Administration of Dimethylcurcumin (ASC-J9) at 75 mg/kg intraperitoneally (i.p.) leads to degradation of both fAR and AR3 in xenografted tumors in vivo, accompanied by a significant reduction in Ki67-positive cells in ASC-J9-treated tumors ^[1].

Treatment with Dimethylcurcumin (ASC-J9) at 50 mg/kg every 48 hours i.p. substantially alleviates SBMA symptoms in AR-97Q mice and mitigates neuromuscular pathological findings. Dimethylcurcumin (ASC-J9)-treated SBMA mice exhibit relatively normal serum testosterone concentrations ^[2].

Mice treated with ASC-J9 display significantly smaller prostate tumor sizes compared to those subjected to conventional androgen deprivation therapy/castration, despite having minimal serum androgen levels ^[3].

Dimethylcurcumin (ASC-J9) induces dose-dependent degradation of fAR and AR3 in various human PCa cells. Moreover, Dimethylcurcumin (ASC-J9) effectively represses AR-targeted genes in CWR22Rv1-fARKD cells. Treatment with Dimethylcurcumin (ASC-J9) at concentrations of 5 or 10 µM significantly inhibits DHT-induced cell proliferation in all three PCa cell lines. Additionally, Dimethylcurcumin (ASC-J9) inhibits AR-targeted genes and cell proliferation by degrading fAR and ectopic AR3 in C81 and C4-2 cells ^[1].

Dimethylcurcumin (ASC-J9) selectively facilitates AR degradation by disrupting the interaction between AR and AR coregulators. ASC-J9 diminishes the aggregation of AR-112Q in cells. Furthermore, Dimethylcurcumin (ASC-J9) inhibits the aggregation of AR-112Q in SBMA PC12/AR-112Q cells ^[2].