| Stereochemistry | ABSOLUTE |
| Molecular Formula | C29H38O4 |
| Molecular Weight | 450.6096 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 6 / 6 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
[H][C@@]12C[C@@](C)(CC[C@]1(C)CC[C@]3(C)C4=CC=C5C(C)=C(O)C(=O)C=C5[C@]4(C)CC[C@@]23C)C(O)=O
InChI
InChIKey=KQJSQWZMSAGSHN-JJWQIEBTSA-N
InChI=1S/C29H38O4/c1-17-18-7-8-21-27(4,19(18)15-20(30)23(17)31)12-14-29(6)22-16-26(3,24(32)33)10-9-25(22,2)11-13-28(21,29)5/h7-8,15,22,31H,9-14,16H2,1-6H3,(H,32,33)/t22-,25-,26-,27+,28-,29+/m1/s1
| Molecular Formula | C29H38O4 |
| Molecular Weight | 450.6096 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ABSOLUTE |
| Additional Stereochemistry | No |
| Defined Stereocenters | 6 / 6 |
| E/Z Centers | 0 |
| Optical Activity | UNSPECIFIED |
Celastrol is a pentacyclic triterpenoid isolated from the root extracts of Tripterygium wilfordii, a perrennial creeping plant indigenous to large area in Southern China. Celastrol possess antioxidant and anti-inflammatory and anticancer action. In the mouse model of rheumatoid arthritis it reduced inflammatory swelling, suppressed humoral and skin response and reduced pathological progression of joint. Celastrol demonstrated efficacy in transgenic mouse model of amyotrophic lateral sclerosis. Anticancer activity of celastrol was shown in xenograft models of prostate cancer. Celastrol suppresses food intake, blocks reduction of energy expenditure, and leads to up to 45% weight loss in hyperleptinemic diet-induced obese (DIO) mice by increasing leptin sensitivity. Celastrol acts by interfering with the activity of Hsp90, IKK-beta and proteasome S26 subunit.
Originator
Approval Year
PubMed
Patents
Sample Use Guides
In collagen-induced arthritis study on mice, celastrol was administered orally at 15 and 30 mg/kg. In model of prostate cancer celastrol was administered at doses 1-3 mg/kg intraperitoneally.
Route of Administration:
Other
The ability of celastrol to inhibit NF-kB activation was studied in vitro in Jurkat cell line. Cells were preincubated with various concentrations of celastrol for 30 min prior to stimulation with TNF-alpha or PMA. After the stimulation, nuclear extracts were prepared and DNA-binding activity of NF-kB in the nuclear extracts was measured by electrophoretic mobility shift assays. Pretreatment of celastrol dose-dependently inhibited DNA-binding activity of NF-kB induced by TNF-a or PMA. The effect was apparent at concentrations of celastrol below 0.3 ug/ml.