Stereochemistry | ACHIRAL |
Molecular Formula | C15H10O5 |
Molecular Weight | 270.2369 |
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=C(O)C=C3O)C2=O
InChI
InChIKey=RHMXXJGYXNZAPX-UHFFFAOYSA-N
InChI=1S/C15H10O5/c1-6-2-8-12(10(17)3-6)15(20)13-9(14(8)19)4-7(16)5-11(13)18/h2-5,16-18H,1H3
Molecular Formula | C15H10O5 |
Molecular Weight | 270.2369 |
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 |
Emodin is a naturally occurring anthraquinone present in the roots of numerous plants and lichens and an active ingredient of various Chinese herbs. Emodin possesses various biological properties and serves as an anti-bacterial and anti-inflammatory agent. Emodin was studied as a potential anti-cancer agent: e.g., it was shown, that compound inhibits the invasion and migration of colon cancer cells in vitro and in vivo by blocking EMT, which is related with the inhibition of Wnt/β-catenin signaling pathway. Besides, emodin effectively ameliorates asthmatic airway inflammation and alternatively activated macrophages (AAMs) polarization, and thus can be a potential agent for the treatment of asthma. It is known that the Inhibition of AAMs is an alternative therapeutic strategy for treating asthma. Some experiments have revealed that emodin can be a beneficial dietary supplement in prolonging lifespan.
Approval Year
PubMed
Patents
Sample Use Guides
murine asthma model: intraperitoneal injection of emodin (20 mg·kg-1·d-1, ip) 1 h prior to DRA (dust mite, ragweed and aspergillus) challenge on days 12-14 significantly decreased pulmonary eosinophil and lymphocyte infiltration, mucus secretion and serum IgE production, as well as IL-4 and IL-5 production in bronchoalveolar lavage fluid.
Route of Administration:
Intraperitoneal
The potential for emodin to inhibit pancreatic cancer cell proliferation was examined using 4 human pancreatic adenocarcinoma cell lines: Mia Paca-2, BxPC-3, Panc-1, and L3.6pl. Forty-eight-hour treatment with 50 muM emodin inhibited proliferation in Mia Paca-2 cells by 42%, BxPc-3 by 38%, L3.6pl by 56%, and Panc-1 by 18% (all P < .01). In three-fourths of the cell lines, emodin treatment resulted in an increase (from 4.7% to 22%) in the cell population number in apoptosis when measured by flow cytometric analysis