Lithocholic acid

For research use only.

Catalog No.S4003

2 publications

Lithocholic acid Chemical Structure

CAS No. 434-13-9

Lithocholic acid is a toxic secondary bile acid, causes intrahepatic cholestasis, has tumor-promoting activity, its toxic effect can be protected after it activates the vitamin D receptor, PXR and FXR.

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10mM (1mL in DMSO) USD 130 In stock
USD 97 In stock
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Selleck's Lithocholic acid has been cited by 2 publications

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Description Lithocholic acid is a toxic secondary bile acid, causes intrahepatic cholestasis, has tumor-promoting activity, its toxic effect can be protected after it activates the vitamin D receptor, PXR and FXR.
FXR [1] PXR [1] vitamin D receptor [1]
In vitro

Lithocholic acid (LCA) is a hydrophobic secondary bile acid that is primarily formed in the intestine by the bacterial 7α-dehydroxylation of chenodeoxycholic acid. LCA causes intrahepatic cholestasis (cessation or impairment of bile flow). LCA activates PXR (pregnane X receptor), and the LCA-induced severe liver damage can be protected by the activation of PXR. [1] LCA is a ligand for farnesoid X receptor (FXR) with EC50 of 3.8 μM. [2] LCA directly binds VDR (vitamin D receptor) with Ki of 29μM, activates VDR (vitamin D receptor) 30 μM, with much more sensitivity than the other nuclear receptors (eg. PXR, FXR), and its toxic effect is thus protected. [3] LCA has tumor-promoting activity, inhibits mammalian DNA Polymerase β with IC50 of 15 μM. [4]

In vivo Administration of LCA and its conjugates to rodents causes intrahepatic cholestasis,a pathogenic state characterized by decreased bile flow and the accumulation of bile constituents in the liver and blood. [1] In DMH (dimethyldydrazine)-induced murine carcinogenesis model, LCA suppresses apoptosis almost completely in premalignant colon. [5] LCA activates VDR, induces expression in vivo of CYP3A, a cytochrome P450 enzyme that detoxifies LCA in the liver and intestine. [3]


Kinase Assay:[3]
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Competitive ligand binding assay.:

Ligand binding is performed using lysates from COS-7 cells transfected with expression plasmids for VDR or RXRα. Binding is performed overnight at 4°C in lysate buffer with 0.71 nM (18 Ci/mmol) [3H]1,25(OH)2D3 and bile acid competitor. Unbound [3H]1,25(OH)2D3 is removed by adsorption to dextran-coated charcoal and the supernatant removed for scintillation counting. Ki values are calculated from a computer fit of competition curves from triplicate assays.
Animal Research:[1]
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  • Animal Models: Mouse
  • Dosages: 0.125 mg/g, twice a day for 4 days.
  • Administration: i.p.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 75 mg/mL (199.16 mM)
Ethanol 47 mg/mL (124.81 mM)
Water Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 376.57


CAS No. 434-13-9
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT02654496 Completed Other: Meal challenge Obesity North Dakota State University January 2016 --

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID