Celastrol - CAS 34157-83-0
Catalog number: 34157-83-0
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C29H38O4
COA:
Certificate of Analysis-Celastrol 34157-83-0 B15W0226  
Description:
Celastrol is a chemical compound isolated from the root extracts of Tripterygium wilfordii (Thunder god vine) and Celastrus regelii. It is a pentacyclic triterpenoid and belongs to the family of quinone methides. It is a potent antioxidant and anti-inflammatory agent. It is a novel HSP90 inhibitor.
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Purity:
>98%
Appearance:
Red powder
Synonyms:
Tripterine; (2R,4aS,6aS,6aR,14aS,14bR)-10-hydroxy-2,4a,6a,6a,9,14a-hexamethyl-11-oxo-1,3,4,5,6,13,14,14b-octahydropicene-2-carboxylic acid; 3-Hydroxy-9β,13α-dimethyl-2-oxo-24,25,26-trinoroleana-1(10),3,5,7-tetraen-29-oic acid; 10-Hydroxy-2,4a,6a,9,12b,14a-hexamethyl-11-oxo-1,2,3,4,4a,5,6,6a,11,12b,13,14,14a,14b-tetradecahydro-picene-2-carboxylic acid
MSDS:
Material Safety Data Sheet-Celastrol 34157-83-0  
Quality Standard:
Enterprise Standard
Quantity:
Grams-Kilos
1.Celastrol supports survival of retinal ganglion cells injured by optic nerve crush
Haksu Kyung, Jacky M.K. Kwong, Vlad Bekerman, Natik Piri*. BRAIN RESEARCH 1609 (2015) 21-30
Celastrol, a quinine methide triterpene extracted from the perennial vine Tripterygium wilfordii (Celastraceae), has been used in traditional Chinese medicine as a natural remedy for inflammation and a variety of autoimmune diseases for hundreds of years. Celastrol has been identified as a potential neuroprotective candidate in a comprehensive drug screen against various neurodegenerative diseases and has since been demonstrated to have cell protective properties in animal models of “protein misfolding” neurodegenerative disorders such as Parkinson's, Hungtington's, Alzheimer's diseases, and amyotrophic lateral sclerosis. The neuroprotective effects of celastrol are associated with the activation of heat shock and antioxidant responses that lead to an induction of an array of cytoprotective genes involved in protein folding/aggregation/turnover and the scavenging and export of reactive species. Furthermore, celastrol was shown to attenuate microglial activation and production of tumor necrosis factor (TNF)-alpha. Since protein misfolding/aggregation, oxidative damage and microglial activation have been associated with the pathogenesis of glaucoma, we hypothesized that celastrol could be a potent multifactorial therapeutic drug for the treatment of this disease.
2.The natural compound celastrol inhibits necroptosis and alleviates ulcerative colitis in mice
Zhenyu Jia, Chunfang Xu, JiaqingShen, Yang He*. International Immunopharmacology 29 (2015) 552-559
Celastrol, also known as Thunder of God Vine, is a triterpene from the root bark of the Chinese medicinal plant Tripterygium wilfordii. Celastrol possesses multiple biological and pharmacological activities, including immune modulation, anti-inflammatory, and anti-tumor activities.The in vivo anti-inflammatory effects of this triterpene have been demonstrated in multiple animal models, including Alzheimer disease, asthma, systemic lupus erythematosus, and rheumatoid arthritis. Moreover, previous studies have revealed that celastrol can ameliorate mouse colitis and human Crohn's disease by inhibiting pro-inflammatory cytokine secretion. In this study, the author hypothesized that the anti-inflammatory activity of celastrol might be mediated by modulating the cellular necroptosis related signal pathway. Therefore, we established a mouse model of UC and explore the mechanism of celastrol in UC treatment.
3.Celastrol Protects against Obesity and Metabolic Dysfunction through Activation of a HSF1-PGC1α Transcriptional Axis
Xinran Ma, Lingyan Xu, Cell Metabolism 22, 695-708, October 6, 2015
Altering the balance between energy intake and expenditure is a potential strategy for treating obesity andmetabolic syndrome. Nonetheless, despite years of progress in identifying diverse molecular targets, biological-based therapies are limited. Here we demonstrate that heat shock factor 1 (HSF1) regulates energy expenditure through activation of a PGC1α-dependent metabolic program in adipose tissues and muscle. Genetic modulation of HSF1 levels altered white fat remodeling and thermogenesis, and pharmacological activation of HSF1 via celastrol was associated with enhanced energy expenditure, increased mitochondrial function in fat and muscle and protection against obesity, insulin resistance, and hepatic steatosis during high-fat diet regimens. The beneficial metabolic changes elicited by celastrol were abrogated in HSF1 knockout mice. Overall, our findings identify the temperature sensor HSF1 as a regulator of energy metabolism and demonstrate that augmenting HSF1 via celastrol represents a possible therapeutic strategy to treat obesity and its myriad metabolic consequences.
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