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InSolution, ≥98%, 10 mM, reversible proteasome inhibitor

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Z-Leu-Leu-Leu-al, Carbobenzoxy-L-leucyl-L-leucyl-L-leucinal, Z-LLL-CHO, Proteasome Inhibitor XI, InSolution MG-132, MG-132
Empirical Formula (Hill Notation):
CAS Number:
Molecular Weight:
MDL number:

Quality Level


≥98% (HPLC)





storage condition

OK to freeze
protect from light

shipped in

wet ice

storage temp.


SMILES string




InChI key


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Amino Acid Sequence


General description

Potent, reversible, and cell-permeable proteasome inhibitor (Ki = 4 nM). Reduces the degradation of ubiquitin-conjugated proteins in mammalian cells and permeable stains of yeast by the 26S complex without affecting its ATPase or isopeptidase activities. Activates c-Jun N-terminal kinase (JNK1) and inhibits NF-κB activation (IC50 = 3 µM).

Biochem/physiol Actions

Cell permeable: yes
Product does not compete with ATP.
Reversible: yes
Target IC50: 3 µM in inhibiting NF-κB activation
Target Ki: 4 nM as proteasome inhibitor


Packaged under inert gas


Toxicity: Irritant (B)

Physical form

A 10 mM (1 mg/210 µl) or (5mg/1050 µl) solution of MG-132 (Cat. No. 474790) in DMSO.

Other Notes

Meriin, A.B., et al. 1998. J. Biol. Chem.273, 6373.
Adams, J., and Stein, R. 1996. Ann. Rep. Med. Chem.31, 279.
Lee, D.H., and Goldberg, A.L. 1996. J. Biol. Chem.271, 27280.
Wiertz, E.J.H.J., et al. 1996. Cell84, 769.
Read, M.A., et al. 1995. Immunity2, 493.
Rock, K.L., et al. 1994. Cell78, 761.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class

10 - Combustible liquids




188.6 °F - (Dimethylsulfoxide)


87 °C - (Dimethylsulfoxide)

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D H Lee et al.
The Journal of biological chemistry, 271(44), 27280-27284 (1996-11-01)
We have studied whether various agents that inhibit purified yeast and mammalian 26 S proteasome can suppress the breakdown of different classes of proteins in Saccharomyces cerevisiae. The degradation of short-lived proteins was inhibited reversibly by peptide aldehyde inhibitors of
E J Wiertz et al.
Cell, 84(5), 769-779 (1996-03-08)
Human cytomegalovirus (HCMV) down-regulates expression of MHC class I products by selective proteolysis. A single HCMV gene, US11, which encodes an endoplasmic reticulum (ER) resident type-I transmembrane glycoprotein, is sufficient to cause this effect. In US11+cells, MHC class I molecules
A B Meriin et al.
The Journal of biological chemistry, 273(11), 6373-6379 (1998-04-16)
Inhibition of the major cytosolic protease, proteasome, has been reported to induce programmed cell death in several cell lines, while with other lines, similar inhibition blocked apoptosis triggered by a variety of harmful treatments. To elucidate the mechanism of pro-
Clarissa Braun et al.
Cell stress, 5(12), 176-182 (2021-12-18)
Programmed cell death protein 4 (PDCD4) exerts critical functions as tumor suppressor and in immune cells to regulate inflammatory processes. The phosphoinositide 3-kinase (PI3K) promotes degradation of PDCD4 via mammalian target of rapamycin complex 1 (mTORC1). However, additional pathways that
M A Read et al.
Immunity, 2(5), 493-506 (1995-05-01)
Multiple cell adhesion proteins are up-regulated in vascular endothelial cells in response to TNF alpha and other inflammatory cytokines. This increase in cell adhesion gene expression is thought to require the transcription factor NF-kappa B. Here, we show that peptide

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