Celastrol (NSC 70931)

For research use only.

Catalog No.S1290 Synonyms: Tripterine

6 publications

Celastrol (NSC 70931) Chemical Structure

CAS No. 34157-83-0

Celastrol (NSC 70931, Tripterine) is a potent proteasome inhibitor for the chymotrypsin-like activity of a purified 20S proteasome with IC50 of 2.5 μM. Celastrol induces apoptosis and autophagy via the ROS/JNK signaling pathway. Celastrol inhibits dopaminergic neuronal death of Parkinson's disease through activating mitophagy.

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Selleck's Celastrol (NSC 70931) has been cited by 6 publications

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  • SK-BR-3, A549, HCT-116 and BT-474 cells were incubated with or without X66 for 1 h before exposed to GM, celastrol or MG132 for 8 h. Cell lysates were analyzed by Western blot with indicated antibodies.

    Oncotarget, 2016, 7(20):29648-63.. Celastrol (NSC 70931) purchased from Selleck.

    Effects of compound 10 and celastrol on client proteins degradation. Both compound 10 and celastrol induces decreases of Hsp90 client proteins (Akt and Cdk4) through a concentration -dependent manner by Western blot. Meanwhile, compound 10 and celastrol have no effect on the expression level of Hsp90.

    Eur J Med Chem, 2017, 136:63-73. Celastrol (NSC 70931) purchased from Selleck.

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Choose Selective Proteasome Inhibitors

Biological Activity

Description Celastrol (NSC 70931, Tripterine) is a potent proteasome inhibitor for the chymotrypsin-like activity of a purified 20S proteasome with IC50 of 2.5 μM. Celastrol induces apoptosis and autophagy via the ROS/JNK signaling pathway. Celastrol inhibits dopaminergic neuronal death of Parkinson's disease through activating mitophagy.
Features A potent antioxidant and anti-inflammatory drug.
Targets
20S proteasome [1]
(Cell-free assay)
2.5 μM
In vitro

Celastrol at 5 μM inhibits the chymotrypsin-like, PGPH-like, and trypsin-like activities of the purified 20S proteasome by 80%, 5%, and <1%, respectively, whereas at 10 μM, it inhibits these three proteasomal activities by ∼90%, 15%, and <1%, respectively. Celastrol significantly inhibits the proteasomal chymotrypsin activity in PC-3 cells in a concentration-dependent manner. Celastrol at 2.5 μM to 5 μM induces caspase-3 activity by 4.7-fold to 5.5-fold in PC-3 cells. Celastrol (5 μM) treated cells, the levels of the proteasome target proteins, IκB-α and Bax, are increased after 1 hour and further increased to its peak for 4 hours to 12 hours. Celastrol (2.5 μM) treatment induces proteasome inhibition by 40%, as shown by the decreased levels of chymotrypsin-like activity and increased accumulation of ubiquitinated proteins in LNCaP cells. Celastrol (2.5 μM) induces apoptosis in the Celastrol-treated LNCaP cells, as shown by increased levels of caspase-3 activity (up to 3.5-fold), PARP cleavage, and apoptotic morphology. [1] Celastrol (300 nM) is found to suppress LPS-induced production of TNF-alpha and IL-1beta by human monocytes and macrophages. Celastrol (100 nM) also decreases LPS-induced expression of class II MHC molecules by microglia. Celastrol strongly inhibits LPS and IFN-y-induced NO production with IC50 of 200 nM in macrophage lineage cells. Celastrol strongly inhibits TNF-α and IFN-γ-induced NO production with IC50 of 200 nM in endothelial cells. [2] Celastrol (2.5 μM) potentiates the apoptosis induced by TNF and chemotherapeutic agents and inhibits invasion, both regulated by NF-kappaB activation, in KBM-5 cells. Celastrol (2.5 μM) suppresses the expression of TNF induced the expression of gene products involved in antiapoptosis (IAP1, IAP2, Bcl-2, Bcl-XL, c-FLIP, and survivin), proliferation (cyclin D1 and COX-2), invasion (MMP-9), and angiogenesis (VEGF) in KBM-5 cells. Celastrol (5 μM) is found to inhibit the TNF-induced activation of IkappaBalpha kinase, IkappaBalpha phosphorylation, IkappaBalpha degradation, p65 nuclear translocation and phosphorylation, and NF-kappaB-mediated reporter gene expression. [3] Celastrol inhibits proliferating of RPMI 8226, KATOIII, UM-SCC1, U251MG and MDA-MB-231 cells with IC50 of 0.52 μM, 0.54 μM, 0.76 μM, 0.69 μM and 0.67 μM, respectively. Celastrol (1 μM) inhibits growth of RPMI 8226 with a decrease in the levels of cyclin D1 and cyclin E, but concomitant increase in the levels of p21 and p27. Celastrol induces apoptosis in RPMI-8226 cells indicated by the activation of caspase-8, bid cleavage, caspase-9 activation, caspase-3 activation, PARP cleavage and through the down regulation of anti-apoptototic proteins. Celastrol (1 μM) suppresses Akt pathway and activates JNK kinase in RPMI-8226 cells. [4]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
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NB-EBc1 MoHodWhVWyCjc4PhfS=> NW\rboF5eUiWUzDv[kBx\WSrYYTybYMh[2GwY3XyJINmdGxibHnu[ZMhfG9iaXTlcpRq\nlibYXseIlxdGVib4Dwc5J1fW6rdHnld{Bnd3JiZIL1[{Bz\XC3coDvd4lv\zpiQ3;u[olzdWG2b4L5JJNkemWnbjDmc5IhVkJvRVLjNUBk\Wyucx?= MYO8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQTR|NUGzPUc,Ojl2M{WxN|k9N2F-
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Rh30 M{LQZZFJXFNiYYPzZZk> M1XsT5FJXFNib3[gdIVlcWG2cnnjJINidmOncjDj[YxtKGyrbnXzJJRwKGmmZX70bYZ6KG23bITpdIxmKG:ycH;yeJVvcXSrZYOg[o9zKGS{dXegdoVxfXKyb4Ppcoc7KEOxbn\pdo1ifG:{eTDzZ5Jm\W5iZn;yJHJpOzBiY3XscJM> M4LRS|xiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ7NEO1NVM6Lz5{OUSzOVE{QTxxYU6=
Saos-2 NVe5NpRZeUiWUzDhd5NigQ>? NGrKNFFyUFSVIH;mJJBm\GmjdILpZ{Bk[W6lZYKgZ4VtdCCuaX7ld{B1dyCrZHXueIlngSCvdXz0bZBt\SCxcIDvdpR2dmm2aXXzJIZweiCmcoXnJJJmeHW{cH;zbY5oQiCFb37mbZJu[XSxcomgd4Nz\WWwIH\vdkBU[W:|LUKgZ4VtdHN? NEPGNnY9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{OUSzOVE{QSd-Mkm0N|UyOzl:L3G+
OHS-50 NEe3Zm1yUFSVIHHzd4F6 MXfxTHRUKG:oIIDl[IlifHKrYzDjZY5k\XJiY3XscEBtcW6nczD0c{Bq\GWwdHnmfUBufWy2aYDs[UBweHCxcoT1col1cWW|IH\vdkBlenWpIILldJVzeG:|aX7nPkBEd26oaYLtZZRwenlic3Py[YVvKG[xcjDPTHMuPTBiY3XscJM> M2nldFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ7NEO1NVM6Lz5{OUSzOVE{QTxxYU6=
SK-N-SH MlvMdWhVWyCjc4PhfS=> MlrsdWhVWyCxZjDw[YRq[XS{aXOgZ4Fv[2W{IHPlcIwhdGmwZYOgeI8hcWSnboTp[pkhdXWudHnwcIUhd3Cyb4L0eY5qfGmnczDmc5Ih\HK3ZzDy[ZB2enCxc3nu[|ohS2:wZnnycYF1d3K7IIPjdoVmdiCob4KgV2suVi2VSDDj[Yxtew>? Ml3NQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjl2M{WxN|koRjJ7NEO1NVM6RC:jPh?=
HCT116 MY\BcpRqeHKxbHnm[ZJifGm4ZTDhd5NigQ>? NHPmfo01QCCqcoO= NF\YZZdCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjDWFEyPiClZXzsd{Bi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBKSzVyIE2gOU4zPiEQvF2u M1vvcVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ7NEi2PVU1Lz5{OUS4Olk2PDxxYU6=
HepG2 M3XyNmFvfGmycn;sbYZmemG2aY\lJIF{e2G7 MkfnOFghcHK| NYfxZ2xiSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDI[ZBIOiClZXzsd{Bi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBKSzVyIE2gOk4yPyEQvF2u MmK3QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjl2OE[5OVQoRjJ7NEi2PVU1RC:jPh?=
A549 MmnQRY51cXC{b3zp[oVz[XSrdnWgZZN{[Xl? NXSxUXlzPDhiaILz M4jRSGFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iQUW0PUBk\WyuczDh[pRmeiB2ODDodpMh[nliTWTUJIF{e2G7LDDJR|UxKD1iNj61PUDPxE1w MVG8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQTR6Nkm1OEc,Ojl2OE[5OVQ9N2F-
MCF7 NEn6OlZCdnSrcILvcIln\XKjdHn2[UBie3OjeR?= MnnROFghcHK| MUPBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE2FRkegZ4VtdHNiYX\0[ZIhPDhiaILzJIJ6KE2WVDDhd5NigSxiSVO1NEA:KDZwOESg{txONg>? NEXzWo49[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{OUS4Olk2PCd-Mkm0PFY6PTR:L3G+
HEK293 NYfI[ZFYS3m2b4TvfIlkcXS7IHHzd4F6 NHjHWYVEgXSxdH;4bYNqfHliYXfhbY5{fCCKRVuyPVMh[2WubIOgLGNQNUGGRErNRX8xODdrOzDDR|UxKGK7IHPlcIwhfmmjYnnsbZR6KGG|c3H5JIlvKESPRV2gLFExLSCIQmOpJI1m\GmjIIXzbY5oKFSFIIDsZZRmeyxiYomgVoV{[Xq3cnnuJGYpPTZyL{W5NEktKEOFNUCgQUAxNjh|NzFOwG0v MY[8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyzNFE6QDJxJ{7DbGVOSkx:L3G+

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
HIF-1α; 

PubMed: 25383959     


Celastrol enhanced HIF-1α expression in multiple cell lines. MCF-7, HeLa, PC-3 and H1299 cells were treated with the indicated doses of Celastrol for 12 h under 3% hypoxia, and western blotting was used to detect the HIF-1 proteins.

Akt / p-Akt / p-p70S6K ; 

PubMed: 25383959     


Celastrol induced AKT/p70S6K activation under normoxia and hypoxia. HepG2 cells were challenged with the indicated doses of Celastrol for 6 h under normoxia or hypoxia. The protein levels were analyzed by western blotting with the corresponding antibodies. 

PARP / p53 / p21 / cIAP1 / Bcl-xl / Bcl-2 ; 

PubMed: 25383959     


Celastrol transiently activates p53 under normoxia but persistently activates p53 under hypoxia. HepG2 cells were cultured in normoxia or hypoxia with or without 4 µM Celastrol for the indicated times. The proteins were detected by western blotting. 

IκBα / p-IKKα/β ; 

PubMed: 28388439     


Inhibition of TNFα-induced IKKα/β phosphorylation and IκBα degradation by celastrol. Cells treated with celastrol and/or TNFα (20 ng/mL) for 30 min were analyzed by western blotting (WB).

iNOS / COX-2 / Arg-1 ; 

PubMed: 29040966     


Effects of celastrol on the expression of iNOS, COX‐2 and arginase-1 in LPS-stimulated RAW264.7 cells. After 24 h treatment with LPS and/or celastrol, the cellular proteins were analyzed by Western blotting with specific antibodies and GAPDH (as loading control). The blots (n = 3) were quantified by a densitometric method. Representative blots were shown

Chk2 / p-Chk2 / Cyclin B1 / Cdc25c / p-Cdc25c ; 

PubMed: 31053160     


U251, U87-MG and C6 cells were treated with celastrol (0, 0.3, 1, 3 and 10 μM) for 24 h. The levels of cell cycle-associated protein expressions were analyzed by western blotting. β-actin was used as an internal control.

25383959 28388439 29040966 31053160
Immunofluorescence
p21 / Nur77 ; 

PubMed: 28388439     


Colocalization of Nur77 with p62. Representative images illustrate colocalization of transfected endogenous Nur77 (E) or transfected GFP-Nur77 (F) with p62 in HepG2 cells after treatment with 4 μM celastrol and 20 ng/mL TNFα for 1 hr, analyzed by immunostaining. Scale bar, 10 μm.

28388439
Growth inhibition assay
Cell viability; 

PubMed: 29040966     


Cytotoxicity of celastrol. Following 48 h treatment, RAW264.7 cells were determined for the cell viability by a colorimetric MTT assay relative to the untreated controls (n = 3). **, p < 0.01 (Celastrol vs Control).

29040966
In vivo Celastrol (3 mg/kg) results in significant inhibition (up to 70%) of tumor growth in male nude mice bearing PC-3 tumors, associated with increased p27 levels and Bax level. Celastrol (3 mg/kg) results more apoptotic tumor cells with the appearance of various PARP cleavage fragments in tumor of male nude mice bearing PC-3 tumors. Celastrol (3 mg/kg) causes 35% of tumor inhibition, associated with decreased proteasome activity and decreased expression of AR protein in nude mice bearing C4-2B tumors. [1] Celastrol (3 mg/kg) is found to suppress strongly joint swelling and other manifestations of adjuvant arthritis in mice. Celastrol (0.2 mg/kg) significantly improves the performance in memory, learning and psychomotor activity tests in rats. [2]

Protocol

Kinase Assay:[1]
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Inhibition of purified 20S proteasome activity:

A purified rabbit 20S proteasome (0.1 μg) is incubated with 40 μM of various fluorogenic peptide substrates in 100 μL assay buffer (20 mM Tris-HCl (pH 7.5)), in the presence of Celastrol at different concentrations or in the solvent DMSO for 2 hours at 37 ℃, followed by measurement of inhibition of each proteasomal activity.
Cell Research:[4]
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  • Cell lines: RPMI 8226, KATOIII, UM-SCC1, U251MG and MDA-MB-231 cells
  • Concentrations: ~5 μM
  • Incubation Time: 2 hours
  • Method: The anti-proliferative effect of celastrol on various human tumor cell lines is determined by the MTT uptake method. Briefly, 5×103 cells are incubated with Celastrol in triplicate in a 96-well plate at 37 ℃. MTT solution is then added to each well. After a 2 hours incubation at 37 ℃, extraction buffer (20% SDS, 50% dimethylformamide) is added, cells are incubated overnight at 37 ℃, and the optical density is then measured at 570 nm using a Tecan plate reader.
    (Only for Reference)
Animal Research:[1]
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  • Animal Models: nude mice bearing C4-2B tumors
  • Dosages: 3 mg/kg
  • Administration: Intraperitoneal injection
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 90 mg/mL (199.72 mM)
Water Insoluble
Ethanol Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 450.61
Formula

C29H38O4

CAS No. 34157-83-0
Storage powder
in solvent
Synonyms Tripterine
Smiles CC1=C(C(=O)C=C2C1=CC=C3C2(CCC4(C3(CCC5(C4CC(CC5)(C)C(=O)O)C)C)C)C)O

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)
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Step 2: Enter the in vivo formulation ()
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Bio Calculators

Molarity Calculator

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (mg) = Concentration (mM) × Volume (mL) × Molecular Weight (g/mol)

  • Mass
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*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

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* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

  • Serial Dilutions

  • Computed Result

  • C1=C0/X C1: LOG(C1):
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Molecular Weight Calculator

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Total Molecular Weight: g/mol

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

Instructions to calculate molar mass (molecular weight) of a chemical compound:

To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

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Proteasome Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID