| Stereochemistry | ABSOLUTE |
| Molecular Formula | C37H56O11 |
| Molecular Weight | 676.8339 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 19 / 19 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
[H][C@]12C[C@@]3(C)[C@]4([H])CC[C@]5([H])[C@]6(C[C@@]46C[C@@H](OC(C)=O)[C@]3(C)[C@@]1([H])[C@H](C)C[C@]7(O[C@H](O)[C@@]8(C)O[C@@H]78)O2)CC[C@H](O[C@]9([H])OC[C@@H](O)[C@H](O)[C@H]9O)C5(C)C
InChI
InChIKey=NEWMWGLPJQHSSQ-PSDKAYTQSA-N
InChI=1S/C37H56O11/c1-17-12-37(29-34(7,47-29)30(42)48-37)46-20-13-32(5)22-9-8-21-31(3,4)23(45-28-27(41)26(40)19(39)15-43-28)10-11-35(21)16-36(22,35)14-24(44-18(2)38)33(32,6)25(17)20/h17,19-30,39-42H,8-16H2,1-7H3/t17-,19-,20+,21+,22+,23+,24-,25+,26+,27-,28+,29-,30+,32+,33-,34+,35-,36+,37-/m1/s1
Actein is tetracyclic triterpenoid compound isolated from the rhizome of Cimicifuga foetida L. In North America, the cimicifuga species had a long medicinal history, mainly used to treat diarrhea, sore throat, and rheumatism. Actein inhibits the activity of the Na,K-ATPase, which affects calcium metabolism. The primary target of actein may relate to calcium metabolism since this agent altered the expression of several genes related to calcium. Although actein was shown to exhibit other pathological functions, such as prevention of oxidative damage to osteoblast and regulation of lipid disorder, the major role of actein is played on its anticancer activity, particularly in breast cancer.
Originator
Approval Year
PubMed
Patents
Sample Use Guides
MC3T3-E1 osteoblastic cells were pretreated with actein (0.01–1 uM) for 1 h and then exposed to 100 nM 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for 48 h. Cell viability was again measured using the water-soluble tetrazolium (WST) assay. Actein-pretreated cells had increased viability compared to those treated with TCDD only, in a concentration-dependent manner. The TCDD-induced increased apoptosis was also restored to a level similar to that in the control group by pretreatment with 1 uM actein. Pretreatment with actein also prevented TCDD-induced autophagic activity in a concentration-dependent manner. Taking these findings together, pretreatment with actein protected MC3T3-E1 osteoblastic cells from TCDD-induced apoptosis
SUBSTANCE RECORD
