acp-196 has been researched along with Agammaglobulinemia* in 2 studies
1 review(s) available for acp-196 and Agammaglobulinemia
| Article | Year |
|---|---|
Btk Inhibitors as First Oral Atherothrombosis-Selective Antiplatelet Drugs?
Bruton's tyrosine kinase (Btk) is essential for B cell differentiation and proliferation, but also platelets express Btk. Patients with X-linked agammaglobulinemia due to hereditary Btk deficiency do not show bleeding, but a mild bleeding tendency is observed in high dose therapy of B-cell malignancies with ibrutinib and novel second-generation irreversible Btk inhibitors (acalabrutinib and ONO/GS-4059). This review discusses recent studies that may explain this apparent paradox and gives mechanistic insights that suggest a unique potential of low dose irreversible Btk inhibitors as atherothrombosis-focused antiplatelet drugs. Topics: Adenine; Administration, Oral; Agammaglobulinaemia Tyrosine Kinase; Agammaglobulinemia; Animals; Arteries; B-Lymphocytes; Benzamides; Blood Platelets; Cell Differentiation; Genetic Diseases, X-Linked; Hemorrhage; Humans; Imidazoles; Mice; Piperidines; Platelet Aggregation Inhibitors; Platelet Membrane Glycoproteins; Protein Kinase Inhibitors; Pyrazines; Pyrazoles; Pyrimidines; Signal Transduction; Thrombosis | 2019 |
1 other study(ies) available for acp-196 and Agammaglobulinemia
| Article | Year |
|---|---|
Inhibition of Btk by Btk-specific concentrations of ibrutinib and acalabrutinib delays but does not block platelet aggregation mediated by glycoprotein VI.
Ibrutinib and acalabrutinib are irreversible inhibitors of Bruton tyrosine kinase used in the treatment of B-cell malignancies. They bind irreversibly to cysteine 481 of Bruton tyrosine kinase, blocking autophosphorylation on tyrosine 223 and phosphorylation of downstream substrates including phospholipase C-γ2. In the present study, we demonstrate that concentrations of ibrutinib and acalabrutinib that block Bruton tyrosine kinase activity, as shown by loss of phosphorylation at tyrosine 223 and phospholipase C-γ2, delay but do not block aggregation in response to a maximally-effective concentration of collagen-related peptide or collagen. In contrast, 10- to 20-fold higher concentrations of ibrutinib or acalabrutinib block platelet aggregation in response to glycoprotein VI agonists. Topics: Adenine; Agammaglobulinaemia Tyrosine Kinase; Agammaglobulinemia; Benzamides; Blood Platelets; Carrier Proteins; Genetic Diseases, X-Linked; Humans; Mutation; Peptides; Piperidines; Platelet Activation; Platelet Function Tests; Platelet Membrane Glycoproteins; Protein Kinase Inhibitors; Pyrazines; Pyrazoles; Pyrimidines | 2018 |