(R)-MG132
(Synonyms: N-[(苯基甲氧基)羰基]-L-亮氨酰-N-[(1S)-1-甲酰基-3-甲基丁基]-D-亮氨酰胺,(S,R,S)-(-)-MG-132; Z-Leu-D-Leu-Leu-al) 目录号 : GC41233
(R)-MG132是一种蛋白酶体抑制剂，IC50为100 nM。
Cas No.:1211877-36-9
Sample solution is provided at 25 µL, 10mM.
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Related Biological Data
Penetration efficiency of peptide KKP.(E) Fluorescence intensity quantification of FITC-labeled KKP1 (7.5 μM) treated with different time points (with or without the MG132 treatment) corresponding to the fluorescence microscopy shown in(D).
(R)-MG132 (GC41233) was obtained from GLPBIO (Montclair,CA, USA).
Acs Pharmacol Transl 6.1 (2022): 76-87. PMID: 36654751 IF: 5.9998 -
Related Biological Data
HNK increases protein ubiquitination by inhibiting proteasome activity. e NB4 cells were treated with HNK (0 or 30 μM) for 24 h, and the cells were collected for 20S protease activity determination. 1 μM (R)-MG-132 was used as a positive control.
In the presence or absence of (R)-MG-132(1 μM)(GLPBIO), the same amount of 30 μg protein, 20 μM fluorescent substrate (Suc-Leu-Leu-Val-Tyr-AMC) and a proper amount of buffer were distributed into a black 96-well plate with transparent substrate.
Apoptosis (2021): 1-14. PMID: 33550458 IF: 4.67
Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
(R)-MG132 is a proteasome inhibitor with an IC50 of 100 nM. This compound effectively hinders the proteolytic function of the 26S proteasome complex, leading to induced autophagy and apoptosis. Moreover, (R)-MG132 exhibits notable efficacy in inhibiting tumor growth[1-2].
(R)-MG132(10- 40 μM ; 3-24h) suppressed the proliferation of C6 glioma cells and also inhibited the chymotrypsin-like activity of the proteasome[3]. (R)-MG132(1 μM;24h) triggers the nuclear translocation of AIF by down-regulating the ERK and Akt/mTOR pathways[4]. The combination of GSK-470 and (R)-MG132 (200 nM; 24 hours) leads to nearly complete inhibition of AKT activity and mTORC1/mTORC2 activity[5].
(R)-MG132(10μg/kg; i.p; daily for 7days) regulated the AMPK signaling pathway, thereby modulating apoptosis and inflammation, enhancing hemodynamics, and inhibiting ventricular structural remodeling in a myocarditis mouse model [6]. Treatment with (R)-MG132(0.1mg/kg; i.p) significantly mitigated cancer cachexia, as evidenced by reduced weight loss, altered carbohydrate metabolism, decreased muscle atrophy, increased spontaneous activity, and extended survival time in tumor-bearing mice[7].
[1]. Harhouri K, Navarro C, et.al. MG132-induced progerin clearance is mediated by autophagy activation and splicing regulation. EMBO Mol Med. 2017 Sep;9(9):1294-1313. doi: 10.15252/emmm.201607315. PMID: 28674081; PMCID: PMC5582415.
[2]. Tsubuki S, Saito Y, , 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. doi: 10.1093/oxfordjournals.jbchem.a021280. PMID: 8830056.
[3]. Fan WH, Hou Y, , et.al. Proteasome inhibitor MG-132 induces C6 glioma cell apoptosis via oxidative stress. Acta Pharmacol Sin. 2011 May;32(5):619-25. doi: 10.1038/aps.2011.16. Epub 2011 Apr 18. PMID: 21499287; PMCID: PMC4002511.
[4]. Ko JK, Choi CH, , et.al. The proteasome inhibitor MG-132 induces AIF nuclear translocation through down-regulation of ERK and Akt/mTOR pathway. Neurochem Res. 2011 May;36(5):722-31. doi: 10.1007/s11064-010-0387-9. Epub 2011 Jan 4. PMID: 21203833.
[5]. Zhang J, Yang C, , et.al. PDK1 inhibitor GSK2334470 synergizes with proteasome inhibitor MG‑132 in multiple myeloma cells by inhibiting full AKT activity and increasing nuclear accumulation of the PTEN protein. Oncol Rep. 2018 Jun;39(6):2951-2959. doi: 10.3892/or.2018.6369. Epub 2018 Apr 12. PMID: 29658600.
[6]. Zhang XM, Li YC, et.al. MG-132 attenuates cardiac deterioration of viral myocarditis via AMPK pathway. Biomed Pharmacother. 2020 Jun;126:110091. doi: 10.1016/j.biopha.2020.110091. Epub 2020 Apr 8. PMID: 32278272.
[7]. Zhang L, Tang H, et.al. MG132-mediated inhibition of the ubiquitin-proteasome pathway ameliorates cancer cachexia. J Cancer Res Clin Oncol. 2013 Jul;139(7):1105-15. doi: 10.1007/s00432-013-1412-6. Epub 2013 Mar 28. PMID: 23535871; PMCID: PMC7087863.
(R)-MG132是一种蛋白酶体抑制剂，IC50为100 nM。该化合物有效阻碍26S蛋白酶体复合物的蛋白水解，导致诱导自噬和凋亡。(R)-MG132具有显著的抑制肿瘤生长的作用[1-2]。
(R)-MG132(10- 40 μM ; 3-24h)抑制C6胶质瘤细胞的增殖，并抑制蛋白酶体的凝乳胰蛋白酶样活性[3]。(R)-MG132(1 μM;24h)通过下调ERK和Akt/mTOR通路触发AIF的核易位[4]。GSK-470和(R)-MG132(200 nM; 24 hours)的结合导致AKT活性和mTORC1/mTORC2活性几乎完全抑制[5]。
在心肌炎小鼠模型中，(R)-MG132(10μg/kg; i.p; daily for 7days)调节AMPK信号通路，从而调节细胞凋亡和炎症，增强血流动力学，抑制心室结构重构[6]。(R)-MG132(0.1mg/kg; i.p)治疗可显著减轻肿瘤恶病质，荷瘤小鼠体重减轻、碳水化合物代谢改变、肌肉萎缩减少、自发活动增加和生存时间延长[7]。
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 2.1026 mL | 10.513 mL | 21.0261 mL |
| 5 mM | 0.4205 mL | 2.1026 mL | 4.2052 mL |
| 10 mM | 0.2103 mL | 1.0513 mL | 2.1026 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。