Product Name:Celastrol bulk powder
Botanic Source:The God Vine(Tripterygium wilfordii hook.f)
CAS No:34157-83-0
Colour: Reddish orange crystal powder with characteristic odor and taste
Specification:≥98% HPLC
GMO Status:GMO Free
Packing: in 25kgs fiber drums
Storage:Keep container unopened in cool, dry place,Keep away from strong light
Shelf Life:24 months from date of production
Celastrol Powder is the active ingredient in Tripterygii Radix, which is the dry root and rhizome of the God Vine. There are four species in total, namely Tripterygium wilfordii Hook.f, Tripterygium hypoglaucum Hutch, Tripterygium regelii Sprague et Takeda, and Tripterygium forresti Dicls.
Diterpenoids: triptolide(cas no.38748-32-2), Tripdiolide( cas no.38647-10-8), etc.
Triterpenoids: Celastrol(cas no.34157-83-0), Wilforlide A(cas no.84104-71-2), etc.
Alkaloids:Wilforgine(cas no.37239-47-7), Wolverine (cas no.11088-09-8), wilforidine, etc.
Tripterygium is a pentazine triterpene found naturally in Tripterygium wilfordii. It is effective in treating rheumatoid arthritis. Triptolide prevents the proteasome and nuclear factor Kb from functioning.
Celastrol (Tripterin) is a proteasome inhibitor with anti-inflammatory and antioxidant activities. It effectively and preferentially inhibits the chymotrypsin-like activity of the 20S proteasome with an IC50 of 2.5 μM.
Tripterine is a powerful antioxidant and anti-inflammatory agent. It is a new HSP90 inhibitor (disrupts the Hsp90/Cdc37 complex), has anti-cancer effects (anti-angiogenesis – inhibits vascular endothelial growth factor receptor expression); antioxidant (inhibits lipid peroxidation) and anti-inflammatory activity (Inhibits the production of iNOS and inflammatory cytokines)
Biological Activity:
Celastrol (Tripterin) down-regulates basal and DNA-damaging agent-induced FANCD2 monoubiquitination, followed by protein degradation. Celastrol treatment eliminates IR-induced G2 checkpoint and enhances ICL drug-induced DNA damage and inhibitory effects on lung cancer cells by depleting FANCD2. Celastrol has significant inhibitory and apoptosis-inducing effects on DU145 cells cultured in vitro in a time- and dose-dependent manner. Celastrol’s anti-prostate cancer effect is partly through down-regulating the expression level of hERG channels in DU145 cells, suggesting that Celastrol may be a potential anti-prostate cancer drug, and its mechanism may be to block hERG channels. Celastrol improves experimental colitis in IL-10-deficient mice by inhibiting the PI3K/Akt/mTOR signaling pathway and upregulating autophagy. Celastrol has the potential to inhibit cytochrome P450 activity and may cause herbal interactions. Celastrol induces apoptosis in TNBC cells, suggesting that apoptosis may be mediated through mitochondrial dysfunction and the PI3K/Akt signaling pathway. Celastrol induces apoptosis and autophagy through the ROS/JNK signaling pathway. Celastrol inhibits dopaminergic neuron death in Parkinson’s disease by activating mitochondrial apoptosis.
Celastrol’s role in cancer chemosensitization:
Chemotherapy remains the main treatment option for cancer patients. However, chemotherapy often must be combined with other drugs to minimize adverse side effects and avoid drug resistance. Natural products are increasingly used as adjuvant therapies in combination with existing chemotherapy regimens to enhance treatment efficacy. One promising example of such a natural medicine is a triterpene compound called celastrol, which may have great potential for use as a chemical sensitizer. Originally identified from Thunder God Vine, it negatively regulates multiple oncogenic molecules such as NF-κB, topoisomerase II, Akt/mTOR, HSP90, STAT3, and Notch-1. These can lead to an anti-inflammatory response, inhibit tumor growth and survival, and eliminate angiogenesis. This chapter briefly summarizes the potential role of celastrol as a chemosensitizer and the underlying molecular mechanisms mediating its reported chemosensitizing effects in various cancers.
