Stereochemistry | ACHIRAL |
Molecular Formula | C15H10O4 |
Molecular Weight | 254.2375 |
Optical Activity | NONE |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
CC1=CC2=C(C(O)=C1)C(=O)C3=C(C=CC=C3O)C2=O
InChI
InChIKey=LQGUBLBATBMXHT-UHFFFAOYSA-N
InChI=1S/C15H10O4/c1-7-5-9-13(11(17)6-7)15(19)12-8(14(9)18)3-2-4-10(12)16/h2-6,16-17H,1H3
Molecular Formula | C15H10O4 |
Molecular Weight | 254.2375 |
Charge | 0 |
Count |
MOL RATIO
1 MOL RATIO (average) |
Stereochemistry | ACHIRAL |
Additional Stereochemistry | No |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Optical Activity | NONE |
Chrysophanic acid (Chrysophanol) is a member of the anthraquinone family abundant in rhubarb, a widely used herb for obesity treatment in Traditional Korean Medicine. Chrysophanol has been shown to induce cell death in different types of cancer cells. Chrysophanol inhibits EGF-induced phosphorylation of EGFR and suppresses activation of AKT and mTOR/p70S6K. Chrysophanol also effectively suppresses breast cancer cell proliferation and facilitates chemosentivity through modulation of the NF-κB signaling pathway. A treatment of chrysophanol could reduce significantly the
clinical signs and the levels of inflammatory mediators in a colitis model caused by DSS treatment.
The anti-inflammatory activities of chrysophanol could be attributed, at least in part, to
the inhibition of proinflammatory cytokine production (TNF-α and IL-6), COX-2, and iNOS protein
expression. These effects of chrysophanol are caused by the inhibition of LPS-induced NF-κB
activation, IκB-α degradation, and caspase-1 activation. These results provide experimental evidence
showing that chrysophanol might prove useful in the treatment of inflammatory diseases.
CNS Activity
Originator
Approval Year
PubMed
Patents
Sample Use Guides
Experimental
colitis in mice was induced by a 5% DSS dissolved in the drinking water for 7 days.
Chrysophanol was administered at doses of 5 mg/kg once a day for 7 days prior to 5% DSS
supplement.
Route of Administration:
Oral
Chrysophanol (80 and 120 uM) significantly blocks cell proliferation when combined with the mTOR inhibitor, Rapamycin. Chrysophanol inhibits EGF-induced phosphorylation of EGFR and suppresses activation of AKT and mTOR/p70S6K, and significantly blocks cell proliferation. Chrysophanol dose dependently decreases CCK-8 and the viability of EGFR-overexpressing SNU-C5 cells. Chrysophanol treatment dose-dependently decreases EGF induced phosphorylation of EGFR at Tyr1068. Chrysophanol (80 and 120 uM) reduces the phosphorylation levels of mTOR at Ser2448. Chrysophanol (80 and 120 uM) also decreases the phosphorylation levels of p70S6K at Thr389.