ESH CLL 2026 | Key lessons from the ibrutinib era in CLL

Yes, so what we have learned from this experience of BTK inhibitor is that you can, there is no such, in some situations you don’t have that much correlation between the depth of the response and the length of the response. So this is exactly what we have with continuous treatment with BTK inhibitor, and that this strategy is effective for patients that are at high risk of genomic instability, such as those with TP53 alteration. So conversely, we learned about the toxicity and how we could improve the routine management of this toxicity, how to anticipate these, and how to set new drugs with less impact on this adverse event, such as the cardiac adverse event, which is key for BTK inhibitors. So the other lesson we learned is that it’s a good target because there is actually plenty of BTK-targeted drugs. So we talked about the covalent BTK inhibitors, but there is the non-covalent BTK inhibitors that do not depend on a specific residue to bind to BTK, so they are effective even if there is mutated BTK with this C481 mutation. And in addition, even more recently, we have emerged the BTK degraders that not only decrease the enzymatic effect of BTK, but also completely degrade the protein, avoiding any of the roles of the BTK, which could be beyond the enzymatic role of BTK. And so this approach is also very effective in patients who were previously treated already with covalent BTK inhibitors or non-covalent BTK inhibitors. But resistance never ends, and there is also a mutation of BTK affecting different types of BTK inhibitors, but we have to learn how to play with these different compounds and the optimal order for using these drugs.

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