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The World’s Leading Authority for Chronic Lymphocytic Leukemia Patients
Eight more days of Decadron in the next 11, then unless I have some untoward reaction, I will stop getting dosed inpatient and needing premedication. YAHOO!
It’s an immune therapy because we harness our immune system to kill the cancer. No toxic chemotherapy.
BTK is a good therapeutic target in CLL because it is only critical for the function of B-cells, and thus loss of BTK is not lethal for the patient.
Following discontinuation of a non-covalent Bruton tyrosine kinase inhibitor (BTKi), venetoclax is clinically active in patients with CLL or Richter transformation who have not received it in the past. CAR-T therapy may also be an option, but this requires further study.
Bruton tyrosine kinase (BTK) degraders are a new therapeutic area that might be able to overcome mutations that cause resistance to BTK inhibitors.
A newly published paper in the New England Journal of Medicine found that pirtobrutinib shows efficacy in patients with heavily pretreated chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL) who had received a covalent Bruton tyrosine kinase inhibitor (BTKi).
Acalabrutinib produced durable responses in patients with chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL) at higher risk of disease progression.
Pirtobrutinib can extend the benefits of Bruton tyrosine kinase (BTKi) in patients with CLL / SLL who are resistant to covalent BTKi
The noncovalent BTK inhibitor nemtabrutinib shows promising antitumor activity and a manageable safety profile in highly relapsed/refractory patients with chronic lymphocytic leukemia CLL / SLL.
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