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ERB-26 is a syntheticestrogen and a selectiveagonist of the ERβ.[1][2] It is the activeenantiomer of the racemic mixtureERB-79.[1] Whereas ERB-79 shows 484-fold selectivity for the ERβ over the ERα,[3] ERB-26 differs slightly in that it is even more selective, showing greater than 1,000-fold selectivity for transactivation of the ERβ relative to the ERα.[1] Its EC50 value for the ERβ is 0.21 nM (4-fold weaker than estradiol) and for the ERα is 260 nM (10,000-fold weaker than estradiol).[1] It has no antagonistic activity at either receptor.[1] ERB-26 is active in prevention of prostate cancer development in preclinicalmodels.[1] In contrast to ERB-26, the selective ERα agonist ERA-45 induced prostate cancer development in preclinical models when it was given in combination with testosterone, whereas testosterone alone did not do so.[1] These findings suggest opposing roles of the ERα and ERβ in the prostate gland.[1] The chemical structure of ERB-26 does not appear to have been disclosed.
^ abcdefghAttia DM, Ederveen AG (2012). "Opposing roles of ERα and ERβ in the genesis and progression of adenocarcinoma in the rat ventral prostate". Prostate. 72 (9): 1013–22. doi:10.1002/pros.21507. PMID22025007. S2CID12951793.
