保存条件 ：4°C
保质期 ：详见说明
英文名 ：MG-132
库存 ：充足
供应商 ：杭州昊鑫生物
CAS号 ：133407-82-6
规格 ：10mg
MG-132 (Synonyms: Z-Leu-Leu-Leu-al; MG132)
MG-132 (Z-Leu-Leu-Leu-al) 是一种有效的，可逆的蛋白酶体 (
proteasome) 抑制剂，
IC50 为 100 nM。MG-132 有效阻断 26S 蛋白酶体复合物的蛋白水解活性。MG-132 是一种肽醛，是自噬 (
autophagy) 激活剂。MG-132 还诱导凋亡 (
apoptosis)。
| 生物活性 |
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] |
体外研究
(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]. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Cell Viability Assay[3]
| Cell Line: |
C6 glioma cells |
| Concentration: |
10, 20, 30, 40 μM |
| Incubation Time: |
24 hours |
| Result: |
Significantly reduced the viability of C6 glioma cells beginning at 6 h in both time- and concentration-dependent manners and showed the IC50 of 18.5 μM at 24 hours. |
|
| |
体内研究
(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]. MCE has not independently confirmed the accuracy of these methods. They are for reference only.
| Animal Model: |
5- to 6-weeks old female athymic nude mice (EC9706 xenograft) |
| Dosage: |
10 mg/kg |
| Administration: |
I.p.; daily for 25 days starting 5 days after EC9706 cells injection |
| Result: |
Significantly inhibited tumor growth of the EC9706 xenograft without causing toxicity to the mice. |
|
| 分子量 |
475.62 |
| 性状 |
Solid |
| Formula |
C26H41N3O5 |
| CAS 号 |
133407-82-6 |
| 运输条件 |
Room temperature in continental US; may vary elsewhere. |
| 储存方式 |
| Powder |
-20°C |
3 years |
| In solvent |
-80°C |
6 months |
| |
-20°C |
1 month |
|
| 溶解性数据 |
In Vitro: DMSO : 100 mg/mL (210.25 mM; Need ultrasonic)
配制储备液
| 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 |
* 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。
In Vivo: 请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂： ——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶
- 1.
请依序添加每种溶剂： 10% DMSO 40% PEG300 5% Tween-80 45% saline Solubility: ≥ 1.67 mg/mL (3.51 mM); Clear solution
- 2.
请依序添加每种溶剂： 10% DMSO 90% (20% SBE-β-CD in saline) Solubility: 1.67 mg/mL (3.51 mM); Suspended solution; Need ultrasonic
- 3.
请依序添加每种溶剂： 10% DMSO 90% corn oil Solubility: ≥ 1.67 mg/mL (3.51 mM); Clear solution
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该产品被引用文献
| 参考文献 |
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[1]. Harhouri K, et al. MG132-induced progerin clearance is mediated by autophagy activation and splicing regulation. EMBO Mol Med. 2017 Sep;9(9):1294-1313. [Content Brief] [2]. Fan WH, et al. Proteasome inhibitor MG-132 induces C6 glioma cell apoptosis via oxidative stress. Acta Pharmacol Sin. 2011 May;32(5):619-25. [Content Brief] [3]. Tsubuki S, et al. Differential inhibition of calpain and proteasome activities by peptidyl aldehydes of di-leucine and tri-leucine. J Biochem. 1996 Mar;119(3):572-6. [Content Brief] [4]. Fiedler MA, et al. Inhibition of TNF-alpha-induced NF-kappaB activation and IL-8 release in A549 cells with the proteasome inhibitor MG-132. Am J Respir Cell Mol Biol. 1998 Aug;19(2):259-68. [Content Brief] [5]. MacLaren AP, et al. p53-dependent apoptosis induced by proteasome inhibition in mammary epithelial cells. Cell Death Differ. 2001 Mar;8(3):210-8. [Content Brief] [6]. Han YH, et al. The effect of MG132, a proteasome inhibitor on HeLa cells in relation to cell growth, reactive oxygen species and GSH. Oncol Rep. 2009 Jul;22(1):215-21. [Content Brief] [7]. Dang L, et al. Proteasome inhibitor MG132 inhibits the proliferation and promotes the cisplatin-inducedapoptosis of human esophageal squamous cell carcinoma cells. Int J Mol Med. 2014 May;33(5):1083-8. [Content Brief] [8]. Matsumoto Y, et al. Enhanced efficacy against cervical carcinomas through polymeric micelles physically incorporating theproteasome inhibitor MG132. Cancer Sci. 2016 Jun;107(6):773-81. [Content Brief] [9]. Bonuccelli G, et al. Proteasome inhibitor (MG-132) treatment of mdx mice rescues the expression and membrane localization of dystrophin and dystrophin-associated proteins. Am J Pathol. 2003 Oct;163(4):1663-75. [Content Brief]
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