M8699
(R)-MG132
≥98%, Proteasome inhibitor
동의어(들):
Z-L-Leu-D-Leu-L-Leu-al
제품 이름
(R)-MG132,
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-VABKMULXSA-N
SMILES string
CC(C)C[C@@H](C(N[C@H](C(N[C@H](C=O)CC(C)C)=O)CC(C)C)=O)NC(OCC1=CC=CC=C1)=O
assay
≥98%
solubility
DMSO or DMF: 25 mg/mL
storage temp.
−20°C
Quality Level
Application
(R)-MG132 has been used in ubiquitination assay and is used as a proteasome inhibitor.
Biochem/physiol Actions
MG132 (carbobenzoxy-Leu-Leu-leucinal) is a tri-peptide aldehyde. It possesses antitumor activity and boosts cytostatic/cytotoxic effects of chemo- and radiotherapy. (R)-MG132 is a potent, membrane-permeable proteasome inhibitor. It can inhibit proteasome activity in lysates of J558L multiple myeloma cells and EMT6 breast cancer cells. The (R)-MG132 stereoisomer is a more effective inhibitor of chymotrypsin-like (ChTL), trypsin-like (TL), and peptidylglutamyl peptide hydrolyzing proteasome (PGPH) activities than the (S)-MG132.
Physical form
crystalline solid or supercooled liquid
저장 등급
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Alternative promotion and suppression of metastasis by JNK2 governed by its phosphorylation.
Hu S, et al.
Oncotarget, 8(34), 56569-56569 (2017)
Studies of the synthesis of all stereoisomers of MG-132 proteasome inhibitors in the tumor targeting approach.
Mroczkiewicz M, et al.
Journal of Medicinal Chemistry, 53(4), 1509-1518 (2010)
A Mad2-Mediated Translational Regulatory Mechanism Promoting S-Phase Cyclin Synthesis Controls Origin Firing and Survival to Replication Stress.
Gay S, et al.
Molecular Cell, 70(4), 628-638 (2018)
Fang Guo et al.
Molecular neurobiology, 54(10), 7597-7609 (2016-11-11)
Autophagy and the ubiquitin proteasome system (UPS), as two major protein degradation pathways, coordinate with each other in regulating programmed cell death. Autophagy can compensate for the UPS impairment-induced cell dysfunction and apoptosis. However, it is not clear how cells
J Yang et al.
Oncogene, 36(34), 4828-4842 (2017-04-11)
PIM1 is a proto-oncogene, encoding a serine/threonine protein kinase that regulates cell proliferation, survival, differentiation and apoptosis. Previous reports suggest that overexpression of PIM1 can induce cellular senescence. However, the molecular mechanism underlying this process is not fully understood. Here
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