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Encapsulation Of Foscarnet In Liposomes Modifies Drug Intracellular Accumulation, In Vitro Anti‐HIV-1 Activity, Tissue Distribution, And Pharmacokinetics

N. Dusserre, C. Lessard, N. Paquette, S. Perron, L. Poulin, M. Tremblay, D. Beauchamp, A. Désormeaux, M. Bergeron
Published 1995 · Biology, Medicine

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ObjectiveTo improve the in vitro anti-HIV-1 activity, intracellular accumulation in macrophages, and in vivo pharmacokinetics, and tissue distribution of foscarnet (trisodium phosphonoformate; PFA) by encapsulation in liposomes. MethodsThe accumulation of free, and liposome-encapsulated PFA was determined in monocyte-macrophage RAW 264.7 cells, and human premonocytoid U937 cells. The antiviral activity was evaluated in U937 cells infected with HIV-1IIIB. Tissue distribution, and pharmacokinetics of free, and liposomal PFA were determined in female Sprague-Dawley rats following the administration of an intravenous bolus dose (10 mg PFA/kg). ResultsThe entrapment of PFA in liposomes resulted in a higher drug accumulation in both U937, and RAW 264.7 cells. A slightly greater efficacy against HIV-1IIIB replication into U937 cells was observed upon encapsulation of PFA into liposomes. Improved pharmacokinetics was observed upon entrapment of PFA in liposomes. Much higher drug levels were found in plasma for the liposomal formulation. The systemic clearance of the liposomal drug was 77 times lower than that of free drug. The encapsulation of PFA in liposomes greatly enhanced the drug accumulation in organs of the reticuloendothelial system. ConclusionThe encapsulation of PFA in liposomes modified the tissue distribution, and plasma pharmacokinetics of the antiviral agent, resulting in a marked improvement of drug accumulation in organs involved in HIV immunopathogenesis, and in a greater PFA bioavailability. The antiviral activity of liposomal PFA was slightly greater than that of free drug in HIV-1IIIB-infected U937 cells.



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