Table 3.
Drug interactions
| Drug | CYP | Mechanism | ||
|---|---|---|---|---|
| 2C9 | 2C19 | 3A4 | ||
| Contraindications | ||||
| Rifampin | ○ | Because of induction of the CYP3A4 metabolism by rifampin, rifampin decreased the steady-state C max and AUC of VRCZ | ||
| Rifabutin | ○ | Because of induction of the CYP3A4 metabolism by rifabutin, rifabutin decreased the steady-state C max and AUC of VRCZ | ||
| Because of inhibition of the CYP3A4 metabolism by VRCZ, VRCZ increased the steady-state C max and AUC of rifabutin | ||||
| Efavirenz | ○ | ○ | ○ | Because of induction of the CYP2C19 and 2C9 metabolism by efavirenz, efavirenz decreased the steady-state C max and AUC of VRCZ |
| Because of inhibition of the CYP3A4 metabolism by VRCZ, VRCZ increased the steady-state C max and AUC of efavirenz | ||||
| Ritonavir | ○ | ○ | Because of induction of the CYP2C19 and 2C9 metabolism by ritonavir, ritonavir decreased the steady-state C max and AUC of VRCZ | |
| Carbamazepine | ○ | Because of induction of the CYP3A4 metabolism by carbamazepine, carbamazepine decreased the steady-state C max and AUC of VRCZ | ||
| Barbital | ○ | Because of induction of the CYP3A4 metabolism by barbital, barbital decreased the steady-state C max and AUC of VRCZ | ||
| Phenobarbital | ○ | Because of induction of the CYP3A4 metabolism by phenobarbital, phenobarbital decreased the steady-state C max and AUC of VRCZ | ||
| Pimozide | ○ | Because of inhibition of the CYP3A4 metabolism by VRCZ, VRCZ increased plasma concentration and risk of cardiotoxicity (QT prolongation, torsade de pointes, cardiac arrest) of pimozide | ||
| Quinidine | ○ | Because of inhibition of the CYP3A4 metabolism by VRCZ, VRCZ increased plasma concentration and risk of cardiotoxicity (QT prolongation, torsade de pointes, cardiac arrest) of quinidine | ||
| Ergotamine | ○ | Because of inhibition of the CYP3A4 metabolism by VRCZ, VRCZ increased plasma concentration of ergot derivative and an increased risk of ergotism (nausea, vomiting, vasospastic ischemia) of ergotamine | ||
| Triazolam | ○ | Because of inhibition of the CYP3A4 triazolam metabolism by VRCZ, VRCZ increased plasma concentrations and potential of triazolam | ||
| Cautions | ||||
| Phenytoin | ○ | ○ | Because of induction of the CYP3A4 metabolism by phenytoin, phenytoin decreased the steady-state C max and AUC of VRCZ | |
| Because of inhibition of the CYP2C9 metabolism by VRCZ, VRCZ increased the steady-state C max and AUC of phenytoin | ||||
| Inhibitor of HIV protease (excluded indinavir): saquinavir, amprenavir, nelfinavir | ○ | Because of inhibition of the CYP3A4 metabolism by VRCZ, VRCZ increased plasma concentration of HIV protease inhibitor | ||
| Because of inhibition of the CYP3A4 metabolism by HIV protease inhibitor, HIV protease inhibitor increased plasma concentration of VRCZ | ||||
| (n*) nucleoside reverse transcriptase inhibitor (NNRTI): Delavirdine | ○ | Because of inhibition of the CYP3A4 metabolism by NNRTI, NNRTI increased plasma concentration of VRCZ | ||
| Because of induction of the CYP3A4 metabolism by NNRT, NNRT decreased plasma concentration of VRCZ | ||||
| Because of inhibition of the CYP3A4 metabolism by VRCZ VRCZ increased plasma concentration of NNRTI | ||||
| Cyclosporine | ○ | Because of inhibition of the CYP3A4 metabolism by VRCZ, VRCZ increased the steady-state C max and AUC of cyclosporine | ||
| Tacrolimus | ○ | Because of inhibition of the CYP3A4 metabolism by VRCZ, VRCZ increased the steady-state C max and AUC of tacrolimus | ||
| Warfarin | ○ | Because of inhibition of the CYP2C9 metabolism by VRCZ, VRCZ increased the prothrombin time of warfarin | ||
| Omeprazole | ○ | ○ | Because of inhibition of the CYP2C19 and 3A4 metabolism by VRCZ, VRCZ increased the steady-state C max and AUC of omeprazole | |
| Midazolam | ○ | Because of inhibition of the CYP3A4 metabolism by VRCZ, VRCZ increased plasma concentration of midazolam | ||
| HMG-CoA reductase inhibitor | ○ | Because of inhibition of the CYP3A4 metabolism by VRCZ, VRCZ increased plasma concentration of HMG-CoA reductase inhibitor | ||
| Diazepam | ○ | ○ | Because of inhibition of the CYP2C9 and 3A4 metabolism by VRCZ, VRCZ increased the steady-state AUC and elimination half-life of diazepam | |
| Zolpidem | ○ | ○ | Because of inhibition of the CYP2C9 and 3A4 metabolism by VRCZ, VRCZ increased the steady-state C max and AUC of zolpidem | |
| Sulfonylureas; tolbutamide | ○ | Because of inhibition of the CYP2C9 metabolism by VRCZ, VRCZ increased plasma concentration of sulfonylureas | ||
| Vinca alkaloids anticancer agents | ○ | Because of inhibition of the CYP3A4 metabolism by VRCZ, VRCZ increased plasma concentration of vinca alkaloids | ||
| Vincristine | ||||
| Vinblastine | ||||
| Oxycodone | ○ | Because of inhibition of the CYP3A4 metabolism by VRCZ, VRCZ increased the steady-state C max and AUC of oxycodone | ||
| Fentanyl | ○ | Because of inhibition of the CYP3A4 metabolism by VRCZ, VRCZ increased the steady-state AUC of fentanyl | ||
| Ibuprofen | ○ | Because of inhibition of the CYP2C9 metabolism by VRCZ, VRCZ increased steady-state C max and AUC of ibuprofen | ||
| Diclofenac | ○ | Because of inhibition of the CYP2C9 metabolism by VRCZ, VRCZ increased steady-state C max and AUC of diclofenac | ||
| Oral contraceptive; norethindrone and ethinyl estradiol | ○ | ○ | Because of inhibition of the CYP2C19 metabolism by norethindrone and ethinyl estradiol, norethindrone and ethinyl estradiol increased steady-state C max and AUC of VRCZ | |
| Because of inhibition of the CYP3A4 metabolism by VRCZ, VRCZ increased steady-state C max and AUC of norethindrone and ethinyl estradiol | ||||
| St. John’s wort | ○ | ○ | Because of induction of the CYP3A4 and 2C19 metabolism by St. John’s wort, St. John’s wort decreased the steady-state AUC of VRCZ | |
| Overseas reference | ||||
| Sirolimus | ○ | Because of inhibition of the CYP3A4 metabolism by VRCZ, VRCZ increased the steady-state C max and AUC of sirolimus | ||
| Digoxin, cimetidine, ranitidine | No change | |||