Coadministration has not been studied. Tolbutamide is mainly metabolized by CYP2C9 and to a lesser extent by CYPs 2C8 and 2C19. In vitro and in vivo data indicate that ritonavir is a weak inducer of CYP2C9 and could potentially decrease tolbutamide concentrations, but to a moderate extent. Monitor clinical effect and increase tolbutamide dosage if needed.

Coadministration has not been studied. Metformin is mainly eliminated unchanged in the urine (via OCT2) and elvitegravir/cobicistat is unlikely to inhibit OCTs at clinically relevant concentrations. However, cobicistat reversibly inhibits MATE1, and concentrations of metformin may be increased when coadministered. Careful patient monitoring and dosage adjustment of metformin is recommended.

Coadministration has not been studied. Metformin is mainly eliminated unchanged in the urine (via OCT2) and elvitegravir/cobicistat is unlikely to inhibit OCTs at clinically relevant concentrations. However, cobicistat reversibly inhibits MATE1, and concentrations of metformin may be increased when coadministered. Careful patient monitoring and dosage adjustment of metformin is recommended.

Coadministration has not been studied. Exenatide is primarily eliminated by glomerular filtration therefore no interaction is expected at the level of drug elimination. However, caution is needed when coadministering rilpivirine and GLP-1 agonists such as exenatide due to their potential to inhibit gastric secretion and thereby reduce the absorption of rilpivirine. Furthermore, exenatide has the potential to slow gastric emptying. Consider taking rilpivirine 4 hours before the GLP-1 agonist.

Coadministration has not been studied. Glipizide is mainly metabolized by CYP2C9. In vitro and in vivo data indicate that ritonavir is a weak inducer of CYP2C9. Lopinavir/ritonavir could potentially decrease glipizide concentrations, although to a moderate extent. Monitor clinical effect and increase glipizide dosage if needed.

Coadministration of metformin (500 mg twice daily) was studied with dolutegravir (50 mg once or twice daily) in 15 subjects. Coadministration with once daily dolutegravir increased metformin Cmax and AUC by 66% and 79%, whereas coadministration with twice daily dolutegravir increased metformin Cmax and AUC by 111% and 145%. A dose adjustment of metformin should be considered when starting and stopping coadministration of dolutegravir with metformin in order to maintain glycaemic control. The US Prescribing Information suggests limiting the total daily dose of metformin to 1000 mg when starting metformin or dolutegravir. However, limiting metformin to 1000 mg daily may result in subtherapeutic exposures in obese people living with HIV as administration of metformin (1000 mg) and dolutegravir (50 mg daily) to obese women living with HIV (n=15; mean BMI of 45.6 kg/m2 (range 35.6-56.7)) resulted in metformin and dolutegravir concentrations which were approximately half of that in historical non-obese healthy volunteers. Monitoring renal function during coadministration and monitoring blood glucose when starting and stopping coadministration is recommended. As metformin is eliminated renally, patients with moderate renal impairment may be at increased risk for lactic acidosis due to increased metformin concentrations.

Coadministration has not been studied. Gliclazide is metabolized mainly by CYP2C9 and to a lesser extent by CYP2C19. In vitro and in vivo data indicate that ritonavir is a weak inducer of CYP2C9. Lopinavir/ritonavir could potentially decrease gliclazide concentrations, although to a moderate extent. Monitor clinical effect and increase gliclazide dosage if needed.

Coadministration has not been studied. Glimepiride is mainly metabolized by CYP2C9. In vitro and in vivo data indicate that ritonavir is a weak inducer of CYP2C9. Lopinavir/ritonavir could potentially decrease glimepiride concentrations, although to a moderate extent. Monitor clinical effect and increase glimepiride dosage if needed.

Coadministration has not been studied. Liraglutide is degraded by endogenous endopeptidases therefore no metabolic interaction is expected. However, caution is needed when coadministering rilpivirine and GLP-1 agonists such as liraglutide due to their potential to inhibit gastric secretion and thereby reduce the absorption of rilpivirine. Consider taking rilpivirine 4 hours before the GLP-1 agonist.

Coadministration has not been studied but lopinavir/ritonavir could potentially increase saxagliptin exposure as saxagliptin is mainly metabolized by CYP3A4/5. The US Prescribing Information for saxagliptin states the recommended dose of saxagliptin to be 2.5 mg once daily when coadministered with strong cytochrome P450 3A4/5 (CYP3A4/5) inhibitors, (e.g., atazanavir, indinavir, nelfinavir, ritonavir, saquinavir).

Coadministration has not been studied. Exenatide is primarily eliminated by glomerular filtration therefore no interaction is expected at the level of drug elimination. However, caution is needed when coadministering rilpivirine and GLP-1 agonists such as exenatide due to their potential to inhibit gastric secretion and thereby reduce the absorption of rilpivirine. Furthermore, exenatide has the potential to slow gastric emptying. Consider taking rilpivirine 4 hours before the GLP-1 agonist.

Coadministration has not been studied. Liraglutide is degraded by endogenous endopeptidases therefore no metabolic interaction is expected. However, caution is needed when coadministering rilpivirine and GLP-1 agonists such as liraglutide due to their potential to inhibit gastric secretion and thereby reduce the absorption of rilpivirine. Consider taking rilpivirine 4 hours before the GLP-1 agonist.

Coadministration has not been studied. Glimepiride is mainly metabolized by CYP2C9. In vitro and in vivo data indicate that ritonavir is a weak inducer of CYP2C9 and could potentially decrease glimepiride concentrations, although to a moderate extent. Monitor clinical effect and increase glimepiride dosage if needed.

Coadministration has not been studied. Glipizide is mainly metabolized by CYP2C9. In vitro and in vivo data indicate that ritonavir is a weak inducer of CYP2C9 and could potentially decrease glipizide concentrations, although to a moderate extent. Monitor clinical effect and increase glipizide dosage if needed.

Coadministration has not been studied. Gliclazide is metabolized mainly by CYP2C9 and to a lesser extent by CYP2C19. In vitro and in vivo data indicate that ritonavir is a weak inducer of CYP2C9 and could potentially decrease gliclazide concentrations, although to a moderate extent. Monitor clinical effect and increase gliclazide dosage if needed.

Coadministration has not been studied. Nateglinide is metabolized mainly by CYP2C9 (70%) and to a lesser extent by CYP3A4 (30%) and in vivo data indicate that ritonavir is a weak inducer of CYP2C9. The net clinical effect of this interaction is difficult to predict as lopinavir/ritonavir could potentially decrease nateglinide concentrations (induction CYP2C9) or increase nateglinide concentrations (inhibition CYP3A4). Monitor clinical effect and adjust nateglinide dosage as needed.

Coadministration has not been studied. Nateglinide is metabolized mainly by CYP2C9 (70%) and to a lesser extent by CYP3A4 (30%) and in vivo data indicate that ritonavir is a weak inducer of CYP2C9. The net clinical effect of this interaction is difficult to predict as ritonavir could potentially decrease nateglinide concentrations (induction CYP2C9) or increase nateglinide concentrations (inhibition CYP3A4). Monitor clinical effect and adjust nateglinide dosage as needed.

Coadministration has not been studied. Tolbutamide is mainly metabolized by CYP2C9 and to a lesser extent by CYPs 2C8 and 2C19. In vitro and in vivo data indicate that lopinavir/ritonavir is a weak inducer of CYP2C9 and could potentially decrease tolbutamide concentrations, but to a moderate extent. Monitor clinical effect and increase tolbutamide dosage if needed.

Coadministration has not been studied. Repaglinide is metabolized by CYP2C8 and CYP3A4 and is a substrate of the hepatic transporter OATP1B1. Ritonavir dosed as a pharmacokinetic booster is a weak inducer of CYP2C8 and a strong inhibitor of CYP3A4. Lopinavir/ritonavir could potentially increase repaglinide concentrations. Monitor clinical effect and decrease repaglinide dosage if needed.

Coadministration has not been studied. Repaglinide is metabolized by CYP2C8 and CYP3A4 and is a substrate of the hepatic transporter OATP1B1. Ritonavir dosed as a pharmacokinetic booster is a weak inducer of CYP2C8 and a strong inhibitor of CYP3A4. Ritonavir could potentially increase repaglinide concentrations. Monitor clinical effect and decrease repaglinide dosage if needed.

Coadministration has not been studied. Pioglitazone is metabolized mainly by CYP2C8 and to a lesser extent by CYPs 3A4, 1A2 and 2C9. Elvitegravir/cobicistat could potentially increase pioglitazone concentrations, although to a moderate extent. No a priori dosage adjustment is required. Emtricitabine and tenofovir-DF do not interact with this metabolic pathway.

Coadministration has not been studied. Pioglitazone is metabolized by mainly CYP2C8 and to a lesser extent by CYPs 3A4, 1A2 and 2C9. Ritonavir dosed as a pharmacokinetic booster is a weak inducer of CYP2C8 and a strong inhibitor of CYP3A4. Ritonavir could potentially increase pioglitazone exposure, although to a moderate extent. No a priori dosage adjustment is required.

Rosiglitazone is metabolized mainly by CYP2C8 and to a lesser extent by CYP2C9. Ritonavir is a weak inducer of CYP2C8 and CYP2C9. Lopinavir/ritonavir could potentially decrease rosiglitazone concentrations, but to a moderate extent. Data from 4 HIV+ subjects showed no significant effect of rosiglitazone on lopinavir Cmax, AUC or Cmin. No a priori dosage adjustment is needed.

Coadministration has not been studied. Pioglitazone is metabolized mainly by CYP2C8 and to a lesser extent by CYPs 3A4, 1A2 and 2C9. Elvitegravir/cobicistat could potentially increase pioglitazone concentrations, although to a moderate extent. No a priori dosage adjustment is required. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway.

Coadministration has not been studied. Pioglitazone is metabolized by mainly CYP2C8 and to a lesser extent by CYPs 3A4, 1A2 and 2C9. Ritonavir dosed as a pharmacokinetic booster is a weak inducer of CYP2C8 and a strong inhibitor of CYP3A4. Lopinavir/ritonavir could potentially increase pioglitazone exposure, although to a moderate extent. No a priori dosage adjustment is required.

Coadministration has not been studied. Rosiglitazone is metabolized mainly by CYP2C8 and to a lesser extent by CYP2C9. Ritonavir is a weak inducer of CYP2C8 and CYP2C9 and could potentially decrease rosiglitazone concentrations, but to a moderate extent. No a priori dosage adjustment is needed.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant drug-drug interaction is unlikely. Rosiglitazone is metabolized mainly by CYP2C8 and to a lesser extent by CYP2C9. Rilpivirine at a dose of 25 mg once daily is unlikely to have a clinically relevant effect on the exposure of medicinal products metabolised by CYP enzymes.

Metformin is mainly eliminated unchanged in the urine (via OCT2). Coadministration of metformin (850 mg single dose) and rilpivirine did not significantly change metformin pharmacokinetics.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as exenatide is primarily eliminated by glomerular filtration. However, as exenatide slows gastric emptying it is advisable to take ritonavir at least 1 hour before an exenatide injection. [Note: this interaction is not specific for ritonavir, but for any medication taken with exenatide.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as exenatide is primarily eliminated by glomerular filtration. However, as exenatide slows gastric emptying it is advisable to take lopinavir/ritonavir at least 1 hour before an exenatide injection. [Note: this interaction is not specific for lopinavir/ritonavir, but for any medication taken with exenatide.]

Coadministration with lopinavir/ritonavir has not been studied. Linagliptin is mainly eliminated as parent compound in faeces and metabolism by CYP3A4 represents a minor elimination pathway. Coadministration of linagliptin (5 mg single dose) and ritonavir (200 mg twice daily for 3 days) increased linagliptin AUC and Cmax by 2-fold and 3-fold respectively, but these changes were not considered to be clinically relevant. Lopinavir/ritonavir could potentially increase linagliptin concentrations, however, this increase is unlikely to be clinically significant as the drug is mainly eliminated unchanged and has a large safety window.

Linagliptin is mainly eliminated as parent compound in faeces and metabolism by CYP3A4 represents a minor elimination pathway. Coadministration of linagliptin (5 mg single dose) and ritonavir (200 mg twice daily for 3 days) increased linagliptin AUC and Cmax by 2-fold and 3-fold respectively, but these changes were not considered to be clinically relevant as the drug is mainly eliminated unchanged and has a large safety window.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Sitagliptin is primarily eliminated in urine as unchanged drug (active secretion by OAT3, OATP4C1, P-gp) and metabolism by CYP3A4 represents a minor elimination pathway. There is little potential for an interaction with tenofovir via competition for these transporters.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Sitagliptin is primarily eliminated in urine as unchanged drug (active secretion by OAT3, OATP4C1, P-gp) and metabolism by CYP3A4 represents a minor elimination pathway. There is little potential for an interaction with emtricitabine via competition for these transporters.

Coadministration has not been studied. Sitagliptin is primarily eliminated in urine as unchanged drug (active secretion by OAT3, OATP4C1, P-gp) and metabolism by CYP3A4 represents a minor elimination pathway. Metabolism may play a more significant role in the elimination of sitagliptin in the setting of severe renal impairment or end-stage renal disease (ESRD). Lopinavir/ritonavir could potentially increase sitagliptin concentrations. However, this increase may not be clinically significant as the drug is mainly eliminated unchanged and has a large safety window. The European SPC for sitagliptin warns that potent CYP3A4 inhibitors (i.e., ritonavir) could alter the pharmacokinetics of sitagliptin in patients with severe renal impairment or ESRD but this has not been assessed in a clinical study.

Coadministration has not been studied. Sitagliptin is primarily eliminated in urine as unchanged drug (active secretion by OAT3, OATP4C1, P-gp) and metabolism by CYP3A4 represents a minor elimination pathway. Metabolism may play a more significant role in the elimination of sitagliptin in the setting of severe renal impairment or end-stage renal disease (ESRD). Ritonavir could potentially increase sitagliptin concentrations. However, this increase may not be clinically significant as the drug is mainly eliminated unchanged and has a large safety window. The European SPC for sitagliptin warns that potent CYP3A4 inhibitors (i.e., ritonavir) could alter the pharmacokinetics of sitagliptin in patients with severe renal impairment or ESRD but this has not been assessed in a clinical study.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Sitagliptin is primarily eliminated in urine as unchanged drug (active secretion by OAT3, OATP4C1, P-gp) and metabolism by CYP3A4 represents a minor elimination pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as exenatide is cleared mainly by glomerular filtration.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. After ingestion of acarbose, the majority of active unchanged drug remains in the lumen of the gastrointestinal tract to exert its pharmacological activity and is metabolised by intestinal enzymes and by the microbial flora.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as exenatide is cleared mainly by glomerular filtration. However, as exenatide slows gastric emptying it is advisable to take Genvoya at least 1 hour before an exenatide injection. [Note: this interaction is not specific for Genvoya, but for any medication taken with exenatide.]

Coadministration has not been studied. Sitagliptin is primarily eliminated in urine as unchanged drug (active secretion by OAT3, OATP4C1, P-gp) and metabolism by CYP3A4 represents a minor elimination pathway. Metabolism may play a more significant role in the elimination of sitagliptin in the setting of severe renal impairment or end-stage renal disease (ESRD). Elvitegravir/cobicistat could potentially increase sitagliptin concentrations. However, this increase may not be clinically significant as the drug is mainly eliminated unchanged and has a large safety window. The European SPC for sitagliptin warns that potent CYP3A4 inhibitors (i.e., ritonavir) could alter the pharmacokinetics of sitagliptin in patients with severe renal impairment or ESRD but this has not been assessed in a clinical study. Emtricitabine and tenofovir derived from tenofovir alafenamide are unlikely to interfere with the renal transporters involved in sitagliptin’s active secretion.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as exenatide is cleared mainly by glomerular filtration. However, as exenatide slows gastric emptying it is advisable to take Stribild at least 1 hour before an exenatide injection. [Note: this interaction is not specific for Stribild, but for any medication taken with exenatide.]

Coadministration has not been studied. Sitagliptin is primarily eliminated in urine as unchanged drug (active secretion by OAT3, OATP4C1, P-gp) and metabolism by CYP3A4 represents a minor elimination pathway. Metabolism may play a more significant role in the elimination of sitagliptin in the setting of severe renal impairment or end-stage renal disease (ESRD). Elvitegravir/cobicistat could potentially increase sitagliptin concentrations. However, this increase may not be clinically significant as the drug is mainly eliminated unchanged and has a large safety window. The European SPC for sitagliptin warns that potent CYP3A4 inhibitors (i.e., ritonavir) could alter the pharmacokinetics of sitagliptin in patients with severe renal impairment or ESRD but this has not been assessed in a clinical study. Emtricitabine and tenofovir are unlikely to interfere with the renal transporters involved in sitagliptin’s active secretion.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. After ingestion of acarbose, the majority of active unchanged drug remains in the lumen of the gastrointestinal tract to exert its pharmacological activity and is metabolised by intestinal enzymes and by the microbial flora. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically relevant drug interaction is unlikely as exenatide is cleared mainly by glomerular filtration. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glibenclamide is mainly metabolized by CYP3A4 and to a lesser extent by CYP2C9. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gliclazide is metabolized mainly by CYP2C9 and to a lesser extent by CYP2C19. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically relevant drug interaction is unlikely. Glimepiride is mainly metabolized by CYP2C9. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glipizide is mainly metabolized by CYP2C9. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Linagliptin is mainly eliminated as parent compound in faeces with metabolism by CYP3A4 representing a minor elimination pathway. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metformin is mainly eliminated unchanged in the urine (via OCT2). Emtricitabine and tenofovir derived from tenofovir alafenamide are unlikely to interfere as they are excreted by different renal transporters. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nateglinide is mainly metabolized by CYP2C9 (70%) and to a lesser extent CYP3A4 (30%). Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pioglitazone is metabolized mainly by CYP2C8 and to a lesser extent by CYPs 3A4, 1A2 and 2C9. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Repaglinide is metabolized by CYP2C8 and 3A4 and clinical data seem to indicate that it is a substrate of the hepatic transporter OATP1B1. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rosiglitazone is metabolized mainly by CYP2C8 and to a lesser extent by CYP2C9. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Saxagliptin is mainly metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Sitagliptin is primarily eliminated in urine as unchanged drug (active secretion by OAT3, OATP4C1, P-gp). Emtricitabine and tenofovir derived from tenofovir alafenamide are unlikely to interfere with the renal transporters involved in sitagliptin’s active secretion. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tolbutamide is mainly metabolized by CYP2C9 and to a lesser extent by CYPs 2C8 and 2C19. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically relevant drug interaction is unlikely as vildagliptin is inactivated via non CYP mediated hydrolysis. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied, but based on metabolism and clearance a clinically significant interaction is unlikely as liraglutide is degraded by endogenous endopeptidases.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. After ingestion of acarbose, the majority of active unchanged drug remains in the lumen of the gastrointestinal tract to exert its pharmacological activity and is metabolised by intestinal enzymes and by the microbial flora. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glibenclamide is mainly metabolized by CYP3A4 and to a lesser extent by CYP2C9. Rilpivirine at a dose of 25 mg once daily is unlikely to have a clinically relevant effect on the exposure of medicinal products metabolised by CYP enzymes. Emtricitabine and tenofovir alafenamide do not interact with glibenclamide metabolic pathway. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gliclazide is metabolized mainly by CYP2C9 and to a lesser extent by CYP2C19. Rilpivirine, emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glipizide is mainly metabolized by CYP2C9. Rilpivirine, emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Linagliptin is mainly eliminated as parent compound in faeces with metabolism by CYP3A4 representing a minor elimination pathway. Rilpivirine at a dose of 25 mg once daily is unlikely to have a clinically relevant effect on the exposure of medicinal products metabolised by CYP enzymes. Emtricitabine and tenofovir alafenamide do not interact with linagliptin metabolic pathway.

Coadministration with rilpivirine, emtricitabine and tenofovir alafenamide has not been studied. Metformin is mainly eliminated unchanged in the urine (via OCT2). Coadministration of metformin (850 mg single dose) and rilpivirine did not significantly change metformin pharmacokinetics. Emtricitabine and tenofovir derived from tenofovir alafenamide are unlikely to interact as they are excreted by different renal transporters. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nateglinide is mainly metabolized by CYP2C9 (70%) and to a lesser extent by CYP3A4 (30%). Rilpivirine, emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pioglitazone is metabolized mainly by CYP2C8 and to a lesser extent by CYPs 3A4, 1A2 and 2C9. Rilpivirine, emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Repaglinide is metabolized by CYP2C8 and CYP3A4 and clinical data seem to indicate that it is a substrate of the hepatic transporter OATP1B1. Rilpivirine, emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rosiglitazone is metabolized mainly by CYP2C8 and to a lesser extent by CYP2C9. Rilpivirine, emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Saxagliptin is mainly metabolized by CYP3A4. Rilpivirine at a dose of 25 mg once daily is unlikely to have a clinically relevant effect on the exposure of medicinal products metabolised by CYP enzymes. Emtricitabine and tenofovir alafenamide do not interact with saxagliptin metabolic pathway. 

Coadministration has not been studied but based on metabolism and clearance a clinically relevant drug interaction is unlikely. Sitagliptin is primarily eliminated in urine as unchanged drug (active secretion by OAT3, OATP4C1, P-gp) and metabolism by CYP3A4 represents a minor elimination pathway. Rilpivirine at a dose of 25 mg once daily is unlikely to have a clinically relevant effect on the exposure of medicinal products metabolised by CYP enzymes. Emtricitabine and tenofovir derived from tenofovir alafenamide are unlikely to interfere with the renal transporters involved in sitagliptin’s active secretion. 

Coadministration has not been studied but based on metabolism and clearance a clinically relevant drug interaction is unlikely. Tolbutamide is mainly metabolized by CYP2C9 and to a lesser extent by CYPs 2C8 and 2C19. Rilpivirine, emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as vildagliptin is inactivated via non-CYP mediated hydrolysis. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glimepiride is mainly metabolized by CYP2C9. Rilpivirine, emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is metabolised by UGTs and is a substrate of P-gp, BCRP, OAT3 and OATP1B1/1B3. Although lopinavir/ritonavir inhibits P-gp and OATP, data with verapamil (a P-gp inhibitor) and rifampicin (an OATP1B1/1B3 inhibitor) suggest a clinically relevant effect on empagliflozin is unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is metabolised by UGTs and is a substrate of P-gp, BCRP, OAT3 and OATP1B1/1B3. Although ritonavir inhibits P-gp and OATP, data with verapamil (a P-gp inhibitor) and rifampicin (an OATP1B1/1B3 inhibitor) suggest a clinically relevant effect on empagliflozin is unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. Although cobicistat inhibits P-gp, BCRP and OATP1B1/3, data with verapamil (a P-gp inhibitor) and rifampicin (an OATP1B1/1B3 inhibitor) suggest a clinically relevant effect on empagliflozin is unlikely.

Coadministration has not been studied. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. Although cobicistat inhibits P-gp, BCRP and OATP1B1/3, data with verapamil (a P-gp inhibitor) and rifampicin (an OATP1B1/1B3 inhibitor) suggest a clinically relevant effect on empagliflozin is unlikely. Although an increased risk for bone fractures and decreased bone mineral density has been reported for other sodium glucose cotransporter 2 inhibitors, coadministration with tenofovir alfenamide is unlikely to be problematic in terms of additive bone toxicity as tenofovir alafenamide results in 90% lower systemic exposure of tenofovir compared to tenofovir disoproxil.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. Empagliflozin does not inhibit or induce CYPs and does not inhibit UGTs. There is no evidence that efavirenz induces the UGTs involved in empagliflozin metabolism or interacts to a significant level with the transporters involved in empagliflozin disposition.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. Empagliflozin does not inhibit or induce CYPs and does not inhibit UGTs. There is no evidence that etravirine induces the UGTs involved in empagliflozin metabolism or interacts to a significant level with the transporters involved in empagliflozin disposition.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. Nevirapine is unlikely to affect the metabolism of empagliflozin and empagliflozin is unlikely to affect nevirapine concentrations as it does not inhibit or induce CYPs and does not inhibit UGTs. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. Rilpivirine is unlikely to affect the metabolism of empagliflozin and empagliflozin is unlikely to affect rilpivirine concentrations as it does not inhibit or induce CYPs and does not inhibit UGTs. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. Rilpivirine is unlikely to affect the metabolism of empagliflozin and empagliflozin is unlikely to affect rilpivirine concentrations as it does not inhibit or induce CYPs and does not inhibit UGTs. Although an increased risk for bone fractures and decreased bone mineral density has been reported for other sodium glucose cotransporter 2 inhibitors, coadministration with tenofovir alafenamide is unlikely to be problematic in terms of additive bone toxicity as tenofovir alafenamide results in 90% lower systemic exposure of tenofovir compared to tenofovir disoproxil.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. Maraviroc is unlikely to affect the metabolism of empagliflozin and empagliflozin is unlikely to affect maraviroc concentrations as it does not inhibit or induce CYPs and does not inhibit UGTs. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. Dolutegravir is unlikely to affect the metabolism of empagliflozin and empagliflozin is unlikely to affect dolutegravir concentrations as it does not inhibit or induce CYPs and does not inhibit UGTs. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. Raltegravir is unlikely to affect the metabolism of empagliflozin and empagliflozin is unlikely to affect raltegravir concentrations as it does not inhibit or induce CYPs and does not inhibit UGTs. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. 

Coadministration has not been studied but based on the metabolism and clearance a pharmacokinetic interaction is unlikely as empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3, but there is little potential for an interaction via competition for these transporters. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3, but there is little potential for an interaction via competition for these transporters.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. Although an increased risk for bone fractures and decreased bone mineral density has been reported for other sodium glucose cotransporter 2 inhibitors, coadministration with tenofovir alafenamide is unlikely to be problematic in terms of additive bone toxicity as tenofovir alafenamide results in 90% lower systemic exposure of tenofovir compared to tenofovir disoproxil.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rosiglitazone is metabolized mainly by CYP2C8 and to a lesser extent by CYP2C9. A clinically relevant drug-drug interaction with nevirapine is not expected. Nevirapine concentrations were determined before and after 28 days of treatment with rosiglitazone (4 mg) in 4 subjects. There was a consistent trend to reductions in nevirapine Cmax (5%), Cmin (11%) and AUC (4%). No dose adjustment is required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rosiglitazone is metabolized mainly by CYP2C8 and to a lesser extent by CYP2C9. A clinically relevant drug-drug interaction with etravirine is not expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. No dose adjustment is required with twice daily or once daily raltegravir.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metformin is primarily eliminated by the kidney and in vitro data suggest that it is a substrate of the renal transporter OCT2. An interaction is unlikely as emtricitabine is primarily excreted by different renal transporters.

Coadministration has not been studied but based on metabolism and clearance a clinically relevant drug interaction is unlikely. Metformin is primarily eliminated by the kidney and in vitro data suggest that it is a substrate of the renal transporter OCT2. A clinically relevant drug interaction is unlikely as tenofovir is primarily excreted by different renal transporters.