(1R-(1R*,3S*,5R*,6R*,9R*,11R*,15S*,16R*,17R*,18S*,19E,21E,23E,25E,27E,29E,31E,33R*,
35S*,36R*,37S*))-33-((3-Amino-3,6-dideoxy-beta-D-mannopyranosyl)oxy)-1,3,5,6,9,11,17,37-octahydroxy-15,16,18-trimethyl-13-oxo-14,39-dioxabicyclo(33.3.1)nonatriaconta-19,21,23,25,27,29,31-heptaene-36-carboxylic acid

Absorption
C max is 0.5 to 2 mcg/mL.

Distribution
Plasma protein binding is more than 90%. Distributed to inflamed pleura, peritoneum, synovium, and aqueous humor.

Metabolism
Metabolic pathways are unknown.

Elimination
Elimination half-life is approximately 15 days. Plasma t ½ is about 24 h. Excreted slowly over a period of weeks to months by the kidneys, with approximately 40% appearing in the urine over a 7-day period.

Antineoplastic agents
Concurrent use may enhance potential for arrhythmias, bronchospasm, renal toxicity, and shock.

Azole antifungal agents (eg, fluconazole, ketoconazole)
Antagonism between amphotericin B and the antifungal agent may occur.

Corticosteroids and corticotropin
Increased potential for hypokalemia.

Cyclosporine, tacrolimus
May increase nephrotoxic effects.

Digitalis glycosides
Amphotericin B–induced hypokalemia may potentiate digitalis toxicity.

Flucytosine
Increased risk of flucytosine toxicity.

Leukocyte transfusions
Acute pulmonary toxicity has been reported in patients receiving IV amphotericin B and leukocyte transfusions. Do not give concurrently.

Nephrotoxic agents (eg, aminoglycosides)
Possible synergistic nephrotoxicity.

Skeletal muscle relaxants (eg, tubocurarine)
Amphotericin B–induced hypokalemia may enhance curariform effect of skeletal muscle relaxant.

Zidovudine
Closely monitor renal and hematologic function if used with amphotericin B.