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SML1135

Sigma-Aldrich

MG-132(R)

≥95% (HPLC)

Synonym(s):

Z-L-Leu-D-Leu-L-Leu-al

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5 MG
$584.00

$584.00

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5 MG
$584.00

About This Item

Empirical Formula (Hill Notation):
C26H41N3O5
CAS Number:
1211877-36-9
Molecular Weight:
475.62
MDL number:
MFCD28580122
UNSPSC Code:
12352200
PubChem Substance ID:
329825671
NACRES:
NA.32

$584.00

Please contact Customer Service for Availability

product line

SAFC Hitech®

Quality Level

200

Assay

≥95% (HPLC)

form

powder

solubility

DMSO: soluble

storage temp.

−20°C

SMILES string

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

InChI

1S/C26H41N3O5/c1-17(2)12-21(15-30)27-24(31)22(13-18(3)4)28-25(32)23(14-19(5)6)29-26(33)34-16-20-10-8-7-9-11-20/h7-11,15,17-19,21-23H,12-14,16H2,1-6H3,(H,27,31)(H,28,32)(H,29,33)/t21-,22+,23-/m0/s1

InChI key

TZYWCYJVHRLUCT-ZRBLBEILSA-N

Gene Information

human ... CTSB(1508), NFKB1(4790), PSMA1(5682)

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This Item
M8699474787474790
MG-132(R) ≥95% (HPLC)

SML1135

MG-132(R)

(R)-MG132

M8699

(R)-MG132

MG-132, ≥95% by HPLC Potent, reversible, and cell-permeable proteasome inhibitor (Ki = 4 nM).

474787

MG-132, ≥95% by HPLC

MG-132 A cell-permeable, potent, reversible proteasome inhibitor (Ki = 4 nM).

474790

MG-132

form

powder

form

-

form

powder

form

solid

assay

≥95% (HPLC)

assay

≥98%

assay

≥95% (HPLC)

assay

≥98% (HPLC)

product line

SAFC Hitech®

product line

-

product line

-

product line

-

storage temp.

−20°C

storage temp.

−20°C

storage temp.

−20°C

storage temp.

−20°C

solubility

DMSO: soluble

solubility

DMSO or DMF: 25 mg/mL

solubility

DMSO: 25 mg/mL, ethanol: 25 mg/mL

solubility

DMSO: 20 mg/mL, ethanol: 20 mg/mL

Quality Level

200

Quality Level

200

Quality Level

100

Quality Level

100

Biochem/physiol Actions

MG-132(R) is a potent, membrane-permeable proteasome inhibitor.[1] It induces neurite outgrowth in PC12 cells at 10 M. MG-132(R) blocks cleavage of poly(ADP-ribose) polymerase and apoptosis in thymocytes. However, MG-132(R) also activates c-Jun N-terminal protein kinase (JNK-1), which initiates apoptosis in response to cell stress. Proteasome inhibition induces accumulation of heat shock protein mRNA, activation of heat-shock proteins, and enhanced thermotolerance in various cell types.

Legal Information

SAFC Hitech is a registered trademark of Sigma-Aldrich Co. LLC

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

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Certificates of Analysis (COA)

Lot/Batch Number
0000408632
0000368535
0000408632
0000368535
13150510

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Xueyan Zhao et al.
Developmental and comparative immunology, 106, 103632-103632 (2020-01-29)
Tightly regulation of NF-κB signaling is essential to innate and adaptive immune responses, but its regulatory mechanism remains unclear in various organisms, especially teleost fish. In this study, we reported that IRF3 attenuates the inhibitory effect of IκBα on NF-κB
Yalong Wang et al.
Neuroscience letters, 739, 135402-135402 (2020-09-26)
Synaptotagmin-11 (Syt11) is associated with schizophrenia and Parkinson's disease (PD) and is a critical substrate of parkin, an E3 ubiquitin ligase linked to PD. Previously we reported that Syt11 regulates multiple membrane trafficking pathways in neurons and glia. However, the
Shashipavan Chillappagari et al.
Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society, 20(1), 140-148 (2020-06-15)
The stress-regulated enzyme hemeoxygenase-1 (HO-1) contributes to the cell response towards inflammation and oxidative stress. We previously reported on curtailed HO-1 expression in cystic fibrosis (CF) bronchial epithelial (CFBE41o-) cells and CF-mice, but the molecular mechanisms for this are not
Ling-Yun Chu et al.
Scientific reports, 7(1), 12472-12472 (2017-10-01)
Pro-inflammatory cytokines are known to induce endothelial cell autophagy, but the role of autophagy in regulating the expression of pro-inflammatory molecules has not been characterized. We hypothesized that autophagy facilitates expression of endothelial adhesion molecules. TNFα and IL-1β induced autophagy
Corinna Wentzel et al.
Nature communications, 9(1), 267-267 (2018-01-20)
Here we explore the relationship between presynaptic homeostatic plasticity and proteasome function at the Drosophila neuromuscular junction. First, we demonstrate that the induction of homeostatic plasticity is blocked after presynaptic proteasome perturbation. Proteasome inhibition potentiates release under baseline conditions but
View All Related Papers

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