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    CAS No. 34157-83-0 Price $40 / 20mg
    Catalog No.CFN99198Purity>=98%
    Molecular Weight450.61Type of CompoundTriterpenoids
    FormulaC29H38O4Physical DescriptionRed powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Our products had been exported to the following research institutions and universities, And still growing.
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    Biological Activity
    Description: Celastrol is a potent proteasome inhibitor for the chymotrypsin-like activity of a purified 20S proteasome with IC50 of 2.5 μM. Celastrol is also a novel HSP90 inhibitor, it has anti-proliferative, anti-inflammatory, anti-tumor , antiangiogenesis, and antioxidant activities. Celastrol inhibits Plasmodium falciparum enoyl-acyl carrier protein reductase and inhibits VEGF receptors expression.
    Targets: Bcl-2/Bax | Caspase | VEGFR | HIF | NF-kB | Akt | HSP (e.g. HSP90) | ROS | JNK | Bcr-Abl | HIV | MAPK | TNF-α | IL Receptor | AP-1 | GLUT | HO-1 | NO
    In vitro:
    Am J Chin Med. 2015;43(1):137-48.
    Celastrol induces mitochondria-mediated apoptosis in hepatocellular carcinoma bel-7402 cells.[Pubmed: 25657108]
    Celastrol is a natural terpenoid isolated from Tripterygium wilfordii, a well-known Chinese medicinal herb that presents anti-proliferative activities in several cancer cell lines.
    Here, we investigated whether Celastrol induces apoptosis on hepatocellular carcinoma Bel-7402 cells and further explored the underlying molecular mechanisms. Celastrol caused a dose- and time-dependent growth inhibition and apoptosis of Bel-7402 cells. It increased apoptosis through the up-regulation of Bax and the down-regulation of Bcl-2 in Bel-7402 cells. Moreover, Celastrol induced the release of cytochrome c and increased the activation of caspase-3 and caspase-9, suggesting that Celastrol-induced apoptosis was related to the mitochondrial pathway.
    These results indicated that Celastrol could induce apoptosis in Bel-7402 cells, which may be associated with the activation of the mitochondria-mediated pathway.
    PLoS One. 2014 Nov 10;9(11):e112470.
    Celastrol stimulates hypoxia-inducible factor-1 activity in tumor cells by initiating the ROS/Akt/p70S6K signaling pathway and enhancing hypoxia-inducible factor-1α protein synthesis.[Pubmed: 25383959]
    Celastrol, a tripterine derived from the traditional Chinese medicine plant Tripterygium wilfordii Hook F. ("Thunder of God Vine"), has been reported to have multiple effects, such as anti-inflammation, suppression of tumor angiogenesis, inhibition of tumor growth, induction of apoptosis and protection of cells against human neurodegenerative diseases. However, the mechanisms that underlie these functions are not well defined.
    In this study, we reported for the first time that Celastrol could induce HIF-1α protein accumulation in multiple cancer cell lines in an oxygen-independent manner and that the enhanced HIF-1α protein entered the nucleus and promoted the transcription of the HIF-1 target genes VEGF and Glut-1. Celastrol did not influence HIF-1α transcription. Instead, Celastrol induced the accumulation of the HIF-1α protein by inducing ROS and activating Akt/p70S6K signaling to promote HIF-1α translation. In addition, we found that the activation of Akt by Celastrol was transient. With increased exposure time, inhibition of Hsp90 chaperone function by Celastrol led to the subsequent depletion of the Akt protein and thus to the suppression of Akt activity. Moreover, in HepG2 cells, the accumulation of HIF-1α increased the expression of BNIP3, which induced autophagy. However, HIF-1α and BNIP3 did not influence the cytotoxicity of Celastrol because the main mechanism by which Celastrol kills cancer cells is through stimulating ROS-mediated JNK activation and inducing apoptosis. Furthermore, our data showed that the dose required for Celastrol to induce HIF-1α protein accumulation and enhance HIF-1α transcriptional activation was below its cytotoxic threshold.
    A cytotoxic dose of Celastrol for cancer cells did not display cytotoxicity in LO2 normal human liver cells, which indicated that the novel functions of Celastrol in regulating HIF-1 signaling and inducing autophagy might be used in new applications, such as in anti-inflammation and protection of cells against human neurodegenerative diseases.
    Bioorg Med Chem. 2014 Nov 1;22(21):6053-61.
    Celastrol inhibits Plasmodium falciparum enoyl-acyl carrier protein reductase.[Pubmed: 25284249]
    Enoyl-acyl carrier protein reductase (ENR), a critical enzyme in type II fatty acid biosynthesis, is a promising target for drug discovery against hepatocyte-stage Plasmodium falciparum.
    In order to identify PfENR-specific inhibitors, we docked 70 FDA-approved, bioactive, and/or natural product small molecules known to inhibit the growth of whole-cell blood-stage P. falciparum into several PfENR crystallographic structures. Subsequent in vitro activity assays identified a noncompetitive low-micromolar PfENR inhibitor, Celastrol, from this set of compounds.
    Celastrol Description
    Source: The herbs of Tripterygium wilfordii Hook. f.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
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    PMID: 29328914

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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.2192 mL 11.0961 mL 22.1921 mL 44.3843 mL 55.4803 mL
    5 mM 0.4438 mL 2.2192 mL 4.4384 mL 8.8769 mL 11.0961 mL
    10 mM 0.2219 mL 1.1096 mL 2.2192 mL 4.4384 mL 5.548 mL
    50 mM 0.0444 mL 0.2219 mL 0.4438 mL 0.8877 mL 1.1096 mL
    100 mM 0.0222 mL 0.111 mL 0.2219 mL 0.4438 mL 0.5548 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Kinase Assay:
    Cancer Lett. 2008 Jun 8;264(1):101-6.
    Celastrol inhibits the growth of human glioma xenografts in nude mice through suppressing VEGFR expression.[Pubmed: 18343027 ]
    Celastrol, a compound purified from Tripterygium wilfordii whose preparations have been used for clinical treatment for rheumatoid arthritis, has been demonstrated to have antiangiogenic activity, and be inhibitory against mice tumor growth by a few recent studies. However, whether its antiangiogenic activity plays a role in the Celastrol-mediated suppression of tumor growth and the molecular basis of anti-tumor activity are poorly understood.
    In this study, we found that Celastrol inhibited the growth of human glioma xenografts in mice, which concurred with the suppression of angiogenesis. Interestingly, while Celastrol had no effect on either the expression of VEGF or its mRNA levels, Celastrol treatment lowered the expression levels of its receptors (VEGFR-1 and VEGFR-2) and their mRNA levels.
    These findings suggest that Celastrol have potential to be used as an antiangiogenesis drug through its role in suppressing VEGF receptors expression that might consequently reduce the signal transduction between VEGF and VEGFR.
    Toxicol Appl Pharmacol. 2014 Oct 1;280(1):42-52.
    Celastrol ameliorates HIV-1 Tat-induced inflammatory responses via NF-kappaB and AP-1 inhibition and heme oxygenase-1 induction in astrocytes.[Pubmed: 25064159]
    HIV-1 Tat causes extensive neuroinflammation that may progress to AIDS-related encephalitis and dementia. Celastrol possesses various biological activities such as anti-oxidant, anti-tumor, and anti-inflammatory activities.
    In this study, we investigated the modulatory effects of Celastrol on HIV-1 Tat-induced inflammatory responses and the molecular mechanisms underlying its action in astrocytes. Pre-treatment of CRT-MG human astroglioma cells with Celastrol significantly inhibited HIV-1 Tat-induced expression of ICAM-1/VCAM-1 and subsequent monocyte adhesiveness in CRT-MG cells. In addition, Celastrol suppressed HIV-1 Tat-induced expression of pro-inflammatory chemokines, such as CXCL10, IL-8, and MCP-1. Celastrol decreased HIV-1 Tat-induced activation of JNK MAPK, AP-1, and NF-κB. Furthermore, Celastrol induced mRNA and protein expression of HO-1 as well as Nrf2 activation. Blockage of HO-1 expression using siRNA reversed the inhibitory effect of Celastrol on HIV-1 Tat-induced inflammatory responses.
    These results suggest that Celastrol has regulatory effects on HIV-1 Tat-induced inflammatory responses by blocking the JNK MAPK-AP-1/NF-κB signaling pathways and inducing HO-1 expression in astrocytes.
    Cell Research:
    Cancer Lett. 2010 Apr 28;290(2):182-91.
    Celastrol, a novel HSP90 inhibitor, depletes Bcr-Abl and induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation.[Pubmed: 19819619 ]
    T315I Bcr-Abl in chronic myelogenous leukemia (CML) is the most notorious point mutations to elicit acquired resistance to imatinib.
    In the present study, we investigated the effect of Celastrol on CML cells bearing wild-type Bcr-Abl or T315I-mutant. The results revealed that Celastrol potently downregulated the protein levels of Bcr-Abl, and inhibited the growth in CML cells in vitro and in nude mouse xenografts regardless of Bcr-Abl mutation status. Celastrol induced mitochondrial-dependent apoptosis.
    In conclusion, Celastrol exhibits potent activity against CML cells bearing wild-type Bcr-Abl or -the T315I-mutant.
    Prog Neuropsychopharmacol Biol Psychiatry. 2001 Oct;25(7):1341-57.
    Celastrol, a potent antioxidant and anti-inflammatory drug, as a possible treatment for Alzheimer's disease.[Pubmed: 11513350]
    In the brains of patients with Alzheimer's disease (AD) signs of neuronal degeneration are accompanied by markers of microglial activation, inflammation, and oxidant damage. The presence of nitrotyrosine in the cell bodies of neurons in AD suggests that peroxynitrite contributes to the pathogenesis of the disease. A drug with antioxidant and anti-inflammatory activity may prevent neuronal degeneration in AD.
    Celastrol, a plant-derived triterpene, has these effects. In low nanomolar concentrations Celastrol was found to suppress the production by human monocytes and macrophages of the pro-inflammatory cytokines TNF-alpha and IL-1beta. Celastrol also decreased the induced expression of class II MHC molecules by microglia. In macrophage lineage cells and endothelial cells Celastrol decreased induced but not constitutive NO production. Celastrol suppressed adjuvant arthritis in the rat, demonstrating in vivo anti-inflammatory activity. Low doses of Celastrol administered to rats significantly improved their performance in memory, learning and psychomotor activity tests.
    The potent antioxidant and anti-inflammatory activities of Celastrol, and its effects on cognitive functions, suggest that the drug may be useful to treat neurodegenerative diseases accompanied by inflammation, such as AD.