Tenofovir disoproxil fumarate
Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.
| ID | DRUG-TENOFOVIR-DF |
|---|---|
| Type | Drug |
| Aliases | TDFTenofovir DFVireadТенофовіру дизопроксил фумарат |
| Status | reviewed 2026-05-18 |
| Diseases | None declared |
| Sources | SRC-AASLD-HBV-2024 SRC-NIH-AIDS-2024 |
Drug Facts
| Class | Nucleotide analog reverse transcriptase inhibitor (NRTI / NtRTI) — HBV polymerase + HIV-1 reverse transcriptase |
|---|---|
| Mechanism | Acyclic nucleotide analog prodrug; the parent compound tenofovir is phosphorylated intracellularly to tenofovir diphosphate, which competitively inhibits HBV polymerase / HIV-1 reverse transcriptase and terminates the nascent viral DNA chain after incorporation. Active against wild-type HBV, lamivudine-resistant HBV, and HIV-1; no activity against HCV. |
| Typical dosing | Chronic HBV (adult): 300 mg PO once daily with food, indefinite duration (long-term suppression). HIV-1 (adult): 300 mg PO once daily as component of combination ART. Renal adjustment required: CrCl 30-49 → 300 mg q48h; CrCl 10-29 → 300 mg q72-96h; HD → 300 mg weekly after dialysis. Pediatric (≥2 y, ≥10 kg): 8 mg/kg PO daily, max 300 mg. Continue HBV therapy long- term — abrupt discontinuation risks severe HBV reactivation / acute hepatitis flare (black-box warning). |
| Ukraine registered | True |
| NSZU reimbursed | True |
| Ukraine last verified | 2026-05-18 |
Warnings
- Lactic acidosis and severe hepatomegaly with steatosis (class effect of NRTIs)
- Severe acute exacerbation of hepatitis B upon discontinuation in HBV-infected patients — monitor LFTs ≥several months after stopping
- Risk of HIV-1 resistance in HIV/HBV coinfected patients treated for HBV alone without full ART
Notes
STUB — v0.2 prevention-workstream authoring; pending two-Clinical-Co-Lead signoff per CHARTER §6.1 dev-mode. First-line oral antiviral for chronic HBV per AASLD-2024; one of three preferred agents (TDF, TAF, entecavir). Long-term HBV suppression is the etiologic-prevention pathway for HBV- driven HCC and HBV-associated B-cell NHL (the v0.2-A prevention scope). TDF carries a higher signal of nephrotoxicity and bone-density loss than TAF — prefer TAF in older adults, baseline renal impairment, or osteopenia/osteoporosis. Also a backbone of HIV-1 ART (commonly co- formulated with emtricitabine ± efavirenz / rilpivirine). The cancer- prevention rationale spans both HBV-mediated HCC reduction (the dominant effect — meta-analyses show ~50-70% HCC risk reduction with sustained viral suppression) and chronic-HBV-associated NHL risk reduction (smaller but consistent signal). Two-Co-Lead signoff queued for v0.2-A clinical review.
Used By
Access Pathways
AP-ART-NSZU-HIV- ART regimens (Biktarvy and alternatives) via НСЗУ HIV programme
Contraindications
CI-TENOFOVIR-SEVERE-RENAL- CI-TENOFOVIR-SEVERE-RENAL