KT-579 demonstrated consistent disease-modifying activity comparable or superior to approved and clinically active therapies in multiple preclinical lupus models 

KT-579 Phase 1 healthy volunteer trial ongoing, with data expected in 2H26

WATERTOWN, Mass., June 08, 2026 (GLOBE NEWSWIRE) -- Kymera Therapeutics, Inc. (NASDAQ:KYMR), a clinical-stage biopharmaceutical company advancing a new class of oral small molecule degrader medicines for immunological diseases, today announced the presentation of new preclinical data for KT-579, its potent, selective, oral IRF5 degrader, demonstrating disease-modifying activity in 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 TNFα, IL-6, IL-12 and IFNβ. 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.