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| 25mg |
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Purity: ≥98%
Dimethylcurcumin (formerly known as ASC-J9; GO-Y025) is an androgen receptor (AR) degradation enhancer that effectively suppresses castration resistant prostate cancer cell proliferation and invasion. Dimethylcurcumin suppresses renal cell carcinoma progression by targeting an androgen receptor-dependent HIF2α/VEGF signaling pathway.ASC-J9 treatment enhanced BCG efficacy to suppress bladder cancer cell proliferation via increasing the recruitment of monocytes/macrophages that involved the promotion of BCG attachment/internalization to the bladder cancer cells through increased integrin-α5β1 expression and IL6 release.
| Targets |
androgen receptor (AR) degradation enhancer
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|---|---|
| ln Vitro |
In a range of human PCa cells, dimethylcurcumin (ASC-J9) can degrade fAR and AR3 in a dose-dependent manner. In CWR22Rv1-fARKD cells, dimethylcurcumin (ASC-J9) can also efficiently block genes that are targeted by AR. In all three PCa cell lines, dimethylcurcumin (ASC-J9) (5 or 10 µM) effectively reduced DHT-induced cell proliferation. Dimethylcurcumin (ASC-J9) breaks down fAR and ectopic AR3 in C81 and C4-2 cells, which suppresses the development of cells and genes targeted by AR [1]. Dimethylcurcumin (ASC-J9) breaks off the connection between AR and AR coregulators, hence preferentially promoting the degradation of AR. Cells accumulate less AR when ASC-J9 AR-112Q is present. SBMA PC12/AR-112Q cell aggregation of AR-112Q is inhibited by dimethylcurcumin (ASC-J9) [2].
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| ln Vivo |
In xenograft tumors, dimethylcurcumin (ASC-J9) (75 mg/kg, i.p.) degrades fAR and AR3, and tumors treated with SC-J9 exhibit a significant reduction in Ki67-positive cells [1]. In AR-97Q mice, intraperitoneal injections of 50 mg/kg dimethylcurcumin (ASC-J9) every 48 hours markedly reduced the symptoms of SBMA and enhanced neuromuscular pathology. Serum testosterone concentrations in SBMA animals treated with dimethylcurcumin (ASC-J9) are comparatively normal [2]. When compared to mice getting traditional ADT/castration with low serum androgen levels, mice treated with ASC-J9 showed noticeably reduced prostate tumor sizes [3].
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| Enzyme Assay |
Western Blot Analysis, Quantitative Real-time Polymerase Chain Reaction, and Luciferase Reporter Assay [1]
Cells were cultured and treated with or without ASC-J9 for 24 hours in 10% charcoal-dextran-stripped fetal bovine serum (CD-FBS) media. Cell lysates were harvested and subjected to Western blot analysis. Quantitative real-time polymerase chain reaction (qPCR) was performed in triplicate with a Bio-Rad iCycler system (Bio-Rad, Hercules, CA); and messenger RNA (mRNA) levels of PSA, TMPRSS2, FKBP5, and GAPDH were measured. Cells were transiently transfected with mouse mammary tumor virus luciferase reporter (MMTV-Luc) or ARE4-Luc plus pRL-TK as internal control. Luciferase activities were measured using GloMax 20/20 Luminometer (Promega, Madison, WI). |
| Cell Assay |
Cell Growth Assay[1]
Cells were treated with vehicle, 1 nM dihydrotestosterone (DHT), 5 µM Casodex, and 5 or 10 µM ASC-J9 in 10% CD-FBS medium. The media were replenished every other day, and we followed the standard MTT assay protocol. |
| Animal Protocol |
In Vivo Tumor Growth Assay [1]
Animal procedures were conducted in accordance with the protocol approved by the University of Rochester Committee on Animal Resources. CWR22Rv1 cells (1 x 106 cells per site) were injected into both anterior prostates (orthotopic) of castrated nude mouse after 2 weeks of implantation. The mice were randomly divided into two groups (four mice/eight tumors each group) and either received 75 mg/kg ASC-J9 intraperitoneal injection or vehicle control every other day. After 4 weeks of treatment, all mice were killed to examine the tumor growth. Body weights and mice activity were measured weekly. |
| References |
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| Molecular Formula |
C23H24O6
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|---|---|
| Molecular Weight |
396.43306
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| Exact Mass |
396.157
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| Elemental Analysis |
C, 69.68; H, 6.10; O, 24.21
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| CAS # |
52328-98-0
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| Appearance |
Light yellow to red solid powder
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| Density |
1.2±0.1 g/cm3
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| Boiling Point |
588.6±50.0 °C at 760 mmHg
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| Melting Point |
129-130 °C
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| Flash Point |
201.8±23.6 °C
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| Vapour Pressure |
0.0±1.7 mmHg at 25°C
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| Index of Refraction |
1.608
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| LogP |
4.05
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| SMILES |
O=C(/C=C(O)/C=C/C1=CC=C(OC)C(OC)=C1)/C=C/C2=CC=C(OC)C(OC)=C2
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| InChi Key |
ZMGUKFHHNQMKJI-CIOHCNBKSA-N
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| InChi Code |
InChI=1S/C23H24O6/c1-26-20-11-7-16(13-22(20)28-3)5-9-18(24)15-19(25)10-6-17-8-12-21(27-2)23(14-17)29-4/h5-15,24H,1-4H3/b9-5+,10-6+,18-15-
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| Chemical Name |
(1E,4Z,6E)-1,7-bis(3,4-dimethoxyphenyl)-5-hydroxyhepta-1,4,6-trien-3-one
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| Synonyms |
ASC-J9; ASC-J-9; ASC J9; GO-Y025; GO-Y 025; GO Y025;
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ≥ 50 mg/mL (~126.13 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.17 mg/mL (5.47 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 21.7 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.2 mg/mL (5.5 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + + 45% Saline For example, if 1 mL of working solution is to be prepared, you can take 100 μL of 21.7 mg/mL of DMSO stock solution and add tO + 400 μL of PEG300, mix well (clear solution); Then add 50 μL of Tween 80 to the above solution, mix well (clear solution); Finally, add 450 μL of saline to the above solution, mix well (clear solution). Preparation of saline: Dissolve 0.9 g of sodium chloride in ddH ₂ O and make up to 100 mL to obtain a clear and transparent saline solution. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.5225 mL | 12.6126 mL | 25.2251 mL | |
| 5 mM | 0.5045 mL | 2.5225 mL | 5.0450 mL | |
| 10 mM | 0.2523 mL | 1.2613 mL | 2.5225 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
 ASC-J9 suppresses AR-targeted genes, AR transactivation, and cell growth through AR degradation in CRPC cells.Neoplasia.2012 Jan;14(1):74-83. |
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 Therapeutic effect of ASC-J9in vivo. (A) Evaluation of tumor volumes of CWR22Rv1 xenografts after ASC-J9 treatment.(B) Body weight determination during ASC-J9 treatment. (C) Histologic examination of tumor tissues after ASC-J9 treatment.Neoplasia.2012 Jan;14(1):74-83. |
 ASC-J9 suppresses AR-targeted genes and cell growth by degradation of fAR and ectopic AR3 in C81 and C4-2 cells.Neoplasia.2012 Jan;14(1):74-83. |
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