Dimethylcurcumin (ASC-J9) (ASC-J9) is an androgen receptor degradation enhancer. It effectively suppresses castration-resistant prostate cancer cell proliferation and invasion.

Dimethylcurcumin 在不同的人类前列腺癌细胞中以剂量依赖的方式降解 fAR 和 AR3。在 CWR22Rv1-fARKD 细胞中，Dimethylcurcumin 也能有效地抑制 AR 靶基因。Dimethylcurcumin (5 或 10 μM) 显著抑制三种前列腺癌细胞线中 DHT 诱导的细胞增长。Dimethylcurcumin 通过降解 C81 和 C4-2 细胞中的 fAR 和异位 AR3 来抑制 AR 靶基因和细胞生长 [1]。ASC-J9 减少细胞中 AR 聚集的 AR-112Q。Dimethylcurcumin 抑制 SBMA PC12/AR-112Q 细胞中的 AR-112Q 聚集 [2]。

Dimethylcurcumin（75 mg/kg，腹腔注射）能在体内降解异种移植肿瘤中的fAR和AR3，并且经ASC-J9处理的肿瘤显示Ki67阳性细胞显著减少[1]。Dimethylcurcumin（50 mg/kg，每48小时一次，腹腔注射）显著改善了AR-97Q小鼠的脊髓性肌萎缩症状，并改善了神经肌肉病理学发现[2]。与接受经典ADT/去势治疗且血清雄激素水平较低的小鼠相比，ASC-J9处理的小鼠展示了显著更小的前列腺肿瘤体积[3]。

For the cell survival assay, the PC12/AR-112Q and PC12/AR-10Q cells are cultured as described previously and incubated cells in the presence of 10 μg/mL doxycycline for 24 h. Then the cells are treated with a vehicle, 5 μM Dimethylcurcumin or 10 μM Dimethylcurcumin, along with 1 nM DHT, and determined cell viability using Trypan blue staining at specific time intervals [2].

CWR22Rv1 cells (1×10^6 cells per site) are injected into both anterior prostates of the castrated nude mice after 2 weeks of implantation. The mice were randomly divided into two groups (four mice/eight tumors each group) and either receive 75 mg/kg Dimethylcurcumin intraperitoneal injection or vehicle control every other day. After 4 weeks of treatment, all mice are killed to examine the tumor growth. Body weights and mice activity are measured weekly [1].