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Fig. 1 · Structure
Cat. No.
A10192
CAS No.
34157-83-0
Formula
C29H38O4
Mol. Weight
450.6

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Celastrol

Cat. No. A10192 CAS 34157-83-0

Celastrol is a triterpenoid antioxidant compound isolated from the Chinese Thunder of God vine (T. wilfordii). In an isolated rat liver assay of lipid peroxidation, celastrol had an IC50 value of 7 µM, equivalent to about 15 times the antioxidant potency of α-tocopherol.

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Publications for Celastrol

3 publications citing this product

  1. Xuechun Wang, .et al. , Int J Mol Sci, 2023, Mar 8;24(6):5204 PMID: 36982279
  2. R. San Gil, .et al. , bioRxiv, 2020, Jan
  3. Abdin AA, .et al. , Eur J Pharmacol., 2014, 742:102-12 PMID: 25218987
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Biological Activity

Bioactivity / Mechanism

In a purified-protein system, celastrol reduced Hsp90–Cdc37 complex formation in pull-down and ELISA assays. Premixing with DTT blocked this effect, while a modified celastrol analog was substantially weaker. These results support a thiol-sensitive interaction effect under the tested conditions; they do not establish a unique cellular target. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
20S proteasome N/A
20S proteasome 2.5 μM

Cellular Effect

Cell Line Activity Value Description Reference
1A9 ED50 0.091 μg/mL Cytotoxicity against human 1A9 cells after 3 days by SRB assay [PMID: 14640511]
1A9 ED50 0.11 μg/mL Cytotoxicity against human 1A9 cells after 6 days by SRB assay [PMID: 14640511]
1A9/ptx-10 ED50 0.1 μg/mL Cytotoxicity against human 1A9/PTX10 cells after 3 days by SRB assay [PMID: 14640511]
1A9/ptx-10 ED50 0.11 μg/mL Cytotoxicity against human 1A9/PTX10 cells after 6 days by SRB assay [PMID: 14640511]
A 172 IC50 2.31 μM Antiproliferative activity against human A-172 cells assessed as reduction in cell viability incubated for 96 hrs by MTT assay [PMID: 34968902]
A2780 IC50 1.84 μM Antiproliferative activity against human A2780 cells incubated for 48 hrs by MTT assay [PMID: 31279299]
A-431 ED50 2.4 μg/mL Cytotoxicity against human A431 cells after 72 hrs by sulforhodamine B assay [PMID: 8158155]
A549 IC50 > 100 μM Antiproliferative activity against human A549 cells expressing Hsp90-Cdc37 protein assessed as inhibition of cell growth incubated for 48 hrs by MTT assay [PMID: 35238566]
A549 IC50 > 100 μM Antiproliferative activity against human A549 cells expressing Hsp90 protein assessed as inhibition of cell growth incubated for 48 hrs by MTT assay [PMID: 35238566]
A549 IC50 > 100 μM Antiproliferative activity against human A549 cells expressing Cdc37 protein assessed as inhibition of cell growth incubated for 48 hrs by MTT assay [PMID: 35238566]
A549 ED50 0.25 μg/mL Cytotoxicity against human A549 cells after 3 days by SRB assay [PMID: 14640511]
A549 IC50 0.98 μM Antiproliferative activity against human A549 cells assessed as inhibition of cell growth incubated for 96 hrs by MTT assay [PMID: 35290844]
A549 IC50 1.1 μM Cytotoxicity against human A549 cells assessed as inhibition of cell growth measured after 96 hrs by MTT assay [PMID: 35255689]
A549 IC50 1.28 μM Cytotoxicity against human A549 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay [PMID: 31051401]
A549 IC50 1.43 μM Antiproliferative activity against human A549 cells after 48 hrs by MTT assay [PMID: 30316059]
A549 IC50 1.48 μM Antiproliferative activity against human A549 cells assessed as inhibition of cell growth incubated for 48 hrs by MTT assay [PMID: 31725288]
A549 IC50 1.56 μM Antiproliferative activity against human A549 cells after 72 hrs by MTT assay [PMID: 28865279]
A549 IC50 1.56 μM Antiproliferative activity against human A549 cells after 72 hrs by MTT assay [PMID: 28688281]
A549 IC50 1.68 μM Antiproliferative activity against human A549 cells assessed as inhibition of cell growth incubated for 48 hrs by MTT assay [PMID: 35238566]
A549 IC50 1.8 μM Antiproliferative activity against human A549 cells assessed as inhibition of cell proliferation measured after 48 hrs by MTT assay [PMID: 34170694]

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In Vitro Studies

In PC-3 and DU145 prostate cancer cells, 30-min celastrol treatment was associated with cytosolic IκBα accumulation and reduced nuclear RelA. The tested concentrations were 2 µM in PC-3 cells and 1–2 µM in DU145 cells. These protein-distribution changes are consistent with suppression of NF-κB signaling in these models. [2]

Disruption of Hsp90–Cdc37 complex formation in a purified-protein system

Biochemical assay · Purified human Hsp90α or Hsp90β with Cdc37; yeast Hsp82 also tested in pull-down assays. [1]

Celastrol reduced complex formation in GST pull-down and ELISA assays. Geldanamycin and its tested derivatives did not reproduce the disruption. Dihydrocelastrol diacetate was weaker, and premixing celastrol with DTT abolished the observed disruption. Washout experiments retained inhibition after Hsp90 pretreatment but not Cdc37 pretreatment. These assay observations do not establish a unique cellular target or a binding constant.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Hsp90–Cdc37 complex formationConcentration-dependent reduction; no fitted binding IC50 is supplied for the selected assays.[1]
Chemical and pretreatment controlsDTT premixing blocked disruption; the modified analog was weaker. Inhibition persisted after Hsp90 pretreatment and washing, while Cdc37 pretreatment followed by washing did not inhibit subsequent binding.[1]

Literature-Reported Treatment Conditions

Treatment concentration
Pull-down: 1, 10 and 100 µM celastrol in Figure 1D human Hsp90β panel; ELISA: 1, 5, 10, 50, 100 and 200 µM in Figures 1E and 3B–C.
Exposure duration
Protein pretreatment: 30 min at 30 °C; subsequent Cdc37 incubation: 1 h at 4 °C in the reported binding procedures.
Method
Compound pretreatment before adding the binding partner; selected washout assays remove free compound before adding the partner.
Vehicle
DMSO control.
Co-treatment
DTT (1 mM) was a separate mechanistic premixing control, not a therapeutic combination.
Reported limits
No fitted IC50 or binding affinity; Figure 1E says triplicate experiments but does not establish independent protein preparations or define every error bar.
Methods and source locations

Compound reported in the paper: Celastrol; Compound label in the paper: cel / Cel

Evidence applies to reported parent celastrol in purified-protein assays; it does not validate an Adooq lot.

Figures 1C–E, 2A–C, 3A–C and captions; Experimental Procedures: Chemicals, GST Pull-down Assay, ELISA Microtiter Plate Assay

Hsp90–Cdc37 complex formation: GST pull-down with immunoblot detection; ELISA with bound-protein detection relative to control. — Figure 1D–E and captions; Results: Celastrol Inhibits Hsp90-Cdc37 Complex Formation

Chemical and pretreatment controls: GST pull-down; reciprocal immobilization and washout ELISA. — Figure 2A–C; Figure 3A–C and captions

NF-κB-associated protein redistribution in prostate cancer cells

Cell-based study · Human PC-3 and DU145 prostate cancer cell lines. [2]

After 30 min, celastrol was associated with higher cytosolic IκBα and lower nuclear RelA than the control lanes. Fractionation blots included tubulin and PARP compartment/loading markers. The experiment supports pathway-associated protein redistribution; it does not identify which molecular target is responsible.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cytosolic IκBα and nuclear RelA abundanceQualitative immunoblot: increased cytosolic IκBα and reduced nuclear RelA after celastrol treatment.[2]

Literature-Reported Treatment Conditions

Treatment concentration
PC-3: celastrol 2 µM; DU145: celastrol 1 or 2 µM. PC-3 positive comparator: MG132 10 µM.
Exposure duration
30 min.
Method
Single-compound cell treatment, followed by cytosolic/nuclear fractionation and immunoblotting.
Vehicle
DMSO is labeled in the PC-3 control lane; DU145 control is labeled 0 µM.
Co-treatment
None; MG132 was a separate comparator.
Reported limits
Final cellular DMSO percentage and independent replicate count for the Figure 5 blots are not specified in the inspected caption/methods. No densitometric effect size or potency is inferred.
Methods and source locations

Compound reported in the paper: Celastrol; Compound label in the paper: Cel

Reported parent-compound experiments; no Adooq material or lot validation.

Figure 5A–B and caption; Results: Celastrol Suppresses the Constitutive NF-κB Activity; Methods: Reagents and Cell Culture, Western Blot, Subcellular Fractionation

Cytosolic IκBα and nuclear RelA abundance: Subcellular fractionation followed by Western blot; tubulin and PARP controls. — Figure 5A–B and caption

In Vivo Studies

In female athymic nu/nu mice bearing PC-3 xenografts, celastrol at 1 mg/kg by oral gavage, five days per week for three weeks, reduced tumor volume versus vehicle at the last dosing time point (day 18; P < 0.05). Tumor tissue showed lower Ki67/CD31 staining and greater TUNEL staining. The result is specific to this preclinical model. [2]

Oral celastrol in a PC-3 xenograft model

Animal study · Female athymic nu/nu mice, 5 weeks old, with bilateral subcutaneous PC-3 xenografts; treatment started at reported tumor volume of 100 mm³. [2]

Oral celastrol reduced tumor volume at the last dosing time point versus vehicle (P < 0.05). Tumor sections showed reduced Ki67/CD31 staining and increased TUNEL staining; tumor lysates showed IκBα accumulation. These are preclinical associations, and this study does not establish clinical efficacy or isolate a single causal molecular target.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Tumor volume at last dosing (day 18)Lower than vehicle; P < 0.05. Figure 6A labels n = 18 for vehicle and n = 12 for celastrol; the caption describes these as numbers of mice.[2]
Proliferation, apoptosis, vascular staining and tumor IκBαQualitatively lower Ki67 and CD31 staining, higher TUNEL staining, and increased tumor IκBα versus vehicle.[2]

Conditions shared by the study groups

Route
Oral gavage (p.o.).
Frequency
5 days per week.
Treatment course
3 weeks; last dosing/tumor measurement reported as day 18.
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Vehicle controlVehicle comparator arm.Reference group for tumor-volume and tissue comparisons.[2]
Celastrol
1 mg/kg		Vehicle group.Lower endpoint tumor volume versus vehicle (P < 0.05); tissue staining changes described in the parent study.[2]
Vehicle control
Model: PC-3 xenografts in female athymic nu/nu mice.
Reported limits: Vehicle composition was not retrieved from the cited prior work. Figure 6A caption calls n the number of mice; bilateral-tumor aggregation is not described here.
Celastrol
Model: PC-3 xenografts in female athymic nu/nu mice.
Reported limits: Vehicle composition was not retrieved from the cited prior work. Figure 6A caption calls n the number of mice; bilateral-tumor aggregation is not described here.
Methods and source locations

Compound reported in the paper: Celastrol; Compound label in the paper: Cel

Reported parent-compound experiments; no Adooq material or lot validation.

Figure 6A–D and caption; Methods: Animal Study, Reagents and Cell Culture, Statistical Analysis; Results: Anti-tumor Effect of Celastrol Involves NF-κB Attenuation in PC-3 Xenografts

Tumor volume at last dosing (day 18): Tumor volume calculated as (length × width²)/2; two-tailed Student’s t-test reported in Statistical Analysis. — Figure 6A and caption; Animal Study; Statistical Analysis

Proliferation, apoptosis, vascular staining and tumor IκBα: Immunohistochemistry/TUNEL and Western blot with GAPDH loading control. — Figure 6B–C and caption

Vehicle control · Animal Study; Figure 6A–C and caption

Celastrol · Animal Study; Figure 6A–C and caption

Specifications

Manufacturer Adooq Bioscience
CAS Number 34157-83-0
Formula C29H38O4
Molecular Weight 450.6
SMILES
CC1=C(C(=O)C=C2C1=CC=C3[C@]2(CC[C@@]4([C@@]3(CC[C@@]5([C@H]4C[C@](CC5)(C)C(=O)O)C)C)C)C)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 82 mg/mL (181.97 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Tao Zhang, Yanyan Li, Yanke Yu, et al. Characterization of Celastrol to Inhibit Hsp90 and Cdc37 Interaction Journal of Biological Chemistry (2009). PMID: 19858214 DOI: 10.1074/jbc.M109.051532 Source material
  2. [2] Yao Dai, Jeffrey DeSano, Wenhua Tang, et al. Natural Proteasome Inhibitor Celastrol Suppresses Androgen-Independent Prostate Cancer Progression by Modulating Apoptotic Proteins and NF-kappaB PLoS ONE (2010). PMID: 21170316 DOI: 10.1371/journal.pone.0014153 Source material

Publications

3 publications citing this product

  1. Xuechun Wang, .et al. , Int J Mol Sci, 2023, Mar 8;24(6):5204 PMID: 36982279
  2. R. San Gil, .et al. , bioRxiv, 2020, Jan
  3. Abdin AA, .et al. , Eur J Pharmacol., 2014, 742:102-12 PMID: 25218987

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