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Endoxifen and other metabolites of tamoxifen inhibit human hydroxysteroid sulfotransferase hSULT2A1
Abstract   Open access   Peer reviewed

Endoxifen and other metabolites of tamoxifen inhibit human hydroxysteroid sulfotransferase hSULT2A1

Edwin Squirewell, Xiaoyan Qin and Michael W. Duffel
The FASEB journal, Vol.27(S1), pp.892.9-892.9
04/2013
DOI: 10.1096/fasebj.27.1_supplement.892.9
url
https://doi.org/10.1096/fasebj.27.1_supplement.892.9View
Published (Version of record) Open Access

Abstract

Tamoxifen is a breast cancer therapeutic that has been shown to cause endometrial cancer in some women following treatment. hSULT2A1 is an enzyme that catalyzes the formation of an α-sulfooxy derivative of tamoxifen that is reactive towards DNA. Moreover, hSULT2A1 functions in the metabolism of steroid hormones such as dehydroepiandrosterone (DHEA) and pregnenenolone (PREG). We hypothesize that major metabolites of tamoxifen regulate the catalytic activity of hSULT2A1, either through direct inhibition or through serving as alternate substrates for the enzyme. Our studies show that endoxifen is a potent inhibitor of hSULT2A1-catalyzed sulfation of PREG and DHEA with Ki values of 3.5 μM and 2.8 μM, respectively. 4-Hydroxytamoxifen and N-desmethyltamoxifen had Ki values of 12.7 μM and 9.8 μM, respectively, for sulfation of PREG, whereas Ki values of 19.4 μM and 17.2 μM were observed for these metabolites when determining the sulfation of DHEA. A Ki of 9.1 μM was observed for tamoxifen-N-oxide when DHEA was used as a substrate, and this increased to a Ki value of 16.9 μM when PREG was utilized as a substrate. Subsequent assays indicated that N-desmethyltamoxifen was a substrate for the enzyme. These results may be useful in interpreting ongoing clinical trials of endoxifen and in improving the design of related molecule

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