Celastrol - CAS 34157-83-0
Not Intended for Therapeutic Use. For research use only.
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Celastrol (tripterine) is a chemical compound isolated from the root extracts of Tripterygium wilfordii (Thunder god vine) and Celastrus regelii. Celastrol is a pentacyclic triterpenoid and belongs to the family of quinone methides. In in vitro and in vivo animal experiments, celastrol exhibits antioxidant, anti-inflammatory, anticancer, and insecticidal activities. It has been shown to have obesity-controlling effects in mice.
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Certificate of Analysis-Celastrol 34157-83-0 B15W0226  
Material Safety Data Sheet-Celastrol 34157-83-0  
Canonical SMILES:
Hsp90 | HSP
Catalog Number Size Price Stock Quantity
B0084-187070 10 mg $198 In stock
B0084-187070 1 g $798 In stock
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Chemical Structure
CAS 34157-83-0 Celastrol

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Reference Reading

1.Protective Effects of Celastrol on Diabetic Liver Injury via TLR4/MyD88/NF-κB Signaling Pathway in Type 2 Diabetic Rats.
Han LP1, Li CJ1, Sun B1, Xie Y1, Guan Y1, Ma ZJ1, Chen LM1. J Diabetes Res. 2016;2016:2641248. doi: 10.1155/2016/2641248. Epub 2016 Jan 19.
Immune and inflammatory pathways play a central role in the pathogenesis of diabetic liver injury. Celastrol is a potent immunosuppressive and anti-inflammatory agent. So far, there is no evidence regarding the mechanism of innate immune alterations of celastrol on diabetic liver injury in type 2 diabetic animal models. The present study was aimed at investigating protective effects of celastrol on the liver injury in diabetic rats and at elucidating the possible involved mechanisms. We analyzed the liver histopathological and biochemical changes and the expressions of TLR4 mediated signaling pathway. Compared to the normal control group, diabetic rats were found to have obvious steatohepatitis and proinflammatory cytokine activities were significantly upregulated. Celastrol-treated diabetic rats show reduced hepatic inflammation and macrophages infiltration. The expressions of TLR4, MyD88, NF-κB, and downstream inflammatory factors IL-1β and TNFα in the hepatic tissue of treated rats were downregulated in a dose-dependent manner.
2.Synergism between NF-kappa B inhibitor, celastrol, and XIAP inhibitor, embelin, in an acute myeloid leukemia cell line, HL-60.
Pazhang Y, Jaliani HZ1, Imani M, Dariushnejad H. J Cancer Res Ther. 2016 Jan-Mar;12(1):155-60. doi: 10.4103/0973-1482.150407.
AIM OF STUDY: Embelin and celastrol, inhibitors of XIAP and NF-κB proteins respectively, have been derived from natural sources and shown anti-tumor activities against different cancer cell lines. Some interactions have recently been discovered between XIAP and NF-κB pathways, but the effects of these inhibitors in combination have not been investigated yet. We have studied possible synergistic effects of embelin in combination with celastrol, in an acute myeloid leukemia model, HL-60 cell line.
3.Celastrol attenuates oxidative stress in the skeletal muscle of diabetic rats by regulating the AMPK-PGC1α-SIRT3 signaling pathway.
Guan Y1, Cui ZJ2, Sun B1, Han LP1, Li CJ1, Chen LM1. Int J Mol Med. 2016 May;37(5):1229-38. doi: 10.3892/ijmm.2016.2549. Epub 2016 Apr 5.
Oxidative stress plays a key role in the pathogenesis of diabetic myopathy. Celastrol provides a wide range of health benefits, including antioxidant, anti-inflammatory and antitumor effects. We hypothesized that celastrol may exert an antioxidant effect in the skeletal muscle of diabetic rats. In the present study, MnSOD activity was determined by spectrophotometry. The protein levels were evaluated by western blot analysis and mRNA content was quantified by RT‑qPCR. We firstly found that the levels of AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor coactivator 1α (PGC1α), silent mating-type information regulation 2 homolog 3 (Sirt3) and manganese superoxide dismutase (MnSOD) were all decreased in the skeletal muscle of diabetic patients. Male rats with diabetes were also treated with the vehicle or with celastrol at 1, 3 and 6 mg/kg/day for 8 weeks. The administration of celastrol at 3 and 6 mg/kg attenuated the deterioration of skeletal muscle, as shown by histological analysis, decreased the malondialdehyde (MDA) level and increased the glutathione (GSH) level assayed by enzyme-linked immunosorbent assay (ELISA) method.