ERB-26

Today, we want to talk about ERB-26. This is a topic that has gained great relevance in recent times, and it is important to study it in depth to understand its impact on our society. Throughout this article, we will explore different aspects of ERB-26, from its origin and evolution to its influence in various areas. In addition, we will analyze the different perspectives that exist on ERB-26, in order to offer a comprehensive and objective vision. Without a doubt, ERB-26 is a topic that invites us to reflect and debate, and we are sure that this article will be enriching for our readers.

ERB-26
Clinical data
Drug classEstrogen; Selective ERβ agonist

ERB-26 is a synthetic estrogen and a selective agonist of the ERβ.[1][2] It is the active enantiomer of the racemic mixture ERB-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 preclinical models.[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.

See also

References

  1. ^ a b c d e f g h Attia 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. PMID 22025007. S2CID 12951793.
  2. ^ Nelson AW, Tilley WD, Neal DE, Carroll JS (2014). "Estrogen receptor beta in prostate cancer: friend or foe?". Endocr. Relat. Cancer. 21 (4): T219–34. doi:10.1530/ERC-13-0508. PMID 24402043.
  3. ^ Dulos J, Vijn P, van Doorn C, Hofstra CL, Veening-Griffioen D, de Graaf J, Dijcks FA, Boots AM (2010). "Suppression of the inflammatory response in experimental arthritis is mediated via estrogen receptor α but not estrogen receptor β". Arthritis Res. Ther. 12 (3): R101. doi:10.1186/ar3032. PMC 2911889. PMID 20497523.



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