Celastrol

Catalog No.S1290 Synonyms: Tripterine

Celastrol Chemical Structure

Molecular Weight(MW): 450.61

Celastrol is a potent proteasome inhibitor for the chymotrypsin-like activity of a purified 20S proteasome with IC50 of 2.5 μM.

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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 is a potent proteasome inhibitor for the chymotrypsin-like activity of a purified 20S proteasome with IC50 of 2.5 μM.
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 MoPZSpVv[3Srb36gZZN{[Xl? MojDUoV2em:ycn;0[YN1cW:wIHHnZYlve3RiYnX0ZU1idXmub3nkJJBmeHSrZHWgNU01Oi2rbnT1Z4VlKHSxeHnjbZR6KGmwIHj1cYFvKFOKLWPZOXkh[2WubIOgZZN{\XO|ZXSgZZMhdGGldHH0[UBl\Wi7ZILv[4Vv[XOnIILlcIVie2VuIFXDOVA:OC5yM{e2OEDPxE1? NUfYPZo3OTlzM{i4OVk>
human SGC7901 cells NXzTfohmTnWwY4Tpc44h[XO|YYm= MmTLOFghcA>? MYHBcpRq[2GwY3XyJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iU1fDO|kxOSClZXzsd{Bie3Onc4Pl[EBieyClZXzsJJN2en[rdnHsJIFnfGW{IES4JIhzeyCkeTDNWHQh[XO|YYmsJGlEPTB;MD6xOUDPxE1? NUjVWJpxOjV6MUK5OlY>
HeLa cells MYrGeY5kfGmxbjDhd5NigQ>? NIG2NIJKdmirYnn0bY9vKG:oIF7GMYtieHCjQjDhZ5Rqfmm2eTDpckBpfW2jbjDI[WxiKGOnbHzzJIJ6KFOHQWCgdoVxd3K2ZYKgZZN{[XluIFnDOVA:OC5zNTFOwG0> MXmyNFQ3QTh6Nx?=
human MCF7 cells NVyxUWlVS3m2b4TvfIlkyqCjc4PhfS=> NIHnV4Y4OiCq Ml;sR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUWNHPyClZXzsd{Bie3Onc4Pl[EBieyCpcn;3eIghcW6qaXLpeIlwdiCjZoTldkA4OiCqcoOgZpkhVVSVL2DNV{Bie3OjeTygTWM2OD1yLkG1N{DPxE1? M17zdVI2PzV4Mkm5
human 293T cells M{W5UmZ2dmO2aX;uJIF{e2G7 NF74ZYk{OCCvaX7z NVrzTldWUW6qaXLpeIlwdiCxZjDMVHMucW6mdXPl[EBPTi2tYYDwZWIh[WO2aY\heIlwdiCrbjDoeY1idiB{OUPUJINmdGy|IHnuZ5Vj[XSnZDDmc5IhOzBibXnud{Bnd2yub4fl[EBjgSC2cnXheIVlKHerdHigUHBUKG[xcjC2JIhzeyCkeTDkeYFtNWy3Y3nm[ZJie2VicnXwc5J1\XJiYYPzZZktKEmFNUC9NE4yPyEQvF2= M3fsS|IyOzl|MEC0
mouse RAW264.7 cells M4e5TmZ2dmO2aX;uJIF{e2G7 NE[4RZkyQCCq MWXJcohq[mm2aX;uJI9nKEySUz3zeIlufWyjdHXkJG5Hc2GycHHCJIFkfGm4YYTpc44hfHKjboPm[YN1\WRiaX6gcY92e2ViUlHXNlY1NjdiY3XscJMh[W[2ZYKgNVghcHK|IHL5JIx2[2moZYLhd4UhemWyb4L0[ZIh\2WwZTDhd5NigSxiSVO1NF0xNjJizszN M4racVIzPzB3MEKw
human SMMC7721 cells NULIR5VPTnWwY4Tpc44h[XO|YYm= MVi0PEBp MW\BcpRq[2GwY3XyJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iU13NR|c4OjFiY3XscJMh[XO|ZYPz[YQh[XNiY3XscEB{fXK4aY\hcEBi\nSncjC0PEBpenNiYomgUXRVKGG|c3H5MEBKSzVyPUCuOVgh|ryP MWeyOVgyOjl4Nh?=
human 293T cells MYLDfZRwfG:6aXRCpIF{e2G7 M4\xR2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJFI6O1RiY3XscJMh[XO|ZYPz[YQh[XNiY3XscEB3cWGkaXzpeJkh[nliZIXhcE1tfWOrZnXyZZNmKHKncH;yeIVzKGG|c3H5MEBKSzVyPUCuOlch|ryP M1n1OVIyOzl|MEC0
human MGC803 cells MU\GeY5kfGmxbjDhd5NigQ>? NEDaO4k1QCCq Mle4RY51cWOjbnPldkBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF3HR|gxOyClZXzsd{Bie3Onc4Pl[EBieyClZXzsJJN2en[rdnHsJIFnfGW{IES4JIhzeyCkeTDNWHQh[XO|YYmsJGlEPTB;MT61OUDPxE1? NGnRSIEzPThzMkm2Oi=>
human SK-N-SH cells MV;DfZRwfG:6aXRCpIF{e2G7 NYPDZWx5PzJiaB?= MmXyR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gV2suVi2VSDDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSVIHHzd4F6NCCFQ{WwQVEvPiEQvF2= M3XM[|E6PTB{MEW3
human LNCAP cells NGfiflRHfW6ldHnvckBie3OjeR?= M3OxR2FvfGm2dX3vdkBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFzOR2FRKGOnbHzzMEBKSzVyPUKuOUDPxE1? NWfXVnljOjB4Mke1OVY>
HeLa cells MkHTSpVv[3Srb36gZZN{[Xl? MnT2N{Bp MlWwRY1xdGmoaXPheIlwdiCxZjDIV2YyKHS{YX7zZ5JqeHSrb37hcEBi[3Srdnn0fUBqdiCqdX3hckBJ\UyjIHPlcIx{KGG|c3Xzd4VlKGG|IHfyZY52dGViZn;ycYF1cW:wIIDy[ZRz\WG2ZXSg[o9zKDNiaILzJIJ6KGmvbYXuc4N6fG:laHXtbYNidCC|dHHpcolv\yxiRVO1NF0zNjZizszN MlL4NVk2ODJyNUe=
human RPMI8226 cells NIrrOotIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NXq2cWdlT3Kxd4ToJIlvcGmkaYTpc44hd2ZiaIXtZY4hWlCPSUiyNlYh[2WubIOsJGlEPTB;MzFOwG0> NXzzVpN4OThzNkSxPVc>
human HeLa cells MVPDfZRwfG:6aXRCpIF{e2G7 M4PyNlczKGh? M2X0PWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGhmVGFiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VWyCjc4PhfUwhUUN3ME2zJO69VQ>? M4jSfFE6PTB{MEW3
rat PC12 cells NWLJdYlzTnWwY4Tpc44h[XO|YYm= NWrUdIFQS3m2b4Dyc5Rm[3SrdnWgZYN1cX[rdImgZYdicW6|dDD0MWJRUC2rbnT1Z4VlKGOnbHyg[IFu[WenIHnuJJJifCCSQ{GyJINmdGy|IHHzd4V{e2WmIHHzJINmdGxidnnhZoltcXS7LDDJR|UxRTNwMUWg{txO NGLxU2EzODZ{N{W1Oi=>
human HepG2 cells NG\q[lhHfW6ldHnvckBie3OjeR?= M13jflQ5KGh? MYDBcpRq[2GwY3XyJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iSHXwS|Ih[2WubIOgZZN{\XO|ZXSgZZMh[2WubDDzeZJ3cX[jbDDh[pRmeiB2ODDodpMh[nliTWTUJIF{e2G7LDDJR|UxRTRwMEGg{txO NHzxOWIzPThzMkm2Oi=>
human NCI-H460 cells M1PCNGN6fG:2b4jpZ:Kh[XO|YYm= NVrrTZR3S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVkOLLVi0OlAh[2WubIOgZYZ1\XJib4\ldo5q\2i2IHnuZ5Vj[XSrb36gZpkhVVSWIHHzd4F6NCCLQ{WwQVEzNjNizszN Moj1NlE6PDJ5NkW=
human THP1 cells NVO1WGFETnWwY4Tpc44h[XO|YYm= M3vFZlI1KGh? M{XHXWlv\HWldHnvckBw\iCjcH;weI9{cXNiaX6gWHJCUUxvcnXzbZN1[W62IHj1cYFvKFSKUEGgZ4VtdHNiYX\0[ZIhOjRiaILzJIJ6KGGwbnX4bY4uXiC|dHHpcolv\yxiRVO1NF0yPSEQvF2= MWOyNFg3PDN2Mh?=
human MCF7 cells MnvESpVv[3Srb36gZZN{[Xl? MnHENlQhcA>? Mm\KTY5pcWKrdHnvckBw\iCKU2C5NEBqdiCqdX3hckBOS0Z5IHPlcIx{KGG|c3Xzd4VlKGG|IGLh[kBl\We{YXTheIlwdiCjdDC1JJRqdWW|IFnDOVAh[W[2ZYKgNlQhcHK|IHL5JHdme3Sncn6gZoxwfCCjbnHsfZNqew>? NVTBVFVpOjV5NU[yPVk>

... Click to View More Cell Line Experimental Data

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]
+ Expand

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]
+ Expand
  • 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]
+ Expand
  • Animal Models: nude mice bearing C4-2B tumors
  • Formulation: 10% DMSO, 70% Cremophor/ethanol (3:1), and 20% PBS
  • 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
Synonyms Tripterine

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID