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ESH CLL 2026 | Treatment sequencing for patients with CLL who relapse after covalent BTKi
Jennifer Brown, MD, PhD, Dana-Farber Cancer Institute, Boston, MA, discusses treatment sequencing for patients with chronic lymphocytic leukemia (CLL) who relapse after covalent BTK inhibitors (BTKi), highlighting venetoclax-based therapy and non-covalent BTKi as key options while noting that the optimal sequence remains uncertain. This interview took place at the ESH CLL 2026 congress in Stockholm, Sweden.
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Transcript
So patients who have disease relapsing after covalent BTK inhibitors have two primary options, venetoclax-based option or now a non-covalent BTK inhibitor option. I think we have more and stronger data for the venetoclax-based option, but certainly depending on patient preference or circumstances, and especially in older patients or those with more comorbidities, continuing with another BTK inhibitor may be easier...
So patients who have disease relapsing after covalent BTK inhibitors have two primary options, venetoclax-based option or now a non-covalent BTK inhibitor option. I think we have more and stronger data for the venetoclax-based option, but certainly depending on patient preference or circumstances, and especially in older patients or those with more comorbidities, continuing with another BTK inhibitor may be easier. We certainly don’t know for sure if there is a preferred sequence at present. I would say, though, that if there are BTK inhibitor mutations that have come out after the covalent BTK inhibitors, giving patients a break with venetoclax may potentially change that clonal architecture and give them a chance to get a longer benefit later from the non-covalent, but that’s speculative at present. Right now, I don’t think the non-covalent BTKIs really change the sequencing algorithm. We have such long, mature data with the covalent BTKIs that I think people should still choose those first for their CLL patients. But the emerging data with pirtobrutinib do look interesting, and we’ll have to see what really comes out of that data in terms of the resistance mechanisms for pirtobrutinib.
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