Parasites of the genus Plasmodium responsible for Malaria are obligate intracellular pathogens residing in mammalian red blood cells, hepatocytes, or mosquito midgut epithelial cells. Regarding that detailed knowledge on the sphingolipid biosynthetic pathway of the apicomplexan protozoan parasites is scarce, different stages of Plasmodium falciparum were treated with tamoxifen in order to evaluate the effects of this drug on' the glycosphingolipid biosynthesis. Thin layer chromatography, High performance reverse phase chromatography and UV-MALDI-TOF mass spectrometry were the tools used for the analysis. In the ring forms, the increase of NBD-phosphatidyl inositol biosynthesis was notorious but differences at NBD-GlcCer levels were undetedable. In trophozoite forms, an abrupt decrease of NBD-acylated GIcDHCer and NBD-GlcDHCer in addition to an increase of NBD-PC biosynthesis was observed. On the contrary, in schizonts, tamoxifen seems not to be producing substantial changes in lipid biosynthesis. Our findings indicate, that in this parasite, tamoxifen is exerting an inhibitory action on Glucosylcer-amidesynthase and sphingomyelin synthase levels. Moreover, regarding that Plasmodium does not bio-synthesize inositolphosphoceramides, the accumulation of phosphatidylinositol should indicate an inhibitoiy action on glycosylinositol phospholipid synthesis. (C) 2018 Elsevier Inc. All rights reserved.