Doxorubicin (DOX) was coupled to human low density lipoprotein (LDL) to form a complex (LDL-DOX). When injected into mice, LDL-DOX was more accumulated in liver than free DOX. In contrast, LDL-DOX was less accumulated in heart than free DOX. In in vitro studies on human hepatoma (HepG2) cells, although the cellular uptake of LDL-DOX was higher than that of DOX, the anti-proliferative effect of LDL-DOX on these tumor cells was smaller than that of LDL. However, when LDL-DOX or DOX was administered to nude mice bearing HepG2 cells implanted on the shoulder, the anti-proliferative effects on the tumor cells of both drugs were similar. Histological analyses indicated that organization of myocardial filaments was disrupted and vacuolization was observed in DOX-treated group when compared with control group whereas LDL-DOX-treatment did not exhibit any damage in the host's heart. Enzymatic analyses also demonstrated that plasma lactate dehydrogenase activity, which is a common indicator of heart damage, was elevated in DOX-treated group when compared with control group whereas the activity of this enzyme was unchanged in LDL-DOX-treated group. The results in present study indicate that LDL can be used as a targeted carrier for DOX because LDL-DOX can exhibit similar anti-proliferative effect as DOX on tumor but reduce the DOX-induced cardiotoxicity in the host.