You know, I was really excited about the Meet the Experts session today and yesterday as well. Yesterday we had over 300 people. Today it was a lot earlier, so not as many, but the news is still the same. We have a lot of developments in Waldenstrom’s, a lot of new drugs that are actually making their way through the pipeline that I think will continue to benefit our patients. And these days, what we’re very much concerned about is what do we do with our patients who fail the covalent BTK inhibitors like ibrutinib or zanubrutinib or acalabrutinib...
You know, I was really excited about the Meet the Experts session today and yesterday as well. Yesterday we had over 300 people. Today it was a lot earlier, so not as many, but the news is still the same. We have a lot of developments in Waldenstrom’s, a lot of new drugs that are actually making their way through the pipeline that I think will continue to benefit our patients. And these days, what we’re very much concerned about is what do we do with our patients who fail the covalent BTK inhibitors like ibrutinib or zanubrutinib or acalabrutinib. And what’s important, I think, for all of us to recognize all the new options. We’ve got non-covalent BTK inhibitors like pirtobrutinib with nice data in Waldenstrom showing that we can get high response rates and durable activity. We talked about BCL2 inhibitors like venetoclax, but we also have new agents to get excited about, the BTK degraders. This is really a big chapter, I think, for Waldenstrom’s because we’re seeing high rates of activity in the relapsed/refractory setting. And the degraders, particularly the BGB-16673 that we have mutation data with shows activity even in those patients with covalent and non-covalent BTK inhibitor acquired mutations in BTK. So I am excited. And the initial data looks really great. You know, upwards of 80% of the patients are having a major response. There’s durability with the BGB-16673 degrader. We’re also excited about Nurix. They’re also developing a BTK degrader. We’ve seen a little bit less data associated with that, but still very high rates of response in Waldenstrom patients. BCL2 inhibition, sonrotoclax. It’s nice to actually see how this agent is also making its way in the development of Waldenstrom. So I wanted to share all that with our audience today. What I wish I could have shared with them is progress in cellular therapies. And we’re still really new at the game to bring in these new and exciting agents. But here at ICML, what’s been great is the learning curve here. Learning about these new cellular therapies, the T-cell engagers, the bispecifics targeting CD19 and CD20, hearing about the CAR T-cells, and particularly some of the dual CAR-T’s that target 19 and 20 or 19 and BCMA. I think these represent very active agents, quite worthy of investigation in Waldenstrom’s, and we’re just starting doing that. I think by next ICML we will finally have the data for these cellular therapies. But this is really progress in the making.
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