| Identification | Back Directory | [Name]
ASC-J9 | [CAS]
52328-98-0 | [Synonyms]
GO-Y 025
Dimethylcurcumin
Dimethylcurcumin, ≥95%
(1E,4Z,6E)-1,7-Bis(3,4-dimethoxyphenyl)-5-hydroxy-1,4,6-heptatrien-3-one
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)
Dimethylcurcumin【(1E,4Z,6E)-1,7-Bis(3,4-dimethoxyphenyl)-5-hydroxy-1,4,6-heptatrien-3-one】
| [EINECS(EC#)]
2017-001-1 | [Molecular Formula]
C23H24O6 | [MOL File]
52328-98-0.mol | [Molecular Weight]
396.43 |
| Chemical Properties | Back Directory | [Melting point ]
129-130℃ | [Boiling point ]
588.6±50.0 °C(Predicted) | [density ]
1.191 | [storage temp. ]
Store at -20°C | [solubility ]
insoluble in EtOH; insoluble in H2O; ≥16.65 mg/mL in DMSO | [form ]
solid | [pka]
8.34±0.60(Predicted) |
| Hazard Information | Back Directory | [Uses]
Dimethylcurcumin selectively enhances the degradation of androgen receptor. Dimethylcurcumin is a related compound of Curcumin (C838500). | [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 |
|
|