Dimethylcurcumin

Research use only, not for human use.

Dimethylcurcumin (ASC-J9) is an androgen receptor degradation enhancer. It effectively suppresses castration-resistant prostate cancer cell proliferation and invasion.Dimethylcurcumin is able to degrade fAR and AR3 in a dose-dependent manner in various human PCa cells. Dimethylcurcumin can also effectively suppress AR-targeted genes in CWR22Rv1-fARKD cells.

Dimethylcurcumin (ASC-J9) is an androgen receptor degradation enhancer. It effectively suppresses castration-resistant prostate cancer cell proliferation and invasion.Dimethylcurcumin is able to degrade fAR and AR3 in a dose-dependent manner in various human PCa cells. Dimethylcurcumin can also effectively suppress AR-targeted genes in CWR22Rv1-fARKD cells. Dimethylcurcumin (5 or 10 μM) significantly suppresses the DHT-induced cell growth in all three PCa cell lines. Dimethylcurcumin suppresses AR-targeted genes and cell growth by the degradation of fAR and ectopic AR3 in C81 and C4-2 cells. ASC-J9 reduces the AR aggregated AR-112Q in cells. Dimethylcurcumin suppresses the aggregation of AR-112Q in SBMA PC12/AR-112Q cells.Dimethylcurcumin (75 mg/kg, i.p.) degrades both fAR and AR3 in the xenografted tumors in vivo and ASC-J9-treated tumors have significantly decreased Ki67-positive cells. Dimethylcurcumin (50 mg/kg every 48 h, i.p.) substantially ameliorates the SBMA symptoms in AR-97Q mice and ameliorates neuromuscular pathological findings. ASC-J9-treated mice show significantly smaller prostate tumor sizes when compared with those receiving classic ADT/castration with little serum androgen.(In Vitro):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):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.

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.

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.

ASC-J9,GO-Y025

Endocrinology/Hormones

Androgen Receptor (AR)

Androgen Receptor

Others

Acne vulgaris

52328-98-0

396.43

C23H24O6

>98% (HPLC)

DMSO:48 mg/mL (121.08 mM);Water:Insoluble

O=C(/C=C(O)/C=C/C1=CC=C(OC)C(OC)=C1)/C=C/C2=CC=C(OC)C(OC)=C2

——

(-20℃)

With Ice Pack

≥ 2 years