Description |
Cholic acid is a major primary bile acid produced in the liver and usually conjugated with glycine or taurine. It facilitates fat absorption and cholesterol excretion.
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Target |
Human Endogenous Metabolite
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In Vitro |
Cholic acid competitively binds Na+/taurocholate cotransporting polypeptide (NTCP) on HepG2 cells and significantly inhibits the uptake of Cholic acid (CA)-nanoliposomes (LPs)-Doxorubicin (DOX)-HCl, which indicates that CA-LPs-DOX-HCl are also uptaken via NTCP-mediated endocytosis pathway[1].
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In Vivo |
Cholic acid feeding leads to increased CYP2D6 expression in CYP2D6-humanized mice. As a cholestasis model, Tg-CYP2D6 mice are fed a Cholic acid (CA)-supplemented diet for over 1 week. The treatment is known to increase bile acid pool size by 2-fold and to replace ~90% of bile acids with CA, recapitulating the features of cholestatic conditions in humans[2].
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Cell Assay |
HepG2 cells are pretreated with the inhibitors NaN3 (1 mg/mL), Genistein (50 μg/mL), MβCD (10 mM), Nystatin (50 μg/mL), Chlorpromazine (10 μg/mL), and Cholic acid (1 mg/mL) for 30 min. After removing the inhibitors, the cells are incubated with CA-LPs for 2 h, and the cellular uptake of LPs is determined in the "In vitro cellular uptake assays" section[1].
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Animal Admin |
Mice[2] Tg-CYP2D6 mice are fed with normal chow (control) or 1% (w/w) Cholic acid-supplemented diet (CA) for 14 days (n=4 mice/group). Alkaline phosphatase (ALP) and alanine aminotransferase (ALT) activities are measured in mouse serum.
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Density | 1.2±0.1 g/cm3 |
Boiling Point | 583.9±50.0 °C at 760 mmHg |
Flash Point | 321.0±26.6 °C |
Exact Mass | 408.287567 |
PSA | 97.99000 |
LogP | 2.62 |
Vapour Pressure | 0.0±3.7 mmHg at 25°C |
Storage condition | 2-8°C |