Science and Technology
 ARD enhancer compounds, such as ASC-J9®, are believed to alter the tertiary structure of the AR protein upon encountering the receptor in the cytoplasm. This results in the disassociation of AR from its chaperon proteins and subsequently leads to loss of structural integrity, drastically reducing AR activation by its ligand, androgens. The alteration of AR tertiary structure and limited binding ability with stabilizing chaperone proteins makes the AR vulnerable to ubiquitination and degradation via the proteasome-mediated pathway.
ARD Enhancers represent a completely novel Mechanism of Action (MOA) which target a known, validated nuclear receptor implicated in a variety of disease states. The MOA has significant advantages over conventional drugs which lower the levels of endogenous ligands such as testosterone or dihydrotestosterone (DHT) and other related steriods. ARD Enhancers selectively reduce the AR and its gene control activity, even in the presence of androgens. Through reducing AR protein levels, an ARD enhancer approach overcomes the impact of AR activation by non-androgen (or non-genetic) ligand pathways and unlike conventional anti-androgens ASC-J9® compounds possesses no partial agonistic activity.
 
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