At ASH 2016 in San Diego, CA, I had the honor of once again interviewing Dr. Wiestner from the NIH (National Institute of Health) about the prototype BTK inhibitor, ibrutinib and how and why it works so well in CLL.
We have known for a while that for its survival and well-being, our cancer is dependent on BCR (B cell receptor) signaling. Blocking BTK (Bruton’s Tyrosine Kinase), blocks that BCR signaling and that blocking usually leads to our cancer’s retreat.
This is a well-understood critical tenet of why ibrutinib works as well as it does, but it is hardly the whole story as we are learning over time.
At the NIH, Dr. Wiestner and his team not only did some of the earliest clinical research on ibrutinib, but also has been doing the bench science on exactly how it works and its impact changes over time.
Please enjoy the interview here: cllsociety.org/2017/02/ash-...
We are all in this together.