800 | THERAPEUTIC POTENTIAL OF NRF2 INHIBITION IN CHRONIC LYMPHOCYTIC LEUKEMIA AND IN COMBINATION WITH CURRENT THERAPY

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NF-κB, and PI3K-AKT-mTOR signaling.Simultaneously, C23 successfully degraded BTK to inhibit cell growth in BTK C481S and BTK L528W mutant cells, which are two most quintessential mutations that confer acquired resistance.C23 significantly suppressed tumor growth in MCL xenograft models with either BTK WT or BTK C481S /BTK L528W mutations.Conclusion: C23 was a highly effective PROTAC targeting BTK degradation for the treatment of MCL with BTK expression or overcoming acquired resistance to covalent and non-covalent BTK inhibitors, underscoring its potential as a novel therapeutic agent for MCL.

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.