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Kymera Therapeutics (KYMR) investor relations material
Kymera Therapeutics Study Result summary
Complete event summary combining all related documents: earnings call transcript, report, and slide presentation.Strategic Overview and Rationale
KT-621 is a first-in-class oral STAT6 degrader targeting Type 2 inflammation in diseases such as atopic dermatitis (AD), asthma, and allergic rhinitis, aiming to provide a biologics-like effect in an oral formulation.
The approach leverages targeted protein degradation to address previously undruggable or hard-to-drug targets, focusing on unmet needs in immunology.
Oral degraders offer continuous pathway suppression, potentially matching or exceeding biologics in efficacy and safety, while improving convenience and access.
The market opportunity is significant, as only a small fraction of eligible patients currently receive advanced systemic therapies, mostly biologics.
KT-621 is positioned to expand access to millions of patients not currently treated with advanced therapies.
Study Design and Patient Population
Open-label, single-arm Phase 1b trial enrolled 22 moderate to severe AD patients across two dose levels (100 mg and 200 mg) for 28 days, followed by 14-day follow-up.
Patients had documented topical corticosteroid failure; prior biologic use allowed after washout.
Dose groups were balanced for gender, age, race, and disease severity; 46% had comorbid asthma or allergic rhinitis, and 23% had prior biologic treatment.
The study included a diverse population, with over half Black or African American and nearly a quarter Hispanic or Latino.
Baseline characteristics were well balanced across cohorts, with high disease burden and frequent comorbid asthma or allergic rhinitis.
Pharmacodynamics and Biomarker Results
KT-621 achieved deep STAT6 degradation (98% in blood, 94% in skin) at both dose levels, maintained through dosing, with strong translation from healthy volunteers to patients.
Robust reductions in Type 2 inflammation biomarkers: TARC (up to 74%), Eotaxin-3 (up to 73%), IgE (up to 14%), IL-31 (up to 56%), and FeNO (up to 56%).
First demonstration of IL-31 and FeNO reduction in AD patients with IL-4/13 pathway blockade.
Transcriptomic analysis of skin biopsies showed significant downregulation of Type 2 and AD-relevant genes, mirroring dupilumab effects.
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