BCL-2 inhibitors (BH3 mimetics)
Oral drugs that switch apoptosis back on in cancer cells that survive by overproducing BCL-2; venetoclax is the model, used in CLL and AML.
What they are
BCL-2 is an anti-apoptotic protein of the outer mitochondrial membrane. Chronic lymphocytic leukaemia and other blood cancers overexpress it to escape programmed cell death. BH3 mimetics block it and release the cell's own death machinery. Venetoclax is the only member in wide use.
Mechanism of action
The drug occupies the BH3-binding groove of BCL-2, the pocket where pro-apoptotic BH3-only proteins (BIM, BID, BAD) would normally be held. Freed BH3-only proteins activate BAX and BAK, the mitochondrial outer membrane becomes permeable, cytochrome c is released and caspases complete apoptosis.
Target: BCL-2 (anti-apoptotic protein of the mitochondrial membrane)
Drugs in this class
Test yourself
Think of the answer, then tap the question to see it.
What does BCL-2 normally do in a cancer cell?
It holds pro-apoptotic proteins in check and keeps the cell alive.
Why are BCL-2 inhibitors called BH3 mimetics?
They imitate the BH3 domain of pro-apoptotic proteins and fill the same groove on BCL-2.
What is the main early risk of starting venetoclax in CLL?
Tumour lysis syndrome.
Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.
Sources: Venetoclax: MedlinePlus Drug Information (MedlinePlus (U.S. National Library of Medicine), 2026); ATCDDD - ATC/DDD Index (WHO Collaborating Centre for Drug Statistics Methodology, 2026).
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Representative model, for educational purposes only.