Kymera Therapeutics, Inc.

Good day, everyone. My name is Shell, and I will be your conference operator today. At this time, I would like to welcome you to the Chimera Therapeutics Third Quarter 2026 results call. All lines have been placed on mute to prevent any background noise. After the speaker's remarks, there will be a question and answer session. If you would like to ask a question during this time, and if you have joined via the webinar, please use the raised hand icon, which can be found at the bottom of your webinar application. If you have joined by phone, please press star 9 on your keypad to raise your hand. At this time, I would like to turn the call over to Justine Koenigsberg, Vice President, Investor Relations. Justine, please go ahead.

Good morning and welcome to Kinera's quarterly update call, which will also include a discussion of the KT579 Phase 1 Healthy Volunteer Results. Joining me this morning with prepared remarks are Nello Mainolfi, our Founder, President, and CEO, Terrence Rooney, 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. In order to have as much time for as many questions as possible, please limit your questions to one. If you would like to ask a question, please use the raise hand icon, which can be found at the bottom of your meeting window. A replay of today's call, including a copy of the corresponding presentation, will be available in the investor section of our website soon after the call concludes. As a reminder, today's presentation 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 10Q 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. Before we begin, we have one housekeeping item. Starting next week, we will enter our previously planned quiet period ahead of our upcoming Stat 6 data. As a result, we don't expect to provide additional commentary on our Stat 6 program until we report those results. With that, I will turn the discussion over to Nello.

Thank you, Justine, and good morning, everyone. Thank you for joining us today. This is a very exciting time for Chimera. We're seeing our scientific vision take shape across our pipeline of oral medicines to address serious inflammatory diseases with KT621, our STAT6 degrader for atopic dermatitis, asthma, and more, and KT579, our RF5 degrader for lupus and potentially other autoimmune diseases. Together, they reflect our goal of developing medicines grounded in strong biology with the potential to reach many more patients than served by available treatments today. I'll start today with an update on KT621 as we approach its Phase 2D AD readout before year-end. I'll then briefly cover the rest of our pipeline before we turn to KT579 Phase 1 results. Our statistics program continues to advance according to plans across both AD and asthma. As shown here, we've advanced KT621 through a series of studies, building on what we learned at each stage to guide the next steps. In Phase 1, we've evaluated KT621 in more than 200 healthy volunteers and observing deep stat6 degradation and facts on downstream biomarkers and a favorable safety and tolerability profile. We then treated 22 patients with AD in Phase 1b, where we saw the first evidence of strong clinical activity in patients. With each study, we built a stronger body of evidence and further de-risked KP621, supporting its advancement into the ongoing Phase IIb studies. In the Broaden II-AD study, we were excited to report that we had completed the 16-week placebo-controlled portion of the study, with the last patient just recently completing their final visit. We expect that the remaining activities to close out this portion of the study will enable us, as planned, to share the KT621 Phase 2D data by year-end. At the same time, we're well into our preparation for the first Phase 3 study in AD, which we plan to initiate assuming both supportive data and alignment with FDA by middle of 2027. Before we move to an update on asthma, as we have shared previously, patients that complete the full 16 weeks of treatment in Broaden 2 are eligible to enter a 52-week open-label extension. Today, we're happy to report that 98% of eligible patients have enrolled into the OLE. Now, turning to asthma, enrollment in the BREAD study continues to progress as planned, with top-line results expected in late 2027. In total, these studies have already enrolled hundreds of participants, providing a robust data set to assess safety and efficacy of these exciting novel mechanisms. And as a reminder, the BREATH study also includes a novel label extension, which together with the ADOLE are designed to further support a long-term safety database for regulatory requirements and the potential registration of KT621. As we approach the Broaden II readout, I wanted to take a moment to put the opportunity for KT621 in AD into perspective. As illustrated on slide 7, published epidemiological reports show that there are approximately 6 to 9 million people in the U.S., 12 years and up, with moderate to severe atopic dermatitis. Despite this high prevalence, only an estimated 400,000 receive advanced systemic therapies, a penetration of only about 5% of the total moderate to severe patient population. As we've been advancing KT621, we've also been conducting market research to better understand the market dynamics of advanced systemic therapies. What we hear from both patients and prescribers is that the main reason for the limited adoption is that many patients don't perceive that their disease state justifies an injectable biologic or a medicine carrying a box warning. That perception creates a significant barrier to the use of currently available advanced therapies. Our market research tells us that patients and physicians want a safe, effective oral treatment. In fact, when we ask what level of efficacy that treatment needs to deliver, we consistently hear that it does not necessarily have to match biologics. We have seen that opportunity play out in other markets. Otezva launched more than a decade ago with roughly half the efficacy of biologics and went on to become a multi-billion dollar franchise. More recently, Icotide, despite efficacy depth by cross-trial comparisons, does not quite match IL-23 biologics, is experiencing one of the strongest launches in psoriasis, bringing new patients to treatment in an already more saturated market. Going back to KT621, a safe and effective oral is what patients are looking for, and that is the profile we aim to deliver. Our focus is to serve the largest segment of moderate to severe AD population, those patients who are either untreated or, in many cases, poorly treated with non-systemic therapies. If we're successful, we believe that KT621 would have the potential to dramatically expand the number of patients accessing advanced therapies. All of that said, and based on the preclinical and phase one data we've generated so far, our scientific expectation remains that BRDN2 efficacy should land in the ballpark of what Dupilumab achieved at week 16 as compared to what was reported in the SOLO1, SOLO2 trials, while recognizing the limitation of comparing results across studies. Beyond KT621, we're also tracking with expectations and timelines across our broader pipeline. Our partner program are both progressing as planned. Sanofi continues to advance KT485, our second generation IRAC4 degrader in a phase one healthy volunteer study that is also expected to enroll HS patients. And Gilead is advancing KT200, our CDK2 molecular glue into IND enabling activities with an IND plan for 2027. With respect to our research pipeline, our undisclosed programs are tracking with our expectations and to support our goal to advance in one program towards development candidate annually. Regarding the disclosure of our next program, given all that we have to share in the fourth quarter with today's KT579 data and the upcoming KT621 Phase 2b readout, we've decided to hold off on that introduction until next year. With all of that said, before I turn the call over to Terrence to share the RS5 Healthy Volunteer data, I wanted to take a bit I want to talk a little bit about the importance of today's IRF-5 data release. We have now successfully advanced multiple degrader programs from target selection and drug discovery through preclinical and into the clinic. This is in fact our seventh first-in-class degrader to enter the clinic, and today we're sharing that we continue to demonstrate impeccable human translation. While each target and molecule is unique and must ultimately prove itself independently, This repeated execution is indicative of the positive and compounding effect of all our learnings and experience across our programs. IRF-5 itself is a highly compelling and genetically validated target that has historically been difficult to drive with conventional drug discovery approaches. And this study is an important first step in establishing our IRF-5 thesis in humans. As you'll hear shortly, KT579, which was well-tolerated in this study, robustly degraded IRF5. Importantly, the prudent IRF5 degradation led to meaningful reduction in multiple disease-relevant biomarkers. With this data in hand, we now plan to move the program with confidence into a Phase Ib lupus trial. The study is designed to establish whether KT579 can demonstrate the biological and clinical activity we would expect based on this mechanism. Overall, the KT579 data represents another important example of our ability to target a highly compelling but historically untracked target, in this case a transcription factor. It also demonstrates our ability to translate our preclinical work into humans in a predictable and compelling way. We've now done this across multiple programs, and with each success, we're building on a strong and increasingly repeatable foundation for selecting the right targets, developing differentiated degraders against them and efficiently translating those programs from discovery into the clinic. I know everyone is eager to get into the data, so with that I'll turn it over to Perrin to walk you through the results. Perrin?