52328-98-0

Basic information

• Product Name: ASC-J9
• Synonyms: (1E,4Z,6E)-1,7-Bis(3,4-dimethoxyphenyl)-5-hydroxy-1,4,6-heptatrien-3-one;Dimethylcurcumin;GO-Y 025;1,4,6-Heptatrien-3-one, 1,7-bis(3,4-diMethoxyphenyl)-5-hydroxy-,(1E,4Z,6E)-;(1E,4Z,6E)-1,7-Bis(3,4-dimethoxyphenyl)-5-hydroxy-1,4,6-heptatrien-3-one (ASC-J9)
• CAS NO: 52328-98-0
• Molecular Formula: C₂₃H₂₄O₆
• Molecular Weight: 396.43306
• EINECS: 2017-001-1
• Mol File: 52328-98-0.mol
• Article Data: 28

Chemical Properties

• Melting Point: 129-130℃
• Boiling Point: 588.6±50.0 °C(Predicted)
• Appearance: /
• Density: 1.191
• Solubility: insoluble in EtOH; insoluble in H2O; ≥16.65 mg/mL in DMSO
• PKA: 8.34±0.60(Predicted)
• CAS DataBase Reference: ASC-J9(CAS DataBase Reference)
• NIST Chemistry Reference: ASC-J9(52328-98-0)
• EPA Substance Registry System: ASC-J9(52328-98-0)

Safety Data

• Hazardous Substances Data: 52328-98-0(Hazardous Substances Data)

Usage

Description

ASC-J9 is a compound with potential applications in various industries due to its unique properties. It is characterized by its ability to selectively enhance the degradation of androgen receptor, making it a promising candidate for pharmaceutical and medical applications.

Uses

Used in Pharmaceutical Industry:
ASC-J9 is used as a therapeutic agent for the treatment of androgen receptor-related conditions. Its selective enhancement of androgen receptor degradation makes it a potential candidate for the development of targeted therapies.
Used in Research and Development:
ASC-J9 is used as a research tool for studying the role of androgen receptor in various biological processes. Its selective degradation properties can help researchers better understand the mechanisms underlying androgen receptor-related diseases and develop novel therapeutic strategies.
Used in Drug Delivery Systems:
Similar to gallotannin, ASC-J9 can also be incorporated into drug delivery systems to improve its delivery, bioavailability, and therapeutic outcomes. The development of novel drug delivery systems for ASC-J9 can enhance its applications and efficacy in targeted therapies.

Biological Activity

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]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 deathdis. 2013,4:e764

Upstream product

• 120-14-9 3,4-dimethoxy-benzaldehyde 
• 123-54-6 acetylacetone 
• 98885-93-9 curcumin 
• 77-78-1 dimethyl sulfate 
• 186581-53-3 diazomethane 
• 74-88-4 methyl iodide 
• 160096-59-3 4',4''-O,O-dimethylcurcumin 
• 458-37-7 curcumin 
• 15390-25-7 (acetylacetonato)borondifluoride 
• 147556-16-9 curcumin 
• 67-68-5 dimethyl sulfoxide 

Downstream Products

• 91998-04-8 (+/-)-di-O-methyl hexahydrocurcumin 
• 55094-78-5 di-O-methyltetrahydrocurcumin 
• 478919-25-4 (E,E)-3,5-bis(3,4-dimethoxystyryl)-1H-pyrazole 
• 884506-35-8 7-(3,4-dimethoxyphenyl)-4-[3-(3,4-dimethoxyphenyl)-acryloyl]-5-hydroxy-hepta-2,4,6-trienoic acid ethyl ester 
• 1039760-70-7 C₃₁H₃₀O₇ 
• 1039760-65-0 C₂₇H₃₃NO₅ 
• 1111745-10-8 C₂₅H₂₈O₇ 
• 1039760-74-1 C₂₆H₂₆O₆ 
• 98886-34-1 (1E,6E)-4-Allyl-1,7-bis-(3,4-dimethoxy-phenyl)-hepta-1,6-diene-3,5-dione 
• 1039760-76-3 C₃₂H₃₂O₆ 
• 1039760-60-5 C₂₇H₃₀O₈ 
• 1111745-24-4 C₄₇H₄₈O₁₂ 
• 1039760-78-5 C₂₆H₂₆O₈ 
• 1038864-69-5 C₂₈H₃₂O₈ 

Relevant articles and documents

The in vitro antitumor activity of arene-ruthenium(II) curcuminoid complexes improves when decreasing curcumin polarity

The antitumor activity of ruthenium(II) arene (p-cymene, benzene, hexamethylbenzene) derivatives containing modified curcumin ligands (HCurcI?=?(1E,4Z,6E)-5-hydroxy-1,7-bis(3,4-dimethoxyphenyl)hepta-1,4,6-trien-3-one and HCurcII?=?(1E,4Z,6E)-5-hydroxy-1,7-bis(4-methoxyphenyl)hepta-1,4,6-trien-3-one) is described. These have been characterized by IR, ESI-MS and NMR spectroscopy. The X-ray crystal structure of HCurcI has been determined and compared with its related Ru complex. Four complexes have been evaluated against five tumor cell lines, whose best activities [IC50 (μM)] are: breast MCF7, 9.7; ovarian A2780, 9.4; glioblastoma U-87, 9.4; lung carcinoma A549, 13.7 and colon-rectal HCT116, 15.5; they are associated with apoptotic features. These activities are improved when compared to the already known corresponding curcumin complex, (p-cymene)Ru(curcuminato)Cl, about twice for the breast and ovarian cancer, 4.7 times stronger in the lung cancer and about 6.6 times stronger in the glioblastoma cell lines. In fact, the less active (p-cymene)Ru(curcuminato)Cl complex only shows similar activity to two novel complexes in the colon cancer cell line. Comparing antitumor activity between these novel complexes and their related curcuminoids, improvement of antiproliferative activity is seen for a complex containing CurcII in A2780, A549 and U87 cell lines, whose IC50 are halved. Therefore, after replacing OH curcumin groups with OCH3, the obtained species HCurcI and its Ru complexes have increased antitumor activity compared to curcumin and its related complex. In contrast, HCurcII is less cytotoxic than curcumin but its related complex [(p-cymene)Ru(CurcII)Cl] is twice as active as HCurcII in 3 cell lines. Results from these novel arene-Ru curcuminoid species suggest that their increased cytotoxicity on tumor cells correlate with increase of curcuminoid lipophilicity.

Influence of side-chain changes on histone deacetylase inhibitory and cytotoxicity activities of curcuminoid derivatives

Using curcuminoids as lead compounds, fifty-nine curcuminoid derivatives with different side chains at the phenolic moiety were synthesized. All compounds were investigated for their histone deacetylase (HDAC) inhibitory activities. The potent pan-HDAC in

A Flexible Strategy for Modular Synthesis of Curcuminoid-BF2/Curcuminoid Pairs and Their Comparative Antiproliferative Activity in Human Cancer Cell Lines

A facile protocol that enables synthetic interconversion of CUR-BF2 and CUR compounds is described that significantly widens the preparative scope of curcuminoids, providing access to larger libraries of compounds, thus enabling comparative antiproliferative and apoptotic study of a larger library of synthetic analogs in cancer cell lines.

Activation of anti-oxidant Nrf2 signaling by enone analogues of curcumin

Inflammation and oxidative stress are common in many chronic diseases. Targeting signaling pathways that contribute to these conditions may have therapeutic potential. The transcription factor Nrf2 is a major regulator of phase II detoxification and anti-oxidant genes as well as anti-inflammatory and neuroprotective genes. Nrf2 is widespread in the CNS and is recognized as an important regulator of brain inflammation. The natural product curcumin exhibits numerous biological activities including ability to induce the expression of Nrf2-dependent phase II and anti-oxidant enzymes. Curcumin has been examined in a number of clinical studies with limited success, mainly owing to limited bioavailability and rapid metabolism. Enone analogues of curcumin were examined with an Nrf2 reporter assay to identify Nrf2 activators. Analogues were separated into groups with a 7-carbon dienone spacer, as found in curcumin; a 5-carbon enone spacer with and without a ring; and a 3-carbon enone spacer. Activators of Nrf2 were found in all three groups, many of which were more active than curcumin. Dose-response studies demonstrated that a range of substituents on the aromatic rings of these enones influenced not only the sensitivity to activation, reflected in EC50 values, but also the extent of activation, which suggests that multiple mechanisms are involved in the activation of Nrf2 by these analogues.