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ESH CLL 2026 | The potential of pirtobrutinib in the treatment of CLL
Matthew Davids, MD, Dana-Farber Cancer Institute, Boston, MA, discusses the potential of pirtobrutinib, a non-covalent BTK inhibitor, in the treatment of chronic lymphocytic leukemia (CLL), highlighting its efficacy in double-refractory settings and its recent approval in the US as a second-line therapy. This interview took place at the ESH CLL 2026 congress in Stockholm, Sweden.
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Transcript
So the non-covalent BTK inhibitor, pirtobrutinib, is very active in that double-refractory setting, but that has kind of spurred the development of earlier lines of therapy with pirtobrutinib. It can be used as a second-line setting, for example. It’s approved in that setting now in the U.S. for patients progressing on a frontline covalent BTK inhibitor. But recent data, phase 3 data, looked at pirtobrutinib as an initial therapy in the BRUIN CLL-313 and 314 trials, comparing it to bendamustine and rituximab in that first study, 313, and compared to ibrutinib directly in the 314 study...
So the non-covalent BTK inhibitor, pirtobrutinib, is very active in that double-refractory setting, but that has kind of spurred the development of earlier lines of therapy with pirtobrutinib. It can be used as a second-line setting, for example. It’s approved in that setting now in the U.S. for patients progressing on a frontline covalent BTK inhibitor. But recent data, phase 3 data, looked at pirtobrutinib as an initial therapy in the BRUIN CLL-313 and 314 trials, comparing it to bendamustine and rituximab in that first study, 313, and compared to ibrutinib directly in the 314 study. So I think the data sets are very intriguing. The response rates of pirtobrutinib as a frontline treatment are very high. But in CLL, with a long natural history, we need to see longer duration of follow-up, particularly around progression-free survival, to understand the potential benefits of non-covalent BTK inhibitors in that setting. And furthermore, we want to see that patients can then respond subsequently to covalent BTK inhibitors after non-covalent inhibitors. And so until we have that level of data, we probably won’t be using the non-covalent inhibitors as frontline therapy, at least not broadly speaking.
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