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The activity of double-stranded RNA-activated protein kinase (PKR) is altered by viral infection as well as by various neuropathologies.[1],[2] A primary phosphorylation target of PKR is eukaryotic initiation factor 2 subunit α (eIF2α), blocking translation and driving apoptosis.3 PKR Inhibitor is an oxindole/imidazole derivative that binds the ATP-binding site of PKR and blocks autophosphorylation with an IC50 value of 186-210 nM.[3] PKR Inhibitor protects human neuroblastoma cells against cell damage triggered by tunicamycin-mediated endoplasmic reticulum stress.[4] It also prevents phosphorylation of Fas-associated protein with a death domain (FADD) in neuroblastoma cells, preventing FADD-dependent activation of caspases and apoptosis.[1] Intraperitoneal administration of PKR inhibitor in rats reduces phosphorylation of PKR and eIF2α in the brain.[5] Similar administration in mice enhances long-term memory storage, including contextual and auditory long-term fear memories.[2]

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