Abstract
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.
Original language | English |
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Pages (from-to) | 1212-1221 |
Number of pages | 10 |
Journal | Thrombosis and Haemostasis |
Volume | 119 |
Issue number | 8 |
DOIs | |
Publication status | Published - Aug 2019 |
Keywords
- ACALABRUTINIB ACP-196
- BRUTONS TYROSINE KINASE
- Btk inhibitor
- CA2+ ENTRY
- COMPLEMENTARY ROLES
- GLYCOPROTEIN-VI
- GPIb
- GPVI
- GPVI-FC
- PLATELET THROMBUS FORMATION
- SRC FAMILY
- TERM-FOLLOW-UP
- X-LINKED AGAMMAGLOBULINEMIA
- X-linked agammaglobulinemia
- bleeding
- platelet
- IBRUTINIB TREATMENT