Moncada-Basualto, MMMoncada-BasualtoAbarca, BelenBelenAbarcaAguilera-Venegas, BenjaminBenjaminAguilera-VenegasBallesteros, RafaelRafaelBallesterosBallesteros-Garrido, RafaelRafaelBallesteros-GarridoGonzalez-Herrera, FabiolaFabiolaGonzalez-HerreraGuzman-Rivera, DanielaDanielaGuzman-RiveraKemmerling, UlrikeUlrikeKemmerlingLapier, MichelMichelLapierMaya, Juan D.Juan D.MayaMoncada-Basualto, MauricioMauricioMoncada-BasualtoOlea-Azar, ClaudioClaudioOlea-AzarPesce, BarbaraBarbaraPesce2025-04-232025-04-23201910.4155/fmc-2018-0242https://sic.vriic.usach.cl/entities/publication/f88f7fbb-461d-447d-b488-fe780c558b47Aim: To study a new series of [1,2,3]triazolo[1,5-α]pyridine derivatives as trypanocidal agents because current antichagasic pharmacologic therapy is only partially effective. Materials & methods: The effect of the series upon Trypanosoma cruzi epimastigotes and murine macrophages viability, cell cycle, cell death and on the metabolites of the sterol biosynthesis pathway was measured; also, docking in 14α-demethylase was analyzed. Results: Compound 16 inhibits 14α-demethylase producing an imbalance in the cholesterol/ergosterol synthesis pathway, as suggested by a metabolic control and theoretical docking analysis. Consequently, it prevented cell proliferation, stopping the cellular cycle at the G2/M phase, inducing cell death. Conclusion: Although the exact cell death mechanism remained elusive, this series can be used for the further rational design of novel antiparasitic molecules. © 2019 Newlands Press.en-US14α-demethylasecell cycle arrestmass spectrometrysqualene/cholesterol-ergosterol balancetriazolopyridine derivativeshttps://doi.org/10.4155/fmc-2018-0242