Regulation of the concentration of cytosolic calcium (Ca2+) is vital for the physiological function of many cell types. Three secondary messengers; inositol 1,4,5 trisphosphate (IP3), nicotinic acid adenine dinucleotide phosphate (NAADP) and cyclic adenosine diphosphate ribose (cADPR); have been identified as being able to induce Ca2+ release from organelle Ca2+ stores. Together these messengers allow for temporal and special coordination of Ca2+ signalling. Acute pancreatitis (AP) is inflammation of the pancreatitis and the surrounding tissue, caused by the improper activation of the digestive enzymes within the acinar cells. This pathological enzymatic activation has been linked to atypical Ca2+ signalling, with mass release from stores; resulting in mitochondrial overload and induction of necrosis. Both the neurotransmitter acetylcholine (ACh) and the hormone cholecystokinin (CCK) induce in release of Ca2+ from stores in pancreatic acinar cells (PAC). ACh has been shown to induce Ca2+ release via generation of IP3, while CCK has been suggested to mobilise Ca2+ via synthesis of NAADP. NAADP is unique from other secondary messengers as it induces calcium release from a thapsigargin resistant (non-endo/sarcoplasmic) store, shown to be composed of acidic organelles. PAC have a large pool of acidic organelles, mainly composed of zygomorphic granules, creating a significant store of NAADP sensitive Ca2+. Targeting this NAADP sensitive Ca2+ store by manipulating NAADP signalling should allow for an increased understanding of the role of Ca2+ in both the physiological and pathological function of PAC. Ned-19 is a NAADP antagonist discovered in a screen of the ZINC chemical library using NAADP’s 3D electrostatic structure. Its ability to inhibit NAADP induced Ca2+ release has been observed in several different mammalian tissue types and Ned-19 has been used to isolate NAADP’s role from that of that the other secondary Ca2+ signalling molecules. Initial experiments into the effect of Ned-19 on physiological Ca2+ signalling in PAC match the pattern expected by the secondary messengers implicated in the function of the stimulants used. With no changes in ACh induced Ca2+ release observed in the presence of Ned-19, but full to partial inhibition of CCK’s ability to increase cytosolic Ca2+ levels. One of the pathological causes of AP is reflux of bile acid in to the pancreases via the common bile duct. The bile acid taurolithocholic-acid-3-sulfate (TLC-S) has been shown to induces large Ca2+ release via a NAADP depend mechanism; however Ned-19 shows only the ability to delay this release and not inhibit it. Further study into Ned-19’s effect on other models of AP and its ability to affect cell fate will provide vital information as to its potential as a treatment for AP.