Version July 2025
Discontinuation of anti-hepatitis B therapy, including tenofovir alafenamide, may result in severe acute exacerbations of hepatitis B. Hepatic function should be monitored closely with both clinical and laboratory follow-up for at least several months in patients who discontinue anti-hepatitis B therapy, including tenofovir alafenamide. If appropriate, resumption of anti-hepatitis B therapy may be warranted.
Chronic hepatitis B (with compensated liver disease):
Children ≥6 years and Adolescents, weighing ≥25 kg: Oral: 25 mg once daily (Ref). Oral antiviral therapy was continued for 1 to 4 years in trials; hepatitis B e antigen (HBeAg) seroconversion has been suggested as a therapeutic end point followed by an additional 12 months of consolidation (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Kidney impairment prior to treatment initiation:
Children ≥6 years and Adolescents: There are no dosage adjustments provided in the manufacturer's labeling (has not been studied). Based on experience in adult patients, no dosage adjustment is likely necessary for patients with CrCl ≥15 mL/minute or in those with end-stage renal disease (CrCl <15 mL/minute) receiving chronic hemodialysis (administer after hemodialysis on dialysis days); tenofovir alafenamide is not recommended in adults with CrCl <15 mL/minute who are not receiving chronic hemodialysis. Monitor closely for adverse effects in patients with renal dysfunction.
Nephrotoxicity during treatment:
Children ≥6 years and Adolescents: Discontinue use in patients who develop clinically significant decreases in renal function or evidence of Fanconi syndrome.
Children ≥6 years and Adolescents:
Mild impairment: No dosage adjustment necessary.
Decompensated impairment: Not recommended.
(For additional information see "Tenofovir alafenamide: Drug information")
Hepatitis B virus infection, treatment: Oral: 25 mg once daily.
Treatment duration: Treatment duration is variable and influenced by hepatitis B e antigen (HBeAg) status, duration of hepatitis B virus (HBV) suppression, and presence of cirrhosis/decompensation (Ref).
Patients without cirrhosis:
HBeAg-positive immune-active chronic hepatitis: Treat until HBeAg seroconversion; after seroconversion, prolonged duration of therapy is often required in patients treated with nucleos(t)ide analogues. Optimal duration is unknown; however, consolidation therapy is generally a minimum of 12 months of persistently normal ALT and undetectable serum HBV DNA levels after HBeAg seroconversion (Ref).
HBeAg-negative immune-active chronic hepatitis: Indefinite antiviral therapy is suggested unless there is compelling rationale for discontinuation (risk/benefit decision); treatment discontinuation may be considered in patients with loss of HBsAg; however, there is insufficient evidence to guide decisions in these patients (Ref).
Patients with cirrhosis:
HBeAg-positive immune-active chronic hepatitis: In patients who seroconvert on therapy, continue antiviral therapy indefinitely due to concerns with decompensation and death, unless there is a strong competing rationale for discontinuation (Ref).
HBeAg-negative immune-active chronic hepatitis: Treatment discontinuation is not recommended due to potential for decompensation and death (limited data) (Ref).
Viral breakthrough : Patients with confirmed viral breakthrough (HBV DNA ≥100 IU/mL with previously undetectable levels [<10 IU/mL] or >1 log increase in HBV DNA compared to nadir), should either be switched to an alternative antiviral monotherapy agent with a high genetic barrier to resistance or receive a second antiviral agent with a complementary resistance profile; consult current clinical practice guidelines for recommended agents (Ref).
Hepatitis B virus reactivation prophylaxis , immunocompromised patients (off-label use): Oral: 25 mg once daily (Ref).
Hepatitis B virus reinfection prophylaxis , post liver transplant (with or without hepatitis B immune globulin) (off-label use): Oral: 25 mg once daily (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
Note: Tenofovir is renally cleared, and exposures are increased in patients with CrCl <30 mL/minute and those receiving hemodialysis (Ref). Close monitoring for adverse effects in the advanced stages of kidney dysfunction is recommended. Kidney function may be estimated using the Cockcroft-Gault formula for dosage adjustment purposes.
Kidney impairment prior to treatment initiation:
Altered kidney function: Oral:
CrCl ≥30 mL/minute: No dosage adjustment necessary (Ref).
CrCl 15 to <30 mL/minute: No dosage adjustment necessary (Ref); however, population pharmacokinetic modeling predicts increased tenofovir plasma AUC0-24 in patients with CrCl 15 to 29 mL/minute receiving once daily dosing compared to those with normal kidney function (1,000 ng*hour/mL versus to 298 ng*hour/mL, respectively) and that administering 25 mg every 48 hours would reduce the risk of toxicity while still achieving adequate intracellular tenofovir concentrations (Ref).
CrCl <15 mL/minute: Use is not recommended (Ref). Alternatively, population pharmacokinetic modeling predicts increased tenofovir plasma AUC0-24 in patients with CrCl <15 mL/minute receiving once daily dosing compared to those with normal kidney function (1,610 ng*hour/mL versus to 298 ng*hour/mL, respectively) and that administering 25 mg every 72 hours would reduce the risk of toxicity while still ensuring sufficient intracellular tenofovir concentrations (Ref).
Hemodialysis, intermittent (thrice weekly): No dosage adjustment necessary; when scheduled dose falls on a dialysis day, administer after dialysis.
Peritoneal dialysis: Limited data available. One case report found that plasma tenofovir and intracellular tenofovir diphosphate trough concentrations were 15-fold and 2-fold higher in a patient on peritoneal dialysis compared to people with normal kidney function. Consider alternative therapies in peritoneal dialysis patients to minimize toxicity and preserve residual kidney function (Ref).
CRRT: No dosage adjustment necessary (Ref).
PIRRT (eg, sustained, low-efficiency diafiltration): No dosage adjustment necessary. When scheduled dose falls on PIRRT days, administer after PIRRT (Ref).
Nephrotoxicity during treatment: Discontinue use in patients who develop clinically significant decreases in renal function or evidence of Fanconi syndrome.
Mild impairment (Child-Pugh class A): No dosage adjustment necessary.
Decompensated cirrhosis (Child-Pugh class B or C): Use is not recommended.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Reported adverse reactions are for adults, unless otherwise indicated.
>10%:
Nervous system: Headache (12%)
Neuromuscular & skeletal: Decreased bone mineral density (children and adolescents: ≥4% at lumbar spine: 6%; ≥4% whole body: 2%; adults: ≥5% at lumbar spine: 11%; ≥7% at femoral neck: 5%)
1% to 10%:
Cardiovascular: Increased serum creatine kinase (grades 3/4: 3%)
Dermatologic: Skin rash (<5%)
Endocrine & metabolic: Increased LDL cholesterol (grades 3/4: 6%)
Gastrointestinal: Abdominal pain (9%), diarrhea (5%), dyspepsia (5%), flatulence (<5%), increased amylase (grades 3/4: 3%), nausea (6%), vomiting (<5%)
Genitourinary: Glycosuria (grades 3/4: 5%)
Hepatic: Increased serum alanine aminotransferase (grades 3/4: 8%), increased serum aspartate aminotransferase (grades 3/4: 3%)
Nervous system: Fatigue (6%)
Neuromuscular & skeletal: Arthralgia (5%), back pain (6%)
Respiratory: Cough (8%)
Frequency not defined:
Endocrine & metabolic: Decreased HDL cholesterol, increased serum triglycerides
Gastrointestinal: Increased serum lipase
Hepatic: Exacerbation of hepatitis B
Postmarketing:
Dermatologic: Urticaria
Hypersensitivity: Angioedema
Renal: Acute kidney injury, Fanconi syndrome, proximal tubular nephropathy, renal tubular necrosis
There are no contraindications listed in the US manufacturer's labeling.
Canadian labeling: Additional contraindications (not in US labeling): Hypersensitivity to tenofovir alafenamide or any component of the formulation
Concerns related to adverse effects:
• Lactic acidosis/hepatomegaly: Lactic acidosis and severe hepatomegaly with steatosis, sometimes fatal, have been reported with the use of nucleoside analogs, alone or in combination with other antiretrovirals. Suspend treatment in any patient who develops clinical or laboratory findings suggestive of lactic acidosis or pronounced hepatotoxicity. Marked transaminase elevation may/may not accompany hepatomegaly and steatosis.
• Kidney toxicity: Kidney toxicity (acute renal failure, Fanconi syndrome, and/or proximal renal tubulopathy) has been reported with use of tenofovir alafenamide–containing products; patients with impaired renal function and those with concurrent or recent nephrotoxic therapy (including nonsteroidal anti-inflammatory drug use) are at an increased risk.
Disease-related concerns:
• Liver impairment: Dosage adjustment may be required.
• HIV-1 and HBV coinfection: Should not be used as a single agent for the treatment of HIV-1 due to resistance development risk.
Other warnings/precautions:
• HIV testing: HIV antibody testing should be offered to all HBV infected patients prior to treatment initiation. If HIV testing is positive, institute an appropriate antiretroviral (HIV-1) combination regimen.
Through disruption in vitamin D metabolism, decreases in bone mineral density (BMD) have been observed with tenofovir alafenamide (TAF) after 48 weeks of treatment; however, the incidence and negative impact on BMD is less than that observed with tenofovir disoproxil fumarate (TDF). Additionally, TAF is associated with less renal toxicity than TDF but equal antiviral efficacy. A higher incidence of dyslipidemia has been reported with TAF than TDF. Do not use TAF and TDF concomitantly (HHS [pediatric] 2022).
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral:
Vemlidy: 25 mg
No
Tablets (Vemlidy Oral)
25 mg (per each): $61.07
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Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral:
Vemlidy: 25 mg
Oral: Administer with food.
Oral: Administer with food.
Store below 30°C (86°F). Dispense in original container.
Treatment of chronic hepatitis B virus infection in patients with compensated liver disease (FDA approved in ages ≥6 years and weighing ≥25 kg and adults).
TAF is an error-prone abbreviation (mistaken as tenofovir disoproxil fumarate)
Substrate of BCRP, OAT1/3, OATP1B1/1B3, P-glycoprotein (Major with inducers), P-glycoprotein (Minor with inhibitors); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential; Inhibits MRP2;
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program
Acyclovir-Valacyclovir: May increase serum concentration of Tenofovir Products. Tenofovir Products may increase serum concentration of Acyclovir-Valacyclovir. Risk C: Monitor
Adefovir: May decrease therapeutic effects of Tenofovir Products. Adefovir may increase serum concentration of Tenofovir Products. Tenofovir Products may increase serum concentration of Adefovir. Risk X: Avoid
Aminoglycosides: May increase serum concentration of Tenofovir Products. Tenofovir Products may increase serum concentration of Aminoglycosides. Risk C: Monitor
Atidarsagene Autotemcel: Antiretroviral Agents may decrease therapeutic effects of Atidarsagene Autotemcel. Risk X: Avoid
Betibeglogene Autotemcel: Antiretroviral Agents may decrease therapeutic effects of Betibeglogene Autotemcel. Risk X: Avoid
Cabozantinib: MRP2 Inhibitors may increase serum concentration of Cabozantinib. Risk C: Monitor
CarBAMazepine: May decrease serum concentration of Tenofovir Alafenamide. Risk X: Avoid
Cidofovir: May increase serum concentration of Tenofovir Products. Tenofovir Products may increase serum concentration of Cidofovir. Risk C: Monitor
Cladribine: Agents that Undergo Intracellular Phosphorylation may decrease therapeutic effects of Cladribine. Risk X: Avoid
Cobicistat: May increase serum concentration of Tenofovir Alafenamide. Risk C: Monitor
Elivaldogene Autotemcel: Antiretroviral Agents may decrease therapeutic effects of Elivaldogene Autotemcel. Management: Avoid use of antiretroviral medications for at least one month, or for the amount of time required for elimination of the retroviral medication, prior to stem cell mobilization and until the all apheresis cycles are finished Risk X: Avoid
Fosphenytoin-Phenytoin: May decrease serum concentration of Tenofovir Alafenamide. Risk X: Avoid
Ganciclovir-Valganciclovir: Tenofovir Products may increase serum concentration of Ganciclovir-Valganciclovir. Ganciclovir-Valganciclovir may increase serum concentration of Tenofovir Products. Risk C: Monitor
Lovotibeglogene Autotemcel: Antiretroviral Agents may decrease therapeutic effects of Lovotibeglogene Autotemcel. Risk X: Avoid
Lumacaftor and Ivacaftor: May increase serum concentration of P-glycoprotein/ABCB1 Substrates (High risk with Inhibitors or Inducers). Lumacaftor and Ivacaftor may decrease serum concentration of P-glycoprotein/ABCB1 Substrates (High risk with Inhibitors or Inducers). Risk C: Monitor
Nirmatrelvir and Ritonavir: May increase serum concentration of Tenofovir Alafenamide. Risk C: Monitor
Nonsteroidal Anti-Inflammatory Agents (Topical): May increase nephrotoxic effects of Tenofovir Products. Risk C: Monitor
Nonsteroidal Anti-Inflammatory Agents: May increase nephrotoxic effects of Tenofovir Products. Management: Seek alternatives to these combinations whenever possible. Avoid use of tenofovir with multiple NSAIDs or any NSAID given at a high dose due to a potential risk of acute renal failure. Diclofenac appears to confer the most risk. Risk D: Consider Therapy Modification
Orlistat: May decrease serum concentration of Antiretroviral Agents. Risk C: Monitor
OXcarbazepine: May decrease serum concentration of Tenofovir Alafenamide. Risk X: Avoid
P-glycoprotein/ABCB1 Inducers: May decrease serum concentration of Tenofovir Alafenamide. Management: Consider alternatives to the use of P-gp inducers with tenofovir alafenamide. If combined, monitor for reduced tenofovir alafenamide concentrations and efficacy, and for the development of resistance. Risk D: Consider Therapy Modification
PHENobarbital: May decrease serum concentration of Tenofovir Alafenamide. Risk X: Avoid
Primidone: May decrease serum concentration of Tenofovir Alafenamide. Risk X: Avoid
Rifabutin: May decrease serum concentration of Tenofovir Alafenamide. Risk X: Avoid
RifAMPin: May decrease serum concentration of Tenofovir Alafenamide. Risk X: Avoid
Rifapentine: May decrease serum concentration of Tenofovir Alafenamide. Risk X: Avoid
Ritonavir: May increase serum concentration of Tenofovir Alafenamide. Risk C: Monitor
St John's Wort: May decrease serum concentration of Tenofovir Alafenamide. Risk X: Avoid
Tacrolimus (Systemic): Tenofovir Products may increase nephrotoxic effects of Tacrolimus (Systemic). Risk C: Monitor
Tipranavir: May decrease serum concentration of Tenofovir Alafenamide. Risk X: Avoid
Contraception is not required to initiate or continue antiretroviral therapy.
Tenofovir alafenamide is a preferred nucleoside reverse transcriptase inhibitor in patients with HIV who are not yet pregnant but are trying to conceive.
Tenofovir alafenamide is not effective for preexposure prophylaxis in persons with vaginal exposure to HIV.
Maximum viral suppression sustained below the limits of detection prior to conception is recommended for all persons with HIV who are planning a pregnancy. Prior to pregnancy, select or make changes to a specific antiretroviral regimen as part of a shared decision-making process. In most cases, recommendations based on data obtained from cisgender women can be applied to transgender and gender diverse people assigned female sex at birth.
Health care providers caring for couples planning a pregnancy when one or both partners are diagnosed with HIV may contact the National Perinatal HIV Hotline (1-888-448-8765) for clinical consultation (HHS [perinatal] 2024).
Algorithms are available for assessing antiviral prophylaxis and treatment of hepatitis B infection in persons not coinfected with HIV who could become pregnant (WHO 2024).
Tenofovir alafenamide has a low level of transfer across the human placenta.
No increased risk of overall teratogenic effects has been observed based on data collected by the antiretroviral pregnancy.
Maternal antiretroviral therapy (ART) may be associated with adverse pregnancy outcomes including preterm birth, low birth weight, and small for GA infants. High viral loads are also associated with adverse outcomes, including preterm birth and pregnancy loss. Treatment improves the health of the pregnant patient and reduces the risk of perinatal transmission. Do not withhold appropriate maternal ART due to concerns for adverse neonatal outcomes. Closely monitor for pregnancy complications. Document in utero ART exposure in the long-term medical record of a child born without HIV; evaluate for potential metabolic dysfunction if significant organ system abnormalities of unknown etiology (particularly of the CNS or heart) develop.
Tenofovir alafenamide is a preferred nucleoside reverse transcriptase inhibitor (NRTI) for pregnant patients with HIV who are antiretroviral naive, who have had ART therapy in the past but are restarting, or who require a new ART regimen (due to poor tolerance or poor virologic response of current regimen). Patients who become pregnant while taking tenofovir alafenamide may continue if viral suppression is effective and the regimen is well tolerated.
Tenofovir alafenamide with emtricitabine or lamivudine is a preferred NRTI backbone for initial therapy in antiretroviral-naive patients who are pregnant. Tenofovir alafenamide is also a preferred component of a regimen when early (acute/recent) HIV infection is detected during pregnancy; genotyping may be required if the person had prior use of long acting cabotegravir for preexposure prophylaxis.
Tenofovir alafenamide plus emtricitabine or lamivudine is a recommended dual NRTI backbone in regimens for pregnant patients who are HIV/hepatitis B virus–coinfected.
The pharmacokinetics of tenofovir alafenamide are not significantly altered during pregnancy and dose adjustment is not required.
ART is recommended for all pregnant people with HIV to maximize their health, maintain the viral load below the limit of an ultrasensitive assay detection, and reduce the risk of perinatal transmission. Start ART prior to conception or as soon as possible during pregnancy. During pregnancy, select or make changes to a specific antiretroviral regimen as part of a shared decision-making process. Patients on fully suppressive regimens prior to pregnancy generally may continue the same regimen considering known pregnancy outcomes and pharmacokinetic data. Monitor pregnant patients more frequently than nonpregnant patients. ART initiated during pregnancy can be modified after delivery. In most cases, recommendations based on data obtained from cisgender women can be applied to transgender and gender diverse people assigned female sex at birth (HHS [perinatal] 2024).
Algorithms are available for assessing antiviral prophylaxis and treatment of hepatitis B infection in pregnant persons not coinfected with HIV. Tenofovir alafenamide may be considered for use during pregnancy (WHO 2024). Patients using tenofovir alafenamide prior to conception should continue use during pregnancy (SMFM [Badell 2024]).
Data collection to monitor pregnancy and infant outcomes following exposure to ART is ongoing. Enroll all patients exposed to antiretroviral medications as early in pregnancy as possible in the Antiretroviral Pregnancy Registry (1-800-258-4263).
Health care providers caring for pregnant patients with HIV and their infants may contact the National Perinatal HIV Hotline (1-888-448-8765) for clinical consultation (HHS [perinatal] 2024).
Hepatitis B virus (HBV):
Prior to starting therapy: HIV testing; SCr, urine glucose and protein; serum phosphate (in patients with chronic kidney disease).
During therapy: Serum electrolytes (including anion gap), SCr, lipid profiles, urine protein and glucose and/or urinalysis, serum phosphate (in patients with chronic kidney disease), serum lactate (if clinical presentation indicates need).
Liver enzymes and HBV RNA plasma levels should be monitored as part of routine hepatitis B disease monitoring. Children with HBV who stop antiviral therapy should be monitored every 3 months for at least 1 year for recurrent viremia, ALT flares, and clinical decompensation (AASLD [Terrault 2018]).
Tenofovir alafenamide, an analog of adenosine 5'-monophosphate, is converted intracellularly by hydrolysis to tenofovir and subsequently phosphorylated to the active tenofovir diphosphate. The active moiety inhibits replication of HBV by inhibiting HBV polymerase.
Protein binding: 80% to plasma proteins.
Metabolism: Tenofovir alafenamide (TAF) is converted intracellularly to tenofovir, then phosphorylated to the active tenofovir diphosphate.
Bioavailability: Increases ~65% with a high-fat meal.
Half-life elimination: 0.51 hours.
Time to peak, serum:
Children ≥4 years and Adolescents ≤15 years: Tenofovir alafenamide: Mean range: 1.1 to 2 hours; Tenofovir: Mean range: 2 to 3 hours (Waalewijn 2023).
Adults: Tenofovir alafenamide: 0.48 hours.
Excretion: Feces (31.7%) and urine (<1%).
Altered kidney function: In patients with CrCl 15 to 29 mL/minute or with end-stage renal disease requiring dialysis, Cmax and AUC of tenofovir were increased.
