Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal form of cancer characterized by drug resistance, urging new therapeutic strategies. In recent years, protein kinases have emerged as promising pharmacological targets for the treatment of several solid and haematological tumors. Interestingly, cyclin dependent kinase 1 (CDK1) is overexpressed in PDAC tissues, and has been correlated to the aggressive nature of these tumors because of its key role in cell cycle progression, and resistance to induction of apoptosis. For these reasons CDK1 is also reported among the main causes of chemoresistance, representing a promising pharmacological target. Herein researchers reported the synthesis of new 1,2,4-oxadiazole compounds, and evaluated their ability in inhibiting cell growth in PATU-T, Hs766T and HPAF-II cell lines, and a primary PDAC cell culture (PDAC3). Compound 6b was the most active compound, with IC₅₀ values ranging from 5.7 to 10.7 μM. Molecular docking studies of 6b into the active site of CDK1 showed the ability of the compound to interact effectively with the adenine binding pocket. Therefore, they assessed its ability to induce the apoptosis (increased of 1.5- and 2-fold in PATU-T and PDAC3 cells, respectively) and to inhibit  CDK1 expression, which was reduced up to 55% in Hs766T. Lastly, compound 6b passed the ADME  prediction studies showing good pharmacokinetic parameters. These data demonstrate that 6b displays cytotoxic activity, induces apoptosis and targets CDK1, supporting further studies for the development of similar compounds against PDAC.