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ASC-J9AR degradation enhancer,antiumor agent

ASC-J9

Catalog No. A3190
Size Price Stock Qty
10mM (in 1mL DMSO) $132.00 In stock
5mg $120.00 In stock
10mg $200.00 In stock
50mg $660.00 In stock

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Sample solution is provided at 25 µL, 10mM.

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Chemical structure

ASC-J9

Related Biological Data

ASC-J9

Biological Activity

Description ASC-J9 is an enhancer of androgen receptor degradation.
Targets PC-3 cell proliferation LNCaP cell proliferation        
IC50 5.9 μM 3.9 μM        

Protocol

Cell experiment [1]:

Cell lines

Human C4-2B/human THP1 cells and mouse TRAMP-C1/mouse RAW264.7 cells.

Preparation method

Soluble in DMSO. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months.

Reaction Conditions

5 μM; 3 days.

Applications

ASC-J9 suppresses macrophage recruitment and suppresses PCa invasion.

Animal experiment [1]:

Animal models

Male 6- to 8-week-old nude mice with orthotopically xenografted 106 TRAMP-C1 cells.

Dosage form

75 mg/kg; i.p. injected three times per week for 3 weeks.

Applications

In mice, ASC-J9 significantly decreases developing distant metastatic tumors in diaphragm and lymph nodes. There are little change in mice body weight among all the mice treated.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

References:

[1]. Lin TH, Izumi K, Lee SO, et al. Anti-androgen receptor ASC-J9 versus anti-androgens MDV3100 (Enzalutamide) or Casodex (Bicalutamide) leads to opposite effects on prostate cancer metastasis via differential modulation of macrophage infiltration and STAT3-CCL2 signaling. Cell Death Dis, 2013, 4: e764.

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Chemical Properties

Cas No. 52328-98-0 SDF Download SDF
Synonyms GO-Y025; Dimethylcurcumin; ASC J9; GO Y025
Chemical Name (1E,4Z,6E)-1,7-bis(3,4-dimethoxyphenyl)-5-hydroxyhepta-1,4,6-trien-3-one
Canonical SMILES COC1=C(C=C(C=C1)C=CC(=CC(=O)C=CC2=CC(=C(C=C2)OC)OC)O)OC
Formula C23H24O6 M.Wt 396.43
Solubility >16.65mg/mL in DMSO Storage Store at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

Background

ASC-J9, is antitumor agent. ASC-J9 suppresses castration-resistant prostate cancer growth via degradation of full-length and splice variant androgen receptors targeting both fAR- and AR3-mediated PCa growth by ASC-J9 may represent the novel therapeutic approach to suppress castration-resistant PCa. ASC-J9 ameliorates spinal and bulbar muscular atrophy phenotype via degradation of androgen receptor.

The androgen receptor (AR) is a type of nuclear receptor that is activated by binding either of the androgenic hormones, testosterone, or dihydrotestosterone in the cytoplasm and then translocating into the nucleus. [1]The binding of an androgen to the androgen receptor(AR) results into a conformational change, in turn, which causes dissociation of HSP, transport from the cytosol into the cell nucleus, and dimerization. The AR dimer binds to a specific sequence of DNA known as HRE which can interact with other proteins in the nucleus, leading to up-regulation or down-regulation of specific gene transcription.[2]

ASC-J9, the AR degradation enhancer, suppressed both macrophage migration and subsequent PCa cell invasion. Additionally, ASC-J9 can regulate pSTAT3-CCL2 signaling using two pathways: an AR-dependent pathway via inhibiting PIAS3 expression and an AR-independent pathway via direct inhibition of the STAT3 phosphorylation/activation through mouse model in vivo with orthotopically injected TRAMP-C1 cells. In conclusion,a new and better therapeutic strategies using ASC-J9 alone or a combinational therapy that simultaneously targets androgens/AR signaling and PIAS3-pSTAT3-CCL2 signaling to better battle PCa growth and metastasis at castration-resistant stage.[3]

References:

1. Lu NZ. et al. "International Union of Pharmacology. LXV. The pharmacology and classification of the nuclear receptor superfamily: glucocorticoid, mineralocorticoid, progesterone, and androgen receptors". Pharmacol. Rev. 2006, 58 (4): 782–97.

2. Heemers HV, Tindall DJ. "Androgen receptor (AR) coregulators: a diversity of functions converging on and regulating the AR transcriptional complex". Endocr. Rev. 2007, 28 (7): 778–808.

3. Lin TH. et al. “Anti-androgen receptor ASC-J9 versus anti-androgens MDV3100 (Enzalutamide) or Casodex (Bicalutamide) leads to opposite effects on prostate cancer metastasis via differential modulation of macrophage infiltration and STAT3-CCL2 signaling.” Cell Death

Dis. 2013,4:e764

.