MG-132
CAS No. : 133407-82-6
(Synonyms: Z-Leu-Leu-Leu-al; MG132)
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|---|---|---|
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| 10mg | $80 | In-stock |
| 25mg | $180 | In-stock |
| 50mg | $290 | In-stock |
| 100mg | $450 | In-stock |
| 200mg | $620 | In-stock |
| 500mg | $980 | In-stock |
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| Cat. No. : | HY-13259 |
| M.Wt: | 475.62 |
| Formula: | C26H41N3O5 |
| Purity: | >98 % |
| Solubility: | DMSO : ≥ 50 mg/mL |
MG-132 (Z-Leu-Leu-Leu-al) is a potent proteasome and calpain inhibitor with IC50s of 100 nM and 1.2 μM, respectively. MG-132 effectively blocks the proteolytic activity of the 26S proteasome complex. MG-132, a peptide aldehyde, also is an autophagy activator. MG-132 also induces apoptosis[1][2][3].
IC50 & Target:IC50: 100 nM (Proteasome), 1.2 μM (Calpain)[1][3]
In Vitro:MG-132 (Z-Leu-Leu-Leu-al) initiates neurite outgrowth in PC12 cells at a low concentration (30 nM) and is a very strong inhibitor of 20S proteasome[3].
MG-132 (10 μM; 1 hour) reverses the effects of TNF- α on I κ B degradation and NF-κ B activation in A549 cells[4].
MG-132 (0.75-5 μM; 24 hours) potently induces p53-dependent apoptosis in KIM-2 cells by 26S proteasome inhibition[5].
MG-132 (10-40 μM; 24 hours) significantly reduces the viability of C6 glioma cells in both time- and concentration-dependent manners and shows the IC50 of 18.5 μM at 24 hours[6].
MG-132 (18.5 μM; 24 hours) induces down-regulation of anti-apoptotic proteins Bcl-2 and XIAP and up-regulates expression of pro-apoptotic protein Bax and caspase-3[6].
In Vivo:MG132 (10 mg/kg; i.p.; daily for 25 days starting 5 days after EC9706 cells injection) significantly inhibits tumor growth of the EC9706 xenograft without causing toxicity to mice[7].
MG-132 (1 mg/kg; i.v.; twice a week for 4 weeks) shows potent tumor inhibitory effect against mice bearing HeLa tumors[8].
MG-132 (1-10 μg/kg/24 hours; subcutaneously implanted osmotic pumps; for 8 days) greatly increases the expression levels of β-dystroglycan, α-dystroglycan, α-sarcoglycan, and dystrophin in skeletal muscle lysates in mice (six-month-old male C57BL/10ScSn DMD mdx mice)[9].
Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.
MG-132, characterized by a short plasma half-life and poor blood-brain barrier permeability, is administered via stereotactic intranigral injection (0.4 μg) to achieve sustained local proteasome inhibition, successfully inducing Parkinson's disease-like pathology in the substantia nigra[10].
Administration: MG-132 (0.4 μg in 4 μL) • stereotaxically injected into the substantia nigra at the target site (Bregma AP, 3.2 mm, ML, 2.0 mm, DV, 4.7 mm) in the right side
(2) Injection should be extremely slow (e.g., 0.5 μL/min), and the needle should be left in place for several minutes after injection to prevent fluid reflux and mechanical damage that could affect model specificity.
(3) The control side must use the same solvent as the drug solution (1% DMSO in PBS) to eliminate the influence of the solvent itself.
Histology analysis: Nigral tyrosine hydroxylase-positive (TH+) neurons loss
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