Abstract:Here, we propose a novel therapeutic concept named drugnavigated clearance system (DNCS), in which a "navigator" decreases the concentration of a target etiologic factor in the blood by steering it to an unusual metabolic pathway. The navigator is composed of protein A (ProA) and dextran sulfate (DexS) and it successfully navigated antibodies (ABs), a model etiologic factor of dilated cardiomyopathy, to hepatocytes in vitro in the presence of low-density lipoprotein (LDL). ProA captured the Fc region of the ta… Show more
“…The drug-navigated clearance system (DNCS) is a novel therapeutic concept, in which the levels of an etiologic factor of a metabolic disease are decreased by artificially switching its metabolic processing pathways. 1,2 A "navigator" drug is critical for this switching: these navigator molecules capture the etiologic factor of interest in the blood and steer it toward another metabolic processing pathway. To achieve this, a typical navigator molecule consists of a capturing part and a steering part; for a highly efficient switching, the former needs to bind strongly to the etiologic factor, while the latter should exhibit a high affinity to surface receptors on a designated metabolic organ.…”
Kidney dysfunction increases the blood levels of β2-microglobulin (β2-m), triggering dialysis-related amyloidosis. Previously, we developed a navigator molecule, consisting of a fusion protein of the N-terminal domain of apolipoprotein E...
“…The drug-navigated clearance system (DNCS) is a novel therapeutic concept, in which the levels of an etiologic factor of a metabolic disease are decreased by artificially switching its metabolic processing pathways. 1,2 A "navigator" drug is critical for this switching: these navigator molecules capture the etiologic factor of interest in the blood and steer it toward another metabolic processing pathway. To achieve this, a typical navigator molecule consists of a capturing part and a steering part; for a highly efficient switching, the former needs to bind strongly to the etiologic factor, while the latter should exhibit a high affinity to surface receptors on a designated metabolic organ.…”
Kidney dysfunction increases the blood levels of β2-microglobulin (β2-m), triggering dialysis-related amyloidosis. Previously, we developed a navigator molecule, consisting of a fusion protein of the N-terminal domain of apolipoprotein E...
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