Skip to main content
. 2014 May;88(10):5263–5276. doi: 10.1128/JVI.03688-13

TABLE 1.

Chemicals used to inhibit specific death pathways in H-1PV-infected PDAC cells

Inhibitor Source Specific process/target Mechanism of action and specific intracellular effects Effective dose range Dose used
Z-VAD-FMK R&D Systems Apoptosis (pan-caspases) Cell permeative, irreversibly binds to caspases' catalytic sites; caspase inactivation might cause a shift toward necrosis 50 nM–100 μM 10 μM
3-MA Sigma Autophagy Cell-permeating autophagic sequestration blocker; class III phosphatidylinositol 3-kinase (PI3K) inhibitor 5–10 mM 1 mM
Ac-LVK-CHO Calbiochem Cathepsin B Water-soluble cathepsin B inhibitor 10–50 nM 50 nM
CA-074 Me Sigma Cathepsin B Cell-permeating, irreversible, selective cathepsin B inhibitor; activity depends on intracellular esterases 1–10 μM 1 μM
Z-FL-COCHO Calbiochem Cathepsin S Slow, tight-binding, reversible inhibitor of cathepsin S 1–2 nM 1 μM
IM-54 Calbiochem Oxidative stress-induced necrosis Cell-permeating selective inhibitor of H2O2-induced necrosis; does not display antioxidant properties 1–10 μM 10 μM
Necrostatin-1 Sigma Necroptosis (RIP1 kinase) Inhibits RIP1 kinase and nonapoptotic cell death; inhibits MMP in TNF-α-treated Jurkat cells 20–300 μM 20 μM