Hereditary pancreatitis (HP) is an inflammatory genetic condition typically caused by uncontrolled activation of trypsin within the pancreas. Discrepancies in key HP genes such as the cationic trypsinogen gene PRSS1 and the trypsin inhibitor SPINK1 leads to difficulties when attempting to model the mutations which drive HP within animal models. Patient derived pancreatic organoids present the opportunity to better study this condition, providing a platform to model gene mutations which have not been successfully replicated in animal models. We have grown organoids both from healthy pancreas and from PRSS1 mutant HP samples. Pancreatic organoids were derived from samples taken from islet isolations, with HP samples originating from patients undergoing total pancreatectomy with islet auto transplantation (TPIAT). These organoids were embedded within a Matrigel matrix and cultured with a complex organoid growth medium. Phase contrast microscopy images were taken to track organoid growth over time. Organoids were further characterized via qPCR and immunohistochemistry to determine whether they maintained an acinar phenotype and gene expression relevant to HP. Furthermore, a colorimetric assay was used to determine the level of active trypsin within both normal and HP organoids, allowing for insight into the effect of patient PRSS1 mutations. Organoids were successfully grown from HP samples and displayed growth comparable to those of normal pancreas. Characterization of these organoids showed expression of acinar genes including PRSS1 and amylase, alongside the presence of ductal genes such as Krt19, indicating the beginnings of acinar to ductal metaplasia (ADM). This gene expression data was corroborated in immunohistochemistry staining, showing a gradual loss in acinar protein in favor of a ductal phenotype. We have demonstrated one of the first instances of growing organoids from HP patient samples, displaying that they maintain the expression of relevant acinar genes for a time, although they gradually transition to a more duct like state over the course of culturing. These organoid models have the potential to provide a platform for deeper research into HP, including a better understanding of unique patient gene mutations and the development of new treatments.