Mechanism of transportation SIS3 ic50 through liposome The limitations and benefits of liposome drug carriers lie critically on the interaction of liposomes with cells and their destiny in vivo after Bortezomib in vitro administration. In vivo and in vitro studies of the contacts with cells have shown that the main interaction of liposomes with cells is either simple adsorption (by specific interactions with cell-surface components, electrostatic forces, or by non-specific weak hydrophobic) or following endocytosis (by

phagocytic cells of the reticuloendothelial system, for example macrophages and neutrophils). Fusion with the plasma cell membrane by insertion of the lipid bilayer of the liposome into the plasma membrane, with simultaneous release of liposomal content into the cytoplasm, is much rare. The fourth possible interaction is the exchange of bilayer components, for instance cholesterol, lipids, and membrane-bound molecules with components of cell membranes. It is often difficult to determine what mechanism is functioning, and more than one may function at the same time [42–44]. Fusogenic liposomes and antibody-mediated liposomes in cancer therapy It has been infrequently well-known that a powerful

anticancer drug, especially one that targets selleck kinase inhibitor the cytoplasm or cell nucleus, does not work due to the low permeability across a plasma membrane, degradation by lysosomal enzymes through an endocytosis-dependent pathway, and other reasons. Thus, much attention on the use of drug delivery systems is focused on overcoming these problems, ultimately leading to the induction of maximal ability of anti-cancer drug. In this respect, a new model for cancer therapy using a novel drug delivery Thymidine kinase system, fusogenic liposome [45], was developed. Fusogenic liposomes are poised of the ultraviolet-inactivated Sendai virus and conventional liposomes. Fusogenic liposomes effectively and directly deliver their encapsulated contents into the cytoplasm using a fusion mechanism

of the Sendai virus, whereas conventional liposomes are taken up by endocytosis by phagocytic cells of the reticuloendothelial system, for example macrophages and neutrophils. Thus, fusogenic liposome is a good candidate as a vehicle to deliver drugs into the cytoplasm in an endocytosis-independent manner [45]. Liposomal drug delivery systems provide steady formulation, provide better pharmacokinetics, and make a degree of ‘passive’ or ‘physiological’ targeting to tumor tissue available. However, these transporters do not directly target tumor cells. The design modifications that protect liposomes from unwanted interactions with plasma proteins and cell membranes which differed them with reactive carriers, for example cationic liposomes, also prevent interactions with tumor cells. As an alternative, after extravasation into tumor tissue, liposomes remain within tumor stroma as a drug-loaded depot.