Kymera Therapeutics, Inc. Common Stock 2026 Q3 Earnings Call

Justine, please go ahead. Good morning and welcome to Kymera's quarterly update call, which will also include a discussion of the KT-579 phase I healthy volunteer results.

Joining me this morning with prepared remarks are Nello Mainolfi, our Founder, President, and CEO, Terence 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 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. 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 Kymera. We're seeing our scientific vision take shape across our pipeline of oral medicines to address serious inflammatory diseases with KT-621, our STAT 6 degrader for atopic dermatitis, asthma, and more, and KT-579, our IRF5 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 KT-621 as we approach its phase II-B AD readout before year-end. I'll then briefly cover the rest of our pipeline before we turn to KT-579 phase I results. Our STAT 6 program continues to advance according to plans across both AD and asthma.

As shown here, we've advanced KT-621 through a series of studies, building on what we learned at each stage to guide the next steps. In phase I, we've evaluated KT-621 in more than 200 healthy volunteers in observing deep STAT 6 degradation, effects on downstream biomarkers, and a favorable safety and tolerability profile. We then treated 22 patients with AD in phase I-B, 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 KT-621, supporting its advancement into the ongoing phase IIb studies. In the BROADEN2 AD study, we're excited to report that we have 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 KT-621 phase IIb data by year-end. At the same time, we're well into our preparation for the first phase III 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 BROADEN2 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. Turning to asthma, enrollment in the BREADTH 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 this exciting novel mechanism. As a reminder, the BREADTH study also includes an open label extension, which together with the AD OLE, are designed to further support a long-term safety database for regulatory requirements and the potential registration of KT-621. As we approach the BROADEN2 readout, I wanted to take a moment to put the opportunity for KT-621 in AD into perspective. As illustrated on slide seven, published epidemiological reports show that there are approximately 6 million 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 KT-621, 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. OTEZLA launched more than a decade ago with roughly half the efficacy of biologics and went on to become a multibillion-dollar franchise.

More recently, icotrokinra, despite efficacy that, 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 KT-621, 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 are successful, we believe that KT-621 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 I data we have generated so far, our scientific expectation remains that BROADEN2 efficacy should land in the ballpark of what dupilumab achieved at week 16 as compared to what was reported in the SOLO 1, SOLO 2 trials, while recognizing the limitation of comparing results across studies. Beyond KT-621, we are also tracking with expectations and timelines across our broader pipeline. Our partner programs are both progressing as planned. Sanofi continues to advance KT-485, our second-generation IRAK4 degrader, in a phase I healthy volunteer study that is also expected to enroll HS patients. Gilead is advancing KT-200, our CDK2 molecular glue, into IND-enabling activities with an IND planned for 2027. With respect to our research pipeline, our undisclosed programs are tracking with our expectations and to support our goal to advancing 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 KT-579 data and the upcoming KT-621 phase IIb readout, we have decided to hold off on that introduction until next year. With all of that said, before I turn the call over to Terence to share the IRF5 healthy volunteer data, I wanted to talk a little bit about the importance of today's IRF5 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 are 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. IRF5 itself is a highly compelling and genetically validated target that has historically been difficult to drug with conventional drug discovery approaches. This study is an important first step in establishing our IRF5 thesis in humans. As you will hear shortly, KT-579, which was well-tolerated in this study, robustly degraded IRF5. Importantly, the potent IRF5 degradation led to meaningful reductions 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 KT-579 can demonstrate the biological and clinical activity we would expect based on this mechanism.

Overall, the KT-579 data represent another important example of our ability to target a highly compelling but historically undrugged 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 have now done this across multiple programs, and with each success, we are 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 will turn it over to Terence to walk you through the results.