2-methoxyestradiol (2-ME2) sulfation: Possible metabolic pathway

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2-ME2 is an endogenous estrogen metabolite that inhibits the proliferation of breast and other human cancer cell lines. 2-ME2 also has potent anti-angiogenic and anti-tubulin properties, and it may inhibit estrogen-induced carcinogenesis in the mammary gland. We set out to test the hypothesis that 2-ME2 might be a substrate for sulfate conjugation and, therefore, that individual variations in the sulfation of 2-ME2 might contribute to individual differences in its metabolism, pharmacokinetics and therapeutic efficacy. As a first step, we tested 2-ME2 as a substrate for 1 human sulfotransferase (SULT) isoforms - as well as all of the common allozymes for SULT1A1 and 1A2. Substrate kinetic studies were conducted in two stages - starting with concentrations over 5 orders of magnitude, followed by determination of Km values over a narrow concentration range. 2-ME2 was a sulfate acceptor substrate for SULT1A1* 1, *2, *3; 1A2*1, *2, *3; 1A3; 1E1; 2A1; 2B1a and 2B1b, with apparent Km values of 2.5, 5.2, 1.6; 4.2, 111, 5.3; 91; 0.067; 8.3; 4.1 and 4.1 μM, respectively. These results suggest that individual pharmacogenetic variation in sulfate conjugation might contribute to individual differences in 2-ME2 pharmacokinetics and therapeutic effect.

Original languageEnglish (US)
Pages (from-to)P75
JournalClinical pharmacology and therapeutics
Issue number2
StatePublished - Dec 1 2001

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)


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