NF-κB blockade with oral administration of dimethylaminoparthenolide, delays prostate cancer resistance to androgen receptor inhibition and inhibits AR variants.

NF-κB activation has been linked to prostate cancer (PCa) progression and is commonly observed in castrate-resistant disease. It has been suggested that NF-κB-driven resistance to androgen deprivation therapy (ADT) in PCa cells may be mediated by aberrant androgen receptor (AR) activation and AR splice variant production.