Description:This invention is a novel drug molecule that binds directly to the FKBP52 protein to disrupt both FKBP52 and beta-catenin regulation of AR activity leading to the inhibition of androgen dependent gene expression and androgen-dependent prostate cancer cell proliferation. In addition to the inhibition of FKBP52 and beta-catenin simultaneously, this novel drug molecule will inhibit a number of other relevant targets in prostate cancer (e.g. glucocorticoid and progesterone receptor), and will likely bypass antiandrogen-induced disease resistance.
Abstract:Embodiments of the current invention include methods and compositions for regulating the activity of hormone receptors.
Issue Date: 06/16/2020
Application Date: 05/17/2018
Post Date: 09/13/2019
UTEP Docket No: 2014-009