The co-administration of Descovy is not recommended with rifampicin. Interaction not studied with either of the components of Descovy. Co-administration of rifampicin, a P-gp inducer, may decrease tenofovir alafenamide plasma concentrations, which may result in loss of therapeutic effect and development of resistance.

Coadministration is expected to decrease concentrations of tenofovir alafenamide and is not recommended.

The drug interaction between tenofovir alafenamide (TAF) and rifampicin was evaluated in an open-label, three period sequential PK study in virologically suppressed people with HIV on antiretroviral treatment and co-treated with rifampicin. Steady-state tenofovir-diphosphate (TFV-DP) and plasma tenofovir concentrations were measured during three treatment periods: 1) TDF + rifampicin, 2) TAF + rifampicin and 3) TDF one month after completing TB treatment. TAF and TDF were dosed at the standard daily dose (25 mg and 300 mg) and were combined with efavirenz (600 mg) and either emtricitabine (200 mg) or lamivudine (300 mg). Eighteen participants were enrolled. TAF + rifampicin was associated with a TFV-DP AUC0-24h geometric mean ration (GMR) of 5.58 (95% CI 4.34, 7.17) and 5.43 (3.90, 7.55) when compared with TDF + rifampicin and TDF only, respectively. The plasma tenofovir AUC0-24h GMR was 0.07 (0.06, 0.09) when treatment with TAF + rifampicin was compared with both TDF + rifampicin and TDF only. This study showed that TAF and rifampicin coadministration was associated with higher tenofovir-diphosphate concentrations than TDF, both with and without rifampicin thereby confirming previous findings among healthy volunteers. This study supports the administration of standard dose of TAF with rifampicin in TB/HIV-1 infected people.

The pharmacokinetics of tenofovir alafenamide and tenofovir diphosphate were determined in healthy volunteers following administration of tenofovir alafenamide alone (25 mg once daily, with emtricitabine) and with rifampicin (600 mg once daily). Rifampicin decreased tenofovir alafenamide AUC and Cmax by 55% and 50%. Plasma tenofovir Cmax, C24 and AUC decreased by 65%, 55% and 54% respectively. Intracellular tenofovir diphosphate (i.e. active entity) concentrations Cmax, C24 and AUC decreased by 38%, 43% and 36%, respectively, but AUC was still 4.21-fold higher than that achieved with standard dose tenofovir-DF alone (300 mg once daily). Rifampicin did not alter emtricitabine pharmacokinetics.

The pharmacokinetics of tenofovir alafenamide and tenofovir diphosphate (TDF-DP) were determined following administration of tenofovir alafenamide alone (25 mg once daily, with bictegravir and emtricitabine) or tenofovir alafenamide (25 mg twice daily, with bictegravir and emtricitabine) and rifampicin (600 mg once daily). Following twice daily administration with rifampicin, the plasma AUC of tenofovir alafenamide and its active intracellular metabolite (TFV-DP) were modestly decreased by ~14% and ~24% when compared to tenofovir alafenamide once daily alone. This modest change is not expected to alter the efficacy of tenofovir alafenamide.