Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Chemical Compound Review:

Desoxycholic acid 4-[ (3R,5R,8S,9S,10S,12S,13R,14S,1 7R)-3,12...

Synonyms: Droxolan, Pyrochol, Degalol, Septochol, Cholerebic, ...

Bramlett, K.S. et al., Carubbi, F. et al., Chiang, J.Y. et al.

Chiang, Kimmel, Weinberger, Stroup,

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Disease relevance of Desoxycholic acid

Higher doses of THDCA or TUDCA did not reduce toxicity induced by 350 micromol/l DCA, but were much less toxic than an equimolar dose of DCA alone [1].

High impact information on Desoxycholic acid

In HepG2 cells, all bile acids (25 microM) were able to repress CYP7A1/luciferase reporter activity, and only CDCA and DCA further repressed reporter activity when cotransfected with RXRalpha/FXR [2].
The rank order and absolute potency was conserved (CDCA IC(50) = 8.7 microM, DCA IC(50) = 27.2 microM, UDCA and CA inactive) consistent with bile acid repression of CYP7A1 being mediated by FXR [3].
Chenodeoxycholic acid (CDCA) was the most potent and efficacious compound in the SRC-1 recruitment assay (EC(50) = 11.7 microM) followed by deoxycholic acid (DCA; EC(50) = 19.0 microM) [3].
In cytoprotection experiments, the addition of 50 micromol/l THDCA decreased only slightly (-5%) AST release induced by 350 micromol/l DCA, while the addition of 50 micromol/l TUDCA was significantly effective (-23%; P<0.05) [1].

References

Comparative cytotoxic and cytoprotective effects of taurohyodeoxycholic acid (THDCA) and tauroursodeoxycholic acid (TUDCA) in HepG2 cell line. Carubbi, F., Guicciardi, M.E., Concari, M., Loria, P., Bertolotti, M., Carulli, N. Biochim. Biophys. Acta (2002) [Pubmed]
Farnesoid X receptor responds to bile acids and represses cholesterol 7alpha-hydroxylase gene (CYP7A1) transcription. Chiang, J.Y., Kimmel, R., Weinberger, C., Stroup, D. J. Biol. Chem. (2000) [Pubmed]
Correlation of farnesoid X receptor coactivator recruitment and cholesterol 7alpha-hydroxylase gene repression by bile acids. Bramlett, K.S., Yao, S., Burris, T.P. Mol. Genet. Metab. (2000) [Pubmed]

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