Results 11 to 20 of about 22,142 (188)

Synergistic effect of venetoclax and ibrutinib on ibrutinib-resistant ABC-type DLBCL cells [PDF]

open access: yesBrazilian Journal of Medical and Biological Research
Despite the widespread use of R-CHOP therapy in diffuse large B-cell lymphoma (DLBCL), the therapeutic efficacy for this disease remains suboptimal, primarily due to the heterogeneity of refractory and/or relapsed diseases.
Fengbo Jin   +8 more
doaj   +3 more sources

Mitigating Ibrutinib‐Induced Ventricular Arrhythmia and Cardiac Dysfunction With Metformin [PDF]

open access: yesCancer Innovation
Background Ibrutinib is a first‐line drug that targets Bruton's tyrosine kinase for the treatment of B cell cancer. However, cardiotoxicity induced by ibrutinib is a major side effect that limits its clinical use.
Pengsha Li   +13 more
doaj   +4 more sources

Ibrutinib Inhibits Angiogenesis and Tumorigenesis in a BTK-Independent Manner

open access: yesPharmaceutics, 2022
BTK inhibitor (BTKi) Ibrutinib carries an increased bleeding risk compared to more selective BTKis Acalabrutinib and Zanubrutinib, however, its impact on vascular endothelium remains unknown.
Jia Liu   +6 more
doaj   +2 more sources

Electrocardiographic Changes Associated With Ibrutinib Exposure

open access: yesCancer Control, 2020
Although ibrutinib-associated atrial and ventricular arrhythmias have been well described, there is little information about ibrutinib’s effects on other electrocardiographic parameters, particularly the QT interval.
Michael G. Fradley MD   +9 more
doaj   +3 more sources

Extrahepatic metabolism of ibrutinib [PDF]

open access: yes, 2021
Ibrutinib is a first-in-class Bruton's kinase inhibitor used in the treatment of multiple lymphomas. In addition to CYP3A4-mediated metabolism, glutathione conjugation can be observed.
Rood, Johannes J M   +9 more
core   +3 more sources

Mechanism of Covalent Binding of Ibrutinib to Bruton’s Tyrosine Kinase revealed by QM/MM Calculations [PDF]

open access: yes, 2020
Ibrutinib is the first covalent inhibitor of Bruton’s tyrosine kinase (BTK) to be used in the treatment of B-cell cancers. Understanding the mechanism of covalent inhibition is crucial for the design of safer and more selective covalent inhibitors that ...
Angus, Voice   +4 more
core   +1 more source

Ibrutinib-related uveitis: A case series

open access: yesAmerican Journal of Ophthalmology Case Reports, 2022
Purpose: Four cases of ibrutinib-related uveitis are presented, which are to the best of our knowledge the first in the literature. Possible mechanisms of ibrutinib-mediated uveitis are explored.
Zelia K. Chiu   +4 more
doaj   +1 more source

Ibrutinib plus Obinutuzumab as Frontline Therapy for Chronic Lymphocytic Leukemia Is Associated with a Lower Rate of Infusion-Related Reactions and with Sustained Remissions after Ibrutinib Discontinuation: A Single-Arm, Open-Label, Phase 1b/2 Clinical Trial NCT0231576

open access: yesAdvances in Hematology, 2022
Ibrutinib-based therapies are costly and require continuous administration. We hypothesized combining BTK inhibition with anti-CD20 monoclonal antibodies would yield deep remissions allowing discontinuation.
Januario E. Castro   +11 more
doaj   +1 more source

Ibrutinib suppresses LPS-induced neuroinflammatory responses in BV2 microglial cells and wild-type mice

open access: yesJournal of Neuroinflammation, 2018
Background The FDA-approved small-molecule drug ibrutinib is an effective targeted therapy for patients with chronic lymphocytic leukemia (CLL). Ibrutinib inhibits Bruton’s tyrosine kinase (BTK), a kinase involved in B cell receptor signaling.
Hye Yeon Nam   +8 more
doaj   +1 more source

Characterization of atrial fibrillation adverse events reported in ibrutinib randomized controlled registration trials

open access: yesHaematologica, 2017
The first-in-class Bruton’s tyrosine kinase inhibitor ibrutinib has proven clinical benefit in B-cell malignancies; however, atrial fibrillation (AF) has been reported in 6–16% of ibrutinib patients.
Jennifer R. Brown   +26 more
doaj   +1 more source

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