The Chronic Lymphocytic Leukemia Channel is supported with funding from AstraZeneca (Diamond), AbbVie (Platinum), Johnson & Johnson (Gold), BeOne Medicines (Silver) and Lilly (Silver).
VJHemOnc is an independent medical education platform. Supporters, including channel supporters, have no influence over the production of content. The levels of sponsorship listed are reflective of the amount of funding given to support the channel.
EHA 2026 | Emerging third-generation BTK-targeted therapies for CLL: overcoming BTK resistance
Paolo Ghia, MD, Vita-Salute San Raffaele University, Milan, Italy, discusses the promise of third-generation agents, including the BTK inhibitor nemtabrutinib and the BTK degrader tacabrutideg, to overcome resistance to covalent BTK inhibitors in chronic lymphocytic leukemia (CLL). Dr Ghia also highlights the importance of fixed-duration treatment to prevent patients from becoming refractory to therapy. This interview took place at the 31st Congress of the European Hematology Association (EHA) in Stockholm, Sweden.
These works are owned by Magdalen Medical Publishing (MMP) and are protected by copyright laws and treaties around the world. All rights are reserved.
Transcript
Both are the third generation BTK inhibitors like tantabrutinib or the BTK degrader. It is a completely new class of drugs. Here we are presenting data on the BGB-16673, which has now a name, tacabrutideg. And these are compounds that have been developed to go beyond the classic covalent BTK inhibitors and to overcome the mutations and the resistance that can occur with the continuous treatment with covalent BTK inhibitors...
Both are the third generation BTK inhibitors like tantabrutinib or the BTK degrader. It is a completely new class of drugs. Here we are presenting data on the BGB-16673, which has now a name, tacabrutideg. And these are compounds that have been developed to go beyond the classic covalent BTK inhibitors and to overcome the mutations and the resistance that can occur with the continuous treatment with covalent BTK inhibitors. Both classes are very effective in this category of patients. The problem is that we should really avoid reaching the point where the patient becomes refractory to drugs. So that’s the whole idea behind fixed duration treatment, with the idea, as we have shown already in the CAPTIVATE study many years ago, that indeed when we expose the patient to a combination of therapies for a year or a little bit longer than a year, then they will not develop mutations in the BTK molecules, for example, and in particular, they don’t seem to become resistant, so that we can continue using the same drugs over and over.
This transcript is AI-generated. While we strive for accuracy, please verify this copy with the video.
Read more...
