This is really a great time for Waldenström’s macroglobulinemia because we’re seeing important advances being made. Thanks really, to our better understanding of the genome. We have a number of new agents being developed, including the BTK inhibitors, CXCR4 inhibitors, BCL2 inhibitors, all of which are showing great promise for this disease. BTK inhibitors represent really a bright spot in this disease...
This is really a great time for Waldenström’s macroglobulinemia because we’re seeing important advances being made. Thanks really, to our better understanding of the genome. We have a number of new agents being developed, including the BTK inhibitors, CXCR4 inhibitors, BCL2 inhibitors, all of which are showing great promise for this disease. BTK inhibitors represent really a bright spot in this disease. These were rationally developed since our discovery of the MYD88 mutation, and recognizing that this mutation actually drives BTK signaling. Since about 95 to 97% of patients carry these MYD88 mutations, this is actually a big deal. And what we’ve seen from all the trials that have been done to date is very high rates of activity for BTK inhibitors, regardless of whether we’re talking about ibrutinib, zanubrutinib, acalabrutinib, tirabrutinib. Even now the non-covalent pirtobrutinib is showing very nice activity in this disease. And so it’s an exciting time. And really there remains a number of questions around the use of BTK inhibitors, including when do we use them? How do we sequence them relative to chemoimmunotherapy? How do we optimize their use, and with what agents can we combine them? The future is very bright. We know they work. We know that they have very long durable responses, and now really it’s about, where do we place them? How do we use them? And what’s the best way to use them?