ABSTRACT
Our understanding of the fate of liposomes in vivo took a sharp turn in the late 1980s, following the work from two independent laboratories, T. M. Allen's at the University of Alberta1·5 and my own, at the University of California, San Francisco (UCSF).6-10 These studies demonstrated that the inclusion of a small percentage of some specific glycolipids and phospholipids had a dramatic effect in increasing the circulation time of liposomes in blood T 112 • Moreover, it was also shown that the long T 112 was correlated with higher uptake by implanted tumors in mice.6· 10 This has greatly expanded the potential of liposomes as drug carriers, and some formulations have already shown promise for increasing the efficacy of chemotherapeutic agents in recent clinical trials. 11 · 13 Such liposomes were initially given the name "SteaJth®"2·14 on the basis of their avoidance of rapid detection and uptake by the reticuloendothelial system (RES). More recently they have been characterized as "sterically stabilized", 15 ·16 on the basis of their enhanced stability and reduced reactivity to plasma proteins and cell surface receptors.
