Celastrol

Short Summary : Antioxidant, anti-inflammatory and immunosuppressive agent

Category : Ubiquitination/ Proteasome|Proteasome

Purity : 0.9849

CAS Number : 34157-83-0

Formula : C29H38O4

Molecular Weight : 450.61

SMILE : CC1=C(C(=O)C=C2C1=CC=C3C2(CCC4(C3(CCC5(C4CC(CC5)(C)C(=O)O)C)C)C)C)O

Solubility : >22.6mg/mL in DMSO

Storage : Store at -20°C

Description : Celastrol is a potent proteasome inhibitor [1].Proteasomes are protein complexes that degrading unneeded or damaged proteins by proteolysis.Celastrol is a potent proteasome inhibitor and an antioxidant, anti-inflammatory and immunosuppressive agent. In a cell-free proteasome activity assay, Celastrol inhibits the chymotrypsin-like activity of a purified rabbit 20S proteasome at 2.5umol and human prostate cancer cellular 26S proteasome at 1-5 μmol. In PC-3 and LNCaP (AR-positive) cells, Celastrol results in the accumulation of ubiquitinated proteins and proteasome substrates (IKB-A, Bax, and p27), and induction of apoptosis [1]. In KBM-5 cells, Celastrol enhances TNF-induced apoptosis by 2% to 92%. In the tumor cells, Celastrol inhibited TNF-induced tumor-cell invasion by 12-fold [2]. In human PBMCs, Celastrol inhibited LPS-induced TNF-α production with IC50 value of 70 nM and LPS-induced IL 113 production with IC50 value of 30nM in a dose-dependent way [3].In PC-3 tumor–bearing nude mice, Celastrol (1-3 mg/kg/d,1-31 days) inhibited the tumor growth by 65-93% [1]. References:[1]. Yang H, Chen D, Cui QC, et al. Celastrol, a triterpene extracted from the Chinese “Thunder of God Vine,” is a potent proteasome inhibitor and suppresses human prostate cancer growth in nude mice. Cancer Res, 2006, 66(9): 4758-4765.[2]. Allison AC, Cacabelos R, Lombardi VR, et al. Celastrol, a potent antioxidant and anti-inflammatory drug, as a possible treatment for Alzheimer’s disease. Prog Neuropsychopharmacol Biol Psychiatry, 2001, 25(7):,1341-1357.[3]. Sethi G, Ahn KS, Pandey MK, et al. Celastrol, a novel triterpene, potentiates TNF-induced apoptosis and suppresses invasion of tumor cells by inhibiting NF-kappaB-regulated gene products and TAK1-mediated NF-kappaB activation. Blood, 2007, 109(7): 2727-2735.

Download datasheet