Some amphiphilic cations block the mitochondrial apoptosis-induced channel, MAC

Sonia Martinez-Caballero, Laurent M. Dejean, Kathleen W. Kinnally

    Research output: Contribution to journalArticlepeer-review


    The mitochondrial apoptosis-induced channel (MAC) forms in the outer membrane of mitochondria early in apoptosis and this activity is altered by physiological levels of cytochrome c. While cyclosporine A and lidocaine have no effect, dibucaine induces a fast blockade of MAC with an IC50 of 39 μM. In contrast, the IC50 for propranolol and trifluoperazine are 52 and 0.9 μM, respectively, and these drugs likely destabilize the open state of MAC. These agents, and others not yet identified, should be valuable tools in the study of apoptosis. Profiling MAC's pharmacology may generate novel therapeutic regimes for disease.

    Original languageEnglish (US)
    Pages (from-to)35-38
    Number of pages4
    JournalFEBS Letters
    Issue number1-3
    StatePublished - Jun 18 2004


    • Apoptosis
    • Bax
    • Cytochrome c
    • Ion channel
    • MAC, mitochondrial apoptosis-induced channel
    • Mitochondrial apoptosis-induced channel
    • PTP, permeability transition pore
    • Patch clamp
    • Pharmacology
    • Tim, translocase of the inner membrane

    ASJC Scopus subject areas

    • Biophysics
    • Structural Biology
    • Biochemistry
    • Molecular Biology
    • Genetics
    • Cell Biology


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