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• W1594592166 abstract "The steroid hormone receptors, the Androgen Receptor (AR), Estrogen Receptors (ER┙ and ER┚), Glucocorticoid Receptor (GR), Mineralocorticoid Receptor and Progesterone Receptor (PR), have been crucial targets for drug discovery even before their existence was known or understood. The drugs on the market for this sub-class of the nuclear hormone receptors constitute a significant pharmacopeia for the treatment of a vast array of conditions and ailments. Despite the breadth of drugs targeted toward this family, they remain an important target for the pharmaceutical industry. Key considerations when designing drugs for any family, beyond the on-target pharmaceutical action and safety, is to ensure specificity against related targets, exploration of the most appropriate routes of administration and desirable pharmacokinetic (PK) profiles. Developing non-steroidal modulators for the steroid receptor family has been a key strategy employed to achieve these goals, although there appears to be growing consensus that not being steroidal is insufficient to justify new drugs on its own (Hermkens et al, 2006). Unlike targeting many families, steroid hormone receptor drug discovery also has to balance the need to elicit either agonistic or antagonistic responses depending on the desired indication. The history of drug discovery for the steroid hormone receptors has tended to follow a common path, beginning with the application of purified endogenous hormone and followed by the application of the first synthetic analogs with improved PK properties or selectivity. For some of the receptors this period was followed by the design of antagonists, including non-steroidal structures. More recently, steroid hormone drug discovery has been" @default.
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• W1594592166 date "2012-01-11" @default.
• W1594592166 modified "2023-09-27" @default.
• W1594592166 title "Drug Design Approaches to Manipulate the Agonist-Antagonist Equilibrium in Steroid Receptors" @default.
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• W1594592166 doi "https://doi.org/10.5772/28124" @default.
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