Recently, a novel cyclopeptide <i>Diffusa Cyclotide-3</i> (DC3), isolated from <i>Hedyotisdiffusa</i>, has been experimentally demonstrated to inhibit the survival and growth of LNCap cells, which typically express T877A-mutated AR, the most frequently detected point mutation of AR in castration-resistant prostate cancer (CRPC).
Chen and colleagues report that a T878A androgen receptor mutation occurs in a subset of patients progressing while receiving abiraterone, suggesting that this may be a therapeutically exploitable mechanism of abiraterone resistance in castration-resistant prostate cancer.