19-norandrosterone is the main phase I metabolite of the synthetic androgenic anabolic steroid (AAS) 19-nortestosterone (or nandrolone). Once formed 19-norandrosterone undergoes conjugation reaction catalyzed mainly by the uridine diphospho glucuronosyltransferases (UDPGTs) to form the corresponding glucuro-conjugated. Due to the fact that the presence of 19-norandrosterone in urine is not unambiguously linked to the intentional administration of nandrolone or its precursors, but also to the natural production (i.e during pregnancy), interference through other drugs (i.e. administration of progestinic agents), ingestion of meat from treated animals, and degradation processes during storage (active urine), a threshold value of 2 ng/mL was set by the World Anti-Doping Agency (WADA). In other words, a urinary concentration of 19-norandrosterone below 2 ng/mL represents a negative result, and no supplementary analytical investigation (i.e. IRMS analysis) is required. Factors (physiological and environmental), interfering with the glucuronidation rate of 19-norandrosterone might alter its urinary levels increasing the risk to give incorrect results in occasion of doping control tests. Here the ability of non-prohibited agents (benzodiazepines, antifungals and non-steroidal anti-inflammatory drugs) in altering phase II metabolic profile of 19-norandrosterone was evaluated by in vitro assays. Our results show that the glucuronidation of 19-norandrosterone is principally carried out by UGT2B7 and UGT2B17 isoenzymes and to a lesser degree by the UGT1A3, UGT1A4, UGT2B4 and UGT2B10 isoforms. Furthermore, our data also show that in the presence of ketoconazole and miconazole, a marked decrease in glucuronidation rate of 19-norandrosterone was registered; moderate variations were instead measured in the presence of diclofenac and triazolam and no appreciable modifications were registered in the presence of the others agents considered.