Comparative Pharmacology
Head-to-head clinical analysis: FOSCARNET SODIUM versus HEPSERA.
Peer-Reviewed Evidence
Head-to-head clinical analysis: FOSCARNET SODIUM versus HEPSERA.
FOSCARNET SODIUM vs HEPSERA
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Foscarnet is an organic analog of inorganic pyrophosphate that selectively inhibits the DNA polymerase activity of herpesviruses, including cytomegalovirus (CMV) and herpes simplex virus (HSV), at the pyrophosphate binding site without requiring activation by thymidine kinase. It also inhibits HIV reverse transcriptase.
Acyclic nucleotide analog of adenosine monophosphate; inhibits hepatitis B virus (HBV) DNA polymerase by competing with the natural substrate dATP, causing DNA chain termination after incorporation into viral DNA.
Induction: 60 mg/kg IV every 8 hours for 14–21 days, followed by maintenance: 90–120 mg/kg IV once daily. Infuse at no more than 1 mg/kg/min via central or peripheral line.
10 mg orally once daily.
None Documented
None Documented
Terminal elimination half-life is approximately 48 hours (range 24-88 hours), reflecting prolonged intracellular retention; clinical context necessitates dose adjustment for renal impairment and monitoring of renal function.
Terminal elimination half-life is approximately 6-9 hours in patients with normal renal function. In renal impairment, half-life is prolonged (up to 18 hours in moderate impairment, >30 hours in severe impairment). Steady-state is achieved within 5-7 days.
Primarily excreted unchanged by the kidney via glomerular filtration and tubular secretion; >80% of dose recovered in urine within 24 hours; minimal biliary or fecal excretion (<5%).
Primarily renal; 70-90% of an oral dose is excreted unchanged in urine via active tubular secretion and glomerular filtration. Biliary/fecal elimination accounts for <5%.
Category A/B
Category C
Antiviral
Antiviral