1. Metabolic Enzyme/Protease
  2. Proteasome

MG-132 

Cat. No.: HY-13259 Purity: >98.0%
Handling Instructions

MG-132 is a potent, reversible, and cell-permeable 20S proteasome inhibitor which inhibits proteasomal chymotrypsin-like peptidase activity with an IC50 of 24.2 nM.

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

MG-132 Chemical Structure

MG-132 Chemical Structure

CAS No. : 133407-82-6

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Customer Review

Customer Validation

    MG-132 purchased from MCE. Usage Cited in: Sci Rep. 2017 Jun 7;7(1):2929.

    p53 and Cell apoptosis. MCF7 and MDA-MB-231 cells are treated with 80 μM ω-3 FFAs, 20 μM ATRA alone or in combination for 48 h. The expression of PARP and p53 protein. β-Actin is used as an internal control.

    MG-132 purchased from MCE. Usage Cited in: Antioxid Redox Signal. 2018 Sep 22.

    Nrf2 and Keap1 degradation in NIH-3T3 cells when protein synthesis is inhibited by 50 μM Cycloheximide (n=3).

    MG-132 purchased from MCE. Usage Cited in: Cell Death Dis. 2018 May 22;9(6):604.

    AGS cells are pretreated with 25 and 50 nM Bortezomib for 1 h, and then incubated with 500 nM Torin 1 for 24 h. After pretreatment with PPI for 24 h in pH 7.4 or pH 6.5 condition, Rapamycin (1 μM) or Torin 1 (500 nM) is added for another 24 h. The protein level of SQSTM1 is measured by western blot analysis.

    MG-132 purchased from MCE. Usage Cited in: Antioxid Redox Signal. 2018 Sep 22.

    The western blot assay shows that Tan-IIA and GKT137831 inhibit Smad3 activation in response to TGF-β1 by dephosphorylation.

    MG-132 purchased from MCE. Usage Cited in: Cell Death Dis. 2018 May 22;9(6):604.

    Western blot analysis of ER stress-related proteins after PPI treatment for 48 h in both pH 7.4 and pH 6.5 conditions. Cells treated with Thapsigargin (TG, 0.5 and 1 μM) or Tunicamycin (Tu, 2.5, 5 and 10 μg/mL) for 24 h served as positive controls.

    MG-132 purchased from MCE. Usage Cited in: Sci Rep. 2017 Jun 7;7(1):2929.

    Caspase signaling pathway. MCF7 and MDA-MB-231 cells are pretreated with 10 µM Z-VAD-FMK and BOC-D-FMK for 1 h and then exposed to 80 μM ω3-FFAs and 20 μM ATRA for 48 h. The expression of PARP protein.

    MG-132 purchased from MCE. Usage Cited in: Antioxid Redox Signal. 2018 Sep 22.

    Tan-IIA increases the endogenous induction of Nrf2 induction and this effect is further enhanced by cotreatment with the proteasome inhibitor MG-132.

    MG-132 purchased from MCE. Usage Cited in: Cell Death Dis. 2018 May 22;9(6):604.

    AGS cells transfected with HA-tagged SQSTM1 plasmid, are treated with 25 μg/mL Cycloheximide (CHX) over a 240-min time period or treated with 100 μg/mL PPI for 48 h in pH 7.4 conditions, and then followed by 25 μg/mL CHX over a 240-min time period.

    MG-132 purchased from MCE. Usage Cited in: Cell Death Dis. 2018 May 22;9(6):604.

    Different concentrations of two classical proteasome inhibitors Bortezomib and MG132 are added. AGS cells are either untreated or treated with Bortezomib (25 nM) or MG132 (0.1 μM) for 24 h in the absence or presence of baf A1 (100 nM).

    MG-132 purchased from MCE. Usage Cited in: Oncotarget. 2016 May 10;7(19):27176-84.

    PIG3 silencing does not affect the degradation of HIF-1α protein under hypoxia. Forty-eight hours after transfection with PIG3-siRNA or negative control siRNA, CAKI cells are pretreated under hypoxia for 4 h followed by treatment with 100 μg/mL Cycloheximide (CHX) to block protein synthesis for the indicated times. The mean values from two experiments are connected by the lines. Protein levels are analyzed by Immunoblotting, GAPDH is employed a loading control. All the experiments above are cond

    MG-132 purchased from MCE. Usage Cited in: Biochem Biophys Res Commun. 2017 Sep 2;490(4):1168-1175.

    SR-B1 protein is degraded by proteasome pathway. (A) SR-B1 is degraded in a CHX dose-dependent manner in CHO-K1 cells. (B) Time course of SR-B1 degradation in CHO-K1 cells treated with CHX.

    MG-132 purchased from MCE. Usage Cited in: Biochem Biophys Res Commun. 2017 Sep 2;490(4):1168-1175.

    Treatment of CHO-K1 cells with proteasome inhibitor, MG-132 results in elevated SR-B1 protein levels. The cells with MG-132, a potent proteasome inhibitor that inhibit ubiquitin/proteasome-dependent protein degradation, and MG-132 treatment significantly enhances cellular SR-B1 protein level.

    MG-132 purchased from MCE. Usage Cited in: J Inorg Biochem. 2017 Jul 19;175:92-100.

    TPEN-triggered PML-RARα degradation in NB4 cells is reversed by MG-132 treatment. NB4 cells are treated with 5 μM TPEN with or without the presence of 1 μM MG-132 for the indicated durations (0–12 h) and then lysed. The lysates are analyzed for PML-RARα and RARα protein levels by western blotting.

    MG-132 purchased from MCE. Usage Cited in: Cancer Lett. 2017 Dec 1;410:112-123.

    Immunoprecipitation of ubiquitin from lysates of U-2 OS cells expressing CHOP after treatment with different concentrations of MG7 for 48 h. Cells are incubated with MG132 (20 mM) for 4 h before harvest. Cell lysates are immunoblotted with the indicated antibodies.

    MG-132 purchased from MCE. Usage Cited in: Eur J Med Chem. 2018 Feb 1;146:251-259.

    In the absence of MG132, the protein degradation pathways are intact, the Tau protein level is significantly decreased in peptide 1-treated group.

    MG-132 purchased from MCE. Usage Cited in: Biochem Pharmacol. 2018 Feb 21;150:280-292.

    Expression of c-Myc in MKN-45 cells treated with Lanatoside C and SB216763 at indicated concentrations for 24 h.

    MG-132 purchased from MCE. Usage Cited in: Cell Prolif. 2018 Aug;51(4):e12451.

    Immunoblot analysis of CDK4 in cells treated with 4 μM of CGN for 24 hours in the presence and absence of MG132.

    MG-132 purchased from MCE. Usage Cited in: Front Pharmacol. 2018 Apr 19;9:377.

    Immunoblot levels of highly molecular weight (HMW)-ubiquitinated proteins and pSer129-α-syn after inhibiting the ubiquitin-proteasome system (UPS) by various concentrations of MG132 (0.25, 0.5, and 1 μM) in SH-SY5Y cells.

    MG-132 purchased from MCE. Usage Cited in: Université de Montréal. Octobre 2017.

    Unsynchronized control and ARF6 cells are treated with DMSO or MG132 (10 μM) for 1h or 4h, lysed and total ubiquitinated proteins are determined using western blot (n=3).

    MG-132 purchased from MCE. Usage Cited in: Mol Plant Pathol. 2018 Dec;19(12):2623-2634.

    Destabilization of BRC1 mediated by SWP1 is inhibited by proteasome inhibitors Epoxomicin and MG132.

    MG-132 purchased from MCE. Usage Cited in: Biochim Biophys Acta Mol Basis Dis. 2018 Oct;1864(10):3322-3338.

    The neonatal rat cardiomyocytes (NRCMs) are treated with MG132 (10 μM). The protein expression level of PPARα in the indicated group.

    MG-132 purchased from MCE. Usage Cited in: Biochim Biophys Acta Mol Basis Dis. 2018 Oct;1864(10):3322-3338.

    LAZ3 knock-down decreases NRF2 expression and nuclear translocation, while only the PPARa agonist (GW7647) can prevent this inhibition. Both PPARγ agonist (GW1929) and PPARδ agonist (GW0742) can not reverse these inhibitions.

    MG-132 purchased from MCE. Usage Cited in: EBioMedicine. 2018 Aug;34:243-255.

    Protein synthesis is inhibited by Cycloheximide (Cyclo).

    MG-132 purchased from MCE. Usage Cited in: EBioMedicine. 2018 Aug;34:243-255.

    MPC1 protein expression in primary mouse hepatocytes incubated with pyruvate for 8 h in the presence of MG-132.

    MG-132 purchased from MCE. Usage Cited in: bioRxiv. July 20, 2018.

    The half-life of p53 protein is detected in GYS2 overexpressed cells by added with Chlorhexidine (CHX, 20 μg/mL) for different times.

    MG-132 purchased from MCE. Usage Cited in: bioRxiv. July 20, 2018.

    Cells are transfected with GYS2 siRNA and pre-incubated with MG-132 (20 μM) for 12 h. Cell lysate are immunoprecipitated by anti-Ub and immunoblotted by anti-p53.

    MG-132 purchased from MCE. Usage Cited in: Biochem Pharmacol. 2018 Oct;156:511-523.

    The accumulated poly-ubiquitinated protein is detected by Western blotting after J-Lat 10.6 cells are treated with DMSO, PR-957 (100 nM), PR-957 (150 nM) or MG132 (500 nM) for 48 h.

    MG-132 purchased from MCE. Usage Cited in: Biochem Pharmacol. 2018 Oct;156:511-523.

    Western blot detection of the p-TEFb component CDK9, Cyclin T1 and CDK9 phosphorylation on Thr186, as well as its downstream RNA poly II CTD and phosphate CTD after J-Lat 10.6 cells are treated with PR-957 in dose-dependent manner.

    MG-132 purchased from MCE. Usage Cited in: Biochem Pharmacol. 2018 Oct;156:511-523.

    J-Lat 10.6 cells are treated with DMSO, PR-957 (150 nM) or Carfilzomib (40 nM) alone with or without the HSF1 inhibitor KRIBB11 (1.25 µM) for 48 h. Then the cells are lysed, and Ser320 phosphorylated HSF1, total HSF1 and p24 are detected by Western blot with the corresponding antibodies.

    MG-132 purchased from MCE. Usage Cited in: J Exp Clin Cancer Res. 2018 Aug 15;37(1):193.

    Western blot is performed in HCC-LM3 cells transfected with HJURP knockdown lentivirus and treated with DMSO or MG132.

    MG-132 purchased from MCE. Usage Cited in: Oncol Lett. 2018 Nov;16(5):5900-5906.

    pVHL interacts with NEK8 and promotes NEK8 degradation through the proteasome ubiquitination signaling pathway.

    MG-132 purchased from MCE. Usage Cited in: Oncol Lett. 2018 Nov;16(5):5900-5906.

    Treatment with the 26S proteasome inhibitor, MG 132 (10 µM), rescues the downregulation of NEK 8 in the pVHL overexpressing SGC 7901 cells.

    MG-132 purchased from MCE. Usage Cited in: J Exp Clin Cancer Res. 2018 Oct 3;37(1):240.

    Decrease of ERCC6 expression can be rescued with proteasome inhibitor MG132. Subconfluent SKOV3 cells are treated with FL118 and MG132 alone or in combination as shown for 8 h, followed by western blot analyses with ERCC6 antibody.

    MG-132 purchased from MCE. Usage Cited in: Cell Cycle. 2018;17(13):1591-1601.

    The protein level of CCNB1 in different groups is analyzed by Western blot; MG132 significantly increases the protein level of CCNB1 in oocytes from CRS group mice. Western blotting showing the reduced expression of securin is rescued by MG132 in CRS group mouse oocytes.

    MG-132 purchased from MCE. Usage Cited in: Mol Immunol. 2018 Nov 13;104:69-78.

    Western analysis of proteins expression with treatment of IKK-16 or MG-132.
    • Biological Activity

    • Protocol

    • Technical Information

    • Purity & Documentation

    • References

    Description

    MG-132 is a potent, reversible, and cell-permeable 20S proteasome inhibitor which inhibits proteasomal chymotrypsin-like peptidase activity with an IC50 of 24.2 nM.

    IC50 & Target

    IC50: 24.2 nM (chymotrypsin-like activity)[1]

    In Vitro

    Dose-dependent inhibition of cell growth is observed in HeLa cells with an IC50 of approximately 5 μM MG132 for 24 h. MG132 inhibits the growth of HeLa cells via inducing the cell cycle arrest as well as triggering apoptosis[2]. MG-132 inhibits C6 glioma cell proliferation in a time- and dose-dependent manner (the IC50 value at 24 h is 18.5 μM). MG-132 (18.5 μM) suppresses the proteasome activity by about 70% at 3 h. MG-132 induces apoptosis via down-regulation of antiapoptotic proteins Bcl-2 and XIAP, up-regulation of pro-apoptotic protein Bax and caspase-3, and production of cleaved C-terminal 85 kDa PARP. MG-132 also causes a more than 5-fold increase of reactive oxygen species[3]. The IC50 of MG-132 against HeLa, CaSki, and C33A cervical cancer cells viability after 48 h of incubation is 2.1, 3.2, and 5.2 μM, respectively[4].

    In Vivo

    The in vivo antitumor activity of MG-132 against cervical cancer is examined using s.c. xenograft models. MG-132 is injected at 1 mg/kg using the following schedule: days 1, 4, 8, 12, 15 18, 23, and 26 for mice bearing HeLa tumors. The growth inhibition rates of MG132 compared to control is 49%[4]. MG-132 (i.p., 0.1 mg/kg/day) attenuates pressure-overload-induced cardiac hypertrophy and improves cardiac function in abdominal aortic banding (AAB) rats through regulation of ERK1/2 and JNK1 signaling pathways[5].

    Solvent & Solubility
    In Vitro: 

    DMSO : ≥ 160 mg/mL (336.40 mM)

    *"≥" means soluble, but saturation unknown.

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 2.1025 mL 10.5126 mL 21.0252 mL
    5 mM 0.4205 mL 2.1025 mL 4.2050 mL
    10 mM 0.2103 mL 1.0513 mL 2.1025 mL
    *Please refer to the solubility information to select the appropriate solvent.
    References
    Kinase Assay
    [3]

    After growing on six-well plates (3×105 cells/well) for 24 h, C6 glioma cells are treated with either PBS (control) or 18.5 μM MG-132 for 3, 6, 12, or 24 h at 37°C. Cells are thoroughly scraped from the culture dishes with a cell scraper and washed with cold PBS. After centrifugation for 10 min at 800×g, the cell pellets are suspended in ice-cold buffer (50 mM Tris-HCl, pH 7.5, 20 μM ATP, 5 mM MgCl2, 1 mM dithiothreitol, and 20% glycerol) and homogenized with a Pyrex glass microhomogenizer (20 strokes). The homogenate is centrifuged at 15 000×g for 10 min at 4°C to obtain supernatant. Protein concentration is determined using protein assay kits. A total of 10 μL (1 μg/μL) of each freshly made supernatant is incubated in a 96-well plate at 37°C for 30 min with 10 μL of 300 μM of Succinyl-LLVY-AMC and 85 μL of assay buffer (20 mM Tris-HCl, pH 7.5, and 20% glycerol). Release of fluorescent AMC is measured with a spectrofluorometer at 440 nm with an excitation wavelength of 380 nm[3].

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

    Cell Assay
    [3]

    C6 glioma cells are seeded onto 96-well microplates (3×104 cells/well) and cultured for 24 h. The cells are treated with PBS or MG-132 final concentrations of 10, 20, 30, and 40 μM, respectively. Cell viability is assessed using an MTT assay at 3, 6, 12, and 24 h after MG-132 treatment. The absorbance value at 570 nm is read using an automatic multi-well spectrophotometer. C6 glioma cells (3×105 cells/well) are allowed to grow on coverslips in 6-well culture plates for 24 h. The cells are then treated with either PBS (control) or 18.5 μM MG-132 at 37°C for 24 h. Cells growing on glass coverslips are fixed in methanol for 5 min at room temperature. The fixed cells are washed twice with PBS and then incubated with Hoechst 33342 for 5 min at room temperature and observed under a fluorescence microscope. Fragmented or condensed nuclei are scored as apoptotic[3].

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

    Animal Administration
    [4][5]

    Mice[4]
    C.B-17/lcr-scid/scidJcl mice are inoculated s.c. with HeLa, CaSki, or C33A (1×107 cells). Tumors are allowed to grow for 1 week. Mice are killed and tumors are removed. Tumors are then cut into 2-mm diameter pieces and s.c. transplanted in C.B-17/lcr-scid/scidJcl mice (n=6 per group). One week after inoculation, mice are treated with i.v. injection of saline (control), MG-132 (1 mg/kg/dose) twice a week for 4 weeks. The volume (V) of tumors is measured before every injection, as estimated using equation V=a×b2/2 where a and b are major and minor axes of the tumor measured by a caliper, respectively.
    Rats[5]
    Male Sprague-Dawley rats (8 weeks old, 180-230 g) are used to establish pressure-overload model. All animals are separated into four groups (10 rats per group): (i) vehicle-treated sham group; (ii) MG-132-treated sham group; (iii) vehicle-treated abdominal aortic banding (AAB) group; and (iv) MG-132-treated AAB group. Under intraperitoneal pentobarbital (50 mg/kg) anesthesia, AAB is created using a 5-0 suture tied twice around the abdominal aorta in which a 21-gauge needle is inserted. The needle is then retracted yielding a 70-80% constriction with an outer aortic diameter of ~0.8 mm. In the sham surgery rats, the same surgery is performed except the aorta is constricted. At Day 3 after the surgery, MG-132-treated rats are intraperitoneally injected with 0.1 mg/kg/day of MG-132 for 8 weeks. All control animals are injected with a corresponding volume of vehicle only (0.1% DMSO).

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

    References
    Molecular Weight

    475.62

    Formula

    C₂₆H₄₁N₃O₅

    CAS No.

    133407-82-6

    SMILES

    O=C(OCC1=CC=CC=C1)N[[email protected]](C(N[[email protected]@H](CC(C)C)C(N[[email protected]](C([H])=O)CC(C)C)=O)=O)CC(C)C

    Storage

    4°C, protect from light

    *The compound is unstable in solutions, freshly prepared is recommended.

    Shipping

    Room temperature in continental US; may vary elsewhere

    Purity: >98.0%

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    Cat. No.: HY-13259