The Bruton tyrosine kinase inhibitor PCI-32765 blocks B-cell activation and is efficacious in models of autoimmune disease and B-cell malignancy
By L. Honigberg, Ashley M. Smith, M. Sirisawad, E. Verner, D. Loury, B. Chang, Shyr-Jiann Li, Z. Pan, D. Thamm, Richard A. Miller and 1 more. Proceedings of the National Academy of Sciences of the United States of America, 2010
1,495 citations recorded by the source corpus.
Subfields: Genetics, Immunology
View Paper: https://www.semanticscholar.org/paper/48743db7e7fcf67c3ae7359f032f8ce49c045e8d
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
Citations in the corpus
- Ibrutinib is an irreversible molecular inhibitor of ITK driving a Th1-selective pressure in T lymphocytes. (2013, background): “This dose range is consistent with serum concentrations observed in vivo during pharmacokinetic studies of ibrutinib in both mouse and human trials.(18,36) To validate these findings in human patients, serial serum cytokine levels were investigated in relapsed or refractory CLL patients receiving ib”
- Role of Bruton’s tyrosine kinase in B cells and malignancies (2018, background): “Acalabrutinib also binds C481 and lacks irreversible targeting to alternative kinases, such as EGFR, ITK, TXK, SRC family kinases and JAK3.”
- Ibrutinib versus Ofatumumab in Previously Treated Chronic Lymphoid Leukemia (2014, neutral): “Neutropenia 42 (22) 32 (16) 28 (15) 26 (14)”
- Developing irreversible inhibitors of the protein kinase cysteinome (2013, neutral): “However, to date only six distinct cysteine sites have been unequivocally demonstrated to be targeted by a covalent inhibitor: the cysteine at the lip of the ATP-binding site targeted by the covalent EGFR, BMX, and BTK inhibitors; the cysteine in the P loop region targeted by FGFR; the cysteine in t”
- Bruton tyrosine kinase inhibitor ibrutinib (PCI-32765) has significant activity in patients with relapsed/refractory B-cell malignancies. (2013, methodology): “5 nmol/L) that inhibits BCR signaling in human B cells via specific active-site occupancy.(16) In vitro, ibrutinib is JOURNAL OF CLINICAL ONCOLOGY O R I G I N A L R E P O R T VOLUME 31 NUMBER 1 JANUARY 1 2013”
- Three-year follow-up of treatment-naïve and previously treated patients with CLL and SLL receiving single-agent ibrutinib. (2015, neutral): “Disease progression 1 (3) 21 (21) 22 (17)”