SEARCHING FOR THERAPIES  Some compounds have shown promise in reducing intracellular trypsin activation, which triggers acute pancreatitis. Calmodulin, a cytosolic calcium-binding protein found in normally functioning acinar cells, prevents ethanol from eliciting the release of substantial amounts of Ca2+ from intracellular stores, which can prematurely activate trypsin. Small peptide activators of calmodulin (such as CALP-3) can be added to the outside of acinar cells to help mobilize calmodulin and prevent the toxic effects of high alcohol concentrations. Calmodulin helps prevent trypsin activation by binding to inositol trisphosphate receptors (IP3Rs), which inhibits Ca2+ release from ZGs. Caffeine has been shown to have similar inhibitory effects on IP3Rs in ZG membranes (A).There is also the potential for small molecule therapies that interfere with CRAC function and thus alter the influx of extracellular Ca2+ (B).
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