Results 11 to 20 of about 16,400 (167)

CD52 and OXPHOS—potential targets in ibrutinib-treated mantle cell lymphoma

open access: yesCell Death Discovery, 2022
Altered features of tumor cells acquired across therapy can result in the survival of treatment-resistant clones that may cause minimal residual disease (MRD).
Viktoria Fuhr   +7 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

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

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   +1 more source

RETRACTED ARTICLE: Ibrutinib facilitates the sensitivity of colorectal cancer cells to ferroptosis through BTK/NRF2 pathway

open access: yesCell Death and Disease, 2023
Ibrutinib is a drug that inhibits the protein Burton’s tyrosine kinase and thereby the nuclear translocation of Nrf2, which played a key role in mediating the activation of antioxidants during stress conditions and ferroptosis resistance.
Jin-Feng Zhu   +8 more
doaj   +1 more source

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   +1 more source

A ROR1 small molecule inhibitor (KAN0441571C) induced significant apoptosis of ibrutinib‐resistant ROR1+ CLL cells

open access: yeseJHaem, 2021
ROR1 – a receptor tyrosine kinase – is overexpressed in CLL. Ibrutinib, a Bruton's tyrosine kinase inhibitor, is clinically effective in CLL but patients may develop resistance. We evaluated the effect of an ROR1 inhibitor, KAN0441571C, in CLL cells from
Amineh Ghaderi   +9 more
doaj   +1 more source

Modulation of myeloid and T cells in vivo by Bruton’s tyrosine kinase inhibitor ibrutinib in patients with metastatic pancreatic ductal adenocarcinoma

open access: yesJournal for ImmunoTherapy of Cancer, 2023
Background In preclinical studies of pancreatic ductal adenocarcinoma (PDAC), ibrutinib improved the antitumor efficacy of the standard of care chemotherapy.
Li Zhang   +28 more
doaj   +1 more source

Proteome‐Wide Target Identification Using Reactive Metallo‐Scaffolds (r‐mS): A Platform for Metallodrug Discovery

open access: yesAngewandte Chemie, EarlyView.
Re‐envisioning the Ligandable Proteome: Reactive Metallo‐Scaffolds (r‐mS) combine non‐covalent protein engagement by a metallo‐scaffold with covalent cysteine capture through a tethered chloroacetamide warhead. Chemoproteomic profiling reveals unique enzyme engagement including ligases, kinases and methyltransferases, highlighting opportunities for ...
Jessica E. Waters   +15 more
wiley   +2 more sources

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