Molecular Formula | C23H24O6 |
Molar Mass | 396.43 |
Density | 1.191 |
Melting Point | 129-130℃ |
Boling Point | 588.6±50.0 °C(Predicted) |
Solubility | DMSO |
Appearance | Powder |
pKa | 8.34±0.60(Predicted) |
Storage Condition | -20℃ |
MDL | MFCD12912341 |
Physical and Chemical Properties | Soluble in methanol, ethanol, DMSO and other organic solvents. |
In vitro study | Dimethylcurcumin (ASC-J9) is able to degrade fAR and AR3 in a dose-dependent manner in various human PCa cells. Dimethylcurcumin (ASC-J9) can also effectively suppress AR-targeted genes in CWR22Rv1-fARKD cells. Dimethylcurcumin (ASC-J9) (5 or 10 µM) significantly suppresses the DHT-induced cell growth in all three PCa cell lines. Dimethylcurcumin (ASC-J9) suppresses AR-targeted genes and cell growth by degradation of fAR and ectopic AR3 in C81 and C4-2 cells. Dimethylcurcumin (ASC-J9) selectively promotes AR degradation by disrupting the interaction between AR and AR coregulators. ASC-J9 reduces the AR aggregated AR-112Q in cells. Dimethylcurcumin (ASC-J9) suppresses the aggregation of AR-112Q in SBMA PC12/AR-112Q cells. |
In vivo study | Dimethylcurcumin (ASC-J9) (75 mg/kg, i.p.) degrades both fAR and AR3 in the xenografted tumors in vivo, and SC-J9-treated tumors has significantly decreased Ki67-positive cells. Dimethylcurcumin (ASC-J9) (50 mg/kg every 48 h, i.p.) substantially ameliorates the SBMA symptoms in AR-97Q mice, and ameliorates neuromuscular pathological findings. The Dimethylcurcumin (ASC-J9)-treated SBMA mice have relatively normal serum testosterone concentrations. ASC-J9-treated mice show significantly smaller prostate tumor sizes when compared with those receiving classic ADT/castration with little serum androgen. |
Reference Show more | 1. [IF=4.946] Lai Yanni et al."3D-quantitative structure–activity relationship and antiviral effects of curcumin derivatives as potent inhibitors of influenza H1N1 neuraminidase."Arch Pharm Res. 2020 May;43(5):489-502 |
biological activity | Dimethylcurcumin (ASC-J9, Dimethyl curcumin, GO-Y025) is a androgen receptor (AR) degradation promoter that can inhibit the growth of castration-resistant prostate cancer by degrading androgen receptors of full and spliced variants. |
target | TargetValue AR () |
Target | Value |
in vitro study | Dimethylcurcumin (ASC-J9) is able to degrade fAR and AR3 in a dose-dependent manner in various human PCa cells. Dimethylcurcumin (ASC-J9) can also effectively suppress AR-targeted genes in CWR22Rv1-fARKD cells. Dimethylcurcumin (ASC-J9) (5 or 10 m) significantly suppresses the DHT-induced cell growth in all three PCa cell lines. Dimethylcurcumin (ASC-J9) suppresses AR-targeted genes and cell growth by degradation of fAR and ectopic AR3 in C81 and C4-2 cells. Dimethylcurcumin (ASC-J9) selectively promotes AR degradation by disrupting the interaction between AR and AR coregulators. ASC-J9 reduces the AR aggregated AR-112Q in cells. Dimethylcurcumin (ASC-J9) suppresses the aggregation of AR-112Q in SBMA PC12/AR-112Q cells. |
in vivo study | Dimethylcurcumin (ASC-J9) (75 mg/kg, I. p.) degrades both fAR and AR3 in the xenografted tumors in vivo, and SC-J9-treated tumors has significantly decreased Ki67-positive cells. Dimethylcurcumin (ASC-J9) (50 mg/kg every 48 h, I. p.) substantially ameliorates the SBMA symptoms in AR-97Q mice, and ameliorates neuromuscular pathological findings. The Dimethylcurcumin (ASC-J9)-treated SBMA mice have relatively normal serum testosterone concentrations. ASC-J9-treated mice show significantly smaller prostate tumour sizes when compared with those receiving classic ADT/castration with little serum androgen. |
Chemical properties | Soluble in organic solvents such as methanol, ethanol, and DMSO. |