Celastrol

For research use only.

Catalog No.S1290 Synonyms: Tripterine

4 publications

Celastrol Chemical Structure

CAS No. 34157-83-0

Celastrol (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 has been cited by 4 publications

2 Customer Reviews

  • 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 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 purchased from Selleck.

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Biological Activity

Description Celastrol (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
human SH-SY5Y cells MlXGSpVv[3Srb36gZZN{[Xl? MkfhUoV2em:ycn;0[YN1cW:wIHHnZYlve3RiYnX0ZU1idXmub3nkJJBmeHSrZHWgNU01Oi2rbnT1Z4VlKHSxeHnjbZR6KGmwIHj1cYFvKFOKLWPZOXkh[2WubIOgZZN{\XO|ZXSgZZMhdGGldHH0[UBl\Wi7ZILv[4Vv[XOnIILlcIVie2VuIFXDOVA:OC5yM{e2OEDPxE1? NUTw[4VOOTlzM{i4OVk>
human SGC7901 cells MVjGeY5kfGmxbjDhd5NigQ>? M1rsTlQ5KGh? MVjBcpRq[2GwY3XyJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iU1fDO|kxOSClZXzsd{Bie3Onc4Pl[EBieyClZXzsJJN2en[rdnHsJIFnfGW{IES4JIhzeyCkeTDNWHQh[XO|YYmsJGlEPTB;MD6xOUDPxE1? MXOyOVgyOjl4Nh?=
HeLa cells NIXwTXNHfW6ldHnvckBie3OjeR?= MVvJcohq[mm2aX;uJI9nKE6ILXvhdJBiSiCjY4Tpeol1gSCrbjDoeY1idiCKZVzhJINmdGy|IHL5JHNGSVBicnXwc5J1\XJiYYPzZZktKEmFNUC9NE4yPSEQvF2= M33XXlIxPDZ7OEi3
human MCF7 cells MXXDfZRwfG:6aXRCpIF{e2G7 NVftPYFbPzJiaB?= M4LkcWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1ETjdiY3XscJMh[XO|ZYPz[YQh[XNiZ4Lve5RpKGmwaHnibZRqd25iYX\0[ZIhPzJiaILzJIJ6KE2WUz;QUXMh[XO|YYmsJGlEPTB;MD6xOVMh|ryP NXe3XHdMOjV5NU[yPVk>
human 293T cells NH\seJJHfW6ldHnvckBie3OjeR?= M3;P[VMxKG2rboO= MU\Jcohq[mm2aX;uJI9nKEySUz3pcoR2[2WmIF7GMYtieHCjQjDhZ5RqfmG2aX;uJIlvKGi3bXHuJFI6O1RiY3XscJMhcW6ldXLheIVlKG[xcjCzNEBucW6|IH\vcIxwf2WmIHL5JJRz\WG2ZXSge4l1cCCOUGOg[o9zKDZiaILzJIJ6KGS3YXytcJVkcW[ncnHz[UBz\XCxcoTldkBie3OjeTygTWM2OD1yLkG3JO69VQ>? MYeyNVM6OzByNB?=
mouse RAW264.7 cells MlnZSpVv[3Srb36gZZN{[Xl? NHLGPVgyQCCq M3nXN2lvcGmkaYTpc44hd2ZiTGDTMZN1cW23bHH0[YQhVk[tYYDwZWIh[WO2aY\heIlwdiC2cnHud4Zm[3SnZDDpckBud3W|ZTDSRXczPjRwNzDj[YxteyCjZoTldkAyQCCqcoOgZpkhdHWlaX\ldoF{\SC{ZYDvdpRmeiCpZX7lJIF{e2G7LDDJR|UxRTBwMjFOwG0> NUDlOJFsOjJ5MEWwNlA>
human SMMC7721 cells Mne0SpVv[3Srb36gZZN{[Xl? M3jrS|Q5KGh? M2LONmFvfGmlYX7j[ZIh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDTUW1EPzd{MTDj[YxteyCjc4Pld5Nm\CCjczDj[YxtKHO3co\peoFtKGGodHXyJFQ5KGi{czDifUBOXFRiYYPzZZktKEmFNUC9NE42QCEQvF2= MXOyOVgyOjl4Nh?=
human 293T cells NYO5[GFwS3m2b4TvfIlkyqCjc4PhfS=> M4TaT2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJFI6O1RiY3XscJMh[XO|ZYPz[YQh[XNiY3XscEB3cWGkaXzpeJkh[nliZIXhcE1tfWOrZnXyZZNmKHKncH;yeIVzKGG|c3H5MEBKSzVyPUCuOlch|ryP MnfnNlE{QTNyMES=
human MGC803 cells M{DZUmZ2dmO2aX;uJIF{e2G7 MXq0PEBp NX;pS2xlSW62aXPhcoNmeiCjY4Tpeol1gSCjZ3HpcpN1KGi3bXHuJG1ISzhyMzDj[YxteyCjc4Pld5Nm\CCjczDj[YxtKHO3co\peoFtKGGodHXyJFQ5KGi{czDifUBOXFRiYYPzZZktKEmFNUC9NU42PSEQvF2= M2PZSFI2QDF{OU[2
human SK-N-SH cells NXfBPZNMS3m2b4TvfIlkyqCjc4PhfS=> MWO3NkBp M37NWWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJHNMNU5vU1igZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KE2WUzDhd5NigSxiQ1O1NF0yNjZizszN M2XROFE6PTB{MEW3
human LNCAP cells NX\neppNTnWwY4Tpc44h[XO|YYm= NXr3[nBkSW62aYT1cY9zKGGldHn2bZR6KGGpYXnud5QhcHWvYX6gUG5ESVBiY3XscJMtKEmFNUC9Nk42KM7:TR?= M{e5dFIxPjJ5NUW2
HeLa cells NFTtSYZHfW6ldHnvckBie3OjeR?= MnfwN{Bp NXnTUJQySW2ybHnmbYNifGmxbjDv[kBJW0ZzIITyZY5{[3KrcITpc45idCCjY4Tpeol1gSCrbjDoeY1idiCKZVzhJINmdGy|IHHzd4V{e2WmIHHzJIdz[W63bHWg[o9zdWG2aX;uJJBz\XS{ZXH0[YQh\m:{IEOgbJJ{KGK7IHntcZVvd2O7dH;jbIVucWOjbDDzeIFqdmmwZzygSWM2OD1{Lk[g{txO MUKxPVUxOjB3Nx?=
human RPMI8226 cells MoHmS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? M3;nUGdzd3e2aDDpcohq[mm2aX;uJI9nKGi3bXHuJHJRVUl6MkK2JINmdGy|LDDJR|UxRTNizszN NG[zW3YyQDF4NEG5Oy=>
human HeLa cells NULR[2FKS3m2b4TvfIlkyqCjc4PhfS=> MVu3NkBp NF3CRZBEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBJ\UyjIHPlcIx{KGGodHXyJFczKGi{czDifUBOXFNiYYPzZZktKEmFNUC9N{DPxE1? NH;URmIyQTVyMkC1Oy=>
rat PC12 cells M4qzU2Z2dmO2aX;uJIF{e2G7 NIj3PYREgXSxcILveIVkfGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IIStRnBJNWmwZIXj[YQh[2WubDDkZY1i\2ViaX6gdoF1KFCFMUKgZ4VtdHNiYYPz[ZN{\WRiYYOgZ4VtdCC4aXHibYxqfHluIFnDOVA:Oy5zNTFOwG0> Ml60NlA3Ojd3NU[=
human HepG2 cells MWHGeY5kfGmxbjDhd5NigQ>? MXe0PEBp MXPBcpRq[2GwY3XyJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iSHXwS|Ih[2WubIOgZZN{\XO|ZXSgZZMh[2WubDDzeZJ3cX[jbDDh[pRmeiB2ODDodpMh[nliTWTUJIF{e2G7LDDJR|UxRTRwMEGg{txO MnTTNlU5OTJ7Nk[=
human NCI-H460 cells M2CwW2N6fG:2b4jpZ:Kh[XO|YYm= NHy4SYpEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBPS0lvSES2NEBk\WyuczDh[pRmeiCxdnXycolocHRiaX7jeYJifGmxbjDifUBOXFRiYYPzZZktKEmFNUC9NVIvOyEQvF2= M16zNFIyQTR{N{[1
human THP1 cells MlnWSpVv[3Srb36gZZN{[Xl? NFe0SoczPCCq NXPXcFI2UW6mdXP0bY9vKG:oIHHwc5B1d3OrczDpckBVWkGLTD3y[ZNqe3SjboSgbJVu[W5iVFjQNUBk\WyuczDh[pRmeiB{NDDodpMh[nliYX7u[Zhqdi2YIIP0ZYlvcW6pLDDFR|UxRTF3IN88US=> NULEPHhJOjB6NkSzOFI>
human MCF7 cells NU\jcXFITnWwY4Tpc44h[XO|YYm= NXjEeJNlOjRiaB?= M2izeWlvcGmkaYTpc44hd2ZiSGPQPVAhcW5iaIXtZY4hVUOINzDj[YxteyCjc4Pld5Nm\CCjczDSZYYh\GWpcnHkZZRqd25iYYSgOUB1cW2nczDJR|UxKGGodHXyJFI1KGi{czDifUBY\XO2ZYLuJIJtd3RiYX7hcJl{cXN? MoG2NlU4PTZ{OUm=

... 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

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID