molecules. Importantly, because of this profile, we believe they can potentially reach much broader patient populations, creating significant opportunities for the modalities broadly and for Kymera specifically. As you think about our immunology pipeline, if we can build a portfolio of molecules that provide comparable pathway inhibition to biologics, as we believe we can, but one with the convenience of oral dosing, we believe the potential is enormous. We have a lot happening across our pipeline, including activities in an early pipeline that we haven’t yet disclosed. We’re at the cutting edge of protein degradation, using this technology to address fundamental clinical and commercial needs and opportunities. I believe our unique approach has resulted in one of the most robust, high-value pipelines in the industry. I’m very proud of the continued execution and innovation by our team to support our future growth. I will now pass it to Jared to walk you through in more detail our clinical and soon-to-be clinical pipeline.

Thanks, Nello. Starting with our IRAK4 program, in the fourth quarter, our partner Sanofi initiated two KT-474 Phase 2 trials, one in hidradenitis suppurativa and one in atopic dermatitis. Enrollment in both trials is ongoing, with top-line data expected to be reported in the first half of 2025. Importantly, with the start of these trials and the dosing of the first HS and AD patients that we disclosed late last year, we collectively earned $55 million in development milestones from Sanofi, which we have already received. We and Sanofi are enthusiastic about the potential for this program. In addition to the two initial indications, we continue to discuss and explore additional potential indications, and we will plan to share more details as we are able in the future. Moving now to our two recently announced preclinical immunology programs. KT-621, our once-daily oral STAT6 degrader is slated to enter the clinic later this year. What makes this program particularly exciting is that the IL-4/IL-13 pathway has been exceptionally well validated. KT-621 targets STAT6, which is an essential transcription factor to the IL-4/IL-13 signaling pathway and the central driver of type 2 inflammation in allergic diseases. By degrading STAT6, we believe we can selectively block this pathway fully and importantly, this pathway only, potentially phenocopying upstream biologics such as dupilumab. At our R&D Day, we shared what we believe is a very compelling set of preclinical data that supports the high level of enthusiasm and confidence we have in this program. Specifically, in our preclinical studies, we have demonstrated full inhibition of the IL-4/IL-13 pathway in all relevant human cell contexts, with picomolar potency superior to dupilumab and exquisite selectivity. We also demonstrated very high levels of activity in multiple well-established preclinical models that give us confidence in the potential of KT-621 to deliver biologic-like activity as we advance this program into clinical trials later this year. If we are able to replicate our strong preclinical data in the clinical setting, which is something we have accomplished with our clinical stage programs, we believe KT-621 would be poised to be a best-in-class therapeutic option for multiple indications, representing a multibillion-dollar opportunity. We are currently in the midst of IND-enabling studies and expect to advance KT-621 into Phase 1 testing in the second half of 2024 with data from that study in 2025. We also recently unveiled KT-294, our potential first-in-class oral TYK2 degrader. We believe KT-294 also has a potential biologics-like profile, creating an opportunity to treat a range of autoimmune and inflammatory diseases. We believe degradation of TYK2 has the potential to overcome the challenges of small molecule TYK2 inhibitors, which have limitations due to lack of selectivity, limited target engagement and/or lack of potent activity against type 1 interferon. Importantly, we believe TYK2 degradation could allow us to recapitulate the human loss of function biology of near full pathway inhibition of type 1 interferon, IL-12, and IL-23, while also sparing IL-10, representing a best-in-class TYK2 agent. Our plan is to move this program into first-in-human studies in 2025. Across our immunology portfolio, we intend to present preclinical data from the STAT6 and TYK2 programs at multiple scientific and medical meetings this year, starting with the American Academy of Dermatology Annual Meeting next month. We also expect multiple clinical data readouts from these programs next year. To summarize, in the first half of 2025, we plan to share top-line data from the KT-474 Phase 2 trials as well as data from the KT-621 Phase 1 study which, as mentioned, is planned to start later in 2024. So switching gears to our oncology portfolio, we expect additional proof of concept data readouts for both KT-333 and KT-253 this year. Both programs have demonstrated initial encouraging anti-tumor activity in liquid and solid tumors and are progressing through dose escalation in line with our expectations. For KT-333, our STAT3 degrader, we shared data at ASH in December demonstrating early signs of anti-tumor activity at doses that were generally well tolerated and associated with substantial STAT3 knockdown in blood and tumor. Our preclinical to clinical translation showed strong objective responses in both CTCL and in Hodgkin’s lymphoma, as well as induction of an interferon-gamma response in tumor and blood that pre-clinically was shown to enhance the response of solid tumors to anti-PD-1 drugs. We believe this supports KT-333’s potential to address both hematological malignancies as a single agent and solid tumors as a potential novel combination therapy with anti-PD-1 or other targeted therapies. Our intent is to complete dose escalation in the Phase 1a study in 2024, at which point we will share the trial results and disclose our plans for the next phase of development for the program. And lastly, KT-253, our MDM2 degrader. This is another really exciting program. Arm A of the Phase 1a in solid tumors and lymphomas is ongoing, and in November we reported clinical data demonstrating evidence of target engagement in p53 pathway activation, as well as initial anti-tumor activity and a lack of the traditional hematological toxicity seen with small molecule inhibitors. We also announced that we commenced enrollment in Arm B for patients with high-grade myeloid malignancies, including AML. For both arms of the study, enrollment is progressing in line with our expectations. Like with STAT3, we expect to complete dose escalation in 2024, at which point we will disclose our plans for the next phase of development for the program. As part of our development plans later this year, we also expect to present comprehensive preclinical and clinical translational data across liquid and solid tumors that will inform a patient selection strategy for KT-253 in ongoing and future clinical studies. I’ll now turn the presentation over to Bruce for a review of the Q4 financials.

Thanks, Jared. I’ll quickly review the fourth quarter financial results, and you can certainly reference the tables in the back of the press release today. As Nello mentioned, with the advancement of 474 into the Phase 2 trials in HS and AD we earned $55 million in milestones from Sanofi. We received $40 million of that in the fourth quarter, the other $15 million, which was recorded as receivable at year-end, that payment was received in the early part of 2024. These milestones were added to the total consideration received under the Sanofi collaboration, with a portion recognized as revenue in the fourth quarter and the remainder in deferred revenue. At the end of the quarter, our deferred revenue balance totaled on the balance sheet approximately $54.7 million. That reflects partnership revenue that we expect to receive over the next several years, excluding the receipt of any potential future milestones. With respect to operating expenses, R&D for the quarter totaled $53 million. Of that, about $5.3 million was non-cash stock-based compensation. The adjusted cash R&D spend of $47.7 million, excluding that stock-based compensation, was up 13% from the comparable quarter a year ago. On the G&A side, our spending for the quarter was $14.2 million, of which $5.6 million was non-cash stock-based comp. The adjusted G&A spend of $8.6 million, again excluding stock-based comp, is a 5% increase year-over-year. Finishing up with our cash balance, as stated earlier, at the end of 2023 it was $436 million, including the $300 million of net proceeds from our equity offering last month and the $15 million that I referenced from Sanofi that was received early this year. That brought our unaudited cash and equivalent balance as of January 9 to approximately $745 million. That is expected to provide a runway into the first half of 2027, enabling us to deliver the next stage of growth and data readouts, including, as Jared mentioned, the KT-474 Phase 2 data, our oncology proof of concept results this year, and then several critical clinical inflection points for our STAT6 and TYK2 programs. So that’s what we had for you today in terms of prepared remarks. And now we’d be happy to answer any questions.

Thank you. We will now begin the question-and-answer session. The first question comes from Vikram Purohit from Morgan Stanley. Please go ahead.

Hi, good morning. Thanks for taking our questions. We had two, both on immunology. First, you alluded to in your prepared remarks potential pipeline expansion for 474. To the extent possible, I was wondering if you could speak a bit about what’s going to feed into that decision and how the data sets we get in the first half of next year for HS and AD might be related to how you think about with Sanofi, where to go next with this molecule? And then a similar question for 621 and 294. What will you be assessing from the initial clinical data we’re going to be getting next year to help prioritize indications for subsequent development in I&I indications? Thank you.

Thanks, Vikram. So maybe I’ll start. With 474, it’s just a bit more challenging because, as you know, this is in collaboration with Sanofi, so we’re not at liberty to disclose several things around decision-making and timing. But as we said in the past, the reason why we built this program several years ago—actually, we said today that IRAK4 and STAT3 were the first programs in 2016-2017. The idea around IRAK4 degradation is the opportunity to generate and develop a broad anti-inflammatory drug with a good tolerability profile. In our goal, there’s always been this possibility and high probability to move beyond skin indications. We’ve disclosed some of the other potential indications that one could pursue: it could be respiratory, it could be rheumatology, it could be GI. When we’re ready with our partner Sanofi to disclose the path forward, we’ll be happy to do so. Personally, I don’t believe that a skin indication will necessarily inform the probability of success of this drug in other types of diseases. However, confirming the safety and activity in longer-term Phase 2 studies will bolster confidence to then move into other indications. For STAT6 and TYK2, I think it’s early for us to comment on decision-making beyond early clinical studies. We could spend hours talking about your question—maybe just at a high level. For STAT6, we’ve been saying now for a few months that the value proposition is an oral degrader that can match the biologics-like activity of upstream monoclonal antibodies such as dupilumab. We’ve shown with our preclinical data that we can match that type of phenotype. Some would argue we’re more potent than it in certain contexts, but maybe we don’t have to go there. We have a pretty exciting blueprint of development plans in front of us. For us, it’s imperative that we enter humans and demonstrate this beautiful translation that we’ve seen with other programs of target knockdown, predictable safety, predictable PK/PD. We have a very elegant biomarker strategy that we’ll be talking about later in the year that we believe will allow us to validate the ability to match the type of pathway inhibition that upstream biologics do. For TYK2, again, we know what other TYK2 inhibitors are missing: selectivity, target engagement depth, and the ability to block all other scaffolding functions. What good looks like for us is a loss of function-like phenotype, and we know what that looks like based on human genetics. That's what we want to confirm in Phase 1. Once we’re there, Jared and his team will be happy to share more details about the late development plan.

Thank you. The next question is from the line of Michael Schmidt from Guggenheim. Please go ahead.

This is Paul on for Michael. Thanks for taking our questions. Mine are on KT-333. The first one is on your bar for pursuing a development in solid tumors. I believe that the ASH data had about a third of the patients with stable disease. Would higher rates of stable disease and biomarker data be sufficient to advance the program into combinations? Or would you really need to see some objective responses to commit to evaluation in solid tumors? And then second is just how does your thinking now for STAT3 and autoimmune fit into your current pipeline? And are you waiting for 333 data to evolve further before making further commitments? Thank you.

Sure. I think with regard to your question on the bar for solid tumors, as you noted, we have had some patients who have had prolonged stable disease. That is of course of interest to us. As we enroll patients onto the study and continue to dose escalate, we look for opportunities to bring on solid tumor patients that can give us a better idea as to what our activity will be as a monotherapy in solid tumors. All along we’ve been guiding that we expect that ultimately, if we move this into solid tumors, it would be as a combination approach, especially with anti-PD-1 combinations, which is something we’re very interested in based on our promising preclinical data and what we’ve shown with our biomarkers. We’re also looking at additional targeted agent combinations pre-clinically. What will inform moving forward with solid tumors will be a combination of what we continue to learn pre-clinically with combination studies and whether we see continued signals of activity as a monotherapy, either stable disease or even preferably major responses. With regards to major responses, we are seeing those in hematological malignancies, including Hodgkin’s lymphoma and cutaneous T-cell lymphoma. That continues to be of interest to us, and we’ll continue to bring on patients in the ongoing Phase 1a study to further explore activity there.

Yes, thanks, Jared. That’s great. On the STAT3 I&I, I want to go back to our strategy, which we discussed at the R&D Day. We believe we exist to bring together the power of the technology and unmet needs that are clinical, commercial, and the opportunity to use this technology to accomplish things that cannot be done with other technology. When we marry those three together, we’ll go all in. As you’ve seen with IRAK4, STAT6, and TYK2, we have a very clear value proposition. I hope you feel that way too. These are complete degradation of targets that lead to exceptional anti-inflammatory profiles that are well tolerated. With STAT3, it’s a program we know well. The reason you haven’t seen us disclose more details on STAT3 I&I is that we currently don’t have all the information in hand to say whether it fits the profile of the types of programs we’ve articulated so far. When we do, we will disclose more.

Thank you. The next question comes from Eli Merle from UBS. Please go ahead.

Hi, this is Jasmine on for Eli. Thanks so much for taking the question. What’s your latest thinking on whether you would take both STAT3 and MDM2 into Phase 2? Or is the thinking that you’ll prioritize one over the other, given your focus on immunology? What would your threshold for success be for each program when thinking about the go/no-go decisions?

Great question. I think our decisions are driven by data. For example, decisions we’ve made on programs we discontinued, even though the molecule was behaving well and was well-tolerated, were driven by a comprehensive analysis. We’ll apply that same rigor to all programs in our pipeline, whether in immunology or oncology. To invest in these two oncology programs, we need to see opportunities to impact broad patient populations. Our go criteria for both programs will be driven by opportunities in hematological and solid tumors. We should wait until we disclose more data later in the year on what our strategy will be. For STAT3, we’ve shown something novel: this is an active target and we have an active drug. We’ve shown a small data set in December, and at ASH we will present more later in the year. The same is true for MDM2; we will show more data later in the year.

Thank you. The next question comes from the line of Geoff Meacham from Bank of America. Please go ahead.

Hi, good morning. This is Susan on for Geoff. Thanks for taking our question. Can you walk us through what the strategy is for indication selection for the immunology programs, the STAT6 and the TYK2? Commenting specifically on maybe the competitive landscape or what kind of data you’ll look at prior to initiating first-in-human studies.

I want to address this at a high level. As we get into the clinic with the healthy volunteer studies for STAT6 and TYK2, we will feel more comfortable discussing late-stage development for several reasons. One reason is that we don’t need to disclose that now. The competitive landscape is something I don’t believe we need to discuss yet. For STAT6, I don’t believe there are well-tolerated oral drugs in indications where dupilumab has been approved. There’s a huge potential in a variety of indications without naming them. While all of those will get more competitive, given large investments in immunology, we believe we are in a unique position going forward. Once we disclose our development plans, you’ll see how we may be really competitive in terms of timing and trial design. With regards to TYK2, there’s a different landscape, as there are several small molecule TYK2 inhibitors available, but there is still room to match biologics like IL-23 and type 1 interferon. I think that is the gap we’re going to fill with our programs. So just remain patient as we finalize designs; they will come as we get into the Phase 1 study.

Thank you. The next question comes from Thomas Smith from Leerink. Please go ahead.

Hi, this is Will on for Thomas. Thanks for taking our questions. A couple on the ZEN and ADVANTA trials. Can you give us a sense of how enrollment is progressing thus far and any color on patient enthusiasm and willingness to enroll? When enrollment is complete for those trials, are you planning to share that information or just wait until the data release? And then I have a follow-up.

Great. Thanks for the question. Sanofi is running both of those Phase 2 trials. If you look on clintrials.gov, you can see the publicly stated timelines for estimated primary completion for both studies, which is in the first half of next year. To our knowledge, both studies are still on track to meet those timelines. That's pretty much all we can say right now regarding how those are staying on track. Our understanding is that there is significant enthusiasm among the various sites that are being engaged, as these are both global studies. That’s encouraging in terms of what we’ve heard from Sanofi. Again, we expect both those studies to readout on the publicly stated timelines. In terms of sharing data, that will be something that Sanofi and Kymera will need to work out in terms of exactly how that will look next year when those readouts are expected to occur.

Thank you. The next question comes from Kelly Shi from Jefferies. Please go ahead.

Hi, good morning. This is Yun for Kelly. Thanks very much for taking the questions. Are you able to share the status of dose escalation in STAT3 and MDM2? Have you reached the targeted 90% degradation that you thought could be required for clinical efficacy? And for I&I indications, are you looking at a specific threshold like the 90% in oncology that you think you will have to achieve? Based on your experience with oncology indications, how confident are you that the preclinical degradation data will translate into human data? Thank you.

I think there are three questions there. Our general approach is not to provide updates on recruitment statuses during quarterly calls. We disclose updates when we present data at medical meetings. We have a plan in place for that, and believe we will be presenting our data in high-impact medical meetings in 2024. Regarding STAT3, we have reached the targeted degradation. We are continuing dose escalation because we’re targeting maximum tolerated doses, which, as we’ve seen pre-clinically, seems to be above our targeted degradation. For MDM2, it’s hard to comment based on just three or four patients’ worth of data that we shared in November. Stay tuned for our next update, where it will be clearer. All our programs, whether in oncology or immunology, have reached targeted degradation in the clinic with a good safety profile. We expect that for STAT6 and TYK2, the same will happen. The immunology profile in preclinical data indicates that degrading STAT6 between 80% and 90% can match dupilumab activity in asthma and AD models. We target complete STAT6 degradation while knowing that we can explore in the clinic, just like with TYK2. Once we generate data, we can discuss late-stage design. The Phase 1 design will resemble the IRAK4 program for immunology.

Thank you. The next question comes from Adam Vogel with Wells Fargo. Please go ahead.

Hey, thank you for taking my call today. I’m on for Derek. Just a few quick questions on the oncology pipeline. Can you walk us through further what data you expect to share from KT-253? Will you be reading out data from both arms A and B? Given your deepening focus and efforts in I&I, will you be looking to partner either with 333 or 253 in the future? Thank you.

So our plan for this year is to complete dose escalation across both studies, the 333 and 253 Phase 1a trials, to establish the maximum tolerated dose and to present those data at a medical meeting later in the year. This will include updates on enrollment, the types of patients we’re including, and for 253, yes, we’re enrolling in both the solid tumor, lymphoma Arm A and the high-grade myeloid malignancy Arm B. We’ll show what types of patients we have enrolled, what the safety profile looks like, and what PD and clinical efficacy we’re seeing, which will give us insights into where we want to go for the next stage of development for these programs. We’ve been conducting preclinical and clinical work to understand patient selection for both liquid and solid tumors with 253.

I want to address the second part. Our decisions on partnerships are driven by opportunities, return on investment, and patient impact. Our current immunology pipeline consists of extremely valuable programs. If our oncology programs translate in the way we hope based on preclinical data, they could also be valuable programs. We will consider whether partnership for 333 or 253 makes sense. It’s essential to establish with our current strategy the best positions for maximum value creation. We have clearly committed heavily to immunology. The question is what are the key value drivers for advancing the oncology programs and whether collaborations represent the best path forward.

Thank you. The next question comes from Marc Frahm from TD Cowen. Please go ahead.

Thanks for taking my questions. Nello, with IRAK4, when we get the data next year, Sanofi will make their own decision on going forward or not. However, you will also have an opt-in decision. How will you approach the opt-in? What do you want to see that would commit Kymera’s resources early on, and how important is the Phase 1 data from STAT6 and TYK2 for that decision?

That’s a great question, requiring a nuanced answer. First, we are extremely bullish on IRAK4. Our value proposition has grown with data. This could potentially be one of the largest drugs in inflammatory diseases. We have early positive data, but we recognize we don’t know how active this drug is until we run a well-powered randomized study, which we are doing with Sanofi. The value proposition for this drug is, in our view, that it is an active oral drug with a good safety profile in indications that extend beyond HS and AD. If the drug fulfills that profile, we believe opting in will be an easy decision. If we have successful Phase 1 programs for STAT6 and TYK2, we will have different cost of capital, enabling us to sustain the growth of the company. Thus, the decision to opt-in will be clearer if the primary program meets our criteria.

Thank you. The next question comes from Brad Canino from Stifel. Please go ahead.

Good morning. This is Brad. Perhaps expanding on prior questions, can you describe the scope of the disclosure expected for MDM2 this year? Are you reading out data from both arms A and B? Will you clearly flag key data elements to watch? Following the disclosure, will you be positioned to outline the broader development thesis?

High level, what is the totality of our data? We plan on providing a comprehensive update later in the year. Our hope is to complete dose escalation in both arms, the solid tumor, lymphoma arm, and the heme malignancy arm. We will provide updates on safety, PD, and efficacy, establishing a differentiation from MDM2 small molecule inhibitors. If those elements come together in 2024, the decisions around continuing investment will be straightforward. While there’s excitement around immunology programs, we also want to address the 2024 data releases for the oncology programs as there is potential to change how we think about this target. Jared, can you provide more details on patient data?

We plan to provide a comprehensive update later in the year for 253. We aim for a large data set from dose escalation across solid tumors, lymphomas, and leukemias, along with insights for patient stratification. Our goal is to show a differentiated therapeutic index from MDM2 small molecule inhibitors by demonstrating superior safety and potentially superior efficacy. We want to present a data set that will highlight this differentiation.

Thank you. The next question comes from Kalpit Patel with B. Riley Securities. Please go ahead.

Hey, good morning, and thanks for taking the question. One for the STAT6 and TYK2 programs: you’ve shown data from the proteome study to confirm selectivity and rule out off-target effects. Can you share how many proteins were identified in those studies and what the coverage rate was in those proteome studies? Thank you.

We’re not going to share more data on that program today as we want to maintain our competitive advantage. However, we have high proteome coverage, typically detecting over 11,000 proteins in each study. We conduct our studies across various cell types to ensure comprehensive coverage of the proteome. The data show we degrade just STAT6, and the same applies to the TYK2, IRAK4, and STAT3 programs.

Thank you. The next question comes from Andy Chen with Wolfe Research. Please go ahead.

Hi, this is Emma on behalf of Andy. Focusing on TYK2, what are the weaknesses you see with current TYK2 inhibitors on the market, and how much headroom is there for improvement with a potential degrader entrant like KT-294?

To clarify, as we mentioned before, there are several layers of differentiation. Small molecule inhibitors block the kinase function and some scaffolding functions but not fully. Degradation leads to a loss-of-function-like phenotype, as shown in our data, and is needed to match the upstream biologics' full pathway blockade. Current approved drugs can influence IL-10 negatively, which could be detrimental for GI indications. Our degrader presents a potential to reach a better target profile as it does not suffer from these shortcomings. We do not have an exact measure yet regarding clinical outcomes, but biologics reach high responses in specific indications, while small molecules fall short. We believe we can fill that gap with our candidate, potentially even exceeding existing therapy outcomes.

This concludes our question-and-answer session. I would like to turn the conference back over to Justine Koenigsberg for any closing remarks.

Thank you. On behalf of the Kymera team, we’d like to thank everyone for joining us this morning and look forward to keeping you updated on our progress. In the meantime, please don’t hesitate to reach out if there are any additional questions following today’s call. Thank you.

Thank you. The conference has now concluded. Thank you for attending today’s presentation. You may now disconnect.