PKR Inhibitor III, 7DG

A cell-permeable gedunin analog that directly targets PKR via reversible interaction inhibits PKR-mediated cellular events by disrupting PKR signaling complexes assembly, such as IκK complex and inflammasome/pyroptosome, resulting in effective blockage of LPS-induced IκBβ degradaion (20 µM) and protection against anthrax toxin LT-induced caspase-1 activation as well as subsequent pyroptosis (10 µM) in murine macrophage J774 cultures. PKR is also known to mediate LT-induced apoptosis via its kinase activity in LPS-primed Macrophages derived from C57BL/6 with a resistent NLRP1 allele, inhibitable by C16 (Cat. Nos. 527450 & 527451), but not by 7DG, while LT-induced pyroptosis in J774 cultures is insensitive to C16 treatment.

A cell-permeable gedunin analog that directly targets PKR via reversible interaction without competing against ATP binding and inhibits PKR-mediated cellular events by disrupting PKR signaling complex assembly, such as IκK complex and inflammasome/pyroptosome, resulting in effective blockage of LPS-induced IκBβ degradaion (20 µM 7DG added 2 h prior to 10 ng/mL LPS) and protection against anthrax toxin LT-induced caspase-1 activation as well as subsequent pyroptosis (by 50% and 100%, respectively, at 5 and 10 µM; 2 h 7DG pretreatment prior to 6 h LT incubation) in J774A.1 BALB/c-derived murine macrophage J774 cultures. PKR is also known to mediate LT-induced apoptosis via its kinase activity in LPS-primed Macrophages derived from C57BL/6 with a resistent NLRP1 allele, inhibitable by C16 (Cat. Nos. 527450 & 527451), but not by 7DG, while LT-induced pyroptosis in J774 cultures is inhibited by 7DG, but insensitive to C16 treatment.

Cell permeable: yes

Primary Target
PKR

Reversible: yes

Packaged under inert gas

Toxicity: Standard Handling (A)

Following reconstitution, aliquot and freeze (-70°C). Stock solutions are stable for up to 6 months at -70°C.

Hett, E.C., et al. 2013. Nat. Chem. Biol.9, 398.

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