Other grades of this product :
| Product Name: | ASC-J9 | | Synonyms: | 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);(1E,4Z,6E)-1,7-Bis(3,4-dimethoxyphenyl)-5-hydroxy-1,4,6-heptatrien-3-one;Dimethylcurcumin;GO-Y 025;Dimethylcurcumin, ≥95%;Dimethylcurcumin【(1E,4Z,6E)-1,7-Bis(3,4-dimethoxyphenyl)-5-hydroxy-1,4,6-heptatrien-3-one】
;Indiscriminate | | CAS: | 52328-98-0 | | MF: | C23H24O6 | | MW: | 396.43 | | EINECS: | 2017-001-1 | | Product Categories: | | Mol File: | 52328-98-0.mol |
| ASC-J9 Chemical Properties |
| Melting point | 129-130℃ | | Boiling point | 588.6±50.0 °C(Predicted) | | density | 1.191 | | solubility | insoluble in EtOH; insoluble in H2O; ≥16.65 mg/mL in DMSO | | form | solid | | pka | 8.34±0.60(Predicted) |
| ASC-J9 Usage And Synthesis |
| 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 |
| ASC-J9 Preparation Products And Raw materials |
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