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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Disposition of bisantrene in humans and rabbits: evidence for intravascular deposition of drug as a cause of phlebitis.

The investigational antitumor agent bisantrene (9,10-anthracenedicarboxaldehyde bis[(4,5-dihydro-1H-imidazol-2-yl)hydrazone] dihydrochloride) causes frequent local complications of phlebitis and thromboses in patients receiving the drug by peripheral venous infusion. Bisantrene pharmacokinetics was studied in five patients. Plasma elimination was biphasic with t1/2 alpha of 65 min and t1/2 beta of 1142 min; the mean apparent volumes of distribution of the central compartment and peripheral compartments were 185 and 1662 liters/sq m, suggesting extensive uptake, binding, or deposition of drug. Total body clearance was 735 ml/min/sq m, and 11.3% of drug was excreted in urine. One hr after bisantrene (260 mg/sq m) at 1 mg/ml in 5% dextrose was infused into the marginal ear vein of a rabbit, the vein was congested with blood and contained 2.1 mg precipitated bisantrene. After 24 hr, the vein was clotted and contained 1.18 mg precipitated drug. Precipitation of bisantrene appears to be related to the low solubility of the drug at physiological pH. Maximum solubility of bisantrene in human and rabbit serum was 12.7 micrograms/ml. Intravascular precipitation of bisantrene may be responsible for phlebitis and thromboses in humans receiving the drug by i.v. infusion.[1]

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