BTK inhibitors
Oral drugs that switch off Bruton tyrosine kinase, the hub of B-cell receptor signalling, in CLL and other B-cell cancers.
What they are
Bruton tyrosine kinase (BTK) inhibitors (suffix «-brutinib») treat chronic lymphocytic leukaemia, mantle cell, marginal zone and follicular lymphoma and Waldenström macroglobulinaemia. Ibrutinib was the first; acalabrutinib and zanubrutinib are more selective covalent inhibitors.
Mechanism of action
B-cell receptor signalling passes through BTK. Covalent inhibitors bond to cysteine 481 in the ATP site and switch BTK off for the life of the protein. Malignant B cells lose their survival signals and die.
Target: Bruton tyrosine kinase (BTK)
Drugs in this class
Others in the class
- Ibrutinib and acalabrutinib (their pages sit under kinase inhibitors)
- Pirtobrutinib
- Orelabrutinib, tirabrutinib
Test yourself
Think of the answer, then tap the question to see it.
Which residue do covalent BTK inhibitors bond to?
Cysteine 481 of BTK.
Why are BTK inhibitors usually held around surgery?
Because of their bleeding risk.
Which three class adverse effects of BTK inhibitors matter most?
Bleeding, infection and atrial fibrillation.
Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.
Sources: ATCDDD - ATC/DDD Index (WHO Collaborating Centre for Drug Statistics Methodology, 2026); Zanubrutinib: MedlinePlus Drug Information (MedlinePlus (U.S. National Library of Medicine), 2024); eEML - Electronic Essential Medicines List (World Health Organization, 2025); RCSB PDB - 6J6M: Co-crystal structure of BTK kinase domain with Zanubrutinib (RCSB Protein Data Bank, 2026).
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Representative model, for educational purposes only.