N-Desmethyltamoxifen, the principal metabolite of tamoxifen in humans, serves as an efficacious modulator of ceramide metabolism within human AML cells by inhibiting ceramide glycosylation, hydrolysis, and sphingosine phosphorylation. Although it demonstrates weak antiestrogenic properties, it acts as a protein kinase C (PKC) inhibitor with a potency ten times greater than that of tamoxifen.

N-desmethyltamoxifen, resulting from the CYP3A4/5-mediated catalysis of tamoxifen, is the major primary quantitative metabolite of tamoxifen. N-desmethyltamoxifen (20-500 ng/ml; 48 hours) has a profound inhibitory effect upon all seven glioma lines (T98G, U87, U138, U373, ALW, AUK, CAS cells). N-desmethyltamoxifen (1.5-10 μM; 114 hours) suppresses the growth of MCF 7 human mammary carcinoma cells. [1][2][3].