Announcement • Jun 09

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Kymera Therapeutics Presents New Preclinical Data for Kt-579, Oral Irf5 Degrader, At Eular and Focis Congresses

Kymera Therapeutics, Inc. presented new preclinical data for KT-579, its potent, selective, oral IRF5 degrader, demonstrating disease-modifying activity in lupus models. KT-579 demonstrated consistent disease-modifying activity comparable or superior to approved and clinically active therapies in multiple preclinical lupus models. The findings show that by selectively targeting and degrading IRF5, KT-579 offers a novel oral approach for complex, heterogeneous autoimmune diseases driven by multiple validated inflammatory pathways, including Type I interferons, pro-inflammatory cytokines and autoantibody responses. These data were presented at the European Alliance of Associations for Rheumatology (EULAR) Annual Meeting held June 3-6, 2026, in London, UK, and will be presented at the Federation of Clinical Immunology Societies (FOCIS) Annual Meeting being held June 9-12, 2026, in San Francisco, CA. The Company previously reported data demonstrating KT-579’s compelling profile in preclinical studies using human primary cell systems, patient-derived cells and in vivo disease models of lupus, rheumatoid arthritis, and inflammatory bowel disease showing activity comparable or superior to existing standards of care. New data presented at EULAR and FOCIS further validate KT-579’s broad and consistent activity across preclinical models of lupus. In healthy donor and lupus patient-derived human cells, with or without a common SLE-associated polymorphism, KT-579 selectively degraded IRF5, blocked TLR-induced IRF5 nuclear translocation, and reduced key downstream inflammatory mediators, including Type I IFN and pro-inflammatory cytokines, as well as plasmablast differentiation and IgG production. In vivo, KT-579 demonstrated dose-dependent IRF5 degradation and inhibition of TLR7- and TLR9-induced cytokine release, including TNFa, IL-6, IL-12 and IFNß. Across multiple lupus models spanning low to high Type I IFN signaling, KT-579 treatment led to reductions in disease-relevant biomarkers, including proteinuria, serum autoantibodies and kidney pathology, with activity comparable or superior to approved and clinically active agents tested. Together, these findings demonstrate consistent modulation of pro-inflammatory, Type I IFN and B cell-driven pathways, supporting KT-579’s potential as a first-in-class, oral approach in lupus and other chronic autoimmune diseases. The KT-579 Phase 1 healthy volunteer trial is ongoing. The Phase 1 study is evaluating the safety, tolerability, pharmacokinetics and pharmacodynamics of single- and multiple-ascending doses of orally administered KT-579 compared to placebo. The key study aim is to show that KT-579 can robustly degrade IRF5 in blood at doses that are safe and well tolerated. The functional impact of IRF5 degradation on the induction of Type I interferons, pro-inflammatory cytokines, and inflammatory pathway gene transcripts will also be assessed with whole blood ex vivo stimulation assays. The Company expects to report data from the trial in the second half of 2026 and, following the healthy volunteer study, plans to initiate a patient proof-of-concept trial, likely in lupus. European Alliance of Associations for Rheumatology (EULAR) Title: First-in-class Oral IRF5 Degrader, KT-579, Demonstrates Selective and Potent In Vitro and In Vivo Activity in Human Cellular Assays and Mouse Models of Lupus Type/Session: Poster, Poster View VIII Date/Time: Saturday, June 6, 2026, at 10:15 AM BST Federation of Clinical Immunology Societies (FOCIS) Title: Potent and Selective First-in-Class Oral IRF5 Degrader, KT-579, Inhibits Endosomal TLR-Induced Responses in SLE Derived PBMCs and Significantly Reduces Disease Activity in the MRL.lpr Mouse Lupus Model Type/Session: Poster, Autoimmune Diseases Date/Time: Thursday, June 11, 2026, at 7:00 PM PT Copies of the EULAR and FOCIS posters will be available in the Resource Library section of Kymera's website. KT-579 is an investigational, first-in-class, oral degrader of IRF5, a genetically validated transcription factor and master regulator of immunity, and currently in Phase 1 testing. By selectively degrading IRF5, KT-579 is designed to modulate multiple disease-driving pathways simultaneously, including Type I interferons, pro-inflammatory cytokines and autoantibody responses, offering the potential for biologics-like activity in a convenient oral medicine. In preclinical studies, KT-579 degraded IRF5 across multiple preclinical species and in all disease-relevant tissues. In preclinical models of lupus, rheumatoid arthritis (RA), and inflammatory bowel disease (IBD), KT-579 activity was equal to or more efficacious than small molecule inhibitors and biologics currently marketed or in the clinic. In preclinical safety studies, KT-579 did not show any adverse effects of any type at all doses tested. KT-579 has the potential to be the first novel mechanism with broad utility in diseases where effective and well tolerated oral therapies are needed, such as lupus, IBD, RA, Sjögren's and others.

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Kymera Therapeutics Presents New Preclinical Data for Kt-579, Oral Irf5 Degrader, At Eular and Focis Congresses

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