1. Metabolic Enzyme/Protease
  2. Proteasome
  3. Tripterin

Tripterin (Synonyms: Celastrol)

Cat. No.: HY-13067 Purity: 99.91%
Handling Instructions

Tripterin (Celastrol) is a proteasome inhibitor which potently and preferentially inhibits the chymotrypsin-like activity of a purified 20S proteasome with IC50 of 2.5 μM.

For research use only. We do not sell to patients.

Tripterin Chemical Structure

Tripterin Chemical Structure

CAS No. : 34157-83-0

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10 mM * 1 mL in DMSO USD 88 In-stock
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Customer Review

Based on 12 publication(s) in Google Scholar

Other Forms of Tripterin:

Top Publications Citing Use of Products

    Tripterin purchased from MCE. Usage Cited in: RSC Adv. 2016,6, 42537-42544.

    Celastrol is able to increase HSP70 protein expression by more than 1.8-fold in PC-3 cells after 24 h of incubation.

    Tripterin purchased from MCE. Usage Cited in: Mol Biosyst. 2016 Dec 20;13(1):83-91.

    Validation of selected targets of Celastrol identified by competitive proteomics. Western blotting (by using anti-GSTO1 and anti-PDI antibodies) of the pull-down samples upon labeling with IA-yne.

    Tripterin purchased from MCE. Usage Cited in: Life Sci. 2018 Jul 15;205:136-144.

    Effects of Celastrol (CEL) on the expression of F4/80 in plantar skin. CEL treatment suppresses macrophage expression in plantar skin. Western blot assay shows significantly downregulated F4/80 levels in 10 and 20 μg/paw CEL groups.

    Tripterin purchased from MCE. Usage Cited in: Cell Death Dis. 2018 May 22;9(6):601.

    Serum-starved HK-2 cells are pretreated with or without indicated concentrations of Celastrol (CEL) for 1 h and then stimulated with TGF-β1 (10 ng/mL) for 24 h. Representative western blots and quantification data of CB2R expression in HK-2 cells are presented.
    • Biological Activity

    • Protocol

    • Purity & Documentation

    • References

    • Customer Review


    Tripterin (Celastrol) is a proteasome inhibitor which potently and preferentially inhibits the chymotrypsin-like activity of a purified 20S proteasome with IC50 of 2.5 μM.

    IC50 & Target

    IC50: 2.5 μM (20S proteasome)[1]

    In Vitro

    Tripterin (Celastrol) significantly inhibits the proteasomal chymotrypsin activity in PC-3 cells in a concentration-dependent manner; at 2.5 μM it reaches ~55% inhibition, comparable to its potency to a purified 20S proteasome (IC50=2.5 μM). Furthermore, increased levels of IκB-α, Bax, and p27 are observed, three well known target proteins of the proteasome in PC-3 cells treated with Celastrol[1].

    In Vivo

    Treatment of PC-3 tumor-bearing nude mice with Tripterin (Celastrol) (1-3 mg/kg/d, i.p., 1-31 days) results in significant inhibition (65-93%) of the tumor growth[1]. Following treatment with 3 and 6 mg/kg Tripterin (Celastrol), the levels of malondialdehyde (MDA) are significantly decreased by 35.2 and 36.7% (P<0.05), respectively. Treatment with 3 and 6 mg/kg Tripterin (Celastrol) markedly restores the GSH level (P<0.05) to almost normal levels[2].

    Molecular Weight




    CAS No.



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    Room temperature in continental US; may vary elsewhere.

    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    DMSO : 33.33 mg/mL (73.97 mM; Need ultrasonic)

    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 2.2192 mL 11.0961 mL 22.1921 mL
    5 mM 0.4438 mL 2.2192 mL 4.4384 mL
    10 mM 0.2219 mL 1.1096 mL 2.2192 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

      Solubility: ≥ 2.5 mg/mL (5.55 mM); Clear solution

    *All of the co-solvents are provided by MCE.
    Kinase Assay

    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 or Oridonin at different concentrations or in the solvent DMSO for 2 hours at 37°C, followed by measurement of inhibition of each proteasomal activity[1].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Cell Assay

    Prostate cancer cells (5,000-8,000) are plated in each well of a 96-well plate and then treated with either DMSO, Tripterin (Celastrol), or Oridonin at different concentrations for 12 to 16 hours, followed by an additional 2-hour incubation with Z-Gly-Gly-Leu-AMC (at 40 μM). After that, the proteasome activity is measured using the whole plate[1].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration

    Male nude immunodeficient mice NCRNU-M, aged 5 weeks, are used. On day 0, human prostate cancer PC-3 or C4-2B cells (5-10×106) suspended in 0.1 mL of serum-free RPMI 1640 are inoculated s.c. in the right flank of each mouse (four mice per group). For the first experiment using PC-3 cells, on day 14 after inoculation, the animals started daily i.p. injection with either 50 to 100 μL of a vehicle [10% DMSO, 70% Cremophor/ethanol (3:1), and 20% PBS], and 1.0 or 3.0 mg/kg of Tripterin (Celastrol) . Tumor sizes are measured daily using calipers and their volumes are calculated using a standard formula: width2×length/2. Body weight is measured weekly. To study whether the proteasome is inhibited in an early phase of the experiment, after 3 days of treatment, one control and one 3.0 mg/kg Tripterin (Celastrol) -treated mouse is sacrificed. The rest are sacrificed after 16 days of treatment when control tumors reach 1,400 mm3. For the second PC-3 tumor experiment, 12 days after inoculation, mice are randomly divided into three groups and treated with either control, Tripterin (Celastrol) , or Oridonin at 1.5 mg/kg daily for the duration of the study (31 days). In another experiment, to study the effects of Tripterin (Celastrol) on AR expression, nude mice bearing C4-2B tumors receive daily i.p. injection of the vehicle or 3.0 mg/kg Tripterin (Celastrol) .
    Male Sprague-Dawley (SD) rats (n=90, 6 weeks old), weighing 161±9 g, are randomly divided into the control (NC) and the high energy diet (HED) groups. In the control group, the animals receive a standard chow diet, while the rats in the HED group are fed with an additional high energy emulsion. After 8 weeks on their respective diets, Streptozotocin (STZ; 45 mg/kg) dissolved in 0.1 mol/l citrate buffer (pH 4.5) is injected into the caudal vein of the rats in the HED group to establish a model of T2DM, while the rats in the control group are injected with sodium citrate buffer. The rats with blood glucose levels ≥16.7 mM at 7 days after the STZ injection are selected as the model of diabetes. On average, 80% of the rats injected with STZ met these criteria. At 1 week following the injection of STZ, the rats with successfully-induced diabetes are randomly divided into the diabetes model (DM) group, the Tripterin (Celastrol) low-dose group (1 mg/kg/day), the Tripterin (Celastrol) middle-dose group (3 mg/kg/day) and the Tripterin (Celastrol) high-dose group (6 mg/kg/day) (n=15 rats per group). The rats in the treatment groups are administered Tripterin (Celastrol) by gavage, whereas the rats in the NC and DM groups are administered an equal amount of distilled water (2 mL). Following 8 weeks of the respective treatments, rats are anesthetized with an intraperitoneal injection of sodium pentobarbital (30 mg/kg body weight) and tissue samples are collected for analysis. The paravertebral muscle is excised from the rat bodies, and is cut perpendicularly along the longitudinal axis and fixed in phosphate-buffered 20% formaldehyde. Histological paraffin-embedded sections (5 µm) are then prepared for H&E staining. The sections of paravertebral muscle are snap-frozen in liquid nitrogen and stored at −80°C until further analysis.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.


    Purity: 99.91%

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    TripterinCelastrolProteasomeAutophagyMitophagyApoptosisMitochondrial AutophagyInhibitorinhibitorinhibit

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