The exact mechanism of in vivo biodistribution and disposition is vary depending on the fat composition, size, charge and degree of surface / steric hydration. Route of administration will also affect the properties of liposomes in vivo. Immediately after intravenous administration, liposomes are usually wrapped with serum proteins and taken by RES cells and finallyeliminated.



Plasma proteins will interact with the liposomes include albumin, lipoproteins (eg HDL and LDL and other cell-related proteins. Some proteins such as HDL will change in the liposome phospholipid double layer of fat, therefore it will hear the stabilization of liposomes. This process can potentially cause premature leakage or dissociation of drugs from liposomes. In the case of acid or liposomes that are sensitive to pH, protein binding would damage pH sensitive liposomes. fat-protein interactions can also dramatically reduced the transfection activity of DNA-cationic complexes in vivo fatty .

Giving large size of liposomes subcutaneously and intramuscularly may be trapped at the injection site and will provide a drug depot. In another case, liposomes that are small (50-80 nm) given subcutaneously will be captured in the spleen and eventually distributed into the blood circulation. The mechanism of increased localization of liposomes caused by the restriction of particle size spleen channels. Dependence on the size of the latex and carbon particles ever observed upper limit on the size of the channel estimate lymph nodes become 20-39 nm. Therefore, complex drug-fat-> 40-50 nm will be captured in the spleen as entering system limfatik.