The corporation's (injectable) nanoemulsion formulations, which are especially useful for "actively targeted" chemotherapy, comprise several key lipid components that can be adjusted for specific applications. [For a detailed review of the relevant scientific and patent literature, associated know-how, advantages over competing technologies, target markets, etc., see recent book: D'Arrigo, J.S. (2011) Stable Nanoemulsions: Self-Assembly in Nature and Nanomedicine, 436 pp., Elsevier Science, Amsterdam and Oxford.] Briefly, the above 2011 book reviews and analyzes much experimental (in vivo) data which collectively demonstrate that this type of stable lipid nanoemulsion, upon intravenous injection, is capable of "active targeting" of various lipophilic drugs to hyperproliferative-disease sites (such as tumors, neuro-injury scar tissue, etc.) -- which commonly overexpress certain cell-surface receptors. These overexpressed receptors fall within the category known as "lipoprotein receptors", which includes notably the (class B) scavenger receptor referred to as SR-BI.
This "active" targeting behavior of the FilmixTM lipid nanoemulsion vehicle (via the process of receptor-mediated endocytosis), involving SR-BI receptors, has direct relevance to the (rapidly targeted) chemotherapy of autoimmune diseases -- especially rheumatoid arthritis (and also inflammatory bowel disease). For example, Mullan et al. [Am. J. Pathol. 176:1999-2008 (2010)] have recently reported that in rheumatoid arthritis (RA) disease the acute-phase reactant called Serum Amyloid A (SAA) apolipoprotein, which is strongly expressed in "rheumatoid arthritis synovial membrane" (RA SM), serves to induce angiogenesis, adhesion molecule expression, and matrix metalloproteinase production through alternative signaling via SR-BI. (These results are consistent with a separate report by Baranova et al. [J. Biol. Chem. 280:8031-8040 (2005)] who assert that the results of their own study demonstrate that (the human version of) SR-BI serves as an endocytic SAA receptor, and is involved in SAA-mediated cell signaling events associated with the immune-related and inflammatory effects of SAA [see also D'Arrigo (2011) reference above] ). As concerns the specific results of the above Mullan et al. (2010) study, quantitative expression/localization of SR-BI in RA SM, RA fibroblast-like cells (FLCs), and micro-vascular endothelial cells (ECs) was assessed by Western blotting and immunohistology/fluorescence. SR-BI was strongly expressed in the RA SM lining layer and endothelial/perivascular regions (in comparison to osteoarthritis SM or normal control synovium). Differential SR-BI expression on RA FLC lines (n = 5) correlated closely with SAA responsiveness. Moreover, these authors demonstrated that the pro-inflammatory actions of SAA in RA FLCs and ECs can be blocked by specific antibodies directed against SR-BI. In conclusion, since SR-BI is expressed in RA synovial tissue and mediates SAA-induced pro-inflammatory pathways, a novel strategy for immunomodulatory chemotherapy of rheumatoid arthritis may well be accomplished by "actively" targeting the overexpressed SR-BI (by utilizing the Filmix nanoemulsion drug-delivery vehicle).
In addition, as noted in the above Mullan et al. (2010) study, SAA is also known to induce the secretion of the pro-inflammatory cytokine "interleukin-1ß" (IL-1ß). This fact is of further interest since Ikeda et al. [Life Sci. 83:43-49 (2008)] point out that IL-1ß is a pro-inflammatory cytokine responsible for the onset of a broad range of autoimmune diseases, such as inflammatory bowel disease and rheumatoid arthritis. Consequently, a novel strategy for immunomodulatory treatment of inflammatory bowel disease may also be accomplished by "actively" targeting overexpressed SR-BI (by utilizing the Filmix nanoemulsion drug-delivery vehicle).