So in the last EHA meeting I presented the data on BGB-16673 that is a BTK degrader. So this is a new concept of BTK inhibition in which these agents actually degrade the BTK both with the wild type and the mutant form by tagging BTK for degradation through the cell-proteasome pathway. In the last follow-up, at 8.2 months, we observed that these agents had a significant preliminary antitumor activity that was demonstrated by a high efficacy with an overall response rate of 84% and about one third of patients achieving a VGPR, so a deep response...
So in the last EHA meeting I presented the data on BGB-16673 that is a BTK degrader. So this is a new concept of BTK inhibition in which these agents actually degrade the BTK both with the wild type and the mutant form by tagging BTK for degradation through the cell-proteasome pathway. In the last follow-up, at 8.2 months, we observed that these agents had a significant preliminary antitumor activity that was demonstrated by a high efficacy with an overall response rate of 84% and about one third of patients achieving a VGPR, so a deep response. And these responses were really rapid. We could see it by the time to first response, this was in median one month. And the improvement, the significant improvement in responding patients for cytopenia. So they showed a recovery of cytopenia in about two months of treatment. So all this data, in particular in this kind of population of heavily treated patients with the enriched for high-risk genomic aberration for Waldenstrom, supported the use of these drugs in dissecting or relapsed refractory patients with Waldenstrom after covalent BTK inhibitor.
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