| Synonyms |
2-furo[2,3-h][1]benzopyranone; Isopsoralen |
| IUPAC Name |
furo[2,3-h]chromen-2-one |
| Molecular Weight |
186.17 |
| Molecular Formula |
C11H6O3 |
| Canonical SMILES |
C1=CC2=C(C=CO2)C3=C1C=CC(=O)O3 |
| InChI |
1S/C11H6O3/c12-10-4-2-7-1-3-9-8(5-6-13-9)11(7)14-10/h1-6H |
| InChIKey |
XDROKJSWHURZGO-UHFFFAOYSA-N |
| Boiling Point |
360.00to362.00°C.at760.00mmHg |
| Melting Point |
135-142 °C. |
| Flash Point |
173.1±23.7 °C |
| Purity |
97 % (HPLC) |
| Density |
1.389 ± 0.06 g/cm3 |
| Solubility |
Chloroform, not well in ether and alcohol, not in water |
| Appearance |
White Solid. |
| Shelf Life |
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly |
| Storage |
Store at 2-8°C, keep in dry cool place |
| Complexity |
284 |
| Exact Mass |
186.031693 |
| Index Of Refraction |
1.667 |
| In Vitro |
Angelicin also inhibited the migration of non-small cell lung cancer (NSCLC) A549 cells in a Transwell assay in a dose-dependent manner. In addition, after angelicin treatment, the expression levels of Bax, cleaved caspase-3 and cleaved caspase-9 were increased, and Bcl-2 expression was decreased. Moreover, the results indicate that angelicin inhibits NSCLC growth not only by downregulating cyclin B1, cyclin E1 and Cdc2, which are related to the cell cycle, but also by reducing MMP2 and MMP9 and increasing E-cadherin expression levels. Furthermore, extracellular signal-regulated kinase (ERK)1/2 and c-Jun NH2-terminal protein kinase (JNK)1/2 phosphorylation increased in parallel with the angelicin treatments. The inhibition of ERK1/2 and JNK1/2 by specific inhibitors significantly abrogated angelicin-induced cell apoptosis, cell cycle arrest and migration inhibition. |
| In Vivo |
The cervical cancer cells were more sensitive to angelicin than cervical epithelial cells. At its IC30, angelicin inhibited the proliferation of HeLa and SiHa cells by blocking the cell cycle at the G1/G0 phase and inhibiting other malignant behaviors, including colony formation, tumor formation in soft agar, migration and invasion. At the IC50, angelicin induced cell death potentially by promoting apoptosis. By identifying the hallmarks of autophagy, it was observed that angelicin treatment caused the accumulation of microtubule associated protein 1 light chain 3-β (LC3B) in the cytoplasm of HeLa and SiHa cells. Western blotting results demonstrated that cleaved LC3B-II and autophagy related proteins (Atg)3, Atg7 and Atg12-5 were upregulated following angelicin treatment. It was also determined that the phosphorylation of mTOR was induced by angelicin treatment. Furthermore, the inhibition of angelicin-induced mTOR phosphorylation did not disrupt its inhibitory effect on autophagy, indicating that angelicin inhibited autophagy in an mTOR-independent manner. |
| PSA |
43.35000 |
| Target |
IC50 value: 49.56 μM (cellular cytotoxicity); 5.39 μg/ml (28.95 μM) (against MHV-68) |
| Vapor Pressure |
9.7X10-6 mm Hg at 25 °C (est) |
| XLogP3-AA |
2 |
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