Kymera Therapeutics, Inc.

Good day, everyone. My name is Stefan and I'll be your conference operator today. At this time, I'd like to welcome you to the Chimera Therapeutics first quarter 2026 results call. All lines have been placed on mute to prevent any background noise. After the speaker's remarks, there'll be a question and answer session. If you would like to ask a question during this time, and if you've joined via the webinar, please use the raised hand icon, which can be found at the bottom of your webinar application. If you've joined by phone, please dial star nine on your keypad to raise your hand. At this time, I'd like to turn the call over to Justine Konigsberg, Vice President of Investor Relations.

Good morning and welcome to Chimera Therapeutics quarterly update conference call. Joining me today are Nello Mainalfi, our founder, president, chief executive officer, Jared Golub, our chief medical officer, and Bruce Jacobs, our chief financial officer. Following our prepared remarks, we will open the call for questions from our covering analysts. Please use the raise hand icon to indicate you'd like to ask a question, and we kindly ask that you limit your question to one so we can accommodate everyone. But before we begin, I would like to remind you that today's discussion will include forward-looking statements subject to risks and uncertainties described in our most recent Form 10-Q filed with the SEC, Please note any forward-looking statements speak only as of today's date, and we undertake no obligation to update them. With that, I will now turn the call over to Nello.

Thanks, Justine, and thanks, everyone, for joining us this morning. Next week marks the 10-year anniversary of Chimera's founding, and it represents more than just a milestone. We have stepped into a new chapter where we believe the strong foundation we've built over the past decades positions us to deliver transformative medicines for patients around the world. In the past 10 years, we've built unique capabilities, including our heat-finding approach to identify ligands to historically undrug proteins, Building on that, creating new rules on how we identify drug-like, highly specific and potent degraders. Importantly, key insights to deliver high fidelity of clinical translation. And finally, creative early clinical studies to de-risk clinical development, late clinical development. We have continued to refine our target selection strategies, such as we believe we built one of the most compelling oral small molecule pipeline in the industry. As we look to the next decades, our guiding principles remain unchanged. We'll continue to focus on both sides, demonstrate early proof of concept to support our investments and build medicines that we believe can change the standard of care for many diseases. And we'll obviously be looking to make the final step, becoming a fully integrated global commercial company that delivers groundbreaking medicines for patients around the world. And it's these principles that have shaped our innovative and increasingly differentiated pipeline. We're laser focused on our wholly owned program, such as KT621, KT579, where we're applying targeted protein degradation to well-validated disease-relevant pathways in immunology. At the same time, we're extending our reach through partnership, like our work with Gilead, advancing KT200, our first molecular group program, and Sanofi with IREC4. What ties it all together is our commitment to pursuing high-value disease-driving targets with precision and to do it repeatedly across different therapeutic areas. The sharp focus and the consistency of results we've delivered is what gives us confidence, not just in individual programs, but in our ability to broaden and expand our pipeline. We've done a lot of groundwork over the past few years as we sit here today. We're well positioned to execute on our strategy and deliver on the groundbreaking promises of our programs. Our immediate priority is execution of the two KT621 face-to-face studies. In atopic dermatitis, we're on track to complete enrollment this year in the Broaden2 study, and we expect data by mid-2027. We continue to be encouraged by the level of interest from both investigators and patients, and it's clear the enthusiasm for the trial is high. We're tracking with our internal expectations for asthma as well, where the breadth study readout is expected by the end of 2027. As we advance these studies, we'll continue to assess a broader development strategy, including areas such as COPD, EOE, chronic rhinositis, and others to maximize the value of the program. Turning to IRF-5, we expect to report healthy volunteer data from the KT579 phase one study in the second half of 2026. The overall goal is to demonstrate that we can safely degrade the target and the biology translates in humans in a way that's consistent with what we've seen preclinically. IRF5 has been a target of particular interest across the industry for a very long time. Gerard will spend more time on the opportunity, but what's compelling here is that by selectively degrading IRF5, we have the potential to impact multiple key drivers of disease with a single mechanism. If we think about lupus specifically, we're addressing autoantibodies, type 1 interferon, pro-inflammatory cytokines, all through one pathway. While individual drugs can address each specific pathway, we believe a single mechanism, such as an RF5 degrader, has the potential to address all pathways and potentially have greater therapeutic potential. We also have several opportunities emerging in an early research pipeline and expect to disclose the next target later this year when we reach development candidate. Before I move on, I wanted to touch briefly on our Gilead collaboration. We recently announced that Gilead has made the decision to advance KT200, our CDK2 molecular glue, which could enter the clinic as early as next year. This program is a great example of the power of Chimera's R&D capabilities. Our ability to reach a target like CDK2 with a highly selective molecular glue really speaks to the depth and reach of our capabilities. CCNE-amplified tumors need specific agents to address the underlying biology. CDK2's selective blockade has not been achieved by any investigational drugs, in my opinion. mostly because of the homology and cross reactivity with CDK1. We designed an absolutely selective molecular glue degrader to achieve this target product profile. I'm thankful to Gilead for believing in this program early on and now for taking KT200 Chimera Therapeutics discovered development candidate into development. Special thanks to our CDK2 team for delivering this molecule in record time. So everything we're doing across all this program is to build long-term value. This isn't just about incremental progress. It's about our commitment to developing medicines that we believe can change treatment paradigms and expand access to important treatment options. KT621 is the best example of our strategy in action. Our continued engagement with KOLs reinforced the growing anticipation for a therapeutic that can potentially fundamentally change the treatment paradigm in type 2 inflammatory diseases. As you all know, we have shared compelling data sets, including most recently AAD. With that as a backdrop, I thought it was worth stepping back and framing what makes this opportunity so compelling. When it comes to treating these conditions, patients and physicians are often forced to make trade-offs. What they want most is simple, a safe, effective, and convenient option. We believe KT621 is well positioned to meet that need, with the potential to deliver the efficacy of biologics and the convenience of an oral pill. And that matters because patients' preference is clear. Given the option, many would choose oral therapy over the burden of injections, especially for chronic diseases that require long-term treatments. In fact, most patients are being treated with suboptimal therapies, such as topical creams, which can be massively ineffective. So with inhaled medicines, often because they or their prescribers are not comfortable moving to advanced systemic injectable therapies. KT621 can change this dynamic completely. Allow patients that are not well treated by these local therapies to access a simple, accessible, effective, and trusted oral pill. So when you put it all together, the mechanism, the clinical profile, and the simplicity of administration, we believe KT621 can stand on its own as the potential to represent a true paradigm shift. As a result, our focus is to expand the market and redefine what patients and physicians should expect from treatments. When you take a broader view, the scale of opportunity really comes into focus. This is a slide you've seen before, but it's worth revisiting because it highlights just how much untapped potential still exists in type two inflammatory diseases, particularly for new entrants that can expand the market. Importantly, nearly 50 million patients could benefit from better therapies. This opportunity is not just about taking share from existing treatments. It's about reaching the much larger population of patients who are untreated or undertreated today. We're already doing the work to better understand the patient population, market dynamics, and access landscape. And these insights are guiding our development and ultimately our commercial strategy. If successful, KT621 could become the preferred option and potentially shift treatment earlier in the disease course, where earlier intervention could meaningfully reduce disease burden and progression. At ALD and through recent advisory board meeting, the feedback has been consistent. There is clear demand for a convenient, effective oral auction and strong excitement around this mechanism. With that, I'll turn it over to Jared to discuss our clinical pipeline a bit more, including KT579. Jared?